Greg Miller

Professor of Psychology


Psychologist Greg Miller's research focuses on how stress affects health. In recent years, he has become especially interested in stressors that occur during early life, and how they might get biologically embedded in people in a manner that reverberates across the lifespan. To study issues like this, his lab brings together theories and methods from across the behavioral and biomedical sciences. His long-term goal is to establish a behaviorally and biologically plausible understanding of the connections between stress and health. 

Miller has received a number of honors and awards for his research, including the Young Investigator Award from the Society for Behavioral Medicine, Herbert Weiner Early Career Award from the American Psychosomatic Society, and Distinguished Scientific Award for Early Career Contributions to Health Psychology from the American Psychological Association. His research has received funding from the National Institutes of Health, Brain and Behavior Research Foundation, and Canadian Institutes of Health Research.

Miller completed a clinical internship at the Western Psychiatric Institute and Clinic and a subsequent postdoctoral fellowship in health psychology at Carnegie Mellon University. Before joining Northwestern, he was a faculty member at Washington University in St. Louis from 2000 to 2003 and at the University of British Columbia from 2003 to 2012.

Current Research

Long-term Biological Consequences of Childhood Poverty. Socioeconomic status (SES) during early life is an important determinant of vulnerability to cardiovascular disease in adulthood. Because these effects are not simply a result of the more direct influences of social standing in adulthood, they raise challenging mechanistic questions about how early-life SES gets embedded in the long term. This project, which has finished data collection and is supported by a grant from the National Institute of Child Health and Human Development, explores an epigenetic programming hypothesis to explain this process. It posits that psychosocial experiences associated with low early-life SES are programmed in the genome via epigenetic mechanisms, or acquired changes in genomic activity that are not due to changes in the DNA sequence. In a study of 420 volunteers, Miller's team of researchers is testing the hypothesis that individuals who spent their early years in low-SES environments were exposed to greater family turmoil, developing vigilant, pessimistic outlooks on life. The researchers further expect that these experiences have become embedded in the immune system through epigenetic modifications. In turn, they are expressed as a pro-inflammatory phenotype from adolescence through adulthood. This phenotype will be characterized by activation of pro-inflammatory transcription control pathways and increased concentrations of the inflammatory biomarkers C-reactive protein and interleukin 6. This project will shed light on the biobehavioral mechanisms underlying SES disparities, with implications for preventative interventions.

Health Consequences of Caring for a Family Member with Cancer. Research indicates that caring for a family member with a chronic illness not only diminishes quality of life, but also contributes to the development and progression of certain medical illnesses. Little is known, however, about the mechanisms through which caregiving “gets inside the body” to influence disease—or the coping strategies and personal resources that enable some to thrive under these demanding conditions, while others struggle. Miller's recently completed project recruited family caregivers of brain cancer patients whose noncaring controls were matched on demographics. All subjects completed four assessments over one year, timed to occur after surgical recovery, at completion of radiotherapy, at completion of chemotherapy, and again two months later. Each sequence included detailed measures of coping, resources, and distress, as well as two days of ambulatory monitoring for output of the hypothalamic pituitary adrenal (HPA) and sympathetic adrenal medullary (SAM) axes. Blood was drawn to assess systemic inflammation and metabolic symptoms; it was also used for genome-wide expression microarrays on subjects’ monocytes. These arrays will provide an in vivo transcriptional fingerprint of caregiving, revealing how it modifies critical signaling pathways in cells of the immune system. Together, these data will help address two overarching questions: What are the mechanisms by which caregiving accentuates vulnerability to disease? What kinds of coping strategies and personal resources facilitate adjustment to caregiving?

Selected Publications

Journal Articles
Cohen, S., D. Janicki-Deverts, W. Doyle, G. Miller, et al. 2012. Chronic stress, glucocorticoid receptor resistance, inflammation, and disease riskProceedings of the National Academy of Sciences 109(16): 5995–99.

Chen, E., G. Miller, M. Kobor, and S. Cole. 2011. Maternal warmth buffers the effects of low early life socioeconomic status on pro-inflammatory signaling in adulthood. Molecular Psychiatry 16(7): 729–37.

Chen, E., and G. Miller. 2012. “Shift-and-persist” strategies: Why being low in socioeconomic status isn’t always bad for health. Perspectives on Psychological Science 7(2): 135–58.

Miller, G., E. Chen, and K. Parker. 2011. Psychological stress in childhood and susceptibility to the chronic diseases of aging: Moving towards a model of behavioral and biological mechanisms. Psychological Bulletin 137(6):959–97.

Miller, G., M. Lachman, E. Chen, T. Gruenewald, A. Karlamangla, and T. Seeman. 2011. Pathways to resilience: Maternal nurturance as a buffer against the effects of childhood poverty on metabolic syndrome at midlife. Psychological Science 22(12): 1591–99.

Miller, G., and E. Chen. 2010. Harsh family climate in early life presages the emergence of a proinflammatory phenotype in adolescencePsychological Science 21(6): 848–56.

Miller, G., E. Chen, and S. Cole. 2009. Health psychology: Developing biologically plausible models linking the social world and physical health. Annual Review of Psychology 60:501–24.

Miller, G., E. Chen, A. Fok, H. Walker, A. Lim, E. Nicholls, S. Cole, and M. Kobor. 2009. Low early-life social class leaves a biological residue manifested by decreased glucocorticoid and increased proinflammatory signaling. Proceedings of the National Academy of Sciences 106(34): 14716–21.

Miller, G., E. Chen, J. Sze, T. Marin, R. Doll, R. Ma, and S. Cole. 2008. A functional genomic fingerprint of chronic stress in humans: Blunted glucocorticoid and increased NF-kB signalingBiological Psychiatry 64(4): 266–72.

Cohen, S., D. Janicki-Deverts, and G. E. Miller. 2007. Psychological stress and diseaseJournal of the American Medical Association 298(14): 1685–87.

Miller, G. E., E. Chen, and E. Zhou. 2007. If it goes up, must it come down? Chronic stress and the hypothalamic-pituitary-adrenocortical axis in humansPsychological Bulletin 133(1): 25–45