Selenium in Thyroid Care: Clinical Insights and Applications
This transcript has been edited for clarity.
Kaniksha Desai, MD: Welcome back, everyone, to the Thyroid Stimulating Podcast. This podcast was created in partnership with the American Thyroid Association to discuss up-to-date diagnosis and management of a wide array of thyroid diseases. I’m your host, Dr Kaniksha Desai. Today we’re exploring a fascinating topic that often flies under the radar: selenium and its role in thyroid health.
Selenium is a trace element with powerful antioxidant properties, and it’s pretty much crucial for the proper function of your thyroid gland. In fact, it’s essential for the conversion of thyroid hormone, and research suggests that selenium supplementation may help reduce inflammation in certain thyroid conditions, like thyroid eye disease.
How do we know how much we need, and can it really make a difference in managing all thyroid disorders? Lastly, how do we ensure that we get enough from our diet? Stay tuned as we unpack these questions and more, with insights from the latest studies and practical advice for your patients.
Joining us today is Dr Trevor Angell, an associate professor of clinical medicine in the Department of Medicine’s Division of Endocrinology and Diabetes at Keck School of Medicine of USC. Dr Angell’s clinical research focuses on the diagnosis and treatment of thyroid diseases, including thyroid nodules, thyroid cancer, and thyroid disorders during pregnancy.
He has published numerous articles in JAMA Surgery, Thyroid, and the Journal of Clinical Endocrinology & Metabolism. He is also currently the editor-in-chief of the American Thyroid Association’s journal, Clinical Thyroidology. Thank you so much for taking the time to join us today to talk about selenium and the thyroid gland.
Trevor E. Angell, MD: Thank you, Dr Desai. It’s a pleasure to be here.
Desai: I want to start with the basics. What is the role that selenium plays in thyroid health? How does it influence thyroid hormone production and metabolism?
Angell: Selenium is a trace element found in the environment, and it turns out to be an essential component of some critical enzymes in the body, including those for thyroid hormone metabolism.
These are the deiodinase enzymes, of which there are three, and they’re called selenoproteins because of the presence of selenium in their structure. These deiodinase enzymes are responsible for production and conversion of thyroid hormones in the body, such as T4 to T3, within the tissues and within the cells. That means that the deiodinase enzymes are important to thyroid hormone actions in the body, and they need selenium. It is a crucial piece of thyroid hormone production and how we use it.
Desai: Many people are concerned about selenium deficiency. Can you tell me about the symptoms of selenium deficiency and how that would directly affect how the thyroid functions?
Angell: Selenium deficiency fortunately ends up being pretty rare. There are populations, because of where they are, that are particularly selenium deficient. We know, from looking at those people, that severe selenium deficiency can involve myocarditis, cardiomyopathy, muscle weakness and pain, hypopigmentation, white nail beds, and hypothyroidism.
I think mild selenium deficiency may have symptoms much more nonspecific, or often may have no symptoms at all. Muscle and joint pains are certainly something that’s been listed as potentially problematic, anemia as well, and again, problems with nails.
Even though thyroid hormone conversion would likely be reduced with selenium deficiency, somewhat surprisingly, we don’t see as much hypothyroidism in selenium-deficient populations as we might expect, even when selenium is relatively deficient. That may be because of other compensations that may exist, but we may not be able to see thyroid hormone abnormalities in all people when selenium is low.
Another effect on thyroid function is thyroid autoimmunity, and that’s a little bit of a separate question, where selenium has many roles in the immune system as well. An association with thyroid autoimmunity is something that has been observed across many studies.
Desai: Who’s this population that’s at risk? Are you and I at risk or is there a certain group of people that might be at risk?
Angell: As I mentioned, the environmental presence or absence of selenium represents one of the major risks. People who live in places with a selenium deficiency in the soil, traditionally, have been a group at risk.
Because of the movement of food, because of supplementation that exists in many places, it’s really not a significant issue in the United States, but it certainly may exist significantly globally.
Other populations that really need to be aware of it can be strict vegetarians because even though selenium will be in some plant products, meat products with concentrated plant sources are a rich source of selenium. People with some medical conditions — people who are on hemodialysis, people living with HIV, and those on parenteral nutrition — are all at risk for selenium deficiency.
Desai: What about patients with gastric bypass?
Angell: I think that is less clear, but it’s certainly worth noting, given the range of deficiencies that they do have, that that could be a problem as well.
Desai: So it’s a very small population overall but still important to consider. Tell me more about this link with thyroid autoimmune diseases like Hashimoto, Graves, and thyroid eye disease.
Angell: Another place where selenium has a critical role is in antioxidant activity, such as glutathione peroxidase and other places. This may broadly relate to inflammation and free radicals, in particular. The effect of selenium in cells can be to increase the antigen expression and how immunologic they might be. Selenium, for example, could lower the reactivity of T cells and increase regulatory T cells. That affects the immune balance and local inflammation.
What does that all mean for the thyroid? Deficiency of selenium, an increase in free radicals, may cause some thyroid damage and responsiveness of the immune system, which is then activated and creates things like thyroid autoantibodies, like thyroid peroxidase, that we see in Hashimoto’s, and then that, in turn, is going to affect thyroid function, most usually with hypothyroidism in some people.
Desai: Tell me a little bit more about thyroid eye disease and how selenium improves that inflammation.
Angell: This is an area where we have some really good data. This comes from a New England Journal of Medicine article in 2011, which was a randomized controlled trial of patients with mild thyroid eye disease who were treated with 100 μg of selenium twice a day or placebo.
This study showed improvement in eye involvement, progression of thyroid eye disease, and quality of life. Of the patients treated with selenium, 70% showed improved quality of life compared with only 20% in the placebo group. Now, these were mostly inflammatory signs rather than proptosis, which has become a subject in more recent studies, but really an evident benefit for selenium in these patients.
Desai: The recommended dose, at least for thyroid eye disease, was 100 μg per day twice a day; would that be what we recommend patients get?
Angell: That was the dose in that study. Other studies have used 200 μg once a day, but 200 μg per day total.
Desai: What happens if I take 400 or 600 or 1000 μg? Is more better?
Angell: Unfortunately, more is not always better. The recommended dietary intake of selenium is around 55-70 μg per day, and so those treatment doses are a little bit higher than that. Most recent data on the average intake in the United States were around 100 μg per day, and the upper limit is considered to be 400 μg per day.
What happens if you do take too much? There have been cases of supplements that were mislabeled where patients have received too much or, unfortunately, where people did think more would be better. There are symptoms of acute selenium toxicity that can include muscle tenderness, tremor, flushing, gastrointestinal symptoms, hair loss, even heart failure or kidney failure. It can be very serious.
Desai: We want to get the correct amount, which is more than the daily recommended dose of 50 μg. We’re shooting for around 200 μg, and 400 μg is the maximum recommended. You talked a little bit about supplements, so that’s one way of getting selenium; but what if somebody wanted to be a little more natural and get it from vegetables or nuts? I know that Brazil nuts are common. Where else can we get selenium from in our diet?
Angell: Selenium does exist naturally in the soil, so there are going to be those plant-based sources. Brazil nuts are maybe what people are most familiar with. Interestingly, many types of mushrooms, like shiitake and button mushrooms, are good sources. Many green vegetables, and also seeds and barley, are good sources of selenium.
As I mentioned, animal products are good sources of selenium, as long as the dietary sources for those animals have been selenium-containing.
Desai: If you’re taking selenium, is there any reason to monitor selenium levels? Should you check selenium to see if you’re deficient when you’re diagnosed with thyroid disease? How do we know if we’re getting enough?
Angell: Selenium deficiency, fortunately, would be very rare. Levels of selenium less than 7 μg/dL are consistent with severe deficiency. Deficiency often would take place when the intake is less than about 10-20 μg per day.
Probably the measurement of selenium in most patients in that case isn’t going to be necessary. We’re unlikely to find selenium levels in patients who aren’t at risk, that are really going to be indicative of severe deficiency, that we know are going to be associated with thyroid problems necessarily. Certainly, if someone has some compatible symptoms, clinicians should always be aware of the possibility, I think.
As far as monitoring thyroid hormone status or making management decisions, our thyroid function testing, such as TSH or free T4, are going to be far and away much better measures of the treatment that people need than what a selenium level would be. Generally, I would say there’s no need to be checking or monitoring levels in that setting or in people taking supplementation, as long as we have no reason to be concerned that they now have toxicity.
Desai: If you’re taking selenium with, say, levothyroxine for Hashimoto’s or methimazole for thyroid eye disease, is there any sort of interaction with selenium and these medications?
Angell: That’s a great question. I would counsel all patients who are taking any sort of vitamin that they need to take it significantly removed from their levothyroxine. We often say 2 hours, maybe even 4 hours later if someone’s taking a multivitamin, iron, calcium.
I haven’t found anything that clearly shows that is an issue with levothyroxine absorption and selenium. In the absence of really being sure that there wouldn’t be any effect on absorption, I would still make the same recommendation to people — to make sure that it’s separated.
Desai: We talked about thyroid eye disease and we briefly touched on Hashimoto’s. Is there any role for selenium in Hashimoto’s?
Angell: Selenium in Hashimoto’s is a place where we have maybe the biggest body of evidence. There is really some compelling evidence about the effect of selenium on Hashimoto’s in terms of antibody levels, but unfortunately, I think there are some real caveats to this that I want to bring up.
Prospective studies of selenium supplementation and the effect on TPO antibody have been done for a couple of decades. Some have showed significant effects and some have not. That has led to several meta-analyses about this. One meta-analysis of 11 randomized controlled trials showed a significant reduction in TPO antibody levels. The effect was greatest in patients who had higher baseline levels of TPO.
Most recently, in 2024, the CATALYST study was a double-blind, randomized, placebo-controlled study of adult patients with TPO antibodies that were elevated — greater than 100 in that study — and taking levothyroxine, who were treated with 200 μg per day of selenium or placebo. That confirmed a significant reduction in TPO antibody in the selenium group compared with the placebo.
I think what’s important to recognize about the potential immunologic change that’s causing TPO antibodies to be lower is that this hasn’t translated into more concrete clinical benefits. A separate meta-analysis of five randomized controlled trials, looking at other thyroid variables, did not find any effect on TSH level, thyroid appearance on ultrasound, or quality of life.
If we return to that CATALYST trial, the primary outcome was improvement in quality of life after 12 months of selenium therapy. There was no difference found in either the composite score or the hypothyroid symptom score. Additionally, they didn’t find a change in free T3 to free T4 ratio that might be indicative of conversion, and no change in the levothyroxine dosing that people needed.
There’s apparently a benefit on reducing antibody levels somewhat. We don’t know how valuable that might be, but we aren’t seeing outcome changes that would really make this an effective and recommended treatment for people with Hashimoto’s.
Desai: I want to make sure I understand. Selenium does a great job at reducing TPO levels, but it doesn’t really lower your dose of thyroid hormone requirement. It doesn’t really, on a population basis, improve any of the symptoms of hypothyroidism, of brain fog, weight gain, and just feeling generally run down. It doesn’t prevent you from getting started on thyroid hormone replacement in the first place. Really the benefit is just, entirely on paper, reducing TPO levels, which may have some benefit not related to thyroid; but from the thyroid perspective, it’s just decreasing those antibodies — correct?
Angell: Correct. This is probably something pretty common. We can see that preclinical evidence, we know that there are things happening in the cells that selenium is affecting, but how do we translate that to a clinical treatment? How do we find a clinical benefit? Sometimes our studies aren’t able to, but that’s the evidence that we have right now.
Desai: Where do you think the research is going in the future? Is this being researched more? Do you think more research will come out?
Angell: I would assume so, because, again, there’s so much interest in this topic. I will tell you that of the many patients that I see with Hashimoto’s, so many of them ask about a way to cure it or a way to get rid of it, rather than dealing with hypothyroidism itself. I think the smoke that we have, related to selenium and the mechanisms of autoimmunity, is something to pursue, even if we don’t have the fire yet.
Desai: More to come, maybe, in the future. We’ll have you come back and give us an update in a couple of years. I know we covered Graves patients, thyroid eye disease, and Hashimoto’s patients. I actually have many cancer patients that ask me about selenium. Is there any role of selenium in patients with thyroid cancer or in shrinking nodules?
Angell: In terms of selenium supplementation for patients with thyroid nodules or thyroid cancer, there doesn’t seem to be nearly the same role that would exist. We’ve been talking about the effect of selenium on how the immune system might respond to the thyroid. In patients who have had thyroid cancer, predominantly those people won’t have a thyroid anymore after surgical treatment.
The role of selenium in having a thyroid nodule may be unknown, but there doesn’t appear to be any particular role of selenium in thyroid nodules forming, persisting, or growing. When we talk about the deiodinase enzymes and the need for selenium in conversion, I think that would apply to anyone taking thyroid medication.
Desai: This was a wonderful conversation. Thank you for joining. Do you have any last-minute tips for our listeners on selenium? What do you do for your own patients in practice?
Angell: Primarily, when patients ask about their thyroid disease and what additional steps they can take to try to improve their conditions, I take that very seriously. I do have a discussion about selenium that goes over some of the data we’ve talked about, including the limitations, but that there’s the option for them to use nutrition and natural sources to try to benefit their health, with the recognition that we, obviously, really do want to avoid potential side effects that might exist.
Desai: Thank you so much. Thank you, everyone, for listening to this episode of the Thyroid Stimulating Podcast. Please stay tuned to hear about our next episode, which will be on AI and its role in the thyroid.
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