This is an early draft of an article I recently published, with Richard
Pillard, in the "Harvard Mental Health Letter" entitled something like "The
Innateness of Sexual Orientation." (Copyright be damned.) Unfortunately, I
don't discuss Hamer's recent X-linkage finding in "Science." 

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	Recently much media attention has focused on the question of what causes
some people to be homosexual and others to be heterosexual. There are at
least two reasons for this attention. First, gay rights issues have been
prominent on the national agenda, and some commentators have argued that
etiology is pertinent to their resolution. Second, scientists have recently
reported several studies supporting the possibility that sexual orientation
is primarily innate, rather than psychosocially determined. The worth and
implications of these studies have been hotly debated. We believe that at
least some of the studies are scientifically valuable and that biological
theories of sexual orientation are the most promising currently being
investigated. 
	Two lines of evidence suggest that sexual orientation is influenced by
innate processes: neuroendocrine (including neuroanatomical) and genetic
studies. Neuroendocrine theories are more fully developed and have spurred
far more research. At the same time, however, cumulative empirical support
for neuroendocrine influences is perhaps more tenuous than that for genetic
influences. 

Neuroendocrine Studies

	Neuroendocrine views were originally motivated by the observation that gay
men are like most women in being attracted to men; lesbians are like most
men in their attraction patterns. The neuroendocrine view posits a process
that is analogous to the differentiation of the external genitalia, about
which much is known. At the risk of oversimplifying, the basic
neuroendocrine hypothesis is that sexual orientation is determined by the
early (probably prenatal) effects of androgens on relevant neural
structures. If these structures are effectively exposed to high levels of
androgens, then they are masculinized, and attraction to women will result
in adulthood. If they are not exposed to high levels of androgens (either
because there are low amounts of androgens or because the relevant tissues
are insensitive to their effects), the structures do not masculinize, and
attraction to men will result. Several lines of research support the
likelihood of neurohormonal influences on human sexual orientation, and we
consider them from the least to the most direct. 
	Studies of rodents have shown clearly that some sex-typical sexual
behavior can be affected by altering early androgen levels. Adult female
rats and mice that received male-typical doses of androgens sufficiently
early will, under certain circumstances, display some male mating behaviors
such as mounting and reduced lordosis. Conversely, males deprived of early
androgens will show the opposite pattern of behavior. It has been widely
acknowledged--by both sides of the biology debate--that neither mounting
nor lordosis behavior is directly analogous to human sexual orientation, in
which the sex of attraction is primary. Nevertheless, these studies have
been heuristically valuable in suggesting how sex-typical behavior
differentiates under the influence of early androgen exposure. Furthermore,
some recent studies of various nonhuman species have supported the
possibility of neuroendocrine influences on preference for male versus
female partners. 
	Perhaps the single most reliable finding in all of homosexology is that
gay men and lesbians recall, on average, substantially more gender atypical
behavior in childhood than do heterosexuals of the same sex. Gay men often
report that they were considered Òsissies,Ó and lesbians Òtomboys,Ó though
there are plenty of exceptions in both groups. This supports the idea that
homosexual people have been subject to some influences more typical of the
opposite sex and is thus consistent with a neuroendocrine hypothesis. 
Furthermore, studies of primates including humans have shown that some
patterns of sex-typical childhood behavior can be altered if fetuses are
exposed to unusual levels of androgens. Female rhesus monkeys exposed
prenatally to high levels of androgen show elevated rates of male-typical
(rough-and-tumble) play behavior.
	Similar findings have come from studies of girls and women with congenital
adrenal hyperplasia (CAH). CAH is a genetic disorder that causes a fetus to
secrete large amounts of androgens from the adrenal glands, enough so that
newborn girls with the condition often have virilized genitalia. Several
studies have found high rates of masculine behavior in girls with CAH,
including preference for masculine toys, increased rough-and-tumble play
activity, and other ÒtomboyishÓ behavior. Even more importantly, some
studies have found elevated rates of homosexual feelings among adult women
with CAH compared to control women. Women prenatally exposed to DES, a
chemical that causes masculinization of sexual behavior in some animals,
also have an elevated rate of homosexual feelings. At the same time, it
should be noted that only a minority of women with a history of DES
exposure or CAH admit to homosexual feelings. Furthermore, there is no
model of male homosexuality that maps as neatly onto the hypothesized
neuroendocrine route as does CAH for female homosexuality.
	The study most relevant to neuroendocrine theories of male homosexuality,
and certainly the most widely-discussed biological finding, is that of
Simon LeVay. LeVay examined the brains of gay men who had died of AIDS, as
well as those of presumably heterosexual men and women who had died of a
variety of causes. He studied cell-groups (nuclei) in an area of the
hypothalamus that had been implicated by animal work as important to
sexually-dimorphic sexual behavior. Two of the nuclei had previously been
shown to be larger in men than in women, and LeVay found the same sex
difference for one of the nuclei (INAH-3) when he compared heterosexual men
and women. More important for sexual orientation, he found that INAH-3 was
as small in gay as in heterosexual women. The differences were statistical
rather than absolute, i.e., there were some gay men and heterosexual women
with INAH-3 as large as those of most heterosexual men. This shows that the
size of INAH-3 cannot be the sole cause of sexual orientation; indeed, it
may not be a cause at all. But it does suggest that some aspects of the
brainÕs sexual differentiation are shared by gay men and heterosexual
women, and it is noteworthy that these include a portion of the brain that
animal work shows to be involved in sexual behavior.
	LeVayÕs study has been intensively scrutinized, and several criticisms
have been made. These include the concern that the difference may have been
due to AIDS, that the ÒheterosexualÓ sample could have included some
homosexual subjects (because medical records did not include sexual
histories), and that the observed difference could have been an effect,
rather than a cause, of homosexuality. These criticisms are unimpressive.
Some of the heterosexual men died of AIDS as well, and their average INAH-3
volume was no smaller than that of heterosexual men who died of other
causes. Recent surveys have suggested that the incidence of homosexuality
is rather low, and so it is unlikely that the heterosexual control groups
contained a significant proportion of homosexual people. (And if they had,
LeVay would have been even less likely to find the results he did.)
Finally, although the possibility that the anatomical differences resulted
from behavioral differences cannot be dismissed altogether, research on
some other mammalian species suggests that sex differences in the
hypothalamus develop early in response to innate hormonal influences and
are not modified by later experiences. 
	At least one other neuroanatomical study has found an association between
male sexual orientation and brain structure that tracks the heterosexual
sex difference. Laura Allen and Roger Gorski found the anterior commissure
of the corpus callosum to be relatively larger in heterosexual women and
homosexual men compared with heterosexual men. This portion of the brain is
unlikely to be directly involved in sexual behavior. Rather, the study
suggests that neuroendocrine influences may have more general effects. 
 
Genetic Studies

	Our own work has investigated the origins of sexual orientation using
techniques from human behavioral genetics. We have attempted to elucidate
the degree to which people who differ in their sexual orientations do so
for genetic versus environmental reasons. Both male and female sexual
orientation run in families, with gay men having more gay brothers and
lesbians more lesbian sisters than do same-sex heterosexuals. (It is less
clear at this point if gay men have more lesbian sisters, and vice versa.)
Of course, this is insufficient to show that genes matter, because a trait
can run in families for environmental reasons as well (e.g., Catholicism).
In order to distinguish between genetic and familial environmental
influences, more sophisticated designs are necessary. Perhaps the most
widely used design in human behavioral genetics is the classical twin
study, in which monozygotic (MZ) and dizygotic (DZ) twin pairs are examined
for their similarity on the trait of interest. The rationale for this
design is that because both MZ and DZ twins are typically reared together,
they are equally similar environmentally. However, MZ twins are identical
to each other genetically, while DZ twins are only as genetically similar
as ordinary brothers. Thus, if MZ twins are more similar than DZ twins on
average in their sexual orientation, the importance of genetic factors is
supported. An explicit assumption of this design is that the environmental
factors important for sexual orientation are no more similar for MZ than
for DZ twins. This "equal environments assumption" has been criticized.
However, in studies of other personality traits, those aspects of the
environment that are particularly similar for MZ twins (such as being
dressed alike) have not appeared to be very important in causing behavioral
similarity.
	There have been several twin studies of sexual orientation. The earliest,
by Franz Kallmann in 1952, found an amazing 100% concordance rate among 37
male MZ twin pairs, compared to a much lower rate of 12% for 26 male DZ
twin pairs. Kallmann's study had enough methodological problems that its
specific results, particularly the 100% MZ concordance rate, cannot be
taken very seriously. On the other hand, no one has provided a satisfying
explanation of how the methodological problems could wholly discredit
evidence for genetic influences. Thus, it is somewhat surprising to us that
nearly 40 years passed before others attempted to follow up his promising
results systematically. 
	The largest genetic studies to date have been our own, one with men and
one with women. These studies included not only MZ and DZ twins, but a
third group, homosexual subjects with adoptively-related same-sex siblings,
who are genetically least similar and thus should be least similar in their
sexual orientations. Our two studies obtained results that were quite
similar to each other. In the male study, MZ twins of our gay index
subjects had a 52% chance also of being gay, compared to a 22% rate for
their DZ twins and an 11% chance for their adoptive brothers. In the female
study, MZ twins had a 48% chance of also being lesbian, compared to a 16%
rate for DZ twins and a 6% rate for adoptive sisters. Note that similarity
in sexual orientation corresponded closely with genetic similarity in both
studies. 
	Quantitative analyses provide heritability estimates of the relative
proportion of genetic causation, and our heritabilities were consistently
above 50%. Thus, both studies were consistent with moderate to strong
genetic influences on sexual orientation. Of course, both studies yielded
figures lower than the 100% suggested by Kallmann. Two newer twin studies
more or less supported ours. One found concordance rates that were lower
than ours, the other found higher rates, but both found MZ higher than DZ
rates. 
	All recent studies find that MZ twins often differ in their sexual
orientations, which shows that sexual orientation cannot be completely
explained by genes. Environment must play its part. On the other hand, we
emphasize that environmental pathways can be biological as well as
psychosocial. One of the most interesting questions to stem from the recent
twin studies is what environmental factor could affect MZ twins differently
enough to give them opposite sexual orientations. 
	One other twin study is worth mentioning because it contained what many
consider to be the ideal (if rare) subjects: twins reared apart. In this
study both of two male pairs were concordant for adult homosexual feelings
and behavior, which would be highly unlikely if genetic factors were
unimortant. Although none of four female pairs was concordant, this sample
was too small to be conclusive; of course it provided no support for
genetic factors affecting female sexual orientation.
	Although we believe the available evidence is strongly suggestive of
genetic influence on sexual orientation for both men and women, one serious
methodological limitation of available studies prevent them from being
definitive. The studies have recruited subjects via advertising in gay- and
lesbian-oriented publications. They may have had an overrepresentation of
concordant pairs because such studies might be more appealing to gay men
and women with gay twins. Such bias is not very serious unless it was
stronger for MZ than for DZ twins, and we have no reason to suspect that
such differential bias occurred. But only a study using systematic
ascertainment could exclude this possibility, and unfortunately none
exists. 
	Research that helps settle some questions raises new ones. By what pathway
do genes lead to the expression of atypical childhood behavior and
homosexual orientation? Our studies have usually been discussed as
supportive of neuroendocrine theories, and genetic influences might indeed
be neuroendocrine. One could imagine a gene that led a fetus to secrete
unusually high or low levels of prenatal androgens during brain
differentiation, or alternatively, to be especially sensitive or
insensitive to androgens. But genetic influences on sexual orientation
would not have to be neuroendocrine in nature. For example, genes could
influence personality (say, independent thinking or unconventionality) that
could increase the chance of adopting a homosexual identity. For reasons we
discuss later, we doubt that the indirect route through personality is
typical, and instead believe that genetic influences operate via a
neuroendocrine pathway. But our studies have had nothing so far to say
about this.

The Biology Debate

	A thorough and thoughtful critique of the biological evidence has been
provided by Byne and Parsons, in a recent version of Archives of General
Psychiatry. They argue that the biological case is quite weak. Byne has
asserted that reviewing the biological evidence is akin to "adding zeroes"
because no one study is methodologically strong enough to establish the
biological case definitively. While we agree that no one study has
established the case for biological factors, we disagree that their sum is
"zero" evidence in favor of biological hypotheses. It is difficult if not
impossible to do perfect studies using human subjects. But if different
kinds of studies with different research strategies (with different
methodological inadequacies) converge to similar conclusions, then the
critic who rejects the cumulative evidence begins to sound strained. For
example, disregarding other research one might reasonably worry (as Byne
and Parsons do) about the role of postnatal socialization of girls with
CAH, since some are born with virilized genitalia and they and their
parents know about their condition, and for this reason may be treated more
like boys. But what if one knows that the only studies that have
investigated this possibility have failed to confirm it? Furthermore, it
has been well-established that androgen administered at critical periods
can masculinize female rhesus monkey's play and sexual behaviors. How
likely is it that the apparently analogous behavioral masculinization of
some CAH females has a completely separate explanation?
	 A second complaint we have of Byne and Parsons' otherwise useful critique
is its one-sided perfectionism. Scientific theories are not evaluated in a
vacuum. Rather, their evidentiary basis and plausibility are compared to
those of the competition. There have been two main psychosocial competitors
to innate theories of sexual orientation: psychoanalysis and socialization
theory. Psychoanalytic theories of homosexuality, which have stressed the
role of family psychodynamics, suffer from the same well-known problems as
does the corpus of psychoanalysis, particularly the inadequacy of
impressionistic data collected during psychotherapy under uncontrolled
conditions. Although there has been some support for the psychoanalytic
prediction that fathers are somewhat distant from their gay sons, this is a
rather small effect that is easy to explain on other grounds, such as
fathers' intolerance of their sons' gender-atypical behavior.  
	In contrast to psychoanalytic theory, which has largely been abandoned by
mainstream science, theories describing the socialization of gender roles
are quite respectable. We are certain that some sex differences result from
socialization by parents, peers, and society. We are nearly as certain that
differential socialization by these agents cannot explain why some people
become homosexual and others heterosexual. For example, there is no good
evidence suggesting that parents of homosexual people socialize their
children differently than do parents of heterosexual people; indeed, the
available evidence suggests they do not. Socialization theory of sex
differences emphasizes processes such as positive reinforcement of
conventional gender norms and modeling. But in our society homosexual
people are obviously not rewarded for their unconventional behavior, and
the vast majority of their potential role models are heterosexual. If
anything, socialization mechanisms in our society have been arranged to
insure heterosexual outcomes. 
	Byne and Parsons recognize the necessity of providing a plausible
competitor to the theories they criticize. Their attempt is an amalgam of
psychoanalytic and socialization theories, suggesting that boys with
certain familial influences and (genetically-influenced) personality traits
might have unusual "nonerotic experiences in childhood that may contribute
to the subsequent emergence of homoerotic preferences." This "theory" has
the unusual dual deficiencies of vagueness and implausibility. It is vague
because the personality traits, familial influences, and childhood
experiences are mostly unspecified. It is implausible because, for example,
there is no personality characteristic besides childhood gender typicality
that has been shown to differ between homosexual and heterosexual people.
Thus, Byne and Parsons have failed to provide a plausible alternative
theory to explain the data that biological theories have generated and more
generally, to account for the development of sexual orientation. 
	We do not argue that the biological evidence is strong enough to settle
the debate over origins of sexual orientation. We acknowledge the need for
replication of the most promising studies, including LeVay's, Allen and
Gorski's, and our own. Nevertheless, we are far more optimistic than some
critics of the biological evidence about the ultimate utility of biological
approaches for explaining human sexual orientation. The biological theories
are far more promising than any existing psychosocial theory, and they
deserve the attention of scientists and funding agencies so that the
"biology debate" can be resolved in the laboratory, as it certainly cannot
be in these pages.