Birth Cohort Studies

by

Christy G. Woolcott, Linda Dodds

• LAST REVIEWED: 13 January 2014
• LAST MODIFIED: 13 January 2014
• DOI: 10.1093/obo/9780199756797-0075

Introduction

Birth cohorts have been established and studied for over half of a century, but the past two decades have seen a surge in the number of birth cohorts established and in the accompanying research. In part, this proliferation has been fueled by the recognition of the importance of the in utero environment on later life health outcomes. The potential of birth cohort studies with follow-up across the life span to help in the understanding of the etiology of numerous health conditions is enormous. Although there is a distinction between pregnancy cohorts, where information collection begins in pregnancy, and birth cohorts, where information begins to be collected at birth, the term birth cohort has been used to refer to both study designs. An inherent assumption in birth cohort research is the longitudinal follow-up of the cohort with follow-up that could continue indefinitely. The frequency and length of follow-up after birth varies, but, increasingly, the importance of continued follow-up well into adulthood is noted. The notion of life course studies has emerged from the recognition that early life events influence adult health and social development. Early sociological research by Glen Elder, who recognized the net effects of experiences and social context throughout the life course, has been followed by modern cohorts that take a very multidisciplinary approach to explore a range of exposure and outcome measures (e.g., biomedical factors, social and economic factors). Pregnancy has been the logical starting place for collecting data through the life course. Among the critical periods of development, fetal life is thought to be among the most important. Further, the emerging role of epigenetics and the potential for fetal exposures to have a life-long effect in offspring health is becoming an important area of study. Birth cohorts and life course designs offer opportunities but, at the same time, present challenges. This review highlights several longstanding and more recently developed birth cohorts, exposure-specific birth cohorts, and resources for finding information on existing birth cohorts. We do not restrict the outcomes to any life-stage, but childhood outcomes are more predominant because many cohorts are not yet mature enough to address longer-term outcomes. However, it should be noted that some very long-standing birth cohorts are now following offspring well into adulthood and the later years of life. For the purposes of this bibliography, birth cohorts covered in this review are primarily prospective cohorts of women recruited in pregnancy (or pre-conception) or soon after delivery. However, a few exceptions are found in the Historical Perspectives section. As much as possible, a variety of geographic areas around the world have been represented.

Theoretical Basis and Hypotheses

Developmental concepts and hypotheses provide the rationale for assembling birth cohort studies and guide their methodology. The brief commentary by Friedman 2010 gives an introduction to Wilson’s six principles of teratogenicity, which include the idea that susceptibility depends on exposure dose and timing and manifestations resulting from exposure may range from functional disorders to death. Barker, et al. 1993 develops the concept of fetal programming as an origin of adult disease, now known as the Barker hypothesis. Gluckman and Hanson 2006 is a valuable resource of the now voluminous literature about the developmental origins of health and disease concept that considers a broad range of exposures during early life and adult diseases. The proposed evolutionary and molecular mechanisms of teratogenicity and developmental programming provide the underlying causal framework of associations observed in birth cohort studies and suggest hypotheses that could be tested regarding mediating variables. For example, Waterland and Michels 2007 discusses epigenetics, heritable changes in gene expression potential that do not involve changes in DNA sequence that may be the main intermediate effect of early life exposures that lead to adult disease. Bateson, et al. 2004 explains the phenomenon of developmental plasticity in which organisms express specific adaptive responses to their environments.

• Barker, D. J. P., P. D. Gluckman, K. M. Godfrey, J. E. Harding, J. A. Owens, and J. S. Robinson. 1993. Fetal nutrition and cardiovascular disease in adult life. The Lancet 341.8850: 1421–1422.

  DOI: 10.1016/0140-6736(93)91224-A

  Barker argues that fetal undernutrition is related to adult-onset cardiovascular disease and its risk factors. To support his argument, he brings forward evidence from animal studies and human cohorts, the latter using birth weight and other growth indicators as proxies of fetal nutrition. Available online for purchase or by subscription.

• Bateson, P., D. Barker, T. Clutton-Brock, et al. 2004. Developmental plasticity and human health. Nature 430:419–421.

  DOI: 10.1038/nature02725

  A protective “helmet” appears in offspring of the crustacean Daphnia if mothers have been exposed to chemical traces of a predator. The authors give such examples of developmental plasticity and discuss this phenomenon in humans as a predictive adaptive response to fetal nutrition cues and its cost when the prediction is incorrect. Available online for purchase or by subscription.

• Friedman, J. M. 2010. The principles of teratology: Are they still true? Special Issue: 50th Anniversary of the Teratology Society. Edited by S. A. Rasmussen, C. Chambers, B. F. Hales. Birth Defects Research Part A, Clinical and Molecular Teratology 88.10: 766–768.

  DOI: 10.1002/bdra.20697

  This paper presents a very short review of basic principles of teratogenicity put forward by Wilson in 1977. It comments that the principles still hold but much progress has been made since about the specific mechanisms that underlie them. Available online for purchase or by subscription.

• Gluckman, P. D., and M. A. Hanson. 2006. Developmental origins of health and disease. Cambridge, UK: Cambridge Univ. Press.

  DOI: 10.1017/CBO9780511544699

  This extensive text with thirty-seven chapters covers the basis of the developmental origins of health and disease hypothesis, a broad range of exposures that could affect development (e.g., nutrition, environmental chemicals, hypoxia), and a wide range of plausible human health effects (e.g., obesity, asthma, behavior).

• Waterland, R., and K. B. Michels. 2007. Epigenetic epidemiology of the developmental origins hypothesis. Annual Review of Nutrition 27:363–388.

  DOI: 10.1146/annurev.nutr.27.061406.093705

  This article presents an understandable but not overly simplified overview of epigenetic mechanisms such as DNA methylation and histone modification. It also reviews the epidemiologic evidence for associations between epigenetic variation and many adult diseases. Available online for purchase or by subscription.