However a new study by Stice and colleague in the latest Science edition has shown that the less number of dopamine receptors is a cause rather than a consequence of obesity. This they did by studying a genetic variation, A1 allele of the TaqIA restriction fragment length polymorphism , that leads to lesser number of dopamine receptors. They found that having this allele increased the risk for obesity and using FMRI they were also able to show that this was mediated by reduced dopamine signaling in the striatum.

Here is the abstract of the study:

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.

Now this should not be news to readers of this blog, because this was exactly what I had proposed in my earlier blog pots. Low number of dopamine receptors leading to lower dopamine rush, leading to overeating and obesity. It is heartening to see the same being confirmed; though we will need more evidence to settle the direction of causality.