When your testicles have shrunk to the size of a cashew nut then it takes about a year to restore them and become fertile again.
Exogeneous T was once studied as a male contraceptive. The reason why it never took off is that fact that the effect it has on fertility is very different from one person to the other. While some still have decent numbers on TRT, some other stay infertile for life.
That’s wrong. It wasn’t used as a male contraceptive because it isn’t effective as a contraceptive. It also doesn’t take a year to get fertile again. You are speaking in facts that aren’t facts.
It is a contraceptive, the problem - as stated above - is the high intersubject variability in the inhibition of spermatogenesis.
And with prolonged use - when your testis are shrunk to the size of a nut - it can take up to 12 months or even longer to regain fertility.
And there are some reports on strucutal sperm defects after TRT or steroid abuse.
Patel et al., 2019
Unfortunately, the contraceptive effect of testosterone is not reliable. This has been proven in multiple studies, including two by the World Health Organization (WHO) Task Force on Methods for the Regulation of Male Fertility [14,15,25]. These two studies found an azoospermia rate of 64% to 75% in 6 months with testosterone enanthate [6,7]. A sperm concentration of 3 million/mL was used as a threshold for effective suppression of spermatogenesis in this study [14,15]. In a Chinese study of a monthly intramuscular TU injection, an azoospermia rate of 93% to 98% was achieved after 6 months with 1 million/mL as the criteria for effective suppression [25,26]. The different rates of azoospermia can be explained by the variable criteria and by ethnic differences in testosterone response [26,27]. These studies confirm the effectiveness of testosterone as a contraceptive, and provides evidence that men who desire fertility should not be prescribed TRT.
Kohn et al., 2018
A TMC of greater than 5 million sperm was achieved by 46 men (70%). Both increased age and duration of testosterone use directly correlated with time to sperm recovery at both 6 and 12 months of hCG/SERM therapy. Age more consistently limited sperm recovery, while duration of testosterone use had less influence at 12 months than at 6 months. Only 64.8% of azoospermic men achieved a TMC greater than 5 million sperm at 12 months, compared with 91.7% of cryptozoospermic men, yet this did not predict a failure of sperm recovery.
Liu et al, 2006
Multivariate Cox’s analysis showed higher rates of recovery with older age, Asian origin, shorter treatment duration, shorter-acting testosterone preparations, higher sperm concentrations at baseline, faster suppression of spermatogenesis, and lower blood concentrations of luteinising hormone at baseline. The typical probability of recovery to 20 million per mL was 67% (61-72) within 6 months, 90% (85-93) within 12 months, 96% (92-98) within 16 months, and 100% within 24 months.
McBride & Coward, 2016
Data specifically looking at recovery of spermatogenesis after cessation of AAS are scant, but case reports suggest that recovery is feasible within 4–12 months although some patients may require up to 24–30 months to return to sperm concentrations of >20 × 106 ml-1. It cannot be understated that given the inherent variability in patient characteristics and AAS agent(s) used, a uniform recovery of the HPG axis cannot be expected in all patients.
An interesting read is also Kovac et al, 2016
MEN REGRET ANABOLIC STEROID USE DUE TO A LACK OF COMPREHENSION REGARDING THE CONSEQUENCES ON FUTURE FERTILITY
DeSouza et al., 2001
Structural sperm and aneuploidies studies in a case of spermatogenesis recovery after the use of androgenic anabolic steroids
Histopathlogy
Experiments in animal models mainly report AAS‐induced Leydig cell alterations, but cellular morphology anomalies have also been reported 12. The decrease in this population of cells is accompanied by low testosterone and LH levels in all papers reviewed, especially in those papers reporting on adult animal models. Immunohistochemical findings have suggested decreased steroidogenesis in testicular tissue, hence spermatogenesis was considered unchanged by some other authors. Nethertheless, specific end‐stage spermatogenesis impairment, with a lack of advanced forms of spermatids, has been described 13. After AAS discontinuation, Leydig cells tend to proliferate but remain below the regular counts, even after longer periods 14. Clearly, long‐lasting, or possibly persistent effects of AAS use cannot be ruled out.
Impact on semen quality
The use of a combination of hCG and steroids is a common practice among AAS users. The goal is to avoid the impact of LH suppression after long‐term AAS administration, which may lead to a persistent state of hypogonadism and low‐quality semen. Restoration of spermatogenesis has been described; however more abnormal and hypokinetic spermatozoa are found, even after hCG ‘post‐cycle’ use, showing a potential for persistent alterations after the discontinuation of AAS use 15.
Apoptosis
Apoptosis has been reported to play an important role in the regulation of germ cell populations in the adult testis. Recently, the correlation between apoptosis and high AAS doses and exercises has been experimentally assessed in animal models. Shokri et al . report a significant increase in the rate of apoptosis after nandrolone administration, an increase clearly amplified by physical exercise 16. Shokri et al . also report an evident impairment in semen quality among the same set of individuals, in the same conditions. Testicular histopathological evaluation according to Johnsen’s method 17 has also been performed, revealing low quality spermatogenesis.
Aneuploidies and ultrastructural changes in spermatozoa
The innovative use of both transmission electron microscopy and fluorescence in situ hybridization (FISH) has recently been reported in an AAS user sperm sample, searching for genetic and ultrastructural consequences of steroid abuse. Immaturity, necrosis and apoptosis were assessed, and a high percentage of structurally normal spermatozoa were found, which showed the absence of a correlation between AAS and ultrastructural sperm changes. In contrast to these findings, FISH sperm analysis revealed XY and chromosomes 1 and 9 disomies, suggesting anomalies in the meiotic process and genetic damage among AAS users 18.
Moretti et al., 2007
Our findings confirm the recovery of spermatogenesis but suggest a possible relationship between altered meiotic segregation and the abuse of androgenic anabolic steroids.
@johann77
You posted 2000 words with some shit in bold to say it makes you have less sperm that not taking T but still enough sperm to get someone pregnant. I worked with the top fertility docs in NYC (I’m in medical device sales) and when I got on TRT I asked about fertility and they all said it’s basically zero chance that TRT alone can make you infertile for life. With the technology today they can get many people who were considered completely unable to have kids 10 years ago conceiving today.
I don’t mean that as a personal dig as I appreciate your consise contributions I just know there are many people under the assumption that TRT means they will never be able to have kids and will put off seeking the relief they need because of that. I was one of them.
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@dextermorgan
In a scientific discussion one provides data and evidence and not just a statement like this is shit.
I am posting medical/scientific literature which is a bit less biased then I have friends or I know somebody. The ‘shit in bold’ is from peer reviewed medical literature.
I have a PhD in biochemistry, 4 years postdoctoral training in molecular medicine, 4 years of experience in laboratory medicine, 10 years of experience in drug discovery and R&D and published 35 articles in journals like Cell and Nature. I know first hand of a clinical program which investigated into the option of exogeneous T as a contraceptive in the 2000s. It wasnt a 100% effective in preventing pregnancies (in agreement with the literature), and unfortunately 3 persons out of about 1500 participants couldnt reach a sperm count of 20 Mil/ml 36 months after discontinuation of T and thus were considered subfertile. None of them could achieve a life pregancy 48 months after discontinuation. Luckily they were able to have kids with the help of ART (testicular sperm aspiration in combination with ICSi), I think this is the technology you are referring to.
I am not saying that there is a high risk for permanent damage, I agree that typically spermatogenesis is kicking in 4 to 12 months after discontinuation, but I am saying that the risk is not 0.
I understand what you’re saying. I’m just saying that I believe you’re wrong.
@dextermorgan
I think you are a smart and educated men highly interested in the topic of TRT. And i appreciate your helpful input into this topic. I acknowledge that I wont be able to convince you, but maybe you anyhow find the time to read the following article, it needs only about 15 min and it is publicly available in PMC.
It the first study into sperm recovery after prolonged testosterone substitution. It presents a model to predict the probability to recovery to a meaningful number/conc of sperm depending on age and length of T use.
Have a great day @dextermorgan
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Will this make Test. Bioavailability increase? It was flagged low
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