<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Belsky DW</submitter><funding>Economic and Social Research Council</funding><funding>NICHD NIH HHS</funding><funding>NIA NIH HHS</funding><funding>Jacobs Foundation</funding><funding>Medical Research Council</funding><funding>Ministry of Business, Innovation and Employment</funding><funding>National Institute on Aging</funding><pagination>644-651</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5506399</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(4)</volume><pubmed_abstract>Therapies to extend healthspan are poised to move from laboratory animal models to human clinical trials. Translation from mouse to human will entail challenges, among them the multifactorial heterogeneity of human aging. To inform clinical trials about this heterogeneity, we report how humans' pace of biological aging relates to personal-history characteristics. Because geroprotective therapies must be delivered by midlife to prevent age-related disease onset, we studied young-adult members of the Dunedin Study 1972-73 birth cohort (n = 954). Cohort members' Pace of Aging was measured as coordinated decline in the integrity of multiple organ systems, by quantifying rate of decline across repeated measurements of 18 biomarkers assayed when cohort members were ages 26, 32, and 38 years. The</pubmed_abstract><journal>Aging cell</journal><pubmed_title>Impact of early personal-history characteristics on the Pace of Aging: implications for clinical trials of therapies to slow aging and extend healthspan.</pubmed_title><pmcid>PMC5506399</pmcid><funding_grant_id>P30AG028716</funding_grant_id><funding_grant_id>P30 AG034424</funding_grant_id><funding_grant_id>R01AG032282</funding_grant_id><funding_grant_id>R01 AG032282</funding_grant_id><funding_grant_id>ES/M010309/1</funding_grant_id><funding_grant_id>1R01AG049789</funding_grant_id><funding_grant_id>MR/P005918/1</funding_grant_id><funding_grant_id>P30 AG028716</funding_grant_id><funding_grant_id>P2C HD065563</funding_grant_id><funding_grant_id>R01 AG048895</funding_grant_id><funding_grant_id>P30AG034424</funding_grant_id><funding_grant_id>R01 AG049789</funding_grant_id><funding_grant_id>R01AG048895</funding_grant_id><pubmed_authors>Cohen HJ</pubmed_authors><pubmed_authors>Moffitt TE</pubmed_authors><pubmed_authors>Kraus WE</pubmed_authors><pubmed_authors>Belsky DW</pubmed_authors><pubmed_authors>Caspi A</pubmed_authors><pubmed_authors>Ramrakha S</pubmed_authors><pubmed_authors>Poulton R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Impact of early personal-history characteristics on the Pace of Aging: implications for clinical trials of therapies to slow aging and extend healthspan.</name><description>Therapies to extend healthspan are poised to move from laboratory animal models to human clinical trials. Translation from mouse to human will entail challenges, among them the multifactorial heterogeneity of human aging. To inform clinical trials about this heterogeneity, we report how humans' pace of biological aging relates to personal-history characteristics. Because geroprotective therapies must be delivered by midlife to prevent age-related disease onset, we studied young-adult members of the Dunedin Study 1972-73 birth cohort (n = 954). Cohort members' Pace of Aging was measured as coordinated decline in the integrity of multiple organ systems, by quantifying rate of decline across repeated measurements of 18 biomarkers assayed when cohort members were ages 26, 32, and 38 years. The</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Aug</publication><modification>2025-04-18T14:56:31.946Z</modification><creation>2019-03-27T02:50:06Z</creation></dates><accession>S-EPMC5506399</accession><cross_references><pubmed>28401731</pubmed><doi>10.1111/acel.12591</doi></cross_references></HashMap>