Summary: A new study reports people who have a family history of alcohol use disorder release more dopamine in the ventral striatum as a response to the expectation of receiving an alcoholic drink than those without a family history of alcoholism.
People with a family history of alcohol use disorder (AUD) release more dopamine in the brain’s main reward center in response to the expectation of alcohol than people diagnosed with the disorder, or healthy people without any family history of AUD, reports a new study in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging.
“This exaggerated reward center stimulation by expectation of alcohol may put the [individuals with family history] at greater risk of alcohol use disorder, and could be a risk factor in itself,” said first author Lawrence Kegeles, MD, PhD, of Columbia University.
The study examined a range of risk for AUD, including 34 healthy participants with no family history of AUD, 16 healthy participants with a family history of the disorder (referred to as the family-history positive, or FHP, group), and 15 participants diagnosed with AUD. Dr. Kegeles and colleagues used PET brain scanning to measure the amount of dopamine release in areas of the brain important for reward and addiction. The participants underwent the brain scans after receiving either an alcohol drink–a cocktail of vodka, tonic, and cranberry–or a placebo drink without the vodka. Although the participants didn’t know the order in which they would receive the drinks, if they received the placebo drink first they were cued into expecting the alcohol drink next.
All three groups had similar dopamine release-levels in response to the alcohol, suggesting that alcohol-induced dopamine release is normal in AUD. However, “we found that the FHP participants had a much more pronounced response to the placebo drink than the other groups, indicating that expectation of alcohol caused the FHP group to release more reward center dopamine,” said Dr. Kegeles. The release of dopamine into the reward center is thought to reinforce alcohol consumption and possibly contribute to risk of AUD.
“This research finding exemplifies how advances in imaging brain chemistry using PET scanning can provide new insights into how differences in brain function in people with a family history of alcoholism can explain their own potential for addiction,” said Cameron Carter, MD, Editor of Biological Psychiatry: Cognitive Neuroscience and Neuroimaging.
The study did not follow the participants to determine whether the exaggerated dopamine response actually predicted development of AUD at a higher rate, so more studies will be needed to determine if this abnormality really does increase risk of the disorder.
Source: Rhiannon Bugno – Elsevier
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Original Research: Abstract for “Enhanced Striatal Dopamine Release to Expectation of Alcohol: A Potential Risk Factor for Alcohol Use Disorder” by Lawrence S. Kegeles, Guillermo Horga, Rassil Ghazzaoui, Rachel Rosengard, Najate Ojeil, Xiaoyan Xu, Mark Slifstein, Ismene Petrakis, Stephanie S. O’Malley, John H. Krystal, and Anissa Abi-Dargham in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging. Published April 20 2018.
Enhanced Striatal Dopamine Release to Expectation of Alcohol: A Potential Risk Factor for Alcohol Use Disorder
We used positron emission tomography imaging with [11C]raclopride to examine the effects of consumption of alcohol or placebo beverage by participants with alcohol use disorder (AUD) compared with healthy participants with and without family history of AUD. We sought to assess dopamine release following alcohol exposure in relation to AUD risk.
Three groups were enrolled: participants with AUD (n = 15) and healthy participants with family history negative (n = 34) or positive (n = 16) for AUD. Participants consumed a placebo (n = 65) or alcohol (n = 63) beverage in counterbalanced order before positron emission tomography scanning (128 scans). Binding potential (BPND) in the two drink conditions and the percent change in BPND between conditions were evaluated across striatal subregions. Subjective effects of beverage consumption were rated. Effects of group, drink order, and sex were evaluated.
Alcohol resulted in greater dopamine release than did placebo in the ventral striatum (p < .001). There were no main effects of group, drink order, or sex on ventral striatum BPND or percent change in BPND. However, there was a drink order-by-group interaction (p = .02) whereby family history–positive participants who received placebo first had both lower placebo BPND and less difference between placebo and alcohol BPND than all other groups, consistent with expectation of alcohol powerfully evoking dopamine release in this group. Subjective responses showed the same order-by-group interaction.
Hyper-responsivity of the dopaminergic system in family history–positive participants to expectation of alcohol may contribute to the expression of familial risk for AUD.