[quote]J-J wrote:
Cymru wrote:
J-J wrote:
Cymru wrote:
army stud wrote:
J-J wrote:
Well mate TRT is not a temporary fix. It shuts you down as hard as you can be.
The HCG ONLY signals the testes to secrete T, it does nothing for the brain which will remain fully inhibited.
HCG does keep the balls working but does not counter being shut down.
Once you go on TRT the idea is you stay on it… don’t take this decision lightly.
Also you are not going to build slabs of muscle and get tonk on that as it is a therapeutic dose that is a replacement for your natural testosterone - ie. T-R-T. It is not SUPRAphysiological (or not supposed to be - and really doesn’t want to be for health reasons, especially if you have no way to control the estrogen which will be really quite high on T and HCG).
You are young, you may want kids, TRT doesn’t rule this out but it may well make it an issue - and the HCG stimulates the Testes to make T, not sperm.
I suspect there is a little more to this than you have given thought.
May i ask… what was the plan? To go on T injections to ‘fix’ you? I mean… what is the meaning of going on test replacement then exclaiming you dont want to be ‘shut down hard’ again? That is kinda… well.
JJ
It kind of puts me in a crappy predicament. My levels are obviously naturally low for my age but always have been. I would ideally hord all the doctor prescribed injectable test and make it cycle-worthy, opposed to TRT.
BUT I am sitting at a test level of 217 right now and I’m feeling like a 10 year old girl scout.
BUT it’s also very important for me to have kids in the near future.
What if I did the daily HcG and oral test to boost my levels a tad, and once I have a more sustained level, I start the injectable? Won’t taking clomid in conjunction help with the sperm count?
Thanks for the help.
Viable sperm require very high concentrations of testosterone, locally, to ensure viable development. When you take steroids you no longer produce testosterone in the testes so sperm cannot develop. Testosterone from external sources cannot diffuse into the testes in high enough concentrations to ever allow sperm development, no matter how much you took. Clomid will have no impact on sperm count whilst taking any chemical that shuts down natural testosterone production it will never restart your own T production whilst using AS. After AS use is over and your system is clear testosterone etc it can help retart and increase sperm count thus.
The only way to keep sperm healthy whilst on gear is regular HCG use
FSH - does this have absolutely no mention in sperm production?
This is inhibited on steroids and HCG does nothing for it.
JJ - Sperm can develop normally without FSH in the presence of HCG (admittedly at lower concentrations but viable never the less). See the link below - normal sperm production in males who have had their FSH and LH secretion suppressed by exogenous T. Normal sperm production occurs with HCG addition - despite the fact that FSH is not present
http://www.andrologyjournal.org/cgi/reprint/6/3/137.pdf
That is great - thank you - it was something i had wondered about for ages but not found the time or motivation to look up.
If this is the case, then what is the point of FSH? I thought that while T was essential for sperm production - ie. the development of the spermatozoa, FSH was also vital to keep the production ‘line’ going.
Ie. with no T and no FSH one would have low production and low sperm health, with just T the health would be fine but the production would be low - the FSH increases the production.
Is this not quite the case?[/quote]
That is my understanding though research exists (as always!) to refute both ways. ie HCG and T allows no sperm production without FSH and HCG aand T allows full and normal sperm production with FSH!!
When deciding who to side with - I believe you can never prove a negative. Therefore just because no sperm was produced in your trial it does not mean it is not possible. If the research appears sound and sperm production occurred it must be possible. Simplistic I know but I am not sure how else to view it.
I also seem to recall some recent research that suggests that there may be mutations of the FSH receptor in sertoli cells and this may be decisive in wether sperm production can or can t occur with HCG and T.
The abstract below actually suggests full motility and count occurs with FSH only T and HCG (same author as earlier)
J Clin Invest. 1981 Oct;68(4):1044-52. Links
Follicle-stimulating hormone and human spermatogenesis.
Bremner WJ, Matsumoto AM, Sussman AM, Paulsen CA.
The role of follicle-stimulating hormone (FSH) in the control of spermatogenesis is not well established in any species, including man. We studied the effect of an experimentally-induced, selective FSH deficiency on sperm production in normal men. After a 3-mo control period, five normal men received testosterone enanthate (T) 200 mg i. m. weekly to suppress luteinizing hormone (LH) and FSH, until three successive sperm counts revealed azoospermia or severe oligospermia (sperm counts <3 million/ml). Then, while continuing T, human chorionic gonadotropin (hCG) 5,000 IU i. m. three times weekly was administered simultaneously to replace LH activity, leaving FSH activity suppressed. The effect of the selective FSH deficiency produced by hCG plus T administration on sperm production was determined.Sperm counts (performed twice monthly throughout the study) were markedly suppressed during T administration alone (1.0+/-1.0 million/ml mean+/-SE, compared with 106+/-28 million/ml during the control period, P < 0.001). With the addition of hCG to T, sperm counts returned toward normal (46+/-16 million/ml, P < 0.001 compared with T alone). In two subjects, sperm counts during hCG plus T returned into the individual’s control range. Sperm motility and morphology were consistently normal in all men during hCG plus T.Serum FSH levels by RIA were normal (110+/-10 ng/ml) in the control period and were suppressed to undetectable levels (<25 ng/ml) in the T alone and hCG plus T periods. Urinary FSH excretion was markedly suppressed in the T alone (60+/-15 mIU/h-2nd IRP, P < 0.01) and hCG plus T (37+/-9 mIU/h, P < 0.01) periods compared with the control period (334+/-78 mIU/h).We conclude that spermatogenesis as assessed by sperm counts, motilities, and morphologies may be reinitiated and maintained at normal levels in men with undetectable blood FSH levels and urinary excretion of FSH less than that of prepubertal children. This conclusion implies that, although FSH may exert effects on human testicular function, maintenance of normal spermatogenesis and reinitiation of sperm production after short-term suppression by exogenous steroids can occur in spite of nearly absent FSH stimulation.
The paper below appears to confirm HCG and T produce lower sperm concentrations than are possible with addition of FSH
J Clin Endocrinol Metab. 1986 Jun;62(6):1184-92. Links
Chronic human chorionic gonadotropin administration in normal men: evidence that follicle-stimulating hormone is necessary for the maintenance of quantitatively normal spermatogenesis in man.
Matsumoto AM, Karpas AE, Bremner WJ.
The role of FSH in the maintenance of spermatogenesis in man is poorly understood. To determine whether normal serum levels of FSH are necessary for the maintenance of quantitatively normal spermatogenesis, we first studied the effect on sperm production of selective FSH deficiency induced by chronic administration of hCG in normal men. Then, we determined the effect of FSH replacement in some of these men. After a 3-month control period, eight normal men (aged 30-39 yr) received 5000 IU hCG, im, twice weekly for 7 months. Then while continuing the same dosage of hCG, subjects simultaneously received 200 mg testosterone enanthate (T), im, weekly for an additional 6 months. hCG administration alone resulted in partial suppression of the mean sperm concentration from 88 +/- 24 (+/-SEM) million/ml during the control period to 22 +/- 7 million/ml during the last 4 months of hCG treatment (P less than 0.001 compared to control values). With the addition of T to hCG, sperm counts remained suppressed to the same degree. Except for one man who became azoospermic while receiving hCG plus T, sperm motilities and morphologies remained normal in all subjects throughout the entire study. During both the hCG alone and hCG plus T periods, serum FSH levels were undetectable (less than 25 ng/ml), and urinary FSH levels were comparable to those in prepubertal children and hypogonadotropic hypogonadal adults. We replaced FSH activity in four of the eight men in whom prolonged selective FSH deficiency and partial suppression of sperm production were induced by hCG administration. Immediately after the period of hCG plus T administration, T was stopped in four men who continued to receive hCG alone (5000 IU, im, twice weekly) for 3 months. Then, while continuing the same dosage of hCG, these men received 100 IU human FSH, sc, daily (n = 2) or 75 IU human menopausal gonadotropin, sc, daily (n = 2) for 5-8 months. During the second period of hCG administration alone, serum FSH levels were undetectable (less than 25 ng/ml), and sperm concentrations were suppressed (34 +/- 13 million/ml) compared to the control values for these four men (125 +/- 39 million/ml; P less than 0.001). With the addition of FSH to hCG, FSH levels increased (213 +/- 72 ng/ml) and sperm concentrations rose significantly, reaching a mean of 103 +/- 30 million/ml (P less than 0.03 compared to hCG alone).(ABSTRACT TRUNCATED AT 400 WORDS)
Conversely the paper below suggests that FSH must be present to initiate spermatogenesis but T alone is needed for maturation
Ann Endocrinol (Paris). 1999 Jul;60(2):102-6. Links
Role of FSH in male gonadal function.
Simoni M, Weinbauer GF, Gromoll J, Nieschlag E.
Institute of Reproductive Medicine of the University, Münster, Germany.
The production of male gametes depends on the concerted action of the two gonadotropins FSH and LH on the testis. The action of LH is mediated through the production of testosterone by the Leydig cells. Since male germ cells possess neither FSH nor androgen receptors, the action of FSH and testosterone occurs through the Sertoli cells. Although the precise function of these two hormones remains elusive, the existing evidence suggest that both FSH and testosterone are able to stimulate all phases of spermatogenesis. In the male FSH is required for the determination of Sertoli cell number, and for induction and maintenance of normal sperm production. The crucial role of FSH in male gonadal function has been clearly illustrated by the discovery of a patient with an activating mutation of the FSH receptor. This patient had been hypophysectomized because of a pituitary tumor and, under testosterone substitution was unexpectedly fertile in spite of undetectable serum gonadotropin levels and had fathered three children. In this patient we could demonstrate a heterozygous activating mutation of the FSH receptor which resulted in cAMP production independent of FSH stimulation. This finding represents the first description of an activating mutation of the FSH receptor and demonstrates that FSH alone maintains spermatogenesis in man. On the other hand, the effects of the lack of FSH action are unclear. Among five men with a homozygous inactivating mutation of the FSH receptor only one was infertile and spermatogenesis was variably affected in the others. However, serum inhibin B values in these men were not completely suppressed and serum FSH levels were only moderately elevated, indicating the possibility that FSH receptor function was not completely abolished by the mutation. Elimination of FSH action is a prerequisite to suppress completely spermatogenesis for contraceptive purposes, while administration of both LH and FSH is necessary to induce sperm production in patients with hypogonadotropic hypogonadism. Experimental immunization of male monkeys against FSH markedly reduced germ cell proliferation and even induced infertility. At the cellular level, FSH stimulates the cAMP-dependent activation of protein kinase A in Sertoli cells, but the molecular mechanism of FSH action is poorly understood. In the primate, the gonadotropin withdrawal achieved by administration of a GnRH antagonist leads to a premeiotic arrest of germ cell proliferation, probably due to inhibition of the mitotic division of A-pale spermatogonia. Therefore, FSH might be the prime inducer of spermatogonial proliferation, while the successive maturation process could proceed independently of FSH. In summary, clinical and experimental evidence support the concept of an irreplaceble role of FSH in the primate. Only the combination of FSH and testosterone, however, supports a qualitatively and quantitatively fully normal spermatogenesis.
On a side note I am convinced that you can produce sperm whilst taking HCG and T. My first child was conceived after an 8-week cycle of T and dianobol . Looking at the dates she was concievd either at the end of the cycle or after a couple of 1500iu HCG jabs. That tells me something. And before the wise cracks start she is the spitting image of me (although I suppose I can t rule my dad or brother out of the equation)