Vitamin D3 (Cholecalciferol) for ALS
Also known as: Cholecalciferol, Calcitriol, 25-hydroxyvitamin D
Vitamin D deficiency is prevalent in ALS and correlates with faster disease progression and worse prognosis.
Mechanism of Action
Vitamin D3 modulates calcium homeostasis in motor neurons, enhances BDNF and GDNF expression through VDR-mediated gene transcription, reduces neuroinflammation via T-regulatory cell promotion, and supports neuromuscular junction integrity.
General mechanism: Secosteroid hormone. VDR-mediated gene transcription affecting calcium, immunity, neurotrophic factors, cell differentiation, and apoptosis.
Current Evidence
Observational studies show ALS patients have significantly lower vitamin D. Supplementation trials show safety and trends toward slower decline. Optimal levels for neuroprotection unclear.
Clinical Status: Observational data strong. Supplementation trials ongoing. Widely available.
Safety Profile
Safe at recommended doses (1000-4000 IU/day). Hypercalcemia at very high doses. Monitor 25(OH)D levels. Rare: kidney stones.
Key Research Questions
- What 25(OH)D level is optimal for ALS neuroprotection?
- Does vitamin D supplementation slow ALS functional decline?