Epidemiological studies, cholesterol

Pietinen, P., Geboers, J., Kesteloot, H., Coffee consumption and serum cholesterol An epidemiological study in Belgium, Inti J Epidemiol, 17, 98, 1988... 

In epidemiologic studies, ingestion of large amounts of cold-water oily fish was associated with a reduction in CHD risk. Fish oil supplementation has a fairly large effect in reducing triglycerides and VLDL cholesterol, but it either has no effect on total and LDL cholesterol or may cause elevations in these fractions. Other actions of fish oil may account for any cardioprotective effects. 

Sixty to eighty-five percent of the fatty acids in fishery products are either monounsaturated or polyunsaturated. Polyunsaturated fats have been shown to reduce blood cholesterol levels and the same phenomenon exists for fish oils. Epidemiological studies of the Greenland Eskimos show their diet to be high in marine oils and the populaticxi has correspcMidingly low serum cholesterol values (6) (7). 

Subsequent epidemiological studies have supported the association between better health and long-term consumption of diets rich in foods of plant origin. " However, whether this is because such diets minimize exposure to deleterious substances (e.g., oxidized cholesterol, pyrolysis mutagens, salt, saturated fat, etc.), or maximize intake of certain beneficial nutrients (e.g., isothiocyanates and other sulfur-containing plant constituents, mono-unsaturated fatty acids, and poly-unsaturated fatty acids, PPT, poly acetylenes, selenium, terpenes, etc.) or some combination as advocated in the Polymeal concept, remains unknown. " An in vitro study indicates that there may be mechanistic basis for true synergy between PPT and isothiocyanates. ... 

Numerous clinical and epidemiological studies have demonstrated the inverse and independent association between HDL cholesterol and the risk of fatal and nonfatal coronary heart disease events. As a consequence, many national and international guidelines endorse the screening for low HDL cholesterol and define 1.05 mmol/1 (40 mg/dl) as the cardiovascular risk threshold value [18]. 

Different epidemiologic studies have suggested that drinking either green or black tea may lower cholesterol concentration and blood pressure [214,215],... 

It has been suspected that low concentrations of serum cholesterol might be associated with an increased risk of cancer or overall mortality. All fibrates and statins cause cancer in rodents, but the relevance of this finding to man has been questioned (68). In an epidemiological study these risks were almost non-existent after adjusting for confounding factors. 

One hypothesis linking dietary fat to colon cancer is that cholesterol is converted to bile acids which act as promoters of carcinogenesis (58). Epidemiological studies have shown however, (38) that when beef consumption in the United States doubled (between 1940-1970) the incidence of colon cancer mortality was virtually unchanged. In addition, the incidence of colon cancer is the same in Seventh Day Adventists, who eat meat sparingly (59) and Mormons, who consume a conventional diet (60). 

Although most epidemiological studies on the relationships between plasma lipids and coronary heart disease have examined total plasma cholesterol (most of which is apoB-associated cholesterol) as a major risk factor, some case-control studies have shown that apoB-100 (i.e., apoB in LDL and VLDL) is higher in subjects with coronary heart disease than controls (A31, A32, F2, M34, 06, RIO, S43, V6, W14). It may be that apoB is itself a risk factor, and that a raised apoB concentration but normal LDL cholesterol will be a marker for a previously unsuspected group of people at risk from coronary heart disease (S43). An increasing body of evidence suggests that hyper-B-apoproteinemia may be an important risk factor for coronary heart disease. This evidence, and the possibility that apolipoprotein assays (in particular apoB and apoA-I assays) may serve as a better marker of risk for atherosclerosis than the standard lipid measurements, have been discussed by Brunzell et al. (B59). 

Later epidemiological studies demonstrated that the low-density lipoprotein (LDL)-cholesterol, which is the predominant cholesterol carrier, like total cholesterol, was positively associated with the risk of CHD. On the other hand, HDL-cholesterol was negatively associated with the risk of CHD. Even between individuals having the same LDL-cholesterol level, those with a predominance of small, dense LDL particles have a much higher risk of CHD than individuals with a predominance of large, buoyant LDL particles (Gurr et al., 2002). It is notable that the Ci2 o, Ci4 o and Ci6 o fatty acids that increase total and LDL-cholesterol the most, concomitantly increase the levels of anti-atherogenic HDL-cholesterol, such that there can be a beneficial decrease in the total HDL ratio (Mensink et al., 2003). 

Epidemiological studies provide little, if any, evidence to support the hypothesis that saturated fatty acids, even those of chain length Ci2 o - Ci6 o that can elevate serum cholesterol concentration, are associated with the risk of CHD. This may result from the increased plasma HDL-cholesterol concentration produced by saturated fatty acids largely compensating for the adverse effects of these fatty acids on LDL-cholesterol concentration (Hu and Willett, 2000). In addition, saturated fatty acids lower the level of plasma Lp[a], which is considered a significant risk factor for CHD (Mensink et al., 1992). 

Kritchevsky and Kritchevsky (2000) provided a summary of the evidence linking dietary cholesterol to the risk of CHD in 10 cohorts from eight large, well-conducted prospective studies that were reported since 1980, which included the Nurses Health Study, the Health Professionals Followup Study and the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. In eight of the cohorts there was no statistical association between cholesterol intake and the risk of CHD. In one of the positive studies the association was established by simple univariate analysis and was not adjusted for other dietary variables. The other study adjusted only for fat intake. There is no compelling evidence from these epidemiological studies that dietary cholesterol is associated with the risk of CHD. 

Evidence from well-conducted prospective epidemiological studies does not suggest that consumption of saturated fat and cholesterol is associated with an increased risk of CHD. Randomized clinical trials that reduced the intake of saturated fatty acids and cholesterol and increased the intake of polyunsaturated fatty acids to lower plasma cholesterol levels did not significantly improve CHD or total mortality. The minor improvement in CHD events for trials of the potent cholesterol-lowering statin drugs may result, to an unknown extent, from their pleiotropic effects and cannot be used to justify the lipid hypothesis. 

Early investigations into a link between dietary tram fatty acid (TFA) intake and plasma cholesterol level in clinical trials, and CHD in epidemiology studies provided conflicting results. This outcome resulted from small numbers of participants in the trials combined with poor experimental... 

Even though milk fat contains some fatty acids that may elevate plasma total and LDL-cholesterol levels, which are risk factors for CHD, this effect is balanced by concurrent increases in levels of anti-atherogenic HDL-choles-terol. In addition, saturated fatty acids reduce plasma levels of atherogenic Lp[a] and produce a less atherogenic LDL particle size. Dietary intervention studies, where there was a substantial reduction in saturated fat intake and plasma cholesterol levels, did not produce an improvement in CHD or total mortality. Prospective epidemiological studies provide no evidence that saturated fatty acids are a risk factor for CHD. Indeed, in two large studies, saturated fatty acids were inversely associated with risk. 

Cholesterol Experiments from laboratory animal trials (21, 69, 70) have supported epidemiological studies (71) that link hypercholesterolemia and hyperlipoproteinameia, two risk factors for CVD, with dietary cholesterol intake or atherogenic fatty acid ratios. Common to many of these studies are the hndings that consumption of diets rich in cholesterol or saturated fat will result in a reduction of LDL receptors and elevation of LDL cholesterol and total cholesterol. 

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