Congestive heart failure is a chronic, usually progressive myocardial disease characterized by the inability of the heart to pump enough blood to meet the body’s demands.
Symptoms include fatigue, dyspnea, shortness of breath, dependent edema, palpitations, and in severe cases, life-threatening pulmonary edema develops with arrhythmias.
Congestive heart failure can be subdivided into systolic and diastolic dysfunction.
is characterized by impaired contractility of the left ventricle and decreased left ventricular ejection fraction. This is the amount of blood that is pumped out of the left ventricle with each contraction. In contrast, diastolic dysfunction is characterized by impaired left ventricular filling in association with normal left ventricular contractility.
has also been called heart failure with a preserved ejection fraction. While systolic heart failure is more widely recognized than diastolic heart failure, and has been the sub-type of congestive heart failure studies, in most clinical trials, diastolic heart failure appears to be much more common than previously recognized, occurring in as many as 55% of congestive heart failure patients in one study.
Coronary artery disease, hypertension, and previous heart attack are among the most common causes of heart failure. When heart failure is not caused by these conditions, it is often called dilated cardiomyopathy.
Known causes of dilated cardiomyopathy include
infections like viral myocarditis, metabolic disorders, ischemia, and exposure to toxins such as alcohol or mercury. However, many cases are idiopathic, such as postpartum cardiomyopathy. Conventional treatments of heart failure may include sodium and fluid restriction, diuretics, ACE and ARB medications, beta blockers such as lopressor or Tenormin, and digoxin. Advances in treatment have improved the prognosis of patients with heart failure, but mortality remains high with a five-year survivor rate of about 50%. Common causes of death are progressive heart failure and in particular arrhythmias.
Conventional treatments of heart failure is aimed mainly at minimizing the effects of disease, for example, by dilating blood vessels and decreasing the workload of the failing heart. Unlike conventional treatments, nutritional therapies may improve the health and functioning of the diseased myocardium. Therefore, the best results may be achieved by appropriately combining conventional and nutritional therapies.
Patients with congestive heart failure have increased energy requirements because increased energy is utilized by the heart and lungs. Heart failure patients may also be deficient in protein and essential fatty acids as well as a wide range of micronutrients. Factors that lead to malnutrition include poor appetite, increased nutritional requirements, malabsorption and drug-induced nutritional deficiencies such as the diuretics that deplete magnesium, potassium and thiamine. A nutrient-dense diet combined with a broad-spectrum micronutrient supplement may improve cardiac function and enhance overall health.
Limiting sodium intake to no more than 1000 to 2000-mg is generally recommended for heart failure patients. There is also evidence that increasing salt intake can promote the development of acute congestive heart failure. High salt intake results in hypertension, which is an independent risk factor for congestive heart failure.
Chronic alcohol is one of the most common causes of cardiomyopathy. It is a direct toxin to the heart, and also leads to deficiency of various nutrients that are important for the heart function such as magnesium and thiamine.
Magnesium is a co-factor for synthesis of ATP, which provides the energy needed for myocardial contraction. Animals fed a magnesium-deficient diet develop myocardial lesions that resemble those seen in alcohol cardiomyopathies. Low magnesium is common in congestive heart failure patients. Causes include the use of certain diuretics, digoxin, anorexia, and hormonal changes. Even when serum magnesium concentrations are normal, patients with congestive heart failure are likely to have low magnesium levels in the heart tissue. These levels have been found to be 24 to 65% lower in heart failure patients. In patients with heart failure, it was found that intravenous administration of magnesium was effective for short-term control of several ventricular arrhythmias in patients hospitalized with congestive heart failure. The benefits were even seen in patients with normal serum magnesium levels. It has also been reported to decrease the frequency of other arrhythmias.
As a component of the electron-transport chain, Co-Q10 plays a key role in the energy production, and therefore it is essential for all energy-dependent processes including myocardial contraction. The mean blood level of Q10 was significantly lower in patients with dilated cardiomyopathy than controls. In addition, myocardial concentrations of Q10 in patients with cardiomyopathy decreased with increasing disease severity. In numerous uncontrolled and double-blind trials, supplementation with Q10 produced clinical improvements in patients with congestive heart failure or dilated cardiomyopathy; some patients’ benefits were profound. Improvements included increase in functional capacity and reduction in frequency of hospitalizations, and apparent increase in survival time. The dose is extremely important. There are conflicting studies on Q10, which in part, is explained by differences in patient population, the type of Q10, and the administration.
Q10, ‘Statin Drugs and Heart Function
It is important to note that the ‘statins lower Q10 levels and there have been reported cases of dilated cardiomyopathy who improve with Q10 supplementation on a ‘statin drug. In one study, administration of Lipitor to patients without history of heart failure resulted in a worsening of left ventricular diastolic dysfunction. This diverse effect was partially reversed by Q10. Based on these findings, combined with the evidence that Q10 may improve ‘statin-induced myalgia in some patients, Q10 supplementation should be considered for all patients taking ‘statin drugs.
Carnitine plays a role in myocardial energy production by facilitating the transport of fatty acids in the mitochondria. Administration of Q10 has improved dilated cardiomyopathy in some studies.
Severe thiamine deficiencies are a well-known, recognized cause of heart failure, beriberi heart disease. Patients with heart failure may be at increased risk for thiamine deficiency as a result of diuretic-induced urinary thiamine excretion, malabsorption and advanced age. Laboratory evidence of thiamine deficiency have been found in 12 to 98% of patients with congestive heart failure in various studies, depending on the assays. In several studies there has been increase in heart function after thiamine administration.
Potassium plays a role in myocardial contraction, relaxation and the cardiac electrical system. In all forms of heart failure, heart cells lose potassium and magnesium and take-up sodium. This may increase and exacerbate heart failure leading to arrhythmias and increase in sudden death. Potassium depletion in congestive heart failure may be exacerbated by use of diuretics.
The importance of taurine for cardiac function is suggested by the fact that it is actually transported in the myocardium to achieve concentrations several hundred times those in plasma. Taurine has been shown to stabilize cell membranes and increase the contractility of the heart, and has antiarrhythmic effects. It also improves cardiac function, and in some studies have been shown to decrease mortality.
Arginine is a precursor to nitric oxide, which acts as a vasodilator. In a double-blind trial, supplementation with arginine for six weeks resulted in clinical improvement of congestive heart failure. In high doses, it should be supplemented with gamma-tocopherol and the two should be used together.
Omega-3 Fatty Acids
Fatty acids improve endothelial function and should be used in all heart failure patients.
Animals fed on a diet deficient in selenium and vitamin E develop areas of myocardial death and heart failure.
Riboflavin, B6, Folic Acid and Copper
Various studies have shown depletion of these are increased in congestive heart failure.
Low vitamin D status is common in people with congestive heart failure, and it has been suggested that vitamin D deficiency can contribute to development of heart failure by increasing levels of parathyroid hormone. There is also an angiotension-reduction seen with vitamin D administration.
D-ribose, which is a component of ATP is synthesized from glucose-6-phosphate. Patients in heart failure or with coronary artery disease have depleted ATP reserves and this can be repleted by ribose. In a three-week double-blind trial, administration of D-ribose 5-g three times a day significantly improved diastolic function in patients with congestive heart failure.
This supplement is essential for cardiac health.
In double-blind sutures, supplementation of 8-g per day of mixed essential amino acids improved exercise capacity in patients with congestive heart failure.
Numerous clinical studies have shown that used an adjunct with conventional therapy, it significantly improves dyspnea, fatigue, and exercise capacity. There is a positive increase in contractility of the heart muscle.
Combined hormone therapy with growth hormone, testosterone, progesterone, and estrogen used in a Bio-identical administration has been shown to increase contractility and preserve heart function in patients with congestive heart failure and cardiomyopathy, and thyroid, low T3 syndrome in heart failure patients.
Approximately 10 years ago my father developed a mild heart attack and had some decreased heart function on a cardiac ultrasound. After administration of amino acids, growth hormone, testosterone, progesterone as well as antioxidant therapy and nutritionals described above, my father markedly improved and his heart function improved 20%. New therapies include hyperbaric oxygen as well as stem cell administration.
As is often the case with nutritional therapies, patient’s with congestive heart failure may experience greater improvement with a combination of nutrients than with individual nutrients.
In addition, when using combinations of nutrients, as well as natural hormones, hyperbaric oxygen, and stem cells, it may be possible to achieve successful results with lower doses, than those used in clinical trials. Based on the available evidence including my clinical experience, my first treatment would include that which I gave my dad: Magnesium, Q10, carnitine, B vitamins, taurine, selenium, potassium, hawthorn omega-3, ribose . I USE MANY OF THESE INTRAVENOUSLY IF NEEDED . I ALSO USE growth hormone, testosterone and thyroid. OXYGEN THERAPY IS ALSO USED.
Extensive laboratory testing is performed prior to the administration of any of these nutritionals or natural hormones, and then levels are checked and titrated appropriately.
BEST IN HEALTH,
DEAN R. SILVER, M.D.