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KEY WORDS Monounsaturated fatty acids, carbohydrates, saturated fatty acids, dietary
cholesterol, plasma cholesterol
Am J C/in Nuir l988;47:965-9. Printed in USA. © 1988 American Society for Clinical Nutrition 965
966 GRUNDY ET AL
Center, Bonham, TX. This facility provides medical and pay- bles, fruits, meat, whole eggs, egg whites, milk, fats, and oil).
chiatric care, rehabilitation assessments, and other therapeutic The High Sat+Chol diet was rich in products containing butter
measures to ambulatory eligible veterans. Many ofthe patients fat and it included two eggs per day. The High Mono diet was
in the domiciliary-care unit reside for long-term care. The pa- enriched in high-oleic safflower oil and unhydrogenated peanut
tients were selected by the following criteria: 1) they were men- butter. Butter and safflower oil were added to salads, vegetables,
tally competent and willing to volunteer for a dietary study, 2) bread, and toast. The order ofthe dietary periods was random-
they did not have recent history of alcohol or drug abuse; 3) ized. The patients were weighed twice weekly and caloric intake
they were generally healthy and did not have liver or kidney was adjusted to maintain a constant weight throughout the
dysfunction, diabetes mellitus or other endocrine diseases, hy- study. Patients maintained their normal activity level and no
pertension, or congestive heart failure; 4) they were not taking special exercise regimen was employed.
cardiac medications; and 5) they were not markedly over-
weight. Lipid and lipoprozein
The patients ranged in age from 61 to 70 y (mean ± SD, 64 After allowing 1 mo for equilibration on each new diet, the
± 2 y). Their body mass indices ranged from 20.8 to 30.5 patients were sampled three times per week for the last 2 wk of
(mean, 25.9 ± 3.4). At the time ofadmission to the study, aver- the 6-wk period. Blood samples were drawn after a 14-h fast
age lipids and lipoproteins for the group were total cholesterol, and plasma was obtained by centrifugation at 1232 X g for 30
227 ± I 2 (SEM) mg/dL(5.87 ± 0.3 mmol/L); triglycerides, 127 mm. Each plasma sample was analyzed by Lipid Research
± 21 mg/dL (1.43 ± 0.24 mmol/L), low-density-lipoprotein Ginics procedures (13) for levels oftotal cholesterol, triglycer-
(LDL) cholesterol 143 ± 5 mg/dL (3.70 ± 0. 13 mmol/L), and ides, and lipoprotein cholesterol; plasma total cholesterol and
high-density-lipoprotein (HDL) cholesterol 5 1 ± 3 mg/dL (1.3 triglycerides were measured enzymatically (14, 15). The HDL-
Total Cholesterol Triglycerides low intake of saturated fatty acids and cholesterol but
300 200 total fat intakes were twice as high.
According to several reports (6, 20, 2 1), intakes of di-
. etary cholesterol > 500 mg/d produce a diminishing in-
250 - 150 crement in the cholesterol concentration beyond the 500
‘O
:\. mg level. For example,
al (6) for dietary
consider
cholesterol:
the equation of Keys et
200 100
C,
-
.
result ofa decreased intake of cholesterol.
On the High Sat+Chol diet, intakes of saturated fatty
acids averaged 19% of total calories. According to the
150-#{149} 40
C, data ofKeys et al (22) and Hegsted et al (3), all saturated
E
fatty acids do not raise the cholesterol level to the same
extent. Both these reports (3, 22) indicated that the C18
100- 20 .-..-.-.
stearic acid does not raise the total cholesterol level com-
pared with oleic acid. A preliminary study (23) from our
I I I
laboratory in humans confirmed this finding, and several
High High Low High High Low studies in animals are in accord with this response (24-
Sat+ Mono Fat Sat+ Mono Fat 26). Further, several reports (27-29) suggest that medi-
Chol Chol um-chain saturated fatty acids (chain length 4-10) do
FIG 1. Plasmalevels oftotal, LDL, and HDL cholesteroland triglyc- not raise the plasma cholesterol levels. Therefore, if we
erides in 10 patientson High Sat+Chol, High Mono, and Low Fat diets. subtract fatty acids of chain lengths 4, 6, 8, 10, and 18
Each point represents the mean ofsix determinations done during the from the total saturates, the High Sat+Chol diet con-
last 2 wk of6-wk periods. (To convert values forcholesterol and triglyc- tamed only 13% of cholesterol-raising saturated fatty
erides to mmol/L, multiply by 0.02586 and 0.01 129, respectively.)
acids (chain lengths 12, 14, and 16). Keys et al (22) mdi-
cated that these latter saturated fatty acids raise the
saturated fatty acids (High Mono) in which calories were plasma cholesterol by 2.7 mg/dL (0.07 mmol/L) for ev-
consumed mainly as solid foods. These two diets in turn ery 1% ofcalories. Thus for the High Sat+Chol diet com-
were compared to a diet high in both saturated fatty acids pared with the High Mono diet for cholesterol-raising
and cholesterol(High Sat+Chol). The latter diet was em- saturates, the High Mono diet should have caused a
ployed to obtain maximally high levels of cholesterol in mean reduction in plasma cholesterol of 16.2 mg/dL
total plasma and in LDL and HDL subfractions. On the (0.42 mmol/L). This decrease combined with the 1 5 mg/
High Sat+Chol diet, intakes ofboth saturated fatty acids dL (0.39 mmol/L) decrease predicted for the lower cho-
(19% ofcalones) and cholesterol (-9#{174} mg/d) exceeded lesterol intake should have reduced the plasma total cho-
current American intakes, and this cholesterol-raising lesterollevel by 3 1 mg/dL(0.80 mmol/L). This predicted
diet should have provided a plasma cholesterol ceiling by reduction closely approximated the observed mean re-
which the two cholesterol-lowering diets could be com- duction of32 mg/dL (0.83 mmol/L).
pared. In other words, the experimental design not only Both Keys et al (2) and Hegsted et al (3) reported that
facilitated comparison of two cholesterol-lowering diets carbohydrates have approximately the same effect as
but also allowed us to determine the maximal degree of monounsaturated fatty acids on plasma total cholesterol
cholesterol reduction that can be obtained by therapeutic levels. A similar relationship was noted previously in a
diets that are low in both saturated fatty acids and choles- study from ourlaboratory (1 1). The current results are in
terol. The Low Fat diet was equivalent to the American complete accord. On average the plasma total cholesterol
Heart Association Phase III diet for treatment of hyper- fell to the same extent on both High Mono and Low Fat
cholesterolemia (19); the High Mono diet had the same diets. Likewise, the LDL-cholesterol concentration de-
968 GRUNDYETAL
TABLE 1
Plasma lipids and lipoproteins in the three diet periods
mg/dL (mmol/L)
i±SEM;n= 10.
t High Mono and Low Fat significantly different from High Sat+Chol atp < 0.0010.
High Mono and Low Fat significantly different from High Sat+Chol at p < 0.0002.
§ Low Fat significantly different from High Sat+Chol and High Mono atp < 0.0182.
10. Keys A, ed. Coronary heart disease in seven countries. Circulation metabolism in nonresponders to increased dietary cholesterol. Ar-
l970;4l(suppl l):Il-2l1. teriosclerosis 198 1; 1:463-70.
1 1 . Grundy SM. Comparison ofmonounsaturated fatty acids and car- 22. Keys A, Anderson iT, Grande F. Serum cholesterol responses to
bohydrates for lowering plasma cholesterol. N Engl J Med changes in diet. IV Particular saturated fatty acids in the diet. Me-
l986;3 14:745-8. tabolism 1965; 14:776-87.
12. Watt BK, Merrill AL. Composition offoods. Washington, DC: US 23. Bonanome A, Grundy SM. Stearic acid does not raise plasma cho-
Government PrintingOffice, 1963.(US Department of Agriculture lesterol. Clin Res 1987; 35:365A(abstr).
handbook #8.) 24. Wilson RB, Martin JM, Hartroft WS. Dietary control of serum
13. Lipid Research Clinics. Manual oflaboratory operations. I Lipid cholesterol levels in rats fed high-fat, cholate-containing diets. Can
and lipoprotein analysis. US Dept of Health, Education and Wel- J Physiol Pharmacol 1967;44:267-73.
fare, 1974; (DHEW publication [NIH] 75-628.) 25. Renaud 5, Gautheron P. Influence ofdietary fats on atherosclero-
14. Roeschlau P, Bernt E, Gruber W. Enzymatic determination of to- sis, coagulation and platelet phospholipids in rabbits. Atheroscle-
tal cholesterol in serum. J Gin Chem Clin Biochem 1974; 12: rosis 1975;2l:l 15-24.
226-7. 26. Kritchevsky D, Tepper SA, Bises G, Klurfeld DM. Experimental
15. Wahlefeld AW. Triglyceride determination afterenzymatic hydra- atherosclerosis in rabbits fed cholesterol-free diets. Part 10. Cocoa
lysis. In: Bergmeyer HU, ed. Methods ofenzymatic analysis. 2nd
butter and palm oil. Atherosclerosis l982;4l :279-84.
ed. Orland, FL: Academic Presslnc, 1974:1831-35.
27. Hashim SA, Arteaga A, van Itallie TB. Effect ofsaturated medium-
16. Miettinen TA, Ahrens EH Jr, Grundy SM. Quantitative isolation
chain triglyceride on serum lipids in man. Lancet 1960; 1:1105-8.
and gas-liquid chromatographic analysis oftotal dietary and fecal
28. Beveridge JMR, Connell WF, Haust HL, Mayer GA. Dietary cho-
neutral steroids. J Lipid Res 1965;6:4l 1-24.
lesteroland plasmacholesterollevels in man. Can J Biochem Phys-