There is a popular misconception that dietary choles-terol correlates directly with serum cholesterol, when in fact dietary cholesterol, within a range of normal dietary consumption (100–400 mg/day), has only a very small impact on blood cholesterol levels. Eggs represent the principal source of dietary cholesterol in most diets (1 egg yolk = 150–250 mg cholesterol); in their absence, most Western diets would contain considerably less than 100 mg cholesterol/day. The classic but extreme egg-feeding studies showed that feeding of up to six eggs per day (900 mg cholesterol) increased LDL cholesterol acutely. However, the body effectively counters this effect with sensitive, compen-satory mechanisms to deal with an increasing load of dietary cholesterol, one of which is to reduce the amount of cholesterol absorbed in the gut. This com-pensation effectively abolishes any dose–response relationship between dietary cholesterol, over a prac-tically realistic range of intakes, and serum choles-terol. Two factors that may influence the variability in response to dietary cholesterol are dietary saturated fatty acids, which have been shown to augment the cholesterol-raising effects of dietary cholesterol, and a phenomenon of increased susceptibility to dietary cholesterol in some individuals for some, as yet, unknown reason.
To place these dietary influences on blood choles-terol in perspective with other cholesterol-lowering strategies, a metaanalysis of dietary intervention trials undertaken by the World Health Organization (WHO) revealed that dietary modification could achieve reductions in serum cholesterol of between only 4% and 5%. This finding is in sharp contrast to the potent effects of cholesterol-lowering drugs, which can reduce serum cholesterol by 30–40% and have been shown, unequivocally, to reduce the incidence of death from CHD. It also highlights the need to address other risk factors which are more responsive to dietary change.
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