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Archived Comments for: Are statins anti-inflammatory?

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  1. Atherosclerotic

    John Tanner, private

    23 February 2003

    Hello Dr. Ridker, I just came across your article re the anti-inflammatory effect of statin drugs in the cardiovasular system.

    Recently, I have had time to do extensive recent basic science literature review along with considerable antecdotal evidence beginning in the late 1970's along with current clinical research such as yours.

    It appears quite probable that overexpression of Cox 2 with its stimulation of the production of prostaglandin E2/kinins is the mediator of the inflammation known to exist in the coronary arteries of patients with atherosclerotic disease, for example. You and others have reasonably shown that the statin drugs benefit patients independently of their cholesterol lowering effects by acting in an anti-inflammatory manner.

    I would hypothesize that the action of the statins is to inhibit Cox 2 as do Celebrex, Vioxx and Bextra.

    Recent studies on the Atkins diet (Westman, et al Duke University) have shown cholesterol and triglyceride reductions far superior to those found in a matched cohort of subjects on the AHA low fat diet. In fact, the cholesterol and triglyceride reductions were shown to be independent of the weight loss observed, to occur long before the study was concluded, and to be do to food avoidance. No statins, Cox 2 "inhibitors" were administered.

    A large number of antecdotal studies in the late 1970's by Philpott and others have strongly suggested that cholesterol, triglycerides and homocysteine are merely MARKERS of inflammation and are NOT RISK FACTORS in and of themselves.

    I would further suggest that you would have seen the same clinical results that you observed in patients on statins, had you merely put them on very low carbohydrate diets. I would hypothesize that no matter what diet you prescribed, your patients would have shown reduction of cholesterol, triglycerides and homocysteine by treating them with Cox 2 inhibitors. (Incidentally, did any of your patients on statins comment on improved arthritis and general feelings of "well-being"--or were they asked?

    the evidence suggests that those carbohydrates elimintated in Westman's very low carbohydrate diet were those acting as STRESSORS to each individual study participant; that is, one or more of the removed carbohydrate foods was a stressor and as such was the agent(s) that caused the Cox 2 overexprssion. Fat people by their nature are carbohydrate sensitive and fat storers.

    William H. Philpott, MD, (Chocktaw, Oklahome) in the late 1970's demonstrated a significant drop in the pH of the duodenal content following the ingestion of a food known to be a STRESSOR (sensitizer). He demonstrated that a stressor food would act to inhibit pancreatic bicarbonate secretion and to stimulate prostaglandin E2/kinin production and clinical symptoms in any part of the body as determined by the patient's heredity.

    At that time, neither he nor anyone else was aware of the exact mechanism or the cause of the prostaglandin E2/kinin production. Now, it is known to be the result of the Cox 2 overexpression.

    If this chemistry be correct, and if all degenerative diseases (coronary disease as just one of many) are basically inflammatory (tissue acidosis, hypoxia and inflammation as we learned in medical school pathology and physiology class), then it is reasonable to hypothesize that ALL degenerative diseases have a common tissue basis and should be preventable by AVOIDING identified stressor foods in any given patient. When food avoidance is not possible or practical, treatment with ANY Cox 2 inhibitor whether it be Celebrex or Lipitor, etc., (or a statin drug--whichever is cheaper and with less side effects) should suffice.

    Dr. Westman found that 5 GERD patients in his Atkins-AHA diet comparison lost all their symptoms with general carbohyrate avoidance. No study was done, however, to attempt to identify WHICH particular carbohyrate(s) were the stessors--the foods which caused the GERD. He also reported orally to me that several women noted loss of their PMS symptoms while on the very low carbohydrate diet (none on the AHA low fat diet).

    My hypothesis to explain the cause of PMS is loss of estrogen-mediated, protective, anti-inflammatory activity during 3/4 of the menstrual cycle. When the premenstrual estrogen levels drop sufficiently, the inflammatory effects of one or more stressor food(s) manifest. I treated one woman with the most severe PMS I had ever seen by identifying the one food (unusual to be only one) that was the stressor. Her PMS consisted of large ecchymoses over most of her body, edema of her hands and feet and gross enlargement of her breasts. She had been worked up at a major university and told "nothing is wrong". All her hormone studies were normal as we expected. Avoidance of Coca-cola for the month before her next expected period completely eliminated her PMS for good.

    I'm sure you are aware of the current cancer treatment studies underway with Celebrex in combination with chemotherapeutics based on its ability to block prostaglandinE2/kinin production. In addition, it has been reported to reset apoptosis and diminish angiogenesis.

    The fact that almost all the studies are strongly positive in such diverse tissues as lung, prostate, colon, skin, and breast is a stong argument for the unified theory of ALL non-infectious diseases including cancer. In fact, more than one author have hypothesized that prostaglandin E2/kinins are the cause of cancer--if correct, then most cancer can be traced back to food stressors.

    Anyway, thanks for reading to this point. I would very much appreciate your comments and thoughts my various hypotheses. It looks to me as if we are on the verge of a relatively simple clinical treatment regimen for almost all the chronic, degenerative diseases--and maybe cancer. John Tanner, MD

    Competing interests

    None declared