Does HCG suppress to the same extent as exogenous testosterone? I want to take HCG for fertility reasons, but when I come off, will have low T levels?
- Thread starter JCUSN
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Osmanm5897
New Member
Go see Dr.Lipshultz at Baylor University in Houston, that is if you are located there or willing to make the trip.
He knows the Ins and outs of TRT including hcg doses and administration. He has contract with a local compounding pharmacy that will deliver hcg and other meds to your home for cheaper. BTW, he recommends high dose of hcg when coming off testosterone. He prescribed me 3000IU of hcg three times a week, plus a FSH for fertility. It worked like a magic because I was able to impregnate my partner within 90 days and I been on TRT for seven years before coming off it.
Anyways, you might be different and not need all of that so it’s better to go a knowledgeable doctor. Thats all.
No. Anywhere from 15-200 million is normal.
My brother had 90 million sperm when he did his SA without any HCG or clomid. Just naturally.
DixieWrecked
Well-Known Member
Are you using pregnyl brand HCG?
Do you think you would feel just as good if you didn't take the HMG?
Yes. Stopping the HMG had no effect on how I feel, but sperm was not recovered. HcG is a game changer though. I won’t ever stop that in my protocol.
did you notice any change in testicle size dropping hmg?
No. HcG maintains size. HMG is purely sperm production.
If I'm not mistaken, most of the testicular volume is from the sertoli cells, so it would make sense that HMG would increase testicular size more than hCG.
phalloguy100
Active Member
hCG is actually used to recover from Test cycles. It mimics LH, so your pituitary would stop producing LH (the hormone that tells the testicles to produce testosterone)
While on TRT, most folks get 500iu 2-3x per week, sometimes up to 1000iu. The problem is it can also raise estrogen levels. As PCT, dosages would start at 2000-iu to 5000-iu then slowly decrease to 1000-iu.
Clomid tells the pituitary to produce more LH amd FSH, by blocking its estrogen receptors. However, it also causes aromatization in other parts of the body, leading to high estrogen and feeling like crap. I hated it. I haven’t tried encloiphene but it is supposed to be more selective than clomiphene (clomid), so it does not raise estrogen levels.
Whatever you do, check with a doctor who specializes in TRT/fertility. I recommend Defy Medical. They know their stuff!!
While on TRT, most folks get 500iu 2-3x per week, sometimes up to 1000iu. The problem is it can also raise estrogen levels. As PCT, dosages would start at 2000-iu to 5000-iu then slowly decrease to 1000-iu.
Clomid tells the pituitary to produce more LH amd FSH, by blocking its estrogen receptors. However, it also causes aromatization in other parts of the body, leading to high estrogen and feeling like crap. I hated it. I haven’t tried encloiphene but it is supposed to be more selective than clomiphene (clomid), so it does not raise estrogen levels.
Whatever you do, check with a doctor who specializes in TRT/fertility. I recommend Defy Medical. They know their stuff!!
madman
Super Moderator
When it comes to the quality/quantity of sperm let alone testicular volume the combination of hCG + FSH would be more effective as they work synergistically.
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* 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
*Spermatogenesis is largely dependent on the action of FSH on Sertoli cells coupled with high intra-testicular testosterone concentrations. Within the seminiferous tubules, only Sertoli cells possess receptors for both FSH and testosterone. 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
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INTRODUCTION
Testosterone is a pleiotropic hormone that plays various physiological roles in the development of male genitalia in utero and during puberty. Classically, testosterone is a hormone associated with masculinity. Testosterone is used as a treatment for males with late-onset hypogonadism, a condition in men who experience symptoms caused by a decrease in serum testosterone. Symptoms associated with low testosterone can include decreased libido, decreased muscle mass, depressed mood, and/or erectile dysfunction. The use of testosterone replacement therapy (TRT) among men over the age of 40 years has increased more than 3-fold over the last decade [1].
Exogenous testosterone comes in various preparations and each form carries various risks. Along with an increase in hematocrit, a major adverse effect of TRT is diminished sperm production because of the decreased intra-testicular concentration of testosterone and suppression of the hypothalamic-pituitary-gonadal (HPG) axis [2-4]. Suppression of follicle-stimulating hormone (FSH) release from the pituitary gland impairs sperm production and suppression of luteinizing hormone (LH) release inhibits intra-testicular testosterone production
The purpose of this review is to evaluate the contraceptive effect of testosterone, discuss how the use of exogenous testosterone can negatively impact a man’s fecundity, and identify the importance of family planning in men who are planning to receive TRT.
The exogenous administration of testosterone suppresses the release of gonadotropins (FSH and LH) to levels below that required for spermatogenesis. Spermatogenesis is largely dependent on the action of FSH on Sertoli cells coupled with high intra-testicular testosterone concentrations. Within the seminiferous tubules, only Sertoli cells possess receptors for both FSH and testosterone. 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]. 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).
Intra-testicular testosterone is required in spermatogenesis for the formation of the blood-testis barrier (BTB). The BTB is a series of tight and adherens junctions between the Sertoli cells that separates postmeiotic germ cells in the adluminal compartment of the seminiferous tubules from the basal compartment containing the blood supply. During spermatogenesis, the BTB is disrupted and reformed as preleptotene spermatocytes pass through this barrier. In the absence of testosterone stimulation, spermatogenesis can only proceed as far as the prophase 1-leptotene stage of meiosis [7].
Testosterone is also required in maintaining connections between Sertoli cells and the haploid spermatid germ cells. Round spermatids are initially connected to Sertoli cells via desmosomes. As the spermatids mature and elongate, the desmosomes are replaced with stronger, specialized adherens junctions called ectoplasmic specializations, which are maintained until the release of mature sperm. Testosterone aids in this process and increases the efficiency of germ cell attachment to Sertoli cells. Testosterone is also essential for the release of mature spermatozoa from Sertoli cells. It has been shown that in the absence of testosterone stimulation, sperm are not released but are instead phagocytized by Sertoli cells [7].
Ultimately, the low intra-testicular testosterone results in decreased proliferation of spermatogonia, defects in spermiation of mature spermatozoa by Sertoli cells, and accelerated apoptosis of spermatozoa [8- 11]. 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 [12,13].
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