Is there evidence for ‘gay’
genes?
Erin L.S Hoyer
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Introduction
Sexual orientation is a topic of discussion across biology, psychology and various
other disciplines. The nature vs. nurture debate is prominent with regard to this topic and the
debate usually centres on ‘What ‘causes’ homosexuality?’ At present, there is no concrete
genetic basis for homosexuality in either male or female populations and research varies
substantially between the sexes. In Australia, the prevalence of women identifying as
exclusively homosexual is 0.8% (Smith et al. 2003). In male populations across Australia, the
prevalence is varying such as 0.8%-3.0% (varying across states) and 1.6% (wholly across
Australia) identify as exclusively homosexual (Prestage et al. 2008; Smith et al. 2003).
Psychological and biological differences between homosexuals and heterosexuals
have been presented in the scientific literature but whether or not these are genetically
influenced or determined has not been thoroughly researched. The actual location(s) of
gene(s) that may influence or determine homosexuality have not been discovered but there is
evidence suggesting that genetic links may be present and whether the evidence is a product
of environment or genetics is currently debated. The idea of a genetic determinant of sexual
orientation stemmed from cumulating evidence of differences in brain structure, behaviour
and brain function between male and female homosexuals and their heterosexual
counterparts. But here lies a strain between genetic determinism, genetics shifting behaviour
(genetic predisposition) and individual free will. As sexual orientation is a complex variation
in humans, it would be wise to conclude that no one genetic marker will be linked to
homosexuality. We currently do not have the whole picture of our genetic variance as
humans and we remain far from identifying human genes (Camargo et al. 2001) and even
more importantly, the functions of various proteins. By cataloguing genetic variance we may
get closer to various biomarkers for certain traits. A recent estimate of greater than 1%
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variation within an individual genome (Conrad et al. 2010) could support genetic variation
having probable contributions to complex human traits.
Scientific research becomes difficult in this field as the measurement of sexual
orientation relies on psychological scaling, for example, the Kinsey scale. This scale proposes
a 0-6 measurement of sexual orientation with zero meaning exclusive heterosexuality and six
identifying as exclusive homosexuality. Between these two poles, 1-5 represent varying
levels of bisexuality and were included as Kinsey did not want to categorise individuals but
rather ‘the living world is a continuum in each and every one of its aspects’. This complex
human trait is difficult to measure and it is even more difficult to replicate findings across
different populations. This review takes into consideration various aspects of the research
sample and presents evidence for female and male homosexuality. The evidence for
biological differences between male homosexuals and male heterosexuals is much more
numerous and broad in the literature in comparison to female sexual orientation. This lack of
research may stem from social interpretations of female sexuality – for example, the
argument that female sexual orientation is more plastic and more gradient when compared to
male sexual orientation, where male orientation is portrayed or categorized as more bipolar
(i.e. exclusively hetero- or homo- sexual)(Lippa 2007).
For men identifying as homosexual in particular, scientific evidence and theory
present the question – is there a gay gene or genes? For any genetic trait to remain present in
a given population – there must be offspring produced. If homosexual men produce less
offspring them their heterosexual peers – how does male homosexuality remain at low but
consistent levels across populations? There is evidence that homosexual males do produce
less offspring (0.12 children per male vs. 0.58 children per heterosexual male) (Iemmola et al.
2009) and this presents the question of – if sexual orientation is genetically influenced or
determined, how is it being maintained consistently? One theory is that homosexual males are
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not genetically selected against on the X chromosome because the reproductive success of
their female relatives (most importantly, sisters) and this theory presents a solution to the
Darwinian paradox of ‘Survival of the Fittest’ (Iemmola et al. 2009). Earlier predictions
concluded that even a 2% fertility advantage in a heterozygote heterosexual would be enough
to ensure the survival of an allele for homosexuality (MacIntyre et al. 1993) but this
prediction was based on statistical predictions, not research participants.
Biological and Genetic Evidence for Sexual Orientation: Separating the Sexes
The research that stemmed this questioning of sexual orientation as an output of
genetic makeup is greatly psychological and biological. The research focusing on sexual
orientation is more prevalent in regard to males and there are great differences between the
sexes, and thus for this prevent review XX female and XY male specific evidence will be
separated due to the complexity of biological and genetic factors that may influence these.
Female Homosexuality
There is evidence that brain structure differs between heterosexual and homosexual
women. For example, homosexual women were found to have less grey matter in the
temporo-basal cortex, ventral cerebellum and left ventral premotor cortex in comparison with
heterosexual females (Ponseti et al. 2007). Heterosexual females tend to have a larger
perirhinal cortex in comparison to males of either orientation or homosexual females. This
evidence points to a sex atypical differentiation of this part of the brain and its possible
relationship to female homosexuality (Ponseti et al. 2007). Following on from this biological
evidence, lesbian women exhibit fewer and weaker Otoacoustic emissions (OAEs) than
heterosexual females. This result is shifted towards male OAE patterns (Ioehlin 2003) and
contributes to the general theory that homosexual women tend to be shifted towards more
male typical patterns. Another example, homosexual females tend to have increased bone
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growth in the arms, legs and hands within compared to heterosexual females. These females
were more similar to the bone growth of heterosexual males (Martin et al. 2004). Weight,
height and age of menarche as characteristics of comparison did not raise significant results,
but variation within the homosexual group was wider (Bogaert 2009). The much studied
2D:4D finger ratio does not differ between the female groups of sexual orientation (Manning
2007), but is a widely known finding with regard to males and this research will be discussed
later. The evidence for homosexual females having longer bone growth is promising and
presents a theory for why this has occurred – greater steroid exposure during development
(Martin et al. 2004) but this does not take into account whether this is cause of consequence
and the lack of correlation with 2D:4D ratio is surprising as this has been thought to be
influenced by steroid exposure. Another interesting difference found in a study population is
that female homosexuals exhibited a high incidence of type A blood and a high proportion of
Rhesus Factor Minus (Rh-) (Ellis et al, 2008). It is well defined that Rhesus factor and blood
type are genetically determined (chromosome 1 and chromosome 9 respectively) but the basis
of these significant differences in these genetically determined factors is unknown.
Male Homosexuality
Simple physical characteristics have been proposed to be different between
homosexual and heterosexual males. For example, homosexual men have been reported to be
shorter in height on average and lighter in weight than heterosexual men (Bogaert 2009). This
evidence does bring up an interesting point about general physical differences which may
stem from hormonal or steroidal differences but environmental influences on weight are
easily identifiable in today’s society. The 2D:4D finger length has been replicated in male but
not in female populations and also contributes to the theory that steroid exposure influences
sexual orientation, in particular, testosterone (Medland et al. 2010) – but this evidence is only
confined to Caucasians (Manning et al. 2007).
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The previously mentioned evidence with regard to Rhesus Factor and blood type,
statistically high proportions of Rh- and low incidence of type A blood were found in
homosexual men when compared to heterosexual men (Ellis et al. 2008). From the previously
mentioned study pertaining to OAEs - no differences were determined for men (Loehlin
2003). This evidence credits the separation of male and female studies pertaining to sexual
orientation as this measure does not correlate in homosexuals of either gender.
Differential activation in brain regions is evident, for example, homosexual males
produced a significantly smaller reduction in hypothalamic glucose metabolism after a single
dosage of fluoxetine ingestion when compared with heterosexual men (Kinnunen et al. 2004).
Other areas of differential responses included the prefrontal association cortex where glucose
metabolism increased and the cingulated cortex where glucose metabolism decreased in
homosexual men participating. Fluoxetine is an SSRI used in depression and effects
serotonergic neurotransmission but may have secondary effects on the noradrenergic and
dopaminergic systems. This evidence may point to a metabolic difference when comparing
men of each sexual polarity. On the other hand, while viewing sexually arousing stimuli,
males of both orientations did not differ in brain activation in the chosen study targets – the
ventral striatum, centromedial thalamus and ventral pre motor cortex (Ponesti et al. 2006).
There is cumulating literature on the effect of Fraternal Birth Order (FBO) and this
tends to be consistent across cultural samples. The underlying cause of this effect is thought
to be the maternal immune hypothesis. Recent evidence determined that having older
biological brothers increased the odds of homosexuality (Bogaert 2006) but other research
found an increased likelihood of homosexual orientation in younger right handed brothers –
where left handed and ambidextrous younger brothers were unaffected (Blanchard et al.
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2006). In regard to first born males, they found non-right handedness was associated with
increased odds of male homosexuality. Why is there an increased likelihood of homosexual
orientation in younger brothers? There is a link with the gene SMCY where two proteins
produced from this gene can cause an immunological reaction in 37% of mothers with sons
up to 8 years after their last male pregnancy (Piper 2007). The study did not look at sexual
orientation specifically, but this evidence does relate to the influence of genes on
immunology affecting future male births. A question remains unanswered: can the mother’s
immune system affect brain mechanisms underlying sexual orientation (Bogaret 2011)? This
SMCY protein displays an incremental immune response, is expressed in the foetal brain and
is expressed in other parts of the body (brain and sperm cells) but not the whole body in its
entirety. This evidence fits with that only minor physical differences between male
heterosexuals and homosexuals could be present (Bogaret et al. 2011).
The most well known, and publicised study of genetics relating to sexual orientation
is by Hamer et al (1993). The possibility of a gay gene sparked controversy but this research
has not been conclusive as another study resulted in clashing evidence where an absence of
linkage markers at Xq28 was discussed (Rice et al. 1999). If this possible linkage at Xq28
was to be the ‘be all and end all’ genetic marker for male homosexuality, the research
findings would be replicated in various populations and this has not happened.
More recent evidence shows the possibility for microsatellite markers on
chromosomes 7,8 and 10 where 7 and 8 were maternally and paternally linked and 10 is
maternal in origin (Mustanski et al. 2005). This research was a genome wide scan and does
need replication on a more dense scale. The results from this study do not cement a genetic
linkage to male homosexuality, but does add to the cumulative literature. On chromosome 10
(specificially 10q26) where the Mustanski et al. (2005) research found microsatellite markers,
there is evidence that this region can be differentially methylated (Strichman-Almashanu et
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al. 2002) which suggests this region could be susceptible to differential activation and
repression depending on structural components of DNA.
There is no concrete evidence for a gay gene(s), but due to the complexity of human
behaviour it will take an accumulation of research spanning the genome (preferably after we
research protein functions which are currently unknown) to determine any factors that shift
sexual orientation towards one pole or the other. From the evidence of differences between
homosexual and heterosexual individuals in various scientific domains, it would be ignorant
to conclude that there is no genetic influence on this trait.
From reading original research papers and review articles, there is still a research bias
where ‘risk’ for male homosexuality is the basis for the research and probably stems from the
researchers own personal bias towards minorities. The social and ethical arguments for and
against research into biomarkers for homosexuality are important and must be taken into
consideration when reviewing research and conclusions.
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