Is Junk Food Addictive?

Reading time: 4 – 7 minutes

In a recent paper in Nature Neuroscience, two researchers at the Scripps Research Institute in Florida report that obese rats with extended access to what they deemed “palatable food” — bacon, sausage, cheesecake, pound cake, frosting and chocolate — exhibited compulsive like eating behavior, much like rats with extended access to cocaine or heroin [1]. This compulsive eating meant that they continued eating despite negative ramifications, in this case a flash of light signaling an oncoming electric shock administered to their foot. This lack of control over behavior with known negative consequences is a hallmark of both drug addiction and obesity. The investigators found that just like drug addicted rats, these obese rats had fewer striatal (a region of the forebrain) dopamine D2 receptors; this is responsible for the observed dampening of their neural reward responses to the food, which caused them to continue to eat, seeking that elusive high.

Junk food

Previous work by other researchers has suggested that deficits in reward processing may contribute to obesity and that obese people may therefore eat compulsively to compensate [2]. Such deficits are considered essential for the development of substance abuse. However, it was not known if this deficit was a prerequisite for developing obesity, or whether overeating induced the deficit and initiated the cycle.

Scripps researchers Paul Johnson and Paul Kenny tackled the problem by establishing brain stimulation reward thresholds in mice and then splitting them into three groups: rats were given no access, restricted access or extended access to a “cafeteria style” diet known to create obese rats. Only those with extended access became obese, and they exhibited a concomitant deficit in their brain reward function similar to that seen in rats with extended, but not restricted, access to cocaine or heroin.

They next assessed whether the diet reduced dopamine D2 receptors in the striatum, a region of the forebrain activated by stimuli associated with reward. Such a reduction in dopamine D2 receptors is known to contribute to addiction-like reward sensitivity, an increase in reward thresholds causing the affected individual to need more of a given stimulus to experience the same reward. The researchers found that the obese rats with extended access to cafeteria food had fewer dopamine D2 receptors in their striata than other rats. Moreover, these rats exhibited compulsive eating behavior much like the compulsive cocaine abuse observed in rats with extended access to the drug. To prove that the observed decreased number of dopamine D2 receptors was in fact responsible for these effects, Johnson and Kenny artificially reduced the expression of the dopamine D2 receptor gene in a new group of rats. As soon as these rats (engineered to have fewer dopamine D2 receptors) were given extended access to the cafeteria diet, their reward thresholds increased and they continued to eat despite an aversive stimulus.

The authors conclude that in rats, extended access to palatable, high-fat cafeteria food results in overeating, causing decreased levels of dopamine receptors and therefore a decreased responsiveness in brain reward circuitry. This in turn leads to compulsive eating — the rats continued to eat junk food, despite negative ramifications. They researchers conclude by stating that “common hedonic mechanisms may therefore underlie obesity and drug addiction.”

How much can we extrapolate these findings to humans? “The canyons of breakfast cereals and condiments; the freezer cases stacked with ‘home meal replacements’ and bagged platonic peas; the broad expanses of soft drinks and towering cliffs of snacks [3]” we face daily in our supermarkets certainly seems to qualify as extended access to palatable, high fat, energy dense food. Human brain imaging has shown that overconsumption of highly palatable food decreases striatal dopamine D2 receptors, just like drug abuse does. This decrease contributes to reward hyposensitivity in obese people [2]. So when pondering your next treat, watch out: in addition to adding pounds to your waistline, clogging your arteries and rotting your teeth, it may just be addictive.


  1. Johnson and Kenny. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nat Neurosci. 2010 May;13(5):635-41. Epub 2010 Mar 28. DOI: 10.1038/nn.2519
    View abstract
  2. Small et al. Relation between obesity and blunted striatal response to food is moderated by TaqIA A1 allele. Science. 2008 Oct 17;322(5900):449-52.
    View abstract
  3. Michel Pollan. The Omnivore’s Dilemma: A natural History of Four Meals. The Penguin Press, New York 2006
About the Author

Diana Gitig, Ph.D., is a freelance science write based in White Plains, New York. She earned her Ph.D. in Cell Biology and Genetics from Cornell University's Graduate School of Medical Sciences.