Coronary artery disease pathogenesis and treatment urgently requires a paradigm shift. Despite popular belief among doctors and the public, the conceptual model of dietary saturated fat clogging a pipe is just plain wrong. A landmark systematic review and meta-analysis of observational studies showed no association between saturated fat consumption and (1) all-cause mortality, (2) coronary heart disease (CHD), (3) CHD mortality, (4) ischaemic stroke or (5) type 2 diabetes in healthy adults.1 Similarly in the secondary prevention of CHD there is no benefit from reduced fat, including saturated fat, on myocardial infarction, cardiovascular or all-cause mortality.2 It is instructive to note that in an angiographic study of postmenopausal women with CHD, greater intake of saturated fat was associated with less progression of atherosclerosis whereas carbohydrate and polyunsaturated fat intake were associated with greater progression.3
Preventing the development of atherosclerosis is important but it is atherothrombosis that is the real killer
The inflammatory processes that contribute to cholesterol deposition within the artery wall and subsequent plaque formation (atherosclerosis), more closely resembles a ‘pimple’ (figure 1). Most cardiac events occur at sites with <70% coronary artery obstruction and these do not …
Red more: http://bjsm.bmj.com/content/early/2017/03/31/bjsports-2016-097285.full
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BUT...
It fails to mention the role of endothelial function which has been shown to be negatively influenced by saturated fat
It fails to acknowledge that PREDIMED was limited for saturated fat, no difference between groups, but MUFA & PUFA higher for nuts & OVOO
It states the Lyon Heart Study as an evidence of effect, this was a low fat intervention. Shouldnt conclude high fat good based on this
It appears confused, 'alpha linoleic acid, polyphenols & omega 3 fatty acids...'does it mean alpha linolenic acid? If so that is an omega 3
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