Introduction

The fundamental assumption underlying the DOHaD model is that environmental factors acting in early life have consequences which become manifest as an altered disease risk in later life. The concept that multiple phenotypes can arise during development from a single genotype (‘developmental plasticity’) is not new: these different phenotypes are based on the nature of the gene–environment interactions, a feature well recognised in developmental biology and the range of phenotypes that can be induced is termed the reaction norm (Gilbert 2001). Given the universality of developmental plasticity, particular sets of phenotypic outcomes may be manifest as variable disease risk (Bateson et al. 2004). As a result, one part of the reaction norm may be associated with better survival in one type of environment, while another is better suited to a different environment. One example comes from the desert locust Schistocerca gregaria, where factors acting in the larval stage induce a phenotype appropriate for migratory or non-migratory situations (Applebaum and Heifetz 1999, Simpson et al., 2002). Having a wing shape appropriate for a non-migratory lifestyle will compromise the locust in a situation of overcrowding and nutritional compromise.

While in comparative biology the concept of environmentally influenced developmental trajectories has been accepted, its influence on our understanding of human disease has taken time to be accepted. This delay has impacted on how the developmental-origins field has developed since the early epidemiological observations in humans relating birth size to later disease risk (Forsdahl 1977, Barker and Osmond 1986).