Neuroendocrine pathways of addictive behaviour.
Alcohol intake is known to modulate plasma concentrations of neuroendocrine peptides. However, recent results suggest that the endocrine system may not only respond passively to alcohol intake but that, vice versa, it also actively modulates alcohol intake behaviour. The most coherent body of data concerns the hypothalamo-pituitary-adrenocortical (HPA) axis, with low corticotrophin-releasing hormone (CRH) being associated with more intense craving and increased probability of relapse after acute detoxification. Leptin, beta-endorphin and atrial natriuretic peptide (ANP), which indirectly regulate the HPA system, also may modulate the intensity of craving or the intensity of the alcohol withdrawal syndrome. Although most of the currently available data demonstrate association rather than causality between neuroendocrine changes and alcohol-related behaviours, they do provide testable hypotheses and open up perspectives of treating alcohol dependence via manipulation of the neuroendocrine axis.
Kiefer
F
F
Department of Psychiatry and Psychotherapy, University Hospital of Hamburg, Hamburg, Germany. kiefer@uke.uni-hamburg.de
Wiedemann
K
K
D000437:Alcoholism / Q000503:physiopathology* / Q000534:rehabilitation; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000502:physiology; D003346:Corticotropin-Releasing Hormone / Q000097:blood; D000431:Ethanol / Q000009:adverse effects; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000503:physiopathology*; D020738:Leptin / Q000502:physiology; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000503:physiopathology*; D012008:Recurrence; D013223:Statistics as Topic; D013375:Substance Withdrawal Syndrome / Q000503:physiopathology; D001615:beta-Endorphin / Q000502:physiology
D020738:Leptin; D000431:Ethanol; D001615:beta-Endorphin; D009320:Atrial Natriuretic Factor; D003346:Corticotropin-Releasing Hormone