Cholesterol

Most of us know that eating the wrong kinds of fats can increase our risk of developing atherosclerosis, but few are aware of just how important types of fats really are in this process. During the late 1940s and early 1950s, scientists believed that a high consumption of cholesterol was a major cause of atherosclerosis. The earliest theories were based on information collected by pathologists, who discovered large amounts of cholesterol within atherosclerotic plaques obtained from autopsied persons.

Next, clinical doctors began to examine their vascular disease patients for high blood levels of cholesterol. They discovered that people with cholesterol levels at 240 mg/dl were four times more likely to die of a heart attack than those with levels at 220 mg/dl. At 260 mg/dl of total cholesterol, patients were six times more likely to die of a heart attack. They then looked at populations of people around the world who had much lower cholesterol levels and found that those with levels of 120-160 mg/dl had an extremely low incidence of heart disease.

From these early observations, scientists created the cholesterol theory of atherosclerosis, which is based on the idea that cholesterol itself is the cause of the disease. This theory has been repeated so often to the medical community and public that it has been extremely difficult to dislodge from their thinking, despite the fact that we now know only 50 percent of all atherosclerosis cases can be accounted for using the standard cholesterol-based risk-factor index built up over the last several decades. It's interesting to note that, even in the earliest years of research, leading cardiologists strongly resisted the idea that cholesterol was solely responsible for atherosclerosis.

At this same time, the pharmaceutical industry, always looking for a way to expand profits based on new discoveries, began a crash program to develop cholesterol-lowering drugs. In the meantime, clinical doctors began to call for lowering cholesterol in diets. A chief recommendation was to switch from saturated fats—which are found mostly in animal products— to polyunsaturated vegetable oils. Among these "healthy oils," corn oil (and margarine made from corn oil) was hailed as the solution for our society's vascular problems. Manufacturers of vegetable oils and margarine launched extensive advertising campaigns, touting endorsements from the American Heart Association. Suddenly, America was on a cholesterol-lowering binge. Food manufacturers inundated the public with guarantees that their foods were "low in cholesterol" and "heart healthy."

Despite this frenzied enthusiasm for lowering cholesterol, there existed an unheeded rumbling in the medical community, raising serious questions about the validity of the theory. In fact, if we look at all the conventional risk factors combined—hypertension, diabetes, smoking, alcohol abuse, and elevated cholesterol—only half of all atherosclerosis cases can be explained. Other factors must be at work, and their impact is being largely ignored. For example, if elevated cholesterol is the true cause of atherosclerosis in mammals, what about hibernating animals, such as bears, whose cholesterol levels hover around four hundred, and who rarely show signs of atherosclerosis? The same is true in humans.

This is not to say that fats do not play a significant role in atherosclerosis, but it also seems obvious that they do not act alone to produce vascular occlusions. The process actually appears to involve a complex interplay of metabolic events and environmental factors— discussions of which are not nearly as conducive to fifteen-second sound bytes on the evening news, or multi-million dollar day-glo ad campaigns.

It is important to note that medically "acceptable" cholesterol levels are lowered almost every year. Today, most doctors seek levels that are below 200 mg/dl. This is based on the famous Framingham study that found people with cholesterol levels below 175 mg/dl had half the number of heart-attack deaths as those with levels from 250-275 mg/dl. These two extremes were then used to justify a vigorous attack on cholesterol.

One of the biggest problems with the cholesterol theory is that its proponents ignore contributing factors that always seem to accompany high cholesterol. For example, when populations of people known to have low incidences of atherosclerotic-associated diseases (strokes, heart attacks, peripheral vascular disease) are examined, most studies ignore the fact that such groups not only consume fewer cholesterol-containing foods, they also eat more foods high in plant phytochemicals, antioxidant vitamins, minerals, and fiber. Such populations also consume considerably less sugar than people with high rates of atherosclerosis, a consideration I will discuss later in this chapter.

Problems with the Cholesterol Theory

Obviously, there are a few problems with the cholesterol theory, not the least of which is the fact that half of all people who end up having a heart attack or stroke have no conventional risk factors. Unfortunately, modern science, when faced with a paradigm that may endanger funding considerations, tends to ignore such anomalies; yet, investigation of such anomalies in the past has led to radical breakthroughs in our understanding of various diseases. The most glaring problem with the cholesterol theory centers around the fact that all early studies on cholesterol-lowing drugs found no statistical evidence linking reduced cholesterol levels to fewer heart-attack deaths.

The only newer studies that have shown a drug-based reduction in cardiac mortality used cholesterol-lowering drugs that were also antioxidants. It has been hypothesized that the antioxidant effect, not the lowered cholesterol, actually accounts for the enhanced protection. In addition, they have platelet inhibiting properties, which when combined with their antioxidant effects, explains the reduction in heart attacks and strokes. As I will discuss later, there are much safer antioxidants than those you can get in a prescription medication.

One of the biggest secrets in the medical world is the connection between cholesterol drugs and cancer. In a paper that appeared in the Journal of the American Medical Association in 1996, Drs. T.B. Newman and S.B. Hulley discussed the long-term implications of twenty-six million people taking these drugs.299 First, they observed that no long-term studies have been done in humans to determine safety: the millions of people currently taking these drugs are essentially test subjects.

They also point out that a meta-analysis (a composition of many studies) indicated cholesterol-lowering drugs may increase mortality rates caused by other conditions. A review of the available research indicated that all cholesterol-lowering drugs cause cancer in rodents, and that the dose of the drug used in test animals was comparable to that used in humans. This important information is conveniently omitted from the Physicians' Desk Reference (published by Medical Economics Company), which your doctor uses to determine drug risk.

While studies have found that cholestyramine and probucol are not directly carcinogenic, these drugs do act as co-carcinogens, enhancing the carcinogenicity of other chemicals. It is important to stress that all known human carcinogens are also carcinogenic in mice or rats. Given this evidence, and for safety's sake, it seems wise to assume the opposite is true—that animal carcinogens are human carcinogens—unless good experimental evidence to the contrary can be produced.

According to Dr. L.S. Gold and co-workers, of a list of eighty possible carcinogenic hazards to humans, the average cholesterol-lowering drug was ranked second.300 According to FDA safety guidelines, a medication must not produce cancer in test animals at doses twenty-five times the usual dose. The lipid-lowering drugs produce cancer in doses far below this. In addition, some of these drugs also have been shown to damage nerves in the brain stem.

Cardiologists, in a widely covered press release, have recently suggested that even more people should be on lipid-lowering drugs. This is ludicrous, since mild cholesterol elevations can be controlled easily by dietary changes and special supplementation.

Another theory suggests that lipoprotein(a), not LDL cholesterol, is the actual culprit. A recent study found that this special protein is a stronger predictor than cholesterol of heart attack risk.301 It is very sticky and tends to attach to arterial walls. In fact, those with high levels of lipoprotein(a) are 70 percent more likely to have a heart attack than those with lower levels, and people with elevated lipoprotein(a) have ten times the risk as those with elevated LDL cholesterol.

Unlike LDL cholesterol, lipoprotein(a) is not affected by diet, smoking, or other risk factors. It is purely hereditary—but vitamins will reduce levels in your body. Nicotinamide (as inositol hexaniacinate) and vitamin C are especially effective, and a combination of these two can lower levels over 36 percent. Two amino acids, lysine and proline, have also been shown to reduce lipoprotein(a)'s stickiness. Lysine is preferable, since proline can act as a neurotoxin. Five hundred milligrams of lysine three times a day should suffice. Your doctor can track lipoprotein(a) levels to determine dosage adjustments.

Most doctors, even some cardiologists, tell their patients that a high LDL-cholesterol value is bad. What most patients aren't told is that recent evidence indicates that there are actually two forms of the LDL molecule: one small and one large. Because it is easily oxidized, only the small one appears to be harmful. In fact, the larger LDL-cholesterol molecule may be just as protective against atherosclerosis as HDL-cholesterol, the so-called "good" cholesterol.

What this means is that if you get a cholesterol test that doesn't differentiate the two types of LDL, you will not know if your risk is high or not, since most of the LDL may, in fact, be the "good" type. Only a few laboratories test for this difference.

It is also important to know the difference because a higher intake of omega-3 fatty acid can actually increase LDL-cholesterol levels, but it is thought that only the good form is raised by omega-3. This would explain why diets high in omega-3 significantly reduce heart attack and stroke rates, despite raising LDL-cholesterol levels.

While the matter is far from settled, I would caution the reader not to be taken in by the shrill hype over cholesterol. A high intake of a variety of antioxidants, a balance of proper fats, and the use of special supplements will protect most of us from coronary heart disease and stroke.

Your Heart and Nutrition

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