Is high cholesterol a defense mechanism?

[Abooga]

Hello everyone.

According to this study:
http://qjmed.oxfordjournals.org/content/96/12/927
And if I understand correctly, cholesterol may be our bodies´defense mechanism against cardiovascular afflictions, which would explain correlation between high levels of cholesterol and cardiovascular risk, but would mean that we are not to try to lower cholesterol, after all, wouldn´t it? I´d love to hear some more knowledgable posters´ opinion on this.

(I couldn´t find any detailed discussion about this topic, so I´ve just started a thread, if there is already one in existence feel free to point me to it)

 

[casebro]

I don't see much reason to defend the cholesterol theory of heart disease. I suspect some big confounding. Like you say.

I believe calcium is the culprit.

Anecdote: Heart attack at 49. Heart murmurs, kidney disease, calcified aorta, calf muscles show calcium, venous insufficiency. All calcium. So I started taking STS (sodium thiosulfate) daily, 2 grams. LDL came down from 115 to 88. Latest labs, kidneys are excellent, Electrolytes excellent, iron good too. No help for hypertension or diabetes though. Google <TACT study diabetes>, it seems to work on diabetics better.

STS is used for chelation therapy, orally, 10 grams/day. I got mine from a photo lab supply house. Also used for pool chlorine neutralizing after 'shocking' a pool with a huge dose of chlorine. It's large crystals, like rock salt. I run it through the blender, with a couple drops of food coloring, then put it into capsules.

The only question on my mind now is what food has the same stuff? Diet is better than supplement. Proteins are high sulfur. Cabbage too? But I don't think the STS mechanism of action is known.

 

[Giordano]

There are many complexities to the causes of cardoivascular disease and much remains unknown. But there is quite a lot of research that indicates high levels of serum cholesterol play a significant causative role in contributing to cardiovascular disease, not in protecting against to ex post facto. These include:

1. Many genetic models in mice and in people demonstrate that increasing the levels of LDL proteins and/or cholesterol itself increase cardiovascular risk- i.e. these factors contribute to, do not protect from, cardiovascular problems.

2. The same is true of nutritional studies.

3. Statins and other drugs that lower serum cholesterol levels lower the risk of cardio-vascular disease.

4. Cholesterol is a major component of the plaques that ultimately occlude coronary arteries that cause the blockage of circulation that results in heart problems such as angina and, often by causing/capturing a clot results in the acute heart attack itself. The more it builds up the greater the risk

5. It is possible that an initial limited, light deposit of cholesterol on the wall of a blood vessel may an attempt by the body to protect against further damage to the blood vessel- maybe yes, maybe no. But if so, the very large build up of cholesterol plaques found in coronary disease would be an example of this potentially protective mechanism going wildly out of control and actually contributing to the latter clinical disease. In fact many human diseases are caused by misregulation of mechanisms that are protective when operated at a lower, properly regulated level: autoimmunity diseases, blood clots in strokes, some aspects of cancer, some of the dangerous effects of bacterial and viral infections, etc. Too much protection often becomes a disease itself.

Of course much remains unknown and yet other factors contribute. For instance cholesterol levels in the diet are not very predictive of cholesterol levels in the serum, and genetics interact in complex ways with diet, exercise, etc. But it seems pretty convincing that too much serum LDL contributes to cardiac risk rather than simply being associated with it.

 

[casebro]

There are many complexities to the causes of cardoivascular disease and much remains unknown. But there is quite a lot of research that indicates high levels of serum cholesterol play a significant causative role in contributing to cardiovascular disease, not in protecting against to ex post facto. These include:

1. Many genetic models in mice and in people demonstrate that increasing the levels of LDL proteins and/or cholesterol itself increase cardiovascular risk- i.e. these factors contribute to, do not protect from, cardiovascular problems.

They are a thing, but may not pertain to the rest of us.

2. The same is true of nutritional studies.

Trans fats are the only fats shown to be BAAAD. And they are grouped with sat fats, so sat fats look bad too. But studies of any particular sat fat show no detriment.

3. Statins and other drugs that lower serum cholesterol levels lower the risk of cardio-vascular disease.

According to studies by statin makers, 30%. But I know of no actual real world clinical study of efficacy. Do you?

4. Cholesterol is a major component of the plaques that ultimately occlude coronary arteries that cause the blockage of circulation that results in heart problems such as angina and, often by causing/capturing a clot results in the acute heart attack itself. The more it builds up the greater the risk

And calcium deposits are ubiquitous too.

5. It is possible that an initial limited, light deposit of cholesterol on the wall of a blood vessel may an attempt by the body to protect against further damage to the blood vessel- maybe yes, maybe no. But if so, the very large build up of cholesterol plaques found in coronary disease would be an example of this potentially protective mechanism going wildly out of control and actually contributing to the latter clinical disease. In fact many human diseases are caused by misregulation of mechanisms that are protective when operated at a lower, properly regulated level: autoimmunity diseases, blood clots in strokes, some aspects of cancer, some of the dangerous effects of bacterial and viral infections, etc. Too much protection often becomes a disease itself.

Of course much remains unknown and yet other factors contribute. For instance cholesterol levels in the diet are not very predictive of cholesterol levels in the serum, and genetics interact in complex ways with diet, exercise, etc. But it seems pretty convincing that too much serum LDL contributes to cardiac risk rather than simply being associated with it.

And a bit I read was that calcium levels and LDL levels go hand in hand. Much discussion about vitamin K2, and the fact that osteoporosis is a huge risk facotr for artery disease.

Anyway, much possibility for calcium/statin confounding. Possibility, linking to OP, cholesterol is a protectant against calcium in the wrong places?

 

[Red Baron Farms]

There are many complexities to the causes of cardoivascular disease and much remains unknown. But there is quite a lot of research that indicates high levels of serum cholesterol play a significant causative role in contributing to cardiovascular disease, not in protecting against to ex post facto. These include:

1. Many genetic models in mice and in people demonstrate that increasing the levels of LDL proteins and/or cholesterol itself increase cardiovascular risk- i.e. these factors contribute to, do not protect from, cardiovascular problems.

2. The same is true of nutritional studies.

3. Statins and other drugs that lower serum cholesterol levels lower the risk of cardio-vascular disease.

4. Cholesterol is a major component of the plaques that ultimately occlude coronary arteries that cause the blockage of circulation that results in heart problems such as angina and, often by causing/capturing a clot results in the acute heart attack itself. The more it builds up the greater the risk

5. It is possible that an initial limited, light deposit of cholesterol on the wall of a blood vessel may an attempt by the body to protect against further damage to the blood vessel- maybe yes, maybe no. But if so, the very large build up of cholesterol plaques found in coronary disease would be an example of this potentially protective mechanism going wildly out of control and actually contributing to the latter clinical disease. In fact many human diseases are caused by misregulation of mechanisms that are protective when operated at a lower, properly regulated level: autoimmunity diseases, blood clots in strokes, some aspects of cancer, some of the dangerous effects of bacterial and viral infections, etc. Too much protection often becomes a disease itself.

Of course much remains unknown and yet other factors contribute. For instance cholesterol levels in the diet are not very predictive of cholesterol levels in the serum, and genetics interact in complex ways with diet, exercise, etc. But it seems pretty convincing that too much serum LDL contributes to cardiac risk rather than simply being associated with it.

That's a pretty good post. I was about to chime in, but I think you covered it pretty good for Abooga! The best part being this:

Too much protection often becomes a disease itself.

There is of course more to it. But that is a pretty thorough start! Nominated!

 

[Giordano]

They are a thing, but may not pertain to the rest of us.


Trans fats are the only fats shown to be BAAAD. And they are grouped with sat fats, so sat fats look bad too. But studies of any particular sat fat show no detriment.

According to studies by statin makers, 30%. But I know of no actual real world clinical study of efficacy. Do you?


And calcium deposits are ubiquitous too.




And a bit I read was that calcium levels and LDL levels go hand in hand. Much discussion about vitamin K2, and the fact that osteoporosis is a huge risk facotr for artery disease.

Anyway, much possibility for calcium/statin confounding. Possibility, linking to OP, cholesterol is a protectant against calcium in the wrong places?

I would rephrase your first statement to "They are an important thing, but may not pertain to everyone." That is the point I was trying to get across- some things are well established as significant risks in heart disease, but there are many complexities and other factors. What is a big risk for some may be a small or non-existent risk for others. High serum cholesterol (especially as LDL) is a major risk factor for cardio-vascular disease but it is not the only risk, it may not be a risk for everyone, and it interacts with other risk factors. Just like smoking is a major risk factor for lung cancer even though not all smokers will get lung cancer and some non-smokers will. Certainly the evidence that high cholesterol is protective, which is the subject of this thread, is virtually non-existent.

Your statement that "trans fats are the only fats shown to be BAAAD. And they are grouped with sat fats, so sat fats look bad too. But studies of any particular sat fat show no detriment." is overly simplified. There are a lot of studies looking at saturated fats in the absence of trans-fats (i.e. saturated fats from untreated natural food sources) and they indicate that the problem is not just artificial trans-fats. Here is a summary of the American Heart Association:
http://www.heart.org/HEARTORG/Healt...ated-Fats_UCM_301110_Article.jsp#.V-LXx90hzI8

Your statement as to "According to studies by statin makers, 30%. But I know of no actual real world clinical study of efficacy. Do you?"
Yes. Here is one that looks at real world clinical studies and was not financed by statin makers:
http://jama.jamanetwork.com/article.aspx?articleid=2396476

Here is another:
http://jama.jamanetwork.com/article.aspx?articleid=2396478

There are more. Again all metabolic causes of disease are complicated and what is bad for one person may be okay for another. And pharmaceutical companies like to hype their products. But that doesn't mean that one should therefore ignore obvious factors that are important contributers in many cases even if not all, or if there are additional factors involved in the disease as well. It is not all smoke and mirrors.

And a bit I read was that calcium levels and LDL levels go hand in hand. Much discussion about vitamin K2, and the fact that osteoporosis is a huge risk facotr for artery disease.
There are studies that suggest calcium increases heart risk and other studies that suggest it decreases it. Again no simplified conclusion can be reached. Same about vitamin K2. There appears to be a link between osteoporosis and cardiovascular disease but the nature of the link remains unknown and is being studied.

My major point, other than high cholesterol being very unlikely to be protective rather than a risk factor, is that there are no simple answers, but there are known risk factors that must be considered even if they may not be risk factors for everyone and even though there are additional less understood risk factors.

Finally as to: "Anyway, much possibility for calcium/statin confounding. Possibility, linking to OP, cholesterol is a protectant against calcium in the wrong places?
The existing studies do not suggest this is true. And believe me- a lot of studies have been done and in ways that controlled for calcium.

Reaching simple conclusions from what know about cardio-vascular disease is inappropriate, but so is reaching simple conclusions based on what is not known about cardio-vascular disease. If calcium is found to play an important role it would not mean that cholesterol does not.

 

[Giordano]

That's a pretty good post. I was about to chime in, but I think you covered it pretty good for Abooga! The best part being this:

There is of course more to it. But that is a pretty thorough start! Nominated!

Thank you. I study, in part, carbohydrate and lipid metabolism in mice, I am not supported by any company, and I realize that there are no simple explanations. Nonetheless some things are understood even if there is much more to learn.

 

[casebro]

Weeell, lab mice are of known genetics. People vary immensely more.

It's genes that make us not-clams. There are a bazillion variations of not-clams. Your variations are different from mine. The mass studies, like for statins, lump everybody into on supposedly homogeneous mass. Very possible that statins may help a sub-set, and be useless ore even harmful to a smaller set. One cite was that 50% of cardiolgists time is spent treating side effects of statins. I've met waay more than "rare" amounts of people with side effects.

Play devils advocate for me: what if, for 10% of us, calcium is the problem? Would statin studies wherein only 2 1/2 % die, show them?

Off to read your links now.

 

[casebro]

Your statement as to "According to studies by statin makers, 30%. But I know of no actual real world clinical study of efficacy. Do you?"
Yes. Here is one that looks at real world clinical studies and was not financed by statin makers:

http://jama.jamanetwork.com/article.aspx?articleid=2396476

Here is another:
http://jama.jamanetwork.com/article.aspx?articleid=2396478.

.From your first link: "..In this microsimulation model " is NOT real world.

And your second link is about eligibilty standards- who should take statins.

Neither one is about efficacy of statins at preventing end points. The microstimulation makes statins sound good, but is probably based on 30%. I'm looking for whether then30% holds up in the real world, or is it really only 10%? Themicrostimulation gives a QALY of $37,000. If 10% is real, than $104,000, not cost effective. $50K is the cut off.

 

[casebro]

I would rephrase your first statement to "They are an important thing, but may not pertain to everyone." That is the point I was trying to get across- some things are well established as significant risks in heart disease, but there are many complexities and other factors. What is a big risk for some may be a small or non-existent risk for others. High serum cholesterol (especially as LDL) is a major risk factor for cardio-vascular disease but it is not the only risk, it may not be a risk for everyone, and it interacts with other risk factors. Just like smoking is a major risk factor for lung cancer even though not all smokers will get lung cancer and some non-smokers will. Certainly the evidence that high cholesterol is protective, which is the subject of this thread, is virtually non-existent.

Your statement that "trans fats are the only fats shown to be BAAAD. And they are grouped with sat fats, so sat fats look bad too. But studies of any particular sat fat show no detriment." is overly simplified. There are a lot of studies looking at saturated fats in the absence of trans-fats (i.e. saturated fats from untreated natural food sources) and they indicate that the problem is not just artificial trans-fats. Here is a summary of the American Heart Association:
http://www.heart.org/HEARTORG/Healt...ated-Fats_UCM_301110_Article.jsp#.V-LXx90hzI8.

That is a position paper, no studies are even mentions. It recommends, without any science.

It's called "appeal to authority", not "science".

I thought you might compare stearic acid to coconut oil.

And did you know that "the good stuff", monounsaturated fats, are higher in lard than any where else?

 

[Giordano]

Casebro,

You seem determined to disagree with what are very cautious statements. I made it clear that there are risk factors that have been identified in many different kinds of studies by different groups using different approaches. One of these is high serum cholesterol. I made it clear that nonetheless what is a big risk factor for some is not a big risk factor for others. I made it clear that much remains unknown, including how these risk factors interact. I cited some studies and patient advocate position papers, but there are huge numbers of primary research papers and reviews out there; way too many to cite,interpret for you, and undoubtably defend against your perspectives, on an Internet forum. Especialy given that I all I am saying that it is a complex phenomenon and simplified explanations of any kind are inaccurate.

So believe what you wish- frankly I don't care and I don't wish to argue with you. But be careful- I have seen a lot of people hurt their health by believing that a simplistic self-medication/supplement regimen will cure their medical problems. I am not denying that you found a plan that may be working for you. Or not. I don't know, I don't know you or your medical history/test results, and I am a researcher not a medical doctor. But be at least as skeptical of self-treatment and what you read in various corners of the Internet as you are of what your doctors tell you and of the more established medical views.

 

[Abooga]

Thank you vor your informed responses! This issue is indeed quite complex so I guess it makes sense for now to be a bit afraid of hich cholesterol levels. It would´ve been so nice though, if it was suddenly found that we don´t have to worry about cholesterol, wouldn´t it? And that cheese and meat are good for you... Because lately everything that tastes nice is bad for you, meat, sweets, crusty dark potato chips (which I recently learned are carcinogenous), tuna (mercury) etc. etc... Luckily hot chili sauce seems to actually be good and may prevent against cancer. Well, thanks for that at least...

 

[McHrozni]

3. Statins and other drugs that lower serum cholesterol levels lower the risk of cardio-vascular disease.

Wasn't this debunked? Lowering cholesterol has no impact on CVD risk as far as I know.

Of course much remains unknown and yet other factors contribute. For instance cholesterol levels in the diet are not very predictive of cholesterol levels in the serum, and genetics interact in complex ways with diet, exercise, etc. But it seems pretty convincing that too much serum LDL contributes to cardiac risk rather than simply being associated with it.

There are good reasons for that, I find this video a good place to start:



McHrozni

 

[McHrozni]

Thank you vor your informed responses! This issue is indeed quite complex so I guess it makes sense for now to be a bit afraid of hich cholesterol levels. It would´ve been so nice though, if it was suddenly found that we don´t have to worry about cholesterol, wouldn´t it? And that cheese and meat are good for you... Because lately everything that tastes nice is bad for you, meat, sweets, crusty dark potato chips (which I recently learned are carcinogenous), tuna (mercury) etc. etc... Luckily hot chili sauce seems to actually be good and may prevent against cancer. Well, thanks for that at least...

If you overdo on the chili you increase your stomach cancer risk.

Life itself is carcinogenic But just about anything is tolerated if you consume it with moderation.

McHrozni

 

[Red Baron Farms]

Thank you for your informed responses! This issue is indeed quite complex so I guess it makes sense for now to be a bit afraid of high cholesterol levels. It would´ve been so nice though, if it was suddenly found that we don´t have to worry about cholesterol, wouldn´t it? And that cheese and meat are good for you... Because lately everything that tastes nice is bad for you, meat, sweets, crusty dark potato chips (which I recently learned are carcinogenous), tuna (mercury) etc. etc... Luckily hot chili sauce seems to actually be good and may prevent against cancer. Well, thanks for that at least...

The most important thing to remember is all those foods you mentioned are not created equal. An apple is sweet and good for you, but a chocolate eclair with a 32 oz soda to wash it down?......not so much. Both are sweet, but they are quite different in regards to health. I could eat several apples a day (or bananas or whatever you prefer) and probably improve my health, but try the same with chocolate eclairs? Bad move.

Same goes for meat and cheese. They are certainly not created equal.

A review of fatty acid profiles and antioxidant
content in grass-fed and grain-fed beef

A bit of common sense might be in order when it comes to diet.

 

[casebro]

Casebro,

You seem determined to disagree with what are very cautious statements. .......

.... But be at least as skeptical of self-treatment and what you read in various corners of the Internet as you are of what your doctors tell you and of the more established medical views.

I'm only disagreeing with your appeal to authority, and the lack of skepticism on you part.

I asked you to look for some studies backing your claims, and what you showed me did not back your claims. If those cites are what you base your dietary science on, I feel sorry for your mice.

Niow, McHrozni and I would like to see a study done in real world clinical practice that shows a reduction in end points for statin treatment. I believe there is some benefit, just not the 30% improvement quoted by the researchers. The research studies were typically done on people in their 50s, while most end points happen later in life. And typically the studies end when only 2 1/2 % of subjects have died, while real world 40% of us die of cardiovascular disease. And even some of the makers studies show no benefit in all cause mortality.

 

[casebro]

One of my current thoughts on calcium levels is that some of us have hyperabsorption.

Absorption is usualy moderated by vitamin D. Perhaps some of us have an alternative system, genetic, or maybe gut flora make vit D?

Or, milk products per se are not the culprit that some vegans think, nor is it the sat fat. But it's the D3 added to the milk that causes hyperabsorption of calcium? Is there D3 Free milk available?

 

[Giordano]

I'm only disagreeing with your appeal to authority, and the lack of skepticism on you part.

I asked you to look for some studies backing your claims, and what you showed me did not back your claims. If those cites are what you base your dietary science on, I feel sorry for your mice.

Niow, McHrozni and I would like to see a study done in real world clinical practice that shows a reduction in end points for statin treatment. I believe there is some benefit, just not the 30% improvement quoted by the researchers. The research studies were typically done on people in their 50s, while most end points happen later in life. And typically the studies end when only 2 1/2 % of subjects have died, while real world 40% of us die of cardiovascular disease. And even some of the makers studies show no benefit in all cause mortality.

"Ah, I'd like to have an argument, please..." You've got the wrong person if you are thinking that you are debating an advocate of what you disparage as the statin-industry financed, medical dogma on cholesterol and cardio-vascular disease:

1. I am nether an expert on cardio-vascular disease nor a medical doctor. And as I already posted in this thread multiple times, I am not advocating any simple relationship between cholesterol serum levels and cardio-vascular risk. If you look again at my posts you will see that I was agreeing with you that cardio-vascular risk factors are complex and differ for different people. You in turn appear to agree with me that serum cholesterol is one of these factors for at least some people. I am not certain how one can argue with these encompassing, uncontroversial, and cautious viewpoints.

2. I initially assumed that you just were seeking additional information, not hoping to engage in a "prove I am wrong" type of argument. As a biologist I am happy to offer some general information in response to questions, but I am not seeking to debate a pet medical theory, particularly not one manifested as self-medication with "supplements," because I have seldom seen these types of debates yield useful insights to anyone. And I don't see the point here.

3. Some specific responses in regard to your post above:

a. The "appeal to authority" of which you accuse me was my reference to an American Heart Association website in response to one of your questions. By citing a fairly well-respected patient advocacy group, I hoped to provide a useful general summary of the majority viewpoint in this regard while avoiding somehow condensing the huge mass of individual studies out there and while, as requested, not using an industry-based source. BTW, the actual "appeal to authority" fallacy is to cite the opinions of an expert in one area to buttress an argument outside of their area of expertise. It is not a fallcy to to cite an expert's views within the area of their actual expertise. The AHA has long established expertise and interest in cardio-vascular issues and although like any expert they have their own perspective, they provide a good representation of the current consensus. Would it also be an "appeal to authority" fallacy to cite the views of any medical doctor or researcher in the field of cardio-vascular disease?

If you will only accept raw data rather than some "authority's" interpretation of it, feel free to use PubMed or a similar site to find the appropriate primary research publications, although even in these publications the raw data is dissected, integrated, and interpreted by the experts who performed the study. But it will take you several years of 24/7 reading to wade through all these publications. In fact: once you do so how do you intend to interpret this mass of raw data? Some studies will state one thing and others will state another; how will you weight studies done in different ways by different methods (in test tubes, in cells in culture, in lab animals, in different human populations, by genetics, by pharmacology, etc.)? Especially on what basis will you evaluate the inevitable contradictions and apparent inconsistencies that one will find in any large number of studies done in so many different ways if you don't trust the people with related experience and training ("experts") to do so correctly?

b. I also cited two recent studies that apparently are not "end-point real world, right age, etc." enough for you. You are siimilarly dismissive of studies in animals, etc. Apparently studies that don’t support your own viewpoint are lacking in some way or another and I have no doubt that you will similarly find objections with any studies I might cite in the future. Okay, fine. But my own point is only that cardio-vascular disease is complex with some known and much unknown about it, whereass I feel that it is you who are trying to oversimplify this complexity and are heavily invested in your own particular theories.

3. Finally I thank you for your concerns about my mice but I can relieve your worries because don't study cardiovascular disease, cholesterol, statins, etc. in them at all- my interests and focus are other aspects of lipid and carbohydrate metabolism. None of my work has ever been financed by any private company and I myself have no pet theories on cholesterol and cardio-vascular disease. So my mice as safe from my ignorance. I will point out that I cannot morally or legally feed my mice chemicals purchased in a photography supply store, unlike the approach that you are currently using to treat yourself. The university and federal government insists on use of drugs for animals that have been specifically batch tested for safety, purity, and consistency for veterinary or human studies, and all use of animals has to be approved by an independent review board of experts to be certain that we don't put the animals at inadvertant or unanticipated risk by using poorly documented treatments. So I again urge you to be very cautious in your self-treatment scheme. I am happy that you feel it is working for you (I hope it is), but you appear to have accepted that it is safe and effective based on surprisingly little evidence compared to your strong skepticism directed toward far more studied and more widely established medical treatments.

 

[casebro]

"Ah, I'd like to have an argument, please..." You've got the wrong person if you are thinking that you are debating an advocate of what you disparage as the statin-industry financed, medical dogma on cholesterol and cardio-vascular disease:

1. I am nether an expert on cardio-vascular disease nor a medical doctor. And as I already posted in this thread multiple times, I am not advocating any simple relationship between cholesterol serum levels and cardio-vascular risk. If you look again at my posts you will see that I was agreeing with you that cardio-vascular risk factors are complex and differ for different people. You in turn appear to agree with me that serum cholesterol is one of these factors for at least some people. I am not certain how one can argue with these encompassing, uncontroversial, and cautious viewpoints.

2. I initially assumed that you just were seeking additional information, not hoping to engage in a "prove I am wrong" type of argument. As a biologist I am happy to offer some general information in response to questions, but I am not seeking to debate a pet medical theory, particularly not one manifested as self-medication with "supplements," because I have seldom seen these types of debates yield useful insights to anyone. And I don't see the point here.

3. Some specific responses in regard to your post above:

a. The "appeal to authority" of which you accuse me was my reference to an American Heart Association website in response to one of your questions. By citing a fairly well-respected patient advocacy group, I hoped to provide a useful general summary of the majority viewpoint in this regard while avoiding somehow condensing the huge mass of individual studies out there and while, as requested, not using an industry-based source. BTW, the actual "appeal to authority" fallacy is to cite the opinions of an expert in one area to buttress an argument outside of their area of expertise. It is not a fallcy to to cite an expert's views within the area of their actual expertise. The AHA has long established expertise and interest in cardio-vascular issues and although like any expert they have their own perspective, they provide a good representation of the current consensus. Would it also be an "appeal to authority" fallacy to cite the views of any medical doctor or researcher in the field of cardio-vascular disease?

If you will only accept raw data rather than some "authority's" interpretation of it, feel free to use PubMed or a similar site to find the appropriate primary research publications, although even in these publications the raw data is dissected, integrated, and interpreted by the experts who performed the study. But it will take you several years of 24/7 reading to wade through all these publications. In fact: once you do so how do you intend to interpret this mass of raw data? Some studies will state one thing and others will state another; how will you weight studies done in different ways by different methods (in test tubes, in cells in culture, in lab animals, in different human populations, by genetics, by pharmacology, etc.)? Especially on what basis will you evaluate the inevitable contradictions and apparent inconsistencies that one will find in any large number of studies done in so many different ways if you don't trust the people with related experience and training ("experts") to do so correctly?

b. I also cited two recent studies that apparently are not "end-point real world, right age, etc." enough for you. You are siimilarly dismissive of studies in animals, etc. Apparently studies that don’t support your own viewpoint are lacking in some way or another and I have no doubt that you will similarly find objections with any studies I might cite in the future. Okay, fine. But my own point is only that cardio-vascular disease is complex with some known and much unknown about it, whereass I feel that it is you who are trying to oversimplify this complexity and are heavily invested in your own particular theories.

3. Finally I thank you for your concerns about my mice but I can relieve your worries because don't study cardiovascular disease, cholesterol, statins, etc. in them at all- my interests and focus are other aspects of lipid and carbohydrate metabolism. None of my work has ever been financed by any private company and I myself have no pet theories on cholesterol and cardio-vascular disease. So my mice as safe from my ignorance. I will point out that I cannot morally or legally feed my mice chemicals purchased in a photography supply store, unlike the approach that you are currently using to treat yourself. The university and federal government insists on use of drugs for animals that have been specifically batch tested for safety, purity, and consistency for veterinary or human studies, and all use of animals has to be approved by an independent review board of experts to be certain that we don't put the animals at inadvertant or unanticipated risk by using poorly documented treatments. So I again urge you to be very cautious in your self-treatment scheme. I am happy that you feel it is working for you (I hope it is), but you appear to have accepted that it is safe and effective based on surprisingly little evidence compared to your strong skepticism directed toward far more studied and more widely established medical treatments.

Darn. I was hoping you would come back with proof of your statements.

One more question: Then why did you even post in a thread about cholesterol?

Another tid bit of science: Vitamin D is tied to calcium absorption. Cholesterol is the substrate of vitamin D. Statins lower cholesterol.......

 

[jaydeehess]

One of my current thoughts on calcium levels is that some of us have hyperabsorption.

Absorption is usualy moderated by vitamin D. Perhaps some of us have an alternative system, genetic, or maybe gut flora make vit D?

Or, milk products per se are not the culprit that some vegans think, nor is it the sat fat. But it's the D3 added to the milk that causes hyperabsorption of calcium? Is there D3 Free milk available?

Vitamin D as produced in the skin, or adsorbed from foods must first be altered by the kidneys into the active form.
Here is a quick description wrt kidney disease patients.