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The Spine Blog

Friday, September 11, 2015

Is obesity a risk factor for lumbar spinal stenosis?

The etiology of lumbar degeneration and subsequent lumbar spinal stenosis (LSS) has been widely studied but remains poorly understood. Initial theories focused on environmental exposures such as heavy lifting, mechanical vibration, and smoking. Later twin studies suggested a stronger hereditary component, with environmental factors seemingly playing less of a role.1 Most studies on this topic have focused on lumbar disc degeneration rather than on LSS, though the latter is a more common reason for spinal surgery. With increasing rates of both obesity and lumbar surgery, Dr. Knutsson and his colleagues from Sweden designed a study to evaluate the association between obesity and the development of LSS. Using a government database that enrolled over 300,000 Swedish workers from 1971-1993, they identified about 2,400 cases of LSS, defined by a hospital admission for that diagnosis. About 75% of the patients underwent surgery for LSS. At baseline, all workers had their height and weight measured, and characteristics such as occupation and smoking status were recorded. The LSS patients were classified based on their body mass index (BMI) as underweight (BMI<18.5), normal (18.5-25), overweight (25-30), or obese (>30). After controlling for age, sex, job type, and smoking status, they found that the incidence of LSS was more than twice as high in the obese patients as compared to the normal weight patients. Overweight patients had an approximately 70% increase in their likelihood of developing LSS, while underweight patients had an incidence of LSS 40% lower than the normal weight patients. These data suggested a nearly linear relationship between BMI and the incidence of LSS. The same relationships held true when only the LSS patients who underwent surgery were included in the analysis.


This large database study clearly demonstrates a strong correlation between BMI and the risk of developing LSS. Less clear is whether increasing BMI plays a role in the causal chain leading to LSS or if it is simply a marker for other factors that cause LSS to develop. The authors note that increasing body weight leads to greater loads on the lumbar spine, which could increase the rate of degeneration. They also note that obesity is associated with hormonal factors and other comorbidities that could accelerate the degenerative process. Another possibility is that heavyset people may tend to have congenitally narrower canals than their thin counterparts. Additionally, bigger people may be drawn to more physically demanding work, which could contribute to degenerative changes. Obese patients may also be at increased risk for epidural lipomatosis, which could be classified as LSS in hospital billing systems. None of these hypotheses can be tested with a retrospective database study, and most would be impossible to assess in an experimental model. Like most large database studies, this one generates more questions than it answers. The most practical of these questions is “Does avoiding obesity decrease the risk of developing LSS?” If that were true, people have yet another health reason to avoid gaining weight in adulthood (not that we need anymore).


Please read Dr. Knutsson’s article in the September 15 issue. Does this article change how you view risk factors for developing LSS? Let us know by leaving a comment on The Spine Blog.


Adam Pearson, MD, MS
Associate Web Editor





1.            Battie MC, Videman T, Parent E. Lumbar disc degeneration: epidemiology and genetic influences. Spine (Phila Pa 1976) 2004;29:2679-90.