Vitamin D and Thyroid: Why Most Hashimoto's Patients Are Deficient (2026)

Between 60% and 80% of Hashimoto's thyroiditis patients are vitamin D deficient. This is not coincidence. Vitamin D is a secosteroid hormone that directly regulates the immune cells driving thyroid autoimmunity — and the standard medical threshold for "normal" (30 ng/mL) is set for bone health, not immune function. The VITAL trial (2022) demonstrated that vitamin D3 supplementation reduced autoimmune disease incidence by 22% over five years, establishing it as the single most cost-effective intervention for autoimmune prevention. Most Hashimoto's patients need significantly more than the RDA of 600 IU per day to reach immune-relevant levels. Discuss all supplementation with your physician before starting.

Vitamin D as an Immune Regulator

Vitamin D is not a vitamin in the traditional sense. It is a secosteroid hormone — synthesized in the skin from cholesterol under UVB radiation, hydroxylated twice (first in the liver to 25-OH vitamin D, then in the kidneys to the active form 1,25-dihydroxyvitamin D), and active throughout virtually every tissue in the body via the vitamin D receptor (VDR).

The VDR is expressed on nearly all immune cells: T cells, B cells, macrophages, dendritic cells, and natural killer cells. Vitamin D is not merely a bone-health nutrient with incidental immune effects. It is a primary immune regulator that happens to also be critical for calcium metabolism.

How Vitamin D Controls Autoimmune Activity

Vitamin D modulates the immune system through several well-characterized mechanisms:

1. Treg promotion. Active vitamin D (1,25(OH)2D) promotes the differentiation and proliferation of FOXP3+ regulatory T cells (Tregs). These are the cells that maintain self-tolerance and suppress autoreactive lymphocytes — the very cells attacking your thyroid in Hashimoto's. When vitamin D is low, Treg numbers and function decline. (Jeffery et al., Journal of Clinical Investigation, 2009)

2. Th17 suppression. Vitamin D directly inhibits the differentiation of Th17 cells, which produce IL-17 — a cytokine central to autoimmune tissue destruction. The Th17/Treg balance is the master switch of autoimmunity: when it tips toward Th17 dominance, autoimmune attacks intensify. Vitamin D pushes the balance back toward Treg dominance. (Joshi et al., Immunity, 2011)

3. Dendritic cell tolerogenesis. Vitamin D promotes a tolerogenic phenotype in dendritic cells — the antigen-presenting cells that decide whether to activate or suppress an immune response. Tolerogenic dendritic cells present self-antigens (like TPO) in a way that induces immune tolerance rather than attack.

4. B cell regulation. Vitamin D inhibits B cell proliferation, immunoglobulin production, and plasma cell differentiation. Since TPO and TgAb antibodies are produced by B cells and plasma cells, this pathway directly affects antibody titers.

5. Cytokine modulation. Vitamin D reduces pro-inflammatory cytokines (IL-6, TNF-alpha, IL-1beta, IFN-gamma) and increases anti-inflammatory IL-10. This shifts the overall immune environment away from chronic inflammation.

These mechanisms are not theoretical. They are demonstrated in human cell studies and clinical trials, and they explain why vitamin D status correlates so strongly with autoimmune disease activity.

The Vitamin D-Thyroid Connection: What the Evidence Shows

Deficiency Prevalence in Hashimoto's

The association between low vitamin D and Hashimoto's is among the most consistent findings in thyroid autoimmunity research.

Tamer et al. (2011, Thyroid) — In a study of 161 Hashimoto's patients versus 162 healthy controls, vitamin D deficiency (below 25 nmol/L) was significantly more prevalent in the Hashimoto's group. Vitamin D levels inversely correlated with TPO antibody titers: the lower the vitamin D, the higher the antibodies.

Kivity et al. (2011, Autoimmunity Reviews) — Examined the relationship between vitamin D deficiency and autoimmune thyroid disease. Found that vitamin D deficiency was significantly more common in patients with autoimmune thyroid disease compared to healthy individuals, and was specifically associated with the presence of antithyroid antibodies and abnormal thyroid function.

Wang et al. (2015, meta-analysis) — Pooled data from multiple studies confirmed that serum 25-OH vitamin D levels are significantly lower in Hashimoto's patients compared to healthy controls, and that vitamin D deficiency increases the risk of Hashimoto's development.

The Inverse Correlation with TPO Antibodies

The relationship between vitamin D and thyroid antibodies is dose-dependent: as vitamin D levels decrease, TPO antibodies tend to increase. This has been observed across multiple populations and study designs.

Several mechanisms explain this correlation:

• Treg decline at low vitamin D levels reduces immune self-tolerance, allowing anti-TPO B cell clones to expand
• Th17 overactivation increases IL-17-driven tissue destruction and antibody stimulation
• VDR polymorphisms (particularly BsmI, TaqI, ApaI, and FokI) that reduce vitamin D receptor function are overrepresented in Hashimoto's populations, suggesting a genetic link between vitamin D signaling and thyroid autoimmune susceptibility (Feng et al., 2013)

This correlation does not prove that supplementing vitamin D will lower TPO antibodies in every patient — but it establishes that vitamin D deficiency is a modifiable risk factor in Hashimoto's progression.

The VITAL Trial: Vitamin D and Autoimmune Disease Prevention [Grade A]

The VITAL trial (Hahn et al., BMJ, 2022) is the most important vitamin D-autoimmune study to date. It enrolled 25,871 adults in a randomized, double-blind, placebo-controlled design over 5.3 years of follow-up — a scale no other vitamin D autoimmune trial approaches.

Key findings:

• Vitamin D3 at 2,000 IU/day reduced confirmed autoimmune disease incidence by 22% (HR 0.78, 95% CI 0.61-0.99, p=0.045)
• The effect strengthened over time: during years 3-5, the reduction was 39%
• Autoimmune diseases prevented included rheumatoid arthritis, polymyalgia rheumatica, autoimmune thyroid disease, psoriasis, and inflammatory bowel disease
• The trial used only 2,000 IU/day — below the dose most functional medicine practitioners recommend for Hashimoto's

The Seasonal Pattern

Hashimoto's patients often report that symptoms worsen in autumn and winter. This is not subjective bias. Vitamin D levels follow a sinusoidal seasonal pattern — peaking in late summer and reaching their nadir in late winter. At higher latitudes, the winter trough can drop levels by 30-50% compared to summer peaks.

Multiple studies have documented that thyroid antibody levels and Hashimoto's symptom scores follow the inverse pattern: highest when vitamin D is lowest. This seasonal correlation supports the causal hypothesis and has a practical implication — winter supplementation may need to be higher than summer doses to maintain stable levels.

How to Read the Evidence Grades

Optimal Vitamin D Levels for Hashimoto's

The Standard vs. Functional Medicine Ranges

The conventional medical threshold for vitamin D sufficiency is 30 ng/mL (75 nmol/L). This was established primarily for bone health — the level needed to prevent rickets and osteomalacia. It was not set for immune function.

For autoimmune thyroid disease, the functional medicine target is 60-80 ng/mL (150-200 nmol/L). This is supported by several lines of evidence:

• Immune cell studies show that VDR-mediated gene transcription (including Treg differentiation and Th17 suppression) does not reach optimal activity until 25-OH vitamin D exceeds 40-60 ng/mL (Prietl et al., Nutrients, 2013)
• Observational data in Hashimoto's populations show that patients with levels above 60 ng/mL have significantly lower TPO antibody titers than those at 30-40 ng/mL
• The Endocrine Society clinical practice guideline (Holick et al., 2011) recommends 40-60 ng/mL as the preferred range, higher than the Institute of Medicine's 30 ng/mL threshold
• Holick 2007 described the vitamin D deficiency pandemic and argued that the RDA of 600 IU/day is insufficient for most adults, particularly those with autoimmune conditions

Why Most Doctors Under-Dose

The RDA for vitamin D is 600 IU/day for adults under 70 (800 IU for those over 70). This was set by the Institute of Medicine in 2010 for bone health in the general population. For a Hashimoto's patient with a baseline level of 18 ng/mL, 600 IU/day will barely move the needle — it might raise levels by 5-8 ng/mL over several months, still leaving the patient well below immune-optimal levels.

The disconnect between the RDA and the dose needed for immune modulation is the primary reason most Hashimoto's patients remain deficient despite "taking vitamin D." They are taking a bone-health dose, not an immune-health dose.

How to Test Vitamin D

The Right Test: 25-OH Vitamin D

The correct test is 25-hydroxyvitamin D (also written as 25(OH)D or calcidiol). This is the circulating storage form with a half-life of approximately 2-3 weeks. It reflects your body's vitamin D status accurately.

Do not test 1,25-dihydroxyvitamin D (calcitriol) as a screening test. This is the active hormonal form, and its levels are tightly regulated by parathyroid hormone. It can be normal or even elevated in vitamin D deficiency because the body compensates by upregulating conversion. Testing 1,25(OH)2D alone will miss deficiency.

When to Test

• Before starting supplementation — establish your baseline
• After 8-12 weeks of loading dose — confirm response
• Every 6 months on maintenance — ensure stability
• Seasonally if variable — some patients need to test in late winter (February-March) when levels are lowest

Interpreting Your Results

For a comprehensive guide to all thyroid labs including vitamin D, see the Hashimoto's optimal lab ranges guide.

The Dosing Protocol [Grade B]

The following protocol is based on clinical practice guidelines, the Endocrine Society recommendations, and the vitamin D dosing literature for autoimmune patients. Evidence grade is B — consistent clinical data and biological plausibility, but no large Hashimoto's-specific RCT at these exact doses.

Loading Phase for Deficiency

For patients with levels below 20 ng/mL (the majority of newly diagnosed Hashimoto's patients who have never supplemented), a loading phase of 10,000 IU D3 daily for 8 weeks is standard. This raises levels rapidly — typically by 30-50 ng/mL over 8 weeks, depending on body composition and absorption.

Some physicians prescribe a single high-dose bolus (50,000 IU weekly). While this achieves repletion, daily dosing is preferred for immune modulation because it maintains more stable circulating levels. The immune system responds to sustained vitamin D availability, not intermittent spikes. (Martineau et al., 2019)

Maintenance Dose

After the loading phase, 4,000-5,000 IU daily is the standard maintenance dose for autoimmune patients targeting 60-80 ng/mL. This is well within the Endocrine Society's recommended upper limit for daily supplementation (10,000 IU/day) and has been used safely in clinical trials lasting up to 5 years (VITAL trial used 2,000 IU with no safety concerns).

D3 vs D2: Why the Form Matters

Vitamin D3 (cholecalciferol) is the preferred form. It is the form produced naturally in human skin and is significantly more effective than D2 (ergocalciferol) at raising and maintaining serum levels.

A 2012 meta-analysis by Tripkovic et al. (American Journal of Clinical Nutrition) found that D3 was approximately 87% more potent than D2 in raising serum 25-OH vitamin D. D2 has a shorter half-life and lower binding affinity for vitamin D-binding protein, meaning it is cleared from circulation faster.

D2 is sometimes prescribed because it is available in high-dose prescription formulations (50,000 IU capsules). If your physician prescribes D2, it works — but D3 achieves the same result at lower doses with better sustained levels.

Essential Cofactors

Vitamin K2 (MK-7)

Vitamin D increases intestinal calcium absorption. Without adequate vitamin K2, that calcium may deposit in arteries and soft tissues rather than being directed to bones. Vitamin K2 activates two critical proteins:

• Osteocalcin — deposits calcium into bone matrix
• Matrix GLA protein — prevents calcium deposition in arterial walls

The MK-7 form (menaquinone-7) is preferred over MK-4 due to its longer half-life (~72 hours vs ~6 hours), providing sustained activity with once-daily dosing.

Dose: 100-200 mcg MK-7 daily. Higher doses (200 mcg) are recommended during the loading phase when vitamin D intake exceeds 5,000 IU/day.

Magnesium

Magnesium is required at multiple steps of vitamin D metabolism:

• Hepatic hydroxylation (vitamin D to 25-OH vitamin D) requires magnesium-dependent enzymes
• Renal hydroxylation (25-OH to active 1,25(OH)2D) requires magnesium
• Vitamin D-binding protein transport depends on adequate magnesium

Magnesium deficiency impairs vitamin D activation. A patient supplementing 5,000 IU of D3 daily but deficient in magnesium may see suboptimal rises in 25-OH levels — the vitamin D cannot be properly metabolized.

Dose: 300-400 mg elemental magnesium daily. Preferred forms: magnesium glycinate (best tolerated, good absorption), magnesium malate, or magnesium threonate. Avoid magnesium oxide (poor bioavailability, primarily laxative effect).

Take magnesium in the evening — it supports sleep quality, which is independently beneficial for Hashimoto's symptom management.

Take Vitamin D with Fat

Vitamin D is fat-soluble. Taking it on an empty stomach significantly reduces absorption. A study by Mulligan and Licata (2010, Journal of Bone and Mineral Research) found that taking vitamin D with the largest meal of the day (typically the highest fat content) increased serum levels by approximately 50% compared to taking it on an empty stomach.

Practical recommendation: take your D3 + K2 with breakfast or lunch, alongside foods containing fat (eggs, avocado, olive oil, nuts, or a meal with cooking oil).

Supplementation Evidence for Hashimoto's

Mazokopakis et al. 2015 — Vitamin D and Hashimoto's Review [Grade B]

Mazokopakis and Kotsiris (2015, Hellenic Journal of Nuclear Medicine) reviewed the evidence for vitamin D supplementation in Hashimoto's thyroiditis specifically. Their analysis concluded:

• Vitamin D deficiency is more prevalent in Hashimoto's patients than the general population
• Supplementation to achieve levels of 40-60 ng/mL is associated with reduced TPO antibody titers
• The recommended approach is to test 25-OH vitamin D, correct deficiency aggressively, and maintain levels in the 40-60 ng/mL range (note: this is their conservative target; many practitioners now target 60-80 ng/mL)
• Vitamin D supplementation should be considered a component of Hashimoto's management alongside thyroid hormone replacement

Chaudhary et al. 2016 — Vitamin D and TPO Antibodies [Grade B]

Chaudhary et al. (2016, Indian Journal of Endocrinology and Metabolism) conducted an interventional study supplementing vitamin D in Hashimoto's patients with documented deficiency. After 3 months of supplementation:

• Serum 25-OH vitamin D levels rose significantly
• TPO antibodies decreased by approximately 20.3% in the supplementation group
• TSH trended downward but did not reach statistical significance in this sample size
• No adverse effects were observed

The 20% TPO antibody reduction is modest compared to selenium's 40-55% in the best trials, which is expected: vitamin D modulates the upstream immune environment, while selenium directly protects thyroid tissue from oxidative damage. The two mechanisms are complementary, not redundant. For the selenium evidence, see the selenium for Hashimoto's deep-dive.

The VITAL Trial Context

The VITAL trial's 22% autoimmune disease reduction was achieved at only 2,000 IU/day in a general population — not Hashimoto's patients specifically, and not at the 60-80 ng/mL target range. This means:

1. The effect is likely understated for Hashimoto's patients supplementing to higher levels
2. The trial confirms that vitamin D has clinically meaningful autoimmune-preventive effects at the population level
3. For patients with established Hashimoto's, the rationale for supplementation is both preventive (preventing additional autoimmune diseases, which Hashimoto's patients are at elevated risk for) and therapeutic (modulating the immune attack on the thyroid)

Who Needs Higher Doses

Several factors increase vitamin D requirements or reduce the effectiveness of standard doses:

Obesity and Overweight

Vitamin D is fat-soluble and is sequestered in adipose tissue. Obese patients (BMI >30) require approximately 2-3 times the standard dose to achieve the same serum levels as lean individuals. A patient at BMI 35 may need 8,000-10,000 IU daily as a maintenance dose rather than 4,000-5,000 IU. (Wortsman et al., American Journal of Clinical Nutrition, 2000)

This is particularly relevant for Hashimoto's patients, where hypothyroidism-driven weight gain creates a vicious cycle: low thyroid function leads to weight gain, which sequesters more vitamin D, which worsens immune dysregulation, which worsens thyroid function.

Dark Skin

Melanin absorbs UVB radiation — the wavelength required for cutaneous vitamin D synthesis. Individuals with Fitzpatrick skin types IV-VI (moderate brown to dark brown/black) produce significantly less vitamin D from sun exposure and have higher rates of deficiency at every latitude. Supplementation is especially important in this population.

Northern Latitudes

Above approximately 37 degrees north latitude (a line roughly through San Francisco, Denver, and Richmond, Virginia), UVB intensity is insufficient for meaningful vitamin D synthesis during winter months (October through March). In northern Europe, Canada, and the northern US, supplementation during these months is not optional for anyone targeting immune-optimal levels.

GI Malabsorption

Conditions affecting fat absorption reduce vitamin D uptake from supplements:

• Celiac disease (common comorbidity with Hashimoto's)
• Crohn's disease and ulcerative colitis
• History of bariatric surgery
• Chronic cholestasis or pancreatic insufficiency

These patients may require higher oral doses, sublingual vitamin D, or in severe cases, intramuscular vitamin D injections. If you have known GI malabsorption and your 25-OH vitamin D does not rise adequately despite oral supplementation, discuss alternative delivery methods with your physician.

Elderly Patients

Cutaneous vitamin D synthesis declines with age — a 70-year-old produces approximately 75% less vitamin D from the same UVB exposure compared to a 20-year-old. Combined with reduced outdoor activity and dietary changes, elderly patients are among the most consistently deficient populations.

Safety and Toxicity

The Risk Is Real but Rare

Vitamin D toxicity (hypervitaminosis D) occurs when serum 25-OH vitamin D levels exceed approximately 150 ng/mL for sustained periods. The mechanism is straightforward: excessive vitamin D causes excessive calcium absorption, leading to hypercalcemia (elevated blood calcium).

Symptoms of vitamin D toxicity include:

• Early: Nausea, vomiting, poor appetite, constipation, weakness
• Progressive: Excessive thirst, frequent urination (polyuria), confusion
• Severe: Kidney stones, nephrocalcinosis (calcium deposits in kidneys), cardiac arrhythmia

At maintenance doses of 4,000-5,000 IU daily, toxicity is exceedingly uncommon. The Endocrine Society considers up to 10,000 IU/day safe for most adults without monitoring, though we recommend retesting because individual variation in metabolism is significant.

Genetic Hypersensitivity: CYP24A1 Mutations

A small number of individuals carry loss-of-function mutations in the CYP24A1 gene, which encodes the enzyme responsible for breaking down active vitamin D. These patients cannot efficiently inactivate 1,25(OH)2D and are susceptible to hypercalcemia at doses that are safe for the general population.

If you develop symptoms of hypercalcemia (persistent nausea, excessive urination, confusion) at modest vitamin D doses, request a serum calcium test. If calcium is elevated, CYP24A1 genetic testing may be warranted.

Granulomatous Diseases

Patients with sarcoidosis or other granulomatous diseases have macrophages that convert 25-OH vitamin D to active 1,25(OH)2D outside the normal kidney pathway. This can cause hypercalcemia at vitamin D levels that are safe for the general population. If you have a granulomatous condition alongside Hashimoto's, vitamin D supplementation requires close physician supervision with regular calcium monitoring.

Vitamin D vs. Sun Exposure

UVB Considerations

Sun exposure triggers endogenous vitamin D synthesis, which some argue is superior to supplementation because the body self-regulates production (cutaneous synthesis plateaus, preventing overproduction). There is merit to this argument, and moderate sun exposure has additional benefits (nitric oxide production, circadian rhythm regulation, mood).

However, for Hashimoto's patients targeting 60-80 ng/mL, relying on sun exposure alone is impractical for most people:

• Latitude: Above 37 degrees north, no meaningful UVB reaches the surface from October to March
• Time required: 10-30 minutes of midday sun on exposed arms and legs, without sunscreen — difficult for office workers
• Skin type: Darker skin requires 3-6 times longer exposure for equivalent synthesis
• Age: Elderly skin produces far less vitamin D per minute of exposure
• Consistency: Cloud cover, air pollution, glass (blocks UVB), and clothing all reduce synthesis

The Practical Approach

For most Hashimoto's patients, the recommended strategy is supplementation as the foundation with moderate sun exposure as a beneficial addition — not a replacement. Get outside when possible, but do not rely on sunshine to maintain immune-optimal vitamin D levels year-round.

Building Your Vitamin D Protocol

Step 1: Test Your Baseline

Order a 25-OH vitamin D test. If your physician only runs the standard metabolic panel, request it specifically. Many direct-to-consumer lab services also offer this test.

Step 2: Start the Loading Phase (If Deficient)

If your level is below 30 ng/mL, begin the loading phase per the dosing table above. Always include K2 (MK-7, 200 mcg) and magnesium (400 mg) from day one.

Step 3: Retest at 8-12 Weeks

Confirm your level is rising. If it has not reached at least 40 ng/mL after 8 weeks of loading, consider:

• Are you taking it with fat?
• Is magnesium adequate?
• Do you have GI malabsorption?
• Is your BMI above 30 (requiring higher doses)?

Step 4: Transition to Maintenance

Once your level is in the 50-80 ng/mL range, switch to the maintenance dose (4,000-5,000 IU daily). Continue K2 and magnesium.

Step 5: Retest Every 6 Months

Levels fluctuate seasonally. Test in late winter (February-March) to catch the annual nadir. Adjust dosing seasonally if needed — some patients increase to 6,000-8,000 IU during winter months and reduce to 3,000-4,000 IU in summer when they get more sun exposure.

Combining with Other Interventions

Vitamin D is one component of a comprehensive Hashimoto's protocol. It works synergistically with:

• Selenium — addresses the oxidative damage pathway; vitamin D addresses the immune regulation pathway
• Myo-inositol — restores TSH receptor signaling
• AIP diet — removes dietary triggers while vitamin D modulates the immune response
• Omega-3 fatty acids — additional anti-inflammatory support

For a personalized protocol based on your specific condition, labs, and severity, take the free AutoimmuneFinder quiz.

Drug Interactions

Frequently Asked Questions

What level of vitamin D is best for Hashimoto's?

The functional medicine target for Hashimoto's is 60-80 ng/mL, well above the conventional threshold of 30 ng/mL. Observational data consistently shows that patients in this range have the lowest TPO antibody titers and the best Treg function. The Endocrine Society recommends 40-60 ng/mL as the preferred range. For a complete guide to optimal lab ranges, see the Hashimoto's lab targets guide.

How long does it take for vitamin D to help Hashimoto's?

At loading doses (8,000-10,000 IU/day), serum levels typically reach the target range within 8-12 weeks. Immune modulation effects (Treg expansion, Th17 suppression) begin as levels rise but may take 3-6 months to translate into measurable changes in TPO antibody titers. Plan for at least 6 months of optimized levels before assessing the impact on antibodies.

Can I take vitamin D with selenium?

Yes. Vitamin D and selenium work through complementary mechanisms: vitamin D modulates immune cell balance (Treg/Th17), while selenium protects thyroid tissue from oxidative damage via selenoproteins. There is no pharmacokinetic interaction between them. They can be taken at the same meal.

Is it possible to have normal vitamin D and still have Hashimoto's?

Yes. Vitamin D deficiency is a risk factor, not a requirement. Some Hashimoto's patients have adequate vitamin D levels. The disease is multifactorial — genetic predisposition (HLA variants, VDR polymorphisms), other environmental triggers (iodine excess, selenium deficiency, gut permeability, infections), and immune dysregulation all contribute. Optimizing vitamin D helps but does not guarantee disease reversal.

Should I stop supplementing in summer?

Most patients can reduce their dose in summer (to 2,000-3,000 IU/day) if they get regular sun exposure, but should not stop entirely. The exception is patients who spend significant time outdoors in summer — they may maintain adequate levels with minimal supplementation. Test in both summer and winter to establish your personal seasonal pattern.

What about vitamin D from food?

Dietary vitamin D sources (fatty fish, egg yolks, fortified milk) contribute at most 200-400 IU daily in a typical diet. This is insufficient to reach immune-optimal levels. Food sources are a useful addition but cannot replace supplementation for Hashimoto's patients targeting 60-80 ng/mL.

Evidence Summary

Your Next Step

Vitamin D optimization is one of the highest-impact, lowest-risk interventions available for Hashimoto's patients. Combined with selenium, dietary modifications, and a complete supplement protocol, it forms a core part of the evidence-based approach to managing thyroid autoimmunity.

Every Hashimoto's patient has a different starting point — different vitamin D levels, different antibody titers, different medications, different comorbidities. A generic recommendation helps, but a personalized protocol based on your specific situation is better.

Take the free AutoimmuneFinder quiz to get a personalized, evidence-graded protocol tailored to your condition, labs, and goals. It takes under 3 minutes.

This article is for educational purposes only and does not constitute medical advice. Vitamin D supplementation at doses above the RDA should be monitored by a healthcare provider with periodic 25-OH vitamin D and calcium testing. Always consult your physician or endocrinologist before starting or changing any supplement regimen, especially if you take levothyroxine, warfarin, or other prescription medications.