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 이성욱 ( 2011-01-24 09:10:59 , Hit : 2262
 Friends connect on a genetic level

Published online 17 January 2011 | Nature | doi:10.1038/news.2011.23

Published online 17 January 2011 | Nature | doi:10.1038/news.2011.23

Groups of friends show patterns of genetic similarity, according to a study published today in The Proceedings of the National Academy of Sciences1.

The findings are based on patterns of variation in two out of six genes sampled among friends and strangers. But the claim is a hard sell for some geneticists, who say that the researchers have not analysed enough genes to rule out alternative explanations.

The team, led by James Fowler, a social scientist at the University of California, San Diego, looked at the available data on six genes from roughly 5,000 individuals enrolled in unrelated studies, and recorded the variation at one specific point, or single nucleotide polymorphism (SNP), in each gene, and compared this between friends and non-friends.

After controlling for genetic likeness due to sex, age, race or common ancestry, friends still tended to have the same SNP at one position in a gene encoding the dopamine D2 receptor, DRD2. Friends also showed more variation at one position in a cytochrome gene, CYP2A6, than non-friends.

An 'opposites attract' phenomenon may account for the variation in CYP2A6 among friends, say the authors. This result indicates that genetic patterns aren't always the result of friends who connect through similar activities, such as running marathons or playing musical instruments.

Genetic cliques
The ultimate function of DRD2 or CYP2A6 is not clear. But the authors point out that previous studies have associated both genes, albeit controversially, with traits that influence social behaviour: DRD2 with alcoholism and CYP2A6 with 'openness'2,3.

"When people choose friends with similar genotypes, an individual's fitness — or survival until reproduction — not only reflects their own genes but also the genes of the friends they've chosen," says Nicholas Christakis, a social scientist at Harvard University in Cambridge, Massachusetts, and an author on the study. In other words, there might be an evolutionary benefit to having friends with compatible genes, even if you don't have any offspring with them. For example, if people who are naturally less susceptible to bacterial infection hang around together, their collective health as a group multiplies because the bacteria have no vulnerable hosts.

"Assuming they're right, what's interesting about this study is that they find an association at the level of SNPs," says David Sloan Wilson, an expert on the evolution of social groups at Binghamton University in New York. He says that scientists have long known that people gravitate towards like-minded people, but he would have expected genotypic similarities to be far less apparent, because behaviour tends to be influenced by several genes. And there is little reason to suspect that friends with similar characteristics, such as altruism, would be able to detect variations in the underlying genes for that trait.

Too good to be true?
But not everyone is convinced.

"If this was a study looking for shared genes in patients with diabetes, it would not be up to the standards of the field," says David Altshuler, a geneticist at the Broad Institute in Cambridge. "We set these standards after 10 years of seeing so many irreproducible results in gene-association studies."

Because most genes have modest effects on behaviour or health, many scientists assume that thousands of SNPs — rather than six — need to be analysed before a correlation to any trait can be confidently made. Geneticists are often hard-pressed to find one SNP in a million that reproducibly correlates with a disease, says Altshuler. "It's like the team bought six lottery tickets and won the megabucks twice — this is not how things work."

Stanley Nelson, a human geneticist at the University of California, Los Angeles, agrees, adding: "It certainly is a provocative study — I would have loved to have seen it done with information from the rest of the genome."

Fowler defends his decision to focus on six genes, rather than thousands. Genome-wide information wasn't available and, he says, the "transmission disequilibrium" statistical tests that the group ran to control for similarity owing to ancestry are among the strongest in the field of human-genetics studies.

References
Fowler, J., Settle, J. E. & Christakis, N. A. Proc. Natl Acad. Sci USA doi:10.1073/pnas.1011687108 (2011).
LeFoll, B., Gallo, A., Le Strat, Y., Lu, L. & Gorwood, P. Behav. Pharmacol. 20, 1-17 (2009). | Article
Lohmueller, K. E., Pearce, C. L., Pike, M., Lander, E. S. & Hirschhorn, J. N. Nature Genetics 33, 177-182 (2003). | Article | ISI







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