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Perinatal complications and aging indicators by midlife
Idan Shalev1, Avshalom Caspi2, Antony Ambler3
1Department 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.
Insights
Perinatal complications at birth predict accelerated aging by midlife, affecting both cellular aging (leukocyte telomere length) and perceived age. This supports the developmental origins of health and disease theory.
Area of Science:
- Developmental biology
- Gerontology
- Public Health
Background:
- Perinatal complications are linked to increased morbidity and mortality.
- The developmental origins of health and disease theory suggests early-life events impact adult health.
- Mechanisms linking perinatal complications to long-term health outcomes require investigation.
Purpose of the Study:
- To test the hypothesis that perinatal complications predict indicators of accelerated aging by midlife.
- To explore the long-term effects of early-life health events on aging.
Main Methods:
- Prospective longitudinal study of 1037 individuals from birth to age 38 (Dunedin Multidisciplinary Health and Development Study).
- Assessment of perinatal complications (maternal and neonatal).
- Measurement of aging indicators at age 38: leukocyte telomere length (cellular aging) and perceived facial age (tissue integrity).
Main Results:
- Perinatal complications significantly predicted shorter leukocyte telomere length (cellular aging).
- Perinatal complications also predicted older perceived facial age (external aging).
- These associations persisted even after controlling for family history, social risk, and intermediate health measures.
Conclusions:
- Findings support the concept of early-life developmental programming impacting adult aging.
- Perinatal complications are associated with accelerated "internal" (cellular) and "external" (perceived) aging.
- Further research is needed to elucidate the mechanisms of perinatal programming on adult aging.
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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