Fetal Origins of Adult Disease

Abstract

Dr. David Barker first popularized the concept of fetal origins of adult disease (FOAD). Since its inception, FOAD has received considerable attention. The FOAD hypothesis holds that events during early development have a profound impact on one’s risk for development of future adult disease. Low birth weight, a surrogate marker of poor fetal growth and nutrition, is linked to coronary artery disease, hypertension, obesity, and insulin resistance. Clues originally arose from large 20th century, European birth registries. Today, large, diverse human cohorts and various animal models have extensively replicated these original observations. This review will focus on the pathogenesis related to FOAD and examines Dr. David Barker’s landmark studies, along with additional human and animal model data. Implications of the FOAD extend beyond the low birth weight population and include babies exposed to stress, both nutritional and non-nutritional, during different critical periods of development, which ultimately result in a disease state. By understanding FOAD, health care professionals and policy makers will make this issue a high healthcare priority and implement preventative measures and treatment for those at higher risk for chronic diseases.

Social Determinants of Risk and Outcomes for Cardiovascular Disease

“…These findings have been observed in populations that have experienced significant famines but occur in many situations in which malnutrition in the form of lack of food or access to poorly nutritious but highly caloric food exists. 316 Numerous studies support the fetal origins hypothesis by demonstrating an association among low birth weight, placental insufficiency, and cardiovascular and other chronic diseases. Adult-onset systemic hypertension has been associated with birth weight.…”

“…Intrauterine growth retardation is associated with a reduced number and function of pancreatic β cells, resulting in decreased insulin production. 316 This alteration leads to abnormal muscle, liver, and adipocyte insulin signaling and eventually to the development of insulin resistance.…”

Epigenetics and Primary Care

“…If, during that individual' s adult life, nutrients become more plentiful, this predisposition increases the risk of obesity and metabolic syndrome over time. 5 This hypothesis differs from the thrifty genotype hypothesis, another proposed explanation for the increasing levels of obesity in Western society. The thrifty genotype hypothesis holds that populations that evolved over generations to survive in harsh environments cannot adapt to the modern environment because the change was too dramatic to allow for evolutionary adaptation over a short time frame.…”

Life Course Health Development Outcomes After Prematurity: Developing a Community, Clinical, and Translational Research Agenda to Optimize Health, Behavior, and Functioning

“…Intrauterine environment and early postnatal life are now generally accepted as important factors that may lead to increased risk for disease in adulthood (Hofman et al 2004). In particular, low birth weight, a marker of poor fetal growth, is linked to vascular disease, hypertension, obesity, and insulin resistance (Calkins and Devaskar 2011). Although several studies have reported an association between low birth weight and poor adult health outcomes, it remains unclear whether this association exists for children with poor fetal growth born small for gestational age as well as premature babies whose weight is appropriate for gestational age.…”