Resilience to childhood adversity

Abstract

Despite being linked to several negative long-term physical and psychological pathologies in adulthood, childhood adversity elicits variable responses in the sufferer. When searching for explanations for this heterogeneity, the concept of resilience has been postulated as a potential mitigating factor. Gene-environmental interactions are a promising avenue in the study of resilience. The premise of gene-environmental research is that interindividual variability in the response to an environmental stressor is due to an individual’s genetic make-up exacerbating or buffering the impact of that stressor. Herein, gene-environmental findings are illustrated in the context of depression and post-traumatic stress disorder (PTSD). Many of the gene loci found to interact with childhood adversity influence both depression and PTSD possibly due to the high degree of shared heritability between these psychopathologies. Variation in the serotonin transporter gene, SLC6A4, and in FKBP5, a gene coding for a glucocorticoid receptor binding protein, interacts with childhood adversity to influence the development and symptomology of depression and of PTSD. Findings in the field of gene-environmental interactions has led to a proposed 3-hit model whereby 3 hits, genetics, early life experiences and later life stressors, interact to determine whether an individual is vulnerable or resilient to the development of psychopathology. As limitations with the current research are addressed and complementary lines of research are integrated, the insight gained on childhood adversity has the potential to better predict children at risk of the long-term sequelae of adversity and to inform potential intervention and prevention strategies.