ofonorow wrote: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.
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?