ABSTRACT
In Chapters 7 and 8 we have discussed several statistical models for testing associations between birth size and chronic diseases in later life, known as the foetal origins of adult disease hypothesis (FOAD) or Barker’s hypothesis. This hypothesis has attracted considerable attention amongst the medical and epidemiological research communities over the last two decades. In the previous chapters we also showed that the associations between birth size and chronic diseases can often be weak (negative or positive) but then become negative and statistically signi‰cant when current body size is adjusted for in the model as a covariate. In recent years, attention to the foetal origins hypothesis has gradually shifted from birth size to early postnatal growth, and it has been suggested that small birth size in conjunction with compensatory rapid growth in childhood (rather than small birth size per se) might lead to a greater risk of developing chronic adult diseases. As a result, the FOAD hypothesis has been rephrased the developmental origins of health and disease hypothesis (DOHaD hypothesis; Barker 2004; Barker et al. 2005; Gillman 2005). In fact, both FOAD and DOHaD may be viewed as members of a larger theme, that of lifecourse epidemiology, in which researchers are interested in ‘the study of long-term effects on chronic disease risk of physical and social exposures during gestation, childhood, adolescence, young adulthood and later adult life’ (Ben-Shlomo and Kuh 2002). Lifecourse epidemiology involves studies of the ‘biological, behavioural and psychosocial pathways that operate across an individual’s lifecourse, as well as across generations, to in£uence the development of chronic diseases’ (Ben-Shlomo and Kuh 2002).
