Most phenotypic changes in early life have immediate adaptive advantage, for example, altered regional blood flows are a fetal response to placental insufficiency and protect the fetal brain at the expense of fetal somatic growth.
However, many phenotypic effects are the result of developmental plasticity and their appearance may follow the initiating cue after a substantial delay. Some such phenotypic changes induced in utero or in the neonate may confer their primary advantage well after birth by adapting the organism to have a greater chance of survival to reproductive success.
Natural selection will favor conservation of such mechanisms even if they have a cost in later life, after peak reproductive competence has passed. Such costs will become increasingly apparent with greater longevity in a population. There is much evidence that a sub-optimal fetal environment, as reflected in smaller size at birth, is linked to increased risk of coronary heart disease and type 2 diabetes in middle-aged and elderly people 1 , 2.
This relationship is continuous across the normal range of birth size; however, the fundamental processes underpinning it do not relate to the birth size per se, because such size is only one surrogate measure of the fetal environment, particularly in late gestation. Diverse effects on the fetus can have physiological consequences not reflected in birth size, for example, by altering nephron number 3 , and early gestation, environmental cues can influence development without affecting birth weight.
In response to a maternally determined environment perceived as inadequate, the fetus makes irreversible changes to aspects of its development. Thus, relative insulin resistance develops in fetal life in response to maternal undernutrition, and leads to reduced somatic growth and energy conservation after birth to allow the offspring a better chance of survival in a postnatal environment where nutrition is poor.
