Chronic inflammation accompanies most chronic diseases, and diabetes is no exception
Vitamin D has been shown to play a role in glycaemic control and reducing the risk of diabetes.
Increasing evidence points to its anti-inflammatory effect as the primary mechanism of action. For example, vitamin D has demonstrated (in human and animal studies) to improve insulin sensitivity by inhibiting cytokine-induced apoptosis of beta cells.
Because of mixed results from cross-sectional and clinical trials, however, there is no consensus on the effect of vitamin D supplementation on inflammation in diabetes.
A meta-analysis, published in Nutrition Reviews in 2018, quantified the effect of vitamin D supplementation on biomarkers of inflammation in patients with type 2 diabetes.
A systematic review identified 28 randomised controlled trials of vitamin D supplementation that measured inflammatory markers in patients with type 2 diabetes, and a meta-analysis was conducted on 20 trials (1270 participants).
All studies were small, with sample sizes ranging from 15–118 participants. Vitamin D dosages ranged from 200 IU to 6000 IU per day, or from 50,000 IU to 60,000 IU per week.
Some studies used a single bolus dose of 300,000 IU. Intervention duration ranged from 8 weeks to 12 months, with most lasting 12–24 weeks.
Most studies used placebo as the control, but two used usual care and three used calcium supplementation. Eight studies reported inflammatory markers as primary outcomes, and the rest reported them as secondary outcomes.
When compared with a control, vitamin D supplementation significantly lowered C-Reactive Protein (CRP) levels (standard mean difference [SMD] -0.23; 95% CI, -0.37 to -0.09; p=.002), tumour necrosis factor-alpha (TNF-alpha) levels (SMD -0.49; 95% CI, -0.84 to -0.15; p=.005) and erythrocyte sedimentation rate (ESR) levels (SMD -0.47; 95% CI, -0.89 to -.05; p=.03).
Vitamin D supplementation significantly increased leptin levels (SMD 0.42; 95% CI, 0.04-0.81; p=.03). Vitamin D supplementation did not significantly affect adiponectin, interleukin-6 or E-selectin.
Strengths of this meta-analysis included its inclusion only of randomised controlled trials and its careful methodology.
Weaknesses included the small sample sizes of studies and the fact that none of the studies reported long-term outcomes or whether reduced inflammation translated into decreased morbidity or mortality in type 2 diabetes.
Still, this study concludes that vitamin D supplementation appears to have a beneficial effect on inflammatory markers in type 2 diabetes.