Carole Hooven has posted this.
https://x.com/hoovlet/status/1943429446171599126?s=46
🧵"World Athletics drew up its rules in 2018 forcing Semenya and other female athletes with Differences in Sex Development to suppress their testosterone to be eligible for international women’s events." ABC News, today, reporting on a new ruling from the European Court of Human Rights. I'm less concerned with the ruling (you can read about it below) and more concerned with the reporting.
Semenya deserves to be treated with respect and dignity. But Semenya is fighting to compete as a female, against females, at the highest levels of sport. Given this, although it may be uncomfortable, the details of Semenya's condition deserve to be understood and accurately represented in the press and elsewhere. The narrative—that Semenya is a female who has been discriminated against because she happens to be blessed with naturally high testosterone levels—is false.
Semenya reaps the benefits of naturally produced male-typical testosterone because Semenya is male. Semenya has confirmed (see the next post) having XY sex chromosomes, undescended testicles, typical male testosterone levels, and what appears to be a vagina (albeit one that does not connect to a cervix, and without a uterus or fallopian tubes). This is all consistent with the condition called 5ARD (5-alpha reductase deficiency).
5ARD is caused by the lack of an enzyme (5-alpha reductase) that normally catalyzes the conversion of testosterone into to a more potent androgen, dihydrotestosterone, or DHT. DHT is what promotes the development of a penis and scrotum and the descent of the testes into the scrotum in fetal development, and in puberty, causes the growth of thick, dark and dense facial hair, acne, male-pattern baldness, and more. Without DHT, some aspects of physical appearance are feminized, like the skin, and certainly external genitalia.
Affected individuals have a body that responds to male levels of testosterone in all the ways that give males large physical advantages over females in sports: size, strength, power, hemoglobin, etc. (see last post in the thread). The female category exists specifically to protect the ability of females to have a shot at winning.
Accurate reporting on sex matters, especially when it comes to policies designed to protect women, whether in sports, prisons, or on the street.
And
Confirmation that a lack of DHT (the missing androgen in 5ARD) does not reduce strength (from a previous post):
TLDR: "Our data are consistent with studies that have reported no effects of 5α-reductase inhibitors on muscle or bone mass."
I've been asked if men with the DSD 5-ARD (in which ppl cannot convert testosterone into the more potent androgen DHT) experience the typical benefits of male puberty, that would give them an advantage in strength and speed relative to women. This is relevant to questions about whether male athletes with 5-ARD should be allowed to compete in the female category.
This is an excellent question, because it could be the case that DHT is necessary for the development and maintenance of male-typical muscle, lean body mass and strength. If that were the case, then people with 5-ARD might not have a typical male advantage, because the lack of DHT would perhaps lead to a more feminine pattern of fat, lean body mass and strength. I've wondered about this myself and have looked into the evidence.
Perhaps the top researcher in this area, Shalendar Bhasin, who is scrupulous in his methods, has examined this very question. The answer appears to be: no, testosterone does not need to be converted to DHT to exert its typical anabolic effects. These findings are reported in his 2012 study, "Effect of Testosterone Supplementation With and Without a Dual 5α-Reductase Inhibitor on Fat-Free Mass in Men With Suppressed Testosterone Production, A Randomized Controlled Trial." (It is linked to below—and since it's paywalled, I've included the graphs that show comparisons between the placebo and DHT— inhibited conditions, with no difference on the various outcomes.)
The investigators wanted to examine the effects of suppressing DHT on muscle mass, strength, and sexual function. This important because one of the treatments for benign prostatic hyperplasia and male-pattern baldness is to suppress DHT, but clinicians have been concerned about effects on other outcomes that affect health and quality of life. Participants (healthy men, 18 to 50, with normal T levels) had their T blocked, and were given graded doses of T, along with either placebo or a drug that blocked the conversion of T to DHT. So both groups had T, but only one, the placebo group, also had DHT.
After 20 weeks of treatment, changes in lean body mass, muscle, and strength were assessed. There were no significant difference between the placebo and DHT-blocked groups in these outcomes.
For LOTS more detail, here's the relevant text from the results. Please don't ask me questions about the study. Just look at the abstract and results which you can find by Googling. The main point is that while there are predicted effects of the different doses of T received, there were no differences in the outcomes according to whether they had DHT blocked (with dutasteride) or not (placebo).
"Fat-Free Mass Fat-free mass and lean body mass increased in a dose-dependent manner in the placebo and dutasteride [THIS IS THE DRUG THAT BLOCKS CONVERSION OF T TO DHT] groups (Figure 2). The changes in fat-free mass were related to testosterone dose and changes in testosterone concentrations in the placebo and dutasteride groups but did not differ between groups; the dose-adjusted mean difference (placebo minus dutasteride) in fat-free mass was 0.50 kg (95% CI, −0.22 to 1.22 kg; P = .18).
There was no significant interaction between testosterone dose and randomization to dutasteride or placebo, indicating a lack of evidence that the relationship of testosterone dose to change in fat-free mass differed between the dutasteride and placebo groups.
The model-based smoothed regression lines, obtained by generalized additive models, describing the relationship between changes in testosterone concentrations and changes in fat-free mass and lean body mass were similar in the placebo and dutasteride groups. Changes in fat mass were negatively related to testosterone dose and concentrations, but the relationship between change in fat mass and dose did not differ significantly between the placebo and dutasteride groups (P = .41; Figure 2)."
"Muscle strength Leg-press and chest-press strength increased dependently by dose in the placebo and dutasteride groups. Increases in leg-press and chest-press strength were greater with larger doses and higher concentrations of testosterone. These relationships did not differ between the placebo and dutasteride groups (Figure 2)."
Really interesting commentary from the authors on the role of DHT in adult men: "Why then did the steroid 5α-reductase system evolve for androgens?
Forty-six XY males with steroid 5α-reductase deficiency exhibited ambiguous or female external genitalia at birth and poor prostate development, but underwent normal muscle and bone development during pubertal transition. The phenotype of these patients suggests that steroid 5α-reductase plays an essential role in the development of prostate and phallus by providing local amplification of an androgenic signal without systemic hyperandrogenemia during critical periods of sexual differentiation, illustrating nature's extraordinary ingenuity in creating mechanisms for tissue-selective amplification during development.
We speculate that in adult men, in whom this tissue-specific amplification is not essential because the circulating testosterone concentrations are substantially higher than those in the fetus, testosterone and DHT can interchangeably subserve many androgenic functions. When circulating testosterone concentrations are low, intraprostatic DHT formation may become important in maintaining prostate growth, thus buffering the effects of decreasing testosterone levels, which has been suggested by Marks et al.
Our data are consistent with studies that have reported no effects of 5α-reductase inhibitors on muscle or bone mass. Inferences from these trials are limited by the fact that administration of 5α-reductase inhibitors increases testosterone levels, rendering it difficult to ascribe the outcomes to differences in DHT levels alone. In our trial, inhibition of endogenous testosterone by administration of a gonadotropin-releasing hormone agonist eliminated this problem. Additionally, the high-dose dutasteride regimen effectively inhibited both steroid 5α-reductase isoenzymes."
https://x.com/hoovlet/status/1943429451951337931?s=46