Homosexuality
in a Changing World: Are We Being Misinformed?
|
By
Dr. Nadia El-Awady
IslamOnline’s
Health & Science Editor
|
17/02/2003
|
Homosexuality-Related
Research
Much
research has been done over the years to discover the scientific
origins of homosexuality. Mostly it has been to disprove the fact
that homosexuality is a matter of choice. None of the research done
up to this date, however, is conclusive. Only varying theories exist
according to the results of such research.
Research
available on the topic of homosexuality can be divided into three
categories:
1.
Anatomical
differences
2.
Genetic
investigations
3.
Biological
causes
1.
Anatomical differences
Simon
LeVay, a self-proclaimed homosexual, presented research in 1991 that
was much publicized by the media. His report found neuroanatomic
differences between homosexual and heterosexual men. Much of the
field’s current visibility is due to the wide publicity
surrounding this study of INAH3, the third interstitial nucleus of
the anterior hypothalamus, which is normally three times larger in
men than in women. LeVay examined hypothalamic tissue from 19
homosexual men, all of whom died of AIDS; 16 heterosexual men, six
of whom had died of AIDS; and six women of unknown sexual
orientation. He found that INAH3 was two to three times larger in
heterosexual men than in homosexual men.
This
study was the first ever to imply that there were neuroanatomic
differences between homo and heterosexual men; thus, naturally, it
was the subject of much controversy relating to both its scientific
and its social implications. Many homosexual activists argued that
the study bolstered their contentions that some people are born gay
and that becoming gay was not a matter of choice. They thus arrived
at the conclusion that homosexuals should be granted protection
against discrimination. Many scientists, however, assailed LeVay’s
methodology and the conclusions of his work. These counter-arguments
did not receive the same amount of media attention.
Another
neuroanatomical difference between homo and heterosexual men was
reported in 1992 by University of California at Los Angelos
investigators Laura S. Allen, a research scientist, and Roger
Gorski, a professor of neurobiology (L.S. Allen, R. Gorski, Proceedings
of the National Academy of Sciences, 89:7199-202).
The
anterior commissure, a relatively small bundle of axons connecting
the two brain hemispheres, which is larger in women than in men, was
found to be also larger in gay men than it is in heterosexual men.
In a related study, Dick F. Swaab and coworkers at the Netherlands
Institute for Brain Research reported that a hypothalamic structure,
known as the central subdivision of the bed nucleus of the stria
terminalis, is larger in men than in women, and also larger in men
than in male-to-female trans-sexuals. (J.N. Zhou et al., Nature,
378:68-70, 1995).
This
anatomical work came under heavy criticism by William Byne, director
of the Neuroanatomy Laboratory of Neuropsychiatric Disease at New
York’s Mount Sinai Medical Center. “A general problem with this
work is that there have been dozens and dozens of reports of sex
differences in the human brain since the middle of the last century.
But not a single one of these has been corroborated, except for the
one that men tend to have slightly larger brains than women. The
reason for that is that it’s tremendously difficult to do
morphometric studies in the human brain. I would be surprised if
there weren’t sex differences in the human brain, since there are
sex differences in just about every organ system in humans. But to
date, we can’t say with any confidence where the sex differences
are.”
Byne
also thinks that even if the sex differences are real, LeVay’s
findings could have been confounded by the fact that all his
original gay subjects died of AIDS. LeVay maintains that he
controlled this by examining the brains of heterosexual men who died
of AIDS, as well as one gay man who died of other causes. Dr.
William Byne argued that, “[LeVay’s] inclusion of a few brains
from heterosexual men with AIDS did not adequately address the fact
that at the time of death virtually all men with AIDS have decreased
testosterone levels as the result of the disease itself or the side
effects of particular treatments. Thus it is possible that the
effects on the size of the INAH3 (hypothalamus) that he attributed
to sexual orientation were actually caused by the hormonal
abnormalities associated with AIDS.” (E. Byne, "The
Biological Evidence Challenged," Scientific
American (May 1994):
50-5)
Byne
gives as an example the fact that many people with AIDS suffer
testicular atrophy before death, and since gonadal hormones are
known to regulate the size of several hypothalamic nuclei in
animals, disease effects can not be excluded.
Another
weakness of LeVay’s study is that even in his sample there were
exceptions. In other words, there were some homosexuals who had
larger hypothalamic structures than some of the heterosexuals
examined. Even LeVay admits that these exceptions “hint at the
possibility that sexual orientation, although an important variable,
may not be the sole determinant of INAH3 (hypothalamus) size.”
Since
the release of LeVay’s study, other researchers have found that
brain structures can change as a result of life experiences. In
1997, University of California at Berkeley psychologist Marc
Breedlove released a study that showed that sexual activities of
rats actually structurally changed aspects of the brain at the base
of the spinal chord. “These findings give us proof for what we
theoretically know to be the case - that sexual experience can alter
the structure of the brain, just as genes can alter it,” Breedlove
commented. “You can’t assume that because you find a structural
difference in the brain, that it was caused by genes. You don’t
know how it got there.” He also states that, “It is possible
that differences in sexual behavior cause (rather than are caused
by) differences in the brain.” (Pat McBroom, "Sexual
Experience May Affect Brain Structure,"
Berkeleyan
campus newspaper [University of California at Berkeley], 19 November
1997).
Indeed
LeVay himself offered the following criticisms of his own research:
“It’s important to stress what I didn’t find. I did not prove
that homosexuality is genetic, or find a genetic cause for being
gay. I didn’t show that gay men are born that way, the most common
mistake people make in interpreting my work. Nor did I locate a gay
center in the brain. INAH3 is less likely to be the sole gay nucleus
of the brain than part of a chain of nuclei engaged in men and
women’s sexual behavior…Since I looked at adult brains, we
don’t know if the differences I found were there at birth, or if
they appeared later.” LeVay also made an interesting observation
about the emphasis on the biology of homosexuality. He noted,
“…people who think that gays and lesbians are born that way are
also more likely to support gay rights.” (The Innate-Immutable
Argument Finds No Basis in Science. In Their Own Words: Gay
Activists Speak About Science, Morality, Philosophy. A. Dean
Byrd, Ph.D.; Shirley E. Cox, Ph.D.; Jeffrey W. Robinson, Ph.D., Salt
Lake City Tribune: May 27th, 2001).
2.
Genetic Investigations
Twin
Studies
In
studies on male and female homosexuals who are twins, Northwestern
University’s J.M. Bailey and his associates claimed that they
found clear evidence for genetic transmission. In a study of gay
men, 52% of their identical twins, 22% of their fraternal twins of
the same sex, and only 11% of their adopted brothers were also gay
(J.M. Bailey, R.C. Pillard, Archives of General Psychiatry,
48:1089-1096, 1991).
Among
lesbian women, 48% of their identical twins, 16% of their fraternal
twins of the same sex, and only 6% of their adopted sisters were
also lesbian (J.M. Bailey et al., Archives of General Psychiatry,
50:217-223, 1993). Aside from these twin studies, there have been
few, if any, firm results showing neuroanatomical or genetic
correlates for female homosexuality.
The
findings of the male twin study appear to support the argument for
biology, since identical twins share the same genes. However, the
rate of non-twin conformity should mirror that of fraternal twins.
In the Bailey and Pillard study, the rate was only 9.2%. And the
rate in adopted - which, if the biological hypothesis were true,
should have been even lower than non-twin brothers - was actually
higher (11%). (J.M. Bailey, R.C. Pillard, "A Genetic Study of
Male Sexual Orientation," Archives of General Psychiatry
48 [1991]: 1089-96).
In
his analysis of the medical evidence supporting a biological cause
of homosexuality, Dr. William Byne noted other twin studies. He
wrote, “Without knowing what developmental experiences contribute
to sexual orientation, the effects of common genes and common
environments are difficult to disentangle. Resolving this issue
requires studies of twins raised apart.” Other physicians have
also criticized the study for overvaluing the genetic influence.
Byne
also criticizes Bailey’s study noting that subjects were recruited
by ads placed in gay publications. “Some people have suggested
that identical twins who are concordant on a variety of measures are
more likely to respond to these ads than ones who are different,
which would lead to an increased estimate of heritability.”
Bailey
conducted another study, published in the March 2000 issue of the Journal
of Personality and Social Psychology, that revealed that the
genetic influence on homosexuality he supposedly found earlier may
actually be less. He sent a questionnaire to the entire Australian
Twin Registry. Only three pairs of identical male twins were both
homosexuals out of a total of 27 male identical twin pairs in which
at least one was homosexual. Of the 16 fraternal male twins, in none
of the pairs were both homosexuals. Bailey found similar results for
lesbians.
Bailey
says that his data in men lead to an estimate that the overall
heritability of sexual orientation ranges from 25-75%, depending on
a number of assumptions.
Bailey’s
team also asked non-concordant identical twins (one was homosexual,
one not) about their early family environment, and found that the
same family environment was experienced or perceived by the twins in
quite different ways. These differences led later to homosexuality
in one twin, but not in the other. (N. E. Whitehead,
Ph.D;http://www.narth.com/docs/whitehead.html).
N.E.
Whitehead, Ph.D. of the National Association for Research and
Therapy of Homosexuality (NARTH)
ponders over the results of concordant identical twins, whether
their genes could have “made them do it”. He contends that they
didn’t. According to him:
Genes
could be a strong influence for a few, but even for those few,
it is never overwhelming. The record strengths for genetic
influence on behaviors are 79% in a group of highly addicted
women cocaine addicts and about the same or somewhat higher, for
ADHD. Because those figures are not 100%, even among addicts or
those strongly pushed towards some other behavior, there is room
for outside intervention and change. Hence even if homosexuality
is as addictive as cocaine for a few individuals, their genes
didn’t ‘make them do it.’
For
perspective, it is valuable to compare genetic contributions to
homosexuality with the question - is a girl genetically
compelled to become pregnant at 15? Her genes might give her
physical characteristics that make her attractive to boys - but
whether she gets pregnant will depend greatly on whether her
community is Amish or urban, conservative or liberal, whether
they use contraceptives, and whether the parents are away for
the evening.
So
the influence of the genes is very indirect. We can see this by
thinking further - if she was in solitary confinement all her
life, would her genes make her become pregnant? Of course not!
Some influence from the environment (in this case a boy) is
essential! The effects of genes on behaviors are very indirect
because genes make proteins, not preferences.
So
the results of identical-twin studies are critical in
understanding the biological influences on homosexuality. Only
for physical traits like skin color are identical twins 100%
concordant; otherwise they don’t necessarily follow either
their parents’ genes…or their parents’ admonitions! In
this, homosexuality proves to be no different from such
unrelated behaviors as violence, being extroverted, or getting
divorced. All may be influenced by genes, but not overwhelmingly
determined by them.
The
scientific truth is - our genes don’t force us into anything.
But we can support or suppress our genetic tendencies. We can
foster them or foil them. If we reinforce our genetic tendencies
thousands of times (even if only through homoerotic fantasy), is
it surprising that it is hard to change? Similarly, we have a
genetic tendency to eat, but it is possible to foster this
tendency and overeat for the pleasure it brings. If we repeat
that often enough, we will not only reinforce a genetic tendency
to become overweight, but find that “starving” the habit
takes a long time! (http://www.narth.com/docs/whitehead.html)
Another,
quite obvious, example of what Dr. Whitehead is saying is that of
alcoholism. It has been demonstrated that there may be a genetic
predisposition towards the condition. If a person does not drink
alcohol, however, he will not possibly become an alcoholic.
Thus
it is the behavior one assumes during one’s life that determines
the acquisition of a certain genetic predisposition, not the gene
itself.
The
“gay” gene
Dean
H. Hamer, chief of the Gene Structure and Regulation Section of the
National Cancer Institute’s Laboratory of Biochemistry, and his
coworkers, conducted a study of the pedigrees of gay men who also
had gay brothers. Hamer found that such people had an excess of gay
relatives on the mother’s, but not the father’s side of the
family. Reasoning that this might indicate that sexual orientation
might be linked to the X chromosome, Hamer conducted a linkage
analysis to determine if any DNA markers on the X chromosome would
be inherited along with the putative gene for sexual orientation. In
33 of 40 pairs of gay brothers, he found such a marker near the tip
of the long arm of the X chromosome, in a location called Xq28, an
area that contains several hundred genes (D.H. Hamer et al., Science,
261:321-7, 1993). Hamer later replicated this finding in a new
set of families (S. Hu et al., Nature genetics, 11:248,
1995).
Hamer’s
results are often misunderstood. Many believe that the study found
an identical sequence (Xq28) on the X chromosome of all homosexual
brothers. In reality, what it found was matching sequences in each
set of brothers who were both homosexuals. Dr. William Byne argues
that in order to prove anything by this study, Hamer would have had
to examine the Xq28 sequence of gay men’s heterosexual brothers.
Hamer insisted that such an inclusion would have confounded his
study. Byne responded, “In other words, inclusion of heterosexual
brothers might have revealed that something other than genes is
responsible for sexual orientation.”
In
1999, on the other hand, Drs. George Rice, Neil Risch and George
Ebers published their findings in Science after attempting to
replicate Hamer’s Xq28 study. Their conclusion: “We were not
able to confirm evidence for an Xq28-linked locus underlying male
homosexuality.” Moreover, they added that when another group of
researchers (Sanders, et al.) tried to replicate Hamer’s study,
they, too, failed to find the genetic connection to homosexuality.
Ebers
explains:
We’ve
been collecting families that have more than one gay person for
five years, and we’ve gone through something like 400
pedigrees. In those [families] there is really no support for
the idea that male homosexuality is X-linked. The DNA tests that
were done didn’t even support Dean’s idea a bit. There
wasn’t even a trend toward increased sharing of haplotypes
down there at Xq28.
Ebers
speculates that there may be a simple explanation for Hamer’s
finding of maternal transmission:
There
may be an excess of all kinds of things on the maternal side
because mothers know more about their family history than
fathers. Something of a personal nature like this is perhaps
even more likely to be something that you would [learn] from the
maternal side.
(http://www.neurolinguistic.com/proxima/articoli/art-41.htm)
Rice
concluded in the Rice et al study:
It
is unclear why our results are so discrepant from Hamer’s
original study. Because our study was larger than that of
Hamer’s et al, we certainly had adequate power to
detect a genetic effect as large as reported in that study.
Nonetheless, our data do not support the presence of a gene of
large effect influencing sexual orientation at position Xq28. (http://www.narth.com/docs/innate.html)
Byne
offers another possible confounding factor in Hamer’s work:
The
hallmark of X-linked transmission is the absence of
father-to-son transmission…It’s possible that just the
relative absence of father-to-son transmission - because gay men
tend not to have children - could have given Dean the impression
of X-linked transmission in his first pedigree study. (http://www.neurolinguistic.com/proxima/articoli/art-41.htm)
Hamer
himself offered some conclusions regarding genetics and
homosexuality:
We
knew that genes were only part of the answer. We assumed the
environment also played a role in sexual orientation, as it does
in most, if not all behaviors…. Homosexuality is not purely
genetic…environmental factors play a role. There is not a
single master gene that makes people gay…I don’t think we
will ever be able to predict who will be gay. (http://www.narth.com/docs/innate.html)
Citing
the failure of his research, Hamer further writes:
The
pedigree failed to produce what we originally hoped to find:
simple Mendelian inheritance. In fact, we never found a single
family in which homosexuality was distributed in the obvious
pattern that Mendel observed in his pea plants. (http://www.narth.com/docs/innate.html)
Hamer’s
research has been cast into doubt not only by arguments over his
interpretation of the data, but also by allegations of scientific
misconduct. According to a front-page article by John Crewdson in
the Chicago Tribune (June 25, 1995), an anonymous former
member of Hamer’s lab had alleged that Hamer engaged in selective
presentation of data in his 1993 Science paper. Crewdson
reported that an investigation had been launched by the Office of
Research Integrity (ORI) of the United States Department of Health
and Human Services.
An
article on genes and behavior in Science magazine said:
The
interaction of genes and environment is much more complicated
than the simple “violence genes” and intelligence genes”
touted in the popular press. Indeed, renewed appreciation of
environmental factors is one of the chief effects of the
increased belief in genetics’ effects on behavior. The same
data that show the effects of genes also point to the enormous
influence of non-genetic factors. (C. Mann, “Genes and
behavior,” Science 264; 1687 (1994), pp. 1686-1689)
Among
Jeffrey Satinover’s conclusions on the “gay gene” are:
-
There
is a genetic component to homosexuality, but “component” is
just a loose way of indicating genetic associations and linkages.
“Linkage” and “association” do not mean “causation.”
-
There
is no evidence that shows that homosexuality is genetic-and
none of the research itself claims there is. Only the
press and certain researchers do, when speaking in sound bites to
the public.
3.
Biological Causes
In
addition to the neuroanatomical and genetic work, several other
studies argue for a biological basis for sexual orientation. In one,
Lee Ellis indicated that “if the mother experiences a lot of
stress - and it’s got to be severe - during the second trimester
[of pregnancy], there will be a significantly higher chance that her
male offspring would be homosexual when they became sexually
mature” (L. Ellis et al., Journal of Sex Research, 25[1]:
152-7, 1988). Another study published in Behavioral Neuroscience suggests
that, compared with heterosexual men, gay men show a leftward
asymmetry in the number of fingerprint ridges on their thumbs and
little fingers (J.A.Y. Hall, D. Kimura, Behavioral Neuroscience,
108[6]: 1203-6, 1994).
Bailey
reports that a common behavioral finding about male homosexuals
provides additional support for a biological hypothesis. “The most
consistent finding about male homosexuality is that as children, gay
men were feminine boys,” as judged by such factors as lack of
interest in sports or rough play, reputation as a “sissy,” or a
desire to be a girl.
Perhaps
75% of feminine boys grow up to be gay men, which is a huge
increase over expected rates. That’s generally consistent with
a biological hypothesis because you have these boys playing
atypically at a very early age - three to five - in a way they
haven’t been socialized to behave. In fact, they’re often
punished for behaving that way (J.M. Bailey, K.J. Zucker, Developmental
Psychology, 31[1]: 43-55, 1995).
In
1998, researchers Dennis McFadden and Edward G. Pasanen published a
study that evaluated the auditory systems of heterosexuals and
homosexuals. Specifically, the study considered differences in
echo-like waveforms emitted from an inner ear structure of people
with normal hearing. These waves are higher in women than in men,
often attributed to the person’s exposure to androgen in his or
her early development as a fetus.
The
McFadden study found the level of these waveforms in the ears of
self-acknowledged lesbian women ranged between those of men and
those of heterosexual women. The researchers concluded that this
evidence suggests that female homosexuality could be a result of
increased exposure to the male hormone androgen in the womb
(homosexual men did not show the same variation).
The
researchers themselves, however, are not too quick to draw
definitive conclusions. They caution that the results are only
tentative. In the published study, they point out that exposure to
“intense sounds, certain drugs, and other manipulations” can
lower the level of these auditory waveforms. “Thus, it may be that
something in the lifestyles of homosexual and bisexual females leads
them to be exposed to one or more agents that have reduced the
(waveforms), either temporarily or permanently.” Moreover, even if
the hearing differences were caused by an increased exposure to
androgen in the womb, scientists would still be a far cry away from
proving that this exposure is a cause of homosexuality -especially
since the difference was not apparent in the male homosexual sample.
In
March 2000, yet another study on a biological link to homosexuality
surfaced. Scientists reported that finger length indicated how much
exposure a person had had to androgen while in the womb (Williams,
T.J., Pepitone, M.E., Christensen, S.E., Cooke, B.M., Huberman,
A.D., Breedlove, N.J., Breedlove, T. J., Jordan, C.L. &
Breedlove, S.M. (2000): Nature 404, 455-456).
Typically,
people’s index finger is slightly shorter than the ring finger - a
difference that is seen more clearly on the right hand due to
exposure to higher levels of androgen while the human is developing
in the womb. In females, the ring finger and index finger are almost
the same size, but in men the ring finger is generally shorter.
Niel
Whitehead, Ph.D. of NARTH comments on this study by saying:
Williams
et al. reported that the mean finger-length ratio for lesbians
was significantly less than that for heterosexual women, and did
this by comparing the two ratios by a statistical test. They
used a large number of interviewees. In such circumstances,
although the mean finger lengths may be statistically different,
they are often so close that it is not practically useful to say
they are different. That is what has happened in the present
case.
The
original normal distributions can be reconstructed from the
researchers' data, and the results are shown in the figure
below. (With its two large overlapping curves, this figure
assumes that we are comparing an equal number of heterosexual
women and lesbians).
There
is obviously a very large overlap in the two populations
(heterosexual women and lesbians), and although the two means
may be statistically different, the difference is only 1% -
which is a small effect, and not diagnostically useful in any
sense.
Within
the figure is also given the expected distribution of finger
lengths for lesbians, assuming a United States nation-wide
prevalence of 1.7% (which includes bisexual lesbians). For any
finger-length ratio chosen, the lesbians in the population at
large are outnumbered by their heterosexual counterparts by
approximately 60:1.
The
figure shows that there are large numbers of heterosexual women
who have much more "masculine" finger-length ratios
than most lesbians, but this is not considered by the
researchers to be related to their sexual orientation.
Williams
et al. invoke the idea of very high prenatal androgen levels
(for which there is very scant evidence) to explain the
difference in mean finger lengths which they find. But if this
is indeed an explanation, it must rarely affect sexual
orientation. An explanation which involved considerably less
biological extrapolation would be preferable. For example, does
a slightly more masculine pattern for a hand influence the
self-image of a developing girl?
This
study is rather similar to many other reported links between
homosexuality and some biologically based phenomena. Although
statistical connections may be shown, only a small percentage of
subjects with that biological feature actually end up
homosexual. (http://www.narth.com/docs/newstudy2.html)
Prominent
research teams Byne and Parsons, and also Friedman and Downey, each
concluded that there was no evidence to support a biologic theory,
but rather that homosexuality could be best explained by an
alternative model where “temperamental and personality traits
interact with the familial and social milieu as the individual’s
sexuality emerges.” (W. Byne and B. Parsons, “Human Sexual
Orientation: The Biologic Theories Reappraised.” Archives of
General Psychiatry 50, no. 3.)
Are
homosexual attractions innate? There is no support in the scientific
research for the conclusion that homosexuality is biologically
determined (A. Dean Byrd, Ph.D. http://www.narth.com/docs/innate.html).
Sociologist
Steven Goldberg, Ph.D. states:
Virtually
all of the evidence argues against there being a determinative
physiological causal factor and I know of no researcher who
believes that such a determinative factor exists…such
factors play a predisposing, not a determinative role…I know
of no one in the field who argues that homosexuality can be
explained without reference to environmental factors.
He
further says, “Gay criticism has not addressed the classic family
configuration.” It has merely “asserted away the considerable
evidence” for the existence of family factors. Studies which
attempt to disprove the existence of the classic family pattern in
homosexuality are “convincing only to those with a need to
believe.” (S. Goldberg, When Wish Replaces Thought; Why So Much
of What You Believe is False. Buffalo, New York: Prometheus
Books, 1994)
Simon
LeVay writes:
At
this point, the most widely held opinion [on causation of
homosexuality] is that multiple factors play a role. In
1988, PFLAG (Parents and Friends of Lesbians and Gays) member
Tinkle Hake surveyed a number of well-known figures in the field
about their views on homosexuality. She asked: “Many observers
believe that a person’s sexual orientation is determined by
one of more of the following factors: genetic, hormonal,
psychological, or social. Based on today’s
state-of-the-art-science, what is your opinion?” The answers
included the following: “all of the above in concert” (Alan
Bell), “all of these variables” (Richard Green), “multiple
factors” (Gilbert Herdt), “a combination of all the factors
named” (Evelyn Hooker), “all of these factors” (Judd
Marmor), “a combination of causes” (Richard Pillard),
“possibly genetic and hormonal, but juvenile sexual rehearsal
play is particularly important” (John Money), and “genetic
and hormonal factors, and perhaps also some early childhood
experiences” (James Weinrich). (Simon LeVay, Queer Science,
MIT Press, p. 273).
The
role of the media in making information available on such research
as mentioned above is of major importance. The media have been noted
to put the spotlight on “pro-homosexual” research without even
mentioning the fact that there are any arguments related to that
research. It has become taboo in the West to be labeled a homophobe.
Does Western media go to great lengths to prove themselves worthy of
the very active and quite strong gay and lesbian movements? Do they
selectively choose what reaches the reader and what does not, to
that end?
