# Minimal Evidence of Inflammaging in Naturalistic Chimpanzee Populations

## TL;DR

Chimpanzees in naturalistic settings show little evidence of chronic inflammation with age, suggesting that inflammaging may be influenced by lifestyle and environment.

## Contribution

The study provides novel comparative data on inflammation in chimpanzees living in semi-wild conditions versus captivity.

## Key findings

- Serum inflammatory biomarkers in sanctuary chimpanzees were 2–10 times lower than in laboratory chimpanzees.
- Chronic systemic inflammation and DNA damage did not differ between sanctuary and wild chimpanzees.
- A modest age-related increase in suPAR was observed in wild chimpanzees.

## Abstract

Whereas chronic inflammation is a hallmark of aging in many human populations, inflammaging is reduced in groups characterized by frequent physical activity and diets low in processed foods. Since most biomarkers of inflammation require blood sampling, comparative data from our closest primate relatives have been derived from sedentary, captive primate populations whose processed diets are uncharacteristic of the wild.

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.

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.

These results parallel recent findings from humans in demonstrating that chronic inflammation is not a natural consequence of aging but may rather be driven by environmental contexts that are mismatched to the evolutionary history of a given species.