Stress-induced cortisol response is associated with right amygdala volume in early childhood.

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Rodent research suggests that dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and the resulting cortisol stress response can alter the structure of the hippocampus and amygdala. Because early-life changes in brain structure can produce later functional impairment and potentially increase risk for psychiatric disorder, it is critical to understand the relationship between the cortisol stress response and brain structure in early childhood. However, no study to date has characterized the concurrent association between cortisol stress response and hippocampal and amygdala volume in young children. In the present study, 42 young children (M age  = 5.97, SD = 0.76), completed a frustration task and cortisol response to stress was measured. Children also underwent magnetic resonance imaging (MRI), providing structural scans from which their hippocampal and amygdala volumes were extracted. Greater cortisol stress response was associated with reduced right amygdala volume, controlling for whole brain volume, age, sex, and number of cortisol samples. There were no significant associations between cortisol stress response and bilateral hippocampus or left amygdala volumes. The association between right amygdala volume and cortisol stress response raises the non-mutually exclusive possibilities that the function of the HPA axis may shape amygdala structure and/or that amygdala structure may shape HPA axis function. As both cortisol stress response and amygdala volume have been associated with risk for psychopathology, it is possible that the relationship between cortisol stress response and amygdala volume is part of a broader pathway contributing to psychiatric risk.





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Fowler, Carina H, Ryan Bogdan and Michael S Gaffrey (2021). Stress-induced cortisol response is associated with right amygdala volume in early childhood. Neurobiology of stress, 14. p. 100329. 10.1016/j.ynstr.2021.100329 Retrieved from

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Carina Fowler


I am a Ph.D. student in the clinical psychology program. My research takes a broad view of life stress and examines how different stressors alter trajectories of child development. I am particularly interested in the role environmental health plays in shaping emotional and neurobiological development.


Michael Santo Gaffrey

Assistant Research Professor of Psychology and Neuroscience

Michael S. Gaffrey, Ph.D. is an Assistant Professor at Duke University in the Department of Psychology & Neuroscience. He is also Director of Duke’s Early Experience and the Developing Brain (DEED) lab. He received his PhD in Clinical Psychology from the University of Wisconsin, Milwaukee and completed a postdoctoral fellowship in developmental clinical and affective neuroscience at the Washington University School of Medicine. Dr. Gaffrey has also completed advanced training in infant mental health practice and policy through the ZERO-TO-THREE Leadership Development Institute.

Dr. Gaffrey is firmly committed to studying, treating, and advocating for the health and well-being of vulnerable infants and young children. To this end, his research endeavors include the use of behavioral and neuroimaging methodologies to better understand biological pathways underlying risk and resilience to early life stress and related environmental challenges. He is also actively involved in using the tools of developmental neuroscience to better understand how preventive intervention programs targeting infants at risk for negative socioemotional outcomes, including depression and autism spectrum disorder, can be used more effectively. Through the integration of clinical practice and innovative research, Dr. Gaffrey hopes to reduce the impact of risk factors that contribute to unfavorable health outcomes for vulnerable infants and families. Furthermore, Dr. Gaffrey believes we can better foster healthy environments for growing children and ensure the well-being of all infants and families by bringing objective research and practice-based knowledge to policy and public arenas.

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