Statin Use

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

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Statin Use

Post Number:#1  Post by scottbushey » Wed Dec 23, 2009 2:41 am

It is my goal to get a VAP test done soon; in light of recent posts I have made and my lab values, I am wondering why it would be bad going on a statin. If Statins raise LPA and High dose VC lowers it, and if Statins cause a CoQ10 deficiency and I am replacing those losses, why would it be bad going on a statin? Is not what I am doing offsetting that which the statins destroy?

Frustrated.......

Scott

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Re: Statin Use

Post Number:#2  Post by godsilove » Wed Dec 23, 2009 7:18 pm

scottbushey wrote:It is my goal to get a VAP test done soon; in light of recent posts I have made and my lab values, I am wondering why it would be bad going on a statin. If Statins raise LPA and High dose VC lowers it, and if Statins cause a CoQ10 deficiency and I am replacing those losses, why would it be bad going on a statin? Is not what I am doing offsetting that which the statins destroy?

Frustrated.......

Scott


The effect of statins on Lp(a) is still uncertain. A few studies have shown an increase, some have found a decrease, and others have found no significant change.


* Are the side effects a major concern for you? Most are relatively mild and are reversible if you stop taking the medication, but there are rare side effects that can be potentially fatal e.g. rhabdomyolysis.
* Is the cost of statins affordable and does it seem cost-effective?
* Are the benefits significant enough?

Some risks of statins to consider:
- side effects, e.g. muscle pains and myopathies (possibly due to CoQ10 deficiency)
- possible increased risk of developing Type II diabetes (about a 0.6% absolute increase in the JUPITER study)

Benefits to consider:
- reduction in total and LDL cholesterol
- anti-inflammatory effects, which could reduce your hsCRP
- reduction in risk of cardiovascular morbidity and mortality (JUPITER trial showed the number needed to treat (NNT) with Crestor for two years was 95 to avoid an MI, stroke or death from any cause; the NNT for four years was 36)

I've referenced the JUPITER study, but bear in mind that this trial enrolled patients with high hsCRP (>2.0), but relatively low LDL-C (<130). The absolute benefits of statins are generally higher in patients with more risk factors.

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Re: Statin Use

Post Number:#3  Post by ofonorow » Thu Dec 24, 2009 4:37 am

At a high level, the statin is artificially lowering an important substance in your blood stream, i.e., treating a symptom. A substance, cholesterol, that is not only required for good health, but may also be elevated because of dental or other toxicity. So artificially lowering your body's own natural defense mechanism seems to be tempting fate.

Thanks to Pauling/Rath we know that ordinary cholesterol doesn't generally adhere to arterial walls like Lp(a) will, and really poses little threat (and a lot of theoretical benefit as described in Dr. Levy's STOP AMERICA'S #1 KILLER - livonbooks.com). A high Lp(a) number, with small molecular weights, would be a sign of significant CVD risk. (Larger Lp(a) molecules are not as atherogenic.)

Apparently, taking CoQ10 can mitigate many of the risks (e.g. the stories of vegetarian women who were put on statins for "prevention" and lost major internal organs. If a cell doesn't have CoQ10 it dies. A meat diet provides at least 5 to 10 mg of CoQ10.) And the destruction of muscle fiber, explains why many statin users experience muscle pain, and lets not forget the threat of heart failure seems to be connected to CoQ10 depletion.

The effect statins have on lowering CoQ10 was recognized almost immediately, because the CoQ10 researchers were from Merck. (Remember the Merck patent to add CoQ10 to HMG-COA reductase inhibitors). What else may these foreign agents to the body interfere with? The drug companies have been reduced to saying that statins are necessary because of other effects, such as reducing inflammation. However, vitamin C is an excellent way to reduce inflammation, and Thomas Levy introduces a theory in his book is that inflammation is the way we have evolved to "move" ascorbate to the site of injury, as white blood cells are the first to saturate with vitamin C.

As we have discussed previously, because of the magic 95% confidence interval, 1 in 20 studies might produce an erroneous results. In my humble opinion, this is why Pfizer has run more than 400 studies on Lipitor. The odds are that something like 20 studies would erroneously produce a positive result. (Unfortunately, I don't believe they really even have a single one :lol: )

At best, statins might not harm you, but there is surprisingly little evidence given all the studies that they will help you in any way. At worst, these drugs will make matters much worse.
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Re: Statin Use

Post Number:#4  Post by scottbushey » Thu Dec 24, 2009 5:08 am

Owen,
At this point, I believe I have not given the VC therapy long a enough trial; I will continue w/ my dynamic flow to bowel tolerance and add Guggul and Inositol Hex daily.

~My recent Vitamin D test came back at 3; I am increasing that to 7000IU daily.

Thanks again,

Scott

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Re: Statin Use

Post Number:#5  Post by godsilove » Thu Dec 24, 2009 9:42 am

ofonorow wrote:At a high level, the statin is artificially lowering an important substance in your blood stream, i.e., treating a symptom. A substance, cholesterol, that is not only required for good health, but may also be elevated because of dental or other toxicity. So artificially lowering your body's own natural defense mechanism seems to be tempting fate.

Thanks to Pauling/Rath we know that ordinary cholesterol doesn't generally adhere to arterial walls like Lp(a) will, and really poses little threat (and a lot of theoretical benefit as described in Dr. Levy's STOP AMERICA'S #1 KILLER - livonbooks.com). A high Lp(a) number, with small molecular weights, would be a sign of significant CVD risk. (Larger Lp(a) molecules are not as atherogenic.)


LDL does adhere to arterial walls - one way through which this occurs is through binding to proteoglycans in the extracellular matrix of the arterial wall.

In the case of LDL, there are several lines of evidence that indicate that lowering LDL through statins has a benefit and that LDL has a causal role.

There is no evidence that heart risk increases with the number of dental amalgams - in fact, a Swedish study found that there was an inverse association between heart risk and the number of dental amalgams, but this association disappeared once they controlled for factors like socioeconomic status.

Apparently, taking CoQ10 can mitigate many of the risks (e.g. the stories of vegetarian women who were put on statins for "prevention" and lost major internal organs. If a cell doesn't have CoQ10 it dies. A meat diet provides at least 5 to 10 mg of CoQ10.) And the destruction of muscle fiber, explains why many statin users experience muscle pain, and lets not forget the threat of heart failure seems to be connected to CoQ10 depletion.

The effect statins have on lowering CoQ10 was recognized almost immediately, because the CoQ10 researchers were from Merck. (Remember the Merck patent to add CoQ10 to HMG-COA reductase inhibitors). What else may these foreign agents to the body interfere with? The drug companies have been reduced to saying that statins are necessary because of other effects, such as reducing inflammation. However, vitamin C is an excellent way to reduce inflammation, and Thomas Levy introduces a theory in his book is that inflammation is the way we have evolved to "move" ascorbate to the site of injury, as white blood cells are the first to saturate with vitamin C.


CoQ10 supplementation might be a good idea, but primarily based on the precautionary principle. The evidence for its benefits in reducing side effects of statins is still inconclusive.

As we have discussed previously, because of the magic 95% confidence interval, 1 in 20 studies might produce an erroneous results.


A meta-analysis would take this into account - even if one in 20 studies is based on a chance finding, the results of the other 19 would by and large correct this. Recent meta-analyses of statins for both primary and secondary prevention have been positive.

In any case, this assumes that all the primary endpoint results have a p-value of 0.05, when in fact the statistical signficance is even higher for many trials (e.g. for JUPITER it was <0.01, IIRC)

In my humble opinion, this is why Pfizer has run more than 400 studies on Lipitor. The odds are that something like 20 studies would erroneously produce a positive result. (Unfortunately, I don't believe they really even have a single one :lol: )


I don't think Pfizer has run 400 studies on Lipitor - many of them were probably run by universities, government agencies, etc. A search for "atorvastatin" on clinicaltrials.gov yields 376 results. A search for "atorvastatin" with Pfizer as a sponsor yields 87 results. If you look through the results, you'll see that there are studies for a wide variety of indications and in different subpopulations.

At best, statins might not harm you, but there is surprisingly little evidence given all the studies that they will help you in any way. At worst, these drugs will make matters much worse.


Your "at best" scenario is inaccurate, given that the evidence clearly shows that statins do provide a benefit in reducing heart attacks and strokes, and also reducing all-cause mortality. The magnitude of the benefit, however, varies depending on whether it is used as primary prevention (as I assume in Scott's case) or secondary prevention. The benefits are more pronounced in the latter case, since the absolute risk of cardiovascular death is much higher to begin with for these patients.

They are not a magic bullet - successful prevention strategies will address a variety of risk factors and make use of lifestyle interventions as well as pharmacological agents (including supplements) where appropriate. Scott can choose to address other risk factors like his hypertension, high CRP, etc through other interventions, but LDL still poses an independent risk. No one can predict the future, but there are ways to estimate what someone's risk of having a heart attack and stroke in the next 10 years is based on evidence from large cohort studies like Framingham. We also know from a recent meta-analysis that the relative risk reduction in major coronary events is roughly 30%, and the relative risk reduction in deaths is roughly 12%, over a mean follow-up period of 4 years. So if you have a 3% chance of having a heart attack in the next five years, you reduce your absolute risk by about 1%. For some, a 1 in 100 chance of avoiding a heart attack over a five-year period is not worth it - for others, it may be.

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Re: Statin Use

Post Number:#6  Post by ofonorow » Fri Dec 25, 2009 5:19 am

The "400" number is from Pfizer's Lipitor advertising on TV. You say they are lying? Good help me prove it, as I am preparing a letter to Big Brother about the false and misleading advertising promulgated by big pharma.

If statin drugs are so beneficial, I would expect that to be clear from at least 380 of these studies. I submit that the reason so many studies have been run is because the results were otherwise disappointing.

Under the vitamin C theory, humans are missing a substance that strengthens arteries. The therapy is to replace the missing substance.

What is the theory on which medicine gives a poison to heart patients? You can quote all the studies and statistics you want, but without a basic theory, it is mostly noise with an underlying imperative to sell a mutli-billion dollar drug to people who don't really need it.

And I know that LDL can accumulate, but I doubt the effect is important. You ignore the Biesegal work that showed the it was Lp(a) and only Lp(a) (post mortem) in the plaque in aortas. Lp(a) is "sticky", LDL is generally not. (But see Levy's STOP AMERICA'S #1 KILLER about how the arterial wall can compensate for weakness.)

If it were true about the Swedish study and amalgams, then I have lost all respect for Swedish researchers who are obviously bought and paid for. Under the vitamin C theory, dental toxicity might explain the MAJORITY of heart disease because of its effect depleting vitamin C.
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Re: Statin Use

Post Number:#7  Post by godsilove » Fri Dec 25, 2009 6:21 am

ofonorow wrote:The "400" number is from Pfizer's Lipitor advertising on TV. You say they are lying? Good help me prove it, as I am preparing a letter to Big Brother about the false and misleading advertising promulgated by big pharma.


It is a misleading claim, albeit probably not a false one.

If statin drugs are so beneficial, I would expect that to be clear from at least 380 of these studies. I submit that the reason so many studies have been run is because the results were otherwise disappointing.


As I said before, you're looking at different indications - not just heart disease, but things like COPD and certain cancers as well. So it may well be that the studies in specific conditions are postive, whereas the ones in other conditions are almost all negative. And many of these trials are presumably small - if they are disappointing, then Pfizer is probably not going to invest in doing more expensive, larger trials which are necessary if they want the indication added on to the label. For every positive Phase III trial, there is probably at least one positive prelimary trial.

Under the vitamin C theory, humans are missing a substance that strengthens arteries. The therapy is to replace the missing substance.


Where's the evidence that it is missing? You suggest taking megadoses of vitamin C - how much of it actually goes towards supposedly replacing missing ascorbate in arteries, as opposed to being excreted in the urine??

What is the theory on which medicine gives a poison to heart patients? You can quote all the studies and statistics you want, but without a basic theory, it is mostly noise with an underlying imperative to sell a mutli-billion dollar drug to people who don't really need it.


There is a vast literature on LDL and it's role in heart disease, which forms the underlaying basis for LDL-lowering therapies. Anti-inflammatory effects are also postulated to be involved in the consistently observed benefit of statins. This isn't mere statistical noise without any a priori biological plausibility.

And I know that LDL can accumulate, but I doubt the effect is important. You ignore the Biesegal work that showed the it was Lp(a) and only Lp(a) (post mortem) in the plaque in aortas. Lp(a) is "sticky", LDL is generally not. (But see Levy's STOP AMERICA'S #1 KILLER about how the arterial wall can compensate for weakness.)


Do a literature search - a number of studies using different experimental methods show that LDL is found in plaques.

If it were true about the Swedish study and amalgams, then I have lost all respect for Swedish researchers who are obviously bought and paid for.


"Obviously"? Just because a study does not confirm your preconceptions does not mean that there is foul play going on. Do you ever consider that your heroes like Pauling, Rath and Levy could be wrong about certain things?

Under the vitamin C theory, dental toxicity might explain the MAJORITY of heart disease because of its effect depleting vitamin C.


And yet the hypothesis isn't supported by the evidence, since amalgams haven't been shown to cause heart disease.

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Re: Statin Use

Post Number:#8  Post by ofonorow » Sat Dec 26, 2009 4:46 am


Under the vitamin C theory, humans are missing a substance that strengthens arteries. The therapy is to replace the missing substance.


Where's the evidence that it is missing? You suggest taking megadoses of vitamin C - how much of it actually goes towards supposedly replacing missing ascorbate in arteries, as opposed to being excreted in the urine??


Again, you can get up to speed on the now more than 100,000 studies of vitamin C that have been conducted since the 1930s by reading Pauling's HOW TO LIVE LONGER AND FEEL BETTER. You may not agree with him, but at least you would be aware of much of the now "hidden" research that has been conducted.

The obvious answer to "evidence that C is missing" is that if you do not obtain at least 10 mg of vitamin C in the diet for a period of approximately one month - you will die. However, virtually every other animal does not operate under these conditions. They do not require vitamin C in the diet to exist. I wrote a paper to summarize a tiny bit of the extensive vitamin C "evidence", here: http://vitamincfoundation.org/NaturalC.htm

Again, what "theory" are the numerous studies of statin drugs testing? Many of the studies, at least when I still bothered to review them, found that statins do indeed lower cholesterol. No one disputes the remarkable ability of statin drugs to lower cholesterol. However, I know that cholesterol is used to make the sex hormones, vitamin D from sunlight, transports fat soluble vitamins, such as E and CoQ10, is a major component of cell membranes and nerve fiber and brain tissue, is one of natures "detoxifying" materials in the blood stream, and that if one eats less cholesterol, the liver has evolved to produce more!

I also know of reports by Dr. Graveline and others of numerous problems in those taking statins, not the least of which is transient global amnesia. (Dr. Graveline is worried about airline pilots taking these drugs), problems sleeping, increased risk of cancer, muscle aches and pains, CoQ10 reductions leading to heart failure and major organ transplants.

Therefore, I say again, what theory is there that artificially reducing this substance is beneficial, especially to sick heart patients? The "cholesterol theory" is probably the answer, (but then why even mention inflammation?) and holds that elevated cholesterol is the cause, and not a result of heart disease. However, I submit that this theory cannot hold water, and that LDL does NOT generally adhere by itself to the walls of arteries as Lp(a) does (Lp(a) is a form of LDL with a sticky apo(a) component. You can argue with University of Chicago researchers who have studied the "kringles" on the lysine/proline binding sites of the Lp(a) molecule. )

As far as the "expensive urine" claim, the answer is again in Pauling's book, but I submit that we "optidosers" eliminate no more ascorbate than all the other animals do that manufacture ascorbate 24/7 (adjusting for body weight).

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Re: Statin Use

Post Number:#9  Post by Johnwen » Sat Dec 26, 2009 5:36 pm

Has anybody ever read this report of studies????

http://www.trit.us/moderndiseases/statin.html

A little closer to home!

http://www.vitamincfoundation.org/statinalert/

Hay well were at it lets get that HDL up. It's THE GOOD CHOLESTERAL RIGHT??? NOT!!!! :(

http://cholesterol.about.com/lw/Health- ... blems-.htm
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Re: Statin Use

Post Number:#10  Post by ofonorow » Sun Dec 27, 2009 5:52 am

Great, thank you for the Weston Price (first) link. Great summary.

p.s. Makes me curious about what Weston-Price has on vaccinations/mercury and autism?
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Re: Statin Use

Post Number:#11  Post by Dolev » Sun Dec 27, 2009 7:04 am

Price himself, of course, never wrote about vaccines or autism, since his book was published in 1939. The Price-Pottenger Nutrition Foundation does extensive work on cholesterol, since Price's writings are so encouraging of meat eating. They will not even give permission for any of their photos or articles to be used by any organization espousing vegetarianism. I haven't seen much from this foundation, of which I am a member, about vaccines or autism, but here is one audio recording from the PPNF vice-president: http://www.ppnf.org/catalog/ppnf/ppnf_speaks_out.htm
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Re: Statin Use

Post Number:#12  Post by Ralph Lotz » Tue Dec 29, 2009 8:13 am

Where's the evidence that it is missing? You suggest taking megadoses of vitamin C - how much of it actually goes towards supposedly replacing missing ascorbate in arteries, as opposed to being excreted in the urine??


For answers regarding the pharmacokinetics of ascorbic acid read:
Ascorbate, The Science of Vitamin C -Download for $6.00
http://www.lulu.com/product/download/as ... e%29/56725

The other primary factor in the Pauling Therapy is lysine, not lysine alone:
Case Report: Lysine/Ascorbate-Related Amelioration of Angina Pectoris
Linus Pauling

http://faculty.washington.edu/ely/paulinglysine.html
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Re: Statin Use

Post Number:#13  Post by ofonorow » Sat Jan 02, 2010 6:05 am

There is no evidence that heart risk increases with the number of dental amalgams - in fact, a Swedish study found that there was an inverse association between heart risk and the number of dental amalgams, but this association disappeared once they controlled for factors like socioeconomic status.

If it were true about the Swedish study and amalgams, then I have lost all respect for Swedish researchers who are obviously bought and paid for.

"Obviously"? Just because a study does not confirm your preconceptions does not mean that there is foul play going on. Do you ever consider that your heroes like Pauling, Rath and Levy could be wrong about certain things?


This has nagged me because it is quite obvious that this study is meaningless, if not bogus, on its face without having to read it. These days, dental work is practically ubiquitous in the modern world. Almost everybody has some kind of dental work, primarily because of the poor, sugary western diet. So how can you infer anything without looking at people who don't have ANY dental work? (Such peoples have been found to be consistently WITHOUT heart disease.)

A symptom of the western diet is rotting teeth, so while no epidemiological study can claim that amalgams cause (or do not cause) cardiovascular disease, we know that poor, highly refined western diets do play a role in cardiovascular disease, and people's teeth suffer because of it. (In the primitive or non-western societies that Weston Price studied, they did not have to brush their teeth to have cavity-free teeth.)

Ergo, if everyone has some dental work, either amalgams or root canals, how can serious researchers find an inverse relationship between "the number of amalgams" and cardiovascular disease? I don't think it is possible or material. Again,, the interesting question is the rate of CVD in people with and without dental work. (Even so, it might be the diet, and not the mercury/toxicity causing the disease.)

Therefore I guess that this study was funded by a Dental Association.
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Re: Statin Use

Post Number:#14  Post by Johnwen » Sat Jan 02, 2010 8:14 am

There doing research to see if it's the antibodies the body releases in responce to dental problems that maybe the cause of CHD.

http://atvb.ahajournals.org/cgi/content ... type=HWCIT

Heres some more on statins

http://www.newswithviews.com/Howenstine/james23.htm

http://www.spacedoc.net/rest_of_my_story.html
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Re: Statin Use

Post Number:#15  Post by godsilove » Sat Jan 02, 2010 10:20 am

ofonorow wrote:
This has nagged me because it is quite obvious that this study is meaningless, if not bogus, on its face without having to read it. These days, dental work is practically ubiquitous in the modern world. Almost everybody has some kind of dental work, primarily because of the poor, sugary western diet. So how can you infer anything without looking at people who don't have ANY dental work? (Such peoples have been found to be consistently WITHOUT heart disease.)

A symptom of the western diet is rotting teeth, so while no epidemiological study can claim that amalgams cause (or do not cause) cardiovascular disease, we know that poor, highly refined western diets do play a role in cardiovascular disease, and people's teeth suffer because of it. (In the primitive or non-western societies that Weston Price studied, they did not have to brush their teeth to have cavity-free teeth.)

Ergo, if everyone has some dental work, either amalgams or root canals, how can serious researchers find an inverse relationship between "the number of amalgams" and cardiovascular disease? I don't think it is possible or material. Again,, the interesting question is the rate of CVD in people with and without dental work. (Even so, it might be the diet, and not the mercury/toxicity causing the disease.)

Therefore I guess that this study was funded by a Dental Association.


One of Hill's criteria for causality is that there should a dose-response relationship. If amalgams increase one's risk of heart disease, then it stands to reason that the higher the number of amalgams, the higher the risk.


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