The increasing use of testosterone replacement therapy to treat reduced testosterone level in older men has been accompanied by growing concerns over its long-term safety. Two studies examining the cardiovascular and kidney disease risks of receiving testosterone will be presented at Cardiovascular, Renal and Metabolic Diseases: Physiology and Gender.
Previous studies published in November 2013 and January 2014 reported increased risk of cardiovascular disease in men who underwent testosterone therapy. Findings from a new review of the literature support the opposite conclusion. "There is no convincing evidence-based data to suggest increased cardiovascular risks with therapy," stated lead researcher Abdulmaged Traish, PhD. "In fact, the literature is replete with studies demonstrating beneficial effects of testosterone therapy on cardiovascular and overall health," Traish said.
Traish will present "Testosterone Therapy in Men with Testosterone Deficiency: Advances and Controversies" as part of the symposium "Non-reproductive Actions of Sex Hormones and Receptors -- A."
A separate study to be presented at the conference suggests that using testosterone could cause kidney damage in hypertensive men. Researchers from the University of Tennessee Health Science Center found that giving 6β-hydroxytestosterone (6β-OHT), a compound produced by the body's metabolism of testosterone, to male mice lacking testosterone made the mice more susceptible to kidney damage from high blood pressure. An earlier study from this group observed that 6β-OHT increased susceptibility to heart damage caused by high blood pressure.
The hormone angiotensin II (Ang II) raises blood pressure. Mice given Ang II steadily for two weeks had kidney damage due to the resulting high blood pressure and the direct effects of Ang II. In this study, castrated mice, which no longer produce testosterone, and mice missing the gene cytochrome P450 1B1 (CYP1B1), whose protein helps break down testosterone, had less Ang II-induced kidney damage compared with non-castrated, normal mice. When the castrated mice and CYP1B1-missing mice were given 6β-OHT, Ang II-associated kidney damage was more severe. "These data suggest that 6β-OHT contributes to impairment of renal (kidney) function and end-organ damage associated with Ang II-induced hypertension in male mice," according to the researchers. The data also suggest that "CYP1B1 could serve as a novel target for the treatment of renal disease and hypertension," the researchers wrote.
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