PSYCHOENDOCRINOLOGIC MECHANISMS OF LIFE STRESS

Psychological coping with daily life stressors induces endocrine responses by the central and autonomic nervous systems (CNS, ANS) as well as steroid hormone secretion by the hypothalamus-pituitary-adrenal axis. The adrenocortical hormones together with the catecholamines maintain peripheral homeostasis and regulate cardiovascular, metabolic and immune functions during stress reactions. Active coping with intermittent stressors is related to sympathetic nervous system (SNS)-adrenomedullary arousal and to adrenocortical hormone suppression. This is presumed to result in a strong, positive response, emotional stability and enhancement of the immune system, so-called 'positive stress reaction'. During passive, long-term coping, SNS arousal is assumed to be associated with adrenocortical (cortisol) stimulation and immune suppression, so-called 'negative stress reaction'. The consequences include psychosomatic disorders and cardiovascular, gastrointestinal and/or immune diseases. Clinical data on adrenocortical hormone measurements in patients with immune diseases, such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and ulcerative colitis (UC), indicate, however, that the levels of cortisol and dehydro-epiandrosterone sulphate (DHEAS) are reduced or normal, compared to those of other categories of patients and healthy subjects. Furthermore, the basal cortisol levels have also been found to be reduced in children with recurrent psychosomatic abdominal pain (RAP). These data seem to be in contraposition to the generally assumed role of the adrenocortical pathway in the evolution of stress-induced diseases. Studies to assess whether there is a relationship between long-term 'negative' stress reactions and the low adrenocortical hormone levels are lacking, but are needed.