title: Electroencephalogram spectral characteristics after alcohol ingestion in Japanese men with aldehyde dehydrogenase-2 genetic variations: comparison with peripheral changes.
abstract: BACKGROUND
  Electroencephalographic (EEG) activity induced by alcohol ingestion may be influenced by individual differences in alcohol metabolism. Specifically, an absence of the low Km isozyme of aldehyde dehydrogenase (ALDH), found in many Asians, may be related to alterations of EEGs.
  
  
  METHODS
  EEG power spectral changes induced by 0.4 ml/kg of alcohol ingestion were compared in two groups of Japanese subjects: NN (ALDH2*1/1, n = 19) and ND (ALDH2*2/1, n = 12). Peripheral changes in heart rate and facial skin temperature were evaluated after the same treatment. Blood ethanol, acetaldehyde, and catecholamine levels were determined to evaluate mediation of the ethanol metabolite, acetaldehyde, and its indirect action on EEGs through the effects on peripheral systems.
  
  
  RESULTS
  As expected, blood acetaldehyde was about 10-fold higher in the ND subjects compared with the NN subjects during the postingestion period. Ethanol produced characteristic EEG changes during and after ingestion. The ND subjects, however, displayed brief periods of decrease in slow alpha immediately after alcohol ingestion and showed no long-term EEG changes. The EEG changes were parallel to peripheral changes.
  
  
  CONCLUSIONS
  The lack of increased EEG power in the ND subjects may be partly mediated by a direct action of the high concentration of acetaldehyde in the central nervous system that penetrates from the peripheral blood. In addition to this direct action of acetaldehyde, an indirect action, such as feedback from peripheral changes, might prevent the characteristic increase in alpha and beta power observed in the NN subjects.
authors.affiliation: Central Laboratories for Key Technology, Kirin Brewery Co., Ltd., Fukuura, Kanazawa, Yokohama, Japan. nfusae@kirin.co.jp
authors.forename: F T
authors.initials: FT
authors.lastname: Nishimura
authors.forename: T
authors.initials: T
authors.lastname: Fukunaga
authors.forename: H
authors.initials: H
authors.lastname: Nishijo
authors.forename: T
authors.initials: T
authors.lastname: Ono
authors.forename: H
authors.initials: H
authors.lastname: Kajiura And
authors.forename: Y
authors.initials: Y
authors.lastname: Yokomukai
mesh_terms: D000079:Acetaldehyde / Q000378:metabolism; D000328:Adult; D000428:Alcohol Drinking / Q000235:genetics / Q000523:psychology*; D000435:Alcoholic Intoxication / Q000523:psychology; D000444:Aldehyde Dehydrogenase / Q000235:genetics*; D000071396:Aldehyde Dehydrogenase, Mitochondrial; D002395:Catecholamines / Q000097:blood; D002492:Central Nervous System Depressants / Q000494:pharmacology*; D004569:Electroencephalography / Q000187:drug effects*; D000431:Ethanol / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D010525:Peripheral Nerves / Q000187:drug effects*; D012881:Skin Temperature / Q000187:drug effects
chemical_list: D002395:Catecholamines; D002492:Central Nervous System Depressants; D000431:Ethanol; C096127:ALDH2 protein, human; D000444:Aldehyde Dehydrogenase; D000071396:Aldehyde Dehydrogenase, Mitochondrial; D000079:Acetaldehyde