Introduction

We have become accustomed to the idea that many disorders of adult life such as noninsulin-dependent diabetes, hypertension and obstructive airways disease arise through an interaction between a genetically determined susceptibility and influences in the current environment including diet, obesity, smoking and allergen exposure. Recent research, however, suggests that the fetal and early infant environment may play a critical role in programming a lifelong predisposition to a number of common adult diseases. As yet, there is only limited and indirect evidence to suggest major long-term effects of the fetal and perinatal environment in relation to atopic dermatitis (AD). Research into this hypothesis, however, is in its very earliest stages and future epidemiological studies of the fetal environment may provide important insights into the aetiology of AD.

The concept of programming during early development

In fetal life and early infancy different tissues of the body grow during periods of rapid cell division, so-called ‘critical’ periods (Widdowson & McCance, 1975). The timing of these critical periods differs for different tissues; a critical period for reproductive tract development exists, for example, very early in development (Beral & Colwell, 1981), as compared with one for kidney development later in gestation between 26 and 34 weeks of pregnancy (Konje et al., 1996). Growth depends on nutrients and oxygen, and the fetus's main adaptation to the lack of these is to slow its rate of cell division, especially in those tissues which are undergoing critical periods at the time.