Minimal Evidence of Inflammaging in Naturalistic Chimpanzee Populations

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Chronic systemic inflammation, widely considered a fundamental hallmark of biological aging, may simply be an artifact of industrialized lifestyles. A comprehensive study examining the inflammatory and oxidative stress profiles of wild and semi-free-ranging chimpanzees (Pan troglodytes) across the lifespan indicates that inflammaging is not biologically inevitable in our closest evolutionary relatives.

The research establishes that chimpanzees living in naturalistic environments—foraging in large forested habitats and consuming diets devoid of highly processed laboratory chow—maintain remarkably low and stable inflammatory markers as they age. Investigators analyzed urinary and serum biomarkers, finding that C-reactive protein (CRP) and interleukin-6 (IL-6) in sanctuary apes remained far below human clinical thresholds for elevation, and did not significantly increase with age. Furthermore, comparisons with historical data showed sanctuary chimpanzees exhibit CRP and IL-6 levels 2 to 10 times lower than those of captive laboratory chimpanzees.

While minor age-related increases were detected in a single urinary marker for chronic immune activation (suPAR) within the wild cohort, the effect size was marginal. Markers of oxidative lipid damage (isoprostanes) and DNA damage (OHdG) showed no significant accumulation with age across the studied populations.

These findings present a compelling argument for the evolutionary mismatch hypothesis. The data strongly suggests that the age-related inflammatory cascade seen in modern human populations is not an endogenous, hard-wired aging mechanism. Instead, it is likely driven by environmental inputs—specifically, continuous positive energy balance, low physical activity, and processed diets—that are incongruent with primate evolutionary biology. For the longevity sector, this reinforces the primacy of modulating environmental and lifestyle inputs before relying on targeted immunomodulatory pharmacotherapy.

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I was going to ask how the study came to this conclusion when it didn’t compare chimpanzees on different diets, but then I realized that the summary of the paper didn’t think to mention that. Seems like an important point. From the paper itself:

We evaluated aging profiles of inflammation and oxidative stress biomarkers derived from urine and serum samples in semi-free ranging chimpanzees (Pan troglodytes) living in two African sanctuaries (N = 156 health checks, 73 individuals, ages 11–39 years), where diet and physical activity more closely approximates wild conditions than captive laboratory settings. We compared these to urinary markers from wild chimpanzees from Kanyawara, Kibale National Park, Uganda (N = 1849 time points, 50 individuals, ages 10–57 years), as well as published serum data from biomedical laboratories.

Results:

Serum inflammatory biomarker (CRP and IL6) levels in sanctuary chimpanzees were 2–10 times lower on average than those of laboratory chimpanzees. Compared to wild populations, acute immune activity (neopterin) and lipid peroxidation (isoprostanes) were higher in sanctuaries, while chronic systemic inflammation (suPAR) and DNA damage (OHdG) did not differ. We detected a significant but modest age-related increase in one biomarker (suPAR) in the wild sample

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