Differential brain response to a highly palatable drink in chronic low back pain patients.

A mechanistic understanding of the association between chronic pain and obesity is still lacking. One prevailing hypothesis posits that fear of movement, which would exacerbate pain, leads to a sedentary lifestyle, reducing energy expenditure and leading to weight gain. Yet evidence that chronic pain patients move less than pain-free control subjects is at best controversial. Here we test a novel hypothesis that chronic pain patients exhibit altered brain response to food within circuits driving overeating, thereby contributing to weight gain. We measured brain activity in 28 chronic low back pain (CLBP) patients and 31 pain-free healthy control (HC) subjects, matched for age, sex, and body mass index (BMI), during the consumption of a highly palatable, caloric drink with functional MRI (fMRI). The task was designed to engage the reward network, centered around the ventromedial prefrontal cortex, nucleus accumbens, and amygdala, which is often altered in chronic pain patients and implicated in uncontrolled eating. Contrary to prediction, the reward network showed no significant differences between the groups. Instead, patients showed larger activations in regions normally involved in food control tasks and interoception, including the posterior-dorsal insula and primary somatosensory-motor cortex. In contrast, the right angular gyrus, a region engaged when individuals attempt to control food craving, showed reduced activity in patients compared to HC subjects. Taken together, these findings indicate that CLBP alters brain response to palatable foods in circuits that govern control of overeating. This suggests that impaired inhibitory processing, rather than exaggerated reward signaling, may underlie excessive weight gain in chronic pain patients.