The answer is: both.
- If a person suddenly gets a huge amount of iodine via ingestion or other means, it’s generally agreed that a normally functioning thyroid gland will “shut off” or “stop thyroid hormone production” temporarily. This is presumably to protect the gland from being acutely “overdosed” with iodine, and to give the gland time to appropriately upregulate or downregulate the receptors, enzymes, and other processes involved with iodine that it uses to produce thyroid hormone. It’s considered a normal homeostasis response. The body is doing this all day, every day, with every other cell and process as well, and not just the thyroid gland. If higher iodine intake continues longer term, in normal people with healthy thyroid glands, the necessary adjustments will take place to get used to these higher amounts of iodine. For example, in times of iodine excess, iodine will be excreted by the kidneys more instead of being captured by the thyroid gland. And the thyroid gland will then once again “turn on” and start making thyroid hormones again. This is called the “Wolff–Chaikoff Effect”.
- On the other hand, most people are aware that “iodine is needed by the thyroid gland to make thyroid hormones”. This is most certainly true, and if a person is getting too little iodine, the thyroid gland and axis will try to maintain homeostasis and adjust to the smaller amounts of iodine coming in. For example, in times of iodine scarcity, iodine will be recycled in the body instead of excreted by the kidneys. Receptors, enzymes, and other regulatory processes will change to accommodate this decreased iodine intake and make sure that every cell is still getting the iodine it needs despite the fact less iodine is coming in. If a person has been low in iodine for a long time, and suddenly increases their iodine by a tiny amount, the thyroid gland will “turn on” full throttle to capture and utilize this iodine.
In the “old days”, both potassium iodide and Lugol’s Iodine were used to treat Grave’s disease, which is hyperthyroidism. This is because large doses of potassium iodide (iodine) can “shut down” the thyroid gland either temporarily or permanently, or enough so that the person was not hyperthyroid anymore. This is presumably due to the “Wolff-Chaikoff Effect” I mentioned earlier. Currently, patients undergoing thyroidectomies may be given potassium iodide in large amounts for 10 days before the surgery, and right before surgery. If it’s an emergency surgery, a large dose will also be given before surgery. Again, this is because large amounts of potassium iodide will “shut down” the thyroid gland and prevent thyrotoxicosis (hyperthyroid flares) during surgery. How much potassium iodide will be given? Different protocols will vary, but one example is 50 mg (yep, that’s MILLIgrams) three times a day for 10 days before surgery, or 150 mg/day. That’s a lot of iodine – way more than the 150 ug (MICROgrams) recommended per day for the general population. (In fact, 150 mg is equal to 150,000 ug — or a thousand times higher). In this case, it’s being used to prevent thyrotoxicosis (hyperthyroid flares). In this case, surgeons are taking advantage of the “Wolff-Chaikoff Effect” as a protective measure during surgery. But another point to take home from this, is that in general, for most people, as long as you don’t have a true iodine allergy, the rest of the body can handle these large amounts of iodine without a problem. Excess iodine will simply be excreted from the body.
So a large amount (milligrams) of potassium iodide will “shut down” the thyroid gland temporarily. It’s almost like the thyroid gland saying “Hey man, we’ve got enough iodine here in the factory, we’re gonna shut down production!” But a little amount of potassium iodide – usually micrograms, like the small amounts we get in our daily diets – is used by the thyroid gland to manufacture thyroid hormones and keeps the thyroid gland “turned on”. The motto of the normal healthy thyroid gland is “Take what you need and leave (excrete) the rest” when it comes to iodine. No matter how much – or how little – iodine intake occurs, there are numerous homeostasis mechanisms in place to precisely control how much your thyroid gland cells – and all the other cells in your body – are exposed to iodine.
When a person develops thyroid problems, in particular Autoimmune Thyroid Diseases such as Hashimoto’s Thyroiditis and Grave’s disease, as well as Autonomously Functioning Nodules or Thyroid Cancer, all bets are off. The normal homeostatic mechanisms no longer work very well or at all. What this means is that in some people with these conditions, taking large amounts of iodine will “shut off” the thyroid gland permanently instead of just temporarily. In extreme cases, sometimes any amount of iodine, even the tiny microgram amounts, will “shut off” the thyroid gland. On the other hand, the opposite could occur too: sometimes large amounts of iodine can cause or exacerbate hyperthyroidism in people prone to it. And sometimes, even the tiniest amounts of iodine can cause hyperthyroid “flares” in people with AITD or autonomously functioning nodules. Sometimes, even the tiniest amounts of iodine are like “putting gasoline on a fire”. So it all depends on the type of pathology that’s going on with the thyroid gland that determines what will happen when iodine is ingested. This may be true if someone has an unknown subclinical, or “silent” thyroid condition as well. In this case, taking iodine may “unmask” this subclinical thyroid problem, making it appear that iodine is the problem. In reality, the problem may have already existed and taking iodine simply exposed it.
This is why different people with differing thyroid problems will have different responses to taking the exact same amounts of iodine. If you know you’ve got a thyroid problem, I don’t think it’s a good idea to “just take iodine” without understanding the possibilities first. And if you don’t know if you have a thyroid problem, I think it is a good idea to try and find that out first, in particular, if there’s an autoimmune component. Having any of the antibodies not only makes the TSH much less reliable as a thyroid testing screen, but will make taking iodine more complicated as well.
What was happening in my particular case? I have a classic presentation of Hashi’s, with serum TPO antibody titers quite high. Hashi’s is an “iodine organification” problem, which basically means there is a problem with iodine metabolism and homeostasis. I certainly confirmed this for myself with my own experimentation with iodine. And when I was OFF thyroid hormone medication, my thyroid gland cells were exquisitely sensitive to the slightest bit of iodine. The slightest bit of iodine, in microgram amounts, would “shut off” my thyroid gland, and certainly large amounts of iodine did the same.
How long would my thyroid gland remain “shut off”? Well, for as long as the iodine remained in my system, which for me, turned out to be about 5-6 hours. At that point in time, if I didn’t supply more iodine, my thyroid gland would attempt to “turn on” again. But I have Hashi’s, where much of the actual thyroid gland and cells producing thyroid hormone were being destroyed by my immune cells. These cells weren’t working very well anymore. So I didn’t have this nice, controlled, steady start up of thyroid hormone again. Instead, it was like my thyroid gland would “wake up” with a bang, spitting out thyroid hormone in fits and starts. These “fits and starts” were like little thyroid “flares”. They were probably caused by 1) thyroid nodules, which people with Hashi’s often have, and/or 2) immune cells “dive bombing” and destroying the thyroid cells, releasing boluses of the T4 and T3 hormone into the bloodstream. In fact, in my experience, it seemed that these “flares” occurred whenever there was a perceived deficit in thyroid hormone levels within me. I came to see these autoimmune attacks on my thyroid as a last ditch effort of my body attempting to get T3, T4, and Iodine quickly and immediately into my blood stream. Hashi’s and other AITD’s are considered by many to be the end stage disease process of a fundamental problem which lies elsewhere. Based on my own experience, I would tend to agree with this.
To avoid these flares, how about just keep taking the iodine, every 5-6 hours, to keep the thyroid gland “shut off”? This could work, and in fact, when I did my little “iodine trial” while I was ON thyroid hormone medication, this contributed to making sure my thyroid gland stayed “shut off”, thereby ensuring there was no endogenous hormone production occurring (confirmed with labs). But if I was NOT on thyroid hormone medication, the problem with this approach was twofold: 1) I would eventually run out of T3 and T4 if my thyroid gland was not producing it, and 2) The longer my thyroid gland remained “shut off”, the greater the “rebound” effect, or flaring would be once I stopped the iodine. Therefore, I could never really stop the iodine in this case, or I would pay for it big time with flaring after wards.
But my problems were even bigger than just the thyroid gland being affected by iodine. Remember that when I was ON a fully suppressive dose of T3 and T4, if I wanted to take iodine, I was one of those people who are forced to decrease my T3/T4 dose to prevent symptoms of hyperthyroidism. My thyroid gland was completely “shut off” (confirmed with labs), and had nothing to do with this phenomenon. If I felt “hyperthyroid”, it was not because my thyroid gland was spitting out more hormone. In fact, I was decreasing my T3 and T4, so I was getting less hormone. For some reason, in my body, higher levels of iodine meant that my T3 and T4 serum levels had to be lower. And that had nothing to do with my thyroid gland. Which brings us to the next section.