Iodine and Selenium: The Two Nutrients Your Thyroid Can't Live Without

Iodine and selenium are two necessary nutrients your thyroid needs to make thyroid hormone. Iodine is necessary to build thyroid hormones, selenium is needed for the enzymes that build (and convert) thyroid hormone. This post expands on some of the ways that getting too little of either one of these (including avoiding iodine entirely with Hashimoto's… often at the recommendation of endocrinologists) shows up in symptoms.

Should you eliminate iodine from your diet with Hashimoto’s?

When I was diagnosed with Hashimoto's, I quickly stumbled into one of the biggest controversies in thyroid health: iodine.

Half the internet insisted iodine was essential for thyroid health. The other half (and my endocrinologist) warned that anyone with Hashimoto's should avoid it like the plague.

This was back when I still did what my doctor told me to do without question… the result was… not good (more on this below).

As with everything in health, the issue isn’t is iodine good for you or bad for you.

It's about balance.

Your thyroid cannot make thyroid hormone without iodine. Full stop. And, many of us have diets deficient in iodine. Here’s why that matters.

NOTE: If you’ve had your thyroid removed and think “well, this conversation doesn’t apply to me.” Nothing could be further from the truth. Your breasts, your ovaries, (if you’re a guy, your prostate), will thank you for continuing to read.

Iodine Is Part of Thyroid Hormone (it’s in the name)

Although the thyroid weighs only about 20 grams (just over half an ounce), it stores roughly 70-80% of the body's iodine, reason being thyroid hormones themselves contain iodine.

It's literally how the thyroid hormones are named (based on how many iodine atoms they contain):

• T4 contains four iodine atoms – this is the pro-hormone, accounting for about 80% of the total thyroid hormone made daily by the thyroid gland

• T3 contains three iodine atoms – this is the “active” form of thyroid hormone, accounting for about 15-20% of the total thyroid hormone made daily by the thyroid gland

Without iodine, your thyroid lacks one of the necessary raw materials to build these hormones.

Before we move on…

The Halogen Problem: How Bromide, Fluoride, and Chloride Interfere with Thyroid Hormone

Quick revisit to high school chemistry. Remember the periodic table? Iodine sits in the halogen family along with fluorine, chlorine and bromine. And if you've spent any time in the alternative-thyroid world, you've probably heard some version of this:

Fluoride, bromide and chloride compete with iodine for iodine receptors in the thyroid.

Quick sidebar: It might be confusing to read iodine vs. iodide. Same thing with the other halogens.
Iodine is the molecule: I2
Iodide is the atom: I-
Same with bromine/bromide: Br2 / Br- and the other halogens (chlorine/chloride and fluorine/fluoride).

Now, as I was saying. In many circles, the story that these other halogens compete with iodine for receptors in the thyroid is a little bit of a simplification.

For starters, there isn't an “iodide receptor” sitting on (or in) the thyroid.

Second, the binding spots for iodide don’t allow chloride to bind. And thank goodness, because chloride is everywhere.

Basic table salt is sodium chloride. If every member of the halogen family competed equally with iodine simply because it lived in the same column of the periodic table, we'd have a pretty major design flaw.

The actual physiology is much more interesting.

How Iodine Gets Into the Thyroid

Before your thyroid uses iodide to create thyroid hormones, it first has to get it out of your bloodstream and into the thyroid cell.

It does this using the sodium-iodide symporter (NIS) protein. This protein allows active transport of iodide from the blood stream into the cell and brings two atoms of sodium (Na+) along with one iodide atom into the cell.

The NIS symporter is evolutionary-tuned for larger halogens. This means small halogens like chloride and fluoride can't pass through the NIS door.

Bromide in particular can be taken into the thyroid by the sodium-iodide symporter because of its large size (it’s even larger and more diffuse than iodide).

There are molecules that interfere with the NIS, two notable ones:

• Perchlorate (an organochloride molecule) is particularly potent, which has historically been used in experiments to block thyroidal iodide uptake.

  Chloride itself doesn't behave this way.

• Thiocyanate (from cigarette smoke and brassica vegetables… think broccoli, Brussels sprouts, cauliflower, and bok choi… I’ve talked about the goitrogenic effect of these veggies in other articles)

Bromide is more interesting because experimental research shows that high bromide exposure changes iodine metabolism. You may be thinking “well, I’m not exposed to bromide.” Interestingly, back in the 1970s, bromide replaced iodide as a conditioner for flour used to make bread.

Bromides are also commonly used flame/fire retardants in office and home furniture (mattresses, carpet, couch cushions, upholstery, etc.). Now that I’ve hopefully convinced you this is something to pay attention to, let’s get back to the research.

In animal studies, increasing bromide exposure decreased iodide accumulation in the thyroid and increased iodide loss through the kidneys. Bromide also enters thyroid tissue, and brominated tyrosines have been identified in the body (interesting because to create thyroid hormone, the thyroid attaches iodide to tyrosine so finding brominated tyrosine means the thyroid can attach bromide to tyrosine just like it can iodide… in other words, bromide is an endocrine disruptor, interfering with hormone function).

3. Fluoride: A Different Mechanism Entirely

Fluoride (F⁻) is the smallest of the halogens. It doesn't behave like iodide with the sodium-iodide symporter, and TPO (thyroid peroxidase) hasn’t been shown to substitute fluoride for iodide when making thyroid hormone.

So whatever effect fluoride has on thyroid physiology isn't adequately explained by fluoride stealing iodide's spot.

One proposed mechanism is much further downstream.

Fluoride easily complexes with trace aluminum to form aluminofluoride species, including AlF₄⁻. This apparently happens pretty easily especially under acidic conditions (think inside the stomach) and these aluminofluoride compounds mimic phosphate (an extremely common molecule in the body) and can activate G proteins.

Inside the thyroid, fluoride alters G-protein signaling pathways, effectively scrambling the hypothalamic-pituitary-thyroid messaging center and specifically impacting the pituitary’s secretion of TSH.

NOTE: You may recognize TSH, Thyroid Stimulating Hormone, from lab tests… what’s so interesting about this is that TSH can be low or in-range and you still have poor thyroid function something I talk about in other posts.

How does the thyroid build thyroid hormone?

The thyroid uses an enzyme called thyroid peroxidase (TPO) to attach iodine onto the amino acid tyrosine. That reaction requires hydrogen peroxide (of all things).

This means as the thyroid makes thyroid hormones, it generates oxidative stress.

As bad as that sounds, here’s where we have to hold two perspectives at once. The body is constantly involved in processes that produce oxidative species and reducing (anti-oxidant) species. This is how it makes energy. And, health resides when these two are in balance. Which is where selenium enters the picture.

Selenium Is the Thyroid's Fire Department

Selenium is incorporated into several antioxidant enzymes that neutralize hydrogen peroxide before it damages thyroid tissue. One of the most important is glutathione peroxidase.

When selenium levels in the body are low, glutathione peroxidase levels are lower, so there isn’t enough glutathione peroxidase to neutralize the hydrogen peroxide. Hydrogen peroxide lingers longer than it should causing more oxidative stress within the thyroid. Replenish selenium, and the body now has the raw material it needs to make more glutathione peroxidase to quench that oxidative fire.

Selenium Does More Than Protect the Thyroid

Selenium has another critically important job.

As I mentioned earlier, most of the hormone your thyroid produces is T4, a pro-hormone. The active form of thyroid hormone is T3. To become active, T4 must lose one iodine atom. This happens both in the thyroid gland and locally within the tissues of the body.

Every tissue of the body has specialized enzymes that are able to transform T4 the pro-hormone into T3 à this is a super simplified version of what’s really going on, for the full story, head here. The enzymes responsible for this are called deiodinase enyzmes, and these enzymes are selenium-dependent.

Without adequate selenium, converting T4 into T3 becomes much less efficient.

In other words... iodine helps build thyroid hormone.

Selenium helps activate it.

Both are required.

Iodine Deficiency: Impacts beyond the thyroid

When I was first diagnosed with Hashimoto's, I started supplementing selenium at the recommendation of my endocrinologist.

I also stopped taking iodine altogether based on her recommendation. This meant not only did I stop eating seaweed, I also stopped all dairy (dairy is a decent source of dietary iodine).

Within a month, I developed a painful breast cyst. Someway, somehow, I knew these were related. So, I started digging into the research.

The thyroid isn't the only organ that needs iodine.

Breasts.

Ovaries.

The prostate.

The salivary glands.

Even the stomach uses iodine.

Those sodium-iodide symporters I mentioned earlier? They’re found in a surprising number of different tissues of the body the tissues above plus the kidneys, liver, lungs, and the GI tract (among other tissues/organs).

Once I restored iodine while maintaining adequate selenium, the cyst resolved on its own.

Read that again. Once I restored iodine to my diet, the breast cyst resolved on its own.

In case you want to dive deeper into the connection between breast health and iodine, check out my article here.

If you're the woman who's already tried the elimination diets, reacted to every protocol you’ve started, and feel like you don’t know where to turn next, I’ve been where you are.

Doing everything correctly and still stuck in a flare loop.

That's not a compliance issue. That's what happens when isolated fixes get thrown at a body that doesn’t have enough capacity to use those fixes in the first place.

This is the entire premise behind Reclaim Wellness Intensive. It’s not another list of what to add or remove, it is the sequence and the reasoning underneath it. Why it’s impossible to approach health in terms of black and white. Why there is no magic pill or magic nutrient. This is a different way of seeing the body and the strategy I developed to walk my own body out of life limiting symptoms like mast cell activation, chronic urinary urgency/interstitial cystitis, and ultimately, orthostatic intolerance.

FAQs: Iodine and Selenium for Thyroid Health

Q: Should someone with Hashimoto's avoid iodine completely? A: In my mind, absolutely not. Other tissues of the body need iodine. Most notably reproductive organs: breasts, ovaries, (for men, prostate) and other tissue also rely on iodine. Many tissues in the body express sodium-iodide symporters (NIS) to allow iodine into cells.

Q: What does selenium actually do for the thyroid? A: Selenium fuels glutathione peroxidase, the enzyme that neutralizes hydrogen peroxide generated during thyroid hormone production (in simple terms selenium tamps down inflammation naturally generated in the thyroid during creation of thyroid hormone).

Selenium is also required by the deiodinase enzymes that convert T4 into active (or reverse) T3. There are three deiodinase enzymes (D1, D2, and D3) and each tissue of the body expresses these three enzymes in different ratios. Every single one of these enzymes requires selenium for proper function.

Q: Can bromide really interfere with thyroid function? A: Yes. Bromide is a large, diffuse halogen (like iodide). It’s been shown that bromide can enter the cell through the sodium-iodide symporter (NIS) , and animal studies show brominated tyrosine molecules (indicating the thyroid has added bromide rather than iodide to tyrosine, the precursor of thyroid hormone).

Q: Does fluoride block iodine absorption in the thyroid? A: Not through the same mechanism as bromide. Fluoride is too small for the sodium-iodide symporter; the proposed pathway instead involves fluoride-aluminum compounds disrupting signaling between the pituitary and thyroid disrupting the hypothalamic-pituitary-thyroid (HPT) axis and altering TSH expression.

Q: Why would TSH look normal if thyroid function is actually low? A: TSH reflects pituitary signaling, not tissue-level thyroid hormone activity/tissue level thyroid function. Local conversion of T4 to T3 is shown to differ significantly between the hypothalamus (where the hormone cascade starts) and pituitary (which releases TSH).

The Bigger Picture

Iodine is a necessary substrate to build thyroid hormones, T3 and T4. Selenium activates the enzymes that convert T4 (the prohormone) to T3 (the active hormone) or reverse T3 (considered the inactive hormone). Iodine and selenium both have roles in the body beyond the thyroid, and these two nutrients are essential for health.

Related articles

More on iodine and breast health (with references). My original post on this.

Low T3, Normal TSH, and Low Thyroid Symptoms: What’s really going on?

What Low T3 has to do with MCAS, POTS, and Dysuatonomia

References

Gadisi RP, Naicker M and Naidoo S (2025) The extra-thyroidal distribution of sodium iodide symporter. Front. Endocrinol. 16:1567405. doi: 10.3389/fendo.2025.1567405.

Pavelka S. (2004). Metabolism of bromide and its interference with the metabolism of iodine. Physiological Research, 53(Suppl 1), S81–S90. PMID: 15119938.

Buchberger W, Holler W, Winsauer K. (1990). Effects of sodium bromide on the biosynthesis of thyroid hormones and brominated/iodinated thyronines. J Trace Elem Electrolytes Health Dis, 4(1), 25–30. PMID: 2135954.

Vobecký M, Babický A, Lener J, Svandová E. (1996). Interaction of bromine with iodine in the rat thyroid gland at enhanced bromide intake. Biological Trace Element Research, 54(3), 207–212. DOI: 10.1007/BF02784432.

Schomburg L. (2012). Selenium, selenoproteins and the thyroid gland: interactions in health and disease. Nature Reviews Endocrinology, 8, 160–171.

Dohán O, de la Vieja A, Paroder V, et al. (2003). The sodium/iodide symporter (NIS): characterization, regulation, and medical significance. Endocrine Reviews, 24(1), 48–77. DOI: 10.1210/er.2001-0029.

Arthur JR. (1991). The role of selenium in thyroid hormone metabolism. Canadian Journal of Physiology and Pharmacology, 69(11), 1648–1652. DOI: 10.1139/y91-243.