What Twin Studies Tell Us about Homosexuality: Nature vs. Nurture
James R. Aist
(Note: Numbers in parentheses refer to specific, numbered references listed at the end of the article.)
I presented a much broader treatment of possible causes of homosexuality elsewhere (click HERE). Most of the more recent research on possible biological origins of homosexuality has focused on the degree to which genes, along with other prenatal factors such as hormones and epi-genetics, may influence the development of homosexuality. In this regard, the most conclusive and telling results have come from studies of “identical” twins (who both have virtually the exact same complement of genes). Although it is commonly assumed that identical-twin studies reveal the influence of genes per se on a trait or behavior, the results of such studies have the unique advantage of reflecting, in fact, the combined influence of all possible, pre-natal, biological factors (e.g., genetics, epi-genetics, hormones, etc.) on the development of homosexuality in adults (1). This is because identical twins not only share the same complement of genes, but they also share the same pre-natal environment (their mother’s womb), where biological factors are postulated to operate.
Twin Studies: Overview
The design of research studies using identical twins has improved greatly since the mid-1990s, with the advent of large, twin registries which can afford much larger data bases and less biased sampling procedures. The former approach of recruiting identical twins via advertisements in gay and lesbian publications is now known to have a very strong “volunteer effect” that produced the appearance of relatively large genetic effects (1). Nevertheless, even with the use of large twin registries, the number of identical twin pairs found with homosexuality is often very small in individual studies, resulting in a standard deviation that is greater than the calculated genetic effect, meaning that the results are not statistically different from zero. In other words, the genetic influence or contribution in several of these studies may actually be zero, making definitive conclusions impossible. Whitehead and Whitehead (1) have presented and discussed, in some detail, these and other problems inherent in twin studies of homosexuality and have presented reasons to expect that the genetic influence on, or contribution to, homosexuality will eventually be agreed to be in the 10%-15% range (i.e., weak). One reason for this (anticipated) lower actual genetic influence is that epi-genetic effects operating through identical twins sharing one placenta probably represent about 15% of the total influence that has been attributed to genetics in published twin studies (2).
Twin Concordance Studies
The “pair-wise concordance” answers the simple question, “Where one twin of an identical pair is homosexual, what percentage of co-twins is also homosexual”. The mathematical formula for pair-wise concordance of identical twins is C/C+D, where C is the number of concordant (similar) twin pairs and D is the number of discordant (dissimilar) twin pairs found in the study. For example, if C=1 and D=9, then the pair-wise concordance would be 1/1+9=1/10 or 10%. This result would indicate that for every twin pair with both members being homosexual, there are 9 twin pairs with only one homosexual member.
Using data provided in several reports of large, twin registry studies in different countries, I performed a meta-analysis and calculated the range of pair-wise concordance to be 9.9% to 31.6%, with the average being 13.0% for males, 13.3% for females, and 13.2% when the raw data for males and females were combined. These pair-wise concordance values indicate that for every twin pair with both members being homosexual, there are 7 twin pairs with only one homosexual member. Now, compare this result to the range of theoretically possible outcomes where no twin pairs would both be homosexual (= 0%) and where all twin pairs would both be homosexual (= 100%) and you can see, intuitively, that a pair-wise concordance of only 13.2% would indicate a real, but relatively minor, contribution of genetics to homosexuality. This minor role is similar to the estimated level of genetic contribution to virtually any kind of human behavior (3) and is known to be non-determinative and, in many cases, treatable by therapy and/or counseling. For instance, the best example to date of a genetically related behavior (mono-amine oxidase deficiency leading to aggressive behavior) has shown itself remarkably responsive to counseling (3). Therefore, on the basis of pair-wise concordance in identical twins, it seems appropriate to conclude that there is, at the most, only a minor genetic contribution to the development of homosexuality, and that this relatively minor influence can be overcome (i.e., nullified) through behavioral therapy (1), which we know to be a fact (4, 5).
The other measure of concordance in twin studies is “proband-wise” concordance. This estimate of concordance is necessary in order to use both identical and fraternal twins in a study to disentangle the relative contributions to homosexuality of genetic and non-genetic (environmental) factors. The formula used is 2C/2C+D, which, compared to the formula for pair-wise concordance, gives much more weight to the individual twins (probands). The effect is to greatly increase, relative to pair-wise concordance values, the apparent genetic contribution to homosexuality in identical twin studies. To illustrate this point, if we use the example given above where the pair-wise concordance calculates to be 1/10 = 10.0%, the proband-wise concordance calculates to be 2/11 = 18.2%. Although it is less intuitive, proband-wise concordance is generally believed to give a better overall estimate of “genetic influence” than does pair-wise concordance.
Classical Twin Studies
While pair-wise concordance gives an intuitive indication of the genetic influence on homosexuality as expressed in identical twins, it does not provide information on what factors may provide the remaining, non-genetic influence. To answer this question, researchers are using other measures, broader-ranging questionnaires and more sophisticated statistical procedures to evaluate such things as heritability, additive genetic effects and postnatal environmental influences. In order to be able to put the results of classical twin studies into perspective, it is important to keep in mind that, by convention in the twin study literature in general, a genetic contribution of around 25% is considered weak, of around 50% is considered moderate and of 75% or more is considered strong (6).
In a meta-analysis, Whitehead (6), using the results from seven of the recent twin registry studies that were designed to reveal contributions of both genetic and non-genetic factors to homosexuality, found that the mean contribution of genetics to male homosexuality was around 22%, and to female homosexuality, around 33%. Because of the relatively large standard deviations in the data, these two values were not statistically different from each other. Thus, the mean genetic contribution to male homosexuality in these studies is weak and to female homosexuality is weakly moderate. Such levels of genetic contribution indicate a real but weak-to-weakly moderate and indeterminate role of genetics in the development of homosexuality. For comparison, other traits that have around 50% (moderate and indeterminate) genetic contribution in twin studies include such things as divorce and alcoholism, while puberty has a 90% (strong and determinate) genetic contribution (1). Furthermore, the non-shared, post-natal environmental contribution to homosexuality is moderate to strong, around 64%-78%, has a relatively small standard deviation and is consistently around the same percentage (6), indicating that homosexuality is influenced primarily by post-natal environmental factors and experiences that are not directly related to prenatal, biological contributions of any kind or combination.
The recent study by Zietsch, et al. (7) can be used to illustrate representative research results obtained with large samples from twin registries. They used a very large sample (9,884) of twins from the Australian Twin Registry, one of the largest samples to date for twin studies of homosexuality. In this sample, there were 1,840 identical twin pairs (1,133 female and 707 male). Their calculated value of only 24% for the proband-wise concordance for homosexuality indicates a weak genetic influence. Moreover, their calculated figure of 31% for heritability of homosexuality also indicates a weak genetic component. This leaves around 68% of the variance represented by post-natal, “shared environment” and “residual” environmental influences combined.
In view of the fact that twin studies have shown that the combined influence of all possible, pre-natal, biological factors (e.g., genetics, epi-genetics, hormones, etc.) on the development of homosexuality in adults is only weak-to-moderate, it is important to understand that all of the biological theories combined can address only this weak-to- weakly moderate amount of influence, while ignoring the far more important post-natal influences (e.g., culture, parental divorce, and having a homosexual parent). Furthermore, twin studies clearly support the inference, based on results obtained through therapy and counseling (4, 5), that post-natal, environmental influences have a far greater role in the development of homosexuality than do pre-natal, biological influences. Thus, where the development of homosexuality is concerned, twin studies have demonstrated that nurture is far more important than nature.
(For more articles on HOMOSEXUALITY, click HERE)
1. Whitehead, N. and B. Whitehead. 2012. Chapter 10. Twin studies: The strongest evidence.(click HERE)
2. Whitehead, N. 2010. Genetic Influence On SSA Significantly Overestimated? (click HERE)
3. Whitehead, N. and B. Whitehead. 2012. Summary. (click HERE)
4. Whitehead, N. and B. Whitehead. 2012. Chapter 12. Can sexual orientation change? (click HERE)
5. Aist, J. 2012. Homosexuality: Good News! (click HERE)
6. Whitehead, N.E. 2011. Neither Genes nor Choice: Same-sex Attraction is Mostly a Unique Reaction to Environmental Factors. Journal of Human Sexuality 3:81-114. (click HERE)
7. Zietsch, B., et al. 2012. Do Shared Etiological Factors Contribute to the Relationship between Sexual Orientation and Depression? Psychological Medicine 42:521-532.