Neuroendocrine studies of depressive illness.
Interest in possible neuroendocrine disturbances in endogenous depression is prompted by two lines of evidence: (1) clinical features of the illness suggest hypothalamic dysfunction; (2) the brain neurotransmitters implicated in depression also regulate neuroendocrine function. Our research reveals a marked, sustained hypersecretion in cortisol in severe depressive illness, which is apparently unrelated to stress and sleep disturbance, and which is associated with a distortion of the 24-hour cortisol secretory pattern. The hypersecretion is manifested primarily in the late afternoon, evening, and early morning hours, when cortisol secretion is normally inhibited. Growth hormone responses to hypoglycemia (but not to L-dopa) are also significantly reduced in endogenous depression, even when factors of age and the menopause are controlled. Postmenopausal depressed women appear to secret significantly less LH than normal postmenopausal women. Since all of these hormonal abnormalities can be reproduced by depletion of brain noradrenalin, the findings provide support for the the hypothesis of reduced functional noradrenergic activity in certain forms of depression.
D000368:Aged; D001007:Anxiety; D002940:Circadian Rhythm; D003863:Depression / Q000097:blood*; D005260:Female; D013006:Growth Hormone / Q000097:blood*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D007003:Hypoglycemia / Q000139:chemically induced; D007328:Insulin; D007986:Luteinizing Hormone / Q000097:blood*; D008875:Middle Aged; D005082:Physical Exertion; D012890:Sleep
D007328:Insulin; D007986:Luteinizing Hormone; D013006:Growth Hormone; D006854:Hydrocortisone