Exploration of the Inter-Relationships Between Obesity, Physical Inactivity, Inflammation, and Low Back Pain

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Abstract

Study Design.

Retrospective analysis wherein 103 patients were considered, and 76 patients were included: 49 were classified as chronic non-specific low back pain (CNSLBP) (Study group) and 27 had identifiable cases of specific chronic low back pain (LBP) (Control group).

Objective.

Elucidate markers of systemic inflammation in patients with CNSLBP.

Summary of Background Data.

Mechanisms of LBP are poorly understood. Pro-inflammatory cytokines are increased in obesity and involved with pain modulation; we previously proposed a theoretical model of their mediating role in LBP.

Methods.

Demographic information was acquired via questionnaire, chart review, and blood test data. Univariate analysis identified factors associated with CNSLBP and markers of systemic inflammation. A receiver operating curve and Youden Index were used to select optimal cut-off points for elevated C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Multivariable logistic regression analysis calculated the adjusted strength of relationship between factors that were proposed in our theoretical model for CNSLBP.

Results.

Unadjusted CRP was significantly correlated with ESR (R = 0.63, P < 0.0001) and body mass index (BMI) (R = 0.38, P = 0.0015). Physically inactive patients had significantly higher CRP (6.1 vs. 1.2, P = 0.0050). ESR was significantly correlated with number of comorbidities (R = 0.34, P = 0.0047), BMI (R = 0.38, P = 0.0014), and age (R = 0.36, P = 0.0026). Physically inactive patients (10.4 vs. 3.6, P = 0.0001) and females (11.2 vs. 6.4, P = 0.0422) had significantly higher ESR. Adjusted analyses indicated significant relationships between physical inactivity and markers of systemic inflammation (adjusted odds ratios for ESR and CRP: 15.9, P = 0.0380; 15.2, P = 0.0272, respectively), and between elevated CRP and CNSLBP (adjusted odds ratio: 8.0, P = 0.0126).

Conclusion.

Systemic inflammation may act as a mediator for physical inactivity and obesity in the pathogenesis of CNSLBP.

Conclusion.

Level of Evidence: 2

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