Stress has long been considered an important factor influencing both the initiation of substance use and the risk of relapse, yet the exact pathways through which it acts remain incompletely defined. Contemporary addiction frameworks propose that stressful experiences can heighten susceptibility to drug use, particularly in individuals with pre-existing vulnerabilities. A substantial body of animal research demonstrates that exposure to stress increases drug-seeking behaviour and enhances the reinforcing effects of addictive substances. Although human studies provide indications that stress elevates craving and contributes to relapse, findings often rely on correlational designs and show considerable inconsistency. Parallel evidence from developmental research highlights another dimension of this relationship. Prenatal drug exposure and early-life stress appear to affect overlapping neural systems involved in emotional regulation, stress responses, and reward processing. Children exposed to substances in utero often exhibit developmental and neurobehavioral deficits, but the extent to which environmental stress contributes to these outcomes is still unclear. Controlled experiments in animal models show that both perinatal substance exposure and early stress can lead to long-lasting changes in brain structure and neurotransmitter function, potentially increasing later vulnerability to addictive behaviours. Overall, existing evidence suggests that stress plays a meaningful role in shaping both the emergence and persistence of drug use, while early developmental experiences may further modify this risk. However, key questions remain regarding how these mechanisms operate in humans. A deeper understanding of the interaction between stress, neural adaptation, and addictive behaviour is essential for improving prevention efforts and developing more targeted treatment strategies for substance use disorders.
Ak et al. (2026) studied this question.