I’m using hcg 400iu”s twice a week on Sunday and weds . I picked these days because my testosterone injections are on Monday and Thursdays and my thought process is I want to limit how much hcg converts to estrogen . So by waiting till the day before my next injection my test levels will be lower equaling less excess estrogen conversion . Is my thinking correct or am I just wasting my time and should inject both the same day ? Thanks again everyone
Hcg on trt . Best time ?
- Thread starter Rogue702
- Start date
U can inject same time but you’ll have more benefit from waiting 12-24 hours. Hcg keeps your natural endocrine system working by triggering the hypothalamus and leydig cells to produce testosterone naturally and keeps your balls normal. Exogenous testosterone turns this off.
madman
Super Moderator
I would be much more concerned with the dose used/injection frequency.
Most are injecting 250-500IU 2-3 times/week.
Top it off that you need to keep in mind how high a trough FT level you are running on such protocol (dose T/injection frequency).
There is no best and you need to find what works for you.
Most are injecting hCG 2-3 times/week and some even EOD or daily.
madman
Super Moderator
*Additional autocrine, paracrine, and endocrine factors within the hypothalamus, pituitary, and testis can function to further modulate the HPG axis in complex ways including endocannabinoids, GnRH, kisspeptin, norepinephrine, growth hormone, interleukins, and TGF-β. 28 Therefore, the HPG axis represents a dynamic, but tightly regulated, system at multiple levels resulting in spermatogenesis, among other things.
Unfortunately even when using hCG along with exogenous testosterone the HPTA is still shutdown.
hCG is a direct luteinizing hormone (LH) analog and mimics LH.
*An additional benefit of HCG is that it acts directly on the testicle, provoking a prompt response relative to indirect medications like CC that rely on the pituitary synthesis of LH. It is for this reason that HCG therapy has become a cornerstone in male fertility treatment. Unfortunately, its cost, subcutaneous route of administration, and relatively short half-life (33 hours) prevent it from being used for most hypogonadal patients as primary therapy [58].
LH stimulates the Leydig cells in the testes to produce ITT (intra-testicular testosterone).
The main benefits are inducing and/or maintaining spermatogenesis and prevention/minimization of testicular atrophy.
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NORMAL SPERMATOGENESIS
Normal spermatogenesis is dependent on appropriate signaling from the HPG axis. This signaling initially consists of a pulsatile release of gonadotropin-releasing hormone (GnRH) from the hypothalamus via the portal system to the pituitary gland where stimulation results in gonadotropin release. Luteinizing hormone (LH) from the pituitary stimulates Leydig cells in the testis to produce testosterone and leads to intratesticular production of insulin-like growth factor 1 (IGF-1), which plays an integral role in Leydig cell LH receptor upregulation, steroidogenesis, and maturation.19,20 Follicle-stimulating hormone (FSH) from the pituitary stimulates Sertoli cells in the testis, which supports spermatogonial differentiation and maturation. Both FSH and maintenance of high intratesticular testosterone (ITT) levels (50–100 fold higher than serum) in response to LH are critical for normal spermatogenesis to occur.21–24 Historically, Sertoli cell-produced androgen-binding protein was thought to be responsible for such high ITT levels, but recent data suggest that other factors are also involved.25 Interestingly, animal studies have demonstrated that the absence of FSH signaling results in impaired spermatogenesis whereas loss of sufficiently high ITT levels results in the absence of spermatogenesis.26
Regulation of the HPG axis occurs via feedback inhibition. Endogenous testosterone directly inhibits GnRH and LH release at the hypothalamus and pituitary levels, respectively, leading to downstream attenuation of testosterone production. Testosterone also indirectly regulates gonadotropin secretion via estrogen, derived from testosterone conversion peripherally by the aromatase enzyme. Estrogen exhibits a greater effect on LH secretion than FSH although additional FSH feedback inhibition occurs with inhibin B secreted from Sertoli cells. Inhibin B levels have been considered a surrogate for spermatogenesis; for example, men with spermatogenetic defects express lower inhibin B levels.27 Additional autocrine, paracrine, and endocrine factors within the hypothalamus, pituitary, and testis can function to further modulate the HPG axis in complex ways including endocannabinoids, GnRH, kisspeptin, norepinephrine, growth hormone, interleukins, and TGF-β. 28 Therefore, the HPG axis represents a dynamic, but tightly regulated, system at multiple levels resulting in spermatogenesis, among other things.
INFLUENCE OF EXOGENOUS ANDROGENS ON SPERMATOGENESIS
The use of exogenous androgens can influence the HPG axis by similar mechanisms as endogenous testosterone by exerting negative feedback in a dose- and duration-dependent fashion, resulting in reductions in ITT, blunting of FSH production, and ultimately decrease or complete cessation of spermatogenesis.29
PHARMACOLOGIC AGENTS TO RESTORE OR MAINTAIN SPERMATOGENESIS
Gonadotropins: hCG and FSH Human chorionic gonadotropin (hCG) is a naturally occurring protein produced by the human placenta with a serum half-life of approximately 36 h. Structurally, hCG shares an identical α-subunit with LH and FSH. However, hCG has a unique β-subunit that is virtually identical to the LH β-subunit except that it has an additional 24 amino acid tail at the amino terminus of the protein, which is highly glycosylated and leads to both a longer circulating half-life of hCG (~36 h) versus LH (~30 min) and increased receptor activity. The increased LH receptor activity, along with its longer half-life, makes it a clinically useful LH analog. Initially extracted from the urine of pregnant females, naturally occurring hCG has demonstrated efficacy at restoring spermatogenesis.38 Newer, recombinant hCG has emerged and is considered equivalent to urinary sources pharmacologically although further study is warranted to confirm its equivalency to urinary forms in restoring spermatogenesis.39 Similarly, FSH has traditionally been derived from the urine of postmenopausal women in the form of human menopausal gonadotropin (HMG). A large proportion of naturally occurring HMG consists of copurified urinary proteins inactive at the FSH receptor, with a lesser proportion containing a blend of FSH, LH, and hCG.40 Therefore, similar to hCG, refinements have led to the production of highly purified urinary HMG, and more recently recombinant FSH (rFSH), to achieve higher specificity for the FSH receptor. To date, direct comparisons between the two have not occurred for use at inducing spermatogenesis in men, but data from use in women suggest that rFSH is equivalent to urinary preparations and can avoid the theoretical risk of Creutzfeld–Jakob disease;38,40 therefore, rFSH is the preferred method of pharmacologic delivery of FSH in men.
Maintenance of spermatogenesis before beginning or during TRT or AAS use
A second scenario is a patient who wishes to preserve existing spermatogenesis before beginning TRT or AAS use. Maintenance of normal ITT levels is critically necessary to maintain spermatogenesis. hCG has proven to maintain ITT levels with doses as low as 500 IU every other day.56,57 Clinical data evaluating higher doses of hCG given as monotherapy (500–2500 IU twice weekly), or low-dose hCG (500 IU every other day) in combination with TRT, have demonstrated satisfactory results for maintaining spermatogenesis,57,58 and either would be a good choice as recommended by these authors.
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MAINTENANCE OF FERTILITY WITH CONCURRENT TESTOSTERONE USE
Preserving testicular function and reproductive ability remains an ongoing challenge to practitioners prescribing TTh. Exogenous testosterone is known to decrease intratesticular testosterone and thus impair spermatogenesis. Indeed, in 1996 the World Health Organization investigated weekly injections of 200 mg testosterone enanthate (TE) as a form of contraception. The task force demonstrated that TE caused azoospermia in approximately 75% of men after only 6 months of use [71]. Both the American Urological Association and the Endocrine Society published guidelines in 2018 which recommend against TTh in men wishing to preserve fertility [2,72]. Current evidence suggests, however, that adjuvant medications can be prescribed in an effort to maintain testicular health and fertility while receiving TTh.
Coadministration of HCG with TTh has been shown to help preserve spermatogenesis in men by maintaining physiologic intratesticular testosterone levels throughout treatment. In 2005, Coviello et al [58] demonstrated that TTh caused intratesticular testosterone levels to drop by 94% in otherwise healthy, reproductive-aged men. However, adding subcutaneous 250 IU HCG every other day to their TTh regimen prevented this precipitous fall with intratesticular testosterone levels only dropping 7% from baseline. Furthermore, men who received TTh and 500 IU of HCG every other day actually experienced an increase in their intratesticular testosterone by 26% [58]. This study showed that intratesticular testosterone could be reliably maintained while on TTh. Future studies would prove that spermatogenesis itself, and thus the male’s fertility, could likewise be persevered throughout therapy.
*Many men receiving TTh may not be interested in fertility but still, wish to maintain normal testicular size. It is recommended that these individuals take 1,500 IU HCG weekly while on TTh. This dose is thought to be enough to maintain adequate levels of intratesticular testosterone in order to minimize testicular volume loss. Some men feel that periodically cycling off of TTh is symptomatically beneficial but this is an anecdotal observation and primarily a matter of patient preference.
madman
Super Moderator
*Additional autocrine, paracrine, and endocrine factors within the hypothalamus, pituitary, and testis can function to further modulate the HPG axis in complex ways including endocannabinoids, GnRH, kisspeptin, norepinephrine, growth hormone, interleukins, and TGF-β. 28 Therefore, the HPG axis represents a dynamic, but tightly regulated, system at multiple levels resulting in spermatogenesis, among other things.
*An additional benefit of HCG is that it acts directly on the testicle, provoking a prompt response relative to indirect medications like CC that rely on the pituitary synthesis of LH. It is for this reason that HCG therapy has become a cornerstone in male fertility treatment. Unfortunately, its cost, subcutaneous route of administration, and relatively short half-life (33 hours) prevent it from being used for most hypogonadal patients as primary therapy [58].
*An additional benefit of HCG is that it acts directly on the testicle, provoking a prompt response relative to indirect medications like CC that rely on the pituitary synthesis of LH. It is for this reason that HCG therapy has become a cornerstone in male fertility treatment. Unfortunately, its cost, subcutaneous route of administration, and relatively short half-life (33 hours) prevent it from being used for most hypogonadal patients as primary therapy [58].
Fernando Almaguer
Well-Known Member
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