More on brain changes in obesity:
An April 2011 Nature article by French researchers demonstrated that diet-induced obesity in miniature pigs leads to decreased activation of the prefrontal cortex, a brain region used for “inhibition of inappropriate behavior, satiety, and meal termination.” The brain activation was determined by regional blood flow as measured by SPECT imaging.
Like the pigs, obese men also show reduced activation of their prefrontal cortex, and it’s not known whether these brain changes cause obesity, or obesity causes the brain changes.
Either way, less neural activation of this brain region may at least partly explain why overweight people find it hard to put the fork down.
This paper concludes that “reduced activation of prefrontal cortex observed in obese humans is probably an acquired feature of obesity since it is also found in minipigs with a diet-induced obesity” (emphasis added).
If diet-induced obesity indeed causes reduced prefrontal cortex activation, then this may lead to a vicious cycle: one’s diet causes weight gain, which diminishes one’s brain signaling to stop eating, leading to more food intake and weight gain, causing further reduced brain signaling, and so forth.
Here’s the abstract:
Compared to lean subjects, obese men have less activation in the dorsolateral prefrontal cortex, a brain area implicated in the inhibition of inappropriate behavior, satiety, and meal termination. Whether this deficit precedes weight gain or is an acquired feature of obesity remains unknown. An adult animal model of obesity may provide insight to this question since brain imaging can be performed in lean vs. obese conditions in a controlled study. Seven diet-induced obese adult minipigs were compared to nine lean adult minipigs housed in the same conditions. Brain activation after an overnight fasting was mapped in lean and obese subjects by single photon emission computed tomography. Cerebral blood flow, a marker of brain activity, was measured in isoflurane-anesthetized animals after the intravenous injection of 99mTc-HMPAO (750 MBq). Statistical analysis was performed using statistical parametric mapping (SPM) software and cerebral blood flow differences were determined using co-registered T1 magnetic resonance imaging (MRI) and histological atlases. Deactivations were observed in the dorsolateral and anterior prefrontal cortices in obese compared to lean subjects. They were also observed in several other structures, including the ventral tegmental area, the nucleus accumbens, and nucleus pontis. On the contrary, activations were found in four different regions, including the ventral posterior nucleus of the thalamus and middle temporal gyrus. Moreover, the anterior and dorsolateral prefrontal cortices as well as the insular cortex activity was negatively associated with the body weight. We suggested that the reduced activation of prefrontal cortex observed in obese humans is probably an acquired feature of obesity since it is also found in minipigs with a diet-induced obesity.