I for one don't believe she did. From what I gather, she claims that they qualify as disorders because they are not what we evolved "for"
No. They are disorders because they cause deleterious outcomes for those who have those conditions.
Same as having twins in a species where the young are so large and so heavily dependent that that's more likely to kill both infants and the mother than for both to survive. Yet any description of the human reproductive system and strategy is incomplete without the datum that we have 0.5-1% twin pregnancies.
They present with actual fucking harm experienced by the people who have them. In some cases the negative health issues are fairly obvious (such as with Kallman Syndrome, where there's a significant risk of osteoporosis and a host of other conditions), some are less obvious and largely present as sterility.
Sterility counts as "actual fucking harm" only in the case of people who
want kids. Unless by "actual fucking harm" you mean "an actual fucking reduced inclusive fitness".
You're mixing two topics here. Disorders appear in any number of species, in any number of situations, and are generally based on the deleterious nature of the conditions on the individual with that condition. This is a separate issue from my discussion of the nature of sex.
Sex is an evolved mechanism present in most reproductive species. Some few species do not reproduce sexually, they reproduce via division (bacteria, for example) or via more complex "mating sets" like many algaes. But a huge number of species - especially vertebrates - reproduce sexually. That method of reproduction is the product of evolution. Way, way, wayyyyyyy back hundreds of millions of years ago, our ancestral species evolved so that reproduction occurred as a result of the merging of two different sized gametes. The two gametes have different roles in the creation of offspring, and those gametes place different demands on the bodies that produce them. As a result of those different demands, these species that reproduce via two different sized gametes (called anisogamous species) evolved different anatomical structures and processes. While the anatomies themselves differ from species to species, what is universal is that within any anisogamous species, we can observe that one body type has evolved to support the production of small motile gametes (sperm), and a different body type has evolved to support the production of large sessile gametes (ova).
Only if you wear your normative-teleological glasses.
What has evolved is a network of genes, mechanisms and triggers for the development of the gonads and genitals that are largely shared between the sexes, a subset of which is responsible for - usually - steering the development towards one of two prototypical realisations. You could argue that the
reason this system evolved is that those two prototypes are efficient at bringing each others gametes into contact and providing the environment for the fertilised ovum to complete its development to the point where it can survive outside the womb in an environment close to what our ancestors were exposed to, but that doesn't change the fact that what
has evolved is the system as a whole.
Evolution doesn't design features from scratch an merge them to the production branch only when they have been thoroughly tested. Evolution takes what it has and tweaks a few parameters until it finds a local optimum, a point at which no adjacent point has overall better results, and runs with it. Furthermore, no gene or even high level trait operates in isolation, they are embedded in a network of other genes and a bagful of epigenetic and environmental factors (shake well), and what constitutes a local optimum is dependent on the specifics of the environment. Sometimes, often, the local optimum predictably produces individuals with a less than ideal configuration at a certain rate. The textbook example of this (because of its simplicity, where basically only one gene is involved) is the sickle cell trait. If you have one copy of the variant gene, it gives you increased resistance to malaria, if you have two, it gives you the sickle cell disease. The result is a stable ratio of a variant that can cause a disease not because of an incomplete adaptation but as the local optimum in the environment. The same can be said for twin births: Presumably evolution could produce a variant of any of the genes involved in the operation of the follicle stimulating hormone which lowers its production or its efficiency to the point were twin births become excessively rare - but it doesn't because doing so would increase the number of cycles skipped entirely and reduce overall fertility so much so that the damage done by an occasional twin birth is outweighed. Evolution presumably
could twist and tweak the levels of a messenger protein involved in the maturation of the gonads such that literally every XX individual develops functional ovaries, but with the background noise of variation in the dozens of other genes involved and of epigenetic and environmental factors, any easy way to do that would probably increase the number of infertile male offspring. So, while what drives the evolution of the reproductory apparatus in humans is the complimentary nature of male and female gametes, and the ability of the male anatomy to deliver theirs to where the female anatomy helps it to mature, the outcome of that selection isn't half of the population as perfect incubators and the other half as perfect inseminators. That's just not how biology works. The outcome of that evolution is, in humans, a range of variation with two peaks at two phenotypes that are mutually compatible in the production of offspring, but see bees for a very different outcome.
We have observed that even when the individual does not actually produce gametes, they still conform to one of those two basic anatomical structures. We can also note that no other body type has evolved - there is no other distinct phenotype that has ever been observed within anisogamous species.
We have definitely observed that the growth of those phenotypes can be derailed, can display incomplete or ambiguous development, can even in some very rare cases display a mixture of typically male and typically female elements. But it is also clear in those cases that there are deleterious effects from those developments, often including the inability to reproduce. It's also clear that such conditions aren't within the range of normal range of human development. And it's abundantly clear to anyone without an ideological axe to grind that these are not evolved phenotypes in and of themselves.
You mean they were not "intended"? They are not what drives the selection? Yeah, so? That doesn't make them go away.
Some people wish to argue that these conditions are either unique sexes of their own, or that they indicate that sex is "bimodal" or "a spectrum". Those arguments are flawed, and demonstrate a considerable lack of understanding of the process of evolution as well as the nature of sexual reproduction across all mammals, all birds, nearly all vertebrates, a huge portion of arthropods, and a whole lot of plants.
Regarding the remainder of your post, I will once again reiterate that evolution has no intent, no objective, it does not select. Evolution is a process, a mechanism. It's a gigantic pachinko machine played out over millions of years.
That right there in the last paragraph is why breaking down the range of variation of a species into "normal" and "abnormal", and categorising it into "evolved phenotypes" and "disorders" is nonsensical. Evolution has given us largely shared developmental trajectories for male and female gonads and genitals that usually produces either one or the other but is prone to produce intermediate forms at a low but non-zero rate when a part of it is disturbed by environmental factors or when an assortment of usually benign variants of seemingly unrelated genes conspire to shift the trajectory. Everything about those less frequent outcomes is the product of evolution.
