Study Evaluates Complex Relationship Between Eating and Chronic Pain Interview with:
Paul Geha, M.D
Assistant Professor of Psychiatry
University of Rochester Medical Center
Rochester, NY 14620

Dr. Geha  What is the background for this study? 

Response: Chronic pain and obesity are interrelated; chronic pain is more common in obese individuals and obese individuals have a higher occurrence of chronic pain conditions such as low-back pain.  The mechanisms behind this association are poorly understood.  In this line of work we are trying to offer an explanation for how chronic pain could lead to obesity. 

We build on two previous facts established in the literature to come up with a new theory. 

First, it is well known that the current obesity epidemic is due to overeating in an environment where highly caloric food is cheap and readily available (e.g., fast food).

Second, our brain imaging research on chronic pain patients established that chronic pain affects the brain motivational pathways (or emotional brain) which are directly involved in feeding decisions, especially the ones that come after satiety.  As such, the emotional brain has been implicated in the decision to overeat on top of satiety. We therefore hypothesized that chronic pain would be associated with disrupted eating behavior that could lead to overeating because of changes in the emotional brain of patients. This is a new approach because the prior thinking posited that obesity and chronic pain are interrelated either because of increased inflammation originating from the increased fat mass or from the fear of movement that patients may have leading to a more sedentary lifestyle. While both theories may be correct, they have never been confirmed.

The current paper builds on a finding we published in PAIN 2014 where we established disrupted eating behavior in patients with chronic low-back pain affecting mainly high-fat foods but not sugary drinks.  In that work we asked patients with long-standing history of chronic low-back pain to sample without consumption pudding with increasing concentration of fat and a sugary drink with increasing concentration of sucrose.  While the sensory experience of the food items was normal in the patients, they reported less pleasure (“liking”) from tasting the fatty pudding but not the sugary drink. On a different session, we brought back the patients and offered them to consume as much as they wanted the pudding that they liked the most during the first testing session. Participants were asked to come hungry.   Chronic back-pain patients showed that their liking and hunger ratings did not predict how much they ate.  Healthy controls showed a linear relationship between liking and hunger ratings and how much they ate. 

In the manuscript we just published in PLOS One we continued this line of work to understand how this disrupted eating behavior sets in as low-back pain develops or subsides.  We wanted to know whether disrupted eating behavior develops in conjunction with chronic pain or because of it.  Hence, we recruited patients with new onset low-back pain (6-12 weeks duration) and tested them in the same way described in our PAIN 2014 paper at baseline and then again at one year as some of them recovered from pain while others became chronic low-back pain because pain persisted at one year follow-up.  In this manuscript we also collected brain images that would allow-us to measure volumes of a key structure in the emotional brain, the nucleus accumbens.  The function of the latter structure is to translate our motivation (e.g., wanting to eat) to actions (e.g. the motor response needed to reach for the food). We wanted to know whether we can link the disrupted eating behavior to measures in the emotional brain. This question was based on our previous finding where we observed that patients at risk of becoming chronic pain or patients already in the chronic phase have a compromised accumbens (i.e. smaller than normal).  What are the main findings?

Response: We found that the relationship of new onset back-pain and chronic-back pain to liking and caloric intake from high fat food to be complex.  At baseline, when the pain was still new, back-pain patients showed decreased liking and disrupted relationship between liking and caloric consumption as we found in the chronic group in the PAIN 2014 work.  However, when we separated the groups by those who persisted in pain at one year, and those who recovered we surprisingly found that this pictured stemmed from the recovering patients and not the patient at risk whose eating behavior was normal.  At one year follow-up the recovered patients started showing signs of normalization of eating behavior but the patients with persistent pain still had a normal eating behavior. A separate cross-sectional sample of patients with chronic low-back pain was also studied here as in PAIN 2014 and showed disrupted eating behavior (i.e., reproduced the previous results).

These results prompted us to conclude that the final picture of disrupted eating behavior sets in after pain becomes chronic, most likely, years down the line. Another interesting finding was that the volume of the compromised nucleus accumbens strongly predicted liking reports of high-fat pudding in the chronic-low back pain sample and in the patients who became chronic after a new bout of low-back pain but not in patients who recovered from back pain or in healthy controls suggesting that the emotional brain becomes a more important player in food perception and caloric ingestion when patients are at risk of or are actually in chronic pain. What should readers take away from your report?

Response: IThese results along with the PAIN 2014 work are the first to examine the complex relationship between eating and chronic pain and provide the first evidence that the perception of pleasure and how pleasure from food relates to satiety are changed in acute and chronic-pain and could explain why chronic pain patients end-up overweight/obese. It has long been suspected that chronic pain patients have altered pleasure perception, but it was not directly measured and tested as such. These results also confirm that chronic pain is also a disease of motivation and hedonic perception and can alter how we perceive pleasurable things in life. What recommendations do you have for future research as a result of this work?

Response: Many questions remain unanswered. This is a relatively small study but quite consistent with our previous results. Nevertheless, these results need to be reproduced and tested in larger samples and other chronic pain conditions, especially ones highly associated with obesity and motivational changes such as fibromyalgia. We also need to study these findings in males and females separately because the sexes have different experiences and different predispositions to chronic pain. Interventions to modulate pleasure perception such as opioid blockers or opioid agonists like commonly used pain killer should be used to study perception of food pleasure in chronic pain patients to understand in better details the molecular mechanisms of these phenomena. This an important question because the emotional brain is rich in opioid receptors and clinical observations confirm the effect of opioid medications on motivation and pleasure. It is also a highly impactful question since prescription opioid pain killer are the main cause of the current opioid epidemic; hence, understanding how pleasure goes awry in chronic pain patients might help us understand the highly addictive effects of prescription opioids.

No disclosures


Yezhe Lin, Ivan De Araujo, Gelsina Stanley, Dana Small, Paul Geha. Chronic pain precedes disrupted eating behavior in low-back pain patients. PLOS ONE, 2022; 17 (2): e0263527 DOI: 10.1371/journal.pone.0263527

The information on is provided for educational purposes only, and is in no way intended to diagnose, cure, or treat any medical or other condition. Always seek the advice of your physician or other qualified health and ask your doctor any questions you may have regarding a medical condition. In addition to all other limitations and disclaimers in this agreement, service provider and its third party providers disclaim any liability or loss in connection with the content provided on this website.

Last Updated on February 17, 2022 by