Early Growth, Cardiovascular and Renal Development: The Generation R Study

Abstract

Cardiovascular disease is a major health problem in the adult general population. Epidemiological studies strongly suggest that early life events have an important role for the susceptibility to develop cardiovascular disease in later life. In the 1980’s, Barker and Osmond showed that areas of Britain with the highest neonatal mortality rates early in the 20th century also had the highest incidence of cardiovascular disease in adults, many decades later1. Birth weight is an important predictor of neonatal mortality. After these observations, many epidemiological studies consistently showed that low birth weight is associated with adult health outcomes such as cardiovascular disease, type 2 diabetes and kidney disease. It was also noted that the risk of cardiovascular disease was highest in subjects who show a postnatal catch-up growth after being born with a low birth weight6. These observations resulted in the “fetal origins of adult disease” hypothesis, also currently known as the “Developmental Origins of Health and Disease “ Hypothesis (DOHaD-hypothesis). This hypothesis states that a suboptimal fetal environment leads to developmental adaptations that permanently alter growth, physiology and metabolism, with long-term consequences for adult health. More recently, this hypothesis has been adapted to a more general “developmental plasticity hypothesis”, which proposes that an organism may develop in different ways, depending on the environment it is exposed to. Investigating specific adverse fetal exposures and early growth may provide new insights in mechanisms underlying the associations of low birth weight with adult disease. Different aspects of early development might be important in determining future risk of adult cardiovascular and renal diseases.