For all of the lurkers out there:
Please be advised that intersex people have not only asked for their complex medical conditions not to be used to prop up trans identities, as other posters have already stated above, but also that the views expressed by Semp in their second post about intersex people is an example of interphobia.
Interphobia is the othering of people who experience differences in sex development due to complex medical reasons.
All intersex people are either male or female.
There is neither a spectrum of sex on a sliding scale between male and female nor is there a third (ie other) category of sex.
For anyone who wishes to know more, here is an excellent explainer by an intersex advocate (from Twitter):
Right, we’re still struggling with the idea that there’s only two sex classes and that intersex people do not prove the ability to change sex, or do not exist on a spectrum. So, let’s look at sex determination and differentiation (thread)…
Sex is determined at the point of conception. This is known as primary (or gonadal) sex. In mammals, primary sex determination is chromosomal. In most cases, the female is XX and the male is XY. Every individual must have at least one X chromosome.
These chromosomes then dictate development. The presence of a Y chromosome is a crucial factor for determining sex in mammals as it carries a gene that encodes a testis-determining factor. In other words, it tells the gonads to develop into testis rather than ovaries.
To be really clear about this, even a person with XXXXY chromosomes would be male because of the Y. Someone with only one X (XO) chromosome would still be female and their body would begin making ovaries (although they would not develop fully as the second X chromosome is needed)
From this we move onto secondary sex determination, or sex differentiation. Secondary sex determination affects the bodily phenotype outside the gonads. A male mammal has a penis, seminal vesicles, and prostate gland.
A female mammal has a vagina, cervix, uterus, oviducts, and mammary glands. In many species, each sex has a sex-specific size, vocal cartilage (aka Adam’s apple), and musculature.
These secondary sex characteristics are usually determined by hormones secreted from the gonads. However, in the absence of gonads, the female phenotype is generated.
If the Y chromosome is absent, the gonadal primordia develop into ovaries. The ovaries produce oestrogen, a hormone that enables the development of the Müllerian duct into the uterus, oviducts, and upper end of the vagina.
If the Y chromosome is present, testes form and secrete two major hormones. The first, AMH, destroys the Müllerian duct. The second hormone, testosterone, masculinizes the foetus, stimulating the formation of the penis, scrotum, and other portions of the male anatomy,
This also inhibits the development of the breast primordia. Thus, the body has the female phenotype unless it is changed by the two hormones secreted by the foetal testes.
Now, I know someone will be quick to pop up and say, “but MRKH, there are XX males and XY females), this is where the SRY gene (sex-determining region of the Y chromosome) comes into play, so let me explain….
The major gene for the testis-determining factor resides on the short arm of the Y chromosome. Individuals who are born with the short arm but not the long arm of the Y chromosome are male, while individuals born with the long arm but not the short arm are female.
Right on the end of the short arm of the short arm is where we find the SRY gene. This gene is called SRY, and there is extensive evidence that it is indeed the gene that encodes the human testis-determining factor.
SRY is found in normal XY males and in the rare XX males, and it is absent from normal XX females and from many XY females. Another important gene in sex determination is SOX9. XX humans who have an extra copy of SOX9 develop as males, even though they have no SRY gene.
Secondary sex determination in mammals also involves the development of the female and male phenotypes in response to hormones secreted by the ovaries and testes. The formation of the male phenotype involves the secretion of two testicular hormones.
The first of these hormones is AMH, the hormone that causes the degeneration of the Müllerian duct. The second is the steroid testosterone. This hormone causes the urogenital swellings to develop into the scrotum and penis.
The existence of these two independent systems of masculinisation is demonstrated by people having AIS. These XY individuals have the SRY gene, and thus have testes that make testosterone and AMH.
However, they lack the testosterone receptor protein, and therefore cannot respond to the testosterone made by their testes. Because they are able to respond to estrogen made in their adrenal glands, they develop the female phenotype.
However, despite their distinctly female appearance, these individuals do have testes, and even though they cannot respond to testosterone, they produce and respond to AMH. Thus, their Müllerian ducts degenerate.
These people develop as normal but sterile women, lacking a uterus and oviducts and having testes in the abdomen.
In summary, because this is a long enough thread, primary sex is determined at conception, the foetus then follows one of several differential routes. This may be a complicated process with lots of variables, but it does not a sex spectrum make.
We’re all just male or female, this is decided before we are even born, and science is able to explain it and categorise us accordingly. The end.
If you want to read about this in more detail, I recommend this paper (it's long but fascinating)
And also this paper, which is quite technical and heavy going but has links to lots of other research and some handy illustrations.