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Re: Study: Animal products necessary to reap the benefits of the ketogenic (Atkins) d
n-3 Fatty acids prevent whereas trans-fatty acids induce vascular inflammation and sudden cardiac death
Cambridge Journals Online - Abstract
In contrast to n-3 PUFA, the consumption of TFA from processed fats has no known health benefits. In fact, TFA are felt to be associated with harm, even at low levels of intake. TFA occur naturally at relatively low levels in meat and dairy products as a by-product of fermentation in ruminant animals; however, during the process of partial hydrogenation of vegetable oils, some cis double bonds are converted to trans, some become saturated and others migrate along the acyl chains resulting in a wide range of unnatural geometric and positional fatty acid isomers(15). As compared with the consumption of an equal number of calories from saturated or cis unsaturated fats, the consumption of TFA raises levels of LDL cholesterol, reduces levels of HDL-C and increases the ratio of total cholesterol to HDL-C, a powerful predictor of the risk of CHD(16). Recent studies have shown that TFA were independently associated with an increased risk of CVD, and contributed to disease through multiple mechanisms(3). For example, TFA (1) influence PG balance promoting thrombogenesis(17), (2) perturb essential fatty acid metabolism by inhibiting the conversion of linoleic acid to arachidonic acid and to other n-6 PUFA, which cause changes in the phospholipid fatty acid composition in the aorta(18), (3) activate systemic inflammatory responses, including substantially increased levels of IL-6, TNF-?, TNF receptors and monocyte chemoattractant protein(19), (4) increase levels of several markers of endothelial dysfunction, including soluble ICAM-1 (sICAM-1), soluble VCAM-1 and E-selectin(20), and (5) impair endothelial function, as reflected by a reduction in brachial artery flow(21). These observations suggest that TFA play a substantial role in the development of CHD. Clearly, TFA consumption causes a pro-inflammatory response within the vascular system.
n-3 Fatty acids prevent whereas trans-fatty acids induce vascular inflammation and sudden cardiac death
Cambridge Journals Online - Abstract
In contrast to n-3 PUFA, the consumption of TFA from processed fats has no known health benefits. In fact, TFA are felt to be associated with harm, even at low levels of intake. TFA occur naturally at relatively low levels in meat and dairy products as a by-product of fermentation in ruminant animals; however, during the process of partial hydrogenation of vegetable oils, some cis double bonds are converted to trans, some become saturated and others migrate along the acyl chains resulting in a wide range of unnatural geometric and positional fatty acid isomers(15). As compared with the consumption of an equal number of calories from saturated or cis unsaturated fats, the consumption of TFA raises levels of LDL cholesterol, reduces levels of HDL-C and increases the ratio of total cholesterol to HDL-C, a powerful predictor of the risk of CHD(16). Recent studies have shown that TFA were independently associated with an increased risk of CVD, and contributed to disease through multiple mechanisms(3). For example, TFA (1) influence PG balance promoting thrombogenesis(17), (2) perturb essential fatty acid metabolism by inhibiting the conversion of linoleic acid to arachidonic acid and to other n-6 PUFA, which cause changes in the phospholipid fatty acid composition in the aorta(18), (3) activate systemic inflammatory responses, including substantially increased levels of IL-6, TNF-?, TNF receptors and monocyte chemoattractant protein(19), (4) increase levels of several markers of endothelial dysfunction, including soluble ICAM-1 (sICAM-1), soluble VCAM-1 and E-selectin(20), and (5) impair endothelial function, as reflected by a reduction in brachial artery flow(21). These observations suggest that TFA play a substantial role in the development of CHD. Clearly, TFA consumption causes a pro-inflammatory response within the vascular system.
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