Most patients with CHF symptoms have been shown to be significantly malnourished. Specific deficiencies that have been found in the failing myocardium include: a reduction in L-carnitine, CoQ10, creatine, and thiamine, which are important nutrient cofactors for myocardial energy production; a relative deficiency of taurine, an amino acid integral to intracellular calcium homeostasis; and increased myocardial oxidative stress with a reduction of antioxidant defenses. Deficiencies of carnitine or taurine result in dilated cardiomyopathy in animals and humans. Each of these deficiencies can be corrected through dietary supplementation. A comprehensive restoration of adequate myocyte nutrition is critical to any therapeutic strategy designed to benefit patients suffering from CHF.15,16 Supplementation that results in higher myocardial levels of CoQ10, taurine, and carnitine levels is associated with a reduction in left ventricular end-diastolic volume in patients with left ventricular dysfunction.17
Successful complementary treatment requires formulating an individualized protocol that addresses the various pathophysiological changes that occur during the development and progression of CHF. The goal of utilizing natural agents in treating are:
- Restoring neurohormonal and metabolic integrity
- Improving myocardial energy and pumping function
- Decreasing oxidation stress
- Restoring mineral balance
- Decreasing vascular resistance
- Preventing risk of thrombosis
- Preventing arrhythmia or improving rhythm disorder
- Using nutrients that can improve the conditions of diseases that cause CHF
The keys to enhancing cardiovascular health are effectively managing the negative effects of stress, antioxidant protection, strengthening the heart and vessels, and reducing the occurrence of calcification through chelation therapy.
Supplements for Cardiovascular Health
Coenzyme Q10 CoQ10 has been used for decades as a nutritional supplement for cardiovascular disease.18 It is found in high concentrations within the mitochondrial membranes of organs that have significant energy requirements, and is essential for the high-level functioning of the heart. CoQ10 is involved in energy production19-22 and exerts antioxidant23 and membrane stabilizing24 effects. The first clinical application of CoQ10 in cardiovascular disease was reported in 1967.25 Since that time, numerous studies have evaluated the use of CoQ10 to treat CHF. As the most important element of the respiration chain of each cell, CoQ10 plays a particular role in improved heart muscle function because of the heart muscle cells’ high bioenergy demand. Most studies have found CoQ10 to have beneficial effects on the heart’s ejection fraction,26-28 end-diastolic volume index,27,29 development of pulmonary edema,30 and other CHF symptoms.31,32 In one study, withdrawal of CoQ10 resulted in decreasing cardiac function and symptoms.33 Two other studies suggested improvement in CHF survival rates when CoQ10 was added to conventional therapy.34,35
While the optimal dose of CoQ10 for treating CHF has not been defined, studies have utilized dosages ranging from 30 to 600 mg daily, and most practitioners prescribe 100-300 mg daily.
Carnitine Another vitamin-like substance, carnitine, is essential in the transport of fatty acids into the myocardium and mitochondria for energy production. Carnitine appears to have beneficial effects on CHF.36 If the heart does not have a good oxygen supply, then carnitine levels decline quickly. Several double-blind clinical studies have shown that carnitine improves cardiac function in CHF patients.37-39 The longer carnitine was used, the more dramatic the improvement. After six months of use, patients’ ejection fraction increased by 12.1% and 13.6%, respectively.38,39 Chronic administration of carnitine has been shown to improve ventricular function, reduce systemic vascular resistance, and increase exercise tolerance.38,40 The dosage used in most studies is 1-3 grams daily.
Taurine The amino acid taurine is an important nutrient found in very high concentrations in excitable tissue. Its lack in heart muscle cells is a particularly frequent cause of heart failure. Generally, CHF responds favorably to taurine therapy. In double-blind studies, taurine supplementation has been shown to reduce signs and symptoms of CHF.41,42 Taurine promotes natriuresis (sodium excretion) and diuresis (urine excretion), and minimizes many of the adverse actions of angiotensin II, including the induction of cardiac hypertrophy, volume overload, and myocardial remodeling. Since ACE inhibitors are the mainstay treatment for CHF, taurine supplementation is extremely important.43 The recommended dosage is 2-3 grams daily.
Hawthorn (or its related species) Herbs in the hawthorn family have been used in the treatment of cardiovascular diseases.44 Clinical studies have found that standardized extracts of these herbs show promise as supplementary agents for the treatment of left ventricular dysfunction.45-48 Other trials consistently demonstrate hawthorn’s ability to improve exercise tolerance as well as symptoms associated with mild to moderate CHF.49,50 Its effectiveness has been demonstrated repeatedly in double-blind studies.45,47,51 Hawthorn extract shows some beneficial effects in animal and human studies, including enhanced heart pumping efficiency (improved contractility), ACE inhibition, antidysrhythmic effects, and mild reduction in systemic vascular resistance.49,52,53
The recommended daily dose ranges from 160 to 900 mg.
Magnesium Magnesium plays an important role in the functioning of the cardiovascular system. A decrease in magnesium has been linked with tachydysrhythmias (fast, irregular heartbeats) and increased mortality in CHF patients.54 The research shows that use of magnesium supplements in these situations may be beneficial for treating and preventing life-threatening conditions. Magnesium supplements can be administered safely either orally or by injection depending on the situation.55,56 In one study, patients with severe CHF took a supplement of 300 mg of oral magnesium citrate daily for 30 days. In some of these patients, oral magnesium supplementation was effective in achieving substantial increments in intracellular magnesium.55
Alpha Lipoic Acid Scientists at The Linus Pauling Institute measured DNA damage in rat hearts and found that old hearts produce three times more free radicals than young hearts. The scientists then gave old rats alpha lipoic acid for just two weeks before their death. Necropsy findings showed that heart muscle cells from these old rats given alpha lipoic acid did not differ from those of un-supplemented young rat hearts. The scientists concluded their study report by stating that “the aging rat heart is under increased mitochondrial-induced oxidative stress, which is significantly attenuated by lipoic acid supplementation.”
Since oxidative stress plays a role in the development and progression of CHF, it would appear prudent for CHF patients to supplement with at least 250 mg of alpha lipoic acid each day.57
- Vitamin C: energy supply for the metabolism of each cell
- Vitamin E: for anti-oxidative protection
- Vitamins B1, B2, B3, B5, B6, and B12: bioenergy carriers of cellular metabolism, particularly for the heart muscle cells; for heart function and pumping, and physical endurance
- L-arginine: vasodilatory effects (2-5 grams daily)
- Creatine: for cardiac function
- Fish oil supplementation
- Potassium (if CHF is associated with hypokalemia or low potassium levels).
It is important to stress that no supplement or diet can cure CHF. Age is the most powerful risk factor for heart disease. Because of the system-wide effects of andropause and menopause, hormones like testosterone may offer cardiovascular protection. Everyone recognizes that the risk of developing CHF increases with age, but the fact that the increased risk may be tied to reduced gonadal testosterone production has not yet been completely accepted by practitioners of conventional medicine.
The normal condition of a living organism is a delicate balance between anabolic and catabolic processes. CHF results when catabolic influences come to predominate, leading to the accumulation of excess cholesterol, impaired carbohydrate metabolism, decreased fibrinolysis, and other well-known symptoms. The dominance of catabolic process is associated with a rise in the cortisol, a decline in DHEA and decreased testosterone levels. These changes correlate with changes in the body mass index and clinical severity of heart failure, suggesting a possible causal link between the two.58,59 The primary anabolic hormone is testosterone; the primary catabolic hormone is another steroid, cortisol.
Neuroendocrine function has a very close relationship with metabolism and is usually abnormal in CHF patients.60 Several studies show these patients have relatively low levels of DHEA, testosterone, estrogen, and IGF-1.61-66