The Role of Deuterium 2H in the Pathogenesis of Heart Failure as Deduced by Food Studies from Six Individual Cases

Abstract

Heart failure results from the loss of structural integrity of the heart and/or a decrease in the rate of maximal ATP production. In cases of relatively preserved structural integrity, a decrease in ATP production in the mitochondria leads to a decrease in the cardiac stroke volume, thereby increasing the heart rate required to maintain the cardiac output. For many years, the exact location of this defect in the metabolic energy cycle remained elusive. Evidence is presented here to show that it is not a single metabolic substrate involved but rather the heavy isotope of hydrogen 2H, deuterium, that is jamming the ATP nanomotors slowing the rate of ATP production. During the digestion of a meal, the cardiac heart rate is shown to be very sensitive to the level of deuterium contained in the fatty acids recently consumed. During strenuous exercise in the fasting state, the enzyme adipose triglyceride lipase (ATGL) is found to mobilize the highest deuterium triglycerides more rapidly than the healthier lower deuterium triglycerides, converting the adipose tissue into a deuterium-depleted energy pool. This is believed to contribute to the low resting heart rates frequently observed in athletes. In vulnerable individuals, i.e., those weakened by disease(s) or space explorers in a weightless environment, the decreased ability to perform strenuous exercise leads to higher deuterium levels in their adipose tissue compromising their ATP production. In these individuals, maintaining healthy deuterium levels is best achieved by an increased intake of lower deuterium-containing foods.