Institute for Genome science and Policy and
PubMed | University of Otago, Institute for Genome science and Policy and, Pennsylvania State University, Duke University and 3 more.
Type: Journal Article | Journal: Pediatrics | Year: 2014
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.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.Perinatal complications predicted both leukocyte TL ( = -0.101; 95% confidence interval, -0.169 to -0.033; P = .004) and perceived age ( = 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.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.