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The Statesman


    BNL Scientists Explore Food-Addiction Link

    Researchers at the U.S. Department of Energy’#146;s Brookhaven National Laboratory(BNL) have found that the mere display of food is associated with a significantelevation in brain dopamine, a neurotransmitter associated with feelings ofpleasure and reward.

    This activation of the brain’#146;s dopamine motivation circuits is distinctfrom the role the molecule plays when people actually eat, and may be similarto what addicts experience when they crave drugs.

    ‘Eating is a highly reinforcing behavior, just like taking illicit drugs,’said psychiatrist Nora Volkow, the study’#146;s lead investigator.

    ‘But this is the first time anyone has shown that the dopamine systemcan be triggered by food when there is no pleasure associated with it sincethe subjects don’#146;t eat the food.’ Volkow added. ‘This providesus with new clues about the mechanisms that lead people to eat other than justfor the pleasure of eating, and in this respect may help us understand why somepeople overeat.’

    Brookhaven scientists have done extensive research showing that addictive drugsincrease the levels of dopamine in the brain, and that addicts have fewer dopaminereceptors than non-addicts.

    Last year, in an effort to understand the relationship of the dopamine systemto obesity, researchers found that obese individuals also had fewer dopaminereceptors than normal control subjects.

    In the new study, the scientists investigated the role of dopamine in foodintake in healthy, non-obese individuals. The researchers used positron emissiontomography (PET), a brain-scanning technique, to measure dopamine levels inten food-deprived volunteers.

    Each volunteer was given an injection containing a radiotracer, which is aradioactive chemical ‘tag’ designed to bind to dopamine receptorsin the brain. Thus, the investigators were able to estimate the concentrationof dopamine in the brain.

    Study subjects’#146; brains were scanned four times over a two-day period,with and without food stimulation, paired with and without an oral dose of methylphenidate.

    Methylphenidate (Ritalin) is known to block the reabsorption of dopamine intonerve cells. The researchers wanted to see if it would amplify any subtle changesin dopamine levels.

    For food stimulation, the volunteers were presented with foods they had previouslyreported as their favorites. As a control, during scans when food stimulationwas not used, subjects were asked to describe in as much detail as possibletheir family genealogy.

    Study participants were also instructed to describe, on a scale of one to ten,whether they felt hungry or desired food prior to food stimulation and thenat five-minute intervals for a total of forty minutes.

    The researchers found that food stimulation in combination with oral methylphenidateproduced a significant increase in extra-cellular (outside of cells) dopaminein the dorsal striatum.

    There was also a correlation between the increase in dopamine triggered byfood stimulation and methylphenidate and the changes in self-reports of ‘hunger’and ‘desire for food.’

    ‘This suggests the dopamine increases during the food/methylphenidatecondition reflect the responses to food stimulation and not the isolated effectsof methylphenidate,’ Volkow said.

    The study demonstrates that methylphenidate, when used at low doses, amplifiesweak dopamine signals. It also shows, for the first time, that the dopaminesystem in the dorsal striatum plays a role in food motivation in the human brain.

    This relationship was not observed in the ventral striatum, which includesthe nucleus accumbens, the area of the brain thought to be responsible for foodreward.

    ‘We and others previously thought the nucleus accumbens was the primarybrain region associated with regulating food intake by modulating reward andpleasure while eating,’ said study co-author Gene-Jack Wang. ‘Thesefindings challenge that belief.’

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