tients” reported in the literature (18 ng/mL vs 12 ng/ mL). There is both in vitro and in vivo evidence that vitamin D is a neurotrophic substance and modulates neuromuscular function and neuronal growth and differentiation. Its role in diabetic neuropathic pain is uncertain. Vitamin D insufficiency may potentiate diabetic nerve damage and may impair nociceptor function, resulting in pain at a threshold of serum 25D concentration higher than that in the nondiabetic population. While primary hyperparathyroidism has been associated with nonspecific musculoskeletal symptoms, the improvement of pain in our subjects following vitamin D repletion could not be attributed to a decrease in parathyroid hormone level. There was no evidence of secondary hyperparathyroidism at baseline, and the decrease in parathyroid hormone level following vitamin D repletion was not statistically significant, indicating that the improvement in symptoms was independent of parathyroid status. The definition of vitamin D sufficiency is an ongoing debate in the literature. While vitamin D insufficiency is generally defined as a serum 25D concentration of less than 20 ng/mL, the optimal level of vitamin D most beneficial to bone health is not known. From the point of view of osteoporosis prevention, there is an argument in aiming at a serum 25D concentration of above 24 ng/ mL, since bone resorption markers have been shown to be significantly higher in individuals below this threshold. The mean (SD) serum 25D concentration at 3 months in our study was 30 (5) ng/mL, which correlated with significant pain reduction. Achieving adequate serum 25D concentration ( 24 ng/mL) may not only help to prevent osteoporosis in patients with type 2 diabetes but may also relieve neuropathic pain. Our study was neither blinded nor randomized, resulting in the possibility of treatment bias. However, vitamin D has definite proven benefit in the prevention of osteoporosis, which is prevalent in the diabetic population. Vitamin D has been increasingly recognized for its pleiotropic effect, including improvement in glycemic control. It is also free of adverse effects. Because the treatment of diabetic neuropathic pain is generally unsatisfying for patients and is associated with significant adverse effects, we advocate a trial of vitamin D supplementation in vitamin D–insufficient patients with neuropathic pain. It is unlikely to have any harmful effects and may offer not only pain relief but also beneficial effects on bone health and glycemic control. In conclusion, vitamin D insufficiency is underrecognized and may be a significant contributor to neuropathic pain in type 2 diabetes. Vitamin D supplementation may be an effective “analgesic” in relieving neuropathic pain.