Interaction between FKBP5 gene and childhood trauma on psychosis, depression and anxiety symptoms in a non-clinical sample. (November 2017)

• Record Type: Journal Article
• Authors: de Castro-Catala, Marta; Peña, Elionora; Kwapil, Thomas R.; Papiol, Sergi; Sheinbaum, Tamara; Cristóbal-Narváez, Paula; Ballespí, Sergi; Barrantes-Vidal, Neus; Rosa, Araceli
• Is Part Of: Psychoneuroendocrinology. Volume 85(2017)
• Page Start: 200
• Page End: 209
• Publication Date: 2017-11
• Subjects: Schizotypy -- Psychotic-like experiences -- Depression -- Anxiety -- Childhood trauma -- FKBP5 gene -- Gene-environment interaction; Psychoneuroendocrinology -- Periodicals; Endocrinology -- Periodicals; Neurology -- Periodicals; Psychiatry -- Periodicals; Neuropsychoendocrinologie -- Périodiques; 616.8
• DOI: 10.1016/j.psyneuen.2017.08.024
• Languages: English
• ISSNs: 0306-4530

Abstract

Highlights: Association between childhood trauma subscales and subclinical psychosis, depressive and anxiety symptoms. FKBP5 genetic variability in 3′ moderates the association between physical abuse and anxiety (GxE). FKBP5 genetic variability in 5′ moderates the association between physical abuse and anxious-depressive symptoms (GxE). Physical abuse subscale is the most related to the anxious-depressive phenotype. Abstract: Background: Childhood trauma has been associated with a heightened risk for presenting clinical and non-clinical psychopathology in adulthood. Genes related with the stress response, such as the FK506 binding protein 51 ( FKBP5 ), are plausible candidates moderating the effects of childhood trauma on the emergence of such symptoms later on. The present study aimed to explore the moderating role of FKBP5 genetic variability on the association of different types of childhood trauma with subclinical psychosis, depression and anxiety in a non-clinical sample. Methods: Schizotypy, psychotic-like experiences, depression and anxiety symptoms and childhood trauma were assessed in 808 young adults. Two FKBP5 haplotypic blocks were detected: block 1 (rs3800373 − rs9296158 − rs1360780) and block 2 (rs9470080 − rs4713916). Subjects were classified in two groups according to whether they carried or not the risk haplotype previously described in the literature (block 1: CAT and block 2: TA). Linear regression analyses were used to study (i) the main effects of childhood trauma and FKBP5 haplotype blocks and (ii) their interaction effects on the mentioned forms of psychopathology. Results: All childhood trauma scales, except sexual abuse, were associated with schizotypy, psychotic-like experiences, depression and anxiety symptoms. None of the analysed symptoms was associated with the main effects of FKBP5 genetic variability. However an interaction effect between block 1 and physical abuse was observed on anxiety, with lower scores in CAT carriers. This effect was driven by SNP 1 and 2. Moreover, an interaction effect between block 2 and physical abuse was identified on the variables tapping depressive and anxiety symptoms. Specifically, non-TA carrier subjects who were exposed to physical abuse were found to be at higher risk for depressive and anxiety symptoms. These effects were driven by SNP 5. No interaction effect was observed for the other variables. Conclusions: Our data suggest that exposure to childhood physical abuse may increase the risk for sub-clinical depressive and anxiety symptoms depending on FKBP5 genetic variability. Further research is needed to better elucidate the role of FKBP5 on mental health in clinical and non-clinical cohorts.