Evolutionary Sense of Sex and Gender

This essay is Professor Jenny Graves' contribution to Iconoclast, a book of collected works edited by La Trobe University alumnus Dr Mark Halloran. It has been reproduced here with the permission of Dr Halloran.

The genetics of sex and gender is full of contradiction. That’s why I love it.

Sex development and expression breaks all the evolutionary laws of survival of the fittest.

Y chromosomes that self-destruct, men who love other men and forgo having kids, men and women who believe they were meant to be the other sex and will do anything to make sex change a reality. Nor are humans alone in their confusion.

The natural world is full of sexual contradiction. Sex chromosomes with mixed messages, sex change, fierce female moles and nurturing male emus, gay sheep.

Like it or not, men and women are very different genetically, anatomically and behaviourally. But within each sex there is tremendous variation, so that for most traits distributions overlap.

There are short men and tall women, fierce females and nurturing males.

Why sex?

We take the male/female divide for granted, but when you think about it, sex doesn’t seem to make evolutionary sense.

Sex is expensive, requiring animals to attract a mate and fight off competitors as well as making sperm and eggs, the ultimate waster of time and energy. And anyway, our genes would be better off if we cloned ourselves, as do many plants – and even some lizards.

That way all our genes would make it into the next generation, rather than having to go halves on offspring as we do.

Generations of geneticists have puzzled over this, and there are many theories1.Mostly these assume that there must be some very big advantage in combining varieties of our 20,000 genes.

Sex throws together two genomes, and there is a mechanism to mix them up each time a man or woman make sperm or eggs. A process called recombination takes place as the first step in sorting out a single copy of each chromosome for sperm or eggs. Recombination literally splices one part of mum’s chromosome 1 to the other part of dad’s chromosome 1, so that most chromosomes in the egg or sperm are patchworks of mum’s and dad’s gene variants.

Why could this be important? The classic explanation was that recombination continually creates new combinations of variants that could do well in new environments. A more recent refinement is that, specifically, new combinations of proteins on the surfaces of our cells bamboozle would-be pathogens that are always bombarding us2. This idea receives support from studies of animals like cheetahs and Tasmanian Devils that are running out of genetic variability, and seem to be very sensitive to being wiped out by a pathogen that sweeps through a colony of near-clones. This probably explains why female-only species of lizards evolved rather recently; they don’t last long.

Sex chromosomes are nothing but trouble

I’ll start from the start with sex genes and chromosomes, which break all the rules of proper function and evolution.

As most people know, women have two copies of a medium-sized chromosome called the X, and males have only a single copy (that’s why it’s called the “X for unknown”; its name has nothing to do with its shape). Men also have an extra small chromosome, called the Y, which women completely lack. So, men and women have different genomes.

The genome, a metre or so of DNA carrying about 20,000 genes, is chopped up into 23 handy sized DNA molecules that are bound with protein and bunch up when the cell divides so we see them as “chromosomes” (that is “staining bodies”) under the microscope. We – and other mammals – carry two copies of the genome, one from mum and one from dad. That’s why chromosomes come in pairs, two copies of the biggest chromosome 1, two copies of chromosome 2 etc, in both males and females. That’s called diploidy, and it is generally considered to be a good thing because if some accident befalls a gene, say on chromosome 1, there is a backup copy. In fact, if you have only a single copy of any of the 22 ordinary chromosomes, you don’t even make it to be born.

Sex chromosomes are different in many ways. The X looks normal enough, with more than 1000 genes that encode all sorts of functions including housekeeping enzymes, visual pigments, blood clotting factors – not at all dedicated to femaleness. It is its differential dosage in males and females that causes problems.

The first problem is that males have only a single copy, so men have no backup if any X-borne gene is mutated (witness the much greater frequency of boys with colour blindness or diseases like haemophilia and mental retardation). The second problem is the dosage difference between the sexes, which is hard on genes that must interact with genes on other chromosomes in a 1:1 way. To avoid problems with this dosage difference, there is a complex system that genetically inactivates the genes on one or other X in cells of females. If this doesn’t work, you die.

As well as their single X, men have a male-specific chromosome called the Y. A pathetic little chromosome bearing hardly any genes, it seems to be composed mainly of junk DNA, simple sequences repeated over and over so it binds fluorescent molecules and literally glows in the dark. It contains hardly any genes; only 27 in the region that is present only in males. Several have amplified into many copies, though some (or most) of these copies have been disabled by mutation.

The Y may look a bit pathetic but one of its 27 genes determines that the embryo that bears it is male. This gene, called SRY (Sex Determining Region on the Y)3, directs other genes to turn a little “genital ridge” of cells in the embryo into a testis. The testis makes male hormones, and the embryo develops into a baby boy. In XX embryos with no SRY the genital ridge develops as an ovary and the baby is born a girl.

The Y has a peculiar set of genes. Its 27 genes are a very specialised set. Several are dedicated to male functions like making sperm, and others seem to be there because they are necessary in a double dose in males as well as females.

Nor does the X have a standard set of genes. There are a disproportionate number dedicated to male reproduction. The reason for this seems to be that because genes on the X are present in a single copy in men, they are exposed rapidly to selection – those that advantage males will do better. Harder to explain is that there are five times as many genes on the X as you’d expect that are involved in intelligence4; perhaps they accumulated because females preferred to mate with smart males who had smart variant genes on the X. Darwin called this sexual selection, and it can lead to very rapid evolution – perhaps explaining how human brains doubled in size over just a few million years.

One curious factor is that some genes are good in one sex but not the other. Genes for making sperm are not much use in a female, and genes for making eggs are no use in a male. There are even some genes that are good for one sex but bad for the other - these are called “sexually antagonistic”, and are well known from studies in a range of animals including fruit flies5.

So, sex chromosomes don’t work very well. Like many peculiarities we observe in nature, they are better understood in terms of evolution, than of function.

How did sex chromosomes evolve to be so odd?

Isn’t evolution supposed to get rid of things that don’t work well and favour ever better solutions? Well, no. Evolution, rather than working to some grand design, does not know where it is going and simply patches things up so they more-or-less work. Here I’ll explain how our sex chromosomes came to be so peculiar – and are getting more damaged all the time.

The X and Y chromosomes look very different, and bear very different sets of genes, so you will be surprised to discover that they evolved from a perfectly normal pair of chromosomes, like chromosome 1, that had nothing to do with sex6. The first evidence for the autosomal origin of the human XY pair was that the very top bit of the X and Y is the same. When the chromosomes pair and sort themselves out into sperm, the X and Y pair up in this little region, and recombination (the breaking and rejoining of pieces of the X and Y) takes place. The rest of the Y does not pair with the X or anything else – it is all alone in the world.

Another curious thing is that most of the genes on the human Y, even those with male-specific functions in sperm (even SRY itself), have copies on the X from which they obviously evolved7. So, the conclusion is that the Y chromosome started off with the same 1000+ genes as the X.

Indeed, we know from studying many animals, that our X and Y were once an ordinary chromosome pair; they still are in birds and turtles, which have quite different sex genes and sex chromosomes. In birds sex chromosomes are the other way around, ZZ specifies male and ZW female; a sex gene on the Z chromosome called DMRT1 operates via dosage difference; two copies specifies male and one copy female. Even platypus have different sex chromosomes, more like birds than like other mammals.

How did this happen? It all started with the evolution of SRY, the sex determining gene, which evolved from an ancient gene with functions largely in the central nervous system. A simple rearrangement that repositioned this gene so it worked in the embryonic gonad gave it new powers, to switch on other genes in the testis determining pathway. So, a respectable brain-determining gene became a testis determining gene.

The acquisition of a sex determining gene was the kiss of death for this proto-Y chromosome, and led to the loss of nearly all its active genes. There are many ideas about why genes get lost from the Y, and people write books on this. Put simply, the Y chromosome suffers from being always in a testis. The testis is a dangerous place to be because making sperm takes many cell divisions, each one an opportunity for a gene mutation to take place. The Y also suffers from being alone in the cell because recombination can’t take place to restore a good Y chromosome by patching together the good bits of two mutated Y chromosomes.

The process of gene loss is still going on, as we see from the many men who are infertile because part of their Y chromosome has been deleted. So how rapid is gene loss and what is the future of the Y? We can date the start of our sex chromosomes to about 160 million years ago because they are not shared outside mammals, or even by platypuses, from which we diverged 180 million years ago. So, we can calculate that if the remaining genes on the Y continue being inactivated and lost at the same rate, the whole Y will be gone in about 6 million years8.

What will happen when the human Y disappears in 6 million years? Well, providing humans survive that long (which seems increasingly unlikely), a new sex gene on another chromosome may take over. This has already happened in two groups of rodents, and in each, a new sex determining system has driven a wedge between species. So, if you come back in 6 million years, you may find no humans – or several hominid species. Scary thought!

Sex chromosomes are the posterchild of the evolutionary principle I call “Dumb Design”. No sensible creator would ever have designed sex chromosomes that cause so much genetic havoc and are well on the road to self-destruction.

Genes and sexual development

The Y may be small and peculiar, but it packs a developmental wallop. We knew this 60 years ago when it was discovered that babies born with unusual combinations of sex chromosomes were male if they had a Y chromosome and female if they didn’t, no matter how many X chromosomes they had. And babies with parts of a Y were male only if they had the top bit of the Y, implying that a gene near in this region directed male development of the foetus.

Indeed, a gene was discovered on the Y in 1990 that directs male development of the embryo. SRY turns on other genes that instruct a ridge of cells on the embryonic kidney to become a testis. It’s a complicated pathway of at least 60 genes, full of checks and balances, that turns on or off genes. So, you have SRY activating a gene that in turn activates other genes in the testis pathway, and as well inhibits genes in the ovary pathway. Likewise, in the absence of SRY, a gene in the ovary pathway activates other genes in this pathway, and also supresses a gene in the testis pathway9. It’s a real pushmi-pullyu.

The embryonic testis makes male hormones (androgens), and these hormones direct the development of male genitals of a baby boy, and continue to exert their effects after birth in morphology, muscle strength and fat distribution, hair growth, voice pitch and behaviour, and, after puberty, the production of sperm. In the absence of SRY, other genes turn on to differentiate the same ridge of cells to become an ovary, which makes female hormones that direct female development and egg production.

The genetic differences between men and women go far beyond just this one gene, or the pathway of sex determination, and may exert their effects independently of hormone production. There are another 26 genes on the male-specific part of the human Y, and some of these encode proteins that are needed for making sperm.

Surprisingly, looking at which of our 20,000 or so genes are turned on in different tissues shows astonishing differences between men and women. Fully one third of our genome (more than 7000 genes) is expressed differently in men and women in one tissue or another. And not just in breasts and gonads, but other supposedly neutral tissues like liver and kidney10. These differences are likely to underpin many of the differences, long known but only recently acknowledged, in the susceptibility of men and women to many diseases, and the different efficacy of treatments11.

And most shockingly, many genes are expressed differently in the brains of men and women12. Add to this the observation that the male-specific SRY gene is expressed in the brain and seems to have a role in the susceptibility of men to Parkinson’s disease13.

There have been fierce arguments over decades as to whether sex differences extend to the brain and behaviour. Do men have superior spatial ability or women superior verbal ability? Are men on average more aggressive and risk-taking? I am not qualified to take sides in these debates, but will just comment that it would be remarkable if brain development did not respond differently to the demonstrated differences in gene activity in men and women.

Sex and career choices

A great deal has been written and discussed about the role of sex differences in abilities, career choice and progression, and very many schemes have been enacted to increase women’s participation in STEM. In science, it is obvious that sex is a major factor in choice of study as early as primary school, and for decades there have been wails of dismay about the low enrolment of young women into science, particularly engineering, computer science and maths. There are programs on programs (many in which I have enthusiastically participated) to lure girls into science during school and university, and to keep them there during their careers. Drop-out rates are higher for women, and we talk about “the leaky pipeline” that delivers few women into senior positions14.

My own path through science might look very straight and confident, and when asked, I would aver that I did not suffer from discrimination – at least while I was a modest junior academic (things got nastier as I became more senior). However, subtle discouragement and discrimination was there at every turn, and the temptation to leave the pipeline was presented many times. It seemed so normal that it had no name.

I remember the occasion, in sixth grade, when our class was asked what careers we would choose. Most of the little girls wanted to be air hostesses and the little boys’ firemen. I learned how to spell “architect”, which served me well over the next decade. But my (girls’) school did not teach maths in the final year (modern history was deemed more suitable for young ladies), and I was one of only two girls in my final year university physical chem class (guaranteeing exclusion from the study groups and cheating consortia). Biology was a better mix, and I was in awe of a very brilliant woman lecturer “Mrs Mayo”, the wife of “Dr Mayo”, another lecturer – only later did I discover that both had DPhils from Cambridge.

Postgraduate research was in quite a close-knit little group, but the pattern was still exclusion from corridor cricket and late-night excursions to buy “floaters” at the Adelaide Town Hall.

After a PhD at the University of California, appointment as the only woman in a blokey department in Melbourne rapidly taught me not to accept the classic female roles (one of my lucky breaks was to reject an early invitation to organize the departmental Christmas party), and to observe closely how my male colleagues came to amass their space and equipment and technical help. The real turning point came when I became pregnant; a point at which well-bred young women were expected to politely resign their tenured jobs for a lifetime of casual demonstratorships – the biggest source of leaks to the pipeline. Fortunately, I could not succumb because I was at the time sole breadwinner while my husband studied.

Negotiating first a teaching and research career, building up a lab of enthusiastic young people gave me some immunity from the quiet sexism of Academia, but winning the L’Oreal-UNESCO For Women in Science prize in 2006 made me realise that being good at my job is not enough.

This is when I started taking seriously efforts to remove sexism from academia. I have spent a major part of my 50 year career on various women in science committees, institutional, Australian, and international. For 40 of these years, we produced report after report, saying much the same thing. We must remove barriers to employment of women. We must make STEM education more female friendly. We need good role models, good mentors for young women in science. But only in the last decade has there been an appetite to do something to enact plans to attract more women into science and keep them there. It is quite thrilling to me to see the fruits of our efforts in programs like Science in Australia Gender Equity (SAGE)15 modelled on the Athena Swan program that strongarms and rewards institutions to make practical changes, not just in words and covenants, but on the ground.

But what is the end-point of these schemes? Can we measure progress toward this endpoint? The simple answer has been that we should not rest until enrollments in computer science are 50% women, and until our professors of physics are 50% women. Oh, and our nurses, too, and primary school teachers of course. On this measure, we are a long way behind, with women constituting only about 15% of engineering enrolees, and 10% physics professors.

But is 50% realistic? And is it desirable? We simply don’t know whether girls’ preference for arts and sociology is purely social, or is at least partly genetically determined. It is obviously at least partly social (for instance women make choices more compatible with running a household and bringing up kids) and I would like to see redress on workload balance between partners. But I would hate to insist on a 50:50 distribution of men and women in engineering and physics just to make up the numbers.

Evolution of sexual behaviour

Sex is essential for reproduction, so it is a big part of “Darwinian fitness” that drives the success of our species, any species. (Fitness is not measured as strength or health, but simply as the number of descendants who inherited our genes). This means that any trait that increases the chances of leaving children will be selected. And any trait that increases the chances that the children will leave children. Conversely, any variant that means that the bearer has fewer or less healthy and fertile children will be ruthlessly expunged by natural selection.

These traits can be anything; favourable variants that make eggs longer-lived, sperm more active. Or that enhances success in attracting a willing partner who will help bear your genes into the next generation. “Mate choice” covers all the factors that go into selecting a mate, including being attracted by outward signs of fertility (at the core of men’s fascination with breasts and hips), and being turned off by a smell that denotes a too-close genetic relationship. There is evidence that this information is delivered via the many variants at the Major Histocompatibility Complex (MHC) (called Human Lymphocyte Antigen, HLA in humans), a large region of the vertebrate genome that contains a set of very variable genes that code for cell surface proteins involved in adaptive immunity16. Then come all the factors that go into attracting a mate, including elaborate mating displays if you’re a fly or a bird, or appearance and behaviour in mammals including humans.

Geneticists are always interested in conditions that are common even though they would not seem to fulfill the criteria of evolutionary fitness, and sexual behaviour offers several that have defied logic.

One of these is male homosexuality, which, by any reckoning, is common in all ages and all cultures, even those that impose drastic social sanctions. In 1998 the first convincing study was published showing that a gene variant (“gay gene”) on the X chromosome was associated with homosexuality17. This caused a furore in the conservative South of the USA, where homosexuality was seen as a “lifestyle choice”, and a genetic factor was incompatible with the dictum that “God cannot create a sinner”. However, corroborative evidence of several “gay genes”, detected by different strategies, makes it clear that homosexuality is at least partly driven by genetic variants.

This is not at all surprising. Almost every trait you can think of, including other behaviours (like toilet flushing and belief in a god18), is at least partly genetic. Much evidence comes from twin studies; identical twins show more concordance in the behaviour than fraternal twins (and it may be even more because recent research shows that identical twins may not be as genetically identical as we supposed because of mutations occurring in one or the other after the developing egg is split into two).

Homosexuality is also common in other species, including many mammals. In fruit flies, a single mutation in a gene changes mating behaviour in males so that they direct their flap-flap, tap-tap mating displays to other males19. And indeed, variants in many genes affect fly mating. We are no different, not even that much more complicated.

What is surprising is how common homosexuality is, given that gay men have far fewer offspring than straight men. You would think that gay genes would not make it in a competition for Darwinian fitness.

Many years ago, during an interview with Phillip Adams alongside a gay men’s rights activist, I suddenly twigged. Maybe homosexuality is a typical sexually antagonistic gene variant. The gay gene, I surmised, was really a “male-loving” variant of a mate-choice gene present in everyone. In a male it will lean toward homosexual partnering, and few offspring. But the same “male-loving” gene variant in his female relatives will push his sisters and aunts to partner earlier and compensate by having more children. So, this gene variant is overall successful, and is kept in high frequency in the population by positive selection in women20.

If this were true, you would expect to find the number of children mothered by the female relatives of gay men to be higher than average. And a few years later, studies in Italy confirmed that it is, indeed, 30% higher, enough to offset the fewer children born to gay men21. I would predict that the same argument can be made for lesbian women, although there are few data. They simply have a preponderance of “female-loving” variants of a gene or genes. You might expect their male relatives to share these “female loving” variants, to partner earlier and have more kids.

I would be surprised if there were not tens or hundreds of genes, variants within which affect mate choice in both men and women. I see them as typical “sexually antagonistic” genes that in one sex curtail reproduction, but in the other sex boost it. So, evolution works in sometimes counter-intuitive ways to produce a spread of normal variation that we see in sexual behaviour, just as in visible traits like height.

Sex and gender

Sex and gender are quite different concepts, and it is important to differentiate them. Sex is the different biological and physiological characteristics of males and females, such as genes, chromosomes, hormones, reproductive organs. Natal sex refers to the biological sex you were born with. Gender is how you identify yourself within (or even outside) the broad swathe of maleness or femaleness.

Sex, as I have discussed, is controlled by genes whose effects have been channelled by evolution into two alternative developmental pathways that yield male or female development. This is why sex is referred to as “binary”, although there are a few individuals in whom development lies between or outside these two channels. Biological sex is pretty hard to change in mammals including humans; you can change the outward manifestations and even the hormones, but genes and chromosomes are unreachable.

But nature throws up variants in several ways. For a start, there are significant numbers of children born with a mutation in one or other of the 60-odd genes that translate the presence or absence of SRY into development into a man or a woman. Some of these variants – for instance a mutation in SRY itself, or a mutation in the molecule that responds to male hormone – produce physically normal girls, who discover that they have a Y chromosome only when they fail to menstruate at puberty and prove to have no functioning ovary and only half a vagina. And there are boys with two X chromosome who possess an SRY gene that has been transferred to the X chromosome.

Other mutations are harder to deal with as they produce babies with some intermediate characteristics that can change during development, so sex is uncertain and advice on sex of rearing is fraught. Children with a block early in the gonad differentiation pathways have “streak” gonads that have not developed in either direction, and they develop outwardly as female. At the other end of severity, some variants are downright life-threatening unless treated.

Although it is not possible to repair the genes or chromosomes of these children, some parents, fearful of bullying and exclusion, opt for genital surgery. Not surprisingly, many of these children with Disorders (or “Differences”) of Sexual Development (DSD) grow up feeling discontented with their parents’ choices, and tell heart-rending stories of deception and a lack of acceptance. Patient groups advocate leaving decisions till puberty, but this leaves a DSD child vulnerable and means surgery is less satisfactory. In some countries in which treatment is not available, DSD children (and often their families) face discrimination, neglect and even death. There is no right answer; the practice today is to minimise any treatment until the child is old enough to make decisions on this aspect of their lives, and avoid removing any genital tissue22.

Unlike sex, gender is anything but binary23. Rather than being channelled into two alternative pathways, gender is a broad spectrum, in which a person may consider themselves at any point, regardless of natal sex. A person may define themselves as cisgender (same as natal sex), transgender (different from natal sex), non-binary or even gender-neutral.

Whereas it’s hard to change biological sex, there are many ways of crossing gender lines, and this has always held great fascination across many cultures. History, literature, opera is replete with stories of women posing as men, and men posing as women to fight or avoid wars, woo or escape lovers. My personal favourite is watching a woman sing the role of a man posing as a woman in Der Rosenkavalier.

On the more serious side, there are people, young and old, whose sex chromosomes and genes, and sexual development is biologically standard, but who are convinced, often from an early age, that they were born the wrong sex. In severe cases of “gender dysphoria”, patients have an intense wish to transition to the sex of choice, and may opt to undergo surgery. The rates of male-to-female transition is 1/200, and female-to-male is 1/400, quite high compared to biological variants.

Again, treatment is fraught. Children who profess to be transgender are at least accorded respect and listening, but the concern is now that being gender fluid has become quite trendy for high school students. Caution has been urged in rushing major surgery and treatment with puberty blockers because at least half change their minds at puberty.

Again, there is some evidence that gene variants play a part in gender dysphoria. Several studies implicate “the usual suspects”, including genes involved in hormone pathways. This sort of variation is not unusual for any trait, morphological or behavioural. The puzzle, again, is why gender dysphoria is so common when transwomen and transmen are infertile unless they preserve their eggs or sperm, so do not commonly hand down their gene variants24,25.

I wonder whether these genes, too, may be classic “sexually antagonistic” variants. I suggest that there are variants of these genes that predispose to femininity or masculinity, and everyone inherits a mixture that affects their gender identity. At one extreme are women and men who inherit a lot of feminine-leaning traits; the men may become transgender and have no children while their female relatives who share the same variants partner earlier and have more children. Conversely, among people who inherit masculine leaning traits, manly men may have more children, compensating for female-to-male transmen who have few.

Sex, gender and sport; there is no level playing field

As transgender becomes more accepted and transmen and transwomen more frequent, there are issues to sort out. Some are relatively easy, like labels for toilets, some just take understanding and getting used to like use of appropriate personal pronouns. Others are insoluble.

One of the insoluble issues is the status of DSD people and transwomen in elite sport. Like it or not, men have, on average, significantly greater muscle strength, heart function and lung capacity than women, and sex tests have been a part of the Olympics for a century to prevent men gate-crashing women’s athletic events. Originally a sex test was the presence of a sex chromatin body (the inactive X chromosome) in the cheek epithelial cells. This was rightly decried as discriminating against women with only a single X, so gave way to (expensive and slow) chromosome tests, then to direct screening for the presence of the SRY gene. But this was pointed out to discriminate against girls having a Y chromosome but a mutant SRY or androgen receptor. Indeed, XY girls with an AR mutation are overrepresented in elite sport; not because they have an androgen advantage (although their bodies make testosterone, it cannot be utilized by the cell), but because they are taller courtesy of a growth gene on the Y chromosome.

Some of the high-profile cases have concerned women who are not intersex or transgender at all, but simply have traits that put them way ahead. The most celebrated is that of an Indian runner with extremely high levels of testosterone; although by any test she is female, her testosterone levels are naturally higher even than the average for men. Undoubtedly this gives her an advantage of muscle strength and sustainability. But to me it seems that banning her from competition makes no more sense than banning an ultra-tall basketballer (or a horse like Phar Lap with an enormous heart for that matter).

Adding to this confusion are now significant numbers of transwomen who were born and grew up as XY males but have had sex change surgery, androgen suppression and estrogen therapy.

Understandably, it is very important for transwomen to feel accepted as women in the community, and sport has always been an effective means of achieving identity and acceptance. Many transwomen speak movingly of the importance of their hockey or water polo team to their sense of self.

Yet a growing number of sporting organizations are now under pressure to ban transwomen from competing in women’s sport, citing (incontrovertible) evidence that the presence of androgen early in their lives as boys gave them a permanent advantage in strength, heart and lung performance, even if they take androgen-suppressing drugs. Bodies such as the Olympic committee are tying themselves into knots trying to be fair26.

So how can we create a level playing field? It seems to me that the playing field can never be level. Elite athletes, although they invest enormously in training and coaching, are bound to be on the extremes of many distributions, and we can’t ban them all. Perhaps we need to compete in categories like children’s sport (e.g., Under 14 C grade basketball) or the Paralympics (e.g., Triathlon PT1). I look forward to representing Australia in the Over-80 medium height low androgen Olympic netball team.

Why are we so obsessed with sex and gender?

Sex is, of course, the most dramatic normal variation between humans. It’s the first thing you notice about a new acquaintance.

Many of these problems I have discussed are problems only because we are so intolerant of difference. What’s the big deal? We are not freaked out by differences in height or facial characteristics or intellectual ability, yet parents are horrified if their newborn is diagnosed with a DSD. Paediatricians and genetic counsellors have told me that parents of DSD kids are often traumatised beyond reason. “I’d rather my baby had a serious heart problem,” one new mother was heard to remark. Often the rush to surgery is fuelled by fears that DSD children will be routinely bullied for their anatomical differences – fears that, sadly, are not misplaced. Children can be very cruel.

Perhaps the fears of parents of DSD children are intensified by primal distress that their own genes will not be passed on to future generations; parents are looking at the end of their lineage.

Why are we so intolerant of differences in sexual development? Why are we resistant to the ideas of variation in sexually different traits? They are not terribly rare in humans, and also occur throughout the animal kingdom. Examples abound in nature of females that act like males; for instance, female hyenas and moles aggressively claim the top spot in the hierarchy as the result of high androgen levels that drive male-like genitals as well as aggression. Or emus in which it is the male that incubates the eggs and takes care of the chicks.

And why are we so appalled – and so titillated – by the concept of changing sex? Plenty of other animals do it routinely. There are whole species of fish that start out one sex then transition to the other when they get big enough. Some start off female, then transition of males when they get big enough to defend a harem. Others start of as males and transition to females when they are big enough to lay a lot of eggs.  My favourite is the blue wrasse, a fish species in which a dominant (blue-headed) male guards a harem of demure gold-striped females. If this male is removed, the biggest female becomes male. She changes her behaviour in minutes, colour in hours, and by 10 days has swapped her ovaries for testes that are making sperm27. What a ride!

If we look around, we see that humans occupy a tiny spot in the grand panoply of sexual differences in morphology and behaviour. We can do a lot by removing rampant discrimination against minorities that occupy outlier positions on distributions of sexual traits. This has happened remarkably rapidly for gay men and women in most western countries, although there are still nations that sanction homosexuality.

But other problems arise with suspicions that people could use transgender as a means of infiltrating – and even attacking – women, for instance in restrooms or prisons. Or claiming a physical advantage on the track. Everything can be abused, and we have to guard against siding with the perpetrators, as well as the victims, of sexual discrimination.

Maybe we are programmed by the evolutionary necessity to find a good mate to provide a superior genome for our kids and hopefully some parental care. And maybe we are programmed by the evolutionary necessity to evaluate the competition, comparing ourselves and anxiously assessing the chance that our genes will make it into the next generation – increasing our Darwinian fitness. It may not be sensible to ignore these biological imperatives, but like other traits evolution endowed us with (like our lethal love of sugar, which evolved so we would choose ripe and nutritious fruit), we can learn to control our urges and rationalise our choices to such an extent that we can celebrate the enormous variation in all aspects of human sex and gender.


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This essay is Professor Jenny Graves' contribution to Iconoclast, a book of collected works edited by Dr Mark Halloran. It has been reproduced here with the permission of Dr Halloran.

Professor Jenny Graves is an evolutionary geneticist who exploits our distant relationship to Australian animals to discover how animal genes and chromosomes evolved, and how they work. She uses this unique perspective to explore the origin, function and fate of human sex genes and chromosomes, (in)famously predicting the disappearance of the Y chromosome.

Jenny studied at Adelaide University (BSc, MSc) and the University of California Berkeley (PhD). She lectured at La Trobe University, then at ANU she founded and directed the Comparative Genomics Group and an ARC Centre of Excellence. She returned to La Trobe as Distinguished Professor and Vice Chancellor’s Fellow.

Jenny has produced three books and more than 400 research articles. She received the international L’Oreal-UNESCO prize (2006), appointment as Companion of the Order of Australia (AC 2010) and the Prime Minister’s Prize for Science (2017). She was elected to the Australian Academy of Science (1999), and the US National Academy of Science (2019).