PainRelief.com Interview with:
Paul Geha, M.D
Assistant Professor of Psychiatry
University of Rochester Medical Center
Rochester, NY 14620

PainRelief.com:  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).