Although media reports on genes are often misleading, this research shows how both positive and negative experiences influence how genetic variants affect the brain and thereby behavior. Maybe influence is not the correct word, ‘are associated with’ or ‘are correlated with’ seems more correct, as I look at the research. On the other hand, the interaction seems highly probable to me and the study is interesting as it shows how thinking about genes isn’t necessarily deterministic in nature (pun intended).
From the press release:
Every single high school student aged 17 to 18 years old in Västmanland, a Swedish county, was invited to participate in the study, and 1,337 agreed to do so. They anonymously completed questionnaires reporting on delinquency, family conflict, experiences of sexual abuse, and the quality of their relationship with their parents. They also provided a sample of saliva from which the researchers extracted DNA.
The Monoamine oxidase A (MAOA) gene is a key enzyme in the catabolism of brain neurotransmitters, monoamines, especially serotonin. Catabolism is the breaking down of complex materials and the releasing of energy within an organism. “About 25% of Caucasian men carry the less active variant of MAOA. Among them, those who experience physical abuse in childhood are more likely than those who are not abused to display serious antisocial behaviour from childhood through adulthood,” Hodgins explained. “Among females it is the high activity variant of the MAOA gene that interacts with adversity in childhood to increase the likelihood of antisocial behaviour.”
The brain-derived neurotrophic factor (BDNF) gene modulates neuronal plasticity. The term neuronal plasticity refers to our brain cells’ ability to reorganize pathways and connections throughout our lives. “The low expressing variants of BDNF are carried by approximately 30% of individuals and some previous studies had shown that this variant was associated with aggressive behaviour if carriers were exposed to aggressive peers. The third gene we studied was the serotonin transporter 5-HTTLPR,” Hodgins said. “The low activity variant of this gene is carried by approximately 20% of individuals. Among carriers of this low activity variant, those exposed to adversity in childhood are more likely than those who are not to display antisocial and aggressive behaviour.”
“We found that the three genetic variants interacted with each other and with family conflict and sexual abuse to increase the likelihood of delinquency, and with a positive parent-child relationship to decrease the risk of delinquency,” Hodgins explained. “Among carriers of the low activity variants of all three genes, those exposed to family conflict or sexual abuse or both reported high levels of delinquency while those who reported a positive and warm relationship with their parents reported little or no delinquency.” Thus, the same genetic variants were associated with high and low levels of delinquency depending on exposure to negative or positive environments.
In conclusion, variants of three common genes, MAOA, BDNF, and 5-HTTLPR, interacted with each other and with negative environmental factors to increase the risk of delinquency and with a positive environmental factor to decrease the risk of delinquency in a large sample of teenagers. “These findings add to those from other studies to show that genes affect the brain, and thereby behaviour, by altering sensitivity to the environment,” Hodgins said.
Abstract of the study:
Background. Previous evidence of gene-by-environment interactions associated with emotional and behavioral disorders is contradictory. Differences in findings may result from variation in valence and dose of the environmental factor, and/or failure to take account of gene-by-gene interactions. The present study investigated interactions between the brain-derived neurotrophic factor gene (BDNF Val66Met), the serotonin transporter gene linked polymorphic region (5-HTTLPR), the monoamine oxidase A (MAOA-uVNTR) polymorphisms, family conflict, sexual abuse, the quality of the child–parent relationship, and teenage delinquency.
Methods. In 2006, as part of the Survey of Adolescent Life in Västmanland, Sweden, 1337 high-school students, aged 17–18 years, anonymously completed questionnaires and provided saliva samples for DNA analyses.
Results. Teenage delinquency was associated with two-, three-, and four-way interactions of each of the genotypes and the three environmental factors. Significant four-way interactions were found for BDNFVal66Met×5-HTTLPR×MAOA-uVNTR×family conflicts, and for BDNF Val66Met×5-HTTLPR×MAOA-uVNTR×sexual abuse. Further, the two genotype combinations that differed the most in expression levels (BDNF Val66Met Val, 5-HTTLPR LL, MAOA-uVNTR LL (girls) and L (boys) vs BDNF Val66Met Val/Met, 5-HTTLPR S/LS, MAOA-uVNTR S/SS/LS) in interaction with family conflict and sexual abuse were associated with the highest delinquency scores. The genetic variants previously shown to confer vulnerability for delinquency (BDNF Val66Met Val/Met×5-HTTLPR S×MAOA-uVNTR S) were associated with the lowest delinquency scores in interaction with a positive child–parent relationship.
Conclusions. Functional variants of the MAOA-uVNTR, 5-HTTLPR, and BDNF Val66Met, either alone or in interaction with each other, may be best conceptualized as modifying sensitivity to environmental factors that confer either risk or protection for teenage delinquency