Stephanie J. Wilson, Janice Kiecolt-Glaser, and William A. Woody
This is an advance summary of a forthcoming article in the Oxford Research Encyclopedia of Psychology. Please check back later for the full article.
Inflammation is central among the immune system’s responses to threat, and its markers provide invaluable tools for studying health and disease across the lifespan. Key to battling acute infection and a natural consequence of tissue damage, inflammation triggers a cascade to destroy pathogens and promote healing. Of particular research focus in the past 20 years, chronic, systemic inflammation—in the absence of specific infection or wounding—serves as a hallmark of most “diseases of aging,” including cardiovascular disease, atherosclerosis, Alzheimer’s disease, osteoporosis, and diabetes, among many others. This low-grade, persistent inflammation appears to damage tissue and contributes to dysfunction in the cardiovascular and endocrine systems, among others; the exact mechanisms remain lively topics of ongoing study.
Research in the past two decades has revealed that inflammation rises in response to psychosocial stress. Indeed, chronic stress boosts the likelihood of elevated inflammation, inflammatory diseases, and death. Stress can also speed age-related increases in inflammation, exacerbating an already dysregulated inflammatory response to threat. In one classic example, chronically stressed dementia family caregivers saw four-fold hikes in inflammation compared to non-caregiving controls.
Inflammation’s relevance spans the life course—from childhood to adulthood, to death. Both infection-related inflammation and stress in childhood presage elevated inflammation and poor health in adulthood. In turn, higher inflammation in adulthood foreshadows frailty and functional decline, among a host of chronic conditions, in older age. In conclusion, mounting evidence suggests that inflammation impacts health and disease across the lifespan and can capture how the effects of stress “get under the skin.”