The mainstream medical consensus is that high intakes of dietary cholesterol are the cause of atherosclerosis and that this increases the risk of cardiovascular disease. However, this theory is provably erroneous, as a large body of evidence in the literature shows that dietary cholesterol is not the cause of cardiovascular disease. For example, one study published in the American Journal of Clinical Nutrition in 19891 investigated the absorption, excretion, synthesis and inter-population variation of cholesterol amongst 63 middle aged men. The cholesterol intake of the subjects was assessed using the 7-day food diary method. The main finding of the study was that endogenous synthesis of cholesterol was negatively associated with both fractional and absolute cholesterol absorption rates. This supports other evidence and suggests that cholesterol synthesis is regulated by cholesterol absorption, whereby higher intakes of cholesterol cause a compensatory decrease in the synthesis rates.
That synthesis rates are modulated to reflect the intake of cholesterol has been known for some time. This is the main argument against dietary cholesterol being able to cause cardiovascular disease. Studies using eggs (here) have shown that increases in dietary cholesterol from of egg yolks results in no change to the plasma cholesterol levels because synthesis rates are thought to compensate for the increase in dietary intake. Further, studies that have shown associations between cholesterol or saturated fat intake and plasma levels of cholesterol carrying lipoproteins have generally not been rigorous in controlling for dietary fibre. Dietary fibre is a confounding variable because it is known that high intakes of fibre cause a decrease in plasma levels of certain cholesterol carrying lipoproteins. That diets high in saturated fat and cholesterol tend to also be low in fibre causes problems with such studies.
Another problem with studies investigating the effects of dietary cholesterol on plasma cholesterol levels is that inclusion of subjects with metabolic disorders associated with cholesterol metabolism can bias the results. The original Framingham study that reported higher intakes of cholesterol for those with more severe atherosclerosis was criticised because the authors failed to remove those subjects with familial hypercholerolaemia. Inclusion of subjects with metabolic syndrome is also problematic because the disorder is characterised by metabolic abnormalities in lipoprotein metabolism. Studying the effects of cholesterol on subjects with metabolic syndrome is acceptable if the study population is correctly identified as such. Including such subjects in a study of healthy individuals is however misleading. In the above cited study, body mass index was negatively associated with the cholesterol absorption rate. This suggests that obese subjects have upregulated cholesterol synthesis rates, perhaps due to the presence of metabolic syndrome.
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