05) Error bars denote standard deviation of the experimental mea

05). Error bars denote standard deviation of the experimental mean. An asterisk (*) indicates statistical significance. The increase in serum testosterone levels for the 1200 mg Temsirolimus per day of Resettin®/MyTosterone™ treatment group after 14 days

was not statistically significant in comparison to the placebo group. However, there was a statistically significant decrease in the DHT levels in the 800 mg/day and 1200 mg/day Resettin®/MyTosterone™ treatment groups compared to their respective placebo control groups (Figure 3; ANOVA-RM; p < 0.05). Consistent with this data were the baseline-subtracted serum DHT levels in the 1200 mg/day Resettin®/MyTosterone™ treatment group which significantly decreased when compared to the serum DHT levels of the 1200 mg/day placebo control group (Figure 3; ANOVA-2; p < 0.05). These findings suggest that Resettin®/MyTosterone™ at the tested concentrations (800 mg/day and 1200 mg/day) do not significantly impact the serum CHIR-99021 in vivo levels of testosterone in sedentary men, but may have an impact on reducing serum E2 and DHT levels, which may in turn prevent the further reduction of testosterone levels. Selleckchem STI571 Figure 3 Baseline subtracted serum DHT levels

in placebo- and Resettin®/MyTosterone™-treated participants. Shown are the serum DHT levels from participants after 3, 7 and 14 days of 800 mg/day placebo or Resettin®/MyTosterone™ (a), or 1200 mg/day placebo or Resettin®/MyTosterone™ (b) as determined by ELISA. Each experimental group had between 9 and 10 participants, and results are indicative of one trial. There was a statistically significant decrease in the DHT levels in the 800 mg/day and 1200 mg/day Resettin®/MyTosterone™ treatment

group compared to their respective placebo control groups (ANOVA-RM; p < 0.05). Error bars denote standard deviation of the experimental mean. An asterisk (*) indicates statistical significance. Conclusions Deficiencies in testosterone production and the deregulation of testosterone’s anabolic activities are hallmarks of an aging endocrine system [1]. It is well-established that decreases in testosterone level are associated with a variety of medical problems, including a decline in cognitive function, loss of libido, triclocarban loss of lean muscle mass and strength, and reductions in bone mineral density [2–4]. While the administration of exogenous testosterone can greatly ameliorate the deleterious effects of a testosterone deficiency, adverse side effects such as an imbalance in the hypothalamic-pituitary axis associated with this type of treatment option [16,20]. By naturally increasing endogenous testosterone levels, the goal is to target the human body’s own well-regulated hypothalamic-pituitary-gonadal axis, whose function is to maintain homeostasis.

Comments are closed.