Influences acting in utero and in early childhood

The search for the environmental causes of ischaemic heart disease is generally guided by a ‘destructive’ model, where the causes to be identified are thought to act in adult life and accelerate destructive processes such as the formation of atheroma, rise in blood pressure, and loss of glucose tolerance. By contrast, a ‘developmental’ model for the disease focuses on causes acting on the baby and argues that in responding to undernutrition and other adverse influences, the baby ensures its continued survival and growth at the cost of premature death from ischaemic heart disease and other chronic disorders.

Low birthweight is associated with increased rates of ischaemic heart disease and the related disorders—stroke, hypertension, and type 2 diabetes. These associations, which have been extensively replicated in studies in different countries, extend across the normal range of birthweight, and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. They are thought to be consequences of developmental plasticity—the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development.

Impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. The placenta is likely to play a key role in programming the baby.