You might want to check out this link
SIRT1 longevity gene linked to Cholesterol.
http://www.imminst.o...o...st&p=270857
From your link-
"Researchers have been curious to find out whether SIRT1 has similar effects. In the new MIT study, researchers found that low SIRT1 levels in mice lead to cholesterol buildup in cells such as macrophages, a type of immune cell, due to reduced activity of a protein called LXR (liver X receptor). LXR is responsible for transporting cholesterol out of macrophage cells. When full of cholesterol, the macrophages can generate plaques that clog arteries. SIRT1 boosts LXR activity, so that cholesterol is expelled from macrophages and out of the body by HDL."
What I read is that macrophages have extra cholesterol within their cell walls. I tried to find a study that shows macrophages cause plaque. All I can come up with is an
association with plaque. Recent clinical and experimental evidence indicates that inflammatory processes in the vascular wall are the decisive factor that accounts for the rate of lesion formation and clinical development in patients suffering from atherosclerosis. The macrophages are there because inflammation is there. I think it is a stretch to blame high cholesterol in the macrophage cells for the formation of the plaque. It is smoke, but not a fire. A connection, but not yet proof that serum cholesterol is a cause of plaque. I don't think there is an explanation yet how cholesterol is the cause, research seems to be focused on inflammation, not cholesterol as a cause.
Your link is an example of why I think identifying cholesterol as bad is harmful. It causes a lot of useless speculation about ways to reduce cholesterol and get a new patented cholesterol lowering block buster drug. The effect of statins is very minor. That's why the enthusiasm for the 85 mg aspirin. The small dose of aspirin has almost the same risk reduction as statins. The aspirin is an anti-inflammatory, and statins are also anti-inflammatory.
Fifty years of statistics has not proven that total cholesterol is a predictor of plaque. A component of cholesterol, oxidized LDL is implicated, and it is easy to imagine an oxidized LDL particle causing inflammation. And there is statistical evidence that oxidized LDL could be the cause of the inflammation. But there is no evidence that serum cholesterol in and of its self is associated with plaque. So precision, by not using the word "cholesterol" as a synonym for "oxidized LDL",will stop the spinning of wheels exampled in the article you quoted. And maybe, someday, cholesterol will get the respect it should.
Matt, don't take this personally, the media blitz about the dangers of cholesterol has been well financed, effective, and long going. Many believe the story, and I know, abandoning the story was not easy for me. When a statement is internalized it is very difficult to examine its truth. But imprecision has reached the point where it is causing damage to research.