I needed to disable self sign-ups because I’ve been getting too many spam-type accounts. Thanks.
Cholesterol hypothesis debate thread
Is atherosclerosis caused by high cholesterol?
"If LDL‐cholesterol and ΔLDL‐cholesterol do not correlate with degree of atherosclerosis or with atherosclerosis growth, why does a high cholesterol predict cardiovascular disease? The answer may be that cardiovascular disease is not synonymous with atherosclerosis. A high LDL or total cholesterol may be secondary to uncontrolled factors that promote cardiovascular disease in other ways and cause hypercholesterolaemia at the same time, for instance lack of physical activity,58 mental stress,59 smoking, and obesity.60 It is generally assumed that their effect on cardiovascular disease is mediated through the high cholesterol, but this may be a secondary phenomenon. Physical activity may benefit the cardiovascular system by improving endothelial function,61 or by stimulating the formation of collateral vessels;62 mental stress may have a harmful influence on adrenal hormone secretion, smoking increases the oxidant burden; in these all situations the high cholesterol may be an epiphenomenal indicator that something is wrong. This argument also explains why some studies found atherosclerotic growth to be associated with initial or on‐study LDL‐cholesterol, but not with ΔLDL or total cholesterol. If the amount of LDL‐cholesterol in the blood were the determining factor, atherosclerotic growth should have been associated with ΔLDL‐cholesterol as well and to a higher degree."
"‘The more LDL there is in the blood, the more rapidly atherosclerosis develops.’ This 1984 statement by the Nobel Award winners Michael Brown and Joseph Goldstein1 has dominated research on atherosclerosis since then. As shown here, this hypothesis appears to be falsified by the fact that degree of atherosclerosis, and atherosclerotic growth, were independent on the concentration or the change of LDL‐cholesterol in almost all studies. The role of LDL‐cholesterol for atherosclerosis growth has been exaggerated, a finding with consequences for the prevention of cardiovascular disease. For instance, as the statins exert their beneficial influence on the cardiovascular system by several mechanisms, it may be wiser to search for the lowest effective dose instead of the dose with maximal effect on LDL‐cholesterol. Neither should an elevated LDL‐cholesterol be the primary target in cardiovascular prevention, as recently claimed by the American National Cholesterol Education Program, and researchers should direct more attention to other hypotheses.
I may have overlooked studies that have found an association between changes of LDL‐cholesterol or other lipid fractions, and atherosclerotic progression. However, although the presence of exposure‐response is not sufficient proof in itself of causality, it is difficult to explain its absence."
I think subclinical chronic Hypervitaminosis A promotes heart disease in at least three ways.
One way is via increased endothelium collagen turnover and the direct effects of excess retinoic acid on the endothelium.
Another way is by causing subclinical chronic Hypovitaminosis C leading to a lack of ascorbate needed to correctly repair damage to the endothelium as Pauling described.
Another way is that due to Hypovitaminosis C the enzyme pathway that converts cholesterol and oxysterols to bile acids is inhibited.