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We evaluated whether the difference between attained and genotype-predicted adult height (\u201cheight-GaP\u201d) would associate with prospectively ascertained early-life growth adversity and later-life all-cause and cardiovascular mortality.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Data were first analyzed from the Avon Longitudinal Study of Parents and Children (ALSPAC;\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u20094582; 56\/43% female\/male) and UKBiobank (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u2009483,385; 54\/46% female\/male). Genotype-predicted height was calculated using a multi-ancestry polygenic height score. Height-GaP was calculated as the difference between measured and genotype-predicted adult height. Early-life growth conditions were ascertained prospectively via standardized procedures (ALSPAC) and mortality via death register (UKBiobank). Regression models examined: (i) adult height-GaP as the outcome with early-life growth conditions as predictors; and (ii) mortality as the outcome with adult height-GaP as predictor. All models were adjusted for age, sex, genotype-predicted height and genetic ancestry. Analyses were replicated in the Dunedin Multidisciplinary Health and Development Study (DMHDS;\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u2009855; 49\/51% female\/male) and the Multi-Ethnic Study of Atherosclerosis (MESA;\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u20096352; 52\/48% female\/male).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Here we show that among ALSPAC participants (median [IQR] age: 24 [18-25] years at height-GaP assessment), lower gestational age at birth, greater pre- and post-natal deprivation indices, tobacco smoke exposure and less breastfeeding are associated with larger adult height-GaP deficit (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.01). Among UKBiobank participants (mean\u2009\u00b1\u2009SD age: 56\u2009\u00b1\u20098 years at height-GaP assessment), height-GaP deficit is associated with death from all-causes (adjusted hazard ratio comparing highest-to-lowest height-GaP deficit quartile [aHR]: 1.25 95%CI: 1.21\u20131.29), atherosclerotic cardiovascular disease (aHR: 1.32 95%CI: 1.23\u20131.42) and coronary heart disease (aHR: 1.64 95%CI: 1.49-1.81). Early- and later-life height-GaP associations replicate in DMHDS and MESA.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This study introduces a precision index of early-life growth adversity deployable in adulthood to investigate the developmental origins of longevity and improve health equity across the life course.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1038\/s43856-025-01245-3","type":"journal-article","created":{"date-parts":[[2025,11,18]],"date-time":"2025-11-18T08:15:02Z","timestamp":1763453702000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Quantifying the impact of early life growth adversity on later life 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