The nutritional basis of the fetal origins of adult disease

It is now widely accepted that the risks of a number of chronic diseases in adulthood may have their origins before birth. Such diseases include non insulin-dependent diabetes mellitus, hypertension and coronary heart disease. Professor David Barker and colleagues in Southampton have produced a large proportion of the data in this field over the last decade, 1 although the relationship between early life events and adult disease had been raised many years earlier. 2 Most of this work has been based on epidemiological studies wherein cohorts of subjects whose birth records were available have been traced into adulthood. They have shown that measurements made on babies at birth, including birthweight, length, body proportions and placental weight, are strongly related to either later disease incidence (coronary heart disease mortality, noninsulin-dependent diabetes) 3,4 or risk factors for those diseases (hypertension, glucose intolerance, hyperlipidaemia). 1,5,6 Such relationships have been shown to hold in many different populations and are apparent from early childhood. 7,8 The basis of these epidemiological observations is proposed to be that of programming. That is, an event operating at a critical or sensitive period results in a long-term change in the structure or function of the organism. Programming is a well-established biological phenomenon, and there are many common and well-known examples. Female rats given testosterone during the first 4 days of life develop a male pattern of gonatotropin secretion after puberty, and despite normal ovarian and pituitary function, fail to develop normal patterns of female sexual behaviour. 9 Administration of androgen at 10 days of age has