Biography
Annelise Madison is a PhD Candidate in Clinical Psychology (Health Track) at The Ohio State University. During the 2023 - 2024 academic year, she is a Clinical Psychology Intern at VA Boston Healthcare System. During her graduate career, she studied psychoneuroimmunology under the mentorship of Dr. Jan Kiecolt-Glaser at the Institute for Behavioral Medicine Research. She is interested in the physiological correlates of stress and depression, including inflammation, vaccine responses, acute stress reactivity, and the gut-brain axis. Most recently, she has focused on the social stress model, which spurs inquiry into:
The physiological and psychological impact of chronic, repetitive, or acute social stress, especially conflict or exclusion, in relation to close others vs. unfamiliar others
Pre-existing psychosocial factors that modulate the physiological or psychological impact of social stress
Individual differences that predict psychological sensitivity to chronic inflammation or acute inflammatory rises (provoked by various inflammatory stimuli, including social stressors)
Factors that facilitate habituation vs. sensitization to repeated social stressors
Psychoneuroimmunology-informed interventions that meaningfully reduce the physiological, immunological, and psychological impact of social stress
Dysfunctional gut-brain or brain-immune signaling that, especially in the context of chronic or repetitive social stress, may underlie medically unexplained symptoms (e.g., chronic pain, fatigue) or vulnerability to long-COVID
To address treatment resistance: (1) Reducing depressive/anxiety symptoms/perceived stress via evidence-based psychotherapeutic interventions (e.g., ACT) to facilitate better responses to immunomodulating treatments (e.g., for autoimmune disorders, cancer, and vaccines); (2) Identifying depressed patients who would best respond to proinflammatory cytokine antagonists, as opposed to standard-of-care depression treatment
Personalized, preventative medicine: Boosting stress resilience to help prevent autoimmune disease onset and inflammation-driven depressive symptoms, especially in those who are most at risk (e.g., those with genetic vulnerability, those who experience frequent social stress)