LOW DOSE STATINS?
"Red yeast rice contains a statin (a natural product of a fungus) and thus is no different to a drug-company manufactured statin. Unfortunately, there are two reported cases of rhabdo after taking RYR, even though a daily dose was probably much lower that the commonly prescribed dose of statins."
..."Although it is far to early to rejoice, there is compelling reason to believe that statin dosing considered minuscule by today's standards may truly be a "friend to man" in the future, with near absence of our present scourge of side effects."...
The long term use jury is till out - although the cholesterol issue has pretty much hit the dust. Personally. I'd steer clear of any drugs and stick to nutrients...
See: Orthomolecular Solutions to Heart Disease
Chris Gupta
-------------------------LOW DOSE STATINS (orginal is here)
Now that the results of long term studies of statin use have been published, few would argue the effectiveness of statin drugs in reducing cardiovascular disease risk. To be sure, other substances having nothing or little to do with our alleged nemesis, cholesterol, also have demonstrated considerable benefit in this regard. Such therapies include omega 3, Coenzyme-Q10, vitamins B6, B12 and folic acid, anti-oxidants and even buffered aspirin. But in considering only the statins, study after study has shown the benefit of these agents in reducing the risk of heart attack and stroke, whether used for primary or secondary prevention. However, almost buried in this barrage of positive results is our growing research evidence that this reduction of cardiovascular disease morbidity and mortality from statin use has occurred independently of cholesterol effect. Regardless of the cholesterol level of the subject at the start of statin therapy, whether normal or high and regardless of the level of cholesterol reduction, whether great or small or none at all, statins, originally felt to work solely as an inhibitor of cholesterol biosynthesis, appear to work independently of cholesterol. Just what is going on here? Weren't we all taught years ago that only by decreasing serum cholesterol by haranguing our patients these past 35 years as to the merits of a low fat/low cholesterol diet and by writing expensive prescriptions for a long list of increasingly potent cholesterol "busting" drugs could we expect to reduce cardiovascular disease risk? And now we find statin benefit independently of any cholesterol factor. Isn't cholesterol still "public health enemy number one"? Can't we still use the "C" word to frighten small children?
Adding to this evolving puzzle about the cause of cardiovascular disease is the work of Kilmer McCully, who, despite massive obstacles of opposition to any concepts of arteriosclerosis and atherosclerosis contrary to a cholesterol causation, successfully demonstrated to the then reluctant scientific world that homocysteine elevation is a major player in cardiovascular disease, relegating cholesterol's appearance in plaques as that of an "innocent bystander". Adding to cholesterol's innocence is its vital role in our body - mediator of synaptic transmissions, precursor of vital hormones and the most abundant biochemical in our brains. Only in its unnatural, oxidized form does cholesterol exhibit toxicity. Sort of ruins your weekly shopping trip through the pastry aisles, doesn't it? Can you find a decent cookie of cake, free of the "oxy" form of cholesterol.? I doubt it! Does this mean back to fresh eggs and whole milk? Think about it!
Despite this evidence of a new non-cholesterol factor in cardiovascular disease risk, our nutritional and pharmaceutical world remains steadfastly focused on cholesterol, the villain. Most of our primary care physicians today, marching lockstep to drug company guidelines, prescribe whatever dose of powerful statins is required to lower serum cholesterol, even though this same cholesterol is increasingly considered to be irrelevant. Statins work by another mechanism, drug company researchers say. They relieve inflammation in the endothelial lining of blood vessels - this reduces sclerotic change. And recently, the greedy eye of our statin "monster" (for that is what it has become in terms of economic and social impact) is focusing on extending the use of statins to organ transplant recipients and victims of autoimmune diseases such as rheumatoid arthritis. Why, because they work!
To read Shovman's excellent review in Cutting Edge Reports of "The anti-inflammatory and immuno-modulatory properties of statins is like entering the topsy-turvy world of Alice in Wonderland, where the effect of lowering one's immune defenses, which most of us intuitively feel is of doubtful benefit, can be interpreted as good for the organ transplant recipient and autoimmune disease victim but bad for most infectious disease and cancer risk. One must admire this "positive spin" ability usually seen only in the Washington political arena. The good I see from the large numbers of excellent studies having to do with this new statin role of attenuating our immune system is that the attention of our clinicians is now beginning to be focused on the true cause of arteriosclerosis and atherosclerosis and the realization will soon dawn that cholesterol is conspicuously absent in the "usual suspects" line-up. When, we might ask, will the doctors who write the prescriptions begin to question the merit of a cholesterol lowering dose of statin drug when cholesterol is not an issue? Although the results of the ongoing low dose statin trials will not be known for several years, we already have some tantalizing clues.
One of the most relevant comes from Japan where Matsuzaki reported the results of a 6-year followup of 47,294 Japanese patients treated with low dose Zocor (5-10 mg daily) for their hypercholesterolemia. Most would consider statin doses in this range to be borderng on sub-therapeutic, yet even with this low statin dose, there resulted substantial lowering of cardiovascular disease mortality. I cite this study as one of the very first to examine the effectiveness of low doses of statins on cardiovascular disease risk independent of cholesterol effect.
Since the development of statin drugs, the end-point for judging effectiveness has been the cholesterol response. If cholesterol seemed reluctant to be lowered, a higher dosage of statin was the almost automatic response. Our focus on cholesterol as the culprit has led us to higher and higher statin dosages over the years as target levels for our serum cholesterol have been progressively lowered. Today it is almost standard that the starting dose be at least 20 to 40 mg, of Liptor or Zocor, (or its equivalent in the other statins) and 80mg doses have become increasingly common. All of this is justified to bring down the sometimes stubbornly elevated cholesterol in a current research climate where every day reveals increased irrelevancy of cholesterol.
Since cholesterol response no longer seems to be a valid end-point in determining statin dose, the entire strategy for dosing these drugs must be reviewed, using a marker of inflammation as anendpoint, not cholesterol. The effectiveness of statins on cardiovascular disease risk at radically lower dosages must be defined. Using Lipitor as an example, the relative benefit on cardiovascular disease of 5 mg and even 2.5 mg should be studied. As Jay Cohen has emphasized in his book, "Over Dose",.most side effects of the statin drugs would never have occurred if the philosophy, "start low, go slow" on statin dosing were applied. The obvious problem with this philosophy is the apparent lack of a meaningful end-point that defines anti-inflammatory success. C-reactive protein is an inflammatory marker that has shown considerable usefulness in defining high risk for cardiovascular disease but, unfortunately, it is non-specific. Inflammation anywhere in the body from chronic unsuspected infectious disease such as low-grade prostatitis, urethritis, cholecystis, gingivitis, cervicitis, or diverticulitis or even the onset of the common cold may trigger falsely positive CRP test results, meaningless in terms of underlying arterial inflammation. A far more specific test when available for wide spread use may be the increasingly well-known transcription factor, nuclear factor-kappa B (NF-kB).
This vital substance appears to be the basis of our entire complex of anti-inflammatory and immuno-modulatory reactions. All statns have been proven to inhibit NF-kB, some far more strongly than others but a curious observation has been noted, which if validated, will be of considerable importance. This observation is that only small doses of statin drugs are necessary for surprising inhibition of NF-kB and doubling or tripling this dose results in only modest increases in inhibitory effectiveness. This effect parallels that of aspirin on platelet inhibition. Small doses (81mg) are very adequate for this purpose and tripling or quadrupling aspirin dose serves only to increase side effects with little or no increase in platelet effect. Incidentally, this reaction also is mediated by NF-kB.
Although it is far to early to rejoice, there is compelling reason to believe that statin dosing considered minuscule by today's standards may truly be a "friend to man" in the future, with near absence of our present scourge of side effects.
posted by Chris Gupta on Friday September 24 2004
updated on Saturday September 24 2005URL of this article:
http://www.newmediaexplorer.org/chris/2004/09/24/low_dose_statins.htm
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