News Release

When mistreated children act out later in life: Brain gene may play a role, study says

Peer-Reviewed Publication

American Association for the Advancement of Science (AAAS)

This news release is also available in French.

Variations in a gene that helps regulate several behavior-related brain chemicals may partly explain why some mistreated children later develop antisocial behavior, while others do not, according to an international study. The authors, from the U.K., the U.S., and New Zealand, report their findings in the journal Science, published by the American Association for the Advancement of Science.

If their findings can be replicated, they may help efforts to identify children with a particular risk for developing behavior problems or committing crimes as adults, said study author Terrie Moffitt of King's College London and the University of Wisconsin. Because there are so many degrees of antisocial behavior, the researchers expect many additional gene-environment interactions to be involved.

"This is not really the story of a gene that has a risk for antisocial behavior. It's the story of the interplay between a gene and the experience of maltreatment," Moffit said.

Among the males in the study, those who had a variation of a certain gene and had experienced childhood maltreatment made up 12 percent of the whole male population. They made up 22 percent of the group that became antisocial as adults, however. That makes the combination a significant risk factor for antisocial behavior, comparable to the major risk factors for heart disease, according to the researchers.

Moffitt and her colleagues studied the MAOA gene, which encodes an enzyme that works on several different neurotransmitters, the chemical messengers that hop from one neuron to another.

"In its normal role, the enzyme has a sort of clean-up function. It stays in the synapse between two neurons and clears away excess neurotransmitters. I think of it as a little Pacman," Moffitt said.

A common variation of the gene produces a less-active enzyme, which isn't as efficient at clearing away excess neurotransmitters. Some previous studies have linked the enzyme's activity levels with aggression, according to the Science authors.

The MAOA gene occurs on the X chromosome. The study focused on males, because they have just one MAOA gene and were therefore simpler to study. Moffitt speculated that one reason females are generally less antisocial than males might be that, with two X chromosomes, they have a better chance of inheriting the high-activity version of the gene.

The team studied a population of young people in New Zealand, whose life histories have been recorded at various intervals since they were born. Moffitt's team measured instances of maltreatment during the first ten years of life, including rejection by the child's mother assessed when the child was three years old, frequent changes of the primary caregiver, and physical and sexual abuse.

They also evaluated the test subjects' records of antisocial behavior, which is generally defined as "behavior that violates the rights and safety of others," according to Moffitt. Specifically, they used the American Psychiatric Association's criteria for adolescent conduct disorder and antisocial personality disorder, court records for violent crimes, and evidence of aggressive personality traits from a psychological assessment at age 26.

The researchers determined which version of the MAOA gene each test subject had. They found that maltreated children with the less active version of the gene were more likely to develop behavioral problems than were those with the more active version.

Merely looking at the genetic variation in the population without considering who had experienced maltreatment revealed no pattern related to later behavior, the authors found.

The unusual study population was a key aspect of the research, Moffitt explained. In 1972, the New Zealand government began a study of birth complications, recording a wide range of information on all the infants born within one year in a certain hospital.

The study expanded its scope as it followed the children through later years. Unlike a study of people in prison or in a medical setting, this group represents a complete cross section of a population, Moffitt said.

The high-activity version of the gene seems to have a protective effect against stress, according to Moffitt. It might someday be possible, she said, to screen people for this version of the gene and for others that might make people more resistant to trauma than others.

"It's interesting that most people are worried about screening because they are looking for disease risk. In this case it may be a genetic strength," Moffitt said.


The other authors of the study are Avshalom Caspi, Joseph Clay, Jonathan Mill, Ian W. Craig, and Alan Taylor, of King's College, London, U.K; Avshalom Caspi is also at the University of Wisconsin, in Madison, Wisconsins, U.S.; and Judy Martin and Richie Poulton of the Dunedin School of Medicine, the University of Otago, New Zealand.

The study was funded by the Health Research Council of New Zealand, the University of Wisconsin Graduate School, and by grants from the U.K. Medical Research Council and the U.S. National Institute of Mental Health.

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