Just because they have not found it does not mean it does not exist.
But what does this have to do with folic acid and B12?
And what does folic acid and B12 have to do with heart disease? According to Pauling and Levy and Bush - not much.
Moderator: ofonorow
Just because they have not found it does not mean it does not exist.
But what does this have to do with folic acid and B12?
ofonorow wrote:Wait a minute, this "new work on folic acid and B12" reinforces the importance of lowering cholesterol?? My brain hurts...
And what does folic acid and B12 have to do with heart disease? According to Pauling and Levy and Bush - not much.
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.
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?)
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.)
In 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.
Johnwen wrote: Doctors are bewildered by some people who they try all kinds of BP meds on and none seem to work within the prescriped guidelines and diruretics seem to be the only course of treatment only to find out after awhile they stop working also. L-Arginnine doesn't work either.
Homocysteine plays a role in cadiovascular disease in that it blocks the production of Nitrous Oxide which prevents the arteries from relaxing causing stress on the endothiel lining which can break down any weakened areas causing the healing cascade of events to occur.
Actually, sustained release arginine does lower BP in hypertensive individuals, but doesn't lower normal BP
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