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There is increasing evidence for the role of adverse childhood experiences in the occurence of mood disorders (MD). A great number of studies have shown that there is a correlation between MD and parental indifference, neglect and sexual and physical abuse. Angst et al., in a 20-year longitudinal study, suggested that childhood family issues have a robust correlation with the chronicity of bipolar and unipolar MD, and adverse childhood experiences give rise to low self-esteem and anxious personality. The presence of childhood trauma (CT) has found to be associated with increases in rates of substance abuse, early age of onset, rapid cycling, and suicide. There is severe CT in half (49%) of bipolar MD patients.
Individuals with CT have both an overall increased risk for depression and a substantially increased sensitivity to the depressogenic effects of stressful life events. The relation between CT and stressful life events is dose dependent and correlated with the intensity of the neuroticism. It has been shown that the severity of CT predicts an early age of onset and the number of life time depressive episodes, and that it is associated with more comorbidity. Increased rates of emotional CT, depressive symptoms and anxiety have been reported in treatment resistant group of patients.
Childhood adverse life events are associated with various neuroendocrine and neuroanotomical changes. There is a 6 times larger ACTH response to stress in depressive female patients who reported CT. These patients also have an increased cortisol response and heart rate response to psychosocial stress. Women, who have reported CT but were not depressed, have exhibited normal cortisol responses, despite having increased an ACTH response. This can be interpreted as resilience against depression, an adrenal adaptation to central sensitization. It has been reported that decreased hippocampal volume (18%) in depression is related to CT and that the hippocampal volumes of depresssive patiens who did not report CT were equal to those of the control group. Repeated bursts of CRF in response to stress during development and increased cortisol reactivity over the course of time may contribute to smaller hippocampi after childhood trauma exposure, leading to further sensitization of the stress responses. These results would suggest that there are biologically distinct subtypes of depression as a function of childhood trauma.
The effect of CT on predisposition to illness is associated with genotype. The s/s allele of the serotonin transporter gene, the gene polymorphism of BDNF and the CRF-1 gene have been shown to be related to vulnerability to trauma effects.
CT is associated to decreased response to pharmacological treatment. Among chronically depressed patients with no history of early trauma, combination treatment was most effective in attaining remission compared to pharmacotherapy and psychotherapy. In contrast, in chronically depressed patients with early-life trauma, remission rates were significantly higher for psychotherapy alone versus pharmacotherapy. Combination treatment did not have any further advantage over psychotherapy alone. Improved effects of cognitive and behavioral therapies, group therapies and EMDR have been reported in various studies. Questioning about CT in MD patients seems to be important for treatment planning, assessment of risks and prophylactic interventions.