Puberty blockers

This is a page where I intend to collect peer-reviewed evidence about puberty blockers and related issues.

I am very interested to read peer-reviewed studies on the effects of puberty blockers on trans children. If you know of any, please contact me.

What are they?

Puberty blockers are also known as a "gonadotropin-releasing hormone agonist" (GnRH agonist). Non-proprietary (non-commercial) names often end in "-relin".

An agonist is a substance that mimics a naturally occurring substance and causes the same reaction in a receptor cell as the natural counterpart would.

A gonadotropin is the name for various hormones (-tropin) produced by sex organs (gonado-, i.e. of the gonads) in males and females.

A GnRH agonist can therefore cause an increase or decrease in the production of a specific sex hormone. Puberty blockers cause a decrease in the hormones that cause sperm production, ovum production, and the physical changes of puberty in both males and females.

Long term effects of puberty blockers on fertility

In all sexes

"Transgender adolescents may wish to preserve fertility, which may be otherwise compromised if puberty is suppressed at an early stage and the patient completes phenotypic transition with the use of cross-sex hormones." Source, 2014.

• This means that puberty blockers alone do not compromise fertility. In order for fertility to be compromised, puberty blockers must be replaced with cross-sex hormones. If puberty blockers are stopped, fertility would return.

In desisting males

• 9 males, treated for precocious puberty (not trans). They stopped taking the puberty blockers in early teens, and sperm production was normal thereafter. Peer-reviewed study, published 2000.
  • "No alteration in semen analysis was found (n=6, sperm count, 106/ml: 52.0 ± 18.7; normal motility (%): 49.5 ± 18.7; atypical morphology (%): 44.5 ± 11.4)."
  • It should be noted that these males stopped taking the puberty blockers earlier than I suspect desisting trans teens would. (Early teens and late teens respectively.)

• 'In adult men with gonadotropin deficiency, sperm are noted in seminal fluid by 6 to 12 months of gonadotropin treatment. However, sperm numbers when partners of these patients conceive are far below the “normal range”.' Article, 2017.
  • Source 1, 1998, 42 males. "Spermatogenesis as evidenced by the appearance of sperm in the ejaculate was induced in 54/57 courses." This is a study comparing treatment methods for males who do not produce enough gonadotropin naturally and suffer infertility as a result. The focus was testicular volume and pregnancy outcomes. Treatment resulted in a higher pregnancy rate and an increased testicular volume.
  • Source 2, 1999, 8 males. "Among the eight men who commenced r-hFSH treatment, seven demonstrated sperm output at a median of 6 months and five achieved the target sperm output ... at a median of 9 months of FSH treatment. ... Three men produced pregnancies in their partners ... We conclude that r-hFSH is well tolerated and effective in inducing testis growth, spermatogenesis and fertility in gonadotrophin-deficient men."
  • Note: An adolescent male taking GnRH agonists to reduce sex hormones (such as a young teen on puberty blockers for trans-related reasons) could be said to have a gonadotropin deficiency, and one might extrapolate from this study that a male taking a GnRH agonist to reduce sex hormones may also experience a lower sperm count when he desists and his natural and healthy gonadotropin levels assert themselves. However, I'm not a doctor but I feel I should mention that a young teen having sex hormones suppressed and then unsuppressed in adulthood (as in the case of an adolescent male who concludes that he isn't transgender) is a different situation than an adult male who has naturally been low in gonadotropin for his adult life and is taking an agonist to attempt to correct that. Therefore, this evidence is indirect, and the conclusion that a male might have a low sperm count after taking puberty blockers for a short time is an assumption. The evidence would also lead to the assumption that fertility may be reduced and not negated in the majority of cases; the results of the above studies suggest that testicular volume would increase (as in puberty) and sperm would start to be produced, even if gonadotropin were introduced after the age of 16 and indeed far into adulthood.

In desisting females

In females with precocious puberty no infertility has been observed after taking puberty blockers; menstruation, uterus and ovary size, ovulation rates and fertility rates are normal when they resume. There is no information about how long it takes for ovulation to develop or resume.

• Peer-reviewed article (2017). "The primary risks of pubertal suppression in GD/gender-incongruent adolescents may include ... compromised fertility if the person subsequently is treated with sex hormones" (i.e. puberty blockers are not sterilising on their own).
  • source 1 (2008), 87 females.
  • source 2 (2010), 92 females.
• Note: These cisgender girls stopped taking puberty blockers in order to start puberty at a typical age, earlier than one would generally expect adolescent females to stop taking puberty blockers upon concluding that they are not trans. (Early teens and late teens respectively.) However, the length of time the puberty blockers were taken by the cis girls in these papers is comparable.