Beer Flavor Provokes Striatal Dopamine Release in Male Drinkers: Mediation by Family History of Alcoholism

• Published in: Neuropsychopharmacology (New York, N.Y.) Vol. 38; no. 9; pp. 1617 - 1624
• Main Authors: Oberlin, Brandon G, Dzemidzic, Mario, Tran, Stella M, Soeurt, Christina M, Albrecht, Daniel S, Yoder, Karmen K, Kareken, David A
• Format: Journal Article
• Language: English
• Published: England Nature Publishing Group 01.08.2013
• Subjects: Adult; Alcohol use; Alcoholism; Alcoholism - genetics; Alcoholism - psychology; Beer; Behavior, Addictive - metabolism; Behavior, Addictive - psychology; Brain; Conditioning, Classical; Corpus Striatum - metabolism; Cues; Dopamine; Dopamine - metabolism; Dopamine Antagonists; Ethanol; Family Health; Functional Neuroimaging; Genetic Predisposition to Disease - genetics; Humans; Intoxication; Male; Medicine; Neurosciences; Original; Raclopride; Tomography; Indiana; United States > US; Indianapolis Indiana
• ISSN: 0893-133X; 1740-634X; 1740-634X
• DOI: 10.1038/npp.2013.91

Striatal dopamine (DA) is increased by virtually all drugs of abuse, including alcohol. However, drug-associated cues are also known to provoke striatal DA transmission- a phenomenon linked to the motivated behaviors associated with addiction. To our knowledge, no one has tested if alcohol's classically conditioned flavor cues, in the absence of a significant pharmacologic effect, are capable of eliciting striatal DA release in humans. Employing positron emission tomography (PET), we hypothesized that beer's flavor alone can reduce the binding potential (BP) of [(11)C]raclopride (RAC; a reflection of striatal DA release) in the ventral striatum, relative to an appetitive flavor control. Forty-nine men, ranging from social to heavy drinking, mean age 25, with a varied family history of alcoholism underwent two [(11)C]RAC PET scans: one while tasting beer, and one while tasting Gatorade. Relative to the control flavor of Gatorade, beer flavor significantly increased self-reported desire to drink, and reduced [(11)C]RAC BP, indicating that the alcohol-associated flavor cues induced DA release. BP reductions were strongest in subjects with first-degree alcoholic relatives. These results demonstrate that alcohol-conditioned flavor cues can provoke ventral striatal DA release, absent significant pharmacologic effects, and that the response is strongest in subjects with a greater genetic risk for alcoholism. Striatal DA responses to salient alcohol cues may thus be an inherited risk factor for alcoholism.