Stressful experiences can be both constructive and destructive to the body and brain. In the short term, acute stressful experiences mobilize adaptive changes in physiology and behavior that help to meet the demands of environmental challenges and protect against threats to internal homeostasis. Over the long term, however, chronic stressful experiences and the recurrent activation of the autonomic, neuroendocrine, and cardiovascular stress-response axes can lead to maladaptive changes in physiology and behavior that undermine health, cognition, mood, and longevity. Over the lifespan, chronic and recurrent stressful experiences can also impair the functional and structural integrity of multiple bodily and brain systems, which may play a role in the pathophysiology of stress-related psychiatric disorders and chronic medical conditions.
Research by Dr. Gianaros and his colleagues uses human functional and structural neuroimaging methods to understand how the brain links stressful experiences with risk for developing cardiovascular disease in particular. To date, this research has shown that a network of corticolimbic brain areas, including areas in the medial prefrontal cortex, amygdala, and insula, are involved in mediating autonomic-cardiovascular stress reactions that are associated with cardiovascular disease risk. From a translational neuroscience perspective, these findings extend lesion, early gene expression, and electrical and chemical stimulation studies in animal models that also demonstrate an important role for the same corticolimbic areas in autonomic-cardiovascular stress reactivity. More recent structural neuroimaging work has shown that chronic stress and hypertension are associated with changes in corticolimbic morphology, which may be involved in adverse changes in mood, cognitive function, and regulatory control over autonomic-cardiovascular physiology. Building on this work, we are now directly examining the relationships between indicators of stress-related brain activity and morphology with biomediators and endpoints of cardiovascular disease risk.
Gianaros, P.J., Hariri, A.R., Sheu, L.K., Sutton-Tyrrell, K., Muldoon, M.F. and Manuck, S.B. Preclinical atherosclerosis covaries with individual differences in reactivity and functional connectivity of the amygdala. Biol Psychiatry, 65, 943-950, 2009.
Gianaros, P.J., Sheu, L.K., Remo, A.M., Christie, I.C., Crtichley, H.D. and Wang, J.J. Heightened resting neural activity predicts exaggerated stressor-evoked blood pressure reactivity. Hypertension, 53, 819-825, 2009.
Gianaros, P.J. and Sheu, L.K. A review of neuroimaging studies of stressor-evoked blood pressure reactivity: Emerging evidence for a brain-body pathway to coronary heart disease risk. NeuroImage, 47, 922-936, 2009.
Gianaros, P.J., Horenstein, J.A., Hariri, A.R., Sheu, L.K., Manuck, S.B., Matthews, K.A. and Cohen, S. Potential neural embedding of parental social standing. Soc Cog Affect Neurosci, 3, 91-96, 2008.
Gianaros, P.J., Matthews, K.A., Jennings, J.R., Sheu, L.K., Manuck, S.B. and Hariri, A.R. Individual differences in stressor-evoked blood pressure reactivity vary activation, volume, and functional connectivity of the amygdala. J Neurosci, 28, 990-999, 2008.