13/03/2026
Mental stress, either acute or chronic, produces certain physiological responses via the CNS. The body's adaptive responses to stress stimuli are mediated by an intricate system, which includes the hypothalamus-pituitary-adrenocortical (HPA) axis and the sympathoadrenal system. Dysregulation of the system by repetitive or chronic stress may induce continually increased adrenocortico-tropic hormone (ACTH) and corticosteroid levels, increase the production of monoamines and proinflammatory cytokines within the brain, and thus contribute to a variety of somatic and psychiatric disorders including hypertension, atherosclerosis, functional disorders of the digestive system, several immunological disorders, affective disorders, or anxiety.
From a clinical point of view, much evidence has accumulated that disturbances in the HPA axis with elevated circulating plasma levels of ACTH and Cortisol play a pivotal role in depression. As it is also known that administered corticosteroids induce hypercholesterolemia, hypertriglyceridemia, and hypertension and that elevated morning Cortisol concentrations are correlated with coronary artherosclerosis, a relationship between depression and vascular diseases seems plausible. However, in recent years, a paradoxical phenomenon has emerged from neurobiological studies on the effect of chronic stress, as a number of studies have provided evi dence that the adrenal gland is hypoactive in some stressrelated states, resulting in hypocortisolism.
This enhanced negative feedback sensitivity of glucocorticoid receptors or a persistent lack of Cortisol availability can be observed in posttraumatic stress disorder and in other conditions such as chronic fatigue syndrome, fibromyalgia (FM), and rheumatoid arthritis. It was proposed that traumatized or chronically stressed individuals may have an increased vulnerability for stress-related somatic disorders. In case you want to explore more, read my articles here: https://www.patreon.com/betterbrain
Reference: Bondy B. (2003)