Summary: Adolescent anxiety is rising worldwide, and a new Perspective argues that its origins may begin much earlier than previously thought—even before birth. The authors emphasize how maternal stress, the quality of early caregiving, and environmental signals during prenatal and early postnatal life shape the brain circuits responsible for emotion regulation and executive function, setting trajectories that can increase risk for anxiety during adolescence.
Early-life cues can tune a child’s developing stress and emotional systems to expect a particular environment. That tuning may be adaptive when early expectations match later reality, preparing a child to respond to danger. However, when early predictions do not match the child’s later environment—especially amid rapid social and technological change—those adaptations can become maladaptive, manifesting as heightened anxiety during the teenage years.
Key points
- Prenatal and early influences: Maternal stress and the quality of caregiving help shape neural systems involved in emotional regulation and cognitive control.
- Predictive adaptive responses: Early environmental signals may prime children for expected threats; if those predicted threats do not occur, the resulting heightened sensitivity can lead to anxiety.
- Policy and prevention: Addressing adolescent anxiety effectively requires prevention strategies that begin in early life and coordinate health, education, and social services.
Source: AAAS
In a Perspective piece, Mark Hanson and Peter Gluckman examine how maternal stress, caregiving quality, and early environmental conditions influence the development of executive function and emotional regulation in children, and how these developmental pathways may contribute to anxiety disorders in young people.
Research shows a notable increase in anxiety disorders among adolescents aged 12 to 19, particularly in developed countries such as the United States. This rise cannot be fully explained by recent acute stressors like the COVID-19 pandemic, which suggests that longer-term developmental and societal changes are important contributors.
Hanson and Gluckman review evidence indicating that signals from the prenatal environment and the earliest caregiving experiences guide the maturation of brain systems that control stress responses, emotion regulation, and executive capacities. These systems are plastic during early life and responsive to biochemical and social cues, including maternal hormone signals and the emotional context provided by caregivers.
From an evolutionary perspective, anxiety has adaptive value because it enhances vigilance and the ability to detect threats. In many animals, maternal cues reflecting environmental stressors—such as crowding, predator presence, or resource scarcity—can alter offspring development to improve survival in expected future conditions. In humans, similar mechanisms may operate: early-life cues can set patterns of neural and behavioral responses intended to fit anticipated circumstances.
Mechanisms that mediate these effects include epigenetic modifications that change gene expression in neural pathways linked to stress regulation. These molecular changes can have lasting influences on how individuals respond to stress and regulate emotion. However, when the environment a child experiences later in life diverges from the conditions anticipated in early development, the same adaptations that were once advantageous can become maladaptive, increasing the likelihood of anxiety disorders or inappropriate socioemotional responses.
The authors highlight that the modern social and technological landscape is changing more rapidly than in previous generations. This rapid change can widen the gap between early developmental predictions and real-world conditions, potentially amplifying vulnerabilities programmed by prenatal and early-life experiences. As a result, mental health burdens among young people may grow unless preventative strategies are implemented.
Hanson and Gluckman argue for a lifecourse approach to mental health policy. Preventive measures should begin in early childhood—supporting expectant parents, strengthening caregiving environments, and integrating health, education, and social welfare policies to promote healthy brain development. Such coordinated, early interventions could reduce the number of young people who develop anxiety disorders and improve population mental health over time.
About this neuroscience and anxiety research news
Author: Science Press Package Team
Source: AAAS
Contact: Science Press Package Team – AAAS
Image: The image is credited to Neuroscience News
Original Research: Open access. “Growing anxious–Are preschoolers matched to their futures?” by Mark A. Hanson et al., published in Science.
Abstract
Growing anxious–Are preschoolers matched to their futures?
Anxiety can serve an adaptive evolutionary function by promoting vigilance toward potential threats. Across species, maternal and perinatal signals reflecting stressors such as population density, predators, and food availability can alter the development of offspring stress responses, producing predictive adaptive responses that may enhance fitness in expected environments.
At a mechanistic level, epigenetic changes in neural pathways are implicated in how environmental factors influence gene expression and developmental outcomes. When early-life predictions align with later reality, these adaptations may be beneficial. But if anticipated conditions do not materialize, an overexpression of anxiety or poorly matched socioemotional regulation can reduce an individual’s personal or social functioning, and contribute to anxiety disorders.
Understanding anxiety disorders through the lens of developmental mismatch suggests that prevention and early intervention—focused on the prenatal period, caregiving environments, and the early childhood years—could be crucial in reducing the rising burden of mental health problems among adolescents.