The topic of iodine and hashimotos disease stirs up something deep in me. I think it is because of the constant warnings I see from thyroid “specialists” that assert that using iodine with hashimotos is like throwing gas on a fire when it isn’t… well it can be if done incorrectly, but I’ll share that in a few minutes.
Iodine levels have dropped 50% over the last 30 years yet the incidence of thyroid disease has increased at an alarming rate. Many people are suffering more than ever from hypothyroidism and at its worst autoimmune thyroid disease and cancer. It is estimated that 20 million Americans have a form of thyroid disease. Up to 60% of those with the disease are unaware they have a condition. Women are 5-8 times more likely to have a thyroid problem than men are. With these numbers how can iodine be to blame when it has been removed from our food supply and is depleted in our soils? It isn’t – it has been wrongly accused of a crime it did not commit.
So lets talk about what happens in an autoimmune thyroid condition. Autoimmune conditions in general in the body represent something that is not normal. The body’s immune system is intelligent in knowing that it doesn’t belong. With an autoimmune thyroid condition this is often related to the thyroid tissue itself. The tissue undergoes oxidative stress due to inflammation within the cells. This can cause mutations of the tissue which results in antibodies coming to the rescue of the body to “attack it” and get it back in order. However in a thyroid autoimmune condition this state can continue to be an issue despite the best efforts of the antibodies to remove the problem. One underlying cause of hashimoto’s is an iodine deficiency.
Please excuse the drawings but I wanted to relay specific information and every pre-made drawing did not share the total picture I wanted to convey.
So let’s walk through the process of iodide in the cells. Please keep in mind that this is not a detailed “walk through” but one to get the general pathway. The pituitary gland stimulates the TSHR via TSH. This then acts upon the NIS (Na+I-) symporter to tell the cell to take iodide into the cell. The NIS is located at the basolateral membrane. This process of pulling into the cell requires ATPase. Iodide is pulled into the thyroid follicular cell where thyroglobulin is made in the endoplasmic reticulum (left center of the cell). Then comes the oxidation of iodide. Iodide within the follicular cell moves to the apical surface of the plasma membrane before entering into the follicular lumen. This transport is regulated by a sodium independent iodide/chloride transporter called pendrin. Iodide is then oxidized to iodine.
Then organification of thyroglobulin occurs where iodination of tyrosine residues within the thyroglobulin (Tg) molecule occurs.
Organification is where iodine becomes a part of lipids, proteins and cholesterol. Organification signals a binding to an organic molecule. So in this case iodine is bound to thyroglobulin to make hormones. Another critical thing can occur at this point when enough iodine is supplied, and it is the often an excluded topic in this discussion. When iodine is available in amounts of at least 100x the RDA (15 mgs) iodo-lipids like delta-iodolactone are created. This is the process of iodine being organified to lipids. Without higher levels of iodine available, insignificant amounts are created. The RDA was defined as a method by which the body would create thyroid hormones and prevent goiter. No consideration was given for these iodolipids and their thyroid cell regulatory effect.
The first iodination that occurs forms monoiodotyrosine or MIT. The second is diiodityrosine or DIT. MIT forms T1, DIT forms T2 and then the MIT and DIT couple together to form thyroid hormones T3 and T4. One MIT + one DIT form T3. Two DITs form T4. This reaction is activated by thyroid peroxidase (TPO). The H2O2 used in this process is a result of the NADPH Oxydase system.  This process is inhibited by certain iodolipids. [2-3] The same iodolipids appear to control damage from excess iodine.
The indirect action of I2 could be exerted by its formation of covalent bonds to specific lipids such as arachidonic acid (AA) or eicosapentaenoic acid, forming 6-iodo-5-hydroxy-8,11,14-eicosatrienoic acid (also called 6-iodolactone; 6-IL) or alpha-iodohexadecanal, respectively. These iodocompounds have been detected in thyroid tissue of rat, pig, horse, and human origin, and they mimic some of the inhibitory effects of excess I? on several thyroid parameters. 
Thyroid hormone creation is the only result of iodide being supplied at the RDA of 150 mcgs. Thyroid hormones are then stored inside thyroid follicles as colloid. These hormones can meet the potential thyroid hormone needs for several months. We’ll stop with the pathway description at this point since we have covered both the areas of concern in hashimotos. The Tg and TPO processes. It is TPO Ab and Tg Ab that are measured in Hashimotos conditions.
When we look at the image below we can see the two areas that experience oxidative stress. The first is at the follicular cell level with damage to the nucelus / DNA. This results in nodular goiters and eventually thyroid cancer. Several things like heavy metals, halide toxicity and low nutrient levels can cause this damage in the cells. But for the purpose of evaluating TPO and Tg Ab’s we will look to the other area. The oxidative stress in the thryoid hormone creation is the main area of concern.
So what goes wrong in an autoimmune thyroid condition?
- Oxidative damage – This can result from too much H2O2 that damages TPO.
- Selenium deficiency – Selenium is a key nutrient in approximately 11 different enzymes. There are two selenoenzymes involved in the thyroid process. Glutathione peroxidase and iodothyronine deiodinase. The important selenoenzyme in autoimmune conditions is Glutathione peroxidase. It contains both antioxidant and protective properties from oxidative damage. Glutathione peroxidase can react with the H202 to reduce it to water. This is a valuable function in the reduction of the oxidation in the cells which can cause inflammation. This is why selenium is recommended as part of the iodine supplementing protocol.
- Iodine deficiency – remember those iodolipids we discussed earlier? Here’s why it matters. If you supplement with iodine in doses less than the 15 mgs (or more – because one size never fits all) you will begin the journey of iodine through the cells to where the oxidation process begins. But how does the body deal with that oxidation and limiting the damage to the cells? The first thing thing is the glutathione peroxidase that we just discussed. The other are iodolipids – specifically delta iodolactone. When you supply low amounts of iodide you are stoking the fire and it is like putting fuel on the flame because no iodolipids – or too few are created. But when you give the body more than it needs for thyroid hormone creation you get a bonus – iodolipids that work to protect the thyroid gland from the damage. These iodolipids also work at the cellular regulatory level in inducing apoptosis (programmed cell death) of any abnormal cells that may be created. Thus the body doesn’t need to use antibodies to ‘clean up the mess’.  The inflammatory process can be reduced and the oxidative damage will also be reduced resulting in relief of the antibody attack.
- The other issue – Magnesium. It is recommended that magnesium is used as part of the full protocol . Magnesium is also important in numerous enzyme reactions in the body. If we look at the oxidation process we will see that calcium is part of it. When the oxidation is too high, another “antidote” to this is to supply magnesium.
(Thank you to Dr Brownstein who created this format for illustration)
5. Finally Vitamin C – This is another nutrient that is recommended in the protocol that helps to maintain balance. Vitamin C offers support against oxidant stress on the thyroid gland. It also works to heal the symporters that pull iodine into the cells. Many of the thyroid cells especially in thyroid cancer lose their ability to uptake iodine.
You may also see B2 and B3 mentioned in relation to iodine and hashimotos. These nutrients can be beneficial in supporting the ATPase process to support the uptake of iodine. In individuals with hashimotos it may help to increase energy and the feeling of well being.
I realize this is a tough subject to work your way through but I hope that this has helped to start the process of understanding why doctors such as Dr David Brownstein and his partners have had incredible success in supplementing with iodine in their autoimmune thyroid patients. Other less vocal doctors using iodine in their practices in high doses are seeing benefits as well. The key is to follow the protocol of support nutrients along with not being timid about the dosing of iodine. Have no fear. Iodine has been used safely and effectively for 200 years!
My hope is that all of you find healing and happiness and I believe that iodine can be a big part of that healing.
Stephanie Identification of delta-iodolactone in iodide treated human goiter and it inhibitory effect on proliferation of human thyroid follicles.  Thyroid autoregulation: evidence for an action of iodoarachidonates and iodide at the cellular membrane level.  Thyroid autoregulation Inhibition of goiter growth and of cyclic AMP formation in rat thyroid by iodinated derivatives of arachidonic acid.  Evidence that iodolactones are the mediators of inhibition by iodine on thyroid  The role of iodine and delta-iodolactone in growth and apoptosis of malignant thyroid epithelial cells and breast cancer cells.