Klara Alfonso
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The mean fat-free mass gained by the placebo groups was 0.8 kg (95% CI, â0.1 to 1.7 kg) when receiving 50 mg/wk of testosterone enanthate, 3.5 kg (95% CI, 2.1 to 4.8 kg) for 125 mg/wk, 5.7 kg (95% CI, 4.8 to 6.5 kg) for 300 mg/wk, and 8.1 kg (95% CI, 6.7 to 9.5 kg) for 600 mg/wk. The mean fat-free mass gained by the dutasteride groups was 0.6 kg (95% CI, â0.1 to 1.2 kg) when receiving 50 mg/wk of testosterone enanthate, 2.6 kg (95% CI, 0.9 to 4.3 kg) for 125 mg/wk, 5.8 kg (95% CI, 4.8 to 6.9 kg) for 300 mg/wk, and 7.1 kg (95% CI, 6.0 to 8.2 kg) for 600 mg/wk. The 5Îħ-Reductase Trial was a randomized controlled trial of healthy men aged 18 to 50 years comparing placebo plus testosterone enthanate with dutasteride plus testosterone enanthate from May 2005 through June 2010.
Ideally, for hair loss prevention you would want to have an anabolic in your body that fulfills all of the anabolic properties of Testosterone and simultaneously has as minimal of an androgenic effect as possible. A small retrospective study reported that finasteride was effective in the treatment of acne in women with normal testosterone levels. In 1997, Merck was successful in obtaining FDA approval for a second indication of finasteride (1Â mg) for treatment of male pattern hair loss, which was marketed under the brand name Propecia. In parallel, circulating levels of testosterone increase by approximately 10%, while local concentrations of testosterone in the prostate gland increase by about 7-fold and local testosterone levels in hair follicles increase by around 27â53%. In the United States, finasteride and minoxidil are the only two FDA-approved drugs for the treatment of male pattern hair loss as of 2017. We randomly assigned 43 hypogonadal men to twice daily oral doses of 150, 250 or 400 mg testosterone with 0.25 mg dutasteride, 400 mg testosterone alone or 0.25 mg dutasteride alone for 28 days in a multicenter study. Exogenous testosterone (T) alone or with finasteride increases physical performance, grip strength, and lean body mass in older men with low serum T.
Within groups, Kruskal-Wallis rank sum tests were used to assess dose relationships. Free testosterone and free DHT were calculated.34 Sex-hormone binding globulin and luteinizing hormone were measured using immunofluormetric assays with sensitivities of 2.5 nmol/L and 0.1 U/L, respectively.26,35 The interassay coefficient of variation for the testosterone assay was 7.7% at 241 ng/dL of testosterone, 4.4% at 532 ng/dL of testosterone, and 3.3% at 1016 ng/dL of testosterone. Testosterone and DHT were measured using liquid chromatography tandem mass spectrometry32,33 with sensitivities of 2 and 5 ng/dL, respectively. Strength was reassessed within 2 to 7 days; if the measurements were within 5%, the better of the 2 measurements was recorded.25,26 Sexual function was assessed using the International Index of Erectile Function.27 Additionally, we used the Male Sexual Health Questionnaire for a more comprehensive assessment of sexual desire28 than is provided by the International Index of Erectile Function. The primary outcome was change in fat-free mass from baseline measured by dual-energy x-ray absorptiometry.
The dutasteride and placebo groups did not differ in any domain of sexual function. Our study had greater than 90% power to detect a 25% difference in outcomes between the placebo and dutasteride groups. Additionally, the high-dose dutasteride regimen effectively inhibited both steroid 5Îħ-reductase isoenzymes. In tissues with low steroid 5Îħ-reductase activity such as muscle and bone, intratissue DHT concentration is very low relative to testosterone and can be discounted, and the androgen effect attributed largely to testosterone. Our data, when viewed together with published literature on the effects of 5Îħ-reductase inhibitors in patients with benign prostatic hyperplasia, are the most consistent with the second model in which DHT amplifies the effects of testosterone in tissues with high 5Îħ-reductase activity.
Sexual dysfunction has been reported as an adverse event in clinical trials of 5Îħ-reductase inhibitors in men with benign prostatic hyperplasia, who have high background rates of sexual dysfunction. Men assigned to dutasteride were similar at baseline to those assigned to placebo. These drugs are extremely androgenic and do an amazing job at boosting libido. The more of an androgen load you have, the more hair follicle miniaturization you have. While this can be accomplished via a variety of mechanisms involving the androgen receptor, one of the most promising ways to potentially facilitate this in my opinion would be by incorporating a less androgenic hormone (like a SARM) in conjunction with Estrogen for hormone replacement therapy. This is evidenced time and again in women who have high Estrogen levels, Progesterone levels equivalent to men the majority of the year (1 ng/mL or under), and low androgen levels. Estrogen elevation is definitely not the cause of androgenic alopecia, and neither are any of the other random values I mentioned.
Ideally, for hair loss prevention you would want to have an anabolic in your body that fulfills all of the anabolic properties of Testosterone and simultaneously has as minimal of an androgenic effect as possible. A small retrospective study reported that finasteride was effective in the treatment of acne in women with normal testosterone levels. In 1997, Merck was successful in obtaining FDA approval for a second indication of finasteride (1Â mg) for treatment of male pattern hair loss, which was marketed under the brand name Propecia. In parallel, circulating levels of testosterone increase by approximately 10%, while local concentrations of testosterone in the prostate gland increase by about 7-fold and local testosterone levels in hair follicles increase by around 27â53%. In the United States, finasteride and minoxidil are the only two FDA-approved drugs for the treatment of male pattern hair loss as of 2017. We randomly assigned 43 hypogonadal men to twice daily oral doses of 150, 250 or 400 mg testosterone with 0.25 mg dutasteride, 400 mg testosterone alone or 0.25 mg dutasteride alone for 28 days in a multicenter study. Exogenous testosterone (T) alone or with finasteride increases physical performance, grip strength, and lean body mass in older men with low serum T.
Within groups, Kruskal-Wallis rank sum tests were used to assess dose relationships. Free testosterone and free DHT were calculated.34 Sex-hormone binding globulin and luteinizing hormone were measured using immunofluormetric assays with sensitivities of 2.5 nmol/L and 0.1 U/L, respectively.26,35 The interassay coefficient of variation for the testosterone assay was 7.7% at 241 ng/dL of testosterone, 4.4% at 532 ng/dL of testosterone, and 3.3% at 1016 ng/dL of testosterone. Testosterone and DHT were measured using liquid chromatography tandem mass spectrometry32,33 with sensitivities of 2 and 5 ng/dL, respectively. Strength was reassessed within 2 to 7 days; if the measurements were within 5%, the better of the 2 measurements was recorded.25,26 Sexual function was assessed using the International Index of Erectile Function.27 Additionally, we used the Male Sexual Health Questionnaire for a more comprehensive assessment of sexual desire28 than is provided by the International Index of Erectile Function. The primary outcome was change in fat-free mass from baseline measured by dual-energy x-ray absorptiometry.
The dutasteride and placebo groups did not differ in any domain of sexual function. Our study had greater than 90% power to detect a 25% difference in outcomes between the placebo and dutasteride groups. Additionally, the high-dose dutasteride regimen effectively inhibited both steroid 5Îħ-reductase isoenzymes. In tissues with low steroid 5Îħ-reductase activity such as muscle and bone, intratissue DHT concentration is very low relative to testosterone and can be discounted, and the androgen effect attributed largely to testosterone. Our data, when viewed together with published literature on the effects of 5Îħ-reductase inhibitors in patients with benign prostatic hyperplasia, are the most consistent with the second model in which DHT amplifies the effects of testosterone in tissues with high 5Îħ-reductase activity.
Sexual dysfunction has been reported as an adverse event in clinical trials of 5Îħ-reductase inhibitors in men with benign prostatic hyperplasia, who have high background rates of sexual dysfunction. Men assigned to dutasteride were similar at baseline to those assigned to placebo. These drugs are extremely androgenic and do an amazing job at boosting libido. The more of an androgen load you have, the more hair follicle miniaturization you have. While this can be accomplished via a variety of mechanisms involving the androgen receptor, one of the most promising ways to potentially facilitate this in my opinion would be by incorporating a less androgenic hormone (like a SARM) in conjunction with Estrogen for hormone replacement therapy. This is evidenced time and again in women who have high Estrogen levels, Progesterone levels equivalent to men the majority of the year (1 ng/mL or under), and low androgen levels. Estrogen elevation is definitely not the cause of androgenic alopecia, and neither are any of the other random values I mentioned.
