Saturated Fat and Blood Triglycerides

As described in Section 4.2, there has been a dogma in the literature for many years indicating that the consumption of saturated fat is causal in dyslipidemia— specifically hypercholesterolemia, specifically raised LDL. This hypercholesterolemia is proposed in turn to be causally related to the development of atherosclerosis. Atherosclerosis is the most common manifestation of cardiovascular/cerebrovascular disease. This dogma is perpetuated by a large (and hence powerful in terms of consensus) group of researchers. If the dogma were correct, then we should be able to identify a correlation between the intake of saturated fat in the diet and the incidence of cardiovascular and/or cerebrovascular accidents. Siri-Tarino et al. (2010) undertook just such an analysis of nearly 350,000 individuals over 6-23 years of followup. Their analysis showed no coincidence between increased saturated fat intake and either cerebrovascular or cardiovascular accidents. The Siri-Tarino et al. (2010) work patently suffers from publication bias (Section 4.2.1). The effect of the bias in this case is an artificially increased risk ratio, despite which their study steadfastly shows no increase in risks. The work of Siri-Tarino and colleagues has been corroborated via at least one other meta-analysis (de Souza et al. 2015). Further, there is some suggestion that lowered intake of saturated fat is associated with increased risk of death from both ischemic and hemorrhagic strokes (Yamagishi et al. 2010). A recent meta-analysis (Sachdeva et al. 2009) looks at the level of blood lipids (HDL, LDL, and triglycerides) in patients at the time of their admission to hospital for treatment of atherosclerosis- driven pathologies. The expected relationship under the lipid/CVD hypothesis is an increase in the number of patients who fall into each LDL bin range as the LDL level increases, and also an increase for each increasing triglyceride bin value, as well as a decrease for each increasing HDL bin value. Again, in short (Section 4.1.1), these relationships were absent. Finally, one of the currently accepted risk factors for cardiovascular and cerebrovascular accidents is increased adiposity (Hubert et al. 1983). With that in mind, Cohen et al. (2015) have suggested that people have been largely following the Dietary Guidelines for Americans (and presumably similar parallel Western nation documents indicating and advocating high-carbohydrate, low-fat intakes) during the period 1965-2011. This period of adherence to this apparently fallacious advice is coincidental with the onset, progression, and ever-worsening current obesity pandemic, as well as the diabetes pandemic. Both problems appear to be related to the glycemic loading concomitant with carbohydrate consumption, which was added to the diet to replace the fat erroneously removed.

In summary, there is apparently no valid reason to restrict or limit the intake of saturated fats, with the caveat that to maintain health in the long term, the restriction of carbohydrates appears critical (Section 4.3.1), as does the restriction of polyunsaturated fatty acids (PUFAs) (Section 4.3.3). Ignoring either Sections 4.3.1 or 4.3.3 may render Section 4.3.2 fruitless with respect to the long-term health of individuals.

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