Aspirin & hCG

[Michael Scally MD]

So, while I am stirring the pot, is there any concern for taking ASA (Aspirin) while using hCG?

 

[CensoredBoardsSuck]

Re: Comprehensive Guide to PCT

So, while I am stirring the pot, is there any concern for taking ASA (Aspirin) while using hCG?

Am J Physiol. 1999 Dec;277(6 Pt 1):E1032-7.
Aspirin inhibits androgen response to chorionic gonadotropin in humans. Aspirin inhibits androgen response to chorionic... [Am J Physiol. 1999] - PubMed - NCBI
Conte D1, Romanelli F, Fillo S, Guidetti L, Isidori A, Franceschi F, Latini M, di Luigi L.

Abstract

Eicosanoids play an important role in the regulation of the hypothalamic-pituitary axis; less clear is their role in testicular steroidogenesis. To evaluate the involvement of cyclooxygenase metabolites, such as prostaglandins, in the regulation of human testicular steroidogenesis, we examined the effects of a prostaglandin-blocker, aspirin, on plasma testosterone, pregnenolone, progesterone, 17OH-progesterone, androstenedione, dehydroepiandrosterone, and 17beta-estradiol response to human chorionic gonadotropin (hCG) in normal male volunteers in a placebo-controlled, single-blinded study. To test the efficacy of aspirin, seminal prostaglandin E(2) levels were also determined. hCG stimulation increased peripheral levels of testosterone, 17OH-progesterone, androstenedione, dehydroepiandrosterone, and 17beta-estradiol, without affecting circulating pregnenolone and progesterone values. Aspirin significantly lowered seminal prostaglandin E(2) levels, whereas it did not modify steroid concentrations not exposed to exogenous hCG. Moreover, the drug significantly reduced the response of testosterone, 17OH-progesterone, androstenedione, and dehydroepiandrosterone to hCG, as assessed by the mean integrated area under the curve, whereas it did not influence 17beta-estradiol response. In conclusion, aspirin treatment inhibits androgen response to chorionic gonadotropin stimulation in normal humans. The action of aspirin is probably mediated via an effective arachidonate cyclooxygenase block.

 

[ApeShitFuckJacked]

Re: Comprehensive Guide to PCT

Thanks Scally and CBS that is actually very important info.

Lots of guys take aspirin and wouldn't even think twice.

Especially bros with inflamed joints.

 

[Michael Scally MD]

Moreover, the drug significantly reduced the response of testosterone, 17OH-progesterone, androstenedione, and dehydroepiandrosterone to hCG, as assessed by the mean integrated area under the curve, whereas it did not influence 17beta-estradiol response.

The E2 just caught my eye! Why?

Damn, CBS, I need to go back and reread and review.

 

[MythotiK]

Very interesting, thank you sir's

 

[CensoredBoardsSuck]

We report that mild analgesics at pharmaceutical doses can directly cause multiple endocrine disturbances in the human adult testis, particularly in the interstitial compartment. The three molecules tested exerted both anti-androgenic and anti-prostaglandinic effects, somehow differing according to their nature, and to some extent, according to their dose. Paracetamol appeared to be the weaker inhibitor of PG secretion, and not to disrupt INSL3 production, whereas INSL3 production was inhibited by aspirin and 10?4 M indomethacin. Consistent with the anti-androgenic effect on cultured human testis, and as a validation for these observations, we found that mild analgesics also reduced steroidogenesis by 10–43% from the control values in human steroid-producing NCI-H295R cells.



We report the first evidence that direct exposure to mild analgesics can result in several endocrine disturbances, causing an unbalance in the hormonal activity of the adult testis in short-term culture. The active doses of analgesics were of the same order of magnitude as plasma concentrations during standard analgesic intake. Our study demonstrates that the testicular PG system is highly susceptible to these molecules. However, the interactions between different testicular hormones under COX-disruptive conditions, in particular the relationship between PGs and testosterone, remain unclear. Our findings are consistent with the concerns recently raised both by epidemiological studies on mild analgesic consumption and by in vitro experiments on the potential targeting of PGs by endocrine disruptors. The present in vitro results highlight the risks associated with the abusive use of mild analgesics for the testicular endocrine system in men.
​

Hum Reprod. 2013 Jul;28(7):1890-8.
Paracetamol, aspirin and indomethacin display endocrine disrupting properties in the adult human testis in vitro. http://www.medscape.com/viewarticle/808447
O. Albert, C. Desdoits-Lethimonier, L. Lesné, A. Legrand, F. Guillé, K. Bensalah, N. Dejucq-Rainsford, B. Jégou


Abstract and Introduction

Abstract

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.









Hum Reprod. 2012 Apr;27(4):1191-201.
Intrauterine exposure to mild analgesics during pregnancy and the occurrence of cryptorchidism and hypospadia in the offspring: the Generation R Study. Intrauterine exposure to mild analgesics during p... [Hum Reprod. 2012] - PubMed - NCBI
Snijder CA1, Kortenkamp A, Steegers EA, Jaddoe VW, Hofman A, Hass U, Burdorf A.

Abstract

BACKGROUND: Recently, over-the-counter mild analgesic use during pregnancy has been suggested to influence the risk of reproductive disorders in the offspring. We examined the influence of maternal exposure to mild analgesics during pregnancy on the occurrence of cryptorchidism and hypospadia in their offspring.

METHODS: Associations between maternal exposure to mild analgesics during pregnancy and cryptorchidism or hypospadia in the offspring were studied in 3184 women participating in a large population-based prospective birth cohort study from early pregnancy onwards in the Netherlands (2002-2006), the Generation R Study. Cryptorchidism and hypospadia were identified during routine screening assessments performed in child health care centres by trained physicians. The use of mild analgesics was assessed in three prenatal questionnaires in pregnancy, resulting in four periods of use, namely, periconception period, first 14 weeks of gestation, 14-22 weeks of gestation and 20-32 weeks of gestation. Logistic regression analyses were used to study the associations between maternal exposure to mild analgesics and cryptorchidism and hypospadia.

RESULTS: The cumulative prevalence over 30 months of follow up was 2.1% for cryptorchidism and 0.7% for hypospadia. Use of mild analgesics in the second period of pregnancy (14-22 weeks) increased the risk of congenital cryptorchidism [adjusted odds ratio (OR) 2.12; 95% confidence interval (CI) 1.17-3.83], primarily due to the use of acetaminophen (paracetamol) (adjusted OR 1.89; 95% CI 1.01-3.51). Among mothers of cryptorchid sons, 33.8% reported (23 of 68) the use of mild analgesics during pregnancy, compared with 31.8% (7 of 22) of mothers with a boy with hypospadia and 29.9% (926 of 3094) of mothers with healthy boys.

CONCLUSIONS: Our results suggest that intrauterine exposure to mild analgesics, primarily paracetamol, during the period in pregnancy when male sexual differentiation takes place, increases the risk of cryptorchidis





Epidemiology. 2010 Nov;21(6):779-85.
Maternal use of acetaminophen, ibuprofen, and acetylsalicylic acid during pregnancy and risk of cryptorchidism. Maternal use of acetaminophen, ibuprofen, and a... [Epidemiology. 2010] - PubMed - NCBI
Jensen MS1, Rebordosa C, Thulstrup AM, Toft G, Sørensen HT, Bonde JP, Henriksen TB, Olsen J.

Abstract

BACKGROUND: Cyclooxygenase (COX) inhibitors-acetaminophen, ibuprofen and acetylsalicylic acid-have endocrine-disruptive properties in the rainbow trout. In humans, aspirin blocks the androgen response to human chorionic gonadotropin (hCG), and, because hCG-stimulated androgen production in utero is crucial for normal testicular descent, exposure to COX inhibitors at vulnerable times during gestation may impair testicular descent. We examined whether prenatal exposure to acetaminophen, ibuprofen, and acetylsalicylic acid was associated with increased occurrence of cryptorchidism.

METHODS: Our study used data on 47,400 live-born singleton sons of mothers enrolled in the Danish National Birth Cohort during 1996-2002. Cryptorchidism was identified in 980 boys during childhood, of whom 565 underwent orchiopexy. The use of acetaminophen, ibuprofen, and acetylsalicylic acid during pregnancy was assessed in 3 computer-assisted telephone interviews and 1 self-administered questionnaire. We estimated adjusted hazard ratios (HRs) of cryptorchidism by Cox regression analysis.

RESULTS: Exposure to acetaminophen during both the first and second trimesters was associated with increased occurrence of cryptorchidism (HR = 1.33 [95% confidence interval = 1.00-1.77]). Exposure for more than 4 weeks within the postulated time-window of programming testicular descent (gestational weeks 8-14) was associated with a HR of 1.38 (1.05-1.83) for cryptorchidism. Exposure to ibuprofen and acetylsalicylic acid was not associated with cryptorchidism.

CONCLUSION: Maternal intake of acetaminophen for more than 4 weeks during pregnancy, especially during the first and second trimesters, may moderately increase the occurrence of cryptorchidism.