Does hCG boost libido by stimulating 5-alpha-reductase?

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FunkOdyssey

Well-Known Member
I started a previous thread to unravel the mystery of why hCG improves libido in some men, which generated some good discussion but didn't reach any firm conclusions:


Now comes a youtube video from Cortex Labs that claims hCG improves libido by stimulating 5-AR activity and increasing DHT production:


This actually sounds plausible to me for a few reasons:
  • My ratio of Free T to DHT increased on testosterone injections compared to my natural baseline. In one case, I tested a below baseline DHT with a free T that was almost double baseline.
  • There seems to be a theme with the endocrine system where hormones that stimulate the secretion of downstream hormones also stimulate the metabolism of those downstream hormones into more active versions. For example, TSH increases the conversion of T4 into T3, so people on T4 only therapy with suppressed TSH may have below baseline production of T3. This is hypothesized to cause poor outcomes and continued hypothyroid symptoms.
  • My libido on injections is pretty garbage except for a short while after dose increases.
  • My libido on cream with the high DHT levels was much better.
  • People that are suffering long-term sexual dysfunction from the use of 5-AR inhibitors, SSRIs, accutane, etc seem to report more success with hCG than TRT.
Has anyone tested their DHT levels with and without hCG and observed differences at comparable free T levels? Or a significant change in the ratio of Free T to DHT?

I think this guy may be onto something and he has inspired me to start taking hCG seriously as worthy of experimentation. He expresses some controversial ideas around absolute levels of estradiol being more important than the T:E2 ratio and the need to control E2 (particularly to gain the best results from hCG) that I think are worth discussing also.
 
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madman

Super Moderator

8. Side effects of HCG treatment

Since HCG treatment raises serum testosterone levels, it can lead to similar side effects as seen in direct TRT, including gynecomastia, high blood pressure, acne, hair loss and raises in estrogen potentially leading to gynecomastia
. However, unlike supplementation with supraphysiological doses of testosterone as seen in doping, physiological serum testosterone increases triggered by HCG supplementation only rarely result in side effects (Table 2). Moreover, as compared to TRT, HCG treatment seems to have fewer side effects with regard to affecting hematocrit, estradiol, prostate volume, and PSA increases [15]. Interestingly, serum testosterone seems to peak at 72 hours post HCG injection and significantly correlates with estradiol peaks observed 24 hours after injection [38]. Therefore similar to TRT, even though not in line with guidelines, ancillary drugs such as aromatase inhibitors, selective estrogen receptor modulators, or 5α-reductase inhibitors are used off-label in some rare cases of severe side effects due to increased serum estradiol or DHT levels.





*Take-home point:

A replacement regimen with combined hCG/rFSH mimics physiologic steroid hormone profiles better than a substitution with exogenous testosterone. The documented differences in steroid profiles on testosterone replacement in hypogonadal males with absent or severely reduced endogenous LH and FSH secretion may have long-term consequences for health and wellbeing. Specifically, body composition, bone health, glucose, and lipid metabolism, salt and water balance, cognition, mood, sleep, and sexual function could be affected. The steroidogenic differences could also be relevant for gonadotropin-suppressive treatments with long-acting testosterone preparations in males with primary hypogonadism. To what extent this hypothesis is true, should be addressed in future clinical studies.






Combined treatment of CHH males with hCG and rFSH resulted in steroid hormone profiles similar to those of healthy men, but this was not the case, while exogenous testosterone was used for replacement. Serum steroid hormone levels on the different treatment modalities in CHH males and matched controls are summarized in Table 1 and plotted individually in Figure 3 and Figure 4. While CHH patients were on T substitution, decreased serum concentrations of some members of the classical Δ4 pathway of androgen biosynthesis (progesterone (p=0.0104), 17-OH-progesterone (17 OHP) (p<0.0001)) and of the alternative T pathway steroid androstenediol (p=0.004)) were observed, compared to controls. The marker steroid of the backdoor DHT pathway androstandiol (p=0.025), was slightly increased.

The testosterone metabolites DHT and 17-ß estradiol (E2), the Δ5 steroid 17-pregnenolone, the sulfated form of the Δ5 pathway steroid dehydroepiandrosterone DHEA, i.e. dehydroepiandrosterone sulfate (DHEAS), androstenedione (A4) and all measured 11-oxygenated C19 androgens (11-keto-testosterone (11-K-T), 11-keto-dihydro-testosterone (11-K-DHT) and 11-keto-androstenedione (11-K-A4)) were comparable to those of controls.

By contrast, normal concentrations were found for most steroid hormones in the serum of CHH males, while they were on hCG/rFSH replacement. Specifically, steroid profiles resembled those of healthy male controls, regarding the Δ 4 pathway of androgen biosynthesis (17-OHP) and the metabolite DHT, the marker steroid of an alternative T pathway via androstenediol, the Δ5 pathway steroids Δ5 steroid 17- pregnenolone, DHEAS and A4 and all aforementioned 11-oxygenated C19 androgens (11-K-A4, 11-K-T, 11-K-DHT). Serum progesterone was slightly decreased (p=0.0104), the testosterone metabolite E2 and the backdoor DHT pathway steroid androstanediol were increased (both p<0.0001).

Our results indicate that the treatment of CHH males with gonadotropins results in steroid hormone profiles similar to those of healthy men, with few exceptions (E2, progesterone). However, this is not the case using a regimen based on exogenous testosterone. If testosterone is applied, steroidogenic pathways in testicles of CHH males remain unstimulated. By contrast, if hCG +rFSH are used, the LHCG receptor in Leydig cells is activated 14. In response, multiple steroids of the classical steroidogenic cascade are synthesized by the gonads, including the classic potent androgens T and DHT. This explains the differences observed in serum steroid levels in CHH males on the two different replacement regimens.




Limitations

One limitation of the present study, regarding the investigation of gonadotropin-effects is that hCG was used to replace LH.
This substance may have slightly different properties regarding the activation of LHCG receptors 55. However, at present, rLH is not licensed for clinical use in males.



Summarized results and conclusions

These biochemical studies of serum steroid hormone patterns in CHH males on two different androgenic replacement regimens contribute to our knowledge of human steroidogenesis, specifically androgen production and it's regulation. Gonadotropins contribute to steroid production along the classic Δ4 pathway, by stimulation of 17-OHP production. In addition, gonadotropins co-activate an alternative pathway of T biosynthesis from DHEA via androstenediol.

However, Δ5 biosynthesis of 17-OH-pregnenolone, DHEA(S) seems fully gonadotropin-independent, and the production of androstenedione is largely gonadotropin-independent. Thus, an “adrenal-peripheral tissues-testicular collaboration” regarding androgen synthesis by classic or alternative pathways seems possible.

The 11-oxygenated C19 androgen pathway is activated independently of gonadotropins. The activity of the three DHT backdoor pathways (converging in androstanediol biosynthesis) is not increased by gonadotropins.

A replacement regimen with combined hCG/rFSH mimics physiologic steroid hormone profiles better than a substitution with exogenous testosterone. The documented differences in steroid profiles on testosterone replacement in hypogonadal males with absent or severely reduced endogenous LH and FSH secretion may have long term consequences for health and wellbeing. Specifically, body composition, bone health, glucose, and lipid metabolism, salt and water balance, cognition, mood, sleep, and sexual function could be affected. The steroidogenic differences could also be relevant for gonadotropin-suppressive treatments with long-acting testosterone preparations in males with primary hypogonadism. To what extent this hypothesis is true, should be addressed in future clinical studies.






Figure 4

-Serum steroid hormone concentrations of CHH males from alternative/backdoor pathways of androgen biosynthesis

-Serum androstenediol concentrations, representing the alternative pathway of testosterone formation, in CHH males on hCG/rFSH and T replacement, compared to those of healthy controls.

-Serum androstanediol concentrations, representing the backdoor pathway of DHT formation in CHH males, on gonadotropin and T replacement, and in healthy controls.

-Serum 11K T and 11 K DHT concentrations, representing the 11-oxygenated C19 androgen pathway in CHH males, on gonadotropin and T replacement, and in healthy controls.

Screenshot (26938).png

Screenshot (26939).png

Screenshot (26940).png





DHT

DHT serum levels were comparable to controls in CHH males during hCG/rFSH replacement but were slightly increased after the patients were switched to exogenous testosterone, indicating that
the pathways of DHT production are more active if exogenous testosterone is provided. DHT is known to result mainly from 5-alpha reduction of testosterone 45 and from the aforementioned backdoor pathway in adrenal and prostatic tissues. DHT exerts the strongest bioactivity on the AR 46.


17ß-estradiol

17ß-estradiol (E2), a major metabolite of testosterone, was found to be slightly elevated as compared to controls while patients were undergoing gonadotropin replacement. About 50-75 % of circulating E2 is derived from extragonadal aromatization of testosterone by fat, bone, brain, testes and other tissues 47. Although we matched for serum T in both cohorts, mean serum T levels were slightly higher during gonadotropin application, compared to the situation during T treatment. This explains why T was aromatized to a greater extent during hCG/rFSH substitution. Alternatively, the higher E2 levels could be interpreted as an enhancement of aromatase activity by hCG/rFSH. E2 acts on estrogen receptors alpha and beta (ERα and ERβ) that are present in reproductive organs, brain, bone, blood vessels, liver, and skin and breast tissue. Many biologic effects, hitherto attributed to testosterone are conveyed by estradiol: estrogen action is important for the regulation of spermatogenesis; E2 is involved in the regulation of the somatotropic axis, it mediates epiphyseal closure in bones, improves bone mineralization and bone microarchitecture, decreases fat mass, thereby favoring lean body mass. In addition, it positively affects glucose metabolism by enhancing insulin sensitivity and conveys vasomotor stability 48-50.
 
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