Those people who use their public platforms to argue that the case is not proven for testosterone (T) being a performance enhancer (PE) for genetic females, are either several studies short of a valid opinion, and/or are beating an ideological drum with one hand and with the other, conducting a chorus that loudly proclaims all those who have concerns about women’s sports are ignorant and / or bigots.
There has been loud condemnation of an Otago University study which calls for a weighting system to be introduced to allow transgender women (TW) to compete fairly in female sports events. This has been attacked by various people – including some extremely problematic claims of incompetence and /or bigotry. Some people have allowed their ideological fervour to cloud their judgment to the point where, if I were them, I’d be worried about a libel suit.
Jack Byrne, a human rights researcher at Trans Action, in an RNZ piece, cited a 2014 study (drawing on data collected in 2011) that was published in The Journal of Clinical Endocrinology and Metabolism.
Byrne claimed the study showed "no clear scientific evidence proving that a high level of testosterone is a significant determinant of performance in female sports," and he further claimed that a literature review in Sports Medicine found no direct and consistent research that transgender female athletes have an advantage in sport. (1)
Apart from the highly selective nature of that quote, the 2014 study claimed no such thing and it is worrying that RNZ, as NZ’s flagship of quality journalism, seems either not to have read the study, or chose to ignore both its purpose and its findings.
The study was concerned with “establishing valid normative serum androgen values” – i.e. a standard reference range (SRR) for elite female athletes – "to help develop the blood steroidal model of the Athlete Biological Passport and by so doing, to improve policies around hyperandrogenism in female athletes."
It was not directly concerned with the issues around transgender athletes who compete in female events; it did not screen for a Y chromosome, and nor did it carry out specific diagnostic tests for polycystic ovary syndrome (PCOS) an endocrine disorder which elevates T levels and has implications for female reproductive health.
The statement Byrne was drawing on is :
“With the exception of data extracted from doping programs in female athletes in the former German Democratic Republic (GDR), there is no clear scientific evidence proving that a high level of T is a significant determinant of performance in female sports.”
That data has been used both to demonise the GDR and as the basis for sports governing bodies' and the World Anti-Doping Agency's (WADA) ban on all anabolic and androgenic substances.
If that data is now being claimed to not be clear scientific evidence proving that a high level of exogenous T is a significant determinant of performance in female sports- then all criticism of the GDR should cease immediately because it has been exposed as pure agit prop.
But, the truth is that exogenous T is a potent performance enhancer in genetic females – for evidence of that you only have to look at what happens to the strength related athletic performance of trans men (genetic females who transition) who are granted an automatic therapeutic use exemption (TUE) for exogenous T use, and for whom there are no limits on that use in competition. (Obvious health implications aside)
There is also strong evidence to suggest that higher endogenous T levels enhance performance, in power events especially.
A study of endurance athletes cited in the 2014 study reported that the:
“hyperandrogenic subgroup (T concentration 1.9 ± 0.2 nmol/L) showed a more anabolic body composition, a higher total bone mineral density (BMD), and upper to lower fat mass ratio as well as the highest maximal oxygen uptake and performance values in general than did oligomenorrheic or amenorrheic athletes with normal androgen levels (1.1–1.2 ± 0.4 nmol/L).”
The researchers also cited other studies that have reported an almost 2 to 1 over-representation of women with PCOS in female Olympic athletes (37% vs 20% in the general population). Importantly, "the PCOS subgroup showed a higher T concentration and free androgen index than those observed for regularly menstruating or non-PCOS Olympian athletes.”
They concluded:
“This last recruitment bias supports the assumption that there is an ergogenic effect of T in high-level female athletes.” (2)
Although the 2014 study was not designed to diagnose PCOS, the researchers felt that several of the athletes in the study had this endocrine disorder. (3)
“In our present cohort, the 99th percentile for T concentration is calculated at 3.08 nmol/L. It is close to the 2.78 nmol/L threshold proposed as one of the criteria for the diagnosis of PCOS and the 3.0 nmol/L cutoff proposed by others to detect hyperandrogenism.”
They also noted that the calculated prevalence of athletes with a hyperandrogenic 46 XY DSD in their cohort gave them a ratio of 7.1 per 1000. Because they did not screen for SRY, they note that the actual prevalence of 46XY DSD was possibly even higher. (4)
In light of studies that have estimated a 46 XY DSD occurrence at a rate of 1 in 20,000 in the general population, this study’s reported prevalence is approximately 140 times higher than expected in the general population.
The researchers noted that the 46XY athletes in their study tended to be younger and showed a higher T concentration than the female athletes who were known to have been doping.
In summary: the researchers noted the significantly higher proportion of elite female athletes whose T level was at or above the diagnostic level PCOS plus, what appears to be a highly skewed representation of athletes with a 46XY DSD. (5)
It may be argued that this study does not categorically prove T is a PE for genetic females but it provides strong evidence to suggest it is nonsensical to argue that it proves it is not.
The fact remains - and this is an issue the Otago researchers have tried to grapple with - if there were not separate events for women and men - in most sports, women would never make the podium.
The background to this is complicated. The IOC and IAAF adopted a quick and arbitrary solution to the complex organisational and ethical problems posed by both athletes with 46 XY DSDs and transgender athletes competing in female sports, which was to set a limit for all competitors in female events of below 10 nmols/L ie the lower end of the male SRR - unless athletes were able to prove they had complete androgen insensitivity.
This arbitrary definition was chosen in the absence of normative statistics of androgen levels in an elite athlete female population – hence the 2014 study.
A study "Serum androgen levels and their relation to performance in track and field" was commissioned by the IAAF after its hyperandrogenism rule was challenged in the Court of Arbitration for Sport. The study which has been criticised for methodological flaws, found there was a performance advantage to female athletes with higher endogenous T level in several track and field events, ranging from 4.5% to 1.2%.
The IAAF/IOC then complicated the matter further this year by lowering the level to 5 nmols/L for some track events only, which was perceived as targeting a specific cohort of African middle distance runners, Caster Semenya among them. (6)
There is a range of factors which enable people to reach elite levels of any given sport; some are naturally occurring physiological advantages, others are cultural and socio-economic. Sports is not a level playing field but the single biggest divider is the performance difference between female and male athletes – averaging 10-12% and rising to 25% in power events like weight lifting.
Against the blithe and often spectacularly ill-informed or ideologically motivated assertions that testosterone is not a proven factor in female athletic performance, transgender athlete Kristin Worley, who surgically transitioned in 2001, successfully argued for an increase, on health grounds, in the amount of exogenous testosterone her sporting body (the UCI) permitted her to take. (7)
Others, like Rachel Mackinnon, argue that any imposed limit on endogenous testosterone is a violation of trans women’s human rights, ie only TW should determine their levels of androgen suppression, if any.
Clearly for both of these cohorts of people who went through a male puberty - in which the average athletic advantage that males have over females is triggered by testosterone - the amount of androgens and ratio of male to female hormones that their genetically male bodies need in order to be able to perform athletically and to maintain general health, is of great concern.
Having had an orchiectomy, athletes like Worley no longer produce any appreciable amount of T naturally and some want to increase the allowed exogenous level to enable them to compete at a level commensurate with their competitive drive - which may be highly problematic if, as some have argued, exogenous T is a more potent performance enhancer than endogenous T.
Some TW athletes, like MacKinnon, who have not had an orchiectomy see any requirement to reduce TW’s endogenous T to be unfairly discriminatory given other women have no imposition on their naturally occurring T.
The point in question here is whether higher T levels and going through a T triggered and fuelled puberty – and possibly even the possession of the Y chromosome itself - confers an average performance advantage (PA) over 46XX women.
We may all agree that performance advantage is complex and multi-faceted and that the PA of trans women and 46XY DSD women with partial androgen insensitivity will not be as great as that of genetic males, but it is highly likely to be enough to skew female sports significantly – especially in events in which power and strength are major factors.
Notes:
(1) Byrne is not the only person to misrepresent this study; sports writer Andy Brown made the same claims in 2015 and the statement that a literature review finds gaps in the research into trans athletes is hardly controversial or remarkable given everyone knows there isn’t enough – yet – and there needs to be.
(2) They discounted congenital adrenal hyperplasia as a possible cause of virilization in the study cohort. “Among our studied population, none of the 13 athletes with a 17-hydroxyprogesterone serum concentration above 8 nmol/L showed increased T or A4 (data not presented), ruling out the possibility of an untreated 21-hydroxylase deficiency, the most common form of congenital adrenal hyperplasia, as a cause of the high T levels.
(3) PCOS is an endocrine disorder which, in severe forms, has implications for overall and specifically reproductive health. Women with PCOS are either more likely to enter/succeed in sports, or possibly there is something about training regimes for female athletes (most rely on male data) which affects endocrine health. Another big question is where the incidence and/or severity of this endocrine disorder is increasing as a result of increasing exposure to endocrine disrupting chemicals in the wider environment.
(4) Four had 5α-reductase deficiency and two had partial androgen insensitivity.
(5) The androgen sensitivity levels of those 46XY athletes is not known but as athletes with 46XY DSD with complete androgen insensitivity are over represented in elite female sports the question has been raised at to whether the possession of a Y chromosome itself confers a performance advantage.
(6)Caster Semenya has refused to take androgen suppressing drugs to lower her endogenous T level to the new level of 5 nmols/L – which is still well above the top of the level for natal women.
(7) Worley’s claim and the arguments underpinning it should be noted by all those who have enthusiastically embraced the medical and surgical transitioning of children. If a post-pubertal orchiectomy leaves a person unable to maintain a general level of health, let alone be competitive in a sport, without higher exogenous T levels than are permitted by a sports governing body, what might happen to the overall health and wellbeing of children whose genetic puberty is suppressed with drugs and who have a counter puberty induced with cross sex hormones, and whose endocrine health thereafter must be maintained by constant doses of a mix of synthetic male and female hormones?
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