<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Duchowny KA</submitter><funding>NCATS NIH HHS</funding><funding>NIA NIH HHS</funding><pagination>eadj6411</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10917337</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(10)</volume><pubmed_abstract>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 "get under the skin" to influence physical well-being. Using data from the Study of Muscle, Mobility, and Aging (&lt;i>n&lt;/i> = 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&lt;sub>max&lt;/sub>) 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 -0.08 SD (95% confidence interval = -0.13, -0.02) lower ATP&lt;sub>max&lt;/sub>. 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.</pubmed_abstract><journal>Science advances</journal><pubmed_title>Childhood adverse life events and skeletal muscle mitochondrial function.</pubmed_title><pmcid>PMC10917337</pmcid><funding_grant_id>P30 AG021332</funding_grant_id><funding_grant_id>R01 AG059416</funding_grant_id><funding_grant_id>R00 AG066846</funding_grant_id><funding_grant_id>UL1 TR001420</funding_grant_id><funding_grant_id>R56 AG059416</funding_grant_id><funding_grant_id>P30 AG024827</funding_grant_id><pubmed_authors>Molina AJA</pubmed_authors><pubmed_authors>Hepple RT</pubmed_authors><pubmed_authors>Kramer PA</pubmed_authors><pubmed_authors>Kritchevsky SB</pubmed_authors><pubmed_authors>Coen PM</pubmed_authors><pubmed_authors>Duchowny KA</pubmed_authors><pubmed_authors>Cummings SR</pubmed_authors><pubmed_authors>Diaz-Ramierz LG</pubmed_authors><pubmed_authors>Toledo FGS</pubmed_authors><pubmed_authors>Newman AB</pubmed_authors><pubmed_authors>Marcinek DJ</pubmed_authors><pubmed_authors>Lui LY</pubmed_authors><pubmed_authors>Cawthon PM</pubmed_authors><pubmed_authors>Mau T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Childhood adverse life events and skeletal muscle mitochondrial function.</name><description>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 "get under the skin" to influence physical well-being. Using data from the Study of Muscle, Mobility, and Aging (&lt;i>n&lt;/i> = 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&lt;sub>max&lt;/sub>) 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 -0.08 SD (95% confidence interval = -0.13, -0.02) lower ATP&lt;sub>max&lt;/sub>. 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.</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Mar</publication><modification>2025-04-19T10:00:16.892Z</modification><creation>2025-04-19T10:00:16.892Z</creation></dates><accession>S-EPMC10917337</accession><cross_references><pubmed>38446898</pubmed><doi>10.1126/sciadv.adj6411</doi></cross_references></HashMap>