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首页医源资料库在线期刊美国临床营养学杂志2002年75卷第2期

Reply to DJ McNamara

来源:《美国临床营养学杂志》
摘要:nlDearSir:McNamarasuggeststhattheeffectofdietarycholesterolonbloodlipidsisconstantwhatevertheinitialconcentration。Asaresult,therelativeeffectofdietarycholesterolontotalcholesterolwouldbelowerandthatonHDLwouldbehigherinsubjectswithhighertotalcholester......

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Martijn B Katan, Rianne M Weggemans and Peter L Zock

Wageningen Centre for Food Sciences and Wageningen University Bomenweg 2 6703 HD Wageningen Netherlands E-mail: martijn.katan{at}staff.nutepi.wau.nl

Dear Sir:

McNamara suggests that the effect of dietary cholesterol on blood lipids is constant whatever the initial concentration. As a result, the relative effect of dietary cholesterol on total cholesterol would be lower and that on HDL would be higher in subjects with higher total cholesterol and lower HDL concentrations. This suggestion is contradicted by studies showing that the response of total cholesterol to dietary cholesterol and fats is greater in subjects with higher baseline concentrations of cholesterol (1,2). However, this finding does not exclude the possibility that the elevated response to dietary cholesterol in subjects with high baseline cholesterol concentrations is mainly due to HDL. We therefore plotted the effect of the consumption of an extra 200 mg dietary cholesterol/d (equivalent to the cholesterol in one egg) on the ratio of total to HDL cholesterol as a function of the mean baseline cholesterol concentration in 17 studies (3). There was a tendency for the change in the ratio of total to HDL cholesterol to be lower when baseline cholesterol concentrations were higher (Figure 1): the slope of the change in the ratio as a function of baseline cholesterol was -0.046 per mmol/L (95% CI: -0.082, -0.009 mmol/L). The negative slope was caused by 2 groups of subjects with baseline total cholesterol concentrations >6 mmol/L (232 mg/dL); both groups were from the same study (4). In the 22 other groups of subjects, the effect of dietary cholesterol on the ratio was the same irrespective of the baseline total cholesterol concentration. Thus, the adverse effect of dietary cholesterol on the ratio of total to HDL cholesterol might be limited to subjects with baseline serum cholesterol concentrations <6 mmol/L. However, this finding needs to be verified in subjects with baseline cholesterol concentrations >6 mmol/L because the finding is based on the results of only one study (4).


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FIGURE 1. . The effect of a 200-mg/d increase in dietary cholesterol on the ratio of total cholesterol to HDL cholesterol. The 17 studies provided 24 data points. Each point is the mean of 9–70 subjects.

 
McNamara also states that "a decade of epidemiologic studies indicates that eggs and dietary cholesterol are not significant factors in heart disease risk" and cites the results of 2 prospective cohort studies (5) to support this statement. However, he ignores the findings of 2 earlier prospective cohort studies that found a significant association between dietary cholesterol and the risk of coronary heart disease (6,7). These observations, together with data showing that dietary cholesterol causes atherosclerosis and coronary heart disease in animals, including primates (8), should give us pause before deciding that dietary cholesterol does not affect heart disease risk in humans. Extrapolations from animal models to humans are often unreliable, but the data are too consistent and strong to be dismissed totally.

We agree that the effect of eating eggs on coronary heart disease risk, calculated from the ratio of total to HDL cholesterol, is small compared with the risk associated with being overweight. However, dietary cholesterol might increase the risk of coronary heart disease through intermediates other than serum cholesterol concentration alone. This suggestion is supported by the findings of Stamler and Shekelle (8), who analyzed the association of cholesterol intake with the risk of coronary heart disease in 4 prospective studies. Stamler and Shekelle concluded that there was an independent additional increase in risk associated with a higher dietary cholesterol intake over and above the greater risk induced by the resultant increase in serum cholesterol. Be that as it may, many people do not find it a major hardship to cut back on egg intake, whereas most people find it impossible to lose weight permanently. We fully support advice to lose weight, to replace saturated fats with unsaturated fats in the diet, and to increase exercise levels, but most people have exhausted the easy ways to achieve these goals. Meanwhile, there are small steps—dietary and other—that people can take to improve their chances of staying healthy; together, these steps may lead to an appreciable effect. Moderate egg consumption is one of these steps.

Finally, we did not say that "eggs make no important contributions to the diet." Eggs are a useful, low-cost source of protein and certain vitamins. What we said was that "in view of the relatively small contribution of eggs to the intake of nutrients that may be beneficial in preventing coronary heart disease, the recommendation to limit the consumption of eggs may still be valid for the prevention of coronary heart disease" (3).

REFERENCES

  1. Katan MB, Beynen AC. Characteristics of human hypo- and hyperresponders to dietary cholesterol. Am J Epidemiol 1987;125:387–99.
  2. Keys A, Anderson JT, Grande F. Serum cholesterol responses to changes in the diet. III: Differences among individuals. Metabolism 1965;14:766–75.
  3. Weggemans RM, Zock PL, Katan MB. Dietary cholesterol from eggs increases the ratio of total cholesterol to high-density lipoprotein cholesterol in humans: a meta-analysis. Am J Clin Nutr 2001;73:885–91.
  4. Knopp RH, Retzlaff BM, Walden CE, et al. A double-blind, randomized, controlled trial of the effects of two eggs per day in moderately hypercholesterolemic and combined hyperlipidemic subjects taught the NCEP step I diet. J Am Coll Nutr 1997;16:551–61.
  5. Hu F, Stampfer MJ, Rimm EB, et al. A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 1999;281:1387–94.
  6. Shekelle RB, MacMillan Shryock A, Paul O, et al. Diet, serum cholesterol, and death from coronary heart disease—The Western Electric Study. N Engl J Med 1981;304:65–70.
  7. McGee DL, Reed DM, Yano K, Kagan A, Tillotson J. Ten-year incidence of coronary heart disease in the Honolulu Heart Program. Relationship to nutrient intake. Am J Epidemiol 1984;119:667–76.
  8. Stamler JS, Shekelle RB. Dietary cholesterol and human coronary heart disease. Arch Pathol Lab Med 1988;112:1032–40.

作者: Martijn B Katan
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