ofonorow wrote:Studies have shown that people with higher levels of homocysteine in their blood have a higher risk of coronary events. This study aimed to establish whether that link is causal, and if lowering homocysteine artificially would be beneficial.
I have seen many studies, or at least reports, over the years, and none have shown that artificially lowering Hsc is all the beneficial. So if this is new, it isn't really news. (But if this got mixed up with a statin study, who knows how legit the results are?)
Keep in mind that this study was started several years ago, and yes, in the time since it was started there have been other studies which have shown that lowering homocysteine through supplementation has not been an effective strategy. So yes, the outcome is not surprising, but I believe this is the longest and largest study to date looking at this issue and it probably puts the nail in that coffin. Also, it may not be "news" because the findings were reported at a medical conference about a year ago and you may have heard about it then.
Hsc is apparently like cholesterol, that is, a SYMPTOM of CVD. We should all know that treating symptoms rarely cures anything. (Too bad all this work, money and effort can't be directed at finding out whether the Pauling therapy has any value. Why not spend the time and effort studying a theory proposed by the world's ONLY 2 -time unshared Nobel prize winner? Why not study what Pauling/Rath claim is the CAUSE of CVD, and his suggested treatment?!? Bizzaro world.)
I came across this article which is an interesting read because it's an interview with someone who one of the pioneers of this hypothesis (and may have some parallels with the Pauling/Rath hypothesis):
http://www.chiro.org/nutrition/FULL/Kil ... y_MD.shtmlIn science, determining
causality is never an easy task, especially when complex biological systems are involved. There was some evidence to suggest that that the association between homocysteine levels could be causal, e.g. patients with homocystinuria often have thrombotic complications, as well as animal studies.
I should point out that even though a number of trials have failed to support the hypothesis that lowering homocysteine through B-vitamin supplementation can reduce cardiovascular events, they don't necessarily falsify the hypothesis that high levels of homocysteine can cause cardiovascular disease. It is still possible that chronic high levels of homocysteine can result in cardiovascular disease, but that the effects are irreversible (hence supplementation after the fact may not reduce risk). It is also possible that B vitamins increase CV risk through an independent mechanism which nullifies the benefit of lowering homocysteine. I'm not saying that any of these explanations are likely, but just to illustrate that it's not always straightforward (if new evidence convincingly showed that alternative explanations could account for the failure of these trials, the homocysteine issue may have to be approached with a different strategy).
Now with regards to Pauling's hypothesis that "chronic scurvy" is the cause of heart disease - the evidence is hardly compelling, in my view. Pauling has never shown that "chronic scurvy" actually exists in humans. Vitamin C has already been tested in randomized trials, and in doses of 500 mg it has not been effective in unselected populations (thus it suggests that epidemiological studies only show a correlation between low levels of ascorbate and heart disease and aren't showing a causal link). Of course, it doesn't mean that 18 grams of vitamin C per day isn't effective - but at this point, there's little published evidence to show that it would be. The fact that Pauling has two Nobel prizes is irrelevant.
Now, it's possible that vitamin C could be effective in a select group of patients (e.g. those with high Lp(a)). Maybe it needs to be given with lysine, and maybe it needs to be administered in high doses to have a substantial effect on Lp(a). But at this point - and correct me if I'm wrong - there is no published study showing that Pauling therapy substantially reduces Lp(a) levels. So at this moment in time, there's no justification for a large study in hundreds of patients. But given the recent evidence supporting the hypothesis that Lp(a) plays a causal role, there may be justification for a small trial designed to see if Lp(a) levels can be reduced with Pauling therapy. If the trial is positive, it may provide justification for a larger trial designed to see if using this strategy in patients with high Lp(a) levels will reduce the risk of cardiovascular events.