Geographical studies provoke the hypothesis that early environmental d
eprivation may be linked to disease in adult life. There is indeed mou
nting evidence from longitudinal studies that markers of poor fetal gr
owth such as weight at birth are associated with later disorders inclu
ding hypertension. The notion that an adverse event at a critical stag
e of fetal development could predispose to disease in adulthood is kno
wn as the programming hypothesis. In the case of hypertension, possibl
e mechanisms include changes in arterial compliance caused by abnormal
ities in fetal blood flow, peripheral insulin resistance and disordere
d beta cell function with high circulating levels of insulin precursor
s, and reduced nephron mass with abnormalities of salt and fluid excre
tion. If the programming hypothesis is correct, risk of cardiovascular
disease in adulthood could be reduced by improvements in maternal nut
rition in pregnancy.