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Egg Nutrition Center 1050 17th Street, NW Suite 560 Washington, DC 20036 E-mail: enc{at}enc-online.org
Dear Sir:
Although the report by Weggemans et al (1) confirms the findings from many recent reported analyses that dietary cholesterol has a small effect not only on plasma total and LDL cholesterol but also on plasma HDL cholesterol (2–4), their interpretation of the findings contradicts more than a decade of epidemiologic studies showing that dietary cholesterol is not a contributor to heart disease risk. The reviews by Howell et al (2), Clarke et al (3), McNamara (4), and Weggemans et al indicate that a 100-mg/d change in dietary cholesterol increases plasma total cholesterol concentrations by 0.06 mmol/L (2.3 mg/dL), LDL cholesterol by 0.05 mmol/L (1.9 mg/dL), and HDL cholesterol by 0.01 mmol/L (0.4 mg/dL). However, Weggemans et al conclude from their analysis that dietary cholesterol increases the ratio of total to HDL cholesterol and that adding an egg a day to the diet increases heart disease risk by 2%. This conclusion is difficult to accept given that a decade of epidemiologic studies indicates that eggs and dietary cholesterol are not significant factors in heart disease risk (5, 6).
The problem is that although dietary cholesterol–mediated changes in total, LDL-, and HDL-cholesterol concentrations are constant relative to the dose, changes in the ratio of LDL to HDL cholesterol are a function of the actual value of each variable. For example, patient X with LDL and HDL concentrations of 3.1 mmol/L (120 mg/dL) and 1.0 mmol/L (40 mg/dL), respectively, has an LDL-HDL ratio of 3.00. Theoretically, adding an egg a day to this patient's diet would increase LDL and HDL concentrations to 3.2 mmol/L (123.8 mg/dL) and 1.1 mmol/L (40.8 mg/dL), respectively, resulting in a ratio of total to HDL cholesterol of 3.03, similar to the ratio of 0.04 predicted by Weggemans et al. In contrast, patient Y with LDL and HDL concentrations of 4.1 mmol/L (160 mg/dL) and 1.0 mmol/L (40 mg/dL), respectively, has a ratio of 4.00. Adding an egg a day to this patient's diet would increase the LDL concentration to 4.2 mmol/L (163.8 mg/dL), the HDL concentration to 1.1 mmol/L (40.8 mg/dL), and the ratio of LDL to HDL cholesterol by 0.01–4.01, not the predicted change of 0.04. Thus, an individual with a very low risk of myocardial infarction could, theoretically, increase their risk by 1.5%, whereas an individual with a high risk could increase their risk by 0.5%. These values represent maximal estimates because, as shown by Weggemans et al, the response of plasma LDL cholesterol to dietary cholesterol was attenuated when the ratio of polyunsaturated to saturated fatty acids (P:S) in the background diet was >0.7 [an increase of 0.04 mmol/L (1.4 mg/dL) with a diet low in saturated fat compared with an increase of 0.06 mmol/L (2.2 mg/dL) with a diet high in saturated fat with each additional increase of 100 mg cholesterol/d], whereas the response of plasma HDL cholesterol is unchanged. Under these conditions there would be no measurable change in the ratio of LDL to HDL cholesterol in our 2 hypothetical patients after adding one egg a day to their diets (ratio: 3.00–3.01 in patient X and 3.99–4.00 in patient Y).
More importantly, I am surprised at the unfortunate interpretation of Weggeman et al's finding that egg restriction can reduce the risk of heart disease. Statistical significance and biological importance must be viewed as distinct concepts. The assertion that eating an egg a day increases the risk of heart disease by 2% (but only in those with low ratios of LDL to HDL cholesterol and a low dietary P:S) needs to be put in perspective relative to other risk factors: 1) the 72% increase in risk associated with a body mass index (in kg/m2) of 25–28.9 relative to a body mass index < 23 (7), 2) the 42% decrease in risk associated with the replacement of 5% of energy from saturated fat with 5% from unsaturated fat (8), and 3) the 51% decrease in risk associated with 1.5 h of vigorous walking 1 d/wk (9).
The fact that no studies in the past decade have reported a significant relation between either egg consumption or dietary cholesterol intakes and heart disease risk (5) is consistent with the view that the hypothesis that dietary cholesterol is a risk factor for heart disease should be dismissed. A small, statistically significant increase in the ratio of total to HDL cholesterol has little biological importance concerning heart disease risk when considered relative to those dietary and lifestyle factors that do in fact contribute to heart disease risk. Concerning the suggestion by Weggeman et al that eggs make no important contributions to the diet, I refer them to a recent supplement of the Journal of the American College of Nutrition (10) in which the merits of egg consumption are documented. In an evaluation of the relation between dietary cholesterol and the risk of heart disease, it is crucial to not only have accurate estimates of risk but also a practical perspective of what a risk estimate represents.
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