The most publicized research studies on the causes of homosexuality have been
those examining the role of genetics. Indeed, a number of studies have attempted
to assess the heritability of the homosexual orientation. The primary way of
examining the genetic contribution to a given behavior or disposition such as
sexual orientation is through twin studies. The premise is that by comparing
monozygotic (MZ) twins (who share 100% of their genetic code), dizygotic (DZ)
twins and biological siblings (who both share approximately 50% of their genetic
code), and adopted siblings (who have none of their genetic code in common),
researchers can glean an understanding of whether a trait is heritable and to
what extent (Billings & Beckwith, 1993).
However,
in order to truly assess the effects of genes, one has to control or neutralize
the contribution of environmental factors in the development of the
characteristic in question. Such environmental factors could include anything
from position in the womb, maternal nutrition, and the hormonal milieu of the
uterine environment to post-natal care, early illnesses, parenting style, family
constellation, education, socialization, and so forth. These influences can have
profound effects not only on a person’s behavior but even on their biological
make-up.
Thus,
researchers are coming to recognize that the hard division of nature—nurture is
no longer tenable. It is always a “both—and”, especially in traits as
complicated as sexual orientation. It is important to note that several of the
factors listed above pertain to the prenatal environment. In this period of
development, the environment can have profound effects on the organism, and this
will be discussed further below.
In
the most desirable type twin study, researchers examine MZ twins who were
separated at birth and reared apart. This is considered the ideal in behavioral
genetics. As the reasoning goes, since such twins have the same genetic code but
are reared in different environments, any behavioral similarities they manifest
likely have a strong genetic basis. Unfortunately, these situations are rare,
and they are extremely so if the trait being studied is itself uncommon.
Homosexuality is just such a case.
A
great deal of research in recent years has shown that roughly 2-3% of men in the
United States are homosexual (Fay, Turner, Klassen, & Gagnon, 1989; Rogers
& Turner, 1991; Leigh, 1993; Billy, Tanfer, Grady, & Klepinger, 1993;
Seidman & Reider, 1994; Black, Gates, Sanders, & Taylor, 2000). The
figure is even smaller for women, approximately 1-2% (Diamond, 1993; Laumann,
Michael, Gagnon, & Michaels, 1994; Wellings, Field, Johnson, & Wadworth,
1994).
Thus,
locating MZ twins who were separated at birth and of whom at least one twin
developed a homosexual orientation is unfeasible. Moreover, such a twin study
(MZ twins reared separately) does not in fact neutralize the environment to the
extent that researchers surmise. The reason for this is that MZ twins, even if
they are separated from the moment of birth forward, still shared the same,
profoundly influential environment for the previous nine months. Thus, every
twin study, no matter how elegant in design, cannot fully tease apart the
effects of genes and environment.
Researchers
try to cope with these difficulties by comparing MZ twins who were reared
together with other sibling pairs such as DZ twins, normal biological siblings,
and adopted siblings with no biological relation between them. Bailey and
Pillard (1991) followed this general paradigm by examining family patterns of
adult males with homosexual orientation who had either a MZ twin, DZ twin, or
adopted brother. These researchers found a concordance rate (if one twin was
homosexual, the other was as well) of 52% among the male MZ twins who were
reared together in the study. The figure for female MZ twins was 48%.
Likewise,
male DZ twins reared together showed a concordance rate of 22% (16% for women)
but this was not significantly different from the rate for adoptive brothers
(Bailey & Pillard, 1991). What this study shows is that there may be a
genetic component to homosexuality, but there appear to be substantial
environmental factors as well. Why else would the concordance rate among MZ
twins be so much less than 100% and why would there be any concordance at all
among adoptive brothers?
Though
far from conclusive, this study by Bailey and Pillard was highly influential.
Several such twin studies followed, and, taken together, the lowest concordances
found for homosexuality among MZ twins was 47% for men and 48% for women
(Bailey, Dunne, & Martin, 2000). However, the samples of twins included in
these studies were largely recruited through advertising in gay or lesbian
publications. This creates the possibility of “ascertainment bias”.
In
other words, “twins deciding whether to participate in a study clearly related
to homosexuality probably considered the sexual orientation of their co-twins
before agreeing to participate” (Bailey et al., 2000, p. 533). This non-random
sampling, of course, would result in biased data. Bailey, Dunne, and Martin
(2000) overcame this methodological weakness by using a large sample (N=4901) of
adult twins recruited from the Australian Twin Registry. In that study, the
researchers identified 27 pairs of male twins in which at least one of the men
was homosexual. However, only 3 of these pairs were concordant (both twins were
homosexual).
Thus,
3 of 27 pairs of male twins (approximately 11%) were concordant on homosexuality
in this systematic study. Likewise, only 3 of 22 pairs of female twins
(approximately 14%) were concordant. These researchers conclude, “These rates
are significantly lower than the respective rates for the two largest prior twin
studies of sexual orientation…. This suggests that concordances from prior
studies were inflated because of concordance-dependent ascertainment bias”
(Bailey, et al., 2000, p. 533). They go on to state,
Consistent
with several studies of siblings… we found that sexual orientation is familial.
In contrast to most prior twin studies of sexual orientation, however, ours did
not provide statistically significant support for the importance of genetic
factors for that trait (p. 534).
This
does not rule out the possibility that there is a genetic component to
homosexuality but rather suggests that “sexual orientation is inherited, if
at all, in a complex manner” (Bailey & Pillard, 1995, p.144, emphasis
added).
A
second line of research examining the supposed genetic basis for homosexuality
employs the molecular analysis of blood samples from relatives of homosexuals
and a method called linkage analysis, which maps genes onto chromosomal regions,
to identify the specific gene or genes that influence sexual orientation. Based
on evidence that “gay men have more homosexual uncles and cousins through the
maternal line than on the paternal side” some researchers have attempted to
identify an X-linked gene that influences male sexual orientation (Rahman &
Wilson, 2003, p. 1342).
Hamer,
Hu, Magnuson, Hu, and Pattatucci, (1993) initially reported findings consistent
with this hypothesis that implicated the chromosomal region Xq28 in the
heritability of male homosexuality. A similar though weaker relationship was
reported later by members of the same research group (Hu et al., 1995).
However,
the methods used in these studies and therefore the reported results have been
called into question. Risch, Whleeler, and Keats (1993) criticized the research
design and statistical methods used by Hamer et al. (1993) and asserted that
their conclusions might not be supported by the data. In addition, Rice et al.
(1999) attempted to replicate the previously reported link between Xq28 and male
homosexuality using similar methods in independently conducted genetic studies,
but their results did not support the Xq28 hypothesis. Indeed, these researchers
stated,
It
is unclear why our results are so discrepant from Hamer’s original study.
Because our study was larger than that of Hamer et al., we certainly had
adequate power to detect a genetic effect as large as was reported in that
study. Nonetheless, our data do not support the presence of a gene of large
effect influencing sexual orientation at position Xq28 (Rice et al., 1999, p.
668).
These
issues were again revisited in the journal Science in 1999 (Hamer et
al., 1999; Rice, Risch, & Ebers, 1999). It is clear from these articles that
because scientists are treading on new methodological ground, there is no simple
solution to this question. The methods being used in these studies have not been
tested and verified in studying a trait as complex as sexual orientation. Hamer
et al. (1999) defended their approach and attempted to meta-analyze four studies
in this area concluding that they collectively support the Xq28 hypothesis.
However,
Rice, Risch, & Ebers (1999) pointed out that if only those studies carried
out by independent investigators are considered, which is necessary to reduce
potential biases, no researchers outside Hamer’s own group has found support for
the Xq28 hypothesis: “Thus, the conclusion remains that the original studies of
Hamer and colleagues are not replicated” (Rice, Risch, & Ebers, 1999, p.
806).
A
study conducted by Bailey et al. (1999) also examined the hypothesis that
homosexuality is the result of an X-linked gene using more stringent standards
in recruitment analysis than many previous studies. Three sampling techniques
were utilized: recruitment from an HIV clinic, a gay pride parade, and through
homophile publications. All participants were interviewed about familial
patterns of non-heterosexuality. Only the sample attained through magazine
advertisement knew of this purpose of the study. The researchers found a rate of
occurrence of homosexuality among brothers of a homosexual male ranging from
7.3% to 9.7%.
This
suggests a modest familial (not necessarily genetic) component to the origin of
male homosexuality. Bailey et al. (1999) also found a slight increase in the
appearance of female homosexuality among sisters of gay men. However, the
familial patterns of homosexuality observed in this study did not support the
Xq28 hypothesis. “This study found no evidence that male sexual orientation is
influenced by an X-linked gene” (Bailey et al., 1999, p. 84).
One
final study worth mentioning was recently conducted by Mustanski, DuPree,
Nievergelt, Bocklandt, Schork, and Hamer (2005). Using blood samples of 456
individuals from 146 unrelated families, the researchers conducted for the first
time a search of the entire human genome for a genetic basis to male
homosexuality. Though three gene regions resulted in elevated values, none were
large enough to generate a statistically significant result. In addition, they
found no evidence of a link to the Xq28 region. Thus, as stated above, research
into the genetic basis for homosexuality, taken as a whole, is inconclusive.
While there may be a modest heritability to such an orientation, the existence
of an overriding gay gene seems highly unlikely at this time.
Another
biologically based line of research bearing on the question of the etiology of
homosexuality deals with the pre-natal environment. As already alluded to, fetal
development is a remarkably crucial time in the development of the human
organism. In particular, brain systems develop rapidly during this period and
are quite sensitive to hormonal and other biochemical influences.
Normally
in a male child, his testes will begin producing testosterone during the fetal
period which masculinizes various body structures and systems. (Girls produce
androgens as well from their adrenal glands, though usually in much smaller
quantities than boys who produce them in their testes and adrenals.) Besides the
obvious differences such as genitalia, musculature, etc., this masculinzation
process affects the development of various brain structures and, thus, their
functions (see chap. 8 of Baron-Cohen, 2003). The development of the child in
the womb can also be influenced by the mother’s hormone levels. It has been
hypothesized that abnormal hormone levels or other deviations during the fetal
period could be responsible for the development of non-heterosexual orientations
(for reviews, see Mustanski, Chivers, & Bailey, 2002; Rahman & Wilson,
2003).
Researchers
have made various attempts to study such an effect upon the development of
homosexual orientations. While for ethical reasons, experimenters cannot
manipulate the hormonal milieu of the prenatal environment in humans, they can
study cases in which such abnormalities occur naturally to see if a homosexual
orientation is more likely to result. In addition, a certain amount can be
learned from animal studies. Finally, somatic and neuropsychological variables
known to be strongly affected by prenatal hormones can be compared in adults to
see if they differ according to sexual orientation.
All
of these methods have been utilized, and it appears that in some respects,
female homosexuals appear to have experienced increased prenatal androgenization
compared to heterosexuals (more masculine auditory systems and waist-to-hip
ratio, higher salivary testosterone levels, less desire to give birth, etc.).
Likewise, on some measures homosexual men appear to have been less androgenized
than heterosexual men (more female-like pubertal onset, weight, height,
cognitive spatial abilities, and language abilities; higher rates of non-right
handedness).
However,
on other measures homosexual men appear hypermasculine, i.e. exposed to greater
quantities of androgens (more masculine relative finger lengths, possibly larger
penises [according to two studies: Nedoma & Freund, 1961; Bogaert &
Hershberger, 1999], and possibly hypermasculine auditory systems [see McFadden,
2002]). Some differences in the size and shape of certain adult brain structures
have also been identified across sexual orientation categories, but it is
unknown whether these neural differences cause or are consequent upon homosexual
lifestyles. After all the brain is a “plastic” structure that changes throughout
life in response to one’s genetic/biological endowment, experiences, and
behaviors.
Thus,
the data on the role of prenatal androgens are very complex, and no scholarly
consensus exists on how to integrate and interpret them. If abnormal androgen
levels are what drive these differences, they appear to affect males and females
differently since homosexual men and homosexual women do not always differ from
their heterosexual counterparts on the same variables.
Moreover,
the data on homosexual men are mixed. Rahman and Wilson (2003) put forward the
hypothesis that perhaps a genetic factor in some men alters the distribution of
androgen receptors in various brain structures. Thus, when exposed to prenatal
androgens at whatever level, the result will be that some brain structures will
be more masculinized than normal and others will be less masculinzed than normal
because of the redistribution of the receptors. While this makes a good deal of
sense, the research has not yet shown this to be the case.
Perhaps
the most well replicated phenomenon related to the causes of homosexuality is
the “fraternal birth order effect”. To put it simply, “Several studies, which
collectively examined over 7000 subjects, have shown that homosexual men have,
on average, a greater number of older brothers than do comparable heterosexuals”
(Ellis and Blanchard, 2001, p. 543).
Thus,
something about being born later in a line of several brothers seems to increase
the likelihood of male homosexuality. Researchers believe that the fraternal
birth order effect per se is not the ultimate causal factor of male
homosexuality in these cases but that there is some other mechanism in place
that mediates the effect. However, what this causal mechanism is is still highly
debated. Most favor a biological explanation such as a fluctuation in prenatal
androgens or increased maternal immune system response related to multiple,
successive male pregnancies.
Another
possibility with mixed empirical support suggests that maternal stress, which
could increase with the births of multiple sons, may alter fetal development in
such a way as to increase the likelihood of a homosexual orientation. Stress
hormones are in fact produced in the adrenal glands (and are therefore,
androgens or at least androgen-like) and can interfere with normal fetal
development.
Other
explanations for the fraternal birth order effect are psychosocial in nature and
posit such potential causes as ostracization of boys by older brothers or
increased early sex play among boys with several older brothers (see James,
2004a; 2004b). Presently, however, the fraternal birth order effect remains
largely unexplained in the absence of any overwhelmingly conclusive
evidence.
Moreover,
it is important to note that according to researchers only 14.8% to 15.2% of
homosexual men can attribute their orientation to this effect (Cantor,
Blanchard, Paterson, & Bogaert, 2002). Though it is a well established and
easily identifiable phenomenon connected with the genesis of male homosexuality,
the fraternal birth order effect does not appear to be the primary cause of
homosexuality in the majority of gay men. Nothing analogous to this effect has
been found in women.
In
light of the foregoing, it is important to recall that sexual orientation does
not emerge immediately upon conception and birth but takes time to develop
throughout childhood, adolescence, and even adulthood. Thus, there is a great
deal of room for experience to affect this process. Consequently, researchers
investigating the various factors discussed above agree that rather than causing
homosexual orientation directly these influences likely precipitate a set of
pre-homosexual traits and dispositions that in turn increases the likelihood of
adult homosexuality (Bailey & Zucker, 1995; Dunne, Bailey, Kirk, &
Martin, 2000).
The
term coined for this is childhood gender nonconformity (CGN), which simply
refers to a certain conglomeration of sex atypical traits (physical,
psychological, and behavioral features). CGN is known to be consistently
associated with later homosexual orientations as well as many of the biological
and familial factors discussed above (Bailey & Zucker, 1995). However, since
not everyone with CGN develops an adult homosexual orientation, there must be
some environmental influences that contribute to such a development. These could
include for instance failed relationships with one’s parents and/or peers.
Indeed,
classic psychodynamic theory held that male homosexuality was primarily caused
by a maladaptive family pattern in which the father is weak and distant and the
mother is over-controlling (roughly the reverse is posited for females). While
there has been very little data in the last 20 years supporting these specific
claims, research does emphasize the importance of relationships in the
development of sexual orientation. For instance, an interesting study by
Landolt, Bartholomew, Saffrey, Oram, and Perlman (2004) examined the
relationship between CGN and rejection from parents and peers in a sample of 191
gay and bisexual men. They found, “Gender nonconforming behavior in childhood
was associated with maternal, paternal, and peer rejection” among these gay and
bisexual men (p. 124).
Another
recent study, though methodologically weak, found that among a sample of
Catholic seminarians, those admitting a homosexual orientation also reported
“more emotional distance from their fathers than heterosexual seminarians”
(Seutter & Rovers, 2004, p. 46).
Bem
(1996; 2000) proposed a model of sexual orientation development which he dubbed
the “exotic becomes erotic” theory. He proposes that biological variables
influence childhood temperaments which in turn affect a child’s degree of gender
conformity. A child who has nonconforming traits and behaviors feels him/herself
to be different from peers. This “feeling different” from same-sex peers can
evolve into an erotic attraction in adolescence:
An
individual’s protracted and sustained experience of feeling different from same-
or opposite-sex peers throughout childhood and adolescence produces a
correspondingly sustained physiological arousal that gets eroticized when the
maturational, cognitive, and situational factors coalesce to provide the
critical defining moment (Bem, 2000, p. 539).
While
these various accounts all have merit to them and a certain ring of truth, one
aspect of the development of a homosexual orientation not explicitly tapped in
any of them is the role of child sexual abuse (CSA) and other early sexual
experiences. There seems to be a link between CSA perpetrated by men (or older
males) against boys that predisposes these boys to later identify as
homosexual.
Indeed,
one reviewer states, “The effects of sexual victimization on male children,
placed in the context of the prevailing concept of masculinity, include mental
disorders, the probability of becoming rapists and incest offenders as adults,
and the development of homosexual identification” (Vander Mey, 1988, p. 61).
Several studies support this claim. For instance, Finkelhor (1984) found a
statistically significant relationship between CSA victimization and later
homosexual activity in adulthood (cited in Dimock, 1988). In a study of 25 adult
males who had been sexually abused in childhood, the majority of these men
experienced “masculine identity confusion” characterized by “confusion regarding
sexual preference and… male roles” (Dimock, 1988, p. 208). Homosexual feelings
and/or behaviors were common among these men. Noting that “the literature
reports that there may be a significant number of gay men who have been sexually
abused as children,” Schwartz (1994) presented clinical data from eight men who
had been victims of CSA. “Six of the eight men identified themselves as
homosexual in their sexual identity; two were heterosexual. Of the two
heterosexuals, one continuously questioned his sexual orientation” (Schwartz,
1994, p. 182).
Likewise,
Johnson & Shrier (1985) compared 40 male victims of CSA and an age-matched
control group and found that 47.5% of the CSA victims went on to develop a
homosexual orientation and another 10% became bisexual. “The study group
identified themselves as currently homosexual nearly seven times as often and
bisexual nearly six times as often as the control group” (Johnson & Shrier,
1985, p. 374).
These
small studies finding an increased likelihood of homosexual identification in
male victims of CSA are corroborated by at least twelve more recent and
systematic ones that have all documented elevated rates of CSA among homosexual
men (Saewyc, Pettingell, & Skay, 2004; Kalichman et al., 2004; Ratner et
al., 2003; Garcia, Adams, Friedman, & East, 2002; Dolezal &
Carballo-Diéguez, 2002; Tomeo et al., 2001; Paul et al., 2001; Krahé et al.,
2001; Paris et al., 1995; Doll et al., 1992; Baier et al., 1991; Haverkos,
Bukoski, & Amsael, 1989; for reviews see Relf, 2001; Holmes & Slap,
1998). For instance, using a nonclinical sample of 942 participants, Tomeo et
al. (2001) found that 46% of homosexual men had been sexually abused as a child
by a man. This was significantly greater than the 7% rate found among
heterosexual men in that study. Among a sample of 307 Latin American men who
have sex with men (MSM), Dolezal and Carballo-Diéguez (2002) observed “that
early sexual contact [with males] is common among these men.
Fifty-nine
percent had had some sexual/genital contact prior to their 13th
birthday. In the majority of those cases, they had a partner who was at least 4
years older than they were” (p. 169-170). Finally, in a systematic study of 2881
MSM, Paul et al. (2001) found that one fifth had experienced CSA. They
state,
Our
study confirms and extends prior research indicating high prevalence levels of
childhood sexual abuse (CSA) among MSM. Such prevalence levels might be higher
if we had elicited data about experiences involving non-contact sexual
victimization (i.e., sexual exposure or exhibitionism). Overall, these men’s CSA
experiences were characterized by high levels of penetrative sex, physical
force, and perceptions of these events as distressing (Paul et al., 2001, p.
575).
Interestingly,
some research suggests that boys who have gender nonconforming traits such as
effeminate physical features are rated as more attractive by adults than a
control group of typical boys (Zucker, Wild, Bradley, & Lowry, 1993).
Even
in cases where such young men and boys do not report the experience as abusive,
early sexual contact with other males is common prior to identifying oneself as
gay. For instance, Dawood et al. (2000) found that one third of their sample of
gay men with gay brothers had engaged in sexual activity with their siblings in
childhood. “Among the 21 participants who indicated that some form of sex play
occurred, levels of activity included touching and mutual masturbation (N=16),
giving or receiving fellatio (N=9), and anal intercourse (N=4)” (p. 161). A
recent study of 961 Dutch gay and bisexual men “found that 68% of respondents
engaged in their first same-sex experience before coming-out” (Schindhelm &
Hospers, 2004, p. 585). Another study found that 58% of homosexual and bisexual
men came to their sexual identity through a sex-centered sequence, i.e. one in
which same-sex activity preceded their identification as gay or bisexual (Dubé,
2000).
In
a study comparing homosexual men and women, researchers discovered that
homosexual men were more likely to pursue sex before identifying themselves as
gay, whereas for women the context of their homosexual identity development was
more emotionally oriented (Savin-Williams & Diamond, 2000).
This
last finding raises an interesting but challenging issue: sexual orientation in
men and women is markedly different and develops in divergent ways. Summarizing
research in this area, Diamond (2003) states,
Women
show greater variability than men in the age at which they consciously question
their sexuality, and the age at which they pursue their first same-gender sexual
contact…. Also, women place less emphasis on the sexual component of their
lesbian or bisexual identification, both during and after the questioning
process…, and are more likely to report that their sexuality is fluid and chosen
versus fixed and biologically given… (p. 185).
Thus,
for men, a homosexual orientation seems to involve a strong inclination to
engage in sexual activity with other men. Whereas, for women the question of
sexual orientation is much more caught up in affectional bonding and is more
often a matter of conscious choice than an irresistible urge.
This
review of the research shows us that many known factors (and there are likely
still more unknown factors) are implicated in the development of homosexuality,
but no one factor seems powerful enough to trump them all. Rather, the adult
homosexual has probably arrived at that orientation through a complex,
idiosyncratic combination of biological, experiential, and volitional factors.
This process seems clearly divergent for men and women and likely differs from
individual to individual among gays and among lesbians.
Andrew J. Sodergren, Psy.D.
Mensagens
