Below is some information regarding our understanding of cholesterol and its link between health and disease
(here) is a study showing that 75% of heart attack patients were not at high risk for an attack based on the current cholesterol guidelines. This is a tricky situation as drug manufactures resort to claiming that more and more people are in the “at risk” category and therefore candidates for cholesterol lowering medications. Ever on the lookout for increased market share, drug companies have even convinced the the American Academy of Pediatrics that giving cholesterol lowering medications to kids as young as eight is a good idea. As reported by the New York Times ()
Even the mechanism by which cholesterol lowering drugs work is also being examined. Emphasis is now being placed on the study of the C-Reactive Protein, which is an an indication of inflammation. Here is what the a American Heart Association journal (here) says in regards to the “inflammation hypothesis” and its link to coronary artery disease (CAD).
“Despite intensive basic and clinical investigation, coronary artery disease remains the principal cause of death and disability in the United States. In recent years, the appreciation of arterialinflammation as an important risk factor has had considerable implications for changing our approach to managing these patients.1,2 Arterial inflammation has emerged as central to the progression of atherothrombosis.3 Of the markers of inflammation, the high-sensitivity C-reactive protein (CRP) is the most studied, with evidence that it may also play a direct pathogenic role in atherosclerotic lesion formation.4– 11 In the absence of active infection, measurements of CRP are reasonably reproducible, comparable to measurements of total cholesterol.12,13 Additionally, elevated CRP appears to be a more potent risk factor than other mediators of inflammation, such as tumor necrosis factor-, interleukin-6, or serum amyloid A.4,14 A group of pharmacotherapies that are currently available, such as aspirin, statins, angiotensin converting enzyme inhibitors (ACE-Is), thienopyridines, and peroxisome proliferator-activated receptor (PPAR) agonists have been shown, in addition to their other properties, to reduce CRP and/or arterial inflammation. Although it is clear that elevated CRP denotes increased risk and emerging evidence suggests that there are novel therapies that result in lowering of CRP, the most important unanswered question is whether suppression of inflammation and consequent lowering of CRP will translate into a decrease in clinical events.15 Surprisingly, despite the importance of the question, the “inflammation hypothesis” of intentional CRP suppression as compared with standard care has not yet been tested. Such a prospective study of patients with established cardiovascular disease and elevated baseline CRP in which incremental pharmacotherapy would be guided by reassessments of the CRP marker could allow formulation of a rational therapeutic strategy instead of an approach of “polypharmacy” for every patient.”
Another more “active” method of controlling CRP is through a Paleo approach to eating. This route will control insulin levels (here), remove gut irritating foods, infuse a ton of antioxidants, and adjust ones Omega 3/Omega 6 balance to its proper place. All that is missing is some Vitamin D, good sleep, and some healthy stress management tools (Nor Cal Margarita anyone?).
This video never gets old. As Robb Wolf (here) has said, “It would be funny if people were not dying from this stuff.”
For further read check out Uffe Ravnkov”s (book) “The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease” or visit his site (here).
In his book “The Cholesterol Con” (here) Dr. Malcolm Kendrick discussing the lack of correlation between cholesterol levels in the blood and heart disease.