
The majority of the early work conducted by David Barker and colleagues utilised data from historical cohorts born in the 1930s and benefited from meticulous birth records, often kept by the same individual over long periods of time. This approach has enabled clear relationships between not only the size and shape of an infant at birth but also its accompanying placental mass and later hypertension to be established. Subsequently, the recruitment of long-term historical records from Finland has enabled longitudinal studies of infant growth to be related to adult insulin sensitivity. More recently, the use of nutritional interventions of preterm formula in randomised controlled studies has emphasised the impact of inappropriate growth in early infancy on later disease risk. However, with more contemporary studies and the rise in both childhood and adult obesity it is now apparent that the translation of findings from such studies into current lifestyle interventions is very difficult. This situation results, at least in part, from the complexity of the biological processes involved and the challenge of effecting lifestyle changes in activity and dietary intake. At the same time, the causes of the ongoing epidemic of obesity, and the predicted increase in associated renal diseases and CVD, are multifactorial and may be either exacerbated, or reduced, by early dietary exposure.
One consistent theme that is apparent from both historical and contemporary studies is that changes in nutrition at specific stages of pregnancy can have very different outcomes. This finding is not unexpected as different organs have critical and precise developmental windows that may be compromised, or enhanced, and thereafter permanently set for the rest of that individual’s life. Importantly, adaptations of this type appear not only to be dependent on the
period in which the mother’s diet is altered but also the diet to which she is rehabilitated. The extent to which mother's diet relates to changes in placental function and/or foetal growth remains less clear, but there is a need to match global pre- and postnatal nutritional requirements in order to avoid accelerated growth and the concomitant increased risk of later obesity and metabolic complications. Importantly, however, intergenerational acceleration mechanisms do not appear to make an important contribution to levels of raised childhood BMI within the population. Epidemiologically, maternal obesity is consistently linked with a predisposition for children overweight and obesity. The underlying mechanisms of such transmission of obesity remains however poorly understood as major confounding factors such as reduction of breastfeeding time duration, transmission of eating habits and genetic predisposition remains to be considered carefully. Consistent findings in humans corroborated by animal studies have established the importance of the maternal nutritional status on the later determination of long term metabolic health outcomes in the offspring. Thus, a risk for an early prenatal programming of cardiovascular diseases, obesity, impaired glucose tolerance have been established in both humans and animal models. Nevertheless, these effects have been shown following periods of maternal nutrient restriction. However, recent animal studies have observed that similar metabolic programming adaptations are very likely to happen following maternal over-eating and obesity.
Obesity has reached epidemic proportions globally, with more than one billion adults overweight, and at least 300 million clinically obese. It is recognised as a major contributor to the global burden of chronic disease and disability.
Obesity becomes a critical international public health issue known to promote a major risk for the development of several metabolic disorders such as hypertension, type II diabetes and cardiovascular diseases. In Western societies, the incidence of obesity has increased dramatically over the past two decades across the majority of age ranges. Indeed, not only is this increase in incidence not slowing, it is likely to worsen as the prevalence of childhood obesity is rising at an even faster rate and, up to 80% of obese adolescents remain obese as adults. Critically, as obesity is prevalent among women of reproductive age, it is important that appropriate dietary advice is provided before and during and after pregnancy if potential problems related to excess maternal weight gain and/or compromised placental and fetal growth throughout this period is to be avoided. In view of the complications associated with pregnancy in obese women, and the escalating costs to health care, many intervention studies are underway world-wide with the primary aim of improving pregnancy outcome. Although a secondary objective, these offer the potential to address the hypothesis of the developmental origins of obesity through prospective follow-up studies in the child from intervention and control arms of the RCTs.
The PREOBE research project aimed to obtain genetic and biochemical & immunological biomarkers for the programming of obesity in early stages of life by studying pregnant women with obesity or gestational diabetes, and by analyzing how these conditions impact on foetal growth and on biomarkers of risk to develop Obesity and a phenotype of Metabolic Syndrome in their offspring during the first months of life.