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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
When testicle size increases, what happens?
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<blockquote data-quote="madman" data-source="post: 187913" data-attributes="member: 13851"><p>Regarding preventing/minimizing testicular atrophy if you are currently on trt then adding in hCG using an effective dose should be all you need mind you hCG +FSH would most likely keep the testes volume fuller/larger.</p><p></p><p>If you are concerned with fertility then hCG + rhFSH may be needed/more effective in some cases.</p><p></p><p></p><p></p><p></p><p><span style="color: rgb(0, 0, 0)"><strong>Testosterone Is a Contraceptive and Should Not Be Used in Men Who Desire Fertility</strong></span></p><p><span style="color: rgb(184, 49, 47)">Amir Shahreza Patel, Joon Yau Leong, Libert Ramos, Ranjith Ramasamy </span></p><p></p><p></p><p><strong>PHYSIOLOGY OF TESTOSTERONE</strong></p><p></p><p>In healthy adult men, testosterone production is precisely regulated by the HPG axis. Higher cortical centers in the brain signal the hypothalamus to secrete gonadotropin-releasing hormone (GnRH) in a pulsatile fashion. GnRH in turn stimulates the release of LH and FSH from the anterior pituitary which modulates testosterone production from the Leydig cells and spermatogenesis by the Sertoli cells, respectively. As testosterone levels increase, negative feedback suppression is exerted on the androgen receptors in the hypothalamic neurons and pituitary gland, thereby inhibiting the release of GnRH, FSH, and LH [5].</p><p></p><p><em><span style="color: rgb(184, 49, 47)">The exogenous administration of testosterone suppresses the release of gonadotropins (FSH and LH) to levels below that required for spermatogenesis. <u><strong>Spermatogenesis is largely dependent on the action of FSH on Sertoli cells coupled with high intra-testicular testosterone concentrations</strong></u><strong>.</strong> </span><span style="color: rgb(44, 130, 201)">Within the seminiferous tubules, only Sertoli cells possess receptors for both FSH and testosterone</span><span style="color: rgb(184, 49, 47)">. Numerous signaling pathways are activated when FSH binds to FSH receptors on these cells. It acts synergistically with testosterone to increase fertility and the efficiency of spermatogenesis [6]. </span></em><span style="color: rgb(44, 130, 201)"><em>The inhibition of LH release by exogenous testosterone leads to the suppression of endogenous testosterone production by the Leydig cells. The decreased intra-testicular testosterone combined with the suppression of FSH leads to decreased germ cell survival and maturation (Fig. 1).</em></span></p><p></p><p></p><p></p><p></p><p><strong><em><span style="color: rgb(184, 49, 47)">*</span></em></strong><em>Ultimately, the low intra-testicular testosterone results in <span style="color: rgb(0, 0, 0)">decreased proliferation of spermatogonia, defects in spermiation of mature spermatozoa by Sertoli cells, and accelerated apoptosis of spermatozoa [8- 11].</span></em><strong><em><span style="color: rgb(184, 49, 47)"> <u>Since 80% of testicular volume consists of germinal epithelium and seminiferous tubules, a reduction in these cells is usually manifested by testicular atrophy and this reflects the loss of both spermatogenesis and Leydig cell function</u> [12,13] </span></em></strong></p><p><strong><em></em></strong></p><p><strong><em></em></strong></p><p><strong><em></em></strong></p><p><strong><em><span style="color: rgb(0, 0, 0)">*</span><span style="color: rgb(184, 49, 47)"><u>Adjunctive hCG and clomiphene can be used with TRT to maintain testicular size and intra-testicular testosterone concentrations </u>[52]. </span></em></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong><span style="color: rgb(0, 0, 0)">Indications for the use of human chorionic gonadotropic hormone for the management of infertility in hypogonadal men </span><span style="color: rgb(184, 49, 47)">(2018)</span></strong></p><p><span style="color: rgb(184, 49, 47)">John Alden Lee, Ranjith Ramasamy </span></p><p></p><p></p><p><em><span style="color: rgb(184, 49, 47)">Luteinizing hormone (LH) in the male is produced by the anterior pituitary in response to pulsatile secretion of gonadotropic releasing hormone (GnRH) from the hypothalamus. It acts on Leydig cells in the testicles promoting the production of testosterone.</span></em> <span style="color: rgb(44, 130, 201)"><em>In men with hypogonadotropic hypogonadism (HH), or men with decreased LH secondary to exogenous testosterone use, <u><strong>the lack of LH results in severely decreased intratesticular testosterone levels. Without intratesticular testosterone, spermatogenesis is impaired, and by replacing lost LH production with hCG, spermatogenesis can be restored by restoring adequate levels of intratesticular testosterone</strong></u><strong>.</strong></em></span></p><p></p><p></p><p></p><p></p><p><span style="color: rgb(184, 49, 47)"><em>Finally,<u><strong> hCG has also been used to reduce some of the side effects of TRT, mainly preventing testicular atrophy</strong> </u>and helping maintain response to TRT by “cycling off” TRT with a periodic replacement of therapy with hCG. </em></span></p><p></p><p></p><p></p><p></p><p><strong>Indications for hCG in combination with TRT </strong></p><p></p><p><span style="color: rgb(0, 0, 0)"><u>Preserving spermatogenesis with TRT</u></span></p><p></p><p>Exogenous steroid use impairs spermatogenesis by promoting negative feedback on both the hypothalamus and the pituitary gland. This reduces the pulsatile secretion of GnRH and LH respectively. The loss of LH secretion shuts down the production of testosterone by Leydig cells which in turn significantly reduces intratesticular testosterone levels. This altering of the hypothalamus-pituitary-gonadal (HPG) axis and drop of intratesticular testosterone can lead to azoospermia within 10 weeks of starting TRT (10). Even more alarming is the fact that up to 10% of men can remain azoospermic after the cessation of TRT.</p><p></p><p><em><span style="color: rgb(184, 49, 47)"><u><strong>hCG therapy can help preserve spermatogenesis in men undergoing TRT by maintaining intratesticular testosterone levels</strong></u><strong>.</strong> </span><span style="color: rgb(44, 130, 201)">It was has been shown that follicle-stimulating hormone (FSH) alone cannot initiate or maintain spermatogenesis in hypogonadal (11) men leading to the discovery of the importance of intratesticular testosterone in spermatogenesis.</span><span style="color: rgb(184, 49, 47)"> <u><strong>In healthy eugonadal men selected to undergo TRT, it was shown that their intratesticular testosterone levels dropped by 94%</strong></u><strong>.</strong> </span></em><span style="color: rgb(44, 130, 201)"><em>However, in those who received 250 IU SC every other day along with TRT, their intratesticular testosterone levels only dropped 7%. Additionally, men who received TRT and 500 IU of hCG every other day, and an increase in intratesticular testosterone by 26% was observed (12). This proved that co-administering low dose hCG could maintain intratesticular testosterone in those undergoing TRT. </em></span><em><span style="color: rgb(44, 130, 201)">It was later shown that not only is intratesticular testosterone increased with co-administration hCG but spermatogenesis is preserved as well at one year follow up (13). These studies proved that by concomitant hCG administration with TRT spermatogenesis and thus potentially fertility could be preserved. </span></em></p><p></p><p>Based on this evidence an algorithm was suggested for the simultaneous treatment of hypogonadism and preservation of fertility (14). All men wishing to preserve fertility while on TRT should have a baseline semen analysis (SA). Next, it is important to determine the appropriate dosing regimen of hCG based on the timeline for the desired pregnancy. For men who wish to obtain pregnancy within six months, it was suggested to discontinue TRT and start 3,000 IU of hCG intramuscular, or subcutaneous every other day. SA should then be performed every two months. Clomiphene citrate 25–50 mg PO daily can be added or omitted to promote FSH production (15). We suggest including of clomiphene citrate in all men who are already oligospermic or azoospermic. It can be omitted in men who are initiating TRT and hCG simultaneously and have normal semen parameters.</p><p></p><p>If Semen parameters fail to improve and FSH remains low, Gonal-f (recombinant FSH) 75 IU every other day can be added. In men who desire pregnancy within 6–12 months, TRT can be continued with co-administration of 500 IU of HCG every other day ± clomiphene citrate can be used. When planning for pregnancy in greater than 12 months TRT should be cycled off every six months replaced by a four-week cycle of 3,000 IU of hCG every other day.<span style="color: rgb(184, 49, 47)"> <strong><em><u>For men who do not desire to preserve fertility testicular size can be maintained while undergoing TRT with 1,500 IU of HCG given weekly. Which is enough to maintain pre-TRT levels of intratesticular testosterone (11)</u>.</em></strong> </span>Table 1 summarizes recommendations for preserving spermatogenesis in men on TRT (16).</p></blockquote><p></p>
[QUOTE="madman, post: 187913, member: 13851"] Regarding preventing/minimizing testicular atrophy if you are currently on trt then adding in hCG using an effective dose should be all you need mind you hCG +FSH would most likely keep the testes volume fuller/larger. If you are concerned with fertility then hCG + rhFSH may be needed/more effective in some cases. [COLOR=rgb(0, 0, 0)][B]Testosterone Is a Contraceptive and Should Not Be Used in Men Who Desire Fertility[/B][/COLOR] [COLOR=rgb(184, 49, 47)]Amir Shahreza Patel, Joon Yau Leong, Libert Ramos, Ranjith Ramasamy [/COLOR] [B]PHYSIOLOGY OF TESTOSTERONE[/B] In healthy adult men, testosterone production is precisely regulated by the HPG axis. Higher cortical centers in the brain signal the hypothalamus to secrete gonadotropin-releasing hormone (GnRH) in a pulsatile fashion. GnRH in turn stimulates the release of LH and FSH from the anterior pituitary which modulates testosterone production from the Leydig cells and spermatogenesis by the Sertoli cells, respectively. As testosterone levels increase, negative feedback suppression is exerted on the androgen receptors in the hypothalamic neurons and pituitary gland, thereby inhibiting the release of GnRH, FSH, and LH [5]. [I][COLOR=rgb(184, 49, 47)]The exogenous administration of testosterone suppresses the release of gonadotropins (FSH and LH) to levels below that required for spermatogenesis. [U][B]Spermatogenesis is largely dependent on the action of FSH on Sertoli cells coupled with high intra-testicular testosterone concentrations[/B][/U][B].[/B] [/COLOR][COLOR=rgb(44, 130, 201)]Within the seminiferous tubules, only Sertoli cells possess receptors for both FSH and testosterone[/COLOR][COLOR=rgb(184, 49, 47)]. Numerous signaling pathways are activated when FSH binds to FSH receptors on these cells. It acts synergistically with testosterone to increase fertility and the efficiency of spermatogenesis [6]. [/COLOR][/I][COLOR=rgb(44, 130, 201)][I]The inhibition of LH release by exogenous testosterone leads to the suppression of endogenous testosterone production by the Leydig cells. The decreased intra-testicular testosterone combined with the suppression of FSH leads to decreased germ cell survival and maturation (Fig. 1).[/I][/COLOR] [B][I][COLOR=rgb(184, 49, 47)]*[/COLOR][/I][/B][I]Ultimately, the low intra-testicular testosterone results in [COLOR=rgb(0, 0, 0)]decreased proliferation of spermatogonia, defects in spermiation of mature spermatozoa by Sertoli cells, and accelerated apoptosis of spermatozoa [8- 11].[/COLOR][/I][B][I][COLOR=rgb(184, 49, 47)] [U]Since 80% of testicular volume consists of germinal epithelium and seminiferous tubules, a reduction in these cells is usually manifested by testicular atrophy and this reflects the loss of both spermatogenesis and Leydig cell function[/U] [12,13] [/COLOR] [COLOR=rgb(0, 0, 0)]*[/COLOR][COLOR=rgb(184, 49, 47)][U]Adjunctive hCG and clomiphene can be used with TRT to maintain testicular size and intra-testicular testosterone concentrations [/U][52]. [/COLOR][/I] [COLOR=rgb(0, 0, 0)]Indications for the use of human chorionic gonadotropic hormone for the management of infertility in hypogonadal men [/COLOR][COLOR=rgb(184, 49, 47)](2018)[/COLOR][/B] [COLOR=rgb(184, 49, 47)]John Alden Lee, Ranjith Ramasamy [/COLOR] [I][COLOR=rgb(184, 49, 47)]Luteinizing hormone (LH) in the male is produced by the anterior pituitary in response to pulsatile secretion of gonadotropic releasing hormone (GnRH) from the hypothalamus. It acts on Leydig cells in the testicles promoting the production of testosterone.[/COLOR][/I] [COLOR=rgb(44, 130, 201)][I]In men with hypogonadotropic hypogonadism (HH), or men with decreased LH secondary to exogenous testosterone use, [U][B]the lack of LH results in severely decreased intratesticular testosterone levels. Without intratesticular testosterone, spermatogenesis is impaired, and by replacing lost LH production with hCG, spermatogenesis can be restored by restoring adequate levels of intratesticular testosterone[/B][/U][B].[/B][/I][/COLOR] [COLOR=rgb(184, 49, 47)][I]Finally,[U][B] hCG has also been used to reduce some of the side effects of TRT, mainly preventing testicular atrophy[/B] [/U]and helping maintain response to TRT by “cycling off” TRT with a periodic replacement of therapy with hCG. [/I][/COLOR] [B]Indications for hCG in combination with TRT [/B] [COLOR=rgb(0, 0, 0)][U]Preserving spermatogenesis with TRT[/U][/COLOR] Exogenous steroid use impairs spermatogenesis by promoting negative feedback on both the hypothalamus and the pituitary gland. This reduces the pulsatile secretion of GnRH and LH respectively. The loss of LH secretion shuts down the production of testosterone by Leydig cells which in turn significantly reduces intratesticular testosterone levels. This altering of the hypothalamus-pituitary-gonadal (HPG) axis and drop of intratesticular testosterone can lead to azoospermia within 10 weeks of starting TRT (10). Even more alarming is the fact that up to 10% of men can remain azoospermic after the cessation of TRT. [I][COLOR=rgb(184, 49, 47)][U][B]hCG therapy can help preserve spermatogenesis in men undergoing TRT by maintaining intratesticular testosterone levels[/B][/U][B].[/B] [/COLOR][COLOR=rgb(44, 130, 201)]It was has been shown that follicle-stimulating hormone (FSH) alone cannot initiate or maintain spermatogenesis in hypogonadal (11) men leading to the discovery of the importance of intratesticular testosterone in spermatogenesis.[/COLOR][COLOR=rgb(184, 49, 47)] [U][B]In healthy eugonadal men selected to undergo TRT, it was shown that their intratesticular testosterone levels dropped by 94%[/B][/U][B].[/B] [/COLOR][/I][COLOR=rgb(44, 130, 201)][I]However, in those who received 250 IU SC every other day along with TRT, their intratesticular testosterone levels only dropped 7%. Additionally, men who received TRT and 500 IU of hCG every other day, and an increase in intratesticular testosterone by 26% was observed (12). This proved that co-administering low dose hCG could maintain intratesticular testosterone in those undergoing TRT. [/I][/COLOR][I][COLOR=rgb(44, 130, 201)]It was later shown that not only is intratesticular testosterone increased with co-administration hCG but spermatogenesis is preserved as well at one year follow up (13). These studies proved that by concomitant hCG administration with TRT spermatogenesis and thus potentially fertility could be preserved. [/COLOR][/I] Based on this evidence an algorithm was suggested for the simultaneous treatment of hypogonadism and preservation of fertility (14). All men wishing to preserve fertility while on TRT should have a baseline semen analysis (SA). Next, it is important to determine the appropriate dosing regimen of hCG based on the timeline for the desired pregnancy. For men who wish to obtain pregnancy within six months, it was suggested to discontinue TRT and start 3,000 IU of hCG intramuscular, or subcutaneous every other day. SA should then be performed every two months. Clomiphene citrate 25–50 mg PO daily can be added or omitted to promote FSH production (15). We suggest including of clomiphene citrate in all men who are already oligospermic or azoospermic. It can be omitted in men who are initiating TRT and hCG simultaneously and have normal semen parameters. If Semen parameters fail to improve and FSH remains low, Gonal-f (recombinant FSH) 75 IU every other day can be added. In men who desire pregnancy within 6–12 months, TRT can be continued with co-administration of 500 IU of HCG every other day ± clomiphene citrate can be used. When planning for pregnancy in greater than 12 months TRT should be cycled off every six months replaced by a four-week cycle of 3,000 IU of hCG every other day.[COLOR=rgb(184, 49, 47)] [B][I][U]For men who do not desire to preserve fertility testicular size can be maintained while undergoing TRT with 1,500 IU of HCG given weekly. Which is enough to maintain pre-TRT levels of intratesticular testosterone (11)[/U].[/I][/B] [/COLOR]Table 1 summarizes recommendations for preserving spermatogenesis in men on TRT (16). [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
When testicle size increases, what happens?
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