Processing and Nutrition of Fats and Oils (Institute of Food Technologists Series)
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Encyclopedia of Food Sciences and Nutrition
Selected type: Hardcover. Added to Your Shopping Cart. View on Wiley Online Library. This is a dummy description. Likewise, there is general agreement that lauric acid does not increase the risk of CVD when it replaced carbohydrate on an equal energy basis.
Although palmitic acid also is generally regarded as hypercholesterolemic and that it results in similar increases in total and LDL cholesterol as trans fats, the picture is less clear than for myristic acid. However, these same groups estimated replacement of carbohydrate by palmitic acid or trans fats results in similar increases in LDL cholesterol level.
Mensink et al found replacement of carbohydrate by palmitic acid, like a similar replacement by lauric acid, resulted in an increase in HDL level. However, the increase in HDL was less than the increase for lauric acid. The effect of palmitic acid on serum lipid and lipoprotein patterns is further confounded by the apparent modifying influence of dietary linoleic acid on the hypercholesterolemic effect of palmitic acid. Increasing the level of linoleic acid in the diet from 2.
Although, as mentioned above, there is support for the belief that stearic acid, unlike the other long chain saturated fatty acid, is not hypercholesterolemic, recent studies do not support this premise. Aro et al also found that stearic acid was not neutral with respect to its effect on serum lipid and lipoprotein patterns. In addition, there is epidemiological evidence Hu et al, that stearic acid increases the incidence of CVD.
Thus, in conclusion, there may be a serious question as to whether any of the long-chain saturated fatty acids are a satisfactory substitute for trans fats. There has been increasing interest recently in CVD risk factors other than those associated with fasting serum lipid and lipoprotein levels. The response of plasma lipids, in particular triacylglycerides TAG Footnote 30 , during the absorption of dietary fat has gathered appreciable interest over the past few years because humans, by eating regular meals, are usually in a postprandial state.
Thrombosis clot formation , endothelial dysfunction, and inflammation are increasingly acknowledged to be risk factors for CVD. However, these non-lipid risk factors have only been studied for a short time. As a result, the volume of data on the relationships of dietary fat to these risk factors and the confidence that can be placed on these relationships is much less well established than the relationships between dietary fat and plasma lipids and lipoproteins.
Exaggerated postprandial lipemia can give rise to chylomicron remnants which are known to be atherogenic. Thus there has been increasing interest in the relationship between postprandial lipemia and atherosclerosis. Several studies, over the past few years, have reported on postprandial lipemia in response to specific fatty acids. In general these studies show that the lipemia following a high fat meal is due primarily to TAG in triacylglyceride-rich lipoproteins TRL , namely the chylomicrons absorbed fat and VLDL fraction which are primarily of hepatic origin.
These studies also show the peak concentration of chylomicron TAG occurs between 3 and 4 hours following a high fat meal and then decreases to or near pre-meal levels by hours postprandial. These studies also have found that a high oleic acid meal tends to produce the highest peak concentration and the greatest load incremental TAG levels throughout the measurement period while a high stearic acid meal produces the lowest peak concentration and load.
Postprandial patterns for meals containing high levels of trans fatty acids or linoleic acid generally follow the same pattern as oleic acid whereas meals containing high levels of palmitic acid follow patterns more analogous to those of stearic acid.
Processing and Nutrition of Fats and Oils
It has been hypothesized that the lower TAG levels following a high stearate meal are due to lower absorption of stearic acid but this theory does not explain the lower levels following a high palmitate meal. Overall the results of these studies do not indicate a particularly adverse effect of trans isomers or any of the long chain saturated or unsaturated fatty acids on lipemic response following a high fat meal.
In addition, the fact that the effects of individual fatty acids on postprandial lipemia do not mimic their effects on lipid and lipoprotein CVD risk factors raises doubt about the role, if any, and thus the importance of postprandial lipemia on the development of CVD. Positive relationships have been found between CVD and several elements in the haemostatic system, such as factor VII activity, platelet function and plasminogen factors.
Likewise, FVIIc levels did not differ from baseline values for subjects fed a high oleate diet for 16 weeks following an 8-week run-in on a high Sat diet. Thus, observations to date do not indicate a relationship between fasting FVII activity and the type or amount of dietary fat.
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By contrast FVIIc levels were found to increase following a high fat meal. However, the increase was only significant following palmitate, oleate and trans fatty acids. The postprandial increases were not statistically significant following stearate and MCT. Thus, postprandial FVIIc levels did not follow the usually accepted pattern of CVD risk associated with trans fat and individual fatty acids.
The role of platelet function in CVD is not well defined even though platelet activation is recognized as a factor in arterial thrombosis. One of the problems encountered in assessing the effect of fat on platelet function is the lack of a satisfactory measure of platelets function in humans. Platelet function usually is assessed by measuring the tendency for platelets to aggregate in response to an agonist added collagen, ADP, arachidonic acid, etc.
No difference in agonist-induced platelet aggregation was found among subjects who consumed a high stearate and a high palmitate diet for 4 weeks even though rate of aggregation increased from baseline levels. On the other hand, platelet aggregation tended to decrease from baseline values, which followed a run-in period on a high saturated fat diet, when subjects were changed to moderate or high oleate diets. The diurnal activity of tissue plasminogen activator tPA , another factor involved in clot formation, was higher on a high palmitate diet than on a high trans fat diet.
In fact, the levels and pattern on the high trans diet were similar to those on a high PUFA diet even though the activity on the PUFA diet did not differ statistically from that on the palmitate diet. It is interesting to note that one research group found tPA activity correlated with postprandial TAG levels. On the other hand, stearate was found to result in significantly higher fibrinogen levels whereas trans fat, oleate, or a mixture of lauric, myristic and palmitate had no effect on fibrinogen levels.
These findings suggest that although stearate has minimal effect on serum LDL levels it may have an adverse effect on haemostasis. Some of the most convincing evidence of a relationship between dietary fat and non-lipid CVD risk factors has been found for biomarkers of systemic inflammation and endothelial dysfunction. This evidence has come from both epidemiological and experimental studies. There also is evidence that stearic acid and combination of lauric-myristic-palmitic acids may increase the levels of biomarkers relative to oleic acid.
Although there is increasing interest in the relationship between dietary fat and non-lipid CVD factors, because lipid and lipoprotein risk factors do not account for the total incidence of CVD, there is insufficient data to establish a meaningful relationship between type and amount of dietary fat and non-lipid CVD risk factors. The one exception may be the effect of trans fatty acids on surrogate measures of systemic inflammation and endothelial function. Stearic acid, trans fatty acids, and dairy fat: effects on serum and lipoprotein lipids, apolipoproteins, lipoprotein a , and lipid transfer proteins in healthy subjects.
Am J Clin Nutr ; Trans fatty acids and coronary heart disease. New Engl J Med ; High-density lipoprotein cholesterol as a predictor of coronary heart disease risk. Atherosclerosis ;SS Stearic acid absorption and its metabolizable energy value are minimally lower than those of other fatty acids in healthy men fed mixed diets. J Nutr ; Inflammatory bio-markers and cardiovascular risk prediction. J Intern Med ; The effect of palmitic acid on lipoprotein cholesterol levels and endogenous cholesterol synthesis in hyperlipidemic subjects.
Lipids ;S The effect of palmitic acid on lipoprotein cholesterol levels. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation ; Consumption of a solid fat rich in lauric acid results in a more favourable serum lipid profile in healthy men and women than consumption of a solid fat rich in trans -fatty acids.
J Nutr a; Replacement of dietary saturated fatty acids by Trans fatty acids lower serum HDL cholesterol and impairs endothelial function in healthy men and women. Arterioscler Thromb Vasc Biol b; Eritsland J. Safety considerations of polyunsaturated fatty acids.
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Cholesterolaemic effect of palmitic acid in relation to other fatty acids. Grundy SM. Comparison of monounsaturated and carbohydrates for lowering plasma cholesterol in men. Hamazaki T and Okuyama H. The Japan Society for Lipid Nutrition recommends to reduce the intake of linoleic acid. A review and critique of the scientific evidence. World Rev Nutr Diet ; Hayes KC and Khosla P.
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