Possible Explanation of Male Homosexuality as a Result of Birth Order
"Proportion of homosexual men who owe their sexual orientation to fraternal
birth order" American Journal of Human Biology 2004; 16: 151-157, Ray Blanchard
and Anthony Bogaert, abstract below.
A Possible Explanation of this Report.
Copyright James Michael Howard, Fayetteville, Arkansas, U.S.A.
It is my hypothesis (1985) that male homosexuality results from low
dehydroepiandrosterone (DHEA) in utero. Specifically, I refer to low maternal
DHEA since the mother provides DHEA for herself and her fetus. (This is derived
from my principal hypothesis that DHEA was selected by evolution because it may
optimize replication and transcription of DNA. Therefore, growth and
development of all tissues, especially the brain, is affected by DHEA levels.)
I suggest low DHEA, during a critical time, reduces growth and development of
the part of the brain involved in sexual orientation. That is, low DHEA results
in a less robust development. This effect may be influenced by birth order
involving males.
It is also my hypothesis that testosterone evolved to direct the use of DHEA.
That is, testosterone increases growth and development of tissues by directing
more of available DHEA for use by "testosterone-target-tissues." I think
estradiol acts identically but testosterone exerts a stronger effect.
Therefore, this differential use of DHEA by estradiol or testosterone may
determine sexual expression of multi-potent tissues, as well as their size, by
inducing differential gene expression. I suggest the same effect controls
growth and development of the brain. In this case I have to assume that sexual
determination occurs before sexual orientation. My point is that testosterone
may be involved in use of DHEA for this process and levels of available DHEA may
affect growth and development of the brain involved in sexual orientation.
DHEA levels decline in women following a first birth and remain low for some
time. "A cross-sectional study (measuring serum DHAS and DHA only) was then
carried out in a series of parous and nulliparous women. The serum DHAS
sulfate] and DHA levels were markedly and significantly lower in parous
than in nulliparous women, as expected. There was no significant relationship
between serum DHAS or DHA levels and months elapsed (up to 150) since last
delivery, indicating that the changes last at least for this period of time.
There was no significant relationship between serum DHAS or DHA levels and
parity (one to three previous pregnancies), indicating that the changes occur
only after a first pregnancy." (J Clin Endocrinol Metab. 1987 Jan;64(1):111-8).
I suggest this may be the source of this subset of homosexual men. That is,
this reduction of maternal DHEA may be a gradual decline which is then
periodically affected by male fetal testosterone production. As subsequent
males are conceived, they develop in a reduced DHEA environment which is further
reduced by the use of this low DHEA by fetal testosterone-target-tissues.
(Evidently, since this effect has not been identified in the case of foregoing
sisters, estradiol may be not sufficient to induce this effect. However, with
increases in data base size, this may be ultimately be identified.) I suggest
the findings of Blanchard and Bogaert may be explained by this mechanism. That
is, each consequtive male is exposed to less maternal DHEA, which is then
further reduced by fetal testosterone, and growth and development of specific
parts of the brain is less robust, resulting in homosexual orientation.
More:
http://www.bio.net/bionet/mm/neur-sci/2004-April/057991.html