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Testosterone Replacement, Low T, HCG, & Beyond
When Testosterone Is Not Enough
How does 125IU of HCG ED affect hormones production while on TRT?
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<blockquote data-quote="madman" data-source="post: 188783" data-attributes="member: 13851"><p>Higher doses of hCG would have a greater impact on T, e2, and upstream hormones.</p><p></p><p></p><p></p><p></p><p>[URL unfurl="true"]https://academic.oup.com/jcem/article/95/8/3806/2596941[/URL]</p><p></p><p><strong>Dose-Dependant Increase in Intratesticulaar Testosterone by Very Low-Dose Human Chorionic Gonadotropin in Normal Men with Experimental Gonadotropin Deficiency </strong></p><p><strong></strong></p><p><strong>*<span style="color: rgb(184, 49, 47)">Prior studies have shown that serum 17-hydroxyprogesterone, which is secreted by the testes in high concentrations, is a good correlate of IT-T (<a href="https://www.excelmale.com/forum/javascript%3A;" target="_blank">20</a>, <a href="https://www.excelmale.com/forum/javascript%3A;" target="_blank">21</a>).<u> However, in our study 17-hydroxyprogesterone was not significantly correlated with IT-T. This difference is likely due to the significantly lower IT-T concentrations induced in this study by the lower doses of hCG used</u>. </span></strong></p><p></p><p></p><p></p><p></p><p>------------------------------------------------------------------------------------------------------</p><p><strong><span style="color: rgb(0, 0, 0)">Serum 17-hydroxyprogesterone strongly correlates with intratesticular testosterone in gonadotropinsuppressed normal men receiving various dosages of human chorionic gonadotropin </span><span style="color: rgb(184, 49, 47)">(2008)</span></strong></p><p></p><p></p><p></p><p><em><span style="color: rgb(184, 49, 47)"><strong>Previous work investigating <u>the response of the testis to hCG has demonstrated that serum concentrations of T precursors such as 17-hydroxyprogesterone (17OH-P), androstenedione (A), and DHEA are increased by hCG administration </u>(16). </strong>Therefore, we hypothesized that serum concentrations of these T precursors might correlate with ITT and potentially provide a serum biomarker of ITT and Leydig cell function. </span></em></p><p></p><p></p><p><strong>Result(s):</strong> <em><span style="color: rgb(184, 49, 47)"><strong>With T administration alone, serum 17OH-P decreased significantly and <u>increased significantly when 500 IU hCG was administered</u>.</strong> End-of-treatment ITT strongly correlated with serum 17OH-P. Moreover, serum 17OH-P, but not androstenedione or DHEA, was independently associated with end-of-treatment ITT by multivariate linear regression</span></em></p><p></p><p></p><p><strong>DISCUSSION </strong></p><p></p><p>In the present work, we demonstrated a significant association between serum concentrations of 17OH-P and ITT in men receiving TE and various dosages of hCG. <strong><em><span style="color: rgb(184, 49, 47)">Serum 17OH-P decreased by roughly 60% in men receiving placebo, <u>whereas it increased by 70% in men at the highest dose (500 IU) of hCG</u>.</span></em></strong> Although 17OH-P did not correlate with ITT at baseline, it was very strongly correlated with ITT on treatment, both when absolute concentration and when the change from baseline was taken into account. Moreover, end-of-treatment concentrations of serum 17OH-P were significantly associated with ITT after correction for other variables using linear regression. <strong><em><span style="color: rgb(184, 49, 47)">Although the overall correlation between ITT and serum 17OH-P was strong, <u>in the lowest-dose hCG group the ITT increased much more than the serum 17OH-P</u>. <u>This implies that serum 17OH-P might not be as sensitive to changes in ITT mediated by lower levels of hCG stimulation as it is to the larger increases in ITT stimulated by higher doses of hCG</u>.</span></em></strong></p><p></p><p></p><p><em><span style="color: rgb(184, 49, 47)"><strong>Most of the circulating 17OH-P in men is likely of testicular and not adrenal origin. Orchiectomy reduces circulating levels of 17OH-P by approximately 70% (19, 20), <u>a reduction very similar to that seen in our group of subjects receiving exogenous T and placebo (and therefore having little circulating LH activity)</u>.</strong> <strong><u>Therefore, roughly 30% of circulating 17OH-P is likely of nontesticular, presumably adrenal, origin. </u></strong><u>T</u><strong><u>he testicular secretion of 17OH-P is known to be second only to that of T, with T accounting for 70% of steroid output and 17OH-P accounting for 20%</u> (21). </strong></span></em></p><p><em><span style="color: rgb(184, 49, 47)"><strong></strong></span></em></p><p><em><span style="color: rgb(184, 49, 47)"><strong></strong></span></em></p><p><em><span style="color: rgb(184, 49, 47)"><strong>[ATTACH=full]11094[/ATTACH]</strong></span></em></p></blockquote><p></p>
[QUOTE="madman, post: 188783, member: 13851"] Higher doses of hCG would have a greater impact on T, e2, and upstream hormones. [URL unfurl="true"]https://academic.oup.com/jcem/article/95/8/3806/2596941[/URL] [B]Dose-Dependant Increase in Intratesticulaar Testosterone by Very Low-Dose Human Chorionic Gonadotropin in Normal Men with Experimental Gonadotropin Deficiency *[COLOR=rgb(184, 49, 47)]Prior studies have shown that serum 17-hydroxyprogesterone, which is secreted by the testes in high concentrations, is a good correlate of IT-T ([URL='https://www.excelmale.com/forum/javascript%3A;']20[/URL], [URL='https://www.excelmale.com/forum/javascript%3A;']21[/URL]).[U] However, in our study 17-hydroxyprogesterone was not significantly correlated with IT-T. This difference is likely due to the significantly lower IT-T concentrations induced in this study by the lower doses of hCG used[/U]. [/COLOR][/B] ------------------------------------------------------------------------------------------------------ [B][COLOR=rgb(0, 0, 0)]Serum 17-hydroxyprogesterone strongly correlates with intratesticular testosterone in gonadotropinsuppressed normal men receiving various dosages of human chorionic gonadotropin [/COLOR][COLOR=rgb(184, 49, 47)](2008)[/COLOR][/B] [I][COLOR=rgb(184, 49, 47)][B]Previous work investigating [U]the response of the testis to hCG has demonstrated that serum concentrations of T precursors such as 17-hydroxyprogesterone (17OH-P), androstenedione (A), and DHEA are increased by hCG administration [/U](16). [/B]Therefore, we hypothesized that serum concentrations of these T precursors might correlate with ITT and potentially provide a serum biomarker of ITT and Leydig cell function. [/COLOR][/I] [B]Result(s):[/B] [I][COLOR=rgb(184, 49, 47)][B]With T administration alone, serum 17OH-P decreased significantly and [U]increased significantly when 500 IU hCG was administered[/U].[/B] End-of-treatment ITT strongly correlated with serum 17OH-P. Moreover, serum 17OH-P, but not androstenedione or DHEA, was independently associated with end-of-treatment ITT by multivariate linear regression[/COLOR][/I] [B]DISCUSSION [/B] In the present work, we demonstrated a significant association between serum concentrations of 17OH-P and ITT in men receiving TE and various dosages of hCG. [B][I][COLOR=rgb(184, 49, 47)]Serum 17OH-P decreased by roughly 60% in men receiving placebo, [U]whereas it increased by 70% in men at the highest dose (500 IU) of hCG[/U].[/COLOR][/I][/B] Although 17OH-P did not correlate with ITT at baseline, it was very strongly correlated with ITT on treatment, both when absolute concentration and when the change from baseline was taken into account. Moreover, end-of-treatment concentrations of serum 17OH-P were significantly associated with ITT after correction for other variables using linear regression. [B][I][COLOR=rgb(184, 49, 47)]Although the overall correlation between ITT and serum 17OH-P was strong, [U]in the lowest-dose hCG group the ITT increased much more than the serum 17OH-P[/U]. [U]This implies that serum 17OH-P might not be as sensitive to changes in ITT mediated by lower levels of hCG stimulation as it is to the larger increases in ITT stimulated by higher doses of hCG[/U].[/COLOR][/I][/B] [I][COLOR=rgb(184, 49, 47)][B]Most of the circulating 17OH-P in men is likely of testicular and not adrenal origin. Orchiectomy reduces circulating levels of 17OH-P by approximately 70% (19, 20), [U]a reduction very similar to that seen in our group of subjects receiving exogenous T and placebo (and therefore having little circulating LH activity)[/U].[/B] [B][U]Therefore, roughly 30% of circulating 17OH-P is likely of nontesticular, presumably adrenal, origin. [/U][/B][U]T[/U][B][U]he testicular secretion of 17OH-P is known to be second only to that of T, with T accounting for 70% of steroid output and 17OH-P accounting for 20%[/U] (21). [ATTACH type="full" alt="Screenshot (2177).png"]11094[/ATTACH][/B][/COLOR][/I] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
When Testosterone Is Not Enough
How does 125IU of HCG ED affect hormones production while on TRT?
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