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Pastimes : Heart Attacks, Cancer and strokes. Preventative approaches

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From: LindyBill4/28/2016 9:57:08 PM
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they are slowly starting to acknowledge that the cholesterol/sat-Fat theory of CAD is dead - and it has been obvious for a long time now(at least to me) that CAD appears to mostly be a disease mediated by the immune system. We now know that this thesis pushed on us by Keys and his buddies was fraudulent science - twisted facts, cherry-picking, withheld data etc.

My understanding of how Statins do their good bit ( and they really don't help all that much ) is by turning down inflammation. Other drugs that lower LDL don't appear to work (if defined as all cause mortality ).

circ.ahajournals.org

"CONCLUSION

Our understanding of atherosclerosis has evolved beyond the view that these lesions consist of a lifeless collection of lipid debris. Current evidence supports a central role for inflammation in all phases of the atherosclerotic process. Substantial biological data implicate inflammatory pathways in early atherogenesis, in the progression of lesions, and finally in the thrombotic complications of this disease. Clinical studies affirm correlation of circulating markers of inflammation with propensity to develop ischemic events and with prognosis after ACS. Intralesional or extralesional inflammation may hasten atheroma evolution and precipitate acute events. Circulating acute-phase reactants elicited by inflammation may not only mark increased risk for vascular events, but in some cases may contribute to their pathogenesis. This new insight into the role of inflammation in the pathobiology of atherosclerosis has initiated important new areas of direct clinical relevance. We can use inflammatory markers today for risk stratification. Future studies will gauge their utility as guides to monitor therapy. Finally, the quest to identify proximal stimuli for inflammation, as one pathogenic process in atherogenesis or trigger to lesion complication, may yield novel therapeutic targets in years to come"

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