The fetal origins hypothesis states that fetal undernutrition in middle to late gestation, which leads to disproportionate fetal growth, programmes later coronary heart disease. Animal studies have shown that undernutrition before birth programmes persisting changes in a range of metabolic, physiological, and structural parameters. Studies in humans have shown that men and women whose birth weights were at the lower end of the normal range, who were thin or short at birth, or who were small in relation to placental size have increased rates of coronary heart disease. We are beginning to understand something of the mechanisms underlying these associations. The programming of blood pressure, insulin responses to glucose, cholesterol metabolism, blood coagulation, and hormonal settings are all areas of active research. The BMJ's recent editorial on the fetal origins hypothesis stated that it rests only on the “very general” proposition that fetal undernutrition causes coronary heart disease. 1 This is incorrect. The hypothesis states that coronary heart disease is associated with specific patterns of disproportionate fetal growth that result from fetal undernutrition in middle to late gestation. 2 3