Dietary fats epidemiological studies

Epidemiologic studies indicate that diets high in total fat and saturated fat and low in certain fibers are associated with an increased risk for colon cancer. In addition, certain dietary fibers and cruciferous vegetables have been associated with a reduced risk in several populations consuming the diets high in total fat. 

Wynder and Shigematsu (15) were the first to suggest that nutritional factors in general and specifically differences in fat intake may be responsible for the international variation in colon cancer incidence. Subsequent descriptive epidemiologic studies have found a strong positive association between colon cancer mortality or incidence in different countries and per capita availability in national diets of total fat (4,16) and of animal fat, estimated from food balance sheets. Such international correlations may be supportive of a hypothesis, but they should be interpreted with caution because the dietary data were based not on actual intake information but on food disappearance data. 

The epidemiologic data, relative to dietary fiber, has been supported by animal studies but experiments with dietary fat have been conflicting and generally do not indicate a fat effect. Other dietary factors which associate with colon cancer in animal studies are deficits of lipotropes and of vitamin A. 

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). 

Epidemiological studies show that dietary fat and protein are most frequently correlated with colon cancer incidence in man (10-14). A number of studies in laboratory animals suggest that dietary fat enhances colon tumor incidence (15) although others have failed to show such enhancement (16). Summarized in this communication are animal experiments conducted by our laboratory to examine the effects of dietary protein on DMH induced carcinogenesis, mutagenesis, and toxicity. 

Overall, epidemiological evidence from within-population studies does not support an independent role for dietary fat or fat subclasses in the risk of colon cancer. However, the evidence does not preclude the possibility that certain fatty acids, such as co-6s and co-3s, may exert opposing influences. 

Evidence from well-conducted epidemiological studies does not support any meaningful associations between the intake of total fat, fat type or individual fatty acids and the risk of colon, breast or prostate cancer. Final proof of a null effect should come from randomized clinical trials. However, such trials seem unlikely because initiation of tumors may occur early in life, whereas the clinical symptoms arise late in life. The cost of appropriate trials would be prohibitive. Further advances, however, may come from improved dietary assessment and a better understanding of, and adjustment for, confounding factors in epidemiological studies. 

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. 

A role for milk fat in cancer risk has not been examined adequately in epidemiological studies, because milk fat is not consumed as a single dietary item, but as a component of dairy products and dairy products also contain non-lipid components with anti-cancer potential (Parodi, 2001a, b). On the other hand, seven studies were found in the literature, where milk fat or butter diets were compared with diets containing equal amounts of polyunsaturated vegetable oils or margarine in animal models of colon, breast, and skin cancer. All seven studies showed that there was less tumor development with milk fat-based diets (Parodi, 2004). 

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. 

Both the total fat intake and the ratios between FAs of different classes influence the activity of immune cells. Such information was initially obtained through epidemiological human studies, and studies conducted with cultured cells and animal models. These studies showed that EFAs are required for the growth and maintenance of the immune cells, and free FAs are produced and secreted during the activation of these cells. A number of intervention studies regarding the effects of the amount and composition of dietary fat on human immune response have been conducted, results of which are discussed in the following sections. 

Research on cis-trans isomerization (CTI) of lipid double bonds focused both on the conversion that occurs in some bacteria enzymatically and on trans isomers that are present in mammalian cells after a dietary supplementation of chemically modified fats [3,4]. It is known that cis/trans isomeric mixtures of fats result from vegetable and fish oils manipulated through partial hydrogenation or deodoriza-tion processes that are frequently utilized in the food industry. Nutritional and epidemiological studies revealed some harmful effects of these unnatural lipids for human health. However, it must be pointed out that in the chemical manipulation of oils the structures of trans fatty acid residues consist of geometrical and positional isomers with unshifted and shifted double bonds compared with the natural cis compounds. With the name trans lipids we indicate these unnatural geometrical and positional isomers. It has to be mentioned for clarity that there... 

SERUM LIPOPROTEINS AND CARDIOVASCULAR EFFECTS In most countries, the risk of mortality due to coronary heart disease (CHD) is correlated with a high dietary intake of saturated fat and elevated serum cholesterol levels. France is an exception to this rule, with relatively low mortality from CHD despite the consumption of high quantities of saturated fats by the French (the French paradox ). Epidemiological studies suggest that widespread wine consumption... 

The rationale for an association between dietary fat intake and cancer comes from epidemiologic studies that observed ethnic differences in the incidence of cancer, which were linked to differences in fat intake (Kolonel et al., 1981). Initially, total fat intake was thought to be of primary importance, but now evidence supports a role of... 

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