It is estimated that 12% of people will have a thyroid problem in their lifetime. This week we’ll take a look at three supplements that could help or harm your thyroid.
Dr. R’s Fast Facts
- Iodine, vitamin D and selenium can all impact thyroid health through affecting the immune system and potentially increasing or reducing chances of autoimmunity.
- The most common cause of hypothyroidism in westernized countries is an autoimmune process known as Hashimoto’s Thyroiditis.
- Hypothyroidism is diagnosed when TSH is high and T4 is low.
- Some studies show that you can lower the antibodies associated with Hashimoto’s with selenium. However, these studies may be biased.
- Recommended dosage of selenium is 200mcg per day.
- There is much association data showing that patients with Hashimoto’s or hypothyroidism have low vitamin D levels. Recently, a study showed treatment with Vitamin D decreased TPO antibodies.
- Recommended vitamin D levels between 40-50 ng/mL.
- Replete vitamin D deficiency with a dose between 2,000IU-10,000IU per day.
- Best source of vitamin D is good, safe sun exposure.
- 24-hour urinary iodine is the gold standard for iodine testing.
- The research shows the best-established environmental factor contributing to thyroid autoimmunity is excess iodine.
- A low iodine diet has been shown to help thyroid autoimmunity. A low iodine diet is defined as less than 100mcg of iodine per day but one should always be above 20mcg per day to avoid iodine deficiency.
- Recommended daily iodine intake should be between 150mcg-1100mcg per day with a sweet spot around 450mcg.
In This Episode
Fast facts … 00:00:38
Episode intro … 00:03:24
Recap of hypothyroidism … 00:04:04
Selenium and hypothyroidism … 00:10:41
Vitamin D and hypothyroidism … 00:16:36
Iodine and hypothyroidism … 00:21:39
One last look at vitamin D … 00:41:47
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Welcome to Dr. Ruscio Radio, discussing the cutting edge in health, nutrition, and functional medicine. To make sure you’re up to date on this and other important topics, visit DrRuscio.com and sign up to receive weekly updates. That’s D-R-R-U-S-C-I-O.com.
The following discussion is for educational purposes only and is not intended to diagnose or treat any disease. Please do not apply any of this information without first speaking with your doctor.
Now, let’s head to the show!
Susan McCauley: Hey, everyone, this is Susan McCauley from Evolve Nutrition, bringing you this week’s Fast Facts.
Iodine, vitamin D, and selenium can all impact thyroid health through affecting the immune system and potentially increasing or reducing chances of autoimmunity. The most common cause of hypothyroidism in Westernized countries is an autoimmune process known as Hashimoto’s thyroiditis. Hypothyroidism is diagnosed when TSH is high and T4 is low. Some studies show that you can lower the antibodies associated with Hashimoto’s with selenium. However, these studies may be biased. Recommended dosage of selenium is 200 mcg per day. There is much association data showing that patients with Hashimoto’s or hypothyroidism have low vitamin D levels.
Recently, a study showed treatment with vitamin D decreased TPO antibodies. Recommended vitamin D level is between 40 and 50 ng/mL. Replete vitamin D deficiency with a dose between 2000 IU and 10,000 IU per day. The best source of vitamin D is good, safe sun exposure. A 24-hour urinary iodine test is the gold standard for iodine testing. The research shows the best-established environmental factor contributing to thyroid autoimmunity is excess iodine. A low-iodine diet has been shown to help thyroid autoimmunity. A low-iodine diet is defined as less than 100 mcg per day of iodine, but one should always be above 20 mcg per day to avoid iodine deficiency. Recommended daily iodine intake should be between 150 mcg and 1100 mcg per day, with a sweet spot around 450 mcg per day. OK, that’s it for the Fast Facts. Now, on to the show.
Dr. Michael Ruscio: Hey, guys. Welcome to Dr. Ruscio Radio. This is Dr. Ruscio, and I am here with Susan McCauley from Evolve Nutrition. Hey, Susan. How are you?
SM: I’m doing great. I have my gingerade kombucha, and I’m ready to rock on the topic today.
DR: Nice. I just had a few chocolate-covered espresso beans.
SM: Ooo, you’re really ready to rock!
DR: A little brain boost here, hopefully!
SM: I could not do that in the afternoon. I am a “zero caffeine after about 11 a.m.” person. It really affects my sleep.
DR: Yeah. I hear you. I’m pushing it, but hopefully it won’t interfere with my sleep tonight.
SM: Happy Monday to you, too, huh?!
DR: Yeah, thanks!
SM: So what do we have going on today?
DR: Well, today I thought we could touch in on some factors regarding thyroid, selenium, vitamin D, and then do a little bit deeper of a dive on iodine. We have done a pretty elaborate discussion on iodine in the past, but I’m not sure if some of the newer people to what we’re doing have had a chance to go through that. So I thought we’d revisit the iodine and kind of weave into that dialogue selenium and vitamin D.
SM: OK, and for everybody’s pleasure, I will include the iodine podcast links (1a) (1b) (1c) as well, so they can go back and they don’t have to go searching around for them. They’ll be right there in the show notes.
Recap of Hypothyroidism
DR: Yeah, let’s jump into a discussion on your thyroid and how selenium, vitamin D, and iodine affect that. Really, the main way in which iodine, selenium, and vitamin D affect your thyroid is through affecting your immune system and potentially affecting autoimmunity.
Just really briefly in recap, the most common cause of hypothyroidism in Westernized countries is an autoimmune process. Typically it manifests as Hashimoto’s that causes gradual and progressive damage to the thyroid gland, which then does not enable the gland to produce adequate levels of thyroid hormone, and thus then one becomes hypothyroid. Hypothyroid typically manifests as kind of a wide compendium of symptoms, but it can include things like fatigue, weight gain, depression, feeling cold, brain fog, low sex drive, digestive problems, high cholesterol, dry hair and skin and nails, poor memory, and morning headaches, just to name a few key symptoms.
This is a fairly common issue, hypothyroidism, that is, and thyroid concerns on the behalf of many patients, because the symptoms of hypothyroidism are so broad that many people who are suffering from some kind of symptoms when they start looking up stuff on the internet run across thyroid as being a possibility, so it’s definitely something that’s important to have a good understanding about.
Again, in recap, the most common cause of hypothyroidism is thyroid autoimmunity, and selenium, vitamin D, and iodine have a pretty strong impact on thyroid autoimmunity.
Susan, anything there you want to add before I dive a little deeper in?
SM: No. Most people, I think, come to me and think that they have a thyroid issue and it’s because of the inability to lose weight and the fatigue, and they really find no comfort or solace or diagnostic ability in their general practitioner because they’ve been offered either antidepressants or antianxiety medication or that it’s all in their head, so the topic of hypothyroidism is really usually always high up on my list.
DR: Mm-hmm. I should say that conventional medicine is good at diagnosing true hypothyroidism because true hypothyroidism is pretty straightforward to diagnose. It manifests as high TSH and low T4. Most of those people are going to need—at least for a short period of time—some thyroid hormone medication to help get their thyroid hormone levels back into the normal range.
Now, there’s also this not-quite-fully-diagnosable hypothyroidism, kind of this in between, known as subclinical hypothyroid, which we discussed previously. Either subclinical or standard hypothyroid, it’s a very good idea to look at if the underlying cause is autoimmunity, and in most cases, it’s going to be. For some people that haven’t yet become hypothyroid, truly diagnosable hypothyroid, they may have an autoimmune problem brewing under the surface that could eventually manifest as hypothyroid. So it’s important to have a look at the immunity/autoimmunity component of this to either help with further deterioration or to prevent from becoming true hypothyroid later.
SM: Which is really funny because I had a friend whom I also consulted with. Her TSH was really high, and I said, “You know, you really need to have your doctor test your antibodies and your T4. We want to really see what’s going on here,” and they all but refused to give her the antibody tests. It’s really interesting.
DR: Well, from a conventional perspective, in many cases, they don’t really treat the autoimmunity.
DR: There’s not a drug that’s been approved to treat the autoimmunity, and to be truthful, according to the published medical literature, there’s not really a diet that’s been shown consistently to lower antibodies. Of course, we’ve all heard about gluten-free diets helping in many applications, but there’s not really a lot of conventional science for a conventional doctor to pull from there to substantiate that, so that’s where, I think, that position comes from. That’s why we’re fortunate to have multiple opinions on this, and when we kind of come into the functional medicine camp, we’re a little bit more progressive in how we look at this.
Although, that being said, from a practical standpoint, there are two main factors that predict if someone will become hypothyroid later, and that is the initial elevation of the TSH—the higher someone is, the higher the likelihood that they are going to become truly hypothyroid—and also the elevation of the antibodies. There’s some evidence showing that the higher the antibodies, the higher the likelihood that someone will later become hypothyroid.
What that does for the conventional doctor, in most cases, is prompt them to be a little bit more thorough in their follow-up so that they know when to put someone on thyroid hormone, which is fine in and of itself, that’s part of the equation, but it’s also good to have a doctor who’s going to look at these things a little bit more differently, which is why I always recommend people have one conventional doctor for an issue and one functional doctor for an issue so that you can get kind of the best of both worlds. The functional doctor—or a conventional doctor who’s trained in the functional stuff—can walk you through some of what we’ll talk about today.
Coming to your friend, let’s say she did have the antibodies run and they did find Hashimoto’s. What are some things that she could do? This is not going to be an exhaustive treatment narrative on Hashimoto’s, but we are going to cover three very important facets, which again are selenium, vitamin D, and iodine.
Selenium and Hypothyroidism
DR: The first is regarding selenium. There have been a few studies that have shown that selenium can lower the antibodies associated with Hashimoto’s. There was one study (2) that showed approximately a 37 percent reduction in Hashimoto’s antibodies, specifically the antibodies known as TPO, or thyroid peroxidase, which is a very simple lab marker that can be run through any conventional lab very cheaply, very easily. So a 37 percent reduction after 200 mcg of selenium for a number of weeks, and they also showed some positive impact on actually the structure of the thyroid gland via monitoring them with ultrasound.
Essentially the way an ultrasound works, ultrasound, of course, is sound, and sound, depending on the density of tissue, produces different echoes. If you knock on a solid wood door compared to a really kind of cheap wood frame door, you get a different type of echo. The echo reading, so to speak, the ultrasound reading, tells you about the structure of the thyroid gland. The same study I’m referencing showed that the thyroid gland structure was either preserved or even in some cases recovered some of its health, and there was even recently—and we reviewed this in the newsletter a few weeks ago—a follow-up study (3) showing that selenium, magnesium, and CoQ10 taken together can prevent and even reverse some of the structural damage associated with Hashimoto’s. So we have a couple of clinical trials that show some exciting potential for selenium in those with thyroid autoimmunity.
However, there also have been reviews (4) performed that have shown that some of these studies could be at a very high risk of bias, meaning the researchers potentially unintentionally projected a bias onto the study, onto the setup, onto the results, that may mean that the benefit of the selenium wasn’t a true benefit, but it was externally influenced by the researchers, and this was according to a 2013 review published in the Cochrane Database. The Cochrane Database, one of the noteworthy things that they do is they review studies to make sure there’s not bias. Because if I wanted to, I could set up a study that I would be sure would produce a positive impact.
SM: Oh, yeah.
DR: To give people both sides of the evidence here, which we like to do, there are a couple of clinical trials, which are very high level evidence, that are very hopeful and show encouraging results. However, there may be bias.
Now, what do we do in that situation? Well, because selenium is fairly cheap and is very safe and, of course, noninvasive, a short-term trial of selenium I don’t think is a bad idea, and I think, based upon the evidence, we can very reasonably justify that. If it was a surgical intervention or something that was much more invasive or much more expensive and we had this kind of data, I’d be a bit more reserved, but because this is essentially vitamin support, so to speak, that’s cheap and has a very low incidence of causing any type of side effect, trying selenium is certainly a good idea.
SM: Right. That was my first question that came to mind: What’s the downside to selenium? I really don’t know of any. It’s a good mineral. We can be deficient in it because of the quality of soil that we have today. I know Brazil nuts have a lot of selenium, but I don’t remember the last time I ate a Brazil nut!
DR: Right, and if people wanted to try to get in the good dietary intake, I would just simply do a google search and look for foods that are highest in selenium and try to incorporate those more so into your diet, or try to use the 200 mcg of selenium a day, which is what has been used in most of the studies.
There have been some studies showing that long-term dosing of selenium may cause some negative side effects. If my memory serves me correctly, I believe there were certain skin cancers that were potentiated by selenium. So it comes back to one of the things that we always harp on, which is trying to find the minimum dose for the minimum period of time. What you should not do is be the person who says, “I have Hashimoto’s. I’m going to be on selenium forever.” That would not be well guided. What would be intelligent would be to use selenium for a number of months, look at your antibodies, and once your antibodies are in the acceptable range—anywhere around 100 to 300 for the TPO antibodies, in my opinion, is reasonable—once you’ve achieved that level, then I would back off the selenium, stop taking the selenium, and reevaluate in a few months. Chances are your antibodies will maintain that acceptable level because you’ve probably repleted the deficiency and you’re OK.
With everything, I think it’s best to find the minimum dose for the shortest duration that produces the effect. It’s just important for me to make that distinction.
SM: Then with the antibody levels, you would also kind of fact check that with your symptoms and how you feel, correct? I’ve heard some people feel better with a little bit higher or a little bit lower. It just depends on the person.
DR: Absolutely. There was recently a podcast and a video that we did, talking about interpreting lab values. Context is such an important part of that, absolutely. We’re not going to drive this solely based upon on someone’s antibody levels. Absolutely.
Vitamin D and Hypothyroidism
DR: Now, there’s another important nutritional intervention, which is vitamin D. There’s a lot of association data (5) showing that those with thyroid autoimmunity, those with hypothyroid, those with Hashimoto’s, have low vitamin D. But association is an observation, and I was thinking about how I could explain in an easy way the relevance of levels of evidence. If we all remember back a little while ago, we talked about how the lowest level of evidence is mechanisms. One level up is observations, or associations in this case, and then the highest level is clinical trial data, and I think this analogy may help people visualize that.
Let’s say you wanted to become financially free. You want to have enough money not to worry about anything. We’re trying to figure out what you can do to become wealthy, then. Mechanism data, like a cell culture or something like that, that is like saying, “People who are wealthy have more money going into their bank account than coming out of their bank account.” OK. That’s interesting, it’s helpful kind of, but does it really tell you what to do in order to become wealthy?
SM: No, it doesn’t tell you how to get there.
SM: That’s the equation: More coming in than going out.
DR: Right, so that’s a mechanism.
One level up would be observation. “People who grew up in this town or went to this college had a higher incidence or higher chance of becoming wealthy.” OK. Also interesting, but does that really tell you what you can do to become wealthy? You can’t go back in time and change where you went to school or where you grew up.
The highest level would be interventional data, and this would be akin to saying, “Seventy percent of the people that followed this investment strategy became millionaires within five years.” That is like an interventional trial. That tells you something you can do to produce the result that you desire.
Is that helpful, Susan?
SM: Definitely. It really gives you the levels of understanding of the information you get from the situation. The bank account in and out really doesn’t give you very much. Anybody knows that, that if you have more money coming in than going out that you have more wealth!
DR: Right. What that is analogous to is if someone shows an interesting study about what happens in a thyroid cell when you give that person selenium. A cell model is akin to the bank account. Just because selenium did this interesting antiinflammatory thing in the cell, it doesn’t really tell you how to prevent Hashimoto’s, and that’s where we need the clinical trial data or what would be the, “Seventy percent of the people that followed this investment strategy…” and so on and so forth.
Coming back to the vitamin D, we have the association of vitamin D, or the observation that people who are low in vitamin D have a higher chance of having Hashimoto’s, but what we really need is a study showing that giving vitamin D would actually lower or improve the thyroid autoimmunity. There was a landmark study (6) published recently in this regard, which we reviewed in the newsletter a few weeks ago, where vitamin D supplementation did cause a significant decrease in TPO antibodies. This is one of the first studies that has really shown that treatment with vitamin D caused a positive effect, and we’ll put the link and also an interesting table from that study in the transcript. That’s very interesting.
SM: Yeah, and it goes back to last week, when we were recording about homocysteine, and we know we can lower homocysteine with B vitamins, but does that really have any positive outcomes on cardiovascular disease? I’m not going to give away the ending, You can go listen to the podcast, but we asked that question. and now here we’re asking the same question, and there’s actually a study that says, yes, it does have an effect on people.
DR: Precisely. So selenium and vitamin D are two easy ways to have potentially good benefit for your thyroid immune health or thyroid autoimmunity.
Now, the last piece, and the one that I think is the most well understood in terms of the medical literature, but the least well understood in terms of what you get on the internet, probably because of people making recommendations based upon lower-level science, is iodine.
Iodine and Hypothyroidism
DR: Now, we’ve reviewed iodine before. The mechanism of iodine is very alluring. I’ll put an image from Guyton’s Textbook of Medical Physiology in the notes, where we can very clearly see—and in green I’ve highlighted some of the key points here—there’s a thyroid cell, and you see you need iodine to go into the thyroid cell to eventually come out as part of thyroid hormone. The mechanism is very suggestive that you need to take iodine to increase your thyroid hormone levels to treat hypothyroid. However, that’s not really the case, and we’ll come back to that in a second.
There are one or two things I just want to quickly note here. Again, we elaborated on these in our last episodes. The iodine skin patch test has not been scientifically validated and is used nowhere in the peer-reviewed medical literature. It was something that was put together by… I guess you could say an iodine enthusiast. I think it was put together with the best intentions, but this was a test where the normal values were arbitrarily assigned, which is really, really poor science. Now, the test that is used in the scientific literature is a 24-hour urinary iodine or a spot urinary iodine test, and that’s really what people should be using if they want to quantify iodine deficiency, not the skin patch test.
What impact does iodine have on thyroid autoimmunity? Well, I’ll give one or two quotes from the medical literature. “The best-established environmental factor is excess dietary iodine” (7). This is in regards to thyroid autoimmunity. Another quote: “Increased iodine consumption is strongly implicated as a trigger for [thyroid inflammation].” There have been numerous other papers that have echoed this (8).
In 2002, the journal of Autoimmunity Reviews published a paper (9) with a few interesting quotes. One quote: “A body of clinical and epidemiological evidence points to excessive ingestion of iodine as an environmental agent.” This is regarding thyroid autoimmunity. This is maybe one of the most important quotes: “Iodine [supplementation] has been shown to increase the incidence and severity of [Hashimoto’s].” “[W]e have been able to show that iodine enhances [Hashimoto’s] in a dose-dependent manner.” What’s important about that is dose-dependent means the higher your intake, the worse the thyroid autoimmunity becomes.
Now, if that wasn’t enough, we have a wealth of population observational studies. What these studies are showing is, here’s a population, and then we either add iodine to the water, to the bread, to the dairy, to replete iodine levels in the population. In Sri Lanka (10a), in Turkey (10b), in Brazil (10c), in China (10d), and in Greece (10e), they have all shown that with adding iodine to the food supply there has been an increase in autoimmunity. In other review papers (10f), they have found the same things, including another study in Greece (10g), China (10h), Northwest Greece (10i), and again, another study in Denmark (10j).
So there’s a very, very high level of support showing this association between adding iodine to the food supply and autoimmunity. However, I hope people are asking, is there any clinical data? Are there any interventional studies that really kind of firm this up? Because it’s one thing to show association, but it’s another thing to show clinical effect from an intervention. And there are. There are some interventional studies, and we’ll put the links in here.
There was an African population where they added iodine to the food supply, and they noticed that hypothyroidism and thyroid autoimmunity both increased. They then removed iodine from the food supply, and they noticed that the prevalence of all abnormalities decreased after removal of excessive iodine from the drinking water system (11a). There’s one study showing that removing iodine helps with hypothyroid and thyroid autoimmunity.
There have been four other interventional studies showing that restricting iodine intake can reverse hypothyroidism (11c) (11d). In fact, there was even one study—and we’ll put the links for all these in the notes—where they put people on a low-iodine diet, their thyroid functional normalized, and then they put them back on a higher-iodine diet, and their hypothyroidism returned (11b).
SM: So is low iodine intake less than 150 mcg per day?
DR: Yes. Good memory. As a nutritional consultant, I would expect you to have that one pegged, Susan.
DR: Kudos! Yes, the low-iodine diet is typically defined as less than 100 mcg a day.
SM: Oh, 100 mcg, not 150 mcg. I said 150 mcg.
DR: Oh, thanks.
SM: I got it wrong.
DR: Well, you were close.
DR: So less than 100 mcg a day. Now, one of the reasons that the autoimmune Paleo diet—and even the Paleo diet, in general—may work well for thyroid autoimmunity is because it inadvertently restricts many of the sources of iodine: breads, which are fortified with iodine; dairy, which is fortified with iodine; table salt, which is fortified with iodine; and then using sea salt instead, which is a poor source of iodine. And if you’re doing all the way to the autoimmune protocol and restricting eggs, another source of iodine. So my speculation is one of the reasons why the Paleo diet—and even more so, the autoimmune Paleo diet—may work well for hypothyroid and for thyroid autoimmunity is because of the restriction of iodine.
SM: Unless you add copious amounts of seaweed and other high-iodine sources that are approved on those diets.
DR: Right, and I want to come back to kelp in a minute because there’s a very important point there.
DR: But I should mention one other study (12), and this was the most relevant, I think, to those in the US because it looked at a US population. They took a group of patients that had Hashimoto’s and they put one group on a low-iodine diet and the other group maintained just a normal diet. In the iodine-restricted group, 78 percent regained their thyroid function while only 45 percent did in the non-restricted group.
So when I say that iodine has its hand in autoimmunity, this is very, very well verified, and I hope what people will not do is wander their way onto some website where there’s all this really cool mechanism stuff and maybe a picture of a thyroid gland and iodine going in as a cartoon and coming out as thyroid hormone, because that is irrelevant, guys. What’s relevant is what the clinical trials show, and so we see very favorable effects for thyroid autoimmunity when restricting iodine intake.
SM: Yeah. The human body isn’t always as simple as, oh, we need iodine to make thyroid hormone; therefore, more iodine is better. There are too many intricacies in the human body to have simple equations like that be factual.
DR: Right. It’s more complicated than an arrow with iodine going into the gland and on the other side thyroid hormone coming out. There’s way more that happens than that. Those diagrams are good to teach simple concepts, but concepts and clinical medicine are two very different things.
SM: And there’s a huge camp on the internet that promotes the use of high-dose iodine for hypothyroidism.
DR: Mm-hmm. Now, we may be able to negate some of that potential detriment from high-dose iodine by using selenium, and some have asked that question on some of our social media pages. Is it really the iodine, or is it the fact that we’re deficient in selenium? To tell you the truth, we’re not really deficient in iodine. If you look at most of the population data through things like the National Institutes of Health, the US population is not deficient in iodine, but what we do have is pretty rampant autoimmunity, probably because of—or at least in part because of—the very hygienic environment in which we live and our microbiomes getting all screwed up because of sterile conditions and antibiotic use early in life, increased Cesarean births, decreased breastfeeding, lack of contact with dirt and germs in our environment. That is a more plausible reason for the hypothyroidism than is the population becoming frankly deficient in iodine.
SM: Right, and in fact, that’s why we started getting our food supply supplemented because there were only actually small pockets—correct?—of the United States where there were goiters. It was a true iodine deficiency, so they started just putting it in salt, basically, which is used for all the processed foods. But today we don’t have that situation, and I’m not sure what would happen if we took the iodine out of the table salt that everybody uses.
DR: Right. The other side of the coin there is that may cause goiter if the intake goes too low. What I think the most prudent recommendation is, is just to obtain a normal recommended dietary intake, which we’ll go over in just a second.
But there’s one other thing I wanted to speak to that may account for why some people can take iodine and not suffer any detriment from it because those people are certainly out there. And this is not to say that iodine never has a time and a place. For example, for fibrocystic breast disease, there have been some very impressive clinical trials showing that iodine can have a very favorable impact. However, for thyroid autoimmunity and for hypothyroid, I think it’s pretty clear that this is a very risky gamble, to use high-dose iodine, because high-dose iodine has been shown to cause both thyroid autoimmunity and hypothyroidism, the very things people are trying to remedy.
Why some people may be able to be hypothyroid or Hashimoto’s and take higher doses of iodine and not seem to have any negative effect from that may be because of a healthy and intact sodium/iodide symporter. The sodium/iodide symporter is essentially your absorption-and-excretion mechanism for iodine. In people who are healthy, they have the ability to absorb what they need and excrete what they don’t. Now, when the sodium/iodide symporter is altered or not functioning properly, then you can’t excrete excess and it may build up, and that is one of the main factors that may cause these negative effects seen with high iodine intake. Interestingly, two of the main factors that can cause alterations or impairment of the sodium/iodide symporter are inflammation and toxicity. This is fairly common. Especially if someone is not feeling well, inflammation certainly is going to be very common.
Now, there are proposed ways of assessing the sodium/iodide symporter; however, in the two years since I’ve come across these, I’ve never found it clinically relevant to need to do that. I say that because there are many things that we learn about, but I try to always bring things back to a practical clinical process, and these have never really worked their way into the clinical process because we’re always going to want to work on improving someone’s inflammation and their gut health, which is also going to help with inflammation and detoxification, and in doing that, it has never really seemed relevant or necessary to directly assess someone’s sodium/iodide symporter. I just say that because I know that there is this… almost instinct sometimes to…
SM: Test things?!
DR: Yes. Something new is something new that we need to run out and test. I am open to it, and I think there may be a time and a place, but I’ve gotten very good results with thyroid patients in the clinic, and I haven’t ever tested this, so just to help anchor people and keep them from getting swept away into interesting academics.
So to bring this home, some tips on iodine intake: We’ve already talked about how inadvertantly through avoiding or lowering iodine through the Paleo diet and autoimmune Paleo diet may be why these diets are helpful for thyroid autoimmunity. A low-iodine diet would be less than 100 mcg per day, but one should always stay above 20 mcg per day (13) because prolonged periods below 20 mcg per day may potentiate true iodine deficiency, which we also do not want. And please don’t misinterpret what I’m saying about restricting iodine. Restricting iodine is one thing; intentionally creating an iodine deficiency is another.
I would say that if you really wanted to give this a try, to be below 100 mcg, just go as shy of 100 mcg as you can and don’t think that lower is better and try to get down to zero iodine intake, because that may cause problems on the other end of the spectrum. What I typically do is just have someone follow the Paleo or the autoimmune Paleo diet, and I haven’t really needed to give people strict recommendations on iodine in most cases.
Now, daily intake should be—this is kind of the recommended dietary intake ranges—anywhere from 150 mcg a day up to 1100 mcg per day. That’s the reasonable recommended dietary allowance range, so to speak. Based upon some of the studies, a sweet spot where you can get the benefit from iodine without risking detriment from iodine may be at 450 mcg per day. That’s based upon some of the studies showing different populations consuming different amounts of iodine and what is the intake that prevents deficiency and things like goiter and also does not increase the chances of excessive iodine and the hypothyroidism and the thyroid autoimmunity that excessive iodine can propagate. That seems to be maybe 450 mcg, this kind of average sweet spot.
If you have active thyroid autoimmunity and you want to try a dietary approach to manage that, you could try less than 150 mcg for a little while and reevaluate. Then for a long-term position to settle in on, somewhere around 450 mcg may be ideal.
Now also, when repleting, if someone does have a true deficiency—which is rare and should be quantified not by the iodine skin patch test, but by ideally a 24-hour urinary iodine-to-creatinine ratio test, which is available through any conventional lab—then taking 1 mg up to a max of 10 mg a day along with 200 mcg of selenium is a good strategy for repletion.
Now, I should also mention that kelp may not be an ideal way of repleting iodine because it has been shown that kelp is high in iodine and iodide may be better for those with thyroid autoimmunity. There are different forms of iodine. We say iodine oftentimes, but there’s iodide and iodine, and it’s actually the potassium iodide which you see in many different forms of iodine supplements that has shown to be slightly safer, and it has been shown in some of these population studies where high kelp intake has been ingested that the kelp seems to be potentially particularly detrimental because of the high iodine content. I used to recommend people replete with kelp and kelp flakes, and I stopped doing that after reviewing some of the literature showing that kelp runs a higher risk.
I have the references for that, but I’m sorry, I was not able to get all that together for this episode. If you ask, I won’t have the chance to fish those out. At some point, we’ll probably do a follow-up and provide all those references, but they’re buried deep within my couple hundred pages of thyroid research notes, and I just didn’t have the chance to dig them out.
Also, regarding repletion, it’s a very good practice before you try to replete an iodine deficiency if you do have one, to investigate any source of inflammation, particularly because of the sodium/iodide symporter. We also discussed toxicity as a potential way of causing problems with that. The main toxin is perchlorate, which is found in ammunitions and gunpowder and firework powder. However, usually by using a water filter that will work its way out of your system fairly readily, so as long as you’re adhering to good diet and lifestyle practices, the toxin/perchlorate issue for negatively affecting the sodium/iodide symporter doesn’t seem to be a huge deal. But the inflammation certainly can be, and that’s why before you take iodine, if you are iodine deficient, as diagnosed by the urinary iodine test, then address inflammation before taking any supplemental iodine.
SM: I have a funny, really quick story about perchlorate. We had a spill in my neck of the woods 25 years ago, and it was a disclosure when we bought our house, so we immediately put in a water filter, which a couple of weeks ago we had to take offline for the weekend because it wasn’t working right, and oh, my goodness, the smell of our water and the way it felt and the way it tasted after six years of drinking filtered water. I always think everyone’s all, “What’s this filter? We don’t really need it. It’s expensive.” Now I will make sure that thing is running every minute of the day because it tasted and smelled horrible.
DR: Yeah, once you get used to filtered water, it’s hard to go back to regular. Totally.
One Last Look at Vitamin D
SM: Do we have time to back up to vitamin D really quickly? I just have one question.
DR: Yeah, sure.
SM: When we talked about selenium and we talked about iodine, we talked about dosing, but when we got to vitamin D, do you have any recommended vitamin D levels from the research or how much we should supplement with or what type of supplements we should use?
DR: Yes. We did… I don’t know if it was one or a two-part series on vitamin D (14).
SM: Oh, yeah!
DR: Susan, if you could grab the link for that, too, that would be awesome.
SM: Yeah, I will.
DR: We gave a little bit more of a comprehensive outline there. I like vitamin D between the levels of 40 and 50, and in terms of repletion, anywhere from 2000 IU per day up to anywhere from 6000 IU to 10,000 IU a day seems to be reasonable.
There may be a case for going a little bit higher in someone that has autoimmunity; however, that’s more right now based upon supposition than it is actual science. We do have a deficiency—no pun intended—in the research regarding what the ideal supplement regimen for vitamin D in autoimmune conditions is. It’s an area right now where there’s a gap in the research. We have association data for autoimmune conditions showing low vitamin D, but we have very little showing that if we give vitamin D we have a favorable impact on these conditions, meaning there are very few studies that have been done trying to answer that question. This thyroid one was one of the first.
Some have speculated that higher vitamin D may be helpful. The highest I would like to see someone would be at the upper end of 50. That’s where I think you run the least risk of a potential negative from going too high with vitamin D. It’s a very important point because we often think that if a little bit is good, more is better, but the more I look at many of these issues from both sides, I find that there’s really this physiological sweet spot.
SM: It’s a bell curve.
DR: Yeah, exactly. I would say in the 50s would be at the higher end of a reasonable range, and I wouldn’t go much beyond that.
If someone wanted to be practical about this and just run an experiment and say, “Well, let me get my level to 75 for three months and then evaluate my thyroid antibodies during that process,” if they notice a substantial dip, then maybe you want to experiment with that longer under the supervision of your doctor. I’m not closed off to a different approach, but if you’re going to experiment, then just be a little bit practical in how you do it. There’s not an answer here, so if someone had nonresponsive thyroid autoimmunity, trying a short course—while supervised—of higher vitamin D, while correlating that with their thyroid antibody levels, may be something to do. We don’t really know, so that would just be something to do cautiously and under the supervision of someone that can really help you with that.
SM: And only change the vitamin D! Don’t change, like, four things at once and then expect to find out if one thing is affecting the other.
SM: Then also, from those podcasts, your best source of vitamin D is good, safe, effective sun exposure.
DR: Absolutely. That’s a very important reminder. Thank you for making that.
SM: Yeah, we go into depth about it. Was it the minimum… I don’t remember…
DR: The minimum erythemal dose.
SM: Yeah, the minimum erythemal dose. I just walked for 40 minutes in a tank top—to all you people in North Dakota that are freezing right now!—so I got my minimum erythemal dose today!
SM: Any words of wisdom to wrap us up today?
DR: No. I think that will do it.
SM: OK. Well, head on over to the blog post if you have any questions or comments or experiences that you would like to share with us, and we’ll see you next week with another great topic.
DR: Thanks, Susan. Thanks, guys.
SM: Take care. Bye-bye.
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➕ Resources & Links
1. (3:53) Previous Dr. Ruscio Radio iodine podcasts:
a Thyroid & Iodine – Part 1
b Thyroid & Iodine – Part 2
c Thyroid Nodules, Goiter and Iodine
2. (10:52) J Clin Endocrinol Metab. 2002 Apr;87(4):1687-91. doi: 10.1210/jcem.87.4.8421.
3. (12:17) BBA Clin. 2014 Dec 31;3:113-22. doi: 10.1016/j.bbacli.2014.12.005. eCollection 2015 Jun.
4. (12:42) Cochrane Database Syst Rev. 2013 Jun 6;(6):CD010223. doi: 10.1002/14651858.CD010223.pub2.
5. (16:44) Thyroid. 2011 Aug;21(8):891-6. doi: 10.1089/thy.2009.0200. Epub 2011 Jul 13.
6. (20:14) Hell J Nucl Med. Sep-Dec 2015;18(3):222-7.
7. (23:33) J Autoimmun. Nov-Dec 2009;33(3-4):183-9. doi: 10.1016/j.jaut.2009.09.001. Epub 2009 Oct 9.
8. (23:43) Thyroid. 2006 Mar;16(3):289-93. doi: 10.1089/thy.2006.16.289.
9. (23:46) Autoimmun Rev. 2002 Feb;1(1-2):97-103. doi: 10.1016/s1568-9972(01)00016-7.
10.(24:42) Observational studies on iodine and thyroid autoimmunity:
a) Mazziotti, G., Premawardhana, L., Parkes, A., Adams, H., Smyth, P., Smith, D., Kaluarachi, W., Wijeyaratne, C., Jayasinghe, A., de Silva, D., & Lazarus, J. (2003). Evolution of thyroid autoimmunity during iodine prophylaxis–the Sri Lankan experience, European Journal of Endocrinology Eur J Endocrinol, 149(2), 103-110.
b) Thyroid. 2006 Dec;16(12):1265-71. doi: 10.1089/thy.2006.16.1265.
c) Camargo, R. Y. A., Tomimori, E. K., Neves, S. C., G S Rubio, I., Galrão, A. L., Knobel, M., & Medeiros-Neto, G. (2008). Thyroid and the environment: exposure to excessive nutritional iodine increases the prevalence of thyroid disorders in São Paulo, Brazil, European Journal of Endocrinology, 159(3), 293-299.
d) Zhonghua Yi Xue Za Zhi. 2004 Jul 17;84(14):1171-4.
e) Christos Zois, Ioanna Stavrou, Chrysoula Kalogera, Eugenia Svarna, Ioannis Dimoliatis, Konstantinos Seferiadis, and Agathocles Tsatsoulis.Thyroid.May 2003.485-489. http://doi.org/10.1089/105072503322021151
f) Endokrynol Pol. 1992;43 Suppl 1:53-69.
g) Hormones (Athens). Jan-Mar 2007;6(1):25-35.
h) N Engl J Med. 2006 Jun 29;354(26):2783-93. doi: 10.1056/NEJMoa054022.
i) Thyroid. 1999 Mar;9(3):279-83. doi: 10.1089/thy.1999.9.279.
j) Clin Endocrinol (Oxf). 2011 Jul;75(1):120-6. doi: 10.1111/j.1365-2265.2011.04008.x.
11. (25:51) Interventional studies on iodine and thyroid autoimmunity:
a) J Clin Endocrinol Metab. 2002 Dec;87(12):5499-502. doi: 10.1210/jc.2002-020692.
b) J Clin Endocrinol Metab. 1986 Aug;63(2):412-7. doi: 10.1210/jcem-63-2-412.
c) Thyroid. 2003 Jun;13(6):561-7. doi: 10.1089/105072503322238827.
d) Thyroid. 2001 May;11(5):501-10. doi: 10.1089/105072501300176462.
12. (28:31) Yonsei Med J. 2003 Apr 30;44(2):227-35. doi: 10.3349/ymj.2003.44.2.227.
13. (35:43) http://ods.od.nih.gov/factsheets/Iodine-HealthProfessional/
14. (42:16) Vitamin D: overlooked causes of chronically low vitamin D, supplementation hype and sun exposure – Episode 6