Studies: Anabolic-steroid induced HTPA shutdown/azoospermia & recovery treatments

The following studies relate to treatments for anabolic steroid-induced HTPA shutdown and recovery.

Also, consider the fact that Finasteride is listed as a Testosterone analogue.

These documents may aid you with visits to doctors, to help you argue a case for boosting your post-Fin T levels.


Impotence related to anabolic steroid use in a body builder. Response to clomiphene citrate.
pubmedcentral.nih.gov/picren … obtype=pdf


Androgenic Anabolic Steroid Use and Severe Hypothalamic-Pituitary Dysfunction: a Case Study
thieme-connect.com/ejournals … 2003-39089

E. van Breda1, H. A. Keizer1, H. Kuipers1, B. H. R. Wolffenbuttel2
1 Department of Movement Sciences , Nutrition and Toxicology Research Institute Maastricht (NUTRIM), University, Maastricht, the Netherlands
2 Department of Endocrinology, University Hospital Maastricht, Maastricht, the Netherlands

The data of the present case demonstrate that the abuse of androgenic anabolic steroids (AAS) may lead to serious health effects. Although most clinical attention is usually directed towards peripheral side effects, the most serious central side effect, hypothalamic-pituitary-dysfunction, is often overlooked in severe cases.

Although this latter central side-effect usually recovers spontaneously when AAS intake is discontinued, the present case shows that spontaneous recovery does not always take place. We suggest that hypothalamic-pituitary dysfunction should always be considered in the differential diagnosis in athletes seen with typical presentation of anabolic steroid use.

In order to regain normal hypothalamic-pituitary function, supraphysiological doses of 200 μg LH-RH should be considered when the physiological challenge test with LH-RH (50 μg) fails to show an acceptable response.


Anabolic steroid induced hypogonadism treated with human chorionic gonadotropin
pmj.bmj.com/cgi/content/abstract/74/867/45
GV Gill
Endocrine Unit, Walton Hospital, Liverpool, UK.

A case is presented of a young competitive body-builder who abused anabolic steroid drugs and developed profound symptomatic hypogonadotrophic hypogonadism.

With the help of prescribed testosterone (Sustanon) he stopped taking anabolic drugs, and later stopped Sustanon also. [u]Hypogonadism returned, but was successfully treated with weekly injections of human chorionic gonadotropin for three months.

Testicular function remained normal thereafter on no treatment. The use of human chorionic gonadotropin should be considered in prolonged hypogonadotrophic hypogonadism due to anabolic steroid abuse. [/u]


Testicular responsiveness to human chorionic gonadotrophin during transient hypogonadotrophic hypogonadism induced by androgenic/anabolic steroids in power athletes.
ncbi.nlm.nih.gov/sites/entre … d_RVDocSum

Martikainen H, Alén M, Rahkila P, Vihko R.

Serum concentrations of testosterone, 17-hydroxyprogesterone, estradiol and several other unconjugated and sulphated steroids were analyzed before and after a single dose of hCG in 6 power athletes, who had used high doses of testosterone and anabolic steroids for 3 months.

The study was carried out 3 weeks after cessation of drug use, but the study subjects were still characterized by hypogonadotrophic hypogonadism.

The mean concentrations of serum LH and FSH were 2.6 +/- 0.3 and 1.1 +/- 0.03 mIU/ml (mean +/- SEM), respectively, and the concentrations of several precursors and metabolites of testosterone were lower than those before drug use.

In contrast, circulating concentrations of steroid sulphates were not decreased, with the exception of dehydroepiandrosterone sulphate.

After hCG injection serum testosterone and 5 alpha-dihydrotestosterone concentrations increased significantly, whereas no increases in estradiol and 17-hydroxyprogesterone concentrations were observed.

These results demonstrate that during transient hypogonadotrophism in adult men, the testicular responsiveness to a single injection of hCG is similar to that in prepubertal boys without any sign of steroidogenic lesion at the 17,20-desmolase step.

Therefore, the appearance of the possibly estradiol-mediated inhibition at the level of C21-steroid side-chain splitting in testosterone biosynthesis seems to be dependent on priming by gonadotrophins.

PMID: 3747510 [PubMed - indexed for MEDLINE]

Mew, I remember pointing out to you at some point before that research exists showing that finasteride has absolutely no affinity for the androgen receptor.

However: Dysfunction caused by finasteride appears to be the exception rather than the rule…Perhaps those for whom finasteride has caused HPTA shutdown have some sort of novel androgen receptor polymorphism that confers affinity to finasteride…that would be interesting…

While that may be true, the fact of the matter is a number of us here (including yourself) have or are experiencing hypogonadism/reduced T levels, similar to how some anabolic steroid users experience HTPA shutdown after coming off the juice.

All I’m saying is these treatments have been used to help AAS abusers recover, and thus might aid a person’s case with docs, when presenting with similar “low T” issues post-Fin.

Mew, nice finds!! Right on man, good idea!!!

So it sounds to me like maybe you are getting ready to go get some treatment??? No??

Current Concepts in Anabolic-Androgenic Steroids

ajs.sagepub.com/cgi/content/full/32/2/534


Selected bit:

Exogenous AAS administration produces a dose-dependent depression of luteinizing hormone and follicle-stimulating hormone via the negative feedback loop of the hypothalamic-pituitary-gonadal axis.46,56 The adverse endocrine effects are gender specific.

In males, this endocrine suppression can lead to hypogonadotrophic hypogonadism, testicular atrophy, reduced sperm count, decreased sperm motility, abnormal sperm morphology, infertility, and changes in libido.14,46,55 These effects generally worsen with larger doses of AAS taken for longer periods of time.56 This AAS-induced hypogonadal state is transient and reversible after discontinuation of AAS.96

However, restoration of hypothalamic-pituitary homeostasis, endogenous testosterone, and spermatogenesis takes between 3 and 12 months,14,46,55,96 and AAS-induced hypogonadism may require treatment with human chorionic gonadotrophin.34

AAS can also produce feminization (gynecomastia) in males, from the aromatization of exogenous testosterone to estrogen metabolites.

So now the call is for HCG.
Its Clomid, HCG, and Arimidex I think.
I wish I could get in with Shippen, and was close.

I wonder how many people (# of people) from this site have gone and been treated by Shippen for this shit…

On an offtopic note, why don’t Crisler or Shippen contact Merck about treating people with serious issues from fin-use? I saw one post on an internet board where Crisler informed about the symptoms his patients have after fin, but this information would be MUCH more useful if posted to Merck and the right authorities. No matter how small our minority is, anyone considering this drug should be informed about the potential dangers, even if the chance is extremely small. I for one would not have taken it had I known there was even a remote chance that it would lead to all this.

Good luck!
This same sort of thing is happening with the Lasik Eye surgery Dry Eye epidemic. People are having rough times with Lasik complications, dry eye being the most common. It is ruining people’s lives too, and people are not beimng properly informed. This is all because IT IS A BUSINESS… A business is not going to give someone the impression that ‘there is a chance this could happen to you’. Otherwise, anyone who can read, and with half a brain, would not take their chances.

I dont think Merck is going to risk losing business with their billion dollar money maker, ground breaking drug that is popular all over the world.

Idk, those are my thoughts

Selected passage below might be useful to bring with to a doctor’s appointment.

renalandurologynews.com/Anab … le/108887/

Anabolic Steroids: What Urologists Should Know

"… Because non-specialists may not be keeping up with the literature on this subject, it is up to the urologist to adjust the treatment regimen. This usually means using medications to “jump start” the pituitary gland’s production of LH.

Commonly used agents are clomiphene citrate (Clomid) and LH analogs such as human chorionic gonadotropin (HCG), sometimes with synthetic FSH treatment. Aro-matase inhibitors also may be enlisted to combat low testosterone levels in infertile males. All these medications require careful monitoring by the urologist."

FULL PDF: nature.com/ijir/journal/v15/ … 00981a.pdf

Clomiphene increases free testosterone levels in men with both secondary hypogonadism and erectile dysfunction: who does and does not benefit?
Clomiphene increases free testosterone levels in men with both secondary hypogonadism and erectile dysfunction - who does and does not benefit.pdf (134 KB)

2006 - Complete reversal of adult-onset isolated hypogonadotropic hypogonadism with clomiphene citrate

fertstert.org/article/PIIS00 … 7/fulltext

PDF attached.
Complete reversal of adult-onset isolated hypogonadotropic hypogonadism with clomiphene citrate.pdf (286 KB)

ooooo Mew that is a good one…going through it right now…interesting…

So what is does tell us about our sitaution. I mean how it can be applied to our sitatuation. can we cure our selves this way?