Amabile Borges Dario1, Manuela Loureiro Ferreira2, Kathryn Refshauge3, Alejandro Luque-Suarez4, Juan Ramon Ordoñana5, Paulo Henrique Ferreira3. 1. Discipline of Physiotherapy, Faculty of Health Sciences, University of Sydney, PO Box 170, Lidcombe, Sydney 1825, Australia. Electronic address: adar3900@sydney.edu.au. 2. The George Institute for Global Health, Sydney Medical School, University of Sydney, PO Box M201, Missenden Rd, NSW 2050, Australia; Institute of Bone and Joint Research, The Kolling Institute, Sydney Medical School, University of Sydney, Reserve Road, St Leonards, NSW 2605, Australia. 3. Discipline of Physiotherapy, Faculty of Health Sciences, University of Sydney, PO Box 170, Lidcombe, Sydney 1825, Australia. 4. Discipline of Physiotherapy, University of Málaga, Avenida Cervantes, 2, 29071 Malaga, Spain. 5. Murcia Twin Registry, Department of Human Anatomy and Psychobiology, University of Murcia, Campus de Espinardo, 30100 Murcia, Spain; IMIB-Arrixaca, HUVA Virgen de la Arrixaca, 30120 Murcia, Spain.
Abstract
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.
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.
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