Inflammation, traditionally seen as a hallmark of aging, may not be a universal human experience, according to new research from Columbia University’s Mailman School of Public Health. The study indicates that “inflammaging”—chronic, low-grade inflammation associated with aging—is likely a result of industrialized lifestyles and varies significantly across different global populations.
The researchers examined data from four distinct groups: two industrialized populations—the Italian InCHIANTI study and the Singapore Longitudinal Aging Study (SLAS)—and two Indigenous, non-industrialized populations—the Tsimane of the Bolivian Amazon and the Orang Asli of Peninsular Malaysia. While similar inflammaging patterns were observed in the industrialized groups, these patterns were absent in the Indigenous groups where inflammation levels were primarily driven by infection rather than age.
“In industrialized settings, we see clear links between inflammaging and diseases like chronic kidney disease,” said lead author PhD, associate professor at Columbia Mailman School. “But in populations with high infection rates, inflammation appears more reflective of infectious disease burden than of aging itself.”
The study found that while Indigenous populations like the Tsimane had high levels of inflammation, these did not increase with age or lead to chronic diseases common in industrialized societies. Chronic conditions such as diabetes and heart disease are rare or largely absent among these Indigenous groups.
“These findings really call into question the idea that inflammation is bad per se,” Cohen stated. “Rather, it appears that inflammation—and perhaps other aging mechanisms too—may be highly context dependent. On the one hand, that’s challenging because there won’t be universal answers to scientific questions. On the other, it’s promising because it means we can intervene and change things.”
Researchers used a panel of 19 cytokines—small immune-signaling proteins—to assess inflammation patterns. These markers aligned with aging in Italian and Singaporean datasets but did not replicate among the Tsimane and Orang Asli.
“These results point to an evolutionary mismatch between our immune systems and the environments we now live in,” Cohen explained. “Inflammaging may not be a direct product of aging but rather a response to industrialized conditions.”
The authors suggest reevaluating how aging and inflammation are measured across populations and emphasize creating standardized tools considering environmental context. “Factors like environment, lifestyle—such as high physical activity or a very low-fat diet—and infection may all influence how the immune system ages,” Cohen noted.
The study was supported by various institutions including the Impetus program, French National Research Agency (ANR), Deutsche Forschungsgemeinschaft (DFG), and NIH’s National Institute on Aging.
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