The developing fetus requires an adequate supply of fatty acids, in particular PUFA, for optimal growth and development. Little is known about the transfer of fatty acids by the placenta into the fetal circulation. However, the molecular form in which fatty acids are transferred into the fetal circulation may influence their metabolism and hence their availability to specific tissues. The aim of the present study was to determine which lipid pools in the fetal circulation become enriched in fatty acids from the placenta by comparing the fatty acid compositions of individual lipid pools between umbilical venous (UV) and umbilical arterial (UA) plasma. Plasma from the UV and UA was collected after delivery from ten uncomplicated pregnancies, and the fatty acid composition of each lipid class was determined by GC. Total NEFA concentration in the UV was twofold higher than in the UA (P < 0·05) due to enrichment in 16 : 0, 16 : 1n-7, 18 : 1n-9, 18 : 1n-7, 18 : 2n-6, 20 : 3n-6, 20 : 4n-6, 24 : 0 and 22 : 6n-3. Total cholesteryl ester concentration was twofold higher in the UV than in the UA (P < 0·05) due to enrichment in 16 : 0, 16 : 1n-7, 18 : 0, 18 : 1n-9, 18 : 1n-7, 18 : 2n-6 and 20 : 4n-6. There were no significant UV–UA differences in the total concentration or composition of TAG or phosphatidylcholine. The present study demonstrates differential enrichment across the placenta of fatty acids into specific lipid pools in the fetal circulation. Such partitioning may facilitate supply of individual fatty acids to specific fetal tissues.

The early hominids and their successors, the nomadic hunter–gatherers, were evolutionarily adapted to an omnivorous diet. Their food was well balanced nutritionally and they acquired adequate supplies with relatively little expenditure of energy. The complete change to a fixed agricultural lifestyle (the Neolithic revolution) took place only some 12 000 years ago and was the most momentous event in human history. Being tied to the land that they worked led eventually to the city states and the great civilisations of history, which brought with them wars and epidemics of infectious diseases. Much more serious were the insidious effects of the new cereal-based diet which persisted until the twentieth century. Not only was it labour intensive, but also for the bulk of the population it was often deficient in vitamins, minerals and energy, particularly at certain times of the year. Time-series analysis reveals a regular short wavelength oscillation in the grain supply that persisted for at least 350 years and dominated the population dynamics of pre-industrial England. In addition to reducing fertility, it acted primarily via its effects on the nutrition of the pregnant woman. Malnutrition during one of the critical trimesters of pregnancy could have far-reaching effects not only on the health of the fetus and neonate but also on the illnesses of later, adult life. These consequences were insidiously and inevitably carried forward to the subsequent generations. Girls who were born with a low birth weight produced daughters and granddaughters of low birth weight, irrespective of their nutrition during childhood. These intergenerational, knock-on effects established a vicious circle from which there was little chance of escape.

Nutrition plays a central role in linking the fields of developmental neurobiology and cognitive neuroscience. It has a profound impact on the development of brain structure and function and malnutrition can result in developmental dysfunction and disease in later life. A number of diseases, including schizophrenia, may be related to neurodevelopmental insults such as malnutrition, hypoxia, viruses or in utero drug exposure. Some of the most significant findings on nutrition and neurodevelopment during the last three decades, and especially during the last few years, are discussed in this review. Attention is focused on the underlying cellular and molecular mechanisms by which diet exerts its effects. Randomized intervention studies have revealed important effects of early nutrition on later cognitive development, and recent epidemiological findings show that both genetics and environment are risk factors for schizophrenia. Particularly important is the effect of early nutrition on development of the hippocampus, a brain structure important in establishing learning and memory, and hence for cognitive performance. A major aim of future research should be to elucidate the molecular mechanisms underlying nutritionally-induced impairment of neurodevelopment and specifically to determine the mechanisms by which early nutritional experience affects later cognitive performance. Key research objectives should include: (1) increased understanding of mechanisms underlying the normal processes of ageing and neurodegenerative disorders; (2) assessment of the role of susceptibility genes in modulating the effects of early nutrition on neurodevelopment; and (3) development of nutritional and pharmaceutical strategies for preventing and/or ameliorating the adverse effects of early malnutrition on long-term programming.

Exposure to either an increased or decreased level of intrauterine nutrition can result in an increase in adiposity and in circulating leptin concentrations in later life. In animals such as the sheep and pig in which fat is deposited before birth, leptin is synthesised in fetal adipose tissue and is present in the fetal circulation throughout late gestation. In the sheep a moderate increase or decrease in the level of maternal nutrition does not alter fetal plasma leptin concentrations, but there is evidence that chronic fetal hyperglycaemia and hyperinsulinaemia increase fetal fat mass and leptin synthesis within fetal fat depots. Importantly, there is a positive relationship between the relative mass of the ‘unilocular’ component of fetal perirenal and interscapular adipose tissue and circulating fetal leptin concentrations in the sheep. Thus, as in the neonate and adult, circulating leptin concentrations may be a signal of fat mass in fetal life. There is also evidence that leptin can act to regulate the lipid storage, leptin synthetic capacity and potential thermogenic functions of fat before birth. Thus, leptin may act as a signal of energy supply and have a ‘lipostatic’ role before birth. Future studies are clearly required to determine whether the intrauterine and early postnatal nutrient environment programme the endocrine feedback loop between adipose tissue and the central and peripheral neuroendocrine systems that regulate energy balance, resulting in an enhanced risk of obesity in adult life.

The fetal-origins hypothesis suggests that maternal and fetal nutrition can have a profound and sustained impact on the health of the offspring in adult life. Although there is abundant literature reporting on the associations between birth weight and disease risk factors, only a handful of studies have been able to examine the relationship between maternal nutrition in pregnancy with the health of offspring in adult life directly. Between 1942 and 1944, nearly 400 pregnant women were recruited into a dietary study to determine whether the wartime dietary rations were sufficient to prevent nutritional deficiencies. Detailed biochemical and clinical assessments were conducted for each of the women, who were followed-up until after delivery. More than 50 years later, approximately one-quarter of the adult offspring were recruited into a study to explore the possible impact of maternal nutrition in pregnancy on CHD risk factors, including glucose tolerance, blood pressure and components of the lipid profile. Results from the present study provide no evidence to support the hypothesis that birth weight or maternal nutrition in pregnancy are associated with CHD risk factors in adult life.

The mechanism by which maternal Fe deficiency in the rat causes fetal growth retardation has not been clearly established. This study compared the effects on the fetuses from dams fed a control diet with two groups of dams fed Fe-restricted diets. One Fe-restricted group was fed the Fe-restricted diet for 1 week prior to mating and throughout gestation and the second Fe-restricted group was fed the Fe-restricted diet for 2 weeks prior to mating and throughout gestation. On day 21 of gestation Fe-restricted dams, and their fetuses, were anaemic. Fetal weight was reduced in both Fe-restricted groups compared with controls. Expression of hypoxia-inducible factor (HIF)-1α and vascular endothelial growth factor (VEGF) are induced by hypoxia. The levels of HIF-1α mRNA were highest in placenta, then in kidney, heart and liver but were not different between the groups. Levels of plasma VEGF were not different between the groups. Maternal plasma triacylglycerol was decreased in the 1-week Fe-restricted dams compared with controls. Maternal plasma cholesterol and free fatty acid levels were not different between the groups. In fetal plasma, levels of triacylglycerol and cholesterol were decreased in both Fe-restricted groups. In maternal plasma, levels of a number of amino acids were elevated in both Fe-restricted groups. In contrast, levels of a number of amino acids in fetal plasma were lower in both Fe-restricted groups. Fetal plasma lactate was increased in Fe-restricted fetuses but fetal plasma glucose and β-hydroxybutyrate were not affected. These changes in fetal metabolism may contribute to fetal growth retardation in this model. This study does not support the hypothesis that the Fe-restricted fetus is hypoxic.