ofonorow wrote:[color=#0000FF] [upated] I am happy that we have people at the forum who are willing to defend statin drugs. The value of these drugs should be debated. A central issue is whether increased cholesterol is really a risk factor, and if so, what does it mean to be a CVD "risk factor." For example, is mucous a "risk factor" for the common cold? One generally gets a sinus drip everytime one gets a cold, but would controlling the mucous, as in an antihistimine, control the cold?
A risk factor need not be causal, agreed, and by definition it need not be. Cholesterol is quite assuredly a risk factor for certain types of cardiovascular diseases - given the evidence from multiple epidemiological studies, as well as the observation that those afflicted with familial hypercholesterolemia are a higher risk than the general population. A meta-analysis done in 2007 from 61 different prospective studies (including over 800,000 people) showed quite convincingly that high total cholesterol is correlated with increased ischaemic heart disease mortality risk. The association is strongest in the 40-59 age group, but declines in older age groups (for both men and women, even when adjusted for systolic blood pressure and smoking status). The study did not however show any correlation between total cholesterol and total stroke mortality. Nonetheless, total cholesterol also increased risk of mortality from vascular conditions other than IHD or stroke.
We know through several large clinical trials that statins reduce all-cause mortality. A meta-analysis conducted by the Cholesterol Treatment Trialist's (CTT) group in 2005 demonstrates that statins reduce the risk of all-cause mortality and mortality from coronary heart disease, proportional to the reduction in LDL-cholesterol. A 1 mmol/L reduction in LDL, for instance, reduced both mortality as well as the incidence of major vascular events in the treatment arm.
Given that statins are known to have pleiotropic effects, it could be that they bring about their beneficial effects through other mechanisms. In that case, the lowering of LDL-cholesterol would simply serve as a marker of treatment efficacy, since these pleiotropic effects (e.g. reduction in CRP) are proportional to the cholesterol-lowering ones. Given the paradoxical epidemiological evidence that cholesterol is not associated with total stroke mortality, yet statin therapy lowers this risk, it is possible that other pleiotropic effects rather than reduction in cholesterol are beneficial in the case of stroke.
Nonetheless, basic science research has suggested that LDL-cholesterol can be thrombogenic, thus there is also evidence of a causal link between cholesterol and heart disease.
As I said before, cholesterol is just one of many risk factors associated with heart disease. The benefits of statin use vary depending on what other risk factors a person has. Thus, the use of statins are probably not cost-effective nor even clinically beneficial in certain groups of patients. However, there are those who will probably benefit from it. Thus, it is important for patients to understand what their absolute risk of suffering a major vascular event is and decide accordingly whether statin use is worthwhile.
Higher cholesterol has been correlated with CVD, just as one could correlate mucous to the cold, and we could also correlate tennis shoes and ownership of microwave ovens. Of interest is what risk factors cause or contribute to heart disease. Is elevated cholesterol really a risk factor or is it a side effect of (body's reaction to) heart disease? There is no evidence that I am aware of that cholesterol in the blood causes atherosclerosis.
Studies have shown that cholesterol is thrombogenic, and the link between cholesterol and atherosclerosis is supported by animal models. Nonetheless, whether there is a direct causal link is a moot point, considering that lowering cholesterol has been shown to reduce the risk of heart disease.
I would be happy to examine some of the hundreds of studies that have been conducted on statin drugs, but again, if the study has not released the raw data, then it is not subject to scientific review and I will not waste my time. (We have noted a pattern during the earlier statin studies, when they were releasing the data, that the studies were ended just before the placebo group began doing better w/r to the statin group. It really has amazed me that statins would do better than placebo in any study, for any amount of time, knowing what we know about the depletion of Coq10. The factors that allow statins to look beneficial are low dosages, and lack of overt heart disease, ending the study early, etc.)
So you have seen raw data from some statin studies? I'm just curious - what does this "raw data" consist of?
It should be noted that ten-year studies of statin use have shown a benefit; many trials are stopped based on predetermined criteria - if there is evidence of clear harm or benefit in the treatment arm, the study is stopped after this preplanned interim analysis since it is not considered ethical to subject the treatment group to further harm or to deny the control group of a treatment that could benefit them.
Cholesterol is part of the body's defense system, it helps remove toxins, transports essential nutrients, etc. When you stop eating enough cholesterol, your body initiates a process to create more in the liver. The fact that Lipitor lowers cholesterol and "works" in that sense is beyond dispute. Whether artificially lowering cholester is a good or very bad thing for heart patients is subject to debate, and should be debated. According to the unified theory, increased cholesterol production, especially Lp(a) (a form of LDL cholesterol) is an adaption to strengthen damaged arteries caused by too little vitamin C (leading to too little collagen in the arterial wall). Why would you want to remove this defense mechanism from heart patients?
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.
This article by a pharmacist is worth reading in this regard, as it compares the standard Lipid Theory of CVD with the Pauling/Rath Unified Theory: http://www.ourhealthcoop.com/pauling.htm
A PLUMBER’S TAKE ON “PLUGS” IN THE SYSTEM
So what’s wrong with the Lipid Theory? Any plumber looking at the Lipid Theory model would say, “It simply doesn’t make sense.”
Let’s start by thinking about “sludge” in a plumbing system. Sludge tends to plug up the smallest pipes in the system first—not the largest.
Likewise, if the system is cardiovascular, you would expect sludge (plaques) to build up first in the capillaries and arterioles, long before appearing in the carotid and coronary arteries. The first blockages, similarly, you would expect to occur way downstream of the pump, not in close proximity to the heart, where the pressure is the greatest.
Yet, this is not the way cholesterol plugs up arteries. It’s the exact reverse. So a plumber’s take would be that something else is happening.
You mean blockages like in retinal vessels? I'm sure you've also heard of peripheral artery disease. Blockages are usually detected in larger arteries first, because these are most likely to be symptomatic. But blockages do occur in smaller arteries.
And yes, the rare condition of hypercholesteremia is the (only?) case I can think of where prescribing these cholesterol-lowering, CoQ10 depleting drugs make sense, but then, only with advice to supplement CoQ10. (Unfortunately, few American doctors even know what CoQ10 is or does.) And the worst case is hyper Lp(a) cholesteremia, extremely high levels of Lp(a), something that if a child gets, their life expectancy is very short.
Note that cholesterol drugs, however, do not generally lower Lp(a), they increase Lp(a) levels.
Why would you think it is beneficial in this case, if high cholesterol isn't a problem?
Do you also have any references to studies showing that cholesterol drugs increase Lp(a) levels?