Effects of high-dose cholecalciferol on serum markers of inflammation and immunity in patients with early chronic kidney disease.
Alvarez. J A JA; Zughaier. S M SM; Law. J J; Hao. L L; Wasse. H H; Ziegler. T R TR; Tangpricha. V V
Key Findings
- High‑dose cholecalciferol lowered serum MCP‑1 after 12 weeks in early CKD patients.
- The MCP‑1 reduction was not maintained after one year of supplementation.
- No significant changes were seen in other inflammatory markers or LL‑37 levels.
- In lab cells, active vitamin D also reduced MCP‑1 secretion when the cells were stimulated.
Practical Outcomes
- For biohackers, a short‑term high‑dose vitamin D regimen may temporarily blunt one inflammatory marker (MCP‑1), but there’s no evidence of lasting benefit or broader immune effects. It suggests that using large intermittent doses of vitamin D for chronic inflammation control is not reliably effective, and regular monitoring would be needed if trying this approach.
Summary
A year‑long study gave people with early kidney disease a high dose of vitamin D (50,000 IU weekly then every other week). After 12 weeks their blood level of the inflammation signal MCP‑1 went down, but the effect faded by the end of the year. Other immune markers, including the peptide LL‑37, didn’t change.
Abstract
Vitamin D has anti-inflammatory and immune-regulating properties. We aimed to determine if high-dose cholecalciferol supplementation for 1 year in subjects with early chronic kidney disease (CKD) improved circulating markers of inflammation and immunity. In this double-blind, randomized, placebo-controlled trial, 46 subjects with early CKD (stages 2 and 3) were supplemented with oral cholecalciferol (50 000 IU weekly for 12 weeks followed by 50 000 IU every other week for 40 weeks) or a matching placebo for 1 year. Serum tumor necrosis factor-α, interleukin-6, monocyte chemoattractant protein-1 (MCP-1), interferon gamma-induced protein-10 and neutrophil gelatinase-associated lipocalin were measured at baseline, 12 weeks and 1 year. Serum cathelicidin (LL-37) was measured at baseline and 12 weeks. An in vitro experiment was performed to investigate the effect of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) treatment on MCP-1 secretion in THP-1 monocytes activated with lipopolysaccharide (LPS) and Pseudomonas aeruginosa. By 12 weeks, serum MCP-1 decreased in the cholecalciferol group (66.2±2.5 to 60.8±2.6 pg/ml, group-by-time interaction P=0.02) but was not different from baseline at 1 year. Other markers of inflammation and immunity did not change. In vitro, LPS- and Pseudomonas-activated monocytes treated with 1,25(OH)2D3 had significantly less MCP-1 secretion compared with untreated cells. High-dose cholecalciferol decreased serum MCP-1 concentrations by 12 weeks in patients with early CKD, although the decrease was not maintained for the remainder of the year. In vitro results confirm an MCP-1-lowering effect of vitamin D. Future studies should determine if vitamin D-mediated reductions in MCP-1 concentrations reflect improved clinical outcomes.
Study Information
pubmed
2013
2013-01-30T00:00:00.000Z
10.1038/ejcn.2012.217
54
47