Life Course Approach

Historical Background

The idea of childhood origins of risk for adult diseases was present in epidemiology and public health thinking during the first half of the 20th century. This paralleled the development of a life course approach in disciplines, such as developmental psychology, demography, sociology, anthropology, human development, and the biological sciences. After World War II, however, the adult risk factor model of disease, with its focus on clinical and biochemical markers in adults, became the dominant model within chronic disease epidemiology. The identification of the major adult lifestyle risk factors for coronary heart disease (CHD) solidified the success of this approach.

Nonetheless, since the late 1970s and 1980s, a growing body of evidence has documented the potential effects of poor growth, undernutrition, and infectious disease in early life and on the risk of adult cardiovascular and respiratory disease. The most influential of the research from this period originated from David Barker and colleagues in the United Kingdom, who used historical cohort studies to investigate the long-term effects of in utero biological programming associated with maternal and fetal undernutrition. The subsequent proliferation in the 1990s of research on the fetal origins of CHD, which often focused on the proxy of birth weight, met with initial resistance from proponents of the primacy of well-established adult risk factors. Life course epidemiology emerged partly as a synthesis of the two approaches, demonstrating that early life factors may act cumulatively or interactively with adult exposures to influence health and disease in later life.

Conceptual Models

Several conceptual models have emerged within the life course approach to health. One of these, the critical period model, focuses on the importance of the timing of exposure. It holds that biological programming occurring during critical periods of growth and development in utero and in early infancy has irreversible effects on fetal structure, physiology, and metabolism. This model is the basis of the fetal origins of adult disease hypothesis, elaborated by Barker and colleagues and now known as the developmental origins of health and disease (DOHaD), to reflect an expanded developmental time frame.

Research in DOHaD has suggested that the highest risk of CHD, central distribution of body fat, insulin resistance, type 2 diabetes, and the metabolic syndrome may be associated with a phenotype of lower birth weight coupled with a higher body mass index in childhood or adulthood. Many of these studies have explored the potential risk associated with accelerated postnatal catch-up growth. Researchers hypothesized that predictive adaptive responses by [Page 593]the fetus and infant lead to irreversible changes that may, when coupled with environments in childhood and adult life that differ from the one anticipated during early life, increase the risk of adult disease. Populations in the developing world undergoing urbanization and the nutritional transition to Western lifestyles may thus be particularly susceptible to this developmental mismatch risk pattern. Studies have also explored gene-environment interactions, including potential epigenetic modification of fetal genes by the in utero environment.

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