{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T02:49:39Z","timestamp":1791946179320,"version":"4.3.4"},"reference-count":61,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"10","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Adv."],"published-print":{"date-parts":[[2024,3,8]]},"abstract":"<jats:p>\n            Social stress experienced in childhood is associated with adverse health later in life. Mitochondrial function has been implicated as a mechanism for how stressful life events \u201cget under the skin\u201d to influence physical well-being. Using data from the Study of Muscle, Mobility, and Aging (\n            <jats:italic>n<\/jats:italic>\n            = 879, 59% women), linear models examined whether adverse childhood events (i.e., physical abuse) were associated with two measures of skeletal muscle mitochondrial energetics in older adults: (i) maximal adenosine triphosphate production (ATP\n            <jats:sub>max<\/jats:sub>\n            ) and (ii) maximal state 3 respiration (Max OXPHOS). Forty-five percent of the sample reported experiencing one or more adverse childhood events. After adjustment, each additional event was associated with \u22120.08 SD (95% confidence interval = \u22120.13, \u22120.02) lower ATP\n            <jats:sub>max<\/jats:sub>\n            . No association was observed with Max OXPHOS. Adverse childhood events are associated with lower ATP production in later life. Findings indicate that mitochondrial function may be a mechanism for understanding how early social stress influences health in later life.\n          <\/jats:p>","DOI":"10.1126\/sciadv.adj6411","type":"journal-article","created":{"date-parts":[[2024,3,6]],"date-time":"2024-03-06T18:58:51Z","timestamp":1709751531000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":18,"title":["Childhood adverse life events and skeletal muscle mitochondrial function"],"prefix":"10.1126","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9771-8454","authenticated-orcid":true,"given":"Kate A.","family":"Duchowny","sequence":"first","affiliation":[{"name":"Institute for Social Research, University of Michigan, Ann Arbor, MI, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5187-2149","authenticated-orcid":true,"given":"David J.","family":"Marcinek","sequence":"additional","affiliation":[{"name":"Department of Radiology, University of Washington, Seattle, WA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4278-6438","authenticated-orcid":true,"given":"Theresa","family":"Mau","sequence":"additional","affiliation":[{"name":"California Pacific Medical Center Research Institute, San Francisco, CA, USA."},{"name":"Department of Epidemiology and Biostatistics, University of California, San Francisco, CA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1621-9309","authenticated-orcid":true,"given":"L. 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