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Chromosomes and gametes: sex in biology

XY and XX correlate with sex but do not define it. The definition is functional: which gamete pathway does the body develop? The SRY gene on the Y chromosome triggers that pathway — chromosomal abnormalities shift it, but leave the binary system intact.

The molecular cascade

Around the sixth embryonic week, SRY (Sex-determining Region Y) activates SOX9 expression in the gonadal crest. This leads to Sertoli and Leydig cells, testosterone production, and regression of the Müllerian system. Without SRY, the gonadal crest develops into an ovary, and the Müllerian system is retained until the uterus, fallopian tubes, and upper vagina. The cascade has been confirmed by thousands of experiments in mammals. The trajectory begins at conception and is completed well before birth — see the gamete definition on biological sex .

Karyotype is correlation, not a definition.

In more than 99.98% of cases, the phenotype follows neatly from the karyotype: 46,XX → female; 46,XY → male. In DSDs, a discordance between chromosomes and gonads sometimes arises—which itself can be explained biologically. None of these conditions introduces a third sex. They disrupt existing trajectories and thereby actually reinforce the dichotomy. The definition of sex is functional (gamete production), not chromosomal—karyotype is highly correlating evidence, not a definition.

The DSD conditions at a glance

The often-cited "spectrum proofs" are in reality pathological deviations within the existing binary:

• Klinefelter (47,XXY) — male trajectory, reduced fertility. No third gender.
• Turner (45,X0) — female trajectory, gonadal dysgenesis. No third sex.
• XYY (Jacobs syndrome) — male trajectory, normal fertility. No third gender.
• 5α-reductase deficiency (5-ARD) — 46,XY, male trajectory with impaired external virilization until puberty. No third sex.
• CAIS — 46,XY with complete androgen insensitivity; phenotypically female but testes intact. A developmental disorder, no proof of identity.
• CAH — adrenal cortex disorder; in 46,XX girls partially masculinized anatomy. Female trajectory remains.

Cumulative frequency of actual DSDs: ~0.018% (Sax 2002). The often-cited 1.7% (Fausto-Sterling) is a statistical trick in which late menarche and hypospadias are included.

Colin Wright's chair analogy

Wright compares sex to the concept of "chair." Chairs vary: three legs, four legs, an armrest, reclining model, office chair, stool. Some chairs are broken, missing a leg, or designed as sofas. No one concludes from this that "chair" is a spectrum, or that a third category, "table chair," exists. The variation lies within the category; it does not invalidate the category. The same applies to sex: DSD variation lies within male or female, not in between. See the broader critique of sex versus gender and the circular reasoning used to eliminate this distinction.

No genetic marker for gender identity

Karyotype, hormones, and gonads are measurable. Gender identity is not. There is no gene, no biomarker, no test by which a "trans-XX" or "cis-XY" can be objectively distinguished — see no genetic marker and no measurable marker . What remains is self-reporting as the only source .

What hormone therapy does and does not do

Hormone therapy alters secondary sexual characteristics — not gamete production, not chromosomal sex, not gonadal architecture. A trans woman remains genetically and gametically male; see trans woman . This is not "transphobia" but physiology. The Cass Final Report (2024) and the earlier SBU and NICE evaluations point to the irreversibility of many medical interventions that cannot cope with this biological reality.