Due to time constraints, this post is less review than description of results. However, I wanted to post something on this study in advance of some commentary coming from Michael Bailey on the topic.
Here is the reference and abstract:
Abstract: The existence of genetic effects on gender atypical behavior in childhood and sexual orientation in adulthood and the overlap between these effects were studied in a population-based sample of 3,261 Finnish twins aged 33–43 years. The participants completed items on recalled childhood behavior and on same-sex sexual interest and behavior, which were combined into a childhood gender atypical behavior and a sexual orientation variable, respectively. The phenotypic association between the two variables was stronger for men than for women. Quantitative genetic analyses showed that variation in both childhood gender atypical behavior and adult sexual orientation was partly due to genetics, with the rest being explained by nonshared environmental effects. Bivariate analyses suggested that substantial common genetic and modest common nonshared environmental correlations underlie the co-occurrence of the two variables. The results were discussed in light of previous research and possible implications for theories of gender role
development and sexual orientation.
Common Genetic Effects of Gender Atypical Behavior in Childhood
and Sexual Orientation in Adulthood: A Study of Finnish Twins
K. Alanko, P. Santtila, N. Harlaar, K. Witting, M. Varjonen, P. Jern, A. Johansson, B. von der Pahlen, & N. K. Sandnabba. Arch Sex Behavior.
The sample was obtained via a registry maintained by the Central Population Registry of Finland which includes all twin pairs born in 1971 or earlier. The researchers requested information from the twins and received responses from 36% of those surveyed (3,604). For various reasons, the authors assume representativeness of their sample, although I think they might be open to some challenge on this point given the response rate.
The authors used Zucker’s Recalled Childhood Gender Identity/Gender Role Questionaire and Sell’s Assessment of Sexual Orientation. The SASO assesses both behavior and attractions via four items:
Item 1: During the past year, on average, how often were you sexually attracted to a man (woman for female participants)? The response alternatives were: never, less than 1 time per month, 1–3 times per month, 1 time per week, 2–3 times per week, 4–6 times per week, daily. Item 2: During the past year, on average, how often did you have sexual contact with a man (woman for female participants)? The response alternatives were the same as for Item 1 above. Item 3: How many different men (women for female participants) have you had sexual contact with during the past year? Item 4: During the past year, on average, how many different men (women for female participants) have you felt sexually attracted to? The response alternatives to Items 3 and 4 were: none, 1, 2, 3–5, 6–10, 11–49, 50–99, 100C. The participants were given numerical scores so that a response of ‘‘none’’/‘‘never’’ gave a score of 0 and a response of ‘‘100 or more’’/‘‘daily’’ gave a score of 7.
Here are the correlations of twins sharing traits of sexual orientation and gender atypical behavior.
Correlations were higher for identical twins than fraternal twins for both traits, especially for women. About the genetic contribution to GAB and sexual orientation, the authors said:
Significant genetic effects were found for women and men for both GAB and sexual orientation, as was our second hypothesis. The heritability estimates for childhood GAB were 51% and 29%, and for sexual orientation 45% and 50%, for women and men, respectively.
These numbers are higher than past studies and may be related to the nature of the sampling although this is not clear.
The authors also found a relationship between GAB and sexual orientation.
Our first aim was to study the phenotypic correlations between childhood GAB and adult sexual orientation. Significant correlations of moderate sizes were found, indicating that the two phenomena were related. The strength of the phenotypic association was higher for male participants, implying that childhood GAB was a stronger predictor of adult sexual orientation for men.
The authors note that these data in conjunction with past studies lead them to propose the possibility of several pathways to homosexual attractions.
There might, in other words, be different genotypes for different kinds of homosexuality. It might also be possible that the relative importance of shared environment and genetic influences vary during development. It is plausible that parents influence their children directly only as long as they live at home (Knafo et al., 2005; Plomin et al., 2001). Bailey et al. (2000) found that GAB predicted about 30% of the variance in men’s sexual orientation. As neither the phenotypic nor the genetic correlations were unity in the present sample, GAB preceded a homosexual orientation for some participants, whereas gender typicality preceded a homosexual orientation for other participants.
What did not show up was any significant role of shared environment for men. A small amount of the effect could be attributed to shared environment for women. Another data point suggesting that the pathways to adult sexual orientation are different for men and women.
Stay tuned…
Sorry if I’m throwing a spanner in the works, but has it not now been established that identical twins don’t, as was previously and more or less universally assumed, have absolutely identical genes?
http://www.sciencedaily.com/releases/2008/02/080215121214.htm
B.T. Carolus,
Very funny!
B.T.Carolus
HAHAHA! I love that comic.
You are right and I do understand that studies need to be repeated. But at this point I think everyone gets it. SSA is part genetic and part environment.
This puts it in the same category as virtually every other phenomenon that mankind has discovered.
Drowssap:
Technically, the scientific method demands repetition of the experiment in order to confirm results. Although I do agree with you that sometimes this becomes overkill. And there are pieces of this particular study that I just don’t find convincing (and I don’t just mean the idea that 3,600 Finnish twins can/should be generalized to the world’s population).
At risk of becoming the comic depositor:
http://xkcd.com/242/
This is the part I don’t understand.
We know from a dozen other studies that SSA is part genetic and part environment.
So if we already know the answer why do scientists keep running the same study over and over again? Does it really matter if SSA is 2% heritable or 22% heritable or 42% heritable? Does the difference mean anything? What if a future study finds that SSA is 0% or 100% heritable? Scientists will dismiss that research because it doesn’t match the other studies. The entire exercise seems like it’s geared to find the same answer over and over again.
In any case Ulcers and many other non-genetic phenomenon show “heritability”.
Here is a study on genetics and peptic ulcers. In case you didn’t know peptic ulcers are caused by bacteria and yes human genes also play an important role. Which phenomenon don’t have a genetic and environmental component? I can’t think of many.
It’s as if scientists ran a study each morning to determine if the sun was going to come up.
Thanks Warren.
In response to several questions above, this passage from the study might help:
For some genetics may be quite relevant, for others not so much. This is a global measure of why variation occurs between groups and cannot be applied to individuals. Probably no gay gene, although one cannot tell from this study since no DNA work was done. The authors simply compared the concordances among the various twin types (MZ, DZ) on sexual attractions and GAB.
While this is discussed often in these circles, I believe the nonshared environment can include different experiences in the womb (chorions). Thus hormones and the like are considered environment and not genetics.
Sanders from Chicago will have more on the specific genetic contributions when his team reports, probably not until later this year.
Whoops, that first paragraph above was supposed to be blockquoted–they are Timothy’s words in answer to one of my questions. Sorry.
I’m not speaking to this study specifically, but researchers often compare identical twins to fraternal twins to determine the extent to which something is genetic. Identical twins share the same genes while fraternal twins do not.
Thanks. Yes, I am familiar with the practice of giving concordance figures for a whole assortment of subjects under research , and I understand that it’s very helpful for researchers to compare/contrast the concordance figures using fraternal and identical twins.
However, in reading over the last couple of years about things like panic/anxiety attacks, depression, etc (which tend to run in families and thus have often been termed “genetic, ” which may or may not be true), I note that some researchers have been trying to distinguish what might be “genetic” (in the Mendelian sense) from what they feel might be more accurately termed “biological.” While they agree, of course, that at the base of everything lies our genetics, they disagree on whether something should be termed “genetic” if it requires a non-genetic trigger (biological reaction) to cause it to be expressed.
For example, I know there is some heritability to migraine headaches. However, w/out the trigger (for some it appears to be reaction to a very specific food ingredient while for others the trigger might be the more nebulous trigger of “stress”), the migraine doesn’t occur.
carole,
I’m not speaking to this study specifically, but researchers often compare identical twins to fraternal twins to determine the extent to which something is genetic. Identical twins share the same genes while fraternal twins do not.
Thus when you see something with such a huge variance (25% v. 50%) you can pretty much know that genes come into play.
However, because there was not 100% allignment in genetic twins, then genes aren’t 100% of the answer for 100% of the situations.
This looks like junk science designed to get results to fuel more junk science.
As soon as someone finds the sexual attraction circuit in animals and later in humans nobody will remember that these studies were ever conducted.
Might as well throw up another question before Warren returns to answer…
If this was based on mathematical analyses from the questionnaires rather than loci analyses of DNA, then how would “genetic effects” be distinguished from “biological effects” (as in uterine or other developmental events, etc?)
Thanks.
@Timothy Kincaid & Ann:
I am on my way out the door right now but I will add something later that addresses your excellent questions. Also, Michael Bailey has agreed to provide more specifics on the topic later this week. There is no one more qualified to discuss twin studies on this topic than Michael.
There might, in other words, be different genotypes for different kinds of homosexuality.
This is interesting to see – different kinds of homosexuality. Does it mean that there are different variations, components, dimensions, and/or degrees to what some say is all or nothing?
Warren:
Genuine non-rhetorical question here: Would it be fair to say that this study suggest the following?
There is indeed a gay gene (or genes). However,
1. This gene may not be a factor in the orientation of all homosexual persons, and
2. in those persons in whom a gene was a contributor, it may not have been the sole contributor.
FWIW, I don’t have any problem with researchers continuing to do such studies, even imperfect ones. At the end of the day, I am willing to bet that some kind of biological (prenatal hormonal) or possibly genetic predisposition plays a role (but is not the sole cause) in the onset of same-sex attraction. It wouldn’t change my viewpoint about it one iota, but it would make sense to me. I recall being gender nonconforming since I was a very small child. Later environmental factors also were key for me, I believe. I just think it’s a mixed bag.
Warren, help me here:
The use of the terms “Quantitative genetic analyses” and “genetic effects” leave me in need of clarification.
I think I know the answer but need to make sure: in this study did the researchers use a mathematical model to quantify heritability, and I am right that they didn’t do actual DNA testing of the twins?