Serotonin (5-HT), a key central nervous system neurotransmitter, is involved in regulating a broad range of psychological traits, behaviors, and physical functions including mood, sleep, appetite, and sexual activity. The serotonin transporter protein (5-HTT), which terminates the action of serotonin by facilitating its reuptake from the synapse, appears to be part of the pathway leading to psychiatric disorders and has been a target of widely used pharmacological treatments. It is thus not surprising that the gene associated with serotonin transport (SLC6A4) has been the focus of extensive research. More than a decade ago, a polymorphism in the promoter region of the gene encoding 5-HTT, referred to as 5-HTTLPR, was identified by Heils et al. [1]: a 44bp deletion/insertion generated two alleles of 5-HTTLPR, with the 14-repeat short (S) variant having less transcriptional activity and lower serotonin uptake than the 16-repeat long (L) variant. Researchers speculated that the differential transcriptional activity caused by this polymorphism would influence complex traits and diseases, including affective disorders [1, 2].
