Summary: A new global study challenges the long-held belief that chronic inflammation is a universal marker of aging. Researchers compared industrialized populations with Indigenous groups and found that “inflammaging” is strongly tied to lifestyle and environmental exposures.
While inflammation rises with age in industrialized societies, it remains stable and infection-driven in non-industrialized populations, and crucially, does not lead to chronic disease. These findings suggest that aging biomarkers like inflammation may not be biologically universal but rather shaped by specific cultural and ecological contexts.
Key Facts:
- Context-Specific Inflammation: Inflammation increased with age in industrialized settings but not in Indigenous populations.
- Infection vs. Aging: Elevated inflammation in non-industrialized groups was driven by infection, not age-related degeneration.
- No Universal Markers: The study calls into question the use of global aging biomarkers, urging context-aware tools instead.
Source: Columbia University
Inflammation, long considered a hallmark of aging, may not be a universal human experience, according to a new study from Columbia University Mailman School of Public Health.
The research suggests that “inflammaging”—chronic, low-grade inflammation associated with aging—appears to be a byproduct of industrialized lifestyles and varies significantly across global populations.

The findings are published in Nature Aging.
Researchers analyzed data from four populations: two industrialized groups—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 the inflammaging signature was similar between the two industrialized populations, it did not hold in the Indigenous groups, where inflammation levels were largely driven by infection rather than age.
“In industrialized settings, we see clear links between inflammaging and diseases like chronic kidney disease,” said lead author Alan Cohen, PhD, associate professor of Environmental Health Sciences at Columbia Mailman School and faculty member of the Butler Columbia Aging Center.
“But in populations with high infection rates, inflammation appears more reflective of infectious disease burden than of aging itself.”
Interestingly, while the indigenous populations, particularly the Tsimane, had high constitutive levels of inflammation, these did not increase with age and, crucially, did not lead to the chronic diseases that plague industrialized societies.
In fact, most chronic diseases – diabetes, heart disease, Alzheimer’s, etc. – are rare or largely absent in the Indigenous populations, meaning that even when young Indigenous people have profiles that look similar on the surface to those of older industrialized adults, these profiles do not lead to pathological consequences.
“These findings really call into question the idea that inflammation is bad per se,” said Cohen.
“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.”
The study used a panel of 19 cytokines—small immune-signaling proteins—to assess inflammation patterns. While these markers aligned with aging in the Italian and Singaporean datasets, they did not replicate among the Tsimane and Orang Asli, whose immune systems were shaped by persistent infections and distinct environmental exposures.
Key findings include:
- Approximately 66 percent of Tsimane had at least one intestinal parasitic infection; over 70 percent of Orang Asli had a prevalent infection.
- Inflammaging markers were strongly linked to chronic disease in industrialized populations, but not in Indigenous groups.
- The study challenges the assumption of universal aging biomarkers, suggesting instead that immune-aging processes are population-specific and heavily influenced by the exposome—the totality of environmental, lifestyle, and infectious exposures.
“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 call for a reevaluation of how aging and inflammation are measured across populations and emphasize the need for standardized, context-aware tools. “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,” said Cohen. “Understanding how these elements interact could help develop more effective global health strategies.”
Co-authors are listed in the manuscript.
Funding: The study was supported by the Impetus program, the French National Research Agency (ANR) under the Investments for the Future (Investissements d’Avenir) program, grant ANR-17-EURE-0010; the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under project ID 499552394 (SFB 1597/1) and grant HE9198/1-1, and the Intramural Research Program of the NIH, National Institute on Aging.
About this aging and inflammation research news
Author: Stephanie Berger
Source: Columbia University
Contact: Stephanie Berger – Columbia University
Image: The image is credited to Neuroscience News
Original Research: Closed access.
“Nonuniversality of inflammaging across human populations” by Alan Cohen et al. Nature Aging
Abstract
Nonuniversality of inflammaging across human populations
Inflammaging, an age-associated increase in chronic inflammation, is considered a hallmark of aging. However, there is no consensus approach to measuring inflammaging based on circulating cytokines.
Here we assessed whether an inflammaging axis detected in the Italian InCHIANTI dataset comprising 19 cytokines could be generalized to a different industrialized population (Singapore Longitudinal Aging Study) or to two indigenous, nonindustrialized populations: the Tsimane from the Bolivian Amazon and the Orang Asli from Peninsular Malaysia.
We assessed cytokine axis structure similarity and whether the inflammaging axis replicating the InCHIANTI result increased with age or was associated with health outcomes.
The Singapore Longitudinal Aging Study was similar to InCHIANTI except for IL-6 and IL-1RA. The Tsimane and Orang Asli showed markedly different axis structures with little to no association with age and no association with age-related diseases.
Inflammaging, as measured in this manner in these cohorts, thus appears to be largely a byproduct of industrialized lifestyles, with major variation across environments and populations.