Swedish twin study: Q & A with J. Michael Bailey

Recently, I posted here and here about a new study from Sweden involving twins and sexuality (Niklas Långström, Qazi Rahman, Eva Carlström, Paul Lichtenstein, (2008). Genetic and Environmental Effects on Same-sex Sexual Behaviour: A Population Study of Twins in Sweden. Archives of Sexual Behaviour, June 7, published online.) To get additional perspective on this new report, I asked prominent sexuality researcher, J. Michael Bailey from Northwestern University to comment. My thanks to Dr. Bailey for his time and expertise.

Throckmorton: How are the models used in twin studies able to separate the family influence into genetic and shared environmental effects? Clearly the environmental factors shared by twins do not look influential in this study. Many critics of this kind of work will wonder how the shared family environment cannot be influential. Hence, the question about how we can tell the family influence is genetic and not from the common parenting or social environment.

Bailey: Most studies use twins who have been reared together from birth. Shared environment is the environment shared by siblings reared together, and thus, identical twins and fraternal twins are equally similar in their shared environment (provided they were reared together, they share all of it). Nonshared environment consists of environmental factors not shared even by siblings in the same household. Nonshared environment is the kind of environment that causes differences even between identical twins reared together. The logic of the common twin study (as opposed to the rare study of identical twins reared apart) depends on their being two types of twins that vary in their genetic similarity. The assumption is that this is the only salient way that such twins differ–other differences are presumed not to have an affect on the trait of interest. If this assumption is true, then one looks to see whether identical twins are more similar than fraternal twins. If they are, this is evidence for genetic effects. To the extent that identical and fraternal twins are equally similar to each other (and more similar than random people are to each other), this suggests there are shared environmental factors. To the extent that identical twins reared together are different from each other, this supports the importance of the nonshared environment.

Throckmorton: What are the advantages of this study over your 2000 population based study (Bailey et al, 2000)? What are the limitations in contrast to your work?

Bailey: I think this study is comparable in quality to our 2000 study, although our measures of sexual orientation were more comprehensive.

Throckmorton: In the new twin study, the genetic effects are estimated at 35-39% for men and 18-19% for women. Since we are not assuming one gene codes for sexual orientation, do you have thoughts about what genetic mechanism(s) could be at work? The pedigree studies have had mixed results, have they not?

Bailey: Studies such as this one provide little if any insight into the nature of genetic mechanisms. Rather, they estimate the magnitude of genetic effects, whatever those effects are. Pedigree studies are studies that look at patterns of similarity in families, and there has been some inconsistency, with some studies finding evidence consistent with X-linkage, and others not finding such evidence. But virtually all studies have found higher rates of homosexuality among family members of gay men.

Throckmorton: The estimates of the effect of non-shared environmental factors are very high. The authors indicate that hormones in utero could be an aspect of the non-shared environment. Given that these twins shared the same womb, what kinds of non-shared effects are they referring to?

Bailey: No one knows how this can happen. First of all, nonshared environment is the kind of environment that causes identical twins reared together to be different. This nonshared environment is poorly understood but is clearly important. We know, for example, that if one identical twin has a congenital major brain anomaly such as microcephaly (being born with a very small cortex), the other twin is usually normal. Obviously, this is due to some kind of prenatal environmental factor or event. (It can’t be genetic, because they have the same genes.) We really haven’t a clue what it is.

Differences between identical twins (or fraternal twins for that matter) also reflect measurement error, and the amount of such error depends on how good the measure of sexual orientation (in this case) is. I would say the measure used in the study at hand is okay but not great.

Throckmorton: By the measure of sexual orientation, I assume you are referring to the fact that this study did not assess sexual fantasy or attraction independent of behavior. How do you think a measure of sexual fantasy would impact the results? Do you think we might get lower effects of environment on the inner world?

Bailey: I have no idea, honestly.

Throckmorton: Concerning environment, some critics of pre-natal theories might suggest that twins are not often treated alike and do not really share environments, even though they live in the same house and share the same parents. Is there an empirical answer to this concern?

Bailey: Twin researchers have typically concocted indices of how similarly twins were treated as children. Parents vary in their twin-rearing philosophies, with some favoring “treat ‘em alike” and others favoring “treat ‘em differently.” Typically, these indices don’t predict how similar twins become.

Throckmorton: Could the non-shared environment also include peer influences, different socialization experiences, trauma, etc.?

Bailey: Yes. Regarding sexual orientation, though, there is both anecdotal and empirical evidence that relevant twin differences arise early. For example, gender nonconformity differences in childhood are common and predict orientation differences in adulthood.

Dr. Bailey’s answer to the last question is an intriguing finding. One twin might display gender nonconformity and the other might not. These differences do arise early and cause me to question that they are often in response to parenting differences. The GNC differences however, will likely lead to very different social environments for each twin.

Going forward, research on non-shared environmental factors would shed light on how environment helps to shape the pre-natal givens.

*Bailey, J.M., Dunne, M.P., & Martin, N.G. (2000). Genetic and Environmental influences on sexual orientation and its correlates in an Australian twin sample. Journal of Personality and Social Psychology, 78, 524-536.

Print Friendly

  • Evan

    Throckmorton: By the measure of sexual orientation, I assume you are referring to the fact that this study did not assess sexual fantasy or attraction independent of behavior. How do you think a measure of sexual fantasy would impact the results? Do you think we might get lower effects of environment on the inner world?

    Bailey: I have no idea, honestly.

    There are many possibilities that Prof. Bailey probably refrained from discussing because it’s tricky to translate results from one study based on a certain methodology to another constrained by a different approach. I’ll try to address at least one right now for the sake of exploring any possible ideas on the subject.

    Discordance between reported attractions, behaviours and identification can be observed if we look at results from Dunne et al (2000). This study was conducted on a sample of 1824 Australian male twins aged between 19 and 52 years. The participants were surveyed, among others, for same-sex attraction (SSA), non-hetero identity (NHI) and same-sex behaviour (SSB).

    14.5% of all males reported ever having SSAs. A subset of SSA-ed men, 46.3%, preferred to see themselves as heterosexual. 60.7% of SSA-ed men (8.8% of all subjects) also reported same-sex behaviour.

    85.6% of the sample reported never having SSAs. 7.5% of males who never had SSAs had at least one same-sex partner and experience (6.4% of entire sample).

    15.2% of all males reported same-sex behaviour.

    In the sample studied by Dunne & colleagues, the number of males who had at least one same-sex experience (15.2%) was slightly larger than the number of males who had SSAs (14.5%) and more than double the number of males who self-identified as homosexuals (6.4%).

    We can conclude that at least at the level of reports, attractions correlate strongly with behaviour. However, the absolute percentage of men who engaged in homosexual behaviour without reporting same-sex attractions (6.4%) is greater than the absolute percentage of men who reported same-sex attractions but no same-sex behaviour (5.7%). Apparently, the underlying factors that lead to behaviour are not specific to the psychological orientation. Therefore, I think that we should bear in mind when interpreting this kind of studies that genetic and environmental factors are likely to play different roles in people who engage in same-sex behaviours compared to people who experience same-sex attractions.

    Dunne M.P.; Bailey J.M.; Kirk K.M.; Martin N.G., The subtlety of sex-atypicality, Archives of Sexual Behavior, Volume 29, Number 6, December 2000, pp. 549-565(17).

  • Drowssap

    We know, for example, that if one identical twin has a congenital major brain anomaly such as microcephaly (being born with a very small cortex), the other twin is usually normal. Obviously, this is due to some kind of prenatal environmental factor or event. (It can’t be genetic, because they have the same genes.)

    I looked this one up because I had never heard of it.

    Microcephaly

    UK incidence rate: 1.02 per 10,000 births

    When you start to find things around 1 in 10,000 kids the cause can be virtually anything. Why Microcephaly impacts one twin and not the other can likewise be anything. Rare stuff can be crazy stuff.

    But homosexuality isn’t like that.

    Male, preferential homosexuality occurs in around 1 in 30 men. Right there you know that homosexuality occurs to due environmental factors that impact nearly everyone. Most people that run into this factor won’t become gay but quite a few do. That’s how things work.

    I wonder if there are prenatal things as common as homosexuality that rarely impact both identical twins. If one twin is gay, the other is straight about 80% of the time. Does anything else work like that? I really don’t know.

    I guess what I’m really asking is why do scientists view homosexuality as almost certainly prenatal in origin? To me it appears a safe bet that it’s probably postnatal most of the time.

  • Drowssap

    A) Homosexuality is set in motion by multiple, random environmental factors that occur throughout the population

    B) Homosexuality is set in motion by just a few environmental factors that occur randomly throughout the population

  • Evan

    Drowssap,

    I think the argument was the possibility of prenatal factors to act differently on identical twins even if they share the same placenta and have almost identical genomes. But there are other occurences like differences in fingerprints, which are due to prenatal factors and which point to the same conclusion that somehow they do not go through the same process in the the same way.

    It is also possible that focusing on twins for the evident advantages of studying the separate contribution of genetic, unique and shared factors, may come with some errors specific to the fact that identical twins are not a typical occurence in human births (1 in about 333 births). There could be genetic effects specific to this type of occurence stemming from the small genetic differences between identical twins (see Bruder et al, Phenotypically Concordant and Discordant Monozygotic Twins Display Different DNA Copy-Number-Variation Profiles, The American Journal of Human Genetics 82, 763–771, March 2008; the report is here).

  • Evan

    You can also check the Scientific American report, which is less technical: Identical Twins’ Genes Are Not Identical.

  • Drowssap

    Evan

    The differences between identical twins increase as they age, because environmentally triggered changes accumulate. But twins can also begin their lives with differences, according to Bruder’s study, and that calls into question their very name.

    “Maybe we shouldn’t call them identical twins,” Harvard’s Bieber says. “We should call them ‘one-egg twins.’”

    I knew that gene expression changes which genes are active throughout our lives. When genes become useful they have the propensity to kick on. On the flip side if they prove detrimental genes have the ability to turn off.

    However I didn’t know that identical twins could start out different to begin with.

    On a related note:

    Clones would start out with precisely the same genes active because a clone is built from a fully expressed, adult strand of DNA. Is that correct or am I missing something on clones?

  • Evan

    I don’t know much about cloning types, Drowssap. I suppose they copy DNA material and they get a full duplicate of whatever they want to clone.

    But how monozygocity is caused no one knows right now. Neither do they know how identical identical twins really are. Apparently they’re not fully identical and that can cause different phenotypes, including different types of diseases (like the one mentioned in the interview). Many things can happen along the way from DNA duplication to expression. It doesn’t necessarily mean that events in the womb are the main influencing factors.

    Here’s one study that focuses on the epigenetic differences that appear in the life of identical twins during their lifetime. One relevant quote:

    By using whole-genome and locus-specific approaches, we found that approximately one-third of MZ twins harbored epigenetic differences in DNA methylation and histone modification. These differential markers between twins are distributed throughout their genomes, affecting repeat DNA sequences and single-copy genes, and have an important impact on gene expression. We also established that these epigenetic markers were more distinct in MZ twins who were older, had different lifestyles, and had spent less of their lives together, underlining the significant role of environmental factors in translating a common genotype into a different phenotype. Our findings also support the role of epigenetic differences in the discordant frequency/onset of diseases in MZ twins.

  • Drowssap

    The logic of the common twin study (as opposed to the rare study of identical twins reared apart) depends on their being two types of twins that vary in their genetic similarity. The assumption is that this is the only salient way that such twins differ–other differences are presumed not to have an affect on the trait of interest.

    Somebody needs to do another brain wiring study like “PET and MRI show differences in cerebral asymmetry and functional connectivity between homo- and heterosexual subjects.” This time do it on identical twins.

    Take 10 pairs of identical twins, 1 straight the other gay.

    Check to see if the same areas of brain wiring are more feminine in the gay twin than the straight twin.

    Since…

    The results cannot be primarily ascribed to learned effects, and they suggest a linkage to neurobiological entities.

    … we’d have a pretty definitive answer.

    Oh how I wish I had a million bucks to donate. Does anybody know how much research like this costs?

  • Evan

    Drowssap,

    A brainscan costs around five thousand dollars each, I think. But the problem is:

    Scanning the brains of discordant twins at adult age would not say much about what caused any different patterns that might be found. You would have to do a longitudinal study, scanning the brains of a group of twin pairs from their earliest years to adulthood to observe any significant changes in volumes, connectivity or activation. That is, if you can find some predictor of future orientation which is already present at the earliest age when brainscans can be performed. Such enterprise would be quite expensive and time-consuming. The risks are also big: you can fail to predict orientations and get useless data, some of them might quit halfway through the process, or if orientation is established before brainscans are performed you would only witness effects and the causes would remain out of sight.

    I think a better approach would be to have a good and reliable collection of candidate genes and try to see how their expression would contribute to any observed brain patterns (and which could be attributed to other environmental causes). The Savic study is the second one, after last year’s Safron et al, which points to something in the amygdala region. They should zero in on that region and see if anxiety is a byproduct of orientation or a component. I think it’s a secondary component which fits Daryl Bem’s description of childhood ‘feelings of apprehension’ in the presence of same-sex peers. (What about the children who were not gender-nonconforming?…) The amygdala seems to take the punch of emotional interpretation, but in order for one gender to be perceived as unfamiliar, as Bem described it, there must also be something underexpressed in the one who perceives and does not fully identify with the perceived gender. Now that’s the hardest part to imagine what it could be. I’ve been talking on this blog about a handful of possible elements, from aggressiveness to anything that can work with(in) perception, like proprioception and brain maps of gender. I have no idea how they can look for aggressiveness expression in the brain which would have a bearing on gender perception (not on something else). It would be ideal if you could turn on or off some very specific brain areas and see which one makes the greatest difference then zero in on that area.

  • http://aebrain.blogspot.com Zoe Brain

    My thoughts on the subject

    I invite critique – by Warren, by Bailey, by anyone with some knowledge of the subject.


CLOSE | X

HIDE | X