Idan Shalev1, Avshalom Caspi2, Antony Ambler3, Daniel W Belsky4, Simon Chapple5, Harvey Jay Cohen6, Salomon Israel7, Richie Poulton5, Sandhya Ramrakha5, Christine D Rivera8, Karen Sugden9, Benjamin Williams9, Dieter Wolke10, Terrie E Moffitt2. 1. Department of Biobehavioral Health and The Network on Child Protection and Well-Being, Social Science Research Institute, The Pennsylvania State University, University Park, Pennsylvania; ius14@psu.edu. 2. Departments of Psychology & Neuroscience and Psychiatry and Behavioral Sciences, Institute for Genome Sciences and Policy, and Social, Genetic, and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, United Kingdom; 3. Social, Genetic, and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, United Kingdom; Dunedin Multidisciplinary Health and Development Research Unit, Department of Preventive and Social Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand; 4. Center for the Study of Aging and Human Development, Duke University Medical Center, Durham, North Carolina; Social Science Research Institute, Duke University, Durham, North Carolina; 5. Dunedin Multidisciplinary Health and Development Research Unit, Department of Preventive and Social Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand; 6. Center for the Study of Aging and Human Development, Duke University Medical Center, Durham, North Carolina; 7. Departments of Psychology & Neuroscience and. 8. Center for Developmental Science, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; and. 9. Institute for Genome Sciences and Policy, and. 10. Department of Psychology, Lifespan Health and Wellbeing Group and Division of Mental Health and Wellbeing, Warwick Medical School, The University of Warwick, Coventry, United Kingdom.
Abstract
BACKGROUND: Perinatal complications predict increased risk for morbidity and early mortality. Evidence of perinatal programming of adult mortality raises the question of what mechanisms embed this long-term effect. We tested a hypothesis related to the theory of developmental origins of health and disease: that perinatal complications assessed at birth predict indicators of accelerated aging by midlife. METHODS: Perinatal complications, including both maternal and neonatal complications, were assessed in the Dunedin Multidisciplinary Health and Development Study cohort (N = 1037), a 38-year, prospective longitudinal study of a representative birth cohort. Two aging indicators were assessed at age 38 years, objectively by leukocyte telomere length (TL) and subjectively by perceived facial age. RESULTS: Perinatal complications predicted both leukocyte TL (β = -0.101; 95% confidence interval, -0.169 to -0.033; P = .004) and perceived age (β = 0.097; 95% confidence interval, 0.029 to 0.165; P = .005) by midlife. We repeated analyses with controls for measures of family history and social risk that could predispose to perinatal complications and accelerated aging, and for measures of poor health taken in between birth and the age-38 follow-up. These covariates attenuated, but did not fully explain the associations observed between perinatal complications and aging indicators. CONCLUSIONS: Our findings provide support for early-life developmental programming by linking newborns' perinatal complications to accelerated aging at midlife. We observed indications of accelerated aging "inside," as measured by leukocyte TL, an indicator of cellular aging, and "outside," as measured by perceived age, an indicator of declining tissue integrity. A better understanding of mechanisms underlying perinatal programming of adult aging is needed.
BACKGROUND: Perinatal complications predict increased risk for morbidity and early mortality. Evidence of perinatal programming of adult mortality raises the question of what mechanisms embed this long-term effect. We tested a hypothesis related to the theory of developmental origins of health and disease: that perinatal complications assessed at birth predict indicators of accelerated aging by midlife. METHODS: Perinatal complications, including both maternal and neonatal complications, were assessed in the Dunedin Multidisciplinary Health and Development Study cohort (N = 1037), a 38-year, prospective longitudinal study of a representative birth cohort. Two aging indicators were assessed at age 38 years, objectively by leukocyte telomere length (TL) and subjectively by perceived facial age. RESULTS: Perinatal complications predicted both leukocyte TL (β = -0.101; 95% confidence interval, -0.169 to -0.033; P = .004) and perceived age (β = 0.097; 95% confidence interval, 0.029 to 0.165; P = .005) by midlife. We repeated analyses with controls for measures of family history and social risk that could predispose to perinatal complications and accelerated aging, and for measures of poor health taken in between birth and the age-38 follow-up. These covariates attenuated, but did not fully explain the associations observed between perinatal complications and aging indicators. CONCLUSIONS: Our findings provide support for early-life developmental programming by linking newborns' perinatal complications to accelerated aging at midlife. We observed indications of accelerated aging "inside," as measured by leukocyte TL, an indicator of cellular aging, and "outside," as measured by perceived age, an indicator of declining tissue integrity. A better understanding of mechanisms underlying perinatal programming of adult aging is needed.
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