Researchers at the Kumamoto University School of Medicine report that there is a close association between blood levels of dehydroepiandrosterone sulfate (DHEAS) and the severity of heart failure. Heart failure (congestive heart failure) is the end stage of heart disease; it affects more than 2 million people in the United States alone. Simply defined, heart failure (CHF) occurs when the output of the heart is insufficient to meet the demands of the body. Left ventricular dysfunction is a common feature of heart failure and recent research has shown that blood plasma levels of A- and B-type natriuretic peptides are elevated in CHF patients. The more severe the CHF the lower the DHEAS levels. The study involved 49 male patients (mean age of 61 years, range 38-75 years) with left ventricular dysfunction and 32 age-matched controls with no heart disease. The researchers confirmed that DHEAS levels decline markedly with age, but noted that this decline was only present in healthy controls. In CHF patients DHEAS levels were low regardless of age. The average DHEAS level in the CHF patients was 79 micrograms/dL as compared to 132 micrograms/dL in the controls. DHEAS levels in patients with severe CHF were significantly lower than in patients with a milder grade of CHF. There were no significant differences in plasma levels of cortisol between the patients and the controls. The plasma cortisol/DHEAS ratio was significantly associated with the levels of A-type natriuretic peptide and the levels of thiobarbituric acid-reactive substances (TBARS). TBARS are a powerful indicator of oxidative stress. The researchers conclude that oxidative stress may play a role not only in CHF, but also in the lowering of DHEAS levels in CHF patients. They also mention that glutathione, a powerful antioxidant, may help reverse the suppression of DHEAS synthesis observed in CHF patients.
Moriyama, Yasushi, et al. The plasma levels of dehydroepiandrosterone sulfate are decreased in patients with chronic heart failure in proportion to the severity. Journal of Clinical Endocrinology & Metabolism, Vol. 85, April 2000, pp. 1834-40