Vitamin D3

vitamin Verified

Specifically for Hashimoto's Thyroiditis

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Why it works for Hashimoto's Thyroiditis:

Immune modulation: Vitamin D receptors are present on many immune cells. Active vitamin D can tilt responses away from inflammatory Th17 cells and support regulatory T cells (Tregs), mechanisms relevant to autoimmune thyroid disease. Reviews summarise these pathways and their potential relevance to Hashimoto’s. Office of Dietary Supplements

Association with deficiency: Low vitamin D status is common in Hashimoto’s and correlates in several studies with higher thyroid autoantibodies and disease activity (association ≠ causation). Frontiers

How to use for Hashimoto's Thyroiditis:

1) Check baseline vitamin D status (25-hydroxyvitamin D, 25(OH)D).

The NIH ODS considers ≥50 nmol/L (≥20 ng/mL) generally adequate for bone and overall health; >125 nmol/L (>50 ng/mL) is linked to potential adverse effects. Routine screening in healthy adults is not recommended by several bodies, but checking is reasonable if deficiency is suspected or before high-dose therapy. Office of Dietary Supplements

2) Daily maintenance dosing if not deficient.

For most adults, typical intakes are 600–800 IU/day; the tolerable upper intake level (UL) for adults is 4,000 IU/day unless a clinician directs otherwise. Office of Dietary Supplements

3) Repletion if deficient.

In RCTs of Hashimoto’s with deficiency, researchers commonly used 50,000 IU vitamin D₃ weekly for ~8–12 weeks, then switched to maintenance dosing; these protocols reduced antibody levels in several trials (details below). Such higher doses should be supervised and followed by retesting. Semantic Scholar

4) Coordination with levothyroxine (if you take it).

Vitamin D itself doesn’t meaningfully interfere with levothyroxine, but many vitamin D products come with calcium—and calcium/iron do block levothyroxine absorption. Take levothyroxine on an empty stomach and separate it from calcium/iron-containing products by ~4 hours. Drugs.com

5) Monitoring.

If you replete deficiency, most clinicians recheck 25(OH)D (and calcium) after ~8–12 weeks; in Hashimoto’s research, some teams also track anti-TPO/anti-TG and routine thyroid labs (TSH, FT4). Follow your treating clinician’s plan. Office of Dietary Supplements

Scientific Evidence for Hashimoto's Thyroiditis:

Meta-analyses / systematic reviews

RCT meta-analysis (2021): Vitamin D supplementation reduced anti-TPO and anti-TG titers in Hashimoto’s compared with control; effects on thyroid hormones were less consistent. SAGE Journals
Narrative/systematic syntheses (2023–2024): Reviews of supplements in Hashimoto’s (including vitamin D) report antibody reductions in multiple trials, while emphasizing study heterogeneity and the adjunctive—not curative—role of vitamin D. Frontiers

Randomized and controlled trials (examples)

Iran RCT (double-blind, placebo-controlled): Vitamin D-deficient Hashimoto’s patients received 50,000 IU/week for 8–12 weeks; anti-TPO fell significantly vs placebo. Semantic Scholar
China RCT (2023): Prospective randomized controlled trial reported improvements in thyroid autoimmunity markers and hormones after vitamin D supplementation. e-century.us
Immunologic RCT (2019): Double-blind trial in women with Hashimoto’s showed vitamin D altered CD4⁺ T-cell subsets (supporting Treg/Th17 modulation). Nature

Recent umbrella review focused on general disease prevention

The Endocrine Society’s 2024 guideline addresses vitamin D for prevention in various populations (not Hashimoto’s-specific) and does not recommend broad high-dose use in replete adults, underscoring the need for targeted supplementation. OUP Academic

Specific Warnings for Hashimoto's Thyroiditis:

Toxicity / hypercalcemia: Excess vitamin D can cause hypercalcemia, hypercalciuria, kidney injury, arrhythmias; toxicity usually occurs with supplement overuse. High serum 25(OH)D levels (typically >150 ng/mL [>375 nmol/L]) are seen in toxicity. Do not exceed 4,000 IU/day long-term without medical supervision. Office of Dietary Supplements

Medication interactions:

Thiazide diuretics increase hypercalcemia risk when combined with vitamin D; digoxin/cardiac glycosides risk is higher with concurrent calcium + vitamin D; orlistat and bile-acid sequestrants can reduce absorption; enzyme-inducing anticonvulsants and corticosteroids can lower vitamin D status. Discuss with your clinician/pharmacist. gpnotebook.com
Levothyroxine: No direct interaction with vitamin D, but separate from calcium/iron to protect thyroid pill absorption. Drugs.com

Kidney stones / calcium supplements: Combined high calcium and vitamin D can increase stone risk in some settings; monitor calcium if you’re on high-dose vitamin D or have stone history. Office of Dietary Supplements

Not a cure for Hashimoto’s: Even with antibody reductions, vitamin D hasn’t been shown to reverse autoimmune thyroiditis or eliminate the need for thyroid hormone when hypothyroid. Keep standard care in place and adjust only with your clinician. thyroid.org

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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

0% effective

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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