Alcohol, slow wave sleep, and the somatotropic axis

When alcohol is a large proportion of daily nutrient energy, the network of signals for energy homeostasis appears to adapt with abnormal patterns of sleep and growth hormone (GH) release along with gradual acquisition of an addictive physical dependency on alcohol. Early relapse during treatment of alcoholism is associated with a lower GH response to challenge, perhaps re flecting an altered balance of somatostatin (SS) to somatotropin releasing hormone (GHRH) that also affects slow wave sleep (SWS) in dependent patient s. Normal patterns of sleep have progressively shorter SWS episodes and lon ger rapid eye movement (REM) episodes during the overall sleep period, but the early sleep cycles of alcoholics have truncated or non-existent SWS epi sodes, and the longer REM episodes occur in early cycles. During SWS delta wave activity, the hypothalamus releases GHRH, which causes the pituitary t o release GH. Alcohol-dependent patients have lower levels of SWS power and GH release than normal subjects, and efforts to understand the molecular b asis for this maladaptation and its relation to continued alcohol dependenc e merit encouragement. More needs to be learned about the possibility of de creasing alcohol dependency by increasing SWS or enhancing GHRH action. Pub lished by Elsevier Science Inc.