Jonathan D Schaefer1, Avshalom Caspi2,3, Daniel W Belsky4,5, Honalee Harrington2, Renate Houts2, Salomon Israel2,6, Morgan E Levine7, Karen Sugden2,8, Benjamin Williams2,8, Richie Poulton9, Terrie E Moffitt3,10. 1. Department of Psychology and Neuroscience, Duke University, Durham, North Carolina. jds116@duke.edu. 2. Department of Psychology and Neuroscience, Duke University, Durham, North Carolina. 3. Social, Genetic, and Developmental Psychiatry Centre, Institute of Psychiatry, King's College, London, UK. 4. Social Science Research Institute, Duke University, Durham, North Carolina. 5. Department of Medicine, Duke University School of Medicine, Durham, North Carolina. 6. Department of Psychology, Hebrew University, Jerusalem, Israel. 7. Department of Human Genetics, University of California, Los Angeles, California. 8. Center for Genomic and Computational Biology, Duke University, Durham, North Carolina. 9. Dunedin Multidisciplinary Health and Development Research Unit, Department of Psychology, University of Otago, Dunedin, New Zealand. 10. Department of Psychiatry and Behavioral Sciences, Duke University, Durham, North Carolina.
Abstract
OBJECTIVES: Early-life intelligence has been shown to predict multiple causes of death in populations around the world. This finding suggests that intelligence might influence mortality through its effects on a general process of physiological deterioration (i.e., individual variation in "biological age"). We examined whether intelligence could predict measures of aging at midlife before the onset of most age-related disease. METHODS: We tested whether intelligence assessed in early childhood, middle childhood, and midlife predicted midlife biological age in members of the Dunedin Study, a population-representative birth cohort. RESULTS: Lower intelligence predicted more advanced biological age at midlife as captured by perceived facial age, a 10-biomarker algorithm based on data from the National Health and Nutrition Examination Survey (NHANES), and Framingham heart age (r = 0.1-0.2). Correlations between intelligence and telomere length were less consistent. The associations between intelligence and biological age were not explained by differences in childhood health or parental socioeconomic status, and intelligence remained a significant predictor of biological age even when intelligence was assessed before Study members began their formal schooling. DISCUSSION: These results suggest that accelerated aging may serve as one of the factors linking low early-life intelligence to increased rates of morbidity and mortality.
OBJECTIVES: Early-life intelligence has been shown to predict multiple causes of death in populations around the world. This finding suggests that intelligence might influence mortality through its effects on a general process of physiological deterioration (i.e., individual variation in "biological age"). We examined whether intelligence could predict measures of aging at midlife before the onset of most age-related disease. METHODS: We tested whether intelligence assessed in early childhood, middle childhood, and midlife predicted midlife biological age in members of the Dunedin Study, a population-representative birth cohort. RESULTS: Lower intelligence predicted more advanced biological age at midlife as captured by perceived facial age, a 10-biomarker algorithm based on data from the National Health and Nutrition Examination Survey (NHANES), and Framingham heart age (r = 0.1-0.2). Correlations between intelligence and telomere length were less consistent. The associations between intelligence and biological age were not explained by differences in childhood health or parental socioeconomic status, and intelligence remained a significant predictor of biological age even when intelligence was assessed before Study members began their formal schooling. DISCUSSION: These results suggest that accelerated aging may serve as one of the factors linking low early-life intelligence to increased rates of morbidity and mortality.
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