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Fat mass and fat distribution are associated with low back pain intensity and disability: results from a cohort study

updated

Tags: etiology, classics, back pain, inflam-sys, pro, pain problems, spine

Two articles on PainSci cite Hussain 2017: (1) Complete Guide to Low Back Pain(2) Chronic, Subtle, Systemic Inflammation

PainSci notes on Hussain 2017:

This important paper shows evidence of the metabolic roots of back pain, and perhaps other kinds of chronic pain as well. The majority (82%) of 5000 Australians reported back pain on a questionnaire, and in 27% of them it was bad enough to be disabling. When compared to their fat mass fat distribution — known indicators of metabolic disorders — a clear pattern emerged: back pain intensity and disability go up with measures of fat mass and distribution. This data does not suggest that weight is a “mechanical” problem — greater weight causing greater stress on spinal joints. Instead, it suggests that “systemic metabolic factors associated with adiposity play a major role in the pathogenesis of LBP.” The weight isn’t the problem, but the biochemistry of being out of shape.

This is a particularly excellent example of what I mean when I argue that we need to look beyond trivial physical stresses and biomechanical factors to the messy “wet” factors in chronic pain, the things that make us more vulnerable to painvulnerable

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

BACKGROUND: Determining the association between body composition and low back pain (LBP) will improve our understanding of the mechanisms by which obesity affects LBP, and inform novel approaches to managing LBP. The aim of this study was to examine the relationship between body composition and LBP intensity and disability.

METHODS: A total of 5058 participants (44% men) of the Australian Diabetes, Obesity and Lifestyle Study were assessed for LBP intensity and disability using the Chronic Pain Grade Questionnaire (2013-2014). Body mass index (BMI) and waist circumference were directly obtained. Fat mass and percentage fat were estimated from bioelectrical impedance analysis at study inception (1999-2000).

RESULTS: Eighty-two percent of participants reported LBP, of whom 27% also reported LBP disability. BMI, waist circumference, percent fat, and fat mass were each positively associated with LBP intensity and disability at 12 years after adjustment for potential confounders. LBP intensity and disability showed significant dose-responses to sex-specific quartiles of BMI, waist circumference, percent fat and fat mass. For example, the adjusted OR for LBP intensity in women increased with increasing fat mass quartiles [Q1: 1, Q2: 1.05 (95%CI 0.84-1.32); Q3: 1.25 (1.00-1.57); and Q4: 1.78 (1.42-2.24); p < 0.001].

CONCLUSIONS: Fat mass and distribution are associated with LBP intensity and disability, suggesting systemic metabolic factors associated with adiposity play a major role in the pathogenesis of LBP. Clarifying the mechanisms will facilitate developing novel preventive and therapeutic approaches for LBP.

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