There was a bit of confusion yesterday involving my post about the defeat of Italian female boxer Angela Carini by Algerian boxer Imane Khelif, who in all likelihood is male but identifies as female. The bout was over in 42 seconds after Khelif delivered a few powerful blows to Carini’s head. She then refused to shake hands with Khelif, cried, and then explained that she was fighting for her late father (she later apologized for the unsportswomanlike gesture of not congratulating her opponent). Most of the videos that accompanied the tweets have been taken down by the Olympics for copyright reasons, but I found one on Emma Hilton’s site:
The first thing I’d like to clear up is my use of the word “transwoman” to refer to Khelif. I meant it to refer to the big brouhaha in sport and gender, which refers to the contested presence of genuine transwomen (i.e., natal males who transition to a female gender identity) competing against women in women’s sports. I kept using the term when applying it to Khelif, but Khelif may indeed have assumed that he/she was a biological female since birth, since Khelif was raised as a female from birth in Algeria. If that’s the case, then Khelif didn’t really “transition”. If you use the “trans” term loosely, I suppose you could say that Khelif transitioned from the biological condition of being a male to having the identity of a woman, but since this wouldn’t have been a conscious transition, I thus gladly retract the use of the term “transwomen” for Khelif. One could, I suppose, call Khelif an “intersex” person, but those afflicted with disorders of sex development (DSDs) prefer the term “person with a disorder of sex development”. Also, definitions of “intersex” vary among researchers.
But that’s a semantic issue. The main question is this: was Khelif a biological male, went though male puberty, and then wound up with the strength, size, speed, and punch-strength advantages that go along with male puberty—advantages that do not go away fully even with testosterone-suppression? All evidence points to “yes”, and my judgment was based on the fact that Khelif had an XY karyotype, the physical appearance and size of a man, and had previously failed testosterone tests and, on that basis, was denied the opportunity to box women.
Now the only way to ascertain for sure what Khelif’s sex was is to do an ultrasound or some kind of noninvasive examination to see if there are ovaries (making a female) or testes (making a male) or both (making a very rare hermaphrodite). This hasn’t been done, but the conclusion of those with more expertise than I is that it’s probable that Khelif was a biological male with a DSD and had gone through male puberty, thus having the same advantage against biological women as either a transwoman or, in Khelif’s case, a male afflicted with a DSD who has suppressed his testosterone. If this is the case, the Olympics screwed up in its last-minute method of determining whether an athlete can compete against biological women (the IOC has said that each sport should make its own rule). At the bottom I say what I would judge to be necessary and sufficient tests to determine whether a person is qualified to compete against biological women.
Let’s look at someone who knows the ins and outs of this: Carole Hooven of Harvard University, author of the well known book T: The Story of Testosterone, the Hormone that Dominates and Divides Us. There is a chapter on sports and gender, too. It’s an excellent book and I recommend it highly.
Hooven issued a long tweet yesterday explaining Khelif’s likely condition. And yes, Khelif appears to be a male with a DSD. Go to the tweet to read the whole thing:
Here’s an excerpt from the long tweet (my bolding). Note that it’s all about one particular DSD, suggesting that this is what Hooven thinks that Khelif has:
First: People living with DSDs should be treated with compassion and understanding, and receive any heath care they need. These can be challenging conditions for individuals and their families. But when male athletes have DSDs that give them an advantage over females, and they compete in the female category, this raises concerns about safety and fairness, and forces discussion of the relevant physical traits.
Athletes with XY DSDs who have testes (usually internal), XY sex chromosomes, male-typical levels of testosterone, and functional androgen receptors are often described as females with “hyperandrogenism,” i.e., abnormally high levels of testosterone. They experience physical benefits of this high testosterone during puberty, which translate into athletic advantages over females. The issue for sports is that athletes with the XY DSD 5-alpha reductase deficiency (5-ARD), may be socialized as female, may be legally female, and may live and identify as female; but they are male.
These individuals are usually born with female-appearing genitalia, which can lead to being sexed as female. Here’s why. 5-ARD is caused by a mutation in the gene that codes for the enzyme 5-alpha reductase, which converts testosterone into a more potent androgen, DHT. This androgen interacts with the androgen receptor, like testosterone, and is necessary for the typical development of male external genitalia (penis and scrotum) and the prostate. Without DHT, female-typical external genitalia develop. At the end of this monster post is a graphic of the relevant steroid production pathway, from my book T: The story of Testosterone.
DHT is also responsible for male-pattern baldness and dark, coarse facial hair, which is why people with the condition have smooth skin that can give a feminine appearance.
The “decision makers” are aware that athletes with 5-ARD are male, and that they experience the benefits of male puberty. The requirement to reduce their testosterone to typical female levels isn’t discriminatory, since these are males who are asking to compete in the female category. But more significantly, all the relevant scientific evidence shows that reducing male T in adulthood does not undo the physical benefits of male puberty.
And the relevant reference:
Here’s more detail about T, DHT, and male advantage in strength and speed.
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 paper is actually free; click on the link below to go to it, and follow the link to “get pdf” or go to the pdf directly here:
The paper shows, as Hooven notes above, that this DSD has its normal effects on the body even though testosterone isn’t converted to the androgen DHT. In other words, 5-ARD males produce testosterone that, even though not converted to DHT, sill has its normal effects on masculinizing the body.
A bit on the condition from the National Library of Medicine:
The presentation of patients with a deficiency of 5α-RD2 can vary. This condition is an autosomal recessive disorder of sex development associated with the mutation in the SRD5A2 gene. No direct association has been seen between the phenotype and the genotype in this disorder. Two individuals with the same gene defects in SRD5A2 can present with completely different phenotypes. This shows that other additional genes probably control the phenotype and the gene under discussion.[8]
The newborns might have genitalia resembling labia majora, which would be unfused labioscrotal folds. The phallus in these children may look more like a clitoris than a penis.[9] At the same time, the internal genitalia in these children include seminal vesicles, epididymis, vas deferens, and ejaculatory duct, and one may not see any Mullerian structures. The testes in these children might be present in the inguinal sac, and very rarely, they can also be found within the abdomen. These children tend to be raised as females until puberty, when they start exhibiting virilization.[5] At puberty, the phallus may grossly enlarge to form a penis, the testes may descend into the unfused labioscrotal folds, the voice deepens, and a beard starts growing. The development of all these secondary sexual characteristics during puberty does not need the presence of DHT but only the presence of testosterone.[9]
Carole also gives a strong recommendation to this free podcast:
So the questions that people are probably asking (my questions and my answers):
a.) Does Khelif have a DSD? Almost certainly, since the chromosomes, testosterone levels, and physiognamy suggest that Khelif is a biological male, but the genitalia probably are female-like, although we don’t know for sure. At any rate, there was some phenotypic trait that caused Khelif to be raised as a female.
b.) Was the DSD XY DSD 5-alpha reductase deficiency (5-ARD)? It’s likely since Hooven discusses it at length. This is in fact the same DSD that Caster Semenya had: according to the BBC:
The 2018 rules meant that Semenya could not compete in female track events over this distance without taking testosterone-reducing drugs.
She appealed against World Athletics’ proposal at the Switzerland-based Court of Arbitration for Sport (Cas), but eventually lost in what amounted to a landmark case in 2019.
It was in the Cas ruling that Semenya’s specific DSD was confirmed as 46 XY 5-ARD (5-alpha-reductase deficiency). People with this particular DSD have the male XY chromosomes. Some are assigned female or male at birth depending on their external genitalia.
Semenya told BBC Sport that she was “born without a uterus” and born “with internal testicles” and said: “I am a woman and have a vagina”.
Cas said, external athletes like Semenya with 5-ARD have “circulating testosterone at the level of the male 46 XY population and not at the level of the female 46 XX population”, which gives them “a significant sporting advantage over 46 XX female athletes”.
Given that Semenya has the equipment (though perhaps not the ability) for making sperm, Semenya is biologically male. So is Khelif, though people are loath to say it or use the pronoun “he” (check their Wikipedia entries). It’s possible that Khelif has another DSD, PAIS D (partial androgen insensitivity syndrome), but this is less likely based on phenotype; and this condition is rarer.
. . . which leads us to the next question:
c.) Is Khelif a man? if he has 5-ARD and went through male puberty, producing testosterone at higher male levels (these don’t overlap with female levels), levels that require suppression to meet sports standards, the answer is yes. Female-like genitalia don’t make someone a biological woman if they have testes (see above).
But there is one last question, and the most relevant one.
d.) Should Khelif be competing in women’s boxing? Given what we know of his size, strength, and performance, as well as his XY status and what must have been high testosterone, the answer is, at present, no. Suppressing testosterone in his case will not eliminate any athletic advantages Khelif accrued by going through male puberty. But further investigation would be useful (see below).
e.) How should sports organizations determine if someone has a sex-based athletic advantage? Ideally, it should be a three-part test. First, are there testes or ovaries? If there are testes, that’s already a sign of male advantage, particularly when accompanied by an XY karyotype. Further tests can examine testosterone levels and exposure as well as sequencing of the DNA to see if there are genetic mutations causing DSDs. But there’s already enough information from Khelif’s obvious athletic advantages and his XY karyotype to mandate banning him/her from boxing until these other issues are examined.
Finally, let me add that most people having DSDs are not athletes in the limelight, and in fact have to deal with medical, emotional, and social issues that arise in conjunction with having DSDs. These people should not be regarded as freaks, have the same moral and legal equality as the non-afflicted, and should be treated with empathy
h/t: Carole Hooven for discussion and clarification
