Selected Annotated Bibliography on Fats

Keys, A., Anderson, T., Mickelson, O., Adelson, S. F., and Fidanza, R. (1956). Diet and Serum Cholesterol in Man: Lack of Effect of Dietary Cholesterol.” Journal of Nutrition. May 10; 59(1):39-56.

Conclusions: The foregoing evidence is definitive, we think, in showing that variations in the intake of cholesterol over the whole range of natural diets do not influence the serum level of physically normal adult men so long as other elements in the diet are constant.

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Fernandez, M. L. (2006) Dietary cholesterol provided by eggs and plasma lipoproteins in healthy populations. Curr Opin Clin Nutr Metab Care. 2006 Jan;9(1):8-12.

Conclusions: For these reasons, dietary recommendations aimed at restricting egg consumption should not be generalized to include all individuals. We need to acknowledge that diverse healthy populations experience no risk in developing coronary heart disease by increasing their intake of cholesterol but, in contrast, they may have multiple beneficial effects by the inclusion of eggs in their regular diet.

Krumholz, H. M. et al. (1994). Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years. JAMA 1994; 272(17):1335-1340.

Conclusions: Our findings do not support the hypothesis that hypercholesterolemia or low HDL-C are important risk factors for all-cause mortality, coronary heart disease mortality, or hospitalization for myocardial infarction or unstable angina in this cohort of persons older than 70 years.


Morris, J. N. et al. (1963). Diet and plasma cholesterol in 99 bank men. Br Med J. 1963 March 2; 1(5330): 571-576.

Conclusion: Animal fat intake ranged from 55 to 173 grams per day, and blood cholesterol ranged from 154 to 324 mg/dL, yet there was no relationship whatsoever between the two. They crunched the data every way they knew how, and could not find any discernible association between dietary animal fat intake and blood cholesterol.


Nichols, A. B., et al. (1976). Daily nutritional intake and serum lipid levels. The Tecumseh study. Am J Clin Nutr 1976 Dec;29(12):1384-92.


Conclusion: Cholesterol and triglyceride levels were unrelated to quality, quantity, or proportions of fat, carbohydrate or protein consumed in the 24-hr recall period.



Okayama, A. et al. (1993). Changes in total serum cholesterol and other risk factors for cardiovascular disease in Japan, 1980-1989. International Journal of Epidemiology (1993) 22(6): 1038-1047.

Conclusions: “The highest death rate observed was among those with lowest cholesterol (under 160mg/dl); lowest death rate observed was with those whose cholesterol was between 200-259mg/dl.” In other words, those with the lowest cholesterol had the highest death rate, and those with cholesterol levels that would today be called “dangerous” had the lowest death rate.


Ravnskov, U. (2003). High cholesterol may protect against infections and atherosclerosis. Quarterly Journal of Medicine (2003;96:927-34).

Conclusions: Our findings do not support the hypothesis that hypercholesterolemia or low HDL-C are important risk factors for all-cause mortality, coronary heart disease mortality, or hospitalization for myocardial infarction or unstable angina in this cohort of persons older than 70 years.

Ravnskov, U. (2002). A hypothesis out-of-date: The diet-heart idea. J Clin Epidemiol. 55 (2002): 1057-1063.

Conclusions: An almost endless number of observations and experiments have effectively falsified the hypothesis that dietary cholesterol and fats, and a high cholesterol level play a role in the causation of atherosclerosis and cardiovascular disease. The hypothesis is maintained because allegedly supportive, but insignificant findings, are inflated, and because most contradictory results are misinterpreted, misquoted or ignored.


Ravnskov, U. (1998). The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. J Clin Epidemiol. 1998 Jun;51(6):443-60.

Conclusions: A fat diet, rich in saturated fatty acids (SFA) and low in polyunsaturated fatty acids (PUFA), is said to be an important cause of atherosclerosis and cardiovascular diseases (CVD). The evidence for this hypothesis was sought by reviewing studies of the direct link between dietary fats and atherosclerotic vascular disease in human beings. The review included ecological, dynamic population, cross-sectional, cohort, and case-control studies, as well as controlled, randomized trials of the effect of fat reduction alone. The positive ecological correlations between national intakes of total fat (TF) and SFA and cardiovascular mortality found in earlier studies were absent or negative in the larger, more recent studies. Secular trends of national fat consumption and mortality from coronary heart disease (CHD) in 18-35 countries (four studies) during different time periods diverged from each other as often as they coincided. In cross-sectional studies of CHD and atherosclerosis, one group of studies (Bantu people vs. Caucasians) were supportive; six groups of studies (West Indians vs. Americans, Japanese, and Japanese migrants vs. Americans, Yemenite Jews vs. Yemenite migrants; Seminole and Pima Indians vs. Americans, Seven Countries) gave partly supportive, partly contradictive results; in seven groups of studies (Navajo Indians vs. Americans; pure vegetarians vs. lacto-ovo-vegetarians and non-vegetarians, Masai people vs. Americans, Asiatic Indians vs. non-Indians, north vs. south Indians, Indian migrants vs. British residents, Geographic Study of Atherosclerosis) the findings were contradictory. Among 21 cohort studies of CHD including 28 cohorts, CHD patients had eaten significantly more SFA in three cohorts and significantly less in one cohort than had CHD-free individuals; in 22 cohorts no significant difference was noted. In three cohorts, CHD patients had eaten significantly more PUFA, in 24 cohorts no significant difference was noted. In three of four cohort studies of atherosclerosis, the vascular changes were unassociated with SFA or PUFA; in one study they were inversely related to TF. No significant differences in fat intake were noted in six case-control studies of CVD patients and CVD-free controls; and neither total or CHD mortality were lowered in a meta-analysis of nine controlled, randomized dietary trials with substantial reductions of dietary fats, in six trials combined with addition of PUFA. The harmful effect of dietary SFA and the protective effect of dietary PUFA on atherosclerosis and CVD are questioned.


Schatz, I. J. et al. (2001). Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: A cohort study. The Lancet, 2001, Vol. 358(9279):351-355.

Conclusion: “Long-term persistence of low cholesterol concentration actually increases the risk of death. Thus, the earlier the patients start to have lower cholesterol concentrations, the greater the risk of death.”


Siri-Tarino, P. W., Sun, Q, Hu, F. B., Krauss, R. M. (2010). Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Journal of Clinical Nutrition. 2010 ajcn.27725; First published online January 13, 2010. doi:10.3945/ajcn.2009.27725.

Conclusions: A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.

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