Introduction

The concept of the developmental origins of adult disease was initially based on epidemiological observations relating evidence of a constrained fetal environment to a greater risk of metabolic and cardiovascular disorders in adult life. It was later recognised that those at greatest risk also have an increased propensity to developing obesity in childhood and during adult life (Barker and Osmond 1988, Hales and Barker 1992, Gluckman and Hanson 2004). The interest in the later effects of early environmental events has since been generalised to include possible prenatal effects on offspring behaviour and cognition. In this chapter, we review the existing human and animal literature on the early-life influences on offspring cognitive function and behaviour.

Human studies

Recently, interest has grown in the possibility of a relation between birthweight and subsequent cognitive function. Early research focused on comparisons between individuals of low birthweight (LBW) or small for gestational age (SGA) and those with normal birthweights (e.g., Ounsted et al. 1983, Pharoah et al. 1994, Strauss 2000). These studies showed that LBW and SGA individuals had an increased incidence of neurological deficits and/or poorer cognitive skills throughout childhood. Subsequent research has examined whether this relationship persists across the normal range of birthweights (e.g. Sorenson et al. 1997, Matte et al. 2001, Richards et al. 2001, 2002, Shenkin et al. 2001, Jefferis et al. 2002). The consensus from this research is that the relationship does hold across the range of normal birthweights, but that the effect is small.