Summary: Brain circuits that drive motivation and pleasure become active when a person experiences pain. New research links these changes to altered eating behavior and helps explain why some people with chronic pain are at greater risk of overeating and weight gain.
Source: University of Rochester
Background
People with chronic pain frequently face challenges with their weight, but the underlying biology connecting pain and eating behavior has been unclear. Researchers at the Del Monte Institute for Neuroscience investigated how pain changes the brain’s response to rewarding foods and whether these changes could explain shifts in food preferences and appetite control.
The team focused on how the brain perceives fat and sugar, using customized gelatin desserts and puddings to vary fat, sugar, and texture while measuring participants’ pleasure ratings and brain activity.
Key findings
The study found that responses to sugary foods were not substantially altered across groups, but fat-rich foods produced notable differences. Among people with acute low-back pain, those who recovered within a year tended to lose pleasure in the fat-rich pudding and showed disrupted satiety signaling—the gut-to-brain signals that tell us we are full. In contrast, patients whose pain persisted at one year did not show the same immediate change in liking for fat.
Chronic low-back pain patients, however, reported that over time high-fat, high-carbohydrate foods such as ice cream and cookies became difficult for them, and brain scans revealed disrupted satiety signaling in this group as well. Importantly, these shifts in food liking were not accompanied by an overall change in caloric intake in the early stages, suggesting that altered food preference rather than decreased activity may contribute to weight gain in some pain patients.
Role of the nucleus accumbens
Structural brain imaging pointed to the nucleus accumbens, a small region known for its role in motivation, decision-making, and hedonic reward, as a key player. Patients who initially changed their eating behavior but later recovered had normal-appearing nucleus accumbens structure. By contrast, patients whose eating behavior remained normal early on but who later developed chronic pain had a smaller nucleus accumbens volume.
The nucleus accumbens volume predicted pleasure ratings for fat-rich foods only in chronic low-back pain patients and in those who transitioned from acute to chronic pain. This pattern suggests the accumbens becomes increasingly important for motivated behavior as pain becomes chronic, and that structural differences in this region may influence who is likely to develop persistent pain and related changes in eating behavior.
Interpretation and implications
Paul Geha, M.D., the study’s lead author, explains that these results point to physiological mechanisms that link chronic pain to altered eating behavior and, potentially, the development of obesity. The findings indicate that obesity in people with chronic pain may not be solely attributable to reduced physical activity; instead, pain-related changes in how the brain processes rewarding food—particularly fat—may shift preferences and disrupt satiety.
Earlier work by the same group also found that a smaller nucleus accumbens can signal higher risk for pain chronification. Together, these studies suggest that structural and functional differences in limbic brain regions could help identify individuals at risk for both persistent pain and maladaptive eating changes.
Study team and funding
Additional authors include Yezhe Lin, Ph.D., and Gelsina Stanley of the University of Rochester; Ivan de Araujo, Ph.D., of Icahn School of Medicine at Mount Sinai; and Dana Small, Ph.D., of Yale University. The research was funded by the National Institute on Drug Abuse.
About this pain research news
Author: Kelsie Smith Hayduk
Source: University of Rochester
Contact: Kelsie Smith Hayduk – University of Rochester
Image: The image is in the public domain
Original Research: Open access. “Chronic pain precedes disrupted eating behavior in low-back pain patients” by Paul Geha et al. PLOS ONE
Abstract
Chronic pain precedes disrupted eating behavior in low-back pain patients
Chronic pain is associated with reduced pleasure and motivation, a constellation of changes that has been linked to alterations in limbic brain circuits and may contribute to higher obesity risk among pain patients. How these behavioral changes emerge in relation to the development of chronic pain has been unclear.
This study examined eating behavior in low-back pain patients before and after some patients transitioned to chronic pain, comparing them with patients whose pain subsided and with healthy controls. The investigators focused on hedonic perception of fat-rich foods and its relationship to nucleus accumbens structure, given that this region is implicated in both hedonic feeding and chronic pain processes.
The results showed that sub-acute back pain patients who recovered and chronic low-back pain patients both exhibited disrupted eating behaviors, while sub-acute patients who remained in pain at follow-up showed intact eating behavior. Neurologically, the link between perceived pleasure from fat-rich food and nucleus accumbens volume was strong only in chronic patients and in those who became chronic after an acute episode, suggesting that accumbens changes are associated with the emergence of disrupted eating once pain chronifies.
The study concludes that disrupted eating behavior arises after pain becomes chronic and is accompanied by structural alterations in the nucleus accumbens, implicating limbic circuitry in the intersection of chronic pain, hedonic feeding, and obesity risk.