Beer’s Taste Alone Can Trigger Desire for Drink

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The latest research shows that even the taste of beer is sufficient to activate the brain‘s pleasure circuits.

“It’s the first drink that gets you drunk,” Alcoholics Anonymous warns its members, reminding alcoholics that even a sip can set off cravings. Now the latest research offers support for this effect, providing evidence that a tiny taste of beer raises dopamine levels in desire-related brain regions, especially in people with a family history of alcoholism.

The study, published in Neuropsychopharmacology, involved 49 male beer drinkers with an average age of 25; , seven were alcoholics and the remainder were either social or heavy drinkers. Twelve had a parent or sibling who had alcoholism.

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For the experiment, led by David Kareken, director of neuropsychology at Indiana University School of Medicine, the participants first received a small dose of a radioactively-labelled compound that occupies dopamine receptors, which are activated by alcohol and can produce feelings of desire and pleasure, depending on their location. The agent allowed researchers to track changes in dopamine levels and locate where dopamine was more or less plentiful as the volunteers reacted to various tastes. While the participants had PET images taken of their brains, they received small spritzes of water, Gatorade or their favorite brand of beer on their tongues. They then rated the taste of the spray on its intensity and pleasantness.

Because the amount of beer consumed was so small, any changes in dopamine levels were not likely due to the alcohol content in the sprays — any variations in the brain chemical could be attributed to expectations and associations linked to the taste of the beverage.  Prior research in both humans and animals showed that dopamine tends to be released from a brain region called the ventral striatum when pleasure is anticipated or expected— so dopamine is often released from this part of the brain before a drug is taken or during sexual desire.

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The research confirmed these findings, showing that simply tasting beer raised dopamine levels in the right side of the ventral striatum.

And not surprisingly, family history made a difference:  people with a family history of alcoholism had a four fold greater dopamine response compared to those without such a history. “[T]hose individuals who had close family members diagnosed for alcoholism showed dopamine increases in response to beer taste, raising the question whether a heightened conditioning, or an unusual ability of conditioned rewards to increase dopamine activity, underlies the development of alcohol (and perhaps other drug) abuse,” said Dai Stephens, professor of psychology at the University of Sussex, in a statement released by the Britain’s Science Media Foundation.  Stephens was not associated with the research.

Interestingly, the alcoholic participants did not show any heightened dopamine response compared to those with a family history of alcoholism. But because the volunteers were only in their 20s, it’s possible that any changes in the sensitivity of the dopamine response due to chronic heavy drinking might not have developed yet— or the number of participants might have been too small to show such changes.

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The findings also don’t establish whether this increased dopamine activation is responsible for generating addictive behavior. “There is a debate as to whether more or less dopamine release corresponds with addiction risk,” the authors write. Some research suggests, for example, that some people may have a reduced response to the pharmacological effects of alcohol, and can drink without suffering the physiological effects that alcohol can have on decision-making and inhibitions.

What the results do suggest, however, is that people with a family history of alcoholism have a greater dopamine response and therefore may harbor a greater desire for alcohol. That may not necessarily lead to problem drinking, and more research will be needed to clarify how dopamine activation and alcoholism are related.