Mapping the association between back pain and type 2 diabetes: A cross-sectional and longitudinal study of adult Spanish twins

Abstract

BackgroundBack pain and type 2 diabetes often co-occur, resulting in greater impact on people’s health and complexity in their care. Plausible causal mechanisms for this association have been proposed, yet the nature of the link remains unclear. We therefore explored the direction of the association between type 2 diabetes and chronic back pain in twins, controlling for genetics and early environmental confounding.Methods2,096 and 1,098 twins were included in the cross-sectional and longitudinal analyses, respectively. Any or severe (≥ 9) low back pain (LBP), neck pain (NP), and spinal pain (concurrent LBP and NP) and type 2 diabetes were investigated. Sequential analyses were performed using logistic regression. Firstly, twins were analysed unpaired (adjusted age and gender): total sample analyses. Then, to control for genetic and shared environmental factors, a co-twin case-control analysis was performed including monozygotic and dizygotic twin pairs discordant for back pain (cross-sectional only).ResultsIn the cross-sectional total sample analyses, type 2 diabetes was associated with chronic spinal pain (OR 1.61; 95%CI 1.12 to 2.31), severe chronic spinal pain (OR 3.33; 95%CI 1.47 to 7.53), chronic NP (OR 1.37; 95%CI 1.01 to 1.85), severe chronic NP (OR 2.28; 95%CI 1.24 to 4.21), and severe chronic LBP (OR 1.63; 95%CI 1.00 to 2.64). After further adjustment for genetic and shared environmental factors, none of the associations remained significant. The longitudinal analyses indicated that the presence of type 2 diabetes did not increase the risk of future back pain, or vice-versa, after two to four years.ConclusionsChronic back pain (spinal pain, NP, or LBP) was associated with the prevalence of type 2 diabetes. Associations are stronger for severe cases of pain. Future research should investigate the temporal relationships between these conditions with longer follow up in twins.

Differential Effect of Long-Term Systemic Exposure of TNFα on Health of the Annulus Fibrosus and Nucleus Pulposus of the Intervertebral Disc

“…Suppression of endogenous TNFα in the context of TNFα overexpression is expected based on published data examining the TNFα concentration of these mice in response to lipopolysaccharide (LPS) stimulation . Increased systemic cytokine concentrations, in particular TNFα, characterize conditions such as obesity and smoking that are implicated in increasing the risk of disc disease–associated LBP . Establishing a severe model of systemic inflammation thus allowed the evaluation of its effect on disc health.…”

“…(18) Increased systemic cytokine concentrations, in particular TNFα, characterize conditions such as obesity and smoking that are implicated in increasing the risk of disc disease-associated LBP. (34)(35)(36)(37) Establishing a severe model of systemic inflammation thus allowed the evaluation of its effect on disc health.…”

Williams Flexion Exercise for Low Back Pain: A Possible Implementation in Rural Areas

“…A Spanish study on twins found a positive correlation between type 2 diabetes mellitus and LBP in their cross-sectional analysis. The study suggested that there might be a common risk factor ascribed to both diseases because the causal relationship only observed when confounding factors are controlled [20].…”

Changes of Metabolic Disorders Associated Peripheral Cytokine/Adipokine Traffic in Non-Obese Chronic Back Patients Responsive to Burst Spinal Cord Stimulation

“…Metabolic disorders such as obesity, diabetes, and cardiovascular disease are suspected to be associated with chronic, low‐grade systemic inflammation. Potential associations between refractory chronic lower back pain of different origins and metabolic disorders such as obesity, diabetes, hypertension, metabolic syndrome, and cardiovascular disease have been investigated in preclinical and human studies resulting in conflicting findings . In particular, the molecular pathomechanisms connecting metabolic disorders, back pain, and co‐existing co‐morbidities are assumed to be related to a disbalanced central brain‐immune communication combined with peripheral inflammation .…”

“…Potential associations between refractory chronic lower back pain of different origins and metabolic disorders such as obesity, diabetes, hypertension, metabolic syndrome, and cardiovascular disease have been investigated in preclinical and human studies resulting in conflicting findings . In particular, the molecular pathomechanisms connecting metabolic disorders, back pain, and co‐existing co‐morbidities are assumed to be related to a disbalanced central brain‐immune communication combined with peripheral inflammation . Based on the complex peripheral interactions that occur between pro‐ and anti‐inflammatory cytokines (interleukin [IL]‐6, IL‐10, and IL‐13 and tumor‐necrosis factor [TNF‐α]) and other mediators such as pro‐ and anti‐obesity biomarkers (leptin [LP], adiponectin [AN], and ghrelin [GH]), other molecules (i.e., biomarkers) are believed to contribute to the development and maintenance of both types of chronic conditions (pain—metabolic disorder) .…”