Introduction

The placenta plays a unique role in supporting the fetal allograft throughout gestation, protecting against immune rejection whilst also serving to supply oxygen and nutrients to, and remove carbon dioxide and waste products from, the fetus. As the nutrient interface between mother and fetus, the placenta may passively or actively transfer nutrients to the fetus or metabolise them en route. In addition the placenta produces a variety of peptide and steroid hormones that affect placental, maternal and fetal metabolism and development. The developmental origins of health and adult disease hypothesis proposes that alterations in fetal development, or adaptations of the fetus to alterations in the normal amount or pattern of substrate supply across the placenta, lead somehow to cardiovascular and metabolic disease in adult life. There is now abundant evidence both from human epidemiological studies and from animal studies that maternal nutrition may ‘programme’ the offspring for adult disease. This effect may be direct but it is more likely to be mediated in some manner by placental structure and/or function regulating the amount or composition of nutrients transferred. Does the placenta therefore play an active or a passive role in programming? Reduced fetal and placental weights are both associated with fetal programming. However, it is argued that, rather than reduced placental weight (and function) being linked to reduced fetal weight in a cause-and-effect relationship, reduced weight(s) might be a surrogate marker for an adverse intrauterine experience.