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.
18 genetic variants have been identified which appear to be associated with alcohol use disorder and heavy drinking. Of these genes, five were overlapped, eight were associated with heavy consumption and five were linked to an increased risk of AUD. The study concluded that while heavy drinking is a risk factor for alcoholism, it is not a sufficient cause of the disorder.
Contrary to popular belief that brain changes begin to normalize immediately after ceasing alcohol consumption, a new study reveals damage to the brain continues during the first weeks of abstinence.
Administering oxytocin blocks the enhanced motivation for drinking alcohol that fuels alcohol use disorder by blocking GABA signaling in the central nucleus of the amygdala.
Men with alcohol use disorder have diminished brain activity in areas associated with emotional processing, memory and social processing, compared to women with AUD. The findings may lead to gender-specific treatments to help relieve addition to alcohol.
Genome-wide study identifies five novel alcohol use risk loci which can pass on the risk of developing alcohol abuse disorder from parents to children.
Drinking small amounts of alcohol, like one pint of beer or a large glass of wine, significantly impairs our feeling of being in control of our actions. A new study reveals even one beer can lead to overconfidence in driving ability and make us act in inappropriate, potentially dangerous ways. The study begs the question, are current alcohol limits for driving truly safe?
Neuroimaging study reveals teens with more gray matter in the caudate nucleus and left cerebellum were at increased risk of problem alcohol use over time. The findings reinforce the idea that brain structure differences may contribute to both psychiatric and substance use disorders.
For those with a genetic predisposition for alcohol use disorder (AUD), being in a romantic relationship appears to reduce the high risk to succumbing to alcohol abuse. This protective effect is limited to males only, suggesting males with a genetic risk for AUD may benefit more from romantic relationships.
Neural patterns of activity in the medial prefrontal cortex associated with the intention to drink alcohol are influenced by the genetic risk for alcohol use disorder.
Ketamine reduced alcohol intake in male rat models of alcohol use disorder but increased the desire for alcohol in low-consumption females.