Cholesterol And Heart Disease

The Big Heart Disease Lie

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Much of what we are told by our most trusted authorities ends up being the exact OPPOSITE of what is true and should be heeded. And this isn't to say that the people telling us these "facts" are lying to us. That's a value judgment that cannot fairly be made. But the fact remains that the public often ends up with the worst possible advice that it can be given. This advice is typically far worse than no "guidance" from the authorities at all. Typical examples of this "opposite" advice include the promotion of water fluoridation, the promotion of mercury amalgam fillings, the promotion of commercially available milk as a positive nutrient, and even the promotion of margarine over butter in the diet.

"Avoid foods that are high in cholesterol." This is yet another example of thoroughly misguided advice from our so-called health authorities.

The irrational attack on the effects of cholesterol on health has resulted primarily from the chronic misinterpretation of statistical data. High cholesterol levels are statistically associated with higher rates of heart disease. This is a fact that has been conclusively demonstrated. However, a statistical association does not mean

McGraw-Hill's Tenns of Use there is a cause-and-effect relationship. Cause-and-effect means there is an association, but an association alone does not assure cause-and-effect. Just because the police consistently show up at the scene of a crime doesn't mean that you can later conclude that the police committed the crime. But if we were to use the same statistical reasoning in this police example as modern science uses in the cholesterol-heart disease relationship, we could proceed directly to this ridiculous conclusion without any further thought. If a factor is actually protecting against an unhealthy (and usually unperceived) force, and that factor reliably emerges when that force is present, that factor and not the unhealthy, hidden force will typically get blamed for the damage. This is especially so when the unhealthy force has never really been discovered or recognized. Just like the police at the crime scene, you simply cannot conclude that the paramedics must have initially hurt the victims they are trying to save just because they are physically present with the victims.

Yet this faulty reasoning is precisely what we encounter in the case of cholesterol. The scientific literature has consistently and reliably correlated elevated cholesterol levels with increased coronary heart disease. Further, multiple clinical trials in which cholesterol levels were medically lowered resulted in the reduction of coronary heart disease. These trials have convinced the medical establishment that there must be a cause-and-effect relationship between cholesterol and heart disease. To a very limited degree, there is some truth to this concept. But as we shall see, cholesterol is much more a good guy than a bad guy, protecting the body far more than harming the body.

Even though the cholesterol-lowering trials have demonstrated that lower coronary heart disease death rates correlate with lower cholesterol levels, increases in deaths from a variety of noncardiac causes have also been noted as the cholesterol levels have been lowered. Golomb reviewed many of these trials and found a statistically significant increase in deaths resulting from suicide, accidents, and violence as cholesterol levels were lowered.1 And these increases in death essentially equaled the decreases in death from coronary heart disease! Therefore, when viewed in terms of ultimate survival, the reduction in cardiac deaths from lowering cholesterol was offset by the increase in deaths from noncardiac causes. No net survival benefit could be claimed from the reduction of cholesterol with medication.

Furthermore, this net lack of survival benefit from cholesterol-lowering drugs does not even take into account any of the side effects of taking such medication. Lazarou et al. published a study that showed that in the United States in 1994, adverse drug reactions were the sixth-leading cause of death.2 The data did not even include another 2.2 million patients who were seriously injured by their prescription medications. Also not included was the fact that roughly equal numbers of patients died or were seriously injured due to errors of their health care providers. But don't avoid seeing your doctor. Just know that no treatment program comes without cutting both ways. Be an active partner with your health care practitioner in whatever therapies that you take or undergo.

As with nearly all prescription drugs, the commonly prescribed anticholesterol preparations have a large number of potentially significant negative effects on an individual's blood chemistries and overall health. This latest generation of cholesterol-lowering drugs, known collectively as "statins," produces undesirable side effects as often as one-third of the time, depending upon the particular statin chosen. Statins are designed to interfere with the normal function of the liver in its natural synthesis of cholesterol. These drugs so effectively interfere with this normal liver function that the Physicians' Desk Reference advises under its warnings for statins that liver function tests be performed routinely before and indefinitely during therapy.

A better general rule of thumb in any approach to the treatment of any disease is to attempt to eliminate the process causing the disease rather than interrupt the body's natural response to that disease process. It's okay to treat disease symptoms, but not to the exclusion of treating the reason why the disease is there in the first place.

High cholesterol levels develop in response to the presence of toxins; the toxins are neutralized by the cholesterol. It follows that the removal of those toxins is the most reasonable way to lower elevated cholesterol levels. Furthermore, the effect of statins on the liver also serves to lower the levels of metabolites other than cholesterol. One of these is coenzyme Q10, a substance vital to the production of energy in all the cells of the body. Not unexpectedly, fatigue can be seen in patients who take these cholesterol-lowering drugs. This can be explained not only by the lower levels of coenzyme Q10, but also by the fact that the lowered cholesterol levels result in less neutralization of circulating toxins.

Since I am a cardiologist, some readers might wonder what my recommendations might be for the individual who has a cholesterol level above 300 milligrams per deciliter (mg%) with a fairly strong family history for cardiac disease. I would probably prescribe a statin or other cholesterol-lowering drug on a short-term basis. In a study by Shih et al., mice exposed to pesticide poisoning who were deliberately fed a high-fat, high-cholesterol diet were more susceptible to developing fatty plaques in their arteries, the type of condition that leads to heart attacks.3 This suggests that very high cholesterol levels, even though they protect against toxicity, can still directly promote arterial blockages. The body's protective mechanisms can possess their own toxicity when they are exaggerated enough and chronic enough. Therefore, I do not summarily dismiss lowering very high cholesterol levels with medication.

However, I would not choose to lower anyone's levels below 240 to 250 mg%, and I would simultaneously attempt to remove and/ or neutralize as much toxicity as possible. This is not to say that I consider a cholesterol level of 240 to 250 mg% optimal. Rather, it is as low as I would choose to go as long as there was significant toxicity present that needed elimination or neutralization. When toxin levels have been minimized, most people will tend to end up with a cholesterol level between 160 and 220 mg%. Such levels generally will not be reached until all significant dental toxins have been removed and the gut is functioning as nontoxically as possible, with good foods properly combined and properly digested. Some high-quality meats must be included in these foods, since a vegetarian diet will not generally sustain cholesterol levels high enough to neutralize one's daily toxin exposure. And although many supplements could be used to boost immune function that will be discussed later, one supplement that would have to be used regularly in high dosage would be vitamin C. It would best be taken as sodium ascor-bate powder, in divided doses totaling about 10 to 15 grams daily, as a very general guideline only. For those with kidney disease or those who do not keep themselves well-hydrated with adequate water on a daily basis, the dose should be lower. For those who get diarrhea from oral vitamin C, the dose should be kept below that provoking level, unless the diarrhea is tolerable, since both the toxin-neutralizing effects of the vitamin C in the gut and the more rapid bowel transit times are highly desirable. Of course, these suggestions and any others throughout this book should only be done in cooperation with your chosen health care provider. No blanket suggestions serve all people well.

Another interesting point regarding statin anticholesterol agents deserves mention. It had always been assumed that the only way heart disease is lessened by such drugs results directly from the lowering of the cholesterol levels and nothing else. However, John et al. discovered that fluvastatin, a specific statin drug, increased the bioavailability of nitric oxide in the arteries.4 Nitric oxide helps the arteries to expand in caliber, a function that could help prevent heart attacks in much the same way as nitroglycerin and other nitrate drugs given to cardiac patients.

Furthermore, Ridker et al. have recently shown that at least one statin drug significantly reduces levels of C-reactive protein.5 Inflammation throughout the body has been correlated with higher levels of this C-reactive protein. Consistent with this antiinflammatory effect, Ross et al. have demonstrated that statin drugs can decrease the incidence of nonfatal stroke.6 Without further studies, however, there is no way to know for certain which biochemical effect of the statin drug is predominating. The lowering of the cholesterol may be a relatively incidental "side effect" accompanying a more important artery-dilating effect or inflammation-lowering effect.

Perhaps a drug that increases nitric oxide levels without lowering cholesterol levels could decrease cardiac deaths without increasing the noncardiac deaths that are seen when cholesterol levels are lowered. Or perhaps any of a number of known anti-inflammatory drugs could also lower cardiac deaths without elevating noncardiac deaths. Presumably neither of these drug approaches would involve the disadvantage of using statin drugs, where lowering cholesterol levels also reduces the neutralization of toxins.

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