Is it Sensible to Reduce Sodium in CVD Patients?

[ofonorow]

That cholesterol has vital functions in the body is not of dispute and is missing the point. The same can be said of sodium and potassium, yet no sensible person would suggest that any reduction of sodium intake is harmful. If one's cholesterol levels are extremely low, the one should not be taking statins.

By the way, I'd love to see studies demonstrating that increased cholesterol production is an adaptation to strengthen damaged arteries. No need for raw data - published findings would be sufficient. I'm also interested to know how this applies to people with familial hypercholesterolemia.

I guess I am not a sensible person. I know of medical research data (from Dr. David Brownstein's book SALT) that found that for people with hypertension and on a low sodium diet, they are something like 400 times more likely to suffer a heart attack. The reason is apparently a change in hormonal balance caused by the sodium restriction. When sodium is restricted, the body adjusts its hormones to preserve what little sodium is available, leading to the problem. This is off topic, but the health problem is apparently highly refined sodium chloride - table salt, and not sodium per se, as our blood stream has (or ought to have) the salt consistency of the ocean.

Now back to cholesterol, what is your definition of low? If it is below 360 mg/dl, then I suppose we are in agreement. No one whose cholesterol is lower than 360 mg/dl should be taking statins.

As far as the "published" papers on cholesterol being an adaption, what do you make of the absence of such papers? Actually the PRIMARY paper, the Pauling/Rath Unified Theory paper, was refused for publication by the National Academy of Sciences USA. But all is not lost as the paper was published in the distinguished Journal of Orthomolecular Medicine which I believe can be opened at this link: http://www.google.com/url?sa=U&start=5& ... n8R62NuK0A Enjoy

[godsilove]

That cholesterol has vital functions in the body is not of dispute and is missing the point. The same can be said of sodium and potassium, yet no sensible person would suggest that any reduction of sodium intake is harmful. If one's cholesterol levels are extremely low, the one should not be taking statins.

By the way, I'd love to see studies demonstrating that increased cholesterol production is an adaptation to strengthen damaged arteries. No need for raw data - published findings would be sufficient. I'm also interested to know how this applies to people with familial hypercholesterolemia.

I guess I am not a sensible person. I know of medical research data (from Dr. David Brownstein's book SALT) that found that for people with hypertension and on a low sodium diet, they are something like 400 times more likely to suffer a heart attack. The reason is apparently a change in hormonal balance caused by the sodium restriction. When sodium is restricted, the body adjusts its hormones to preserve what little sodium is available, leading to the problem. This is off topic, but the health problem is apparently highly refined sodium chloride - table salt, and not sodium per se, as our blood stream has (or ought to have) the salt consistency of the ocean.

Now back to cholesterol, what is your definition of low? If it is below 360 mg/dl, then I suppose we are in agreement. No one whose cholesterol is lower than 360 mg/dl should be taking statins.

As far as the "published" papers on cholesterol being an adaption, what do you make of the absence of such papers? Actually the PRIMARY paper, the Pauling/Rath Unified Theory paper, was refused for publication by the National Academy of Sciences USA. But all is not lost as the paper was published in the distinguished Journal of Orthomolecular Medicine which I believe can be opened at this link: http://www.google.com/url?sa=U&start=5& ... n8R62NuK0A Enjoy

I think you've misunderstood me. I'm not saying that all reductions in sodium are safe; I'm saying that any reduction in sodium is not necessarily bad and is desirable in some cases. Extremely low intake of salt can be dangerous (e.g. in combination with too much water intake can result in hyponatremia), but a moderate reduction usually is not - and is probably beneficial in some cases (I'm not sure which study(ies)Brownstein is referring to, as the ones I have seen do not show an increase in heart attacks). Likewise with cholesterol, the reduction with statin drugs is probably in a safe range (>160 mg/dL) as "normal" cholesterol levels tend to be in this range. Extremely low cholesterol can be a bad thing, just as high cholesterol can be. The same applies to several other vital substances in our body. For instance, blood glucose can be too high, or it can be too low. Glucose is essential for humans, but does that mean that any intervention that lowers blood glucose levels is bad? Certainly if the reduction is too drastic it could be, but if glucose levels remain in a person's normal range, then it most probably isn't.

[Frank]

Sorry about addressing this issue, but the subject heading is about sodium.

I am a little confused about the term "low sodium". With the current western diet, with packaged foods etc, a "reduced sodium" diet could mean 2000mg/day. On the other hand the paleolithic diet, without packaged food, but with plenty of fruit and vegetables, the sodium content could be as low as 500-1000mg/day. I don't think that paleolithic dieters think of themselves as being on a low sodium diet. I don't think that humans 10,000 years ago were on a low sodium diet.

However, anyone on a diet without much vegetables, fruit or packaged food would be on a really low sodium diet. Since sodium is essential, this type of diet, I would think may be dangerous.

Am I incorrect about this line of reasoning?

[ofonorow]

Don't be sorry and a good point about the current western diet.

The issue of sodium or glucose levels in the blood do not seem to me to be relevant to the issue of cholesterol. Arguing that it is wise to control abnormal levels of various indicators does not justify the artificial regulation of serum cholesterol. But lets consider how the body treats each case.

If blood sugar levels get too high, the body releases more insulin into the blood in an attempt to prevent us from lapsing into a coma. I believe that interventions that support what the body would do naturally is an orthomolecular approach and warranted.

If sodium levels are abnormal the body compensates, and it is my understanding that more sodium is expelled in this case through the urine. So drinking water is wise when sodium intake is increased (and we get thirsty when we take in sodium.) As Frank pointed out, it is hard these days to get "low" sodium in the diet.

Lets consider cholesterol. Unlike sodium or glucose, the only symptom of "elevated cholesterol" is feeling good. In other words, if we didn't have the blood test, no one would know that their cholesterol was elevated, at least in the range 160 mg/dl to 360 mg/dl. Furthermore, when cholesterol is restricted in the diet, the body compensates by producing more! This is the well-known feedback mechanism in the liver, and medicine by giving statins, rather than supporting the body in this fashion, works against the interest of the human body by interfering with this feedback mechanism.

[Frank]

As you pointed out, Owen, when we reduce cholesterol intake via the diet the liver produces more. The reason for this is that the body requires more. According to the unified theory, the body requires the extra cholesterol to do repair work, and uses the cholesterol instead of vitamin c, if there isn't enough. As you have pointed out numerous times, increasing vitamin c reduces cholesterol, because it's not needed.

As you you have pointed out before, with enough vitamin c, cholesterol eventually should drop to 180 mg/dl. I have recently had a blood test with a cholesterol result of 5.0 mmol/l. I believe that this converts to about 195 mg/dl. I am taking only 4000mg of ascorbic acid because I get gas if I take more. I have to take it from these readings that my body doesn't want more than 4000mg of ascorbic acid. How do I get the cholesterol down to 180 mg.dl? I have some metal tooth fillings but no root canals.

[godsilove]

Sorry about addressing this issue, but the subject heading is about sodium.

I am a little confused about the term "low sodium". With the current western diet, with packaged foods etc, a "reduced sodium" diet could mean 2000mg/day. On the other hand the paleolithic diet, without packaged food, but with plenty of fruit and vegetables, the sodium content could be as low as 500-1000mg/day. I don't think that paleolithic dieters think of themselves as being on a low sodium diet. I don't think that humans 10,000 years ago were on a low sodium diet.

However, anyone on a diet without much vegetables, fruit or packaged food would be on a really low sodium diet. Since sodium is essential, this type of diet, I would think may be dangerous.

Am I incorrect about this line of reasoning?

It is of course a relative term, as are "low-fat" and "high-carb".

[godsilove]

[color=#0000FF]
The issue of sodium or glucose levels in the blood do not seem to me to be relevant to the issue of cholesterol. Arguing that it is wise to control abnormal levels of various indicators does not justify the artificial regulation of serum cholesterol. But lets consider how the body treats each case.

If blood sugar levels get too high, the body releases more insulin into the blood in an attempt to prevent us from lapsing into a coma. I believe that interventions that support what the body would do naturally is an orthomolecular approach and warranted.

Or it doesn't release more insulin, and the diabetic patient blacks out without the necessary intervention.

If sodium levels are abnormal the body compensates, and it is my understanding that more sodium is expelled in this case through the urine. So drinking water is wise when sodium intake is increased (and we get thirsty when we take in sodium.) As Frank pointed out, it is hard these days to get "low" sodium in the diet.

Of course the body has ways of regulating sodium - but you seem to assume that this ability is perfectly in order in everybody. Some people have higher sodium sensitivity than others (and it can contribute to fluid retention).

If the "normal" Western diet contains a relatively high diet, then it boggles the mind as to why lowering the intake of sodium would be harmful.

Lets consider cholesterol. Unlike sodium or glucose, the only symptom of "elevated cholesterol" is feeling good. In other words, if we didn't have the blood test, no one would know that their cholesterol was elevated, at least in the range 160 mg/dl to 360 mg/dl.

What's the symptom of reduced Vitamin C? I'm not talking about levels low enough to give you scurvy, but levels in most people that you and Pauling would probably consider "deficient"?

I've been taking Vitamin D supplements for the past few weeks - based on my location and the low amount of sunlight exposure, I would assume that my levels of Vitamin D were suboptimal. Yet, the only definitive way to know would be to take a blood test. I don't "feel" any different after supplementing than I did before.

You might argue that there are more long term effects of these deficiencies, but then the same applies to high levels of cholesterol (and probably extremely low levels of it as well).

Furthermore, when cholesterol is restricted in the diet, the body compensates by producing more! This is the well-known feedback mechanism in the liver, and medicine by giving statins, rather than supporting the body in this fashion, works against the interest of the human body by interfering with this feedback mechanism.

Again, you assume that this feedback mechanism is fully functional in everybody. An extreme example is those with familial hypercholesterolemia.

[ofonorow]

What's the symptom of reduced Vitamin C?

Cardiovascular disease, bruising, susceptibility to colds and infections, lack of energy, poor reaction to stress, more illnesses than I can list.


As far as the other points above, you have not addressed the issue that when medicine treats cholesterol by artificially lowering it, it is countering the natural tendency of the body, in all cases, not just during illness.

[godsilove]

What's the symptom of reduced Vitamin C?

Cardiovascular disease, bruising, susceptibility to colds and infections, lack of energy, poor reaction to stress, more illnesses than I can list.

In the same vein, it could be argued based on the available data, that the long term symptoms of high cholesterol are various vascular problems.

As far as the other points above, you have not addressed the issue that when medicine treats cholesterol by artificially lowering it, it is countering the natural tendency of the body, in all cases, not just during illness.

It's not drastically different from administering insulin to a diabetic, or allopurinol as a preventitive treatment for gout. You seem to be assuming that whatever feedback mechanism exists in humans to control serum cholesterol is in perfect working order for everybody.
Many diseases exist precisely because the body is not functioning as it should.

[ofonorow]

I think you are making too fine a point. Medicine adds insulin because it is missing. In type I because the body no longer can make it. (In type II adding insulin may kill the patient.)

To make the analogy with cholesterol better, if medicine instead reduced insulin levels, rather than injected them, perhaps to reduce sugar levels in cells for example, when a healthy body would have produced more, then you have a better analogy with what medicine does w/r to cholesterol. This would be acting in a manner which counteracts the natural tendency of the human body. I believe this is exactly what medicine does when it administers an antihistimine to control mucous (the mucous was produced for a reason, to help expel foreign particles/germs) and when medicine administers cholesterol-lowering drugs.

Your assumption is that the natural reaction of the body, at least in the case of cholesterol, is harmful. I disagree, and believe that the natural reaction of the body is based on (perhaps billions of years) of evolution, and to administer treatments that run counter to evolution must demonstrate substantial benefit. Of course this leads to the argument about vitamin C and evolution, but my argument stands that man is the exception, not the rule w/r to vitamin C blood levels, and supplementing vitamin C is correcting for a recent error in evolution (See the Unified Theory). Elevated cholesterol is connected, according to Pauling/Rath as an adaption to compensate for the arterial weakness caused by low vitamin C.

WIth the now thousands of studies, please identify a repeatable experiment that supports your contention that a symptom of high cholesterol is a set of vascular problems. There is obviously a connection, but what causes what? My counter-argument is that high cholesterol itself is the symptom of vascular problems. (Problems caused by too little vitamin C in our diets. This is supported by the lack of similar CVD in animals that make their own vitamin C, and the presence of CVD in guinea pigs - animals that cannot make C - when they are deprived of vitamin C.

[godsilove]

I think you are making too fine a point.

The cusp of my argument is simple - if an "optimal" level of any substance in the body exists, then by definition it is possible to have too much of something or too little of it. Hyperglycemia, hyponatremia, hypercholesteremia, hypervitaminosis A, etc. Hence, reducing something that may be in excess quantities is not harmful, and in some cases is beneficial.

Medicine adds insulin because it is missing. In type I because the body no longer can make it. (In type II adding insulin may kill the patient.)

Precisely, and with Type II diabetes we are forced to use different treatment strategies to control blood glucose levels. Type II diabetes is also an example of a disease where the body's feedback mechanisms are out of whack, for whatever reason.

To make the analogy with cholesterol better, if medicine instead reduced insulin levels, rather than injected them, perhaps to reduce sugar levels in cells for example, when a healthy body would have produced more, then you have a better analogy with what medicine does w/r to cholesterol.

How is that a better analogy? Why would you want to reduce insulin levels in someone with Type I diabetes?

If there were a way to safely stimulate insulin production in Type I diabetics, it would be a viable treatment option. The problem of course is that the body attacks the very cells that secrete insulin (again, an example of where the body despite its wonderful intricacies is out of order).

The management of Type II diabetes is analogous to statin therapy to reduce cholesterol. Poor management of blood glucose can have long term adverse effects; would you argue against lowering blood glucose simply because glucose is an essential nutrient for cells? It seems to me that you are making a similar argument vis-a-vis cholesterol. I don't think anyone denies that cholesterol has a role to play in the body; but that alone does not mean that the body regulates it optimally in every individual.

Your assumption is that the natural reaction of the body, at least in the case of cholesterol, is harmful. I disagree, and believe that the natural reaction of the body is based on (perhaps billions of years) of evolution, and to administer treatments that run counter to evolution must demonstrate substantial benefit. Of course this leads to the argument about vitamin C and evolution, but my argument stands that man is the exception, not the rule w/r to vitamin C blood levels, and supplementing vitamin C is correcting for a recent error in evolution (See the Unified Theory). Elevated cholesterol is connected, according to Pauling/Rath as an adaption to compensate for the arterial weakness caused by low vitamin C.

It's special pleading to argue that vitamin C is the only "error" of evolution. The line of argument also tends to anthropomorphize the process of evolution. With most things, traits that have a survival advantage also have costs. The increasing size of our brains came at the cost of more painful childbirth and increased infant mortality rates. Our wonderful immune system sometimes turns on the body it evolved to protect. Furthermore, traits beneficial in one environment can be deleterious in another. If you look at the pace of human migration, technological and cultural advancement over the last few millenia, evolution probably has had little time to catch up in many cases.

WIth the now thousands of studies, please identify a repeatable experiment that supports your contention that a symptom of high cholesterol is a set of vascular problems. There is obviously a connection, but what causes what? My counter-argument is that high cholesterol itself is the symptom of vascular problems. (Problems caused by too little vitamin C in our diets. This is supported by the lack of similar CVD in animals that make their own vitamin C, and the presence of CVD in guinea pigs - animals that cannot make C - when they are deprived of vitamin C.

If cholesterol is simply the body's reaction to vascular problems, then why do baseline levels of high LDL predict greater vascular risk even before the fact? Furthermore, why have multiple studies shown a proportional reduction in risk with LDL-lowering strategies?

What is the signalling mechanism that tells the body to produce more cholesterol? Has this been verified experimentally?

[ofonorow]

The cusp of my argument is simple - if an "optimal" level of any substance in the body exists, then by definition it is possible to have too much of something or too little of it. Hyperglycemia, hyponatremia, hypercholesteremia, hypervitaminosis A, etc. Hence, reducing something that may be in excess quantities is not harmful, and in some cases is beneficial.

That is a big "if" and a lot of "may"bes. In the case of insulin, sodium, even vitamin A, etc. the correct range can be easily demonstrated because the consequences are serious when the metabolism begins to fail.

Your argument would be valid if, for example, it was known that some people produce too much insulin and that a health benefit could be induced by reducing serum insulin in such people to the optimal level. Such a case is contrived, and it seems likely that such people would die before anyone figured out what the problem was, even if there was a drug to attack insulin production. This process is called evolution. But in theory, some people with this strange condition might be helped. This is the argument you are using to justify lowering cholesterol. You assume that for some reason the natural body response to increase its production in the face of lower supplies is incorrect. Your assumption is based on various studies that apparently show a benefit, no matter how small, to people with CVD after lowering their cholesterol.

The problems with all these studies are numerous and at the core are the self-interests of the parties running these highly focused studies. We are not told and therefore do not know what other factors play a more important role in these findings.

Dr. Levy has uncovered considerable experimental evidence that cholesterol is one of the body's natural toxic defense mechanisms. In other words, cholesterol levels in experimental animals can be made to rise simply by inducing toxins. Conversely, when the toxic load is reduced, the cholesterol levels follow suit. (If you have been following this forum, you know that cardiologist Levy began researching this after noticing that cholesterol levels in his patients dropped immediately after they had their dental amalgams removed.)

It makes no sense to me from any theoretical standpoint to give CVD patients drugs that deplete their CoQ10 levels, a substance required for energy in every heart cell. (The heart and pancreas have the highest CoQ10 concentrations, and that is why these studies avoid discussing side effects, such as pain, fatigue and other "issues" caused by the CoQ10 depletion.) Furthermore, cholesterol has a role in helping the body rid itself of toxins. Even the makers of the statin drugs have backed off the emotionally appealing claim that lowering cholesterol works by reducing cholesterol levels in the blood. (Today it is an anti imflammatory property, etc.) No one seriously thinks that elevated cholesterol in the blood causes the lesions that lead to atherosclerotic plaques around the heart.

If cholesterol is simply the body's reaction to vascular problems, then why do baseline levels of high LDL predict greater vascular risk even before the fact? Furthermore, why have multiple studies shown a proportional reduction in risk with LDL-lowering strategies?

What is the signaling mechanism that tells the body to produce more cholesterol? Has this been verified experimentally?

I do not accept the premise that high LDL predicts greater vascular risk, but since LDL by definition includes some Lp(a), I can understand the confusion. Pauling said the risk is Lp(a) cholesterol, which are LDL molecules with a "sticky" apolipoprotein(a) on the surface. (It turns out they vary in size by a factor of 1000 and the small molecules are much more atherogenic.) Pauling began to understand the importance of Lp(a) after the Biesegal team in Germany discovered Lp(a) only - no LDL - in the aortic plaques analyzed post mortem. http://www.paulingtherapy.com/archive/refs.html#R2
TITLE: Lipoprotein(a) in the arterial wall.
AUTHOR: Beisiegel U; Rath M; Reblin T; Wolf K; Niendorf A


Ordinary LDL does not have any adhesive properties that I am aware of so there is little reason for it to attach to a damaged vascular wall.

The argument of "before the fact" does not take into account cause/effect. I am willing to grant you that people with elevated cholesterol are more likely to be suffering CVD, (aka chronic scurvy) but I do not accept the notion that artificially lowering a CVD patient's cholesterol improves their health or increases their life span, any more than I believe that people taking an antihistimine are really controlling their underlying infection. They are treating a symptom, which happens to be a primary defensive mechanism of the immune system - mucous.

The signaling mechanism is in the liver and so well established that I believe even modern medicine teaches it. But who knows, here is an article that purports to tell us a probable method: http://www.ajcn.org/cgi/content/abstract/8/5/645

[godsilove]

The cusp of my argument is simple - if an "optimal" level of any substance in the body exists, then by definition it is possible to have too much of something or too little of it. Hyperglycemia, hyponatremia, hypercholesteremia, hypervitaminosis A, etc. Hence, reducing something that may be in excess quantities is not harmful, and in some cases is beneficial.

That is a big "if" and a lot of "may"bes. In the case of insulin, sodium, even vitamin A, etc. the correct range can be easily demonstrated because the consequences are serious when the metabolism begins to fail.

Your argument would be valid if, for example, it was known that some people produce too much insulin and that a health benefit could be induced by reducing serum insulin in such people to the optimal level. Such a case is contrived, and it seems likely that such people would die before anyone figured out what the problem was, even if there was a drug to attack insulin production.

There are rare cases where the body secretes too much insulin e.g. in insulinomas. Usually the beta-cell tumors are removed surgically, but if the patient is not suitable for surgery, drug treatment is used to decrease the secretion of insulin.

This process is called evolution. But in theory, some people with this strange condition might be helped. This is the argument you are using to justify lowering cholesterol. You assume that for some reason the natural body response to increase its production in the face of lower supplies is incorrect. Your assumption is based on various studies that apparently show a benefit, no matter how small, to people with CVD after lowering their cholesterol.

It's more than just an assumption. If the body's natural responses were perfectly in order, many diseases probably wouldn't exist or would be extremely rare. One only needs to observe cases of autoimmunity or endocrinological disorders where the body clearly is not able to regulate itself properly.

If you want to use the evolution argument, you have to take into consideration that the average individual in the Western world now has a drastically different lifestyle from his ancestors who were subjected to thousands years of natural selection. Think about it - modern humans have been around for a few thousand years; on the other hand, as a species Homo sapiens has been around for 200,000 years. And many of our traits have a history that goes far beyond that. I also think that the extremely adaptationist view you take is incorrect. Natural selection is not the only force that drives evolution; much of it is also due to genetic drift, i.e. chance.

The problems with all these studies are numerous and at the core are the self-interests of the parties running these highly focused studies. We are not told and therefore do not know what other factors play a more important role in these findings.

There are statin studies that are not funded by industry, if that is the biggest problem you see with them. Most of these are observational studies, but they still show a benefit for statin use. For instance, there was a recent publication in the Archives of Internal Medicine where they did a retrospective population-based study on statin use in Israel. The authors got data from an HMO which kept records such as prescription data, hospital admissions, etc. They found that there was a decrease in all-cause mortality amongst those who took statins. Furthermore, the benefit was higher amongst those who took statins for a higher proportion of time during the study period. Another interesting finding was that those taking statins or doses associated with higher reductions in LDL-cholesterol also had lower all-cause mortality. The study of course has its weaknesses, and it is possible that the benefits are exaggerated due to confounding. However, this does confirm observations from industry-funded RCTs.

http://archinte.ama-assn.org/cgi/conten ... IOI80171-7

Dr. Levy has uncovered considerable experimental evidence that cholesterol is one of the body's natural toxic defense mechanisms. In other words, cholesterol levels in experimental animals can be made to rise simply by inducing toxins. Conversely, when the toxic load is reduced, the cholesterol levels follow suit. (If you have been following this forum, you know that cardiologist Levy began researching this after noticing that cholesterol levels in his patients dropped immediately after they had their dental amalgams removed.)

I'm not sure how you went from point A to point B. Consuming a diet high in trans-fats has also been shown to increase cholesterol levels; however, one would not conclude that this is the body's way of expelling trans-fats.

I'm not sure that dental amalgams contribute to higher cholesterol, unless you have something more than just anecdotal evidence to go by.

It makes no sense to me from any theoretical standpoint to give CVD patients drugs that deplete their CoQ10 levels, a substance required for energy in every heart cell. (The heart and pancreas have the highest CoQ10 concentrations, and that is why these studies avoid discussing side effects, such as pain, fatigue and other "issues" caused by the CoQ10 depletion.) Furthermore, cholesterol has a role in helping the body rid itself of toxins.

Can you show that statins deplete CoQ10 to levels that have an adverse clinical effect? It's one thing to have a hypothetical mechanism, but it's quite another to show that this is actually the case in a clinical setting. If the benefits of reducing LDL-cholesterol outweigh the risks (including reductions in CoQ10), then it certainly does make sense for me to treat suitable CVD patients with statins.

Even the makers of the statin drugs have backed off the emotionally appealing claim that lowering cholesterol works by reducing cholesterol levels in the blood. (Today it is an anti imflammatory property, etc.) No one seriously thinks that elevated cholesterol in the blood causes the lesions that lead to atherosclerotic plaques around the heart.

Hardly...the Lipitor ads still talk about cholesterol. The product monographs and treatment guidelines still address cholesterol. Reducing cholesterol in at risk individuals remains the standard of care, and with good reason - the evidence supports this intervention.

That cholesterol may have additional effects through other mechanisms does not invalidate this.

I do not accept the premise that high LDL predicts greater vascular risk, but since LDL by definition includes some Lp(a), I can understand the confusion. Pauling said the risk is Lp(a) cholesterol, which are LDL molecules with a "sticky" apolipoprotein(a) on the surface. (It turns out they vary in size by a factor of 1000 and the small molecules are much more atherogenic.) Pauling began to understand the importance of Lp(a) after the Biesegal team in Germany discovered Lp(a) only - no LDL - in the aortic plaques analyzed post mortem. http://www.paulingtherapy.com/archive/refs.html#R2
TITLE: Lipoprotein(a) in the arterial wall.
AUTHOR: Beisiegel U; Rath M; Reblin T; Wolf K; Niendorf A

Ordinary LDL does not have any adhesive properties that I am aware of so there is little reason for it to attach to a damaged vascular wall.

I must be missing something. The abstracts in your link do not indicate that only Lp(a) is found in plaques.

The argument of "before the fact" does not take into account cause/effect. I am willing to grant you that people with elevated cholesterol are more likely to be suffering CVD, (aka chronic scurvy) but I do not accept the notion that artificially lowering a CVD patient's cholesterol improves their health or increases their life span, any more than I believe that people taking an antihistimine are really controlling their underlying infection. They are treating a symptom, which happens to be a primary defensive mechanism of the immune system - mucous.

It's unfortunate that you do not accept the benefits of cholesterol-lowering treatments in spite of the available evidence. While I agree that this strategy should not be pursued in all individuals, I certainly think that at-risk individuals who can afford and tolerate treatment should consider it.

The signaling mechanism is in the liver and so well established that I believe even modern medicine teaches it. But who knows, here is an article that purports to tell us a probable method: http://www.ajcn.org/cgi/content/abstract/8/5/645

I'm referring specifically to the putative mechanism by which the body increases cholesterol production in response to lesions in the arterial wall, which is what you are arguing, as I understand. AFAIK, the well-characterized pathways by which cholesterol production is regulated does not support your hypothesis - but then again, I'm not a biochemist.

If, as you say, cholesterol is the effect of pre-existing cardiovascular disease, then what are the biochemical processes that lead to its increased production?

[ofonorow]

I must be missing something. The abstracts in your link do not indicate that only Lp(a) is found in plaques.

From the abstract,
“only a few areas containing only apo B were detected.”

I admit, I picked this up from Pauling during his video lecture, i.e. that only Lp(a) (apo(a)) was found.

Can you show that statins deplete CoQ10 to levels that have an adverse clinical effect? It's one thing to have a hypothetical mechanism, but it's quite another to show that this is actually the case in a clinical setting. If the benefits of reducing LDL-cholesterol outweigh the risks (including reductions in CoQ10), then it certainly does make sense for me to treat suitable CVD patients with statins.

Lets start with the Merck patent 4,933,165 (1990) which states that statin drugs without nutrient supplementation lead to 0.5% myopathies...

United States Patent
4,933,165
Brown
June 12, 1990

Coenzyme Q.sub.10 with HMG-CoA reductase inhibitors
Abstract
A pharmaceutical composition and method of counteracting HMG-CoA reductase inhibitor-associated myopathy is disclosed. The method comprises the adjunct administration of an effective amount of a HMG-CoA reductase inhibitor and an effective amount of Coenzyme Q.sub.10.
http://patft.uspto.gov/netacgi/nph-Pars ... =4,933,165


I happened to notice that the following query finds quite a few related patents,

http://patft.uspto.gov/netacgi/nph-Pars ... D2=&d=PTXT

In other words, Merck was well aware of this effect by 1990, and if you want, I can do a pubmed/medline search for abstracts. They exist.

I'm not sure how you went from point A to point B. Consuming a diet high in trans-fats has also been shown to increase cholesterol levels; however, one would not conclude that this is the body's way of expelling trans-fats.

I'm not sure that dental amalgams contribute to higher cholesterol, unless you have something more than just anecdotal evidence to go by.

One might indeed conclude that higher cholesterol is the means by which the body expells trans fats (actually it is a metal related to nickle which is left in the transfat that is believe to cause the problem, the metal is formed during hydrogenation. So it would be the body's attempt to remove this toxin, not the hydrogenated fat.

Dr. Levy cites the research evidence in one of his book, laboratory studies that illustrate cholesterol rises in response to toxic loads. These are repeatable experiments. The anecdotal evidence of his patients only peaked his interest.

Hardly...the Lipitor ads still talk about cholesterol. The product monographs and treatment guidelines still address cholesterol. Reducing cholesterol in at risk individuals remains the standard of care, and with good reason - the evidence supports this intervention.

That cholesterol may have additional effects through other mechanisms does not invalidate this.

No doubt, but the ads are from the marketing people. I have read comments of researchers in medicine from clinics and medical schools, they seem to understand that data is very weak and look to other reasons. But I know of no scientist who thinks ordinary LDL causes the lesions. In fact, the fact is well established, that the famous “Lysine Binding Sites” that led to the Brown-Goldstein Nobel Prize in medicine – are only found on apo(a) (so Lp(a)) molecules – not ordinary cholesterol. This fact is kept hidden from doctors, who assume these binding sites exist on ordinary cholesterol. We can discuss the “kringle” on the apo(a) where these sites manifest if you want.

If doctors were made aware of that simple fact, they would be focused like a laser on Lp(a) as Pauling was.

It's unfortunate that you do not accept the benefits of cholesterol-lowering treatments in spite of the available evidence. While I agree that this strategy should not be pursued in all individuals, I certainly think that at-risk individuals who can afford and tolerate treatment should consider it.

I am not sure why you say it is unfortunate? The people we inform about Pauling's discoveries usually get well in about two weeks, and most of these people were seriously ill. I do not accept the benefits because in the few studies I looked at, e.g. the Brown statin studies, the raw data (lab measurements) included in the paper favored the placebo group, (insulin was lower, blood sugar was lower, etc.). I thought this would be obvious to any MD reading the paper. Brown admitted dropping, from memory, 187 subjects for various reasons. Five years and they dropped subjects? I infer the reason it takes 5 years to publish statin studies is because the first time they run through the results (just a guess) the results do not look good and so they have learned how to cherry-pick the subjects. I am not making this up. Brown admitted dropping the subjects (not cherry picking) in one of the later papesr, for what sounded like good reasons, but again, there is too much money involved to take these studies seriously, especially when the benefits, plotted side-by-side, statin vs. placebo, are almost identical.

I'm referring specifically to the putative mechanism by which the body increases cholesterol production in response to lesions in the arterial wall, which is what you are arguing, as I understand. AFAIK, the well-characterized pathways by which cholesterol production is regulated does not support your hypothesis - but then again, I'm not a biochemist.

If, as you say, cholesterol is the effect of pre-existing cardiovascular disease, then what are the biochemical processes that lead to its increased production?

My argument is that when serum cholesterol levels drop, the human body has a natural feedback mechanism to increase the production in the liver, and that medicine, by prescribing statins, defeats this feedback mechanism without a sound theory or really good evidence.

It turns out that vitamin C is a “natural” statin, a HMG-CoA Reductase inhibitor,
See:http://www.jbc.org/cgi/content/abstract/261/16/7127
J. Biol. Chem., Vol. 261, Issue 16, 7127-7135, 06, 1986
Inhibition of human leukocyte 3-hydroxy-3-methylglutaryl coenzyme A reductase activity by ascorbic acid. An effect mediated by the free radical monodehydroascorbate
HJ Harwood Jr, YJ Greene and PW Stacpoole

After reading this paper, it looked to me to be the same effect of the statin drugs – without any risk of side effects. And while we have had arguments here how important this effect is (and Pauling has another theory in his book) it is a fact that when vitamin C levels are low, the body produces more cholesterol. So to answer your question, the “biochemical process” is low serum vitamin C, i.e., lower blood and tissue levels than animals which produce their own ascorbate 24/7 .

[godsilove]

From the abstract,
“only a few areas containing only apo B were detected.”

I admit, I picked this up from Pauling during his video lecture, i.e. that only Lp(a) (apo(a)) was found.

I must still be missing something. That statement simply means that places were apo B was not colocalized with something else were rare; but the preceding sentence points out that there are places where apo B colocalized with apo A.

Can you show that statins deplete CoQ10 to levels that have an adverse clinical effect? It's one thing to have a hypothetical mechanism, but it's quite another to show that this is actually the case in a clinical setting. If the benefits of reducing LDL-cholesterol outweigh the risks (including reductions in CoQ10), then it certainly does make sense for me to treat suitable CVD patients with statins.

Lets start with the Merck patent 4,933,165 (1990) which states that statin drugs without nutrient supplementation lead to 0.5% myopathies...

[/QUOTE]

Fair enough; however, I don't think the evidence that it is depleted CoQ10 that results in myopathy. The patent applications means little - one doesn't need to prove that an invention works in order to file a patent for it.

Furthermore, the incidence of myopathy is very low and does not outweigh the benefit (even if one were to assume that 100 patients would have to be treated to save one life).

One might indeed conclude that higher cholesterol is the means by which the body expells trans fats (actually it is a metal related to nickle which is left in the transfat that is believe to cause the problem, the metal is formed during hydrogenation. So it would be the body's attempt to remove this toxin, not the hydrogenated fat.

The observation does not warrant that conclusion. I'm also curious as to how a metal is formed by hydrogenation; I'm no chemist, but that seems implausible to me. Perhaps you mean the metals that are used to catalyze dehydrogenation reactions, but I'd be surprised if these are retained in the products at concentrations higher than what one would find in tap water. If you have evidence to the contrary, I'd be interested to see it.

Dr. Levy cites the research evidence in one of his book, laboratory studies that illustrate cholesterol rises in response to toxic loads. These are repeatable experiments. The anecdotal evidence of his patients only peaked his interest.

I assume this evidence is also published somewhere in the literature?

No doubt, but the ads are from the marketing people. I have read comments of researchers in medicine from clinics and medical schools, they seem to understand that data is very weak and look to other reasons. But I know of no scientist who thinks ordinary LDL causes the lesions. In fact, the fact is well established, that the famous “Lysine Binding Sites” that led to the Brown-Goldstein Nobel Prize in medicine – are only found on apo(a) (so Lp(a)) molecules – not ordinary cholesterol. This fact is kept hidden from doctors, who assume these binding sites exist on ordinary cholesterol. We can discuss the “kringle” on the apo(a) where these sites manifest if you want.

If doctors were made aware of that simple fact, they would be focused like a laser on Lp(a) as Pauling was.[/color]

I'm sure you'll find doctors who are skeptical of the role of cholesterol, just as you might find some scientists who don't accept evolution. But the consensus remains that LDL is a risk factor for heart disease, and that reduction of LDL is an effective treatment strategy for at-risk individuals. This is reflected in treatment guidelines.

Lp(a) may be an independent risk factor, but we already know that there are multiple risk factors for heart disease including genetics, LDL cholesterol, and smoking.

I am not sure why you say it is unfortunate? The people we inform about Pauling's discoveries usually get well in about two weeks, and most of these people were seriously ill. I do not accept the benefits because in the few studies I looked at, e.g. the Brown statin studies, the raw data (lab measurements) included in the paper favored the placebo group, (insulin was lower, blood sugar was lower, etc.). I thought this would be obvious to any MD reading the paper. Brown admitted dropping, from memory, 187 subjects for various reasons. Five years and they dropped subjects? I infer the reason it takes 5 years to publish statin studies is because the first time they run through the results (just a guess) the results do not look good and so they have learned how to cherry-pick the subjects. I am not making this up. Brown admitted dropping the subjects (not cherry picking) in one of the later papesr, for what sounded like good reasons, but again, there is too much money involved to take these studies seriously, especially when the benefits, plotted side-by-side, statin vs. placebo, are almost identical.

Which trial are you talking about?

My argument is that when serum cholesterol levels drop, the human body has a natural feedback mechanism to increase the production in the liver, and that medicine, by prescribing statins, defeats this feedback mechanism without a sound theory or really good evidence.

It turns out that vitamin C is a “natural” statin, a HMG-CoA Reductase inhibitor,
See:http://www.jbc.org/cgi/content/abstract/261/16/7127
J. Biol. Chem., Vol. 261, Issue 16, 7127-7135, 06, 1986
Inhibition of human leukocyte 3-hydroxy-3-methylglutaryl coenzyme A reductase activity by ascorbic acid. An effect mediated by the free radical monodehydroascorbate
HJ Harwood Jr, YJ Greene and PW Stacpoole

After reading this paper, it looked to me to be the same effect of the statin drugs – without any risk of side effects. And while we have had arguments here how important this effect is (and Pauling has another theory in his book) it is a fact that when vitamin C levels are low, the body produces more cholesterol. So to answer your question, the “biochemical process” is low serum vitamin C, i.e., lower blood and tissue levels than animals which produce their own ascorbate 24/7 .

How does low serum Vitamin C contribute to higher LDL? In any case, you're citing an in vitro study as though it definitely shows that this applies to the human body.