Vitamin C Forum

godsilove wrote:Studies have shown that cholesterol is thrombogenic, and the link between cholesterol and atherosclerosis is supported by animal models. Nonetheless, whether there is a direct causal link is a moot point, considering that lowering cholesterol has been shown to reduce the risk of heart disease.

the now often repeated claim that lowering cholesterol has been "shown to reduce the risk of heart disease" is an outright lie

ofonorow wrote:

godsilove wrote: What animal models? I submit that the only animal model known to occur in nature which creates a lesion similar to the human is the guinea pig. This was noticed and first published in 1950. It is possible to create "fatty streaks", in other species with a very high cholesterol diet, but these lesions seem to bear little relation to CVD in humans. (There are clever (non cholesterol) methods known that will create human-like lesions, such as restricting vitamin B6 or copper in the diet of apes.)

By the way, perhaps the strongest animal models of which you speak have been created in recent years through genetic engineering. Mice which have been genetically altered so they cannot produce their own vitamin C rapidly develop atherosclerosis of the aorta.
http://www.pubmedcentral.nih.gov/articl ... d=10639167

Obviously, animal models do not not completely mimic the same pathology as in humans. (Just think of various animal models for mental illnesses) They are however useful to establish proof-of-concept, and to investigate specific molecular and genetic pathways that cannot be experimented on with human subjects. Often, the entire disease process cannot be simulated in a specific animal model; but a specific component of it, e.g. plaque rupture can be mimicked.

The example of the GULO-knockout mouse is quite interesting; nonetheless, upon reading the paper I don't see any indication that the aortic lesions in these mice resemble those found in atherosclerotic humans, nor that is meant to be a model for heart disease.

It might interest you to know that mice models used to study atherosclerosis include apo-E and LDL receptor knockouts.

Furthermore, I believe that the now often repeated claim that lowering cholesterol has been "shown to reduce the risk of heart disease" is an outright lie, unless clarified to some particular sub group on the basis of some limited study. On what do you base this statement?

It's based on multiple, large randomized clinical trials, meta-analyses that systematically review these studies, as well as long term observational studies. I think it's fairly well established that lowering cholesterol (primarily through the use of statins) can reduce the risk of heart disease, although to varying degrees in different subgroups.

Note that it has been reliably shown that increasing vitamin C intake lowers total cholesterol, so I can understand medicine's confusion. When increased vitamin C supplementatio is reducing the "risk of heart disease", a side-effect is lowered cholesterol.

I'd be very intrigued by any RCTs showing that ascorbic acid lowers cholesterol as effectively as statins.

DonHarry wrote:No one is denying that statins lower cholesterol - they do, very well. The point is, as Dr Fonorow mentioned, is there a benefit to reducing a symptom instead of attacking the cause? Vitamin C lowers cholesterol, but only as a side effect of resolving the cause.

Only if you believe (The ever modified) cholesterol hypothesis does it make sense to block cholesterol production.

ofonorow wrote:

I'd be very intrigued by any RCTs showing that ascorbic acid lowers cholesterol as effectively as statins.

viewtopic.php?f=9&t=152

This thread is devoted to the large number of experiments by Emil Ginter on both guinea pigs and humans, and provides an overview. The Ginter work was referenced and discussed by Pauling in 1970 (long before statins) in HOW TO LIVE LONGER...