Fatty acids, dietary total intake effects

We have seen in Section F that the dietary factors linked with the incidence of coronary heart disease reflect complex relations that cannot be simply based on ratios of polyunsaturated to saturated fats. It is now evident that not all saturated, polyunsaturated and monounsaturated fats play the same role in nutrition, n-3 Polyunsaturated fatty acids are not particularly effective in lowering serum cholesterol, but markedly reduce serum triacylglycerols in hypertriglyceridic subjects. The recent tendency has been to make nutritional recommendations on the basis of total fat intake and on the ratio of n-6 to n-3 polyunsaturated fatty acids. Reducing n-6 polyunsaturated fatty acids may be an effective way of utilizing relatively low and more practical amounts of fish oils. 

The details of population dietary guidelines for the quality and quantity of fat intake differ between countries. However, in consideration of prevention of CHD, dietary guidelines generally reflect advice to reduce average total fat intakes to 30-35% dietary energy and to lower saturated fat intakes to approximately 10% of dietary energy. Though the effect of trans fatty acids on the plasma LDL/ HDL ratio is less favorable than that of saturated fatty acids, dietary advice needs to reflect the relative intakes of these two types of fatty acids. Since... 

The relationship between diet and cancer risk is extremely complex (7). Factors that appear to enhance carcinogenesis under one set of conditions may have no effect or even inhibit carcinogenesis under different conditions (2). The link between dietary fat and cancer is complicated by many factors, in particular total calorie intake and fatty acid composition (2). Among the fatty acids that comprise lipid, only linoleic acid is clearly linked to the enhancement of carcinogenesis in rat manunary gland (5), pancreas (4) and colon (5). 

The amount of fat in the ration has little effect on the fat content of milk, but the fatty acid composition of the dietary fat greatly influences that of milk fat (Chapter 4). Neither the total protein content of milk nor the proportions of the individual proteins is greatly influenced by the amount or kind of protein in the diet except at very greatly reduced intakes. Overfeeding with protein does, however, increase the NPN content of the milk (Thomas 1980). Milk of normal composition with the normal content and proportions of proteins can be produced on protein-free diets with urea and ammonium salts as the only sources of nitrogen (Virtanen 1966). 

In contrast to lignans, few studies have been reported regarding the relationship between ALA and breast cancer. In a meta-analysis, Saadatian-Elahi et al. (2004) reported a significant protective effect of total n-3 fatty acids and breast cancer risk. In this assessment, three cohort and seven case-control studies were reviewed. The case-control studies revealed an inverse association between ALA and breast cancer risk. High dietary intakes of ALA were correlated with a reduced breast cancer risk (Franceschi et al., 1996). This study involved 2569 women with breast cancer and the result was supported by a cohort study conducted in the Netherlands (Voorrips et al., 2002). A significant inverse association was found between ALA content in breast adipose tissue and breast cancer risk (Klein et al., 2000 Maillard et al., 2002). Furthermore, ALA to LA ratio close to one was also significantly associated with lower breast cancer risk (Maillard et al., 2002). 

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. 

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. 

As shown in a Swedish cohort of healthy 50-year-old men with 20 years follow-up, proportion of 14 0 and 16 0 in serum cholesterol esters predicted the development of metabolic syndrome, independently of other metabolic and lifestyle factors [105]. Besides serum lipids, proportion of PA in adipose tissue is also related to insulin sensitivity. Unlikely 14 0 and 18 0, which were positively associated with insulin sensitivity, PA inversely correlated with insulin sensitivity in 59 healthy British men and women [134]. Since the authors excluded the effect of dietary intake for any of these SFA, they concluded that the reason is de novo lipogenesis in adipose tissue. In human skeletal muscle phospholipids, SFA [135,135] and especially PA [137] have been negatively associated with insulin sensitivity and Type 2 diabetes, [138] which could partly reflect dietary intake [139], In a Finnish cohort study of 4 years follow-up, impaired fasting glucose and Type 2 diabetes incidence were associated with serum nonesterified 16 0 levels, but were not associated with baseline dietary 16 0 intakes assessed from dietary records [140], Recently published prospective follow-up study showed that erythrocyte membrane fatty acids nominaly predict incident type 2 diabetes [141], In the American Atherosclerosis Risk in Commimities (ARIC) study, 2909 middle-aged men and women were followed for 9 years. The incidence of Type 2 diabetes was associated with total SFA levels of plasma cholesterol esters (also observed for 16 0 independently) and phospolipids (also for 16 0 and 18 0) [101]. In a more recent 4-year case-... 

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