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What Doctors Don't Tell You

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September 2019 (Vol. 4 Issue 7)

Cholesterol: caught in the act

About the author: 

Cholesterol: caught in the act image

The entire approach of lowering cholesterol is faulty

The entire approach of lowering cholesterol is faulty. The Framingham Project, which followed a Massachusetts study group over time, found a significant correlation between total cholesterol and heart attack risk only in males from their low 30s to their early 60s (Atlantic, 1989; September: 37-70). Extrapolating these findings to everyone violates more than common sense.

Why is cholesterol lowering wrong? This lipid does not participate in initial arterial injury; it may not pile up in arteries or accumulate in the blood for months after such injury (Atheroscle-rosis Review, 1983; 11: 157-246). It was caught at the scene of the crime like a schoolboy seen throwing the last snowball after a window was already broken. Not only is cholesterol essential for innumerable body functions, but four fifths is generated in the body.

Rising levels of cholesterol, uric acid and others are among the body's defensive responses to arterial injury (Proc Nat Acad Sci, 1982; 79: 6858-62). They are signs of disease like a fever, not the disease or "risk factors" themselves (Lancet, October 8, 1988: 839-41). And so artificially lowering cholesterol, like contriving to reduce a fever with aspirin, hinders the body's efforts to protect itself.

US Alternative cardiologist Dean Ornish's patients got better with exercising, lowering stress and eating a vegetarian diet without supplements. Carefully matched, randomly selected control patients on the American Heart Association diet taking their heart specialists' prescribed drugs got worse: their arteries continued to narrow. Ornish attributed the improvement in test patients to their lowered cholesterol (Dr Dean Ornish's Program for Reversing Coronary Heart Disease, New York: Random House, 1990).

Since rising cholesterol is a sign of disease like a fever, not its cause, falling cholesterol cannot improve health any more than a dropping fever cures a patient of pneumonia. The test patients got better because they put little if any oxidised cholesterol into their mouths (Amer J Clin Nutrition, 1979; 32: 40-57); they prevented the formation of oxysterols, or oxidised cholesterol molecules, by avoiding animal protein (Atherosclerosis Review, 1983; 11: 157-246); and their diet provided antioxidant vitamins C, beta carotene and co enzyme Q10 to handle oxysterols from all sources (J Orth Medicine, 1991; 6: 83-98).

But why would nature create LDLs if they kill us? LDLs perform necessary functions. For one, they carry beta carotene and co enzyme Q10. Too little LDL may not carry enough of those and other antioxidants to inhibit growth of tumour cells (Earthletter, 1993; Spring), helping explain why artificially lowering LDL cholesterol promotes cancer.

LDL functions as the steroid forming precursor to deliver anti ageing pregnenolone, the precursor of progesterone and DHEA all required for good health. Further, cholesterol itself serves as an antioxidant to help rid the body of toxins from the environment and diet (Free Rad Biol & Med, 1991; 11: 47-61). This helps explain why the body makes cholesterol rise after arterial damage and makes it drop as plaques are reversed, and further helps explain why excessive lowering of cholesterol promotes cancer.

Lovastatin and its "statin" analogues do much more than lower cholesterol. Inhibiting HMG CoA reductase activity, their mechanism of action increases lipoprotein(a), lowers co enzyme Q10, increases the risk of conditions against which CoQ10 protects, increases the risk of arterial damage and suppresses the immune system.

Suppression of HMG coA reductase activity is one of the mechanisms by which oxysterols damage arterial walls and suppress the immune system (J Biol Chem, 1974; 249: 7306-14; Exp Molec Path, 1984; 41: 249-57). CoQ10 is a powerful antioxidant, and overwhelming international evidence gathered over a quarter century confirms that it is indispensable for human cardiac function in other ways as well. It is deficient in cardiac patients (J Molec Med, 1977; 2: 431-60; Klin Wochenschr., 1988; 66: 583-590; Amer J Card, 1990; 65: 521-3). CoQ10 is intimately involved in the synthesis of adenosine triphosphate (ATP), the basic energy molecule of every cell, and thus in the generation of 95 percent of the body's energy. In congestive heart failure, digitalis, diuretics and vasodilators offered a 25 per cent survival after six years; without drugs, CoQ10 offered 75 per cent (Amer J Cardio, 1990; 65: 521-3).

In patients taking CoQ10, starting concurrent lovastatin lowered levels of the antioxidant 44 to 75 per cent (Proc Nat Acad Sci, 1990; 87: 8931-4); In one Italian study (Proc Nat Acad Sci U.S.A, 1990; 87: 8931-34), the condition of every patient worsened.

After the 200 percent increase in cardiac deaths among test patients using diuretics in the Oslo Heart Trial (American Journal of Medicine, 1980; 69: 725-740), the National Health Institute of Helsinki called for a moratorium on the use of cholesterol lowering drugs.

In view of those results and the evidence, such a moratorium should be made universal and permanent.

!AJoseph Hattersley

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