Interesting - Thank you for that - I had wondered how statins worked and where it all fits in - I am a miniscule bit wiser. It is all so interlinked and complex every door opening onto another.
Journal of Cellular and Molecular Medicine 5 (4) , 378–387 doi:10.1111/j.1582-4934.2001.tb00172.x
http://www.blackwell-synergy.com/doi...2001.tb00172.x
The beneficial effects of statins are the result of their capacity to reduce cholesterol biosyntesis, mainly in the liver, where they are selectively distributed, as well as to the modulation of lipid metabolism, derived from their effect of inhibition upon HMG-CoA reductase. Statins have antiatherosclerotic effects, that positively correlate with the percent decrease in LDL cholesterol. In addition, they can exert antiatherosclerotic effects independently of their hypolipidemic action.
Because the mevalonate metabolism generates a series of isoprenoids vital for different cellular functions, from cholesterol synthesis to the control of cell growth and differentiation, HMG-CoA reductase inhibition has beneficial pleiotropic effects. Consequently, statins reduce significantly the incidence of coronary events, both in primary and secondary prevention, being the most efficient hypolipidemic compounds that have reduced the rate of mortality in coronary patients. Independent of their hypolipidemic properties,
statins interfere with events involved in bone formation and impede tumor cell growth.
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