Gender with a new Twist and a Stutter

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Researchers in Goteburg University and the Karolinska Institute in Gotesburg and Stockholm are researching possible causes for transgender behaviour, basing their research on genes known to affect the sexual development of the brain. The research results are described in the August 2005 issue of Psychoneuroendocrinology.

The findings suggest that transgender behaviour may depend on specific segments of D.N.A. where the code "stutters", repeating a few letters of the code many times. These variants are "all much more common than the frequency of transgender" but the researchers say the stuttering genes may facilitate or prevent transgender.

One variant seemed to be significantly associated with transgender. This gene produces a molecule called E.R.-Beta which acts a gateway controlling the flow of estrogen through the brain during foetal development.

Estrogen is thought to be responsible for "wiring" the brain for masculinity in males before birth, although it is more generally known as a female and feminising hormone. After birth it influences the development of feminine characteristics.

The gene producing the E.R.-Beta receptor contains a "stutter", properly called a "C.A. repeat sequence" which contains the C and A letters of the genetic code repeated many times sequentially.

The researchers found that this repeat sequence was associated with a much higher likelihood of transgender in the study, which included 29 M.T.F. transgenders and 229 non-transgender men.

It is not understood how this receptor contributes to transgender but it is possible that it changes the molecular gateway and allows easier or more difficult transmission of estrogen. The researchers admit that there is no certainty what effect the receptor has and this may not be determined until further research with greater numbers of subjects has been carried out.

The researchers also believe two other genes may influence the risk of becoming transgender but neither of these was decisive on its own. Rather, specific combinations of the three substances seemed to occur among trans-gender subjects.

The other genes were those which encoded the production of aromatase and androgen receptor. These genes are believed to determine how "male" the brain will become. They affect the relative size of some of the structures of the brain, structures which typically are larger or smaller in male and female brains, and may determine the innate gender of the subject.

The frontal cortex and the limbic cortex are bigger in women (reasoning functions and emotions) than they are in men when compared to other parts of the brain. Parts of the parietal cortex and the amygdala (spatial perception and emotion) are bigger in men. Part of the hypothalamus is also thought to be bigger in men. Studies have also shown differences between heterosexual and homosexual males in another part of the hypothalamus but research has never shown that homosexuality and transgender have anything in common biologically other than that they can now be shown to have possible genetic bases.

The idea that genes underlie transgender, at least in the case of M.T.F. transgenders, is gaining support following reports on twin and non-twin siblings with the same genetic stutter, and from families where there are more than one member with the genetic condition.

Gender identity is usually established by the time a child is eighteen months to two years old, according to the Merck Manual of Diagnosis and Therapy, 17th edition.

This supports the anecdotal evidence provided by the vast majority of transgenders, and refutes the theory that transgenders transitioning in middle age or later and claiming to have been transgendered since infancy are lying in order to justify the need to transition at a mature age.

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