The heart works extremely hard. Normally it beats about 100,000 times a day, pumping over 2,000 gallons of blood over tens of thousands of miles of blood vessels throughout the body. This is equal to going around the world twice. When large volumes of heart muscle are damaged by a heart attack, or even a series of smaller heart attacks, the ability of the heart to pump blood is impaired. The heart as a pump may fail for other reasons as well, such as is seen in viral infections of the heart (cardiomyopathy) and as a result of aging changes, or as a result of prolonged hypertension. A study presented at the American College of Cardiology in Detroit of 26,000 people followed over a ten-year period found that the incidence of heart failure was increasing significantly. In fact, since 1989, the number of heart failure cases has doubled! An examination of heart clinics throughout the United States reveals the same dramatic rise in heart failure.
As a result of pump failure, many organs are forced to work with reduced oxygen and nutrient supplies, leading to such problems as shortness of breath with mild exertion, impaired kidney function, and overall fatigue. Gradually the heart begins to enlarge, a condition called congestive heart failure. Because the rest of the body and organs are denied adequate blood supply, free-radical generation increases within these tissues as well. This leads to accelerated aging of the entire body, not just the heart. In time, these organs begin to break down as well, as is seen with kidney failure associated with heart muscle decompensation.
Because the heart has to work so hard, it requires an increased supply of antioxidants and energy supplies. It has been found that falling levels of CoQIO, L-carnitine, and magnesium accompany heart failure. In fact, heart muscle biopsies of cardiac disease patients have shown a CoQIO deficiency in 50-75 percent of cases, with the levels decreasing greatest with increasing severity of the heart disease.325 Other studies have shown this energy-supplying coenzyme to be deficient in numerous cardiac disorders such as mitral valve stenosis, angina, cardiomyopathy, and congenital heart defects. Supplementation with CoQIO and L-carnitine, as well as the other B vitamins, often significantly improves heart muscle contraction and so heart function. This in turn improves the oxygen supply to the other tissues and organs.
Numerous experimental studies have shown the benefits of CoQIO for strengthening heart muscle. A considerable number of human studies have also shown the benefit of this supplement in improving congestive heart failure. For example, in one study of twenty patients with congestive heart failure who were treated with 30 mg of CoQIO per day, 55 percent demonstrated improvement in symptoms after two months.326 Thirty percent of the patients showed a dramatic reduction in fluid buildup in the lungs, a major complication of congestive heart failure.
Some might criticize that more objective testing of heart function would be needed to confirm that the supplement was actually improving heart muscle function. Indeed, examinations measuring stroke volume, cardiac output, ejection fraction, and cardiac index have confirmed that the effect was more than subjective.327
In another large study involving multiple medical centers in Italy, 2,664 patients with mild to moderate congestive heart failure were given CoQIO in doses ranging from 50-150 mg per day. Most (78 percent) received 100 mg per day. Following three months of therapy, the vast majority improved in terms of swelling of extremities, shortness of breath, arrhythmia, heart palpitations, and nighttime urination.328
While the most consistent improvements in cardiac function were associated with mild to moderate heart failure, even severe, advanced heart failure patients have responded to this treatment. For example, in one study involving thirty-four patients with highly advanced congestive heart failure, in which cardiologists gave the patients 100 mg per day of CoQIO, 82 percent of the patients showed improved heart function. Equally impressive was the finding that the survival rate two years later was 62 percent—compared to less than 25 percent survival for patients treated with conventional therapy.
CoQIO has also been shown to reduce significantly the oxidation of LDL cholesterol, a leading culprit in cardiovascular and cerebrovascular disease. In a study done on human volunteers given 300 mg of CoQIO daily for eleven days, researchers found a fourfold increase in the level of CoQIO in the blood, and more importantly, within the LDL cholesterol itself.32" This was found to reduce significantly the risk of the LDL cholesterol becoming oxidized.
So what about the studies that show no effect for CoQIO? (These studies are carried around in the pockets of some skeptical cardiologists.) In most such studies, CoQIO was given alone. As we have seen throughout this book, nothing in human biology works alone, especially with respect to disease. Congestive heart patients, both because of their disease and the numerous medications given by their doctors, suffer numerous nutritional deficiencies, especially of magnesium. In these studies, little attempt is made to identify these deficiencies, much less to correct them.
In addition, few doctors doing clinical research understand the intricacies of nutritional supplementation. For example, CoQIO is a fat-soluble substance. Giving it with water results in poor absorption. It must be given with fats, such as phospholipids or extra-virgin olive oil. Dosing is also important. The best results are obtained with higher doses, such as 300-600 mg a day. And finally, if the heart is severely depleted of numerous nutrients, especially L-carnitine, providing CoQIO will provide far less benefit. Remember these things the next time your cardiologist starts waving his negative study in your face.
It should be appreciated that most cholesterol-lowering drugs also dramatically lower CoQIO levels. Dr. Karl Folkers, of the University of Texas at Austin, addressed this problem in the journal, Proceedings of the National Academy of Sciences, in which he cautioned that as a result of this drug-induced deficiency, patients may experience life-threatening deterioration of heart function.330 Unfortunately, his warning has gone unheeded.
One patient I was seeing for a heart problem wanted to know if CoQIO would help her ninety-five-year-old mother, who was also suffering from heart failure. I answered that, in conjunction with other nutrients, it certainly would. She then told me that her cardiologist had told her to be sure not to give her mother CoQIO.
I thought the statement was a little strange, but on the outside chance the cardiologist might have known of some rare complication occurring in ninety-five-year-olds taking CoQIO, I asked her why he said that. She replied, "He said that studies showed it didn't work." I had to laugh. The medical profession writes millions of prescriptions every year that do not work, yet they never bat an eye to fill their patients' hands full of them.
I recall a pediatrician telling me that he routinely wrote antibiotic prescriptions for viral illnesses in children because the parents wanted an antibiotic for them, and if he didn't prescribe it, they would just take the kid to another pediatrician who would. He didn't want to lose the business, so he gave them a useless and dangerous antibiotic. I hear the same refrain about Ritalin from pediatricians: hypocrisy at its best.
Another metabolic fuel needed by the heart is L-carnitine. It is known that animals have forty times higher levels of L-carnitine in their heart muscles than in their blood. The same is suspected to be true in humans. Because of this huge difference between blood and heart-muscle levels, it is suspected that the heart has a special transport mechanism to push L-carnitine into the heart muscle.331
So what does L-carnitine do? Basically, it allows our cells to metabolize fats (mainly long-chained fatty acids) for energy. In fact, fats supply most of the heart muscle's fuel. It does this by allowing fats to enter the mitochondria, where it is converted into energy—and lots of it.
Studies on children suffering from a certain form of heart failure have shown that their heart-muscle L-carnitine levels were drastically low.332 Surprisingly, many others have blood levels of L-carnitine that are either normal or slightly elevated. The problem appears to be in the mechanism that pushes L-carnitine into the heart muscle. Untreated, these children's hearts progressively enlarge until they fail altogether. By giving very high doses of L-carnitine to these children, doctors have been able to reverse this otherwise fatal condition.
Then, what about adults? We know that there is a virtual epidemic of congestive heart failure in this country, and that the incidence is continually rising. Severe depletion of carnitine from the hearts of patients with congestive heart failure has been demonstrated in numerous studies.333 Several double-blind studies have shown that giving patients with congestive heart failure large doses of L-carnitine significantly improved cardiac function in most,334 and the beneficial effect increased the longer they took the supplement.
It is ironic that doctors prescribe drugs that cost thousands of dollars to treat the complications of heart disease, yet rarely pay attention to one of the most versatile, powerful, and least expensive weapons in their arsenal: magnesium.
Magnesium plays a vital role as a coenzyme (helper) in over three hundred enzyme reactions, many of which control energy production. Numerous studies have shown the value of maintaining normal magnesium levels in persons having cardiovascular disease. For example, one study found that congestive heart disease patients having normal blood levels of magnesium had almost twice the survival rate as those with lower levels.335
Next to potassium, magnesium is the most abundant cation in the body. The body contains 1,000 mM of magnesium, with over 50 percent in the bones, slightly less than 50 percent in the soft tissues (such as muscle, skin, ligaments, and organs), and less than 1 percent in the blood. This is why blood levels of magnesium are so notoriously inaccurate for estimating tissue magnesium levels. The heart muscle normally has one of the highest magnesium levels of any organ.
While many patients with cardiovascular disease have normal blood levels of magnesium, a significant number of these patients will have low tissue levels. Animal studies have shown that chronic depletion of magnesium can significantly worsen elevated levels of triglycerides and cholesterol, and can lower the good type of cholesterol—HDL.336And, as we have seen previously, dogs on a magnesium-free diet subjected to coronary artery occlusion (a heart attack) have heart muscle destruction involving areas twice as large as those on a normal magnesium diet.337
Patients who have sudden heart attacks frequently experience a precipitous fall in magnesium concentration in their blood, with the lowest levels occurring twelve to twenty hours after hospital admission. This is because of the massive release of catecholamines (adrenaline) released after the heart attack, in conjunction with the associated release of fatty acids, that binds the magnesium. Other forms of severe stress have also been shown to cause a significant, sudden drop in magnesium levels, including major burns, infections, trauma, alcohol withdrawal, hypothermia, and during cardiac surgery.
It is also important because of the widespread occurrence of magnesium deficiency based on poor diets. Younger generations are especially at risk because of their dependence on carbonated drinks, junk foods, and diets devoid of the main dietary source of magnesium— vegetables.
One frightening condition associated with low magnesium levels is sudden cardiac death. Experimentally, it is known that if you feed animals a diet deficient in magnesium and then frighten the animals, a significant number will die suddenly. The same is true of humans with low tissue magnesium levels; that is, those who have a diet deficient in magnesium. A combined study of a number of heart attack patients found that magnesium infusions could lower mortality rates by 54 percent compared to patients who did not receive magnesium treatment.338
One effect of magnesium is to increase blood flow through the coronary arteries, which occurs because magnesium is a calcium-channel blocker and dilates blood vessels. This is especially important in cases of sudden cardiac death in young people, and frequently a cause of death in athletes, in which a segment of the coronary artery is hyperactive and goes into spasm. Magnesium can counteract this spasm.339
Another frequent cause of death following a heart attack is the development of uncontrollable irregular heartbeats called an arrhythmia. In one study, ten of thirteen patients who had had a heart attack as well as low magnesium levels, developed arrhythmia afterwards.340 While not all doctors agree that magnesium supplementation can prevent arrthythmias, most agree that it can reduce the incidence of difficult-to-control arrthythmias.
One type of arrhythmia, atrial fibrillation, may be controlled with magnesium supplementation. Supplementation can also reduce the incidence of digitalis-induced atrial tachycardia, a condition in which the heart's atria beat too quickly. We also know that low potassium levels are associated with increased risk for arrhythmia: less well known is the fact that low magnesium also lowers potassium levels. In fact, patients with low potassium often have significant difficulty correcting their potassium deficit until the magnesium deficiency is corrected.
Because it is a slight anti-coagulant, magnesium also helps to reduce heart-attack incidence by thinning the blood.341 This is especially important in individuals who have high fibrinogen levels, a condition that increases blood coagulation. Elevated fibrinogen levels are an independent risk factor for heart attacks and strokes: that means that even if all other studies—triglycerides, LDL cholesterol, and total cholesterol—are normal, you are still at increased risk of having a heart attack.
Not only can magnesium be used to effectively treat people who have already had a heart attack, it can also significantly reduce the incidence of arteriosclerosis. More recent studies have shown that magnesium improves endothelial cell function, reduces entry of cholesterol into the wall of the blood vessel, and acts as an antioxidant.342 Magnesium deficiency has been shown to double free-radical production in cells of various types. These deficient cells are also twice as likely to die under stress as cells grown in a magnesium-containing medium. Cellular glutathione levels are significantly lower in cells made magnesium deficient. Recall that glutathione is one of the most important antioxidant systems in cells, including endothelial cells lining our arteries.
On top of all these benefits, magnesium also plays a major role in protecting the brain, improves blood flow to the kidneys, and improves lung function. These benefits are particularly important to the heart-attack patient, since impaired cardiac function impairs blood flow to all of the organs of the body, especially the brain.
As Benjamin Franklin said over two hundred years ago, "An ounce of prevention is worth a pound of cure." The time to correct low tissue magnesium levels is not after you have heart disease, but before. It will significantly lessen your risk of developing heart disease in the first place. And if you do have a heart attack, sufficient magnesium intake will greatly improve your chances of survival and recovery.
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