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Alcohol Consumers

Alcohol abuse in men has been reported to cause impaired testosterone production, and atrophy of
testes, which can result in impotence, infertility and reduced male secondary sexual characteristics.
[11],[12],[13] However, dose-dependent effects of alcohol on human spermatogenesis are not well
established. [6] Of the 100 alcoholics included in our study, only 12 alcoholics showed normozoospermia
of which nine were mild alcoholics and three were moderate alcoholics, while none of the heavy
alcoholics showed normal semen parameters [Table 2]. Thus alcohol consumption did reduce the
number of normozoospermic cases amongst alcoholics. Of the three semen variables, teratozoospermia,
oligozoospermia and their combined presence (O+T), amongst alcoholics was double or more than that
found in controls, while asthenozoospermia was less frequent amongst alcoholics [Table 2]. This
indicated that sperm motility defects were less frequent amongst Alcoholics in comparison to defects of
sperm morphology and sperm count [Table 2]. A positive correlation with daily alcohol intake was
observed amongst alcoholics, with percentage of cases increasing from mild to heavy alcoholic sub-
groups for all the three variables, A, T and O [Table 2]. These observations were in agreement with few
other studies. [5],[6],[11],[12] The category (A+O+T) again showed higher number of cases (n=20)
amongst alcoholics than in controls (n = 11) [Table 2].

Overall, the number of cases with teratozoospermia (n = 59) amongst alcoholics was much higher than
of controls (n = 34), indicating that it was the most frequently encountered sperm defect amongst
alcoholics [Table 4]. Teratozoospermia was observed in 72% heavy alcoholics and 63% moderate
alcoholics. Oligozoospermia, also showed much higher number of cases amongst alcoholics (n = 51) than
controls, indicated progressive damage to testes in direct relation to increasing daily alcohol intake,
(64% in heavy alcoholics) [Table 4]. Both teratozoospermia and oligozoospermia were statistically
significant amongst alcoholics [Table 4].

Alcohol has been shown to have a deleterious effect at all levels of male reproductive system. Alcohol
interferes in the feedback mechanisms of hypothalamus-pituitary-gonadal (HPG) axis resulting in
impairment of production and secretion of adequate quantity or potency, of leutinizing hormone (LH)
and follicle-stimulating hormone (FSH) leading to deterioration of Sertoli cells More Details. [15] Alcohol
affects the leydig cells and reduces blood levels of testosterone, by reducing its production and
increasing its metabolic clearance. [13] Alcohol also influences the sertoli cell functions, probably by
producing damage to some of the proteins required for sperm cell production that the Sertoli cells
provide. [14] Thus, alcohol induced reduction in levels of testosterone, LH and FSH not only hampers
their normal morphological development and maturation of spermatozoa (producing significant
teratozoospermia), it also slows down the sperm production by testicular germ cells (oligozoospermia),
especially in heavy alcoholics. [15]
Other studies have reported partial to complete spermatogenic arrest amongst moderate to heavy
alcohol consumers, even leading to "sertoli cell only" syndrome in advanced cases, indicating severe
testicular damage. [6],[16] Progressive damage to testes and reduction of sex hormones leads to loss of
secondary sexual characteristics and development of impotence and infertility. [15]

In our study, asthenozoospermia, by comparison, did not show a very strong correlation amongst mild
alcoholics, but appeared in moderate and heavy alcoholics, probably as an additive feature linked to
severe oligo-teratozoospermia.

Cigarette Smokers Top

Smoking is a lifestyle hazard for both active and passive smokers. Although much is known now about
the carcinogens in tobacco cigarette smoke and their resultant effect on organs like lungs and urinary
bladder, their effects on fertility status have been less documented.

In our study, only six smokers qualified as being normozoospermic [Table 3]. This underscored the fact
that smoking certainly had a definite influence on the semen quality, as concluded in several other
studies. [17],[18],[19],[20] Asthenozoospermia was the most dominant semen variable contributing to
the semen quality of smokers (n is equal to four) as well as Controls (n = 37), individually as well as in
combination with other variables like teratozoospermia (A+T) and oligozoospermia, (A+O) and (A+O+T)
[Table 3] and [Table 4]. So asthenozoospermia appeared to be a 'premier' factor contributing to the
infertile status of a male. [20] However viable and morphologically normal spermatozoa may be, if they
are not actively motile, showing linear forward motion in the seminal fluid, they will fail to fulfill their
prime function of traversing the complex route through female genital tract, to seek and fertilize an
ovum. Tragically, however, while assessing the semen quality of an individual, emphasis has always been
laid on the sperm count and sperm morphology. [3],[4]

Isolated asthenozoospermia was seen in 39% light smokers and 19.2% moderate smokers while no such
case was detected amongst heavy smokers [Table 2]. Since in light smokers, even this 'mild' smoking
could produce reduction in the sperm motility in 39% cases, it appeared that there is no "safe" quantity
of cigarette smoking that may not affect the semen quality. In 22% light smokers, teratozoospermia was
observed in addition to asthenozoospermia. Thus, teratozoospermia appeared to be the next anomaly
to develop in the spermatozoa of light smokers, after asthenozoospermia, further reducing the sperm
quality [Table 2]. By comparison, fewer cases showed contribution of oligozoospermia amongst
smokers; still their number was higher than controls [Table 3] and [Table 4].
In heavy and moderate smokers, presence of all the three variables, astheno-, oligo- as well as
teratozoospermia, indicated that heavy smoking apparently had a significant contribution in the
development of morphological abnormalities and reduced sperm counts besides motility defects [Table
3] and [Table 4]. [17],[18] A study on voluntary males of reproductive age showed that after ejaculation,
sperm motility deteriorated much more rapidly in heavy smokers in comparison to controls. [20]

Researchers have variously concluded that toxins in cigarette smoke reach male reproductive system
and their effects, though still under research, are mainly due to their direct interaction with seminal
fluid components and the accessory glands, that contribute their secretions to the seminal fluid, leading
to its increased viscosity, reduced seminal volume and delayed liquefaction time, hence reducing
forward linear progression of spermatozoa, manifesting as asthenozoospermia. [3],[4],[17],[18],[19] In
studies conducted on fertile men, it was observed that fertile men who were smokers showed reduction
in semen volume in comparison to nonsmokers; and this reduction in semen volume was in proportion
to the number of cigarettes smoked. [21],[22] Also, direct exposure of spermatozoa to the toxins in
cigarettes smoke probably tilts the delicate balance of reactive oxygen species (ROS) that are produced
by spermatozoa for their special functions like decapitation etc. Increased quantities of ROS have been
shown to be detrimental to the DNA of spermatozoa, thus producing negative effect on the viability and
morphology of spermatozoa. [23] Our observations were in agreement with these findings.

Smoking plays a role in producing asthenozoospermia, in otherwise normal and viable spermatozoa,
which can be a very subtle 'early indicator' of deterioration in semen quality. Since 37% controls too
showed asthenozoospermia [Table 4], many of these controls might be innocent 'passive smokers' or
getting affected by environmental pollutants, chemicals and other unknown factors awaiting discovery.
[17],[24] A higher level research of such non-Smokers may unmask the influence of these additional
factors.

By contrast, oligozoospermia may also result from other etiological factors, like chronic inflammatory or
infective processes, which needs further exploration. Statistical analysis of the results also underscored
a significant impact of asthenozoospermia and teratozoospermia on the semen quality of smokers, in
comparison to controls.

Our study could highlight that in early stages, alcohol and cigarette smoke constituents target different
aspects of sperm quality; alcohol targeting sperm morphology and spermatogenesis while smoking
impaired active motility of spermatozoa by reducing semen volume, increasing liquefaction time and
direct toxic effect on them, by dissolved smoke constituents in seminal fluid.
Heavy exposure to alcohol and/or smoking ultimately deteriorated all aspects of semen quality.
Synergistic effect of alcohol intake and smoking has been reported to be very detrimental to the
reproductive health of an individual. [4],[5],[7],[24]

Conclusions Top

Asthenozoospermia is the most common anomaly of semen. Its presence can be a very subtle, 'early
indicator' of reduction in the semen quality, which many a times gets overlooked, if the semen sample
shows adequate sperm count and normal morphology.

Alcohol consumption produces progressive damage to sperm morphology and spermatogenesis;

cigarette smoking produces sperm motility defect in light smokers with additive sperm morphology
defects in moderate/heavy smokers. Deterioration in semen quality appeared in direct proportion to the
quantity of alcohol intake and cigarettes smoked. Hence, male partners of infertile couples should
strictly abstain from alcohol consumption and cigarette smoking.
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