Iodine and oral health: the overlooked mineral your mouth needs
Most people associate iodine with thyroid hormones. But this trace element also shapes saliva quality, oral bacterial balance, and gum tissue integrity in ways that dental research is only beginning to map in full.
Iodine matters for your mouth in two distinct ways: it powers salivary defence and it runs your thyroid, which affects everything downstream. Salivary glands concentrate iodine above blood levels to feed the lactoperoxidase system, your continuous antimicrobial defence. Adults need 150 micrograms daily, pregnant women 220, breastfeeding women 290. Topical povidone-iodine has solid evidence as a dental antimicrobial. Chronic deficiency or thyroid dysfunction slows gum healing and shifts oral bacteria. High-dose supplements add no benefit and carry real risks. Iodized salt or a normal mixed diet covers most people.
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TL;DR
Iodine deficiency, rare in well-nourished populations but common in iodine-poor regions, is linked to changes in saliva quality, shifts in oral bacteria, and slower healing of gum tissue. Thyroid dysfunction caused by chronic iodine insufficiency adds a second layer of downstream oral effects. Adequate intake through food or iodized salt is enough for most people. Topical povidone-iodine has real antimicrobial evidence behind it. High-dose supplementation offers no extra oral benefit and carries risks.
This article is informational and not medical or dental advice. It draws on published research, cited below. For your own teeth, talk to your dentist.
What iodine actually does in the body
Iodine is an essential trace element: the body cannot synthesize it and must obtain it from food or supplements. The thyroid gland concentrates iodine to produce thyroxine (T4) and triiodothyronine (T3), hormones that regulate metabolism, growth, and cellular repair throughout every organ system. Adults need around 150 micrograms per day. Pregnant women need 220 mcg, and breastfeeding women need 290 mcg.
Beyond the thyroid, iodine concentrates in several tissues including the salivary glands, gastric mucosa, and mammary glands. The salivary concentration of iodine actually exceeds serum levels, which signals active transport by the glands rather than passive diffusion. This appears to serve a dual role: augmenting the salivary antioxidant system and supporting the lactoperoxidase antimicrobial pathway that operates continuously in the mouth.
In biological systems iodine cycles between iodide (the dietary form), hypoiodous acid (HOI), and other reactive intermediates generated by the enzyme lactoperoxidase. This lactoperoxidase system is one of the mouth's primary natural defenses against bacterial overgrowth, and iodide is one of its key substrates. Understanding this system explains why salivary iodine concentrations have any clinical relevance at all.
When iodine intake is chronically low, the thyroid enlarges (goiter) in an attempt to capture more circulating iodide. Prolonged deficiency leads to overt hypothyroidism, with downstream effects on nearly every tissue including oral tissues. Excessive iodine intake can paradoxically inhibit thyroid hormone synthesis via the Wolff-Chaikoff effect, making both extremes potentially problematic, though clinical problems from dietary overexposure are rare in healthy individuals.
Globally, iodine status is uneven. The World Health Organization estimates that roughly 2 billion people have insufficient intake, concentrated in mountainous inland regions and areas without reliable access to seafood or iodized salt. Mild to moderate deficiency persists in several European countries despite decades of salt iodization programs, with surveys showing median urinary iodine below the 100 mcg/L adequacy threshold in parts of the United Kingdom, Germany, and parts of Scandinavia.
How iodine deficiency shows up in the mouth
The link between iodine deficiency and dental health has been observed epidemiologically for decades, though controlled mechanistic research is still developing. Studies in iodine-deficient regions consistently report higher rates of dental caries compared to iodine-sufficient populations, even after researchers adjust for fluoride exposure and socioeconomic variables.
One proposed mechanism runs through saliva. Saliva is the mouth's primary buffering and remineralizing fluid. Its composition, including flow rate, pH, and mineral content, is governed partly by the systemic hormonal environment. Research published in Caries Research has shown that salivary iodine concentrations track dietary iodine intake, and that lower concentrations correlate with reduced salivary peroxidase activity. Because the peroxidase system generates hypothiocyanate ions that suppress Streptococcus mutans, any weakening of this system can tilt the oral environment toward cariogenicity.
A second mechanism runs through the thyroid. Subclinical hypothyroidism, a state of mildly elevated TSH without overt symptoms, is associated with reduced salivary flow. Xerostomia (dry mouth) is a substantial risk factor for both caries and periodontal disease, because saliva washes away bacteria, neutralizes post-meal acids, and provides the calcium and phosphate ions needed for enamel remineralization. Without adequate saliva, enamel is more vulnerable during acidic periods. Enamel begins to demineralize at pH 5.5, and under dry conditions that threshold is reached and sustained for longer stretches after eating.
Gum tissue is also affected. Iodine-deficient individuals may show signs of gingival inflammation even without heavy plaque accumulation, possibly because hypothyroid states slow connective tissue repair and alter inflammatory signaling. Collagen turnover in the periodontium depends on adequate T3/T4, and reduced synthesis can leave gum tissues structurally weaker over time.
Children face particular risk. Iodine deficiency during fetal development and early childhood can impair dentition formation. Reports from iodine-deficient regions document higher rates of enamel hypoplasia (incomplete enamel formation) and delayed tooth eruption. These effects overlap with those of vitamin D deficiency, making it methodologically difficult to isolate iodine's specific contribution in population studies, but the pattern is consistent enough across different geographic contexts to be taken seriously.
The salivary peroxidase system and iodine's role in it
The salivary peroxidase system is one of those biological defense mechanisms that rarely makes headlines but does an enormous amount of quiet work. It consists of three components: the enzyme lactoperoxidase (produced by the parotid and submandibular salivary glands), hydrogen peroxide (generated by certain oral bacteria and by the oral epithelium), and thiocyanate ions (derived from dietary glucosinolates and secreted into saliva). Together they produce hypothiocyanite, which inhibits the glucose metabolism of cariogenic bacteria.
Iodide can substitute for thiocyanate as a substrate. When it does, the reaction produces hypoiodous acid (HOI), which is even more potently antimicrobial than hypothiocyanite. This dual-substrate capacity means that salivary iodide concentrations directly influence how effectively the peroxidase system suppresses pathogenic bacteria.
Research published in the Journal of Dental Research has explored how salivary peroxidase activity varies across populations and noted that iodide supplementation in vitro enhances the antimicrobial capacity of human saliva against Streptococcus mutans. While in vitro findings do not automatically translate into clinical outcomes, they provide a plausible mechanistic explanation for the epidemiological observation that iodine-deficient populations show worse caries rates.
It is worth keeping this in context. The salivary peroxidase system is not the mouth's only antibacterial defense. Immunoglobulin A, lysozyme, lactoferrin, defensins, and mucins all contribute. Iodine insufficiency would weaken one component of a multi-layered system, which partly explains why the relationship between iodine status and dental outcomes is not uniform across individuals. Some people have higher baseline thiocyanate from cruciferous vegetable consumption, which may partially compensate for lower iodide. Others have lower baseline peroxidase activity for genetic reasons. The system is buffered, which is why deficiency effects are often subtle at an individual level but visible in population-level data.
Thyroid health and its downstream effects on teeth and gums
Salivary flow and dry mouth
Hypothyroidism is a well-documented cause of reduced salivary secretion. Salivary glands require adequate thyroid hormone to maintain their secretory function. A review in the Journal of Periodontology found that hypothyroid patients reported xerostomia significantly more often than euthyroid controls, and that saliva produced under hypothyroid conditions showed lower buffering capacity and reduced calcium content. Both factors raise caries risk meaningfully over time.
Gum healing and collagen repair
T3 and T4 regulate fibroblast activity and collagen synthesis. Fibroblasts are the primary producers of collagen in the periodontium, which includes the gums, periodontal ligament, and alveolar bone. In hypothyroid states, fibroblast proliferation slows, wound healing is delayed, and the inflammatory response to bacterial challenges may become dysregulated. Clinically this can appear as gingivitis that responds poorly to standard oral hygiene improvement, frustrating both patients and clinicians who do not consider systemic thyroid status as a contributing variable.
Macroglossia and taste changes
In severe, long-standing hypothyroidism, the tongue can enlarge due to myxedema, a mucopolysaccharide accumulation in connective tissues. An enlarged tongue affects chewing, speech, and can exert mechanical pressure on teeth, leading to scalloped tongue edges from persistent contact with tooth surfaces. Taste alteration is another oral symptom: hypothyroid patients often describe blunted taste or a persistent metallic quality. While this does not directly damage teeth, it influences dietary choices in ways that can affect caries risk over time.
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Try MinvelleIodine in drinking water: regional variation and dental outcomes
Drinking water is a significant iodine source in some regions and a negligible one in others. Groundwater iodine content depends heavily on local soil geology. Coastal aquifers and deep wells often contain more iodine than surface water in inland mountainous areas. In countries where water naturally contains higher iodine, goiter rates and dental caries rates have historically been lower, independent of fluoride status.
The relationship between water iodine and dental health is sometimes confused with the fluoride story, because both minerals appear in groundwater and both have been studied in relation to caries. Their mechanisms differ substantially. Fluoride's anti-caries effect operates locally at the enamel surface: it substitutes into hydroxyapatite to form fluorapatite, which is more resistant to acid dissolution. Enamel demineralizes at pH 5.5, and fluorapatite withstands slightly lower pH values. Iodine's role is systemic, operating through salivary biochemistry and thyroid-mediated tissue physiology rather than direct enamel chemistry.
A systematic review in Caries Research concluded that both fluoride sufficiency and iodine adequacy appear to independently contribute to lower caries prevalence in studied populations, with the two minerals interacting in complex ways at the systemic level. In regions where both are deficient, the combined effect on dental health is more severe than either alone.
In developed countries where salt is routinely iodized, drinking water iodine is a less critical variable. But as specialty salts including Himalayan pink salt, Celtic sea salt, and artisan finishing salts gain market share, many consumers shift away from standard iodized salt. These specialty products contain little to no iodine. Public health bodies including the British Thyroid Association have noted a gradual decline in population iodine intake correlated with this trend, with particular concern for women of reproductive age who rely entirely on non-iodized salt.
Topical iodine in dentistry: clinical uses and evidence base
While dietary iodine affects oral health through systemic pathways, topical iodine has a more direct and better-documented clinical role as a broad-spectrum oral antiseptic. Povidone-iodine (PVP-I) is a compound of polyvinylpyrrolidone and elemental iodine that releases iodine slowly, providing sustained antimicrobial activity while minimizing the mucosal irritation that free iodine causes.
Caries prevention in high-risk children
Multiple randomized controlled trials have tested professionally applied PVP-I solutions and gels on tooth surfaces in children with elevated caries risk. A Cochrane review of these trials concluded that PVP-I shows promise for caries prevention but that the evidence base is not yet sufficient to recommend it over established fluoride treatments as a first-line option. In fluoride-intolerant patients or communities where fluoride access is limited, PVP-I represents a credible and evidence-supported alternative that deserves continued study.
Periodontal pocket irrigation
PVP-I is used as an irrigant during scaling and root planing procedures (deep cleaning). The rationale: mechanically disrupting biofilm and then flushing with an antimicrobial agent reduces bacterial load more effectively than physical debridement alone. Studies published in Clinical Oral Investigations have reported significant reductions in key periodontal pathogens including Porphyromonas gingivalis and Tannerella forsythia following combined scaling plus PVP-I irrigation versus scaling alone, with corresponding improvements in clinical attachment levels in some trials.
Pre-procedural rinses
Interest in PVP-I rinses increased during the COVID-19 period, when research showed that iodine rapidly inactivates coronaviruses in vitro. Clinical benefit for infection control during dental procedures remains under investigation, but this research renewed interest in iodine's broad antiviral properties. PVP-I as a pre-procedural rinse before aerosol-generating dental work has been adopted in some practices based on in vitro data, though large clinical trials are still needed.
A practical note: PVP-I stains teeth brown with extended use and should not be used by patients with known thyroid disease, iodine allergy, or during pregnancy without medical guidance. It is a clinical and short-term therapeutic tool, not a daily mouthwash substitute.
How much iodine do you need, and what are the best sources?
The recommended dietary allowance is 150 mcg per day for adults, 220 mcg for pregnant women, and 290 mcg for breastfeeding women. The tolerable upper intake level is 1,100 mcg for adults, though chronic intake well above the RDA can still cause thyroid disruption in genetically susceptible individuals before that ceiling is reached.
For most people eating a varied diet with iodized salt, dairy, or fish, meeting the RDA is straightforward. A 100-gram serving of cod provides roughly 170 mcg. A cup of plain low-fat yogurt provides around 75 mcg. Two large eggs contribute approximately 50 mcg. Nori seaweed varies widely but can provide over 100 mcg per sheet. These foods together can easily hit the daily requirement without supplementation.
Groups at higher deficiency risk include:
- People following strict vegan diets without regular seaweed or iodine supplementation
- Those who use non-iodized specialty salts exclusively
- Pregnant and breastfeeding women with low seafood and dairy intake
- People in inland regions with iodine-poor soil and water
- Individuals consuming large amounts of raw cruciferous vegetables and soy, which contain goitrogenic compounds that can interfere with thyroid iodine uptake
For those in at-risk groups, a standard multivitamin typically contains 150 mcg of iodine as potassium iodide, which is sufficient to fill most dietary gaps without approaching the upper tolerable limit. High-dose iodine supplements (1,000 mcg or more) are not warranted for oral health purposes and should be taken only under medical supervision.
Pulling it together: iodine, remineralization, and daily oral care
Iodine will not replace nano-hydroxyapatite or xylitol as a direct remineralizing agent. Its role is upstream: maintaining the hormonal and salivary biochemical environment that allows the mouth's natural defenses to function at full capacity. Think of it as infrastructure. Without adequate iodine, the systems that protect enamel run at reduced capacity even when other oral care habits are excellent.
The practical implications are straightforward. If your diet includes iodized salt, dairy, or fish regularly, your iodine status is almost certainly adequate and no special measures are needed. If you follow a strict plant-based diet or use non-iodized salt exclusively, a basic potassium iodide supplement at 150 mcg/day is a reasonable and inexpensive precaution that dentists rarely mention but that nutritional medicine practitioners frequently flag.
For enamel protection specifically, adequate saliva flow is the most important single natural protector. Saliva buffers acids, washes away bacteria, supplies calcium and phosphate for remineralization, and, via the lactoperoxidase system, keeps cariogenic bacteria in check. Any systemic factor that reduces saliva output raises caries risk over time. Iodine-related hypothyroidism is one such factor, sitting quietly in the background while other variables get more attention.
Chewing remineralizing gum provides a dual benefit here: it stimulates saliva mechanically and delivers active ingredients like nano-hydroxyapatite and xylitol directly to tooth surfaces between meals. Nano-hydroxyapatite, approved as an anti-cavity agent in Japan since 1993 and by the EU's Scientific Committee on Consumer Safety (SCCS) in 2023, integrates directly into enamel's hydroxyapatite lattice. Enamel is approximately 97% hydroxyapatite by weight, making nano-hydroxyapatite a structurally identical repair material rather than a chemical substitute. This kind of targeted remineralization works most effectively when the systemic environment, including thyroid and iodine status, is also sound.
The broader lesson is that oral health is not purely a local hygiene problem. It reflects systemic nutritional status, hormonal balance, and the quality of the biological environment in which teeth live. Iodine is one piece of a complex picture, easily overlooked because its effects are indirect and slow-developing, but meaningful enough that its deficiency leaves a measurable signature in dental health data across populations worldwide.
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Try Minvelle, save 10%Frequently asked questions
Can iodine deficiency cause tooth problems?
Research suggests iodine deficiency may alter saliva composition and is associated with higher rates of dental caries in regions with low iodine intake, though the relationship involves multiple factors.
Does iodine in mouthwash actually work?
Povidone-iodine (PVP-I) mouth rinses have shown broad-spectrum antimicrobial activity in clinical studies, including against Streptococcus mutans, the primary cavity-causing bacterium. Several studies in Clinical Oral Investigations confirm short-term efficacy.
Can I get enough iodine from food alone?
For most people, yes. Seaweed, oily fish, dairy products, eggs, and iodized salt provide adequate iodine. Strict vegans and those who avoid iodized salt face a higher risk of deficiency.
Is iodine supplementation safe for oral health?
At the recommended dietary allowance of 150 mcg per day for adults, iodine is considered safe. Very high doses can suppress thyroid function, which may indirectly affect oral health.
How does thyroid disease linked to iodine deficiency affect the mouth?
Hypothyroidism, which can result from prolonged iodine deficiency, is associated with slower tissue healing, reduced salivary flow, increased susceptibility to periodontal inflammation, and altered taste sensation.
How your salivary glands hoard iodide, and why that matters at the molecular level
Most articles stop at the headline fact that saliva contains iodine. The more interesting question is how it gets there, because the mechanism is the same one your thyroid uses, and it tells you why your mouth never simply runs on whatever iodide happens to be floating in your blood. The workhorse is a membrane protein called the sodium-iodide symporter, usually shortened to NIS. In the salivary glands, NIS sits on the basolateral membrane of the ductal epithelial cells, and it pumps iodide out of the bloodstream and into the gland against its concentration gradient, riding on the inward flow of sodium ions. The result is active accumulation: research using the saliva-to-plasma ratio as a clinical readout treats a value of 20 or higher as the normal floor, which means a healthy gland concentrates iodide to at least twenty times the level circulating in plasma (The Sodium/Iodide Symporter, Molecular Physiology and Applications).
That twenty-fold floor is the part worth sitting with. Your body treats salivary iodide as a priority, not an afterthought. The parotid gland's intralobular ducts are a principal site where iodide is loaded into saliva, and the same transporter handles related anions, which is why studies of dietary nitrate show a comparable concentration of roughly twenty times plasma levels into saliva through the identical pathway (The sodium/iodide symporter is a nitrate transporter in the human salivary gland). The practical reading is that the iodide in your mouth is not a passive spillover from blood. It is actively selected and concentrated, which is exactly what you would expect of a defence system the body wants kept stocked.
Once iodide is inside saliva, it becomes the fuel for the peroxidase reaction described earlier in this article. The enzyme lactoperoxidase uses hydrogen peroxide to oxidise iodide and thiocyanate into hypoiodous acid and hypothiocyanite, two short-lived oxidants that disrupt microbial cells in a broad, non-specific way (Mode of Action of Lactoperoxidase, a Review). Research describes these products as powerful and, importantly, broad in their reach, which is the trait that makes the system hard for bacteria to evolve around: there is no single protein target to mutate, the oxidants simply attack exposed thiol groups across the cell. Understanding this chain, NIS concentrates iodide, lactoperoxidase converts it, and the oxidant does the work, is what turns iodine from a thyroid footnote into a daily participant in oral defence.
What the research actually shows when iodide supply changes
A reasonable next question is whether the amount of iodide you take in actually moves the antimicrobial output in saliva, or whether the system is saturated and indifferent. A human study addressed this directly. Researchers measured salivary analytes in 40 subjects before and after an acute iodine load delivered by the iodinated contrast dye used in coronary angiography. That load was several hundred-fold above the recommended daily allowance of 150 micrograms, and it significantly raised both salivary iodide and salivary hypoiodous acid compared with baseline (Excess iodine exposure acutely increases salivary iodide and antimicrobial hypoiodous acid concentrations in humans). In plain terms, the system is responsive: when more iodide is available, the glands have more substrate to convert, and the antimicrobial oxidant pool grows.
Two cautions keep that finding honest. First, the dose used was a pharmacological extreme, not a dinner plate, so the study shows the pathway responds to iodide, not that flooding yourself with iodine is wise. The American Thyroid Association cautions that habitual intake above roughly 1,100 micrograms a day can itself disturb thyroid function, so more is emphatically not better (American Thyroid Association statement on excess iodine). Second, responsiveness has a downside the research community flags indirectly: the body's halide defence depends on supply, so chronic shortfall starves it. That framing lines up with the deficiency picture covered earlier in this article and explains why researchers treat salivary iodide as a candidate marker of whole-body iodine status rather than a closed, self-sufficient loop (Salivary iodide status as a measure of whole body iodine homoeostasis).
The clinical-use evidence points the same direction from a different entrance. A controlled split-mouth study in 60 patients with chronic periodontitis gave scaling and root planing on one side and the same treatment plus 10 percent povidone-iodine subgingival irrigation on the other. The investigators reported that the povidone-iodine side fared better on the clinical periodontal measures and showed lower counts of key periodontal pathogens such as Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, which they attributed to the broad-spectrum antimicrobial action of the iodine preparation (Efficacy of subgingival irrigation with 10% povidone-iodine as an adjunct to scaling and root planing). Povidone-iodine is a far more concentrated source than anything saliva produces on its own, so this is not proof that dietary iodine treats gum disease. What it does illustrate is that iodine chemistry, applied at the gumline, behaves the way the molecular story predicts: it suppresses the bacteria most associated with periodontal breakdown.
Where this leaves a sensible reader
Pulling the threads together, the case for caring about iodine in the mouth rests on a coherent chain rather than a single dramatic study. The salivary glands actively concentrate iodide through the same transporter the thyroid relies on, holding it at roughly twenty times the level in blood. That stored iodide feeds the lactoperoxidase system, which converts it into short-lived oxidants that keep microbial populations in check. Studies show the output of that system tracks iodide supply, climbing when iodide is abundant, and the research community is testing salivary iodide as a readout of how much iodine the whole body has on hand. None of this means an iodine supplement is a dental product, and it does not cure, prevent, or guarantee anything about your gums or teeth.
The honest practical takeaway is narrow and worth stating plainly. For most people, the move is not to chase iodine for its mouth effects but to make sure overall intake lands in the normal range through ordinary food, since both shortfall and excess carry their own costs (NIH Office of Dietary Supplements, Iodine). Iodised salt, dairy, eggs, and seafood cover the 150-microgram target for most adults without any thinking, and the Linus Pauling Institute lays out the same food-first picture alongside the thyroid biology that makes iodine non-negotiable in the first place (Iodine, Linus Pauling Institute, Oregon State University). If your iodine status is already where it should be, the oral defence system has the substrate it needs, and that is the quiet, unglamorous reason this overlooked mineral earns a place in the conversation about a healthy mouth.
Sources
- Zimmermann MB. Iodine deficiency. Endocrine Reviews. 2009;30(4):376-408.
- Thomas EL et al. Salivary peroxidase systems and oral health. Caries Research. 2004;38(5):437-444.
- Benahmed AG et al. The relationship between iodine status and caries. Clinical Oral Investigations. 2021;25(3):1073-1083.
- Slot DE et al. Povidone-iodine as an anti-plaque agent: a systematic review. Journal of Clinical Periodontology. 2020;47(8):928-938.
- Bajaj S, Prasad S, Gupta A, et al. Oral manifestations in type-2 diabetes and related complications. Indian Journal of Endocrinology and Metabolism. 2012.
- Nederfors T. Xerostomia and hyposalivation. Advances in Dental Research. 2000;14:48-56.
- World Health Organization. Assessment of iodine deficiency disorders and monitoring their elimination. 3rd ed. Geneva: WHO; 2007.
- Venturi S & Venturi M, Nutrition & Health, 2009
- El Mobadder M et al., Journal of Clinical Medicine, 2022
- Sahrmann P et al., Journal of Periodontal Research, 2010
- Dekker BL et al., The Journal of Nutrition, 2021
- The Sodium/Iodide Symporter (NIS): Molecular Physiology and Preclinical and Clinical Applications (PMC5739519): NIS on basolateral membrane of salivary ductal epithelial cells; saliva-to-plasma iodide ratio normal floor >=20
- The sodium/iodide symporter is a nitrate transporter in the human salivary gland (PMC12721291): NIS concentrates nitrate to about 20 times plasma levels in saliva
- Mode of Action of Lactoperoxidase as Related to Its Antimicrobial Activity: A Review (PMC4182067): lactoperoxidase uses H2O2 to oxidise iodide and thiocyanate into hypoiodous acid (HOI) and hypothiocyanite that attack thiol groups
- Excess iodine exposure acutely increases salivary iodide and antimicrobial hypoiodous acid concentrations in humans (PMC9719529): 40 subjects, iodinated contrast load several hundred-fold over the 150 mcg/day RDA significantly raised salivary iodide and HOI
- Salivary iodide status as a measure of whole body iodine homoeostasis? (PMC11063662): scoping review treating salivary iodide as a candidate marker of whole-body iodine status
- Efficacy of subgingival irrigation with 10% povidone-iodine as an adjunct to scaling and root planing: A clinical and microbiological study (PubMed 29072213): split-mouth chronic periodontitis, povidone-iodine adjunct favoured outcomes via broad-spectrum antimicrobial activity
- American Thyroid Association statement on the potential risks of excess iodine ingestion and exposure: intake above ~1,100 mcg/day may cause thyroid dysfunction
- NIH Office of Dietary Supplements, Iodine (Consumer Fact Sheet): 150 mcg/day RDA, food sources, deficiency and excess
- Iodine, Linus Pauling Institute, Oregon State University: iodine function, thyroid biology, intake and deficiency, food-first picture
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Vitamin D and your teeth
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Max, Founder of Minvelle. Reads dental research daily, not a medical professional. Every Minvelle post is fact-checked against primary sources, no LLM-generated content goes live unedited. More on how this brand started.
Last reviewed: June 2, 2026 by Max, Founder of Minvelle.