NICOTINE and SMOKING BENEFITS

By Wanda Hamilton Researchers have long been aware that fewer smokers get Alzheimer's and Parkinson's diseases than non-smokers. Up to April l992, of the 17 studies on Alzheimer's and smoking which had been published in peer-reviewed journals, 13 reported a reduced risk for smokers and only four found no difference between smokers and non-smokers. Similar findings have been published on the effect of smoking and Parkinson's disease. In an article in The Times of London (9/7/93), Dr. James Le Fanu provided an examination of the research on smoking and its apparent protective effect for certain diseases. Dr. Le Fanu stated unequivocally: "Smokers have a 50 per cent reduced risk of developing Alzheimer's--and the more smoked the greater the protection." He also noted that emerging research points to a similar effect of smoking on Parkinson's disease. So striking was the apparent protective effect of smoking on Alzheimer's and Parkinson's that increasingly biomedical researchers are experimenting with nicotine to treat the symptoms of these dread disease in-patients who have been diagnosed as having them. Results from these experiments have all showed promise in alleviating the symptoms of these diseases with the administration of nicotine. The mechanism by which the nicotine in tobacco works to protect smokers is that it increases the number of so-called "nicotinic" receptors in the brain, which in turn influence the production and release of the neurotransmitter acetylcholine. Those who come down with Alzheimer's show a marked loss of "nicotinic" receptors in their brains and thus have reduced levels of acetylcholine, which is necessary for memory and other brain functions. Research has shown that tobacco smoke (and the nicotine therein) inhibits the activity of monoamine oxidase B (MAOB). Experiments on mice which were genetically engineered to be without the gene for MAOB "were resistant to the neurodegenerative effects of MPTP, a toxin that induces a condition reminiscent of Parkinson's disease," (Dr. Jean C. Shih researcher at the University of Southern California, as reported in Reuters, 10/7/97, "Isoenzyme Inhibited by cigarette Smoke May Have Role in Aging and Neurodegeneration"). The findings of Dr. Shih and her colleagues point to a protective effect from smoking on the aging of the brain. Other diseases for which smoking and nicotine appear to be protective are ulcerative colitis, Tourette's Syndrome, and possibly rheumatoid arthritis and colorectal cancer. Below are excerpts from some recent articles and studies on nicotine, Alzheimer's, Parkinson's, cognitive abilities, Tourette's and ulcerative colitis.

"In human studies, reported performance improvements with post-trial administration of nicotine have all involved associated learning (Mangan and Golding l883; Colrain et al, l992; Warburton et al, l992).... Nicotine improves performance by increasing the attentional resources available for such strategic processing," [Rusted JM, et al, "Facilitation of memory by post-trial administration of nicotine: evidence for attentional explanation," Psychopharmacology, 108(4):452-5, l992]. "1. Nicotine improves attention in a wide variety of tasks in healthy volunteers. 2. Nicotine improves immediate and longer-term memory in healthy volunteers. 3. Nicotine improves attention in patients with probable Alzheimer's Disease," [Warburton D M, "Nicotine as a cognitive enhancer," Progress in NeuroPsychopharmacology and Biological Psychiatry, 16(2): 181-91, Mar l992]

"Researchers observed lessening of tic frequency and severity 3 minutes after subjects chewed [nicotine] gum, even more so at 10 minutes." [Rickards E H, "Nicotine gum in Tourette's disorder," American Journal of Psychiatry, 149(3):417, Mar l992. Note: the subjects were all children with Tourette's disorder]. "In humans, nicotine-induced improvement of rapid information processing is particularly well documented.... Preliminary studies have found that some aspects of the cognitive deficit in Alzheimer's disease can be attenuated by nicotine." [Levin E D, "Nicotinic systems and cognitive function," Psychopharmacology, 108(4):417-31, l992] "Improvement in attention, learning, reaction time, and problem solving have been reported.... Different processes, including attention, stimulus evaluation, and response selection, appear to be involved in the effect of nicotine on human information processing." [Le Houezec J, Benowitz N L, "Basic and clinical psychopharmacology of nicotine," Clinics in Chest Medicine, 12(4):681-99, Dec l991]. "Despite the absence of change in memory functioning, these results demonstrate that DAT [Alzheimer's disease] patients have significant perceptual and visual attentional deficits which are improved by nicotine administration." [Jones G M, Sahakian B J, et al, "Effects of acute subcutaneous nicotine on attention, information processing and short-term memory in Alzheimer's disease," Psychopharmacology, 108(4):485-94, l992]. "When you look at people who smoke, and people who don't smoke...you find those who smoke cigarettes are about half as likely to get Parkinson's disease." [Dr. David Morens of the University of Hawaii School of Public Health as quoted in "Stunned docs discover cigarettes stop Parkinson's," by Roger Field, New York Post, 6/15/95. Dr. Morens and colleagues examined 34 studies on smoking and Parkinson's. Their study was published in the June, l995 issue of Neurology]. According to a study conducted at Surrey University and published in the journal Psychopharmacology, smokers are more mentally alert at night than non-smokers. Rosemary Brook, spokeswoman for Surrey University's psychopharmacology unit, said, "The results showed that smokers were subsequently able to perform various tests of reaction, memory recall and other related tasks consistently better than the nonsmokers," [Reported on the BBC News, 4/8/98, "Cigarettes 'keep you sharp after dark'." In a presentation at the 151st annual meeting of the American Psychiatric Association (June 8, l998 in Toronto), Dr. Paul Newhouse of the University of Vermont reported on his research on treating Parkinson's disease with nicotine. "Preliminary analysis shows improvements after acute nicotine administration in several areas of cognitive performance." These areas included reaction time and central processing speed. The researchers also reported that after chronic use of nicotine on Parkinson's patients, motor function and the ability to move also improved. [Reported by Reuters, 6/8/98, "Nicotine patch promising for Parkinson's"]. "The influence of smoking on the risk of developing ulcerative colitis is well documented. Compared with lifetime nonsmokers, the risk is reduced in smokers...." [Tysk C, Jarnerot G, "Has smoking changed the epidemiology of ulcerative colitis?" Scandinavian Journal of Gastroenterology, 27(6):508-12, Jun l992]. "When association between cigarette smoking and UC [ulcerative colitis] are examined, never-smokers are approximately three times more likely to develop UC than smokers. A consistent finding from study to study is that quitters have a mildly increased risk of developing UC which suggests that cigarette smoking may have a protective effect," [Lashner B A, "Inflammatory bowel disease: family patterns and risk factors," Comprehensive Therapy, 18(8):2-4, Aug l992]. "It is beyond doubt that smokers are protected against ulcerative colitis, and the more that is smoked the greater the protection--so those on 25 cigarettes a day or more have a risk as little as one-tenth that of nonsmokers," (Dr. Martin Osbourne, surgeon at the Royal Free Hospital in London, as quoted in the Daily Telegraph, 9/7/93).

THE ANTI-SMOKERS LIED ABOUT OSTEOPOROSIS AND ABOUT ESTROGEN Antismokers grasping at straws: Lying at any cost, even when all the evidence is against them The media flooded the country with the anti-smoker claim that smoking increases osteoporosis (Danielle HW. Osteoporosis of the slender smoker. Arch Intern Med 1976;136:298-304). There was no publicity when the claim was later refuted (Jensen GF. Osteoporosis of the slender smoker revisited by epidemiologic approach. Eur J Clin Investig 1986;16:239-242). The Danielle study used two "ill-defined" patient populations; the second included all 70 year-old women in nine suburbs of Copenhagen, and had more cases, 180 versus 72. The first asserted that there was no relation between weight and bone mass in non-smokers, while the second, and most other studies, have found correlation in both. Most importantly, there was no difference between smokers and non-smokers in the frequency of definite osteoporotic or other fractures. The smokers actually had fewer. Since all the cases were the same age, there is no way to use age adjustment to manipulate the data. Referring to smoking, another researcher has admitted, "this factor is a more manipulable one than some of the other factors which have been shown to be important in the etiology of fracture." A number of studies have found that smokers have slightly higher bone mass and density than nonsmokers, both pre- or post-menopausal. "No association between bone mass and smoking was observed. A subgroup with patterns of substantial combined tobacco and alcohol use having a lower mean bone mass could not be identified" (MF Sowers et al. Prev Med 1985;14:585-596). "Smoking history in pack years did not correlate with bone density at either skeletal site," spine or forearm (MM Luckey et al. J Clin Endocrinol Metab 1989;69:762-770). In the Framingham Study, Felson et al found that "Cigarette smoking was not associated with risk of fracture in any analyses including models without alcohol." This was in 217 cases, 174 of them female, in an ongoing prospective of over 40 years' duration 1988;128(5):1102-1110). (Felson DT et al. Am J Epidemiol

And in a study the next year which separately analyzed radiographs of the white, middle class Framingham subjects, and poorer, more nonwhite HANES I subjects, Felson also found a borderline statistically significant protective association between smoking and osteoarthritis, which was strongest in the heaviest smokers (Arthr Rheum 1989;32:166-172).

However, true to their anti-smoker psychosis, they had to find something bad to say about smoking. Although they admitted that very few of their subjects ever used estrogen, they claimed that smokers did not benefit from estrogen therapy on the basis of a mere 29 ever-users, 8 of them smokers. Never mind that this claim was opposite to that of a large 1982 study which claimed both big risks of fractures, and big benefits from estrogen for smokers. With this study, the anti-smokers could simultaneously fear-monger against smoking and promote pharmacological intervention. But in the "Nurses Study," (D Hemenway, AJPH Dec 1988;78(12):1554-1558), which is possibly

Smoking and Lung Cancer Though there seem to be strong links between smoking and lung cancer, anti-tobacco propaganda often infers that smoking is THE cause of lung cancer, with the implicit message that if smoking could be eliminated, so could lung cancer. This is, of course, false. Smoking is by no means the only risk factor for lung cancer, and in some occupations cigarette smoking appears actually to help protect against getting the disease. Lung cancer is acknowledged to be on the rise both in the U.S. and elsewhere despite the decline in cigarette smoking which began more than 25 years ago. Further, lung cancer among nonsmokers seems to be increasing, while the rate of lung cancer among smokers is decreasing, thanks to the advent of filtered cigarettes, which nearly every study has shown decreases risk anywhere from 20% to 30% (only one such study is listed here).

"Rising lung cancer mortality rates during 1953-1982 were similar for both sexes in all parts of Oregon; the steepest increases were among women living in the coastal counties." "Occupational risk differences among both sexes far exceeded those noted with other risk factors, suggesting that occupational exposures deserve primary emphasis in future efforts at lung cancer control." "Causes of lung cancer other than smoking which are associated with particular occupations will be identified in the hope of eventually reversing the epidemic trend of this disease." 1375. University of Oregon, School of Medicine. Morton, W.E. "epidemiology of Lung Cancer in Oregon." Methods: Following data have been collected:

(1) sex-specific, age-standardized, mean annual death rates for 5-year periods since 1953 for all counties [Portland-Vancouver area] (2) occupations from death certificates since 1963 (3) all cases occurring in the Portland metropolitan area during 1963-1977 by search of tumour registries and hospital record rooms (4) age-adjusted incidence rates by sex for geographic regions, socioeconomic strata, and occupational categories.

"Prospective contribution of pack-years to development of lung cancer was reduced by crosssectional adjustment, but remained significant." But more important than pack years was airflow obstruction. "Data suggest that smokers who will develop lung cancer may be recognized by prior development of ventilatory obstruction." 1006. Johns Hopkins University, School of Hygiene and Public Health. Tockman, M.S.; Anthoisen, N.R.; Wright E.C. "Airways Obstruction and the Risk of Lung Cancer."

AND

"AO was significantly associated with advanced age, male sex, PiZ allete, blood group A antigen, heavy coffee intake (> 3 cups/day) and first degree relationship to a patient with chronic obstructive pulmonary [lung] disease [genetical predisposition]" "Both AO and CB were associated with cigarette smoking and low socioeconomic status." 1005. Johns Hopkins University, School of Hygiene and Public Health. Tockman, M.S.; Khoury, M.J.; Cohen, B.H. "Different Risk Factor Distributions for Airways Obstruction [AO] and Chronic Bronchitis."

"A cross-geographical analysis of lung cancer mortality for white male residents of Harris County for 1979 to 1981 is being made to assess the contribution of air pollution." "Regression techniques will be used to examine the relationship between mortality rates and measures of air pollution while statistically controller for variables that are known to be linked with excess lung cancer mortality, including age, smoking, and socioeconomic status, [emphasis added]" Results not available at time of printing. 1472. University of Texas Health Science Centre, School of Public Health. Buffler, P.A.; Stallones, R. "Air Pollution and Lung Cancer in Harris County, Texas." Funding: EPA (CR807108-01) 10/79-4/84.

Results to date (Sept, 1976-May, 1981): "A possible flattening in the dose-response [between smoking and lung cancer] was found and a low relative risk in an area of the world with one of the highest recorded incidence of lung cancer. The flattening of the dose-response curve occurred with an above-average consumption of 20 cigarettes/day" [emphasis added] 0590. West of Scotland Cancer Surveillance Unit (Glasgow) and University of Michigan, School of Public Health. Gillis, C.R.; Hoie, D.J.; Hawthorne, VIM et al. "Retrospective Case Control Study of Smoking Habits and Lung Cancer in the West of Scotland." Funding: National Institutes of Health (N01-CP-05646).

"Excess risks of lung cancer found in miners and foundry workers could not be fully explained by the high prevalence of smoking among these occupations," [emphasis added]. 0495. University of Zurich, Institute of Pathology (Switzerland). Schuler, G. "Epidemiology of Lung Cancer in Switzerland."

Smoking has a protective effect on immunological abnormalities in asbestos workers. 0429. Institute of Immunology and Experimental Therapy (Poland). Lange, A. "Effect of Smoking on Immunological Abnormalities in Asbestos Workers.

AND

Relative risk of lung cancer for asbestos workers was "highest for those who had never smoked, lowest for current smokers, and intermediate for ex-smokers. The trend was statistically significant. There was no significant association between smoking and deaths from mesothelioma," [emphasis added]. 0565. University of London, School of Hygiene and Tropical Medicine. "Cancer of the Lung Among Asbestos Factory Workers." [Many other studies show similar findings for asbestos workers].

"Over the 22 years of follow-up, exposed workers have had a very high risk of respiratory cancer, mostly of the lung. The risk has been dose related and has been much higher in nonsmokers and ex-smokers than in current smokers. The epidemic began to subside shortly after exposure to chloromethyl ethers ceased. The mean induction-latency period was 17 years. Most of the lung cancers in the moderate and high dose groups have been small cell carcinoma," [emphasis added]. 1388. Hahnemann Medical College and Hospital (Philadelphia). Weiss, W. "Lung Cancer Dueto Chloromethyl Ethers."

Method: "A cohort of 125 workers (91 exposed to chloromethyl ethers) have been followed since 1963, and semi-quantitative estimates of degree of exposure and records of duration of exposure have been maintained. Information on smoking habits was obtained at the beginning of the observation period." "Marked atypia were found only in workers chemically exposed to BCME (4.8 percent of smokers and 6.2 percent of nonsmokers). The biological mechanism for increased injury in nonsmokers...has not yet been determined [emphasis added]." [Index number not recorded]. Labour Protection and Hygiene Centre, Laboratory of Cytology (Romania). Herivan, R.: Constantinescu, V.; Melinte, L. "BCME, Soot, Smoking and Lung Cancer.

"Presence of chronic respiratory symptoms at baseline was inversely related to cessation of smoking. Respiratory impairment was positively associated with smoking cessation, but failed to reach statistical significance," [emphasis added]. 1544. DHHS, PHS, CDC, NIOSH. Ames, R.G. "Respiratory Effects of Exposure to Diesel Emissions in Underground Coal Miners." Funding: NIOSH.

"Lung volume parameters were found to decrease with age, but there was no significant modification related to tobacco consumption."

0241. Institut D'Etudes Et Recherches Pneumophtisiologiques (Institute of Studies on Tuber-culosis). France. Keisbauer, J.P. "Longitudinal Study of the Methods of Early Detection of Respiratory Diseases in a Population of Cab Drivers."

"Neither smokers nor nonsmokers showed any changes in bronchial responsiveness after smoking cigarettes." 0391. Yokohama City University, School of Medicine (Japan). Okubo, T; Suzuki, S; Sano, F. "Acute Effect of Smoking on Bronchial Responsiveness."

"Chronic bronchitis was found more often in suburban inhabitants than in rural inhabitants, a significant difference." "It is concluded that chronic bronchitis is twice as common in the city as in rural areas, however, in both areas, air pollution and cigarette smoking lead to higher incidence." 0427. Copernicus Academy of Medicine (Poland). Nikodemowicz, E.; Owsinski, J.M.; Chomicka, Z. et al. "Influence of Urban Factors on the Incidence of Chronic Bronchitis in Rural Populations."

Smoking and Heart Disease

The connection between smoking and heart disease is far more tenuous than that between smoking and lung disease. Though the medical establishment considers smoking to be a risk factor (among many risk factors) for heart disease, the fact remains that anywhere from 30 to 50% of those admitted to hospitals for coronary problems exhibit none of the known risk factors (including smoking), and that the research is by no means either consistent of conclusive in linking smoking the heart disease. It is true that deaths from heart disease, which is still the number one cause of death, are declining but most researchers attribute this to better surgical and medical techniques, not to a decline in smoking rates, since deaths from heart disease are declining world-wide, even in countries with high smoking rate.

"No statistically significant relationship was found in either community between smoking and coronary heart disease, hypertension or somatic complaints" [emphasis added] 1477. University of Texas School of Allied Health Sciences. Philips, B.U., Jr.; Bruhn, J.G. "Smoking Habits and Reported Illness in Two Communities With Different Systems of Social Support." FUNDING: Univ. of Texas; National Institute of Mental Health. 1981-83.

"Preliminary data indicate greater frequency of anterior infarctions among nonsmokers." "Among patients with unstable angina, smoking was associated with less persistent rest pain and a lower proportion of

smokers had chronic angina of effort prior to hospital admission. Preliminary analysis suggests a marginally lower in-hospital mortality rate among smokers after controlling for age and other prognostic factors." [emphasis added]. 0298. St. Vincent's Hospital, Dept. of Preventive Cardiology and Cardiac Dept. (Dublin, Ireland). Cohort of 898 males and 415 female heart patients. 12/80-1/86.

"Preliminary data indicate a high prevalence of IHD [Ischemic Heart Disease] in South Wales. A significant association between white cell count and IHD defined cross-sectionally is not explained by smoking habits. Prevalent IHD is not explained by smoking habit" [emphasis added] 0598. Medical Research Council, Epidemiology Unit (Wales). Yarnell, J.W.G; Elwood, P.C.; Sweetnam, P.M. "Caerphilly Prospective Study of Ischemic Heart Disease." Cohort study of 2,400 men (aged 44-60) began in 1979. Two samples of women also studied.

"Recent secular trends in sex and age specific mortality from ischemic heart disease, both in the United Kingdom and in the United States, appear to be independent of changes in cigarette consumption." 0564. University of Leeds, Dept. of Medical Physics (England). Burch, P.R.J. "Tests of Causal, Constitutional and Mixed Hypotheses of Associations between Smoking and Disease in Man," 1972 and continuing. Funding: Univ. Leeds.

While smoking was more common among women who had myocardial infarction, "no such difference was observed between women with angina pectoris and other women." Also no significant differences were observed between smoking and nonsmoking women with respect to myocardial infarction and death during the 12-year follow-up. 0464. Sahlgrenska Hospital, Medical Dept. (Sweden). Bengtsson, C.: Lapidus, L; Hallstrom, T. "The Population Study of Women in Gothenburg, Sweden."

"In asymptomatic male aviators (aged 20 to 60), age and ratio of total cholesterol to high density lipoprotein cholesterol are most highly correlated with degree of coronary artery disease found on angiography. After removing the effect of age and this ratio, no statistically significant additional variance is explained by other risk factors [including smoking]." [emphasis added] 1465. Department of Defense, Department of the Air Force, School of Aerospace Medicine (Brooks Air Force Base, Texas). Tolan, G.D.; Honck, P.; Hickman, R. et al. "Multivariate Approaches to the Detection of Asymptomatic Coronary Artery Disease." Funded by USAF. 1971 - continuing.

Pipe smokers have a higher intake of nicotine than cigarette smokers (as measured by serum and urinary cotinine levels). "Since pipe smokers have little excess risk of CHD [chronic heart disease], higher chronic nicotine exposure is unlikely to be the cause of the excess seen in cigarette smokers." 0534. Medical College of St. Bartholomew's Hospital. Dept. of Environmental and Preventative Medicine (England). Wald, M.J.; Bailey, A. "Nicotine and Heart Disease.".

ETS and Heart Disease

"No difference in prevalence of cardiovascular symptoms was found [between those living with smokers and those not]" 0591. West of Scotland Cancer Surveillance Unit, Ruchill Hospital (Scotland). Gillis, C.R.; Hole, D.J.; Hawthorne, V.M. "Health Effects of Exposure to ETS (Environmental Tobacco Smoke] in the West of Scotland." Cohort of 16,171 (45-64 years old) screened in 1972 and 1976.

Smoking and "Throat" Cancer (See also appended bibliography for additional studies on this)

"All countries experienced a sharp increase in lung cancer mortality; [but] laryngeal and oral cavity cancers showed divergent trends (10 countries had steady or decreasing rates). Results suggest that tobacco may not be the major causative factor for laryngeal and oral cavity cancers." [emphasis added] 0244. Institut National de Recherche et de Security (France). Moulin, J.J; Mur, J.M.; Cavelier, C. "Comparative Epidemiology, In Europe, of Tobacco-Related Cancers (Lung, Larynx, Pharynx, Buccal Cavity)." Data is from World Health Organization 1950-1977.

"Secular trends in mortality from oesophageal cancer in the United Kingdom are independent of secular changes in cigarette consumption, but well correlated with secular changes in alcohol consumption...alcohol acts as an indirect causal agent. The proximal causal agent is likely to be a precipitator, such as a microorganism. Genetic predisposition is also implicated" 0564. University of Leeds. Dept. of Medical Physics (England). Burch, P.R.J. "Tests of Causal, constitutional, and Mixed Hypotheses of Associations Between Smoking and Disease in Man." Funding: Univ. of Leeds. 1972 -

continuing.

..."alcohol consumption was the dominant risk factor [for oesophageal cancer" [em. add.] Dept. of HHS, National Cancer Institute. Blot, W.J.; Brown, L.M.; Ershow, A. et al. "Epidemiologic Studies of Tobacco Use and Risk Cancer."

Smoking and Renal [Kidney] Cancer

"Preliminary results implicate relative weight in both men and women as a principal risk factor in renal cell carcinoma. Comparison with population controls failed to implicate cigarette smoking of beverage use as risk factors." [emphasis added] 1363. University of Oklahoma, Health Sciences Canter. Asal, N.R.; Geyer, J. "Risk Factors in Kidney Cancer." Oct. 1981 - Feb., 1985. FUNDING:< National Cancer Institute.

"A weak positive association with cigarette smoking has been found, but only after controlling for selection biases." "Findings appear to confirm previously observed associations with obesity, northeastern European ancestry, renal calculi [kidney stones], and use of phenacetin-containing analgesics." [emphasis added] 1060. Harvard University, School of Public Health, Dept. of Epidemiology. MacMahon, B; Maclure, K.M. "A Casa Control Study of Renal Adenocarcinoma." Method: Used Cancer registries, pathology logs and medical records at 37 participating hospitals in the Boston area and follow-up interviews by phone. FINDING: Harvard School of Public Health; National Cancer Institute.

ETS and Bladder Cancer

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"No association was found for exposure to side-stream smoke, coffee drinking, or artificial sweetener use. The association of several occupations with bladder cancer risk has been found in males..." 1216. American Health Foundation. Wynder, E.L.; Goodman, M.T.; Kabat, G.C., et al. "Studies in Tobacco-Related Cancers." FUNDING: National Cancer Institute.

Smoking and Endometrial, Ovarian and Breast Cancer

"Overall, smoking was not found to be associated with any of the cancers studied." Centres for Disease Control. Epidemiologic Studies Branch. Division of Reproductive Health. Rubin, G.; Tyler, C.W.; Franks, A.L.; Stroup, M. "Smoking and Endometrial, Ovarian, and Breast Cancer." FUNDING: NICHD.

"The risk of breast cancer does not appear to be influenced by cigarette smoking" 1039. Boston University Medical Centre. Drug Epidemiology Unit. Shapiro. S Rosenberg. L.; Kaufman. D. "Multiple Case-Control Study of the Long Term Effects of Drug, Use in the Treatment of Chronic Disease." FUNDING: FDA (U01 FD01222-03) and NICHD [National Institute nf Child Health & Human Development]. Emphasis added.

Smoking and Cervical Cancer

"Sexual Behaviour and socioeconomic indicators predict cervical cancer incidence, as has been demonstrated in numerous other studies.: [emphasis added]" University of Utah. School of Medicine. Lyon J.L. "Epidemiologic Investigation of Cervical Cancer in an Area of Low Incidence " FUNDING: NCI (Dept. of Health &HS)

Smoking and Pregnancy

Some studies have found a correlation between maternal smoking during pregnancy and lower birth weight in babies. However, there are many factors which correlate with low birth weight, and the dominant risk factors seem to be the mother's age and the mother's socioeconomic class. Even those studies which show a correlation between maternal smoking and low birth weight speak of weight differences in grams, not ounces, and one ounce = 28.35

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grams.

Risk factors associated with low birth weight (in rank order):

1. Mother's age (too young or too old) 2. First pregnancy 3. More than two previous stillbirths 4. Lower birth weight of older siblings 5. Small stature and weight of mother 6. Fewer examinations during pregnancy 7. Smoking by mother or father

0360. Department of Public Health. Jichi Medical School (Japan). Nagai. M.; Yanagawa. H.; Kawaguchi, T. et al. "A Study of the Factors Associated With low Birth Weight. A Case-Control Study in Togichi Prefecture Apr. 1982Dec. 1984.

"Women who smoke during pregnancy have full-term babies which, on the average are 5-6 grams [a fraction of an ounce] smaller than full-term babies born to nonsmoking mothers." 0755. University of Colorado. Health Sciences Centre. Moore. L.C. "Maternal O2 Transport During Pregnancy at High Altitude " [emphasis added]

1. Birth weight lower in the smoking group, but the incidence of smoking was higher in young, unmarried women of lower socioeconomic status. Perinatal death was also higher among young, unmarried, low income women. 2. "No differences in antepartum hemorrhage or congenital anomalies between the groups" 3. "Hypertension and postpartum hemorrhage were lower in smokers [emphasis added]."

0045. University of Tasmania, ( Queen Alexandra Hospital, Dept. of Obstetrics & Gynaecology. Correy, J.; Newman. N.: Currarn, J "An Assessment of Smoking in Pregnancy." Method: Since I974, this study was conducted on ALL patients in Tasmania (smoking data was collected since Jan.1981 ). Details of alcohol ingestion and drug use were also included. By 1984 information available on 90% of patients on average birth weight of infants, incidence of low birth weight (less than 2,500 grams), incidence of prematurity, congenital abnormalities, perinatal death antepartum hemorrhage and hypertension in pregnancy.

"The proportion of complications of pregnancy and delivery were similar in smokers and nonsmokers."

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University of Oslo (Norway). Dalaher, K.; Grunfeld, B.; Jansen, A.

"Data do not confirm the suggestion that changes in cord blood vessels similar to those of arteriosclerosis are brought about by maternal smoking during pregnancy. Pathological changes in the cord at term may be found in infants of healthy, nonsmoking mothers..." 0184. Universitat Freiburg, Anatomische: Institut (Germany). Staubesand, J.; Seydewitz, V.; Hugod, C. et al. "Effects of Maternal Smoking on the Neonatal Umbilical Cord."

Parental Smoking, ETS and Children

"...excess influenza virus infection was found for black infants and infants with at least one sibling (especially those with school-age siblings), and rhinovirus infection rates were highest among girls attending daycare. No convincing differences for viral infection or respiratory illness were seen with parental smoking as an isolated factor..." [emph. added] 1462. Baylor College of Medicine, Influenza Research Centre (Texas). Gardner, G.C.; Frank, A.L.; Taber, L.H. "Effects of Social and Family Factors on Viral Respiratory Infection and Illness in the First Year of Life." A longitudinal study,1975 - 1980. This study was published in the Journal of Epidemiology and Community Health 39 (1); 42-48, March, 1984.

"The correlation matrix revealed that maternal education was the variable most significantly inversely correlated with infection... Its statistical significance persisted in the presence of other added factors." "Maternal education appeared to have played a highly significant role in the health of the children studied." [emphasis added] 0878. University of Kansas, College of Health Sciences. Holmes. G.E.; Hassanein, K.M.; Miller. H.C. "Factors Associated with Morbidity Among Breast Fed and Formula Fed Babies." The incidence of infection in babies was studied with regard to a number of factors, including maternal smoking.

Nicotine and Smoking: Benefits

Though the risks of smoking are highly publicized, the medical benefits of smoking are rarely mentioned. The greatest risks of smoking come from the tars released during the combustion of tobacco, and these tars are implicated in lung cancer and other breathing disorders, though even the tar apparently has some beneficial effects in protecting the lungs from some noxious particulate matter (e.g. asbestos). According to many studies, the chief medical benefits of smoking are from the nicotine, which occurs naturally in tobacco as well as in certain vegetables such as tomatoes, potatoes, and red peppers, though in much smaller amounts. Interestingly, these three plants

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originated in the Americas so nicotine was essentially a "New World" substance. Native Americans were well aware of the curative properties of tobacco, and used it both medicinally and ceremonially. Numerous studies have shown the protective effects of smoking with regard to Parkinson's Disease and ulcerative colitis, and an increasing body of research indicates it also helps protect against Alzheimer's Disease and colo-rectal cancer. Since these effects are so well known, wehave not listed them below but have focused instead on a few more obscure medical benefits culled from the 1984-85 CDC bibliography. Brief documentation of the beneficial effects of smoking with regard to Parkinson's, ulcerative colitis, Alzheimer and colo-rectal cancer will appear in an attached appendix of some relevant studies from the 1991 CDC bibliography.

1. Smoking improves human information precessing. 2. Higher nicotine cigarettes produce greater improvements [in information processing] than low-nicotine cigarettes. 3. Nicotine tablets produce similar effects. 4. Nicotine can reverse the detrimental effects of scopolamine on performance 5. Smoking effects are accompanied by increases in EEG arousal and decreases in the latency of the late positive component of the evoked potential."

0574. University of Reading, Department of Psychology (England). Warburton., D.M.; Wesnes, K. "The Effects of Cigarette Smoking on Human Information Processing and the role of Nicotine in These Effects "

"In general, motor performance in all groups improved after smoking." 0530. London University, Institute of Psychiatry. O'Connor, K.P "Individual Differences in Psychophysiology of Smoking and Smoking Behaviour "

"Smokers in general are thinner than nonsmokers, even when they ingest more calories." [Numerous studies, but only two are listed below] 0885. Kentucky State University. Lee. C.J.: Panemangalore. M. "Obesity Among Selected Elderly Females In Central Kentucky." FUNDING: USDA 0942. University of Louisville. Belknap Campus School of Medicine. Satmford, B.A.; Matter, S.; Fell, R.D., et al. "Cigarette Smoking, Exercise and High Density Lipoprotein Cholesterol" FUNDING: American Heart Association.

"...all smokers had less plaque, gingival inflammation and tooth mobility than nonsmokers and similar periodontal pocket depth."

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Veterans Administration, Outpatient Clinic (Boston). Chauncey. H.H,; Kapur, K.K.; Feldmar, R S. "The Longitudinal and Cross-Sectional Study of Oral Health: in Healthy Veterans (Dental Longitudinal Study)

"Smokers have lower incidence of postoperative deep vein thrombosis than nonsmokers." Guy's Hospital Medical School (England). Jones, R.M. "Influence of Smoking on Peri-Operative Morbidity." Hypertension (High blood pressure) is less common among smokers.

"Hypertension prevalence rate among smokers was 3.94 percent; among nonsmokers the rate was 4.90 percent." 0146. Shanghai Institute of Cardiovascular Diseases. Chen, H.Z.; Pan, X.W.; Guo, G. et al. "Relation Between Cigarette Smoking and Epidemiology of Hypertension. AND

"Hypertension and postpartum hemorrhage were lower in smokers." 0045. University of Tasmania (Australia). Correy, J.; Newman, N. Curran, J. "An Assessment of Smoking in Pregnancy."

"RBCs [red blood cells] from cigarette smokers contain more glutathione and catalase and protect lung endothelial cells against O2 [dioxide] metabolites better than RBCs from nonsmokers." [emphasis added] 0759. University of Colorado. Refine, J.E.; Berger, E.M.; Beehler, C.J. et al. "Role of RBC Antioxidants in Cigarette Smoke Related Diseases." Jan 1980 - continuing.

(A number of studies in the 1991 CDC bibliography describe the apparent protective effect of smoking with regard to mouth ulcers).

APPENDIX Following are studies listed in the Centres for Disease control's Bibliography on Smoking and Health, 1991. Many newer studies appear in this more recent CDC bibliography which support the earlier studies listed in the foregoing selected bibliography, including a lower risk of breast cancer, lower risk of endometrial cancer in smoking women; the improvement of fine motor control for smokers; lower incidence of overweight in smokers; lower incidence of high blood pressure among smokers. Below are selected studies which demonstrate the protective effect of smoking in Parkinson's Disease and ulcerative colitis.

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"Several epidemiological studies have indicated that there may be an inverse relationship between smoking and Parkinson's disease." There is an "apparent protective effect of cigarette smoke." 1102. Carr, L.A.; Rowell, P.P. "Attenuation of 1methyl-4-phenyl-1,2,3,6-tetrahydrophyridine- induced neurotoxicity by tobacco smoke." Published in Neuro-pharmacology 29(3):311-4, Mar 1990.

"These results indicate that in sufficient doses chronic treatment with nicotine may be considered in the pharmacological treatment of Parkinson's disease. It remains to be demonstrated whether these protective actions can be extended to include also other injured neurons..." 1190. Janson, A.M.; Fuxe, K.; Agnati, L.F. Jansson, A. et al. "Protective effects of chronic nicotine treatment on lesioned nigrostriatal dopamine neurons in the male rat." Pub. in Progress in Brain Research 79:257-65, 1989.

"Several studies have reported an apparent protective effect of cigarette smoking for the risk of idiopathic Parkinson's disease (IPD). These observations are supported by neurochemical studies..." These findings suggest that the inverse association between smoking and IPD may apply to NIP [neuroleptic-indiced parkinsonism]." 4014. Decina, P.; Caracci, G.; Sandik, R.; Berman, W. et al. "Cigarette smoking and neuroleptic- induced parkinsonism." In Biological Psychiatry 28(6):502-8, Sept. 15, 1990

"There is a low prevalence of smoking in ulcerative colitis. The disease often starts or relapses after stopping smoking." 4101. Prytz, H.; Benoni, C.; Tagesson, C. "Does smoking tighten the gut?" In Scandinavian Journal of Gastroenterology 24(9):1084-8, Nov. 1989.

"These results indicate that nonsmokers and especially ex-smokers of cigarettes have greater risk of UC [ulcerative colitis] and thus confirm the results of other studies." 4134. Lorusso, D.; Leo, S.; Miscianga, G.; Guerra, V. "Cigarette smoking and ulcerative colitis. A case control Study." Hepato-Gastroenterology 36(4): 202-4, Aug. 1989.

Documentation for the protective effect of smoking on Alzheimer's may be found in the 11 studies reviewed in the International Journal of Epidemiology, 1991. There is also documentation for lower incidence of colorectal cancer in JAMA in the early 1980s

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ADDITIONAL BIBLIOGRAPHY Forces Canada wishes to thank Martha Perske for providing the following bibliography:

"...particular attention is paid to the consumption of ethanol [alcohol] which has a major impact on the incidence of human cancer" 91-2046. Doll, R. Lifestyle: An overview. Cancer detection and prevention. 14(6): 589-94, 1990

" There is little direct evidence that cancer prevention has led to any major reduction in cancer incidence or mortality." 91-2068. Claysdon, D.B. " An overview of current and anticipated methods for cancer prevention." Cancer Letters. 50(1):3-9, April 9, 1990.

"...the prevalence of mild and moderate disease [oesophageal cancer] was found to be positively associated with the consumption of burning hot beverages (odds ratio = 4.7), the prevalence of esophagitis among siblings (O.R. = 4.4) and family history (O.R. = 1.8) ... Weaker associations were seen for cigarette smoking and the use of cottonseed oil..." 91-2069. Chang-Claude, J.C.; Wahrendorf, J. et al. " An epidemiological study of precursor lesions of oesophageal cancer among young persons in a high risk population in Hulxian, China." Cancer Research 50(8):2266-74, April 15, 1990.

" The incidence of these cancers appear to be increasing rapidly in response to the increasing level of alcohol consumption in Denmark." 91-2130. Miller, H. "Changing incidence of cancer of the tongue, oral cavity, and pharynx in Denmark." Journal of Oral Pathology and Medicine. 18(4): 224-9, Apr. 1989.

" Cancers of the mouth or pharynx and oesophagus were independently and strongly related to alcohol consumption..."

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91-2147. Ferraroni, M.; Negri, E. et al. " Socioeconomic indicators, tobacco and alcohol in the aetiology of digestive tract neoplasms." International Journal of Epidemiology. 18(3): 556-62, Sep 1989.

"...Linxian, a rural country in North Central China with one of the world,s highest mortality rates for these tumours. Cancer rates tended to raise with increasing intake of wheat or corn... Few persons reported drinking alcoholic beverages. Smoking was reported by 61% of the male cases and was a mild risk factor, related more to cancer of the cardia than of the oesophagus. The risk was increased by 70% among those whose parents had oesophageal or stomach cancer..." 91-2180. Li, J.Y.; Brshow, A.G.; et al [including Blot, W.J.]. "A case-control study of cancer of yhe oesophagus and gastric cardia in Linxian [China]." International Journal of Cancer. 43(5) : 755-61, May 15, 1989.

Odds ratios for oesophageal cancer: Current smokers: 3.8 - Heavy drinkers: 6.0 91-2199 Franceschini, S.; Talamini, R., et al. "Smoking and drinking in relation to cancers of the oral cavity, pharynx, larynx, and oesophagus in Northern Italy." Cancer Research. 50(20) :6502-7, Oct. 15, 1990.

"Highly significant associations with frequent intake of Maize emerged for oral cancer, pharyngeal cancer, and oesophageal cancer (OR = 3.3, 3.2, and 2.8, respectively). The risk elevation could not be explained in terms of difference in education, occupation, tobacco use, or consumption of fresh fruits and vegetables. The unfavourable effect of Maize... was evident only in those individuals who reported heavy drinking... The present findings agree with previous observations from Africa, China, the U.S., and Italy." 91-2202. Franceschini, S.; Bidoli, E.; et al. "Maize (corn) and risk of cancer in the oral cavity, pharynx, and oesophagus in Northeastern Italy." Journal of the National Cancer Institute. 82(17) :1407-11, Sept. 5, 1990.

"The three risk factor showed a strong tendency to be related to cancer only in combination, adding new evidence to the theory that risk factors in cancer act in a synergistic fashion." 91-2322. Grossart-Maticek, R.; Eysenck, H.J. "Personality, smoking, and alcohol as synergistic risk factors for cancer of the mouth and pharynx." Phycological Reports. 67 (3 Pt. 1) : 1024-6, Dec. 1990.

Source: Bibliography On Smoking and Health, 1991. Centres for Disease Control and Prevention.

SMOKERS HAVE REDUCED RISKS OF ALZHEIMER'S AND PARKINSON'S DISEASE Patients with Alzheimer's disease (AD) have a considerably decreased life expectancy, with the entire course of the disease taking an average of about eight years. AD is defined by a specific combination of neuropathologic features that

18

include neuronal loss in particular regions of the brain and a high density of senile plaques and neurofibrillary tangles. It is hard to distinguish during life because of other damage and dementias. As many as 80% of the cases may be unrecognized by general practitioners. Acute administration of low doses of nicotine improved mental processes and may be protective in AD. This possibility was first put forward by Appel, who noted that only 6 out of 30 patients had smoked at any time in their lives. Since that time, nineteen case control studies have been published and are considered here. The overall from these showed a clear negative association, 15 out of 18 studies reporting a lower risk of AD in men and women who had smoked. Of the 19 studies, 15 found a reduce risk in smokers, and none found an increased risk. And smoking is clearly associated with a reduced risk of Parkinson's disease, another disease in which nicotine receptors are reduced. The fact that acute administration of nicotine improves attention and information processing in AD patients adds further plausibility to the hypothesis.

"The risk of Alzheimer's disease decreased with increasing daily number of cigarettes smoked before onset of disease. In six families in which the disease was apparently inherited, the mean age of onset was 4-17 years later in smoking patients than in non- smoking from the same family." (Conelia M. van Duljn MSC Albert Hoffman Md., Erasmus Univ. Md. School) STUDIES AND PUBLICATIONS

Amaducci LA, et al. A case-controlled study of an Italian population. Neurology, 1986, 36:922-931. Barclay L, Kheyfets S. Tobacco used in Alzeimer's disease. Prog. Clin. Bho. Res 0989, 317:189-194. Brenner DE, et al. Relationship between cig. smoking and Alz. disease. Neurology 1993, 43:293-300. Broe GA et al. A case -controlled study of alz. in Australia. Neurology 1990, 40:1698-1707. Chandra V. et al. Case study of the late on-set 'probable Alz. disease'. Neurology 1987, 37:1295-1300. Dewey ME, et al. Risk factors for Dementia. Liverpool, Int. Geriatric Psychiatry 1988, 3:245-249. Ferini-Strambi, et al. Clinical Aspect of Alz. Disease with pre-senile on-set. Neuro Epidem 1990, 9:3449. French LR, et al. Case-control study of dementia of Alz. type. Am J Epidemiol 1985, 121:414-421. Graves, AB, et al. Case controlled study of Alz. disease. Neurol 1990, 28:766-774.

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Grossberg, GT, et al. Smoking as a risk factor for Alz disease. Am. Geriatric Soc. 1989, 37:819. Hebert LE, et al. Relation of smoking and alcohol to Alz disease. Amer. J Epidemiol 1992, 135:347355. Heyman A, et al. Alz disease: a study of epidem aspects. Am Neurol 1984, 15:335-341. Hofman A, van Duijn. Alz disease, Parkinson's disease, and smoking. Neurobiol Aging 1990, 11:295. Jones GMM, et al. Smoking and dementia of Alz type. Neurol Neurosurg Psychiatry 1987, 50:1383. Joya CJ, et al. Risk factors in clinically-diagnosed Alz disease. SA Neuroniol Aging 1990, 11:296. Katzman R, et al. Develop of dementing ill. in 80 yr. old volunteer cohort. Am Neurol 1989, 25:317324. Kondo, K Yamashita I. Case study of Alz in Japan. Biol & Social advances. Excerpta Medica 1990, 49-53. Shalat SL, et. al. Risk factors for Alz. disease. Neurology 1987, 37:1630-1633. Soininen H, et al. Clinical and etiological aspects of senile dementia. Eur Neurol 1982, 21:401-410. Korten AE, et al. Control informant agr. in case control studies of Alz. Int. J Epidie. 1992, 21:11211131. Breteler MMB, et al. Epidemiology of Alz disease. Epidemiol Review 1992, 14:59-82. Lee PN Statistics, Sutto, UK.

ALZHEIMER'S DISEASE IS ASSOCIATED WITH NON-SMOKING Graves' pooled reanalysis found, "A statistically significant inverse relation between smoking and Alzheimer's disease was observed at all levels of analysis, with a trend towards decreasing risk with increasing consumption (p=0.0003). A propensity towards a stronger inverse relation was observed among patients with a positive family history of dementia." Only three studies have ever linked smoking with AD. The reanalysis, in which the author of one participated, noted, "Since veterans may be expected to smoke more than the general population, and since smokers have been found to respond less frequently to questionnaires than non-smokers, the positive result observed for this study may be spurious."

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Contrary to a claim that smokers got AD at a younger age, there was no difference in men. Female smokers were younger among both cases and controls, which proved it to be spurious. Over 4 million people suffer from AD, and annual costs are over $88 billion. There may be 73,000 excess cases per year among non-smokers, with $17.5 billion in excess costs.

Ferini-Strambi L, Smirne S et al. Clinical and epidemiological aspects of Alzheimer's disease with presenile onset: a case-control study. Neuroepidemiol 1990;9:39-49. 63 ADs, ever/never 0.47 (0.23-0.94).

Li G, Shen YC et al. A case-control study of Alzheimer's disease in China. Neurol 1992 Aug;42(8):1481-1488. 70 ADs, >10y 0.92 (0.45-1.87), >20y 0.87 (0.35-2.16).

Hebert LE, Scherr PA et al. Relation of smoking and alcohol consumption to incident Alzheimer's disease. Am J Epidemiol 1992;135(4):347-355. 76 ADs, ever/never 0.7 (0.3-1.4), 40 pyrs 0.8 (0.6-1.1).

Jones GMM, Reith M et al. Smoking and Dementia of Alzheimer type (letter). J Neurol Neurosurg Psychiatry 1987;50:1383. 81 ADs. ever/never 0.63 (from Graves: NON-smokers 1.58).

Grossberg GT, Nakra R et al. Smoking as a Risk Factor for Alzheimer's Disease (letter). J Am Geriatr Soc 1989;37:822. 144 ADs ever/never 0.33 unmatched OR (p<0.01) (from Graves). Reported that female smokers had onset 2 years earlier, non-significant.

Brenner DE, Kukull WA et al. Relationship between cigarette smoking and Alzheimer's disease in a population-based case-control study. Neurol 1993; 43(2):293-300. 152 e/n 0.61 (0.37-0.99).

Graves AB, van Duijn CM et al., for the EURODEM Risk Factors Research Group. Alcohol and tobacco consumption as risk factors for Alzheimer's disease: A collaborative reanalysis of case-control studies. Int J Epidemiol 1991;20(2 Suppl 2):S48-S57. All 8 studies, 899 cases: ever/never 0.78 (0.62-0.98 with Shalat), 0.72 (0.56-0.92 without); <1p 0.84 (0.75-0.92), >1p 0.81 (0.53- 1.27) with. 4 studies with pack-year data, adjusted for education: <15 py 0.68 (0.46-1.01), 15.5-37.0 py 0.58 (0.37-0.89), >37.0 py 0.49 (0.30-0.78). The 8 studies:

Amaducci LA et al. Neurol 1986;36:922-931. 116 ever/never 0.60 (0.26-1.37).

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Broe GA et al. Neurol 1990;40:1698-1707. 168 ever/never 0.79 (0.47-1.31).

Chandra V et al. Neurol 1987;37:1295-1300. 63 ever/never 0.57 (0.24-1.36)

French LR et al. Am J Epidemiol 1985;121(3):414-421. 78 ever/never 0.50 (0.15-0.66).

Graves AB et al. Ann Neurol 1990;28:766-774. 129 ever/never 0.73 (0.43-1.23).

Heyman A et al. Ann Neurol 1984;15:335-341. 46 ever/never 0.97 (0.45-2.13).

Hofman A et al. Neurobiol Aging 1990;11:295. 197 ever/never 0.73 (0.45-1.17).

Shalat SL et al. Neurol 1987;37:1630-1633. 102 ever/never 1.53 (0.74-3.17). NOT SHOWN ON GRAPH:

Appel SH. Alzheimer's disease. In: Brain Neurotransmitters and Receptors in Aging and Age-Related Disorders (Aging, Vol 17). SJ Enna et al, eds. New York: Raven Press 1981. pp 203-207. Observed that only 6/30 patients ever smoked.

Barclay L, Kheyfets S. Tobacco use in Alzheimer's disease. In: Alzheimer's Disease and Related Disorders. Alan R Liss 1989. pp 189-194. 39 ADs vs spouse controls: ever 64.1%/69.2%.

Hirayama T. Health effects of active and passive smoking. In: Smoking and Health 1987. Proc 6th World Conf of Smoking and Health, Tokyo, 9-12 Nov, 1987. Amsterdam, The Netherlands: Elsevier Science Pub, pp. 75-86. Rate ratio 39 male 1.53, 13 female 1.72; 1-14 cigs 1.5, 15-19 2.1, 20+ 2.4. Number of non-smokers not given.

Joya CJ, Pardo CA, Londono JL. (abstr) Risk factors in clinically diagnosed Alzheimer's disease: a case-control study in Colombia (South America). Neurobiol Aging 1990;11:296. 43 ADs. "Tobacco use (>20 cigarettes/day)... tended to be more frequent among cases of AD than controls; however differences were not significant." No detail.

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Katzman R, Aronson M et al. Development of dementing illnesses in an 80-year-old volunteer cohort. Ann Neurol 1989;25:317-324. 32 incident ADs/controls: 28.1%/51.1% ex, 0.0%/10.9% current. Prospective: "In this [75-85 yr old] study population, the incidence of dementia exceeded that of stroke and equalled that of presumed heart attacks."

Mayeux R, Ottman R et al. Genetic susceptibility and head injury as risk factors for Alzheimer's disease among community-dwelling elderly persons and their first-degree relatives. Ann Neurol 1993;33(5):494-501. 138 ADs; "smoking was more frequent in control subjects than in patients," no detail. PARKINSON'S DISEASE IS ASSOCIATED WITH NON-SMOKING (Studies listed by size) Duvoisin RC, Eldridge R et al. Twin study of Parkinson disease. Neurol 1981; 31:77-80. 12 pairs. 1.0 ever/never; 0.4 current; all nonsignificant. Ho SC, Woo J, Lee CM. Epidemiologic study of Parkinson's disease in Hong Kong. Neurol 1989;39:1314-1318. 34 PDs; ever/never 0.6 (0.2-1.3). Tanner CM, Chen B et al. Environmental factors in the etiology of Parkinson's disease. Can J Neurol Sci 1987;14:419-423. 35 PDs; ever/never 0.67 not significant. Bharucha NE, Stokes L et al. A case-control study of twin pairs discordant for Parkinson's disease: A search for environmental risk factors. Neurol 1986; 36:284-288. 41 PDs; ever 0.4, p<0.05; current 0.4 p<0.05. Statistically significant less cigarette smoking by PDs. [*] Doll R, Peto R. Mortality in relation to smoking: 20 years' observations on male British doctors. Br Med J 1976;25:1525-1536. 51 men; current/non 0.36 p<0.01. Ngim C-H, Devathasan G. Epidemiologic study on the association between body burden mercury level and idiopathic Parkinson's disease. Neuroepidemiol 1989;8:128-141. 54 PDs ever 0.61 (0.18-2.03). Hertzman C, Wiens M et al. Parkinson's disease: A case-control study of occupational and environmental risk factors. Am J Ind Med 1990;17:349-355. 57 cases. Age-adj logistic regression ever s 0.40 (0.19-0.86). [*] Grandinetti A, Morens DM et al. Prospective study of cigarette smoking and the risk of developing idiopathic Parkinson's disease. Am J Epidemiol 1994; 139(12):1129-1138. 58 definite PDs, ever smokers 0.39 (0.22-0.70).

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Butterfield PG, Valanis BG et al. Environmental antecedents of young-onset Parkinson's disease. Neurol 1993;43(6):1150-1158. 63 PDs <50y; s p/d 15y prior 0.32 (0.15-0.67). Hofman A, Collette HJA et al. Incidence and risk factors of Parkinson's disease in the Netherlands. Neuroepidemiol 1989;8:296-299. 86 PDs ever 0.6 (0.3-1.0), current 0.7 (0.4-1.4). [*]Sasco AJ, Paffenbarger RS. Smoking and Parkinson's disease. Epidemiology 1990;1:460-465. C-c in 50k Harvard cohort, 96 PDs; smoked at college 1.0; adult current cig 0.51 (0.26-1.0). Most eventual smokers did not smoke at college. Cazzato G, Capus L et al. Abitudine al fumo e morbo di Parkinson. Rivista di Neurologia 1985;55:79-87. 100 PDs; ever/never 0.4 sig. (Baron's calculation). Rajput AH, Offord KP et al. A case-control study of smoking habits, dementia, and other illnesses in idiopathic Parkinson's disease. Neurol 1987;37:226232. 118 PDs; ever 0.7 (0.4-1.2). Reanalysis of subjects of 1984 study, with linear logistic regression. [*] Hammond EC. Smoking in relation to the death rates of one million men and women. In: Haenszel W, ed. USDHEW NCI Monograph 19, 1966. 123 PDs; ever/ never RR 0.76 ages 45-64. Barbeau A, Pourcher E. New data on the genetics of Parkinson's disease. Can J Neurol Sci 1982;9(1):53-60. 124 early onset PD; ever/never OR 0.4 (Baron's Calculation). Jimnez-Jimnez FJ, Mateo D, Gimnez-Roldan S. Premorbid smoking, alcohol consumption, and coffee drinking habits in Parkinson's disease: A casecontrol study. Movement Dis 1992;7(4):339-344. 128 PDs; 11+c, p<0.005. [Mean of Table 1, 0.63 11+/never]. Semchuk KM, Love EJ, Lee RG. Parkinson's disease: A test of the multifactorial etiologic hypothesis. Neurol 1993;43(6):1173-1180. 130 PDs; ever smokers 0.58 (0.33-1.02) adj; 0.48 (0.29-0.80) crude. Stern M, Dulaney E et al. The epidemiology of Parkinson's disease. A casecontrol study of young-onset and old-onset patients. Arch Neurol 1991;48:903-907. 149 PDs; 0.5 (0.3-0.9). Mayeux R, Tang M-X, Marder K, Ct LJ, Stern Y. Smoking and Parkinson's disease. Movement Disorders 1994 Mar;9(2):207-212. 150 PDs. Ever s adj for age & sex 0.8 (0.4-1.5); <30py 0.8 (0.4-1.5), >30py 0.6 (0.3-1.2). Tanner CM, Koller WC et al. (abstr) Cigarette smoking, alcohol drinking and Parkinson's disease: cross-cultural risk assessment. Movement Disorders

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1990; 5(suppl 1):11. US: 150 PDs OR 0.2 p<0.0001. Kondo K. Epidemiological clues for the etiology of Parkinson's disease. Adv Neurol 1984;40:345-351. 166 PDs; ever/never, female 0.6 sig, male 0.4 sig (Baron's calculation). Nefzger MD, Quadfasel FA, Karl VC. A retrospective study of smoking in Parkinson's disease. Am J Epidemiol 1968;88(2):149-158. 198 PDs; ever/never 0.44 sig. Kessler II. Epidemiologic studies of Parkinson's disease. Am J Epidemiol 1972;96(4):242-254. 228 PDs; ever/never,female 0.56 p>0.05, male 0.38 p<0.001. Baumann RJ, Jameson HD et al. Cigarette smoking and Parkinson disease: 1. A comparison of cases with matched neighbors. Neurol 1980;30:839-843; and Haack DG, Baumann RJ et al. Nicotine exposure and Parkinson disease. Am J Epidemiol 1981;114(2):191-200. 237 PDs. ever/never both sexes 0.46 p<0.001. Godwin-Austen RB, Lee PN et al. Smoking and Parkinson's disease. J Neurol Neurosurg Psychiatry 1982;45:577-581. 350 PDs; ever 0.52, current 0.40; doseresponse 1-19=ref., 20+ 0.76 cur. [*] Hellenbrand W et al. Smoking and Parkinson's disease: a case control study in Germany. Int J Epidemiol 1997 Apr;26(2):328-339. 380 PD pts. Ever s 0.5 (0.3-0.7), P<0.00005; current s 0.2 (0.1-0.4), versus never. Dose-response. [*] Kahn HA. The Dorn study of smoking and mortality among U.S. veterans: report on eight and one-half years of observation. In: Haenszel W, ed. USDHEW NCI Monograph 19, 1966. 400 PDs; ever RR 0.36, current RR 0.30, vs. never. Marttila R, Rinne UK. Smoking and Parkinson's disease. Acta Neurol Scand 1980; 62:322-325. 443 PD; ever/never 0.7 significant (Baron's calculation). Kessler II, Diamond EL. Epidemiologic studies of Parkinson's disease. Am J Epidemiol 1971;94(1):16-25. 468 PDs; both sexes ever/never 0.66, p<0.05.

Busenbark KL, Huber SJ et al. Olfactory function in essential tremor. Neurol 1992 Aug;42:1631-1632. yes/no 1/15 PDs, 3/13 normal controls.

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Dulaney E, Stern M (abstr) The epidemiology of Parkinson's disease: A casecontrol study of young-onset versus old-onset patients. Movement Disorders 1990;5(suppl 1):12. 75 onset <40y, 75 >60y. Smoking less frequent, no detail. Golbe LI, Cody RA, Duvoisin RC. Smoking and Parkinson's Disease: Search for a dose-response relationship. Arch Neurol 1986;43:774-778. PDs only, no controls; 3693 questionnaires/30k sent. Claimed no dose-response. [*] Hirayama T. Epidemiological patterns of Parkinson's disease based on a cohort study. Tokyo: Japan Ministry of Health and Welfare, 1985. RR 0.6, trend (Baron). Unknown no. of PDs. [*] Hirayama T. Health effects of active and passive smoking. In: Smoking and Health 1987. Proceedings of the 6th World Conference of Smoking and Health, Tokyo, 9-12 November, 1987. Amsterdam, The Netherlands: Elsevier Science Publishers, pp. 75-86. Smoker mortality ratio male 0.56, female 0.59. Number unknown. Jansson B, Jankovic J. Low cancer rates among patients with Parkinson's disease. Ann Neurol 1985;17:505-509. 406 pts. Ever s M: 35% obs v 70% exp, F 10% v 45% (in general population). No RR given. Morano A, Jimnez-Jimnez FJ et al. Risk-factors for Parkinson's disease: casecontrol study in the province of C ceres, Spain. Acta Neurol Scand 1994 Mar;89(3):164-170. 74 PDs. Analysis combined non- & light smokers, no ORs. ~46%mPD, 29%m controls & 100%fPD, 98.8% f controls non-smokers. Tanner CM, Koller WC et al. (abstr) Cigarette smoking, alcohol drinking and Parkinson's disease: cross-cultural risk assessment. Movement Disorders 1990; 5(suppl 1):11. China: 100 PD 41% s v 49.5% controls; no OR given. Ward CD, Duvoisin RC et al. Parkinson's disease in 65 pairs of twins and in a set of quadruplets. Neurol 1983;33:815-824. 58 PD pairs; Less smoking by PD twins than non-PD, p<0.01. Wechsler LS, Checkoway H et al. A pilot study of occupational and environmental risk factors for Parkinson's disease. Neurotoxicol 1991;12:387-392. 34 PDs. Ever s 50% v 64%, fewer y & cpd. No OR given. [*] Wolf PA, Feldman RG et al. (abstr) Precursors and natural history of Parkinson's disease: The Framingham Study. Neurol 1991 Mar;41(suppl 1):371. 77 PDs. Relationship to non-smoking in men only, no detail. Zuber M, Verdier-Taillefer M-H et al. Smoking and Parkinson's disease: Differences according to age at disease onset. Neuroepidemiol 1991;10:103104. 150 PDs; 44 v 36% nevers, nonsig.

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[*] = prospective study ________________________________________________ Additional references:

Methods for detecting and evaluating ascorbic acid deficiency in man and animals. HB Burch. In: Annals of the New York Academy of Sciences, Vol 92:269-275. Humane requirements for Vitamin C and its use in clinical medicine. GA Goldsmith. In: Annals of the New York Academy of Sciences, Vol 92:230-245. What are people really eating? The relation between energy intake derived from estimated diet records and intake determined to maintain body weight. W Mertz, JC Tsui, JT Judd, S Reiser, J Hallfrisch, ER Morris, PD Steele, E Lashley. American Journal of Clinical Nutrition 1991;54:291-295. Smoking and Vitamin C levels in humans. O Pelletier. American Journal of Clinical Nutrition Nov 1968;21(11):1259-1267. Relationship between leucocyte and plasma ascorbic acid concentrations. HS Loh, CWM Wilson. British Medical Journal 25 Sep 1971;3:733-735.

SMOKING DOES NOT CAUSE CHROMOSOME ANOMALIES Summary of findings of studies of congenital chromosome anomalies:

Christianson RE, Torfs CP. (letter re Hook 1988). Am J Hum Genet 1988;43:545-546. Reanalysis by Cuckle 1990: 28 Down's s 0.81 (0.38-1.71), no age adjustment.

Shiono PH, Klebanoff MA, Berendes HW. Congenital malformations and maternal smoking during pregnancy. Teratol 1986;34:65-71. Kaiser-Permanente prospective. 25 DS 0.2 (0.1-0.9); 23 autosomal 1.1 (0.5-2.7). Age-adjusted reanalysis by Cuckle 1990 31 DS 0.34 (0.08-1.45).

Seidman DS, Ever-Hadani P, Gale R. Effect of maternal smoking and age on congenital anomalies. Obstet Gynecol 1990;76:1046-1050. Rates/1000, all ages [34 calc.] Down's 0p 1.9, <1p 1.8, 1+p 2.0, all nonsignificant. [crude relative risk 0.95, 1.05].

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Palomaki GE, Knight GJ, Haddow JE, Canick JA, Wald NJ, Kennard A. Cigarette smoking and levels of maternal serum alpha-fetoprotein, unconjugated estriol, and hCG: Impact on Down syndrome screening. Obstet Gynecol 1993; 81(5 pt 1):675-678. 35 Downs, s 0.51 (0.15-1.5).

Kelsey JL, Dwyer T, Holford TR, Bracken MB. Maternal smoking and congenital malformations: an epidemiological study. J Epidemiol Commun Health 1978;32:102-107. 52 Down's & sex chromosomes relative risks 1-20c 1.1, 21+c 1.8.

Heinonen OP, Slone D, Shapiro S, eds. Birth defects and drugs in pregnancy. Littleton, MA: Publishing Sciences Group, 1977. Collaborative Perinatal Project prospective. 176 syndromes excluding Downs, [subgroup] 30+c 1.6 MLR; 61 Down NON-smokers 2.0 in MLR. Age-adjusted reanalysis by Cuckle 1990 of Kline 1981 reanalysis, 64 Down's 0.66 (0.40-1.07).

Kline J, Levin B et al. Cigarette smoking and trisomy 21 at amniocentesis. Genet Epidemiol 1993;10(1):35-42. 89 DS. 1-13c 0.5 (0.2-1.4), 14+c 1.2 (0.6-2.7); Cur/nev 0.8 (0.4-1.6).

Cuckle HS, Alberman E, Wald NJ, Royston P, Knight G. Maternal smoking habits and Down's syndrome. Prenat Diag 1990;10:561-567. 1) Antenatal Series: 91 Down's 0.63 (0.33-1.20). 2) Radiation Study: 461 Down's s 1.03 (0.80-1.34); Both age adjusted.

Hook EB, Cross PK. Cigarette smoking and Down syndrome. Am J Hum Genet 1985; 37:1216-1224. 0.56 (0.33-0.95) case-normal, 0.58 (0.34-0.98) case-defect control. Age-adjusted reanalysis by Cuckle 1990: 100 Down's 0.56 (0.30- 1.03).

Van den Eeden SK, Karagas MR, Daling JR, Vaughan TL. A case-control study of maternal smoking and congenital malformations. Paediatr Perinat Epidemiol 1990;4:147-155. 117 Down's. S during pregnancy 0.8 (0.5-1.3).

Stoll C, Alembik Y, Dott B, Roth M-P. Epidemiology of Down syndrome in 118,265 consecutive births. Am J Med Genet 1990;suppl 7:79-83. 139 Downs. 19.4% v 21.6% s [0.90] nonsig.

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Kline J, Levin B, Shrout P, Stein Z, Susser M, Warburton M. Maternal smoking and trisomy among spontaneously aborted conceptions. Am J Hum Genet 1983; 35:421-431. 160 trisomy, 0.85. Age-adjusted reanalysis by Cuckle 1990 0.70 (0.46-0.96).

McDonald AD, Armstrong BG, Sloan M. Cigarette, alcohol, and coffee consumption and congenital defects. AJPH 1992;82(1):91-93. 169 chromosome 1-9c 1.02 (0.7-1.5), 10-19c 0.94 (0.7-1.3), 20+c 0.84 (0.6-1.2).

Lazar P, Gueguen S, Boue J, Boue A. Epidemiologie des avortements spontanes precoces: a propos de 1,469 avortements caryotypes. In: Boue A, Thibault C, eds. Les Accidents Chromosomiques de la Reproduction, Inserm Ministere de la Sante Publique et de la Securite Sociale, 1973, pp. 317-331. Reanalysis by Cuckle 1990, not age-adjusted. 231 other chromosome 0.87 (0.70-1.08); 287 trisomy 0.87 (0.72-1.05).

Malloy MH, Kleinman JC et al. Maternal smoking during pregnancy: No association with congenital malformations in Missouri. AJPH 1989;79(9):1243-1246. 330 chr. 0.99 (0.76-1.28). NOT SHOWN ON GRAPH:

Alberman E, Creasy M, Elliot M, Spicer C. Maternal factors associated with fetal chromosomal anomalies in spontaneous abortions. Br J Obstet Gynaecol 1976;83:621-627. 992 abnormals. "smoking history no longer had a significant effect when [its] relation to maternal age was allowed for," no detail.

SMOKING DOES NOT CAUSE BREAST CANCER

Bibliography on studies - The untold evidence A summary of the largest studies, based on the criteria of: Cigarette smoking and the risk of breast cancer. JR Palmer, L Rosenberg. Epidemiologic Reviews 1993;15(1):145-156. Their review concludes that smoking neither increases nor decreases risk. And, there is no suggestion of a dose/response, which is necessary to infer causation. "For purposes of this review, we excluded studies of prevalent disease... We also excluded studies with insufficient detail (e.g., lacking confidence intervals, number of exposed cases, and definition of the reference category); all of these studies had fewer than 300 cases. We further excluded case- control

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studies in which patients with smoking-related diagnoses were included in the control series," to eliminate biases which falsely lower risks. A dual study by Meara (1989) confirmed that screening studies tended to show risks above 1.0, and that hospital studies tended to show risks below 1.0. When one screening study (Schechter 1985) was updated in 1989, the originally reported risks of up to 3.6 had dropped to 0.9 to 1.2, just by the addition of new cases. Needless to say, the media ballyhooed the early claims, but not the later ones. "In five studies with healthy controls, the participation rates were less than 80 percent, low enough to admit the possibility that some or all of the modest increases in risk observed in smokers were due to bias." The authors of one (Chu et al) admit that "Telephone surveys have indicated that refusal rates in research studies are higher among persons with less education and lower income," who are more likely to smoke, which creates a deficiency of smokers among controls. They estimated a maximum bias of 0.1 in their study, which would make all their results non significant. Contrary to propaganda, "the many epidemiologic studies of endogenous estrogens have not produced a consistent explanation of how the estrogen environment affects risk....The relation between cigarette smoking and endogenous estrogens is also unclear...hormone studies in smokers and non- smokers have failed to demonstrate a consistent association." In other words, "a strong link between estrogen activity and cigarette smoking, or between estrogen levels and breast cancer, has not been demonstrated." The originator of the myth that smokers are estrogen-deficient was one B MacMahon (1982), and all of the 8 breast cancer studies he was involved in were rejected under the reviewers' control bias criteria.

STUDIES WITH OVER 1000 CASES:

Hiatt RA, Fireman BH. Smoking, menopause, and breast cancer. JNCI 1986;76(5): 833836. 1363 cases. <1p 0.95 (0.80-1.11), 1-2p 1.22 (1.05-1.43), 2+p 1.19 (0.88-1.60). Current smokers 1.08 (0.89-1.31).

Ewertz M. Smoking and breast cancer risk in Denmark. Cancer Causes Control1990;1:3137. 1480 cases. 1-4c 0.93 (0.69-1.25); 5-9c 1.05 (0.81-1.35); 10-14c 1.02 (0.82-1.28); 15-19c 1.01 (0.761.35); 20+c 0.75 (0.56-1.00). Current smokers 0.96 (0.74-1.25).

Brinton LA. Cigarette smoking and breast cancer. Am J Epidemiol 1986;123:614-622. (ACS/NCI). 1547 cases. <10c 1.15 (0.9-1.4); 10-19c 1.41 (1.1-1.8); 20-29c 1.15 (0.9-1.4); 30-39c 1.24 (0.9-1.8); 40+c 1.15 (0.8-1.6). Current smokers 1.18 (0.9-1.4).

Field NA, Baptiste MS et al. Cigarette smoking and breast cancer. Int J Epidemiol

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1992;21(5):842-848. 1617 cases; <1/2p 0.88 (0.73-1.06), 1/2-1p1.17 (1.00-1.37), 1 1/2p 0.87 (0.66-1.14), 2p 0.98 (0.70-1.39), >2p 1.16 (0.68-1.96) adjusted. Ever smokers 1.03 (0.90-1.19).

Baron JA, Byers T et al. Cigarette smoking in women with cancers of the breast and reproductive organs. JNCI 1986;77(3):677-680. 1741 cases. 1-14py 0.91(0.75-1.10), 15+py 0.93 (0.761.13).

London SJ, Colditz GA et al. Prospective study of smoking and the risk of breast cancer. JNCI 1989;81(21):1625-1631. 1788 cases. 1-14 c/d 0.98 (0.82-1.17), 15-24 0.99 (0.85-1.15), 25+ 1.02 (0.86-1.22), multivariate.

Palmer JR, Rosenberg L et al. Breast cancer and cigarette smoking: a hypothesis. Am J Epidemiol 1991;134(1):1-9. 1955 cases. <25c 1.2 (0.8-1.9), 25-34 1.2 (0.9-1.8), 35+ 1.1 (0.7-1.8). Current smokers 1.3 (1.1-1.6).

Rosenberg L, Schwingl PJ et al. Breast cancer and cigarette smoking. NEJM 1984;310(2):92-94. 2160 cases. 1-14c 1.3 (0.9-1.8), 15-24c 1.0 (0.8-1.4), 25+c 1.1 (0.8-1.6). Current smokers 1.1 (0.9-1.3).

Chu SY, Stroup NE et al. Cigarette smoking and the risk of breast cancer. Am J Epidemiol 1990; 131(2):244-253. 4720 cases. <15c 1.1 (1.0-1.3); 15-24c 1.2 (1.0-1.3); 25+ 1.2 (1.1-1.4). Current smokers 1.2 (1.1-1.3).

Stockwell HG. Cigarette smoking and the risk of female reproductive cancer. Am J Obstet Gynecol 1987;157:35-40. 5246 cases. <20c 1.3 (1.1-1.5), 20-40c 1.2 (1.0-1.4), >40c 1.2 (0.8-1.6), age adj. EXCLUDED BY PALMER AND ROSENBERG:

Vessey M, Baron J et al. Final report of an epidemiological study. Br J Cancer 1983;47:455462. 1176 cases. Heavy smokers 0.54 crude, 0.67 adj. [Baron 1984: 1-14 c/d 0.77]. Excluded for smoking related disease controls.

Centers for Disease Control. Long-term oral contraceptive use and the risk of breast cancer. JAMA 1983;249:1591-1595. In: Baron JA. Smoking and estrogen-related disease. Am J

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Epidemiol 1984;119(1):9-22. 1473 cases. Data from CDC author: ever smoker 0.99.

Garfinkel L. Cancer mortality in non-smokers: prospective study by the American Cancer Society. JNCI 1980;65:1169-1173. 3096 deaths. [Baron 1984:smokers 1.0. Excluded for inclusion of prevalent cases.]

SMOKING DOES NOT CAUSE BIRTH DEFECTS Bibliography on studies - The untold evidence The 1989 Surgeon General report (Reducing the Health Consequences of Smoking. 25 Years of Progress DHHS Pub No [CDC] 89-8411, 1989) insinuated that maternal smoking causes birth defects by mentioning only two small studies by Lelsey and Himmelberger that showed a risk. In the graphic at the bottom of this page is indicated the amount of excess risk established by each of the studies listed below. Please remember that anything smaller than 2.5 to 3.0 excess risk factor is considered insignificant by the scientific world, thus unworthy of consideration. Even in the highest risk case (Seidman, first on the left) the risk factor is smaller than 2.0. These studies cover a vast amount of cases, thus the base for their conclusions is a broad one. The studies covering less than 1,000 cases are not shown in the graph. Of particular interest is that, when the study considers the actual number of cigarettes smoked each day, there is NO CONSISTENT DOSE-RESPONSE relationship. For example, in the AD McDonald, et al. study, the non-existant "risk" actually became LESS as the number of cigarettes smoked INCREASED. There are several immutable "rules of the road" in the science of risk assessment -- one of them is that a clear and repeatable dose-response (the dose makes the poison) curve be displayed. In the case of maternal smoking and birth defects, there is simply no association. This is clear, unequivocal fact. No spin, no hype. Using scare tactics based on misinterpretations of scientific research to change human behavior is reprehensible, irresponsible and does tremendous damage to the reputations of the vast majority of scientists who conduct careful and meticulous research.

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Seidman DS, Ever-Hadani P, Gale R Effects of maternal smoking and age on congenital anomalies. Obstet Gynecol Dec. 1990;76:1046-1050. Israel, 1921 major defects, smokers 0.94 (0.621.43); minor 1,06 (0.90-1.25).

Kelsey JL, Dwyler T, Halford TR, Bracken MB Maternal smoking and congenital malformations: An epidemiological study. J Epidemiol Commun Health 1978:32:102-107. Retrospective case-control, random control at "several hospital in Connecticut," 1369 cases. 1-10 cigarettes 1.0, 11-20 1.1, 21-30c 1.4, >/= 31c 1.9; all smokers 1.10 (0.97-1.26).

Evans DR, Newcombe RG, Campbell H. Maternal smoking habits and congenital malformations: a population study. BMJ 1979 Jul 21;2:171-173. Cardiff, Wales Noted association with low class. Rates for all 1864 cases: 0 cigarettes 2.8%, 1-9 2.5%, 10-19 2.8%, >/= 20 3.0% [calculated relative risk for smokers 0.89, 1.0, 1.07].

MacDonald AD, Armstrong BG, Sloan M. Cigarette, alcohol, and coffee consumption and congenital defects. AJPH Jan 1992;82(1) : 91-93. 1928 total. 1-9 cigarettes 1.14 (1.0-1.4), 10-19 1.08 (0.9-1.2), 20+ 1.02 (0.9-1.2).

Christianson RE. The relationship between maternal smoking and the incidence of congenital anomalies. Am. J of Epidemiol 1980;112(5):684-695. Kaiser Foundation. "There was no significant differences in the incidence of congenital anomalies" overall. 2077 total cases. RRs white light smokers, male child 1.03, female 0.91; heavy smoker m 1.22, f 1.05; black ls m 0.92, f 0.95; hs m 1.18, f 1.11.

Heinonen OP, Slone D, Shapiro S, eds. Birth defects and drugs in pregnancy. Littleton, MA: Publishing Sciences Group, 1977. Collaborative Perinatal Project prospective. 2277 cases. All malformations, 1050 white 14 cigarettes 0.9, 15-29 1.0, >/= 30 0.9; 1097 black 1.0 1.0 1.0.

Van Den Eeden SK, Karagas MR, Daling JR, Vaughan TL. A case-control study of maternal smoking and congenital malformations. Paediatr Perinatal Epidemiol 1990;4:147- 155. 3048 malformations, smokers 1.0 (0.9-1.1).

Shiono, PH, Klebanoff MA, Berendes HW. Congenital malformations and maternal

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smoking during pregnancy. Teratol 1986;34:65-71. Kaiser-Premanente prospective. 5624 total cases: 592 major, smokers 1.0 (0.8-1.2); 4032 minor, smokers 0.9 (0.8-0.9).

Malloy MH, Kleinman JC, Blakewell JM, Schramm WF, Land GH. Maternal smoking during pregnancy: No association with congenital malformations in Missouri. AJPH 1989 Sep:79 (9):1243-1246. Total 10,223, smokers 0.98 (0.94-1.03).

LESS THAN 1,000 CASES, NOT SHOWN ON GRAPH:

Andrews J, McGarry JM. A community study of smoking in pregnancy. J Obstet Gynaecol Br Commonw 1972 Dec;79 (12):1057-1073. Cardiff, Wales. 509 cases. Non-smokers 2.37%, smokers 2.73% abnormal infants.

Himmelberger DU, Brown BW, Cohen EN. Cigarette smoking during pregnancy and the risk of spontaneous abortion and congenital anomaly. Am J Epidemiol 1978;108 (6) : 470- 479. Trace Anesthetic Study, retrospective mail survey of health professionals, 935 cases, All smokers from 0.90 to 2.34, depending on parity and age.

HOW THE ANTI-SMOKERS LIE ABOUT SMOKING AND VITAMIN C The influence of smoking on Vitamin C status in adults. G. Schectman, JC Byrd, HW Gruchow. American Journal of Public Health, Feb. 1989;79 (2):158-162 Gordon Schectman, whose claim that 91% of smokers are suffering from a Vitamin C deficiency has been uncritically and frequently recycled in the media, is not even qualified to make any dietary recommendations. This is because his findings are based on interviews, not measurement of dietary intake of nutrients. A recent US Department of Agriculture found that even trained peoples' reports do not agree with the results of metabolic ward studies. About 80% under-reported their intakes, while a small minority overreported them. The US RDAs are also based upon careful laboratory study, not sloppy interviews. They were also established at a time when smoking was even more prevalent than now, and could not have failed to either detect or reflect an influence of smoking -- especially of such a magnitude as 200%.

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The RDAs were expressly developed "to provide for individual variations among most normal persons as they live in the United States under usual environmental stress," of which smoking is negligible. Desaturation experiments have shown that smokers use Vitamin C no faster than non-smokers. The recent increase to 100 mg reflects the political strength of health obsessiveness as well, perhaps, as pharmaceutical company desires for profits. At this intake, experiments have shown that tissues will be saturated, with white blood cell levels at 25 to 30 mg/100 ml, and serum levels above 1 mg/100 ml. If intake is increased, WBC and tissue levels will stay the same, while serum levels will rise to a maximum of about 1.89 mg/100 ml. Marginal risk of deficiency doesn't occur until levels of 0.4 mg/100 ml. One cup of orange juice provides about 120 mg of Vitamin C. (The minimum for prevention of scurvy is a little less than 10 mg per day.) If average, healthy people have low levels, it is because they are disregarding dietary advice. Schectman's measurements were of serum Vitamin C. These do not give an accurate measure of tissue levels, which are more important. Particularly at low levels, white blood cell readings are necessary. Serum levels also fluctuate hourly with intake. Higher WBC levels tend to correlate with lower plasma values. Plasma values tend to become lower as metabolic demands decrease, as with age. The mean Vitamin C level he measured in smokers was nearly 90% of saturation. It is impossible that only 9% of smokers get adequate Vitamin C, as he claims. And no ethical researcher would go around telling people that they are sick when they are not. Were properly controlled studies to show that smoking depleted Vitamin C, the proper response would be to notify the media that smokers should have this information in a value neutral statement.

Additional references: Methods for detecting and evaluating ascorbic acid deficiency in man and animals. HB Burch. In: Annals of the New York Academy of Sciences, Vol 92:269-275. Humane In: Annals of requirements for Vitamin C and its use in clinical medicine. GA Goldsmith. the New York Academy of Sciences, Vol 92:230-245. What are people really eating? The relation between energy intake derived from estimated diet records and intake determined to maintain body weight. W Mertz, JC Tsui, JT Judd, S Reiser, J Hallfrisch, ER Morris, PD Steele, E Lashley. American Journal of Clinical Nutrition 1991;54:291-295. Smoking and Vitamin C levels in humans. O Pelletier. American Journal of Clinical Nutrition Nov 1968;21(11):1259-1267.

Relationship Wilson.

between leucocyte and plasma ascorbic acid concentrations. HS Loh, CWM British Medical Journal 25 Sep 1971;3:733-735.

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THE ANTI-SMOKERS LIED ABOUT SMOKING AND VASOCONSTRICTION "Because of the relative ease with which blood flow can be estimated in the human hand and foot, the vascular innervation of these extremities has been extensively studied. It should be stressed, however, that the vasculature of the hand and foot is highly specialized and adapted to serve temperature regulation. Therefore considering vasomotor responses in the hand to be representative of those occurring in other tissues leads to false impressions of vasomotor regulation in the body. Conclusions from the experiments in hand skin cannot be extrapolated to forearm skin, let alone to the other tissues of the body." (IC Roddie. Circulation to the skin and adipose tissue. In: Handbook of Physiology: The Cardiovascular System III. The American Physiological Society. JT Sheperd, FM Abboud, eds. Oxford Univ Press 1983. Chapter 10 pp 285-317.) The hand has primarily vasoconstrictor innervation, while the forearm is primarily vasodilator. But in their endless quest for pseudo-scientific propaganda, the anti-smokers routinely misuse hand skin studies as "supporting evidence" that smoking causes vasoconstriction, ischemia, and various other harmful circulatory effects in virtually every organ of the body. The simplistic line that "smoking causes vasoconstriction" has been one of the most versatile myth-making tools. Nicotine is actually a direct-acting vasodilator when there is no innervation (Fewings JD et al. Brit J Pharmacol 1966;26:567-579; Mitolo-Chiepa D. Boll Soc Ital Biol Sper 1968;44:892-893). Mental stress, exercise, cold pressor test, serotonin, acetylcholine and smoking all constrict a stenosed artery segment, but dilate a normal one. 1991;324:641-648.) (AC Yeung et al. NEJM 1991;325:1551-1556; and P Golino et al. NEJM

But the anti-smokers misrepresent this nonspecific paradoxical constriction of stenotic artery as evidence that smoking causes cardiac ischemia. And they attempt to blame smoking, but not mental arithmetic serotonin, etc., for causing heart disease out of purely ideological motives.

Although muscle perfusion is opposite to that of skin (Redish W et al. Angiol 1968;19:232-237), antismokers lie that smoking reduces blood flow to the muscles, supposedly causing cramps. Because vasoconstrictor action in inhibited at high temperature, the anti-smoker claim that smoking increases the risk of heat stroke is fraudulent. Roddie: "If the circulation to the hand is arrested with a pneumatic cuff... release of the occlusion is followed by flushing of the skin of the hand and an increase in hand skin temperature. The degree of flushing is related to the duration of the ischemia. When the hand is warm, the reactive hyperaemia is greater than when it is cold." If the smokers hands were cold, which they are usually contended to be, that should have been considered in accounting for the slightly decreased reactive hyperaemia that Tur et al. (Angiology 1992;43:328-335) attributed to impaired microvasculature in smokers. And their claim that "reactive hyperaemia plays an important role in protecting, or at least limiting, tissue damage following the ischemia," should be weighed against the

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evidence that it causes damage via free radicals. And how about the hyperaemia following injury, for which we are advised to apply ice? (Because these people are fundamentally hate propagandists, they probably would have claimed the opposite if they had seen more reactive hyperaemia in smokers!) Roddie: "Blood flow in the hands and feet is very labile," and the vessels "undergo waves of constriction and dilation when the subject is comfortably warm..." Hand blood flow tends to fall in response to minor sensor stimuli, and "many stimuli that have an alerting effect cause strong transient vasoconstriction in the hands and feet that last about 60 s."

And in an experiment involving mental arithmetic, JK Wilkin et al. (Arch Dermatol 1987;123:1503-1506) found, "During the period of mental activity, cutaneous blood flow in the finger fell to 59%, digital cutaneous pulse fell to 62%, and heart rate increased by 24% of the subjects' initial baseline values." These changes are of a magnitude larger than those which have been attributed to smoking, which has also been found to have an arousing effect in EEG. However, "Cutaneous blood flow in the malar region [cheek] did not change. Because vasomotor control of the finger skin is principally vasoconstrictor and that of the malar area vasodilator, these results suggest that mental activity unrelated to obvious stress may provoke changes in cutaneous blood flow in areas controlled by sympathetic vasoconstrictor fibres." He also notes that "the face has a poor vasoconstrictor supply and stimuli that provoke intense vasoconstriction on the finger are ineffective on the face." But the anti-smokers have put out reams of hate propaganda claiming to be able to instantly detect a "smokers' face" by its pallor, supposed due to "intense vasoconstriction," and embellished with malicious speculation about "microvascular damage," collagen abnormalities, and wrinkles. The anti-smoker delusion of massive vasoconstriction is integral to their lie that smoking causes high blood pressure. Most studies in the 1960s found that smokers actually has somewhat lower blood pressure (Lasrson PS, Silvette H. In: Tobacco: Experimental and Clinical Studies. A Comprehensive Account of the World Literature. Baltimore: The Williams & Wilkins Co., 1971 pp. 81-83), but it was speculated that smokers' lower weight was the reason. In the following years, a torrent of propaganda obliterated the truth. But a recent ambulatory blood pressure monitoring study by MS Green (Am Heart J 1991;121:1569-1570), plus confirmation from others, has resulted in a sudden rediscovery of the truth.

SMOKING AND THE DECLINE IN HEART ATTACK DEATHS At a superficial glance, declines in smoking and declines in ischemic heart disease (heart attack or myocardial infarction) appear to correlate. From 1963 (the peak year) to 1985, the age-adjusted death rate fell by 42%. But the decline in IHD has been much greater than the decline in smoking. And when the data are analyzed by sex, the discrepancy is even more marked. Smoking has declined less in women than in men (16% v 37%), and even anti-smokers claim less IHD risk in women from smoking, yet the decline in IHD has been proportionally equal in men and women. Women began quitting later than men, but the decline began at the same time. A much greater percentage of older women smoke than in the past, which would supposedly cause an increase in the death rates in those age groups, yet the decline in IHD has been about the same as at younger ages. Women's IHD death rates declined in 26 countries from 1950 to 1978, while men's increased in most of those countries during this time.

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Other factors that doctors like to invoke don't explain the IHD decline, either. Deaths from high blood pressure began declining around 1950, while IHD was still increasing. Death rates fell just as quickly among the old, who did not embrace the exercise mania of the young. IHD increased during the Depression, rather than decreasing as they would if a rich diet caused it. The decline began before there were any large-scale changes in diet, which are not sufficient to account for it anyhow. Nor are improvements in treating heart attacks; 60-70% of deaths still occur outside the hospital. Whatever caused the decline affected both sexes, and all ages and races, simultaneously and equally, with greater strength than any known influence. The 1978 Conference on the Decline in Coronary Heart Disease Mortality (of the National Heart, Blood, and Lung Institute) concluded that they did not know why the rise occurred, why it ended, or why it turned downward. Like other explanations, decreased smoking does not fit the ticket. Main references: Mortality data are from Vital Statistics of the United States 1950-1989.

Higgins MW, Luepker RV. Preface and Appendix. In: Trends in coronary heart disease. Higgins MW, Luepker RV, eds. New York: Oxford Univ Press, 1988. pp vii-x.

Stallones, RA. The Rise and Fall of Ischemic Heart Disease. Sci Am 1980 Nov;243(5):53-59.

Thom TJ, Maurer J. Time trends for coronary heart disease mortality and morbidity. In: Trends in coronary heart disease. Higgins MW, Luepker RV, eds. New York: Oxford Univ Press, 1988. pp 7-15, Ch 1. Smoking and cervical cancer | Details: Type: Bibliographical compendium Further Information As it is clear that antismoking propaganda associates active and passive smoking with almost any disease conceivable, cervical cancer could not be missing on the list. It has been said, in fact, that active and passive smoking causes cervical cancer. However, not even questionnaire-based epidemiology has been able to point at the smokingcervical cancer scare. Already in 1994 serious questions were posed against this "political" association, and it turned out that the weak association could be explained with confouders not properly taken into account in original analyses. More and more, in fact, it is becoming crystal-clear clear that cervical cancer most often has viral origins. Following is a short compendium of documentation from the FORCES Archives demonstrating that, once again, fear, prejudice and superstition to say nothing of political bias have been used to once again hit a style of life that no longer enjoys the favour of the so-called majority. The elite decress what it likes and calls it "science." Absurd contradictions

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Note that despite the publication in April 1996, in JNCI Monograph 21, of the NIH Consensus Statement on cervical cancer that is tantamount to abandoning the claim that smoking causes cervical cancer, in 1997 JNCI still published two completely inaccurate letters attempting to insinuate that there is such a connection (Tokudome S. Semen of smokers and cervical cancer risk. JNCI 1997;89:96-97; and Phillip Whidden [of Association for Nonsmokers' Rights] JNCI 1997;89:520). The Tokudome letter conveyed the falsehood that "tobacco smoke constituents/metabolites or mutagens/carcinogens will be conveyed to the cervical mucus and act as independent initiators/promoters in the carcinogenesis or interact with the oncogenes of HPV" in active smoking. This has been discredited by FX Bosch et al. (Int J Epidemiol 1994 Oct;23(5):11001101, with a repudiation of Whidden by Phillips & Davey Smith on the same page). It was shown to be the result of confounding, because there is no association of smoking with cervical cancer in known HPV positives. Tokudome cited nothing but such presumptively confounded studies blaming ETS for cervical cancer in non-smokers as well. Furtheremore, Tokudome speculated that "tobacco-related mutagens/carcinogens in a smoking sex partner's semen/seminal fluid are applied directly to the cervix mucus membrane during sexual intercourse and may possibly play some role in the pathogenesis of cervical cancer," citing no more support for this than studies showing that condoms, which reduce HPV infections, reduce cervical cancer. Whidden added to this bizarre contention with remarks that "digital stimulation of the vagina by fingers coated with tobacco tars -- might well add up to a significant burden and might provide a trigger for a rise in risk for cervical cancer in women whose long-time male sexual partners are smokers." !! The editors of the Journal of the National Cancer Institute know that it is reckless and irresponsible to publish such speculations in the absence of evidence of any disease in need of explanation by them. Smoking does not cause cervical cancer in the first place. It was falsely blamed for disease caused by HPV. These short letters, however, are very useful tools for antismoking propaganda; and of course they were publicized in the mass media as well, with the implication that with the "prestige" of the Journal of the National Cancer Institute behind them, they must be true. Causal relationship The causal relation between human papillomavirus and cervical cancer. FX Bosch, A Lorincz, N Muoz, CJLM Meijer, KV Shah. J Clin Pathol 2002 Apr;55(4):244-265. Review. "The causal role of human papillomavirus infections in cervical cancer has been documented beyond reasonable doubt. The association is present in virtually all cervical cancer cases worldwide... This association has been evaluated under all proposed sets of causality criteria and endorsed by the scientific community and major review institutes. The finding is universally consistent, and to date there are no documented alternative hypotheses for the aetiology of cervical cancer."

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Worldwide human papillomavirus etiology of cervical adenocarcinoma and its cofactors: implications for screening and prevention. Papillomavirus research update: highlights of the Barcelona HPV 2000 international papillomavirus conference - "One phenomenon of interest in relation to risk of cervical cancer is the so-called male factor. Essentially, this is taken to mean that the sexual behavior of men (for example, the number of sexual partners that they have had) can influence the risk of cervical cancer in their female sexual partners. In this regard, Bleeker et al. presented data showing that 80% of the male sexual partners of women with CIN had penile lesions, of which a substantial portion were infected with HPV, and they speculated that penile lesions in sexual partners of women with CIN are probably productive and that they might play an important role in influencing the course of cervical lesions in these women by continuously reinfecting them with HPV." This is just a small sample of the vast amount of documentatioon that demonstrates that smoking - active or passive - has nothing to do with cervical cancer, and that the Human Papillomavirus is to blame. Yet, still to date, we see attempts to push the responsibility of this cancer on the smokers - either on themselves or on the nonsmokers. Relying on popular ignorance has always been the main path of antismoking propaganda.

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SMOKING AND CERVICAL CANCER May 5, 1996

In a recent paper, A N Phillips and George Davey demonstrated mathematically that smoking could be falsely blamed for cervical cancer by failure to detect all exposure to a causative pathogen with a high risk. Subsequently, Bosch et al re-analyzed their cervical cancer study data to assess whether this had happened. They found that "when HPV [human papillomavirus] positive women are examined, thus removing those with potential undetected HPV, the odds ratios os cervical cancer in five data sets 3 on invasive cancer and 2 of CIN III lesions) were consistently and statistically not different from 1" for cigarette smoking. They concluded, "Real data are thus in agreement with the model proposed by Phillips and Smith". Since the studies claimed by anti-smokers to show that smoking causes cervical cancer invariably fail to test their results in this way, they are therefore making a false and spurious claim based on their own methodological malpractice. This also explains why these studies routinely show cervical cancer risks associated with low education that are equal to or greater than those claimed for smoking, which they never feel compelled to invent any specious theories of biological plausibility to explain. And, these results indicate that studies blaming secondhand smoke for cervical cancer in passive smokers are actually just exploiting the socio-economic similarity between smokers and passive smokers.

THE LETTER FROM ANDREW PHILLIPS AND GEORGE DAVEY SMITH to BOSCH et al. Sir- Whidden suggests that studies underestimate the effect of smoking by comparing smokers with a baseline group who are themselves exposed, albeit passively, to cigarette smoke. Two meta-analyses have estimated the summary relative odds for the 'independent' effect of current smoking compared with non-smoking to be 1.46 and 1.69. [1,2] Even if one believe the effect to be causal, given the modest size of the difference in risk of cervical cancer in women who actively smoke versus those who do not, it seems unlikely that there is substantial difference in risk between non-smokers in a smoking environment and non-smokers in a non-smoking environment. Therefore, even if thew comparison group were nonsmokers in a non-smoking environment the relative odds estimates are unlikely to be much larger. Even so, we illustrated that relative risks of as high as two and above could easily arise merely as a result of the inability to fully adjust for exposure to the sexually transmitted pathogen involved [3] . This was based on plausible estimates of the association between the presence of the aetiological pathogen and both smoking and risk of cervical cancer. The conclusion holds equally whether one is comparing active smokers with all non-smokers or active smokers with non-smokers in a non-smoking environment. Further, in the study which Whidden says 'claims to have proven that second-hand smoking is definitely a risk factor for this cancer [4] the adjusted relative odds associated with passive smoking (which was 2.96) was almost the same as that associated with active cigarette smoking (3.42). As pointed out by Layde [5] since active cigarette smokers are also passive smokers because of the side-stream smoke from their own cigarettes they would be expected -- if passive smoking truly contributes to the development of

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SMOKING AND BRAIN CANCER

Brain Cancer: No Association With Smoking - Since smoking is now erroneously credited with causing almost every ailment known to man, the results of a study conducted on brain cancer is noteworthy because the scientists set out to discover whether smoking is responsible for its increasing frequency in industrial societies. "Some have suggested that cigarette smoking and other tobacco product use may increase the risk of brain tumors because tobacco product use is considered to be the greatest source for human exposure to N-nitroso compounds, which are potent nervous system carcinogens in animal studies. Our investigation, however, did not find a positive association between cigarette smoking, or with use of other tobacco products, and risk of brain cancer." Note that the researchers' focus on N-nitroso compounds, which are labeled "potent nervous system carcinogens" but only in animal studies. One is justified in assuming that these compounds have never been proven to be potent or harmful in the tiny doses obtained from smoking tobacco.

SMOKING DOES NOT CAUSE UROGENITAL BIRTH DEFECTS Bear in mind that 1.0 equals NO EXCESS RISK. Risks of less than 2.0 or results that include "zero" within their range of results (for example, 0.8 - 1.18) are considered extremely weak results and viewed with skepticism by responsible scientists.

Summary of findings of studies of urogenital birth defects, including hypospadias: Seidman DS, Ever-Hadani P, Gale R. Effect of maternal smoking and age on congenital anomalies. Obstet. Gynecol Dec. 1990; 76: 1046-1050. RATES/K, 10 genitourinary 0c 0.4, <1p 1.3, >/=1 p 1.8; 62 hypospadias 0c 3.5, <1p 3.2, >/= 1 p 4.4 [calculated crude relative risk gu 3.25 4.5; hyposp. 0.9 1.26].

Andrews, J, McGarry JM. A community study of smoking in pregnancy. J Obstet Gynaecol Br Commonw 1972 Dec; 79(12): 1057-1073. Cardiff. In %: 64 genitourinary, 39n 0.43, 25s 0.33 [calculated crude relative risk 0.77]

Himmelberger DU, Brown BW, Cohen EN. Cigarette smoking during pregnancy and the risk of spontaneous abortion and congenital anomaly. Am J Epidemiol 1978; 108(6): 470-479. Trace Anesthetic Study, retrospective mail survey of health professionals. Rates/1000 186 urogen s21.32 n 15.81. [calculated crude relative risk 0.74]

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Heinonen OP, Slone D, Shapiro S, eds. Birth defects and drugs in pregnancy. Littleton, MA: Publishing Sciences Group, 1977. Collaborative Perinatal Project prospective. genitourinary 366, no total RR. Hypospadias 187 /= 30c 2.0 (14 cases), >/= 30c 1.7 [subgroup].

Van Den Eeden SK, Karagas MR, Daling JR, Vaughan TL. A case-control study of maternal smoking and congenital malformations. Paediatr Perinatal Epidemiol 1990; 4:147-155. 206 hypospadias 0.8 (0.5-1.1).

McDonald, AD, Armstrong BG, Sloan M. Cigarette, alcohol, and coffee consumption and congenital defects. AJPH Jan 1992; 82(1):91-93. 209 renal/urinary 1-9c 1.55 (1.0-2.5), 10- 19c 1.42 (0.9-2.1), 20+c 1.17 (0.8-1.8).

Christianson, RE. The relationship between maternal smoking and the incidence of congenital anomalies. Am J Epidemiol 1980; 112 (5): 684-695. Kaiser Foundation. Rates/1000: 218 genitourinary never 15.1, 1-19c 15.6, >/=20c 14.1. [calculated crude relative risk 1.03, 0.93]

Evans, DR, Newcombe RG, Campbell H. Maternal smoking habits and congenital malformations: a population study. BMJ Jul 21 1979; 2:171-173. Cardiff. Rates/1000 308 genitourinary 0c 4.6, 1-9c 4.5, 10-19c 4.4, 20+c 4.9. [calculated crude relative risk 0.98, 1.06].

Shiono, PH, Klebanoff MA, Berendes HW. Congenital malformations and maternal smoking during pregnancy. Teratol 1986: 34:65-71. Kaiser-Permanente prospective. 202 crytorchism 1.2 (0.9-1.7); 101 hypospadias 1.0 (0.7-1.6); 536 hydrocele 0.7 (0.6-0.9); 32 other m sex 0.8 (0.4-1.8); 68 other f sex 1.1 (0.7-1.8); 13 renal agenesis 1.1 (0.3-3.6); 18 other renal 0.3 (0.1-1.4); 13 other urogential 1.1 (0.3-3.6). [0.87 overall].

Malloy MH, Kleinman JC, Bakewell JM, Schramm WF, Land GH. Maternal smoking during pregnancy: No association with congenital malformations in Missouri. AJPH 1989 Sep;79(9): 1243-1246. 1622 Genitourinary 0.97 (0.86-1.08).

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SMOKING DOES NOT CAUSE MYOCARDIAL INFARCTION Myocardial infarction: "Glucose level and systolic blood pressure were associated with the incidence of MI, but smoking and lipid measures were not." Oops! Remember all the noise in 1998 about smoking and intimal-medial thickening? Where is the media now?

The American Medical Association seems to be conveniently quiet on this study, though published in its own archives. It does not take great intelligence to understand the reasons. Traditional Risk Factors and Subclinical Disease Measures as Predictors of First Myocardial Infarction in Older Adults The Cardiovascular Health Study

SMOKING DOES NOT CAUSE MUSCULOSKELETAL BIRTH DEFECTS Study after study fails to find ANY consistent, positive correlation between smoking and musculoskeletal birth defects. In fact, many studies show a negative correlation -- that is smoking during pregnancy could result in fewer defects than not smoking. Basically, the lack of consistency in results makes it clear that smoking is not the factor that should be under study in the matter -- it is obvious that other factors are involved.

Andrews J, McGarry JM. A community study of smoking in pregnancy. J Obstet Gynaecol Br Common: 1972 Dec; 79(12): 1057-1073. Cardiff. Crude rates in %: 117 bone, 65n 0.72n, 52s 0.68 [calculated relative risk 0.94].

Kelsey JL, Dwyer T, Holford TR, Bracken MB. Maternal smoking and congenital malformations: an epidemiological study. J Epidemiol Commun Health 1978; 32:102-107. Retrospective case-random controls "at several hospitals in Connecticut." 50 poly-syndactyly 1-20c 0.6, 21+c 1.6; 91 other musculoskeletal 1-20c 0.8, 21+c 1.1.

Himmelberger DU, Brown BW, Cohen, EN. Cigarette smoking during pregnancy and the risk of spontaneous abortion and congenital anomaly. Am J Epidemiol 1978; 108 (6): 470-479. Trace Anesthetic Study, retrospective mail survey. Crude rates/1000: 222 musculoskeletal s23.84, n19.69 [calculated relative risk 1.21].

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McDonald AD, Armstrong BG, Sloan M. Cigarette, alcohol, and coffee consumption and congenital defects. AJPH Jan. 1992;82(1):91-93. 223 musculoskeletal 1-9c 1.07 (0.6-1.8), 10-19c 1.29 (0.9-1.9), 20+c 0.73 (0.5-1.2).

Aro T. Maternal diseases, alcohol consumption and smoking during pregnancy associated with reduction limb defects. Early Human Dev. 1983;9:49-57. Finland, registry, retrospective, 453 cases 1.3 (0.9-2.0) adjusted for age >35, alcohol; 329 isolated RLD 1.7 (1.0-2.8).

Christianson RE. The relationship between maternal smoking and the incidence of congenital anomalies. Am J Epidemiol 1980; 112 (5):684-695. Kaiser Foundation prospective. Crude rate/1000 453 musc/skel never 33.5, 1-19c 23.5, >/= 20c 29.7 [calculated relative risks 1-19c 0.70, >/= 20c 0.89].

Hemminki K, Mutagen P, Saloniemi T: Smoking and the occurrence on congenital malformations and spontaneous abortions: Multivariate analysis. Am J Obstet Gynecol Jan 1 1983; 145:61-66. Finnish Register. 521 musc/skel, any s 1.31/1.02 adj; 335 regular s 1.32/0.90 adj; 218 >/= 5c 1.36/0.75 adj.

Van Den Eeden SK, Karagas MR, Daling JR, Vaughan TL. A case-control study of maternal smoking and congenital malformations. Paediatr Perinatal Epidemiol 1990;4: 147-155. 571 skeletal (171 club foot, 95 poly-, 74 syn- & 14 adactyly, 35 other limb reduction, 215 hip dislocation) 1.1 (0.91.3).

Evans DR, Newcombe RG, Campbell H. Maternal smoking habits and congenital malformations: a population study. BMJ July 21 1979; 2:171-173. Cardiff. Crude rates/1000: 715 musc/skel )o 11.3, 1-9c 9.3, 10-19c 9.9, 20+c 10.4 [calculated relative risk 1-9c 0.82, 10-19c 0.88, 20+c 0.92].

Shiono PH, Klebanoff MA, Berendes HW. Congenital malformations and maternal smoking during pregnancy. Teratol 1986;34:65-71. Kaiser-Permanente prospective. 17 limb reductions 2.2 (0.9-5.8); 34 syndactyly 0.7 (0.3-1.5); 44 skull 1.1 (0.6-2.0); 71 hip dysplasia 0.6 (0.3-1.1); 73 polydactyly 1.0 (0.6-1.6); 80 other musculoskeletal 1.4 (0.9-2.2); 407 other limb 0.9 (0.7-1.1). 726 total.

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Malloy MH, Kleinman JC, Bakewell JM, Schramm WF, Land GH. Maternal smoking during pregnancy: No association with congenital malformations in Missouri. AJPH 1989 Sep;79(9):1243-1246. 3705 musculoskeletal 0.99 (0.92-1.06). Not shown on graph:

Heinonen OP, Slone D, Shapiro S, eds. Birth defects and drugs in pregnancy. Littleton, MA: Publishing Sciences Group, 1977. Collaborative Perinatal Project prospective. 404 musculoskeletal (including polydactyly) smoking nonsignificance in MLR, no detail.

SMOKING DOES NOT CAUSE MULTIPLE MYELOMA

When the Mills study of multiple myeloma among Seventh-Day Adventists claimed in 1990 that smokers had over three times the risk of non-smokers, the national media eagerly trumpeted it as yet another new danger of smoking. This was despite the fact that previous studies actually found a slightly reduced overall risk among smokers, and that Mills' 21 cases represented not even 3% of the multiple myeloma cases studied to that date. It's a classic "little tiny study with a great big headline." Just as important is the basic epidemiological principle that cases and controls should be as ALIKE as possible except in the condition or protocol being studies. Seventh-Day Adventists are not representative of the general population. Their drinking, smoking, dietary and exercise habits are well outside the parameters of the population at large. In effect, using them as a "control group" is not only scientifically unsound; it borders on the absurd.. What is more, even Mills et al. later admitted that "recent evidence from this study has indicated the presence of substantial 'healthy volunteer effect' during the first few years of follow-up, suggesting that it may be inappropriate to compare participants in a study such as this with the general population." Judging by its discrepant finding, which doesn't even agree in direction with others, it probably has a "healthy volunteer effect" operating internally as well, involving the from-birth Adventists more than the converts from whom most of the smokers and ex-smokers were drawn. Most importantly, this Adventist study has been the basis of major anti-smoking propaganda, namely the Repace and Lowrey claim of 5,000 deaths (Environ Int 1985;11:3-22). But the antismoker and the mainstream media have never retracted their false claim. * Mills PK et al. History of cigarette smoking and risk of leukaemia and myeloma: Results from the Adventist Health Survey. JNCI 1990;82:1832-1836. 21 cases <5 cigs per day 3.58 (0.95-13.50); 5-14 2.26 (0.47-10.80); 15+ 3.63 (1.17-11.25). * Linet MS et al. Is cigarette smoking a risk factor for non-Hodgkin's lymphoma or

46

multiple myeloma? Results from the Lutheran Brotherhood Cohort Study. Leuk Res. 1992 Jun-Jul; 16(6-7): 621-624. 21 Cases. Ever 1.3 (0.4-3.9), no dose-response. * Hammond EC, Horn D. Smoking and deaths rates - Report on forty-four months of follow-up of 187,783 men. II. Death rates by cause. JAMA 1958 Mar. 15;166(11):12941308. 28 cases. Regular smokers 0.66. Gallagher RP myeloma. Br. et al. Allergies and agricultural exposure as risks factors for multiple J Cancer 1983;48:853-857. 84 cases, 0.48 not significant. Williams RR, Horm JW. Association of cancer sites with tobacco and alcohol consumption and socioeconomic status of patients: Interview from the Third National Cancer Survey. JNCI 1977 Mar; 58(3):525-547. 40 male cases, by amount smoked: 0.97, 0.37, 1.0; 46 females, 1.25, 2.26, 0.65. Linet MS et al. A case-control study of multiple myeloma in whites: Chronic antigenic stimulation, occupation, and drug use. Cancer Res. 1987;47:2978-2981. 100 cases, male & female. "No increased risk was found for cigarette smoking," no detail. Flodin U et case-referent smokers 0.78 al. Multiple myeloma and engine exhausts, fresh wood, and creosote: A study. Am J Ind Med 1978;12:519-529. 131 cases, male & female. Current (0.4-=1.3). Brown LM et al. Smoking and risk of non-Hodgkin's lymphoma and multiple myeloma. Cancer Causes Control 1992;3:49-55. 173 cases. Any tobacco 1.0 (0.7-1.6); cigarettes only 1.3 (0.8-2.0). * Boffeta LM Cancer Ever 0.9 (0.6et al. A case-control study of multiple-myeloma nested in the American Society prospective study. Int J Cancer 1989;43:554-559. (CPS-II) 282. 1.3) Mantel-Haenszel; 0.9 (0.6-1.4) logistic regression. * Heineman EF et al. A prospective study of tobacco use and multiple myeloma: evidence against an association. Cancer Causes Control 1992;3(1):31-36. Cases = 582 male veterans. Current 0.9 (0.8-1.2). No dose-response. Herrinton LJ 1992 Jul; 3 selfet al. (comment) Smoking and multiple myeloma. Cancer Causes Control (4):391-392. 689 cases. Current 0.8 (0.7-1.1) all respondents; 0.7 (0.5-0.9) respondents. Brownson RC Cigarette smoking and risk of myeloma (letter re Mills). JNCI 1991;83:1036-1037. 824 cases. Ever 1.03 (0.85-1.25) no dose-resp.: <20 1.07 (0.73-1.58), 20+ 1.03 (0.77-1.37).

SMOKING DOES NOT CAUSE CONGENITAL HEART DEFECTS In the graphic at the bottom of this page is indicated the amount of excess risk established by each of the studies listed below. Please remember that anything smaller than 2.5 to 3.0 excess risk factor is considered insignificant by the scientific world, thus unworthy of consideration. Even in the highest risk case (Seidman, first on the left) the risk factor is

47

smaller than 2.0. These studies cover a vaste amount of cases, thus the base for their conclusions is a broad one. The studies covering less than 1,000 cases are not shown in the graph. Where does the competence of health 'authorities' ends and lies begin? ...WHAT "mountain of evidence"?

Seidman DS, Ever-hadani P. Gale R. Effect of maternal smoking and age on congenital anomalies. Obstet Gynecol Deco 1990:76:1046-1050. 62 [calculated from rates/1000] cardiovascular Oc 3.5, (1p 3.9, >/= p 3.5. [calculated crude risk ratio <1p 1.1, >/=1p 1.0].

Andrews J, McGarry JM. A community study of smoking in pregnancy. J Obstet Gynaecol Br Common 1972 Dec; 79(12):1057-1073. Cardiff. 66 cardiovascular system abnormalities. Crude rates: nonsmokers 0.37%, smokers 0.42%. [calculated risk ratio 1.14].

Yerushalmy J. (letter re Fredrick). Nature 1973 Mar 23;242:262. Prospective. All races 38/115 (33%)s CHD v 5158/14,616 (35.3%)s no CHD; White 31/78 (39.7%)s v 3735/9812 (38.1%)s.

Christianson RE. The relationship between maternal smoking and the incidence of congenital anomalies. Am J Epidemiol 1980;112(5):684-695. Kaiser Child Health & Development Study. 12 malformation of circulatory system. Crude rates/1000 never 8.4, ex 10.7, 1-19c 6.6, >/=20c 10.8. [calculated risk ratio 1-19c 0.79, >/=20c 1.29].

Himmelberger DU, Brown BW, Cohen EN. Cigarette smoking during pregnancy and the risk of spontaneous abortion and congenital anomaly. Am J Epidemiol 1978;108(6):470-479. Trace Anesthetic Study, retrospective mail survey of health professionals. 163 cardiovescular malformations, crude rates/1000: smokers 19.07, nonsmokers 13.65 [calc. rel. risk 1.4].

Shiono PH, Klebanoff MA, Berendes HW. Congential Malformations and Maternal Smoking During Pregnancy. Teratol 1986:34:65-71. Kaiser - Permanente Prospective. 62 ventricular septal 0.5 (0.2-096): 22 heart valves 0.3 (0.1-1.1): 92 ductus arteriosus 1.1 (0.7-1.6): 16 unspecified 0.8 (0.3-2.6): 8 transposition 0.4 (0.04-2.9): 9 atrial septal defect 0.7 ( 0.2-3.5): 5 fibroelastosis 1.7 (0.3-10.1): 6 coarctation of aorta 0.5 (0.1-4.3). [calculated overall odds ratio 0.78].

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Evans DR, Newcombe RG, Campbell H. Maternal smoking habits and congenital malformations: a population study. BMJ Jul 21 1979; 2: 171-173. Cardiff. 223 cardiovascular malformations, crude rates/1,000: non 3.6, 1-9c 2.9, 10-19c 3.0, 20+c 2.8. [calculated risk ratios 1-9c 0.81, 10- 19c 0.83, 20+c 0.78].

Fredrick J, Alberman ED, Goldstein H. Possible teratogenic effect of cigarette smoking. Nature 1971 Jun 25;231:529-530. British Perinatal Mortality Survey, retrospective, 34/86 (39.5%)s 1 wk pop, 81/204 (39.7%)s v 4626/15, 719 (29.4%)s CHD 3 mo pop sample. 290 incident, smokers 7.3%, nonsmokers 4.7% [crude risk ratio 1.55]

McDonald AD, Armostrong BG, Sloan M. Cigarette, alcohol, and coffee consimption and congenital defects. AGPH Jan 1992;82(1), 91-93. 3/18 cardiovascular 1-9c 1.03 (0.6-1.6), 10-19c 1.17 (0.8-1.7), 20+c 1.17 (0.9-1.6).

Kelsey JL, Dwyer T, Holford TR, Brecken MB. Maternal smoking and congenital malformations: an epidemiological study J Epidemiol Commun Health 1978; 32:102-107. Retrospective case- random control at "several hospitals in Connecticut" Relative risks: 52 abnormal heart valves 1- 1.3, 0.4; 106 other 0.9, 1.0; 213 septal defects 1.0, 1.4. No combined results.

Van Den eden SK, Karagas MR, Daling JR, Vaughan TL. A case-control study of maternal smoking and congenital malformations. Paediatr Perinatal Epidemiol 1990;4:147-155. 88 patient doctus arteriosus 1.0 (0.6-1.6); 582 other 0.9 (0.7-1.1); 655 total cardiac 0.9 (0.8-1.2).

Milloy MH, Kleinman JC, Bakewell JM, Schramm WF, Land GH. Maternal smoking during pregnancy, No association with congenital Malformations in Missouri. AJPH 1989 Sep; 79 (9): 1243-1246. 123 atrial septal 1.04 (0.70-1.55); 151, valvular 0.74 (0.50-1.09); 447 ventricular septal 0.87 (0.70-1.09); 756 other cardiovascular 1.01 (0.86-1.19); 1341 heart 0.92 (0.82-1.05). NOT SHOWN ON GRAPH:

HEINONEN OP, SLONE D, SHAPIRO S, EDS. Birth defects and drugs in pregnancy. Littleton, MA: Publishing Science Group, 1977, Collaborative Perinatal Project prospective. 404 congenital heart defects, smoking non significant in Multiple Logistic Regression, no details.

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WORLD'S LARGEST AND LONGEST HEART STUDY PRODUCES SOME SURPRISES

Embargoed to Monday August 24th 1998 12:30 Vienna time Press Conference: European Congress of Cardiology, ESC Press Conference Centre Messe Vien, WHO MONICA Project: preliminary analysis of final results 11:30 to 12:20, Monday 24th August 1998. Participants: Dr Hugh Tunstall-Pedoe:Chairperson (Dundee, GB), Dr A Evans (Belfast, GB), Dr Ingrid Martin (WHO Geneva, CH), Dr U Keil (Mnster, DE), Dr K Kuulasmaa (Helsinki, FI)

The European Congress of Cardiology in Vienna this week is seeing preliminary analyses of the final ten-year results of the largest collaborative study of heart disease ever undertaken. These results - on the effects of treatments and risk factors in determining trends in coronary heart attack rates and mortality - which include some early surprises, will create considerable discussion and controversy amongst the worlds experts, although further analyses remain to be done. The near completion of this World Health Organization (Geneva) initiative is a remarkable feat of international research collaboration. Background Twenty years ago investigators in 38 centres in 21 countries got together with the World Health Organization to answer key questions on coronary heart disease and stroke: Why were rates declining rapidly in some countries and increasing in others ? Were changes in disease rates driven directly by changes in factors known to be important in individuals - smoking, blood pressure, cholesterol and obesity ? How well could changing survival and mortality from heart attacks be related to changes in treatment ? o questions which are as topical today, when heart disease generates everincreasing burdens and costs to the worlds ageing populations, as they were when they were first posed.

The Project The resulting collaboration was called the WHO MONICA Project (from MONItoring CArdiovascular disease). Participants, who were locally funded, used standardized methods to study trends in heart disease (and optionally stroke), trends in its treatment, and trends in coronary risk factors in their local populations, but copied their results to a Data Centre in Helsinki, for central analysis. Procedures and results were scrutinized by designated quality control centres, and by panels of international experts. Performances were scored, ranked and circulated. Serious failure led to exclusion from the study, but most investigators worked together for over ten years submitting data which met WHO MONICA Project requirements. Preliminary results from 150 thousand heart attacks, and 180 thousand risk factor records were presented briefly at a "Hot-Line" session by Professor Hugh Tunstall-Pedoe (Dundee, Scotland, head of one of the quality control centres, and long-term member of the MONICA Steering Committee) on Sunday 23rd August and with his MONICA colleagues (named above) at a press conference on the next day. Heart disease rates are declining in most of the populations studied but there is more decline in fatal than in nonfatal attacks and in men than in women. Rates are increasing in some Eastern populations. Survival rates from heart attacks are improving but to a lesser extent than event rates.

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Effective treatments are being adopted at very different rates in different countries. Improving heart attack rates do not always go with better survival. Blood pressure is coming down in most populations, as is smoking but there are differences by sex and age group in the latter. Cholesterol levels are difficult to measure and follow accurately over time, but they are changing little in most MONICA populations. Obesity is increasing in most MONICA populations. AND WHEN THESE ARE PUT TOGETHER

Those populations which, during the period of study, showed the most rapid increase in new treatments tended to be those in which heart attack survival and mortality were improving most but this effect could be nonspecific. Many drugs were being adopted at the same time, and there were regional effects. It was therefore not possible in these preliminary analyses to say which treatments, if any, were the cause. Although there was more relationship in women than in men, changing rates of coronary heart disease in different populations did not appear to relate at all well to the change in the standard risk factors, considered one by one, or in a risk factor score. Large differences in the rate of decline occurred across populations with similar trends in risk factors.

Discussion and possible explanations The latter preliminary finding will cause surprise and controversy, as many had assumed a direct relationship. Professor Hugh Tunstall-Pedoe, speaking for the study, said: "The WHO MONICA Project was set up in the early 1980s to see whether the engines driving the changes in heart disease rates were those known at that time to determine risk in individuals smoking, blood pressure, cholesterol, and to a lesser extent, obesity. Our initial impression, - of no direct relationship overall in this study, despite reported results from individual centres- does not negate the importance of these factors to the individual and to health education. If you get eaten by a crocodile when you are expecting lions and tigers it does not mean that big cats have rubber teeth! We would not have done the study if we had been sure what it would show, and we needed international collaboration to make it possible. The preliminary results are a bit of surprise but not entirely so. "There are several possible explanations for our findings, including problems of measurement, the fact that rates were declining in most populations anyway, and lack of linearity in trends associated with possible time-lags for which preliminary analyses do not allow. Another interesting possibility is that in population terms the contribution of the classical risk factors is swamped by that of other, dietary, behavioural, environmental or developmental factors, of which several have been proposed since the study was launched. Although many enthusiasts will now be staking claims for their favourite candidates, we cannot pass judgement on factors which were not included in the agreed core set of data for the original study. Some of these factors have been looked at in local and MONICA optional studies but will not have the power of a 38 population and ten-year evaluation. Further more sophisticated analysis of the central data that we do have will continue beyond these preliminary findings and will involve more use of our quality scores to weight the results." Dr Ingrid Martin, responsible officer for cardiovascular diseases at the World Health Organization Headquarters in Geneva stated: "The World Health Organization has facilitated, co-ordinated and helped to manage this study since 1979. MONICA has spread best practice in the technology of population surveys and disease monitoring through four continents. It has trained many young people in population aspects of cardiovascular disease. The findings on risk factors in no way diminish their importance for individuals and for public health. That the classical risk factors make major contributions to individual risk has been shown repeatedly in numerous studies, many involving MONICA investigators. They feature in ongoing WHO sponsored prevention programmes. The WHO MONICA Project is adding to our understanding of what is going on, and not taking away anything that was known before. It has

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generated high quality data for local use on what is happening to cardiovascular disease and major risk factors, and created an invaluable international resource. It is a model for other international research collaborations." Enclosure: Press Pack consisting of: List of MONICA sites and principal investigators World Map to show MONICA sites *Ten-year trends in coronary death rates in MONICA populations using MONICA diagnostic criteria. *Ten-year trends in daily smoking in MONICA populations, smoking defined by MONICA criteria *Selected examples of WHO MONICA Project output

NOTE: 1: These findings will be the subject of a special evening discussion session outside the main Congress programme, organized by the WHO MONICA Project and by the European Society of Cardiology Working Group on Epidemiology and Prevention in Hall 16C Messe Vien, Tuesday 25th August 18:30-20:00 NOTE: 2 The WHO MONICA Project is sponsored and co-ordinated by the World Health Organization with contributions from NHLBI (USA) to data analysis and quality control, and European Union funding through BIOMED grants, plus donations from drug companies. The MONICA Data Centre has been supported by Finnish funds. Individual MONICA centres are funded by government bodies and by heart foundations. NOTE: 3 Press release and results have been sent to individual Principal Investigators who can now comment both on the study and on their own local results for their national media and may put out their own statements.

Nicotines effect on fluoride Nicotine, most know of it through smoking and tobacco use. I've always wondered why the US Government is so adamant with anti-smoking and tobacco usage. The carcinogenic properties are bad yes, i do condone smoking but only in small amounts and from organic of hand rolling tobacco, pipe tobacco or Cigars. I do however condone nicotine gum, or other nicotine treatments. Here is why.

Nicotine has an adverse effect on fluoride.

Remember how fluoride inhibits choleric activity? Nicotine excites them, rebounding and undoing fluorides effect. Nicotine is being used as a treatment for ADD and ADHD, Alzheimers, Parkinson's disease. I will not list the rest, for every single ailment fluoride is known to cause, nicotine has the reverse effect.

It makes you wonder, why people who smoke may find a considerably less effect from Prozac and other anti-depressants. Why most people with ADD and ADHD develop into smokers. WHY DO MOST DOCTORS SMOKE?

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Parkinson's disease is your brain's ability to receive and use dopamine from the blockage or death of brain cells in the motor regions. The cause is UNKNOWN. On a side note, Ill mention again how fluoride enters the brain tissue easily and deposits aluminum at will, which has a conspicuous effect of killing brain cells and clogging up dopamine receptors. The most common treatment is levodopa; a drug that increases dopamine levels, so that what receptors and brain cells you have left can receive a better supply of dopamine. Funny, nicotine has the same effect. On a large level. Large enough so that it becomes addictive. Your brain becomes used to the higher dopamine count, so when the dopamine stops coming, your brain says "hey, i want some more 'o' that."

There is a lot more info. Here are some links for your own further research. www.epa.gov, www.fluoridealert.org, Summation - Fluoride & Pineal Gland: Up until the 1990s, no research had ever been conducted to determine the impact of fluoride on the pineal gland - a small gland located between the two hemispheres of the brain that regulates the production of the hormone melatonin. Melatonin is a hormone that helps regulate the onset of puberty and helps protect the body from cell damage caused by free radicals. It is now known - thanks to the meticulous research of Dr. Jennifer Luke from the University of Surrey in England - that the pineal gland is the primary target of fluoride accumulation within the body. The soft tissue of the adult pineal gland contains more fluoride than any other soft tissue in the body - a level of fluoride (~300 ppm) capable of inhibiting enzymes. The pineal gland also contains hard tissue (hyroxyapatite crystals), and this hard tissue accumulates more fluoride (up to 21,000 ppm) than any other hard tissue in the body (e.g. teeth and bone). After finding that the pineal gland is a major target for fluoride accumulation in humans, Dr. Luke conducted animal experiments to determine if the accumulated fluoride could impact the functioning of the gland - particularly the gland's regulation of melatonin. Luke found that animals treated with fluoride had lower levels of circulating melatonin, as reflected by reduced levels of melatonin metabolites in the animals' urine. This reduced level of circulating melatonin was accompanied - as might be expected - by an earlier onset of puberty in the fluoride-treated female animals. Luke summarized her human and animal findings as follows: "In conclusion, the human pineal gland contains the highest concentration of fluoride in the body. Fluoride is associated with depressed pineal melatonin synthesis by prepubertal gerbils and an accelerated onset of sexual maturation in the female gerbil. The results strengthen the hypothesis that the pineal has a role in the timing of the onset of puberty. Whether or not fluoride interferes with pineal function in humans requires further investigation."

TOKYO - Life expectancy for Japanese women already the longest in the world has risen by nearly one year, the Health Ministry said Thursday, citing the latest census data. Female life expectancy increased to 85.52 years in 2005 from 84.60 years in 2000, Health Ministry official Morio Akimoto said.

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The latest figures were calculated based on the fixed census data taken in 2005. The census is taken every five years in Japan. Akimoto said Japanese women's life expectancy remained the world's longest for the 21st straight year, ahead of Hong Kong and Spain, according to U.N. demographic figures. For men, life expectancy rose to 78.56 years from 77.72 years, the fourth-longest in the world after Hong Kong, Iceland, Switzerland, Akimoto said. Japan has long been touted as one of the world's longest-living populations, but experts are worried that changing eating patterns from the traditional fish and ricebased diet to fast food such as hamburgers and instant noodles may soon change this. http://news.yahoo.com/s/ap/20070301/ap_on_he_me/japan_l...A63sOuYGwxibtivMWM 0F

ummm excuse me!! how can this be?? Isnt Japan one of the highest tobacco use rates in the world?? Greece also has massive amounts of smokers and also have extremely high life expectancies.

Interestingly, reading Whitby's book from that link (great reading btw), on page 58-59 (of the book; 30-40 on web page) I find that Co-enzime Q10, CoQ10, hailed as the miracle supplement, for heart, circulation, infections, cancers, Parkinson's,... and just about everything that can go wrong, is actually a tobacco leaf and is manufactured from tobacco. Naturally, it is not mentioned very often, but that is what it is and how it was discovered in 1950s. Now, that is interesting. After reading Whitby one can only say, yep, tobacco is a miracle medicine, as our elders always thought. From every angle one looks the actual facts behind the antismoking propaganda, from biochemistry to animal experiments and the randomized quitting trials, even the statistical rigging in the epidemiology, one arrives to this same conclusion -- tobacco is a miracle drug. No wonder Big Pharma is doing its best to destroy it.

Here is an interesting official confirmation I found abot smoking rodents. The source is the official repository of tobacco documents (obtained during MSA negotiations). On page 97 of the report there is the following study citation & conclusion excerpt:

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"Inhalation Bioassy of Cigarette Smoke in Rats" A. P. Wehrner, et al. (Battele Pacific Northwest Labs, Richland WA) Journal of Toxiology & Applied Pharmacology, Vol. 61: pp 1-17 (1981) The results show that the highest number of tumors occured in the untreated control [non-smoking] rats. The next highest number of tumors occurred in rats subject to sham smoking, i.e. rats which were placed in the smoking machine without smoke exposure, and the lowest number of tumors occurred in the smoke-exposed rats. Among the latter, the largest number of tumors occurreed in rats exposed to smoke from cigarettes having the lowest level of nicotine.

So, among the lab rats, the "full flavor" smokers had the fewest tumors, the "light cigrattes" smokers had more, the sham-smokers even more, and non-smokers had the most. The entire document (pdf file) is a gold mine with many hudreds of fascinating and little publicised reasearch "anomalies" (i.e. the studies in which the data went the "wrong" way) regarding the relation of cancers to smoking. Of course, there is no real anomaly (the reality is surely not perplexed by itself), provided one views the data from the perspective of tobacco smoking being protective against (instead of "the cause of") the diseases studied. The data is anomalous only from the perspectiva in which tobacco smoke is assumed to be the cause of those diseases.

Major Health Advocate Groups state that smoking causes heart disease and deaths;however,since they do not state "HOW", their statements are of little use or believability. Many studies,ie "WhiteHall 1","MRFIT","Framingham", and etc,state that smoking is not a risk factor for heart disease. Since they do not say why this is so,they are of little help either. -----

Lung Cancer and smokers

Let's see; 70% of LC cases are ex-smokers, plus 15% LC cases are never smokers, that means that only about 15% of LC cases are current smokers!!! Not anywhere near the 90% you hear about. Since there are as many ex-smokers(70% of LC's) as current smokers(15% of LC's) in this country, don't quit!

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In Calif., ex's = 70%, non's = 30% = 100%. Smokers do not get LC in Calif. http://www.smokersclubinc.com/modules.php?name=News&file=article&sid=3752 Rise in lung cancer in nonsmokers puzzling MDs 9/30/06

Doctors who treat lung cancer are facing a puzzling trend: every week about 65 Canadians who have never smoked are being told they have cancer in their lungs.

According to the Canadian Cancer Society, an estimated 22,700 Canadians will be diagnosed with lung cancer in 2006 and 19,300 will die of it. Smoking has long been understood to be a key risk factor for lung cancer. But according to information CTV's Avis Favaro received from doctors at Princess Margaret Hospital and the Sunnybrook Regional Cancer Centre in Toronto, 10 to 15 per cent of new lung cancer cases diagnosed are in people who have never smoked. Many have never been exposed to second-hand smoke. Genetics, hormones, second-hand smoke, diet and air pollution are all possible factors. "Many of these people are young," said Dr. Natasha Leighl of the Princess Margaret Hospital. "They're women and this is a population that is increasing. In California, they believe the number of people with lung cancer who have never smoked may now be 30 per cent." Doctors suspect environmental pollution may trigger some cases. In others there may be a genetic link. Many agree the numbers of non-smokers developing long cancer is growing. Although quitting smoking decreases the risk of getting lung cancer, it doesn't mean you don't have to worry. Leighl said 70 per cent of diagnosed cases of lung cancer are in former smokers who said they quit 10 or 20 years ago. Antis;using CDC data that shows that Kentucky has a 32.6% smoking rate and a 223.9/100,000 cancer death rate compared to Utah's 12.8% smoking rate and 144.9/100,000 cancer death rate,claim that smoking causes cancer and thus, cancer

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deaths. Below is a chart using only CDC data. There are some very interesting datum in this chart. For instance;note that both Colorado and The Dist.of Columbia have a 20.4% smoking rate. However,DC ranks 14th on the chart and Colo. ranks 49th! DC has more politicians, it must be the politicians that are causing cancers. Mass.,with a 18.9% smoking rate, ranks 24th and Alaska, with a 29.3%(about 50% higher)smoking rate, ranks 32nd!! New Jersey, with a 19% smoking rate,ranks 22nd and Hawaii,with a 21% smoking rate, ranks 51st!!! Now consider Ky. and Ut. Let's just say that smoking causes all cancers, this is what the antis would say. Ky's 32.6% = 32,600/100,000. 32,600 divided by Ky's 223.9/100,000 death rate = 1 cancer death per 146 Ky smokers. Ut's 12.8% = 12,800/100,000. 12.800 divided by Ut's 144.9/100,000 death rate = 1 cancer death per 88 Ut smokers. 1/88 is much worse than 1/146. If a Ut smoker moved to Ky, he would reduce his risk of dying from cancer by 66%!! Must be the Ky whiskey that has the protective effect. This data may indeed prove something;but,it does not prove that smoking causes cancer deaths. Gary K.

Cancer Death Rates and 95% Confidence Intervals by State (Table 5.1.2MF) Available at http://www.cdc.gov/nchs/data/nvsr/nvsr54/nvsr54_13.pdf. Source: U.S. Cancer Statistics Working Group. United States Cancer Statistics: 2003 Incidence and Mortality. Atlanta (GA): Department of Health and Human Services, Centers for Disease Control and Prevention, and National Cancer Institute; 2007. Rankings by State: 2003, Male and Female, All Sites Rates per 100,000 57

Smoking Rates from CDC- BRFSS Data. http://apps.nccd.cdc.gov/brfss/Trends/trendchart_c.asp?...key=10000&SUBMIT1=Go DEATHS (smoker%-2002) (Deaths/Smokers) (2003 Rate) 1 Kentucky 32.6 1/146 223.9 2 Louisiana 23.9 1/107 222.6 3 Tennessee 27.8 1/131 212.9 4 Mississippi 27.3 1/129 212.0 5 West Virginia 28.3 1/134 211.6 6 Alabama 24.4 1/117 207.7 7 Indiana 27.7 1/134 207.2 8 Arkansas 26.3 1/128 205.5 9 Ohio 26.6 1/130 204.3 10 Maine 23.6 1/116 204.1 11 South Carolina 26.5 1/130 203.7 12 Nevada 26.0 1/128 203.0 13 Missouri 26.5 1/131 201.7 14 Dist.of Columbia 20.4 1/101 201.1 15 Delaware 24.7 1/123 200.4 16 Oklahoma 26.6 1/133 199.7 17 Pennsylvania 24.5 1/124 197.9 18 Virginia 24.6 1/125 197.6 19 Georgia 23.3 1/118 197.4 20 Illinois 22.8 1/116 197.0 21 North Carolina 26.2 1/134 195.6 22 New Jersey 19.0 1/97 195.1 23 Maryland 22.0 1/113 194.9 24 Massachusetts 18.9 1/98 193.0 25 Michigan 24.2 1/125 193.0 26 Oregon 22.5 1/117 192.7 27 United States 23.0 1/121 190.1 28 New Hampshire 23.2 1/122 189.9 29 Washington 21.5 1/113 189.6 30 Rhode Island 22.4 1/118 189.5 31 South Dakota 22.5 1/119 188.9 32 Alaska 29.3 1/155 188.5 33 Wyoming 23.7 1/126 188.4 34 Iowa 23.2 1/124 187.1 35 Texas 22.9 1/123 186.3 36 Kansas 22.1 1/119 185.5 37 Wisconsin 23.3 1/127 182.8 38 Connecticut 19.4 1/107 182.1 39 Vermont 21.2 1/117 181.8 58

40 Idaho 20.6 1/113 181.7 41 Montana 21.2 1/117 181.5 42 Florida 22.1 1/122 181.3 43 Minnesota 21.8 1/120 181.2 44 New York 22.3 1/125 178.6 45 Nebraska 22.7 1/127 178.3 46 North Dakota 21.5 1/121 178.3 47 California 16.4 1/95 172.5 48 Arizona 23.4 1/126 172.3 49 Colorado 20.4 1/120 170.1 50 New Mexico 21.3 1/125 169.8 51 Hawaii 21.0 1/136 154.3 52 Utah 12.8 1/88 144.9

The problem is that most smokers, including many posters in this forum, have been infested by guilt (for allegedly harming themselves) and thus lack drive to defend publicly something they consider a bad habit of their own. It is a clever scheme and until smokers discard the anti-smoker "science", every rotten scrap of it, and realize that tobacco is an ancient medicinal plant, cultivated over milenia for its beneficial and benevolent smoke, thus which is good for them, the smokers will remain at the mercy of the swindlers. Hence, the type of pro-smoker organization which can fight and win, will have to have as its central postulate that smoking is good for smoker. It is true of course that a blind statistics, especially in recent years, will find correlation between smoking and variety of health problems. But that kind of correlation doesn't differentiate which is the cause and which is the consequence. For example, if you observe use of feeding tubes, you will find that their use correlates with spinal injury i.e. among those with spinal injury the feeding tubes will be found more often than among general population. Does that mean the feeding tubes are cause of spinal injuries? Or that banning feeding tubes will reduce occurence of spinal injuries? With smoking, even in the smoker friendly era, some portion of those attracted to smoking were people self-medicating themselves. Thus people in stressful or unhealthy jobs always tended to smoke more. Smoking stimulates internal antioxidants, such as glutathione (essential antioxidant for internal detox from mercury, aluminum, lead...), it is a kind of excercise for the immune system. With the social engineering against smokers, the social and economic pressures have filtered out smokers population, so that those who didn't really need

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to smoke (e.g. those who did it for social reasons, peer pressure) have largely quit, while those still smoking are largely people self-medicating. Hence, the correlation between smoking and various health ailments has increased in recent years. For those still smoking, quitting would not reduce the ailments but would increase them. Asthma and allergies (for which traditionally smoking was considered helpful) have been rapidly rising, while smoking has been decreasing. Alzheimers and Parkinson, have been increasing, too. Smoking is strongly protective against Alzheimer's e.g. when you match people genetically and socio-economically, such as when comparing between family members, smokers have ten times lower risk of Alzheimer's than their nonsmoking relatives! Of course, if you don't match the samples, but compare within general population, the smoking appears only mildly negatively correlated with Alzheimer's, and in recent 5-10 years even slighlty positively correlated. Similarly, smoking is strongly positively correlated with schizophrenia - schizophrenics smoke 23 times more often than general population, and smoke much more heavily than general smokers. Unlike Alzheimer's, schizophrenia usually starts in teens, often well before person has started smoking (or has smoked very little), hence it is obvious that smoking is a form of self-medication among schizophrenics rather than its cause (this has been also shown more explicitly). Even for lung cancer, smoking among asbestos workers was shown to be protective (a non-smoking asbestos worker is much more likely to get asbestos related lung cancer). In famous study by Doll (which was the first to find correlation between smoking & lung cancers), it was found that while lung cancers correlate positively with smoking, it was also found that those who inhale smoke have much lower rates of lung cancers than those who don't inhale! Similar stong protective effects of smoking against lung cancer (induced by radiation) were also demonstrated in controlled experiments on mice. Among nations, Japanese men smoke 2-3 times more often than Americans, yet they have 6-8 times lower rates of lung cancer. Similar paradoxical relations hold among Europeans, where Greeks are the heaviest smokers and have the lowest lung cancer rates. In USA, lung cancer has been rising for decades (most rapidly among non-smokers), and is now at its all time high, while smoking has been declining and is now at its all time low (note that CDC had to rig their counting to hide this fact contradicting their ideology and $$$) . After studying various papers and books (see e.g. Ray Johnstone, Lauren Colby, FORCES), as well as observing myself, my family and people I know, I have concluded that the truth about health effects of smoking is precisely opposite from the presentday conventional wisdom -- smoking is good for smoker. Further, believing antismoker propaganda, even partially, is harmful to smoker (due to witch doctor effect,

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negative placebo). In summary, there is money on our side, the money being currently stolen from us (only few crumbs of which are used against us). Unfortunately, until enough smokers realize that their habit is good for them (despite financial burden from extortion), there won't be organized and effective resistance against the anti-tobacco swindle. The essential first step in getting organized is to neutralize the key psychological weapon used against our will to defend ourselves, the poisonous anti-smoker pseudoscience.

Thu February 21 2008 04:24 PM THE TRUTH ABOUT SMOKING CAUSED DISEASES: TRENDS AND INCIDENCE RATES If smoking was bad for us and caused heart disease and cancers, as the anti-smokers claim,; then, the fact that smoking rates have decreased by 50% over the last 40 years should bring about an equal decrease in heart disease and cancer incidence rates. This decrease has not happened!! http://www.nj.gov/health/ces/reports.shtml Data,Statistics and Reports: Trends in Cancer Incidence and Mortality in New Jersey, 1979-2002 [pdf 312k] (11/28/05) NOTE: U.S. rates are also shown. Tables 5+6,pages 46 and 47 Total cancer incidence rate- U.S.(per 100,000) 1979 male + female total = 861.5 2001 male + female total = 963.4 2004 male + female total = 970.9

www.cdc.gov.mill1.sjlibrary.org/nchs/data/hus/hus06.pdf[/URL] Health,United States,2006 Page 229

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Table 39 (page 1 of 3). Death rates for malignant neoplasms of trachea, bronchus, and lung, by age: United States, selected years 19502004 [Data are based on death certificates] All persons: Deaths per 100,000 resident population All ages, age-adjusted 1970.........2004 37.1.........53.2 This is a 43% increase in lung cancer deaths!! Smoking can not be the major cause of lung cancer!! HEART DISEASE http://www.proteinpower.com/drmike/uncategorized/cancer...disease-and-smoking/ The AHA doesnt particularly want us to know about the incidence of heart disease; they just want us to know that deaths from it are declining. To find the incidence you have to go to a table called Hospital Discharges with Cardiovascular Disease as the First Listed Diagnosis. Hospital Discharges With Cardiovascular Disease as the First Listed Diagnosis United States: 1979-2003 1969 = about 3,200,000 2003 = 6,434,000 As you can see the rate of these discharges is increasing. When you correct for the increase in population over the years, the line doesnt increase as rapidly, but still increases slightly. What does this mean? It means that despite a 50% decrease in smoking rates, that the number of people developing heart disease hasnt dropped at all. If anything it has increased. Smoking cannot be the major cause of Heart Disease!!!

The Truth-part 2 EMPHYSEMA and BRONCHITIS (COPD) This is from the "American Lung Association(ALA)", we know that they would not lie as they are a public health organization and only interested in our welfare. TRENDS IN CHRONIC BRONCHITIS AND EMPHYSEMA MORBIDITY AND MORTALITY;

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AMERICAN LUNG ASSOCIATION; EPIDEMIOLOGY & STATISTICS UNIT; RESEARCH AND PROGRAM SERVICES MAY 2005 COPD Age Adjusted Death Rates Population, 1979-2002 Age-Adjusted Death Rate per 100,000 Persons 1979..... 2002 24.2.......42.0 NOTE: Smoking has gone DOWN by almost 50% over the last 40 years, over the last 20 plus years the COPD death rate has GONE UP BY 74%. Yet, the ALA and other health advocates say that smoking causes Emphysema!!!! Clearly, smoking does not cause Emphysema and Chronic Bronchitis. Smoking and the Asthma Epidemic: The most recent study to exonerate smoking and tobacco smoke as a cause of asthma was published in the British Medical Journal July 8, 2000. In this 20-year, inter generational study, researchers found that the rate of asthma had doubled between l976 and l996, even as the smoking rate dropped by half during that same period. Asthma and hay fever increased for both smokers and non-smokers, but the increase was higher for non-smokers. The steep rise in asthma was dramatically underscored by the fact that prescriptions for steroid inhalants for treatment of the disease rose more than six-fold between l980 and l990 alone. This pattern of precipitous increases in asthma coupled with significantly diminishing smoking rates is not unique to the population described by the Scottish researchers in their BMJ article. In the United States, too, the incidence of adult and childhood asthma has climbed to an unprecedented high during the past twenty years, while smoking and exposure to environmental tobacco smoke [ETS] have decreased significantly during the same period. "...Between 1980 and l995, the number of people reporting asthma in the U.S. more than doubled (from 6.7 million to 13.7 million), a 75% increase in the rate per 100,000 population. The Centers for Disease Control estimates the l998 rate at 17.3 million, a 150% increase since 1980. 63

"...Between l980 and l995, the adult smoking rate decreased from 33.2 to 24.7, a drop of 25%. In the late l990s the overall smoking rate has remained steady at between 24 and 25 percent of the adult population, far less than its peak of 42.6% in l966. The inverse relationship between asthma rates and smoking and between asthma rates and exposure to ETS can be seen quite clearly. Smoking and SHS cannot be causing Asthma!!

American Indian/Alaska Native have the highest smoking rates and the lowest total cancer incidence rate and a much lower lung cancer incidence and mortality rate than most of the other groups.

http://www.statehealthfacts.org/comparetable.jsp?ind=82&cat=2 Smoking Rates for Adults by Race/Ethnicity, 2005 White- Black-American-Indian/Alaska Native 20.9%----20.8%.............34.8% Cancer facts and Figures 2008 In 2005, 6% of adults aged 18 and older had smoked cigars in the past month. American Indian/Alaska Natives (11%) had the highest prevalence of past month cigar use, followed by African Americans (7%),whites (6%). Cancer facts and Figures 2008 Cancer Incidence by Site, Race, and Ethnicity, US, 2000-2004 Incidence- All sites White American/African merican/AmericanIndian/ Alaskan Males+Females Total-980.6--------1,060.6--------603.6 American Indians have a 38% lower cancer incidence than whites!!!

Cancer Incidence and Mortality Rates* by Site, Race, and Ethnicity, US, 2000-2004 Lung & bronchus(total male+female) White--African American--American Indian/Alaska Native Incidence 135.6----164.3--------------90.4 Mortality

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114.7----135.6--------------82.3 American Indians have a 33.33% lower lung cancer incidence rate that whites!! American Indians have a 28% lower lung cancer mortality rate than whites!!!! Over the last 40 years smoking rates have decreased by about 50%, cancer incidence has steadily increased. http://www.nj.gov/health/ces/reports.shtml Data,Statistics and Reports: Total cancer incidence rate- U.S.(per 100,000) 1979 male + female total = 861.5 2001 male + female total= 963.4 (Cancer facts and Figures 2008) 2004 male + female Total = 970.9 Cancer facts and Figures 2008 Who Is at Risk of Developing Cancer? The risk of being diagnosed with cancer increases as individuals age, most cases occur in adults who are middle-aged or older. About 77% of all cancers are diagnosed in persons 55 and older. http://apps.nccd.cdc.gov/brfss/age.asp?yr=2006&state=US&qkey=4394&grp=0 Age: 55-64 Median % Smoke everyday/some days/Former smoker/Never smoked 12.3------3.9---------36.3----------45.3 65+ Median % 6.6-------2.0---------42.5----------48.9 Cancer facts and Figures 2008 Quitting smoking substantially decreases the risk of lung, laryngeal, esophageal, oral, pancreatic, bladder, and cervical cancers. Old age equals most cancers and fewer smokers and more ex-smokers!!

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The risk of developing lung cancer is about 23 times higher in male smokers and 13 times higher in female smokers compared to lifelong non-smokers. SOOOO; if a man wants to decrease his risk of getting lung cancer by about 1/2, all he has to do is have a sex-change and not change his lifestyle. Then; if he/she became an American Indian and went to live on a reservation, he/she would lower his/her risk of getting lung cancer by another 33.33%. DATA FROM THE ACS PROVES THESE FACTS TO BE TRUE!!

The decrease in Lung Cancer mortality is not true,according to the CDC's 'Health,United States,2006'. This report left out many of the people in the US. The only facts that it shows for certain are these: 1. Older people die more often than younger people. 2.Women die from lung cancer less often than men. 3. In spite of the hundreds of millions of dollars spent on tobacco control and smoking prevention and the 'Campaign for Tobacco Free Kids' claim that for every 10% increase in the cost of cigarettes there is a 7% decrease in teen-age smoking,the high school smoking rates have been increasing by quite a lot. 4. Any decrease in lung cancer death rates is probably due to better screening and curative proceedures by the medical folks. More to the point,Lung Cancer incidence has not decreased over the last couple of decades,in spite of the 50% decrease in smoking rates over the last 4 decades. http://www.nj.gov/health/ces/reports.shtml Trends in Cancer Incidence and Mortality in New Jersey, 1979-2002 TABLE 9+10 Lung Cancer Incidence Rates U.S., 1979-2002* Incidence Rate/100,000 1979 male= 95.8 female=31.6 Total = 127.4 2001 male= 77.7 female= 49.1 Total=126.8

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Considering that blacks and white have about the same smoking rate and whites have a lower lung cancer mortality rate, American Indians have a higher smoking rate and a much lower lung cancer mortality rate than either group, the Japanese and Israeli people have very high smoking rates and much lower lung cancer death rates than the US, economic and environmental factors have a much greater impact on LC incidence and death rates than does smoking.

quote: the Japanese and Isreali people have very high smoking rates and much lower lung cancer death rates than the US, economic and environmental factors have a much greater impact on LC incidence and death rates than does smoking. In case your are curious. lung cancer death rate(lcdr) http://www.kidon.com/smoke/percentages3.htm Smokers Prevalence(%)- LCDR/100,000 smokers MALE Japan--- 59.0 ('94)-- --- 81.2 Israel---- 45.0 ('90)----- 84.7 USA ----- 28.1 ('91)---- 305.7 FEMALE Israel---- 30.0 ('90)------- 40.3 Spain---- 25.0 ('93)------- 21.6 USA------ 23.5 ('91)------ 157.0

The real question is just how much does smoking contribute to Lung Cancer and Lung Cancer Deaths? The answer= NOT MUCH!!! This information is not for the antis, they believe what they want to believe and no amount of 'Truth' will influence them. This is for the smokers and will help to free them from the decades of propaganda and brain-washing that they have received. Gary K. This is 'THE TRUTH-5'.

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We will use the map above and female smoking rates from here. http://www.statehealthfacts.org/comparetable.jsp?ind=81&cat=2 In 'The Truth-4', we saw that American Indians/Alaskan Natives had a 35% higher smoking rate and a 28% lower LC Death rate than white smokers. These a just a few of the dose-response comparisons that can be done. Using the map and female smoking rates,we find that New York has a lower smoking rate than Penn.(18.1%-22.3%) and about a 200% higher LC death rate!! The Penn. smoking rate is about 100% higher than Calif's(22.3%-11.3%) and Calif has LC death rate that is about 200% higher!! Iowa and Neb both have a smoking rate slightly higher than does Fla(19.1%-18.8%) and Fla has a LC death rate about 100% higher!! Utah and Calif have about the same smoking rate(9.3%-11.3%) and Calif has a LC death rate that is about 300% higher!! Do the smokers living on the coast of No.and So. Carolina smoke more toxic cigarettes?? lung cancer death rate(lcdr) http://www.kidon.com/smoke/percentages3.htm Smokers Prevalence(%)- LCDR/100,000 smokers MALE Japan--- 59.0 ('94)-- --- 81.2 Israel---- 45.0 ('90)----- 84.7 USA ----- 28.1 ('91)---- 305.7 FEMALE Israel---- 30.0 ('90)------- 40.3 Spain---- 25.0 ('93)------- 21.6 USA------ 23.5 ('91)------ 157.0 For females we see that both Spain and Israel have slightly higher smoking rates and the USA's LC death rate is about 700% and 300% higher!!

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Do Calif women get out more than men? Calif male smoking rate is almost twice the female smoking rate(19.1%-11.3%),and women are supposed to have less risk for LC;about 50% less. Yet; the Calif female LC death rate is 100% greater than the male. Data here: http://apps.nccd.cdc.gov/brfss/age.asp?yr=2006&state=US&qkey=4394&grp=0 shows that old farts like me only have a 8% smoking rate. If there is a high LC death rate in Fla, old age is the cause,not smoking! More comparisons that show smoking is not a major cause of LC deaths. 1.Pa. has a male smoking rate(24.9%) higher than NY(22.7%) and Maine(22.1%). Yet;NY and Maine have about a 100% higher male LC death rate!! 2.Il(21.1%), Ohio(21.8%),Wisc(22%),Minn(20.8%),and Ia(21.7%)all have about the same male smoking rates. Yet,Il and Ohio have about a 100% greater LC death rate.

Something is causing the higher LC death rates in Maine,NY,Ohio, and Ill and it is not smoking!! 3.Why do the men in southern Ohio and Mo have a 100% higher LC death rate than the men in northern Ohio and Mo?? Squeezer; since your Guv Doyle wants a smoking ban for health reasons,you might ask him why the Wis Indians have a higher smoking rate and a lower LC death rate(if SHS is supposed to cause LC)?

"Nicotine enhances memory, study finds Non-smokers could find themselves being prescribed nicotine patches to combat Alzheimer's disease By STEPHEN STRAUSS From Friday's Globe and Mail While sucking on a cigarette definitely is bad for your health, numerous non-smokers may find themselves some day being prescribed nicotine patches to combat Alzheimer's disease.

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In a soon-to-be-published study, scientists in North Carolina will describe how they tested the patches on 11 senior men and women to counter deteriorating memories. After several weeks of treatment, the subjects experienced significant improvements in their abilities to make decisions quickly and recognize objects. The researchers are so impressed with the results that they propose a long-term, multisite study involving a large number of seniors whose memories are frayed.

U.S. and European studies published over the past year indicate that nicotine has a protective effect in laboratory animals whose conditions mimic Alzheimer's. Said Paul Fraser, a researcher with the Centre for Research in Neurodegenerative Diseases at the University of Toronto, "The definitive animal experiment has already been done in Sweden." All this research reinforces the results of small studies on humans by Edward Levin at Duke University's Medical Center laboratory, which found that using nicotine patches on people with Alzheimer's reduced some of their mistakes by 10 to 80 per cent. Some scientists said a lack of funding is part of the reason there have been no large trials examining the nicotine-patch effect on a disease such as Alzheimer's. Because nicotine is in the public domain, the drug's new medical uses cannot be patented. "We could have had answers 10 years ago to the question of whether it is good for Alzheimer's if drug companies had given a go on it," Prof. Kellar said. Instead, several drug companies are trying to develop nicotine look-alikes that they can patent, Prof. Levin said." GLOBE NEWS Studies have been conducted on the therapeutic uses of nicotine for many years. The vast majority of the studies show it DOES improve concentration and short-term memory, along with a host of other benefits. That Big Pharma wants to capitalize on therapeutic nicotine has been established. The problem is, as the article states, nicotine is a naturally occurring substance that can't be patented, so Big Pharma is busy with "nicotinic" compounds which can. You perception that you can concentrate better when you smoke, Peter, is borne out by studies from 20 or more years ago, as well as more recent ones. It also alleviates

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hunger and acts as an analgesic (helps alleviate pain). And for all these reasons, during the World Wars, the brass made sure their troops had plenty of cigs. The problem is, as the article states, nicotine is a naturally occurring substance that can't be patented, so Big Pharma is busy with "nicotinic" compounds which can.

"Smoking lessens risk of Alzheimer's: research"

WINNIPEG - A University of Manitoba scientist is studying a controversial link between smoking and Alzheimer's disease. It's controversial because the research suggests that smokers are actually less likely to get the disease. Dr. Dan Sitar believes it's the nicotine that acts as a protective agent against the development of Alzheimer's. Still, he doesn't advocate smoking or using "the patch" as a way to prevent the disease." http://winnipeg.cbc.ca/template/servlet/View? filename=mb_smokealzheimer20030116

Tobacco: the definitive link in healthy aging.

By Daniel John Richard Date Introduction: It is a fact, all of the world's oldest living people are classified as chain-smokers [1]. A few of them drink daily [1][2][3], one of them even smokes marijuana daily[3]. Posed with these facts, research was to be done as to why this was possible. Sources of Vitamin: Nicotine, Cannibinoid, Opiate The brain contains receptors designed to receive nicotine, cannibinoid, and opiate. Thus, we can be assured that they are necessary components of a balanced diet and are of nutritional value. Nicotine in Tobacco is analogous to Vitamin B3 (Niacin) [4]. The discovery of Vitamin B3 was through tobacco research, and nicotine (nicotinic acid) is also present in wholesome foods. Nicotine is found in Eggplants and Tomatoes, Tobacco, Whole grains, leaves and meat. Consumption of nicotine (niacin) by smoking inhalation of Tobacco is profoundly associated with extreme longevity. [1] To meet the U.S. RDA for niacin (nicotine) (15-20mg/day) requires that a person consume a serving of chicken, a

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serving of turkey, a serving of spinach, and a bowl of fortified cereal; or smoke 2 packs of cigarettes each day. Anandamide is a cannibinoid in chocolate; it binds with the same receptors as THC (marijuana). Consumption of large quantities of Chocolate is known to produce Marijuana like high"[5] The consumption of cannibinoid is associated with extreme longevity. [3][6] The worlds oldest documented persons Jeanne Calment (1875-1997) and Sarah Knauss (1880-1999), were passionately fond of chocolate. Jeanne Calment habitually ate two pounds of chocolate per week until her physician induced her to give up sweets at the age of 119 - three years before her death aged 122. [6] Opiates are found in wholesome foods we eat; Milk, wheat, barley and poppy seeds, all contain significant amounts of opiate proteins that stimulate the exact same opiate binding receptors in the brain as heroin [7] It would seem that because the brain is designed with receptors to receive nicotine, cannabinoid, and opiate; and their sources being inherently attractive sources of food; Marijuana, Chocolate, Tobacco, Bread, Meat, and Dairy; any intelligent and educated person could capably realize that this meant higher nutrition. The Value of Nicotine, Cannibinoid, and Opiate Vitamins in History: Tobacco Man was never meant to run out of Tobacco and experience withdrawal symptoms, it is the fastest producing crop in the world; yielding 1 million seeds per plant. [8] Praised by Native American tribes for its peaceful qualities. They believed smoking allowed for one to communicate with the Great Spirit (North Americanmonotheistic deity) and the Heart of Sky (South American-monotheistic deity). This coincides with the old testament of the bible, which believes that making Burnt Offerings allowed for one to atone for their sin, and become united with the Holy Spirit. The Central American Mazatec Shamans practice Catholicism today, they drink Fermented Tobacco Juice and smoke the leaves of psycho-active jungle herbs (Salvia); they believe that this is the way of Jesus Christ. Cannabis Marijuana is industrially the most useful plant ever cultivated by man; it is praised in the bible for its psychoactive properties [9]. It is scholarly understood that the word Cannabis has its earliest root in the Semitic Language of Hebrew. The ancient Hebrew word for Cannabis is KanehBosem. In the bible, the word was mistranslated to Calamus; though many English bibles noted this error and decided to use Fragrant Cane instead, the rough translation of Kaneh-Bosem. Any intelligent

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person could realize that Kaneh-Bos is the origin of the word Cannabis. The second page of the bible states, And God said, Behold, I have given you every herb bearing seed, which [is] upon the face of all the earth, and every tree, in the which [is] the fruit of a tree yielding seed; to you it shall be for food (Gen 1:29). To the good believers of the bible, this means [all] herbs yielding seed across the face of the earth; including marijuana and tobacco, are wholesome and of nutritional value. The following verses go on to state that these things are Very Good as well. Most believers in the bible believe that Cannabis is bad, because it is illegal. They do not understand that only man has made it illegal, with the intent of inducing malnutrition among the populace. This has succeeded, with the rates of obesity; pharmaceutical companies are now extracting THC from cannabis to use as a weight-loss drug [10]. Chocolate Chocolate is an opiate, cannibinoid, amphetamine, and source of nicotine all mixed together, it was held of the highest economic and religious value by the Indigenous South Americans. [11] Chocolate contains tryptophan. Tryptophan is an essential amino acid. It is the ratelimiting step in the production of the mood-modulating neurotransmitter serotonin. Enhanced serotonin function typically diminishes anxiety. Tryptophan is also broken down by the body into nicotine (niacin). Consumption of chocolate triggers the release of endorphins, the body's endogenous opiates. Enhanced endorphin-release reduces the chocolate-eater's sensitivity to pain. Chocolate contains a group of neuroactive alkaloids known as tetrahydro-betacarbolines. Tetrahydro-beta-carbolines are also found in beer, wine and liquor. Chocolate contains phenylethylamine, structurally identical to amphetamine, well indicating why this food staple is highly addictive. Bread Bread is spoken of highest value in the Holy Bible. Exodus 16:12, I have heard the murmurings of the children of Israel: speak unto them, saying, at even ye shall eat flesh, and in the morning ye shall be filled with bread; and ye shall know that I am the LORD your God. By direct implication, only under the influence of opiates and nicotine found in bread, can man even be able to understand the divines existence. It is also said in the bible, that both Jesus and Moses anointed themselves with holy oil (marijuana containing) and spent 40 days in the desert without eating bread; yet came back gleaming because they had been with Yahweh. This means that if a person has no bread, he can supplement his nutrition with cannabis to remain in a consciousness that is holy. Milk

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Milk, which contains powerful bovine opiate (casomorphine), meant to sedate baby cows; is highly praised in the Holy Quran. Be grateful to the Bounties of Allah, to eat its meat and drink its milk, pure milk, palatable to drinkers." (16:66) The Prophet Mohammad is reported in the Hadith Collection of his records to have encouraged a man to drink more milk than he normally would. The Prophet Mohammad is also said to have never left his house without Kefir. Kefir is a lactose based bacterial culture that cannot factually survive without human care. Kefir also proves beyond reasonable doubt the theory of Creationism. Not only is this organism unable reproduce itself without human care, but historic man did not have the capabilities of creating living organisms that would be dependent upon himself for survival. Kefir contains the most important lacto-bacterias for the human immune-system, and was required by law to be consumed daily by Chernobyl survivors [citation needed]. It is not found naturally occurring in nature, and only capable of reproducing itself if placed in buckets of milk. The Recorded History of Kefir states that God rained it down to man from the sky as a gift, which also serves as the only rational explanation for its existence. Mohammad was reported to have healthily lived for 96 years, and was able to fight war through his elderly age. Alcohol Wine is spoken of frequently in the holy bible and especially recommended, "Drink no longer water, but use a little wine for thy stomach's sake and thine often infirmities. " (Timothy 5:23) If taken literally, we should no longer drink water and instead drink wine exclusively. Jesus turned the water into wine, possibly because water is simply not as wholesome. Wine is typically forbidden to Muslims, only out of ignorance of their own religion, as similarly experienced by Christians with Cannabis. It is stated in the Quran, A similitude of the Garden which those who keep their duty (to Allah) are promised: Therein are rivers of water unpolluted ... and rivers of wine, delicious to the drinkers. -- Sura 47:15 Surely the pious will be in bliss ... their thirst will be slaked with pure wine sealed. -- Sura 83:22,25 How would Muslims ever know the taste of wine, and what to expect in the afterlife, if it is forbidden to them in the first place? I am sure there would be no suicide bombings if they took drinks and relaxed like the Islamic people of Turkey. Health Benefits of Tobacco according to the Scientific Method: Tobacco tar is known to protect against the damaging effects of Asbestos [12], cure Asthma and prevent Breast Cancer [13]. Nicotine has been shown to stop Tuberculosis in its tracks. [14] Carbon Monoxide may prevent Heart attacks and 74

Stroke. [15] Parkinsons Disease is associated with non-smoking [16] Alzheimers disease is associated with non-smoking. [17] Less than 3% of smokers die of lung cancer, even if they smoked chemical ridden generic cigarettes. [18] According to the Journal of Theoretic, Smoking simply does not cause Lung Cancer. [19a] Researchers attempted to induce lung-cancer in thousands of mice through exposure to chronic levels of tobacco smoke (equivalent to 200 cigarettes a day in some cases) every study failed. One study even proved that chronic exposure to tobacco smoke protected mice from cancer induced by nuclear radiation. [19b][c] Tobacco Related Premature death by the Scientific Method: A person is logged as a premature smoking death no matter what age he dies, including the worlds oldest living people [20]. Anti-tobacco research is paid for and governed by the Pharmaceutical industry. [21] The Pharmaceutical industry distributes methamphetamines to children [22], including Desoxyn (Methamphetamine Hydrochloride)[23] Their credibility and integrity is certainly dubious. They happen to be the sole supplier and profiteer of nicotine patches.

Facts and Evidences: Marijuana smoking is not linked to lung cancer, even though it contains more chemicals known to cause Lung Cancer. [24] The Pharmaceutical industry has submitted an ample amount of scientific evidence to convince people of smoking related epidemic, some studies have even shown the complete opposite of the scientific evidence I have chosen to use in my research. It is certain that all of the studies conducted by the pharmaceutical industry are biased to produce anti-smoking propaganda (i.e. using obese smokers as test subjects) (orciting that nicotine dependent fast-food eaters died from their smoking and not from their fast food consumption [20][25] . No conclusive truth can be established from Scientific Study, but people will believe what they are told on Television to be fact anyway. This essay is designed to educate the brain-washed masses with facts. For this purpose, I specifically chose the scientific evidence that supported the fact, worlds oldest living people are chain smokers [1]. Those who disagree will choose the scientific evidence that supports the theory "Smoking causes premature death"[20]

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Scientific evidence is produced of money, and fact is produced of history. Many people have been confused in deciphering the difference between scientific evidence and fact. Under the Iron-Curtain of Corporatism, the facts will not even be known by most people, excluding myself and the readers of this essay. The fact states that the worlds oldest living people were smokers and suffered no ailment from it [1]. Those who rely on Science Fiction (err...evidence) in an attempt to fraudulate the fact say, "Smoking causes premature death".[20] I know that my logic must be superior to that of a "normal" non-smoking human being, and I declare that Fact disproves fiction. The wisest words to have been spoken throughout the recorded history of man. A short segment about Alcohol: Some of the worlds oldest living people were considered "moderate drinkers". Moderate drinking is defined as 1-3 glasses of alcohol a day. The Queen Elizabeth lived 100 years drinking gin cocktails and smoking cigarettes daily. As did George Burns with his 20 cigar a day habit beginning at the age of 12, he is rumored to have also enjoyed ten martinis on a daily basis. Vitamins in Beer? "Unfiltered" Beer is chalk full of B-vitamins, it is known as "liquid bread".[26] Moderate drinking is known to provide over 50 different health benefits[27]. Is all alcohol created equal? Most alcohol on the market is cheap crap, filtered beer is crap, preservatives and chemical flavorings are crap and often added to alcoholic beverages. For a good drink, buy quality Gin that has been distilled at least 3 times. i.e. "Bombay Sapphire", mix it with all natural tonic water and squeeze some grapefruit juice into it. Or try drinking unfiltered beer for a real health experience. Summary: Read my sources, light up, have a drink, and encourage your children to smoke. One should note, that creationism is shown beyond reasonable doubt by paintings from the 15th and 18th centuries [29]

Jesus basically walked around bad-mouthing Pharisees and Saccubacees,

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people back then didn't smoke tobacco yet, so they were living the symptoms of nonsmoking; irritability and hunger. The symptoms of non-smoking made them practically barbaric; The Jews killed Jesus for exercising his fourth amendment. Daniel John Richard Date References: 1: The Evidence - World's Oldest - All Smokers http://www.forces.org/evidence/hamilton/other/oldest.htm 2:Biography of Madame Jeanne Calment http://www.biogs.com/famous/calment.html 3. 120 Year-old Woman Claims smoking pot/tobacco and drinking every day is her secret to long life. http://www.tobacco.org/news/237486.html 4. Encyclopedia entry for Vitamin B3 (Niacin) http://en.wikipedia.org/wiki/Niacin http://www.pdrhealth.com/drug_info/nmdrugprofiles/nutsupdrugs/nia_0184.shtml http://www.umm.edu/altmed/ConsSupplements/VitaminB3Niacincs.html 5. Neuroscience for Kids: Coco http://faculty.washington.edu/chudler/choco.html 6: Psychoactive food: http://www.chocolate.org/ 7. Encyclopedia entry: Gluten-free Casein-free diet. http://en.wikipedia.org/wiki/Gluten-free,_casein-free_diet http://www.greatplainslaboratory.com/gluten-casein.html http://ajpgi.physiology.org/cgi/content/abstract/290/6/G1105 8. Encyclopedia entry: Tobacco http://encarta.msn.com/encyclopedia_761562287/Tobacco.html 9. Cannabis Linked to Biblical Healing http://news.bbc.co.uk/2/hi/health/2633187.stm 10. Cannabis Obesity Drug Trials to Start Yahoo News UK http://uk.news.yahoo.com/30012007/325/cannabis-obesity-drug-trials-start.html 11. History of Chocolate http://www.fieldmuseum.org/Chocolate/history_intro.html 12. Smoking has a protective effect on immunological abnormalities in asbestos workers. 0429. Institute of Immunology and Experimental Therapy (Poland). Lange, A. "Effect of Smoking on Immunological Abnormalities in Asbestos Workers. ---Relative risk of lung cancer for asbestos workers was "highest for those who had never smoked, lowest for current smokers, and intermediate for ex-smokers. The trend was statistically significant. There was no significant association between smoking and deaths from mesothelioma," [emphasis added]. 0565. University of London, School of Hygiene and Tropical Medicine. "Cancer of the Lung Among Asbestos Factory Workers." [Many other studies show similar findings for asbestos workers].

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13. Smokers Paradoxes, the Health Benefits of Smoking http://en.wikipedia.org/wiki/Tobacco_smoking#Health_benefits_of_smoking 14. Shocker: Villain Nicotine slays TB http://www.data-yard.net/10c/nicotine.htm 15. The Carbon Monoxide Paradox http://www.data-yard.net/10b/cm.htm 16. Parkinsons Disease is associated with non-smoking. http://www.forces.org/evidence/carol/carol36.htm 17. Alzheimers Disease is associated with non-smoking. http://www.forces.org/evidence/carol/carol16.htm 18. An Early Warning for Lung Cancer- Less than 3% of smokers die of Lung Cancer. http://www.data-yard.net/3/md0203_1.htm 19a. Smoking Does Not cause Lung Cancer; helps to prevent it http://www.journaloftheoretics.com/Editorials/Editorial%201-4.html b. http://www.vialls.com/transpositions/smoking.html c. "Inhalation Bioassay of Cigarette Smoke in Rats" A. P. Wehrner, et al. (Battele Pacific Northwest Labs, Richland WA) Journal of Toxicology & Applied Pharmacology, Vol. 61: pp 1-17 (1981) The results show that the highest number of tumors occurred in the untreated control [non-smoking] rats. The next highest number of tumors occurred in rats subject to sham smoking, i.e. rats which were placed in the smoking machine without smoke exposure, and the lowest number of tumors occurred in the smoke-exposed rats. Among the latter, the largest number of tumors occurred in rats exposed to smoke from cigarettes having the lowest level of nicotine. 20. Tobacco Will kill 1 billion this century http://www.foxnews.com/story/0,2933,202810,00.html?sPage=fnc.health/cancer 21. State and Institutions: At the service of the Pharmaceutical Industry http://www.forces.org/evidence/files/pharma.htm 22. Psychiatric Drug Facts. http://www.breggin.com/ 23. Encyclopedia entry for Desoxyn (Methamphetamine Hydrochloride) http://en.wikipedia.org/wiki/Desoxyn 24. Pot Smoking not linked to Lung Cancer http://www.entheology.org/edoto/anmviewer.asp?a=246&z=9 25. The association between degree of nicotine dependence and other health behaviors http://eurpub.oxfordjournals.org/cgi/content/abstract/11/4/450 26. Vitamin B Sources, Wikipedia http://en.wikipedia.org/wiki/Vitamin_b#Vitamin_B_sources 27. Alcohol and Health http://www2.potsdam.edu/hansondj/AlcoholAndHealth.html Additional Sources 28. Primary Smoking and Lung Cancer http://www.forces.org/evidence/evid/lung.htm 78

29a. A view of The Madonna with Saint Giovannino"(15th C.) by Domenico Ghirlandaio (1449-1494) http://members.lycos.co.uk/dandate2/ufomadonna.jpg b. A Closer view of The Madonna with Saint Giovannino"(15th C.) by Domenico Ghirlandaio (1449-1494) http://members.lycos.co.uk/dandate2/maryufoclose.jpg c. "The Baptism of Christ"(18th C.) by Aert De Gelder http://members.lycos.co.uk/dandate2/ufojesus2.jpg

"Using normal lung cells, the team found that nicotine levels routinely acquired by smoking will activate cell survival [u]within minutes of exposure.[/u] Theoretically, as long as nicotine is present in the lungs or bloodstream, many of the cells damaged from carcinogens will remain alive, increasing the risk of cancer." The next study will probably show that the effect takes place within [u]seconds[/u]. Or maybe that even the mere thought of smoking triggers the effect. In any case, the report ought to give the producers of nicotine aids to stop smoking pause. But then, that would be in a sane world. At least they are not saying that nicotine causes cancer. An oversight? I thought that had been one of the claims against the stuff. The debate about the adverse health effects of SHS is over, The US Surgeon General's report says so. 2006 SURGEON GENERALS REPORT Now let us look at what the report, pages 13-16, said are some of the things SHS exposure does not cause: 1. The evidence is inadequate to infer the presence of a causal relationship between maternal exposure to secondhand smoke during pregnancy and spontaneous abortion.

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2. The evidence is inadequate to infer the presence of a causal relationship between exposure to secondhand smoke and neonatal mortality. 3. The evidence is not sufficient to infer a causal relationship between maternal exposure to secondhand smoke during pregnancy and preterm delivery. 4. The evidence is inadequate to infer the presence of a causal relationship between exposure to secondhand smoke and congenital malformations. 5. The evidence is inadequate to infer the presence of a causal relationship between exposure to secondhand smoke and cognitive functioning among children. 6. The evidence is inadequate to infer the presence of a causal relationship between exposure to secondhand smoke and behavioral problems among children. 7. The evidence is inadequate to infer the presence of a causal relationship between exposure to secondhand smoke and childrens height/growth. 8. The evidence not sufficient to infer a causal relationship between prenatal and postnatal exposure to secondhand smoke and childhood cancer. 9. The evidence is not sufficient to infer a causal relationship between prenatal and postnatal exposure to secondhand smoke and childhood leukemias. 10. The evidence is not sufficient to infer a causal relationship between prenatal and postnatal exposure to secondhand smoke and childhood lymphomas. 11. The evidence is not sufficient to infer a causal relationship between prenatal and postnatal exposure to secondhand smoke and childhood brain tumors. 12. The evidence is inadequate to infer the presence of a causal relationship between prenatal and postnatal exposure to secondhand smoke and other childhood cancer types. 13. The evidence is not sufficient to infer a causal relationship between parental smoking and the natural history of middle ear effusion. 14. The evidence is inadequate to infer the presence of a causal relationship between parental smoking and an increase in the risk of adenoidectomy or tonsillectomy among children.

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15. The evidence is not sufficient to infer a causal relationship between secondhand smoke exposure from parental smoking and the onset of childhood asthma. 16. The evidence is inadequate to infer the presence of a causal relationship between parental smoking and the risk of immunoglobulin E-mediated allergy in their children. 17. The evidence is not sufficient to infer a causal relationship between secondhand smoke and breast cancer. 18. The evidence is not sufficient to infer a causal relationship between secondhand smoke exposure and a risk of nasal sinus cancer among nonsmokers. 19. The evidence is inadequate to infer the presence of a causal relationship between secondhand smoke exposure and a risk of nasopharyngeal carcinoma among nonsmokers. 20. The evidence is inadequate to infer the presence of a causal relationship between secondhand smoke exposure and the risk of cervical cancer among lifetime nonsmokers. 21. The evidence is not sufficient to infer a causal relationship between exposure to secondhand smoke and an increased risk of stroke. 22. Studies of secondhand smoke and subclinical vascular disease, particularly carotid arterial wall thickening, are not sufficient to infer a causal relationship between exposure to secondhand smoke and atherosclerosis. 23. The evidence is not sufficient to conclude that persons with nasal allergies or a history of respiratory illnesses are more susceptible to developing nasal irritation from secondhand smoke exposure. 24. The evidence is not sufficient to infer a causal relationship between secondhand smoke exposure and acute respiratory symptoms including cough, wheeze, chest tightness, and difficulty breathing among persons with asthma. 25. The evidence is not sufficient to infer a causal relationship between secondhand smoke exposure and acute respiratory symptoms including cough, wheeze, chest tightness, and difficulty breathing among healthy persons.

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26. The evidence is not sufficient to infer a causal relationship between secondhand smoke exposure and chronic respiratory symptoms. 27. The evidence is not sufficient to infer a causal relationship between short-term secondhand smoke exposure and an acute decline in lung function in persons with asthma. 28. The evidence is inadequate to infer the presence of a causal relationship between shortterm secondhand smoke exposure and an acute decline in lung function in healthy persons. 29. The evidence is inadequate to infer the presence of a causal relationship between chronic secondhand smoke exposure and an accelerated decline in lung function. 30. The evidence is not sufficient to infer a causal relationship between secondhand smoke exposure and adult-onset asthma. 31. The evidence is not sufficient to infer a causal relationship between secondhand smoke exposure and a worsening of asthma control. 32. The evidence is not sufficient to infer a causal relationship between secondhand smoke exposure and risk for chronic obstructive pulmonary disease (emphysema and chronic bronchitis). 33. The evidence is inadequate to infer the presence of a causal relationship between secondhand smoke exposure and morbidity in persons with chronic obstructive pulmonary disease. Not much of an assault! Regarding our EPA's 3000 lung cancer deaths from exposure to SHS: The Australian Supreme Court reached this conclusion, officially rejecting the EPA report because: "The [study] results set out in tabular and statistical form did not support the claim of risk." - Federal Focus, Vol VIII, NO. 11, 1993

So far we found and as the literature shows smoking has many benefits: a) Osteo-arthritis reduced threefold (the most for knee arthritis in women) b) Lowered insuline growth factor IGF-1 (in animal experiments this change extends

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lifespan). c) Internal antioxidant SOD doubled (recent article labels the higher SOD "the elixir of ethernal life" based on animal experiments i.e. hard science). d) Reduced MAO B enzyme (smokers in their 60s have MAO B of nonsmokers in their 20s; also here). Lowering of MAO B is the holy grail (deprenyl does it but not as well as tobacco) of life-extension and smart drug circles. e) Telomerase ("fountain of youth") much more active in smokers. f) Glutathione (chief antioxidant in human body) and catalase (another key antioxidant which neutralizes alcohol damage, cyanide,...) doubled in smokers. g) Nicotine suppresses cell death of neurons (it also promotes vascular growth factor, e.g. growth and branching of capillaries). h) Low concentration carbon monoxide (as found in tobacco smoke) protects cells in harsh conditions, such as low oxygen and general cell death. i) Nitric oxide stimulates peripheral circulation (this is the mechanism behind Viagra effect). j) The miracle supplement (for skin, heart, brain rejuvenation) Coenzyme Q10 is extracted from tobacco leaf. k) Raises youth hormonoes DHEA, pregnenolone, testosterone,... ... and so on and on, all hard science (not the wishfully interpreted statistical correlations of usual antismoking "science"). It's just mind boggling how truly good this ancient 'gift of gods' is. And this is all from antismoking scientists, doing the hard science, while straining very hard to somehow give their findings negative spin. Smokers ought to know all this and when they do in sufficient numbers, the antismoking racket will be over instantly. Hence, we need to completely ignore antismokers and also not waste any time on reassuring nonsmokers that SHS is harmless (its only real drawback is that it isn't as beneficial as the primary smoke; but hey, they get what they pay for). Our sole focus must be smokers, to let them know that smoking is not merely harmless but that it is the best thing one can do for ones health, via website and word of mouth (little leaflet with web address can be dropped wherever there are outdoors smokers, as soon FORCES updates and firms up the target web pages, with a clean, crisp, unwavering message presented at multiple depths and levels of scientific detail, along with all supporting materials available on the web site itself). It is not hard to defend this position since all hard science is on our side, while the antismoking propaganda rests entirely on soft "science" (the wishful interpretations of statistical correlations, which on their own are consistent not just with their theory but ours as well; the only difference is that hard science, the real experiments and detailed biochemistry, is entirely on our side). Another aspect we need to watch for in this undertaking is to absolutely stay away from any other political, ideological, philosophical, religious, ethnic,... issue and entanglement. Hence, no gun issues, no global warming, no abortion, no islam, no

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immigration, no home schooling, no sexual orientation or gay marriage, no marijuana or drug war,... etc, however tempting it may be on occasion. We must be very disciplined on this, or our enemies will splinter us in no time. If you are a fellow smoker, that is all that matters and you are sincerely and fully welcome. The only enemy we hate and attack is the Big Pharma (and they have plenty of enemies already e.g. supplement & vitamin industry, natural health folks, elderly being ripped off on medicines, parents of vaccine damaged autistic & ADHD kids, the obese or just people who like tasty foods,... all of them are potential allies, but only in the future, after the main job is done). All others, including loudmouth antismokers or doctors and media, are simply seen as being duped by the main villain and we have nothing against any of them. Boycotts of carefully selected companies & politicians, one at a time, should be left for a later phase, after we have completed the primary task, to spread the word among the 60 million American smokers. Once the receiving FORCES web site is properly prepared, this first phase will take easily less than a year, provided we are single-focused on that sole task. For example, if each smoker, once informed, continues informing one new smoker every two weeks, it will take less than 1 year to have all 60 million American smokers with us! Finally, as a practical matter of economizing resources, the information gathering phase (collecting and downloading scientific papers, searching archives, especially tobacco documents) should be done quietly, low key [...] ... the best initial approach would be to gather competent sympathetic folks, mostly smokers, in newsgroups, healthgroups, among college students and medical personnel,... for a project of collecting, studying and classifying evidence on health benefits of smoking. They simply join a semi-private discussion group, with a WIKI encyclopedia style adjunct and the facility to upload files (PDF, html, images, videos) by trusted members, where all the evidence is gathered and built up, as it crystallizes from the informal discussions into a solid, systematic information (I have much more on the logistics and technical aspects of this process, but on that later). Only then, with the scientific and logical foundation firmed up, would we go out to spread the word among general smokers. Even then, no political or economic action would be undertaken or advocated, but one would merely seek to inform smokers on the other side of smoking issue with a clear, unambiguous message: smoking is good for you. The rest will happen automatically, once the numbers of well informed smokers are sufficient.

Alzheimer's, Parkinson's and schizophrenia risks are cut in half by smoking (at least) and for the patients, taking up smoking greatly alleviates the symptoms and reduces further damage of these diseases. Those who quit smoking, increase their risk of getting these diseases by 50% for each 10 years of non-smoking. For the early onset Alzheimer's (40s and 50s), smoking cuts the risk tenfold.

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The problem is that vast majority of smokers were brainwashed, like the rest of population, that smoking is bad for them and those around them, that smoking is a vice. You can't convince very many people to join in a defense of what they believe is a vice, even if it is their own. For example, how many societies for defense of 'wife beaters' or 'drunken drivers' rights are there? Will 'wife beaters' create any such and join en masse if one were to tell them that their ways of handling family disagreements are eroding and in grave danger? Of course not. In contrast to the present antismoking brainwashing, people have smoked tobacco for over ten millennia and cultivated it for seven millennia as a wholesome medicinal plant, the most potent one humans have ever had. That was a general view, based on thousands years of human experience with tobacco, until just few decades ago, when the antismoking swindle was pulled out of thin air, based on the worst kind of junk science. The antismoking con is making enormous amounts of money, stolen from the smokers, for the conmen behind it, chiefly the pharmaceutical industry (albeit, FORCES only looks at their nicotine replacement "therapy" profits, which is just a tiny tip of their profit iceberg, see few examples here or here, here). Therefore, the message that needs to be passed on to fellow smokers is a simple scientific fact (which is based on hard science, from the antismoking interests themselves) that "Smoking is good for you" (see also a thread here, all posts by "nightlight", where this fact was defended in much more detail against a pack of health zealots; many further facts and links are given in my posts on usenet and speakeasy). The upshot of all the collected scientific evidence is that tobacco smoke is not merely harmless, but it is the most potent medicinal substance and youth elixir, natural or synthetic, bar none, humans have ever known. Once the 50+ million American smokers are aware that 'smoking is good for them', the antismoking swindle will be wiped out instantly. Some thoughts on how to get there from here were given on speakeasy (post-1, post-2, post-3 and post-4). Therefore, the present Multimedia initiative, aiming to educate general public that smoking isn't quite as bad as commonly believed and that SHS is mostly harmless, is not merely a waste of time and resources, but it is explicitly counterproductive since it reinforces in the minds of smokers themselves the fundamental 'big lie' of the antismoking conmen (that smoking is bad at all, when it is exactly the opposite). That 'big lie' was what started the entire con in late 1950s and its effect, in addition to directly harming smoker's health via 'witch doctor effect', is to paralyze smokers from defending themselves against the antismoking parasite. Accepting it leads inevitably to where we are now, only faster the second time around. Hence, smoker organizations should stop wasting time and resources on educating general public about SHS, or trying to organize smokers around liberty issues, since that will keep failing, as it always did, for the reason above.

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The sole focus of smoker organizations in the present situation need to be tens of millions (or 1-2 billions worldwide) of brainwashed smokers and and how to get to them as quickly as possible the simple fact: "smoking is good for you". All the rest will happen automatically.

Cancer Lett. 2007 Feb 8;246(1-2):24-33. Epub 2006 Mar 6.

Smoking is associated with increased telomerase activity in short-term cultures of human bronchial epithelial cells.
Yim HW, Slebos RJ, Randell SH, Umbach DM, Parsons AM, Rivera MP, Detterbeck FC, Taylor JA. Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. Telomerase plays an important role in the maintenance of telomere ends in normal and tumor cells and ectopic expression can immortalize human bronchial epithelial (HBE) cells. We assessed telomerase activation, growth properties and methylation status in the hTERT promoter in a panel of HBE cell cultures in relation to smoking and previous lung cancer history. HBE cells were obtained from a total of 26 subjects, six of whom were lifelong nonsmokers, while 20 subjects had a smoking history, including seven who had lung carcinoma. Telomerase activity was determined using the telomeric repeat amplification protocol (TRAP). Maximum passage number and time to senescence were also determined through extended culturing. The distribution of the telomerase activity between ever-smokers and never-smokers was significantly different (P=0.03, F-test), and there was a strong correlation between telomerase activity and the number of pack-years smoked (P=0.0012, F-test for slope). A small difference in telomerase activity was observed according to lung cancer status (P=0.02, F-test). Telomerase activity was not correlated with maximum passage number after extended culturing or with time to senescence. None of the HBE cultures demonstrated methylation of the hTERT promoter. Our results indicate an association between tobacco carcinogen exposure and telomerase activity in normal bronchial epithelium, although a causative role of tobacco smoking in the (re)activation of telomerase can not be proven. An increase in telomerase activity in normal bronchial epithelium might extend the lifespan of cells at risk for malignant transformation, and thus contribute to lung carcinogenesis.

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Study finds smokers have higher risk of dementia http://news.yahoo.com/s/nm/20070903/hl_nm/dementia_smokers_dc

WASHINGTON (Reuters) - People who smoke are more likely to develop Alzheimer's disease and other forms of dementia than people who have quit or have never smoked, Dutch researchers reported on Sunday. ADVERTISEMENT Smokers over the age of 55 were 50 percent more likely to develop dementia than similar nonsmokers, Dr. Monique Breteler of Erasmus Medical Center in Rotterdam, Netherlands, and colleagues found. Writing in the journal Neurology, Breteler and colleagues said they followed nearly 7,000 people age 55 and older for an average of seven years. Over that time, 706 of the people developed dementia. There is a well-known gene that raises the risk of dementia called APOE4 or apolipoprotein E4. Smoking did not affect the Alzheimer's risk for people who had that gene. But people who did not have the gene had a 70 percent higher risk of Alzheimer's if they smoked. Smoking could cause small strokes, which in turn damage the brain and cause dementia, Breteler said. "Smoking increases the risk of cerebrovascular disease (stroke), which is also tied to dementia," Breteler said in a statement. "Another mechanism could be through oxidative stress, which can damage cells in the blood vessels and lead to hardening of the arteries. Smokers experience greater oxidative stress than nonsmokers, and increased oxidative stress is also seen in Alzheimer's disease." Oxidative stress is a process akin to rusting, in which chemical reactions damage the DNA.

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_________________ Smoke'em if ya got'em!

Why Smokers Feel Good By LiveScience Staff posted: 29 October 2004 6:30 am ET Smokers enjoy their habit because it stimulates the flow of "feel good" chemicals in the brain, according to a new study involving just a handful of test subjects. The system of the brain affected is the same one that is stimulated by heroin and morphine. The study is the first to show smoking affects the brain's natural system of chemicals called endogenous opioids, which also help quell painful sensations and heightening positive emotions, the researchers said in a statement today. The system includes the release of endorphins that produce the oft-sought "runner's high." Participants did not smoke for 12 hours before the test. Then they smoked two cigarettes which had the nicotine removed from them, followed later by two cigarettes with nicotine. Their brains were monitored the whole time, and they were also asked how they felt at each step. "It appears that smokers have an altered opioid flow all the time, when compared with non-smokers, and that smoking a cigarette further alters that flow by 20 to 30 percent in regions of the brain important to emotions and craving," said David Scott, a graduate student in the University of Michigan Neuroscience Program. "This change in flow as seen on a brain scan correlated with changes in how the smokers themselves reported feeling before and after smoking."

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The orange dots on these brain scans show the areas where the biggest changes in opioid activity took place after smokers began smoking a regular cigarette. On the left is the cingulate, where activity increased 20 percent. On the right is the amygdala, where activity decreased by more than 20 percent. Credit: University of Michigan The study involved just six smokers, however, all males in their 20s who said they normally puffed 14 cigarettes a day. Scott and his colleagues say that despite the small number of participants, they were surprised at the large effect on opioid levels. The research will be expanded to include more participants. Further study, the scientists suggest, might reveal why the habit is so hard to kick. "The interaction of tobacco, and especially nicotine, with brain chemistry is a fascinating area that we're just beginning to understand, especially when it comes to correlating neurochemistry with behavior," said study leader Jon-Kar Zubieta, a psychiatrist and neuroscientist at the university. "Just as with the 'hard' drugs of abuse, such as heroin and cocaine, the phenomena of pleasure, addiction, increased tolerance and craving from tobacco are firmly rooted in neurochemistry." The research will be presented Tuesday in San Diego at the annual meeting of the Society for Neuroscience. http://www.livescience.com/health/041129_smoking_feel.html

Schizophrenia
Nearly 90% of schizophrenics smoke [NOTE: most of them chain smoke, yet they have 30-50 percent lower lung & other cancer rates, compared to general population of the same age]. One possible explanation for this phenomenon is that schizophrenics may smoke in part because nicotine may improve their ability to filter out and ignore irrelevant sensory information, which may be related to an impairment

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of inhibitory mechanisms which act to decrease attention to repeated stimuli (sensory gating).

whatsmokersshouldknow.com

What Smokers Should Know...

SMOKING IS GOOD FOR YOU!

Smoking is Good for You!

AKA, Smokers' Paradoxes
Note that the studies referenced are what is known as "hard science" as opposed to the "soft science" of epidemiological studies. Also, notice that the research here is not in tobacco literature or tobacco-funded literature; in fact, many of the studies cited are actually from antismoking literature funded by Big Tobacco Control and/or Big Pharma. For more information, please see the Must Reads. You can find previously cited Therapeutic Effects of Smoking and Nicotine in the FORCES International archives. An easy-to-read but well-referenced paper is ONE FEELS BETTER TEMPERED: An Investigation Into The Beneficial Effects Of Smoking
The miracle supplement (for skin, heart, brain rejuvenation) Coenzyme Q10 is extracted from tobacco leaf. WebMistress: Coenzyme Q10 is also essential in fighting cancer!!!

In Coenzyme Q10: A Miracle Vitamin , Dr. Richard A. Kunin extols the benefits of Coenzyme Q10. He also says:
The energy of oxidation in cells depends on CoQ in partnership with niacinamide (vitamin B3), riboflavin (vitamin B2), and minerals such as iron and copper to effect the movement of electrons and hydrogen protons in the power plant of cell, the mitochondrion. ... Incidentally, tobacco leaf is the champion source, containing 184 mg in a quarter pound. Note that the doctor follows with the disclaimer, "In fact, the Japanese companies make

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their CoQ from tobacco, however it is only released by means of bacterial fermentation not by smoking." The fact remains that CoQ 10 is a natural miracle for the human body and its chief source is tobacco! Those MDs just can't get their heads around the fact that tobacco is a valuable gift from nature! Now take a look at what a pharmacy has to say about natural vs. synthetic CoQ10: The natural CoQ10 in Qmelt is made via fermentation in which a microorganism (in the case of CoQ10, a bacterium or yeast) naturally produces CoQ10. The CoQ10 is then extracted from the organism and concentrated. It is termed natural since it is normally and naturally produced by the yeast or bacterium from which it was taken. This is different from synthetic CoQ10 which is made by taking a compound found in tobacco and then mixing it with other chemicals to form a similar structure of CoQ10. While tobacco is natural, CoQ10 is not taken from tobacco in this synthetic process....the only thing taken from the tobacco is a compound which is used as the starting material for chemically creating CoQ10. That is why it is referred to as a synthetic process. Tobacco or plants in general do not contain significant amounts of CoQ10 The pharmacy "information" is in direct contradiction of what is known by everyone else: (1) tobacco is the chief source of CoQ10 with an abundance of the enzyme and (2) the means by which CoQ10 is extracted is not chemical, although it might involve fermentation. (Note: The fermentation process might involve beets or fermented sugar cane.)

AN IMPORTANT NOTE: The doctor cited above comments on the importance of CoQ in partnership with other nutrients, including niacinamide, AKA nicotinic acid, niacin and vitamin B3. This is a form of nicotine, which could result from the alteration of nicotine as it is very unstable. Please see Facts about Nicotine.
Smoking Reduces Parkinson's Neurology. 1999 Sep 22;53(5):1158. Smoking and Parkinson's disease: a doseresponse relationship Gorell JM, Rybicki BA, Johnson CC, Peterson EL

Department of Neurology, Henry Ford Health System, National Institute of Environmental Health Sciences Center in Molecular and Cellular Toxicology with Human Applications, Wayne State University, Detroit, MI, USA. OBJECTIVE: To determine whether an inverse dose-response relationship exists between cigarette smoking and PD among ever-smokers and ex-smokers. METHODS: Smoking and alcohol consumption were analyzed in 144 PD patients and 464 control subjects, who were frequency matched for sex, race, and age (+/-5 years), in a population-based case-control study of men and women > or =50 years old in the Henry Ford Health System. RESULTS: With never-smokers as the reference category, there was an inverse association between current light smokers (>0 to 30 pack-years) and PD patients (odds ratio [OR], 0.59; 95% CI, 0.23 to

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1.53), and a stronger inverse association of PD with current heavy smokers (>30 pack-years; OR, 0.08; 95% CI, 0.01 to 0.62). When former >30-pack-year smokers were stratified by the interval since quitting, there was an inverse association between those who stopped >20 years ago and PD (OR, 0.86; 95% CI, 0.42 to 1.75), and a greater inverse relationship with those who stopped 1 to 20 years ago (OR, 0.37; 95% CI, 0.19 to 0.72). Alcohol consumption had no independent, significant association with PD, but heavy drinking (>10 drink-years) had a greater effect than light-moderate drinking in reducing but not eliminating the inverse association between smoking and PD. CONCLUSIONS: The inverse dose-response relationship between PD and smoking and its cessation is unlikely to be due to bias or confounding, as discussed, providing indirect evidence that smoking is biologically protective.
Also see Smoking lowers Parkinson's disease risk from Reuters (Mar 20, 2007).

From "Temporal relationship between cigarette smoking and risk of Parkinson disease" (NEUROLOGY 2007;68:764-768):
The lower risk of Parkinson disease among current and former smokers varied with smoking duration, intensity, and recentness. The dependence of this association on the timing of smoking during life is consistent with a biologic effect. Osteo-arthritis reduced threefold (the most for knee arthritis in women) IS OSTEOARTHRITIS IN WOMEN AFFECTED BY HORMONAL CHANGES OR SMOKING? from the journal for British Society for Rheumatology (1993). Internal antioxidant SOD doubled (recent article labels the higher SOD "the elixir of eternal life" based on animal experiments) From Scientists find elixir of eternal life - in a worm By Roger Highfield, Science Editor, "Detailed work showed that the gene can boost levels of proteins called SODs (superoxide dismutase) which mop up free radicals, harmful chemicals linked with aging. The researchers think that this may be a defense mechanism that helps the creatures tolerate starvation." Reduced MAO B enzyme (smokers in their 60s have MAO B of nonsmokers in their 20s; also here). Lowering of MAO B is the Holy Grail (deprenyl does it but not as well as tobacco) of life-extension and smart drug circles. Explained very well by NightLight referencing The American Journal of Psychiatry illustrated by these graphs, and the National Academy of Sciences (September 8, 2003). More can be found on MAO and the importance of MAO-inhibitors in Turkish Journal of Medical Sciences, MAO Inhibitors in Aging: Can They Serve as Protective Agents in Cardiac Tissue Against Oxidative Stress?, Scholar Google and The real eye-opener comes from theNational Institute on Drug Abuse! That's about as far as you can get from being a shill for Big Tobacco! Yet, this antismoking group's

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very own study, "Tobacco Smoke May Contain a Psychoactive Ingredient Other Than Nicotine" (NIDA News, Volume 13, Number 3, July, 1998), states plainly: The amount of the enzyme, called monoamine oxidase (MAO), is reduced by 30 to 40 percent in the brains of smokers, compared to nonsmokers or former smokers, the brain scans show. The reduction in brain MAO levels may result in an increase in levels of dopamine, which scientists associate with the reinforcing effects of drugs of abuse. A note needs to be on the research paper in the American Journal of Psychiatry, Maintenance of Brain Monoamine Oxidase B Inhibition in Smokers After Overnight Cigarette Abstinence. The Abstract includes these remarks: OBJECTIVE: The authors' goal was to replicate a previous finding that smokers have lower brain monoamine oxidase B (MAO-B) levels than comparison nonsmoking subjects ...RESULTS: Average MAO-B levels in smokers in the present study were similar to those found in the previous study and averaged 39% (SD=17) lower than those found in a comparison group of nonsmokers. Brain MAO-B levels did not differ between baseline levels and 10 minutes after smoking. So, the authors of this study were replicating the results that MAO-B levels are lower in smokers!!!

This benefit of inhibiting MAO-B was known as long ago as 1987. From Irreversible inhibition of monoamine oxidase by some components of cigarette smoke, Life Science (1987 Aug 10;41(6):67582), "Inhibitory activity towards monoamine oxidase has been found in a solution of cigarette smoke. The inhibition was irreversible." Alas, one must an actual smoker to benefit. From the abstract of "Smoking a single cigarette does not produce a measurable reduction in brain MAO B in non-smokers" (PubMed):
Positron emission tomography (PET) studies with [11C]L-deprenyl-D2 have shown that brain monoamine oxidase (MAO) B is 40% lower in smokers than in non-smokers. ...These results indicate that the reduction in MAO B in smokers probably occurs gradually and requires chronic tobacco smoke exposure. Telomerase ("fountain of youth") much more active in smokers.

Smoking is associated with increased telomerase activity in short-term cultures of human bronchial epithelial cells, Cancer Letters 2007 Feb 8;246(1-2):24-33. Epub 2006 Mar 6--from the Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.
Glutathione (chief antioxidant in human body) and catalase (another key antioxidant which neutralizes alcohol damage, cyanide,...) doubled in smokers.

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Also explained by NightLight. From The Abstract of Normal alveolar epithelial lining fluid contains high levels of glutathione in the Journal of Applied Physiology (Vol. 63, Issue 1, p. 152-157): The epithelial cells on the alveolar surface of the human lower respiratory tract are vulnerable to toxic oxidants derived from inhaled pollutants or inflammatory cells. Although these lung cells have intracellular antioxidants, these defenses may be insufficient to protect the epithelial surface against oxidants present at the alveolar surface. This study demonstrates that the epithelial lining fluid (ELF) of the lower respiratory tract contains large amounts of the sulfhydryl-containing antioxidant glutathione (GSH). The total glutathione (the reduced form GSH and the disulfide GSSG) concentration of normal ELF was 140-fold higher than that in plasma of the same individuals, and 96% of the glutathione in ELF was in the reduced form. Compared with nonsmokers, cigarette smokers had 80% higher levels of ELF total glutathione, 98% of which was in the reduced form. Studies of cultured lung epithelial cells and fibroblasts demonstrated that these concentrations of reduced glutathione were sufficient to protect these cells against the burden of H2O2 in the range released by alveolar macrophages removed from the lower respiratory tract of nonsmokers and smokers, respectively, suggesting that the glutathione present in the alveolar ELF of normal individuals likely contributes to the protective screen against oxidants in the extracellular milieu of the lower respiratory tract. More studies on antioxidants in people who smoke can be found in the Journal of Applied Physiology. Selective increase of antioxidant enzyme activity in the alveolar macrophages from cigarette smokers and smoke-exposed hamsters. for American Review of Respiratory Disease, (1990 Mar, vol. 141, no 3, p. 678-82). http://www.imminst.org/forum/index.php? s=&act=ST&f=169&t=15654&st=20&#entry170219 Nicotine suppresses cell death of neurons (it also promotes vascular growth factor, e.g. growth and branching of capillaries). (Another advantage of nicotine is that Nicotine Slays TB. The link to this mainstream article is prefaced by this comment, "This article was written in 2001 and since then the ban on smoking in public places and taxing tobacco has grown. Extremely-Drug-Resistant Tuberculosis strains will continue to spread and multiply. The resulting global XDR-TB epidemic will be an untreatable and unstoppable calamity.") Low concentration carbon monoxide (as found in tobacco smoke) protects cells in harsh conditions, such as low oxygen and general cell death.

From CO-RMs: Therapeutic Carbon Monoxide Releasing Molecules (Monday, October 22, 2007; medGadget, Internet journal of Medical Technologies):

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Carbon monoxide (CO), a silent and powerful poison gas, might actually lend itself for a variety of promising clinical applications, according to the researchers from Sheffield University in the UK. Professor Brian Mann and colleagues from the University's Department of Chemistry and hemoCORM Ltd, a spinout company, are working on water-soluble molecules that can deliver CO to tissues to "reduce inflammation, widen blood vessels, increase blood flow, prevent unwanted blood clotting and even suppress the activity of cells and macrophages which attack transplanted organs," according to the university's press release. Nitric oxide stimulates peripheral circulation (this is the mechanism behind Viagra effect). Raises youth hormones, e.g. DHEA, pregnenolone, testosterone,...

Relation of age and smoking to serum levels of total testosterone and dehydroepiandrosterone sulfate in aged men in Geriatrics & Gerontology International (Volume 6 Issue 1 Page 49-52, March 2006), which found these results, "Serum T did not decrease with age, and was significantly higher in smokers than for non-smokers. Serum DHEA decreased with age more sharply in non-smokers than for smokers."
Smoking reduces IGF-1 (insulin-like growth factor 1)--at least in males for sure. In animal experiments, lowered insulin growth factor IGF-1 change extends lifespan.

From Signals from the reproductive system regulate the lifespan of C. elegans (Nature. 1999 May 27;399(6734):308-9), "Mutants with reduced activity of the insulin/IGF-1-receptor homologue DAF-2 have been shown to live twice as long as normal". From Dietary and Lifestyle Correlates of Plasma Insulin-Like Growth Factor-I (IGF-I) and IGF Binding Protein-3 (IGFBP-3): The Multiethnic Cohort (Cancer Epidemiology Biomarkers & Prevention, Vol. 13, 1444-1451, September 2004), "In addition, we observed associations between current smoking and low IGF-I levels..."--and, on p. 1449, table 3 shows that smoking had strongest reduction effect on IGF-1 in males! Hmmmmm.... So, IGF-1 is reduced in people who smoke and animals bred to have reduced IGF-1 have a tendency to double their life spans. That goes a long way toward explaining the reason that the people who have lived longest on this earth are all smokers!
Reduced Incidence of Colorectal Cancer--especially in women.

Cigarette Smoking and the Risk of Colorectal Cancer in Women (Journal of the National Cancer Institute, Vol. 80, No. 16, 1329-1333, October 19, 1988) states, "Colorectal cancer incidence rates for smokers, nonsmokers living with smokers (i.e., passive smokers), and non-smokers in smokefree households were compared in a 12-year prospective study of 25, 369 women who participated in a private census conducted in Washington County, MD, in 1963. Women who smoked had a decreased relative risk of colorectal cancer compared with the risk for nonsmokers (age-adjusted relative risk, 0.76; 95% confidence interval, 0.52-1.10). The risk for passive smokers was similar to that for smokers. The relative risks were significantly reduced for older women; relative risks were 0.42 for smokers and 0.66 for passive smokers over age 65. The data suggest that older women who
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smoke have a lower risk of colorectal cancer than non-smokers. The effect may be mediated by an antiestrogenic effect of smoking." More evidence can be found in this scanned document
People who smoke fare better than nonsmokers when exposed to occupational hazards.

From Lack of combined effects of exposure and smoking on respiratory health in aluminium potroom workersBritish Medical Journal, Occupational and Environmental Medicine (Vol. 56, 468472, 1999):
Smokers in the potroom group had a lower prevalence of respiratory symptoms than never smokers or ex-smokers, which was significant for wheezing (2.6% v 17.4% and 28.6% respectively, both p < 0.01), whereas respiratory symptoms in controls tended to be highest in smokers (NS). No effects of potroom work on the prevalence of respiratory symptoms could be detected. In potroom workers, impairment of lung function due to occupational exposure was found only in non-smokers, with lower results for forced vital capacity (FVC) (98.8% predicted), forced expiratory volume in one second (FEV1) (96.1% predicted) and peak expiratory flow (PEF) (80.2% predicted) compared with controls (114.2, 109.9, and 105.9% predicted; each p < 0.001). Conversely, effects of smoking on lung function were only detectable in non-exposed controls (current smokers v non-smokers: FVC 98.8% v 114.2% predicted; p < 0.01; FEV1 95.5 v 109.9% predicted; p < 0.05)." (NOTE: The key result is that for the exposure controlled group (the potroom workers) the smoking reduced the risk of lung damage sixfold compared to never-smokers.)

For asbestos workers, "Effect of Smoking on Immunological Abnormalities in Asbestos Workers" (Institute of Immunology and Experimental Therapy, Poland) by Lange, A.:
Smoking has a protective effect on immunological abnormalities in asbestos workers.

More for asbestos workers is found in "Cancer of the Lung Among Asbestos Factory Workers" (University of London, School of Hygiene and Tropical Medicine), relative risk of lung cancer for asbestos workers was "highest for those who had never smoked, lowest for current smokers, and intermediate for ex-smokers. The trend was statistically significant. There was no significant association between smoking and deaths from mesothelioma," And again in The Interaction of Asbestos and Smoking in Lung Cancer by G. BERRY1, and F. D. K. LIDDELL (Oxford Journals, Medicine, Annals of Occupational Hygiene, Volume 48, Number 5, p. 459-462, 2004):
Conclusion: The excess relative risk of lung cancer from asbestos exposure is about three times higher in non-smokers than in smokers. The modified measure has been placed within a more versatile model of interaction. If

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interaction is present the relative risk from asbestos exposure changes only slightly between light and heavy smokers, but is higher in very light smokers and non-smokers.

Many other studies show protective effects of smoking for asbestos workers. Similar effects are found for other lung cancer risk factors, including radiation and chemical cancerogen exposures. For example:
From "Lung Cancer Dueto Chloromethyl Ethers" (Hahnemann Medical College and Hospital, Philadelphia) by Weiss, W., "Over the 22 years of follow-up, exposed workers have had a very high risk of respiratory cancer, mostly of the lung. The risk has been dose related and has been much higher in nonsmokers and ex-smokers than in current smokers. The epidemic began to subside shortly after exposure to chloromethyl ethers ceased. The mean induction-latency period was 17 years. Most of the lung cancers in the moderate and high dose groups have been small cell carcinoma,"

From "Respiratory Effects of Exposure to Diesel Emissions in Underground Coal Miners" by Ames, R.G. (DHHS, PHS, CDC, NIOSH. Funding: NIOSH), "Presence of chronic respiratory symptoms at baseline was inversely related to cessation of smoking. Respiratory impairment was positively associated with smoking cessation, but failed to reach statistical significance,"
Reduces schizophrenia symptoms.

From "Investigating the Association Between Cigarette Smoking and Schizophrenia in a Cohort Study," Am J Psychiatry (160:2216-2221, December 2003):
Cigarette smoking may be an independent protective factor for developing schizophrenia. These results are consistent with animal models showing both neuroprotective effects of nicotine and differential release of prefrontal dopamine in response to nicotine. From Cancer in schizophrenia: is the risk higher or lower? in Schizophrenia Research (Volume 73, Issue 2, Pages 333-341) at http://www.schresjournal.com/article/PIIS0920996404002130/abstract : The incidence of cancer in patients diagnosed with schizophrenia was compared with the incidence in the general population. The results showed that the cancer standardized incidence ratios (SIRs) for all sites were significantly lower among men and women with schizophrenia, 0.86 [95% confidence interval (CI) 0.80-0.93] and 0.91 (95% CI 0.85-0.97), respectively. This reduced overall risk was clearest for those born in Europe-America, both men (SIR 0.85, 95% CI 0.74-0.97) and women (SIR 0.86, 95% CI 0.77-0.94). Appetite Suppressant -- no citations. Common sense. Most stimulants are appetite

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suppressants, and nicotine does seem to be a stimulant. Tobacco: the definitive link in healthy aging by Daniel John Richard Date. Reduces incidence of Alzheimer's, among other degenerative diseases.

From The Straight Dope Classics: "A statistically significant inverse association between smoking and Alzheimer's disease was observed at all levels of analysis, with a trend towards decreasing risk with increasing consumption" (International Journal of Epidemiology, 1991) "The risk of Alzheimer's disease decreased with increasing daily number of cigarettes smoked before onset of disease. . . . In six families in which the disease was apparently inherited . . . the mean age of onset was 4.17 years later in smoking patients than in non-smoking patients from the same family" (British Medical Journal, June 22, 1991) "Although more data are needed . . . [an analysis of 19 studies suggests] nicotine protects against AD" (Neuroepidemiology, 1994) Nicotine injections significantly improved certain types of mental functioning in Alzheimer's patients (Psychopharmacology, 1992). One theory: nicotine improves the responsiveness of Alzheimer's patients to acetylcholine, an important brain chemical. "When chronically taken, nicotine may result in: (1) positive reinforcement [it makes you feel good], (2) negative reinforcement [it may keep you from feeling bad], (3) reduction of body weight [by reducing appetite and increasing metabolic rate], (4) enhancement of performance, and protection against: (5) Parkinson's disease, (6) Tourette's disease [tics], (7) Alzheimer's disease, (8) ulcerative colitis and (9) sleep apnea. The reliability of these effects varies greatly but justifies the search for more therapeutic applications for this interesting compound." ("Beneficial Effects of Nicotine," Jarvik, British Journal of Addiction, 1991)
See more on smoking and reduced incidence of Alzheimer's disease. In this compilation of 19 studies, 15 found a reduce risk in smokers, and none found an increased risk. Also noted is the fact that acute administration of nicotine improves attention and information processing in AD patients, which adds further plausibility to the hypothesis. Smoking is Good for You: Absence, Presence, and the Ecumenical Appeal of Indian Islamic Healing Centers In Shop owner says smoking 'doesn't cause disease' a shop owner "tells his customers that smoking calms the nerves and soothes the mind." This is in sync with what Albert Einstein stated upon becoming a lifetime member of the Montreal Pipe Smokers Club at the age of 71, "I believe that pipe smoking contributes to a somewhat calm and

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objective judgment in all human affairs." Evidence that smoking is protective against thyroid cancer

Prepublished from the American Journal of Epidemiology (Sep 2007). From the abstract of pubmed's Alcohol Drinking, Tobacco Smoking, and Anthropometric Characteristics as Risk Factors for Thyroid Cancer: A Countrywide Case-Control Study in New Caledonia. (Unit 754, INSERM, Villejuif, France) by Guignard R, Truong T, Rougier Y, Baron-Dubourdieu D, Gunel P., quote (emphasis added):
Exceptionally high incidence rates of thyroid cancer are observed in New Caledonia, particularly in Melanesian women. To investigate further the etiology of thyroid cancer and to clarify the reasons of this elevated incidence, the authors conducted a countrywide population-based case-control study in this multiethnic population. The study included 332 cases with histologically verified papillary or follicular carcinoma (293 women and 39 men) diagnosed in 1993-1999 and 412 population controls (354 women and 58 men) frequency matched by gender and 5-year age group. Thyroid cancer was negatively associated with tobacco smoking and alcohol drinking, but no inverse dose-response relation was observed. Height was positively associated with thyroid cancer, particularly in men. Strong positive associations with weight and body mass index were observed in Melanesian women aged 50 years or more, with an odds ratio of 5.5 (95% confidence interval: 1.5, 20.3) for a body mass index of 35 kg/m(2) or greater compared with normal-weight women, and there was a clear doseresponse trend. This study clarifies the role of overweight for thyroid cancer in postmenopausal women. Because of the high prevalence of obesity among Melanesian women of New Caledonia, this finding may explain in part the exceptionally elevated incidence of thyroid cancer in this group.

A Few Words of Caution Concerning Filters

From "Cigarettes with defective filters marketed for 40 years: what Philip Morris never told smokers" (Tobacco Control 2002;11:i51-i61): Background: More than 90% of the cigarettes sold worldwide have a filter. Nearly all filters consist of a rod of numerous ( > 12 000) plasticlike cellulose acetate fibres. During high speed cigarette manufacturing procedures, fragments of cellulose acetate that form the mouthpiece of a filter rod become separated from the filter at the end face. The cut surface of the filter of nearly all cigarettes has these
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fragments. In smoking a cigarette in the usual manner, some of these fragments are released during puffing. In addition to the cellulose acetate fragments, carbon particles are released also from some cigarette brands that have a charcoal filter. Cigarettes with filters that release cellulose acetate or carbon particles during normal smoking conditions are defective. and: Conclusions: We have shown that: (a) the filter of today's cigarette is defective; (b) Philip Morris, Inc has known of this filter defect for more than 40 years; (c) the existence of this filter defect has been confirmed by others in independent studies; (d) many methods exist to prevent and correct the filter defect, but have not been implemented; and (e) results of investigations substantiating defective filters have been concealed from the smoker and the health community. The tobacco industry has been negligent in not performing toxicological examinations and other studies to assess the human health risks associated with regularly ingesting and inhaling non-degradable, toxin coated cellulose acetate fragments and carbon microparticles and possibly other components that are released from conventional cigarette filters during normal smoking. The rationale for harm assessment is supported by the results of consumer surveys that have shown that the ingestion or inhalation of cigarette filter fibres is a health concern to nearly all smokers. From "A False Martyr?" from Surreality Times: The "official" explanation for smokers developing less squamous tumors and more adenocarcinoma tumors, is that modern filters on cigarettes cause smokers to inhale more deeply which deposits irritants into the small airways deep in the lungs where adenocarcinomas develop. But - non-smokers don't inhale secondhand smoke through a filter! The anti-smoking industry claims, smokers are now developing andenocarcinomas because they are inhaling cigarette smoke through

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modern filters, specifically. It's the filtering that makes the difference, in smokers, they claim. Non-smokers never inhale SHS through filters, they always inhale unfiltered smoke. That means, if SHS is causing lung cancer in non-smokers, they should be developing Squamous Cell tumours! Unfiltered tobacco smoke = squamous cell tumours, filtered tobacco smoke = andenocarcinoma tumours, according to the American Cancer Society.

Other health risks could be associated with the use of tobacco sheets in cigarette manufacturing. Although "authorities" and "experts" tell us that "there is no safe cigarette"--but then try to legislate for safer cigarettes--the fact is that whole leaf tobacco and organic tobacco are less hazardous. Moreover, whole leaf tobacco burns slower, thus reducing fire hazards.

Pharmaceutical industry creates and funds most of the so-called "grass roots" antismoking organizations and also drives the same antismoking agenda within the FDA, EPA, CDC, AMA,... where their money buys the bureaucrats & lawmakers.

The obvious most immediate motivation, as others noted here, is the sale of the smoking cessation "therapies", see for example recent posts on Robert Wood Johnson Foundation (J&J money and largest stockholder), as well as sites tracking it in more depth: http://groups.google.com/group/alt.support.stop-smoking/browse_frm/th... http://groups.google.com/group/alt.support.stop-smoking/browse_frm/th... Clearing the Air (antismoking money trail investigations)

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http://cleanairquality.blogspot.com/2006/08/its-time-for-full-scale-c... Pharmaceutical industry & antismoking http://www.forces.org/evidence/pharma/index.htm But the smoking cessation therapies are only a small part of the story. The rest of the profit iceberg is that Big Pharma is fighting all traditional health remedies, herbs and folk medicine: http://groups.google.com/group/alt.support.stop-smoking/browse_frm/th... for the same reason -- they are all competing products and by destroying them it establishes its own monopoly over the health market. Yes, it may sound absurd in the current antismoking zeitgeist, but tobacco is one of the most ancient and most revered among the medicinal plants and traditional health remedies: http://groups.google.com/group/alt.smokers/browse_frm/thread/34b73a74... The amount of money made by attacking tobacco is thus vastly grater than just the sales of the smoking cessation pharmaceuticals, since the Big Pharma also provides their own synthetic compounds as substitutes for numerous therapeutic & protective effects of tobacco: http://groups.google.com/group/alt.smokers/msg/81f9269f69c012e7?hl=en& http://groups.google.com/group/alt.smokers/browse_frm/thread/a27152b2... The antismoking movement has another embryonic layer, though, going back to 1950s, which is couple decades before the Big Pharma got into the act. The initial impetus came from the British and US governments, looking for scapegoats to blame for suddenly skyrocketing rates of lung cancers and melanomas, that track well in time and space with the exponential rise in the atmospheric nuclear tests. Something else had to be blamed instead of the obvious and clear culprit, the the radioactive fallout. The brains behind the new blame-diverting strategy was a British doctor, Richard Doll, who made a career out of his unique talent to "scientifically" shift the blame for various cancers (and other diseases over six decades of his "science") from his paymasters and their actions (radiation, asbestos, agent orange, chlorine cancerogens,...) to the victims themselves, their own lifestyle choices (over-cleanliness of their homes, under-cleanliness of their homes, sun, tobacco,...). He was just recently, not long after he died, exposed as a complete scientific

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fraud of the lowest kind, a Dr. Faustus incarnate, by the in-depth investigative report from a UK legal group Injurywatch: http://groups.google.com/group/alt.support.stop-smoking/msg/37bbf9c50... Further analysis of Doll & his antismoking science: http://groups.google.com/group/alt.smokers/msg/acde99339a682316?hl=en& Lung Cancer & Melanoma graphs for 20th century: http://speakeasyforum.com/eve/forums/a/tpc/f/173601742/m/7541044041?r... and how the blame was shifted: http://speakeasyforum.com/eve/forums/a/tpc/f/173601742/m/7541044041?r...

The Scientific Scandal of Antismoking By J. R. Johnstone, PhD (Monash) and P.D.Finch, Emeritus Professor of Mathematical Statistics (Monash)

Science is not always a neutral, disinterested search for knowledge, although it may often seem that way to the outsider. Sometimes the story can be very different.

Smoking and health have been the subject of argument since tobacco was introduced to Europe in the sixteenth century. King James I was a pioneer antismoker. In 1604 he declared that smoking was "a custome lothsome to the eye, hatefull to the Nose, harmefull to the braine, dangerous to the Lungs, and in the blacke stinking fume thereof, neerest resembling the horrible Stigian smoke of the pit that is bottomelesse." But like many a politician since, he decided that taxing tobacco was a more sensible option than banning it.
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By the end of the century general opinion had changed. The Royal College of Physicians of London promoted smoking for its benefits to health and advised which brands were best. Smoking was compulsory in schools. An Eton schoolboy later recalled that "he was never whipped so much in his life as he was one morning for not smoking". As recently as 1942 Prices textbook of medicine recommended smoking to relieve asthma. These strong opinions for and against smoking were not supported by much evidence either way until 1950 when Richard Doll and Bradford Hill showed that smokers seemed more likely to develop lung cancer. A campaign was begun to limit smoking. But Sir Ronald Fisher, arguably the greatest statistician of the 20th century, had noticed a bizarre anomaly in their results. Doll and Hill had asked their subjects if they inhaled. Fisher showed that men who inhaled were significantly less likely to develop lung cancer than non-inhalers. As Fisher said, "even equality would be a fair knock-out for the theory that smoke in the lung causes cancer." Doll and Hill decided to follow their preliminary work with a much larger and protracted study. British doctors were asked to take part as subjects. 40.000 volunteered and 20,000 refused. The relative health of smokers, nonsmokers and particularly ex-smokers would be compared over the course of future years. In this trial smokers would no longer be asked whether they inhaled, in spite of the earlier result. Fisher commented: "I suppose the subject of inhaling had become distasteful to the research workers, and they just wanted to hear as little about inhaling as possible". And: "Should not these workers have let the world know not only that they had discovered the cause of lung cancer (cigarettes) but also that they had discovered the means of its prevention (inhaling cigarette smoke)? How had the MRC [Medical Research Council] the heart to withhold this information from the thousands who would otherwise die of lung cancer?" Five years later, in 1964, Doll and Hill responded to this damning criticism. They did not explain why they had withdrawn the question about inhaling. Instead they complained that Fisher had not examined their more recent results but they agreed their results were mystifying. Fisher had died 2 years earlier and could not reply. This refusal to consider conflicting evidence is the negation of the scientific method. It has been the hallmark of fifty years of antismoking propaganda and what with good reason may well be described as one of the greatest scandals in 500 years of modern science. A typical example of such deception appeared in the same year from the American Surgeon General. This was "Smoking and Health", the first of many reports on smoking and health to be produced by his office over the next 40 years. It declared that in the Doll and Hill study "no difference in the proportion of smokers inhaling was found among male and female cases and controls." Fisher had shown this was not so. Fishers assessment and criticism of the Doll and Hill results is not mentioned, not even to be rejected. Unwelcome results are not merely considered and rejected. They cease to exist. The work of Doll and Hill was continued and followed up over the next 50 years. They reintroduced the question about inhaling. Their results continued to show the inhaling/noninhaling paradox. In spite of this defect their work was to become the keystone of the modern anti-smoking

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movement: Defects count for nothing if they are never considered by those who are appointed to assess the evidence. But their work had a far more serious and crippling disability. From its inception the British doctors study was known to have a critical weakness. Its subjects were not selected randomly by the investigators but had decided for themselves to be smokers, nonsmokers or ex-smokers. The kind of error that can result from such non-random selection was well demonstrated during the 1948 US presidential election. Opinion polls showed that Dewey would win by a landslide from Truman. Yet Truman won. He was famously photographed holding a newspaper with a headline declaring Dewey the winner. The pollsters had got it wrong by doing a telephone poll which at that time would have targeted the wealthier voters. The majority of telephone owners may have supported Dewey but those without telephones had not. A true sample of the population had not been obtained. The new Doll and Hill study was subject to a similar error. Smokers who became ex-smokers might have done so because they were ill and hoped quitting would improve them. Alternatively, they might quit because they were exceptionally healthy and hoped to remain so. Quitting could appear either harmful or beneficial. To avoid this source of error another project, the Whitehall study, was begun. In 1968 fourteen hundred British civil servants, all smokers, were divided into two similar groups. Half were encouraged and counselled to quit smoking. These formed the test group. The others, the control group, were left to their own devices. For ten years both groups were monitored with respect to their health and smoking status. Such a study is known as a randomised controlled intervention trial. It has become increasingly the benchmark, or as it is often referred to, the "gold standard" of medical investigation. Any week you can open The Lancet or British Medical Journal and you will likely find an example of such a trial to determine the benefits or harm of some new therapy. Such trials are fundamentally different to that of Doll and Hill. This is ironic because Hill had published the influential and much-reprinted textbook "Principles of Medical Statistics" where he considers the relative merits of controlled and uncontrolled trials. His praise is reserved for the former. Of the latter he is particularly critical: Such work uses "second-best" or "inferior" methods. "The same objections must be made to the contrasting in a trial of volunteers for a treatment with those who do not volunteer, or in everyday life between those who accept and those who refuse. There can be no knowledge that such groups are comparable; and the onus lies wholly, it may justly be maintained, upon the experimenter to prove that they are comparable, before his results can be accepted." This criticism by Hill can accurately be applied to the Doll and Hill study. According to Hills own criteria, his work with Doll can only be described as second-rate, inferior work. It would be for others to conduct properly controlled trials. So what were the results of the Whitehall study? They were contrary to all expectation. The quit group showed no improvement in life expectancy. Nor was there any change in the death rates due to heart disease, lung cancer, or any other cause with one exception: certain other cancers were

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more than twice as common in the quit group. Later, after twenty years there was still no benefit in life expectancy for the quit group. Over the next decade the results of other similar trials appeared. It had been argued that if an improvement in one life-style factor, smoking, were of benefit, then an improvement in several eg smoking, diet and exercise - should produce even clearer benefits. And so appeared the results of the whimsically acronymed Multiple Risk Factor Intervention Trial or MRFIT, with its 12,886 American subjects. Similarly, in Europe 60,881 subjects in four countries took part in the WHO Collaborative Trial. In Sweden the Goteborg study had 30,022 subjects. These were enormously expensive, wide-spread and time-consuming experiments. In all, there were 6 such trials with a total of over a hundred thousand subjects each engaged for an average of 7.4 years, a grand total of nearly 800,000 subject-years. The results of all were uniform, forthright and unequivocal: giving up smoking, even when fortified by improved diet and exercise, produced no increase in life expectancy. Nor was there any change in the death rate for heart disease or for cancer. A decade of expensive and protracted research had produced a quite unexpected result. During this same period, in America, the Surgeon General had been issuing a number of publications about smoking and health. In 1982, before the final results of the Whitehall study had been published, the then Surgeon General C. Everett Koop had praised the study for "pointing up the positive consequences of smoking in a positive manner". But now for nearly ten years he fell silent on the subject and there was no further mention of the Whitehall study nor of the other six studies, though thousands of pages on the dangers of smoking issued from his office. For example in 1989 there appeared "Reducing the Health Consequences of Smoking: 25 Years of Progress". This weighty work is long on advice about the benefits of giving up smoking but short on discussion of the very studies which should allow the evaluation of that advice: you will look in vain through the thousand references to scientific papers for any mention of the Whitehall study or most of the other six quit studies. Only the MRFIT study is mentioned, and then falsely: "The MRFIT study shows that smoking status and number of cigarettes smoked per day have remained powerful predictors for total mortality and the development of CHD [coronary heart disease], stroke, cancer, and COPD [chronic obstructive pulmonary disease]. In the study population, there were an estimated 2,249 (29 percent) excess deaths due to smoking, of which 35 percent were from CHD and 21 percent from lung cancer. The nonsmoker-former smoker group had 30 percent fewer total cancers than the smoking group over the 6-year follow up." This was untrue, as the Surgeon General was later to admit.

What the MRFIT authors themselves had to say about their work was quite different: "In conclusion we have shown that it is possible to apply an intensive long-term intervention program against three coronary risk factors with considerable success in terms of risk factor changes. The overall results do not show a beneficial effect on CHD or total mortality from this multifactor intervention." (Multiple Risk Factor Intervention Trial Research Group, 1982)

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But in 1990 the Surgeon General published "The Health Benefits of Smoking Cessation" and at last the subject was addressed. The Whitehall study was rejected because of its "small size". A once praiseworthy study had become blameworthy. The MRFIT results were described, this time truthfully: "there was no difference in total mortality between the special intervention [quit] and usual care groups." This and the other studies were rejected because the combined change in other factors - eg diet and exercise - made it impossible to apportion benefit due to smoking alone. This is absurd and illogical reasoning. If, say, a 10% improvement in life expectancy had been found then it might indeed be difficult if not impossible to say how much was due to smoking alone. But there was no improvement. There was nothing to apportion. Nevertheless, with such deceptive words the Surgeon General turned to an unpublished, unreviewed, un-controlled, non-intervention, non-randomised survey conducted for the American Cancer Society ("American Cancer Society: Unpublished tabulations"). The gold standard of modern science was rejected and replaced by the debased currency of what is by comparison little better than opinion and gossip. This rejection of consistent results from controlled trials and the acceptance of far inferior data would not be countenanced in any other area of medical science. Anyone who suggested doing so would be met with howls of derision and questions as to their intelligence if not their sanity. But where smoking and health are being considered this debasement of science is commonplace and passes without comment. In Australia in the same year there appeared a similar publication "The Quantification of Drug Caused (sic) Mortality and Morbidity in Australia" from the Federal Department of Community Services and Health. Its authors waste no time in discussing intervention trials. These receive not a mention, not even to be rejected. Instead the authors turned to several surveys of the kind ultimately used by the Surgeon General. In particular they used yet another study conducted for the American Cancer Society by E.C.Hammond, a gigantic study of a million subjects, another uncontrolled, non-intervention, non-randomised survey. This was a particularly bad choice. The dangers of very large surveys are well known to statisticians: because of their size it is difficult to do them accurately. The flaws in Hammonds work were revealed when the initial results were published in 1954. Hammond himself was later to admit that his study had not been conducted as he had intended and as a consequence his results are to an unknown extent erroneous. But it was worse than that. His work became literally a textbook example of how not to do research. It can be found as example 287 in "Statistics A New Approach" by W.A.Wallis and H.V.Roberts. This was the ignominious and undignified fate of work which should only be quoted as a salutary example of the pitfalls which can await the researcher. Two problems bedevil both Hammonds work and other similar studies. First, some of the volunteers who enrolled their subjects told Hammond that contrary to his instructions they had selectively targeted ill smokers. These results he was able to scrap but necessarily an unknown proportion of his final results must be suspect. Second, as was demonstrated at the time, his subjects were quite unrepresentative of the general public in a number of respects. In particular, there were relatively few smokers. It seems quite plausible that many healthy if indignant smokers would refuse to take part in his trial and this would produce such an aberration. These two vitiating defects are of the kind which have led to the widespread preference for gold standard trials.

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But the continuation of Hammonds work, with its demonstrated faulty methodology, was used by the Australian authors to deduce that smoking causes premature death to the extent of 17,800 per year in Australia. Their conclusions should be compared with the results of a survey by the Australian Statistician in 1991 of 22,200 households, chosen at random. This showed "long term conditions", including cancer and heart disease, to be more common in non-smokers than smokers. Even if they had used sound data to calculate deaths caused by smoking, this still would not have shown that smoking is overall harmful or causes an excess of deaths. Antibiotics kill some susceptible, allergic individuals but this fact does not show that antibiotics reduce life expectancy. If the data used by these authors is examined more closely it can in fact be shown that the mean age at death from smoking-related causes (eg lung cancer) is about 1 year greater than from nonsmoking-related causes (eg tetanus). See: http://members.iinet.net.au/~ray/finch2.pdf for details. This result does not necessarily show that smokers live longer than nonsmokers: smokers as well as nonsmokers die from both nonsmoking-related causes and smoking-related causes. But it is certainly not evidence for the belief that smoking reduces life expectancy. During all this time health authorities have repeatedly and persistently lied to the public. Consider just one of innumerable examples. In June 1988, in Western Australia the Health Department in full page advertisements in local papers declared: "The statistics are frightening. Smoking will kill almost 700 women in Western Australia this year. If present trends continue, lung cancer will soon overtake breast cancer as the most common malignant cancer in women". What was frightening was not the statistics but the fact that a Health Department should lie about them. In 1987 the same Health Department in its own publications had said: "Suggestions by some commentators that lung cancer deaths in women will overtake breast cancer deaths in the next few years look increasingly unlikelyfemale lung cancer death rates have fallen for the last 2 years." It was predicted that breast cancer would far outweigh lung cancer for the next 14 years. What the public were told was not just an untruth but the reverse of the truth. This is classic Orwellian Newspeak. The public are given what George Orwell in "1984" named "prolefeed" lies. Orwell must have smiled wryly in his grave. Above all has been the repeated and world-wide directive that smokers should quit and live longer when every controlled trial without exception has demonstrated this claim to be false. Is there anything that can be said with certainty about the health and life expectancy of smokers and non-smokers? The evidence indicates little difference. One important fact often causes confusion: an agent can be a certain cause of death and yet have the effect of extending life. Smoking could be a major cause of lung cancer or even the only cause yet also be associated with long life. The Japanese are amongst the heaviest smokers in the world. They also live the longest. The Frenchwoman Jeanne Calment smoked for a hundred years before dying at 122 as the worlds oldest ever person. The resolution of this paradox lies in the simple fact that most agents have both good and bad effects on health and life expectancy and it is the net result which is of primary importance. This

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simple but crucial fact is often ignored or forgotten by medical researchers. Coffee causes pancreatic cancer says the newspaper article. Perhaps it does, but if it has a bigger and beneficial effect on heart disease then those who drink coffee may well live longer than those who dont. Hormone replacement therapy may increase the incidence of certain cancers yet still have overall a beneficial effect. (See "The Contrapuntists"). It may now be apparent why there is such a general belief that smoking is dangerously harmful. There are 3 reasons. First, studies which in any other area of science would be rejected as secondrate and inferior but which support antismoking are accepted as first-rate. Second, studies which are conducted according to orthodox and rigorous design but which do not support the idea that smoking is harmful are not merely ignored but suppressed. Third, authorities who are duty-bound to represent the truth have failed to do so and have presented not just untruths but the reverse of the truth. It may be argued that this is news about an old and settled subject. And who cares about smoking anyway. But smoking is really a secondary issue. The primary issue is the integrity of science. This has no use-by date. When the processes of science are misused, even if for what seems a good reason, science and its practitioners are alike degraded.

The Contrapuntists A Parable By P.D. Finch In a few years time an accidental by-product of genetic engineering leads to the discovery that certain living vibrating crystals can be manufactured very cheaply. When encased in a suitable holder and inserted in the ear one can hear, just for a few minutes, until body heat kills the crystal, beautiful melodies, rhythms and fascinating counterpoint. They are marketed as aural contrapuntive devices. Since they are cheap and become very popular, the Government taxes them. Users of the device become known as contrapuntists. Some years later a new disease is identified when an increasing number of people drop dead, suddenly, for no apparent reason. Autopsies reveal a strange deterioration in the brain cells of those affected. An observant pathologist notes that in most of the associated post-mortem examinations an aural contrapuntive device was found in an ear of the deceased and the disease becomes known as SADS, an acronym for Sudden Aural Death Syndrome. Epidemiologists find that people who are not contrapuntists seldom fall victim to SADS and that, in fact, about 98 per

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cent of all such deaths are either current or former contrapuntists. The strength of association between aural contrapuntism and SADS is undeniable, the relative risk is as high as 50, i.e. a contrapuntist has about 50 times the chance of falling to SADS as does a non-contrapuntist. An anti-contrapuntist health campaign is initiated and aural contrapuntive devices are taxed more and more heavily in an attempt to dissuade people from using them. The campaign is very successful and is vigorously supported by an unexpected alliance between animal liberationists, the music industry and the tone-deaf. Attention then shifts to passive aural contrapuntism, viz. the dangers posed by the sidestream melodic overflow from the devices in the ears of contrapuntists, in particular on the occurrence of SADS in non-contrapuntal spouses of contrapuntal men, the harm contrapuntal parents may do their children and the possible ill-effects suffered by the foetus of a contrapuntal pregnant woman. After great initial success, however, the campaign falters when it becomes widely known that even though aural contrapuntism is so strongly associated with SADS, relatively few contrapuntists die from it each year and those that do have lived, on average, about one year longer than do noncontrapuntists and, moreover, at each age, are much more likely to die of other causes than of SADS itself. Politicians realise very quickly that they can now, with a clear conscience and with profit, tax aural contrapuntal devices even more heavily.

1 http://www.la.utexas.edu/research/poltheory/james/blaste/blaste.html 2 Keynes, G (1978), "The Life of William Harvey", Oxford,

3 Lyte, H.C.M. (1899), "A History of Eton College (1440-1898", Macmillan

4 Price, F.W. (ed.) (1942), "A Textbook of the Practice of Medicine", 6th edition, Oxford University Press

5 Doll, R. and Hill, A.B. (1950), "Smoking and carcinoma of the lung", British Medical Journal, ii pp739-48 6 Fisher, R.A. (1959) "Smoking: The Cancer Controversy", Oliver and Boyd

7 Doll, R. and Hill, A.B. (1954), "The mortality of doctors in relation to their smoking habits", British Medical Journal, i pp1451-5

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8 Doll, R. and Hill, A.B. (1964), "Mortality in relation to smoking: ten years' observations of British doctors", British Medical Journal, i pp1460-7 9 Surgeon General (1964), "Smoking and Health" http://www.cdc.gov/tobacco/sgr/sgr_1964/sgr64.htm 10 Rose, G. and P.J.S. Hamilton (1978), 'A randomised controlled trial of the effect on middleaged men of advice to stop smoking', Journal of Epidemiology and Community Health, 32, pages 275-281.

11 Hill, A.B.(1971, 9th ed.) "Principles of Medical Statistics", The Lancet

12 Rose, G., P.J.S. Hamilton, L. Colwell and M.J. Shipley (1982), 'A randomised controlled trial of anti-smoking advice: 10-year results', Journal of Epidemiology and Community Health, 36, pages 102-108

13 Multiple Risk Factor Intervention Trial Research Group (1982), 'Multiple risk factor intervention trial: risk factor changes and mortality results', Journal of the American Medical Association, 248, pages 1465-1477.

14 WHO European Collaborative Group (1986), 'European collaborative trial of multifactorial prevention of coronary heart disease: final report on the 6-year results', Lancet, 1, pages 869-872.

15 Wilhelmsen, L., G. Berglund, E. Elmfeldt, G. Tibblin, H. Wedel, K. Pennert, A. Vedin, C. Wilhelmsson and L. Werks (1986), 'The multifactor primary prevention trial in Goteborg', European Heart Journal, 7, pages 279-288.

16 Miettinen, T.A., J.K. Huttunen, V. Naukkarinen, T. Strandberg, S. Mattila, T. Kumlin and S. Sarna (1985), 'Multifactorial primary prevention of cardiovascular diseases in middle-aged men: risk-factor changes, incidence and mortality', Journal of the American Medical Association, 254, pages 2097-2102.

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17 Puska, P., J. Tuomilehto, J. Salonen, L. NeittaanmSki, J. Maki, J. Virtamo, A. Nissinen, K. Koskela and T. Takalo (1979), 'Changes in coronary risk factors during comprehensive five-year community programme to control cardiovascular diseases (North Karelia project), British Medical Journal, 2, pages 1173-1178.

18 Leren, P., E.M. Askenvold, O.P. Foss, A. Frili, D. Grymyr, A. Helgeland, I. Hjermann, I. Holme, P.G. Lund-Larsen and K.R. Norum (1975), 'The Oslo study. Cardiovascular disease in middle-aged and young Oslo men', Acta Medica Scandinavica [Suppl.], 588, pages 1-38.

19 Surgeon General (1982) The Health Consequences of Smoking - Cancer: A Report of the Surgeon General.

20 Surgeon General (1989) Reducing the Health Consequences of Smoking: 25 Years of Progress: A Report of the Surgeon General: Executive Summary and Full Report

21 Surgeon General (1990) The Health Benefits of Smoking Cessation: A Report of the Surgeon General

22 Commonwealth Department of Community Services and Health, Canberra (1988) "The Quantification of Drug Caused Morbidity and Mortality in Australia".

23 http://members.iinet.net.au/~ray/hammond3.html Wallis, W.A. and Roberts, H.V. (1962) "Statistics: A New Approach", Methuen and Co. Ltd.

24 Australian Bureau of Statistics: Smokers are less likely to have cancer, heart disease 1 Australian Bureau of Statistics, No 4382.0, "1989-90 National Health Survey: Smoking" http://members.iinet.net.au/~ray/19jun2006.htm

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25 Australian Bureau of Statistics: Smokers are less likely to have cancer, heart disease 2 http://members.iinet.net.au/~ray/ABS43820d.jpg

26 Two messages from the Western Australian Health Department Subiaco Post, 28 June 1988: 12 Hatton, W.M. (1987), Cancer Projections: Projections of numbers of incident cancers in Western Australia to the Year 2001, Perth: Epidemiology Branch, Health Department of Western Australia.

Hatton, W.M. and M.D. Clarke-Hundley (1987), Cancer in Western Australia: an analysis of age and sex specific rates, Perth: Health Department of Western Australia. http://members.iinet.net.au/~ray/HealthDept1.jpg http://members.iinet.net.au/~ray/HealthDept2.jpg ----

"Smoking lowers Parkinson's disease risk"

By Megan Rauscher "NEW YORK (Reuters Health) - A new study adds to the previously reported evidence that cigarette smoking protects against Parkinson's disease. Specifically, the new research shows a temporal relationship between smoking and reduced risk of Parkinson's disease. That is, the protective effect wanes after smokers quit. "It is not our intent to promote smoking as a protective measure against Parkinson's disease," Evan L. Thacker from Harvard School of Public Health emphasized in comments to Reuters Health. "Obviously smoking has a multitude of negative consequences. Rather, we did this study to try to encourage other scientists...to consider the possibility that neuroprotective chemicals may be present in tobacco leaves." As reported in the March 6th issue of Neurology, Thacker and colleagues analyzed data, including detailed lifetime smoking histories, from 79,977 women and 63,348 men participating in the Cancer Prevention Study II Nutrition Cohort. During about 9 years of follow-up, 413 subjects developed definite or probable Parkinson's disease.

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Compared to people who had never smoked and were considered to have "normal" Parkinson's disease risk, former smokers had a 22-percent lower risk of Parkinson's disease and current smokers had a 73-percent lower risk. "The results were similar for men and women, and were also similar to the results of studies by many other researchers looking at the same topic," Thacker noted. In former smokers, more years of smoking, fewer years since quitting, more cigarettes per day, and a higher total amount of lifetime smoking were all related to a lower Parkinson's disease risk. The researchers also found that the duration of smoking and the time since quitting influenced risk more than the average daily amount of smoking. "A 30 percent to 60 percent decreased risk of Parkinson's disease was apparent for smoking as early as 15 to 24 years before symptom onset, but not for smoking 25 or more years before onset," the investigators report. "The results of our study," Thacker said, "can probably be explained by something in cigarettes -most likely in the tobacco itself -- actually protecting people against getting Parkinson's disease. That would be the simplest explanation that makes the most sense." Studies to determine if, in fact, there are neuroprotective compounds in tobacco are warranted, the researchers say. "The observation that smokeless tobacco users also have a lower risk of Parkinson's disease suggests that the most likely candidates are not compounds generated by combustion, but rather constituents of the tobacco leaves."
The attributes of tobacco are and have been known for some time to the medical profession. I became aware of this when studying the research of the tobacco industry turned over after the MSA. On PBS's Lehr Report, last night a doctor was describing the likelihood of developing Alzheimers after a heart attack or cancer diagnosis. No mention of how many patients who smoke got the disease, but the one thing that comes to mind first for these patients is to quit smoking or using tobacco in any form. It make take a while for the disease to appear but tobacco stimulates the brain to work faster. Reduced stimulation is bound to have an impact on a brain use to the stimulation or in the case of ADD or ADHD have always needed the stimulation.

Reducing tobacco use only generates more patients for these quacks to treat. They know it and so do I.
You should have advised him to start smoking some strong, clean, additive free tobacco in nonfiltered cigarettes, since nicotine by itself helps only slightly against Parkinson's (it's a bit more helpful for Alzheimer's). Only full tobacco smoke does the trick in either case (reduces Alzheimer's tenfold), by virtue of near doubling of

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dopamine levels (by inhibiting MAO B enzymes by 40%, whose levels increase with age, being the highest in senile elderly, and which destroy dopamine). Interestingly, brief smoking doesn't have this MAO effect, only long term smoking somehow does it. If you look at the brain scans photos of two women age 50:

you can see smoker's brain is about couple decades younger (lower MAO B), despite deceptive coloring scheme which paints the nonsmoker's brain as bright (had they also shown a brain scan of 30 year old person, it would look like that of the smoker there). With their color choices, a 70 year old nonsmoker would look even brighter then the 50 year old shown, while an Alzheimer's patient would appear brilliant white, the whole brain being gunked up with the oxdating MAO enzymes depicted as bright pixels above. (Note how low the antismoking "science" has to stoop to make their case, where dim is shown as bright and bright as dark, aiming its propaganda apparently at the far left tail of the Bell Curve, such as this antismoking genius.) As described earlier, pharmaceutical drug deprenyl (selegiline), which has become all the rage in life-extension circles, is used for smoking cessation "therapy" since it mimics selective MAO B inhibition by tobacco smoke, and is also used in treatments of Parkinson's and Alzheimer's, along with nicotine patches (which upregulates acetylcholine, another vital neurotransmitter along with dopamine). Since dopamine is vital biochemical messenger molecule not just in brain but also in all other organs and tissues, the selective MAO B increase with aging makes other organs, especially heart, go "senile". Tobacco smoking (also long term only) blocks the peripheral MAO B as well (again, nearly halving its levels), keeping thus other organs decades younger from middle age on. Here are few "prematurely aged" chain smokers...

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46 year old chain smoker, 122 year old Jeanne Louise Calment and 90 year old chain smoker Deng Xiaoping

Tobacco Smoke May Contain a Psychoactive Ingredient Other Than Nicotine Nicotine may not be the only psychoactive component in tobacco smoke, according to a study funded in part by NIDA. Using positron emission tomography, an advanced neuroimaging technology, Dr. Joanna S. Fowler and her colleagues at Brookhaven National Laboratory in Upton, New York, have produced images showing that smoking decreases the brain levels of an important enzyme that breaks down the neurotransmitter dopamine. The amount of the enzyme, called monoamine oxidase (MAO), is reduced by 30 to 40 percent in the brains of smokers, compared to nonsmokers or former smokers, the brain scans show. The reduction in brain MAO levels may result in an increase in levels of dopamine, which scientists associate with the reinforcing effects of drugs of abuse. Although nicotine causes increases in brain dopamine, it does not affect MAO levels, research has shown. Thus it appears that another component of tobacco smoke is inhibiting MAO. "Whatever is inhibiting MAO could be acting in concert with nicotine to enhance dopamine's activity by preventing its breakdown," says Dr. Fowler.

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The lighted areas in these brain images show levels of an enzyme called monoamine oxidase (MAO). A marked decrease in MAO is apparent in the brains of smokers compared to those of nonsmokers, but nicotine is not responsible.

The concept that the smoking-related reduction of MAO activity may synergize with nicotine's stimulation of dopamine levels to produce the diverse behavioral effects of smoking suggests that MAO inhibitor drugs may be useful as an additional therapy in smoking cessation efforts, she adds. MAO inhibitor drugs are used to treat depression and Parkinson's disease. One such drug, moclobemide, is already being used experimentally to assist persons trying to quit smoking. Dr. Fowler's research was funded by NIDA, the National Institute of Neurological Diseases and Stroke, and the Department of Energy's Office of Health and Environmental Research. Sources Fowler, J.S.; Volkow, N.D.; et al. Inhibition of monoamine oxidase B in the brains of smokers. Nature 379:733-736, 1996. Fowler, J.S.; Volkow, N.D.; et al. Brain monoamine oxidase inhibition in cigarette smokers. Proceedings of the National Academy of Sciences 93:14065-14069, 1996.

American Spirit: over 10 times more free nicotine than Camel

Posted by Warren on Friday, 29-Jul-2005

I ran into some interesting info on Natural American Spirit cigarettes & tobacco which helps explain their quick rise in popularity: their smoke (normalized per puff) contains 36%
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nicotine in free form (the part that absorbs quickly into bloodstream) vs 2.7% for Camel, 6.3% for Winston, 7.5% for Gauloises Blondes, 9.6% for Marlboro (but only in the first few puffs, drops down to 2.7% in later puffs). I guess that makes NAS tobacco the most inexpensive (per mg of free nicotine) and most healthy (the least amount of tar and carbon monoxide per mg of free nicotine). The links with data (warning -- antismokers sites): http://whyfiles.org/183smoking/2.html http://www.ohsu.edu/news/2003/071803smoke.html http://www.everybody.co.nz/page-1bc70d6f-9a03-4bcf-aa49-9a5dcf819160.aspx http://www.google.com/search?hl=en&q=pankow+camel+nicotine&btnG=Google+Search

Low monoamine oxidase B in peripheral organs in smokers

1. Joanna S. Fowler*,, 2. Jean Logan*, 3. Gene-Jack Wang, 4. Nora D. Volkow, 5. Frank Telang, 6. Wei Zhu, 7. Dinko Franceschi, 8. Naomi Pappas, 9. Richard Ferrieri*, 10. Colleen Shea*, 11. Victor Garza*, 12. Youwen Xu*, 13. David Schlyer*, 14. S. John Gatley, 15. Yu-Shin Ding*, 16. David Alexoff*, 17. Donald Warner*, 18. Noelwah Netusil, 19. Pauline Carter, 20. Millard Jayne, 21. Payton King, and 22. Paul Vaska

+Author Affiliations 1.
*

Chemistry Department and Medical Department, Brookhaven National Laboratory, Upton, NY 11973; and Department of Applied Mathematics and Statistics, Stony Brook University, Stony Brook, NY 11794

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1. Contributed by Joanna S. Fowler, July 9, 2003

Abstract
One of the major mechanisms for terminating the actions of catecholamines and vasoactive dietary amines is oxidation by monoamine oxidase (MAO). Smokers have been shown to have reduced levels of brain MAO, leading to speculation that MAO inhibition by tobacco smoke may underlie some of the behavioral and epidemiological features of smoking. Because smoking exposes peripheral organs as well as the brain to MAO-inhibitory compounds, we questioned whether smokers would also have reduced MAO levels in peripheral organs. Here we compared MAO B in peripheral organs in nonsmokers and smokers by using positron emission tomography and serial scans with the MAO B-specific radiotracers,l-[11C]deprenyl and deuterium-substituted l[11C]deprenyl (l-[11C]deprenyl-D2). Binding specificity was assessed by using the deuterium isotope effect. We found that smokers have significantly reduced MAO B in peripheral organs, particularly in the heart, lungs, and kidneys, when compared with nonsmokers. Reductions ranged from 33% to 46%. Because MAO B breaks down catecholamines and other physiologically active amines, including those released by nicotine, its inhibition may alter sympathetic tone as well as central neurotransmitter activity, which could contribute to the medical consequences of smoking. In addition, although most of the emphases on the carcinogenic properties of smoke have been placed on the lungs and the upper airways, this finding highlights the fact that multiple organs in the body are also exposed to pharmacologically significant quantities of chemical compounds in tobacco smoke.

There is inverse, dose-response relation between smoking and Parkinson's disease (the more pack-years the lower PD risk), and quitting increases the chances for PD, the longer the quit, the more chance for the disease. Here is one prospective study on these relations:

Neurology. 1999 Sep 22;53(5):1158. Smoking and Parkinson's disease: a dose-response relationship Gorell JM, Rybicki BA, Johnson CC, Peterson EL Department of Neurology, Henry Ford Health System, National Institute of Environmental Health Sciences Center in Molecular and Cellular Toxicology with Human Applications, Wayne State University, Detroit, MI, USA. OBJECTIVE: To determine whether an inverse dose-response relationship exists between cigarette smoking and PD among ever-smokers and ex-smokers. METHODS: Smoking and alcohol consumption were analyzed in 144 PD patients and 464 control subjects, who were frequency matched for sex, race, and age (+/-5 years), in a population-based case-control study of men and women > or =50 years 119

old in the Henry Ford Health System. RESULTS: With never-smokers as the reference category, there was an inverse association between current light smokers (>0 to 30 pack-years) and PD patients (odds ratio [OR], 0.59; 95% CI, 0.23 to 1.53), and a stronger inverse association of PD with current heavy smokers (>30 pack-years; OR, 0.08; 95% CI, 0.01 to 0.62). When former >30-pack-year smokers were stratified by the interval since quitting, there was an inverse association between those who stopped >20 years ago and PD (OR, 0.86; 95% CI, 0.42 to 1.75), and a greater inverse relationship with those who stopped 1 to 20 years ago (OR, 0.37; 95% CI, 0.19 to 0.72). Alcohol consumption had no independent, significant association with PD, but heavy drinking (>10 drink-years) had a greater effect than light-moderate drinking in reducing but not eliminating the inverse association between smoking and PD. CONCLUSIONS: The inverse dose-response relationship between PD and smoking and its cessation is unlikely to be due to bias or confounding, as discussed, providing indirect evidence that smoking is biologically protective.

The most striking fact is that for smokers with 30 or more pack-years (OR=0.08), the odds for Parkinson's are reduced compared to the nonsmokers of the same age by a factor 1/0.08=12.5 i.e. more than twelve times. Note also how when the duration of the quitting increases from 'less than 20' to 'more than 20' years, the odds for PD more then double: from 0.37 to 0.86, getting closer to never smokers (OR=1.0). There are also animal experiments with similar results (and no confounding variables). The Big Pharma is certainly making 'great' returns from their billion a year investment into antismoking "science" and propaganda, from all these extra millions of Parkinson's and Alzheimer's patients, who can go on lingering for a decade or more on expensive drugs.

Some more PET scans of MAO B (oxidative gunk which increases with aging) in nonsmoker and smoker (ages 41) in different organs (as discussed above and in this study):
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MAO B graphs for smokers and nonsmokers (paper) show smokers in their sixties having MAO B levels of nonsmokers in their twenties. Bar graphs show that this MAO B inhibition is result of long term smoking (e.g. no significant MAO change after a day of abstinence and a subsequent cigarette). These MAO B rejuvenation effects of smoking are not the result of nicotine but of some other presently unknown magical ingredient of tobacco smoke.

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SCIENCE NEWS March 20, 2007 Smoking lowers Parkinson's disease risk
By Megan Rauscher NEW YORK (Reuters Health) - A new study adds to the previously reported evidence that cigarette smoking protects against Parkinson's disease. Specifically, the new research shows a temporal relationship between smoking and reduced risk of Parkinson's disease. That is, the protective effect wanes after smokers quit. "It is not our intent to promote smoking as a protective measure against Parkinson's disease," Evan L. Thacker from Harvard School of Public Health emphasized in comments to Reuters Health. "Obviously smoking has a multitude of negative consequences. Rather, we did this study to try to encourage other scientists...to consider the possibility that neuroprotective chemicals may be present in tobacco leaves." As reported in the March 6th issue of Neurology, Thacker and colleagues
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analyzed data, including detailed lifetime smoking histories, from 79,977 women and 63,348 men participating in the Cancer Prevention Study II Nutrition Cohort. During about 9 years of follow-up, 413 subjects developed definite or probable Parkinson's disease.
Compared to people who had never smoked and were considered to have "normal" Parkinson's disease risk, former smokers had a 22-percent lower risk of Parkinson's disease and current smokers had a 73-percent lower risk.

"The results were similar for men and women, and were also similar to the results of studies by many other researchers looking at the same topic," Thacker noted.
In former smokers, more years of smoking, fewer years since quitting, more cigarettes per day, and a higher total amount of lifetime smoking were all related to a lower Parkinson's disease risk. The researchers also found that the duration of smoking and the time since quitting influenced risk more than the average daily amount of smoking.

"A 30 percent to 60 percent decreased risk of Parkinson's disease was apparent for smoking as early as 15 to 24 years before symptom onset, but not for smoking 25 or more years before onset," the investigators report. "The results of our study," Thacker said, "can probably be explained by something in cigarettes -- most likely in the tobacco itself -- actually protecting people against getting Parkinson's disease. That would be the simplest explanation that makes the most sense." Studies to determine if, in fact, there are neuroprotective compounds in tobacco are warranted, the researchers say. "The observation that smokeless tobacco users also have a lower risk of Parkinson's disease suggests that the most likely candidates are not compounds generated by combustion, but rather constituents of the tobacco leaves." SOURCE: Neurology, March 6,, 2007 Shocker: 'Villain' nicotine slays TB
Robyn Suriano SENTINEL STAFF WRITER Posted May 22, 2001

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Nicotine might be a surprising alternative someday for treating stubborn forms of tuberculosis, a University of Central Florida researcher said Monday. The compound stopped the growth of tuberculosis in laboratory tests, even when used in small quantities, said Saleh Naser, an associate professor of microbiology and molecular biology at UCF. Naser said nicotine worked better than about 10 other substances also tested. If it proves itself in further study, people might swallow capsules of nicotine or get intravenous doses to stave off their TB in the future.

It could be a potentially white-hat role for one of medicine's great villains. Most scientists agree that nicotine is the substance that causes people to become addicted to cigarettes and other tobacco products. "Can you imagine if we can get something useful out of it?" said Naser, who presented his study to members of the American Society for Microbiology, which is meeting this week at the Orange County Convention Center in Orlando. "It's the best thing I've seen to date. It shows there is some hope that this substance we've hated for so long might be formulated in one way or another to fight infectious diseases." Naser's research team uses naturally occurring substances taken from the jungles of Vietnam to the swamps of Florida in search of ones that might fight disease. He was working with tobacco plants when Naser noticed they were showing some effectiveness in quashing TB. Unsure what specific component was at work, he decided to test nicotine because it is the most-studied compound in the tobacco plant. He got lucky. First nicotine killed regular tuberculosis, and then harder, drug-resistant strains that will not succumb to the usual medicines. It worked even when used in doses smaller than what's found in a single cigarette. Naser said such small quantities are not likely to cause addiction. But no one is suggesting that people with TB take up the potentially deadly habit of smoking. Tuberculosis is highly treatable in most cases but still requires at least six months of antibiotics. When people fail to finish their medications, they can develop dangerous forms of the disease that no longer respond to the standard drugs. There were no cases of drug-resistant TB in Orange County last year, but statewide, the troublesome forms amount to about 1 percent of all cases, said Graydon Sheperd, chief of the bureau of TB and refugee health at the Florida Department of Health in Tallahassee. The contagious disease is caused by a bacteria that is spread through the air when an infected person coughs. There were 1,281 cases of newly diagnosed TB in the state in 1999. Doctors say they welcome the search for more tools to treat the ailment. "The biggest problem we have with TB is compliance. People don't want to take their medications, and we can end up with something that takes even longer to treat," said Dr. Boubker Naouri, TB program manager for the Orange County Health Department. "If we can have better drugs that work faster, it would be a big help." Robyn Suriano can be reached at rsuriano@orlandosentinel.com or 407-420-5487.

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Copyright 2001, Orlando Sentinel

The Carbon Monoxide Paradox

By Neil Sherman HealthScout Reporter

WEDNESDAY, May 9 (HealthScout) -- A killer gas may actually be a lifesaver, surprising research in mice reveals. Researchers discovered that very low levels of carbon monoxide helped mice whose lungs had been starved of blood and oxygen to stave off death. The startling discovery could possibly lead to the use of carbon monoxide -- at the right concentrations -- to help stroke and heart attack victims. "When you give very low levels of carbon monoxide, it actually causes the blood vessels to change some of their properties so that clots dissolve more readily," says lead author Dr. David Pinsky, an associate professor of medicine at Columbia University. "During an emergency -- like a heart attack or stroke or severe infections like sepsis -- clots form rapidly in small vessels, choking off blood flow. In this case, small doses of carbon monoxide turn off the protein which inhibits clot dissolution, therefore allowing clots to dissolve where they wouldn't," he adds. Carbon monoxide, a colorless, odorless gas, is usually toxic. Normally a by-product of the incomplete combustion of fuels, it enters the bloodstream after being inhaled and then mimics the behavior of oxygen without providing its benefits. The gas is transported through the body, gradually starving the body's organs. This increases the body's need for oxygen, and the heart rate increases, which brings on poisoning at a more rapid pace. As poisoning continues, the victim can suffer breathing difficulties, heart damage, brain damage and coma. Without fresh air, the victim can die. Carbon monoxide's close resemblance to nitric oxide alerted Pinsky and his colleagues to its potential. "Nitric oxide has very important biological functions within blood vessels -- it keeps blow flowing, keeps white cells from accumulating, and it keeps blood vessels from dilating," Pinsky explains. "Carbon monoxide can do some of the same things as nitric oxide, because they both bind to molecules of iron in the blood called heme proteins. And both activate an enzyme which signals cells to turn on and turn off various cell functions." "Our hypothesis is that since nitric oxide and carbon monoxide do similar things, if nitric oxide is unavailable to do these normalizing routines in blood vessels, carbon monoxide might take over some of the same functions," Pinsky says.
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To see if carbon monoxide worked like nitric oxide, Pinsky studied normal mice as well as mice that were unable to produce carbon monoxide in reaction to stress. "Under stressful situations, the body reacts by producing carbon monoxide. For a long time it was thought to be an incidental by-product of cell death," he says. Pinsky prevented blood flow to the right lungs of the mice for 30 minutes and then gave them very low levels of carbon monoxide. None of the normal mice survived. But 50 percent of the mice unable to produce carbon monoxide recovered. Carbon monoxide's ability to reverse clot development prevented the lung tissue from dying, allowing the mice to survive, Pinsky says. The findings were published in the May issue of Nature Medicine. So does that mean carbon monoxide could be used to treat heart attack and stroke victims? "With a lot of cautionary notes and a plea for further testing, perhaps," Pinsky responds. "So under a heart attack or stroke or sepsis or organ transplantation, the right amounts of carbon monoxide might be beneficial. But we are not sure yet -- it must be tested." It's not completely surprising that carbon monoxide may prove to be a therapeutic agent, according to Christoph Thiemermann of the William Harvey Research Institute in London. "The words carbon monoxide will for many of us immediately bring to mind the images of air pollution, of cigarette smoke, of suicides by inhalation of car exhaust fumes in closed garages," Thiemermann writes in an editorial accompanying Pinksy's article. "Recently nitric oxide has been elevated from a common air pollutant . . . to an [internal] second messenger of utmost physiological importance," Thiemermann explains. "Therefore, many of us may not be entirely surprised to learn that carbon monoxide can paradoxically rescue the lung from [cardiovascular blockage] injury." Whether carbon monoxide will become a treatment for stroke is still up for grabs, Thiemermann adds. "One could also argue that the use of [blood thinners] might be safer and just as effective as carbon monoxide inhalation in reducing [blood clot] deposition in the lung." What To Do This research is very preliminary. For all practical purposes, the gas remains a killer, so don't throw out your carbon monoxide detector just yet. (You do have a detector, don't you?) For more information on carbon monoxide, visit the Carbon Monoxide Headquarters or the Environmental Health Center. And don't forget these HealthScout stories on carbon monoxide.

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Cigarettes May Have an Up Side

By Paul Recer AP Science Writer Tuesday, May 19, 1998; 4:03 p.m. EDT

WASHINGTON (AP) -- Cigarettes may actually lower the risk of breast cancer among women with a gene mutation linked to high rates of the disease, a study indicates. But the researchers say other health risks of smoking far outweigh the possible benefits. ``Smoking may reduce breast cancer risk for these women, but cigarettes sharply increase the incidence of other cancers,'' said Jean-Sebastien Brunet, lead author of a study being published Wednesday in the Journal of the National Cancer Institute. ``This study is interesting scientifically, but it should not encourage anyone to smoke,'' said Brunet, a researcher at the Women's College Hospital of the University of Toronto in Canada. The study examined the breast cancer history of 372 women who all had mutations of the BRCA1 or BRCA2 genes. By some estimates, about 80 percent of such women will develop breast cancer during their lifetime. Half of the women in the study were smokers and half were nonsmokers. Brunet said that the incidence of breast cancer was 54 percent lower among heavy smokers than among nonsmokers. The effect, he said, was ``dose related''; that is, the more a woman with a BRCA gene mutation smoked, the less likelihood of her developing breast cancer. ``If a woman smoked up to four pack years, the reduction was 35 percent,'' he said. ``For a four or more pack years, the reduction was 54 percent.'' A pack year is equal to smoking one 20-cigarette pack a day for a year. Four pack years would be four packs a day for a year or one pack a day for four years. The study involved only women with the BRCA gene mutation. This mutation occurs, on average, in only one of every 250 women. Among some ethnic groups, the rate can be as high as one in 50. Between 5 percent and 10 percent of all women with breast cancer have a BRCA mutation. Brunet said the study was scientifically valuable because it suggests that some action of smoking or of some of the 1,300 compounds in cigarette smoke may be protective against breast cancer. However, he said, ``we don't have any idea what that compound is.'' Some breast cancers have been linked to estrogen, the female hormone, and cigarette smoking is known to lower production of estrogen, said Brunet. Smoking also is linked to early menopause and to a decreased risk of endometrial cancer, Brunet said.

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However, smoking significantly increases the risk of other, even more dangerous cancers, such of the lung, throat and pancreas. Brunet said he and his 18 co-authors came to their conclusions reluctantly and only after putting the study results to rigorous statistical tests. Further, Brunet said that scientific referees on the Journal also carefully scrutinized the data. ``We did everything we could to test the data, but we would really like for someone to replicate the study just to prove that our data set is correct,'' he said. In a commentary in the journal, Dr. John A. Baron of Dartmouth Medical School and Dr. R. W. Haile of the University of Southern California said that the study ``certainly should not be taken as encouragement for women with (the) mutations to smoke,'' but that it does raise the possibility that something in cigarette smoke could be of benefit for such women. They said more research could lead to a drug that would protect against mutation-related breast cancer, but without the serious health risks of smoking. Copyright 1998 The Associated Press

Research Indicating That Nicotine Holds Potential for NonSurgical Heart By-Pass Procedures Honored by the American College of Cardiology
Stanford University Discovery Licensed by Endovasc

MONTGOMERY, Texas--(BUSINESS WIRE)--March 17, 2000-- Dr. Christopher Heeschen of Stanford University was honored this week by the American College of Cardiology for his research on the effect of nicotine on angiogenesis (new blood vessel growth). His work took third place in the 2,000 entry Young Investigators Competition in the category of Physiology, Pharmacology and Pathology. Dr. Heeschen presented compelling data from research done at Stanford revealing that the simple plant protein, nicotine, applied in small harmless doses, produced new blood vessel growth around blocked arteries to oxygen-starved tissue. The research, involving animal studies, showed that the nicotine agent created more new blood vessels in blocked arteries than any other known growth factor. The new agent could be used to treat failing hearts and limbs with poor circulation. It holds the potential for non-surgical heart bypass procedures.

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Dr. Heeschen commented, ``It is important to note that this is a natural protein and is not gene therapy. Our research demonstrated conclusively that medicinal nicotine given at low doses is a very potent angiogenic.'' Dr. John P. Cooke, director of the Vascular Medicine Research Laboratory at Stanford, stated, ``We went into our research suspecting strongly that nicotine might play a negative role, that it would prevent growth of new blood vessels. In doing our experiments, we were surprised to find that nicotine, which is usually considered harmful, did the opposite. It actually had a potent therapeutic effect on the enhancement and growth of new blood vessels in cases of ischemic (oxygen-starved) vessels. The paradoxical results caused a paradigm shift in our thinking.'' The medicinal application of nicotine does not involve smoking. Endovasc Ltd., Inc. (OTC: ENDV - news), recently acquired the worldwide exclusive license on the patent for the newly discovered growth agent. Dr. David P. Summers, chairman and CEO of Endovasc said, `` We are very gratified that the American College of Cardiology has honored the work on angiogenesis at Stanford. We know that the receptor that controls angiogenesis is specific to the nicotine molecule. There are enormous implications for this discovery in the treatment of heart disease. We hope that medicinal nicotine may provide a multitude of therapeutic options to the clinician's armory.'' About the Company: Endovasc Ltd., Inc. is a biopharmaceutical company using liposomal drug delivery for products for the limbs and heart that have already shown safety and efficacy in the generic form. The company's products and processes are covered by patents and trade secrets for competing in a $2 billion market. The foregoing statements are made under the ``Safe Harbor'' Private Securities Litigation Reform Act of 1995 and may contain forward-looking statements that involve risks and uncertainties that may not be evident at the time of this release.

Nicotine Drugs Hold Promise for Treating Neurological Disease Alzheimer's patients may benefit, scientists say
Carl T. Hall, Chronicle Science Writer

Washington -- Nicotine drugs and skin patches are starting to show remarkable promise in treating neurological diseases that conventional medicines cannot touch, scientists reported yesterday. In one of the more extraordinary twists in modern medicine, the addictive agent in cigarettes -- in patch or gum form to avoid the obvious health risks of smoking -- is now being given in pilot

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studies to Alzheimer's patients to improve mental prowess and to Parkinson's sufferers to improve motor ability. Nicotine and similar drugs in the same chemical class are also being tested for chronic pain problems, obsessive-compulsive disorder, schizophrenia and cocaine addiction. In some cases, experts say nicotine might even protect precious brain cells whose death causes symptoms in Parkinson's, Alzheimer's and other neurodegenerative diseases.
TOURETTE'S SYNDROME

Those studies are all in the early stages, with approved uses many years away. But in at least one case -- Tourette's syndrome -- a treatment could be available as soon as April, if the U.S. Food and Drug Administration approves. Scientists outlined this emerging story of nicotine-as-medicine yesterday at the annual meeting of the American Association for the Advancement of Science. Dr. Paul Sanberg of the University of South Florida, part of a panel of top nicotine experts, reported that the research into nicotine's usefulness for Tourette's had the unexpected result of resurrecting a 1950s- era drug for high blood pressure. The drug, known generically as mecamylamine, appears to give Tourette's sufferers the same relief as nicotine, with fewer side effects. Drugmaker Merck & Co. once sold mecamylamine under the brand name Inversine, and it is still listed as an approved treatment for hypertension in the United States. However, the company stopped making it in the 1970s when more effective blood-pressure drugs were introduced. Known as a nicotinic antagonist, mecamylamine effectively blocks the short-term molecular effects of nicotine, which binds to certain receptor molecules in the brain. Paradoxically, the antagonist drug turns out to have some of the same long-term neurological effects as nicotine, which also shuts down its own receptors in the brain. Sanberg was searching desperately for something to help patients with Tourette's, a condition affecting about 100,000 people in America, marked by facial tics and virtually uncontrollable movements and vocalizations. Symptoms typically arise in childhood, often accompanied by behavioral and other problems that can persist long into adulthood. Scientific investigations pointed to nicotine as a possible therapy because of the peculiar brain chemistry involved. Sanberg first tested nicotine gum, but his youthful patients did not like the bitter taste and had difficulty chewing it correctly. Later, when anti-smoking nicotine skin patches hit the market, Sanberg tried again, but found that the side effects -- nausea and occasional vomiting -- outweighed the benefits. Eventually, he discovered that mecamylamine could achieve the same or even better results as nicotine patches. Most importantly, ``side effects were really minimal,'' Sanberg said.

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`DON'T SMOKE'

Experts at the conference took pains yesterday to emphasize the health risks of nicotine by traditional delivery methods -- cigarettes, chewing tobacco or cigars. ``Don't smoke,'' said Dr. Edward Levin of Duke University, noting that tobacco smoke contains some 4,000 chemicals of which nicotine is only one. The future for medicinal nicotine, however, could be promising. Layton Bioscience Inc., a small biotechnology company based in Sunnyvale, acquired marketing rights to the drug in March 1988 from Merck, which had no interest in pursuing the project on its own given the small size of the market. Layton hopes to win U.S. Food and Drug Administration approval by March 29, which would allow the company to reintroduce the product. Doctors could then prescribe it for any condition they choose, including for Tourette's syndrome. Detailed results of the latest clinical studies are awaiting publication in a medical journal. Based on further studies, meanwhile, Layton eventually plans to seek formal approval for mecamylamine as a Tourette's drug. Other drugs that both block and mimic nicotine are being developed and could also be on the market within a few years.
Even smoking is clearly trumped by another factor or combination of factors, judging by the unusually low incidence of heart attacks in France, Japan and on Kitava. The Kitavans: Wisdom from the Pacific Islands There are very few cultures left on this planet that have not been affected by modern food habits. There are even fewer that have been studied thoroughly. The island of Kitava in Papua New Guinea is host to one such culture, and its inhabitants have many profound things to teach us about diet and health. The Kitava study, a series of papers produced primarily by Dr. Staffan Lindeberg and his collaborators, offers a glimpse into the nutrition and health of an ancient society, using modern scientific methods. This study is one of the most complete and useful characterizations of the diet and health of a non-industrial society I have come across. It's also the study that created, and ultimately resolved, my cognitive dissonance over the health effects of carbohydrate. From the photos I've seen, the Kitavans are beautiful people. They have the broad, attractive faces, smooth skin and excellent teeth typical of healthy non-industrial peoples. Like the Kuna, Kitavans straddle the line between agricultural and hunter-gatherer lifestyles. They eat a diet primarily composed of tubers (yam, sweet potato, taro and cassava), fruit, vegetables, coconut and fish, in order of calories. This is typical of traditional Pacific island cultures, although the relative amounts differ. 131

Grains, refined sugar, vegetable oils and other processed foods are virtually nonexistent on Kitava. They get an estimated 69% of their calories from carbohydrate, 21% from fat, 17% from saturated fat and 10% from protein. Most of their fat intake is saturated because it comes from coconuts. They have an omega-6 : omega-3 ratio of approximately 1:2. Average caloric intake is 2,200 calories per day (9,200 kJ). By Western standards, their diet is high in carbohydrate, high in saturated fat, low in total fat, a bit low in protein and high in calories. Now for a few relevant facts before we really start diving in:

Kitavans are not particularly active. They have an activity level comparable to a moderately active Swede, the population to which Dr. Lindeberg draws frequent comparisons. They have abundant food, and shortage is practically unknown. Their good health is probably not related to genetics, since genetically similar groups in the same region are exquisitely sensitive to the ravages of industrial food. Furthermore, the only Kitavan who moved away from the island to live a modern life is also the only fat Kitavan. Their life expectancy at birth is estimated at 45 years (includes infant mortality), and life expectancy at age 50 is an additional 25 years. This is remarkable for a culture with limited access to modern medicine.

Over 75% of Kitavans smoke cigarettes. Even the most isolated societies have their modern vices.

The first study in the series is provocatively titled "Apparent absence of stroke and ischaemic heart disease in a traditional Melanesian island: a clinical study in Kitava." In it, Dr. Lindeberg presents data from interviews and electrocardiograms (ECG) suggesting that heart disease and stroke are absent or extremely rare on Kitava. The inhabitants are entirely unfamiliar with the (characteristic) symptoms of heart attack and stroke, despite the sizable elderly population. This is confirmed by the ECG findings, which indicate remarkable cardiovascular health. It also agrees with data from other traditional cultures in Papua New Guinea. Lindeberg states: For the whole of PNG, no case of IHD or atherothrombotic stroke has been reported in clinical investigations and autopsy studies among traditionally living Melanesians for more than seven decades, though an increasing number of myocardial infarctions [heart attacks] and angina pectoris in urbanized populations have been reported since the 1960s. Dementia was not found except in in two young Kitavans, who were born handicapped. The elderly remained sharp until death, including one man who reached 100 years of age. Kitavans are also unfamiliar with external cancers, with the exception of one possible case of breast cancer in an elderly woman. Overall, Kitavans possess a resistance to degenerative diseases that is baffling to industrialized societies. Not only is this typical of non-industrial cultures, I believe it represents the natural state of existence for Homo sapiens. Like all other animals, humans are healthy and robust when occupying their preferred ecological niche. Our niche happens to be a particularly broad one, ranging from complete carnivory to plant-rich omnivory. But it does not include large

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amounts of grains or modern industrial foods. In the next few posts, I'll discuss more specific data about the health of the Kitavans, including their body composition, serum lipids, and hormone profile. These data challenge the theory of an "atherogenic lipid profile", the idea that certain blood lipid patterns cause heart disease.

DID YOU KNOW... ...that an Australian study sampling, among other things, individuals over 45 years of age, found that 38.9% of smokers were overweight, versus 49.5% ex-smokers and 44.1% never-smokers? ________________________ DATA FROM: Australian Bureau of Statistics January 1994 report entitled "1980-90 National Health Survey: Lifestyle and Health Australia".

DID YOU KNOW... ...that an Australian study sampling, among other things, individuals over 45 years of age, found that 11.3% of smokers suffered from hypertension, versus 27.0% ex-smokers and 29.0% never-smokers? ________________________ DATA FROM: Australian Bureau of Statistics January 1994 report entitled "1980-90 National Health Survey: Lifestyle and Health Australia".

DID YOU KNOW... ...that an Australian study sampling, among other things, individuals over 45 years of age, found that 6.0% of smokers suffered from heart disease, versus 6.7% never-smokers and 11.4% ex-smokers? ________________________ DATA FROM:

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Australian Bureau of Statistics January 1994 report entitled "1980-90 National Health Survey: Lifestyle and Health Australia".

DID YOU KNOW... ...that in an Australian study, 91.8% of those who never smoked reported a long term illenss, while those who smoked reported 89.0%? When age was taken into consideration, more people who had never smoked than those who did smoke reported one or more long-term illnesses. When the number of years during which a person had been a smoker were taken into account, it was the ex-smokers who fared worse when it came to long term illnesses. ________________________ DATA FROM: Australian Bureau of Statistics January 1994 report entitled "1980-90 National Health Survey: Lifestyle and Health Australia".

DID YOU KNOW... ...that smoking has a protective effect on immunological abnormalities in asbestos workers? Data from: 0429. Institute of Immunology and Experimental Therapy (Poland). Lange, A. "Effect of Smoking on Immunological Abnormalities in Asbestos Workers".

DID YOU KNOW... ... that Hypertension and postpartum hemorrhage are lower in smokers? Data from: 0045. University of Tasmania (Australia). Correy, J.; Newman, N. Curran, J. "An Assessment of Smoking in Pregnancy."

DID YOU KNOW... ... that nonsmokers and especially ex-smokers of cigarettes have greater risk of UC [ulcerative colitis]? Data from: 4134. Lorusso, D.; Leo, S.; Miscianga, G.; Guerra, V. "Cigarette smoking and ulcerative colitis. A case control Study." Hepato-Gastroenterology 36(4): 202-4, Aug. 1989.

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DID YOU KNOW THAT... ... that there is a low prevalence of smoking in ulcerative colitis? And that the disease often starts or relapses after stopping smoking? Data from: 4101. Prytz, H.; Benoni, C.; Tagesson, C. "Does smoking tighten the gut?" In Scandinavian Journal of Gastroenterology 24(9):1084-8, Nov. 1989.

DID YOU KNOW THAT... ... that smoking protects against Parkinson's disease? Data from many studies. Among them: 1102. Carr, L.A.; Rowell, P.P. "Attenuation of 1methyl-4-phenyl-1,2,3,6-tetrahydrophyridine- induced neurotoxicity by tobacco smoke." Published in Neuro-pharmacology 29(3):311-4, Mar 1990. 1190. Janson, A.M.; Fuxe, K.; Agnati, L.F. Jansson, A. et al. "Protective effects of chronic nicotine treatment on lesioned nigrostriatal dopamine neurons in the male rat." Pub. in Progress in Brain Research 79:257-65, 1989. 4014. Decina, P.; Caracci, G.; Sandik, R.; Berman, W. et al. "Cigarette smoking and neuroleptic-induced parkinsonism." In Biological Psychiatry 28(6):502-8, Sept. 15, 1990

DID YOU KNOW THAT... ... that RBCs [red blood cells] from cigarette smokers contain more glutathione and catalase and protect lung endothelial cells against O2 [dioxide] metabolites better than RBCs from nonsmokers? Data from: 0759. University of Colorado. Refine, J.E.; Berger, E.M.; Beehler, C.J. et al. "Role of RBC Antioxidants in Cigarette Smoke Related Diseases." Jan 1980 - continuing.

DID YOU KNOW THAT... ... that Hypertension (high blood pressure) and postpartum hemorrhage are lower in smokers? Data from: 0045. University of Tasmania (Australia). Correy, J.; Newman, N. Curran, J. "An Assessment of Smoking in Pregnancy."

DID YOU KNOW THAT... ... that Hypertension (high blood pressure) is less common among smokers?

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Data from: 0146. Shanghai Institute of Cardiovascular Diseases. Chen, H.Z.; Pan, X.W.; Guo, G. et al. "Relation Between Cigarette Smoking and Epidemiology of Hypertension.

DID YOU KNOW... ... that smokers have lower incidence of postoperative deep vein thrombosis than nonsmokers? Data from: Guy's Hospital Medical School (England). Jones, R.M. "Influence of Smoking on Peri-Operative Morbidity."

DID YOU KNOW... ... that smokers have less plaque, gingival inflammation and tooth mobility than nonsmokers? Data from: Veterans Administration, Outpatient Clinic (Boston). Chauncey. H.H,; Kapur, K.K.; Feldmar, R S. "The Longitudinal and Cross-Sectional Study of Oral Health: in Healthy Veterans (Dental Longitudinal Study)

DID YOU KNOW THAT... ... that Smokers in general are thinner than nonsmokers, even when they ingest more calories? Data from: Numerous studies, but only two are listed below: 0885. Kentucky State University. Lee. C.J.: Panemangalore. M. "Obesity Among Selected Elderly Females In Central Kentucky." FUNDING: USDA 0942. University of Louisville. Belknap Campus School of Medicine. Satmford, B.A.; Matter, S.; Fell, R.D., et al. "Cigarette Smoking, Exercise and High Density Lipoprotein Cholesterol" FUNDING: American Heart Association.

DID YOU KNOW... ... that smoking improves motor performance?

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Data from: 0530. London University, Institute of Psychiatry. O'Connor, K.P "Individual Differences in Psychophysiology of Smoking and Smoking Behaviour "

DID YOU KNOW THAT... Smoking improves human information processing? Higher nicotine cigarettes produce greater improvements [in information processing] than lownicotine cigarettes? Nicotine can reverse the detrimental effects of scopolamine on performance? Smoking effects are accompanied by increases in EEG arousal and decreases in the latency of the late positive component of the evoked potential?

Data from: 0574. University of Reading, Department of Psychology (England). Warburton., D.M.; Wesnes, K. "The Effects of Cigarette Smoking on Human Information Processing and the role of Nicotine in These Effects"

The WHO, in order to "prove" the dangers of ETS, financed the second largest study in the world on secondhand smoke. But the study "backfired" and showed not only that there was no statistical risk of disease on passive smoking, but even a protective effect for those who are exposed to it. Not surprisingly, it is said that the WHO tried to hide the study from the media. For more information click here

Allergy season: Cigarettes to the rescue?

http://www.scienceblog.com/cms/allergy-season-cigarettes-rescue-21093.html A new study shows that cigarette smoke can prevent allergies by decreasing the reaction of immune cells to allergens. Smoking cigarettes has a surprising benefit: cigarettes can protect smokers from certain types of allergies. Now, a study recommended by Neil Thomson, a member of Faculty of 1000 Biology and leading expert in the field of respiratory medicine, demonstrates that cigarette smoke decreases the allergic response by inhibiting the activity of mast cells, the major players in the immune system's response to allergens.

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Researchers at Utrecht University in the Netherlands found that treatment of mast cells with a cigarette smoke-infused solution prevented the release of inflammationinducing proteins in response to allergens, without affecting other mast cell immune functions. The mast cells used in the study were derived from mice, but it is likely that the same anti-allergy effect will hold true in humans. While taking up smoking to cure allergies is unwise, Thomson concludes that the findings presented in this study are "consistent with a dampening of allergic responses in smokers

Lung cancer: when unresolved emotions and diagnosis shorten your life "Surgery, radiation, or chemotherapy" are the three treatment options a person hears soon after they're told they have lung cancer. Lung cancer is the third most prevalent cancer in Georgia according to CDC statistics. We hear that smoking is touted as one of the causes, however is smoking the cause, or is it just correlated with the presence of lung cancer? This is a tough question which we must ask because the results of scientific animal research is ambiguous. Some animals die when subjected to tobacco smoke, whereas some do not. The reason may be to do with a fear of smoke. Lung cancers come in several forms. Discussed here are some of the more prevalent ones, and their emotional causes based on the work of Dr. Ryke Hamer. Dr. Hamer has worked with 6,500 patients with various cancers, many of which were considered "Terminal". Five years later, 6,000 of them were still alive. Those results speak for themselves and far surpass the results achieved by the mainstream medical paradigm. To fully understand what you're about to read, open another tab and read the brief articles about Dr. Hamer's work. There are several types of lung cancer. Here are some of them, along with Dr. Hamer's explanation of how they arise. This information comes from: www.GermanNewMedicine.ca. Bronchial carcinoma This cancer is related to a territorial fear which may happen when we're emotionally unable to move (forward) or maneuver in any direction in response to a big emotional shock. The result can be a sensory problem, or a motor problem. The sensory territorial fear manifests itself during the healing phase as pneumonia.

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Whereas the motor problem may create Asthma-like symptoms, which involves a motor problem with the bronchial musculature i.e. they are unable to move and feel restricted. A territorial fear is usually experienced by men or post-menopausal women. More information is available here. Pulmonary lung cancer Put simply - this is a fear of death brought on by a specific experience. When a patient receives a cancer" diagnosis, this is often experienced as a devastating shock which instantly triggers new cancers. Medicine calls these new cancers metastases. Thus, metastasis can be caused by the emotional shock of a doctor's diagnosis and prognosis. Avoid asking your doctor to tell you how long or short a lifespan you have - it may create an additional cancer. You may even have to tell your doctor to not disclosed their opinion of what your lifespan is. According to Dr. Hamer, many patients can also get a death-fright when they are concerned that a loved one or pet has experienced an accident and may die. More information on lung cancer and the German New Medicine is available here. For more info: James is a fitness, nutrition, and healing coach at www.TotalFitness.net who will guide you to the very best in health and wellness. He's a world-class professional and creator of the Holistic Weight Loss For Life groups. Send James a note.

Hi Dr. Motley, My name is Patty and I have DH. I found long ago that when I smoke it is not as bad. I found studies done on line. I thought you might be interested in them. I would love to do a video on this subject, but we do a lot of children's videos, and I would not want to have one of the kids who watch them click on a smoking one. I have nothing against persons smoking after they reach an age of understanding.

There could be beneficial effects of smoking when it comes to Dermatitis Herpetiformis, DH... immunosuppressive effects of smoking play a role in this autoimmune disease Smith JB, Fenske NA. Cutaneous manifestations and consequences of smoking. J Am Acad Dermatol 1996;34:717-732[Medline].

One study found decreased serum IgA in smokers which may also play a role.

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Ferson M, Edwards A, Lind A, et al. Low natural killer-cell activity and immunoglobulin levels associated with smoking in human subjects. Int J Cancer 1979;23:603609[Medline].

Your videos are very well made and have some great information too. I liked the fluoride one. One of the triggers for DH are bromides so I stay away from anything and anywhere I might come in contact. Thank you for posting all the information, Patty

Much of "addiction" propaganda is aimed at uneducated. While it is true that smoking causes permanent changes in brain (and in other tissues), so does remembering you birthday or your last name or your native tongue. Your entire life is an irreversible unfolding at biochemical, psychological,... economic, social levels. The relevant question is not whether changes are permanent (they mostly are) but whether the changes in your biochemical network induced by tobacco smoking are good or bad for you. All the hard science from antismoking research itself, indicates that tobacco smoking has protective, invigorating and rejuvenating effects on the nervous systems, central and peripheral. In particular regarding the "addiction" causing changes above, tobacco smoking does increase the numbers of nicotinic receptors (which are one of the two main types of cellular receptors; these receptors exist in everyone, unrelated to smoking despite historically accidental suggestive name). These nicotinc receptors are vital for functioning of not just brain but of perhipheral nervous system and ultimately of every cell and organ in your body. Their numbers and functionality decline with age, most dramatically in people with dementias (such as Alzheimer's and Parkinson's). As with MAO levels discussed in the first post (which increase with age, like a gunk in a high precision machinery), the number of well functioning nicotinic receptors is another clock defining your real biological age -- the more well functioning nicotinic receptors you have, the younger and more vital you are. The permanent increase in number of these receptors induced (in the long run, not instantly) by tobacco smoke is most certainly good for you. What the antismoking propaganda refers to is the fact that nicotine itself occupies

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temporarily these receptors, making thus fewer available for acetylcholine for a brief time. This is no different than if you lift a weight, some of muscle cells are certainly temporarily occupied by lifting a "useless" weight. Yet, lifting weights is good for your muscles since in response to periodic increase in their load, they upregulate all biochemical systems needed to support greater load. Hence nicotine from tobacco smoke is a workout for your receptor system, which strengthens it over time. Note that nicotine from patches or other slow delivery systems peddled by pharmaceutical industry doesn't work here nearly as well, since it acts more like getting hold of a weight and holding it up for 10 hours -- it is not a real weight lifting exercise but something which will likely harm your muscles. The nicotine levels from smoking tobacco oscillates and thus it is more like taking 20-30 exercise breaks every day, which is a much better way to do it. You will find the same sleight of hand used for most other effects of tobacco smoking, as illustrated earlier on glutathione example (the same goes for CO and NO, neutrophyls, oxygen & blood supply to heart,...) -- they take a momentary snapshot of some oscillatory effect of smoking, pick the most convenient phase in the process and measure the change, such as decline in some resource and then declare: this is what smoking does to this resource - it depletes it. While it would certainly be bad for your were that were all that is happening to the resource, that is not all that is happening -- the smoking causes oscillation on all such resources and with live systems this is good for them, since it represents a workout of the production & support systems for the resource, strengthening them and upregulating the supplies over time. The recent hoopla on negative cardiovascular effects of secondary smoke after only 30 seconds of exposure is also the gimmick of this kind -- they were talking about the transient mild reduction in reserves of blood carrying capacity to heart, which is actually a very positive effect -- that's why people do aerobics in the first place, to reduce the reserves temporarily so that the suppplies would get upregulated in the long run. Using this kind of "logic" one could also "prove" that sleep is bad for you, since during sleep many of the systems we value for our productive life reduce acitivity or shut down altogether. Just as exercise is "addictive" or having a family is "addictive" or eating and breathing are "addictive" so is the smoking -- people seek it because it is good for them. I wrote a bit more on the smoking "addiction" on another forum.

quote: I've come across information lately that has led me to believe that meat eating and smoking is more analagous than most would probably believe. Humans began eating meat because it had a survival benefit that boosted the evolutionary process. The high protein yielded from meat consumption gave homo sapiens the muscular strength and endurance to prevail and survive. In other words, hypothetically, if one

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were to look at it "naturally" at the time, one could say "humans aren't meant to eat meat. Humans have always been herbivores." ... In summary, the idea of something being "natural" should not have to meet the simple definition of being "organically and historically pre-justified". Just because humans do it now and didn't do it before, is not a reason to summarily dismiss anything. Humans don't just simply adapt to their environments, but adopt them and carry them forward into future generations. One could further argue that humans have become advanced enough to create greater complexities to adopt into themselves, thus carrying the adoption of the symbiotic relationship into the next generation, and further, for a survival benefit. In this way, what doesn't kill you, makes you, and those who follow you, stronger.

Nice observations. When I hear "humans aren't meant to..." from antismokers and other 'god wannabes', I usually ask them whether human hand was "meant to" type on keyboards or just to hold branches, pick fruits and insects and such. The major advances in any realm occur precisely when the systems find a way around "what was meant" and do something which "was not meant" while extracting the net benefit from it.

Light a cigarette and inhale lungfuls of smoke. Good for you? Hardly. But spend time with people suffering from schizophrenia or other forms of severe mental illness, and you'll find many of them going at it like chimneys. Why? Poor judgement about the consequences, perhaps. Or the need for anything to soothe their distress. But there's a third possibility that is much more intriguing. For them, and others with psychiatric and even physical illnesses, smoking amounts to an oddly neglected form of selfmedication. Of course, tobacco smoke - an airborne cocktail of nasty chemicals - is harmful. What's at issue is a single non-carcinogenic ingredient: nicotine. This already has one medically approved application: taken by mouth in the form of gum, or through the skin from an impregnated patch, would-be ex-smokers aim to absorb a dose sufficient to dampen their cravings. And for many trying to kick the habit, particularly when used as part of a complete programme, it works. But though we hear occasional whisperings of other possible benefits of nicotine, they never seem to get taken seriously. In ulcerative colitis, for example, the symptoms...

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Schizophrenia, too, has attracted interest. Surveys have suggested that up to 90 per cent of people with the disorder smoke... Nicotine has been studied in the context of two neurological disorders: Alzheimer's and Parkinson's... Attempts to use nicotine in Parkinson's date back to the 1920s... Nicotine has also been tested in small studies on pain, depression, attention deficit hyperactivity disorder, obesity and anxiety... The usual explanation is that nicotine, a natural material, cannot be patented. Few companies would be prepared to invest in testing it for disorders if, when it was licensed, anyone could make and sell it... Of course, there is also a quite separate reason for the lack of interest: nicotine has an image problem... Nicotine, after all, is only the world's second most popular drug; caffeine is still No 1. "We could take caffeine in a pill if we wanted. I don't want to. I'm sure it's much more addictive when it comes in a cup with a smell, with a look, with a taste, and combined with some social activity." Clearly there is a big difference between being given a drug to treat an illness and seeking it out for non-medical reasons. Fears of inducing nicotine addiction by giving a pill or a piece of gum are, he believes, unwarranted. A longer version of this article appears in the August edition of the monthly newsletter 'Medicine Today' (www.medicine-today.co.uk) Story

Study finds unusual suspect in lung cancer risk Dear Friend, For years I've told you that the link between smoking and cancer has been exaggerated, and I'm not surprised to see that there's another danger factor here that's got nothing to do with lighting up. Researchers at the University of Montreal were stunned to find that that women who had undergone hysterectomies, or had otherwise had menopause medically induced were almost twice as likely to develop lung cancer as women who had gone through "the changes" naturally. Ironically, the study began as a quest to find a link between lung cancer and hormones in women. Can you imagine a worse situation? You have a hysterectomy or get your ovaries

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removed for whatever reason, believing that at the very least you're reducing your risk of the lethal ovarian cancer only to find out that you're nearly doubling your chances of developing an equally deadly disease. Hormones contain growth agents, and they're just as likely to cause cancer cells to grow as they are to help offset the effects of menopause -- which is why there's so much evidence out there which says that women should avoid hormone therapies. The researchers on this study theorize that the lung cancer danger is rooted in the fact that surgically or medically induced menopause results in a woman's estrogen level dropping to radically low levels almost instantly. In the case of naturally occurring menopause, the decline in estrogen is far less extreme, giving the body time to adjust. Other studies have also unearthed the detrimental health effects of removing ovaries. The recent Nurse's Health study found that women who underwent hysterectomies but kept their ovaries tended to live longer than women who had their ovaries removed entirely. Women without ovaries also tended to be at higher risk for theoretically unconnected ailments like heart disease and other cancers -- including lung cancer. If nothing else, I'm hoping that this study helps spread the news that cigarettes are not the sole cause of lung cancer. For too long, the "quit smoking" mantra of the mainstream healthcare community has served as a catch-all solution to this terrible disease. But the truth of the matter is that thousands upon thousands of people die from lung cancer every year -- people who have never even taken a puff of a single cigarette (filtered or otherwise!). Case in point: the tragic death of Diana Reeve, who was felled by lung cancer just seven months after being diagnosed with a disease -- and she had never smoked. She'd never even lived in an environment where she was exposed to second hand smoke, third hand smoke, sidestream smoke or any of the other crazy smoke "exposures" they're always citing as "causes" of cancer. And yet she was taken by the disease as rapidly and mercilessly as someone who'd had a three-pack-a-day habit for forty years. Until doctors want to admit that there's a lot more to lung cancer than preventing people from smoking, I'm afraid we'll never get to the bottom of this disease.

Antis claim that there are "400,000 preventable deaths" caused by smoking. If every smoker quit smoking today, that number of deaths would INCREASE!!

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Error! Hyperlink reference not valid. www.lungcanceralliance.or...tsheet_2008.pdf "In fact, non-smokers(never-smokers..GK) now account for nearly 20 percent of all new lung cancer cases and over 50% of new lung cancer patients are former smokers, many of whom quit decades ago, says the Alliance for Lung Cancer (Alcase), a Vancouver, Wash.-based non-profit group. Current smokers,45 million, account for 30% of the new lung cancer deaths(LCD's) or about 48,000 LCD's per year. Ex-smokers,45 million, account for 50% of the yearly LCD's or 80,000 per year. If the 45 million current smokers became ex-smokers, there would be 32,000 MORE LCD's per year. Smokers will have a 67% GREATER chance of suffering a LCD if they quit. If every smoker quit smoking today,there would be an INCREASE in LCD's and there would be NO decrease in cardiovascular disease deaths!!

Smokers are NOT at a higher risk for cardiovascular disease!!!! Cardiovascular disease events include heart attack, angina, coronary heart disease, stroke, and claudicate (peripheral arterial disease). The Framingham Heart Study is about real people who have been monitored for decades. The two reports below are the results of 40 and about 60 years of data about actual people and their health. The CDC and it's 400,000 deaths is NOT about real people, that number and it's risk factors, is a computer generated GUESS!!

http://www.forces.org/writers/hatton/files/murder.htm It's on the cigarette packet in capital letters: SMOKING CAUSES HEART DISEASE. The most authoritative study on this is certainly the Framingham Heart Study, which is known as the Rolls Royce of studies.

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In this town in Massachusetts, 5,127 men and women have been studied since 1948. They have had the fullest details taken on their health and life-style, and have been checked every two years. Dr. Seltzer of Harvard University discusses this study at length in 'Framingham Study Data and "Established Wisdom" abut Cigarette Smoking and Coronary Heart Disease', Journal of Critical Epidemiology 42, no. 8 (1989). The results of the study show that there is no relationship between smoking and heart disease in women except a very slight favorable one (women who smoke have a very slightly lower rate of angina, not statistically significant). For men, the relative risk starts at 1.3 in smokers of forty or more cigarettes a day. Remember, the risk ratio of 2 has been designated the lower boundary of a weak association, so this means in fact a non-significant association. This risk went down to exactly one, that is, no risk at all, as the subjects aged. When information about certain of the other 300 risk factors for heart disease were taken into account, the relationship between smoking and heart disease was lost. http://www.foxnews.com/story/0,2933,184016,00.html First Lifetime Heart Disease Risk Assessment Developed Lloyd-Jones and colleagues from Northwestern University used data from the Framingham Heart Study, which has followed thousands of people for decades, to calculate lifetime cardiovascular risk among 50-year-olds. The researchers reviewed the medical records of 3,564 men and 4,362 women who did not have any record of cardiovascular disease at age 50. The men and women were followed for several decades and all cases of heart attack, coronary heart disease, angina, stroke, claudication (pain in the legs caused by circulation problems), and death from cardiovascular disease were recorded. When the researchers calculated the impact of modifiable risk factors such as body weight, smoking history, cholesterol levels, and blood pressure, they found that: --Smokers and nonsmokers had similar lifetime risks for cardiovascular disease. The study appears in the Feb. 14,2006 issue of the American Heart Association journal 'Circulation'.

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(SOURCES: Lloyd-Jones, D.M. "Circulation", Feb. 14, 2006, vol. 113: online. Donald M. Lloyd-Jones, MD, ScM, department of preventive medicine, Feinberg School of Medicine, Northwestern University, Chicago. Jorge Plutzky, MD, director, vascular disease prevention program, Brigham and Womens Hospital, Boston.) Here is a better link for the LCA. http://www.lungcanceralliance.org/documents/lungcancer_factsheet_2008.pdf The LCA shows never-smokers as having 15% of the LCD's; but, CDC data here: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5745a3.htm Table Shows that there are about 156,899 total LCD's. Shows that there are about 125,522 LCD's attributed to smoking(current+ex). That is 80% of the LCD's are smoking(current+ex) attributed and 20% attributed to never-smokers. I have been somewhat loose with my %'s; but,as the antis say "it's for a noble cause"!!! Note the cardiovascular diseases(CVD) deaths portion of the table. CDC show about 852,300 total CVD deaths. CDC data here shows that there are about 128,500 CVD deaths attributed to smoking.

That 128,500 is 15% of the total CVD deaths. Sooo,we have 20% of the adult population(current smokers), causing ONLY 15% of the total CVD deaths. Thus;as shown by BOTH the Framingham Study data and the CDC data, smokers DO NOT have an increased risk of CVD deaths. ntis claim that smoking causes cardiovascular diseases(CVD) and that this is proved by the fact that both smoking rates and CVD deaths have declined. However;since heart disease incidence rates have not decreased, the decline in CVD deaths is due to better medical science and not to the decrease in smoking rates. The EPA/NCHS chart here;

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http://oaspub.epa.gov/eims/eims.ROEreport.displayImage?graphrecno=10417

shows that,with the exception of Hypertension, Heart Disease incidence rates have stayed about the same. Since smoking has been shown to reduce tension,it is no wonder that Hypertension incidence has increased by about 25%!! [img]http://oaspub.epa.gov/eims/eims.ROEreport.displayImage? graphrecno=10417[/img]

Ohhh well,for some reason, it will not do a picture. The anti-smokers claim that smoking 'causes' 400,000 deaths per year. The media has never stopped to wonder about how many of those deaths would occur,even if smokers did not smoke? CDC data from the table here: http://www.cdc.gov/mmwr/preview/...ml/ mm5745a3.htm shows that there are an estimated 392,684 smokers deaths from the 19 diseases that are associated with smoking. However;since non-smokers also die from these diseases,these diseases can not be said to be 'caused' only by smoking. The table shows that there are a total of 1,293,886 deaths from these diseases. Smokers are 27%(cigarette 20%,cigar 6%,pipe 1%) of the population included in this data and smokers would be expected to have 27% of those deaths even if they did not smoke. 27% of 1,293,886 is 349,349 smokers deaths occurring even if they did not smoke. 349,349 is 89% of 392,684! Soooo,in the U.S., 89% of the 'so-called smoking caused deaths' would still have occurred if smokers did not smoke!!! As compared to most countries world-wide, the U.S. hhas a rather low adult smoking

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rate. World-wide, well OVER 90% of those 'smoking caused' deaths would still have occurred even if smokers did not smoke!! Pro-ban anti-smoker statistics are very strange!! http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5745a3.htm The link above has the CDC saying it found NO SAF's/SAM's(deaths) below the age of 35. Soooo;if a smoker dies at the age of 34 from lung cancer,it is NOT smoking related. If a non-smoker exposed to SHS/ETS dies at the age of 34 from lung cancer,it is NOT smoking related. If that same smoker were to die at the age of 36, it would be smoking related. If that same non-smoker were to die at the age of 36, it would be smoking related. This is not logical. Also, in the chart,there are all sorts of deaths from respiratory diseases that are smoker related. In fact 86% of the COPD(emphysema,etc) deaths are smoker related. However,there is NOT ONE respiratory disease death said to be due to SHS/ETS exposure!!!! ETS/SHS exposure will 'cause' lung cancer death;but,SHS/ETS exposure does not 'cause' a non-smoker to die from a respiratory disease?? That toooo,is very,very strange!!!
There is still no scientific proof whatsoever that smoking causes cancer. To hide this reality, epidemiology has been elevated to the rank of science in the public perception by dishonest researchers and health authorities backed by media. One particular form of lung cancer stands out. Adenocarcinoma makes up a larger proportion of cancers among never smokers and former smokers than current smokers. It might be fair to establish that adenocarcinoma seems to be a 'non smokers' cancer. Perhaps the smokers are infested by this form of lung cancer, by socializing too much with never smokers. Passive never smoking. Let's ban never smokers from the workplaces of smokers, to protect the smokers from the lung cancers of never smokers.....

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You are welcome to bring in a study demonstrating that tobacco smoking causes lung cancer (e.g. an animal experiment or a randomized intervention trial in humans). Mere statistical correlation between A (smoking) and B (lung cancer) does not prove hypothesis A causes B, since such correlation is also perfectly consistent with a hypothesis that there is some other factor C which causes both, A and B. Since tobacco smoke produces numerous beneficial biochemical and physiological effects in smokers (e.g. upregulation/rejuvenation of glutathione, neutrophiles, vascular growth factor, pregnenolone, IGF1, DHEA, testosterone, # of nicotinic ACh receptors, acetylcholine, dopamine, MAOI B,... ), there are plenty of therapeutic and protective effects against variety of inflammatory and toxic exposures C (where tobacco smoking provides immediate relief e.g. see a recent German study where C=aluminum dusts, and benefit of upregulated glutathione in smokers) but some of which can also be carcinogenic. In that case, correlation of A and B would be analogous to a correlation between the use of sunglasses and sunburns -- people who used sunglasses more hours last year are also more likely to have had more sunburns last year than the non users. Measuring the use of sunglasses is then simply a proxy for measuring person's sun exposure, the actual cause of sunburns. Since the statistical correlation between smoking and lung cancer was known since 1950s, the brute fact that after half a century and the vast amounts of money and resources spent into attempts to demonstrate the causal hypothesis, there is still no such demonstration (many such attempts backfired, proving precisely the oppposite, the protective role of smoking), reinforces the alternative hypothesis into a virtual certainty -- tobacco smoking does not cause lung cancer.

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I am wondering what the effects of smoking would be on exercise if one takes the proper precautions by using organic tobacco and a vaporizer. Most smokers cannot run without getting winded very quickly, and I doubt this could be prevented even under the best circumstances. This alone is a serious drawback.

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Tobacco was traditionally used by soldiers throughout the world, from ancient Native American warriors milennia ago, right up to the war in Iraq. In the British Empire era, smoking was compulsory for students in their elite boys schools (to improve health and get performance edge in sports). The Semai of Malaysia start smoking at age two. Medical textbooks, until 1950s advised smoking for congestive repiratory problems, and even today cold medicines use dopamine boosting for the same reason (which clean tobacco smoke does via multiple synergistic mechanisms much more effectively and more pleasantly). Smoking is also much more prevalent among physical laborers, miners, firemen, blue collar workers,... If you take a look at a recent German study of aluminum workers, it becomes obvious why they smoke more -- smoking reduces respiratory problems (caused in this case by inhalation of aluminm dusts) sixfold compared to nonsmokers. The same "smoker's paradox" was observed numerous times for all kinds of miners and other workers heavily exposed to noxious metallic dusts. They smoke because it tangibly and immediately helps their breathing. So, no, I don't think a clean tobacco smoke would cause any problem. People nowdays do smoke different cigarettes than those our ancestors smoked. The principal difference is that we use filters, which shifts the delicately balanced biochemistry of the inhaled smoke, which was finely tuned over the millenia of cultivation, into some arbitrary artificial range of medicinal ingredients. Hence the biochemical signaling, which is vital for the proper feedback on the dosing and rhytms of the nested cycles (puffs, whole cigaretts, night breaks) is off. Filters also shed synthetic fibers (they even made Kent's filters from asbestos for several years) which, unlike the natural tobacco leaf particles, are non-biodegradable, hence the

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lung cells have to enclose these fibers into the mucous liquid to ease their excretion via cough.

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What about the glycation effects: Tobacco smoke is a source of toxic reactive glycation products http://www.pubmedcentral.nih.gov/articlere...ubmedid=9391127 and we should focus on heart attacks more than cancer: http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum

So, we got the team of Alteon Inc. (pharma) consultants hinting that effects of smoking may be, or may not be, similar to those of diabetes (in mice experiments). So why does smoking mice live longer than nonsmoking mice? In fact tobacco smoking happens to be, among its numerous other therapeutic effects, protective against diabetes (coincidentally, Alteon makes diabetes drugs):

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Nicotine Reduces the Incidence of Type I Diabetes in Mice J. G. Mabley, P. Pacher, G. J. Southan, A. L. Salzman and C. Szab J. Pharmacology and Exp. Therapeutics, Vol. 300, Issue 3, 876-881, March 2002 Nicotine has been previously shown to have immunosuppressive actions. Type I diabetes is an autoimmune disease resulting from the specific destruction of the insulin-producing pancreatic beta -cells. Thus, we hypothesized that nicotine may exert protective effects against type I diabetes. The multiple low-dose streptozotocin (MLDS)-induced model and spontaneous nonobese diabetic (NOD) mouse model of type I diabetes were used to assess whether nicotine could prevent this autoimmune disease. Blood glucose levels, diabetes incidence, pancreas insulin content, and cytokine levels were measured in both models of diabetes, both to asses the level of protection exerted by nicotine and to further investigate its mechanism of action. Nicotine treatment reduced the hyperglycemia and incidence of disease in both the MLDS and NOD mouse models of diabetes. Nicotine also protected against the diabetes-induced decrease in pancreatic insulin content observed in both animal models. The pancreatic levels of the Th1 cytokines interleukin (IL)-12, IL-1, tumor necrosis factor (TNF)-alpha , and interferon (IFN)-gamma were increased in both MLDS-induced and spontaneous NOD diabetes, an effect prevented by nicotine 152

treatment. Nicotine treatment increased the pancreatic levels of the Th2 cytokines IL4 and IL-10. Nicotine treatment reduces the incidence of type I diabetes in two animal models by changing the profile of pancreatic cytokine expression from Th1 to Th2.

Or similarly a more recent experimental study from a different group (demonstrating also the "exercise effect" mentioned earlier in this thread):

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The Expression and Functional Role of Nicotinic Acetylcholine Receptors in Rat Adipocytes Run-Hua Liu, Masanari Mizuta, and Shigeru Matsukura JPET 310:52-58, 2004 To clarify whether nicotine has a direct effect on the function of adipocytes, we evaluated nicotinic acetylcholine receptor (nAChR) expression in adipocytes by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunocytochemistry and the direct effects of nicotine on the production of adipocytokines by enzymelinked immunosorbent assay and Western blot analysis. Receptor binding assays were performed using [3H]nicotine. RT-PCR studies revealed that {alpha}17, 9, 10, {beta}14, {delta}, and {epsilon} subunit mRNAs are expressed in adipocytes. Immunocytochemical experiments also suggested the presence of {alpha}7 and {beta}2 subunits. The receptor binding assay revealed a binding site for nicotine (Kd = 39.2 x 10-9 M) on adipocytes. Adipocytes incubated with nicotine for 12 and 36 h released tumor necrosis factor-{alpha} (TNF-{alpha}), adiponectin, and free fatty acid (FFA) into the medium in a dose-dependent manner with increasing nicotine concentration from 6 x 10-8 to 6 x 10-4 M. However, TNF-{alpha} protein levels in adipocytes incubated for 12 and 36 h decreased in a dose-dependent manner with increasing nicotine concentration from 6 x 10-8 to 6 x 10-4 M. These results show that adipocytes have functional nAChRs and suggest that nicotine reduces TNF-{alpha} protein production in adipocytes through the activation of nAChRs. Nicotine may temporarily lower insulin sensitivity by stimulating the secretion of TNF-{alpha} and FFA, whereas long-term direct stimulation of nAChRs by nicotine in addition to autonomic nervous system stimulation may contribute to better insulin sensitivity in vivo through a modulated secretion of adipocytokines.

As to cardiovascular diseases and smoking, our ancient medicine is again hard to beat for its protective and therapeutic effects (what a coincidence -- Alteon's other specialty are cardiovascular drugs).

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Did you know that the best brands (Japanese, natural complexes) of the miracle heart protector, Coenzyme Q10, are made from tobacco leaf (the richest source of CoQ10)? Do you know about nicotine based heart medicine "Angiogenix" based on the upregulation of vascular growth factor by nicotine described here:

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The product is called "Angiogenix" and is a nicotine-based treatment that appears to grow new blood vessels in the heart. It can be taken orally and, the company says, is non-addicting. The company, located in Texas, is called Endovasc Ltd., Inc. (I didn't know you could be both "limited" and "incorporated," but that's Texas.) Established in 1996, they think big, move fast, and have an impressive record for a young company. The fact that the company has been able to get this potential blockbuster drug all the way to Phase III trials (which means it's well on its way to FDA approval) without incurring any significant debt, in near record time indicates that they are very savvy indeed. It seems Endovasc believes that nutriceutical nicotine-based drinks, fitness bars, or capsules combined with high protein complexes could become super stars among nonprescription products. And these products could produce positive cash flow even sooner than you'd expect because they are not subject to the FDA approval process.

Nicotinic acid and its salts, along with nitric oxide (another vascular stimulator in tobacco smoke, along with CO in low concentration) have been used in heart medications for decades. Unlike the self-selected samples of smokers and nonsmokers considered in the study you cited, the randomized intervention trials (which is how you can find out the direction of causal relations), in which a random subset of smokers is selected for "quit group", show more heart attacks in the 'quit group' than in the control group (those left to smoke as they wish).

This post has been edited by nightlight: 17 April 2007 - 01:21 PM

Additionally it's a historical fact that the California Desert Indians smoked tobacco to cure colds. http://www.tobacco.o...antobcalif.html (Note the above website was developed to research and support lawsuits against tobacco.) In the final analysis, the facts do not add up about the risks of tobacco.

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Of course, none of the above would surprise our ancestors. For example, smoking was compulsory (for health reasons) for the students in elite boys schools of the glorious British Empire: * Johnstone & Hill "Scientific Scandal of Antismoking" The Royal College of Physicians of London promoted smoking for its benefits to health and advised which brands were best. Smoking was compulsory in schools. An Eton schoolboy later recalled that "he was never whipped so much in his life as he was one morning for not smoking". As recently as 1942 Prices textbook of medicine recommended smoking to relieve asthma. http://members.iinet.com.au/~ray/TSSOASb.html Those protective effects of tobacco smoke would surprise even less the British medical team of Dr. C. Y. Caldwell, who studied the Semai people of Maylasia in 1970s. The Semai children are fairly unique in our times since they enjoy the benefits of not merely the occasional whiff of secondary smoke but of the real thing -- the Semai children start smoking at age two (it is a way of weaning them from nursing). Now we are talking protection. Short of ripping them away from their mother's breast to make them smoke before the age of two, you can't get more direct and clear experiment than that. I would imagine animal rights groups here would scream a bloody murder, were scientists to try such experiment even on dogs, let alone primates or humans. Yet here, the parents themselves teach, perhaps even compel, their own toddlers to smoke before they can talk, the way they and their ancestors were taught as far back as anyone can remember. Dr. Caldwell and his team thoroughly examined (which included full chest x-rays) 12000 Semai and, as their paper (Feb 26, 1977 BMJ) reported, they found _not a single_ lung cancer. For more on this, see Dr. Whitby's book (2nd edition, pages 26, 103) which brought this amazing result, completely ignored by the mass media, to public attention: * Dr. W. T. Whitby "Smoking is Good for You" (online book) http://groups.google.com/group/alt.smokers/browse_frm/thread/34b73a74...
> Smoking and secondhand smoke are associated with my diseases such as > emphysema which were not addressed in the study you cited.

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Sorry, I didn't know "your diseases" include emphysema. I can't even imagine how hard it must be for you to participate here, struggling for oxygen every moment. If only you smoked, your lungs might have still been good and healthy.

Namely, as indicated in our previous thread on protective effects of tobacco smoke against lung damage: == Smoking protective against lung damage http://groups.google.com/group/alt.smokers/browse_frm/thread/f4c2f720... the German study of aluminum workers found that, when you control the samples for exposure (e.g. to aluminum vapors & dust), hence when you compare apples with apples, the risk of lung damage (which included decrease in lung capacity & alveolar elasticity) was _six_ times greater for the non-smokers than for smokers. Tobacco smoke is an aerobics for your immune and biochemical detox systems, equivalent of you stepping away from your desk 20-30 times a day for few minutes of pushups and thread-mill exercise. Within weeks you would see quite a bit of difference. Smoking produces analogous toning and stimulating effects on your immune system that conventional exercise does for your muscles and heart (in fact, tobacco smoke exercises & tones cardiovascular system as well). As cited in an earlier post, smokers have nearly twice the levels of glutathione, which is our main internal antioxidant & detox enzyme: == Beneficial effect of tobacco smoking for glutathione: http://speakeasyforum.com/eve/forums/a/tpc/f/613606642/m/4851097471?r... It is therefore perfectly natural that pharmaceutical and medical businesses would fight tobacco with all their might -- tobacco is the single most potent natural medicine humans have ever had. No other natural or synthetic medicine comes even close to the full spectrum of healing magic encoded in this biochemical miracle, the true gift of gods if there ever was one. You didn't perhaps imagine that the Big Pharma execs are willingly pouring billions of their hard earned profits into antismoking "science" and "grass roots" antismoking organizations, or to buy antismoking laws and regulations, just to benefit your or my health, or to spare you from a whiff of secondary smoke? That's what they worry about, your olfactory sensitivities. Yeah, sure. The only benefits the fat Big Pharma & Big Med are concerned about are their own profits. That's how they got to be so big and fat in the first

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place. Hence they do invest heavily into trying to restrict and badmouth (through pseudo-science & their mass media lapdogs) all natural and traditional remedies (see their Codex initiative which will make it very difficult for EU citizens to freely buy regular vitamins and other OTC health remedies). But no natural remedy is a greater danger to their profits than the most ancient and most potent medicinal plant of them all, tobacco. Hence, they _invest_ more money battling tobacco than all the rest of natural remedies put together: == After EU, the Big Pharama after natural remedies in USA: http://groups.google.com/group/alt.smokers/browse_frm/thread/7b173004... == Money trail behind antismoking http://groups.google.com/group/alt.smokers/browse_frm/thread/18ce47ec...

Here is one scientific paper, very heavily cited (263 times), focusing specifically on the glutathione levels and smoking: -----"Normal alveolar epithelial lining fluid contains high levels of glutathione" A. M. Cantin, S. L. North, R. C. Hubbard and R. G. Crystal Journal of Applied Physiology, Vol 63, Issue 1 152-157, Copyright c 1987 by American Physiological Society ABSTRACT The epithelial cells on the alveolar surface of the human lower respiratory tract are vulnerable to toxic oxidants derived from inhaled pollutants or inflammatory cells. Although these lung cells have intracellular antioxidants, these defenses may be insufficient to protect the epithelial surface against oxidants present at the alveolar surface. This study demonstrates that the epithelial lining fluid (ELF) of the lower respiratory tract contains large amounts of the sulfhydryl-containing antioxidant glutathione (GSH). The total glutathione (the reduced form GSH and the disulfide GSSG) concentration of normal ELF was 140-fold higher than that in plasma of the same individuals, and 96% of the glutathione in ELF was in the reduced form. Compared with nonsmokers, cigarette smokers had 80% higher levels of ELF total glutathione, 98% of which was in the reduced form. Studies of cultured lung epithelial cells and fibroblasts demonstrated that these concentrations of reduced glutathione were sufficient to protect these cells against the burden of H2O2 in the range released by alveolar macrophages removed from the lower respiratory tract of nonsmokers and smokers, respectively, suggesting that the glutathione present in the alveolar ELF of normal individuals likely contributes to the protective screen against oxidants in the extracellular milieu of the lower respiratory tract. ----

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Note that smokers (they had 22+/-4 pack years) did not only have 80% more total glutathione in the mucous layer, but also had a greater concentration (98 vs 96) of the reduced glutathione (which is the active, not used up, form). Basically, smoking 20-30 cigarettes has an effect on immune system analogous to the effect on muscles of taking 20-30 exercise breaks through the day and doing pushups and situps for five minutes. Even after few weeks, the gain in the size and strength of the muscles would start showing. You will find some papers, especially the more recent ones as the anti-smoking hysteria has intensified, spin this unambiguous strengthening of the immune system as the increase in the "inflammatory marker" or "stress marker", which while containing a tiny grain of truth, is like characterizing the stronger muscles of body builder as a larger 'mechanical stress or overload markers' or labeling a pay raise as increase in 'decadence and wastefulness markers'. When the anti-smoking "science" has to stoop to this kind of cheap verbal gimmickry to make their case, you know what the real score is. In addition to glutathione, which is the body's master antioxidant and metal detoxifier, many other lesser antioxidants and detoxifiers are similarly strengthened (e.g. check the study list citing and extending this study).

Scientists have ruthlessly sacrificed tens of thousands of mice and rats in this way over the years, deliberately subjecting their lungs to radioactive matter. The documented scientific results of these various experiments are identical. Every mouse or rat obediently contracts lung cancer, and every mouse or rat then dies. Theory has thus been converted to hard scientific fact under tightly controlled laboratory conditions. The suspect agent (radioactive matter) caused the claimed result (lung cancer) when inhaled by mammals. The overall magnitude of lung cancer risk to humans from atmospheric radioactive fallout cannot be overstated. Before Russia, Britain and America outlawed atmospheric testing on August 5, 1963, more than 4,200 kilograms of plutonium had been discharged into the atmosphere. Because we know that less than one microgram [millionth of a single gram] of inhaled plutonium causes terminal lung cancer in a human, we therefore know that your friendly government has lofted 4,200,000,000 [4.2 Billion] lethal doses into the atmosphere, with particle radioactive half-life a minimum of 50,000 years. Frightening? Unfortunately it gets worse. The plutonium mentioned above exists in the actual nuclear weapon before detonation, but by far the greatest number of deadly radioactive particles are those derived from common dirt or sand sucked up from the ground, and irradiated while travelling vertically through the weapons fireball. These particles form by far the 158

largest part of the smoke in any photo of an atmospheric nuclear detonation. In most cases several tons of material are sucked up and permanently irradiated in transit, but let us be incredibly conservative and claim that only 1,000 kilograms of surface material is sucked up by each individual atmospheric nuclear test. Before being banned by Russia, Britain and America, a total of 711 atmospheric nuclear tests were conducted, thereby creating 711,000 kilograms of deadly microscopic radioactive particles, to which must be added the original 4,200 kilograms from the weapons themselves, for a gross though very conservative total of 715,200 kilograms. There are more than a million lethal doses per kilogram, meaning that your governments have contaminated your atmosphere with more than 715,000,000,000 [715 Billion] such doses, enough to cause lung or skin cancer 117 times in every man, woman and child on earth. Before you ask, no, the radioactive particles do not just fade away, at least not in your lifetime or that of your children and grandchildren. With a half-life of 50,000 years or longer, these countless trillions of deadly government-manufactured radioactive particles are essentially with you forever. Circulated around the world by powerful jet streams, these particles are deposited at random, though in higher concentrations within a couple of thousand miles of the original test sites. A simple wind or other surface disturbance is all that is needed to stir them up again and create enhanced dangers for those in the vicinity. The once-innocent activity of playfully kicking sand around on the beach in summer could nowadays easily translate to suicide, if you happen to stir up a few radioactive particles that could stick to your skin or be inhaled into your lungs. Stop poking fun at Michael Jackson when he appears at your local airport wearing a surgical mask over his nose and mouth. He may look eccentric, but Michael will almost certainly outlive most of us. Twelve years after the cataclysmic Trinity test, it became obvious to western governments that things were getting completely out of control, with a 1957 British Medical Research Council report stating that global deaths from lung cancer have more than doubled during the period 1945 to 1955, though no explanation was offered. During the same ten-year period, cancer deaths in the immediate proximity of Hiroshima and Nagasaki went up threefold. By the end of official atmospheric testing in 1963, the incidence of lung cancer in the Pacific Islands had increased fivefold since 1945. Having screwed your environment completely for 50,000 years, it was time for big government to start taking heavy diversionary action. How could people be proved to be causing themselves to contract lung cancer, i.e. be said to be guilty of a self inflicted injury for which government could never be blamed or sued? The only obvious substance that people inhaled into their lungs, apart from air, was tobacco smoke, so the government boot was put in. Poorly qualified medical 159

researchers suddenly found themselves overwhelmed with massive government grants all aimed at achieving the same end-result: Prove that smoking causes lung cancer. Real scientists [especially some notable nuclear physicists] smiled grimly at the early pathetic efforts of the fledgling anti-smoking lobby, and lured them into the deadliest trap of all. The quasi medical researchers were invited to prove their false claims under exactly the same rigid scientific rules that were used when proving that radioactive particles cause lung cancer in mammals. Remember, for any theory to be accepted scientifically, it must first be proven in accordance with rigorous requirements universally agreed by scientists. First the suspect agent [tobacco smoke] must be isolated, then used in properly controlled laboratory experiments to produce the claimed result, i.e. lung cancer in mammals. Despite exposing literally tens of thousands of especially vulnerable mice and rats to the equivalent of 200 cigarettes per day for years on end, medical science has never once managed to induce lung cancer in any mouse or rat. Yes, you did read that correctly. For more than forty years, hundreds of thousands of medical doctors have been deliberately lying to you. The real scientists had the quasi medical researchers by the throat, because pairing the deadly radioactive particle experiment with the benign tobacco smoke experiment, proved conclusively for all time that smoking cannot under any circumstances cause lung cancer. And further, in one large accidental experiment they were never allowed to publish, the real scientists proved with startling clarity that smoking actually helps to protect against lung cancer. All mice and rats are used one-time-only in a specific experiment, and then destroyed. In this way researchers ensure that the results of whatever substance they are testing cannot be accidentally contaminated by the real or imagined effects of another substance. Then one day as if by magic, a few thousand mice from the smoking experiment accidentally found their way into the radioactive particle experiment, which in the past had killed every single one of its unfortunate test subjects. But this time, completely against the odds, sixty percent of the smoking mice survived exposure to the radioactive particles. The only variable was their prior exposure to copious quantities of tobacco smoke. 'Now I am become Death, the destroyer of worlds.' Vishnu, Bhagavad-Gita Government pressure was immediately brought to bear and the facts suppressed, but this did not completely silence the real scientists. Tongue in cheek perhaps, Professor Schrauzer, President of the International Association of Bio-inorganic Chemists, testified before a U.S. congressional committee in 1982 that it had long been well known to scientists that certain constituents of tobacco smoke act as anti-carcinogens [anti-cancer agents] in test animals. He continued that when known carcinogens 160

[cancer causing substances] are applied to the animals, the application of constituents of cigarette smoke counter them. Nor did Professor Schrauzer stop there. He further testified on oath to the committee that no ingredient of cigarette smoke has been shown to cause human lung cancer, adding that no-one has been able to produce lung cancer in laboratory animals from smoking. It was a neat answer to a rather perplexing problem. If government blocks publication of your scientific paper, take the alternate route and put the essential facts on the written congressional record! Predictably, this hard truth drove the government and quasi medical researchers into a frenzy of rage. By 1982 they had actually started to believe their own ridiculous propaganda, and were not to be silenced by eminent members of the scientific establishment. Quite suddenly they switched the blame to other secret ingredients put into cigarettes by the tobacco companies. Yes, that must be it! they clamored eagerly, until a handful of scientists got on the phone and pointed out that these same secret ingredients had been included in the mice experiments, and had therefore also been proved incapable of causing lung cancer. Things were looking desperate for government and the medical community overall. Since the anti-smoking funding had started in the early sixties, tens of thousands of medical doctors had passed through medical school, where they had been taught that smoking causes lung cancer. Most believed the lie, but cracks were starting to appear in the paintwork. Even the dullest of straight C doctors could not really make the data correlate, and when they queried it were told not to ask stupid questions. Smoking causes lung cancer converted to a creed, a quasi religious belief mechanism where blind faith became a substitute for proof. Even blind faith needs a system of positive reinforcement, which in this case became the advertising agencies and the media. Suddenly the television screens were flooded with images of terribly blackened smokers lungs, with the accompanying mantra that you will die in horrible agony if you dont quit now. It was all pathetic rubbish of course. On the mortuary slab the lungs of a smoker and non-smoker look an identical pink, and the only way a forensic pathologist can tell you might have been a smoker, is if he finds heavy stains of nicotine on your fingers, a packet of Camels or Marlboro in your coat pocket, or if one of your relatives unwisely admits on the record that you once smoked the demon weed. The black lungs? From a coal miner, who throughout his working life breathed in copious quantities of microscopic black coal dust particles. Just like radioactive particles they get caught deep in the tissue of the lungs and stay there forever. If you worked down the coal mines for twenty or more years without a face mask, your lungs will probably look like this on the slab.

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Many people ask exactly how it is that those smoking mice were protected from deadly radioactive particles, and even more are asking why real figures nowadays are showing far more non-smokers dying from lung cancer than smokers. Professor Sterling of the Simon Fraser University in Canada is perhaps closest to the truth, where he uses research papers to reason that smoking promotes the formation of a thin mucous layer in the lungs, which forms a protective layer stopping any cancer-carrying particles from entering the lung tissue. This is probably as close as we can get to the truth at present, and it does make perfect scientific sense. Deadly radioactive particles inhaled by a smoker would initially be trapped by the mucous layer, and then be ejected from the body before they could enter the tissue. All of this may be a bit depressing for non-smokers, but there are probably one or two things you can do to minimize the risks as far as possible. Rather than shy away from smokers in your local pub or club, get as close as you can and breathe in their expensive second-hand smoke. Go on, dont be shy, suck in a few giant breaths. Or perhaps you could smoke one cigarette or small cigar after each meal, just three a day to build up a thin boundary mucous layer. If you cannot or will not do either of the above, consider phoning Michael Jackson to ask for a spare surgical mask! Copyright Joe Vialls. 16 July 2003

With the level of negative social pressures put on smokers, the smoking now correlates with variety of illnesses simply because these negative forces tend to affect more those who care more about their health. Further, there is a 'witch doctor effect' (a negative placebo), which damages health of those who believe in the propaganda. Finally, like with much of mass produced foods and beverages, the short term profitability is placed ahead of consumer health (and the long term profitability), hence the mass products have numerous additives which may be harmful in the long term to the consumer. For the latter two reasons, the best smokers can do for their health is to replace the mass market brands with 'make your own' (from real and additive free tobacco leaf) and turn every suggestion from the mass media and the 'health experts' upside down (since it is a money making swindle through and through). The worst off are those who quit due to pressures (e.g. Peter Jennings), since that is marker of those who have internalized the 'witch doctor effect', absorbing its maximum damage, while simultaneously being cut off from any beneficial effects of the tobacco (a sacred plant, bred and selected over millenia for its medicinal and 162

spiritual benefits). The time is on our side, since it won't be long before it will become impossible to blame second hand smoke for anything, since there won't be any. Also, the extortion syndicate now stealing from us is a greedy scum which will move onto other potential victims, and will eventually bite more than they can chew and will be discredited and neutered in everyones eyes. Their ongoing shift against fatsos may just do them in. The present thieves can pull their scam only so many times and make only so many enemies, before they run out of luck and get run out of town.

There is an interesting simultaneous rapid rise in the rates for both types of cancers in the fifties, just as the atmospheric nuclear tests (especially in neighboring USSR) were reaching their peak (these tests were banned not long after the cancer rates rise started). The skin and lungs would be particularly sensitive to airborne radioactive particles, hence the rates of these two cancers show high degree of temporal correlation. Note also how there is another little upward jolt in the rates, especially striking for melanoma rates, in late 1980s, right after the Chernobyl nuclear plant meltdown. In the article they also show how this same correlation (between melanoma & lung cancer) manifests in spatial dimension as well, when data is compared by counties in Sweden, which is to be expected since the air current patterns would deposit radioactive fallout differently at different locations. Another interesting bit buried in the paper is how the statistics around this critical period were difficult to get from the government "health" bureaucrats and how the more recent official way of counting the cancer death rates, the so called 'age adjusted mortality', is artificially making the increase appear smaller (citing discussion after Fig 13): " First of all, data before 1955 has always been locked out from publicly available databases. Secondly, and even worse, trends for obviously exposure-timedependent cancers are effectively neutralised by use of age-standardised ratios (ASR). This procedure assumes that the increasing cancer incidence is a natural effect of growing old and thus the age standardised mortality will stay the same although the population gets older. By doing this, the responsible institutions can show to the authorities that the mortality is in control and in effect not increasing at all despite the fact that it is. " This same statistical gimmick with 'age adjusted rates' was also used by CDC to hide the fact that lung cancers in USA have been on the rise for decades, being now at their maximum, even though the smoking has been declining also for decades, being at its minimum now. The sneaky little mathematical trick of scaling the rates for different years using different multipliers, made the actual increase appear as a

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small decrease in the "new math" (since they multiplied the rates of more recent years with smaller factors), which CDC "scientists" then attributed to the decline in smoking rates.

Here is an interesting official confirmation I found abot smoking rodents. The source is the official repository of tobacco documents (obtained during MSA negotiations). On page 97 of the report there is the following study citation & conclusion excerpt: "Inhalation Bioassy of Cigarette Smoke in Rats" A. P. Wehrner, et al. (Battele Pacific Northwest Labs, Richland WA) Journal of Toxiology & Applied Pharmacology, Vol. 61: pp 1-17 (1981) The results show that the highest number of tumors occured in the untreated control [non-smoking] rats. The next highest number of tumors occurred in rats subject to sham smoking, i.e. rats which were placed in the smoking machine without smoke exposure, and the lowest number of tumors occurred in the smoke-exposed rats. Among the latter, the largest number of tumors occurreed in rats exposed to smoke from cigarettes having the lowest level of nicotine.

So, among the lab rats, the "full flavor" smokers had the fewest tumors, the "light cigrattes" smokers had more, the sham-smokers even more, and non-smokers had the most. The entire document (pdf file) is a gold mine with many hudreds of fascinating and little publicised reasearch "anomalies" (i.e. the studies in which the data went the "wrong" way) regarding the relation of cancers to smoking. Of course, there is no real anomaly (the reality is surely not perplexed by itself), provided one views the data from the perspective of tobacco smoking being protective against (instead of "the cause of") the diseases studied. The data is anomalous only from the perspectiva in which tobacco smoke is assumed to be the cause of those diseases.

Alzheimer's, Parkinson's and schizophrenia risks are cut in half by smoking (at least) and for the patients, taking up smoking greatly alleviates the symptoms and reduces further damage of these diseases. Those who quit smoking, increase their risk of getting these diseases by 50% for each 10 years of non-smoking. For the early onset Alzheimer's (40s and 50s), smoking cuts the risk tenfold.

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I might point out that a lower adult smoking rate(50%) and a greatly reduced SHS exposure rate(87%) over the last 40 years have led to a 121% increase in lung cancer deaths, a 20% increase in COPD(emphysema) deaths since 1990, and since 1980 a 50% increase in asthma deaths. Whatever is causing more and more of our children and adults to contract and die from asthma, lung cancer, and COPD -it's not tobacco smoke and smoking bans will do nothing to stop the slaughter. Gary K. Adult Smoking rate in the early 60's was about 44%,by 1990 that rate had fallen to 23%,a 48% decrease.We can expect that SHS exposure levels were down by the same 48%; thus, SHS exposure levels in 1990 were only 52% of what it was in the early 60's. 2006 Sur.Gen's Report quotes the CDC thusly: (note:cotinine is used to measure SHS exposure-GK) The Health Consequences of Involuntary Exposure to Tobacco Smoke(SG's 2006 Report) Table 10.1, page 575 2005 The Centers for Disease Control and Prevention issues the Third National Report on Human Exposure to Environmental Chemicals, which documents that cotinine levels decreased 68 percent for children, 69 percent for adolescents, and 75 percent for adults from the early 1990s to 2002. 75% of 52 is 39, 52 minus 39 = 13. Thus SHS exposure levels are only 13% of what they were in the 60's, this is an 87% decrease!! Health,United States,2006 Page 229 Table 39 (page 1 of 3). Death rates for malignant neoplasms of trachea, bronchus, and lung, by age: United States, selected years 1950-2004 Lung Cancer deaths (age adjusted) were: 1960 24.1 per 100,000 2004 53.2 per 100,000 This is a 121% increase. http://www.aafa.org/display.cfm?id=8=42 165

The prevalence of asthma has been increasing since the early 1980s across all age, sex and racial groups. Mortality: Since 1980 asthma death rates overall have increased more than 50% among all genders, age groups and ethnic groups. COPD Age Adjusted Death Rates Population, 1979-2002 Age-Adjusted Death Rate per 100,000 Persons 1990 = 35.1 2002 = 42.0 This is a 20% increase. Source: Age Standardization of Death Rates: Implementation of the Year 2000 Standard. National Vital Statistics Reports, Vol. 47 No. 3. Additional Calculations Performed by the American Lung Association, Epidemiology and Statistics Unit. "

BMJ: Occupational and Environmental Medicine, Vol 56, 468-472, 1999 Lack of combined effects of exposure and smoking on respiratory health in aluminium potroom workers K Radon, D Nowak and D Szadkowski Ordinariat fur Arbeitsmedizin der Universitat und Zentralinstitut fur Arbeitsmedizin, Hamburg, Germany. OBJECTIVE: To investigate the combined influence on respiratory health of smoking and exposure in an aluminium potroom. METHODS: In a cross sectional study of 75 potroom workers (23 never smokers, 38 current smokers, 14 ex-smokers) and 56 controls in the same plant (watchmen, craftsmen, office workers, laboratory employees; 18 non-smokers, 21 current smokers, 17 ex-smokers), prevalences of respiratory symptoms and spirometric indices were compared. RESULTS: Smokers in the potroom group had a lower prevalence of respiratory symptoms than never smokers or ex-smokers, which was significant for wheezing (2.6% v 17.4% and 28.6% respectively, both p < 0.01), whereas respiratory symptoms in controls tended to be highest in 166

smokers (NS). No effects of potroom work on the prevalence of respiratory symptoms could be detected. In potroom workers, impairment of lung function due to occupational exposure was found only in non-smokers, with lower results for forced vital capacity (FVC) (98.8% predicted), forced expiratory volume in one second (FEV1) (96.1% predicted) and peak expiratory flow (PEF) (80.2% predicted) compared with controls (114.2, 109.9, and 105.9% predicted; each p < 0.001). Conversely, effects of smoking on lung function were only detectable in non-exposed controls (current smokers v non-smokers: FVC 98.8% v 114.2% predicted; p < 0.01; FEV1 95.5 v 109.9% predicted; p < 0.05). CONCLUSIONS: In a cross sectional survey such as this, the effects of both smoking and occupational exposure on respiratory health may be masked in subjects with both risk factors. This is probably due to strong selection processes which result in least susceptible subjects continuing to smoke and working in an atmosphere with respiratory irritants.

The key result is that for the exposure controlled group (the potroom workers) the smoking reduced the risk of lung damage sixfold compared to never-smokers.

I look at it this way: While it's true that nearly 90% of lung cancers will be found in smokers, what is repeatedly ignored is the fact that less than 10% of smokers overall will ever get the disease. In simple terms, this means that even if you smoke, there's a greater than 90% chance overall that you'll never get lung cancer.(Unless you can find the time to suck down 3 packs a day; then it's reduced to about 85%.....) With that said, though, I am intrigued by the nuclear test theory; especially since places like Greece & Japan have a much higher number of smokers yet a much lower rate of lung cancer. Lung cancer rates in the US, however, are higher, yet far less people smoke. The Anti's simply blame that on secondhand smoke, so they have that covered. Admittedly, I can't figure one thing out. We are the only country thus far to have ever used nuclear weapons. We nuked Hiroshima and Nagasaki in 1945. The fallout from those bombings must still be in the atmosphere. Shouldn't the Japanese have higher rates of lung cancer?

The Japanese also smoke much more. If I correctly understand the evidence Nightlight has provided, the Japanese would instinctually smoke more to seek the protective effects of smoking against the radiation, and that, along with other contributing factors, would reduce their rates of lung cancer.

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If smoking had any role, it protected him all those years from lung cancer by helping remove & clean up more efficiently the industrial pollution & radiation damage. In animal experiments (see links below for references) smoking animals get fewer lung cancers than non-smoking or ex-smoking animals, in a linear dose-response manner -- the more they smoke, up to well over 5 packs a day equivalents, the fewer lung cancers they get. Even after half a century of antismoking "science", they still rely on 'lying with statistics' to make their case and can't get animals to get lung cancers from smoking (even when poor animals are forced to smoke equivalents of a several cartons per day through implanted breathing tubes, their whole lives, yet no increase in lung cancer rates to show). In human _randomized_ intervention trials, smokers randomly selected into the "quit group" (which is not the same sample as self-selected non-pressured quitters) get over 20 percent more lung cancers than those left alone. About 80-90 percent of schizophrenics smoke (it relieves their symptoms and even cuts the risk of getting schizophrenia or its recurrence in half) and most of them are chain smokers, yet at any age they get lung cancers (and most other cancers) at half the rates of general population (which smokes at 20-25 percent rate and significantly fewer cigarettes per smoker). In USA, the average number of lung cancers per cigarette smoked has grown over 8 times since 1950s, while the total number of cigarettes smoked in USA is much smaller now than in 1950s (and fewer cigarettes are consumed per smoker).... and so on, anomaly after anomaly. All hard scientific facts which focus onto the causal role of smoking, come out the "wrong" way, by demonstrating that smoking is protective and not a cause of the lung cancer.

Cigarette Smoking May Lower Parkinson's Risk Tobacco products conferred some protection, although not for those over 75, study says TUESDAY, July 10 (HealthDay News) -- Long-term and current smokers have a lower risk of Parkinson's disease than the general population, researchers say in a report that confirms previous observations that people with Parkinson's disease were less likely to be smokers. Dr. Beate Ritz of the University of California, Los Angeles, School of Public Health and colleagues analyzed data from 11,809 people involved in 11 studies conducted between 1960 and 2004. Of those, 2,816 individuals had Parkinson's disease.

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The data showed that current smokers and those who had continued to smoke within five years of Parkinson's disease diagnosis had the lowest risk. People who quit smoking up to 25 years before diagnosis also had a reduced risk. Other tobacco products such as cigars, pipe tobacco and chewing tobacco showed reduced risk as well. The association between tobacco use and Parkinson's disease disappeared for people older than 75, however. And while the association was strong for people of Caucasian or Asian ancestry, it did not hold for Hispanics or blacks. The researchers wrote that the biochemical basis for the effect is not well understood, but that either nicotine or carbon monoxide may, in fact, protect brain cells that produce dopamine. Dopamine is a chemical produced in the brain that enables the body to coordinate movement. Once 80 percent of the neurons that produce dopamine begin to fail, the symptoms of Parkinson's disease appear. Symptoms include tremors in hands and feet and a lack of flexibility or balance. Writing in the July issue of the Archives of Neurology, the researchers called or further research to understand what chemicals in cigarettes and tobacco might be protective against Parkinson's disease. More information To learn about Parkinson's disease, visit the Parkinson's Disease Foundation. http://www.pdf.org/ -- Madeline Vann SOURCE: Archives of Neurology, news release, July 9, 2007

There is a new thread "Smoking is good for you" with over 450 posts and you can go check it to see how did your "... is a true crank" theory work out (and no, that wasn't the same guy as already noted by other members here; it should be pretty obvious, anyway). It turns out, after all was said and done, and after everyone presented their best arguments and papers, that tobacco smoke is much better than even the farthest claims in this thread. Below are few highlights of the "debate" (since all the hard science was squarely on one side, while the other side could only offer junk science, it was hardly a debate). Before jumping in with your "scientific proof" please check what was discusssed already (add your "proof" there since this thread has been inactive for years). 1. Dogs exposed to radon or radon+smoke: 5% of smoking dogs and 37% of nonsmoking dogs got lung cancers. 2. Massive National Cancer Institute sponsored experiments that backfired terribly, setting back the NCI's workplace smoking bans agenda for over decade.

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3. The crowning experiments (2004, 2005) of six decades of antismoking "science", the pinnacle -- again backfired badly, as they always do -- at the end, more than twice as many smoking animals alive than non-smoking ones. 4. Self-medication with tobacco 5. Common genes for lung cancer & smoking 6. Hazards of quitting (triggers lung cancers in animal experiments) 7. Emphysema/COPD - smoking protective rather than cause 8. How does antismoking "science" lie with stats (how to "prove" that -- Prozac causes depression -- using method of antismoking "science") 9. Heart attacks from SHS myths (is a 'friend saying Boo' more hazardous for your heart than SHS?) 10. Glycotoxins/AGE in tobacco smoke -- backfires 11. Smoking vs Caloric Restrictions, Smoking protects against cancers 12. More on anti-carcinogenicity of tobacco smoke 13. ** why take a chance 14. Smoking and diabetes, insulin sensitivity -- another "proof" backfires 15. How to prove that 'Lifting weights is harmful for muscles' - pinhole vision sleight of hand of antismoking "science" illustrated 16. Oxidative stress, breast cancer, "randomizing non-randomized variables" sleight of hand -- more antismoking junk science claims turned upside-down by facts hard science 17. Can one replicate the health benefits of tobacco smoke (the short list given) using supplements and pharmaceuticals? Even if it were possible, can one do it for < $1 day (cost for a pack of roll-your-own cigarettes with natural, additive free tobacco)? 18. Who knows more about biochemistry of life and its molecular engineering -- one little cell in your little toe or all the biochemists and molecular biologists in the world taken together? Is "Sickness Industry" good for your health?

Tobacco is a potent medicinal plant and youth elixir used for over 8000 years. Antismoking "science" is a money making scam, resting entirely on the worst kind of junk science, created and financed chiefly by the pharmaceutical industry. The big 170

pharma reflexively seeks to suppress other natural medicines and folk remedies as well, especially those that work. Tobacco being the most beneifical natural medicine humans have ever known (tell me which other substance, matural or synthetic, extends the lifespan by 20% in animal experiments, while keeping the brain sharp into the old age, doubles our main internal detox and antioxidant enzymes glutathione, catalase and SOD,...), is the main target of the pharma's attacks on natural medicines.

No one has a bluperint for what Nature or God, or whoever, had in mind for our lungs, our brains, our hands,.... Otherwise you wouldn't be typing this, since surely, your fingers "were not made" for typing on the keyboards, but merely for holding onto branches, picking flees from your buddies backs, grubs to eat,... In nature, anything that works, goes. In biochemistry of live organisms every enzyme, protein or general molecule, has myriad of uses, depending on location and context. Absorbtion of substances via skin or lungs (even eyes, ears, nose,...) has long been used in medicine (have you heard of medicinal creams, patches, inhalers, aromatherapy, medicinal smoke,...). As to the toxic smoke scare stories that you've been kind enough to retell, go back in time to the lightening scorched primordial soup few billions years ago. You will find all those scary, all 'burned' organic molecules, dancing to some cosmic tune, weaving the first life on Earth. If live cells have learned how to do anything at all by now, it is how to process safely the oxidized organic molecules. These are the kinds of organic molecules that gave rise to life and that still make the life go (oxidation/reduction cycle). Keep also in mind that about 100mg (less than third of an aspirin tablet) of tobacco smoke matter absorbed per pack of cigarettes via 75 m^2 lung surface, is dwarfed by tens of thousands larger quantity of matter absorbed daly via digestive system, from foods and beverages. Since virtually every organic molecule you ingest has to undergo biochemical breakdown, before it is used as a building block or for energy (via oxidative processes), the potentially damaging oxidative processes, along with all their 'scary' free radicals byproducts, go on continuously in each of your cells 24/7. The quantities of matter involved in this vast biochemical factory making up your body are many orders of magnitude greater than the 100mg of matter/pack abosorbed from oxidized plant's leaf cells (smoking). There is more oxidation and its byproducts from one peanut or one blueberry, by the time it is fully processed and used up inside your cells, than a smoker ingests from pack of cigarettes (where much of oxidation takes place safely away from your cells). Further, unlike most foods you ingest in thousands times greater quantities than tobacco smoke matter, some unknown components of tobacco smoke upregulate all the main internal antioxidant and detox enzymes -- nearly doubling glutathione, 171

catalase and SOD, which vastly offsets any oxidative stress from the 100mg of tobacco matter ingested. Consequently, among others, smoking doubles smoker's detox rates for virtually any toxic materials (heavy metals, exhaust fumes,...) they are exposed to. Hence people exposed to such toxic materials at work or in their living environment, or those genetically sensitive to them, will instinctively use smoking as self-medication (to protect & help detox from the noxious exposures), resulting in the observed statistical associations of smoking with 'smoking related diseases'. That is no different than association between using sunglasses and sunburns -- those who use sunglasses more, will have more sunburns (and also, the ex-users will have less sunburns than the current users), even though sunglasses are protective against the sun's radiation, and they certainly don't cause sunburns.

In Japan and Korea, 60-70 percent of men smoke, yet they tend to look more youthful than Europeans or Americans with less than half of those smoking rates (Japanese men also have three times lower lung cancer rates and live longer than American men). Back in 1940s and 1950s, actors and other celebrities were largely smokers, they didn't have botox or face lifts, yet they didn't look particularly wrinkled, certainly not more than nonsmokers of that era (some smoking celebrity photos; wikpedia had a large list of smoking who-is-who in Hollywood, which was deleted recently, someone obviously has felt threatened by the unsuitable facts and decided to erase history and improve on truth, Orwell's 1984 or Stalin style; that's is quite typical for vicious antismoking hysterics, even FDR's cigarette was erased from old photos). Many models smoke today, to control weight and their skin looks fine, too. Some of the underlyng biochemical reasons why smoker's skin (and every other marker of youthfulness) would come out younger in any apples to apples comparisons (not just the same genetics, but sun & other exposures, diet, stress, socioeconomic status,...): a) Nicotine stimulates and upregulates growth and branching of blood vessels (via upregulation of vascular growth factor), especially of capillaries, which improves the nutrient delivery and cleanup (antioxidant & detox enzyme supplies) to all tissues, including brain and skin (provided person's intake of nutrients and supplements is adequate). b) Tobacco smoke (not nicotine) upregulates production of glutathione, catalase and SOD (our body's chief internal antioxidant and detox enzymes, sometimes used in cosmetics for skin rejuvenation), to nearly double levels. c) Carbon monoxide in low concentration (as delivered in tobacco smoke) acts as a

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signaling mechanism in human biochemical networks to increase blood circulation, oxygenation and reduce inflammation. d) Nitric oxide in low concentrations (as provided by tobacco smoke) acts as neurotransmitter, signaling to cardiovascular system to increase blood supplies to peripheral tissues (this is the biochemical mechanism behind the Viagra effect). e) Tobacco smoke upregulates levels of "youth hormones" DHEA and testosterone and reduces their decline with age. f) The highest quality brands (Japanese) of the miracle skin supplement and rejuvenator, Conezyme Q10 are produced from tobacco leaf, which is still the best source of natural Co-Q10 (since it includes the full synergistic complex which the cheaper synthetic production methods cannot replicate). g) Deprenyl (selegiline), which mimics the selective MAO B inhibitory properties of tobacco smoke (this is not related to nicotine) and is used in smoking cessation "therapies" for that reason, has become quite popular in life-extension circles, due to its almost magical rejuvenating powers. h) Nicotinic acid (byproduct of oxidized nicotine, as in burning tobacco, delivered directly into arterial bloodstream), along with its salts and various organic compounds, are skin-protective agents, used in cosmetic and pharmaceutical industry.

There is nothing wrong in being dependent on something that is good for you. We are all "addicted" to food, water, air, family, friends, reading,... If something is good for you, transferring the need to replenish it to automated/reflexive systems (the socalled "addiction") is quite useful, time and effort saving transformation. You can also start smoking at any age and still benefit. The longest living man in the world, Shigechiyo Izumi (see at the top of the thread), started smoking at age 70. Some folks, scientifically well educated and health fanatics, who lived four or five decades as nonsmokers, until their lucky day when they decided to educate me, usually at a party or at work, that I ought to quit smoking, it is terribly bad for me,... and then I 'splained to them few things about glutathione, SOD, MAO B,... gave them books, emailed links to papers, and few days later they would ask me where can they order 'organic tobacco'..

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Tobacco is a medicinal plant that increasing percentage of smokers uses instinctively for self-medication (the vicious antismoking pressures have scared and driven away most of those who don't really need it for any such purpose, those who are left are mostly the folks who do need it). Most smokers can't get a pharma drugs, even if they could afford them all, that will double all the key detox & antioxidant enzymes, that is simultaneously dopaminergic and cholinergic without downregulating either of those systems (an apparent paradox), that is also anti-inflammatory at multiple levels, antiapoptotic, protective against sepsis, analgesic, ... (see earlier links for numerous other beneficial effects). There is just nothing else that combines harmoniously that kind of broad spectrum of therapeutic and protective effects and in such depth. Those who are still smoking in the face of ever escalating abuses of smokers, economic, social and psychological, are poor folks for whom no other medicine will do the same thing, or those who can't afford the array of pharmaceuticals needed to cover all the beneficial effects of tobacco smoke that matter to them. Of course, as with any medicine, be it pharmaceutical prescribed by doctors or a remedy/supplement taken on ones own initiative, those who use them will have more health problems than those who don't use them. People using blood pressure meds will have more strokes than those not using them. That doesn't mean blood pressure meds cause stroke. They are obviously meant to prevent them, by lowering the blood pressure, which itself causes strokes. The same reasoning goes for tobacco smoke. For example, consider a miner exposed to toxic, possibly carcinogenic, heavy metal dusts and vapors at work. It just happens that tobacco smoke nearly doubles levels of glutathione, the master detox enzyme in human body, the perfect weapon to bind and excrete the heavy metals from outr body. A miner can't buy, even if he heard of glutathione, a supplement that will nearly double it, simply because there isn't anything that can do it, other than tobacco smoke. Hence, by smoking this miner will nearly double his detox rates, resulting in perceptible relief from the effects of toxic heavy metals. Hence he will have much greater incentive to smoke, especially under the present pressures, than somene sipping lemonade and inhaling purified air all day in a nice, clean suburban home. Indeed miners (or any physical or farm laborers, truck drivers, soldiers, firemen,...) will smoke at much higer rates than general populations -- it helps them detox (among other myriad other potential benefits). Yet, those same toxins that tobacco, via glutathione, catalase & SOD upregulation, partially protects against, will over time damage their health anyway and they will end up with higher rates of 'smoking related diseases' than the suburban white collar folks. And they will also be smoking at higher rates than the white collar workers, That is the mechanism behind statistical correlations of smoking and 'smoking related diseases' on non-randomized samples (each person chose to smoke or not to smoke for their own reasons). Tobacco is by virtue of its therapeutic & protective effects a mere statistical marker for any kind of physical, chemical, emotional and psychological hardship, and it is the latter factors, the harships, that causes diseases attributed (by the pharma sponsored antismoking junk science) to 174

tobacco smoke. The antismoking racket is truly the most evil force in the western world today. It is analogous to someone ripping respirators from patients in hospitals, justifying it by observation that respirator users have shorter lifespans than non-users, while the ex-users of respirators fall in between, hence all those terrible respirators must be ripped from the patients to save them. An their pockets need to be picked in the process to help the breathe easier (tobacco taxes are becoming a pure thievery, e.g. the first law Obama signed, increased sharply the tax on all tobacco products, and on my particular one, the rolling/loose tobacco, by 2200%; thanks Mr. Reverse Robin Hood, at least your lobbyists are happy now). Generally, statistical associations on non-randomized (self-selected subjects) samples, of some substance X with disease D, could equally well be due to the therapeutic/protective effects of X against D (or against some of the real causes of D), as they could be due to the causal role of X in D. To find out which is the case you need hard science (experiments, randomized trials). Yet, all you hear about tobacco smoking, for over six decades now, are the stats on non-randmized samples. Why? Because the hard science comes out the "wrong" way -- the smoking animals live longer, and the randomly selected quit group ends up with more lung cancers or more heart attacks than the control group (smokers left alone).

The real story is that tobacco is androgenic (not very strongly), so if you have trouble getting pregnant or need estrogen boost to get and stay pregnant, suspending smoking, or reducing it down to 2-3 per day would be beneficial (disruption is not good either). If you are normal feminine female, it would have no harmful androgenic effects. While you will find some number of papers about animal experiments, claiming variety of (mostly small) negative effects on fetus, if you check their numbers more carefully, you will discover that they are injecting pregnant mice with pure nicotine (very different substance than tobacco smoke) and at doses typically 12 mg per kg (some even 6+ mg/kg), which for a 75kg (165 lb) pregnant woman would amount to 75-150mg of nicotine (450 for 6mg/kg), which for todays <1mg nic full flavor cigarettes, would come to 4-8 packs of FF cigs per day (or over two cartons for 6mg/kg), obviously all in a massive overdose. What that tells between the lines, is that for anything near normal human smoking levels, there is absolutely no harm they could detect, hence they had to resort to such massive overdoses to show any harm at all (resulting mostly from reduced circulation at those high levels of injected nicotine). Wearing nicotine patch is much closer to those experiments than obtaining equivalent amount of nicotine via tobacco smoke (the researchers apparently avoided tobacco smoke inhalation in these experiments, which is another 'between the lines' fact). 175

The negative effects observed were chiefly due to acute vaso-constrictory effects of pure nicotine, especially when injected (it gets in and no let up from there), in contrast to cyclic self-administered delivery from smoking finely controlled by your own natural feedbacks. Tobacco smoke has also a number of offseting vascular effects (from low dose NO and CO in the smoke), which counter and balance the acute vasoconstricting effects of pure nicotine, effectively nullifying them as far as blood delivery to any tissue. The non-acute effect of nictine is upregulation of vascular growth factor, stimulating growth and branching of blood vessels, hence it improves circulation. Some positive aspects are anti-inflammatory effects and a particularly strong protective effect against pre-eclampsia. There is also a unexplained protective effect of maternal smoking against transmission of H. Pylori infection to baby (fourfold reduction in transmission for smoking mothers). Anti-depressant effects of nicotine are also becoming important in the era when pharma is pushing for the en masse use of clearly harmful antidepressants on pregnant women. I think, the best is to listen to yur own body and you will know what to do and how much. Pregnant women a famous for strange food cravings, knowing apparently exactly what they need.

This post has been edited by nightlight: 28 February 2010 - 04:16 PM

Of course the conclusion is ridiculous if you start with a false premise "keep damaging yourself". The hard science (animal expriments) demonstrates that the premise is not merely formally false but that the net effect of life-long inhalation of tobacco smoke is clearly beneficial for health and longevity. You are welcome to show some hard scientific evidence (experiments) that supports your premise. Otherwise that premise is merely an element of your own personal faith, which you have every right to hold and cherish.

It is not just anecdotes on the world record holders in lifespan. 30 million humans of japan smoke. this is a high percentage of the population. http://en.wikipedia....moking_in_Japan and Japan has highest life expectancy. Cuba similar. see http://www.kidon.com...ercentages2.htm 176

how many competitors had Mme Calment? BILLIONS. BILLIONS of non-smokers. and you assume that she would have lived longer if she did not smoke? world record holders can not make many mistakes. every detail must be perfect. smoking was an important detail.

Tobacco smoke is consequently, highly protective aginst Alzheimer's. This strong protective effect of t.s. against amyloidosis (in humans and lab animals) has been heavily researched.

My position is that tobacco smoking (at the levels of common human smoking) is good for health and longevity and I offer scientific experiments clearly demonstrating the validity of the claim. I don't know of any such experiment or make similar claims about pure nicotine (although, I think it is harmful when taken alone in the long run, without the full synergistic complex of tobacco smoke).

How do you know that these folks were not instinctively self-medicating throughout their lives using tobacco e.g. to help detox gasoline or paint fumes or other scientifically well established (unlike tobacco smoke) carcinogenic exposures. Or perhaps that they didn't have the known alleles within a nicotinic acetylcholine receptor gene cluster which simultaneously made them more likely to get lung cancer, as well as, independently made them more likely to smoke (also here). Correlations on non-randomized samples of some disease D and a substance X, especially when considreing a substance with so many therapeutic and protective effects as tobacco smoke, don't rise even to a level of hint that X causes D, let alone to a proof. Your sample size of 2, emotional appeals aside, makes your case even weaker than "well below the hint level."

It just happens that one among the myriad of beneficial effects of tobacco smoke, in his case due to nicotine, is stimulation of the growth and branching of blood vessels (via nicotine vascular growth factor upregulation; as you can see there is a vast ammount of literature about that effect). Since the greatest concentrations of 177

nictine inhaled via tobacco smoke will be in the respiratory system, especially in lungs, that is where the greatest vascularization will take place. Consequently, the cancers (which are caused by the deliberately bred in genetic defects in this mice for that exact purpose) in the respiratory system will get most nutrients and have the fastest growth. That is precisely what these contractors (former Pfizer scientists & consultants) chose to measure, the growth of tumors in different tissues. Of course, as expected, in the smoking mice they found the most in the lungs, but fewer in the liver and other tissues. The same researchers conducted the same experiment on F344 rats (also a variety bred for cancers, like this mice) and obtained exactly same results, more tumors in the lungs than elsewhere. Although this may appear as something new to an uninformed reader, this effect is well known for more than three decades (the paper quoted below is from 1980 and they cite even older ones, cf. research review p. 97): Chronic Inhalation of Cigarette Smoke by F344 rats W.E. Dalbey at al., Oak Ridge Nat. Lab., Inst. Environ. Health... J. National Cancer Inst., 64 (2): 383-390 (Feb 1980) "Smoke exposure did not change the total number of tumor-bearing animals relative to controls; however [smoke] exposed rats had significantly fewer tumors in the hypophyses, hematopletic-lymphoid system, uteri and ovaries, but an increased number of tumors in the respiratory tracts and dermes." These animal data fit in with the concepts of Prof. Oeser in Berlin and Dr. Lock in Hamburg, that, if properly assessed, the epidemiological data on cancers in general and for specific organs, indicate that total cancer rates have not changed, and that the only thing which has changed is that the increase in one type of cancer is compensated for by a decrease in other organ cancers. Curiously, the researchers in the 2005 mice paper, don't cite anything from this literature trail but purport that they have discovered an animal model for t.s. related lung cancer. Since this is a long known phenomenon unrelated to any alleged causative role of tobacco smoke in cancers (since any vascular growth stimulant will show exactly the same effect), it was discarded decades ago as a candidate for the l.c. model related to t.s. It is a pure vascular growth effect, unrelated to lung carcinogenicity (or the lack thereof) of tobacco smoke. Of course, as soon as you check their survival figures, it becomes clear what a charade the whole "animal l.c. model" claim was -- the smoking mice outlived the non-smoking mice (cf. published paper p. 2001):

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In summary, no there is no animal experiment, demonstrating that inhalation of tobacco smoke causes lung cancer. Of course, S.S. Hecht's review paper (2005) on animal experiments reluctantly acknowledges this failure as well. The antismoking "science" has pursued this 'holy grail' for over six decades, with no expense or efforts spared, and still a dud. No wonder they are still stuck with the inconclusive epidemiological hints -- the hard, conclusive science goes the "wrong" way, so what can they do but remain inconclusive. ---Smoker lungs photos are a cheap fraud, see for example Colby's chapter on that antismoking myth. Since it is not so, the Marlboro question is unnecessary. Although the plain classical (additive free) tobacco leaf, honed over many millenia is certainly better for you than additives & sugars laden 'tobacco sheets' (fake leaf look-alike), just as it is the case with whole natural foods vs additive laden reconstituted food look-alikes in the supermarkets. The two classes of products are optimized to different utility functions, the classical natural stuff (foods or tobacco) is optimized for pleasant, beneficial effects on user, while the supermarket cheap look-alike stuff is tuned to maximize profits of the manufacturer (cheap ingredients, much cheaper to produce).

Smoking kills mostly by causing cardiovascular disease, cancers are a distant second. That is also a myth. See this critical review where all major human randomized intervention trials were examined (one more here a major backfire; there were only handful ever done, because they simply don't "work" for antismoking "science") and they either showed no benefit in randomly selected quit group, or showed outright benefits of smoking for cardiovascular system (randomly selected smoking group had fewer heart attacks). Epidemiology (non-randomized samples) of course lacks resolution to say whether the smoke was protective (self-medication mechanism) or harmful (causal role in a

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disease), since either possibility can produce the same kind of statistical correlations on non-randomized samples.

You know, if this was any other substance than tobacco, people would be going wild over it! Exactly. If someone were to publish results of animal studies, those graphs showing life-extension & lower weight (plus much more), for some secret supplement X you can order online, without saying it was just cigarettes or rolling tobacco & paper, it would create a sensation and a massive demand. And keep also in mind that all those experiments were done under the most unfavorable adversarial conditions -- intensely antismoking scientists doing their very best to maximize the harm from tobacco smoke (e.g. the edge of asphyxiation exposures). And yet it always backfired, for over six decades now (those life-extending mice experiments were from 2005). That's how potent this ancient medicinal miracle plant truly is. Imagine how those graphs would look like if neutral scientists, or god forbid tobacco industry or smokers orgs researchers, did them with objective to maximize the benefits rather than harm. All those gains from the adversarial research (that backfired) would likely double. Nothing stops human smokers from seeking to maximize the benefits, though. The main harm today most of them suffer, is unfortunately from the nocebo (negative placebo, witch doctor) effect --from the omnipresent "smoking kills" death curse from our witch doctors (parroted generously in this thread as well).

All 'class A carcinogens' easily cause cancers on lab animals (much easier than in humans e.g. "animal carcinogen" term) and shorten their lives. All except 'tobacco smoke' which not only fails to cause cancers in lab animals (strangely, though, it can do it only in humans), but it extends the lifespan of lab animals by 20%, while keeping them thinner and sharper into the old age. And all that despite over six decades of vast research efforts to demonstrate this very carcinogenicity. With tobacco everything is somehow the opposite and upside down from everything else in science. Logic included. As a smoker friend observed regarding some FDA pronouncement about smoking, with tobacco more is always worse, but less is always equally dangerous.

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Some benefits of nicotine and smoking for schizophrenics: Quote Encephale. 2008 Jun;34(3):299-305. Epub 2007 Dec 26. [Smoking and schizophrenia: epidemiological and clinical features] [Article in French] Dervaux A, Laqueille X. Service d'Addictologie, centre hospitalier Sainte-Anne, 1 rue Cabanis, Paris, France. a.dervaux@ch-ste-anne.fr FREQUENCY: The prevalence of cigarette smoking is significantly higher among patients with schizophrenia (60-90%) than in the general population (23-30%). While tobacco smoking decreases in the general population (from 45% in the 1960's to 23-30% in the 2000's), smoking in patients with schizophrenia remains high. Patients with schizophrenia smoke more cigarettes than control subjects. Patients smoke more deeply, thereby increasing their exposure to the harmful elements in tobacco smoke. IMPACT OF SMOKING IN SCHIZOPHRENIC PATIENTS: As in the general population, smoking contributes to the reduced life expectancy in patients with schizophrenia. Patients with schizophrenia are at increased risk for cardiovascular disease due to high rates of cigarette smoking. In the Department of Mental Health of the commonwealth of Massachusetts, cardiovascular disease was the factor the most strongly associated with excess mortality. Cardiac deaths were elevated more than six-fold. Weight gain, insulin resistance, metabolic syndrome and diabetes mellitus are frequent in patients with schizophrenia, and may worsen the risk of cardiovascular diseases. It has been reported that the risk for lung cancer in patients with schizophrenia is lower than that of the general population, despite increased smoking. However, in a study conducted in Finland, a slightly increased cancer risk was found in patients with schizophrenia. Half of the excess cases were attributable to lung cancer. IMPROVEMENT OF COGNITIVE DEFICITS: Patients with schizophrenia may use nicotine to reduce cognitive deficits and negative symptoms or neuroleptic side effects. Smoking may transiently alleviate negative symptoms in schizophrenic patients by increasing dopaminergic and glutamatergic neurotransmission in the prefrontal cortex. In patients with schizophrenia, nicotine improves some cognitive deficits: (1) sensory gating deficits and abnormalities in smooth pursuit eye movements associated with schizophrenia are transiently normalized with the administration of nicotine ; (2) high-dose nicotine transiently normalizes the abnormality in P50 inhibition in patients with schizophrenia and in their relatives; (3) in tasks that tax working memory and selective attention, nicotine may improve performance in schizophrenia patients by enhancing activation of and functional connectivity between brain regions that mediate task performance (Jacobsen et al. 2004; Paktar et al.2002); (4) cigarette smoking may selectively enhance visuospatial working memory and attentional deficits in smokers with schizophrenia. However, Harris et al., found that nicotine affects only the attention without effects of nicotine on learning, memory or visuospatial/constructional abilities. In addition, smoking could facilitate disinhibition in schizophrenic patients. PMID: 18558153

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Self-medication mechanism affects self-selected samples no matter what their coarse grained general health status was at the beginning of the study. After all the initial self-selection to smoker, non-smoker in real life occurs usually in teens, when they all seem healthy to standard examinations. Many more teenagers experiment briefly with tobacco than there are smokers later. Those that self-select themselves to stick with it are smokers, those who don't feel the need for it are non-smokers (or if they smoked long enough, ex-smokers). The more subtle biochemical differences (as far as docs are concerned in routine examinations), the level at which the self-medication mechanisms operates at, such as glutathione, catalase & SOD status (and related alleles such as ApoE), exposure to toxins or carcinogens or sensitivity to them, stress in life of any kind (biochemical or psychological), susceptibility to inflammatory or autoimmune irritations (a precursor to all kinds of diseases years later), low dopamine, low DHEA or pregnenolone, telomerase expression/biologocial aging speed (naturally, our ancient miracle medicine, tobacco smoke upregulates telomerase activity, too; see also here)... are all well beyond the normal coarse grained "healthy" grade assigned to all subjects at the beginning of a prospective study. To say nothing of myriad unknown factors and effects of tobacco smoke resulting in self-medication. And of course, the further self-selection, driven by the same self-medication forces, will continue uninterrupted after the initial crude "healthy" evaluation, as their exposures or life stresses of all types change over time. Therefore, the 'prospective' nature od study makes absolutely no difference at all for the self-medication mechanism acting through continuous process of selfselection of the subjects to smoker/non-smoker/ex-smoker (working all analogously to natural selection in evolution but on a small scale to create differences over time). The self-medication does not mean solely a therapy for the existent disease (e.g. RA) but also protective or mitigating effects on the underlying causes of the final disease. This RA examples shows exactly how this happens -- here you show a nonrandomized (self-selected smokers/nonsmokers/exsmokers) study with an RR ~2 for smokers vs nonsmokers for RA. Yet the RA experiment (on mouse model of RA) shows both protective and therapeutic effects of nicotine and even stronger protective effect of tobacco smoke against inflammatory auto-immune damage to cartliage. The underlying autoimmune inflammatory processes which eventually result in clinical RA, start at biochemical level years before the onset of the clinical RA. Tobacco smoke slows down their progression from the start (nicotine does it too, but not as well). Therefore the selfselection process to smoker/non-smoker/ex-smoker does have perfectly viable biochemical self-medication levers to operate on long before and right up to the onset of the clinical RA.

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As to how these women would know to self-medicate i.e. that smoking helps protect them against RA they are susceptible to, I would suggest that a very low grade inflammatory processes produce minor weakness, exhaustion, sleepiness... due to parasympathetic overactivation (just like a mild cold or mild CFS), which tobacco smoke would easily mitigate (by driving up the sympathetic system as well as by suppressing the low grade inflammation itself and its perceptible slightly uncomfortable effects). So they would easily perceive the difference. Of course, the study authors couldn't care less about it, to even mention possible self-medication confounding (based on the well established anti-inflammatory effects of tobacco smoke), let alone quantifying it and taking into account for their final results. Of course, once you take into account the self-medication mechanism the apparent paradox between epidemiological and experimental facts, which the standard antismoking epidemiology ingnores althogether, vanishes. In other words, selfmedication mechanism allows for a coherent explanation of all the known facts and not just of a cherry picked subset of known facts that fit some other agenda (to help inflame anstismoking hysteria and ultimately boost pharma sales of RA drugs in this example), while ignoring others that contradict it (such as contradiction with the effects of tobacco smoke in animal models of RA, or anti-inflammatory effects of TS). Self-medication with tobacco is quite an active research subject. Numerous therapeutic and protective effects of tobacco smoke make it an ideal substance for study of that phenomenon. Historically, during the early spread of tobacco into Europe and then around the world, people everywhere would instinctively start using it for self-medication and that was often its main attraction and force that helped its popularity and acceptance. In much of the undeveloped world, self-medication is still the dominant form of treatment for most health problems, and until the twentieth century and rise of pharmaceutical industry, it was the same in the western world as well. Placebo and nocebo (negative placebo, witch doctor effect) are also important enough, being surprisingly effective (e.g. a witch doctor effect is powerful enough to kill), forms of self-medications that any drug trial has to take them into account. Self-medication isn't restricted to humans either -- animals are as good at it if not better than we are. But even that isn't the final boundary of the phenomenon -- each one of your cells self-medicates its entire life, repairing damages and treating variety of health problems, malfunctions and challenges virtually every moment of its existence. With that level of phenomenon taken fully into account, the self-medication is still the dominant and the most effective form of treatment and healing for each one of us here in the developed world, mighty pharma and the rest of the 'sickness industry' notwithstanding.

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Regarding the self-medication aspect of tobacco use, smokers who quit on their own because they don't feel they really need it any more or that it doesn't do all that much for them considering all the hassle and expense in the current antismoking hysteria (as opposed to quitting in randomized intervention trial, where they quit based on random selection, or being forced to quit e.g. by ending in prison, like the 'first immortal' fellow who promptly got lung cancer there) are analogous to patients who complete using prescription meds or those who leave hospital -- those that completed the treatment are certainly going to be better off than those still being treated. Similarly, the longer someone is using medicines or staying in hospitals, the worse off they will be, just like the association with smoking. Of course, for any individual, the potent life-extending and rejuvenating effects of tobacco smoke, firmly established in animal experiments, imply that smoking will extend lifespan while keeping them thinner and sharper into the old age than that same individual would have been without smoking. There is no paradox here: Note that the therapeutic/protective and harmfull/causative substances have identicall statistical associations with diseases on non-randomized samples. If you ignore the therapeutic/protective effects of some medicine (pharma drug or natural remedy), and applly the same leap correlation => causation as done regarding tobacco smoke by antismoking "science", you could as easily "conclude" that pharmaceuticals kill nearly everyone, since in any age, gender, socioeconomic status... group, the preceding use of pharmaceuticals is among the strongest risk factors positively correlated with the death of a subject (another one in the same category is being in hospital). Yet, simultaneously the use of pharmaceuticals as a rule does extend the lifespan and improves health. No paradox, of course.

With skin care products, the mechanisms of action are and effects are well reasearched and well understood. With smoking, under the present antismoking mass hysteria, one will not find research directly addressing the rejuvenating effects of smoking on the skin. But the results are still there, albeit often buried within some seemingly unrelated research topic. Here are a few such bits of hard science supporting the rejuevenating and beneficial effects of smoking on the skin: a) Nicotine stimulates growth and branching of blood vessels (via upregulation of vascular growth factor), especially of capillaries, which improves the nutrient delivery and cleanup (antioxidant & detox enzyme supplies) to all tissues, including brain and skin (provided person's intake of nutrients and supplements is adequate). As noted earlier, it is already used for this reason in cardiovascular pharmaceuticals. b) Tobacco smoke (not nicotine) upregulates production of glutathione (our body's 184

master antioxidant and detox enzyme), to nearly double the levels of nonsmokers. c) Carbon monoxide in low concentration (as delivered in tobacco smoke) acts as a signaling mechanism in human biochemical networks to increase tissue oxygenation and protect against inflammation and inflammatory damage. d) Nitric oxide in low concentrations (as provided by tobacco smoke) acts as neurotransmitter, signaling to cardiovascular system to increase blood supplies to peripheral tissues (this is the biochemical mechanism behind the Viagra effect as well various circulatory medications). e) Tobacco smoke upregulates the levels of "youth hormones" DHEA, testosterone and pregnenolone, and reduces their decline with age. It also lowers "insuline growth factor" IGF1 (such change in animal experiments results in leaner and more youthful, longer living animals). f) The highest quality brands (Japanese) of the miracle skin rejuvenator, Conezyme Q10 are produced from tobacco leaf, which is still the best source of natural Co-Q10 (since it includes the full synergistic complex which the synthetic production methods cannot replicate). g) Deprenyl (selegiline), which mimics the selective MAO B inhibitory properties of tobacco smoke (this is not due to nicotine) and is used in smoking cessation "therapies" for that reason, has become all the rage in the life-extension circles, due to its almost magical rejuvenating powers. h) Nicotinic acid, along with its salts and various organic compounds, are skinprotective agents, used by cosmetic and pharmaceutical industry.

Since the hard science (in contrast to antismoking pseudo-science which is nothing more than a wishful, self-serving interpretation of statistical correlations) has demonstrated that tobacco smoke is not merely harmless, but that it is a genuine medicinal miracle, then your hate of tobacco smoke and/or smokers, which you are perfectly entitled to, is simply a matter of taste or personal beliefs. Some don't like smells of people belonging to races or ethnic groups other than their own. That's their business and I certainly would not wish to prescribe to you or to them what you ought to like and what to dislike. On the other hand, when you buy things that you believe are good for you or that you like for any reason, you pay sales tax of about 5%. If I buy what I believe is good for me, such as tobacco products, I pay "sin" taxes of different sorts totaling about 500% 185

(MA) of the free market product value. That is an obscene extortion. Further, I don't like smells of some ethnic cousines, yet those ethnic restaurants are allowed to freely operate in my town. Can you imagine, that I am forced to gag every time I have to do some shopping next to such stinky places? Antismokers dislike tobacco smoke and insist that no restaurants are allowed to cater to smokers, that every single restaurant must be forced by law to adapt to the antismokers' tastes. There is no reason that their taste takes precedence over the tastes of smokers and others who don't hate tobacco smoke and/or smokers. Insisting that all restaurants,bars, clubs, theaters, means of mass transportation, offices, hospitals,... must be forcibly reshaped by laws to suit the tastes and fit the subjective belief system of antismokers is an obscene discrimination and abuse of fellow human beings. Therefore, it's not a matter of smokers trying to impose their taste on you, but simply that smokers want to get antismoking parasite off their backs. Your or my particular tastes and beliefs are irrelevant. The antismoking racket, along with its hypertaxation, shameless discrimination and vicious abuse of smokers, is about money, not about your olfactory sensitivites. Each of us has our own tastes and no one cares about that. That's not what the conflict is about. It is about Big Pharma "investing" couple billions dollars (in USA alone) into antismoking "science", antismoking "grass roots" organization, numerous disease organizations, buying of politicians, bureaucrats, antismoking laws, taxes, regulations, incitement of hate, abuse and violence toward smokers through mass media, and getting in return hundreds billions in profits, a small bit of change from nicotine replacements and other cessation "therapies", with the bulk of their loot coming from treating tens of millions of extra victims with Alzheimer's, Parkinson's, schizophrenia, ADHD, depression, diabetes, ulcerative colitis, osteo-arthritis,... any many other conditions, the poor folks who could have avoided these expensive and terrible diseases, had they not been brainwashed and scared away from the ancient medicine, tobacco, by the antismoking hysteria whipped up and paid for by the Big Pharma. The same thieves are coming after your supplements next, so you might wish to subdue your glee for a moment and think it through a bit, before continuing with your chearing for their "denormalization" and extortion of smokers. As with all Big Lies, the antismoking fraud will perish, too. Reality always finds a way to break through and restore its rule, no matter how powerful and invincible any propaganda "matrix" appears at the moment. There are far stronger statistical correlations between the use of breathing ventilators and low productivity, missed days of work, shorter life expectancy,... The current users of ventilators are the least productive (99.93 percent of them don't work at all), the never users are the most productive, while the former users are in

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between and the longer they have been off those ventilators the more productive they are compared to the age matched current users. Everything statistically correlates just like with smokers, except that the corresponding correlations are much stronger for the users of ventilators. Ought not the never users and 'born again' ex-users of ventilators get organized, go to hospitals and start ripping the breathing tubes out of those ventilator addicts, to make those parasites more productive? Those tube sucking parasitic wretches may squirm a bit, yes, but hey, that's just their addiction to those evil ventilators which made 99.93 percent of them unproductive and a burden to the rest of us. After all, there are thousands of those who overcame the same addiction, they got off them evil machines and they are doing just fine now, returning gradually to the fully productive life. Those weaklings still sucking on their tubes ought get some will power, snap out of their addiction and return to the normal productive life as well. Your reasoning is no different in essence than the one caricatured above. People smoke because smoking is therapeutic for them (as plentifully illustrated in this thread and as acknowledged even by the antismoking scientists themselves), just as other people use breathing ventilators, and others use aspirin, because those "addictions" may be therapeutic for their particular problems. The only difference is that mechanisms of some therapeutic benefits are macroscopic and evident to the naked eye, while others operate at the more subtle biochemical levels and are externally perceptible only through the methods of hard science. As already pointed out, what these scientific mercenaries are doing here is a typical pinhole-view sleight of hand, where they highlight through that pinhole some selfserving tiny fragments of a complex dynamics and exclaim 'see how smoking is doing damage here'. At the same time, they chose to overlook that their 'damage' theory flies in the face of the easily reproducible plain fact that smoking mice, even under highly unfavorable conditions (including order of magnitude more smoke and absent dosing and rhythms feedbacks) compared to natural, self-dosed and self-paced human smoking, still lives significantly longer than nonsmoking mice. If smoking had damaging effects on the health of mice as these contractors are conjecturing, than the smoking mice ought to live shorter. Unless, of course, you now decide to redefine the term "health damage" to include the kinds of "health damage" which makes those "health damaged" live significantly longer than those who are not "health damaged." Further, the fact that tobacco smoke may carry compounds which result in AGE metabolites, by itself does not mean that smoking over time will results in increased AGEs if you take up smoking. For example, tobacco smoke (like anything we metabolize, including food in vastly greater quantities compared to 100mg/pack absorbed) will deplete some glutathione, yet smoking over time upregulates glutathione by 80% (while transient depletion from smoke is 10% or less). The net

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effect of smoking is the increased antioxidant and detox capacity of the organism. This is also perfectly analogous to the effect of vaccination -- you introduce a small quantity of an antigen and the net effect is a greater resistance to and quicker elimination of that antigen later, hence lowering of the levels of that antigen in the long run, even though there was transient phase right after the vaccination in which the level of that antigen was elevated temporarily. The "experiments" in the paper you cited are a piece of antismoking art to behold. They did not measure effects of tobacco smoking at all, but rather the of the injection of "aqueous tobacco extracts" and "cigarette smoke condensate" into the "rat tail tendon collagen". Do rats or humans normally smoke with their tail tendon collagens? That's like trying to prove that daily exercising by lifting 50 pound weights is harmful to humans by tying some poor dog to a bench and dropping a 200 pound weight onto his tail tendon collagen, then studying a damage to the tail depending on the height of the drop. Wrong quantity, wrong warm up, wrong position, wrong organ, wrong grip, wrong motion, wrong rhythm and repetitions,.... The only relation of such "experiment" with normal weight lifting is that they used some weights. Everything else is transparently rigged to "prove" (to idiots, I suppose) that weight lifting is terribly harmful and painful. And that is the climax of the antismoking hard "science" after 40+ years of "research"? What a shameless scam. If some gigantic enterprise were to spend 40+ years trying to prove that weight lifting is harmful, spending untold billions of dollars and uncountable human and technological resources, and on the 45th anniversary they do this kind dog 'tail tendon collagen' weight drop experiment as their final "proof", what would you think of it -- is weight lifting really harmful? Wouldn't have they been able to find, with all that money and manpower and technological resources and all these years of hard work, something less ridiculous if there was anything at all, even a tiny, remote whiff of anything at all? All it would really tell me is that weight lifting must in fact be terrific for your health, if that's how far they got, after all the time and resources they spent trying to prove the opposite. That is precisely what this "experiment", the climax of the antismoking hard "science" as of 1997 proves -- smoking is very, very good for you. Finally, there is your fundamental leap of faith at the root of this branch of argument -- "The aging of the skin is caused mostly by this. This may be why smokers are notorious for having old looking skin for their age." Without proper context (the "pinhole view" problem) this is a pure religious statement of antismoking faith. What if one honey roasted peanut yields as much AGEs as the smoking of a pack of cigarettes. Than your daily food (the fact that you need some minimum to live is non 188

sequitur) will yield thousands times more AGEs, hence your leap of faith leads to conclusion that basic eating ages us thousands times faster than smoking. And if you drop two honey roasted peanuts from your daily menu, you can smoke two packs per day without any difference in aging. Smoke just one pack, and you are ahead of the evil AGEs. If you wish to salvage any shred of your argument, bring in a list showing glycotoxic content absorbed by lung cells from a pack of cigarettes, along with glycotoxic loads for some common foods and beverages spanning roughly upper and lower ranges. Without it, you are merely selling your particular religion. For example, using the technical term "risk" one could say without 'technically' lying that wearing a bra every day increases the "risk" of breast cancer 12,500 times. But if someone restates that and says instead, as "journalists" and similar ignorants often do, that wearing bra causes breast cancers, then s/he is outright lying. Almost everything in the cellular biochemistry which is normally good, such as the ability of cells to replicate, becomes bad when cells become cancerous. Nicotine and nitric oxide, indeed, promote vascular growth and peripheral blood circulation, which is normally good for your health, but it becomes bad if you have a cancer. The other side of this "reversal of values" phenomenon is that things that are normally bad for you if you are not cancerous, such as radiation, leg amputation or removal of a lung, chemotherapy,... become good (at least partially) for you. The fact that normally "good" things become "bad" in the context of our present cancer "therapies" is more of a judgment on the misguided and discordant nature of these "therapies" than on things that are good for you (ability of cells to replicate, antioxidants and detox enzymes such as glutathione, better vascularization and circulation, rejuvenated MAO B levels,...). What you have here are three elements: (A) smoking stimulated vascularization, (B) cancer and our current cancer "therapies". These three don't fit well together. Now, our "cancer therapists", the brains behind the component , are declaring that this three way discord is 'all fault of the component (A)'. Does that surprise you? You can understand better this situation if you look at the societies and nations as organisms (which is what they are). In that perspective, having better roads and other infrastructure is good for a nation. Yet, in a war, such as WWII, it proved the undoing for more developed countries, allowing for German tanks to conquer them much faster (in contrast, the backwards and mountaneous Balkans gave Germans much more trouble). You can also note the same two-way "reversal of values" here -destroying your own bridges and roads, which is normally bad for a country, may become good if it will slow down the enemy advance.

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Would then this "reversal of values" phenomenon be a good argument against developing infrastructure (as you are doing above by classifying better vascularization as a negative effect of smoking)? Or for preemptively destroying bridges and roads in peacetime? Of course not. The good roads and other infrastructure, could work for defender, too, if proper war strategy and supporting technology are developed. Had French developed the right kind of army, their developed infrastructure could have helped them more then it helped Germans. Similarly, when medicine comes out of its present dark age and abandons its wrongheaded obsession with chasing and trying to cover up the symptoms, and when it masters the molecular level engineering, the same improved vascularization and circulation could help some advanced nano-medication get to cancer cells easier, while additional antioxidants and detox enzymes, such as glutathione, could help clean up the toxins quicker, once the cancerous cells were destoyed.

Quote Because you could do a human study measuring the effect of smoking on short-lived proteins in a study group of people screened for AGE generating and related diseases, instead?

Just showing that trace amounts of glycotoxins from tobacco smoke can interact with proteints and produce AGEs, does not demonstrate that the effect of smoking is an elevation of AGE levels. After all, since smoking suppresses appetite, smoker will take in less food (this drop in food quantity will be many times larger than the absorbed 100mg/pack of cigarettes), hence take in less glycotoxins from food, resulting in the net decrease of the consumed glycotoxins. For example if you were to take only a pinhole-view biochemcial snapshot of the effects of weight lifting (or similarly of aerobic exercise, vaccine,...) you could "prove" that weight lifting weakens and damages the muscles since, within the conveniently selected pinhole snapshot, the muscle cells can be seen with depleted energy stores and under heavier oxidative stress than baseline, at some point during or shortly after the lifting. That type of reasoning is based on a simple-minded, primitive mechanistic model of the biochemical networks, which is a fundamentally false model and which yields incorrect predictions, be it about the effects of weight lifting on the muscles or about the effects of trace
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levels of glycotoxins from tobacco smoke on the AGE levels in human body. Note that the rat's tail experiment you cited, with the injections of 'tobacco smoke condensates' has as much relation with the effects of smoking on human AGEs levels as does the dropping of a 50 pund weight from the height of 1m on rat's tail has to do with the effects of weight lifting on human muscles. It is about equally non sequitur in both cases. If you do have some more pertinent experiment to cite on this subject, you welcome to bring it in. The rat's tail experiment-like motions don't even pass the laugh test. Quote Others and yourself can do what you want, but with the evidence I have seen on smoking and heart disease and AGEs, I will keep away. It may be that I require a lower threshold of evidence before I reject something as too risky.

Yep, your evidence threshold regarding AGEs seems to be quite low, in fact well into the negative range i.e. the evidence that smoking reduces your AGEs (e.g. just add appetite suppressing effects of smoking on total glycotoxic intake) is still by your threshold judged as evidence against smoking.
There is a new thread "Smoking is good for you" with over 450 posts and you can go check it to see how did your "... is a true crank" theory work out (and no, that wasn't the same guy as already noted by other members here; it should be pretty obvious, anyway). It turns out, after all was said and done, and after everyone presented their best arguments and papers, that tobacco smoke is much better than even the farthest claims in this thread. Below are few highlights of the "debate" (since all the hard science was squarely on one side, while the other side could only offer junk science, it was hardly a debate). Before jumping in with your "scientific proof" please check what was discusssed already (add your "proof" there since this thread has been inactive for years).

1. Dogs exposed to radon or radon+smoke: 5% of smoking dogs and 37% of nonsmoking dogs got lung cancers. 2. Massive National Cancer Institute sponsored experiments that backfired terribly, setting back the NCI's workplace smoking bans agenda for over decade. 3. The crowning experiments (2004, 2005) of six decades of antismoking "science", the pinnacle -- again backfired badly, as they always do -- at the end, more than twice as many smoking animals alive than non-smoking ones.

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4. Self-medication with tobacco 5. Common genes for lung cancer & smoking 6. Hazards of quitting (triggers lung cancers in animal experiments) 7. Emphysema/COPD - smoking protective rather than cause 8. How does antismoking "science" lie with stats (how to "prove" that -- Prozac causes depression -- using method of antismoking "science") 9. Heart attacks from SHS myths (is a 'friend saying Boo' more hazardous for your heart than SHS?) 10. Glycotoxins/AGE in tobacco smoke -- backfires 11. Smoking vs Caloric Restrictions, Smoking protects against cancers 12. More on anti-carcinogenicity of tobacco smoke 13. ** why take a chance 14. Smoking and diabetes, insulin sensitivity -- another "proof" backfires 15. How to prove that 'Lifting weights is harmful for muscles' - pinhole vision sleight of hand of antismoking "science" illustrated 16. Oxidative stress, breast cancer, "randomizing non-randomized variables" sleight of hand -- more antismoking junk science claims turned upside-down by facts hard science 17. Can one replicate the health benefits of tobacco smoke (the short list given) using supplements and pharmaceuticals? Even if it were possible, can one do it for < $1 day (cost for a pack of roll-your-own cigarettes with natural, additive free tobacco)? 18. Who knows more about biochemistry of life and its molecular engineering -- one little cell in your little toe or all the biochemists and molecular biologists in the world taken together? Is "Sickness Industry" good for your health?

It is even more interesting than that -- there is an acetylcholine receptor gene cluster where certain alleles make carriers simultaneosuly and independently more likely to smoke and more likely to get lung cancer (more here). Curiosuly, the father of

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modern scientific statistics R.A. Fisher, speculated that this might be the case in late 1950s, after considering various statistical anomalies of the antismoking data, which in his expert view, didn't quite point, even as a mere hint (which is the most such non-randomized correlations can do), toward the causal role of tobacco smoke.

Quote You speculation that it is vascular growth that caused the increased cancer is a speculation without evidence. Even if true, smoking still caused cancer.

Well, to see how absurd the claim is, translate the "smoking caused lung cancer" interpretation of animal experiments to humans i.e. the results which would be obtained if one could do similar experiments on humans: If you don't smoke, you will live on average 75 years and will be more likely to die from liver, bone or other cancers, while if you smoke, you will live till 90, while remaining sharper and thinner throughout, and will be more likely to die from lung cancer. (Note that 20% increase in lifespan applied above is from the less asphyxiating levels of smoke in the hamster experiments.) While dying from any cancer is surely unpleasant, which deal would you pick if given the choice (actually you are given the choice, since you can choose to smoke or not)? Who should squirm? Since that is what the question comes down to.
The one result of the experiments which is certain and can be agreed on is that nonsmoking caused shorter lifespans of the test animals. There is plenty of evidence for tobacco smoke or nicotine promoting angiogenesis and via that mechanism the existent tumor growth. That's exactly where I found reference for this effect in the first place. Here is one paper using specifically tobacco smoke and mice for this exact purpose. Unlike the "ts-lc model" papers, where autors deliberately ignore the most obvious and well known explanation for their results, choosing to spin their self-serving alternative conjectures out of thin air, here the researchers actually evaluate the angiogenesis effect and properly attribute the tumor growth results to the vascular mechanism. Any promoter of angiogenesis will produce exactly the same result, which has nothing to do with ethiology of lung or any other cancer.

Within the current antismoking climate in the Western world you will not find papers that will explicitly state that quitting causes any harm, let alone lung cancers. In fact the official party line is that quitting significantly reduces harm and lung cancers (resting entirely on the stats on non-randomized/self-selected samples). What tipped me that there is something fishy going with the official party line was paper by a research team of Indian academics with provocative title: "Are lung cancers triggered by stopping smoking?" (pdf), (by A. Kumar et al., Med. Hypotheses

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2007; 68(5):1176.). Although the usual antismoking animus permeates much of the prose, there were few little slipups outside of the Matrix, indicating something interesting may be going on here: "In an overview of personal history in a number of lung cancer patients locally, we are struck by the more than casual relationship between the appearance of lung cancer and an abrupt and recent cessation of the smoking habit in many, if not most cases. The association is more than just casual development of cancer within a few months of eschewing cigarette smoking. ... The striking direct statistical correlation between cessation of smoking to the development of lung malignancies, more than 60% plus, is too glaring to be dismissed as coincidental. ... Nicotine stimulates corticotrophin-releasing factor (CRF) besides increasing the level of adrenocorticotropic hormone (ACTH), both of which interfere with immune systems [2]. Abrupt withdrawal of the addictive drug could trigger derangement of the `smoking-steroid' conferred immunity, priming the healing lung epithelia to dangerous levels uncontrolled cell division. ... Larger studies and mass reviews of case histories in lung cancer patients could throw more light on this, rather unusual clinical observation. No doubt, tobacco kills too many. Or does it?" The concluding question of the paper is not something you would expect any Western researcher to ask, much less seek an answer. Their explanation is mere conjecture, colored with usual conventional antismoking wisdom (body tries to repair the damage from smoking too fast). Yet their curiously worded expression "'smoking-steroid' conferred immunity' indicates that it is in fact the loss of the anti-inflammatory protection of tobacco smoke which let to the runaway cell multiplication and cancer. Of course, since this was not a randomized sample, it is hard to say what it really means. There are too many unknowns among the links and their possible arrangements into the web of causes and effects. With the eyes now opened to this phenomenon, I went back over the animal studies, where in previous readings I didn't notice anything mentioned about the extremely harmful effects of quitting. Previously I assumed that, at worst, quitting would result in a loss of some self-medication function that mattered to that smoker (if any) and the ex-smoker would get prescribed several pharmaceuticals to deal with the same problem at hundred times greater cost (and for some effects there are no as effective substitutes, e.g. doubling of detox enzymes, protection against or delay of onset of Alzheimer's, Parkinson's, schizophrenia, rheumatoid arthritis). Generally, I assumed, the quitting was a mere loss of benefits, so the ex-smoker would end up with the life-expectancy shortened to an equivalent non-smoker, gained 15-20% in 194

weight and became dumber or more senile (due to loss of several nootropic effects). But the above paper suggests it is much worse than mere loss of benefits. As I reread the experimental papers I realized this phenomenon was always there right in front of me, it was noticed and studied by researchers, including the potential treatments (with none other than those same 'scary' tobacco smoke components, which we are told in the other story, before quitting, cause lung cancers), but the very carefully worded, circumspect descriptions had made it invisible to a reader unaware of its existence from some other source. The exemplary in this regard is masterfully weasel-worded recent review of animal experiments by the leading authority in the field, Dr. S.S. Hecht: "Carcinogenicity studies of inhaled cigarette smoke in laboratory animals: old and new" S.S. Hecht, Carcinogenesis 2005 26(9):1488 [p.1489]...The animals were exposed for 5 months, then allowed a 4 month recovery period.... The increases in tumor multiplicity were generally small, from ~1 tumor per mouse to ~2.8, following exposure to 50-170 mg/m3 of total suspended particulates. The increase in tumor multiplicity observed in this model was due to a component of the gas phase of tobacco smoke....The 4-month recovery period is absolutely necessary for observation of increased lung tumor multiplicity, but the reason for this is not clear. [p.1492] Note added in proof: A recent study (W. Stinn et al. 2005) indicated that the recovery period in the A/J mouse smoke inhalation model is necessary to overcome stress induced inhibition of lung tumorigenesis, and that the lack of weight gain during the smoke inhalation period was unrelated to the final tumor multiplicity.

Well, there it is -- increased lung tumors were observed (in A/J mice, a specially bred cancer-mice which gets lung tumors spontaneously), attributed of course to inhalation of tobacco smoke, but somehow, for the smoking to "cause" these lung tumors, the mice has to quit smoking, then it has go through the perversely named "recovery period" (non-smoking) of similar duration as previous smoking, and only then "smoking" will somehow cause increase in tumors. But had they continued smoking instead of ostensibly "recovering" from the ravages of smoking, smoking would not have caused increase in tumors (and it would have even extended their lifespan well beyond that of the non-smoking mice). Orwell was an amateur for these newspeak magicians. What an excruciatingly round about way of saying plainly -- quitting smoking will trigger any latent tumors (that smoking had kept suppressed). But since this is 195

antismoking "science" which provides the "scientific" pretext for hounding and extorting countless millions of human smokers, to force them to quit, Dr. S.S. Hecht simply cannot say it that way. And of curse, as a matter of routine, researchers terminate these experiments (kill mice) safely before the expiration of their natural life-expectancy (otherwise they would have to watch out for the wrath from the vengeful ancient gods of prairies that endowed us this medicinal miracle plant -- the life-extending effects of tobacco smoking). Another experimental paper (G.M. Curtin et al, 2004) explains the "recovery period" somewhat more bluntly: [p. 26] Demonstration of increased tumor formation required that the standardized 20-week exposure period be followed by a 16-week recovery period, during which mice were provided filtered air. Bogen and Witschi (2002) provided justification for the recovery period; more specifically, it was suggested that tobacco smoke exposure suppresses the growth of premalignant foci, and that smoke induced lung tumor risk occurs predominantly via a genotoxic mechanism. Consequently, the recovery period allows tobacco smoke-induced genetic damage to progress to tumors. We should also recall that this scheme also relies on vascular effects of nicotine to demonstrate "carcinogenicity" of tobacco smoke in mice susceptible to lung tumors or in mice seeded with tumors in the beginning of the experiment (they observe rates of growth and misattribute vascular effect to 'genetic damage', which obviously contradicts the fact that extending smoking somehow cancels the effects of the alleged genotoxic damage from smoking during the first half of the experiment). What they are in fact fighting with "recovery period" is the tumor suppressive effects of tobacco smoke (explicitly demonstrated in that [Stinn 2005] experiment), that are overriding the vascular effect on the growth in A/J mice. The recovery period simply removes the carcinogenic protection by tobacco smoke leaving the vascular effect to help the existent tumors (caused by injected seed or from genetically bred traits) in the respiratory system grow faster. So, what is the lesson for humans(smokers and non-smokers) from all this? The basic fact established in animal experiments is that lifelong tobacco smoking will extend lifespan, regardless of genetic predisposition to cancers or carcinogenic exposures. If someone is genetically predisposed to cancers or is exposed to real carcinogens, tobacco smoke will still be protective throughout (e.g. via nearly doubled detox rates as well via the mechanisms mentioned in Indian paper at the top), as the experiment with dogs inhaling radon clearly demonstrated (similarly in other hamster, mice, rat experiments with co-exposures). The vascular effect (better angiogenesis in the lungs, which is normally quite beneficial, such as for physical laborers, athletes, soldiers or the 101 year marathon runners) implies that if a cancer eventually gets started despite the protective effects of tobacco smoke, depending on its location it 196

may grow 'potentially faster' (in respiratory system) or always slower (elsewhere, since the protection still exists, it's just not strong enough, while vascular effect is absent or much smaller). Regarding the case of 'potentially faster' growth for respiratory cancers, the net effect again depends on the precise balance between the ongoing protective effects and the vascular effect, which now amplifies the cancer growth rate (but it helps amplify protective tobacco effects, too). Hence, it is the same kind of battle as elsewhere in the body (where protective effects of TS battle the growth of cancer), except that in the respiratory system, both sides are amplified by the vascular effect. So the net result in the respiratory system is down to the same kind of balance as elsewhere. The case of someone quitting smoking removes the protective effects of tobacco smoke, while leaving the vascular effect (the extra blood vessels and higher circulation remain) to help the cancer, whenever its natural onset begins (from genetic or environmental causes). That is the worst possible combination, worse than had he never-smoked, in which case the vascular effect in the lungs would have been absent. On the other hand, a lifelong smoker is always better off than had he never started smoking. He will live longer and age better than had he not started, regardless of when the cancers are set to start in his case. As the cancer-mice/rat experiments show, even in the cases of the extremely strong propensity to cancers (including in lungs), the net protective effect is beneficial -- smoking mice/rats still outlive the nonsmoking ones (despite the experiments & exposures being optimized to go the other way; human smoker optimizes the exposure in opposite direction than antismoking scientists did for the test animals).

Nightlight, do you believe children should begin smoking? Do you think the earlier you begin smoking, the more pronounced the benefit?

From the ancient pre-Columbian times, starting to smoke was part of the rites of passage. In Europe, in the golden era of British Empire, smoking was compulsory for the students (which meant corporal punishment for boys who refused to smoke) in their elite boy schools, such as Eton (for reasons of health and performance). The most interesting example are Semai people of Malaysia. There was a report in British Medical Journal, Feb 26, 1977 by Dr. C.Y. Caldwell, describing how Semai children start smoking at age two, a kind of 'rites of passage', except it is weaning from nursing by smoking. During the early 1970s, medical researchers curious about this unusual custom, went out to see how bad the 'smoking related diseases' are among Semai, expecting large number of cancers, emphysema,... They took trouble to give full physical, including chest X-rays, to every adult Semai, about 12000 of

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them. To their shock, not a single 'smoking related disease' was found. In animals experiments, researchers have been trying for some years to demonstrate harmful effects of tobacco smoke on fetuses and newborns. The pregnant mice are injected with nicotine and indeed some harm to fetus does occur. The only problem with the "theory" is that the nicotine dosing is 2-6 mg/kg, which for current full flavor cigarettes and a pregnant 175 lb woman would require her to smoke 8 to 24 packs of full flavor cigarettes per day. Considering how eager the antismoking researchers are in proving the harm from smoking, especially to the children, that extreme dosing then tells you that were they able to get any harmful effect with anything less, they would have surely trumpeted that, rather than those ridiculous doses. So, one can onoy conclude that 8 packs a day or more of FF cigs, may cause some harm to fetus (due chiefly from low circulation). There was also a Bulgarian-Italian experiment on very young albino mice set to smoke starting 12 hours from birth. Lung damage, including hyperplasia, lesions (18% were malignant) and numerous benign micro-tumors, totalling in 78% mice after 180230 days. Again, the little problem buried in small print was the dosing -- they had average smoke particle density of 818 mg/m3. Recall the mice studies discussed earlier, where they used 250 mg/m3, which was equivalent to about 4 packs/day (full flavor). Hence albino mice babies here were smoking about 1 whole carton+ 3 packs from the 2nd carton per day (over 21% died right away, likely from asphyxiation). What this tells you between the lines is that anything comparable to human smoking wouldn't show any harmful effect, or even several times that. They had to go up by more than order of magnitude from adult smoker to show the harm on newborns. In any case, that's the science about children smoking -- it is very difficult, short of going to the extreme asphyxiating dosing, to scientifically demonstrate any harm at almost any age, even pre-natally. In my view, due to mildly androgenic hormonal effects, the best age is probably the age of traditional rites of passage, which in our era is when kids get drivers license i.e. somewhere in older teens. That 101 yo marathon runner started smoking at 7, while Jeanne Calment, the oldest human ever (122+), started smoking in her teens (she smoked as a teen with van Gogh in Parisian caffes).

Keep in mind that there are alleles of certain genes (related to acetylcholine receptors, also this one) which make a person more likely to smoke and also independently more likely to get lung cancer, of all things. In my family tree, only my maternal grandmother had a lung cancer, got it in her 60s (neither she nor grandfather ever smoked). Being a 'village healer' (they still have those back in the Balkans), she decided to refuse medical treatment, choosing to treat herself with her herbs and whatever else she did for her healing, and she lived another 20+ years,

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dying of old age in her late 80s. Several years after the diagnosis, she was symptom free by then, my mother (a medical doctor) conviced her to get examined again, and to everyone's surprise the lung cancer was gone, with only some scar tisse visible on the X-rays. But even if there were no such genes, the plain fact is that medicinal/protective and harmful substances will produce the same kind of positive correlations with diseases on non-randomized samples. Such correlations are only a hint for possible harmful causal role. But they are also equally strong hint of a medicinal/protective role. You need hard science to disentangle some unknown web of causes and effects (as it is the case with ethiology of cancers or full biochemical interaction of ts). The problem is that antismoking "science" was stuck in the "hint phase" for six decades now. Consider that you are still quoting mere hints, when the matter should have been resolved by hard science way back in 1950s as R.A. Fisher pointed out and as it does in normal science. They are stuck not for lack of trying (as you can see from animal research being discussed), but because the hard science is telling them what they don't want to hear, it is all going the "wrong" way. So, that's how it came to be that six decades later, the best you got to show above is a hint, the same one they had 1950, just new people, new places, but the same kind of hint as back then. Such hint could mean that smoking is causing 'smoking related diseases' but it could equally well mean that smoking is protective or therapetic against some of the actual causes of those diseases (self-medication mechanism). Since the hard science has already established numerous such medicinal effects including the near doubling of key internal detox & antioxidant enzymes (in animal experiments and human observations), that fact alone provides major boost for selfmedication explanation of much of those 'smoking related diseases' (since the nearly doubled glutathione, catalase & SOD are precisely the defenses that protect against industrial and other forms of carcinogenic & toxic pollution or genetic sensitivities to it). Add to that animal experiments, which whenever they say anything conclusive, they confirm the beneficial net effect of tobacco smoke on live creatures from mice and hamsters, through dogs and small monkeys, despite the researchers doing their best to show exactly the opposite. Can you imagine how much better those graphs I keep showing would look, had someone done those exeriments optimizing them for maximum benefit, we could might well see 40% longer lifespans, instead of "only" 20% longer. The "harm" theory of standard antismoking "science" cannot coherently account or fit in such facts without parting the ways with facts and/or logic. As you can see reading the critiques of its various claims in previous posts here, it often hides the facts that don't fit and it abandons the logic when it doesn't work out the way they wished.

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There are no animal experiments with shortened lifespan of smoking animals, that model anything remotely comparable in dosing/concentration to human smoking, which is the subject of interest here -- is smoking good for you? Nobody is arguing in this thread that "smoking" using Dontenwill's only-in-Germany "smoking" machine is good for anyone (had someone tried those here in USA, PETA would have slashed the researcher's tires and firebombed their labs). It appears you just don't have anything better but to cling onto the same few strawmen argumens, repeated over and over, as if stuck in loop. Keep in mind that "the dose makes the poison". Even plain water, clean and pure as can be, can be very toxic, including lethal, if you overload you kidneys excretion capacity e.g. drink a gallon in half an hour. Your clinging to the Dontenwill's 'only-inGernany' "smoking" machines results, debunked several times already, are no different than arguing that drinking plain water is bad for humans, by citing cases of the letal water toxicity.

Nightlite, will you please explain than the relationship of smoking and COPD?????

I will try to get to every issue brought up. Emphysema, or its umbrella label COPD (which also includes chronic bronchitis), is in fact the best example for the selfmedication mechanism behind the non-randomized correlations of smoking and 'smoking related diseases' and I was hoping someone would bring it up. Emphysema, in essence the destruction of elasticity of alveolar walls, is result of overload of the inflammatory cleanup processes in the lungs. Namely, the inflammatory processes, characterized among others, by the activation of lung neutrophiles (a type of white blood cells which are the first line of defense against all the types pathogens). One of the key weapons in the neutrophiles antibacterial arsenal are enzymes elastase, which are used to dissolve the bacterial membranes to kill them. Of course, like any weapon, they are a double edged sword, capable as easily dissolving the cell walls of ones own lung cells, including alveolar cells, which they routinely do. To minimize that kind of self injury, as soon as the emergency of battling the invading bacteria is over, there is another enzyme, Alpha 1-Antitrypsin (A1AT), produced by liver, which inhibits the activity of elastase, protecting thus ones own alveoli from the damage by elastase. The process is in reality far more complex, due to need to continuously maintain delicate balance between the two opposing requirements, continuously vanquishing bacteria (which we inhale with every breath by the millions and protection against 'civilian collateral damage', destruction of ones own alveolar cells, from the heat of these battles). Emphysema results from both global overload of A1AT system, when it is unable to 200

clean up all the active elastase, allowing thus for progressive damage to alveoli by remaining elastase, and from disrupted local balance between elastase and A1AT activity. The causes of global A1AT overload may be genetic, which is in its extreme forms analogous disease to type 1 diabetes, or a result of any type of liver damage (e.g. from alcoholism, Tylenol or many other pharma products). More delicate local A1AT vs elastase balance can be disrupted by all kinds of malfunctions in the complex biochemical processes needed to maintain it always at some optimum, in the face of continuously changing and fluctuating localized demands throughout the lungs, for either enzyme. Of course, our cellular biochemical networks, are usually well up to this unimaginably complex task. Namely these networks are an implementation of the same kind of self-programming natural distributed computers as human brain, the intelligent adaptable networks architecture (mathematically modeled as neural networks, which are at best toy model for the real thing). They are the true masters of biochemical engineering at the molecular level, far exceeding in their expertise and deep understanding of this realm, the baby-like clumsy babble of all our human-level biological sciences and scientists put together. To provide a bit of bird eye perspective (it will become clear shortly why this is needed), we can note that tobacco plant itself is the same kind of biochemical network as are human biochemical networks. The two networks have evolved an amazing synergistic system over the past eight millennia of mutual intertwining, each using its vast wisdom and expertise of the biochemistry and molecular engineering, to adapt itself and please the best it knows how its partner in this ancient dance. The optimization of the synergy results from the continued feedbacks between the networks. The tobacco smoke is the primary contact subnet of the tobacco plant networks within the human biochemical networks. It interacts first with our cellular networks in the lungs, and within a second or two with our CNS, where feedback actions from human to tobacco networks get formulated. The back-path for this human => tobacco feedback obviously doesn't flow through tobacco smoke, but rather it flows back through our social and economic networks, manifesting and delivering its final report, in the form of tobacco cultivation, protection and taking good care of our partner and its health, as it does of us and our health. Of course, we have similar synergistic relations with countless other networks of various plants we cultivate for food and other uses (e.g. flowers for beauty and scent, wood for furniture, tools, arts,...). The degree of optimization of a synergistic relation is vitally dependent on the rate of information flows back and forth between the synergistic partners. Synergy with tobacco networks has a unique advantage here compared to nearly all other such relations, due to virtually instant feedback, perfectly sharp and clear, being generated within our CNS, within a second or two after a puff. In contrast, feedbacks from foods are very noisy with a much weaker signal, considering that foods undergo a much slower digestive process, preventing unambiguous, information rich clear attribution of any effects to specific food we may have ingested many minutes or hours ago, 201

amid dozens or hundreds of other interactions we may have had since. So, the signal to noise ratio and the rates of information flows in the feedbacks to tobacco is several orders of magnitude higher than analogous feedbacks to the food plants. Consequently, the human-tobacco synergy, which is nearly as old as human synergy with any other plants we use for food, is much more finely optimized for the mutual benefit than any other we have. From this perspective, it is not surprise at all to see the countless therapeutic and protective effects of tobacco smoke or to witness how this biochemical miracle medicine, easily defeats the massive pharma sponsored scientific efforts to make it cause harm to its human partner or to lab animals (by virtue of similar biochemistry with humans, from the plants networks perspective; of course, tobacco is much better for us than it is for animals to which it was not specifilly optimized). No mater how they twist and turn the conditions of their experiments to make it cause harm, everything short of brute mechanical asphyxiation of the lab animals (you could do that kind of "harm" with plain water, too), ends extending the lifespan of animals as well as keeping them sharper and thinner, more youthful throughput. How can that be, wonder the poor pharma contractors. It can be because it was self-programmed into these networks over the millennia of the synergistic, feedback rich intertwining, through processes and knowledge of molecular engineering that human sciences may not reach in thousand years, if ever (there are intrinsic limits to what can be computed, even in principle). Consider as an example, the fact that nicotine is quite toxic; about 60 mg will kill you. Yet it is virtually impossible to make our partner actually kill us through nicotine poisoning through the long optimized form of our interaction -- by smoking. Even the most badass guy trying to impress his buddies, in a 'hold mah beer' moment, by showing he can rapidly chain smoke 60 cigarettes, two or three at once, to get the lethal dose, would be stopped by nausea and vomiting far before he is anywhere near the 3 packs needed. This magical plant will simply not do harm to its synergistic partner. Compare this finely tuned interaction to the pharma substitute nicotine, a patch, crudely optimized, mostly mechanically. You can easily lethally overdose with these -- there is no built in sure-fire overdose protection mechanism that the finely tuned synergy with tobacco has. The same goes for all medicinal aspects of tobacco compared to primitive pharma substitutes. In side effects, protections and overall benefits, there is no contest, like world chess champion (the tobacco biochemical network) playing against a two year old who just learned how to move some of the pieces (pharma and its substitutes for medicinal effects of tobacco). The reason for putting forward this bird eye view sketch of the human-tobacco interaction, in the context of emphysema, is that in this field (much more than in lung cancer field) you will find great many antismoking research papers, claiming to show this or that reaction "impaired" or that enzyme "disrupted",... by this or that component of tobacco smoke. You can read all that, then put the animals in the lab to 202

smoke their whole life and watch how it all will add up, and it will add up the "wrong" way -- all those "disrupted" and "impaired" smoking animals will live longer and will do much better than their "unimpaired" and "undisrupted" cohorts. Those claims are basically pinhole vision sleight of hand -- they show you a pinhole view of something much larger and more complex, that not only the reader doesn't know what it truly means in the overall computations by the unimaginably complex biochemical networks, but the authors don't understand all that much more beyond their simple minded toy models of what is going on. They are like a five year old, looking at the electrical readings of this or that pin on this or that chip of a computer running a program, and claiming to be able to interpret for you what the program running in the computer is doing. It is beyond preposterous. You will also hear similar scare stories about glycation, AGE and free radicals and oxidative damage... from tobacco smoke. All such scare stories fall under the same pinhole vision gimmick, or kid with pin voltmeter readings explaining to you what the program in the computer is doing, all equally preposterous, blind leading the blind. One tiny cell in your little toe knows and understands more about biochemistry and molecular level engineering of live processes than all the biochemists and molecular biologists in the world all put together. The same goes for lung cell and tobacco plant cell. E.g. any one of them knows how to engineer and build a live cell from scratch at a molecular level, something our primitive biological sciences couldn't even begin to dream about, let alone equal such feat. Unlike cancers, where the holy grail of coercing inhaled tobacco smoke to cause lung cancer is still a mystery to antismoking "science" (despite some self-serving claims, which were debunked in this thread), it is not all that difficult to overwhelm or disrupt the lungs through mechanical or chemical irritation, especially of well selected strain of mice or hamster, and produce emphysema like damages. The local A1AT vs elastase balance is a highly delicate and complex process which is not difficult to disrupt with primitive simulations of human smoking or through massive overdose or through use of individual components of tobacco smoke. Such process requires the equally delicate, feedback rich interaction loop with tobacco smoke, the way it was optimized within this perfectly tuned synergy, to be able to flow without disruptions. The key problem with simulated smoking in animals and testing for emphysema-like damages, is that simulated smoking lacks any feedback, which is the dominant feature of human smoking. The natural human smoking is a rhythmic, gentle dance driven by information rich biochemical feedbacks, unfolding in a hierarchy of nested cycles of twining in and twining out motions of the two networks, as puffs come and go, alternating with plain air in between, all wrapped into cigarette level cycles, then several daily and longer cycles. Every step of this twining in and out dance, choreographed into perfection through millennia of synergy by countless millions of humans and even greater numbers of tobacco plants, performed with instant feedbacks controlling every tiniest action of hands, mouth, throat, lung muscles and nerves, along with myriad even 203

smaller actions down to cell levels, all along the path of interactions. (Of course, after the initial learning to smoke phase, almost none this process is occurring at the conscious level, having become the second nature.) That's the kind of process that this synergy has tuned as the manner of the beneficial interaction, that causes no irritation or disruption of our internal biochemical processes in the lungs. In contrast, with simulated "smoking" the air in a chamber is filled up with thick smoke for several hours, usually delivering equivalent of 3-5 packs/day, but all compressed into 2-6 hours. There is no let up, animal can't move away, alternate plain air with smoke, change the pace and rhythm of interaction with tobacco network the way it was programmed and optimized to interact with human networks. Under such conditions of "smoking", there will be emphysema-like and damage-like effects on the lungs. Of course, the descriptions of these changes and adaptations in the antismoking literatures sound scary and visually appear much worse than they actually are. After getting an earful of medical jargon describing all those horrible damages, you would expect little rodent to drop dead right there. Yet, he goes on about his little life, in pursuit of his little happiness, ready to outlive those wholesome, healthy lung looking cohorts. Biochemical networks are extremely smart, adaptable and resilient. The changes are mostly defense mechanisms and adaptations to primitive simulations and mishandling, like calluses one may get from not putting gloves on before lifting weights. They may look bad, but they are basically completely benign defensive formations and are minimally disruptive (for most activities, although one can contrive some for which they would be so). That this is indeed so, benign defensive and adaptive reconfigurations, is confirmed if you watch for the net effect of such "damage" over the lifespan of the animals -- the emphysema-like "smoke-damaged" animals will substantially outlive, and in a better shape, than the protected, smoke-undamaged controls. In short, this finely optimized synergy still manages to produce the net benefits, despite having to take long adaptive detours from the more optimal procedures. It shows again how unbelievably strong are the built in smart safeguards against any real damage, no matter how hard those antismoking researchers tried to coerce it to cause harm. The biochemical networks of this magical plant are much too smart for them. At the more fundamental level, tobacco smoke is highly protective against emphysema and bronchitis, since both diseases include chronic inflammatory processes as the key step of their etiology. The multutudes of anti-inflammatory effects of tobacco smoke are one of its most distinguishing traits, recognized and appreciated since ancient times. The early spread of tobacco smoking through Europe was kicked off when the physicians for royalties started prescribing to their royal patients tobacco for coughs, flu, bronchitis, asthma, arthritis.. and variety of other inflammatory and auto-immune diseases. While some of these effects are due to nicotine, there others which only the full synergistic complex can deliver (e.g. see the recent rheumatoid arthritis experiment on mice, trying to tease out the this very difference). 204

The conventional antismoking epidemiology, with its strict taboo against even mentioning medicinal effects of tobacco smoke, let alone measuring them and accounting for this strong self-medication confounding, cannot easily detect the protective effects of tobacco smoke against COPD, since the confounding skews the signal, often resulting in the apparent effect with exactly opposite sign from the pure signal (as one also expects to see from any medication and a disease, if one completely ignores the medication's therapeutic effects). The excellent example of the power of this skewing effect within the antismoking epidemiology is the above rheumatoid arthritis -- while epidemiology has declared smoking as "risk factor" for RA (which it is, within its taboo space, that discards the confounders) and advises patients to quit smoking (so the pharma can sell genuinely hazardous and damaging cortico-steroids for substitutes), the experiment above show how the tobacco smoke (and nicotine alone but to a lesser extent) protects cartilage from the incipient autoimmune damage, delaying the onset of clinical RA, and then continues protection by slowing down the breakdown of cartilage and progression of the disease (while also having analgesic effects that alleviate the painful symptoms, but this wasn't an issue with mice experiment above). Yet, despite its best efforts to ignore potent anti-inflammatory effects of TS and its confounding role, the antismoking epidemiology occasionally inadvertently allows the nature of the research subjects and situation, to almost eliminate the confounding by equalizing the parameters they don't want to mention or measure. Most often this happens when studying workers in harsh, toxic/carcinogenic working conditions, where the nature of sample (workers all in the same place), equalizes toxic exposures among subjects. As expected, and as seen in NCI hamsters experiments as well (which tested for exposure to workplace toxins and carcinogens + smoke), the smoking workers, with their nearly doubled detox rates fare much better (within variations in genetic susceptibilities) than never-smokers, while ex-smokers fare worse than either (as expected, see discussion on harmfulness of quitting). When the usually reliable ally, the stats on non-randomized samples backfires like that, making the correlations go the "wrong" way, the antismoking "scientists" cannot now check the deliberately overlooked effects of tobacco smoke on glutathione, catalase and SOD, to properly explain the observation. Instead they simply declare that the smoking workers must be the genetically strongest ones, since to smoke in that kind of harsh environment, you have to be internally stronger than non-smokers and that offsets the bad effects of smoking. Nothing is ever measured to test the conjecture, and since there can be no other explanation within the antismoking Matrix, who needs tests. The name for this wishfully imagined phenomenon is "Healthy Smoker Effect" (see also here, here). It is most often brought up in relation to COPD and its inflammatory precursors. A good example is this study of German aluminum potroom workers (Occup Environ Med 1999;56:468-472), (pdf) which illustrates all of the above points. Aluminum is potent pro-inflammatory toxin and the potroom workers inhale its vapors and dusts, leading to emphysema type damages. In this case, such 205

emphysema type damages were found only in non-smokers, while respiratory symptoms, such as cough, wheezing... were 6.7 times lower in smokers than in never-smokers, and 11 times lower than in ex-smokers (these poor dupes get the worst of everything, they are sicker than they need to be and they have less fun). This study was discussed in more detail in this thread (search for "aluminum" for several posts) Dr. Siegel's blog (tobacco control doc).

Tobacco is a potent medicinal plant and youth elixir used for over 8000 years. Antismoking "science" is a money making scam, resting entirely on the worst kind of junk science, created and financed chiefly by the pharmaceutical industry. The big pharma reflexively seeks to suppress other natural medicines and folk remedies as well, especially those that work. Tobacco being the most beneifical natural medicine humans have ever known (tell me which other substance, matural or synthetic, extends the lifespan by 20% in animal experiments, while keeping the brain sharp into the old age, doubles our main internal detox and antioxidant enzymes glutathione, catalase and SOD,...), is the main target of the pharma's attacks on natural medicines.

First the "smoker" sister's skin looks like a typical result of sun damage. Second, she wasn't a smoker at all (for 20+ years already, and she smoked 16 years only at younger age). In contrast, here are some young looking older chain smokers:

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46 year old and 75 year old (and at 81) chain smokers since their early teens In Japan and Korea, 60-70 percent of men smoke, yet they tend to look more youthful than Europeans or Americans with less than half of those smoking rates (Japanese men also have three times lower lung cancer rates and live longer than American men). Back in 1940s and 1950s, actors and other celebrities were largely smokers, they didn't have botox or face lifts, yet they didn't look particularly wrinkled, certainly not more than nonsmokers of that era (some smoking celebrity photos; wikpedia had a large list of smoking who-is-who in Hollywood, which was deleted recently, someone obviously has felt threatened by the unsuitable facts and decided to erase history and improve on truth, Orwell's 1984 or Stalin style; that's is quite typical for vicious antismoking hysterics, even FDR's cigarette was erased from old photos). Many models smoke today, to control weight and their skin looks fine, too. Some of the underlyng biochemical reasons why smoker's skin (and every other marker of youthfulness) would come out younger in any apples to apples comparisons (not just the same genetics, but sun & other exposures, diet, stress, socioeconomic status,...): a) Nicotine stimulates and upregulates growth and branching of blood vessels (via upregulation of vascular growth factor), especially of capillaries, which improves the nutrient delivery and cleanup (antioxidant & detox enzyme supplies) to all tissues, including brain and skin (provided person's intake of nutrients and supplements is adequate). b) Tobacco smoke (not nicotine) upregulates production of glutathione, catalase and SOD (our body's chief internal antioxidant and detox enzymes, sometimes used in cosmetics for skin rejuvenation), to nearly double levels. c) Carbon monoxide in low concentration (as delivered in tobacco smoke) acts as a signaling mechanism in human biochemical networks to increase blood circulation, oxygenation and reduce inflammation. d) Nitric oxide in low concentrations (as provided by tobacco smoke) acts as neurotransmitter, signaling to cardiovascular system to increase blood supplies to peripheral tissues (this is the biochemical mechanism behind the Viagra effect). e) Tobacco smoke upregulates levels of "youth hormones" DHEA and testosterone and reduces their decline with age. f) The highest quality brands (Japanese) of the miracle skin supplement and rejuvenator, Conezyme Q10 are produced from tobacco leaf, which is still the best source of natural Co-Q10 (since it includes the full synergistic complex which the cheaper synthetic production methods cannot replicate). 208

g) Deprenyl (selegiline), which mimics the selective MAO B inhibitory properties of tobacco smoke (this is not related to nicotine) and is used in smoking cessation "therapies" for that reason, has become quite popular in life-extension circles, due to its almost magical rejuvenating powers. h) Nicotinic acid (byproduct of oxidized nicotine, as in burning tobacco, delivered directly into arterial bloodstream), along with its salts and various organic compounds, are skin-protective agents, used in cosmetic and pharmaceutical industry.

All that antismoking con has got show for the vast expenditures of six decades in intense research to demonstrate scientifically any harm from inhalation of tobacco smoke at all, are mere vague hints -- the statistical correlations of smoking with socalled 'smoking related diseases' on non-randomized samples (i.e. on selfselected classes of subjects: 'smokers', 'never-smokers' and 'ex-smokers'). Such correlations on their own are equally consistent with therapeutic/protectve role of tobacco smoke as they are with a causal role in those diseases. Taking further into account (a) the vast number of therapeutic/protective effects of tobacco smoke discovered within hard science (experiments, see links from earlier posts in this thread), along with (b) dead silence of antismoking "science" about these firmly established beneficial effects, while sticking exlcusilvely with junk science methods (since hard science routinely comes out the "wrong" way for their mission), along with animal experiments (which backfired, having been funded by antismoking interests) demonstrating directly and unambiguously that smoking animals live longer (20%), stay thinner and sharper, leads any rational person to a simple conclusion -- smoking is good for you.

There is nothing wrong in being dependent on something that is good for you. We are all "addicted" to food, water, air, family, friends, reading,... If something is good for you, transferring the need to replenish it to automated/reflexive systems (the so-called "addiction") is quite useful, time and effort saving transformation.

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You can also start smoking at any age and still benefit. The longest living man in the world, Shigechiyo Izumi (see at the top of the thread), started smoking at age 70. Some folks, scientifically well educated and health fanatics, who lived four or five decades as nonsmokers, until their lucky day when they decided to educate me, usually at a party or at work, that I ought to quit smoking, it is terribly bad for me,... and then I 'splained to them few things about glutathione, SOD, MAO B,... gave them books, emailed links to papers, and few days later they would ask me where can they order 'organic tobacco'...

Tobacco is a medicinal plant that increasing percentage of smokers uses instinctively for self-medication (the vicious antismoking pressures have scared and driven away most of those who don't really need it for any such purpose, those who are left are mostly the folks who do need it). Most smokers can't get a pharma drugs, even if they could afford them all, that will double all the key detox & antioxidant enzymes, that is simultaneously dopaminergic and cholinergic without downregulating either of those systems (an apparent paradox), that is also anti-inflammatory at multiple levels, antiapoptotic, protective against sepsis, analgesic, ... (see earlier links for numerous other beneficial effects). There is just nothing else that combines harmoniously that kind of broad spectrum of therapeutic and protective effects and in such depth. Those who are still smoking in the face of ever escalating abuses of smokers, economic, social and psychological, are poor folks for whom no other medicine will do the same thing, or those who can't afford the array of pharmaceuticals needed to cover all the beneficial effects of tobacco smoke that matter to them. Of course, as with any medicine, be it pharmaceutical prescribed by doctors or a remedy/supplement taken on ones own initiative, those who use them will have more health problems than those who don't use them. People using blood pressure meds will have more strokes than those not using them. That doesn't mean blood pressure meds cause stroke. They are obviously meant to prevent them, by lowering the blood pressure, which itself causes strokes. The same reasoning goes for tobacco smoke. For example, consider a miner exposed to toxic, possibly carcinogenic, heavy metal dusts and vapors at work. It just happens that tobacco smoke nearly doubles levels of glutathione, the master detox enzyme in human body, the perfect weapon to bind and excrete the heavy metals from outr body. A miner can't buy, even if he heard of glutathione, a supplement that will nearly double it, simply because there isn't anything that can do it, other than tobacco smoke. Hence, by smoking this miner will nearly double his detox rates, resulting in perceptible relief from the effects of toxic heavy metals. Hence he will have much greater incentive to smoke, especially under the present pressures, than somene sipping lemonade and inhaling purified air all day in a nice, clean suburban home. Indeed miners (or any physical or farm laborers, 210

truck drivers, soldiers, firemen,...) will smoke at much higer rates than general populations -- it helps them detox (among other myriad other potential benefits). Yet, those same toxins that tobacco, via glutathione, catalase & SOD upregulation, partially protects against, will over time damage their health anyway and they will end up with higher rates of 'smoking related diseases' than the suburban white collar folks. And they will also be smoking at higher rates than the white collar workers, That is the mechanism behind statistical correlations of smoking and 'smoking related diseases' on non-randomized samples (each person chose to smoke or not to smoke for their own reasons). Tobacco is by virtue of its therapeutic & protective effects a mere statistical marker for any kind of physical, chemical, emotional and psychological hardship, and it is the latter factors, the harships, that causes diseases attributed (by the pharma sponsored antismoking junk science) to tobacco smoke. The antismoking racket is truly the most evil force in the western world today. It is analogous to someone ripping respirators from patients in hospitals, justifying it by observation that respirator users have shorter lifespans than non-users, while the exusers of respirators fall in between, hence all those terrible respirators must be ripped from the patients to save them. An their pockets need to be picked in the process to help the breathe easier (tobacco taxes are becoming a pure thievery, e.g. the first law Obama signed, increased sharply the tax on all tobacco products, and on my particular one, the rolling/loose tobacco, by 2200%; thanks Mr. Reverse Robin Hood, at least your lobbyists are happy now). Generally, statistical associations on non-randomized (self-selected subjects) samples, of some substance X with disease D, could equally well be due to the therapeutic/protective effects of X against D (or against some of the real causes of D), as they could be due to the causal role of X in D. To find out which is the case you need hard science (experiments, randomized trials). Yet, all you hear about tobacco smoking, for over six decades now, are the stats on non-randmized samples. Why? Because the hard science comes out the "wrong" way -- the smoking animals live longer, and the randomly selected quit group ends up with more lung cancers or more heart attacks than the control group (smokers left alone).

My mother (medical doctor) didn't smoke at all, while my father (also doctor, surgeon) smoked heavily, right around her while she was pregnant. Her younger sister smoked as well, and she smoked right through her pregnancies without my mother or any other doctor advising her to quit. We had their friends doctors at the house all the time, all males smoking with all their kids around them (this was all back in the 'old country', where antismoking didn't yet arrive at that time). The real story is that tobacco is androgenic (not very strongly), so if you have trouble getting pregnant or need estrogen boost to get and stay pregnant, suspending 211

smoking, or reducing it down to 2-3 per day would be beneficial (disruption is not good either). If you are normal feminine female, it would have no harmful androgenic effects. While you will find some number of papers about animal experiments, claiming variety of (mostly small) negative effects on fetus, if you check their numbers more carefully, you will discover that they are injecting pregnant mice with pure nicotine (very different substance than tobacco smoke) and at doses typically 12 mg per kg (some even 6+ mg/kg), which for a 75kg (165 lb) pregnant woman would amount to 75-150mg of nicotine (450 for 6mg/kg), which for todays <1mg nic full flavor cigarettes, would come to 4-8 packs of FF cigs per day (or over two cartons for 6mg/kg), obviously all in a massive overdose. What that tells between the lines, is that for anything near normal human smoking levels, there is absolutely no harm they could detect, hence they had to resort to such massive overdoses to show any harm at all (resulting mostly from reduced circulation at those high levels of injected nicotine). Wearing nicotine patch is much closer to those experiments than obtaining equivalent amount of nicotine via tobacco smoke (the researchers apparently avoided tobacco smoke inhalation in these experiments, which is another 'between the lines' fact). The negative effects observed were chiefly due to acute vaso-constrictory effects of pure nicotine, especially when injected (it gets in and no let up from there), in contrast to cyclic self-administered delivery from smoking finely controlled by your own natural feedbacks. Tobacco smoke has also a number of offseting vascular effects (from low dose NO and CO in the smoke), which counter and balance the acute vasoconstricting effects of pure nicotine, effectively nullifying them as far as blood delivery to any tissue. The non-acute effect of nictine is upregulation of vascular growth factor, stimulating growth and branching of blood vessels, hence it improves circulation. Some positive aspects are anti-inflammatory effects and a particularly strong protective effect against pre-eclampsia. There is also a unexplained protective effect of maternal smoking against transmission of H. Pylori infection to baby (fourfold reduction in transmission for smoking mothers). Anti-depressant effects of nicotine are also becoming important in the era when pharma is pushing for the en masse use of clearly harmful antidepressants on pregnant women. I think, the best is to listen to yur own body and you will know what to do and how much. Pregnant women a famous for strange food cravings, knowing apparently exactly what they need.

It is not just anecdotes on the world record holders in lifespan. 30 million humans of japan smoke. this is a high percentage of the population. 212

http://en.wikipedia....moking_in_Japan and japan has highest life expectancy. Cuba similar. see http://www.kidon.com...ercentages2.htm how many competitors had Mme Calment? BILLIONS. BILLIONS of non-smokers. And you assume that she would have lived longer if she did not smoke? World record holders can not make many mistakes. Every detail must be perfect. Smoking was an important detail.

Let's check our theories when we both reach 120. Recalling also that the only two humans who ever made it to that age were smokers, I'll stick with mine.

Check the real Dontenwill et al 1973 (pdf) paper for yourself. They acknowledge (p. 1802) that their 300x smoke concentration (on nose & larynx than on bronchi or lungs) was the essential aspect required to show the damaging effects (on nose & larynx) observed as well as (p. 1802): "However the effective dose acting on the larynx of the experimental animal is many times greater than the effective dose per surface area in the respiratory tract of man." If you look further the related papers of this group (at the same site, use search form, look for early 1970s), you will see that they were the folks who made the Syrian Golden Hamster the next 'great hope' of antismoking research, after their skin experiments showing that applying high contentration of liquid smoke condensate (in solvents) to hamster skin caused lesions (many thousands times greater concentrations than in human smoking). The series of their reports preceding this paper shows iterations of their machine and concentrations (e.g. see this paper), a test run for the main show (they call it "pilot study"), as they sought to replicate those liquid condensate concentrations within the nose & larynx (they couldn't deliver it to lungs without outright asphyxiating or drowning the animal in the

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condensate). If you read the main paper, it is clear that the their "smoking" machine is not even remotely close in any way to human smoking (in many other ways than just astronomical concentrations, or solvants) -- they were in effect scorching the nasal cavity & larynx of the hamsters with their "many times greater" smoke concentrations, replicating their skin experiments inside the nose & larynx. So, no, this experiment doesn't help your postion at all. In fact, if it demonstrates anything of interest to science, it is how extremely difficult it is to coerce this ancient medicinal plant to cause any harm at all to smoker. Regular inhalation just won't do. They had to go into these kinds of extreme exposure methods and concentrations, amounting to pure animal torture, to barely induce some harm. This 'great hope' of antismoking "research" vanished into the memory hole shortly thereafter, when National Cancer Institute sought to scientifically show damage from smoking in work place (in preparation for smoking bans intended for 1970s) and contracted a large study on Syrian Golden Hamsters. Since it was clear they couldn't sell in USA the Dontenwill's machine method as anything remotely resembling smoking, they used regular air inhalation. Unfortunately for them, the 'great hope' backfired horribly, showing exactly the opposite from what they wished to show -tobacco smoke was protective against variety of industrial toxins and carcinogens, and smoking animals in all groups outlived (by about 20%) the non-smoking animals (pdf, p. 40): With the exception of the two asbestos-exposed groups (Groups 5 and 6), the groups exposed to cigarette smoke lived significantly (p<0.05) longer than their sham-smoke-exposed cohorts. The hamsters exposed to asbestos plus cigarette smoke also outlived their sham-smoke-exposed cohorts; however the difference was not statistically significant. Asbestos decreased the lifespan of the asbestos-exposed groups and thereby masked, to a degree, the difference in the survival between the smoke-exposed animals and their sham-smoke-exposed cohorts which is so readily apparent in other groups (Figure 23).

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Resized to 99% (was 1052 x 757) - Click image to enlarge

So much for the 'great hope'. The NCI disaster had set back their smoking bans agenda by 10-15 years, until some genius at EPA came up with a great idea -- why bother with science and experiments at all, when the plain lying with numbers will do. As the mice & rat experiments from 2004, 2005 (discussed earlier) show, nothing has changed much on the scientific front since then -- the smoking mice and rats still outlive the non-smoking ones, despite all the efforts of the researchers to get the opposite result. This ancient 'gift of gods' just would not do harm. That's how good it is. Lesson for smokers: don't chain smoke 90 cigarettes in a row every day for the rest of your life using 'Dontenwill-73' "smoking" machines. They will burn holes through your nose and throat and this will hurt quite a bit and it may slightly reduce your lifespan. Use cigarette holders or pipes instead -- they are an enjoyable way to smoke and as a bonus, it will extend your lifespan by about 20% compared to non-smokers,

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while keeping you thin and sharp into the old age. A pack a day keeps doctors away.

It just happens that one among the myriad of beneficial effects of tobacco smoke, in his case due to nicotine, is stimulation of the growth and branching of blood vessels (via nicotine vascular growth factor upregulation; as you can see there is a vast ammount of literature about that effect). Since the greatest concentrations of nictine inhaled via tobacco smoke will be in the respiratory system, especially in lungs, that is where the greatest vascularization will take place. Consequently, the cancers (which are caused by the deliberately bred in genetic defects in this mice for that exact purpose) in the respiratory system will get most nutrients and have the fastest growth. That is precisely what these contractors (former Pfizer scientists & consultants) chose to measure, the growth of tumors in different tissues. Of course, as expected, in the smoking mice they found the most in the lungs, but fewer in the liver and other tissues. The same researchers conducted the same experiment on F344 rats (also a variety bred for cancers, like this mice) and obtained exactly same results, more tumors in the lungs than elsewhere. Although this may appear as something new to an uninformed reader, this effect is well known for more than three decades (the paper quoted below is from 1980 and they cite even older ones, cf. research review p. 97): Chronic Inhalation of Cigarette Smoke by F344 rats W.E. Dalbey at al., Oak Ridge Nat. Lab., Inst. Environ. Health... J. National Cancer Inst., 64 (2): 383-390 (Feb 1980) "Smoke exposure did not change the total number of tumor-bearing animals relative to controls; however [smoke] exposed rats had significantly fewer tumors in the hypophyses, hematopletic-lymphoid system, uteri and ovaries, but an increased number of tumors in the respiratory tracts and dermes." These animal data fit in with the concepts of Prof. Oeser in Berlin and Dr. Lock in Hamburg, that, if properly assessed, the epidemiological data on cancers in general and for specific organs, indicate that total cancer rates have not changed, and that the only thing which has changed is that the increase in one type of cancer is compensated for by a decrease in other organ cancers. Curiously, the researchers in the 2005 mice paper, don't cite anything from this literature trail but purport that they have discovered an animal model for t.s. related lung cancer. Since this is a long known phenomenon unrelated to any alleged 216

causative role of tobacco smoke in cancers (since any vascular growth stimulant will show exactly the same effect), it was discarded decades ago as a candidate for the l.c. model related to t.s. It is a pure vascular growth effect, unrelated to lung carcinogenicity (or the lack thereof) of tobacco smoke. Of course, as soon as you check their survival figures, it becomes clear what a charade the whole "animal l.c. model" claim was -- the smoking mice outlived the non-smoking mice (cf. published paper p. 2001): Resized to 100% (was 1043 x 815) - Click image to enlarge

In summary, no there is no animal experiment, demonstrating that inhalation of tobacco smoke causes lung cancer. Of course, S.S. Hecht's review paper (2005) on animal experiments reluctantly acknowledges this failure as well. The antismoking "science" has pursued this 'holy grail' for over six decades, with no expense or efforts spared, and still a dud. No wonder they are still stuck with the inconclusive epidemiological hints -- the hard, conclusive science goes the "wrong" way, so what can they do but remain inconclusive.

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You can check the previous posts for more detailed discussion (for brevity I skipped here discussion of other interesting aspects of these experiments).

The plain experimental fact is that lifelong inhalation of tobacco smoke (within the range of doses comparable to common human smoking) extends lifespan of test animals (by about ~20% in hamster experiments). What makes it even firmer scientifically, is that it was established by the strongly adversarial researchers -- the scientists seeking and doing their best to prove exactly the opposite. There is nothing you can establish in science more strongly than under such adversarial conditions. And you haven't offered anything that refutes this fact (the flawed, meandering logic won't do either). As to other related issues (which are irrelevant for the validty of the facts above), I would disagree that CR is the sole or even the most important mechanism behind the established life-extending effects of tobacco smoking. For example: (1) -- Raising the levels of SOD was hailed few years ago as new "elixir of eternal life". Smoking nearly doubles SOD (in animal experiments and human observations). Upregulation of catalase and glutathione would have similar protective and antiaging/lifextending effects. (2) -- Then the selective MAO B inhibition by selegiline is often hailed as a fountain of youth. Tobacco smoke does that too (40% inhibition). It additionally stimulates release of dopamine & norepinephrine. (3) -- Anti-inflammatory effects of tobacco smoke are numerous (pdf), and only some of them are due to nicotine (e.g. check the recent rheumatoid arthritis paper using mice experiments designed to differentiate between nicotine and additional tobacco smoke specific anti-inflammatory effects). There is a vast amount of research of this topic, probably because of its uniquely wide spectrum of mechanisms through which it accomplishes these effects. For example, in addition to the long known corticosteroid anti-inflammatory mechanism, it was recently discovered that it also operates through the CNS vagus mechanism. Any of the above effects, along with dozens more (you can find them through the links I posted earlier in this thread), could explain some aspects of the life-extending effects of tobacco smoke (only some are nicotine specific). Over the last several years, I have folowed this forum and sci.life-extension newsgorup, along with any medical news on longevity, and any time some new biochemical mechanism was brought up as being life-extending or rejuvenating or fountain of youth..., I checked the literature on the effects (tobacco smoke OR nicotine) on that mechanism and 218

virtually every time (with occasional rare ambiguity) this ancient miracle medicine would pull that same biochemical lever in the "good" direction indicated in the 'fountain of youth' du jour announcement. Coincidentally, practically all the tobbaco research backing up these findings was done by none other than the same big pharma which publicly badmouths tobacco, finances practically all of the antismoking "science" and propaganda (creating & sponsoring antismoking "grass roots" grups) and buys antismoking laws and regulations. Yet, behind the scenes the same tobacco-hating pharma is quietly and very intensly researching and uncovering in great depths countless therapeutic and protectivel effects of tobacco smoke (obviously trying to figure out how to replicate those effects with some patented substances of their own). This seemingly peculiar pattern of research makes it pretty obvious why is the big pharma investing billions in antismoking. It is clearly not all about selling nicotine gums and patches, or other cessation products (although sales of these aren't small change either). Yes, you can probably replace some, perhaps many, of the known beneficial effects of tobacco smoke with different supplements or pharamaceuticals. Or you can just use one supplement, the 'most precious gift of gods', at the fraction of the cost (it is still so, despite astronomical taxes on tobacco, bought by pharma, can you guess why?) and get all the known effects, plus likely even many more still undiscovered, all working in a perfectly tuned harmonious synergy that only a product finely tuned to perfection over eight thousand years by couple billions of lifelong test subjects. There is simply no other single substance/supplement/drug of any kind that does all that and that does it so well. That's what the hard science shows. As to "safer" methods -- animal experiments unambiguously refute suggestion that tobacco smoke is "unsafe" (at the levels of common human smoking, or even at higher e.g. in mice & rat experiments discussed earlier, the exposure levels were right at the edge of asphyxiation, which is well beyond the human smoking exposure levels). Those smoking hamsters, whether exposed to hazardous industrial toxins or just to tobacco smoke alone, outlived their non-smoking cohorts. Rats and mice too. Smoking dogs tolerated radon exposure much better than non-smoking dogs (e.g. 5% radon induced cancers in smoking dogs vs 37% in non-smoking dogs).... And all that under the most severe adversarial research conditions. (Just imagine the magnitude of the beneficial effects had the smokers organizations or tobacco industry contracted similar experiments, optimizing the exposure methods for the most beneficial effects rather than for the most harmful ones.) Therefore, the causal role of tobacco smoke in those beneficial life-extending effects is as firmly established as hard science can establish anything. The "hazard' you keep looping back to, is at a completely another level of scienctific certainty -- the statistical associations on non-randomized samples. Such associations are equally consistent with protective/therapeutic role of tobacco as

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they are with the harmful role. Since the therapeutic/protective role is already established firmly and unambiguously within the hard science (animal experiments), the only coherent theory that is consistent with both sets of facts is that those non-randomized associations observed in human epidemiology are the result of therapeutic/protective role of tobacco smoke (i.e. smokers are self-medicating with tobacco smoke, each one for their own specific subset of the well established beneficial effects). In contrast, assuming the "harmful role" from those associations requires pretty incoherent and torturous position according to which tobacco smoke is simultaneously protective therapeutic for animals and harmful to humans.

The oxidized cells of a tobacco leaf again. This boogy man of antismoking propaganda in grade school health classes, was addressed in earlier post (2nd half). Recall also that much of what you ingest as food gets eventually oxidized inside your cells/mitochondria, by the time it is fully metabolized and used up for energy production, while with inhaling of oxidized tobacco leaf cells (smoking) the most violent and damaging part of oxidative reactions is not only taking place outside of your cells, but outside of your body altogether. Of course. All 'class A carcinogens' easily cause cancers on lab animals (much easier than in humans e.g. "animal carcinogen" term) and shorten their lives. All except 'tobacco smoke' which not only fails to cause cancers in lab animals (strangely, though, it can do it only in humans), but it extends the lifespan of lab animals by 20%, while keeping them thinner and sharper into the old age. And all that despite over six decades of vast research efforts to demonstrate this very carcinogenicity. With tobacco everything is somehow the opposite and upside down from everything else in science. Logic included. As a smoker friend observed regarding some FDA pronouncement about smoking, with tobacco more is always worse, but less is always equally dangerous.

The self-medication does not mean solely a therapy for the existent disease (e.g. RA) but also protective or mitigating effects on the underlying causes of the final disease. This RA examples shows exactly how this happens -- here you show a nonrandomized (self-selected smokers/nonsmokers/exsmokers) study with an RR ~2 for smokers vs nonsmokers for RA. Yet the RA experiment (on mouse model of RA) shows both protective and therapeutic effects of nicotine and even stronger protective effect of tobacco smoke 220

against inflammatory auto-immune damage to cartliage. The underlying autoimmune inflammatory processes which eventually result in clinical RA, start at biochemical level years before the onset of the clinical RA. Tobacco smoke slows down their progression from the start (nicotine does it too, but not as well). Therefore the selfselection process to smoker/non-smoker/ex-smoker does have perfectly viable biochemical self-medication levers to operate on long before and right up to the onset of the clinical RA. As to how these women would know to self-medicate i.e. that smoking helps protect them against RA they are susceptible to, I would suggest that a very low grade inflammatory processes produce minor weakness, exhaustion, sleepiness... due to parasympathetic overactivation (just like a mild cold or mild CFS), which tobacco smoke would easily mitigate (by driving up the sympathetic system as well as by suppressing the low grade inflammation itself and its perceptible slightly uncomfortable effects). So they would easily perceive the difference. Of course, the study authors couldn't care less about it, to even mention possible self-medication confounding (based on the well established anti-inflammatory effects of tobacco smoke), let alone quantifying it and taking into account for their final results. Of course, once you take into account the self-medication mechanism the apparent paradox between epidemiological and experimental facts, which the standard antismoking epidemiology ingnores althogether, vanishes. In other words, selfmedication mechanism allows for a coherent explanation of all the known facts and not just of a cherry picked subset of known facts that fit some other agenda (to help inflame anstismoking hysteria and ultimately boost pharma sales of RA drugs in this example), while ignoring others that contradict it (such as contradiction with the effects of tobacco smoke in animal models of RA, or anti-inflammatory effects of TS).

Self-medication with tobacco is quite an active research subject. Numerous therapeutic and protective effects of tobacco smoke make it an ideal substance for study of that phenomenon. Historically, during the early spread of tobacco into Europe and then around the world, people everywhere would instinctively start using it for self-medication and that was often its main attraction and force that helped its popularity and acceptance. In much of the undeveloped world, self-medication is still the dominant form of treatment for most health problems, and until the twentieth century and rise of pharmaceutical industry, it was the same in the western world as well. Placebo and nocebo (negative placebo, witch doctor effect) are also important enough, being surprisingly effective (e.g. a witch doctor effect is powerful enough to kill), forms of self-medications that any drug trial has to take them into account. Self-medication isn't restricted to humans either -- animals are as good at it if not

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better than we are. But even that isn't the final boundary of the phenomenon -- each one of your cells self-medicates its entire life, repairing damages and treating variety of health problems, malfunctions and challenges virtually every moment of its existence. With that level of phenomenon taken fully into account, the self-medication is still the dominant and the most effective form of treatment and healing for each one of us here in the developed world, mighty pharma and the rest of the 'sickness industry' notwithstanding. They did find quite a few interesting therapeutic and protective effects, although the pharma was much better at it and nearly everything I cite is from pharma funded research (with some from government institutions) . Here is an article on the subject of tobacco industry research covering some of their findings and a pharmaceutical company Targacept spawned by RJR researchers to tap into some of this potential. You can find much more about tobacco industry's research of beneficial health effects of tobacco smoke at TobaccoDocuments.org if you are interested. Regarding the self-medication aspect of tobacco use, smokers who quit on their own because they don't feel they really need it any more or that it doesn't do all that much for them considering all the hassle and expense in the current antismoking hysteria (as opposed to quitting in randomized intervention trial, where they quit based on random selection, or being forced to quit e.g. by ending in prison, like the 'first immortal' fellow who promptly got lung cancer there) are analogous to patients who complete using prescription meds or those who leave hospital -- those that completed the treatment are certainly going to be better off than those still being treated. Similarly, the longer someone is using medicines or staying in hospitals, the worse off they will be, just like the association with smoking. Of course, for any individual, the potent life-extending and rejuvenating effects of tobacco smoke, firmly established in animal experiments, imply that smoking will extend lifespan while keeping them thinner and sharper into the old age than that same individual would have been without smoking. There is no paradox here: Note that the therapeutic/protective and harmfull/causative substances have identicall statistical associations with diseases on non-randomized samples. If you ignore the therapeutic/protective effects of some medicine (pharma drug or natural remedy), and applly the same leap correlation => causation as done regarding tobacco smoke by antismoking "science", you could as easily "conclude" that pharmaceuticals kill nearly everyone, since in any age, gender, socioeconomic status... group, the preceding use of pharmaceuticals is among the strongest risk factors positively correlated with the death of a subject (another one in the same category is being in hospital). Yet, simultaneously the use of pharmaceuticals as a rule does extend the lifespan and improves health. No paradox, of course.

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There are also many contradictory statistics out there for those who care to look. Native Americans have half the rate of lung cancer of white Americans even though they smoke much more. Very few Chinese women smoke and yet they have one of the highest lung cancer rates in the world. Lung cancer rates practically everywhere have been rising since about 1930 and in some cases (e.g. American women) have not peaked yet, despite the fact that smoking rates have gone steadily down. Japan, one of the worlds heaviest-smoking nations, is also in the top two or three in life expectancy. Japanese rates of lung cancer and heart disease have nevertheless been rising for the last 3 decades - at the same time as their smoking rate has gone down. Perhaps this is because their diet and lifestyle have become increasingly Americanised. I really dont know. All Im saying is that inconvenient facts should be investigated, rather than swept under the carpet. Antismokers maintain that smoking is responsible for about 90% of lung cancer deaths. But the Lung Cancer Alliance, a US lobby group, maintains that a half of lung cancer victims have never smoked. THE SMOKING-RELATED DISEASE This is one of the antismokers cleverest inventions. To say that a disease is smoking-related is not the same as saying that it is directly caused by smoking, or that there is any actual proof of anything. It means simply that someone has decided that smoking may be a factor in that disease. Over the last couple of decades, more and more diseases have been added to the list, often with very little evidence. Heart disease was one of the first, even though it has something like 300 risk factors, and some major studies (for instance, that of the citizens of Framingham, Massachusetts, which has been going on since 1948) have shown not only that the link with smoking is weak, but that moderate smokers have less heart disease than nonsmokers. Recent media scares have claimed that smoking may cause impotence or infertility. But people smoked more during the two world wars than at any other time in history, and what did we have in the 1950s? A baby boom! Other scares have found their way onto cigarette packets.

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Smoking causes ageing of the skin says one. Well, maybe, for some people, but there are clearly more important factors. Like the sun. And ageing. THE DOSE MAKES THE POISON This is an old, but often ignored, scientific axiom. What it means is that there are safe and unsafe levels of everything. A little bit of arsenic is just fine. A significantly large amount of orange juice could kill you. But antismokers are now trying to sell us a scientific absurdity: that smoking is dangerous at any level. 1.USWM smokers have a lifetime relative risk of dying from lung cancer of only 8 (not the 20 or more that is based on an annual death rate and therefore virtually useless).

2. No study has ever shown that casual cigar smoker (<5 cigars/wk, not inhaled) has an increased incidence of lung cancer.

3.Lung cancer is not in even in the top 5 causes of death, it is only #9.**

4.All cancers combined account for only 13% of all annual deaths and lung cancer only 2%.**

5. Occasional cigarette use (<1 pk/wk) has never been shown to be a risk factor in lung cancer.

6.Certain types of pollution are more dangerous than second hand smoke.3

7. Second hand smoke has never been shown to be a causative factor in lung cancer.

8.A WHO study did not show that passive (second hand) smoke statistically increased the risk of getting lung cancer.

9.No study has shown that second hand smoke exposure during childhood increases their risk of getting lung cancer.

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10.In one study they couldn't even cause lung cancer in mice after exposing them to cigarette smoke for a long time.23

11. If everyone in the world stopped smoking 50 years ago, the premature death rate would still be well over 80% of what it is today.1 (But I thought that smoking was the major cause of preventable death...hmmm.) I would be very cautious about the supposed high readings of mercury in tobacco smoke. Russ, you should check the smoke from other materials, wood, leaves,... since the meter may be falsely responding to the ions in the smoke. Also the smoke from a stand alone cigarette vs the exhaled smoke should be tested i.e. the smoke may act as chelator of mercury from the lungs of a toxic person, hence the exhaled smoke would contain more Hg for the same reason that urine contains more Hg after DMSA or DMPS provocation. The extremely high readings, though, are most indicative of the false reading. Namely, all references from anti-smoking research on the composition of tobacco smoke give about 1-5 nanograms of Hg per cigarette (e.g. see this paper, p. 18), which is 5/1000 micrograms per cigarette i.e. you would need to smoke a carton of cigarettes for 1 microgram of mecury! For your 100 micrograms per m3 reading, you would need to burn 100 cartons into 1m3. Note also that these 5 ng is the outer end of the measurements, the best shot of the science strongly biased against tobacco smoke (they make big bucks out of peddling its alleged dangers, see below). If you are a mercury toxic smoker, you may be harming yourself by quitting (or by not taking up smoking, as you will see below). Tobacco smokers have about 80% more glutathione in active form than non-smokers (smoking is a kind of exercise of immune system). One of beneficial effects of this excess glutathione is about tenfold reduction in rates of Alzheimer's disease of smokers vs non-smokers among ApoE4 allele carriers (these are people with poor detox of mercury from brain and particularly susceptible to Alzheimer's; ApoE4 frequency increases from south to north Europe, hence Nordic countries are most affected by amalgams among Europeans). Tobacco smoke is also highly therapeutic for Parkinson's disease and schizophrenia (possibly due to increase in dopamine and MAO inhibition). Note that Alzheimer's, Parkinson's and schizophrenia share great deal of symptoms with mercury toxicity of the brain and smoking is significantly therapeutic for all three diseases. So be very careful before jumping into the hands of the Big Pharma, with their nicotine replacements and antidepressants (which don't help at all for your own

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glutathione stimulation by tobacco smoke). Odds are you will cause yourself much more harm than good. Tobacco is an ancient medicinal plant and the present anti-smoking propaganda is driven chiefly by the profits of the Big Pharma (also Big Med & "health" bureaucracies), which created and funded almost all of the anti-smoking groups and funds much of the anti-smoking "science" directly (and the rest indirectly via the "health" bureaucracies). The profits of the Big Anti-tobacco come not just from the obscene taxes on cigarettes (imagine suddenly having to pay $100,000 for a car you can now buy for $25,000), but also from selling nicotine replacements, antidepressants (tobacco smoke is therapeutic for anxiety & depression), allergies and asthma (smoking used to be advised by medical textbooks & doctors for these ailments until 1950s), Parkinson's, Alzheimer's, schizophrenia... The ancient medicinal plant, tobacco, is a competitor for the Big Pharma. Many tens of billions are extorted from smokers every year under the cover of the anti-smoking hysteria they whipped up. Few crumbs from the loot go into buying the best anti-smoking "science", "health" bureacrats, politicians, anti-smoking laws and regulations the money can buy. To get a bit more balanced picture on the subject of tobacco smoking (and avoid harming yourself by falling for the media brainwashing), check the following references: 1. The Scientific Scandal of Antismoking by J. R. Johnstone & P. D. Finch 2. "In Defense of Smokers" by L. A. Colby 3. "Smoking is good for you" by Dr. W. T. Whitby 4. Therapeutic Effects of Smoking (misc. scientific references; also article "World's Oldest -- All Smokers) 5. LF thread on WHO study showing that secondary smoke is protective against lung cancer (lots of discussion and other links) 6. SE thread Tobacco Smoking is Protective Against Lung Cancer (more links & references cited in the discussion; see also on immune stimulus & correlations with diseases) Now, of course, additive and pesticide laden supermarket cigarettes, like much of supermarket foods, are junk and likely harmful. Filters are also harmful since they shed non-biodegradable fibers. On the other hand, additive free, organically grown pure tobacco leaf, such as American Spirit, rolled in thin paper (on how to "roll your own" and "stuff your own") 226

or used in a pipe, is the way it was meant to be done, the way our grandfathers smoked it. Tobacco was cultivated for thousands of years as the sacred medicinal plant and real science (unlike the anti-tobacco junk science) is only beginning to uncover some of its magic. Nicotine is just one tiny bit of its medicinal power (that's why nicotine patches or antidepressants don't work for quitting; e.g. they don't stimulate glutathione or act as MAO inhibitors). For example, Coenzyme Q10, the miracle supplement, is actually tobacco leaf, it was discovered there and the best brands are still manufactured from tobacco leaf, even though it can be now synthesized artificially (see Whitby's book #3, also #6). Note also that the anti-smoking propaganda is peddled largely by the same actors (FDA, CDC, EPA, AMA, NCI) and backed up by the same kind of pseudo-science (and money that buys it) that peddle the theory that "mouthful of mercury is safe and effective" and "thimerosal injected into babies causes them no harm". The same guys, the same alphabet soup agencies, the same money and and the same bought "science". So, read the materials for yourself, all sides of the story, but before anything else, listen and trust signals from your own body. A single cell in your little toe knows more about biochemistry, genetics and detox at the molecular level than all the science and technology in the world put together. If you were to take all of the world's medical, biochemical and pharmaceutical science & technology in one gigantic team, give them all the money and resources they want and ask them to create one live cell from scratch, they wouldn't even know how to create one organelle, a tiny organ of cell, let alone a whole live cell (or to say nothing about a vastly more complex human organism). Yet, the little "dumb" cells, which are actually unamaginably complex biochemical networks (i.e. distributed, self-programming natural computers of the same kind as human brain), create new live cells from scratch every day all day long, without breaking a sweat, as it were. Tobacco Smoke May Contain a Psychoactive Ingredient Other Than Nicotine

But for as far as what I have researched, SMOKING ALONE does not produce those gross and commonly fatal effects of smoking. Smoking alone cannot cause Buergers disease, you need to be 30 years old and above and a male to have it. Smoking alone cannot cause Raynauds disease, you need to be 40 years old and above and female to have it. Smoking alone cannot cause Deep Vein Thrombosis, you still need to be obese, hyperlipidemic, have been using oral contraceptives for a long time, have a history of diabetes and myocardial infarction. You cant have Pneumonia by smoking alone, you also need to have inhaled air pollution, you need to be immunocompromised, you need to have accidentally aspirated food, you need to be over fatigued, you cannot have Peptic ulcer disease just by smoking, because it needs to be on your blood lines, you need to be alcoholic, you need to have irregular diet, you need to have drank caffeine instead of eating foods, a microbial invasion should have caused peptic ulcer disease and many more.

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http://www.ljdiaz.com/18-benefits-of-cigarette-smoking/ Here are 18 benefits of cigarette smoking. 1. Smoking improves human information processing Higher nicotine cigarettes produce greater improvements [in information processing] than low-nicotine cigarettes Nicotine can reverse the detrimental effects of scopolamine on performance Smoking effects are accompanied by increases in EEG arousal and decreases in the latency of the late positive component of the evoked potential Data from: 0574. University of Reading, Department of Psychology (England). Warburton., D.M.; Wesnes, K. The Effects of Cigarette Smoking on Human Information Processing and the role of Nicotine in These Effects 2. Smoking improves motor performance Data from: 0530. London University, Institute of Psychiatry. OConnor, K.P Individual Differences in Psychophysiology of Smoking and Smoking Behaviour 3. Smokers in general are thinner than nonsmokers, even when they ingest more calories Data from: Numerous studies, but only two are listed below: 0885. Kentucky State University. Lee. C.J.: Panemangalore. M. Obesity Among Selected Elderly Females In Central Kentucky. FUNDING: USDA 0942. University of Louisville. Belknap Campus School of Medicine. Satmford, B.A.; Matter, S.; Fell, R.D., et al. Cigarette Smoking, Exercise and High Density Lipoprotein Cholesterol FUNDING: American Heart Association. 4. Smokers have less plaque, gingival inflammation and tooth mobility than nonsmokers Data from: Veterans Administration, Outpatient Clinic (Boston). Chauncey. H.H,; Kapur, K.K.; Feldmar, R S. The Longitudinal and Cross-Sectional Study of Oral Health: in Healthy Veterans (Dental Longitudinal Study) 5. Smokers have lower incidence of postoperative deep vein thrombosis than nonsmokers

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Data from: Guys Hospital Medical School (England). Jones, R.M. Influence of Smoking on Peri-Operative Morbidity. 6. Hypertension (high blood pressure) is less common among smokers Data from: 0146. Shanghai Institute of Cardiovascular Diseases. Chen, H.Z.; Pan, X.W.; Guo, G. et al. Relation Between Cigarette Smoking and Epidemiology of Hypertension. 7. Hypertension (high blood pressure) and postpartum hemorrhage are lower in smokers Data from: 0045. University of Tasmania (Australia). Correy, J.; Newman, N. Curran, J. An Assessment of Smoking in Pregnancy. 8. RBCs [red blood cells] from cigarette smokers contain more glutathione and catalase and protect lung endothelial cells against O2 [dioxide] metabolites better than RBCs from nonsmokers Data from: 0759. University of Colorado. Refine, J.E.; Berger, E.M.; Beehler, C.J. et al. Role of RBC Antioxidants in Cigarette Smoke Related Diseases. Jan 1980 continuing. 9. Smoking protects against Parkinsons disease Data from many studies. Among them: 1102. Carr, L.A.; Rowell, P.P. Attenuation of 1methyl-4-phenyl-1,2,3,6-tetrahydrophyridineinduced neurotoxicity by tobacco smoke. Published in Neuro-pharmacology 29(3):311-4, Mar 1990. 1190. Janson, A.M.; Fuxe, K.; Agnati, L.F. Jansson, A. et al. Protective effects of chronic nicotine treatment on lesioned nigrostriatal dopamine neurons in the male rat. Pub. in Progress in Brain Research 79:257-65, 1989. 4014. Decina, P.; Caracci, G.; Sandik, R.; Berman, W. et al. Cigarette smoking and neurolepticinduced parkinsonism. In Biological Psychiatry 28(6):502-8, Sept. 15, 1990 10. There is a low prevalence of smoking in ulcerative colitis? And that the disease often starts or relapses after stopping smoking Data from: 4101. Prytz, H.; Benoni, C.; Tagesson, C. Does smoking tighten the gut? In Scandinavian Journal of Gastroenterology 24(9):1084-8, Nov. 1989. 11. Nonsmokers and especially ex-smokers of cigarettes have greater risk of UC [ulcerative colitis]

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Data from: 4134. Lorusso, D.; Leo, S.; Miscianga, G.; Guerra, V. Cigarette smoking and ulcerative colitis. A case control Study. Hepato-Gastroenterology 36(4): 202-4, Aug. 1989. 12. Hypertension and postpartum hemorrhage are lower in smokers Data from: 0045. University of Tasmania (Australia). Correy, J.; Newman, N. Curran, J. An Assessment of Smoking in Pregnancy. 13. Smoking has a protective effect on immunological abnormalities in asbestos workers Data from: 0429. Institute of Immunology and Experimental Therapy (Poland). Lange, A. Effect of Smoking on Immunological Abnormalities in Asbestos Workers. 14. The WHO, in order to prove the dangers of ETS, financed the second largest study in the world on secondhand smoke. But the study backfired and showed not only that there was no statistical risk of disease on passive smoking, but even a protective effect for those who are exposed to it. Not surprisingly, it is said that the WHO tried to hide the study from the media. For the In-depth info Click HERE 15. That in an Australian study, 91.8% of those who never smoked reported a long term illenss, while those who smoked reported 89.0% When age was taken into consideration, more people who had never smoked than those who did smoke reported one or more long-term illnesses. When the number of years during which a person had been a smoker were taken into account, it was the ex-smokers who fared worse when it came to long term illnesses. Data From: Australian Bureau of Statistics January 1994 report entitled 1980-90 National Health Survey: Lifestyle and Health Australia. 16. That an Australian study sampling, among other things, individuals over 45 years of age, found that 6.0% of smokers suffered from heart disease, versus 6.7% never-smokers and 11.4% ex-smokers Data From: Australian Bureau of Statistics January 1994 report entitled 1980-90 National Health Survey: Lifestyle and Health Australia.

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17. Australian study sampling, among other things, individuals over 45 years of age, found that 11.3% of smokers suffered from hypertension, versus 27.0% ex-smokers and 29.0% never-smokers Data From: Australian Bureau of Statistics January 1994 report entitled 1980-90 National Health Survey: Lifestyle and Health Australia. 18. Australian study sampling, among other things, individuals over 45 years of age, found that 38.9% of smokers were overweight, versus 49.5% ex-smokers and 44.1% never-smokers Data From: Australian Bureau of Statistics January 1994 report entitled 1980-90 National Health Survey: Lifestyle and Health Australia. Now those were the 18 benefits of smoking, well I do not advocate smoking, its just that I felt the need to blurt out the things that people disregard. There is always a need to be open minded. Always know the two faces of the mirror. I even had the inspiration to write this article because of my favorite show House MD. Here is a clip of House, prescribing his patient with cigarettes. (From: House MD Season 1 Episode 5 Damned If You Do) If you have been smoking, all I can say is continue it, because if you do stop, you will just have to tread on the torturous feeling of withdrawal process, and your body might get startled by the process, making your body system vulnerable. If you havent started yet, then better think twice. Might as well never to try it, because it is where it all begins.

Facts on Smoking You are Not Told, or Why George Burns Lived to 100!

by Robert R. Barney

We are running a series of articles in our YOUR HEALTH TODAY section which I think will absolutely blow most of our readers today! Over the past 40 years, we have been overwhelmed with the evils of smoking. The message has basically been, SMOKE ONE CIGARETTE and YOU WILL DIE A DAY YOUNGER! Have you ever thought of any benefits of smoking? Honestly, could there be any benefits? Well I did my own investigation and guess what? Smoking in moderation may actually be GOOD for you! I know that smacks in the face of everything science and
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government has been telling us, but sometimes governments LIE! Here are just a few examples of FACTS I bet you don't know: -- Q10 is made from Tobacco -- Smoking Reduces both Parkinson Disease AND Alzheimers! -- Smoking increases certain hormones and can act similar to Viagra! -- A Reduced risk in women who smoke to Colon Cancer -- Moderate Cigar or Non-Filtered Cigarettes may actually help you live Longer I realize that this sounds like I have gone bonkers, but friends, every statement I have made has proven science behind it and I document it below! Drinking wine can kill you. If you drink two to thee bottles of wine a day, you will probably be at a much greater risk of developing a host of diseases related to alcoholism, yet we know that those who drink a glass a day statistically live longer than tea-tottlers. The same seems to apply to smoking. Very low doses of smoking (a Cigar or two once a week or two or three NON-FILTERED cigarettes a day) actually helps our bodies. It has been documented for years that Japanese men out smoke American men yet have lower incidences of lung cancer! ( http://cebp.aacrjournals.org/cgi/content/full/10/11/1193 ) One looks at people like George Burns who lived to be 100, smoking a cigar his entire life. Would he have lived to 150 if he didn't smoke? Well, the evidence I am presenting suggests that he lived that long BECAUSE he smoked. If you notice,whenever I mentioned cigarette smoking, I always wrote of NON-FILTERED cigarettes. Again, big businees like the tobacco companies and our government know that the filters on these cigarettes are much more harmful than the tobacco smoke! More than 90% of the cigarettes sold worldwide have a filter. Nearly all filters consist of a rod of numerous ( > 12 000) plastic-like cellulose acetate fibres. During high speed cigarette manufacturing procedures, fragments of cellulose acetate that form the mouthpiece of a filter rod become separated from the filter at the end face. The cut surface of the filter of nearly all cigarettes has these fragments.
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In smoking a cigarette in the usual manner, some of these fragments are released during puffing. In addition to the cellulose acetate fragments, carbon particles are released also from some cigarette brands that have a charcoal filter. Cigarettes with filters that release cellulose acetate or carbon particles during normal smoking conditions are defective. Philip Morris, Inc has known of this filter defect for more than 40 years. results of investigations substantiating defective filters have been concealed from the smoker and the health community. The tobacco industry has been negligent in not performing toxicological examinations and other studies to assess the human health risks associated with regularly ingesting and inhaling non-degradable, toxin coated cellulose acetate fragments and carbon microparticles and possibly other components that are released from conventional cigarette filters during normal smoking. The rationale for harm assessment is supported by the results of consumer surveys that have shown that the ingestion or inhalation of cigarette filter fibres are a health concern to nearly all smokers. (From Cigarettes with defective filters marketed for 40 years: what Philip Morris never told smokers (Tobacco Control 2002;11:i51-i61):) Check out a host of stories we have on this subject on http://journals.aol.com/plaintruthtoday/your-health-today Notes and References 1) The miracle supplement (for skin, heart, brain rejuvenation) Coenzyme Q10 is extracted from tobacco leaf! http://www.ritecare.com/prodsheets/and-503000.html Dr. Ricjard A. Kunin extols the benefits of Coenzyme Q10. He also says: The energy of oxidation in cells depends on CoQ in partnership with niacinamide (vitamin B3), riboflavin (vitamin B2), and minerals such as iron and copper to effect the movement of electrons and hydrogen protons in the power plant of cell, the mitochondrion. Incidentally, tobacco leaf is the champion source, containing 184 mg in a quarter pound. Note that the doctor follows with the disclaimer, "In fact, the Japanese companies make their CoQ from tobacco, however it is only released by means of bacterial

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fermentation not by smoking." The fact remains that CoQ 10 is a natural miracle for the human body and it's chief source is tobacco! 2) Smoking Reduces Parkinson's Disease: Studies world-wide has notice that smokers have a significally lower incidence of getting the disease, yet this is never mentioned in any of the anti-smoking campaigns. Neurology. 1999 Sep 22;53(5):1158. Smoking and Parkinson's disease: a dose-response relationship Gorell JM, Rybicki BA, Johnson CC, Peterson EL Department of Neurology, Henry Ford Health System, National Institute of Environmental Health Sciences Center in Molecular and Cellular Toxicology with Human Applications, Wayne State University, Detroit, MI, USA. Also see Smoking lowers Parkinson's disease risk from Reuters (Mar 20, 2007). From Temporal relationship between cigarette smoking and risk of Parkinson disease (NEUROLOGY 2007;68:764-768): 3) The by-product of smoking (Nitric Oxide) helps in opening our arteries! Nitric oxide stimulates peripheral circulation (this is the mechanism behind Viagra effect).Low concentration carbon monoxide (as found in tobacco smoke) protects cells in harsh conditions, such as low oxygen and general cell death 4) Smoking actually increases GROWTH Hormones! Like testosterone and DHEA. source: Geriatrics & Gerontology International (Volume 6 Issue 1 Page 4952, March 2006)Relation of age and smoking to serum levels of total testosterone and dehydroepiandrosterone sulfate in aged men in , which found these results, "Serum T did not decrease with age, and was significantly higher in smokers than for non-smokers. Serum DHEA decreased with age more sharply in non-smokers than for smokers."

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5) Smoking reduces IGF-1 (insulin-like growth factor 1)--at least in males for sure. In animal experiments, lowered insuline growth factor IGF-1 change extends lifespan. 6) Reduced Incidence of Colorectal Cancer--especially in women. Cigarette Smoking and the Risk of Colorectal Cancer in Women (Journal of the National Cancer Institute, Vol. 80, No. 16, 1329-1333, October 19, 1988) states, "Colorectal cancer incidence rates for smokers, nonsmokers living with smokers (i.e., passive smokers), and non-smokers in smoke-free households were compared in a 12-year prospective study of 25, 369 women who participated in a private census conducted in Washington County, MD, in 1963. Women who smoked had a decreased relative risk of colorectal cancer compared with the risk for nonsmokers (age-adjusted relative risk, 0.76; 95% confidence interval, 0.521.10). The risk for passive smokers was similar to that for smokers. The relative risks were significantly reduced for older women; relative risks were 0.42 for smokers and 0.66 for passive smokers over age 65. The data suggest that older women who smoke have a lower risk of colorectal cancer than non-smokers. The effect may be mediated by an antiestrogenic effect of smoking." 7) People who smoke fare better than nonsmokers when exposed to occupational hazards. From Lack of combined effects of exposure and smoking on respiratory health in aluminium potroom workersBritish Medical Journal, Occupational and Environmental Medicine (Vol 56, 468-472, 1999): 8) Cigarette smoking may be an independent protective factor for developing schizophrenia. These results are consistent with animal models showing both neuroprotective effects of nicotine and differential release of prefrontal dopamine in response to nicotine. From Cancer in schizophrenia: is the risk higher or lower? in Schizophrenia Research (Volume 73, Issue 2, Pages 333-341) at http://www.schresjournal.com/article/PIIS0920996404002130/abstract :
The incidence of cancer in patients diagnosed with schizophrenia was compared with the incidence
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in the general population. The results showed that the cancer standardized incidence ratios (SIRs) for all sites were significantly lower among men and women with schizophrenia, 0.86 [95% confidence interval (CI) 0.800.93] and 0.91 (95% CI 0.850.97), respectively. This reduced overall risk was clearest for those born in EuropeAmerica, both men (SIR 0.85, 95% CI 0.74 0.97) and women (SIR 0.86, 95% CI 0.770.94). Appetite Suppressant -- no citations. Common sense. Most stimulants are appetite suppressants, and nicotine does seem to be a stimulant.

9) Tobacco: the definitive link in healthy aging by Daniel John Richard Date. Reduces incidence of Alzheimer's, among other degenerative diseases. "A statistically significant inverse association between smoking and Alzheimer's disease was observed at all levels of analysis, with a trend towards decreasing risk with increasing consumption" (International Journal of Epidemiology, 1991) "The risk of Alzheimer's disease decreased with increasing daily number of cigarettes smoked before onset of disease. . . . In six families in which the disease was apparently inherited . . . the mean age of onset was 4.17 years later in smoking patients than in non-smoking patients from the same family" (British Medical Journal, June 22, 1991) "Although more data are needed . . . [an analysis of 19 studies suggests] nicotine protects against AD" (Neuroepidemiology, 1994) Nicotine injections significantly improved certain types of mental functioning in Alzheimer's patients (Psychopharmacology, 1992). One theory: nicotine improves the responsiveness of Alzheimer's patients to acetylcholine, an important brain chemical. When chronically taken, nicotine may result in: (1) positive reinforcement [it makes you feel good], (2) negative reinforcement [it may keep you from feeling bad], (3) reduction of body weight [by reducing appetite and increasing metabolic rate], (4) enhancement of performance, and protection against: (5) Parkinson's disease, (6) Tourette's disease [tics], (7) Alzheimer's disease, (8) ulcerative colitis and (9) sleep apnea. The reliability of these effects varies greatly but justifies the search for more therapeutic
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applications for this interesting compound." ("Beneficial Effects of Nicotine," Jarvik, British Journal of Addiction, 1991) See more on smoking and reduced incidence of Alzheimer's disease. In this compilation of 19 studies, 15 found a reduce risk in smokers, and none found an increased risk. Also noted is the fact that acute administration of nicotine improves attention and information processing in AD patients, which adds further plausibility to the hypothesis. Smoking is Good for You: Absence, Presence, and the Ecumenical Appeal of Indian Islamic Healing Centers In Shop owner says smoking 'doesn't cause disease' a shop owner "tells his customers that smoking calms the nerves and soothes the mind." This is in sync with what Albert Einstein stated upon becoming a lifetime member of the Montreal Pipe Smokers Club at the age of 71, "I believe that pipe smoking contributes to a somewhat calm and objective judgment in all human affairs."

Smoking Does Not Cause Lung Cancer! (According to

WHO/CDC Data)*
By: James P. Siepmann, MD

Yes, it is true, smoking does not cause lung cancer. It is only one of many risk factors for lung cancer. I initially was going to write an article on how the professional literature and publications misuse the language by saying "smoking causes lung cancer"1,2, but the more that I looked into how biased the literature, professional organizations, and the media are, I modified this article to one on trying to put the relationship between smoking and cancer into perspective. (No, I did not get paid off by the tobacco companies, or anything else like that.) When the tobacco executives testified to Congress that they did not believe that smoking caused cancer, their answers were probably truthful and I agree with that statement. Now, if they were asked if smoking increases the risk of getting lung cancer, then their answer based upon current evidence should
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have be "yes." But even so, the risk of a smoker getting lung cancer is much less than anyone would suspect. Based upon what the media and antitobacco organizations say, one would think that if you smoke, you get lung cancer (a 100% correlation) or at least expect a 50+% occurrence before someone uses the word "cause."

http://www.journaloftheoretics.com/Editorials/Vol1/e1-4.htm Nicotine's protective effect against neurodegenerative disorders

While the health risks of tobacco are well known, several studies have shown that people with a history of cigarette smoking have lower rates of neurodegenerative diseases like Parkinson's and Alzheimer's disease. However, the explanations for nicotine's neuroprotective effects continue to be debated. Now a team of neuroscientists at the University of South Florida College of Medicine presents new evidence of an anti-inflammatory mechanism in the brain by which nicotine may protect against nerve cell death. Their study was published today in the Journal of Neurochemistry. http://www.medicalnewstoday.com/articles/6544.php

J Cardiol. 2006 Oct;48(4):193-200. [Article in Japanese] Katayama T, Iwasaki Y, Yamamoto T, Yoshioka M, Nakashima H, Suzuki S, Honda Y, Yano K.
Department of Cardiology, Kouseikai Hospital, Nagasaki. snowman-kt@syd.odn.ne.jp

OBJECTIVES: Smokers with acute myocardial infarction have lower mortality rates than non-smokers despite increased risk for coronary artery disease. This study assessed the effects of smoking on complications and outcomes after acute myocardial infarction, and investigated the relationship between the clinical factors and the paradoxical effects of smoking in patients receiving primary coronary intervention. METHODS: Subjects were 367 consecutive patients with acute myocardial infarction who were admitted within 24 hr of onset and underwent successful coronary intervention, 165 (45%) of whom were smokers.

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RESULTS: The smoking group contained significantly more male patients, and the smoking group was significantly younger than the non-smoking group (p < 0.0001). The value of acute phase brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) were significantly lower (BNP: 250 +/- 366 vs 448 +/513pg/ml, p = 0.0002; ANP: 48 +/- 77 vs 74 +/- 82pg/ml, p = 0.005) in the smoking group. Peak creatine kinase time from onset was significantly earlier (12.9 +/- 9.3 vs 16.1 +/- 10.0 hr, p = 0.049) in the smoking group. Left ventricular ejection fraction in the chronic phase was significantly better in the smoking group (58 +/- 13% vs 52 +/- 14%, p = 0.03). The early ST-segment resolution rate was higher in the smoking group (81% vs 67%, p = 0.003), and there were significantly fewer patients with heart failure in the smoking group than in the non-smoking group (28% vs 41%, p = 0.01). The cardiac mortality rate during 6 months was significantly lower in the smoking group (3% vs 9%, p = 0.01). The beneficial effects of smoking on the prognosis were related with the differences in sex and age of the study group. CONCLUSIONS: The reason why smokers with acute myocardial infarction have lower mortality rates than nonsmokers, the "smoker's paradox", may be related to less damage to the microvascular function after primary coronary intervention, with lower BNP and better left ventricular ejection fraction. "Smoker's paradox" in patients with acute myocardial infarction receiving primary coronary intervention
PMID: 17066622 [PubMed - indexed for MEDLINE]

Abstract

Gingival recession in smokers and non-smokers with minimal periodontal disease

Hans-Peter Mller, School of Dental Medicine, University of Heidelberg, Sabine Stadermann, School of Dental Medicine, University of Heidelberg, German Armed Forces Central Hospital, Koblenz; and Achim Heinecke, Institute for Medical Informatics and Biostatistics, University of Mnster, Germany

Background/aims: Smoking is a major risk factor for destructive periodontal disease. There is limited information with regard to effects of smoking in subjects with minimal periodontal destruction. The aim of the present investigation was to assess the development of gingival recession in young adult smokers and non-smokers. Methods: 61 systemically healthy young adults, 19 to 30 years of age completed the final examination. 30 volunteers smoked at least 20 cigarettes per day, whereas 31 subjects were nonsmokers. Clinical periodontal conditions were assessed 4 within a time period of 6 months. Site-specific analyses considering the correlated structure of data were performed. Results: At the outset, 50% of subjects presented with gingival recession at 1 or more sites. There was no significant difference in the prevalence of gingival recession between non-smokers and smokers. Severe recession in excess of 2 mm affected about 23% non-smokers but only 7% smokers. Some further gingival recession developed during the 6-month observation period. In a multivariate logistic regression analysis, the risk for recession development appeared not to be influenced by smoking status after adjusting for periodontal probing depth, recession at baseline, tooth

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brushing frequency, gender, jaw, tooth type and site. Conclusions: Present data did not support the hypothesis that smokers are at an increased risk for the development of gingival recession.

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