Introduction
The developmental origins of health and disease (DOHaD) hypothesis suggests that the prenatal environment plays a foundational role in shaping long-term health trajectories. While individual exposures such as maternal substance use or pregnancy complications have long been linked to neurodevelopmental risks, real-world scenarios rarely involve isolated stressors. Instead, adverse prenatal exposures (APEs) frequently co-occur, creating a cumulative burden that may fundamentally alter the brain’s structural maturation. A landmark study recently published in JAMA Psychiatry by Zhi et al. (2026) provides compelling evidence that this cumulative burden not only predicts persistent psychopathology into midadolescence but is also associated with distinct alterations in the pace of cortical thinning, a hallmark of adolescent brain development.
