Aspirin and Androgens Compilation (Anti-Peat-ish)

Green Dot

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This is just what I've personally found. I hope someone can refute these studies.

Effect of aspirin on semen quality: A review​

According to the PubMed data base, there are at least fifty published articles that link between aspirin and semen quality. However, such link has yet to be comprehensively discussed and summarised.

This work reviews and summarises the effect of aspirin on semen quality and sperm fertility characteristics, and hence on semen fertilising ability. To achieve this contribution, an electronic search of PubMed and Scopus databases was conducted for original manuscripts, presented from January 1974 through September 2019, via the keywords "aspirin" and "acetylsalicylic acid" versus "sperm" and "semen."

In summary, there is a scientific research consensus that reveals negative effects of aspirin on semen quality.

Still, clinical studies that directly examine the effect of aspirin on the main semen quality parameters are needed to support this conclusion.

Mechanistically, the negative documented effect of aspirin on semen quality parameters may be attributable to decreased synthesis of testosterone, reduced function of nuclear factor kappa-light-chain-enhancer of activated B cells, decreased formation of testicular prostaglandins, reduced production of seminal nitric oxide and increased oxidative injury to sperm.


Paracetamol, aspirin and indomethacin display endocrine disrupting properties in the adult human testis in vitro​

Study question: Do mild analgesics affect the endocrine system of the human adult testis?

Summary answer: Mild analgesics induce multiple endocrine disturbances in the human adult testis in vitro.

What is known already: Mild analgesics have recently been incriminated as potential endocrine disruptors. Studies of the effects of these widely used molecules on the androgenic status of men are limited and somewhat contradictory. This prompted us to investigate whether these compounds could alter the adult human testicular function. We therefore assessed in parallel the effects of paracetamol, aspirin and indomethacin on organo-cultured adult human testis and on the NCI-H295R steroid-producing human cell line.

Study design, size, duration: Adult human testis explants or NCI-H295R adrenocortical human cells were cultured with 10(-4) or 10(-5) M paracetamol, aspirin or indomethacin for 24-48 h. The effect of 10(-5) M ketoconazole, used as an anti-androgenic reference molecule, was also assessed.

Participants/materials, setting, methods: Testes were obtained from prostate cancer patients, who had not received any hormone therapy. The protocol was approved by the local ethics committee of Rennes, France and informed consent was given by the donors. Only testes displaying spermatogenesis, as assessed by transillumination, were used in this study. Hormone levels in the culture media were determined by radioimmunoassay (testosterone, insulin-like factor 3), Enzyme-Linked Immunosorbent Assay (inhibin B) or Enzyme Immunosorbent Assay [prostaglandin (PG) D2, and PGE2]. Tissues were observed and cells counted using classical immunohistochemical methods.

Main results and the role of chance: The three mild analgesics caused multiple endocrine disturbances in the adult human testis. This was particularly apparent in the interstitial compartment. Effective doses were in the same range as those measured in blood plasma following standard analgesic treatment. The production of testosterone and insulin-like factor 3 by Leydig cells was altered by exposure to all these drugs. Inhibin B production by Sertoli cells was marginally affected by aspirin only. Our experiments also revealed that mild analgesics display direct anti-PG activity, which varied depending on the drug used, the dose and the duration of exposure. Nevertheless, associations between the alteration of the PG and testosterone profiles were not systematically observed, suggesting that a combination of mechanisms of endocrine disruption is at play.

Limitations, reasons for caution: Our studies were performed in vitro.

Wider implications of the findings: We provide the first evidence that direct exposure to mild analgesics can result in multiple endocrine disturbances in the human adult testis. Caution, concerning the consumption of mild analgesics by men, should be strengthened, particularly in high-risk population subgroups such as elite athletes.


Paracetamol (acetaminophen), aspirin (acetylsalicylic acid) and indomethacin are anti-androgenic in the rat foetal testis​

More than half the pregnant women in the Western world report taking mild analgesics. These pharmaceutical compounds have been associated with congenital cryptorchidism in humans, the best-known risk factor for low semen quality and testicular germ cell cancer.

Furthermore, some of these mild analgesics exert potent anti-androgenic effects in the male rat and several endocrine-disrupting compounds, known to alter masculinization, have also been shown to be potent inhibitors of prostaglandin (PG) synthesis similar to mild analgesics.

Using a 3-day ex vivo organotypic model system based on gestational day 14.5 rat testes, we herein show that testosterone production was inhibited by paracetamol, at doses of 0.1 μm to 100 μm. Similar results were obtained for aspirin (1-100 μm) and indomethacin (10 μm). The production of the other Leydig cell hormone, Insl3, was not disrupted by exposure to paracetamol. Investigations of the gross anatomy of the testis as well as Leydig cells number and rate of gonocyte apoptosis after the 3 days of ex vivo differentiation showed no significant effect of the analgesics tested compared with controls.

These data indicate therefore that mild analgesics specifically inhibit testosterone production in rat foetal testes in vitro and that these compounds had no effect on gonocyte survival. Parallel determinations of prostaglandin D2 (PGD2) production indicated that the effects of paracetamol and aspirin on PGD2 and testosterone were not connected, whereas the effects of indomethacin were correlated.

We conclude that mild analgesics exert direct and specific anti-androgenic effects in rat foetal testis in our experimental setup and that the mechanism of action is probably uncoupled from the inhibition of PG synthesis.
 

Xref

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The review is of extremely low quality. I can't see any pictures of testis Leydig cell which usually indicate abnormality.
The one human example he mentioned had "NSAIDs (mainly aspirin)".
 

TheCedar1

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"Study design, size, duration: Adult human testis explants"

Don't bother at this point, if the testes were extracted from humans, obviously reducing prostaglandins would have a negative effect on T production, because the testes AREN'T EVEN CONNECTED TO THE ORGANISM AND THE ENDOCRINE SYSTEM

Prostaglandins are inflammatory markers, they get released as a response to inflammation around the body, including the testes, the prostaglandin pgd2 for example, is released when your leydig cells are dysfunctional to the point you don't produce T, so it gets released in an attempt to repair and restart T production. Having high PGD2 is actually a sign of testicular dysfunction, not high T.

Seriously, its like the aspirin rat studies online, they take explanted testes of animals, look for prostaglandins, and then automatically assume this applies to normal humans with a functioning endocrine system. Do better research
 

tankasnowgod

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Meanwhile, Haidut posted this study a while ago, showing that giving aspirin to humans (and not extracted testes from prostate cancer patients) lowers cortisol and increases testosterone-

 

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