Transsexuality is the result of hormone swings during fetal development.  By now the data is conclusive and irrefutable--based on animal models, naturally occurring human mutations, and human experimentation.

    Transsexuality can and has been artificially induced with over 95% reliability.

PHYSIOLOGIC BASIS:  Initial brain development & gender definition begin in the embryo 15 days after fertilization and depend on MATERNAL & local cellular factors.  Gonad differentiation begins 21 days after fertilization.  Fetal testosterone first appears (males only) between at 6-8 weeks- gestation--which then dictates all subsequent sexual development.

Thus there's a critical time between 15 days post-fertilization and 6 weeks gestation when the brain is developing independent of gonadal secretion.  During this time MATERNAL CORTISOL (stress hormone) is linked to embryonic testosterone production.

ANIMAL MODELS:   In the animal world transsexual equivalents are known as Freemartins.  For example, every time a cow bears mixed-sex twins (one male and one female calf), the female calf will be a Freemartin due to testosterone leakage through the placenta.  The calf is fully female biologically:  uterus, vagina, ovaries, etc.  But because of the fetal testosterone exposure, she has the basic personality of a steer (castrated male bovine)--male personality (gender) but female biology = transsexual.  

For many species a 1-3 week “window of opportunity” has been determined during which testosterone exposure will produce a freemartin.  Testosterone exposure outside of the window doesn’t.  For example the critical time is 18-27 days post-conception in rats.  In a Rhesus monkey it's 40-60 days post conception.

If mice are injected with testosterone but lack cellular testosterone receptors, they don’t change their behavior.  If mice produce defective testosterone they don’t acquire male behavior.  (Actual mechanisms of differentiation--fetal enzyme induction, etc--have been worked out in great detail.  To find out more, read Nature's Choice by Cheryl Weill, Routledge 2009)

NATURALLY OCCURRING HUMAN MUTATIONS:  Testosterone Insensitivity Syndrome is the human equivalent of the mouse experiment mentioned above.   XY chromosomes & testes are present in the newborn, while uterus & vagina are not present.  Functional testosterone is produced, but the cells lack receptors for the testosterone.  100% of those children have FEMALE gender (personality) & gender identity.

For example in Congenital Adrenal Hyperplasia a biologic female (XX chromosomes, ovaries, vagina & uterus) is exposed during fetal development to testosterone produced by the Adrenal glands.  Two-thirds of those children develop MALE gender; half develop male gender identity.   Only ONE-THIRD of these children have a female gender, in spite of female biology.

HUMAN EXPERIMENTATION:  During the 1950-1980’s it was commonplace to do genital surgery on newborn males if their genitals didn’t look quite right.  (See Old Paradigm to find out why)  In other words a newborn with male gender & gender identity plus male biology was surgically transformed into a newborn with male gender & gender identity but now with female biology--an artificially created transsexual.  The infants were then raised as girls, an imposed wrong-gender expression.

If post-natal influences had any impact at all on gender & gender identity, at least some of those infants would have grown up enjoying dolls and hopscotch.  In fact NONE of them grew into feminine girls.  ALL of them had male core personalities (gender--rough & tumble play, competitive, spatial, analytical, etc) even though they went through childhood treated as girls.  All of them were miserable because of the mismatch between their innate gender identity and their biology.  About one third later underwent surgery to go back to their original state (gender male, male gender identity, male biology).   (Reiner  et al New England Journal of Medicine 350(4): 333-41, Jan. 22, 2004)

...Just like naturally occurring transsexuals.