Key points are not available for this paper at this time.
The impact of early life stress on neurobiological vulnerability to obsessive-compulsive disorder (OCD) is a major focus of psychiatric research. Individuals with OCD frequently report that psychosocial stress exacerbates their symptoms, with many attributing the onset of symptoms to stressful life events. However, the exact pathophysiological relationship between stress and OCD is not well understood. Stress has been shown in preclinical studies to have significant effects on cortico-striatal and limbic circuitry, including neuronal atrophy in the frontal cortices, dorsomedial striatum, and hippocampus, as well as neuronal hypertrophy in the dorsolateral striatum and amygdala. These neurobiological effects may contribute to an imbalance between goal-directed and habitual behaviour, which is associated with OCD symptoms. Furthermore, genetic and environmental factors, including early life stress, play an essential role in the advancement of OCD. Understanding gene-environment interactions and pathogenic mechanisms is critical to advancing precision medicine and improving treatment outcomes for OCD and related disorders. This review emphasises the need for additional research into how early life stress interacts with genetic factors to cause the behavioural, cellular, and molecular changes seen in OCD. Integrating global mental health and translational neuroscience approaches shows potential for enhancing our understanding and treatment of OCD and related disorders.
Debnath et al. (Mon,) studied this question.