There was a significant difference in serum concentration of 25 hydroxyvitamin D in patients with LBP in comparison to subjects without LBP. The serum concentration of 25 hydroxyvitamin D was significantly lower in patients with LBP and 42.85% and 22.22% of them had vitamin D deficiency and insufficiency, respectively. However, 14.54% and 27.27% of subjects without LBP showed vitamin D deficiency and insufficiency, respectively. According to the findings, subjects with lower serum 25 hydroxyvitamin D concentration (vitamin D deficiency or insufficiency) were 2.39 times more likely to exhibit LBP than subjects with normal vitamin D status. In a similar study in women with LBP, Hypovitaminosis D (25 hydroxyvitamin D < 40 ng/ml) was found in 49/60 patients with LBP (81%) and 12/20 (60%) of subjects without LBP, with an odds ratio of 2.97 (9). However, Thorneby et al., in a cross-sectional study on individuals with chronic LBP, could not find any significant relationship between vitamin D status and LBP (18). The reason for this variety of findings in studies regarding vitamin D status and LBP could be due to population variations across different societies. In the scientific literature, the Vitamin D status varies in various countries, even in various areas of the same country, in response to diversity in outdoor activity, exposure to the sunlight and dietary habits.
There were significant inverse correlations between weight as well as BMI and serum concentration of 25 hydroxyvitamin D in individuals with LBP. That means higher weight and BMI were associated with lower serum 25 hydroxyvitamin D concentration. Several studies, (19-21) but not all,(22) have suggested lower concentration of serum free 25 hydroxyvitamin D in obesity. Obesity has essential indications for the impression of vitamin D supplementation, and improvements in circulating 25 hydroxyvitamin D concentrations are commonly lower in obese/overweight subjects (23). Effect of diet-induced obesity on biology of fatty tissue may contribute to the obesity-correlated decrease of free 25 hydroxyvitamin D. It has been shown that high-fat diet transcriptionally modifies Cyp2r1, which actively participates in vitamin D3 trapping and latter transformation to 25 hydroxyvitamin D (24). These modifications are related to a reduction of free 25 hydroxyvitamin D in plasma (25).
In the current study, lower serum concentrations of 25 hydroxyvitamin D were associated with higher scores of disability questionnaire. The same pattern of relationship was also found for pain severity. Lower serum concentrations of 25 hydroxyvitamin D were associated with higher scores of LBP in VAS. In favor of findings in the current study, in a retrospective observational study in Turkey by Gokcek et.al. (26) there was an inverse correlation between concentration of 25 hydroxyvitamin D and VAS score in patients with LBP (r = -0.594, P < 0.001). In contrast, in a nested case-control study by Heuch et.al (8), no association was found between 25 hydroxyvitamin D status and risk of chronic LBP (OR per 10 nmol/L 25(OH)D=1.01, 95% CI 0.97 to 1.06). What matters is that the interpretation of the findings of these studies will not be bias-free, regardless of the characteristics of the population studied. The prevalence and severity of vitamin D deficiency is very important in determining the association between the vitamin D status and LBP. In this regard, in the study of Brady et al. (27) on those with 25 hydroxyvitamin D <30 nmol/L, cholecalciferol supplementation led to a significant reduction in back pain disability. It seems that, these relationships are more conspicuous in those populations in which vitamin D deficiency is prevalent.
The exact mechanism linking vitamin D to pain is not completely clarified physiologically. It has been shown that vitamin D is associated with pain feelings through regulation of inflammatory cytokines (28) and modulation of sensory nerves (29). Since there are some receptors of vitamin D present in the central nervous system, there have been theories proposed on relationship between vitamin D and fibromyalgia (30). Vitamin D may also reduce the production of Prostaglandin E2 (PGE2) in fibroblasts which is a crucial factor for pain perception (31).
Limitation
This study had some limitations, however. Firstly, finding representative control participants in the case-control design is not easy. Secondly, we did not determine the dietary intake of vitamin D in the participants. Nevertheless, a smaller quantity vitamin D is acquired from food than from sun exposure. Thirdly, the possibility of reverse confounding is another limitation of this study that should be considered. Severe back pain may limit ones physical activity; reduce one's outdoor activity and sunshine exposure. Fourthly, the sample size was relatively small. Finally, causality cannot be confirmed because of retrospective design, and prospective and interventional studies are required to verify these findings.