Pleasure, Dopamine, and Food Intake

Byron's Comments:

If you don't get enough dopamine release giving you pleasure you will keep eating until you do.

Study Title:

Relation Between Obesity and Blunted Striatal Response to Food Is Moderated by TaqIA A1 Allele.

Study Abstract:

The dorsal striatum plays a role in consummatory food reward, and striatal dopamine receptors are reduced in obese individuals, relative to lean individuals, which suggests that the striatum and dopaminergic signaling in the striatum may contribute to the development of obesity. Thus, we tested whether striatal activation in response to food intake is related to current and future increases in body mass and whether these relations are moderated by the presence of the A1 allele of the TaqIA restriction fragment length polymorphism, which is associated with dopamine D2 receptor (DRD2) gene binding in the striatum and compromised striatal dopamine signaling. Cross-sectional and prospective data from two functional magnetic resonance imaging studies support these hypotheses, which implies that individuals may overeat to compensate for a hypofunctioning dorsal striatum, particularly those with genetic polymorphisms thought to attenuate dopamine signaling in this region.

From press release:

Using brain imaging and chocolate milkshakes, scientists have found that women with weakened “reward circuitry” in their brains are at increased risk of weight gain over time and potential obesity. The risk increases even more for women who also have a gene associated with compromised dopamine signaling in the brain.

The results, drawn from two studies using functional magnetic resonance imaging (fMRI) at the University of Oregon’s Lewis Center for Neuroimaging, appear in the Oct. 17 issue of the journal Science. The first-of-its-kind approach unveiled blunted activation in the brain’s dorsal stratium when subjects were given milkshakes, which may reflect less-than-normal dopamine output.

“Although recent findings suggested that obese individuals may experience less pleasure when eating, and therefore eat more to compensate, this is the first prospective evidence for this relationship,” said Eric Stice, lead author and senior researcher at the Oregon Research Institute (ORI) in Eugene. “The evidence of temporal precedence suggests it is a true vulnerability factor that predates obesity onset. In addition, the evidence that this relation is even stronger for individuals at genetic risk for compromised signaling in these brain regions points to an important biological factor that appears to increase risk for obesity onset.”

Stice, who has a courtesy appointment in the UO psychology department, has studied eating disorders and obesity for 18 years. He was joined in the new research by ORI colleague Sonja T.P. Spoor, Cara Bohon, a UO doctoral student in clinical psychology, and Dana M. Small of the John B. Pierce Laboratory in New Haven, Conn., and the Yale University School of Medicine.

Dopamine is the primary neurotransmitter in the brain’s reward pathways. Food intake is associated with dopamine release, while pleasure from eating correlates with the amount of dopamine release. Previous studies have suggested that obese individuals have fewer dopamine receptors in the brain and have to eat more than lean people to be satisfied.

Using fMRI, Stice’s team measured the extent to which the dorsal striatum was activated in response to an individual’s receipt of a taste of chocolate milkshake or a tasteless solution.

One study involved 43 female college students ranging in age from 18 to 22 with a mean body mass index (BMI) of 28.6. The second study looked at 33 adolescent girls, ages 14-18, with a mean BMI of 24.3. Most of the participants were tested for the presence of a genetic variation known as the Taq1A1 allele, which is linked to a lower number of dopamine D2 receptors.

Researchers tracked changes in BMI over a year. Results showed that participants with decreased striatal activation in response to receiving milkshake and those with the A1 allele were more likely to gain weight over time.

“I was quite excited by the study itself, as it is the first prospective study to utilize fMRI and genetic data to predict unhealthy weight gain,” said Bohon, whose doctoral work is done on both the UO campus and the nearby ORI facility. “The findings suggest that certain biological factors may impact one’s risk for weight gain, which is important in order to better understand how we can eventually intervene and prevent obesity.”

Study Information:

E. Stice, S. Spoor, C. Bohon, and D. M. Small.  Relation Between Obesity and Blunted Striatal Response to Food Is Moderated by TaqIA A1 Allele. Science 2008 October 
Oregon Research Institute, 1715 Franklin Boulevard, Eugene, OR 97403, USA.




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