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 ofactive research.