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----- Original Message -----
Sent: Sunday, March 07, 2004 9:02
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Subject: ugnet_: Drs. Buga /Munini on
Sex, genetics & Human behavoiur
http://www.idr.co.ug/dfwa-u/gallery.htm
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From: "Geoffrey A. B Buga"
<[EMAIL PROTECTED]>
To: <[EMAIL PROTECTED]>
Subject: Re: ugnet_:
Biology of human sexuality
Date: Fri, 15 Oct 1999 07:33:54
+0200
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Hi Dr
Muniini,
I have read both your submissions on homosexuality, and I must
say you did
a very good expose'. Mine was a belated attempt to explain some
aspects of
homosexuality. But the biological explanations are certainly not
enough. I
agree with you that social determinants impact heavily on the
_expression_ of
homosexual tendencies. So tomboys may ultimately grow up to
have husbands
and children, whereas deep down in themselves, some might
still prefer to
have sex with other women. Where the society is more
permissive, such women
may have an opportunity to express their lesbianism.
There is evidence to
suggest that a fair proportion of lesbians were once
tomboys when they were
children. And tomboyism seems to be strongly
associated with perinatal
exposure of a female child to inappropriately
increased levels of
androgens. Whereas such androgen exposure would have
rendered the cyclic
centre of a female rat acyclic (this centre is in the
pre-optic anterior
hypothalamus and parts of the suprachiasmatic portions
of the
hypothalamus), leading to masculinization, defeminization and
infertility,
it has no such drastic effect on monkeys and women who in fact
retain their
fertility.
Most of the recent research continues to
use animal models, and they
confirm that sex steroids influence animal
sexual behaviour during
perinatal life when the brain differentiates, and
after puberty. It seems
to be the view that in mammals, female sexual
behaviour is an inherent
feature of development which we would probably all
revert back to as the
template (much like the gonads and genitalia), and
that male sexual
behaviour is superimposed on this template by exposure to
androgens. The
strange thing is that in rats and mice, the androgens have
to first be
changed into oestrogens in the preoptic anterior hypothalamus
in order to
masculinize the brain! Yet direct administration of oestrogens
into this
area of the brain does not masculinize, and so the oestrogens
in
circulation in females do not quite masculinize the female. Only
exposure
of this female to excess androgens would do so via conversion of
the
androgens into oestrogen. It would therefore seem that the
hypothalamus
prefers to do the conversion for itself and does not like
ready-made
oestrogens. As a result of this, the activity of the enzyme
(P450
aromatase) necessary for this conversion of androgens into oestrogens
is
increased in male rats and mice, and the area is structurally bigger
in
males than females. Other parts of the cortical brain, e.g. the
corpus
callosum, also respond to androgens and oestrogens to display
sexually
dimorphic behaviour.
It is not clear whether androgens have
to be converted into oestrogens in
the brain before masculinization of the
primate and human brain. What is
however, clear is that androgens are
required both in the perinatal period
and in adulthood to maintain the
masculinized state and hence maintain male
sexual behaviour. Social
experience plays a role in this as well.
Thus masculinization is
accompanied by varying degrees of defeminization.
In other words, all males
have some inherent aspects of female sexual
behaviour that could surface
given the right circumstances.
There are really no conclusive studies
involving any particular part of the
brain that controls sexual orientation
and preference that I have come
across. It would also be difficult to
separate higher centre influences
from the hypothalamic ones. In short, we
are really in the dark, and are
likely to remain so because of the
constraints associated with studying the
brain in living human beings.
Postmortem studies cannot give you functional
answers. Your observations
about the PM studies on gays illustrates just
that. The conclusions would
have to be contrived.
Cheers
Geoffrey
Buga
----------
> From: [EMAIL PROTECTED]
> To:
[EMAIL PROTECTED]
> Subject: ugnet_: To Professor Geoffrey Buga re-
biology of human
sexuality
> Date: Tuesday, October 12, 1999 11:10
PM
>
> Hello Geoffrey:
>
> Thank you for a most
enjoyable review of human sexual development. This
is
> a complex
area which, unfortunately, is frequently reduced to polemics
and
>
emotional outbursts instead of reasoned debate. One hopes that your
>
contribution will make the anti-gay crusaders pose and think before
they
> throw the next arrow.
>
> I was intrigued by your
observation: << But later in adulthood, most
tomboys
> display
normal female sexual behavior, and have boyfriends, husbands and
>
children. This would suggest that, as in the monkeys, androgens cause
>
masculinization, but not complete defeminization.>>
>
>
This is possibly the case. However, I wonder how much of the tomboys'
>
eventual feminine role is a consequence of socialization and societal
>
expectations. In other words, since society expects "Alice Akello" to
be
a
> woman, and given that she has the female apparatus to fulfil
the role,
she
> proceeds to play the assigned role, when in fact deep
down she would
rather
> be "male".
>
> One question I
need help with is this: What is the current state of
> knowledge
regarding the role of the brain, specifically the hippocampus
and
>
the hypothalamus, in the determination of one's sexual orientation?
>
> Most of the material that has been published in this regard - at
least
what
> I have read - has not been convincing and some of it is
designed to prove
> that differences exist, rather than examining
whether differences exist.
>
> Of course Simon LeVay's now famous
paper (Scientific American 270
(1994):
> 44-49) in which he claimed
that one group of the Interstitial Nuclei of
the
> Anterior
Hypothalamus (INAH3) were smaller in homosexual men than in
>
heterosexual men
> (and were as small as they were in women) was
received with great
excitement
> by the gay community.
>
> The problem with LeVay's findings is that:
>
> 1. they
have not been corroborated;
>
> 2. all the homosexual men in the
study had died of AIDS. Since we know
that
> men with AIDS have
decreased testosterone levels as a result of the
disease
> or the
drug therapy, it is plausible that the INAH3 changes were a
>
consequence of the hormonal aberrations of AIDS.
>
>
>
There was another study which reported that the Suprachiasmatic
Nucleus
was
> larger in homosexuals than in heterosexuals. I am sorry
I cannot locate
the
> reference for this, but as I recall the study
was also on brains of males
> who had died of AIDS. I am not aware of
this report being corroborated.
>
> Perhaps you and our
neuro-anatomists and neurologists can shade some
light
> on these
issues, and the claims that there are differences between the
> corpus
callosum and anterior commisures of gays and heterosexuals.
>
>
Please accept my belated wishes for a Happy Independence Anniversary!
>
>
> Cheers,
>
>
> Muniini K.
Mulera
__________
bwanika
url:
www.idr.co.ug
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