For more than a decade, the fetal programming hypothesis has taught that insulin resistance and its associated metabolic disturbances result from poor gestational environment, for which low birth weight is a surrogate. Low birth weight, however, is now uncommon in industrialized societies. We have investigated the relevance of birth weight, “catch-up” weight, and current weight to insulin resistance in 300 contemporary British children. Insulin resistance at 5 years was not related to birth weight but was correlated with current weight and weight catch-up in both sexes, more strongly so in girls (r = 0.33, P < 0.001 vs. r = 0.18, P = 0.03), who were intrinsically more insulin-resistant than boys. Weight change merely co-correlated with current weight (r = 0.67, P < 0.01 in both sexes) and did not improve on the prediction of insulin resistance. Most important, insulin resistance at 5 years was the same in children of heavier birth weight, whose weight SD score had not changed, as in those of lighter birth weight, matched for current weight, who had experienced so-called catch-up (boys 0.89 and 0.88 units, respectively, P = 0.96; girls 1.26 and 1.13 units, P = 0.41). Insulin resistance in contemporary children seems to be a function of excess current weight rather than of low birth weight or change in weight. Type 2 diabetes is the outcome of a process—it is not the process itself. The process is one of insulin resistance, in which high levels of circulating insulin reflect the response of the β-cells to a rising blood glucose. Type 2 diabetes emerges when the β-cells are no longer able to compensate (1), whereas the accompanying hyperinsulinemia is independently associated with other metabolic disturbances collectively referred to as the metabolic syndrome (2). These disturbances together account for much of the cardiovascular morbidity of the industrialized world (3,4) and tend not to occur in the absence of insulin resistance. Of the three hypotheses advanced to explain insulin resistance (“thrifty genotype” , “fetal origins” , and “fetal insulin” ), the second, or “Barker” hypothesis, has enjoyed the widest exposure. It sees low birth weight as a surrogate for poor gestational environment and interprets the (inverse) correlation between birth weight and insulin resistance later in life as the result of “fetal programming.” The strongest predictor of future cardiovascular disease reportedly combines low ponderal index (kg/m3) at birth with rapid weight gain thereafter—so-called “catch-up” (8–10). The fetal programming hypothesis was originally formulated on data from metabolic studies conducted in aging males who were born before the second world war. Many of them were born into circumstances of relative poverty, in which low birth weight is more common. However, as Lucas et al. (11) have pointed out, birth weight is likely to be as valid a surrogate for nutritional circumstances after birth as before birth because birth weight and subsequent weight correlate. It may therefore be as logical to ascribe metabolic disturbance later in life to events after birth as to prenatal programming. Furthermore, low birth weight at term (<2,500 g) is nowadays rare in industrialized societies (12), and the privations that prevailed 80 years ago no longer apply to contemporary pregnancies. In this study, we tested the hypothesis in a cohort of young U.K. children that insulin resistance can nowadays be best accounted for by current weight (overfeeding/underactivity) rather than by birth weight (gestational environment/insulin resistance genes) or catch-up weight.