The abstract of a recent PNAS article by Thomas W. McDade (motivated readers can obtain the whole article from me):
Inflammation is one of the most important, and potent, physiological systems in the human body. It is widely assumed that levels of inflammation increase with age and that chronic inflammation contributes to cardiovascular diseases. This understanding of inflammation is based on studies of people living in affluent, industrialized settings with low burdens of infectious disease. A broader view, based on research conducted across a wider range of ecological settings globally, indicates that chronic inflammation is not necessarily a “normal” part of aging and that the association between inflammation and age-related diseases is not inevitable. It also suggests that environments early in development have lasting effects on the regulation of inflammation in adulthood, with implications for diseases of aging.Abstract
Chronic inflammation contributes to the onset and progression of cardiovascular disease and other degenerative diseases of aging. But does it have to? This article considers the associations among inflammation, aging, and health through the lens of human population biology and suggests that chronic inflammation is not a normal nor inevitable component of aging. It is commonly assumed that conclusions drawn from research in affluent, industrialized countries can be applied globally; that aging processes leading to morbidity and mortality begin in middle age; and that inflammation is pathological. These foundational assumptions have shifted focus away from inflammation as a beneficial response to infection or injury and toward an understanding of inflammation as chronic, dysregulated, and dangerous. Findings from community-based studies around the world—many conducted in areas with relatively high burdens of infectious disease—challenge these assumptions by documenting substantial variation in levels of inflammation and patterns of association with disease. They also indicate that nutritional, microbial, and psychosocial environments in infancy and childhood play important roles in shaping inflammatory phenotypes and their contributions to diseases of aging. A comparative, developmental, and ecological approach has the potential to generate novel insights into the regulation of inflammation and how it relates to human health over the life course.