Beer Flavor Provokes Striatal Dopamine Release in Male Drinkers: Mediation by Family History of Alcoholism
Neuropsychopharmacology (15 April 2013)
Brandon G Oberlin, et al.
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 [11C]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 [11C]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 [11C]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.