[INTERVIEW]
Ronda Nelson: You are looking at a thyroid panel, and that thyroid panel has a positive TPO, positive thyroglobulin, maybe even a positive TSI. And one practitioner says, “That is Hashimoto’s.” And another one says, “No, no, that’s Graves’ disease.” But what do those antibodies actually mean, and what are they not telling you?
Today, we’re gonna decode the major thyroid antibodies, where they act, how infections and food cross-reactivity fit into the picture, and I’m gonna tell you how to avoid making the wrong diagnosis. Let’s go.
Well, hello, and welcome back to the podcast — the show, the YouTube, weekly explosion of Ronda’s thoughts over here. So I’m back. Today, we are gonna be talking about the thyroid. It is one of my favorite things to look at, and I think it’s because it’s sorta complicated, and I like that. I like being able to figure out a puzzle. I like putting the pieces together. I like to kinda pull it apart. I sometimes think that complex clinical conditions are, I don’t know, they’re like a dreadlock, or like a real tangled ball of yarn, you know? You have to kinda pull the threads and start to kinda unravel the thing a little bit at a time. I really enjoy that, and I always feel like the thyroid’s sort of at the center of the endocrine tangle, so to speak. There’s always something going on with the, within the — something else within the endocrine system, and the thyroid is the reflector of that a lot of times.
So we’re gonna talk today about thyroid antibodies. This was actually a question that someone asked me recently, and I thought, “Oh, that’s gonna make a great podcast.” So I wanted to share some more information about this with you.
So let’s talk first about thyroid antibodies. We often look at these antibodies as a measure of thyroid function. Let me say that again. We often look at a blood test when there’s positive antibodies, and we say, “Oh, if these antibodies are positive” — let’s say it’s TPO, I’ll talk more about that in a minute — we look at TPO and we go, “Oh, for sure you have Hashimoto’s.” I’ve done it. Excuse me, I’ve done it. I don’t think that’s the best way to handle that, but we’ve all done it, I think.
So we have to look at antibodies as a signal. I want you to think about the antibodies as a signal, not as a diagnosis. So we’re not gonna use that term today. We’re gonna talk about questions instead that we need to — I want you to be thinking about asking. So with every thyroid patient, there’s kind of three questions. I’ve got some more questions for you later, but for now, three things.
If there’s an antibody that you see on a test, whatever the thyroid antibody is, the question is, number one: is the immune system reacting to thyroid tissue, or could it be reacting to something else? Just a valid question, a clinical question you need to ask yourself, which is going to direct then how you’re developing out the care or the protocol that you’re gonna recommend to the patient.
The second question is, is the thyroid actually dysfunctional, or is it functioning normally and we have a positive antibody? That happens all the time. Or you have a positive antibody, the patient is incorrectly told they have Hashimoto’s, but the thyroid’s fine. Do they or don’t they? That’s your job. You gotta figure that out.
The third question is, is there a clinical action or a clinical decision that I need to make? Is there something that needs to be done that’s going to help me move the ball forward for the patient and help the thyroid get better? I would argue that unless the thyroid is behaving poorly — meaning you’re seeing other markers on the test, they’ve got clinical presentation symptoms, you can see clearly hypothyroid, clearly some kind of a thyroid presentation that’s not normal — then yeah, there should be a clinical decision that’s made.
But just because you have a positive antibody does not mean that it’s telling you what the thyroid is doing today. That’s the big takeaway here. Just because the thyroid antibody is positive doesn’t mean that the thyroid is under any pressure from that antibody. Might be, but maybe not. So one does not equal the other. So we have to be thinking about this differently. The antibodies are just an indicator. They’re just a light. They’re just a light that’s telling you something. Is it a red light? Is it a green light? Is it a yellow light? Is it a purple light? Is it a blue light? I don’t know what color the light is, but the thyroid antibodies are just giving you information.
So let’s talk — I’m gonna take this and we’re gonna back it up for those of you that are, you know, new here, or maybe you’re just getting your feet wet with all this. I always like to give a little bit of context.
So first of all, let’s just talk about the immune system, right? The immune system is designed to recognize foreign proteins. That’s what it does. That’s what it’s doing. It’s looking all the time, searching, searching, searching. It’s like the most aggressive, you know, most-wanted patrol, and it’s always looking for something that doesn’t feel or look right. In an autoimmune disease, the immune tolerance starts to kind of break down. Something is provoking it. It’s like recognizing something for something.
Now, there’s always a small amount of immune activity that’s going on because we are always, every day, recognizing foreign things in the body. The immune system is tagging them and getting rid of them. So I’ll say this, don’t mistake what I’m saying, but an autoimmune response, a self-directed immune response — the immune system’s already out looking for things that shouldn’t be there inside the body. It’s already doing that. So when the autoimmune — the normal autoimmune, or the normal immune cleanup process where it’s tagging these foreign proteins and saying, “No, no, you out, you gotta go” — that system, that communication, gets altered and it breaks down. And that’s what happens when we see tissue destruction. There’s something that’s driving that. We’re gonna talk about that.
So the B cells produce the antibodies against the targets that resemble whatever the threat is, and then the T cells and the inflammatory signaling help kind of sustain the response. So you’ve got the two arms, you know, two branches of the — the Army and the Navy, right? You’ve got both of them.
Now, we also have this thing that most of you are familiar with, which is called molecular mimicry, and molecular mimicry occurs when a microbial protein resembles part of — key word right there, part — but when some kind of microbial protein resembles part of a human protein close enough that the immune response goes, “Hmm, I don’t know, maybe there’s something screwy going on,” and that could be a bad guy. And because the immune system is always working so hard to protect us, it’s gonna go after it. So it’s biologically very plausible that that happens. In fact, there is research that shows that that does happen. However, in mainstream medicine, I don’t know that they’re always so on board with this concept. That’s okay. We can take a plausible explanation, and we can run with it, and that’s okay. We can absolutely do that, and if it’s not the right answer, then we just change direction and we do something else. But I do think that it’s very plausible and possible. There’s a lot of ongoing research happening in this field of molecular mimicry as it has to do with autoimmunity, and it is an established concept. It just hasn’t been kind of written in stone, so to speak.
And so when these infectious triggers show up, they can present in a number of ways and in a number of places in the body. So it could be an unresolved infection, like maybe the patient had food poisoning 20 years ago, and now it’s just showing up. Maybe they had some other viral, weird viral thing. I mean, who knows? Could be COVID. Who knows what it could be. But some unresolved infection. Could have been like sepsis, or it could have been bronchitis, or it could be anything. Could also be microbial proteins that resemble a self-tissue — and in this case, we’re talking about the thyroid, but it could be any tissue in the body. But microbial proteins are known to have similar protein signatures or structures or sequences as self-tissue, and it also could just be general shifts in immune regulation and the microbiome. So we sometimes casually — I should say I, and for those of you that listen, I sometimes refer to that as, you know, we call those stealth pathogens. And I think that term, we all kinda know what it means, but we don’t always define what that means. But stealth pathogen just means something that’s in the body that doesn’t necessarily need to be there and may be causing a problem downstream. Something that’s hiding, has cloaked itself, is nestled away, tucked away somewhere, and maybe, may be, might be, could be possibly contributing to a potential autoimmune response.
Do you hear all my caution in here? And I think rightly so, because I think the error that we make — and I’m guilty, so I’m like the pot calling the kettle black here — the error that we make is that we make assumptions, we make generalizations. I think we too often make generalizations about, “Oh, if this, then that.” But how — the body doesn’t work that way. Just because I say turn right and I meant turn left doesn’t mean we should go right. It means someone says, “Hey, wait a minute, are you sure you wanna turn right? Doesn’t the sign say no right turn? Like, go left.” So we have to think, just because we can hear something or see something on a test and go, “Oh, for sure it means that,” it doesn’t have to mean that. It might mean something completely different.
So if you know that there is a documented infection that is driving immune activation — think about ulcerative colitis, we know that there’s infection behind that, or Crohn’s disease, where there’s some things going on, right, there’s an autoimmune response, there’s an active, some kind of an inflammatory trigger — then addressing that infection could very much impact the immune response and inflammatory regulation, 100%. But it’s not always accurate to promise or expect that just because you treat an infection, like with the stealth pathogen work, with myrrh and artemisinin and some of the other herbs — you could call them the group of antimicrobial herbs — if you treat with that, that doesn’t mean that the antibodies are gonna go away. Right? Antibodies could stay positive. In fact, they often do.
So how do you know when you get that test that you’re looking at the antibodies, maybe this is the stable? Maybe they used to be 800, and now you see them and they’re 150, and then you and I — I’ve done it, I’m here, I’m in this camp with you, my friend — we look at it and we’re like, “Oh, you have Hashi’s, looks like you’ve got Hashi’s.” I can’t tell you how many times I’ve done this, and I think that it’s not right. I just don’t think we should do it that way. I think the better thing is to step back and say, “Hmm, maybe this is the normal. How about we get some historical context? How about we look at this a little bit deeper, or more broadly, to see if that indeed is true? Or is it just we’ve resolved the issue and those antibodies are just hanging out there being positive?” It’s okay.
So there is, as most of you are gonna be familiar with, Dr. Vojdani. He was the first person that I really understood. I’ve never met him, I don’t know who he is in person, but I love his work. And he’s associated with Cyrex Labs, and I do use their labs. But with Dr. Vojdani’s work, he introduced the concept years ago that dietary proteins could share similarities with human tissue proteins, meaning that if a certain person were to eat a certain type of food, their unique immune system may have a reaction to that food in the form of an autoimmune response or an immune reaction. It’s not a food sensitivity or an allergy per se. It’s an immune recognition of protein in a food that that individual person’s immune system says, “Yep, that gluten protein right there looks like the thyroid.” And we all know this, right? We do know that a lot of patients, not all, but a lot of patients that have autoimmune thyroid also have sensitivity to certain types of proteins found in wheat. So Dr. Vojdani has done a great job of pioneering that work. So they have some great tests over there. The one test that I like is the Array 4 test, and what that does is it gives us information about what foods an individual’s body may be reacting to that could be — all of this is quotes, right — that could be causing or contributing to an autoimmune response.
This doesn’t mean that every single positive IgG or IgA result represents something that’s clinically meaningful. It’s just information. Like I said earlier, you’re gathering the pieces of your puzzle. You’re like, “Hmm, interesting, that test came back, I did the Array 4, and it came back with wheat was a no, dairy was a no, but chocolate and quinoa were positive.” Interesting. And then you ask the patient, “What are you eating?” And they say, “Oh, I eat quinoa bread every day and chocolate milk with coconut milk every day.” Okay, well, that might explain why those are positive. You have to take that in clinical context with their history, their diet, their lifestyle, all of the things, in order to create that bigger picture.
So now we kind of have some context here. Let’s talk about these antibodies. There’s four of them that we’re gonna cover today.
The first one is the one that you’re probably all familiar with, and that is TPO. TPO stands for thyroid peroxidase, and it is an enzyme, okay? Oxidase is your key there, your clue. It’s an enzyme that’s involved in hormone production inside the thyroid itself, inside the thyrocyte. It’s actually on the membrane of the thyrocyte, on the lumen or the colloid side. So it’s on the apical membrane, inside the cell — inside is kind of general, but anyway, it’s in there. It’s an enzyme, and that helps to synthesize thyroid hormone. It is very strongly associated with Hashi’s, but it can also appear positive in Graves’ disease and also in postpartum thyroiditis. It can also be positive in some other autoimmune conditions and have nothing to do with the thyroid. Let that sink in for a hot minute.
How many times might we have assumed that someone had Hashi’s when the antibody was positive, but it wasn’t because there was an autoimmune issue with the thyroid, but it was because there was something else going on in the body, an associated condition? So these antibodies — I want you to think about them as thyroid-directed autoimmunity, okay? It’s directed at the thyroid, at the actual thyroid cell, at the tissue. So when there is an injury and we have an autoimmune response, it’s going to affect the actual thyrocyte itself. So the immune system is triggered, it recognizes there’s something going on, whether that’s molecular mimicry or food or another whatever. But in this case, with TPO, it often is targeting — better word than “attacking” — the thyrocyte itself. But just because that TPO is positive does not mean or prove that hypothyroidism is present.
I know. So why do we test them then if it doesn’t mean anything? Because it’s just information. It can tell you that there is a possible risk of developing thyroid dysfunction over time. Maybe they’re positive, maybe the thyroid T4, T3, TSH, all that looks fine. Then you’re like, “Great, patient looks fine, they feel fine, everything’s fine.” Okay, well what would your next question be? Might be, “Well, hmm, why would that antibody be high?” I’m not gonna let it go and just go, “Oh well, you’re fine, let’s just keep moving.” I don’t think that’s normal, but I’m gonna be asking different questions like, “Huh, could there be something in the microbiome maybe? I don’t know. Could there be some kind of an infection somewhere? I don’t know. Could there be a food that might be triggering it? I don’t know.” The patient’s not symptomatic, but I’m not gonna let it go. I wanna keep digging and see what I can find out to provide me more context about why that antibody might be high if it doesn’t seem to be affecting the thyroid.
If you see those antibodies at 800 — I had one, one time, this, I always say this was my worst clinical case ever, I talk about it inside Clinical Academy, but it was my worst clinical case ever, and the lab results were up over 8,000. The TPO was. It was crazy. And I thought, “Oh my gosh, this lady’s gonna die.” And I ended up figuring out what the problem was. But the point is that when they’re really, really high, then something’s going on. But I’m talking here about if they’re a little bit on the lower side, you know, you’re not really looking at this as a big glaring red light, red light, danger, danger, danger.
All right, the second antibody is the thyroglobulin antibody, and this is the TGAb, the thyroglobulin antibody. This also is produced inside the thyrocyte, but it’s different. This one doesn’t have to do with the synthesis of hormones as an enzyme. This is actually directed at a protein, the scaffolding protein that the thyroid hormones are built on. And this one too is more commonly associated with Hashi’s, but it can also occur in Graves’ disease. It’s not as common, but it can be. And so you have to take that into consideration as well. Obviously, we’re gonna see far more Hashi’s patients than we will ever see Graves’ patients. But sometimes — and I’ve seen this, you probably have too — sometimes you’ll get these antibodies back and TPO is completely normal and thyroglobulin is detectable. That doesn’t mean that just because TPO is negative that there’s not some kind of thyroid activity going on. We sometimes kind of brush past it and we’re like, “Oh well, TPO is fine, so, I don’t know what that TG antibody is, what it’s representing, but eh, we’re gonna gloss right over it.”
So this antibody, the thyroglobulin antibody, isn’t a measure of hormone production or tissue damage or symptom severity. It really interferes, when this antibody is positive, with thyroglobulin production — production as in the scaffolding, right. You can’t — if I’m gonna build a house and I need scaffolding on the outside of the house in order to get the workers up to build two stories, three stories on my house, I have to have the scaffolding. If I don’t have the scaffolding, how are they gonna get up there? Same thing in the thyroid. Without the scaffolding, the thyroid hormones — the iodine and tyrosine — get attached to that scaffolding. If there’s not enough scaffolding, we’re not gonna have enough thyroid hormone, ’cause I don’t have enough of the backbone, the structure, I don’t have enough of it. So that’s why this thyroglobulin antibody can be problematic, because it can be attacking that thyroglobulin production, meaning that I don’t have enough scaffolding to build my hormones.
So TPO attacks an enzyme. This one is the scaffolding. So these two, they’re very specific. These two tell us — either one of these positive — tell us that the immune system is recognizing, and I’m using that word very specifically, it’s recognizing thyroid components. There’s two components, thyroglobulin and the thyroid peroxidase enzyme. It’s recognizing those components. I did not say targeting, and although it might be, the clearer word is that it’s recognizing it. What it’s not telling us, what these antibodies do not tell us, is why the immune response began. It doesn’t tell us what the trigger was. It doesn’t tell us how active the tissue damage is, and it doesn’t tell us what the thyroid is currently doing. So really, it’s just a sign. It’s just a signal, it’s just a sign.
But the next two antibodies are different, because these two interact with the receptor that receives TSH, which would be the TSH receptor. So TSH is the normal signal from the pituitary to the thyroid-stimulating hormone. TSH receptors are on the thyroid, on the thyroid cell, called the thyrocyte. And the TSH engages with that receptor, and it basically sends a signal to the thyroid that says, “Go, please, we need a little more hormone.” So then the whole process happens, and the thyroid cell releases those hormones — primarily T4, with a little bit of T3 — into the bloodstream. And then off it goes down to do all the rest of the things in the body. So TSH receives a signal from the pituitary, and that causes increased thyroid hormone production. This is perfect. But these next two antibodies can do the same thing, and this is where these guys can be a bit of a problem.
So the first one is called TSI, and this is the question that I had a practitioner ask me not long ago. TSI stands for thyroid-stimulating immunoglobulin — so you automatically know immunoglobulin, protein, right, globulin is in protein. This TSI stimulates the TSH receptor directly, and it mimics TSH, and it basically tells the thyroid, “Go ahead and make more hormone.” Now, TSH isn’t sending the signal — that’s the one that we want, right, coming from the pituitary, that’s the regulatory mechanism, we’ve got the negative feedback back to the pituitary, hypothalamus, all things cascade down, and the thyroid gets a signal when the pituitary says, “Nah, we need a little more hormone.” So TSI can do the same thing. It can interact and stimulate the TSH receptor.
So when you have a positive TSI antibody — and many of you may have never even ordered this, but it’s kinda moving around now, it’s, you know, how things become popular for a hot minute, right, everybody talking about one thing, and this is what everybody’s talking about, so that was the other reason why I wanted to bring this up — so TSI is stimulating the thyroid. Now let’s stop for a minute and think about this. If TSI is stimulating the TSH receptor, and that means that the thyroid is producing a whole bunch of hormones, what might the test results look like? Might it look like there’s a ton of hormone going out? And what would we — could we, might we, if we aren’t paying attention maybe — interpret that as? We might interpret that as Graves’ or hyperthyroid, because there’s way too much hormone. That’s what TSI does, is it stimulates the TSH receptor, and it basically just gives it the go — please produce more hormone — signal.
So if there’s other markers or other signals that maybe there’s Graves’ disease — and typically Graves’ disease is gonna be outside of scope for most wellness practitioners, but not all — that one kind of needs to be medically managed. You can come in and support it for sure, but it does need to be medically managed. But a positive TSI doesn’t necessarily mean that there’s Graves’. It just means that there’s something that’s causing this particular antibody to target the TSH receptor, and the solution’s the same thing — we have to go figure out what it is.
Now, one word of caution that I will give you is that when TSI is positive — if you ever get one back and you have a patient that’s going to be pregnant, is pregnant, wants to be pregnant, trying to be pregnant, et cetera — the OB needs to be managing that, because it can be very, very impactful during pregnancy. So that has to be managed medically. We don’t want to see that, because the TSI can cross the placenta, and that can have an impact on fetal development.
The second antibody that we wanna talk — well, it’s the fourth antibody, but it’s the second one that targets the TSH receptor — this one is called the thyroid receptor antibody. And you could probably tell from the name what it targets, the thyroid receptor, i.e. TSH. But this one is different. This one has three things that it can do. It’s an umbrella term — thyroid receptor antibodies, there are several of them, there’s multiple of them. They do three things: they will either stimulate the receptor, block the receptor, or have very little or no effect.
So what the heck, why would we ever want to look at thyroid receptor antibodies? Well, because if they’re stimulating, it’s going to look like the patient is — could look like the patient’s hyperthyroid. Or it could block, and if it’s blocking, now we’re going to have interference with TSH signaling, and that can then look like hypothyroid.
Are you confused? I know. I’m talking a lot, I know. I should probably make this into a diagram so that it’s a little easier to understand. But this one, the thyroid receptor antibodies, just think of it as like an umbrella — they either block, stimulate, or do nothing. So the blocking ones can cause it to appear as if there is a hypothyroid when there’s nothing wrong with the thyroid itself — it’s that the dang antibody is blocking it at the TSH receptor. It’s basically shutting the receptor down, saying, “Nope, no stimulation from the pituitary, nope, this receptor is closed for business.” And then the body says, “I need thyroid hormones, but I’m not getting them.” And so it looks like it’s hypothyroid.
So using this one as an indicator, you can test for it if you want to. However, without knowing exactly whether it’s stimulating, blocking, or doing nothing, it doesn’t really give you any good information. I would say if you’re stuck, you have a thyroid case that you are working on and you cannot get it unstuck, that patient is just not moving no matter what you do, this could be one that you would want to investigate — thyroid receptor antibodies. And then you can at least see if it’s positive, or if it fits the clinical picture. So it does need a little bit of additional interpretation, but you would wanna use this one alongside all the other normal blood tests for thyroid — TSH, T4, T3, T3 uptake, you know, all the things.
So to recap, are you ready? I know, that was a lot for your little cerebral brain to handle, but here we go. Thyroid-stimulating immunoglobulin, TSI, that stimulates function, where the thyroid receptor antibodies describe the broader family against the TSH receptor. So they’re both active at the receptor site, but TSI stimulates it, whereas the thyroid receptor antibodies — you don’t know whether it’s stimulating, blocking, or doing nothing.
So the other two, the TPO and the thyroglobulin antibodies, those are more — I hate to say “inside the cell,” but they kind of are, one is at the receptor. The two that I just talked about, I should say, are at the receptor. TPO and thyroglobulin antibodies, those are the two that we most commonly order. Those are immune on the inside, basically. They’re at different points, but they’re both inside the thyrocyte.
So you can’t depend — do you see why you can’t just look at these antibodies and go, “Oh, there you go, you’ve got Hashi’s,” or, “You’ve got Graves’,” or thyrotoxicosis, or euthyroid, subclinical thyroid, central hypothyroidism. You can’t know that for sure just by looking at these antibodies.
Now, I wanna just make sure that you’re clear — I wanna talk a little bit more about this as it has to do with pregnancy. If you ever have, again, a TSI or a thyroid receptor antibody, and the person is pregnant, going to be pregnant, just pregnant — just make sure that they’re being medically managed. These also can be relevant for patients who have recently had a contrast, they’ve had radioactive iodine. Sometimes these antibodies will come back positive because it’s reacting to something foreign in the body. They can be relevant obviously for Graves’ disease, even euthyroid. If they’re currently euthyroid, you might find that these antibodies are positive, and also you can find them positive if they’re taking levothyroxine, so thyroid hormone replacement. But most importantly, it’s for pregnancy, because these antibodies can cross the placenta, and so that’s kind of a big deal. So you just wanna make sure that you’re ruling that out.
So now, to wrap it up, my friend, if your brain doesn’t already hurt, you may wanna put this one on repeat. And while you’re doing that, hit the like button, if you would. Just hit the like button, hit the subscribe button, because it does tell YouTube that the content’s valuable, and then they start putting it out to more people.
So here’s the questions that I want to kind of throw back at you. First, we wanna say, which antibody is positive? Well, that’s pretty easy, because we’re gonna have a blood test that we can look at, we can see the antibody that’s positive. What does the antibody target? Where is it targeting? Is it the TSH receptor? So what are the two that are targeted at the TSH receptor? Do you remember? TSI and the thyroid receptor antibodies. So those are at the TSH receptor. The other two are, quote, “inside” — that’s the thyroglobulin and the TPO. So we wanna know, is it inside, or at the TSH receptor?
The third thing you wanna look at is, well, what actually can I see on a blood test with regard to free T4, free T3, total T4, total T3, T3 uptake, et cetera? What are all the other things that are happening with the thyroid as it has to do with the normal markers that we would use to assess thyroid function? And then remember too, as an aside here, that the thyroid produces 90-plus percent of T4. But T4 is not active. It’s a prohormone, meaning that it has the potential and should convert into T3, but low T3 in the body doesn’t necessarily mean that the thyroid is not producing enough T4. Could be that the T4-to-T3 conversion’s all messed up, and that happens very frequently.
So you have to — there’s — see, this is why I love the thyroid, because you gotta think, “Oh, it could be this, it could be this, it could be this, and how am I gonna put all these pieces together and make this very, very simple?” So you wanna know, what’s happening with T4, T3, et cetera. You wanna ask questions like, is the patient on thyroid medication? Are they on Levo, or Armour, or something like that? Are they taking T3? Ugh, I hate it when patients are taking T3. Hate’s a strong word — I don’t like it, because the T3 really messes up that feedback badly. I have yet to find a patient who’s on T3, it doesn’t mess up their gut, and they can never get off. I’m not a fan, because I believe that the thyroid has the potential, just like the entire endocrine system, to right itself.
And if we think about the endocrine system, I talk about it as an endocrine triangle. If we think about the triangle being a three-dimensional triangle, meaning I can pull and stretch it, it can change its three-dimensional shape, and that’s how the endocrine system works. It’s not a linear, one-dimensional or two-dimensional interaction that happens between the glands. It’s very three-dimensional, very active, very living, very fluid. And it wants to repair itself. It wants to be healthy. It wants the signaling to be normal. Our job is to figure out what’s causing the distortion in the signal. What’s causing that three-dimensional triangle, like a pyramid, what’s causing that shape to distort? Is it downstream conversion? Is it interference from another gland in the system? Again, this is why I love the thyroid, because you get to put all the little pieces together.
Another question you wanna ask is, are they taking biotin? Biotin can interfere with thyroid hormones, and so you wanna be looking at that if they’re on any kind of biotin supplement. And a lot of times female patients could be taking, like, a hair, skin, and nail supplement, or they’re taking two or three things that have biotin in it. So you just wanna rule that out. Is the patient pregnant? We know that pregnancy is important. Do they have Graves’ disease? Have they had thyroid surgery where they’ve had it removed? Do they have history of nodules? All of that’s gonna come out in your history with them anyway. You also wanna know, have they done radioactive iodine? I was recently talking to my mom, and she just dropped the bomb — she goes, “Oh yeah, I went in, they did a contrast something or other with that iodine that lights up in your whole body.” And I just dropped my head. I go, “Ugh, I mean, why do parents not listen?” I don’t understand. That’s a side note, but yeah, I don’t get it.
Anyway, back to it. So we also wanna ask, does the clinical presentation match what you’re seeing on the labs? I cannot tell you how many times I have had patients come in and say, “Oh, I have Graves’ disease.” Their skin is dry, they’re constipated, they’re overweight, they are tired all the time, hair’s falling out, and they have a little high T4, T3, and TSH is a little low, and TPO is positive, and maybe thyroglobulin positive, ’cause those are the only two antibodies they had. And I go, “Hmm, your test says one thing, but your body looks like something different.” This lines up with when patients go to the doctor and they go, “Well, I’m looking at your test and everything looks fine, so you’re fine, bye, here’s an antidepressant.” Like, “Go have a great life.” Wait a minute, that doesn’t — I’m not gonna treat the test. In this case, I’m gonna look at the patient and go, “Okay, something doesn’t match, something’s not right, these two things do not belong together.” So we have to just investigate a little bit further. Could there be any other medications that they’re taking? I mean, maybe they’re on some medication that affects the thyroid.
How many times on TV — I don’t have cable, I haven’t had cable or TV in several years, but when I’m at a hotel, or I’m traveling, or at my parents’ house or something, they have the TVs on, and I’ll see these commercials, these drug commercials, and there’s always new things out there, I don’t know anything about them, but almost always they’ll say, you know, “Let your doctor know if you have thyroid or medullary cancer,” or there’s always, almost always, something mentioning the thyroid in there. Interesting, because I believe the thyroid is like the central part of the endocrine system. It’s where the tangle happens. All the other things tangle around it. So getting to the thyroid means we have to untangle all the rest of the things.
And then lastly, I think you have to look at, could there be supplements that they’re taking, like biotin for instance, that might be confusing your results? And then, do you need to refer out? Because I don’t want you to feel — don’t be a hero. If it feels like it’s over your head, it is, and then either get help or refer out. If you even are questioning that there could be something going on that needs to be medically managed, better be safe than sorry. Just refer it out. Don’t let a positive antibody override looking at the bigger clinical picture.
So to close it up, here we go, ready? Number one, TPO and TGB, thyroglobulin antibodies — those are thyroid-directed autoimmunity. TSI and thyroid receptor antibodies — those target the TSH receptor. And then lastly, no antibody should ever be interpreted outside of looking at thyroid function, their medication and supplement history, their clinical presentation, reproductive context — because we know, whether it’s pregnancy or even where she’s at in her reproductive years, is she perimenopause, menopause, post-menopause, where is she at — and then any other clinical findings that you have. So those are so important. We sometimes just get tunnel vision, and I get it, because you’ve got a complex patient, and you see something jumping off the page at you, and we think, “Oh, that’s it, your cholesterol is high, your TPO is high, and your thyroid is… okay, that must be what it is.” But I would encourage you, or challenge you, to stop, take a step back, and think, “Okay, what else could be part of this picture?” Because the endocrine system never, ever operates alone. It doesn’t. It just doesn’t. There’s always going to be several endocrine glands involved.
[CLOSING]
Ronda Nelson: So my friend, if you would like to know more about the thyroid, you are in luck, because on October 17th, I’m teaching a brand-new seminar, an online seminar called Decoding the Thyroid. We’re gonna be looking deeper at thyroid hormone synthesis. We’re gonna be looking at the 11 most common thyroid presentations — I’m gonna go through each one of them with you. Thyrotoxicosis, euthyroid, central hypothyroidism, there’s 11 of them, and we’re gonna go through each one of them. We’re gonna look at markers that you could look at, and we’re gonna look at other things that could be contributing to each one of those things. I’m gonna be talking about possible testing that you may wanna order, and of course, I’m gonna give you my own clinical recommendations about how to optimize the thyroid and how to get that thyroid back up and working.
So register. Registration’s only open for a little bit longer. You go to rondanelson.com/thyroid2026. If you were in my menopause seminar earlier in the year — I think we did it in May — if you were there, then you know that these seminars are not for sissies, but you will walk away with a framework that you can follow, checklists that you’ll follow, so much information about other places that you can connect, how you’re gonna untangle the ball of yarn. What are the threads that you need to pull? And if there’s nothing at the end of the thread and you can untangle it, you throw that thread away and say, “It’s not that.” Great. But we need to be able to know what threads to pull, so I’m gonna teach you how to do all of that.
So positive antibodies doesn’t mean a license to an autoimmune condition, just like being hypothyroid doesn’t mean she’s stuck there either. So come visit me on the thyroid seminar, Decoding the Thyroid, October the 17th, rondanelson.com/thyroid2026. One more thing — if you’re busy that day, it’s okay, go ahead and register, because you’ll get all the slides, all the resources, and there’s always a ton of them, and you’ll have access to the replays. So you don’t have to be in person, that’s just how we roll, because I know your life is busy and a Saturday is a Saturday. I hope to see you there. Thanks for hanging out with me, and I’ll see you next week. Take care.
[END]