Heavy Metals and Hashimoto's: The Thyroid Connection

🦋

What this article is about, and what it is not

This article zooms in on a single sub-topic within the heavy-metal field: the thyroid and Hashimoto's. The general heavy-metal mechanics, the diagnostics and the sources are covered in the heavy-metals overview page. Here we look only at what might make the thyroid so particularly susceptible, and at the honest question of when the suspicion is even worth pursuing.

Thyroid / Hashimoto's Part of the heavy-metal cluster

When the numbers look right and you still feel awful

Many people with Hashimoto's know this trajectory. The diagnosis is made, the levothyroxine is dialled in, the TSH sits in the target range. And yet something lingers: an exhaustion that will not lift, brain fog, weight problems, the diffuse sense that your body keeps working against you.

When you ask why, the answer is usually the same: the cause of Hashimoto's is simply unknown, a mix of genetic predisposition and nonspecific triggers. That is not wrong. But it is not the end of the story either.

This article follows a lead that almost never comes up in that conversation: whether and how a heavy metal, mercury above all, could play a role. What is mechanistically plausible about it, what is established, what remains hypothesis, and when the question is even clinically worth asking. Without fear marketing, and without promising you that a test will dissolve your Hashimoto's.

A reframe before we begin

"Cause unknown" does not mean "there is nothing to check." Heavy metals are not a proven cause of Hashimoto's, and anyone who claims so goes beyond the data. But they are an unusually concrete mechanistic lead. The difference between "proven cause" and "plausible, testable lead" is exactly what almost always gets blurred online. This page keeps it consistently apart.

What you will find in this article Why the thyroid, through its selenoenzymes, could be a plausible target of mercury. The difference between toxic burden and autoimmune trigger. Why your TSH can be normal while too little active hormone reaches the periphery. The selenium question in connection with the heavy-metal question. And an honest list of when the suspicion is worth pursuing and when it is not.

Why the thyroid in particular could be a plausible target

The thyroid is one of the most selenium-rich organs in your body. That is no accident, but a necessity. Three of its central tools are so-called selenoenzymes: enzymes that simply cannot work without the trace element selenium. This is exactly where things get interesting.

Mercury binds selenium with very high affinity. Within the body, it preferentially seeks out the very places where selenium sits. And when the most important thyroid enzymes happen to carry selenium at their core, that creates a biologically understandable line of conflict. This is the heart of this page, and the point most sources skip over.

The two switch points at stake

1. The deiodinases (DIO1, DIO2, DIO3). These enzymes convert the storage hormone T4 into the actually active T3. T4 alone does little for your cells; only T3 switches your metabolism on. The deiodinases carry selenium in their catalytic centre.

2. The glutathione peroxidases (GPx). To make its hormones, the thyroid produces hydrogen peroxide itself, a cell toxin. The GPx, also selenoenzymes, neutralise it again and protect the thyrocyte from its own tool.

Both enzyme families need selenium. Both sit exactly where mercury likes to dock. From this follows the central hypothesis of this page, framed here in a way you will rarely see elsewhere.

The scientific basis for this is well established. Two large mechanistic reviews describe just how dependent the thyroid is on its selenoenzymes.

Mechanistic review

Köhrle and Gärtner summarised what makes the thyroid a selenium hotspot: the three deiodinases as well as the glutathione peroxidases and thioredoxin reductases are all selenoproteins that govern hormone activation and oxidative protection. The thyroid is among the most selenium-rich tissues of all. For you this means: the key enzymes of your thyroid need selenium, and this is exactly where a possible mercury conflict comes in.

Köhrle & Gärtner, Best Pract Res Clin Endocrinol Metab. 2009. DOI: 10.1016/j.beem.2009.08.002

Mechanistic review

Schweizer and colleagues described the thyrocyte's dilemma in more detail: to synthesise hormones, the cell continuously produces hydrogen peroxide and relies on glutathione peroxidases and thioredoxin reductases to protect itself from it. Selenium acts protectively here both directly and indirectly. For you this means: the thyroid works permanently with a cell toxin that it can only neutralise with selenium enzymes, a system that reacts sensitively to anything that blocks selenium.

Schweizer, Chiu & Köhrle, Antioxid Redox Signal. 2008. DOI: 10.1089/ars.2008.2054

How mercury could intervene concretely

The mechanistic reviews show why the thyroid needs selenium. Other work shows what happens when mercury gets in the way. Here the data are strikingly direct at the molecular level, even though they come mostly from cell culture and animal models.

Mercury seeks out the selenium

Methylmercury binds directly to the selenol group of glutathione peroxidase and inhibits its activity. In human cells it was shown that adding selenium softens this effect. This is the molecular evidence for the mercury–selenium antagonism, at exactly the type of enzyme that also protects the thyroid.

Hormone conversion can slow down

In an animal model, the mercury compound thimerosal lowered deiodinase activity in several tissues without changing the amount of enzyme. The researchers suspect direct binding to the selenium centre. Translated: the enzyme is still there, but it works more slowly, and the conversion of T4 into active T3 could suffer.

The pattern also shows up in the whole organism

In chronically mercury-exposed amphibian larvae, the thyroid was structurally damaged, and deiodinase-2 expression and glutathione peroxidase were suppressed. This adds the level of a living organism to the cellular picture, but, like all animal data, remains a hint and not proof for humans.

In vitro · human cells

Chen and colleagues investigated, in human kidney cells, how mercury attacks glutathione peroxidase 4. Methylmercury bound directly to the enzyme's selenol group and inhibited it; adding selenium partly restored the activity and reduced the cell damage. For you this is the direct molecular evidence that mercury blocks exactly those selenium enzymes that also protect the thyroid, and that selenium can counteract it.

Chen et al., Metallomics. 2023. DOI: 10.1093/mtomcs/mfad014

In vivo · rat

Pantaleão and colleagues gave rats the mercury compound thimerosal and measured thyroid hormones and deiodinase activity. The highest dose lowered deiodinase activity in several tissues without changing the amount of enzyme. For you this means: in the animal model, mercury slows down exactly the enzymes that convert T4 into active T3, a possible reason for symptoms despite unremarkable standard values.

Pantaleão et al., Endocr Connect. 2017. DOI: 10.1530/EC-17-0220

In vivo · amphibian larva

Shi and colleagues exposed toad larvae chronically to various mercury concentrations. High doses damaged the thyroid, lowered deiodinase-2 and thyroid hormone receptor expression, and suppressed glutathione peroxidase. For you this rounds out the picture: mercury hits the thyroid via the same selenium-dependent pathways in a whole organism too, not just in cell culture.

Shi et al., Ecotoxicol Environ Saf. 2018. DOI: 10.1016/j.ecoenv.2018.08.058

The core idea in one sentence

A heavy-metal burden could hit the thyroid through a functional selenium deficiency, that is, even when your selenium blood level looks perfectly normal. The selenium is there, but if mercury binds it, it is not available to the enzymes. Important: this functional deficiency is mechanistically plausible and has been shown in cells and animal models, but it has not been directly demonstrated in humans with Hashimoto's. It remains a well-grounded hypothesis, not a finding.

How the generic mercury–selenium mechanics work in detail, that is, the affinity for sulfur and selenium groups across all organs, is the subject of the heavy-metals overview page. Oxidative protection via glutathione is at the same time the interface with detoxification, more on that in the article on glutathione and heavy metals.

Two questions that are constantly confused

This is where the biggest fallacy online lies. Functional blogs throw two completely different things into one pot, and exactly this blending produces either panic or sweeping dismissal. Kept cleanly apart, they are two questions with two different answers.

Level 1 · Function

Toxic burden

Could mercury, by inhibiting the selenoenzymes, disrupt hormone activation and oxidative protection? This is the functional and metabolic level. It is not about autoimmunity but about whether the machine runs more slowly. This level is mechanistically well grounded.

Level 2 · Immune system

Autoimmune trigger

Could mercury, acting as an adjuvant or hapten, immunologically promote an autoimmune reaction against thyroid tissue? This is the trigger level, the actual Hashimoto's question. Here the data are thinnest and most contradictory.

This distinction is the real map, and online it is almost entirely missing. A heavy metal could theoretically burden the function of your thyroid without ever triggering an autoimmune reaction. And conversely, Hashimoto's is an autoimmune disease whose initiation is a separate, immunological process. Anyone who equates "mercury disrupts enzymes" with "mercury causes Hashimoto's" leaps over a decisive gap.

What the trigger level actually offers, honestly considered

For the immunological trigger hypothesis there is an explanatory model, but only weak evidence. The idea: metal ions could activate T cells and, via signalling molecules, kick off systemic inflammation. This is the hapten and adjuvant hypothesis. It comes mostly from small, uncontrolled case series in the orbit of the MELISA test, and it is methodologically weak.

Narrative review · case series · weak

Stejskal and colleagues postulated that metal ions could activate T cells and trigger systemic inflammation via cytokines, and described health improvements after removal of intolerable dental materials. The work provides the immunological explanatory model for the trigger level, but remains hypothesis: small sample size, no control group, proximity to the test provider. For you this means taking this model seriously as a question, not as an answer.

Stejskal et al., Neuro Endocrinol Lett. 2006. PMID: 17261999 (no DOI)

Framing, not hype The MELISA and amalgam strand is the weakest pillar of this entire topic. It works as a generator of hypotheses, not as evidence. If someone tells you that a lymphocyte test proves your Hashimoto's comes from amalgam, they are selling you more certainty than the data support.

Why your TSH can be normal while you do not feel that way

This is one of the most common and most frustrating findings in Hashimoto's: the values are okay, you are not. The key lies in the difference between the central control and what actually arrives in your cells.

The conversion logic, briefly explained

TSH is the control hormone from the pituitary gland. It says how loudly the thyroid should "call out." When enough T4 is circulating in the blood, TSH is satisfied and sits in the normal range. So much for the central level.

But T4 is only the storage form. Only the deiodinases convert it into the active T3 within the cells. If this peripheral conversion is slowed, for example because the selenium-dependent deiodinases are not running smoothly, too little active T3 may arrive where it is meant to act, while TSH and T4 still look unremarkable.

This could explain why some people, despite "good values," still feel exhausted, cold-sensitive and foggy-headed. The control is right, the local execution perhaps not. Important: this is an explanatory model, not a diagnosis that may be made across the board.

Population study · n=1254

Kim and colleagues analysed a Korean environmental-health survey and linked mercury, cadmium and lead to thyroid hormones and calculated deiodinase activity. Urinary mercury was associated with lower total T3 and altered deiodinase activity. For you this means: at the population level there are hints that heavy metals could disrupt the T4-to-T3 conversion, consistent with the deiodinase mechanism, but as an observation, not as proof.

Kim et al., Sci Total Environ. 2021. DOI: 10.1016/j.scitotenv.2020.144227

An important limit

The precise laboratory methodology, that is, which values to measure how and how to interpret them, does not belong in this article. Here it is only about why a normal TSH need not fully explain how you feel. Please never question or stop your levothyroxine therapy on your own. The heavy-metal question is a complementary lead, not a substitute for your endocrinological care.

Selenium in Hashimoto's: why it can help, and why on its own it often is not enough

If any micronutrient has a solid evidence base in Hashimoto's, it is selenium. It is the best-supported lever of this whole topic, and at the same time the bridge to the heavy-metal question. Both hang on the same element.

Meta-analysis of RCTs · k=35

Huwiler and colleagues evaluated 35 randomised trials of selenium in Hashimoto's. Selenium markedly lowered TPO antibodies, and TSH in patients without hormone replacement, independent of levothyroxine therapy, with a safety profile comparable to placebo. For you this means: selenium can measurably lower the thyroid antibodies; it is the best-supported lever in Hashimoto's.

Huwiler et al., Thyroid. 2024. DOI: 10.1089/thy.2023.0556

Cochrane review · k=4 · n=463

The Cochrane review by van Zuuren and colleagues summarised four controlled trials. Selenium lowered TPO antibodies in several studies, but the clinical relevance remained unclear and the evidence was overall incomplete. For you this means: while selenium does lower antibody levels, whether it reliably makes you feel better is not yet proven. Honest framing rather than a promise of cure.

van Zuuren et al., Cochrane Database Syst Rev. 2013. DOI: 10.1002/14651858.CD010223.pub2

Meta-analysis of RCTs · k=7

Kong and colleagues evaluated seven controlled trials. After six months there was a significant reduction in TPO and Tg antibodies; after three months there was still no clear effect. For you this means: selenium can act on the antibodies only over months, not weeks, so patience is part of it.

Kong et al., Medicine (Baltimore). 2023. DOI: 10.1097/MD.0000000000033791

The findings are consistent across many studies: selenium can lower TPO antibodies. Another large meta-analysis confirms this, but points out that the effect on other values is inconsistent.

Meta-analysis of RCTs · k=17 · n=1911

Zuo and colleagues evaluated 17 randomised trials of selenium in autoimmune thyroiditis. Selenium markedly lowered TPO antibodies, whereas TSH and Tg antibodies did not change consistently. For you this means: the antibody effect is robust, but selenium is not a switch that resets the entire thyroid picture.

Zuo et al., Ann Palliat Med. 2021. DOI: 10.21037/apm-21-449

The bridge between the selenium question and the heavy-metal question

Here the circle closes. Selenium is the cofactor of exactly those enzymes that mercury could block. If a heavy metal binds the selenium away, a pure selenium supplement could partly run into the void as long as the burden is not taken into account. This is the link that almost no one makes online: it could be not only about "too little selenium" but about "selenium that does not arrive." What is established is that selenium can lower TPO antibodies and that mercury binds selenium. That, in the Hashimoto's patient, one cancels out the other remains a plausible but unproven hypothesis.

No self-experiment with high-dose selenium Selenium has a narrow therapeutic window; too much over a long time can do harm. Dosing belongs in medical hands and under monitoring, not in self-directed use following a blog tip. This article deliberately gives no dosage figures.

What the human data really show, and what they do not

Now the most honest part. At the mechanistic level the data are concrete. At the level of proof in humans they are thin and contradictory. Anyone who tells you otherwise is hiding half the studies. Let us look at both camps.

Cross-sectional · n=2047

Gallagher and Meliker analysed the US health survey NHANES and examined the association between blood mercury and thyroid autoantibodies in about 2,000 women. Women with the highest mercury had roughly double the odds for thyroglobulin antibodies, while no association showed up for TPO antibodies. For you this means: there is a statistical signal between mercury and one thyroid antibody, but no proof of cause and only for one of the two antibodies.

Gallagher & Meliker, Environ Int. 2012. DOI: 10.1016/j.envint.2011.11.014

Set against this is a whole series of null findings. Two studies found no association with thyroid antibodies despite high or oral mercury exposure respectively.

Controlled cross-sectional · n=82

Barregard and colleagues compared mercury-exposed chloralkali workers with controls. Despite clearly elevated mercury levels, there was no significant difference in autoantibodies; the authors consider a sustained autoimmune reaction at these exposure levels to be rare. For you this is an important counter-finding: high mercury exposure did not automatically lead to thyroid antibodies here, and individual susceptibility seems to be decisive.

Barregard et al., Int Arch Occup Environ Health. 1997. DOI: 10.1007/s004200050193

Case-control study · n=78

Rachmawati and colleagues investigated oral metal exposure, metal allergy and autoimmune markers. Oral mercury, gold or palladium exposure was not associated with autoimmune phenomena; metal-allergic individuals even had thyroid antibodies less often. For you this means, against the blanket equation of amalgam equals autoimmune: in this study there was no association of amalgam mercury with thyroid antibodies.

Rachmawati et al., Autoimmunity. 2015. DOI: 10.3109/08916934.2015.1033688

The honest core

There is no proof that mercury causes Hashimoto's. One positive signal for only a single antibody in one population study, null findings in two others. The direct link between mercury and the classic TPO antibodies is not established in humans.

The most plausible explanation for the contradictions is individual susceptibility: genetics, selenium supply, the rest of the toxin burden. The person at the next table with a similar number of fillings may have no symptoms because their biology buffers the mercury better. That is biology, not imagination, but it remains an explanatory hypothesis.

Why this middle ground is so rare

Conventional-medicine sources almost entirely leave environmental toxins out of Hashimoto's and end at "cause unknown." Functional blogs aggressively take up mercury as a cause and tip over into claimed causation. No one occupies the middle ground cleanly: mechanistically grounded, honestly delimited, with a clear separation of what is established and what is hypothesis. It is exactly this middle ground that this page tries to hold.

When the heavy-metal question is worth asking in Hashimoto's, and when it is not

Not every Hashimoto's has a toxin story, and "go get detoxed" is no responsible piece of advice. But it would be equally wrong to dismiss the question across the board. There are pointers where the thought is genuinely worth pursuing, and there are situations where it tends to mislead.

Pointers where the question can make sense

A relevant mercury history: many or long-worn amalgam fillings, a removal without a protective protocol, or occupational contact with amalgam, for example in dentistry.
Treatment resistance despite well-controlled TSH: the values are right, the levothyroxine fits, and yet your wellbeing remains clearly impaired over a long time.
Persistent exhaustion and brain fog that cannot be explained by the thyroid settings alone.
Further unexplained multisystem complaints that coexist and cannot be assigned to any single organ picture.
Regular consumption of large predatory fish such as tuna or swordfish over years, an often-overlooked methylmercury source.

When the question tends to mislead

A freshly diagnosed Hashimoto's that responds well to treatment: here solid endocrinological care comes first.
No exposure indications whatsoever and a symptom picture that is well explained by the thyroid and known factors.
The expectation that a test or a course of chelation will dissolve the Hashimoto's: this expectation is not supported by the data.

Whether and how one should sensibly measure at all when there is a well-founded suspicion is a separate question. A blanket "test for heavy metals" says little, because a simple spot blood value often does not reveal a burden stored in tissue at all. How a mobilisation test works, you can read in the article on the DMPS challenge test, and which investigative route is suited when, in the post measuring heavy metals in blood or urine.

My stance as a physician

For a Hashimoto's that does not settle despite a cleanly controlled TSH, the question of a mercury history belongs in the conversation, in my view. Not as a promise of cure, but as one of several leads you can check before discarding it. Conventional medicine does the most important thing right here, it secures the hormone supply. What integrative medicine can add is the question of possible contributing factors in the background. The two do not exclude each other.

"Amalgam out, then the Hashimoto's is gone": why it does not work that way

This is the most common forum myth on this topic. It sounds logical and is nonetheless too short-sighted. The honest answer has three parts.

Shutting off the source makes sense

If amalgam really is a relevant source, it makes sense to stop the supply. So far the thought is right. How a removal proceeds safely is the subject of the post removing amalgam and chelating correctly.

The stored burden remains

Mercury already deposited does not disappear just because the filling is gone. It has long residence times in tissue. That is simply half-life mathematics, not a failure of detox. Source gone does not mean burden gone.

An autoimmune reaction once set in motion often continues

Once the immune reaction against the thyroid is under way, it has a momentum of its own. Even if a trigger had originally been involved, its removal does not yet mean reversal. This is why expectation management matters more here than any promise.

Case series · n=35 · weak

Procházková and colleagues replaced the amalgam in 35 metal-allergic autoimmune patients and followed the course with the lymphocyte test MELISA. About 71 percent reported a health improvement, though the strongest improvement was in multiple sclerosis, not primarily in the thyroid. For you this is a hint, not proof: with demonstrated metal sensitivity, shutting off the source might help, but the study is small and without a control group.

Procházková et al., Neuro Endocrinol Lett. 2004. PMID: 15349088 (no DOI)

To this day there is no randomised or prospective human study showing that heavy-metal chelation improves the course of Hashimoto's. This gap must be named openly. The general question of how mercury can even be chelated and with what expectations is dealt with in the article on mercury poisoning and chelation. Gentle, food-based approaches you will find in the post on natural heavy-metal elimination. How dangerous amalgam actually is and what the EU ban means is the subject of the article amalgam fillings and mercury exposure.

Evidence overview: established, plausible, open

So that you keep the overview, here are the key statements of this page with their respective evidence status, without sugar-coating.

Statement	Evidence status	Limitation
Key thyroid enzymes are selenoenzymes	Strongly established	Mechanistic reviews, established textbook knowledge
Mercury binds and inhibits these selenium enzymes	Molecularly established	In vitro and animal model, not measured in the Hashimoto's patient
Selenium lowers TPO antibodies	Meta-analyses of RCTs	Clinical relevance of the antibody reduction uncertain per Cochrane
Functional selenium deficiency at normal blood level	Mechanistically plausible	Not directly demonstrated in humans with Hashimoto's, hypothesis
Heavy metals disrupt the T4-to-T3 conversion	Animal plus observation	Population signal and animal data, no proof of causation
Mercury linked to thyroid antibodies	Contradictory	Signal for TgAb only in one study, two null findings
Mercury as an autoimmune trigger (hapten/adjuvant)	Weak, hypothesis	Small, uncontrolled case series, proximity to conflicts of interest
Chelation improves the course of Hashimoto's	Not established	No randomised or prospective human study available

Transparency disclaimer The mechanistic plausibility, that is, thyroid selenoenzymes and the mercury–selenium antagonism, is well established, but largely preclinical, from cells, animals and reviews. The direct human evidence for a causal link between heavy metals and Hashimoto's is thin and contradictory. What is established: selenium can lower TPO antibodies, and mercury binds selenium. What remains hypothesis: mercury causes Hashimoto's. This page claims no causation and does not present chelation as a solution for Hashimoto's.

The thyroid is a biologically understandable target of mercury. But that does not become a diagnosis, it becomes a question you can check.

Frequently asked questions

Can heavy metals trigger Hashimoto's?

There is no proven causal link. What there is, is an unusually concrete mechanistic plausibility: the central thyroid enzymes are selenoenzymes, and mercury binds selenium with high affinity. That makes the thyroid an understandable target. What is established is the plausibility, not proof in humans.

Can amalgam trigger Hashimoto's?

Amalgam is a plausible mercury source close to the thyroid, but the human data are contradictory. One NHANES analysis found a signal for one antibody, two other studies found no association. Assuming amalgam to be the sole cause goes beyond what the data support. The danger of amalgam itself is covered in more detail in the post on amalgam fillings.

Why is my TSH normal even though I have symptoms?

TSH measures the central control. If the peripheral conversion of T4 into the active T3 by the deiodinases is slowed, too little active hormone may reach the cells while TSH and T4 still look unremarkable. This could explain the common finding that the values are okay but you do not feel okay. It is an explanatory model, not a blanket diagnosis.

Does selenium help with Hashimoto's?

Several meta-analyses show that selenium can measurably lower TPO antibodies. Whether this reliably makes you feel better is less clear; the Cochrane analysis rates the clinical relevance as uncertain. Selenium is the best-supported micronutrient in Hashimoto's, but it is no cure-all and, because of its narrow therapeutic window, belongs under medical supervision.

What does Hashimoto's despite taking selenium mean?

If selenium does not bring the hoped-for effect, there are several possible reasons: too short a duration of intake, other contributing factors, or the hypothesis discussed here that a heavy-metal burden functionally binds the selenium. This connection is plausible but not proven in humans. It is a reason to look more closely, not a reason to panic.

Is it true that Hashimoto's disappears after amalgam removal?

It is not that simple. Shutting off the source makes sense, but mercury already stored remains for years, and an autoimmune reaction once set in motion often continues. There is no human study proving an improvement in the course of Hashimoto's through chelation. Honest expectation management matters more here than any promise of cure.

Which heavy metals could harm the thyroid?

At the centre is mercury, because of its strong selenium antagonism. Population data suggest that cadmium and lead could also be linked to altered thyroid values. The mechanistic data are densest for mercury and thinner for the other metals. The general toxicology of these metals you will find on the heavy-metals overview page.

Should I stop my levothyroxine therapy if I chelate?

No. The hormone replacement therapy secures your basic supply and must not be changed or stopped on your own. The heavy-metal question is a complementary lead, never a substitute for your endocrinological care. Every adjustment belongs in medical hands.

What does glutathione have to do with the thyroid?

The glutathione peroxidases protect the thyrocyte from the hydrogen peroxide it produces itself to make hormones. They are at the same time a central tool of the body's own detoxification. This makes glutathione the interface between thyroid protection and heavy-metal defence. More on this in the post on glutathione and heavy metals.

Could my constant exhaustion come from heavy metals rather than the thyroid?

Exhaustion is nonspecific and can have many causes; the thyroid is only one of them. Heavy metals can burden the mitochondria and energy metabolism and overlay a thyroid picture. The lead symptom exhaustion in the heavy-metal context is dealt with separately in the article constantly tired from heavy metals.

Read on in the heavy-metal cluster

This article is the thyroid deep dive of a larger topic. These posts connect directly to the points touched on here.

⚗️

Heavy Metals Overview

Sources, mechanics, diagnostics in the big picture

Pillar 🦷

Amalgam Fillings

How dangerous the mercury really is

🧪

DMPS Challenge Test

Measuring heavy metals correctly, whether and when

🛡️

Glutathione

The body's own detoxifier and cell protector

🩺

Chelating Mercury

Recognising symptoms and reducing the burden

🔋

Fatigue

When heavy metals slow the mitochondria

Shukri Jarmoukli

Physician, Integrative Medicine · ViveCura Berlin

Focused on environmental medicine, heavy-metal diagnostics and the connection between toxin burden and chronic complaints. Skalitzer Strasse 137, 10999 Berlin. This article is no substitute for medical advice or endocrinological care.

Sources

Tier markers: Clinical = meta-analysis, RCT or case series in humans · Human = population or observation · In vivo = animal model · In vitro = cell culture or mechanistic review. The mechanistic plausibility is largely preclinical; the direct human evidence for causation is thin and contradictory.

Huwiler VV, Maissen-Abgottspon S, Stanga Z et al. Selenium Supplementation in Patients with Hashimoto Thyroiditis: A Systematic Review and Meta-Analysis of Randomized Clinical Trials. Thyroid. 2024;34(3):295-313. DOI: 10.1089/thy.2023.0556 [Meta-analysis, clinical, k=35]
van Zuuren EJ, Albusta AY, Fedorowicz Z, Carter B, Pijl H. Selenium supplementation for Hashimoto's thyroiditis. Cochrane Database Syst Rev. 2013;(6):CD010223. DOI: 10.1002/14651858.CD010223.pub2 [Review, Cochrane, clinical, k=4, n=463]
Kong XQ, Qiu GY, Yang ZB, Tan ZX, Quan XQ. Clinical efficacy of selenium supplementation in patients with Hashimoto thyroiditis: A systematic review and meta-analysis. Medicine (Baltimore). 2023;102(20):e33791. DOI: 10.1097/MD.0000000000033791 [Meta-analysis, clinical, k=7, n=342]
Zuo Y, Li Y, Gu X, Lei Z. The correlation between selenium levels and autoimmune thyroid disease: a systematic review and meta-analysis. Ann Palliat Med. 2021;10(4):4398-4408. DOI: 10.21037/apm-21-449 [Meta-analysis, clinical, k=17, n=1911]
Nordio M, Basciani S. Myo-inositol plus selenium supplementation restores euthyroid state in Hashimoto's patients with subclinical hypothyroidism. Eur Rev Med Pharmacol Sci. 2017;21(2 Suppl):51-59. PMID: 28724185 (no DOI) [RCT, clinical, n=168]
Gallagher CM, Meliker JR. Mercury and thyroid autoantibodies in U.S. women, NHANES 2007-2008. Environ Int. 2012;40:39-43. DOI: 10.1016/j.envint.2011.11.014 [Cohort, cross-sectional, human, n=2047]
Kim MJ, Kim S, Choi S et al. Association of exposure to polycyclic aromatic hydrocarbons and heavy metals with thyroid hormones in general adult population and potential mechanisms. Sci Total Environ. 2021;762:144227. DOI: 10.1016/j.scitotenv.2020.144227 [Cohort, population study, human, n=1254]
Barregard L, Enestrom S, Ljunghusen O, Wieslander J, Hultman P. A study of autoantibodies and circulating immune complexes in mercury-exposed chloralkali workers. Int Arch Occup Environ Health. 1997;70(2):101-6. DOI: 10.1007/s004200050193 [Cohort, controlled cross-sectional, human, n=82]
Rachmawati D, Muris J, Scheper RJ et al. Continuing the quest for autoimmunity due to oral metal exposure. Autoimmunity. 2015;48(7):494-501. DOI: 10.3109/08916934.2015.1033688 [Case, case-control study, human, n=78]
Chen J, Ma M, Wang R et al. Roles of glutathione peroxidase 4 on the mercury-triggered ferroptosis in renal cells: implications for the antagonism between selenium and mercury. Metallomics. 2023;15(3):mfad014. DOI: 10.1093/mtomcs/mfad014 [In vitro, human cells]
Pantaleão TU, Ferreira ACF, Santos MCS et al. Effect of thimerosal on thyroid hormones metabolism in rats. Endocr Connect. 2017;6(8):741-747. DOI: 10.1530/EC-17-0220 [In vivo, rat]
Shi Q, Sun N, Kou H, Wang H, Zhao H. Chronic effects of mercury on Bufo gargarizans larvae: Thyroid disruption, liver damage, oxidative stress and lipid metabolism disorder. Ecotoxicol Environ Saf. 2018;164:500-509. DOI: 10.1016/j.ecoenv.2018.08.058 [In vivo, amphibian larva]
Schweizer U, Chiu J, Köhrle J. Peroxides and peroxide-degrading enzymes in the thyroid. Antioxid Redox Signal. 2008;10(9):1577-92. DOI: 10.1089/ars.2008.2054 [In vitro, mechanistic review]
Köhrle J, Gärtner R. Selenium and thyroid. Best Pract Res Clin Endocrinol Metab. 2009;23(6):815-27. DOI: 10.1016/j.beem.2009.08.002 [In vitro, mechanistic review]
Procházková J, Sterzl I, Kucerova H, Bartova J, Stejskal VDM. The beneficial effect of amalgam replacement on health in patients with autoimmunity. Neuro Endocrinol Lett. 2004;25(3):211-8. PMID: 15349088 (no DOI) [Case, case series, clinical, n=35, methodologically weak]
Stejskal V, Hudecek R, Stejskal J, Sterzl I. Diagnosis and treatment of metal-induced side-effects. Neuro Endocrinol Lett. 2006;27(Suppl 1):7-16. PMID: 17261999 (no DOI) [Review, narrative with case series, human, methodologically weak]