Saturated fatty acids cholesterol effects

It is important to realize that epidemiology can provide only statistical correlations it can give no information about mechanisms. That requires experimental evidence. Many studies with animals and man confirm that certain saturated fatty acids in the diet elevate plasma LDL. This is mainly confined to lauric, myristic and palmitic acids. Those with lower or higher chain lengths have very little effect on blood cholesterol. Careful evaluation of the scientific evidence indicates that the main role of polyunsaturated fatty acids is to prevent the rise otherwise associated with saturated fatty acids. The effects of monounsaturated fatty acids on blood cholesterol were thought to be neutral until recent more carefully controlled studies indicated that they depress LDL and slightly elevate HDL concentrations. 

The intermediate m hydrogenation formed by reaction of the unsaturated ester with the hydrogenated surface of the metal catalyst not only can proceed to the saturated fatty acid ester but also can dissociate to the original ester having a cis double bond or to its trans stereoisomer Unlike polyunsaturated vegetable oils which tend to reduce serum cholesterol levels the trans fats produced by partial hydrogenation have cholesterol raising effects similar to those of saturated fats... 

The reason for the cholesterol-lowering effect of polyunsaturated fatty acids is still not fully understood. It is clear, however, that one of the mechanisms involved is the up-regulation of LDL receptors by poly-and monounsaturated as compared with saturated fatty acids, causing an increase in the catabolic rate of LDL, the main atherogenic lipoprotein. In addition, saturated fatty acids cause the formation of smaller VLDL particles that contain relatively more cholesterol, and they are utilized by extrahepatic tissues at a slower rate than are larger particles—tendencies that may be regarded as atherogenic. 

Considered by FDA to be saturated fatty acids (for labeling purposes) and to have an effect on plasma hpids and cholesterol. 

It is important to bear in mind when discussing the effect of dairy fat in association to heart disease that dairy products contain many different saturated fatty acids that do not exert the same biological response in terms of, for example, cholesterol levels. The saturated fatty acids in milk fat include shorter and medium chain fatty acids (2 0-10 0), lauric acid (12 0), myristic acid (14 0), palmitic acid (16 0), and stearic acid (18 0). Other fatty acids in milk fat are oleic acid (18 1) and linoleic acid (18 2n-6) as indicated in Table 1.2. 

In the SC lipids form two crystalline lamellar phases.27 The mixture of both phases produces the optimal barrier to water loss from SC. The balance between the liquid crystalline and the solid crystal phases is determined by the degree of fatty acid unsaturation, the amount of water, and probably by other yet undiscovered factors. A pure liquid crystal system, produced by an all-unsaturated fatty acid mixture, allows a rapid water loss through the bilayers with a moderate barrier action. The solid system produced with an all-saturated fatty acid mixture causes an extreme water loss due to breaks in the solid crystal phase.6,23 Studies with mixtures prepared with isolated ceramides revealed that cholesterol and ceramides are very important for the formation of the lamellar phases, and the presence of ceramide 1 is crucial for the formation of the long-periodicity phase.27 The occurrence of dry skin associated with cold, dry weather for example, may result from an extensive, elevated level of skin lipids in the solid state. Therefore, a material that maintains a higher proportion of lipid in the liquid crystalline state may be an effective moisturizer.6... 

Since then, there have been numerous studies that investigated the effect of different types and amounts of fat, individual fatty acids and other dietary components on plasma cholesterol level. It is now realized that all saturated fatty acids do not elevate plasma cholesterol levels to the same extent. The short-chain fatty acids, butyric (C4 o), caproic (C6 o), caprylic (Cs o) the medium-chain capric (Cio o) and stearic (Ci8 o) acids,... 

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). 

Clinical studies show that dietary cholesterol is a less potent regulator of plasma cholesterol than are saturated fatty acids. Results from meta-analyses predict that plasma cholesterol response to a 100 mg/day change in dietary cholesterol will be from 0.06 to 0.07 mmol/L. The data show that although dietary cholesterol elevates plasma total cholesterol and LDL-cholesterol level, it also increases the level of HDL-cholesterol such that there is little overall effect on the LDL HDL ratio (McNamara, 2000). 

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. 

In the early 1990s, a series of well-designed clinical studies convincingly demonstrated that TFAs increased plasma total and LDL-cholesterol to levels similar to those produced by saturated fatty acids. More than this, TFAs reduced plasma HDL-cholesterol level. The overall effect was that the ratio of LDL-cholesterol to HDL-cholesterol was approximately double that for an equivalent intake of saturated fatty acids (Ascherio et al., 1999). In addition, TFAs adversely affect other CHD risk factors. Plasma triglycerides and Lp[a] levels are increased (Ascherio et al., 1999) and it was shown recently that consumption of TFAs was associated with a deleterious increase in small, dense LDL particles (Mauger et al., 2003). 

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. 

Medium-chain fatty acids are saturated fatty acids because of the relatively shorter hydrocarbon chain, which does not facilitate unsaturation. The safety of medium-chain triacylglycerol (MCTs) in dietary oil has been debated, and associated effects on cholesterol metabolism remain unclear. Although some studies have shown that... 

There is substantial evidence that indicates that dietary fat can influence significantly not only serum levels of cholesterol and triacylglycerols but also the lipid composition and content of Apoproteins (156-159). Much attention has been placed on the effects of diet on LDL levels, and saturated fatty acid and cholesterol itself have been identified as the major nutritional factors that can raise serum LDL-cholesterol levels. However, LDL cholesterol is only one of the many risk factors for atherosclerosis, and it is not known if oxidative modification of LDL is an equally or more important factor in the pathogenesis of atherosclerosis than total LDL cholesterol per se. More longitudinal studies are needed to answer these questions. If lipid peroxidation is a major risk factor for atherosclerosis, then excess consumption of highly unsaturated fats may not be advisable. 

In addition to dietary cholesterol, saturated fatty acids also are thought to raise semm LDL-cholesterol levels as well as total cholesterol concentrations. The major effect of saturated fatty acids on serum cholesterol appears to be due to a reduction in LDL-receptor activity. It is likely that saturated fatty acids may contribute to a cellular redistribution of cholesterol and cholesterol oxidation derivatives, leading to a favorable environment by these lipid particles to suppress LDL-receptor synthesis. In addition to their effects (directly or indirectly) on LDL-receptor activity, saturated fatty acids also may promote the synthesis of apoB-containing lipoproteins. 

It is now known that not all saturated fatty acids are equally hypercholesterole-mic. For example, medium-chain saturated fatty acids of carbon length 8-10, as well as stearic acid (18 0), have little or no effect on serum cholesterol concentrations. In contrast, evidence indicates that palmitic acid (16 0), the principle fatty acid in most diets, can increase serum cholesterol concentrations in humans. However, in normocholesterolemic humans, dietary palmitic and oleic acids have been shown to exert similar effects on serum cholesterol, suggesting that only humans or animal species sensitive to dietary cholesterol and selected fats ( hyperresponders ) may exhibit significant changes in semm cholesterol in response to dietary fat intake. Myristic acid (14 0) and, to a lesser extent, lauric acid (12 0), which are relatively high in coconut oil, both can raise serum cholesterol and LDL-cholesterol levels. Overall, it is not clear why humans respond so differently to cholesterol or... 

Saturated fatty acids. The adverse effect of saturated fat on blood cholesterol level and its implication in cardiovascular disease has stimulated concern over the level of saturated fatty acids in the diet. Canola oil contains a very low level (<7%) of saturated fatty acids about half the level present in corn oil, olive oil, or soybean oil and about one-quarter the level present in cottonseed oil. Furthermore, canola oil contains only 4% of the saturated fatty acids (viz., lauric, myristic, and palmitic) that have been found to increase blood cholesterol level. Hence, canola oil fits well with the recommendation to reduce the amount of saturated fat in the diet. 

Appreciable research on the effect of canola oil on plasma cholesterol and lipoproteins has been reported. The primary impetus for this research was the finding that dietary monounsaturated fatty acids were as effective as polyunsaturated fatty acids in lowering plasma total and LDL cholesterol (100, 109). These findings also provided a possible explanation for the observation that canola oil was as effective as soybean oil in lowering plasma cholesterol in normolipidemic men (110). Prevailing theory had held that saturated fatty acids raised plasma cholesterol, polyunsaturated fatty acids lowered plasma cholesterol, and monounsaturated fatty acids were neutral, they neither raised nor lowered plasma cholesterol (111, 112). 

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