I write regarding a major new paper released in Science on August 30, 2019, regarding the existence and extent of a hypothetical genetic contribution to the incidence of homosexuality. The paper is titled Large-scale GWAS reveals insights into the genetic architecture of same-sex sexual behavior, by Ganna et al. (paper here; supplement and figures here). As discussed in greater detail below, this paper establishes a small, but statistically significant, correlation between the genome and homosexuality.

“GWAS” means genome-wide association study, a type of analysis in which the entire genome, generally characterized by SNPs (single-nucleotide polymorphisms) is analyzed to identify correlations between the SNPs and the trait being studied. The data sources were extraordinarily large: a UK sample called the “UK Biobank” of about 500,000 individuals (about 400,000 of whom provided usable data regarding sexual orientation); an additional sample of about 75,000 individuals of European ancestry from 23andMe; and a few smaller samples.

The major conclusion was:

In aggregate, all tested genetic variants accounted for 8 to 25% of variation in male and female same-sex sexual behavior.

While results varied for different models and different data sets, they were all statistically significant at well above the 99% confidence level. This is a major contribution to our understanding.

Over about a week in March 2019, I published six Ricochet posts reviewing, summarizing, and critiquing the literature regarding two issues: (1) the genetic, biological, and environmental causes of homosexuality, and (2) the rate of reported change in homosexual orientation. My first such post (here, titled Homosexuality Facts #1: Baby You’re Not Born That Way) evaluated the evidence for a genetic cause for homosexuality, principally based on three major twin studies. My major conclusions were:

1. The proper conclusion is that none of these [twin] studies demonstrates any genetic effect on homosexuality, while all of these studies demonstrate substantial non-shared environmental effect, generally in the 55-65% range.
2. It is incorrect to draw the conclusion that there is no genetic component to homosexuality. This remains to be determined. But it is also incorrect to draw that conclusion that any such component has been established.
3. A genetic basis for homosexuality has not been established, but there are indications of an effect in the 20-40% range, probably somewhat higher for males than females. For comparison purposes, the heritability of IQ appears to be in the range of 57-85%. The heritability of the Big Five personality traits appear to be in the 40-60% range. What we can say, with high confidence, is that homosexuality is not entirely an inborn trait. Baby, you’re not born that way. The environment, potentially including individual choice, is the principal cause.

This new paper by Ganna et al. provides evidence of a statistically significant, genome-wide contribution to the incidence of homosexuality (though perhaps indirectly, as discussed below). It finds no single “gay gene.” It confirms my tentative conclusion in March of a relatively small genetic contribution, indicating that it is even smaller than I expected — probably in the range of 15-20%, where I had estimated 20-40%. The effect seems about equal for males and females, though there is relatively low genetic correlation between the sexes (which means, if I understand the authors correctly, that different SNPs seem to affect males and females but that the overall estimated heritability is comparable).

There is a summary article about the Ganna et al. paper, at the Science website itself (here). It does report the main findings with reasonable accuracy, though with an absurdly misleading title and other misdirection. I will discuss the problems with reporting of these findings in Section III below.

I. The Major Results

From the Science press release:

1. “When the researchers combined all the variants they measured across the entire genome, they estimate that genetics can explain between 8% and 25% of nonheterosexual behavior. The rest, they say, is explained by environmental influences, which could range from hormone exposure in the womb to social influences later in life.”
2. “But the five DNA markers they found explained less than 1% of this behavior, as did another analysis that included more markers with smaller effects. As with other behavioral traits such as personality, there is no single ‘gay gene,’ says Broad team member Andrea Ganna. Instead, same-sex sexual behavior appears to be influenced by perhaps hundreds or thousands of genes, each with tiny effects.”
3. “As the researchers had reported last year, they also found people with these markers were more open to new experiences, more likely to use marijuana, and at higher risk for mental illnesses such as depression. LGBTQ people might be more susceptible to mental illness because of societal pressures, the researchers note.”

The main result appears at the bottom half of Table S11 in the supplement (here), which reports the results of 27 separate analysis — 9 different models and data sets, with each analysis performed on males separately, females separately, and the combined sample. The combined sample yielded lower estimates (ranging from 6.8% to 13.3%), with the authors explaining that “[e]stimates combining males and females are biased downwards because of the relatively low genetic correlation between the sexes.” This was consistent with my prior literature reviews, which indicated that there are significant differences between male and females with respect to both the causes of, and the stability of, sexual orientation.

My impression is that the most sophisticated of the 9 different models were the final two, which appear to be the most complex multivariate analyses applied to the largest samples. These are what I will call the “Multivariate MTAG” and “BOLT-LMM” models (don’t worry about the details; it’s just useful to have a label for them). These results were around the middle of the 8-25% range, as follows:

1. Male: 15.36% – Confidence Interval 11.17-19.55% – p-value >99.9% (Multivariate MTAG)
2. Male: 16.55% – Confidence Interval 12.01-21.10% – p-value >99.9% (BOLT-LMM)
3. Male: 14.36% (average of all 9 models)
4. Female: 13.25% – Confidence Interval 8.61-17.89% – p-value >99.9% (Multivariate MTAG)
5. Female: 20.66% – Confidence Interval 15.42-25.91% – p-value >99.9% (BOLT-LMM)
6. Female: 14.09 (average of all 9 models)

In my view, this provides extremely convincing evidence of a genetic contribution to homosexual behavior, though this contribution may be direct or indirect. It also provides very strong evidence that the genetic contribution is probably around 15% for both males and females.

The second major result was that, while the researchers identified 5 significant SNPs associated with homosexuality, but these were very minor factors, each explaining less than 1% of the incidence of homosexuality. This seems, to me, to demonstrate convincingly that there is no single “gay gene,” nor is there a small number of “gay genes,” which is the conclusion of the authors. Interestingly, of the 5 significant SNPs, 2 were significant in both males and females, 2 were significant in males but not females, and 1 was significant in females but not males.

The third major result is strong correlation of homosexuality with certain personality traits and other behaviors, including: (1) openness to experience (a Big Five personality trait); (2) trait neuroticism (a Big Five trait); (3) smoking; (4) cannabis use; and (5) “risk behavior” (a risk taking variable from the UK Biobank data set). There were also significant correlation between homosexuality and: (1) major depressive disorder, (2) ADHD, and (3) schizophrenia (this was smaller than the other two). These correlations were all statistically significant.

II. My Speculations Regarding Indirect Causation

The correlation between certain personality traits and other behaviors, on the one hand, and sexual orientation, on the other, suggest that the genome-wide association with homosexuality demonstrated in Ganna et al. may be indirect, at least in part. Understanding this would require further study.

As an example, consider openness to experience, one of the Big Five personality traits. The Big Five Wikipedia page describes openness as:

Openness is a general appreciation for art, emotion, adventure, unusual ideas, imagination, curiosity, and variety of experience. People who are open to experience are intellectually curious, open to emotion, sensitive to beauty and willing to try new things. They tend to be, when compared to closed people, more creative and more aware of their feelings. They are also more likely to hold unconventional beliefs. High openness can be perceived as unpredictability or lack of focus, and more likely to engage in risky behaviour or drug taking. Moreover, individuals with high openness are said to pursue self-actualization specifically by seeking out intense, euphoric experiences.

This 2018 paper by Bogaert et al. (abstract only – I can’t access the full paper) states that: “All nonheterosexual groups, particularly bisexual people, averaged higher in openness to experience than did heterosexuals.” This is consistent with the result of the Ganna et al. paper discussed above.

This 2017 paper by Lo et al. indicates that there is a genome-wide correlation with openness, with a heritability estimate of around 10-12% (to see these figures, you need to download the supplemental table at the bottom of the paper). 

It stands to reason that people who are more adventurous and curious, more willing to try new things, and more interested in a variety of experience, would be more likely to experiment with homosexuality. Some might find that they like it (or even become hooked). If there is a genome-wide contribution to openness, and if openness makes one more likely to be homosexual — both of which appear to be true — then part of the genome-wide correlation with homosexuality could be indirect.

There may be other avenues of indirect causation, and it is possible that genetic factors could be triggered by environmental factors to result in a same-sex orientation. It’s complicated, to say the least.

III. Concern About Media Reporting

Reading the Ganna et al. article makes it clear, frankly, that the authors were terrified of running afoul of the SJW mobs. The paper actually concludes with this explanation:

Science Communication Strategy

To communicate the results of the study to the broader audience, we engaged with different LGBTQIA+ (lesbian, gay, bisexual, transgender, queer, intersex, asexual, and other+) and science communication organizations and created multimedia materials for a lay audience.

Genetics may explain up to 25% of same-sex behavior, giant analysis reveals.

We acknowledge that the grouping phrase “nonheterosexuals” has the potential to present messages of othering (that is, undesirable marginalization of another person or group on the basis of their sexual expression) — by defining an “outgroup” in reference to an “ingroup” and implying that “nonheterosexual behavior” may have a negative connotation, whereas “heterosexual behavior” may have a positive one. We wish to make clear that our choice of language is not meant to forward messages of othering on the basis of sexual behavior.

 

. . .

 

As is common in genetic analyses, we dropped individuals from our study whose biological sex and self-identified sex/gender did not match. This is an important limitation of our analyses because the analyses do not include transgender persons, intersex persons, and other important persons and groups within the queer community.We hope that this limitation will be addressed in future work.

 

. . .

 

The topic explored in this study is complex and intersects with sexuality, identity, and attraction and potentially has civil and political implications for sexual minority groups. Therefore, we have

 

Engaged with science communication teams,
Engaged with LGBTQIA+ advocacy groups nationally and within our local institutions, and
Tried to make clear the many limitations and nuances of our study and our phenotypes.

 

We wish to make it clear that our results overwhelmingly point toward the richness and diversity of human sexuality. Our results do not point toward a role for discrimination on the basis of sexual identity or attraction, nor do our results make any conclusive statements about the degree to which “nature” and “nurture” influence sexual preference.

These disclaimers raise concern about either the ideological predisposition of the authors (which I do not know), or their fear of reprisal, or both. However, they are to be commended for going forward with this research and publication.