SMALL BABIES, STRESS HORMONES AND DISEASE IN ADULT LIFE

David Phillips, Medical Research Centre, University of Southampton, UK.

Although there is a large body of evidence linking adverse influences in early life with a raised prevalence of cardiovascular disease and its risk factors, the mechanisms are still poorly understood. Animal studies suggest that prenatal resetting of major hormonal axes controlling growth and development may be one process explaining this link. Of particular interest is the hypothalamic-pituitary-adrenal axis which controls production of the biologically potent stress hormone, cortisol. Exposure of experimental animals to undernutrition or other stressful influences during pregnancy results in the birth of offspring that have increased basal or stress-induced cortisol secretion. A number of studies now suggest that similar processes occur in humans as there are subtle elevations in circulating cortisol concentrations in men and women who were of low birthweight. These cortisol elevations are in turn linked with higher prevalences of cardiovascular risk factors including high blood pressure, glucose intolerance or raised concentrations of plasma lipids. These findings raise the question as to the nature of the processes that adversely affect fetal growth while increasing stress hormone levels in the offspring. Recent studies have began to identify these factors and evidence will be presented suggesting that maternal nutrition and social class are determinants of stress hormone production in the offspring.