:: By Brooke E. O’Neill, AM’04

:: Photography by Dan Dry

Investigations ::

They’re getting high off cold meds, posting lewd photos on MySpace, and developing online gambling addictions. The sins may be new, but problem behavior has long been a rite of passage for U.S. teens. In fact, says behavioral geneticist Kristen Jacobson, troublemaking is so common for Americans between ages 14 and 18 that “it’s almost normative.” Yet individual differences abound. Why do some youths make relatively harmless crank calls while others wield knives and bully classmates? Why do some emerge from adolescence as well-adjusted adults while others sink into a cycle of delinquent behavior? Jacobson, an assistant professor of psychiatry, wants to understand the divergence. With a $1.5 million National Institutes of Health New Innovator Award she won this past September, she’ll study how environmental and genetic influences interact to shape adolescent conduct, including nonviolent delinquency, aggression, and substance abuse.

When delinquency persists past adolescence, Jacobson says, genes may be partly to blame.

“People may be acting out for genetic reasons, but they may be acting out for environmental reasons as well,” says Jacobson. Known as the “bioecological model,” her chosen approach sees individual development as a set of interactions between genes and environmental factors such as family, school, and community. Much of Jacobson’s research on teens has focused on twin studies, and she is associate director of the psychiatry department’s twin-studies program. By comparing identical twins, who share all of their DNA, with fraternal twins, who share only half, geneticists can better pinpoint which behaviors may be genetically linked.

Jacobson describes many of the environmental influences she studies as “grandmother science,” or things a typical grandmother might warn her grandchild about. Peer pressure is one example. “Kids who hang out with other kids who do bad things tend to get in trouble,” she says. In fact, most problem behavior, both aggression and nonviolent delinquency, such as lying to parents and stealing, drops off as teens grow up and leave high school.

Yet some adolescents exhibit more lasting problems. In research conducted in 2003, Jacobson analyzed twin-studies data to identify two pathways of antisocial conduct: adolescent-limited and life-course persistent. Each is characterized by a different degree of heritability, or genetic influence. The first group, which makes up roughly 50–75 percent of troubled teens, describes those whose acting out, influenced mainly by environmental factors, tapers off after adolescence.

Children whose difficulties continue, on the other hand, make up less than ten percent of the population and exhibit higher genetic influence. They often act out earlier in life and score higher on early-childhood tests that measure maternal depression, maternal life stress, low socioeconomic status, single parenthood, home environment, and parental treatment.

As genetic technology improves and more human-development researchers seek out the individual genes that influence behavior, Jacobson continues to stress the importance of environmental variables, which may even alter how genes express themselves. A 2005 study in the Proceedings of the National Academy of Sciences, for example, found variation in identical twins’ DNA methylation levels, a driver of gene expression. Because both siblings have the same gene set, says Jacobson, whose NIH study builds on these findings, such a divergence may result from environmental influences—the level of maternal care in infancy is one example—that cause twins’ genes to express themselves differently.

If the way a parent treats a child can change the body’s biology, Jacobson reasons, so might other environmental influences. Recent functional magnetic resonance imaging (fMRI) studies, for example, link early-life family adversity with decreased activity in the amygdala, the part of the brain related to emotion regulation and believed to play a role in developing aggressive behavior.

Understanding how deviance develops on both genetic and environmental levels could offer new ideas on how to help at-risk teens. Researchers have long observed that children from low socioeconomic environments, a group over-represented by racial and ethnic minorities, show the worst developmental outcomes. Furthermore, the influence of genes on those outcomes may be different from other populations. As a graduate student at Pennsylvania State University, Jacobson coauthored a 1999 paper in Child Development finding that genetic influence on verbal IQ varied depending on parents’ education levels. For children from a highly educated family, genetic influence was greater than for those with less education. In other words, says Jacobson, environmental influences played a larger role on verbal IQ for the disadvantaged.

Over the next five years her NIH study will investigate the environmental, psychosocial, biological, and genetic risk components of delinquency across socioeconomic and racial groups. The multidisciplinary project—one of the only large-scale genetic studies of adolescent delinquency to look at ethnicity and socioeconomic status beyond Caucasians—will use in-school surveys, interviews, computer-based tests of traits like impulsivity, and fMRI to parse the effects of nature and nurture.

The study’s first phase will survey 7,000 middle schoolers in ten Chicago public schools targeted for their socioeconomic and racial diversity. When the data is compiled this May, says Jacobson, it will paint the “broad brushstrokes” overview of how individual, family, peer, school, and community factors encourage or protect against problem behavior in different populations. She will then analyze 400 pairs of siblings who participated in the first phase: 200 pairs who have the same mother and father, 150 half-siblings who share only one parent, and 50 step- and adoptive siblings who are not genetically related. Such variations will help her tease apart how much of an individual’s delinquency is attributable to sharing a household versus sharing genes.

Jacobson emphasizes that her project, an attempt to cull data at several levels, is more exploratory than hypothesis-driven. Thus while it would be premature for her to speculate on what intervention programs might best help at-risk teens, her work should shed light on why some kids struggle while others thrive. For teens whose bad behavior—not to mention whose parents and teachers—cries out for real-world solutions, Jacobson is laying critical groundwork.