In this blog I want to talk about the connection to autoimmune thyroid (mainly Hashimoto’s) and iodine deficiency. I think there is a lot of confusion going around in the health industry about iodine and Hashimoto’s.  But before I discuss this further, I want to provide a little background summary of the disorder and some basic biochemistry.

What is Hashimoto’s?

Hashimoto’s is an autoimmune illness where the body produces antithyroid peroxidase antibodies (anti-TPO) that cause an inflammation of the thyroid gland (Mincer & Jialal, 2021).  Goiter as well as hyperthyroidism and hypothyroidism are common with Hashimoto’s.  Often if there is hypothyroidism, it is the end result of long-standing Hashimoto’s disease.

The incidence of autoimmune thyroid disease is reported to occur in 0.1-5% of the population and quickly rising. Some experts estimate that the incidence is actually closer to 15-20% of the population and is often underreported.

Although conventional medicine has not identified a root cause for Hashimoto’s, I have discovered through my research that Hashimoto’s (and Graves’s disease) are often caused by both iodine deficiency and gluten sensitivity (Brownstein, 2014).  Please keep in mind that nearly all conventional doctors and under the misinformed opinion that iodine supplementation causes autoimmune thyroid diseases.

However, the research does not support this hypothesis. In fact, over the last 40 years, iodine levels have significantly fallen while autoimmune thyroid disorders have been rising in epidemic levels. This also correlates with a rise in iodine deficiency.

Let me give you some examples.  In the US, nearly 60% of women of pregnancy age have iodine deficiency and 15.5% of women in reproductive age are deficient as measured in urinary iodine excretion of levels below 50ug/L (Brownstein, 2014).  The WHO claims that iodine excretion below 50ug/L is classified as moderate/iodide deficiency (Brownstein, 2014). Therefore, if iodine caused autoimmune thyroid problems, you should expect that subjects with autoimmune thyroid disorders would have more iodine in their thyroid, but in fact, they demonstrated to have less.

It boils down to ATP

Our thyroid gland cannot optimally function in a state of iodine deficiency (Chung, 2014).  In a future blog, I will discuss iodine in more detail.  Our mitochondria (energy producing organelles of the cell) contain a process called oxidative phosphorylation to produce ATP (energy).  Within the mitochondria is the NADPH oxidase system.  The production of ATP requires oxygen, magnesium, ADP, vitamins and amino acids (Brownstein, 2014).

Many people with chronic fatigue, autoimmune disorders and fibromyalgia complain they have no energy.  Both Vitamin B2 and B3 are integral cofactors in stimulating oxidative phosphorylation and ATP production.

Hydrogen peroxide- a double edged sword!

Here is the thing.  Hydrogen peroxide is a byproduct of oxidative phosphorylation.  This is a process your body uses to produce energy in the form of ATP.  The production of hydrogen peroxide is critical to the oxidation process of iodine!  Hydrogen peroxide and TPO help to oxidize iodide to form iodine (Brownstein, 2014).

Adequate hydrogen peroxide production is essential for facilitating the oxidation of iodide (Brownstein, 2014).  Without adequate levels, iodine will not be formed from iodide. However, if the production and utilization of hydrogen peroxide is not closely maintained, it can damage the tissue and cause autoimmune thyroid disorders such as Hashimoto’s disease.

The immune system has antioxidant mechanisms to keep from hydrogen peroxide from harming tissues. These include selenium-containing enzyme glutathione peroxidase which functions to keep hydrogen peroxide reduced to water after it oxidizes to iodide.  A deficiency in selenium or precursors to glutathione (glycine, glutamine, cysteine) can impair this defense mechanism.  Once iodine is formed, it undergoes organification and becomes part of cholesterol, lipids and proteins.

RDA levels of iodine is 150ug/day, which can be bound to thyroglobulin to make the thyroid hormones- T1, T2, T3 and T4.  But what most people don’t is it takes larger doses of iodine (as much as 100X RDA) for iodine to produce the important iodo-lipids such as δ-iodolactone.

“Really Dumb Allowances”

Basically, the RDA amounts of iodine barely give the cell enough iodine to make thyroid hormone and prevent goiter. That is often why RDA is often nicknamed “really dumb allowances”.

When you ingest RDA levels of iodine, it can lead to iodine deficiency.  There is not enough iodine to produce iodinated lipids, such as δ-iodolactone and others that puts a brake in the pathway to oxidize iodide.  This may result in a temporary production of TOO MUCH hydrogen peroxide.  This excessive hydrogen peroxide can damage the enzyme TPO.

Too much hydrogen peroxide can damage the enzyme TPO!

When the TPO is damaged, the body responds by producing antibodies to TPO, or anti-TPO antibodies.  A diagnosis of Hashimoto’s requires the presence of anti-TPO antibodies.  As the damage worsens, surrounding proteins such as thyroglobulin can also be damaged, which then can produce anti-thyroglobulin antibodies.

Most people with Hashimoto’s present with antibodies to TPO and thyroglobulin.  Patients with autoimmune thyroid can fluctuate symptomatically between overactive thyroid (hyperthyroidism) and underactive thyroid (hypothyroidism).  They can also suffer from symptoms of both.

In the early stages, too much hydrogen peroxide is damaging the thyroid. As the illnesses progresses, this can cause imbalanced thyroid hormone.  Thyroid hormone is important for ATP production. 

This can lead to fatigue, exercise intolerance, brain fog and muscle aches and pain.

Treatment requires understanding

To understand how to treat this condition, you have to understand the mechanisms behind it.  First, you need enough iodine to produce iodo-lipids such as δ-iodolactone.  You also need to stimulate the NADPH oxidase pathway that is integral to energy production.  That would require providing the cofactors Vitamin B2 (riboflavin) and B3 (niacin) that are cofactors of the NADPH oxidase system that will not only stimulate the mitochondria to product more energy but also provide thyroid cells with enough hydrogen peroxide to properly oxidize iodide.

You can also run a Nutreval and HTMA to identify other vitamin and mineral imbalances that are impairing your energy pathways.

How is it treated conventionally?

The conventional approach to treating autoimmune thyroid disorders revolves primarily around alleviating symptoms of autoimmune illness which involve using medications that block thyroid hormone production.  However, this does not address the underlying cause of the problem. 

Radioactive iodine is often also used to treat autoimmune thyroid disorders, which destroys the thyroid gland.  The theory behind its use is that wherever the radioactive form of iodine binds, the radioactivity will destroy the surrounding cells.  In the case of autoimmune thyroid disorders, the binding of the radioactive iodine to the thyroid gland will destroy the thyroid tissue by the radioactive isotope.

But since excessive thyroid tissue is not the root cause of the problem, this treatment is often ineffective.  Radioactive iodine is also not fully safe. The radioactive iodine will bind to other sites in the body besides the thyroid such in the breasts of women.  In fact, researchers reported a 400% increase in thyroid cancer due to radioactive iodine.

How is it treated nutritionally?

The initial treatment for early or late-stage autoimmune thyroid is to best done nutritionally.  This is by correcting iodine deficiency together with cofactors for energy production by identify them through proper lab testing. These often include your B vitamins, vitamin C, magnesium, and their nutrient partners.

I also recommend everyone to do either a spot urine or 24-hour loading test for iodine, which I do in my lab panels as well.

If iodine levels are low, you need to follow a comprehensive iodine dosing protocol that is a therapeutic for repleting iodine levels.  People often need 12-50mg of iodine per day, which is much more than the RDA, in the form of a combination of iodine and iodide.  It is very important to work with a healthcare provider knowledgeable on how to dose iodine to get results.

In addition, you have to support your energy pathways with the proper cofactors as identified on proper lab testing. I like to use Nutreval and HTMA.

Finally, you have to correct oxidant stress in the thyroid gland and mitochondria with proper antioxidants.  These includes vitamin C, vitamin E, and plant antioxidants and plant compounds like sulforaphane, curcumin, resveratrol.  In fact, there is a strong correlation to many different pathways such as RANTES and INOS with oxidative stress, that I will explain in a future blog.

There are many ways to minimize oxidative stress in the body.  Two of the most important wants are to drink adequate pure water and eat a healthy diet.  Also, ensure you have adequate intake of unrefined sea salt in the body. And finally, make sure you are not deficient in magnesium, and if you are, replete it. Magnesium acts as an antagonist to excess intracellular calcium levels which can fuel the oxidative pathways.

Oxidative stress is like a fire burning in our body.  You can put the fire out by giving your body what it needs, and removing things that are causing it. These include things such as mold toxins, infections, leaky gut and metal and environmental toxicity, EMF’s, stress, and others.

To achieve the best results, schedule a Discovery call with me so we can figure out the proper testing to run to investigate what may be contributing to oxidative stress. The best results are achieved with a comprehensive holistic approach.

Why doe TSH Rise when using iodine?

Sometimes this claim is made when TSH elevates shortly after starting iodine therapy.  This is a normal response and not a reason to stop taking iodine.  TSH is released by the pituitary gland to stimulate the thyroid gland to produce thyroid hormone.  It also helps stimulate the body’s production of the iodine transport molecules (sodium-iodide symporter NIS).

With adequate amounts of NIS, iodine would not be able to enter the cells and be utilized.  The body increases the production of TSH to stimulate more NIS to shuttle more iodine into the thyroid cell to produce more thyroid hormone.  An elevated TSH without clinical signs of hypothyroidism (fatigue, hair loss, headaches), as well as normal T3 and T3 levels does not indicate a hypothyroid condition.

In this case the TSH elevation is normal and expected. This is often due a normal response to the body due to iodine supplementation, and it may remain elevated for 3-6 months before lowering into the reference range.  The lowering THS indicates the body’s iodine stores are increasing.

I believe all individuals with a thyroid problem should have their iodine levels tested alongside an HTMA. Adding on Nutreval will give you a well-rounded Root Cause investigation to your thyroid condition.

Keep in mind, about 1/3 of patients being treated for hypothyroidism will need to lower their dose of thyroid hormone when an iodine deficiency disorder is corrected.  The other 2/3 can maintain their dose.

Contradictions of using iodine

Please note, some people also worry that iodine will induce hyperthyroidism. According to Dr. David Brownstein, MD, one rare condition that can predispose someone to iodine-induced hypothyroidism is in patients that have autonomously functioning module on their thyroid.  This is often referred to as a hot nodule on a thyroid scan.  This can be diagnosed with a thyroid scan, and is often diagnosed after someone has a trial of iodine therapy and the person becomes hyperthyroid after taking the first couple of doses.  These patients must avoid all sources of iodine, such as supplements and foods such as seaweed until the nodule is surgically removed.


Brownstein,D. (2014). Iodine.  Why you Need it, Why you Can’t Live Without It.

Chung H. R. (2014). Iodine and thyroid function. Annals of pediatric endocrinology & metabolism19(1), 8–12. https://doi.org/10.6065/apem.2014.19.1.8

McLeod DS, Cooper DS. The incidence and prevalence of thyroid autoimmunity. Endocrine. 2012 Oct;42(2):252-65. doi: 10.1007/s12020-012-9703-2. Epub 2012 May 29. PMID: 22644837

Mincer DL, Jialal I. Hashimoto Thyroiditis. [Updated 2021 Sep 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459262/