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 no such effect. Similarly, transient immunization of neonatal rats against growth hormone releasing factor results in permanent impairment of pituitary growth hormone secretion and permanent impairment of growth rate. 10 Exposure of neonatal rats to short periods of stimulation, handling or various stressors results in permanent changes in hypothalamic structure and systemic responses to stress. 11 , 12 Since most examples of programming involve a critical period early in life, this phenomenon as the proposed basis of the epidemiological observations is both epidemiologically and biologically plausible. Thus a programming stimulus in fetal life is proposed to lead both to changes in size at birth and also to altered homeostatic mechanisms such as regulation of blood pressure or insulin sensitivity, which in turn result in susceptibility to disease in later life. 13 The question which then arises concerns the nature of the programming stimulus. Undernutrition was proposed early as a likely programming stimulus, although others such as excessive fetal exposure to glucocorticoids have also been proposed. 14 -- 16 This review will focus on nutrition as the hypothesized primary programming stimulus. It will examine the experimental basis for this hypothesis, a number of assumptions and misconceptions surrounding the hypothesis, and the need for caution in applying the results of animal experiments to the human situation. Why nutrition? The proposal that nutrition in fetal life