HcG, Hmg, and Sertoli cells.

[John Bahlmer]

Hey,

For introduction, I am a 24 year old that is taking 200 mg of Test E a week because it makes me feel better, has been helping me gain muscle, and-overall-just feels great. I know it carries its risks, but after alot of research the only two major problems that can't be fixed with proper ancilleries are possible heart issues (Left Ventral Hypertrophy) and fertility. These two issues are severly lacking in clinical research, so I figured I would see if anyone in this forum can help.

Its pretty clear that HcG can prevent testicular atrophy if used while on TRT or on cycle. It does this by keeping the Leydig cells stimulated. The leydig cells are the cells in the testicles responsible for producing testosterone. Although the nuts can ussually be "turned-on" after long term AAS use, sometimes the leydig cells actually die after being chronically understimulated.

From my research, this seems to be pretty much solid fact. My question, however, is, "Do the Sertoli cells, that produce the sperm, sometimes die after being chronically understimulated, even though they can normally be 'turned-on' after long term AAS use or TRT? If this is so, is HmG to Sertoli Cells what HcG is to Leydig cells? If so, then in theory, could periodic use of low-dose HmG be enough to maintain the Sertoli cells as a preventitive measure to keep them from dying off?

That shit is expensive, but I read about some guys using maybe 150 iu a month, divided into like three shots, to keep shit down their stimulated.

I am going to end up being a guinea pig here but any insight would be appreciated

 

[Dr JIM]

First from this thread alone it's quite obvious your "research" is almost exclusively limited to venues such as PED forum, TT blogs or AAS forums. For example;

Your first statement is predicated on the "bro-science" notion the reversal of testicular atrophy with HCG somehow is limited to the awakening of Leydig cells, it is not!

Second HCG has been used and studied as a therapy for infertility in and of itself and while HMG will have a similar effect the additional cost does not justify the added benefit with few exception.

Many forum bros have propagated the belief atrophy of any organ from SKM to gonadal,is syanmyous with cellular aptosis when it's been well established cellular death is primarily genetically predetermined or programmed.

The fact is just like SKM sarcopenic atrophy in the elderly
the dormancy exhibited by S and L cells is largely REVERSIBLE once a functional stimuli is reapplied.

Nonetheless to KNOW to what degree your fertility has been effected requires a SPERM COUNT, period. One can only hope you obtained baseline labs, but I suppose we already know the answer to that question.

More importantly you readily admit you have LVH, the incidence which is reasonably WELL ESTABLISHED to increase, in a cumulative manner, with the use of AAS, including TT.

Consequently, the fact you are self prescribing TT at a time when your TT levels should be at their plateau just "to feel better" in the face of LVH, is like playing Russian roulette, unless you are being followed by a cardiologist and periodic echocardiography.

 

[I Declare WAR!]

He doesn't admit he has LVH.

Please forgive my ignorance, what does SKM stand for?

 

[Dr JIM]

He doesn't admit he has LVH.

Please forgive my ignorance, what does SKM stand for?

Yep, my oversight, thank goodness.

SKM = SKeletal Muscle

 

[John Bahlmer]

I knew you were going to reply Doctor Jim! Good insight. I've done alot of research on a few different venues with and without connections to anobolics. I admit, I haven't looked too much into hcg and fertility not in the context of anobolics and trt. Unfortunately, research is kind of limited and contradictory when it comes to fertility. I read lots of articles showing that fertility usually comes back and the articles that show infertility being permenantly affected pretty much come from people who started while they were really young or people who used heavily for a long time and didn't do any pct. Hcg is pretty cheap, so it gives me peace of mind. Hmg is what I'm really curious about, there's not even bro science on the matter.

 

[Dr JIM]

Unfortunately, research is kind of limited and contradictory when it comes to fertility.

There are WELL OVER 20 evidence based citations with respect to this topic listed ON GOOGLE ALONE and that which may seem contradictory, is more a function of one's ability to interpret the data correctly.

To that end I've no idea what you consider "research" but it's certainly not on par with the contemporary evidence based standard such as MedLine or PubMed!

Good Luck

 

[romaleos]

This may explain the reinvigoration of my testes post cycles/pcts. Mind you I was infertile for ten years AND pre-aas TT was 200-300. After heavy ped use, a child was conceived naturally and Pre-cycle TT is currently 850 natural go figure?

 

[Dr JIM]

This may explain the reinvigoration of my testes post cycles/pcts. Mind you I was infertile for ten years AND pre-aas TT was 200-300. After heavy ped use, a child was conceived naturally and Pre-cycle TT is currently 850 natural go figure?

This is all conjecture on behalf of the OP, as he hasn't conducted any labs nor a sperm count. So until then he could simply reverse the CAUSE and discontinue TT supplementation, right!

Well we ALL know that's not going to happen, thus until what could be morphs into WHAT IS …….. GOOD LUCK!

 

[romaleos]

This is all conjecture on behalf of the OP, as he hasn't conducted any labs nor a sperm count. So until then he could simply reverse the CAUSE and discontinue TT supplementation, right!

Well we ALL know that's not going to happen, thus until what could be morphs into WHAT IS …….. GOOD LUCK!

I know this doc. I just wanted an explanation for my anecdotal experience other than the Lord came down from heaven and tickled my barren testicles to life. Bro science or prayer? Both require a leap of faith outside of real laboratory research. Blind belief is all I got at this point.

 

[Docd187123]

I know this doc. I just wanted an explanation for my anecdotal experience other than the Lord came down from heaven and tickled my barren testicles to life. Bro science or prayer? Both require a leap of faith outside of real laboratory research. It's all I got at this point.

Would you prefer I visited you from the Elysian forests and tickled your barren testes to life? The offer is on the table and without expiration.

 

[Dr JIM]

Both require a leap of faith outside of real laboratory research. Blind belief is all I got at this point.

I guess we'll never know absent lab data that followed your recovery in a chronological fashion. All that being said, another obviously important yet often overlooked factor in this regard is the fertility status of one's SO!

 

[romaleos]

True. Takes two to tango. Outside from low to moderate endometriosis, she was/is tip top fertility wise. Periods were synced to an atomic clock and amazing follicle response when she was on the meds. Embryos were coming out fragmented which I think is more of a problem with my boys than her eggs.

We will never know but I like to believe it was the roids.

 

[John Bahlmer]

Well, Dr.Jim, most of the Data is not conclusive. I read it right, I guarantee you, you don't need to be condescending. The controls are shit; the studies are rarely long term. Its illegal to use steroids in most experiments because they are illegal and therefore considered inhumane, and lots of the reviews seem biased.

What point are you trying to prove, exactly. Are you trying to prove that steroids don't ever cause irreversable infertility? Are you proving that testicular atrophy can't be permenant? Are you trying to prove that Hcg or Hmg isn't healthier on cycle or during TRT than not doing anything? And if it is reversable, will using hcg or hmg on cycle cause the reverse to happen faster?

Better yet, post the study showing hcg and hmg does not prevent infertility, temporary or not, from long term (5 years+) high dose anabolic steroid use?

Show me a paper of a long term study (5 years +) showing that long term, chronic, anobolic steroid use (not TRT), with NO PCT, is not associated with with an increase primary hypogonadism or infertility compared to placebo?

Post as many as you like that fit the criteria.

 

[John Bahlmer]

First from this thread alone it's quite obvious your "research" is almost exclusively limited to venues such as PED forum, TT blogs or AAS forums. For example;

Your first statement is predicated on the "bro-science" notion the reversal of testicular atrophy with HCG somehow is limited to the awakening of Leydig cells, it is not!

Second HCG has been used and studied as a therapy for infertility in and of itself and while HMG will have a similar effect the additional cost does not justify the added benefit with few exception.

Many forum bros have propagated the belief atrophy of any organ from SKM to gonadal,is syanmyous with cellular aptosis when it's been well established cellular death is primarily genetically predetermined or programmed.

The fact is just like SKM sarcopenic atrophy in the elderly
the dormancy exhibited by S and L cells is largely REVERSIBLE once a functional stimuli is reapplied.

Nonetheless to KNOW to what degree your fertility has been effected requires a SPERM COUNT, period. One can only hope you obtained baseline labs, but I suppose we already know the answer to that question.

More importantly you readily admit you have LVH, the incidence which is reasonably WELL ESTABLISHED to increase, in a cumulative manner, with the use of AAS, including TT.

Consequently, the fact you are self prescribing TT at a time when your TT levels should be at their plateau just "to feel better" in the face of LVH, is like playing Russian roulette, unless you are being followed by a cardiologist and periodic echocardiography.

Another point, apoptosis and cell death might be genetically determined , but an aversive stimulus like high doses of testosterone could speed up the process. For example, high doses of DHT don't cause everybody to go bald. But, a susceptible individual who is prone to Male Patter baldness will go bald much quicker when they take Testosterone etc.. If this man would have naturally gone fully bald at 60, but he ends up going bald at 30 after using steroids, did steroids cause his baldness or was it just his genetics. Furthermore, if he controlled his DHT levels and took finestride as a preventative measure he probably would not have gone bald.

 

[I Declare WAR!]

That's kind of a good argument... but you have no evidence.

 

[John Bahlmer]

That's kind of a good argument... but you have no evidence.

Thanks! You're right about the evidence. When I get the free time I'll copy and paste any of the abstracts I find relating to the issue or copy and paste anything I find in a book (i started torrenting e-textbooks to save money for school).

 

[John Bahlmer]

Outcome of gonadotropin therapy for male infertility due to hypogonadotrophic hypogonadism.
Farhat R1, Al-zidjali F, Alzahrani AS.

Author information
Abstract
Data on the management of male infertility secondary to hypogonadotrophic hypogonadism (HH) are limited. We report our extensive experience with intramuscular injections of gonadotropins, one of the two methods used for this purpose. Eighty-seven married men (median age, 28 years) with either congenital (47 men) or acquired (40 men) HH were treated for a median of 26 months (range, 6-57) with intramuscular injections of gonadotropins (HCG/HMG) three times weekly for the purpose of achieving fertility. The outcome was assessed by achievement of one or more pregnancies. Of the 151 courses of HCG/HMG treatment administered to 87 patients, 85 courses (56.3%) were successful, resulting in 85 pregnancies (median pregnancy rate 2, range 1-10) in 35 patients (40%) while 52 cases did not achieve pregnancy. Responders had larger pretherapy testicular volume (9 +/- 3.6 cc) compared to non-responders [(5.7 +/- 2.0 cc), P < 0.0001], but there was no difference in age, LH, FSH or testosterone levels or doses of HCG/HMG used. The pregnancy rate was similar in those with congenital (51.4%) and acquired causes (48.6%) of HH (P = 0.83). Only testicular size was predictive of conception (P < 0.001, odds ratio 1.5, 95% CI 1.21-1.92) while age, pretherapy levels of testosterone, LH, FSH and doses of HCG/HMG did not predict the success of pregnancy. Gonadotropins are moderately effective in achieving one to several pregnancies in HH. Only testicular size is predictive of success in achieving pregnancy. There is no difference in success between those with congenital and acquired causes of HH.

 

[John Bahlmer]

Induction of spermatogenesis in hypogonadotrophic hypogonadism
NB Oldereid T Tanbo　


Physiology and pathophysiology
Hypogonadism in men is a condition involving impaired testicular function resulting in decreased production of various hormones, including http://legemiddelhandboka.no/Legemidler/?frid=Lk-03-endokr-5481 and inhibin B, and reduced or absent sperm production. If the failing gonadal function is secondary to decreased gonadotropin secretion from the pituitary gland, there is a secondary (hypogonadotrophic) hypogonadism.

Inadequate secretion of gonadotropin releasing hormone (GnRH) from the hypothalamus and decreased pituitary causes reduced or absent secretion of follicle stimulating hormone (FSH) and luteinizing hormone (LH), which leads to lack of spermatogenesis and decreased testicular hormone production ( 4 ).Luteinizing hormone stimulates the Leydig cells in the testis to androgen production, so that the intratesticular level of http://legemiddelhandboka.no/Legemidler/?frid=Lk-03-endokr-5481 significantly higher than in serum ( 4 , 5 ). Follicle-stimulating hormone regulates sertolicelleproliferasjonen before and during puberty and helps in the regulation of spermatogenesis, by maintaining different aspects sertolicellemetabolismen. This ensures a favorable intratubulært environment where conditions are suitable for normal spermatogenesis both qualitatively and quantitatively ( 6 ). The endocrine regulation of gonadotropins involve negative feedback mechanisms ofhttp://legemiddelhandboka.no/Legemidler/?frid=Lk-03-endokr-5481 and inhibin B, a glycoprotein produced in the testis, which selectively regulate the secretion of follicle stimulating hormone ( 7 ).

Chorionic gonadotropin (hCG) and luteinizing hormone is structurally very similar and operates in the same receptors on Leydig cells ( 8 ). Injections with chorionic gonadotropin used to stimulate these.

There are various anatomical, functional and genetic causes of hypogonadotrophic hypogonadism (Box 2) (5 ). The clinical picture varies depending on the time of onset of the hypoandrogene condition and whether GnRH deficiency or hypofysesvikten is complete or partial. Most patients diagnosed in adolescence by a lack of puberty. Typical findings of the survey are usually small testes and lack of virilization. By hypoandrogen condition debuts after puberty, the clinical vary widely. Characteristic features are often reduced hair growth, decreased libido and lack of spermatogenesis ( 4 ).

In men with hypogonadotrophic hypogonadism partial or postpubertal onset of an overall hormonal deficiency can injection of chorionic gonadotrophin be sufficient to restore fertility. Most men with congenital hypogonadotrophic hypogonadism need an additional subsidy of follicle stimulating hormone ( 5 ).

Partial failure exists generally milder symptoms, with larger testis volume and better virilization. The response to treatment will occur earlier. By genetic or idiopathic hypogonadotrophic hypogonadism is testicular size significantly less than where both anatomical and functional causes of hormone failure. Men in the last two groups have often undergone a normal onset of puberty, and hypogonadism have with most of these debuted in adulthood. Time to positive effect on spermatogenesis and detection of pregnancy in the partner seems to be significantly shorter in men who have undergone spontaneous puberty.

 

[John Bahlmer]

Male hypogonadotropic hypogonadism: factors influencing response to human chorionic gonadotropin and human menopausal gonadotropin, including prior exogenous androgens.
Ley SB, Leonard JM.

Abstract
Although testosterone (T) therapy is sufficient for maturation and maintenance of secondary sex characteristics in hypogonadal men, gonadotropins are required for stimulation of spermatogenesis. Thirteen men with hypogonadotropic hypogonadism received treatment with hCG, followed in 12 by the addition of human menopausal gonadotropin (hMG). All initially had undetectable serum LH and FSH and low T levels and were azoospermic with small testes. During therapy, all achieved normal male levels of T. Twelve of 13 had marked and continuous increase in testicular volume. Three men had sperm in the ejaculate with hCG treatment alone. All but 1 patient developed sperm in their seminal fluid during combined hCG and h

 

[John Bahlmer]

Pulsatile GnRH or human chorionic gonadotropin/human menopausal gonadotropin as effective treatment for men with hypogonadotropic hypogonadism: a review of 42 cases.
Büchter D1, Behre HM, Kliesch S, Nieschlag E.

Author information
Abstract
Stimulatory therapy with either GnRH or gonadotropins is an effective treatment to induce spermatogenesis and achieve paternity in men with secondary hypogonadism. However, there is still uncertainty about the optimal treatment modality and schedule, the duration of treatment necessary and the influence of interfering factors such as maldescended testes. We have extended our previous series of men treated for secondary hypogonadism and now present our therapeutic experience with 42 cases. Twenty-one patients with hypothalamic disorders (11 with idiopathic hypogonadotropic hypogonadism (IHH) and 10 with Kallmann syndrome (KalS)) were treated with GnRH (group Ia) or human chorionic gonadotropin (hCG)/human menopausal gonadotropin (hMG) (group Ib), and 21 patients with hypopituitarism (group II) were treated with hCG/hMG. A total of 5 7 treatment courses were initiated for induction of spermatogenesis, 36 of these for the purpose of induction of pregnancy in the female partner. Bilateral testicular volumes doubled within 5-12 months of therapy. Spermatogenesis as evidenced by the appearance of sperm in the ejaculate was induced in 54/57 courses. Pregnancies occurred in 26/36 courses. Unilaterally maldescended testes did not preclude patients with IHH or KalS from gaining fertility under therapy and spermatogenesis could be successfully initiated even in some individuals with bilateral maldescended testes. In general there was a tendency for a longer duration of therapy until induction of spermatogenesis in patients with a history of bilateral cryptorchidism. However, this did not reach statistical significance. In patients with IHH or KalS treated with either hCG/hMG or GnRH there were no statistically significant differences in terms of duration to appearance of sperm or pregnancy rates. Even in KalS patients as old as 43 years spermatogenesis could be induced. In repeatedly treated patients stimulation of spermatogenesis tended to be faster while time until induction of pregnancy was significantly shorter in the second treatment course. In conclusion, GnRH or hCG/hMG are effective therapeutic modalities for patients with IHH or KalS. It remains to be determined whether highly purified urinary gonadotropin preparations or recombinant LH and FSH will provide therapeutic advantages.


MG therapy. Two men achieved three pregnancies, and 2 more had semen that produced hamster oocyte penetration assays in the fertile range during the protocol period. Four of 5 who achieved sperm densities greater than 1 million/ml while receiving combined therapy maintained or increased sperm production while receiving continued hCG therapy after hMG was withdrawn. We examined the response to gonadotropin therapy of men who had received previous T therapy and those who had not. There were no differences in rapidity or degree of response, as assessed by rise in serum T, increase in testis volume, or maximal sperm density achieved. Multiple pituitary deficits and cryptorchidism were negative prognostic factors. In summary, the prognosis for successful stimulation of spermatogenesis in men with hypogonadotropic hypogonadism treated with hCG/hMG is good and not adversely affected by prior androgen treatment. Despite undetectable serum FSH levels, hCG treatment was sufficient to both initiate and maintain spermatogenesis in some patients.