We know that torectrapib was excellent at raising "good" HDL cholesterol, while simultaneously increasing the human death rate from heart attack to the point where it couldn't be ignored. We know that the Kitavans have low "good" HDL cholesterol and no heart disease. So we should forget good and bad cholesterol and concentrate on the things that really matter, which are probably
hyperglycaemia, hyperinsulinaemia and wheat. Plus a few other things like trans fats. But the HDL as "good" cholesterol hypothesis will not lie down, although it seems to have been dead for some time. The statins raise HDL, but can be ignored due to their host of confounding pleiotropic effects, inseparable from their cholesterol effects. The current flavour of the month for raising HDL,
since the demise of torcetrpib, appears to be niacin, vitamin B3, in multigram doses.
There is no doubt that niacin elevates HDL cholesterol levels and, according to those who follow these things, decreases overall mortality. Now niacin is a very interesting drug. Oh, at 2.0g a day niacin is a drug, not a vitamin. Its career began with Abraham Hoffer, who is still going strong, back in the 1950s. On the basis that "vitamin" doses of niacin had half emptied the psychiatric wards when the problem of pellagra was solved by Goldberger, Hoffer tried massive doses of B3 on schizophrenic patients. The idea was to see if they had a poor response to "normal" doses of B3 which could be overcome by high doses. It worked.
Hoffer's publication in 1954 was last-authored by Smythies, so I assume he was Hoffer's supervisor.
Smythies is also still going strong and has recently summarised the adrenochrome theory of schizophrenia in one of his many publications.
My guess is that niacin may be working by reducing adrenochrome in the brains of schizophrenics. I've no idea of how this works, but it is interesting to note that adrenochrome is an oxidation product and niacin is an effective antioxidant.
That dynamo of genuine cardiovascular research, Kummerow, has looked at adrenochrome in the blood of hypertensive patients. It's there and it mangles the vascular epithelium. Now, does niacin reduce adrenochrome in the blood stream as well as in the brain? It is, after all, a significant antioxidant and anti inflammatory agent. No one has looked at this as far as I know. I certainly don't know if this is the case, but I'm suspicious.
If it does, who cares about the HDL cholesterol effect? Like the statins, niacin appears to be a useful drug, possibly a very useful drug, chosen for the wrong reason. Unlike the statins, niacin has
relatively little "badness" attached to it. The problem with torcetrapib was that it ONLY adjusted cholesterol levels. Whatever its associated "badness" or "goodness" might have turned out to be.
That's what happens when you spend millions or maybe billions of dollars developing a drug based on a wrong hypothesis.