Four Decades of Stress, Depression, and Close Relationships: Lessons from Psychoneuroimmunology

08/08/2026

AI Summary

Psychosocial adversity reliably alters immune and endocrine function, increasing infections, weakening vaccine responses, slowing wound healing, and heightening inflammation.
Depression sensitises immune function, producing larger inflammatory responses to stressors and accelerating cellular ageing, increasing inflammation related disease risk.
Loneliness, low support and relationship distress amplify stress reactivity, alter gut microbiome and intestinal permeability, but behavioural and nutritional interventions can modify trajectories.

TL;DR (AI Generated)

Human psychoneuroimmunology research has demonstrated that stress, depression, and close relationships reliably shape immune and endocrine function in ways that matter for health.

Across studies of examination stress, laboratory stressors, marital discord, cancer survivorship, and dementia caregiving, psychosocial adversity predicts more infections, weaker vaccine responses and faster erosion of vaccine protection, slower wound healing, heightened inflammation, and accelerated cellular aging.

Loneliness, low support, and distressed relationships can amplify stress reactivity and are linked to greater inflammatory and metabolic vulnerability, including postprandial inflammatory and endothelial responses.

Basic summary

Annu Rev Psychol. 2026 Aug 7. doi: 10.1146/annurev-psych-020226-033326. Online ahead of print.

ABSTRACT

Human psychoneuroimmunology research has demonstrated that stress, depression, and close relationships reliably shape immune and endocrine function in ways that matter for health. Across studies of examination stress, laboratory stressors, marital discord, cancer survivorship, and dementia caregiving, psychosocial adversity predicts more infections, weaker vaccine responses and faster erosion of vaccine protection, slower wound healing, heightened inflammation, and accelerated cellular aging. Depression also sensitizes immune function, producing larger inflammatory responses when individuals encounter stressors. Loneliness, low support, and distressed relationships can amplify stress reactivity and are linked to greater inflammatory and metabolic vulnerability, including postprandial inflammatory and endothelial responses. More recent work has extended these pathways to the gut microbiome and intestinal permeability (leaky gut), integrating microbial, neuroendocrine, and immune mechanisms. Collectively, the evidence supports a biobehavioral model in which social stress accelerates immune aging and increases risk for inflammation-related disease, while behavioral and nutritional interventions can modify these trajectories.

PMID:42566682 | DOI:10.1146/annurev-psych-020226-033326

Document this CPD