Abstract
Depression risk genes in combination with childhood events have been associated with biased processing as an intermediate phenotype for depression. The aim of the present conceptual replication study was to investigate the role of biased automatic approach-avoidance tendencies as a candidate intermediate phenotype for depression, in the context of genes (5-HTTLPR polymorphism) and childhood trauma. A naturalistic remitted depressed patients sample (N = 209) performed an Approach-Avoidance Task (AAT) with facial expressions (angry, sad, happy and neutral). Childhood trauma was assessed with a questionnaire. Genotype groups were created based on allele frequency: LaLa versus S/Lg-carriers. The latter is associated with depression risk. We found that remitted S/Lg-carriers who experienced childhood trauma automatically avoided sad facial expressions relatively more than LaLa homozygotes with childhood trauma. Remitted LaLa-carriers who had not experienced childhood trauma, avoided sad faces relatively more than LaLa homozygotes with childhood trauma. We did not find a main effect of childhood trauma, nor differential avoidance of any of the other facial expressions. Although tentative, the results suggest that automatic approach-avoidance tendencies for disorder-congruent materials may be a fitting intermediate phenotype for depression. The specific pattern of tendencies, and the relation to depression, may depend on the genetic risk profile and childhood trauma, but replication is needed before firm conclusions can be drawn.
Highlights
Major depressive disorder is highly prevalent and is associated with high personal and societal costs [1,2,3]
In line with earlier intermediate phenotype findings, in the current conceptual replication we examined the hypothesized association of automatic approach-avoidance tendencies as a candidate intermediate phenotype for depression with the 5-HTTLPR polymorphism in interaction with childhood trauma
The groups did not differ on age, sex distribution, medication use, Beck Depression Inventory-II (BDI-II) total score, LSAS total score, age of depression onset, or number of past depressive episodes
Summary
Major depressive disorder is highly prevalent and is associated with high personal and societal costs [1,2,3]. The serotonin transporter gene (SLC6A4), and especially a polymorphism in the promoter region (5-HTTLPR), have been linked to depressive symptoms [5]. The 5-HTTLPR polymorphism has a ‘short’ (S) and a ‘long’ (L) form, referring to the number of base pairs in the region. The function of the L allele is influenced by a single-nucleoid polymorphism or SNP (rs25531), which consists of an A and a G allele (La and Lg). The ‘short’ (S) form as well as the Lg variant have been associated with depression risk, because they restrict the transcriptional activity of the promoter, resulting in low functional expression of SLC6A4, and reduced re-uptake of serotonin [6]
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