High-dose vitamin D supplementation may help ward off chronic immune-mediated diseases like type 1 diabetes (T1D), Hashimoto’s thyroiditis, inflammatory bowel disease (IBD), and multiple sclerosis (MS), according to a study recently published in the Journal of Clinical Endocrinology & Metabolism.
Previous studies have shown that vitamin D deficiency has been linked to immune-mediated diseases. (We reported on a study in the April 2014 issue that showed vitamin D deficiency was associated with compromised immune function.) However, as researchers led by Andrew T. Chan, MD, MPH, of Massachusetts General Hospital in Boston write, data demonstrating vitamin D’s direct effects on T-cell function are lacking.
The team conducted an ancillary study of 38 individuals with vitamin D deficiency and untreated pre- or early-stage 1 hypertension. The patients were randomized to either low-dose (400 IU daily) or high-dose (4000 IU daily) vitamin D, taken orally for six months. “We measured CD4+ T-cell activation estimated by intracellular ATP release after stimulation of whole blood with plant lectin phytohemagglutinin collected at baseline (pretreatment) and 2-month follow-up,” the authors write.
They found a significant different in ATP level changes between each treatment cohort – treatment with high doses of vitamin D decreased intracellular CD4+ ATP release by 95.5 ng/ml (interquartile range, −219.5 to 105.8), while treatment with low doses decreased intracellular CD4+ ATP release by only 0.5 ng/ml (interquartile range, −69.2 to 148.5). “In a proportional odds model,” Chan and his team write, “high-dose vitamin D3 was more likely than low-dose vitamin D3 to decrease CD4+ ATP release (odds ratio, 3.43; 95% confidence interval, 1.06–1.11).”
The authors conclude that “high-dose vitamin D3 significantly reduced CD4+ T-cell activation compared to low-dose vitamin D3, providing human evidence that vitamin D can influence cell-mediated immunity.”