AJCN Tufts Nutrition Symposium, Boston Sept 24-26
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American Journal of Clinical Nutrition, Vol. 72, No. 4, 1059, October 2000
© 2000 American Society for Clinical Nutrition


Letter to the Editor

No evidence for a link between consumption of chocolate and coronary heart disease

Penny M Kris-Etherton, Christine L Pelkman, Guixiang Zhao and Ying Wang

Nutrition Department, Pennsylvania State University, 126S Henderson Building, University Park, PA 16802-6504

Dear Sir:

The recent study of Hu et al (1) examined the associations between intakes of individual saturated fatty acids (SFAs) and their food sources in relation to the risk of coronary heart disease (CHD) in 80082 women in the Nurses' Health Study. These investigators reported that after a 14-y follow-up period, the major long-chain SFAs were each individually associated with a small increase in the risk of CHD. In addition, the ratio of polyunsaturated fatty acids to SFAs (P:S) was inversely associated with CHD risk. This latter conclusion is supported by data showing a cardioprotective effect of an increasing P:S. In contrast is the lack of any significant effect of SFAs when the investigators adjusted for various dietary factors, including monounsaturated fat, polyunsaturated fat, trans fat, protein, dietary cholesterol, dietary fiber, and total energy. When these dietary factors were included in the model, every relative risk for each quintile of individual SFA intake and the sum of 12:0–18:0 was not significant. These findings do not diminish the results of the linear regression showing an effect of total SFA intake or the results of the many controlled clinical trials showing adverse effects of SFAs, primarily 12:0-16:0, on important risk factors for coronary disease; however, they do illustrate the important effects of other components of the diet in affecting CHD risk.

The magnitude of the saturated fat effect on the risk of CHD is not clear. On the basis of the linear regression analysis, the investigators reported that for every 5% increase in 12:0–18:0 intake, the risk of CHD would be expected to increase by {approx}29% (ie, by a relative risk of 1.29). However, it is perplexing that in the multivariate analysis the relative risk appears to decrease (not significantly) in the second and third quintiles of intake in the summed long-chain SFA group. Importantly, relative risk increased by l.05 and not by 1.29 between the first and fourth quintiles of total saturated fat intake, at which intake increased by 5%. This is not unexpected given the inherent and well-documented limitations of epidemiologic studies. Nonetheless, there is abundant evidence that 12:0–16:0 increases CHD risk. What remains unclear from this study is the relative contribution of each SFA (including 18:0) as well as the contribution of total SFA to CHD risk within the context of different eating patterns.

Of note, chocolate was not a main contributor to stearic acid or total SFA intake. Chocolate was reported to contribute only 5% to total stearic acid intake. Moreover, only 0.13% of SFAs were stearic acid provided by chocolate. On the basis of the insignificant contribution of chocolate to total SFA intake, the rationale for focusing on chocolate specifically in the accompanying editorial (2) is not obvious. As might be expected from our knowledge of the biological effects of SFAs, the data do show significant effects of the ratio of red meat to poultry and fish consumption as well as of the ratio of high-fat to low-fat dairy products on relative risk of CHD. A clear benefit of increasing the P:S of the diet on CHD risk was also shown. However, chocolate specifically was not shown to affect risk of CHD. This is not unexpected given the very small contribution of chocolate to total SFA intake and the negligible to nonexistent effect of chocolate on the P:S of the diet. Thus, the comment made in the editorial (2) that chocolate is pathogenic clearly is not justified by the data presented in the report by Hu et al (1), on the basis of either chocolate's stearic acid content or its contribution to the P:S.

It is important to maintain our focus on reducing saturated fat intake to reduce the risk of CHD. Little is to be gained by focusing on selected foods, such as chocolate, that contribute little to total SFA intake. Rather, emphasis should be placed on changing the dietary patterns of Americans by targeting the food groups that are major contributors of SFAs and ensuring that other dietary constituents meet contemporary dietary guidelines.

REFERENCES

  1. Hu FB, Stampfer MJ, Manson JE, et al. Dietary saturated fats and their food sources in relation to risk of coronary heart disease in women. Am J Clin Nutr 1999;70:1001–8.[Abstract/Free Full Text]
  2. Connor WE. Harbingers of coronary heart disease: dietary saturated fatty acids and cholesterol. Is chocolate benign because of its stearic acid content? Am J Clin Nutr 1999;70:951–2.[Free Full Text]



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