In this episode, we discuss:
- The myth that Hashimoto’s always leads to hypothyroidism
- The connection between gut health, nutrient absorption, and thyroid function
- Which specific nutrients can help improve symptoms and thyroid function
- The staggering number of patients who are being incorrectly diagnosed as hypothyroid and taking unnecessary medication
- How you can check if your thyroid diagnosis was correct
- Dr. Ruscio’s website
- The Ruscio Institute for Functional Medicine website
- “Symptoms Originally Attributed to Thyroid Dysfunction Were Instead Caused by Suboptimal Gastrointestinal Health: A Case Series and Literature Review” by Michael Ruscio, Gavin Guard, and Joe Mather
- “The Relationship between Gastrointestinal Health, Micronutrient Concentrations, and Autoimmunity: A Focus on the Thyroid” by Michael Ruscio, Gavin Guard, Gabriela Piedrahita, and Christopher R. D’Adamo
- Understand the True Causes of Thyroid Disease free eBook by Chris
Hey, everybody, Chris Kresser here. Welcome to another episode of Revolution Health Radio. This week’s episode is about Hashimoto’s [disease] and hypothyroidism, and in particular, we’re going to look at common misconceptions about these conditions. In this case, the misconceptions are more common within the Integrative and Functional Medicine or alternative medicine communities than they are in the conventional medical world.
I’m going to be discussing this with Dr. Michael Ruscio. He is a doctor, clinical researcher, and author who published studies this year on thyroid health and the gut–nutrient–thyroid axis, which we’re going to be discussing on the show. We’re going to talk about why so many people are misdiagnosed with hypothyroidism and misprescribed thyroid medication. We’re going to talk about the myth that Hashimoto’s [disease] always leads to hypothyroidism or, in some cases, has been conflated with hypothyroidism itself. We’re going to talk about the critical role that gut health plays in thyroid function, and how correcting imbalances in the gut can improve thyroid hormone production, even without medication. We’re going to talk about how gut symptoms can be similar to symptoms of hypothyroidism and how patients can be misdiagnosed with hypothyroidism when they really have underlying gut disorders. We’re going to talk about why people with subclinical hypothyroidism should generally not be prescribed thyroid hormone, despite the fact that they often are in the Integrative and Functional Medicine community, and a whole bunch of other fascinating topics related to thyroid and gut health.
I really enjoyed this episode. I think you will, too, especially if you or anyone you know is struggling with hypothyroidism or thinks they might be struggling with hypothyroidism. Let’s dive in.
Chris Kresser: Mike, pleasure to have you back on the show.
Michael Ruscio: Hey, Chris, thanks for having me.
Chris Kresser: I’m really excited to dive into this conversation. For many years as a clinician, when I saw a patient with thyroid issues, one of the first things I would be looking at [was] the gut because of the connection between the gut and the thyroid. So when you reached out and told me about this focus of yours, I was really keen to get you on the show so we [could] talk a little bit about it. First of all, what led you down this path?
Michael Ruscio: Well, the inception [was] way back when I had an intestinal parasite [in] college. Actually, I think we discussed it before on your show, but we had the same amoeba. That led me to an interest in gut health. As you see more and more patients, there’s this interplay between gut health and thyroid health. Progressively, I’d see more patients who either had Hashimoto’s [disease] or had hypothyroidism, and they were asking, “Do you think improving my constipation or reflux or leaky gut [or] whatever could improve my thyroid?” I started paying more attention to this, and now, maybe six-ish years later, there [are] a few things we’ve uncovered that I think people need to know. [For] as many great facets and discoveries [that] Integrative Medicine has brought to thyroid care, there might be an equal number of errors that we need to correct because they’re harming people, they’re wasting their money, [and] they’re creating undue fear. That’s what I’m really looking forward to unpacking today.
Chris Kresser: Your research team and [you] have published a couple of papers in 2022, patient case studies and a review paper, breaking down nutrient–gut–thyroid relationships. And the case studies were related to how the gut–thyroid connection shows up in clinical practice and what can be accomplished when you take a holistic approach. Why don’t we just dive in there? What [were] some of the clinical pearls and realizations that you came to in your practice, and in these papers, as well?
Prevalence of Hashimoto’s to Hypothyroidism Progression
Michael Ruscio: There’s maybe half a dozen. The first one [is that] I think we should just better define Hashimoto’s [disease] and hypothyroidism because part of this story arc is [that] people might be chasing the wrong issue. They might be looking at [the] thyroid as a cause of all their problems, but it may not actually be. Let’s start with some of the prevalence data. Not to get too nerdy into the numbers, but the numbers here really do matter. If you look at the prevalence of Hashimoto’s [disease], it’s between 5 and 20 percent of the population. What’s interesting is [that], the more discerning you become with the diagnostic criteria, the lower that [number] goes. If we look at just [thyroid peroxidase] (TPO) antibodies, it’s about 19 percent of the population. If we cross-reference TPO and examine [whether] there’s also evidence of histological changes in the gland with an ultrasound, [it] drops from 19 percent to about 5 percent. This is likely because antibody testing is imperfect. It’s helpful, it’s inexpensive, [and] it can be done on a larger scale, but it’s not necessarily perfect.
Let’s say, generously, 20 percent of the population has Hashimoto’s [disease]. Only about 1 percent, technically 0.3 percent, has hypothyroidism. If 20 percent has Hashimoto’s [disease] and about 1 percent has hypothyroidism, that right there tells us that if you have Hashimoto’s [disease], we should not be describing it as, “Oh my goodness, you will become hypothyroid.” The odds are actually quite strongly stacked in your favor that if you have Hashimoto’s [disease], you will not develop hypothyroid. Sure, there are things we want to do proactively that I know we’re on the same page regarding, [such as] diet [and] lifestyle. But I think, from a psychological and a risk perspective, we should make sure to put that out there.
Chris Kresser: Oh man, I can’t tell you how many times I had this conversation in my practice, as I know you have, as well, where people have conflated Hashimoto’s [disease] and hypothyroidism as if they’re the same thing, like you just mentioned. What’s true is that, if you have Hashimoto’s [disease], you do have a higher risk of moving on to hypothyroidism than someone who doesn’t have Hashimoto’s [disease]. But that risk, as you just pointed out, and the simple numbers can attest, is nowhere near 100 percent. Not even remotely close.
Michael Ruscio: Exactly. In fact, it’s well under 50 percent. I know you and I agree on so many of these points, which is why it’s always awesome checking in with you and unpacking some of this stuff. Let’s [talk about] gluten, [as an example]. Maybe someone is being told, “You have Hashimoto’s [disease], [and] it’s going to turn into hypothyroid if you have gluten. We know that everyone with hypothyroidism or Hashimoto’s [disease] should avoid gluten vehemently.” Now, these people carry this into their social lives, and it has a really negative impact on them psychosocially.
Chris Kresser: Yeah, there can be a lot of examples of this. Someone might start [the autoimmune protocol] (AIP) because they have positive thyroid antibodies that are slightly above the reference range. For the listeners, AIP can be a fantastic, effective approach, lifesaving even, for some. [There can be] extreme improvements in quality of life for people who have severe autoimmune disease and for whom it works. But [it] could totally be overkill for someone who has no evidence of any clinical disease like hypothyroidism and just mildly elevated thyroid antibodies, which, as you pointed out, can be abnormal in patients with no other symptoms and is not necessarily indicative of a clinical problem. So it’s a question of scope and scale here. Let’s match the intervention with the scope and scale of the condition.
Michael Ruscio: One hundred percent. Very well said. To your point, also, with the risk, there are some data points that have quantified and tracked people over time to see, [of] those who start off with Hashimoto’s [disease], how many of them actually convert [to hypothyroidism]. This prospective follow-up study from Tehran [is] really the best data point I think we have here. Over their nine-year follow-up, [which is] a pretty good follow-up window, between 9 percent and 19 percent of people converted to full-blown hypothyroidism. So that gives us an idea of what the risk quantification is. I think this is important because all too often, like you said a moment ago, people conflate the two, or they think that if you have Hashimoto’s [disease], [then] you’re guaranteed to be hypothyroid. Along with this, we can look at the level of antibodies. Specifically [of] TPO, [which is] the most accurate and the most helpful to quantify your risk. One of the things I discuss in the clinic with our patients is [that] we want to look at many of these markers on a gradient or on a scale, and not just say, “Well, anything regarding blood glucose above 99 is positive,” but we don’t talk to a patient who has a 102 fasting blood glucose the same as we do if they have a 182. Those are very different conversations, and it seems [like] we don’t grade the elevation of TPO antibodies the same way that we do with so many other things, like blood sugar or blood pressure.
There was a study, albeit small, [that] looked at 21 individuals over a six-year follow-up. They found that only when people had TPO over 500 was there a statistically significant increase in their [thyroid-stimulating hormone] (TSH) over time. The researchers concluded that if you have TPO over 500, this was the relevant cutoff that was associated with progression and risk. The other thing that’s so important to keep in mind with this study is [that], of those 21 people, only one person became hypothyroid. So again, we have to delineate that TPO over 500 puts you at risk, but how at risk are you? It’s probably only about 10 or 15 percent, let’s say, to use rough approximations.
Chris Kresser: Yeah, this is an issue in other autoimmune pathologies and diagnoses, as well. I’m thinking of the anti-nuclear antibody or ANA. There’s a pretty shockingly high percentage of healthy people who have positive ANA antibodies, and that doesn’t mean they have lupus or a serious rheumatological autoimmune condition. There [are] parts of this that we don’t fully understand yet [about] the process of antibody production and why someone who doesn’t have any clinical symptoms or disease would have antibody production. But I agree with you that there’s been a hysteria around this in [the] Functional and Integrative Medicine world. Like you said, it can cause a lot of unnecessary stress and anxiety, which, of course, [is] not what you want if you’re worried about your immune function.
The Nutrient–Gut–Thyroid Axis
Chris Kresser: Let’s talk a little bit about the nutrient–gut–thyroid axis. I was really pleased to see this. I wrote an article many years ago, actually one of the first series I ever wrote on my website [about] thyroid health, and I talked about the gut–thyroid axis. More recently, I’ve been really focused on the role of nutrients in health and disease. So I love how you pulled those together into the nutrient–thyroid–gut axis, or whatever order of those terms that [you prefer]. Tell us about that.
Michael Ruscio: So, this is one of the other components. When we start looking at how important gut health is as it pertains to thyroid function, absorption obviously becomes center stage in that conversation. Just as a quick, tangential tie-in, if someone is [truly] hypothyroid, they may still be struggling because they are inconsistently or incorrectly absorbing their thyroid medication. This has been well documented in people who have [irritable bowel syndrome] (IBS) or ulcers or inflammatory bowel disease or an active [Helicobacter pylori] infection. The reason why their TSH is up and down or their thyroid levels are up and down or their dose keeps modulating [and] they can’t get everything right with their lab work could be inconsistent malabsorption. That malabsorption also ties to things like [vitamin] B12 and iron.
What’s so important about this, and [is] an area I know you’ve discussed quite a bit, is that you could be chasing thyroid hormone medication as the cause for your fatigue, your brain fog, [or] your poor exercise tolerance, [when] it could actually be a [vitamin] B12 deficiency or an iron deficiency. [That’s] just two [examples of what] might be driving that. The importance of the gut here [is] so prominent, and something I think more patients need to be considering [in] the context of, do you first fine-tune your thyroid levels? Or do you look to make sure that you have a nutrient-dense diet and healthy absorption of those nutrients? I would argue [that] it should be the latter first because it’s far more prevalent that we’ll see a need for nutrients than for this uber-fine-tuning of the levels of [thyroxine] (T4) and [triiodothyronine] (T3), let’s say.
Chris Kresser: Absolutely. I know, and I imagine you’ve had similar experiences, [that when] treating people for undetected [gastrointestinal] (GI) conditions like a parasite, [small intestinal bacterial overgrowth] (SIBO), [or] disrupted gut microbiome, I would often warn patients that they may need to [carefully] watch their thyroid levels and thyroid medication, because as their gut health improved, their thyroid function would improve, and then the dose of the medication that they were on would often be too high.
Michael Ruscio: Yeah, such a wonderful thing to have to warn them about.
Chris Kresser: Exactly. “You may need to reduce the dose of your medication as we fix your gut.” There’s probably multiple things happening there. We’re increasing the absorption of nutrients and [improving] thyroid function, [and] we’re decreasing intestinal permeability, which reduces inflammation, which can suppress the conversion of T4 to T3. There [are] so many different mechanisms that we already know about, and probably a lot that we don’t know about, that regulate that gut–thyroid axis.
Michael Ruscio: Exactly, exactly. It’s also important to mention that there’s a tremendous amount of overlap between the symptoms of hypothyroidism and symptoms of suboptimal gut health, [like] fatigue, brain fog, insomnia, constipation, abdominal pain, [and] even dry skin [and] thinning hair. This is another area, coming back to your comment about thyroid hysteria, [where] I just have so many concerns that people are barking up the wrong tree. They’re going, “Thyroid, thyroid, thyroid,” and they’re missing the fact that their fatigue, their brain fog, [or] their dry hair or skin could be due to what’s going on in their gut.
Chris Kresser: Yeah, we could extend that to so many other systems in the body, too—metabolism, cardiovascular health, hormone balance, brain health, cognitive function. There is a profound connection between the gut and all these systems, and it only seems to increase as [the] science progresses and we get more data through full sequencing of the microbiome and understanding those relationships [better]. Our understanding has grown over time of how much of a driver gut health is to overall health.
Nutrients to Help with Thyroid Function
Chris Kresser: Let’s talk a little bit about the specific nutrients. You mentioned iron and [vitamin] B12 as part of the nutrient–GI–thyroid axis. What other nutrients should people be thinking about?
Michael Ruscio: One quick thing on the iron: there’s discussion and debate regarding what an optimal ferritin level is. This researcher, [Dr. Esa] Soppi, in Finland, [has] been proposing that ferritin should not be below 100. In case some people have been confronted with this, we are finding at the clinic that a ferritin target of 100 [is] too high. It’s not practical. But if we can get ferritin to 30 or above, or said another way, if people are below 30 [and we] either increase their iron intake in their diet or supplement them,  is the cutoff that’s most likely to lead to a symptomatic improvement, based upon fatigue or whatever is shifting. So I just want to plant that one footnote. I’m not sure. Have you been trying to figure out what the best ferritin cutoff is on your side, Chris?
Chris Kresser: Yeah. I think you know [that] iron overload has been a big focus for me in my career, and how often that is under diagnosed and under recognized. So I get nervous when I hear about a minimum level of 100, especially in women. The baseline ferritin levels in men and women can differ, and I would consider [100 for ferritin] to be borderline high for women, especially if they’re supplementing with iron. So I agree with you. I would see improvements and changes if I brought ferritin from 15 to 30 or 35, but I wouldn’t see much of a change from 35 to 60, for example. I think there is some individual variation. I’ve definitely had patients who would notice a difference going from 30 to 60. But I don’t think we can make that a general rule.
Michael Ruscio: Agreed. I was excited about the prospect of these suboptimal ferritin levels holding the key to these non-responsive symptoms, so we were tracking this meticulously because, [as] I know you do, we prefer a nutritional solution when we can. But that may have been too aggressive. Excellent point, also, on the iron overload. Like so many things, there’s this Goldilocks zone. More is definitely not better. It’s the right balance that we want to strike. So, to your earlier question about other nutrients, there’s a number [of them], but two that I think are important to keep in mind are selenium and inositol. Selenium, I’m sure your audience has heard, has [a] multifold impact. One [is] lowering TPO antibodies, and there [have] been a few trials looking at subclinical hypothyroidism. This is where the TSH starts to drift up into the positive range. It goes above the upper cutoff of 4.5 to maybe 5, 6, 7, [or] 9. Selenium plus myo-inositol has been shown [to be] very effective in helping increase the likelihood that someone will see their TSH go back to normal. This could be because selenium is anti-inflammatory, as is inositol. Inositol may help with improving sensitivity of the thyroid gland to TSH signaling. And selenium is an antioxidant. So those two, I think, are important to keep in mind. People can target those in their diet via a number of [foods]. This is [where] having a non-heretical position on diet can be helpful, but there are a number of foods that are rich in both of those. I’ll offer those as two for people to consider, that are more so through the lens of autoimmunity.
Did you know one of the most common reasons people suffer with thyroid symptoms and non-responsiveness to thyroid medication is due to problems in the gut? Tune into this episode as Dr. Ruscio discusses his innovative, gut-focused approach to thyroid care. #chriskresser #thyroid #guthealth
Chris Kresser: Yeah, I love that. Selenium, as you mentioned, can be particularly important for Hashimoto’s [disease], in part because it promotes glutathione production, and glutathione helps regulate immune function and reduce autoimmunity. In the [United States], true selenium deficiency is rare, when you look at the statistics. But I’ve also seen studies, and [I’m] curious what you think of this, [showing] that people who have Hashimoto’s [disease] and antibody production may require slightly higher levels of selenium intake than the general population.
Michael Ruscio: Yeah, I think that’s fair. The other thing we can juxtapose with is, what happens when free-living humans in the [United States] are diagnosed with Hashimoto’s [disease] and they supplement with 200 micrograms per day of selenium, let’s say? Not all the studies agree, but there’s clearly a sign of benefit. But the other part of this is [that], if you look at some of the studies that track selenium supplementation for three, six, nine, [and] 12 months, the benefit from selenium tends to drop off around three to nine months. So it’s something that might get them to this optimal topping off of the tank, so to speak, but I think it’s important to clarify [that] people with Hashimoto’s [disease] should not be supplementing with selenium in perpetuity.
Chris Kresser: Yeah, or [in] high doses. Selenium is one of those nutrients that is toxic at higher doses. If you take too much selenium over time, like you said, [you] can store it up, and it can be problematic. It’s not like vitamin C or B12, which don’t have a toxicity threshold that we’re aware of. It’s more like vitamin A, iron, calcium, etc., that you can get in trouble with if you take too much.
Michael Ruscio: Right, right. And of course, there’s vitamin D. I’m sure everyone at this point is probably aware of the importance of vitamin D. I think you and I, Chris, are on the same page that we should be looking at vitamin D as something to predominantly get from the sun. Using our lifestyle as a lever for that and supplementing secondarily, being careful not to be too heavy on the gas pedal with your vitamin D supplementation. Every once in a while, we’ll see someone whose vitamin D level is 90, 100, [or] 110.
Chris Kresser: 125.
Michael Ruscio: Yeah. And again, it’s the same sort of thinking, where more is better. More supplements, more dietary restriction[s]. I think we should try to invert that. We should be looking to expand our diet, eat as nutrient-dense of a diet as we can, and use supplements as minimally as possible. This is more able to be done, I think, when people don’t have this heretical view on autoimmunity, like, “Oh, my God. I’ve got to go so high on vitamin D and selenium because I still have TPO antibodies that are 100, and I heard if I have any antibodies, if I’m not at zero, it means I’m at risk.” That whole paradigm is this self-feeding cycle of overzealously interpreting labs, doubling down on your supplements, [and] going too restrictive with your diet. That’s what I, again, appreciate about your perspective [on], Chris, because I think we’re both on the same page where we’re trying to give people the tools, but make sure they’re not overusing the tools.
Misdiagnosis and Overmedication of Patients with Thyroid Symptoms
Chris Kresser: Yeah, I think [this is] one of the things that happens, [and] I know we’ve talked about this before, in the search for a solution. Which is totally understandable. We’ve both dealt with our own chronic health problems, we know what that’s like, [and] we know how frustrating it can be to not have a solution. If you get a lab result that comes back with some kind of signal, it’s very natural and understandable that we would tend to latch on to that as the answer. [If] you [have] a patient [with] symptoms [like] fatigue, constipation, malaise, depression, dry skin, all of that, and then you get a positive thyroid antibody test with or without [a] slight difference in elevation of TSH, it’s pretty easy to just be like, “I found the answer. This is it. Now if I correct this, everything’s going to get better.” And I don’t blame patients for that, [or] even clinicians. It’s understandable. But often, that leads us in the wrong direction. As you pointed out in this podcast, maybe it’s [actually] more of a gut issue, and taking thyroid medication just because you have slightly elevated thyroid antibodies and slightly elevated TSH with normal T4 and T3 is not the best option. Let’s talk about that, because I think you and I agree on this, as well. There’s a growing trend [that] I’ve seen, or at least saw over the past several years in my practice, where I would see patients coming in [who] were prescribed thyroid medication for subclinical hypothyroidism. This is when their TSH was slightly elevated, but their free T3 and free T4 were totally normal. And my thinking was, “Why?” The thyroid medication’s goal is to raise thyroid hormones. If thyroid hormones are already in the normal or optimal range, why is a thyroid medication being prescribed? What does the research say about this?
Michael Ruscio: I completely agree with you, Chris. It’s so important for us to mention that subclinical hypothyroidism, in the vast majority of cases, like we discussed a moment ago, corrects itself on its own, [and] you can increase those odds with selenium and myo-inositol. But [it also] does not benefit from treatment. We’ve looked at this up, down, left, right, and center. Unless you’re very young, and the definitions [of that] vary from study to study, but we’re talking in your teens, maybe in your early 20s, but unless you’re very young, people do not benefit symptomatically from medication. Now, there’s also been some discussion that those who have a history of infertility may benefit from using, let’s say, levothyroxine to take their TSH from 7 down to 2. However, a recent meta-analysis challenged that. So even for that cohort, there may not be benefit from using thyroid hormone. You will see some reduction in cholesterol, but I don’t think the potential risks associated with using thyroid hormone that you don’t need is worth the minimal reduction in lipids.
But just to play devil’s advocate, that would be the devil’s advocate argument—“Well, what about my mildly elevated lipids?” You’re not going to see a massive change, and no endocrine bodies are recommending to use thyroid hormone replacement in perpetuity for the rest of the person’s life for subclinical hypothyroidism. Definitely not for those who have elevated lipids, because there are better ways to address that. This is one of the main gripes I have with the field is [that] people are often told, “Well, your TSH should be at 2.5, or at two.” What happens here, [and] I think it’s well-intentioned, but it’s definitely incorrect, [is that] providers sometimes look at the goal for when you are medicating an individual who’s hypothyroid. The goal when someone is [a] true hypothyroid and we’re medicating them is to get their TSH down to 2.5 or 2. But we can’t conflate that and say everyone should have a TSH of 2 to 2.5, and if you’re above that, you’re hypothyroid. Your thyroid function is totally fine if your TSH is 3, 3.5, 4, 4.5, even if your TSH is 6, 7, 8, [or] 9. The level at which TSH elevations indicate someone should go on hormone [and] that they’ll benefit from the therapy is when you get above 10. Some recent estimates are suggesting maybe 7. When you’re in this ballpark, this transitional zone from TSH being between 7 and 10, that’s when someone might benefit from thyroid hormone. But these poor people who are being put on hormone who have a 5 or 6 [or] 7 for the TSH, it’s not the right play. This was corroborated by a recent meta-analysis that found that 37 percent of people [who] were on thyroid hormone did not need to be, meaning they were able to come off hormone and were tracked over a six- to eight-week period, and their TSH and their T4 maintained totally normal levels after stopping thyroid hormone. Thirty-seven percent of people. That’s shocking.
Now, if we factored a Functional Medicine cohort into that analysis, it would probably be more like this paper from Greece [in] 2018, published in the journal Thyroid, that found 61 percent of individuals were incorrectly diagnosed. To your question, a lot of this incorrect diagnosis, I think, comes from overzealously prescribing thyroid hormone for subclinical hypothyroidism. This person, let’s say his name is John, goes and sees a different healthcare provider two years later. The healthcare provider reviews his history [and says], “Oh, you’re hypothyroid? Oh, you’re on [levothyroxine]. Okay.” And no one questions it. It just gets buried in their chart, and no one says, “Hang on a second; how were you diagnosed? Who diagnosed you? What was the lab work looking like at [the] time of diagnosis?” I can say that, at our clinic, we now have this as part of our intake paperwork. “Are you hypothyroid? Who diagnosed you?” If it was an Integrative provider, that throws up a big flag. We ask to see the labs that diagnosed them, meaning from before they went on thyroid hormone, and you would be shocked [by] the number of people who are walking around thinking they’re hypothyroid and they’re actually not. Again, corroborated by two great papers recently, one a meta-analysis, finding that 37 percent of people do not need to be on hormone that they’re on.
Chris Kresser: Yeah. I’m not shocked, of course, because I’ve had that same experience and we have the same type of paperwork. The conversation would also go toward, “Okay, was it just TSH that was measured? Did they also measure T4 and T3, free T4 and T3? What were those results? Was there serial testing done?” Because, and I’m sure you came across this in your research, we now know that TSH, which is often the only marker that’s tested in a conventional setting, has a diurnal rhythm. It fluctuates throughout the day. I saw one study a while ago that said you’d have to do something like 30 tests of TSH over a several day period to get a true average reliable result, because it’s fluctuating that much throughout the day. Imagine someone who goes to the doctor, they get a single TSH reading [at] a single moment in time, which is high, and [they] are prescribed thyroid hormone as a result of that. There might be retesting, [but] there might not be. I’ve had patients who were prescribed thyroid hormone on that basis and took it for years without ever being retested, without ever having a T4 or T3 test, or free T4 or T3 test. Then it’s really hard, sometimes, to convince those folks that [it] was not necessarily an evidence-based decision, because they’ve adopted the mentality of, “I have hypothyroidism; I need this medication. I can’t stop it now or else bad things are going to happen.”
Michael Ruscio: Well, one, I guess, ray of optimism from this meta-analysis was that the time on thyroid hormone did not predict if people could successfully discontinue their medication or not. Just as one point of solace for the audience. If you’ve been on hormone for five years [or] 10 years incorrectly, that doesn’t mean that your body’s built up a dependency.
Chris Kresser: Right. That’s really important. I want to talk a little bit about the flip side of that, too. One of the objections that I’ve heard over the years [from] patients who I think were incorrectly diagnosed with hypothyroidism and incorrectly prescribed thyroid hormone, is they’ll say, “But I have more energy.” Or, “It makes me feel better.” And my response is, “Well, cocaine would do that, too. But that doesn’t mean that that’s the solution to your problem.” Thyroid hormone, as a medication, will increase your thyroid hormone levels, and that will have certain physiological effects, regardless of whether you’re [actually] hypothyroid [or not], depending on the person. Just because it produces a certain effect in the body, that doesn’t, in and of itself, justify its use, particularly over a long period of time.
Michael Ruscio: Yes, [I] completely agree. While, on the one hand, yes, it’s important to listen to the individual because you learn so much from listening to people, we also have to factor in for placebo and for the fact that, often, people start on multi-interventional care plans. They could have improved their diet, gone on curcumin, vitamin D, fish oil, and a probiotic, and started taking thyroid hormone all at the same time. And they may have falsely attributed all the benefit, or most of the benefit, to the thyroid hormone. Coming back to placebo, even in studies where people know they are being given a placebo, they still report benefit. All those things are very important to keep in mind. I leave a small crack in the door for [the possibility that] there’s a very tiny subset of people that feel better using thyroid hormone [almost] like an anti-aging support. But I think it’s got to be incredibly small, and more likely, it’s placebo or the other interventions that the person has utilized.
It’s also important to mention that thyroid hormone, as you intimated, is not without risk. A recent study found that the combination formulas of T4 and T3 can, in some cases, increase the risk of stroke and another cardiovascular outcome. I don’t know if it was heart attack or stroke, but there was a 1.6 and 1.7 percent increased risk of, let’s say, stroke and heart attack. I may have the outcome slightly off, but they’re generally representative of two things you don’t want to have. As a juxtaposition, the risk associated with smoking for those conditions is about 2 percent. So it’s not to say that’s a nominal amount of risk. I also want to be careful to say [that] I’m not advocating that anyone who was feeling good on something like a desiccated hormone [should] stop [taking] it. It’s just to impress the point that these medications aren’t without risks. We certainly see people in the clinic who are on thyroid hormone who don’t need to be, and when you look at their symptoms, it’s like, “Geez, you are fatigued, you have insomnia, [and] you have heart palpitations. Yeah, this sounds a whole heck of a lot like overdose.” Because remember that too much thyroid hormone, as [with] hyperthyroidism, can make you tired. It’s always so disheartening when someone’s been struggling with symptoms for a couple of years because they’re on hormone that they don’t need to be on.
Chris Kresser: Yeah, I liken that to coffee. A lot of people have had the experience where coffee will create a temporary lift in energy levels just after you drink it, but in the afternoon, if you have had too much coffee, you feel like you got hit by a truck. Excess thyroid hormone can do that, too, because essentially, it’s goosing the system, and you can’t do that endlessly without paying the price at some point. So I definitely appreciate you bringing that [up].
Checking on the Accuracy of Your Thyroid Diagnosis
Chris Kresser: I want to bring this back to how someone [should] think about this. I’m sure a lot of people are listening to this and now have questions about their own diagnosis, [like] whether they were accurately diagnosed [and] whether they should be taking the medication that they’re taking. What are some questions that folks can ask their provider to help clarify this?
Michael Ruscio: Sure. I think building a checklist is incredibly helpful here. Some of these things, you may or may not want to ask your provider. Who diagnosed you? If the person who diagnosed you is an in-the-box, conventional medical provider, this is one thing I think conventional medicine is doing quite well. If you’re diagnosed by a conventional medical doctor who’s practicing in Integrative and Functional care, or any type of Integrated provider, unfortunately, and no offense to any of my colleagues, this raises suspicion significantly that you could have been misdiagnosed. I would obtain the labs, if you can, that diagnosed you, and look to see if your TSH and your free T4 are within the lab ranges of the conventional labs—not what the provider writes in, not the Functional Medicine ranges, but look to see [if] you [were] flagged high with TSH and flagged low for T4. And if you weren’t, then you might be on hormone that you don’t need. Of course, don’t change anything without checking with a healthcare provider.
The other thing to consider is your digestive health. Do you still have any lingering GI symptoms? If you do, this could be the source of most of your symptoms. Also remember, as I learned myself, [that] it is possible to have a silent gastrointestinal problem that’s only manifesting neurologically, dermatologically, [or] rheumatologically, meaning it’s causing fatigue, brain fog, insomnia, joint pain, [and] skin issues. Just because you don’t have digestive symptoms, [that] does not guarantee your gut health is in good shape. It might still be worth doing a trial on something like a probiotic or another gut intervention. Also remember that the odds are really well-stacked in your favor that if you have Hashimoto’s [disease], it’s not a sentence to hypothyroidism. In fact, you probably won’t become hypothyroid. Hopefully, that knowledge will help people be a little bit more self-supportive and liberal with their diet. I’m not saying that you [should] have pizza and beer every night. But I’d love for you to be able to have pizza and beer when you want and not feel like you’re burning your thyroid gland with inflammation when you do that. Unless you notice a very clear aversion to those foods, [of course]. I think that’s a short list.
Chris Kresser: I would just still say, consider [the] other possibilities. That’s the whole point of this show. Has it been a misdiagnosis, in the sense that maybe the key issue has not been the thyroid all along? Or, even if the thyroid is not functioning optimally, could it not [be] the root cause of what’s going on? [Perhaps] the gut is actually the root cause and a thyroid dysfunction is just a symptom of that underlying problem. That’s another avenue of exploration, for people to look into alternative causes of those symptoms or signs.
Michael Ruscio: Yes, yes, 100 percent. That’s the six-patient case series that we published in Integrative Medicine, the clinician’s journal, where we wanted to share [our learning curve] with providers. There’s one great case study where we tried four different perturbations of medications. There’s a really nifty chart where you can see this patient’s TSH levels. We plot the different interventions with different thyroid medications that were trialed, and the TSH just is not getting to where it needs to be. Finally, she’s given triple therapy probiotic, antimicrobial herbs, and immunoglobulin therapy, [with] no change to her thyroid hormone, and her TSH finally goes into range. There [are] so many cases where we’ve learned that we have to address gut health, either as the true cause of the symptoms or the reason why the person is not responding to thyroid medication to begin with.
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Chris Kresser: Absolutely, yeah. This might seem a bit discouraging in some ways for people who are listening, because it’s a lot to take in, especially if you felt like you’ve already arrived at the diagnosis and were clear about it. But it is really true that it pays to be your own advocate. It’s really important to be a critical thinker about this kind of thing, whether you’re a patient or a clinician, and not just accept the first explanation that’s offered. Really dig in and think in a methodical way about it. That’s never a bad idea, in my experience, whether you’re a clinician or a patient. I want to be clear [that] this is my perspective. I imagine you agree, but let me know if you don’t. It’s not like people who are making these diagnoses have any ulterior motives. They’re trying to help, in most cases, and it’s just that there has been some unfortunate misinformation or misunderstandings around these things. In science, in general, and medicine is part of science, there’s an evolution that happens over time, where understanding improves. That’s what this is about. We’re not throwing anyone under the bus, whether you’re a patient or a clinician. We’re just trying to help clarify what the research has illuminated over the past few years, so that people can hopefully get to the bottom of what’s causing their symptoms and find a solution that works and is safe over the long term.
Michael Ruscio: Yes, we’re all on the same team. Clearly, right? We’re all on the same team. We’re all trying to [either] get better ourselves, if we’re patients, or as healthcare providers. It’s really important that we can be okay with the fact that our field is not going to have everything right all the time. I would offer that for people, because every once in a while, we’ll come across a clinician who digs their heels in. When we’re offering up a new and different hypothesis, it’s almost as if you’re attacking their worldview, and it’s like, whoa. We should be open and constantly reappraising these things, because the probability that we’re right on everything is extremely low. [And] if we’re not right about everything, there are going to be some things we’re wrong on, and we should embrace that. Because the faster we get to those realizations, the better we are clinically and the more expeditiously we can help patients improve. So yeah, I’m totally with you. I’m glad you said that. We’re all on the same team. There’s a few things, I think, in the model of Functional thyroid care that were interesting initial hypotheses, but now we have enough data to reexamine those and kind of course correct how we’re talking about this and how we’re doing our diagnostic workups in our corresponding care plans.
Chris Kresser: As I’ve said in the past, the history of science is the history of most people being wrong about most things, most of the time. That’s objectively true. At every point in history, most of the people who live at that time think that was only true of the past and not in the present. Objectively, progress does happen over time, and it’s true that our understanding is more accurate overall now than it was 100 years ago, and that will be true 100 years from now, as well. It’s pure hubris to think that we know all the answers. It strikes me how, and this is a little bit of a tangent, but physicists get this right. Physicists are gleeful and excited when they find out they’re wrong because that means that there’s something missing in their fundamental understanding of how the universe works and world works, whether we’re talking about the quantum level or the more macro level. I think [that], of all scientists, physicists have the most pure approach to science [and] understanding that everything is just a hypothesis that we’re trying to prove wrong. You never get to full 100 percent proof. And when we find out that we’re wrong, that’s actually an exciting opportunity to get closer to the truth. If only we’d embrace that in medicine and healthcare. But I think that can be a little jarring for people. I’ve tried to explain this to patients, and it’s one thing when you’re talking about the Higgs boson particle, which doesn’t really affect people’s daily life. But if you’re talking about their symptoms and their health, I can understand why people get frustrated with changing ideas and practices over time. But really, that’s the reality. If we want to be honest and intellectually have integrity about our practice, that’s how it is.
Michael Ruscio: Yeah, I couldn’t agree more. One of my mantras is “try to be less wrong.” I think it’s really helpful to think about things that way. On the clinical side, the way we try to communicate this with our patients and think through the problems is [that] there’s no black or white, right or wrong. With all these things, we’re just assigning a certain probability to them. And when you look at these things as probability gradients, you don’t fall into this absolutist, “Well, this thing [is] good or bad, or this diagnosis [is] right or wrong.” But rather, “Well, there’s a 70 percent chance it could be this. And we’re going to continue to look and listen at how your symptoms evolve and, with more data, we’ll either progressively prove or disprove this hypothesis.” This is such a freeing way of reframing clinical care. Because, again, you get out of this binary or false choice of right or wrong. You’re always just trying to turn the direction of what you’re doing clinically, based upon these shifting probabilities.
Chris Kresser: Absolutely. You mentioned this briefly earlier on, [but] I want to highlight it because it’s one of my pet peeves about the conventional view. You can look at that same thing when it comes to lab ranges and diagnoses. It’s a question of probability and scales. It’s usually not a binary yes or no. Even when you have a lab result that’s pointing in a certain direction, you almost always have to put that in the larger clinical context and consider symptoms and history and risk factors. It’s not like, “Oh, your fasting glucose is 98; that’s just fine. Now it’s 99. Okay, you have prediabetes, and now we’re going to mobilize and do something about it.” Nothing in nature works like that, including the human body. It’s a good reminder, in general, whether we’re talking about [the] accuracy of our diagnostic framework, or whether we’re talking about lab test results, [to approach] it with an attitude of curiosity and exploration and willingness to be wrong and keep learning. I think we’ll end up at a better destination when we do that.
Michael Ruscio: Yep.
Chris Kresser: Mike, I loved this. [I] really appreciate you and your perspective and your great work in these areas. Where can people learn more about your work and the studies, as well?
Michael Ruscio: The studies [are] indexed in PubMed. If you go to DrRuscio.com, that’s our hub website [with] access points for everything else. We recently [released] a course on this. I wanted to give people a way of going through this checklist, so to speak, without having to see a doctor, in case it was financially out of their reach. I am in the clinic, and we have a great team of doctors, if anyone needs direct clinical care. There’s also the course, as a lower cost entry point. Then these papers and a bunch of other stuff is available through the main website, DrRuscio.com.
Chris Kresser: Fantastic. Thanks again, Mike. [It’s] always a pleasure to speak with you, and congrats on the publications and the great work.
Michael Ruscio: Thanks, Chris. I appreciate it. Let’s do it again soon. It’s always fun catching up with you.
Chris Kresser: Absolutely. And thanks, everybody, for listening. [I] hope this was helpful. Keep sending your questions to ChrisKresser.com/podcastquestion. We’ll see you next time.
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