Vitamin D3

vitamin Verified

Specifically for Multiple Sclerosis

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Why it works for Multiple Sclerosis:

Immunomodulation. Active vitamin D (1,25-dihydroxyvitamin D) binds the vitamin D receptor (VDR) on immune cells and tends to:

tilt T cells away from pro-inflammatory Th1/Th17 phenotypes and toward regulatory T cells (Tregs),
reduce B-cell activation and inflammatory cytokines,
dampen trafficking of immune cells across the blood–brain barrier.
Good overviews: British Journal of Pharmacology review (2020) and Brain Communications review (2022). BPS Publications

Observational links. Low serum 25-hydroxyvitamin D [25(OH)D] is associated with higher MS risk and more MRI activity/relapses; this is consistent across multiple reviews, but association ≠ causation. Frontiers

How to use for Multiple Sclerosis:

Measure a baseline 25(OH)D level.

25(OH)D is the correct test (not 1,25-dihydroxyvitamin D). Many MS clinics monitor to keep levels in an “adequate” range. Cleveland Clinic

Target range.

MS Canada suggests a target between ~50–125 nmol/L (20–50 ng/mL) (some documents emphasize around ≥75 nmol/L/30 ng/mL). mscanada.ca

Maintenance dosing (outside of research protocols).

Common clinic practice: 1,000–4,000 IU/day of vitamin D3, adjusted to maintain target levels; this aligns with American Academy of Neurology summaries and MS center guidance. Cleveland Clinic
The NIH Office of Dietary Supplements notes an upper intake level (UL) of 4,000 IU/day for adults (without specialist supervision). Office of Dietary Supplements

Re-check & adjust.

Recheck 25(OH)D after 3–4 months and titrate dose to stay in range; monitor calcium if higher doses are used or if risk factors for hypercalcemia exist. Clinic factsheet example and NIH ODS provide testing/dose context. Cleveland Clinic+1

High-dose “pulse” regimens are research-grade.

Some trials used 100,000 IU every 2 weeks or ~14,000 IU/day—do not copy these doses on your own; if considered, this must be done under specialist supervision with labs. (Details in trials below.) JAMA Network

Keep standard MS therapy.

Vitamin D is usually an adjunct to DMTs (e.g., interferon-β, glatiramer, etc.). It is not a replacement for approved DMTs per AAN guideline. aan.com

Scientific Evidence for Multiple Sclerosis:

Key trials/reviews

D-Lay MS (JAMA, 2025) – Monotherapy in CIS / early RRMS

100,000 IU cholecalciferol every 2 weeks vs placebo for 24 months (n=303).
Primary outcome (relapse and/or MRI activity): HR 0.66 (95% CI 0.50–0.87), statistically significant; MRI activity and new/CE lesions also favored vitamin D. Clinical relapse alone was not significantly different. Safety similar to placebo.
⇒ Suggests reduced new disease activity early after CIS, but not yet a replacement for standard DMTs. JAMA Network

SOLAR (Neurology) – Add-on to interferon-β-1a

~14,000 IU/day vs placebo for 48 weeks (n≈232). Primary endpoint (NEDA-3) not met; some MRI outcomes favored vitamin D. American Academy of Neurology

CHOLINE (Neurology: Neuroimmunology & Neuroinflammation) – Add-on to interferon-β-1a

100,000 IU every other week for 96 weeks (n=129). Primary endpoint (annualized relapse rate) not met; in completers, several MRI/EDSS measures favored vitamin D. Classification of evidence: no significant effect on ARR. American Academy of Neurology

VIDAMS (EClinicalMedicine/The Lancet group) – Add-on to glatiramer acetate

5,000 IU/day vs 600 IU/day; designed to test relapse risk reduction. Results did not show a definitive clinical benefit on relapses. (Useful for dosing context as an add-on.) The Lancet

Systematic reviews/meta-analyses

Cochrane and multiple meta-analyses conclude insufficient evidence that vitamin D reduces relapses/disability, with some trends toward fewer new MRI lesions; more/larger trials needed. Cochrane

Specific Warnings for Multiple Sclerosis:

Vitamin D toxicity (hypervitaminosis D) leads to hypercalcemia and hypercalciuria, which can cause kidney stones, renal impairment, arrhythmias, soft-tissue calcifications, and other symptoms (nausea, vomiting, confusion, polyuria/polydipsia, weakness). Toxicity is typically from excess supplements, not sunlight. The NIH ODS fact sheet details this and reinforces the adult UL of 4,000 IU/day absent close medical monitoring. Office of Dietary Supplements

Drug interactions (from NIH ODS):

Thiazide diuretics ↑ hypercalcemia risk with vitamin D.
Orlistat and cholestyramine can reduce absorption.
Glucocorticoids and some antiepileptics can lower vitamin D status.
Monitor levels and calcium if on these medicines. Office of Dietary Supplements

Conditions needing extra caution:

Granulomatous diseases (e.g., sarcoidosis), primary hyperparathyroidism, renal impairment, and a history of nephrolithiasis—risk of hypercalcemia is higher; specialist oversight required. Clinic guidance flags these groups. Cleveland Clinic

Pregnancy: stay within RDA unless specifically advised; very high doses are not routine in pregnancy. Cleveland Clinic

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General Information (All Ailments)

Note: You are viewing ailment-specific information above. This section shows the general remedy information for all conditions.

What It Is

Vitamin D3 (cholecalciferol) is a fat-soluble vitamin that the human body can make on its own when UV-B sunlight hits the skin. It can also be consumed in food (e.g., egg yolks, oily fish, fortified milk) or taken as a supplement. After entering the body, D3 is converted in the liver to calcidiol (25-hydroxyvitamin D), and then in the kidneys to calcitriol — the hormonally active form of vitamin D. These conversions are tightly regulated because vitamin D behaves less like a “vitamin” and more like a hormone with genomic effects.

How It Works

The active form of vitamin D (calcitriol) binds to the vitamin D receptor (VDR), a nuclear receptor present in many cell types. Once bound, the vitamin D–VDR complex regulates the transcription of genes involved in calcium absorption, bone remodeling, immune signaling, and cellular differentiation. One of its clearest roles is to raise blood calcium by increasing absorption from the gut, reducing loss in the kidneys, and mobilizing calcium from bone when needed. Beyond mineral metabolism, vitamin D also modulates innate and adaptive immunity, reduces inflammatory signaling, and influences the differentiation of many tissues — which is why deficiency affects systems far beyond bones.

Why It’s Important

Vitamin D is essential for maintaining mineral balance and skeletal integrity; deficiency can lead to osteomalacia in adults and rickets in children, and even subclinical deficiency increases the rate of fractures and bone loss. Its immunomodulatory actions appear to reduce the incidence or severity of some infections, especially respiratory ones in deficient individuals. Observationally, low vitamin D status has been associated with higher rates of autoimmune disease, cardiovascular disease, metabolic syndrome, some cancers, depression, and all-cause mortality — though association does not prove that supplementation prevents those outcomes. Nevertheless, population-level insufficiency is common due to indoor lifestyles, sunscreen use, higher latitudes, winter seasons, darker skin pigmentation (which reduces cutaneous synthesis), aging skin, and obesity (which sequesters fat-soluble vitamins in adipose tissue).

Considerations

Vitamin D is fat-soluble, so excess can accumulate and cause toxicity (hypercalcemia, kidney stones, vascular calcification), though this is usually from chronic high-dose supplementation, not sunlight or diet. Personal need varies by latitude, season, skin tone, age, body fat, and kidney/liver function, so a single fixed dose is not universally appropriate. Measuring serum 25-hydroxyvitamin D is the standard way to assess status; targets differ by guideline, but values persistently below ~20 ng/mL are generally considered deficient, whereas most toxicity reports involve sustained levels above ~100 ng/mL. Because vitamin D raises calcium absorption, adequate vitamin K2 and magnesium status may help maintain safer calcium handling, while thiazide use, sarcoidosis, and certain granulomatous diseases can increase sensitivity to vitamin D. In pregnancy and lactation, requirements rise, but dosing should still be individualized rather than assumed.

Helps with these conditions

Vitamin D3 is most effective for general wellness support with emerging research . The effectiveness varies by condition based on clinical evidence and user experiences.

Common Cold 0% effective

Flu 0% effective

COVID-19 0% effective

Depression 0% effective

Eczema 0% effective

Menopause 0% effective

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Common Cold

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Immune regulation & antimicrobial peptides. Vitamin D (the active form 1,25-diOH-D) binds the Vitamin D Receptor in immune cells and epithelial ce...

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