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In 1986 David Barker and Clive Osmond published their seminal paper on the relationship between smaller size at birth and the subsequent development of ischaemic heart disease.1 This paper gave birth to the so-called "Barker hypothesis" – that cardiovascular disease and other medical problems such as metabolic disease or osteoporosis may have their origins in utero and early-life. This phenomenon was recently reviewed in the New England Journal of Medicine.2 The relevant epidemiological data and clinical observations are discussed, followed by a description of developmental plasticity and the influence of the genome and epigenome on phenotype. In this issue of ADC, Terry Dwyer and colleagues, further define some aspects of the Barker hypothesis by delineating the role of certain alleles (those that govern corticotropin-releasing hormone) in modifying the relationship between birth weight and adolescent systolic blood pressure. The relationship between the in utero environment and various outcomes was
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