A new study of youths reveals that social scientists’ opinions still vary on the potential of studying how genes interact with social contexts
ATLANTA — Early in the morning on August 14, sociologists crammed into a meeting room here to debate the merits of their unlikely new collaboration with geneticists trying to unravel the roots of behavior.
Attendees at this session of the annual meeting of the American Sociological Association seemed certain of one thing: There’s a long way to go, but it’s a trip worth taking.
Reports that certain gene variants interact with stress or other social forces to promote or protect against depression and other outcomes remain hard to interpret and usually stymie replication attempts. But that has led a growing band of sociologists to redouble efforts to entwine a strand of social nuance around the double helix.
“If we don’t provide input about the importance of social context in mediating genetic effects on behavior, I can assure you that psychologists and psychiatrists won’t do it,” said Michael Shanahan of the University of North Carolina in Chapel Hill.
Evidence presented by the University of North Carolina’s Guang Guo illustrated the excitement and ambiguity surrounding this endeavor. He and his colleagues found that teenage boys who have inherited two copies of a particular gene variant engage in fewer risky behaviors as they get older than their peers who carry at least one copy of another version of the same gene.
Genetic protection against risky behaviors appeared only at ages when such acts were illegal, such as prior to age 21 for drinking alcohol, Guo said. This effect largely vanished at ages when risky behaviors become legal or socially tolerated.
His team analyzed data on 822 white males from a larger national sample. Participants were first interviewed in 1994, at ages 12 to 18. Follow-ups tracked participants to ages 18 to 26.
Carriers of two copies of one common version of the dopamine transporter gene displayed generally lower rates of 10 risky behaviors than males with at least one copy of a different common version of that gene. These self-reported behaviors included attacking others with weapons and other forms of delinquency, having multiple sex partners, drinking alcohol in binges, regularly smoking cigarettes, using marijuana and cocaine and not wearing seat belts in cars.
The dopamine transporter gene affects the efficiency of brain receptors for dopamine, a chemical messenger that mediates feelings of reward and pleasure. Differences between the effects of this gene’s main variants remain unclear.
Age played a prominent role in Guo’s findings. As boys reached ages at which alcohol and cigarette use became legal, the two genetic groups reported using these substances at comparable rates. A protective effect of the critical gene form appeared at all ages for marijuana and cocaine use, both illicit drugs.
Boys carrying the protective gene strapped in with seat belts while driving or riding in cars significantly more often than their male peers did beginning at ages 16 to 17, when they became legally able to drive.
Findings for all risky behaviors held after statistically accounting for participants’ physical maturity, verbal intelligence, popularity with peers, grade point average and church attendance.
Still, noted Kristen Springer of Rutgers University in New Brunswick, N.J., it’s possible that carriers of the protective gene variant mature out of tendencies to engage in risky behaviors more quickly than their peers do, rather than easing up when those acts become legal.
Researchers need to replicate Guo’s provocative findings, a process that has proven elusive for previous gene-environment interaction studies, remarked Jeremy Freese of Northwestern University in Evanston, Ill. In a new study reported at the meeting, Freese and his colleagues failed to find support for an earlier report by another team that carriers of one form of a gene called taq1a are especially vulnerable to doing poorly in school if they had low birth weights.
Replication difficulties often reflect differences in samples of people studied and in measures of environmental factors, such as stress (SN: 7/18/09, p. 10), commented North Carolina's Matt Bradshaw. “Stress occurs at many levels and in different forms,” he said. “It’s very complicated to study gene-environment interplay over the course of people’s lives.”
G. Guo. DAT1 Gene, Risky Behaviors, and the Law. American Sociological Association annual meeting. Aug. 14, 2010. Atlanta. Abstract available at www.asanet.org/2010Program.cfm
J. Freese. Taq1a and Education, Partisanship, Voting, and Other Outcomes: Replication Attempts Using the Wisconsin Longitudinal Study. American Sociological Association annual meeting. Aug. 14, 2010. Atlanta. Abstract available at www.asanet.org/2010Program.cfm
B. Bower. Gene plus stress equals depression debate. Science News. July 18, 2009. Vol. 176, #2, p. 10. Available online [Go to]