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 A Pauling Therapy Study Design Exercise 
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Ascorbate Wizard
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Post I don't understand the question
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I disagree that Hickey's point makes any sense at all.


So you don't believe the pharmaceutical companies would have tested Pauling and Rath's protocol, hoping that they could easily shoot it down? You believe that they simply ignored it, a potential cure? That is your opinion. I happen to agree with Hickey. If Pauling has made a serious error, we would have know about it big time - over and over.

Quote:

Look, if for whatever reason these products don't perform as well as we'd hope (in a trial), wouldn't you want to know this? You receive positive testimonials but what of the people that don't reorder or don't send such testimonials? Are they moving on to other things? Dying? Getting so much better that they leave the entire therapy behind? Who knows?


They don't work for everyone. They seem to work less often lately, possibly because of the new medicated stents. Since these substances are completely nontoxic, people can find out whether it provides relief in their individual case with minimal risk. Of course your doctor won't agree with this statement, but look at what he is offering.

The point that you seem to be dancing around is that what you want doesn't exist - even in the prescription world. Contrary to the daily propagana and the white lab coats, the science behind pharmaceuticals is very poor. Nothing in the pharmaceutical world works on everyone, and these drugs are toxic. Most of the studies have to do with assessing the risk of the toxic effects. This point escapes many people.
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Tell me something. If Dr. Willis proved that 1,500 mg of vitamin C (all by itself) could reverse heart disease ... then why did a study, conducted some forty years later by a colleague of Dr. Pauling (Dr. Rath) find that nearly double that amount of Vitamin C could only HALT the process?


???? Are you saying Rath used 3000 mg of vitamin C? I thought he was using his VitaCore formula? Where did this number come from?

Again, Willis was the first to run these type of studies, and he invented a new X-ray method for looking into the walls of arteries. This was 1950 for heavens sake! And for only 1500 mg daily (500 mg 3 times daily) he showed that 1/3 of the plaques got smaller. From memory, 4 people. 4 people's plaques stayed the same, and 4 people's plaques got slightly worse.

The proof of reversal was in guinea pigs, not humans. There was only one variable, vitamin C, and if you read The Reversibility of Atherosclerosis, you'll see that it is the culmination of his work. In an earlier study, his team proved that 100% of the guinea pigs deprived of one factor - vitamin C - developed atherosclerosis. And 0% of the controls getting the recommended vitamin C for guinea pigs developed this "heart" condition. Other than fraud, which was unheard of in 1950, there is no other explanation.

And that is the point. When experimental results may have been induced by some other factor, we don't really have a good study. I can think of multiple reasons for the Ornish results. There is only one possible reason for the Willis outcomes (again, other than fraud. It is a simple experiment to repeat. And Pauling and Rath did repeat it, but they were looking for Lp(a) in the pigs blood in the 1980s.)

So given that 100% of the pigs develop atherosclerosis on low vitamin C, they induced (and tested in part of the population) that the pigs had plaques. Then they slowly introduced vitamin C, and documented the arterial reversal - thus the reversibility of atherosclerosis by vitamin C. Simple. Clean. Elegant. Convincing. Professional. Good science.

Now, if I wanted to demonstrate reversal in a large population (larger than Willis's 12 subjects) I would want the subjects to have at least 10,000 mg daily. We know some people experience reversals of symptoms on 2500 mg of vitamin C and 2500 mg of lysine, while others apparently require more.

Anyway, back to study design. I am still hoping that this exercise will result in a good, inexpensive protocol. A repeatible experiment that will have no other possible explanation.

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Owen R. Fonorow, Orthomolecular Naturopath


Mon Jun 18, 2007 6:44 pm
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Post Re: I don't understand the question
ofonorow wrote:
???? Are you saying Rath used 3000 mg of vitamin C? I thought he was using his VitaCore formula? Where did this number come from?



Quote:
Composition and Administration of Nutritional Supplement Program


The following daily dosages of nutritional supplements were taken for a period of one year: Vitamins: Vitamin C 2700 mg, Vitamin E(d-Alpha-Tocopherol) 600 IU, Vitamin A (as Beta-Carotene) 7,500 IU, Vitamin B-1 (Thiamine) 30 mg, Vitamin B-2 (Riboflavin) 30 mg, Vitamin B-3 (as Niacin and Niacinamide) 195 mg, Vitamin B-5 (Pantothenate) 180 mg, Vitamin B-6 (Pyridoxine) 45 mg, Vitamin B-12 (Cyanocobalamin) 90 mcg, Vitamin D (Cholecalciferol) 600 IU. Minerals: Calcium 150 mg, Magnesium 180 mg, Potassium 90 mg, Phosphate 60 mg, Zinc 30 mg, Manganese 6 mg, Copper 1500 mcg, Selenium 90 mcg, Chromium 45 mcg, Molybdenum 18 mcg. Amino acids: L-Proline 450 mg, L-Lysine 450 mg, L-Carnitine 150 mg, L-Arginine 150 mg, L-Cysteine 150 mg. Coenzymes and other nutrients: Folic Acid 390 mcg, Biotin 300 mcg, Inositol 150 mg, Coenzyme Q-10 30 mg, Pycnogenol 30 mg, and Citrus Bioflavonoids 450 mg.


http://www4.dr-rath-foundation.org/THE_ ... /pub18.htm


Mon Jun 18, 2007 8:19 pm
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Ascorbate Wizard
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Post One Answer to the question
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The most important finding of this study is that coronary artery disease can be effectively prevented and treated by natural means. This nutritional supplement program was able to decrease the progression of coronary artery disease within the relatively short time of one year, irrespective of the stage of this disease. Most significantly, in patients with early coronary calcifications this nutritional supplement program was able to essentially stop its further progression. In individual cases with small calcified deposits, nutritional supplement intervention led to their complete disappearance (Figure 4).


One answer to your question is that Rath did observe reversals, per above comment, or better results than Willis (1500 mg) who reported in 1953 that some (1/3) of the plaques only "diminished."

Note: These results are better than any drug, especially any result from the many statin studies.

Also, the Rath method focused on calcification, a simple non infasive measureent. I'm not certain about the Willis X-ray technique.


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Tue Jun 19, 2007 5:23 pm
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Post Dr. Rath
Owen,

Dr. Rath only offers evidence of ONE reversal of a "small calcification" (out of a trial that included 55 patients):

Quote:
A total of 55 patients, 50 men and 5 women, with documented coronary artery disease assessed by Ultrafast CT, were recruited for the study.


Quote:
Figure 4 shows the actual Ultrafast CT scans of a 51 year old patient with early, asymptomatic, coronary artery disease. The patientsÕ first Ultrafast CT scan was performed in 1993 as part of an annual routine check-up. The scan film revealed small calcifications in the left anterior descendent coronary artery as well as in the right coronary artery. The second CT scan was performed one year later at which time the initial calcium deposits had further increased. Figure 4.a shows two Ultrafast CT scan images taken before the nutritional supplement program. Subsequently, the patient started on the nutritional supplement program. About one year later the patient received a control scan. At this time point, coronary calcifications were not found (Figure 4b), indicating the natural reversal of coronary artery disease.


One out of 55 is much better than what the allopathic counterparts have to offer but it's probably a lot different than what most people are expecting and are frankly led to believe.

We also don't know what role the other nutrients (and phytochemicals) may have played in the results (of Dr. Rath's study). We don't know if more lysine would have improved the results. We don't know if more or less Vitamin C would have improved the results. In essence, we don't know if Pauling's Therapy (Vitamin C and lysine) would help more or less than Dr. Willis' therapy or Dr. Rath's therapy. There's a lot we don't know. There are however a lot of assumptions being made.


Tue Jun 19, 2007 6:00 pm
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Post another study
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1: Lipids. 1995 Dec;30(12):1179-83.

Antioxidant effects of tocotrienols in patients with hyperlipidemia and carotid stenosis.

Tomeo AC, Geller M, Watkins TR, Gapor A, Bierenbaum ML.

Kenneth L. Jordan Research Group, Montclair, New Jersey 07042, USA.

Antioxidants may have a role in the prevention of atherosclerosis. In the present trial, we investigated the antioxidant properties of Palm Vitee, a gamma-tocotrienol-, and alpha-tocopherol enriched fraction of palm oil, in patients with carotid atherosclerosis.

Serum lipids, fatty acid peroxides, platelet aggregation and carotid artery stenosis were measured over an 18-month period in fifty patients with cerebrovascular disease. Change in stenosis was measured with duplex ultrasonography.
Ultrasound scans were done at six months, twelve months, and yearly thereafter.

Bilateral duplex ultrasonography revealed apparent carotid atherosclerotic regression in seven and progression in two of the 25 tocotrienol patients, while none of the control group exhibited regression and ten of 25 showed progression (P < 0.002).

Serum thiobarbituric acid reactive substances, an ex vivo indicator of maximal platelet peroxidation, decreased in the treatment group from 1.08 +/- 0.70 to 0.80 +/- 0.55 microM/L (P < 0.05) after 12 mon, and in the placebo group, they increased nonsignificantly from 0.99 +/- 0.80 to 1.26 +/- 0.54 microM/L.

Both tocotrienol and placebo groups displayed significantly attenuated collagen-induced platelet aggregation responses (P < 0.05) as compared with entry values. Serum total cholesterol, low density lipoprotein cholesterol, and triglyceride values remained unchanged in both groups, as did the plasma high density lipoprotein cholesterol values.

These findings suggest that antioxidants, such as tocotrienols, may influence the course of carotid atherosclerosis.

PMID: 8614310 [PubMed - indexed for MEDLINE]



http://tinyurl.com/23pzyp


Last edited by Seymore Spectacles on Tue Jun 19, 2007 10:53 pm, edited 1 time in total.

Tue Jun 19, 2007 10:39 pm
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Post even low dosages may slow progression
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1: J Intern Med. 2000 Nov;248(5):377-86.

Antioxidant Supplementation in Atherosclerosis Prevention (ASAP) study: a randomized trial of the effect of vitamins E and C on 3-year progression of carotid atherosclerosis.

Salonen JT, Nyyssönen K, Salonen R, Lakka HM, Kaikkonen J, Porkkala-Sarataho E, Voutilainen S, Lakka TA, Rissanen T, Leskinen L, Tuomainen TP, Valkonen VP, Ristonmaa U, Poulsen HE.

Research Institute of Public Health, University of Kuopio, Kuopio, Finland and Department of Clinical Pharmacology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. jukka.salonen@uku.fi


OBJECTIVES: To study the efficacy of vitamin E and C supplementation on the progression of carotid atherosclerosis, hypothesizing an enhanced preventive effect in men and in smokers and synergism between vitamins.

DESIGN AND SUBJECTS: Double-masked two-by-two factorial trial, randomization in four strata (by gender and smoking status) to receive twice daily either 91 mg (136 IU) of d-alpha-tocopherol, 250 mg of slow-release vitamin C, a combination of these or placebo for three years. A randomized sample of 520 smoking and nonsmoking men and postmenopausal women aged 45-69 years with serum cholesterol >/= 5.0 mmol L-1 were studied.

SETTING: The population of the city of Kuopio in Eastern Finland.

INTERVENTION: Twice daily either a special formulation of 91 mg of d-alpha-tocopherol, 250 mg of slow-release vitamin C, a combination of these (CellaVie(R)) or placebo for three years.

MEASUREMENTS: Atherosclerotic progression, defined as the linear regression slope of ultrasonographically assessed common carotid artery mean intima-media thickness (IMT), was calculated over semi-annual assessments.

RESULTS: The average increase of the mean IMT was 0.020 mm year-1 amongst men randomized to placebo and 0.018 mm year-1 in vitamin E, 0.017 mm year-1 in vitamin C and 0.011 mm year-1 in the vitamin combination group (P = 0.008 for E + C vs. placebo).

The respective means in women were 0.016, 0.015, 0.017 and 0.016 mm year-1. The proportion of men with progression was reduced by 74% (95% CI 36-89%, P = 0.003) by supplementation with the formulation containing both vitamins, as compared with placebo.

CONCLUSIONS: Our study shows that a combined supplementation with reasonable doses of both vitamin E and slow-release vitamin C can retard the progression of common carotid atherosclerosis in men. This may imply benefits with regard to other atherosclerosis-based events.

PMID: 11123502 [PubMed - indexed for MEDLINE]


http://tinyurl.com/2xq2by


Tue Jun 19, 2007 10:49 pm
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Ascorbate Wizard
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Post Good point
I'll look at those additional studies, you posted, but what do you like/dislike about them?

Your point (below) is right on. There are generally too many variables in studies with humans, because you can't control all the variables all the time.

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We also don't know what role the other nutrients (and phytochemicals) may have played in the results (of Dr. Rath's study). We don't know if more lysine would have improved the results. We don't know if more or less Vitamin C would have improved the results. In essence, we don't know if Pauling's Therapy (Vitamin C and lysine) would help more or less than Dr. Willis' therapy or Dr. Rath's therapy. There's a lot we don't know. There are however a lot of assumptions being made.


This is exactly why I personally didn't pay much attention to that Rath study. And why I find the Willis studies, while preliminary, very good. Willis varied one factor - vitamin C.

And again, while the small Willis study in humans was inconclusive (but highly encouraging) it was the Reversal of Atherosclerosis study in guinea pigs that "proved" the vitamin C connection, (I hate to fall in the trap set by medicine and use the word unscientific word "prove"). Willis showed that vitamin C, and vitamin C alone, has the ability to reverse existing plaques in living beings which, like us, do not make their own vitamin C.

This has been repeated. Now, can vitamin C do the same for humans? The Willis study seems to say that a "measly" 1500 mg can about 30-60% of the time. About 2/3 didn't get worse.

The problem with comparing Rath and Willis may be apples and oranges. (And Rath starts out his paper in error, saying that his study is the first of its kind. Maybe with that particular formula, but ignoring the pioneering Willis work is an error. )

Rath studied calcification, and we know from Bush cardioretinometry and Levy, that calcified plaques are much harder to treat and reverse. (I personally believe that the best nutrient for calcified plaques is probably vitamin K.)

While I never really thought much about it, the Willis studies show pictures of the actual arteries, and it may be in fact mean that these pictures rely on calcium in the deposits. It doesn't look like it to me though.

It is a complicating factor that not all plaque/blockage has calcium, and not all arteries with calcium have any blockage impeding blood flow.

This is why agreeing on a measurement - how and what to measure - is important.

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Wed Jun 20, 2007 8:37 am
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Ascorbate Wizard
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Post Good study
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Change in stenosis was measured with duplex ultrasonography.

Ultrasound scans were done at six months, twelve months, and yearly thereafter.


Bilateral duplex ultrasonography revealed apparent carotid atherosclerotic regression in seven and progression in two of the 25 tocotrienol patients, while none of the control group exhibited regression and ten of 25 showed progression (P < 0.002).



Thanks for this. I like this study in that, to my knowledge, it varied one factor - a form of vitamin E. (I'd just like to know the relationship between the researchers and companies that market this particular form of the vitamin.)

I don't know a great deal about ultrasound, but I suspect that as a diagnostic technique, it is getting more refined and accurate all the time. If any reader knows how much such a test costs, that would be helpful. As well as any ideas why they decided to run them so infrequently.

Now, it is my personal opinion that a primary function of vitamin E in the body is to recycle (regenerate) the chronically low levels of vitamin C in most people, especially heart patients. (The Harvard Rimm study that made news about vitamin E was designed based on questionaires in such a way as to ignore any contribution of vitamin C - and the value of vitamin E unexpelctedly "popped out." ) So the study you cite is also a very encouraging study visa vis the Pauling/Rath unified theory.

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Wed Jun 20, 2007 8:49 am
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Ascorbate Wizard
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Post Wow - another very good study
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CONCLUSIONS: Our study shows that a combined supplementation with reasonable doses of both vitamin E and slow-release vitamin C can retard the progression of common carotid atherosclerosis in men. This may imply benefits with regard to other atherosclerosis


Thank you for the second study. This seems to show that even half the Willis dosage may have benefit, especially in conjunction with vitamin E. More support for Willis/Pauling/Rath.

So given this confirming work, what more would you like to see? (I can see people running out to by more vitamin C and vitamin E as we speak..) Lysine? Proline?

As a starting point, we'd want to measure the effect of at least 10,000 mg of vitamin C, 6000 mg lysine, some amount of vitamin E and CoQ10 and magnesium. If ultra-fast CT scan, then vitamin K too. Proline for Lp(a), etc.

As a thought experiment, lets say money is no object. Lets assume we could afford almost any study. What would we like to know?

I'd personally like to measure the following for 2 to 3 months with no intervention, other than ordinary medications. As a Base line.

Ultrasound.
Blood assays (including Lp(a) and cholesterol)
Cardioretinometry
Stress Testing
Arterial Stiffness Index (Computerized Blood Pressure Device)

Then start the intervention (at least 10,000 mg vitamin C) and measure the same measurements weekly for at least 3 months.

Then add 6000 mg lysine, and measure for 3 months.

Then add 300 mg proline, and measure for 3 months.

Etc.

A starting and ending Ultra-Fast CT scan would also be good data.

The point is that this would give us some idea of the value of every component in the Pauling therapy. Of course, it is not perfect, because over time, vitamin C by itself will lower cholesterol, so that delayed affect might be interpreted as the next nutrient.

So ideally, you added one nutrient until no further benefit is noticed, and then add another.

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Wed Jun 20, 2007 9:02 am
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Post Re: Good point
ofonorow wrote:
I'll look at those additional studies, you posted, but what do you like/dislike about them?


Owen,

Thank you for your thoughtful replies. I'll try to address the issues you raise in your first post but I'll wait until I'm home to (more thoroughly attempt to) answer the "dream" study design questions. :)

I like the first study, on tocotrienols, because (as you said) it studies the effect of one (group of) substance(s) and it employs the use of a control group.

I found the second study to be of interest because of what it reveals and does not reveal. First of all, it utilizes relatively small dosages of vitamin C (500mg of time-release C) and a rather conservative dosage of vitamin E (as alpha tocopherol) as well. And yet, it still manages to bring about some effect, primarily in men (also interesting).

I believe this study may provide a small piece of the puzzle. It's impossible to know the relevance of such a study unless we look at it in context of the many other studies that have been are yet to be conducted. I also thought it would be good to bring it up because there is some controversy about the efficacy of time-release C products.

Ultimately, the second study just adds to the number of questions we should acknowledge having:

Quote:
Rath studied calcification, and we know from Bush cardioretinometry and Levy, that calcified plaques are much harder to treat and reverse. (I personally believe that the best nutrient for calcified plaques is probably vitamin K.)


I agree with this statement and I also think that vitamin K, in particular MK7 (a form of vitamin K2) looks promising in this regard.

Quote:
Cardiovascular Benefits of Natural Vitamin K2

Natural Vitamin K2 from food sources has been linked to significant inhibition of calcium accumulation in the arteries. A recent study published the Journal of Nutrition with over 4,800 participants, showed that those with the highest
natural K2 consumption (45mcg) had 50% less arterial calcium accumulation and an equal reduction in risk of cardiovascular events. This was not found for vitamin K1.

Compelling in vivo research may provide the basis for new indications


In a study accepted by the journal Blood, researchers looked at the potential to regress calcification with vitamin K. Arterial calcification was induced in rats in an accepted model. Vitamin K2 supplementation was shown to reduce the previously accumulated arterial calcium precipitates. Additionally, the regression of arterial calcification was accompanied by restoration of arterial distensibility, or elasticity as compared to the control animals. Human research in this area is necessary to confirm these findings.


http://www.plthomas.com/MenaQ7.htm


Wed Jun 20, 2007 11:21 am
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Post Re: Wow - another very good study
ofonorow wrote:

So given this confirming work, what more would you like to see? (I can see people running out to by more vitamin C and vitamin E as we speak..) Lysine? Proline?

As a starting point, we'd want to measure the effect of at least 10,000 mg of vitamin C, 6000 mg lysine, some amount of vitamin E and CoQ10 and magnesium. If ultra-fast CT scan, then vitamin K too. Proline for Lp(a), etc.

As a thought experiment, lets say money is no object. Lets assume we could afford almost any study. What would we like to know?




Owen,

I think the design you proposed would provide a wealth of most welcome information. Here's another study-design that I think might work quite well.

Proposed Design #1


Group Selection

+ We take one group of (middle-aged) participants who are basically just using medication. I think ten people, preferably five men and five women, would do.

+ We take another group of ten (again 5 men and 5 women) middle-aged participants who AREN'T taking medication and provide them with only the most basic nutrients that Pauling called for in his patent. This group is included because I'm assuming that most middle-aged people have some degree of arterial plaque.

+ Finally, we select a group that is very similar to the second group (the non-medicated folks) and we give them an expanded version of the Pauling Protocol. In other words, we add the CoQ10, magnesium, MK7, proline, vitamin E, etc.

Note: Come to think of it, we might want to start with 15 people in each group (because of the small size of the study and the generally expected drop-out rate).

Length of Study and Testing Methods


+ I think the study should span the course of a year. This will allow for real results to manifest.

+ In terms of what diagnostic tests ought to be performed, I generally agree with what you laid out:

+ Just prior to the study's start date and directly after the completion of the study, "we" perform an:

1. Ultrasound.

2. Blood Chemistry * - Cholesterol Panel, Homocysteine, C-Reactive Protein, Lp(a) and a Complete Blood Chemistry Panel including Liver Enzymes (for signs of toxicity)

* I think the blood work should also be conducted at the six-month mark to rule out any unforeseen health problems.

3. Cardioretinometry - This may serve to popularize this new diagnostic test and offer useful information as well.

4. Stress Testing

5. Arterial Stiffness Index (Computerized Blood Pressure Device)

6. Ultra-Fast CT

7. A "Quality of Life" questionnaire. "We" could devise a standard form that would detect matters beyond just the obvious. Did any of these protocols cause any side-effects (including the medicated group). How did each treatment affect other measures of health - overall energy-levels, memory, mood, etc.

The questionnaire would not only point out the differences between the medicated and supplemented groups but it would also point to other worthwhile areas to research in the future.

Tell me what you think of my suggestions. They're just off the top of my head and I'm not a clinician by trade ... so, please be patient with me. :)


Wed Jun 20, 2007 3:43 pm
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Ascorbate Wizard
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Post Memories
Quote:

Group Selection

+ We take one group of (middle-aged) participants who are basically just using medication. I think ten people, preferably five men and five women, would do.

+ We take another group of ten (again 5 men and 5 women) middle-aged participants who AREN'T taking medication and provide them with only the most basic nutrients that Pauling called for in his patent. This group is included because I'm assuming that most middle-aged people have some degree of arterial plaque.

+ Finally, we select a group that is very similar to the second group (the non-medicated folks) and we give them an expanded version of the Pauling Protocol. In other words, we add the CoQ10, magnesium, MK7, proline, vitamin E, etc.

Note: Come to think of it, we might want to start with 15 people in each group (because of the small size of the study and the generally expected drop-out rate).


First, this is bringing back a memory. Dr. Warren Levin was the physician who was willing to conduct the NIH research the first time we submitted a grant request. After they refused, Dr. Levine suggested a study on Lp(a). He advised keeping it focused and simple. We should keep this in mind, because there is an effect on Lp(a) - Dr. Levin noticed it over and over and tried to get a letter about this published in JAMA (which was published in the Townsend Letter for Doctors and Patients http://www.townsendletter.com ) I just posted some email from a person who had very high Lp(a) prior to her adopting the Pauling therapy many years ago.

Now, in your proposal as to subject selection, how do we keep it fair? For example, what if the group on medication has read Levy, and is taking vitamin C without telling the doctors?

That is why I like the idea of selecting anyone on almost any basis, and using each person as their own control. We monitor them for 2-3 months. (I suppose to save money, we would be within ou rights to restrict the study group to those whose plaques are getting worse during the baseline. Unless we wanted to show that the Pauling therapy doesn't make plaques worse in generally healthy people? This can probably be a later study.).

After the baseline measurements show plaques getting worse, the nutritional intervention is added.

This way we are measuring apples to apples. It would provide real knowledge about how well current heart patients are likely to do by simply adding the Pauling Therapy to their current course of treatment.

Again, the value of Willis over Rath is that we know it was the vitamin C that has the effect, where in the Rath study, it could have been one of 20 different substances. So keeping the intervention to a minimum actually provides more useful information. I think to be completely faithful to Pauling the intervention should be 10,000 mg vitamin C and 6000 mg lysine. This is a "can't miss" combination in my opinion, at least for the initial study.

Now, given the cost, what measurements do we absolutely need? Can we invent our own? I like your questionaire, but I would also like a video record, as many people who can't walk across the room, are painting their homes in 30 days. The old picture is worth a thousand words.


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Thu Jun 21, 2007 7:33 am
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'seems to me that this is where animal testing could be a more
informative test:

we know that most animals make C at a certain rate

I assume that they don't make lysine at a 0.6x rate, so

we take two animal groups, we add lysine to one group, not the other

we feed both groups the same--lots of junk food, for example.

when we physically examine for arterial plaque at a later date
we would have a relatively accurate comparison.

perhaps we could include a 3rd group--animals that don't make their
own C. And then another test using those animals that don't make
there own C, but including supplements.

You can see where this is going . . . .

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Thu Jun 21, 2007 8:35 am
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Post Re: Memories
ofonorow wrote:

First, this is bringing back a memory. Dr. Warren Levin was the physician who was willing to conduct the NIH research the first time we submitted a grant request. After they refused, Dr. Levine suggested a study on Lp(a). He advised keeping it focused and simple. We should keep this in mind, because there is an effect on Lp(a) - Dr. Levin noticed it over and over and tried to get a letter about this published in JAMA (which was published in the Townsend Letter for Doctors and Patients http://www.townsendletter.com ) I just posted some email from a person who had very high Lp(a) prior to her adopting the Pauling therapy many years ago.

Now, in your proposal as to subject selection, how do we keep it fair? For example, what if the group on medication has read Levy, and is taking vitamin C without telling the doctors?


I believe we could achieve this in a few different ways.

1. We could test for vitamin C levels prior to accepting them. This information would be useful to have anyway.

2. By carefully screening the potential participants and by making it clear that whatever information they provide will be viewed without judgment. In other words, they would likely admit to using supplements if they're divulging such information to a sympathetic ear - as opposed to their own (probably) judgmental physician.

Most studies have to rely on careful screening and the good judgment of the conductors. If we combine this with the vitamin C test ... I think that should be enough.

ofonorow wrote:

That is why I like the idea of selecting anyone on almost any basis, and using each person as their own control. We monitor them for 2-3 months. (I suppose to save money, we would be within ou rights to restrict the study group to those whose plaques are getting worse during the baseline. Unless we wanted to show that the Pauling therapy doesn't make plaques worse in generally healthy people? This can probably be a later study.).

After the baseline measurements show plaques getting worse, the nutritional intervention is added.

This way we are measuring apples to apples. It would provide real knowledge about how well current heart patients are likely to do by simply adding the Pauling Therapy to their current course of treatment.

Again, the value of Willis over Rath is that we know it was the vitamin C that has the effect, where in the Rath study, it could have been one of 20 different substances. So keeping the intervention to a minimum actually provides more useful information. I think to be completely faithful to Pauling the intervention should be 10,000 mg vitamin C and 6000 mg lysine. This is a "can't miss" combination in my opinion, at least for the initial study.

Now, given the cost, what measurements do we absolutely need? Can we invent our own? I like your questionaire, but I would also like a video record, as many people who can't walk across the room, are painting their homes in 30 days. The old picture is worth a thousand words.



I'm supportive of using Pauling's original C and lysine approach. If it shows some measure of success, we would then have the basis for expanding our research to include other substances that are likely to be beneficial as well.

I also like your idea about the video diaries. We could even provide some guidelines about how such diaries should be recorded.

I think the bare-minimum, in terms of testing would be to have a CBC:

http://www.lef.org/newshop/items/itemLC381822.html

Add to that, the Lp(a) test.

Then, I think we could choose from the following:

a) Intima-media thickness ultrasound may be a safe, informative and relatively inexpensive test that we could employ at the beginning and end of the study.

http://www.uchospitals.edu/specialties/ ... riovision/

b) The Cardioretinometry test is another option that we might be able to use for a nominal fee. Perhaps Dr. Bush (or a colleague of his) might be willing to donate their services or provide assistance for a reduced-rate ... in exchange for the positive exposure the study might provide. I believe that's how Dr. Rath was (in part?) able to use the CT testing.

c) I would love to have a before and after Ultra-Fast CT scan as well but I'm not thrilled about the exposure to radiation that it would subject our participants to. So, if there's a way to avoid this I would prefer it. Still, the information it may yield could make it invaluable.

http://www.labiomed.org/cardiology/ebt/ ... wsweek.htm


Thu Jun 21, 2007 9:04 pm
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w6nrw wrote:
'seems to me that this is where animal testing could be a more
informative test:

we know that most animals make C at a certain rate

I assume that they don't make lysine at a 0.6x rate, so

we take two animal groups, we add lysine to one group, not the other

we feed both groups the same--lots of junk food, for example.

when we physically examine for arterial plaque at a later date
we would have a relatively accurate comparison.

perhaps we could include a 3rd group--animals that don't make their
own C. And then another test using those animals that don't make
there own C, but including supplements.

You can see where this is going . . . .


I think this is a reasonable proposal. It certainly would be more economical. But, I must tell you that I believe a human-trial is what we currently need the most.

If we conduct such studies on rats or guinea pigs ... we'll likely derive some valuable information from them but we won't really know how well that will translate to us (human beings).

The thing we truly need, in my opinion, is real-world evidence that this therapy works (in an objective way) in the population that is most likely to use it (middle-aged to senior men and women).

I fear that an animal study won't do much to impress skeptical users or any potential converts.


Thu Jun 21, 2007 9:20 pm
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