• Ashraf El-Metwally, Marja Mikkelsson, Minna Ståhl, Gary J Macfarlane, Gareth T Jones, Lea Pulkkinen, Richard J Rose, and Jaakko Kaprio.
• Aberdeen Pain Research Collaboration (Epidemiology Group), Department of Public Health, University of Aberdeen, School of Medicine, Polwarth Building, Foresterhill Aberdeen, AB25 2ZD, UK. a.el-metwally@abdn.ac.uk
• Eur Spine J. 2008 Apr 1;17(4):502-8.

AbstractAggregation of low back symptoms in families of children with low back pain (LBP) has been described. However, this may be due to genetic factors or common exposure to environmental factors. The aim of this study was to evaluate the relative contribution of genetic and environmental factors to childhood LBP by comparing the pairwise similarity of LBP in pairs of monozygotic (MZ) and dizygotic (DZ) twin children. Data was collected from 1995 to 1998 from a national sample of Finnish 11-year-old twins born between 1984 and 1987. This study sample constituted of 1,790 twin pairs: 610 MZ pairs, 598 same-sex DZ pairs, 582 opposite-sex DZ pairs. LBP pain was determined by using a validated pain questionnaire designed to assess musculoskeletal pains during the preceding 3 months. The outcome measure, LBP, was considered in three categories: none, once a month and at least once a week. Twin similarity in the report of LBP was quantified by correlations. Variance components for genetic and environmental factors were estimated by using biometric structural equation modelling techniques. The prevalence of LBP at least once a month was 15.7%, and at least once a week was 6.6%. The prevalence of frequent LBP in boys was significantly higher than that in girls (P = 0.04). In both genders, there were no differences in LBP reporting by zygosity (P > 0.2). There were no statistically significant differences between polychoric correlations in male MZ and DZ pairs and between polychoric correlations in female MZ and DZ pairs, suggesting little genetic influence. Results obtained from the best-fitting genetic model suggests that, of the total variance in LBP, 41% (95% CI 34-48) could be attributed to shared environmental factors within families; and 59% (52-66) to unique (unshared) environmental factors. Our results suggest that genetic factors play, at most, a minor role in LBP in children; instead, symptoms seem to be related to a mixture of shared and unshared environmental factors. This study underscore the need for further high-quality research, preferably prospective studies, to identify important modifiable risk factors in order to guide interventions that may prevent LBP in childhood.

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