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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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>\n                      We evaluated aging profiles of inflammation and oxidative stress biomarkers derived from urine and serum samples in semi\u2010free ranging chimpanzees (\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>Pan troglodytes<\/jats:italic>\n                      <\/jats:styled-content>\n                      ) living in two African sanctuaries (\n                      <jats:italic>N<\/jats:italic>\n                      \u2009=\u2009156 health checks, 73 individuals, ages 11\u201339\u2009years), 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                      <jats:italic>N<\/jats:italic>\n                      \u2009=\u20091849 time points, 50 individuals, ages 10\u201357\u2009years), as well as published serum data from biomedical laboratories.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Serum inflammatory biomarker (\n                      <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n                      and\n                      <jats:styled-content style=\"fixed-case\">IL6<\/jats:styled-content>\n                      ) levels in sanctuary chimpanzees were 2\u201310 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 (\n                      <jats:styled-content style=\"fixed-case\">suPAR<\/jats:styled-content>\n                      ) and\n                      <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>\n                      damage (\n                      <jats:styled-content style=\"fixed-case\">OHdG<\/jats:styled-content>\n                      ) did not differ. We detected a significant but modest age\u2010related increase in one biomarker (\n                      <jats:styled-content style=\"fixed-case\">suPAR<\/jats:styled-content>\n                      ) in the wild sample.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ajpa.70211","type":"journal-article","created":{"date-parts":[[2026,2,9]],"date-time":"2026-02-09T09:01:40Z","timestamp":1770627700000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Minimal Evidence of Inflammaging 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