Are you genetically predisposed to antisocial behavior?

December 15, 2014
Credit: George Hodan/public domain

Both positive and negative experiences influence how genetic variants affect the brain and thereby behaviour, according to a new study. "Evidence is accumulating to show that the effects of variants of many genes that are common in the population depend on environmental factors. Further, these genetic variants affect each other," explained Sheilagh Hodgins of the University of Montreal and its affiliated Institut Universitaire en Santé Mentale de Montréal. "We conducted a study to determine whether juvenile offending was associated with interactions between three common genetic variants and positive and negative experiences." Hodgins and her colleagues published the study on December 11, 2014 in the International Journal of Neuropsychopharmacology.

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, , 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 ."

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 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 to increase the risk of delinquency and with a positive environmental factor to decrease the risk of 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.

Explore further: Studying links between EI and delinquency

More information: Kent W Nilsson, Erika Comasco, Sheilagh Hodgins, Lars Oreland, Cecilia Åslund published "Genotypes do not confer risk for delinquency but rather alter susceptibility to positive and negative environmental factors: Gene-environment interactions of BDNF Val66Met, 5-HTTLPR, and MAOA-uVNTR" in the International Journal of Neuropsychopharmacology on December 11, 2014.

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JVK
1 / 5 (1) Dec 15, 2014
http://ijnp.oxfor...p.pyu107
The BDNF Val66Met polymorphism, which consists of a single-nucleotide polymorphism (SNP) G/A substitution at codon 66 (Val66Met), was analyzed as described previously, Val/Val versus Val/Met or Met/Met (Comasco et al., 2013). The Met allele is less active than the Val allele.


See also Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults. http://dx.doi.org...4-0895-5

That experimental evidence also links metabolic networks and genetic networks via a different amino acid substitution. In fact, all experimental evidence of biologically-based cause and effect links nutrient-dependent RNA-directed DNA methylation to RNA-mediated events and amino acid substitutions that differentiate all cell types directly linked to morphological and behavioral phenotypes. See for examples: http://www.ncbi.n...24693353

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