A study led by Columbia University’s Mailman School of Public Health suggests that the link between aging and chronic inflammation may not be as universal as once believed.
The phenomenon known as ‘inflammaging’ — a state of persistent, low-level inflammation commonly associated with ageing — appears to be closely tied to industrialised environments rather than an inevitable part of human biology.
The study, published in Nature Aging, examined data from four distinct populations: two from industrialised settings — participants in Italy’s InCHIANTI study and Singapore’s Longitudinal Aging Study (SLAS) — and two from non-industrialised Indigenous communities — the Tsimane people of Bolivia’s Amazon region and the Orang Asli of Peninsular Malaysia.
The researchers found that while older adults in industrialised societies exhibited clear signs of inflammaging, this pattern was not observed in the Indigenous populations.
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In these communities, inflammation was more commonly linked to infection rather than advancing age.
These findings point to the significant influence of modern lifestyles on biological aging and challenge the idea that age-related inflammation is a universal human experience.
First author Professor Alan Cohen said: “In industrialised settings, we see clear links between inflammaging and diseases like chronic kidney disease. But in populations with high infection rates, inflammation appears more reflective of infectious disease burden than of aging itself.”
In a surprising contrast to industrialised populations, Indigenous groups — particularly the Tsimane people — experience consistently elevated levels of inflammation throughout life, but this does not worsen with age, nor does it result in the chronic illnesses so prevalent in modern societies.
Diseases such as type 2 diabetes, heart disease, and Alzheimer’s, which are common causes of disability and death in industrialised nations, remain rare or virtually absent in these communities.
Even when younger individuals in these populations display inflammatory markers similar to those of older adults in wealthier nations, these markers do not translate into the same disease risks or health complications.
Professor Coehn said: “These findings really call into question the idea that inflammation is bad per se.
“Rather, it appears that inflammation, and perhaps other aging mechanisms too, may be highly context dependent.”
He added: “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.”
To examine patterns of inflammation, researchers measured 19 different cytokines — proteins that play a key role in immune system signalling.
In the Italian and Singaporean participants, these immune markers showed clear associations with ageing.
However, this pattern did not appear in the Tsimane and Orang Asli populations, where immune responses were more heavily influenced by ongoing exposure to infections and unique environmental conditions.
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Professor Cohen explained: “These results point to an evolutionary mismatch between our immune systems and the environments we now live in.
“Inflammaging may not be a direct product of ageing, but rather a response to industrialised conditions.
“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.
“Understanding how these elements interact could help develop more effective global health strategies.”
