Genetics of emotion regulation.

Emotions can be powerful drivers of behavior that may be adaptive or maladaptive for the individual. Thus, the ability to alter one's emotions, to regulate them, should be beneficial to an individual's success of survival and fitness. What is the biological basis of this ability? And what are the biological mechanisms that impart individual differences in the ability to regulate emotion? In this article, we will first introduce readers to the construct of emotion regulation, and the various strategies that individuals may utilize to regulate their emotions. We will then point to evidence that suggests genetic contributions (alongside environmental contributions) to individual differences in emotion regulation. To date, efforts to identify specific genetic mechanisms involved in emotion regulation have focused on common gene variants (i.e. variants that exist in >1% of the population, referred to as polymorphisms) and their association with specific emotion regulation strategies or the neural substrate mediating these strategies. We will discuss these efforts, and conclude with a call to expand the set of experimental paradigms and putative molecular mechanisms, in order to significantly advance our understanding of the molecular mechanisms by which genes are involved in emotion regulation.

No association between two polymorphisms of the serotonin transporter gene and combined type attention deficit hyperactivity disorder.

Several independent studies have reported association between serotonin transporter gene (SLC6A4) polymorphisms and attention deficit hyperactivity disorder (ADHD). Five studies found evidence for association between the long-allele of a 44-bp insertion/deletion polymorphism (5-HTTLPR) and ADHD. Another two studies corroborated this finding while a further six studies did not find such an association. For a second polymorphism within the gene, a variable number tandem repeat (VNTR) within intron 2, one study demonstrated that the 12/12 genotype was significantly less frequent in ADHD cases compared to controls, while a second study found that the 12-allele was preferentially transmitted to offspring affected with ADHD. To provide further clarification of the reported associations, we investigated the association of these two markers with ADHD in a sample of 1,020 families with 1,166 combined type ADHD cases for the International Multi-Centre ADHD Genetics project, using the Transmission Disequilibrium Test. Given the large body of work supporting the association of the promoter polymorphism and mood disorders, we further analyzed the group of subjects with ADHD plus mood disorder separately. No association was found between either of the two markers and ADHD in our large multisite study or with depression within the sample of ADHD cases.