The programming of the stress response network by early-life adversity

Abstract

Adverse conditions early in life have been identified as risk factors for the susceptibility for psychopathology during adolescence and adulthood. A change in the regulation of stress response systems has been discussed as potential mechanism linking early life stress to later psychopathology. Over the past several years, we have gathered data from several independent studies assessing the regulation of the hypothalamic–pituitary–adrenal (hpa) axis, the sympathetic and parasympathetic nervous system, and the volume of key brain structures involved in the regulation of these systems, to investigate the effects of various forms of early life adversity. All studies consistently show effects of early life adversity on the regulation of the stress response systems. However, the directionality of the effect appears to be variable. For cortisol as a marker of the hpa axis, subjects with low early life parental care show signs of changed cortisol awakening response, afternoon cortisol output, and cortisol stress responses, when compared to subjects with average parental care scores. For sympathetic and parasympathetic nervous system, results point to a systematic cross-talk with the hpa axis, depending on specific aspects of early-life adversity. The changes in the regulation of these systems map on to the changes of distinct areas in the central nervous system believed to be involved in the regulation of the stress response systems. Together, the differential regulation of these systems suggest that specific stress response endophenotypes emerge as a consequence of experiences during critical development periods early in life.