How an XY Person Can Develop a “Female‑Typical” Brain Pattern (and vice versa for XX)—Even Without a Named Genetic DSD

Key takeaways

• Sex development unfolds in stages. Genitals differentiate early in the first 2 months of pregnancy, while much of brain sexual differentiation occurs later in the second half of pregnancy. Because these windows only partially overlap, the genital pattern and the brain pattern can diverge. (PubMed)

  
  

• Divergence does not require a classic, named genetic DSD. Non‑genetic factors—like maternal androgen excess (e.g., luteoma of pregnancy or androgenic drugs) or loss of fetal testicular function—can shift fetal hormone exposure and nudge brain development toward the other sex‑typical trajectory. (PubMed Central, Jpag Online, PubMed)

  
  

• Human brains are not binary (“male” vs “female”). Most people show a mosaic of features that are more common in one sex or the other, with lots of overlap. So phrases like “female brain in an XY person” are shorthand for patterns more typical of one sex, not an on/off switch. (PNAS, PubMed)

A quick map of sex development

1. Chromosomes set the plan (XX or XY at conception).

   
   

2. Genitals: Differentiate early, primarily from androgen (testosterone → DHT) action (weeks ~8–12).

   
   

3. Brain: Many sex‑typical brain features organize later, as hormones act on developing neural circuits during mid/late gestation. Because the brain’s timetable lags the genitals, the two can be influenced independently. (PubMed)

How divergence can happen without a named genetic condition

Below are well‑documented non‑genetic (or not necessarily genetic) routes that can alter fetal hormone exposure enough to bias brain organization toward the other sex‑typical pattern—even when karyotype is “typical” and no classic DSD is diagnosed.

1) Maternal androgen excess (temporarily high androgens in the pregnant parent)

• Luteoma of pregnancy (a transient ovarian growth) can secrete androgens and virilize an XX fetus; mom may also become virilized. This resolves after delivery. (PubMed Central, Jpag Online, PubMed)

  
  

• Exogenous/iatrogenic androgens (historic examples include danazol) have caused virilization of XX fetuses in case series; effects depend on dose and timing. (PubMed)

Why this matters for the brain: Androgen surges in critical windows can “masculinize/defeminize” aspects of the brain and behavior—even when chromosomes remain XX. Meta‑analytic and review evidence links higher prenatal androgens to more male‑typical play behavior in humans. (PubMed Central, ScienceDirect)

2) Reduced or lost fetal testicular function in an XY fetus (without a known syndrome)

• Testicular regression (anorchia) / fetal‑onset hypogonadism: An XY fetus that loses testicular function early may lack the normal androgen surge, resulting in undervirilized genitals at birth and, potentially, more female‑typical brain organization. Causes can be non‑genetic (e.g., vascular accidents/torsion). (PubMed Central, Frontiers)

  
  

3) Environmental/hormonal milieu that shifts androgen signaling

• Human data (and extensive animal work) suggest endocrine disruptors (e.g., some phthalates) can reduce androgen‑dependent genital measures (like shorter anogenital distance, AGD), indicating lower androgen action in utero. While AGD ≠ brain identity, it’s a biomarker that the hormonal environment was altered—the same environment that also shapes the developing brain. (PubMed, PubMed Central, Oxford Academic)

In all of these scenarios, the chromosomes haven’t changed—the hormonal environment did. Because brain differentiation happens later and is hormone‑sensitive, it can end up following a path that’s more typical of the other sex, regardless of karyotype or even external anatomy. (PubMed)

What does the science show about “female‑typical” vs “male‑typical” brain patterns?

• Classic postmortem studies found that in endosexual women (XY), a hypothalamic region called the BSTc has female‑typical size/neuron counts, even controlling for adult hormone treatment—evidence that some sex‑typical brain traits reflect early organization. Replications extended these findings. (PubMed)

  
  

• Reviews of neurobiology and gender identity emphasize that prenatal hormones are one contributing factor among many; no single biomarker “diagnoses” identity. (PubMed Central)

  
  

• At the same time, large‑scale MRI work shows most brains are mosaics with overlapping distributions—not two discrete types—so any individual may express a blend of features more common in one sex or the other. (PNAS)

  
  

Bottom line: it’s plausible—and documented—that some XY people organize certain brain systems along a female‑typical path (and some XX people along a male‑typical path) without having a named genetic DSD, because hormone exposure and timing are key drivers of brain sexual differentiation. (PubMed)

What about endosex people (no intersex traits) who feel “cross‑typical”?

Many endosex individuals (no observable intersex traits) experience gender identity or cognitive/behavioral patterns more typical of another sex. This can happen because:

• Brain differentiation is sensitive to hormones in utero, independent of visible genital anatomy. (PubMed)

  
  

• Subtle variability in prenatal hormone exposure (from maternal, placental, environmental, or fetal factors) can nudge brain circuits without producing external intersex traits. Evidence from behavior (e.g., play interests) and biomarkers supports this. (PubMed Central, ScienceDirect, Oxford Academic)

  
  

• Epigenetic mechanisms (changes in gene regulation without altering DNA sequence) likely participate in establishing and maintaining brain sex differences, offering non‑genetic routes to divergence. (PubMed Central, Royal Society Publishing)

A nuanced note on language

• Terms like “female brain” or “male brain” are shorthand for statistical patterns; they don’t imply that any one brain is wholly male or female. Most brains mix features typical of both sexes. (PNAS)

  
  

• Gender identity is multifactorial—biology (including prenatal hormones), life experience, and culture all play roles. No single study explains every person’s experience. (PubMed Central)

Clinical relevance (for patients, families, and clinicians)

• Do not assume that genital appearance or karyotype perfectly predicts later identity or brain organization. Clinical teams should communicate this timing mismatch compassionately when discussing intersex/DSD evaluations or gender questions. (PubMed)

  
  

• If a person reports cross‑typical identity or traits without a classic DSD diagnosis, that experience is consistent with current science on independent developmental windows and hormone‑sensitive brain organization. (PubMed)

  
  

• For gender‑diverse youth and adults seeking care, major medical organizations (e.g., Endocrine Society) provide evidence‑based guidelines emphasizing multidisciplinary evaluation and individualized treatment. (Endocrine Society, Oxford Academic)

References (selected, accessible)

• Timing & independence of genital vs brain differentiation: Swaab & Garcia‑Falgueras (2009); Bao & Swaab (2011). (PubMed)

  
  

• Maternal androgen excess (non‑genetic): Stewart et al., Ovarian luteoma review (2024); Spitzer et al. (2007) case series; Wang et al. (2005). (PubMed Central, Jpag Online, PubMed)

  
  

• Exogenous androgens (danazol) in pregnancy: Brunskill (1992); Rosa (1984). (PubMed)

  
  

• Reduced fetal testicular function in XY: Pirgon et al., Vanishing Testes review (2012); Tack et al. (2023); Grinspon et al. (2014). (PubMed Central, Frontiers)

  
  

• Prenatal androgen exposure & behavior: Hines (2003, 2015); Kung meta‑analysis (2024). (PubMed, PubMed Central, ScienceDirect)

  
  

• Endocrine disruptors as androgen antagonists (AGD evidence): Swan et al. (2005, 2006, 2015). (PubMed, PubMed Central, Oxford Academic)

  
  

• Neuroanatomical studies tied to gender identity: Zhou et al. (1995); Kruijver et al. (2000); review in Arch Sex Behav (2016). (PubMed, SpringerLink)

  
  

• Brains as mosaics, not binaries: Joel et al., PNAS (2015). (PNAS)

  
  

• Epigenetics of brain sex differences: Forger (2016) and related reviews. (PubMed Central, Royal Society Publishing)

  
  

• Clinical guidance: Endocrine Society Clinical Practice Guideline (2017; resource page 2024). (Oxford Academic, Endocrine Society)

FAQ

Does this mean chromosomes don’t matter? Chromosomes matter a lot—for gonadal development and many downstream processes. But they are not the whole story; the timing and levels of hormone exposure—and how tissues respond to those signals—are also crucial. (PubMed)

Can environment alone “flip” the brain’s sex? No single factor “flips” anything. Evidence shows gradients and mosaics, not switches. Environmental factors can shift hormone action during sensitive windows, potentially nudging some brain features toward the other sex‑typical mean. (PNAS)

I’m endosex and feel very cross‑typical—is that consistent with biology? Yes. Atypical or subtle prenatal hormone milieus (maternal, placental, environmental, or fetal) and epigenetic regulation can shape brain circuits independently of external anatomy. (PubMed, PubMed Central)