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Purpose: To investigate the relationship between different measures of obesity and chronic low back pain (LBP) using a within-pair twin case-control design that adjusts for genetics and early shared environment.Methods: A cross-sectional association between lifetime prevalence of chronic LBP and different measures of obesity (body mass index-BMI; percent body fat; waist circumference; waist-hip ratio) was investigated in 1128 female twins in three stages: (i) total sample analysis; (ii) within-pair case-control analysis for monozygotic (MZ) and dizygotic (DZ) twins together; (iii) within-pair case-control analysis separated by DZ and MZ. Odds ratios (OR) and 95% confidence intervals (CI) were calculated.Results: BMI (OR 1.12; 95% CI 1.02-1.26) and percent body fat (OR 1.15; 95% CI 1.01-1.32) were weakly associated with lifetime prevalence of chronic LBP in the total sample analysis but were absent when shared environment and genetic factors were adjusted for using the within-pair case-control analysis. Greater waist-hip ratios were associated with smaller prevalence estimates of chronic LBP in the within-pair case-control analysis with both MZ and DZ twins (OR 0.67; 95% CI 0.47-0.94). However, this association did not remain after the full adjustment for genetic factors in the MZ within-pair case-control analysis.Conclusions: BMI, percent of fat mass and greater depositions of fat and mass around the hips are associated with increases in chronic LBP prevalence in women but these associations are small and appear to be confounded by the effects of genetics and early shared environment. Therefore, our results do not support a causal direct relationship between obesity and chronic LBP. [ABSTRACT FROM AUTHOR]

Background Context: Obesity is commonly investigated as a potential risk factor for low back pain (LBP); however, current evidence remains unclear. Limitations in previous studies may explain the inconsistent results in the field, such as the use of a cross sectional design, limitations in the measures used to assess obesity (eg, body mass index-BMI), and poor adjustment for confounders (eg, genetics and physical activity).Purpose and Design: To better understand the effects of obesity on LBP, our aim was to investigate in a prospective cohort whether obesity-related measures increase the risk of chronic LBP outcomes using a longitudinal design. We assessed obesity through measures that consider the magnitude as well as the distribution of body fat mass. A within-pair twin case-control analysis was used to control for the possible effects of genetic and early shared environmental factors on the obesity-LBP relationship.Patient Sample and Outcome Measures: Data were obtained from the Murcia Twin Registry in Spain. Participants were 1,098 twins, aged 43 to 71 years, who did not report chronic LBP at baseline. Follow-up data on chronic LBP (>6 months), activity-limiting LBP, and care-seeking for LBP were collected after 2 to 4 years.Risk Factors: The risk factors were BMI, percentage of fat mass, waist circumference, and waist-to-hip ratio.Methods: Sequential analyses were performed using logistic regression controlling for familial confounding: (1) total sample analysis (twins analyzed as independent individuals); (2) within-pair twin case-control analyses (all complete twin pairs discordant for LBP at follow-up); and within-pair twin case-control analyses separated for (3) dizygotic and (4) monozygotic twins.Results: No increase in the risk of chronic LBP was found for any of the obesity-related measures: BMI (men/women, odds ratio [OR]: 0.99; 95 % confidence interval [CI]: 0.86-1.14), % fat mass (women, OR: 0.87; 95% CI: 0.66-1.14), waist circumference (women, OR: 0.98; 95% CI: 0.74-1.30), and waist-to-hip ratio (women, OR: 1.05; 95% CI: 0.81-1.36). Similar results were found for activity-limiting LBP and care-seeking due to LBP. After the adjustment for genetics and early environmental factors shared by twins, the non-significant results remained unchanged.Conclusions: After 2 to 4 years, obesity-related measures did not increase the risk of developing chronic LBP or care-seeking for LBP with or without adjustment for familial factors such as genetics in Spanish adults. [ABSTRACT FROM AUTHOR]

Background: The relationship between sedentary lifestyle and low back pain (LBP) remains unclear and previous research has not accounted for genetic and early environmental factors.Purpose: Our aim was to investigate if sedentary behavior is associated with the lifetime prevalence of persistent LBP and the risk of developing persistent LBP, care-seeking due to LBP, and activity limiting LBP when genetics and early environmental factors are accounted for.Study Design: Both cross-sectional and longitudinal designs with a within-pair twin case-control were implemented.Patient Sample: There were 2,148 twins included in the cross-sectional analysis whereas 1,098 twins free of persistent LBP at baseline were included in the longitudinal analysis.Outcome Measures: Sedentary behavior was the explanatory variable. Lifetime prevalence of LBP was the outcome variable in the cross-sectional analysis. The incidence of persistent LBP, care-seeking due to LBP, and activity limiting LBP were the outcome variables for the longitudinal analysis.Methods: This observational study was supported by a grant in 2012. No competing interests were declared.Results: In the cross-sectional analysis, sedentary behavior was slightly associated with an increased prevalence of persistent LBP in females but not in males. This association was not apparent when genetics and early environmental factors were accounted for. We acknowledge that the small sample included in the co-twin analyses have yielded wide confidence intervals, and that caution should be exercised when interpreting and an association may not be ruled out. In the longitudinal analysis, sedentary behavior did not significantly increase the risk of persistent LBP, care-seeking due to LBP, or activity limiting LBP.Conclusions: Sedentary behavior is associated with concurrent LBP. However, this association is weak; it only appears in females and decreases when accounting for genetics. Future studies using a twin design with larger samples should be conducted to further test these findings. [ABSTRACT FROM AUTHOR]