Translations:Fat/37/en: Difference between revisions

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Several [[meta-analysis|meta-analyses]] (reviews and consolidations of multiple previously published experimental studies) have confirmed a significant relationship between saturated fat and high [[serum cholesterol]] levels, which in turn have been claimed to have a causal relation with increased risk of cardiovascular disease (the so-called [[lipid hypothesis]]). However, high cholesterol may be caused by many factors. Other indicators, such as high LDL/HDL ratio, have proved to be more predictive. In a study of [[myocardial infarction]] in 52 countries, the [[apolipoprotein B|ApoB]]/[[apolipoprotein A1|ApoA1]] (related to LDL and HDL, respectively) ratio was the strongest predictor of CVD among all risk factors. There are other pathways involving [[obesity]], [[triglyceride]] levels, [[insulin resistance|insulin sensitivity]], [[endothelium|endothelial function]], and [[thrombogenicity]], among others, that play a role in CVD, although it seems, in the absence of an adverse blood lipid profile, the other known risk factors have only a weak [[atherogenic]] effect. Different saturated fatty acids have differing effects on various lipid levels.

Several meta-analyses (reviews and consolidations of multiple previously published experimental studies) have confirmed a significant relationship between saturated fat and high serum cholesterol levels, which in turn have been claimed to have a causal relation with increased risk of cardiovascular disease (the so-called lipid hypothesis). However, high cholesterol may be caused by many factors. Other indicators, such as high LDL/HDL ratio, have proved to be more predictive. In a study of myocardial infarction in 52 countries, the ApoB/ApoA1 (related to LDL and HDL, respectively) ratio was the strongest predictor of CVD among all risk factors. There are other pathways involving obesity, triglyceride levels, insulin sensitivity, endothelial function, and thrombogenicity, among others, that play a role in CVD, although it seems, in the absence of an adverse blood lipid profile, the other known risk factors have only a weak atherogenic effect. Different saturated fatty acids have differing effects on various lipid levels.