BACKGROUND: The relationships between obesity and both low back pain (LBP) and lumbar disc degeneration (LDD) remain unclear. It is possible that familial factors, including genetics and early environment, affect these relationships. PURPOSE: To investigate the relationship between obesity-related measures (e.g. weight, BMI) and LBP and LDD using twin studies, where the effect of genetics and early environment can be controlled for. STUDY DESIGN: Systematic review with meta-analysis. METHODS: MEDLINE, CINAHL, Scopus, Web of Science and EMBASE databases were searched from the earliest records to August 2014. All cross-sectional and longitudinal observational twin studies identified by the search strategy were considered for inclusion. Two investigators independently assessed eligibility, conducted the quality assessment, and extracted the data. Meta-analyses (fixed or random effects, as appropriate) were used to pool studies' estimates of association. RESULTS: In total, 11 articles met the inclusion criteria. Five studies were included in the LBP analysis and seven in the LDD analysis. For the LBP analysis, pooling of the five studies showed that the risk of having LBP for individuals with the highest levels of BMI or weight was almost twice that of people with a lower BMI (OR 1.8 95% CI 1.6 - 2.0; I2= 0%). A dose-response relationship was also identified. When genetics and the effects of a shared early environment were adjusted for using a within-pair twin case-control analysis, pooling of three studies showed a reduced but statistically positive association between obesity and prevalence of LBP (OR 1.5 95% CI 1.1 - 2.1; I2= 0%). However, the association was further diminished and not significant (OR 1.4 95% CI 0.8 - 2.3; I2= 0%) when pooling included two studies on monozygotic twin pairs only. Seven studies met the inclusion criteria for LDD. When familial factors were not controlled for, body weight was positively associated with LDD in all five cross-sectional studies. Only two cross-sectional studies investigated the relationship between obesity-related measures and LDD accounting for familial factors, and results were conflicting. One longitudinal study in LBP and three longitudinal studies in LDD found no increase in risk in obese individuals, whether or not familial factors were controlled for. CONCLUSIONS: Findings from this review suggest that genetics and early environment are possible mechanisms underlying the relationship between obesity and LBP, however a direct casual link between these conditions appears to be weak. Further longitudinal studies using the twin design are needed to better understand the complex mechanisms underlying the associations between obesity, LBP and LDD.
a1878-1632 (Electronic)