Eating to Live, Living to Eat: Genes May Make Some People More Motivated to Eat, Perhaps Overeat
We knew that.
Here’s a press release from the American Psychological Association:
Newswise — Science has found one likely contributor to the way that some folks eat to live and others live to eat. Researchers at the University at Buffalo, The State University of New York, have found that people with genetically lower dopamine, a neurotransmitter that helps make behaviors and substances more rewarding, find food to be more reinforcing than people without that genotype. In short, they are more motivated to eat and they eat more. . . .
The abstract is after the jump, with the cite to the full paper.
What I found really interesting was a little sentence tucked into the bottom of the press release:
Using overweight men, the group has already found that chemically manipulating dopamine levels alters eating behavior, a finding highly suggestive for pharmaceutical intervention.
Dr. Epstein is a consultant for Kraft Foods, a spinoff from Altria, the cigarette company, so he should have access to really good data.
For my money, I think lorcaserin , which is basically phen-fen without the cardiac problems, is probably going to be first to market — a “Chevy”, not a “Maybach”. This acts on the serotonin receptors to cut appetite (without going to the cardiac receptors, and there is some doubt as to whether the valvopathy originally with Phen-fen was really for real). Lots of other anti-obesity meds in the pipeline, which are probably much more biologically well-reasoned, but, hey, eat less, lose weight. Maybe they should add some dopamine to it.
Food Reinforcement, the Dopamine D2 Receptor Genotype, and Energy
Intake in Obese and Nonobese Humans
Leonard H. Epstein, Jennifer L. Temple, Brad J. Neaderhiser, Robbert J. Salis, Richard W. Erbe, and John J. Leddy University at Buffalo, The State University of New York
The authors measured food reinforcement, polymorphisms of the dopamine D2 receptor (DRD2) and dopamine transporter (DAT1) genes, and laboratory energy intake in 29 obese and 45 nonobese humans 18–40 years old. Food reinforcement was greater in obese than in nonobese individuals, especially in obese individuals with the TaqI A1 allele. Energy intake was greater for individuals high in food reinforcement and greatest in those high in food reinforcement with the TaqI A1 allele. No effect of the DAT1 genotype was observed. These data show that individual differences in food reinforcement may be
important for obesity and that the DRD2 genotype may interact with food reinforcement to influence energy intake.
Keywords: food reinforcement, energy intake, obesity, dopamine, dopamine receptor
Behavioral Neuroscience 2007, Vol. 121, No. 5, 877–886 Copyright 2007 by the American Psychological Association (the link is to the full PDF via Docuticker)
Article: “Food Reinforcement, the Dopamine D2 Receptor Genotype, and Energy Intake in Obese and Nonobese Humans”; Leonard H. Epstein, PhD, Jennifer L. Temple, PhD, Brad. J. Neaderhiser, PhD, Robbert J. Salis, MD, Richard W. Erbe, MD, and John J. Leddy, MD, University at Buffalo, The State University of New York; Behavioral Neuroscience, Vol. 121, No. 5.
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