2 - The ‘developmental origins’ hypothesis: epidemiology

Summary

Introduction

Research worldwide has established that people who were small at birth and had poor growth in infancy have an increased risk of adult coronary heart disease and type 2 diabetes, particularly if this is followed by increased childhood weight gain. There is also evidence linking impaired early growth with other degenerative disorders in later life, including stroke, hypertension, obesity, osteoporosis, obstructive airways disease, reduced cognitive function and poor mental health. The relations between smaller infant size and an increased risk of ill health and adult disease extend across the normal range of infant size in a graded manner. Moreover, recent animal studies and epidemiological data have demonstrated that while maternal thinness and unbalanced diet during pregnancy may have modest effects on size at birth, they are nonetheless associated with raised blood pressure and altered glucose–insulin metabolism and stress responsiveness in the adult offspring. It is now clear that the associations do not simply reflect genetic influences; rather the findings indicate that interactions between the genetic influences and the early-life environment determine disease and susceptibility to adverse influences in the adult environment.

The observations have led to the hypothesis that cardiovascular disease, type 2 diabetes, osteoporosis and obstructive airways disease originate through developmental plastic responses made by the fetus and infant as part of a prediction of the subsequent environment to which it anticipates that it will be exposed.