Folic acid and B12 not effective in secondary prevention

The discussion of the Linus Pauling vitamin C/lysine invention for chronic scurvy

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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#16  Post by Johnwen » Sun Jun 27, 2010 2:04 pm

--could someone
please break down the following sentence:



I thought I clarified this in the sentence after this one which reads!

So homocysteine dosen't directly cause the breakage but contributes to the chemical reactions which can lead to higher pressure traumas of the arteries.
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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#17  Post by w6nrw » Mon Jun 28, 2010 4:02 am

You are correct, johnwen. Thanks
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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#18  Post by Ralph Lotz » Tue Jun 29, 2010 8:53 am

When all else fails, 6 grams daily of betaine (TMG) will lower homocysteine levels.
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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#19  Post by godsilove » Tue Jun 29, 2010 2:07 pm

ofonorow wrote:
Again, here is where a comprehensive theory helps make sense out of the data. If homocysteine (like cholesterol) was a cause of cardiovascular disease, one would expect the effect to be random and fairly distributed throughout the cardiovascular system. For example, one would expect to see higher levels of plaque/CVD where the blood pools and slows. But it is just the opposite. Plaque usually forms close to the heart, where the pressure and forces are the greatest. This is what made Willis (and later others) believe CVD was caused by physical stress (plaque is the body compensating for weakness) and this is the basis of the Pauling/Rath unified theory. It is based on the understanding of what would make the arteries weak (lack of collagen caused by a lack of vitamin C).




All fine in "theory", but where is the actual data supporting these hypotheses?
- What is the evidence that plaque is mostly formed as a response to physical stress (rather than plaque formation leading to physical stress on the artery walls)? What experiments did Pauling/Rath/Willis or anybody else do to test this hypothesis?
- What is the evidence that it is a "lack" of collagen in the arteries of all patients with atherosclerosis?
- What is the evidence that excessive amounts of vitamin C are necessary to have an optimal amount of collagen?

You are entitled to your opinion, and your opinion is apparently shared by most everyone in medicine (who just happen to be part of a business making billions from the treatment of CVD.) Yes, Pauling's prizes are irrelevant, but it is a different thing for Linus Pauling to have made this claim, than for say, Owen Fonorow to make such a claim. He may have been wrong. Why has there been ABSOLUTELY NO PUBLICITY in the mainstream media that he made this claim?


Huh? I'm not sure what kind of publicity you're expecting (and several years after he proposed his theory?). If a well-designed study actually showed that lysine + vitamin C actually prevented heart attacks, then that would be a different matter. The public health implications would be huge - until then, it's unsupported and inconsequential.

I am confused. There is justification for a large study of vitamin B12 and folic acid, but not for investigating vitamin C? You seem pretty selective, considering that there is considerable evidence - when blood levels are actually measured - that low vitamin C does increase mortality, particularly cardiovascular mortality. http://www.ncbi.nlm.nih.gov/pubmed/14594788?dopt=Abstract I know of no such evidence for Hsc/B vitamins, for example.


You're conveniently ignoring the fact that vitamin C trials have been done already.

Going by the epidemiological study you cite, a 20 µmol/L difference in serum ascorbate levels was associated with a relative risk reduction of about 20% for all-cause mortality. If the association was not due to confounding and reflects a true causal relationship, then one would expect that increasing serum concentrations of vitamin C by 20 µmol/L would result in a decrease in all-cause mortality of about 20%. A daily dose of 500mg of vitamin C would increase serum levels by twice that amount. But large randomized trials using this amount have failed to show any benefit.

Homocysteine falls into the same category. There are a number of epidemiological studies which have shown an association between homocysteine and heart disease (Example). But as we've seen, lowering homocysteine with B vitamins does not seem to reduce rates of heart disease.


As for chronic scurvy, take your head out of the sand. It is the number one killer in the United States, and probably the world! (I gather you haven't bothered to read Levy's STOP AMERICA'S #1 KILLER).

But of course, given the billions involved, one could argue that the livelihoods of almost everyone in medicine is at stake, thus I would expect you (and most doctors) to be thoroughly confused. That is apparently the intention of some very smart people.

Too bad this attitude dooms a lot of people, many of them all too young, to a lot of suffering.



I see you've brought out the usual retorts (go read so-and-so's book, or doom-and-gloom for medicine if Pauling is to be believed). :roll:

I'm still waiting to see compelling evidence. If Levy's book is so amazing, I would expect that he has some concrete data demonstrating that (a) "chronic scurvy" actually exists, and (b) it is the "number one killer in America".

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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#20  Post by godsilove » Tue Jun 29, 2010 2:09 pm

Ralph Lotz wrote:When all else fails, 6 grams daily of betaine (TMG) will lower homocysteine levels.


But will this lead to any clinical benefit?

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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#21  Post by Johnwen » Tue Jun 29, 2010 3:26 pm

But will this lead to any clinical benefit?



http://www.rxlist.com/cystadane-drug.htm
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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#22  Post by godsilove » Tue Jun 29, 2010 4:44 pm

Johnwen wrote:
But will this lead to any clinical benefit?


http://www.rxlist.com/cystadane-drug.htm



I mean in people without homocystinuria

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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#23  Post by Johnwen » Wed Jun 30, 2010 2:56 am

I mean in people without homocystinuria


Probably do as much good as people without heart disease who take statins!

http://archinte.ama-assn.org/cgi/conten ... 70/12/1024
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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#24  Post by ofonorow » Wed Jun 30, 2010 3:04 am


All fine in "theory", but where is the actual data supporting these hypotheses?
- What is the evidence that plaque is mostly formed as a response to physical stress (rather than plaque formation leading to physical stress on the artery walls)?


Common knowledge and rational thinking. Do you doubt that cardiovascular disease occurs mostly near the heart in highly predictable locations and arteries? You seek "evidence" that plaque doesn't form uniformly throughout the cardiovascular system, is that what you are asking for? Ask any medical examiner, and perhaps heart surgeon or cardiologist. Dr. George Willis in the early 1950s was a cardiologist. He observed post mortem that plaques always seemed to form in his patients near the heart, and he was probably the first to notice that plaques formed where the physical forces on the arterial walls were the greatest.

It is you my dear skeptic that could debunk this theory, not by asking for data in support (the white swan) but by finding data that plaques are equally likely to form anywhere (the black swan). So you have turned the issue around. Nice try.


What experiments did Pauling/Rath/Willis or anybody else do to test this hypothesis?


Again I refer you to the series of Willis papers on the series of experiments designed to test this specific hypothesis and publishe in the Canadian Journal of Medicine, See: vitamincfoundation.org/pdfs No one in Willis's time new of Lp(a). We have also discussed similar Pauling/Rath experiments on guinea pigs, but this time, measuring Lp(a) (apo(a)) Do I have to cite again?


- What is the evidence that it is a "lack" of collagen in the arteries of all patients with atherosclerosis?


Where is the evidence that there is a lack of collagen in frank scurvy? Yes, for a succinct explanation, read Pauling or view the video. Vitamin C is an important factor in the endogenous production of collagen. It is my understanding that it plays a role in "hydrolyzing" lysine and proline into the collagen helix. (Copper and vitamin B6 also play a role, but they are rarely the critical missing nutrient.) When vitamin C is missing, (in the animals which can no longer produce their own vitamin C, and must therefore get their entire supply form the diet) the body cannot form collagen. Pauling cites Japanese test tube experiments showing that vitamin C must be present. I can look them up if you care..

- What is the evidence that excessive amounts of vitamin C are necessary to have an optimal amount of collagen?

I think you are asking what is the optimal vitamin C intake, which is really what this forum has been trying to determine from anecdotal experience for years. We do know that 10 mgs daily can prevent most people from falling apart - dying from scurvy. I'll turn it around, what conventional or medical study can you cite that has ever tried to find the optimal amount of vitamin C for this or any other purpose?
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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#25  Post by ofonorow » Wed Jun 30, 2010 3:25 am

You're conveniently ignoring the fact that vitamin C trials have been done already.


Trials? Oh come on.. Okay I'll bite - Please cite 5 of these so-called trials of which you speak where multi-gram doses of vitamin C are investigated by unbiased observers (i.e. people not making unconscionable money in the field of medicine.) A tenured professor for example.. (Although that isn't all that protective either - just ask the well known Harvard Medical professor/cardiologist who got dumped (forced to retire from Harvard Medical school) from even suggesting the Pauling/Rath theory might have merit. Yes, I can find his name..)

Going by the epidemiological study you cite, a 20 µmol/L difference in serum ascorbate levels was associated with a relative risk reduction of about 20% for all-cause mortality. If the association was not due to confounding and reflects a true causal relationship, then one would expect that increasing serum concentrations of vitamin C by 20 µmol/L would result in a decrease in all-cause mortality of about 20%. A daily dose of 500mg of vitamin C would increase serum levels by twice that amount. But large randomized trials using this amount have failed to show any benefit.


What large randomized trials are you referring to? These posts of yours make me feel like I am in the twilight zone.

But your point about ascorbate blood levels is interesting and worth analyzing. Note - this study measured blood levels (as opposed to food questionaires. I am not saying that such questionaires can't provide some valuable information.) The way I read the abstract, low vitamin C levels increases mortality, perhaps as much as 50% versus people with high blood levels. And that this was limited to ascorbate levels, and no such association with mortality was found by analyzing vitamin A or vitamin E levels.

Now we know that ascorbate levels in the blood vary in a known range (the kidneys buffer ascorbate) and in the terms I am more familiar with 10 mg leads to a 1 mg/dl level, 100 mg leads to 10 mg/dl level and 150 and above lead to the maximum levels of 15 mg/dl. (If someone can provide a conversion to uMol/L, that would help me. The point is that there is some maximum, and taking more vitamin C won't lead to higher blood levels. (Although levels in the blood can get higher for a short time, but the kidney pumps work to quickly lower the level to 15 mg/dl). So you are right, strictly in terms of mortality, taking 150 mg or 200 mg puts a person in the highest percentile, and we cannot tell from this study whether 500, 1000 or 18,000 mg provides any more benefit. This study is showing that low serum levels are dangerous.
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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#26  Post by VanCanada » Wed Jun 30, 2010 9:21 am

godsilove wrote:- What is the evidence that it is a "lack" of collagen in the arteries of all patients with atherosclerosis?

Pauling explains the vitamin C/collagen relationship beautifully in this 1986 book. He includes diagrams too, which I found to be worth many words in themselves. He was a brilliant scientist and brilliant communicator. If you can read that book and still have these questions then I'm afraid you may be wasting your time on this forum, since if he can't explain it, it may be long time before anyone else can.

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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#27  Post by BaronZemo » Thu Jul 01, 2010 3:56 am

Johnwen wrote:
Actually, sustained release arginine does lower BP in hypertensive individuals, but doesn't lower normal BP


In an ADMA + individual l-arginine will have no effect. If you read the article you posted you see that it says HEALTHY individuals with high Blood Pressure. This precludes individuals who have no responce to BP meds which presents as a problem. In a normal person with proper endothiel function L-Arginine will lower their BP.

http://www.ncbi.nlm.nih.gov/pubmed/19820234



I have high to borderline high bp and have tried arginine (not sustained release however) and it had no effect on bp...do you need sustained release and how much to get the effect?

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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#28  Post by bbtri » Thu Jul 01, 2010 5:36 am

BaronZemo wrote:
Johnwen wrote:
Actually, sustained release arginine does lower BP in hypertensive individuals, but doesn't lower normal BP


In an ADMA + individual l-arginine will have no effect. If you read the article you posted you see that it says HEALTHY individuals with high Blood Pressure. This precludes individuals who have no responce to BP meds which presents as a problem. In a normal person with proper endothiel function L-Arginine will lower their BP.

http://www.ncbi.nlm.nih.gov/pubmed/19820234



I have high to borderline high bp and have tried arginine (not sustained release however) and it had no effect on bp...do you need sustained release and how much to get the effect?

Sustained release has shown better results. In the study I linked to in my previous post, they used 1 gram twice a day. Do you also take Vit C, Vit D, fish oil, and Magnesium? That's what worked for me, along with exercise, but I had been exercising already.

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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#29  Post by Johnwen » Thu Jul 01, 2010 10:32 am

If you haven't had your homocysteine levels checked you might want to give L-Citrulline a try for a couple of weeks. If you still get no responce your going to need to get a homocysteine level check.
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Re: Folic acid and B12 not effective in secondary prevention

Post Number:#30  Post by BaronZemo » Sat Jul 03, 2010 7:29 am


I have high to borderline high bp and have tried arginine (not sustained release however) and it had no effect on bp...do you need sustained release and how much to get the effect?

Sustained release has shown better results. In the study I linked to in my previous post, they used 1 gram twice a day. Do you also take Vit C, Vit D, fish oil, and Magnesium? That's what worked for me, along with exercise, but I had been exercising alreadyyes I take all of those and excersise, but don't take timed release arginine




I take all of those and excersise, but do not take timed released arginine


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