Abstract
The environmental conditions experienced by the developing human during the peri-conceptual, embryonic, fetal, neonatal and adolescent periods, have a profound effect on the future health of that individual. Adverse early-life environmental conditions such as under or over nutrition, stress, vitamin deficiencies, drugs and alcohol exposure can permanently alter the long-term functioning of many organs. These changes significantly increase the risk of developing diseases in adult life such as cardiovascular disease, diabetes and metabolic syndrome, as well as mental health conditions such as attention deficit disorder, autism, and schizophrenia. The now widely studied, yet still mechanistically ill-defined “developmental origins of adult disease” hypothesis, was first proposed by Barker in 1986 [1]. Barker and his colleagues described an association between low birth weight and increased risk of developing ischaemic heart disease in later life. Since then, human epidemiological studies have continued to show a strong association between low birth weight and adult coronary heart disease and hypertension. This hypothesis has since been expanded to show that ‘programming’ can occur independently of low birth weight or growth retardation. Animal models are currently being used to investigate the mechanisms of the developmental origins of adult disease including maternal undernutrition, both global and nutrient specific such as low protein, uterine artery ligation to induce fetal growth restriction and maternal glucocorticoid exposure. Results vary significantly between these models depending on the type, severity and the timing of the insult. What has emerged from many of these studies is that there are key windows of development that are more susceptible to particular insults
Keywords: Fetal programming, glucocorticoids, low protein, maternal stress
4