Ep. 166 – How to Maintain a Healthier Thyroid: Interesting Thyroid Physiology Health & Preventative Care with Dr. Eric Balcavage

Presenter: This is Everyday Wellness, a podcast dedicated to helping you achieve your health and wellness goals, and provide practical strategies that you can use in your real life. And now. here’s your host, Nurse Practitioner Cynthia Thurlow.

Cynthia: Today, we are thrilled to have Dr. Eric Balcavage back. He was in episode 105 talking about thyroid physiology, and chronic illness, and due to huge demand, we have brought him back to dip a little bit deeper into thyroid physiology, biophysiology, detoxification, and chronic illnesses. Dr. Eric is the owner and founder of Rejuvagen, R-E-J-U-V-A-G-E-N, a functional medicine clinic in Chadds Ford, Pennsylvania. He’s also the cohost of Thyroid Answers Podcast where he focuses on answering the pressing questions of those suffering with chronic hypothyroidism symptoms. He also recently coauthored a book called the Thyroid Debacle.

Today, Dr. Eric and I talked a lot about some of the signs and symptoms of subclinical hypothyroidism, fat malabsorption, the use of synthetic versus non-synthetic medications, and really diving into why people can have lab values that are suggestive of them being persistently hypothyroid, despite escalating doses of medications. We talked a lot about peripheral conversion, intracellular conversion, and what this all really amounts to it are reasons why our thyroid is not functioning optimally. So, I hope you’ll really enjoy this conversation. Again, a really deeper dive into cellular response to thyroid physiology, tissues, the immune system, what gets turned on and off things we need to look for, and how to maintain a healthier thyroid.

But thank you again for carving time out of your busy schedule. If you don’t already follow Dr. Eric on Instagram, you need to, because he has incredibly informative– isn’t there like thyroid Thursdays? You have video, and content, and it’s really fantastic. I feel like even as a practitioner, I learn a lot. So, I know that others will as well. How are you doing?

Eric: Thank you. I’m doing great. Thanks for having me on the show, again.

Cynthia: Absolutely. I thought it might be helpful to talk a little bit about– this is my nerdy science side. Let’s talk a little bit about anatomy and physiology. For those who are listening who’ve been diagnosed with hypothyroidism, with an underactive thyroid, and autoimmune hot thyroid, either Hashimoto’s or Graves, let’s talk a little bit about the physiology because I think so many of us, including practitioners, forget the very delicate orchestration and communication that goes on with the HPA access, and thyroid, and how all these other hormones really impact the health of our thyroid. I think this is a great place to start, because I really asked my community what their questions were, and it was pretty consistently in a couple different camps. But I think that’s a great place to start, and I know this is an area in particular that you love discussing. So, let’s dive into anatomy and physiology.

Eric: Well, pretty simple, thyroid hormone is what really controls and regulates metabolism in our cell. There’s two primary thyroid hormones that impact the cell. T4 and T3. T3 is considered the more active form. T4 is more the circulating reserve, the more dominant hormone that’s in circulation, and it’s the one that needs to be converted to T3 to support or stimulate our metabolism. Those thyroid hormones are generated by a gland that’s a butterfly-shaped gland right in the middle of your neck.

What happens is, all the signals from the body, hunger signals, cold signals, fear signals, stress signals, all these signals from your organs or tissues all come into the brain and get integrated. There’s a gland in your brain called your hypothalamus that has to figure all those things out. Then, it drives if the body needs to increase its metabolism, the hypothalamus increases a hormone called TRH, thyrotropin-releasing hormone. TRH then goes to a little gland in your brain just below the hypothalamus, the pituitary gland. The pituitary gland gets a signal to make something called thyrotropin- stimulating hormone, TSH, which almost everybody has heard of already. TSH can then go to your thyroid gland and tell the thyroid gland, “Hey, we need to increase the production of thyroid hormone.” Then the thyroid gland makes thyroid hormone. There’s T1, there’s T2, there’s T3, there’s T4, it makes some other things as well. But T3 and T4 wind up being the primary hormones that are released from the thyroid gland and enter the bloodstream.

Typically, the ratio is about 10 to 1. For every one T4, there’s one T3. So, T4 by majority is the dominant hormone and that’s good, because it’s a pre-hormone or a pro-hormone that’s not– it’s still active. Some people say it’s inactive but it is actually an active hormone. It can actually do some stuff. But it’s not nearly as active as T3, and that’s what most of the cell receptors inside the cell need, is T3. So, T4, T3 dumped into the bloodstream, and when they’re first dumped into the bloodstream, they’re dumped into the bloodstream as free hormone. But to get to all the cells and tissues, they have to then pick up an Uber. So, they need to get an Uber ride to the body, and that Uber ride is typically something called thyroid-binding globulin. So, protein like an Uber, just drives it around the tissue. There’s other binding proteins but by far thyroid-binding globulin is the one, we talk about most dominantly about when we talk about thyroid physiology.

Once that T4 and T3 is in the bloodstream, it’s circulating through the bloodstream, going into the tissues, and when a tissue needs thyroid hormone, that T4 or the T3 that’s made can become separated or free of the thyroid-binding globulin and then be actively transported into the cell, and be converted into T3, and then that can go to the nuclear receptors, to the mitochondrial receptors, or some of the cytoplasmic receptors, and stimulate actions. T4 and T3 can also bind to the outside of the cells and stimulate what we call nongenomic actions. But most of the ones that people think about like, “Hey, I want my hair to grow, I want to lose weight, I want good healthy skin, I want to have a libido, I want my bowels move,” we’re thinking about those types of actions are typically driven by the intracellular mitochondrial genomic actions of T3 in itself.

Cynthia: I think it’s really important for people to understand that there are all these subtle nuances to thyroid. I don’t think I fully appreciated thyroid physiology and these hormones in particular until I was probably in my late 30s, and I was seeing a lot of women, in particular, in their mid to late 40s and early 50s, who were being diagnosed with things like adrenal fatigue. They were told, “Oh, well, your thyroid is subclinically hypothyroid, but not enough to justify putting you on medication.” I just felt like we were missing opportunities with a lot of individuals who probably really warranted a closer look at managing their thyroid more effectively.

Now, for the benefits of the listeners, because this is one of the questions that I did receive, what are some of the things that can impact that conversion from inactive to active thyroid hormone because I know gut health can impact this, whether or not your liver’s detoxing effectively. There are a lot of, again, nuances that can impact the conversion of being able to utilize the thyroid hormones properly and effectively.

When people are thinking about the mitochondria, obviously, those are powerhouses of our cells, really critically important, and we know north of 40 most of us have some degree of mitochondrial dysfunction. Obviously, the healthier you are, the healthier your mitochondria are. But I think there’s this misnomer that our mitochondria just stay healthy all on their own. But it’s a lot of the lifestyle piece, a lot of the how we choose to sleep, what we choose to eat, how we choose to move our bodies, are we insulin resistant? So, let’s unpack that, because that was a question that actually came up two or three times on Instagram when I was polling followers for what they were interested in learning more about.

Eric: I think the way to get into that is the first discuss that thyroid hormone production by the gland is one piece. That’s like the tip of the iceberg. The bigger piece of that is what we don’t see, we don’t measure, and that is what’s inside a cell. That’s like the part of the iceberg that’s underneath the water. So, putting thyroid hormone into the bloodstream, whether it’s from your thyroid gland, or hey, if you don’t have a thyroid gland, you had Graves’ disease, and it was radiated or medicated away, or it’s so dysfunctional that you got diagnosed with primary hypothyroidism, getting thyroid hormone in the bloodstream is part A. Part B is, what happens to that thyroid hormone once it hits the cells and tissues.

What’s important to understand is that every tissue type has different transport mechanisms, different ways to get thyroid hormone into their cells, have different quantities and qualities of what do we call the converting enzymes, what we call the deiodinase enzymes, and all the tissue types have different types of receptors. So, all the tissues don’t regulate thyroid hormone quite the same. That’s important and critically important because if they did, that means every time you dumped out more thyroid hormone to the system, then every tissue would have to have its metabolism revved up at the same time. If there’s a downturn in thyroid hormone physiology, then everything would have to be downregulated at the same time. We wouldn’t want that because if you want to have sex, you need some thyroid hormone to generate sex hormones and got to get things in here but you don’t want to be having a bowel movement in the middle of that sex. You don’t want your bowels moving at the same time you’re having an orgasm. So, in those situations, we need different systems to be upregulated when other systems are downregulated. Maybe not the prettiest picture to think of, but I think that hits home. You don’t want those two things happening at the same time.

The body’s pretty smart. “Hey, I’m going to put this thyroid hormone out there. When you need it, liver, when you need it, you use it. Gut, when you need it, you use it. Brain, when you need it, you use it.” But it’s not like you all have to use it at the same time. Now, we’ve got this issue like, okay, so now it’s available on the cell, do I just bring it in and convert all that T4 to T3? The answer is no. The cells have certain tissues, depending on what’s happening on the cell, is either going to bring more T4 into the cell converted to T3 to increase metabolism, or it’s going to take that T4 or the T3 that’s in the circulation and deactivate it if it doesn’t need it. If it’s deactivating T4, it’s converting it to something called reverse T3, and if it’s deactivating T3, it’s converting it to something called T2, which no clinical labs measure. We don’t know necessarily when that’s happening. That creates problems, which maybe we’ll get into later.

What happens is when a cell wants to increase its metabolism, for the most part, it wants more T3 in the cell, because when T3 binds to the nuclear and mitochondrial receptors, it helps generate energy. It helps make proteins, it helps makes enzymes, it makes healthy cell membranes, it does all these kinds of building block types of things. But T3 binding to other receptors can actually turn off actions and some of the actions that are turned off by T3 binding are actions associated with inflammation and cell defense.

The cell is kind of in one of two states, either in building mode, growing mode, or in cell defense mode. T3 is like the dimmer switch to determine what’s that going to be. Let’s say I’m a cell in the liver, and I’m sensing some type of stress or danger, now I want to slow my metabolism down and I want to defend myself, just like people. I use the analogy with my patients that if you were cooking for your family, you had four burners on making this big meal, one of your kids is sitting at the island and they’re having a great conversation, but then somebody breaks in and starts attacking your child, are you going to continue to cook? Most people would say, “No, I’m not going to continue to cook, I’m going to defend my child.” “Are you going to take the time to turn the burners off?” “Probably not.” “You’re going to pack everything up in glass Tupperware?” “Probably not.” “You’re going to try and throw a load of washing real quick?” “Probably not.” “Are you going to go take a nap?” “Probably not.” “You’re going to go have sex?” “Probably not.”

If I walked in not seeing you defending your child, I would walk in and I would say, “Man, maybe you’re just a terrible mom and housewife,” because I see wash not done, I see kitchen not clean, I see food burning on this stove, maybe I just need to hire a cook, maybe I need to hire a house cleaner, and maybe one of those things. But the reality is, I’m only seeing a part of the picture. Instead of saying, “Wow, this is a terrible situation,” I should really be looking at what else is going on here, and oh, if I hire you a cook, but you’re not going to eat– even if I give you a cook, because you’re defending your child, now I look at and say, “Hey, she’s not doing the wrong thing. She’s not a bad parent, bad mother, bad spouse. She is a great parent, because she’s defending her child.” Our cells are just like us. They want to grow, build muscles, tissues, proteins, all these great things, unless they sense danger. Then they need to slow that stuff down and shift energy to cell defense.

That’s from my perspective, what’s happening for a lot of people, and that’s what I call and I didn’t make the term up, cellular or tissue hypothyroid. This has been talked about in the literature for probably 20 to 30 years now, but nobody’s paying attention to it. We do have a term for it in allopathic medicine is called euthyroid sickness syndrome or nonthyroidal illness syndrome. But in that model, it is pretty much considered that it’s only a disorder of people in critical illness, in a hospital setting who are in critical illness, that’s the only time it happens and that’s not true. I think I just talked about that today, on my Thyroid Thursday is that this mechanism occurs when their cell stressors that initiate danger.

Getting back to what triggers it, there’s lots of things that can trigger the cell stress or what we call the cell danger response. Hypoxia, that’s lack of oxygen getting to the tissues. People are like, “Well, I don’t think I have that.” Do you snore at night? Do you breathe your mouth a lot? Do you have sleep apnea? Yes, yes, yes, Well, you have hypoxia. You’re not getting enough oxygen to the tissues that can trigger a cell stress response or cell danger response, and in that situation, your body, those cells that are receiving hypoxia, our low oxygen state are going to downregulate thyroid metabolism. Why would the body do that? Well, if I don’t have enough oxygen, one of the primary roles of T3 in the cell is that drive the mitochondrial production of ATP, I don’t want to keep driving that process because it produces a lot of oxidative stress or damage. So, the body’s pretty smart like, “Whoa, if I don’t have a lot of oxygen, and now I give a lot of oxygen, that reperfusion process or that increased oxygenation process could really drive a lot of oxidative stress.” So, the body does that on purpose.

Toxins affect the cell, can trigger a cell stress and a downregulation of thyroid hormone. Bacterial, organisms, viruses, these can also trigger that cell stress or dangerous substance. Perceived stress, just emotional stress, physical injury, radiation, everybody’s talking on these things, and we don’t think that they have to create any damage. You see mixed reports, but the science is pretty clear that if you’re sitting there with your phone talking like this all the time, the people that they’ve done in studies have decreased thyroid function, because it creates damage. We live in a Wi-Fi-dominated society. So, is there a potential problem there? Yeah. There’s nutrient restrictions, there’s lots of different things that can have a real impact on it. Even the types of dietary fats you have put them into the system, if they are becoming part of the cell membrane is damaged, oxidized fats, those two can result in some of the process that creates a danger response. , anything that triggers the cell to say, “Wow, this is too much stress. I got to slow the metabolism down.” That includes disrupted sleep patterns, and it includes, which is what happened to me, excessive exercise without recovery.

Cynthia: Mm-hmm. You bring up so many good points, and the irony is that back many years ago, when I was an ER nurse in Baltimore, I was asked to be part of an ER consortium and what I went around and did throughout the Baltimore area, along with other advanced practice nurses and physicians, is I lectured on thyroid emergencies. You mentioned this kind of sick thyroid syndrome, which the extremes are myxedema coma when your thyroid’s grossly and it’s a life-threatening issue, and thyroid storm. So, you have these two extremes. I think in traditional allopathic medicine, that’s what we think of, like you’re really, really sick when those things happen, and everything in between is benign. But I love that you’re acknowledging that the cellular response to all of these toxins or these stressors can really overtax the thyroid gland and make it much less efficient in doing its job and the cellular response to this stress. I think many of us, including healthcare professionals, let’s be honest, we think in terms of organs and glands, and we don’t think about things on a cellular level, and that’s really where it all starts.

I do want to acknowledge that you mentioned poor quality fats. This is another rabbit hole we could dive down. But I would imagine the oxidation, the highly inflammatory seed oils, which I know Dr. Cate Shanahan, we’ve had her on the podcast, talks a lot about, and I definitely try to avoid as much as possible. In fact, we were traveling. We were in Montana for a couple days. I had a business trip. So, my whole family went. Every time we went out to dinner, my husband’s like, “Please don’t say it,” because he said, “I know what you’re thinking. You’re going to say, you don’t want to get salad dressing, because you’re fairly certain you’re going to get seed oils.” I said, “Yes.” [laughs] But we know that even seed oil, canola oil, soybean, cottonseed, sunflower, safflower, those kinds of things actually change the composition of that cellular membrane. So, I would imagine that those are highly toxic as well. I would imagine your trans fats, although we’re not seeing as many as we did before, they can definitely play a role as well. Is there any current research that you have your hands on talking about seed oils and the association between thyroid physiology and the thyroid glands themselves?

Eric: Well, the gland itself, I don’t know. I guess at the cell level, absolutely. So, I would imagine it’s going to impact the thyroid gland itself too. But when you have those damaged fats that are being incorporated into the cell membrane, the cell membrane is not as permeable as maybe it should be or it can become excessively permeable. There’s that fine balance between how much permeability, how easy it is to get things in and out of the cell. If it’s making the cell less permeable, then that drives the hypoxic state. If it makes it more permeable, then we’ve got the potential for excessive amounts of things to come into a cell that probably shouldn’t, and that too can trigger that danger response.

But I do want to say that people are listening to this and we’re talking about thyroid physiology, it’s important for them to understand that you can have hypothyroid signs and symptoms, hyperthyroid signs and symptoms, and have nothing wrong with your thyroid gland. That’s what we’re saying with that nonthyroidal illness syndrome or euthyroid sickness syndrome. From a medical perspective, they’re saying, “Hey, the gland is still functional. You just don’t have enough thyroid hormone impacting the tissues,” or “You have low T3 syndrome,” is another name that’s thrown out there. But this happens quite a bit, and it’s my argument is that, for many people that this tissue level of hypothyroidism and sometimes hyperthyroidism, this starts long before the thyroid gland is ever has any damage to it.

If you’re one of those people that has been told, you don’t have a thyroid problem, even though your hair’s falling out, you’re overweight, you’re fatigued, and you have no libido, and you’re constipated, I know those are hypothyroid symptoms, but your medical doctor may tell you, you don’t have a thyroid problem because your TSH and T4 are normal, I think I have to be fair to allopathic medicine, because what they’re saying is different than what the patient’s often feeling. What the patient may be feeling in that moment is the signs and symptoms of hypothyroidism caused by cellular hypothyroidism or tissue hypothyroidism, but their gland may still be functioning to that point. You might say, “Well, it sounds like what you’re calling cellular hypothyroidism is nonthyroidal illness syndrome, or low T3 syndrome, or euthyroid sickness syndrome. Why aren’t they telling me that?” Well, because the guidelines don’t tell a medical doctor to run a T3 or a reverse T3 on a regular basis. The guidelines pretty much tell a medical physician run a TSH or run a TSH with a reflex to free T4. Those are the only two tests that get run. So, if your TSH is still normal, you’re free T3 may never be run to see that the thyroid gland is already struggling. If your TSH is high, but your free T4 is still hanging on, they are going to be said you’re subclinical. But that doesn’t mean that your thyroid gland is in good shape. That means it’s not producing enough thyroid hormone, and that’s part of the reason why TSH is up. It may be that you have enough T4, but you can’t convert it to T3, and that’s why your TSH is still up. But the doctor is not going to tell you have euthyroid sickness syndrome because they haven’t run any test at all to identify it, and the general consensus is that only happens in critical conditions.

Yet, the literature says, that it happens in many other conditions like hypoxia, like acute and chronic inflammatory states. And what’s one of the states that we see in this country that most people suffer from is chronic low-grade inflammation. If that’s the case, maybe we need to be looking at a bigger panel. But also, to be fair to the medical doctor, they don’t have a tool other than T4 pretty much to provide as an answer. So, I don’t want to be putting extra T4 into a system that doesn’t need it yet because I could drive somebody into a hyperthyroid state. So, I understand the reserve. There’s lots of discussion, I’m sure you know looking at the literature, there’s lots of discussion with, “Should we be providing T4 to people who are in a subclinical state?” Maybe it helps, maybe it doesn’t help. But the answer is, I don’t think you should. This is a patient who still at a cellular hypothyroid state. Yes, they’re probably already into thyroiditis. There’s already damaging occurring. But T4 in this situation isn’t going to work, especially if that T4 is getting deactivated to reverse T3 already, because of the cell danger response, more T4 in that system isn’t going to fix it. Matter of fact, that’s exactly what the body doesn’t want.

So, a medical physician, who’s doing their job, who’s following the guidelines really does have their hands tied. They’re often not going to run more than those two tests, because the guidelines say it’s not medically necessary to diagnose or treat. Insurance companies often don’t want to pay for the extra test because they’re not medically necessary and they don’t want a patient coming back to them three weeks later after they get the blood panel with a $400 bill like, “Why is this not being covered?” “Because your insurance doesn’t cover it, I told you that. They didn’t cover it. Now, you get this big bill,” and you’re going to ask a medical physician, even if those they do get those tests done, what do I do about? And they don’t have a tool if it’s elevated reverse T3. They don’t have a tool to try and fix that. There’s no demand to fix it.

The only other thing that typically occurs, some docs are a little bit more integrated, and they say, “Okay, your T4 is good, but you’re still symptomatic, but your T3 is lower. So, we’ll give you T3 since you don’t seem to be able to do it.” Again, that can normalize the blood but it doesn’t fix the underlying issue or the question, which is why is my cells that are supposed to do most of that conversion not doing it in the first place. Forcing that extra thyroid hormone into the bloodstream doesn’t mean we’re going to optimize cell function. Oftentimes, it actually backfires by putting too much thyroid hormone into the system. Initially, you have a honeymoon period, but then it triggers more of a hyperthyroid state, too much T4 or too much T3, impacting the brain causes mast cells to degranulate, that can create brain fog, and fatigue, and anxiety. Then, the other thing that happens is when you flood the brain with thyroid hormone, you actually increase the peripheral deactivation and actually make the hypothyroid state worse in the peripheral tissues.

One last piece, sorry to keep going, but the literature is clear that almost every form of cancer– let me say this way, 2019 paper, I forget the name of the paper, I’d never thought that anybody would do the study. But what they found is that people who’ve been diagnosed with hypothyroidism and put on thyroid medication have a higher incidence of almost every type of cancer. That’s a big deal. It usually takes five, six years for the outcome of that to occur, and nobody’s going back often and tying that to, “Oh, I put more thyroid hormone into the system, and now I’ve got a patient with any type of cancer.” Not just thyroid cancer, but almost any type of cancer. The question might be, ‘Well, why does that happen?” Because T4’s not getting into the cells to stimulate normal metabolism. It can bind to what we call integrating receptors on the outsides of the cells and cause cell multiplication. Well, now if I have sick cells and I multiply a bunch of sick cells, now we’ve got the development of cancer.

Cynthia: That’s fascinating. I’m trying to absorb all of this. I’ve so many different questions. But for someone that’s listening and if they’re looking to work with someone that’s more integrative or functionally trained, for their own information and really for my own validation, because I have a whole little algorithm that I work off with my own clients and patients, what are the ride and die thyroid labs you would start with, and do you routinely look at the cofactors for thyroid hormone to be looking to see like what’s the vitamin D level, what’s their RBC, zinc, what’s their magnesium level? Is that part of the clinical workup for you? From your perspective, what are the diehard labs that everyone needs to be running, so that they can get the proper information, and so they can really become, because what you’re essentially saying is that a lot of medication management for thyroid is looking at a lab and prescribing a medication, hoping that it works. For full disclosure, and this is another thing that I definitely want to touch on, in September of last year, many people including myself, I’ve been on Nature thyroid, doing fine, stable thyroid hormone levels, and I dive down the rabbit hole after Nature thyroid was recalled. I was on compound and I was on Armour. Now, I’m on synthetics. What’s actually happened is, I’ve gone from having a stable thyroid hormone levels to now, my levels are really low and much to your point about, obviously, this disconnect in my body.

So first, let’s unpack, what are the thyroid labs and do you think it’s important to also be looking at cofactors for healthy thyroid production? Again, it’s looking at things like iodine and iron levels, and magnesium, and zinc, and all those things, is that helpful as well? Then, what has been your mindset philosophy because I’m sure there are a lot of people that are gravitating towards you and your practice, because you are this recognized thyroid expert, because people really feel like they’ve been floundering for the last probably nine months, trying to make sense of what’s working or not working for them. Are their symptoms better, are they worse? How are they showing up after the recall of a lot of the natural desiccated products that were out there?

Eric: Yeah, lots of questions. Hopefully, if I go off track, stop me and get me back on it.

Cynthia: [laughs]

Eric: But when it comes to thyroid hormone– Let’s just say assess somebody. In general, if somebody is taking T4, labs are normal, symptoms are normal, I think that’s great. It works and it does for a lot of people. If it’s just the issue that their thyroid gland doesn’t work, you put T4 in, there’s no problem with the downstream physiology. T4 converts to T3, gets to the cells, stimulates metabolism, all is good. The problem sometimes is that when that doesn’t work, we default to adding T3. Does adding T3 normalize T3? Absolutely, it does. Is there a tendency for reverse T3 to go down? Which is one of the reasons sometimes people provide T3 because they say, “Hey your T4 is converting to reverse T3. Reverse T3 is blocking the receptors. Therefore, we’re going to give you T3, your reverse T3 will go down and everything will be better.”

Initially, if you give somebody T3, they don’t have to go through a conversion process and they can get that into the cell fairly easily, yes, they’re going to feel better. But in time, the body says, “Oh, I didn’t want more T4 and T3.” So, they start deactivating it to T2. The issue with that whole process is that reverse T3 does not block nuclear mitochondrial receptors. That’s never been shown to be the case. We talk about it a lot, we talked about a lot in functional medicine, there’s assumptions that it might happen, deiodinase 3 does go to the nucleus, and it can deactivate T4 and T3 right in the nucleus. But there’s been no science that I’ve seen, I think I’ve read 1200 papers at this point, and never seen anything documented that’s exactly what happens. I’ll hear, if thyroid people experts talk say that because T3 and reverse T3 are mirror images that one can bind– they can block each other out and bind to the same receptor. They are not mirror images. When one iodine is pulled off the inner molecule on, the other is pulled off the outer molecule, so, they are not mirror images. I don’t know why people keep repeating that. I don’t know why we keep repeating the idea that reverse T3 blocks the receptors. It is true. If you give somebody less T4 and give them more T3, their reverse T3 will go down because you don’t have enough T4 to make reverse T3.

So, when I’m looking at somebody, I have to take into context, what medication they’re taking first of all, and what supplements they’re taking. But my start process for everybody is, I want to see a full thyroid panel. TSH, T4 total, T3 total, free T4, free T3, T3 uptake, reverse T3 thyroid antibodies. There’s a three-thyroid index that started in there. I don’t really spend that much time looking at the free thyroid index but those are the base thyroid panel. But you can’t assess somebody started physiology with just those things. So, I think a comprehensive thyroid panel has to be taken in context of the rest of what I call a comprehensive metabolic panel. You’ve been in healthcare. I’ve been in healthcare on both sides as well. A comprehensive metabolic panel means totally different things to 10 different people. So, my panel encompasses a lot of inflammatory markers, CRP, homocysteine, fibrinogen, uric acid, ferritin.

What I want to see is, first of all, where’s the person already? What’s the state that they’re in already? Well, we already know that they’ve primary hypothyroidism, we already know they have Hashimoto’s, they’re already on T4. So, you have to assess the labs in that scenario. I want to determine, is this a person who’s got cellular hypothyroidism? They don’t have very good conversion of T4 to T3. You can really only assess that really well if the person’s not on T3. If they’re on T3, the T3 number is going to be artificially normal. It’s going to be artificially elevated. Because that’s not really what the gland is making, and it’s not really what the peripheral tissues are making.

A good point to the patients is that your thyroid gland, your total T3 production is 30 micrograms. Your thyroid gland only typically makes 5 micrograms. The other 25 micrograms is made by your peripheral tissues. So, peripheral tissue, liver, gut, muscle brings T4 and converts it to T3, and then it goes back out in the bloodstream so another tissue can use it, and then it keeps going until it gets metabolized. The T3 in circulation, most of it is made by peripheral tissue conversion. If you’re seeing a normal T4 and a low T3, that’s not necessarily a thyroid problem, that’s a peripheral tissue conversion issue, and we’d have to ask that question like, “Why would the body not want to convert it T4 to T3?” I want to see that do I have a lower T3 situation? Do I have elevated reverse T3?

Again, you have to take reverse T3 in context. If the person has a normal or functionally normal reverse T3 lab highs like 24, I usually use around 18 as my number, but if I have a patient with less than optimal T4, then that reverse T3 is going to be falsely low potentially. We have to take that into consideration, because if I don’t have a lot of free T4, where I have low total T4, I’m not going to get as much at that T4 to be able to be free to actually convert to reverse T3. Does that part make sense?

Cynthia: Totally.

Eric: Then, the next thing I want to see is, I look at the ratio of T4, T3, and again, those ratios are really only valid if the person’s not on T3, because the T3 will skew the values. So, I want to look at those things. And then, the other thing I want to look at is, where’s my TSH in relation to my values? If somebody is on thyroid hormone and their TSH is still above the functional range and their T4 and free T4 optimal, then that’s a situation where I’ very cautious with that person like, “Be careful. You are not the person who needs to be adding more T4 to this system, because the body’s already starting to have a higher deactivation, and the reason your TSH is staying elevated is because the pituitary gland is trying to get that thyroid gland to try and make a little bit more T3.” Normally, the thyroid gland makes T4, T3 in a 10 to 1 ratio, but I haven’t read that we understand the mechanism. But the pituitary gland is also monitoring T3. When T3 levels are less than optimal, the pituitary gland will try and maintain a higher level of TSH, maybe not make your endocrinologist happy, but it will try and keep that TSH more elevated, because the signal it sends when there’s low T3 is different when there’s low T4.

What happens is, instead of the thyroid gland making T4 to T3 at a ratio of 10 to 1, it can drop it as low as 5 to 1. Then, when the doctor sees that TSH, it’s still 3, you’re still symptomatic, we’re going to force more T4 into the system, they can artificially suppress that TSH, but it takes away with the pituitary gland was trying to do, since the peripheral tissues aren’t converting, the pituitary glands like, “Hey, let’s try and boost this thyroid gland to get to– Come on give us a little bit more T3. Let’s see if we can do it,” and we just blew it by over flooding the system. Then you usually see that with a really jacked reverse T3 on the next lab panel, but I want to look at that whole panel in context.

Then, the next thing I want to do is, if I see that I have this tissue hyperthyroidism going on, what’s the primary driver that some type of stress or inflammatory response, so then I want to go right to my inflammatory markers, and I want to see if I have elevated CRP, elevated homocysteine, elevated fibrinogen, elevated ferritin, elevated uric acid. I want to see if I see markers of inflammation. Sometimes, the only marker of inflammation is CRP. High sensitive CRP, it’s rare. I don’t see it get that a lot, but when I do see it and somebody says, you don’t have an inflammatory condition because we measured CRP. What do you need to make CRP? You need T3 to make that protein. If you already have tissue hypothyroidism, especially, if it’s impacting an area like the liver, you probably aren’t going to have high levels of reverse of CRP. So, you have to take that into consideration as well.

I’m sure you don’t look at one lab value as the end all, be all we look for patterns on bloodwork. Do I have a pattern of inflammation? I just have one marker out of range. Well, does it fit with my patient signs and symptoms? Not really. Okay, let’s retest it next time. Let’s do it in two or three weeks. See if it changes, because labs vary quite a bit because we’re dynamic. So, if I see the inflammatory stuff going on, then I checked that box again. Okay, I’ve got tissue hypothyroidism. I know where you have thyroiditis that’s probably been caused by this tissue hypothyroidism for an extended period of time. I know it’s caused 90% destruction of the gland. Therefore, I know I’ve got a poorly regulated thyroid physiology. I put some T4 and/or T3 in the system, but I still have tissue hypothyroidism and now, I have justification for why that is. I also need to figure out where the inflammation is coming from.

So, the next piece is to look the rest of the blood panel and say, “Okay, what tissues indicate or confirm that there’s a level of tissue hypothyroidism?” So, that’s where I’ll start looking at the rest of the lab panels. I’ll look at the blood sugar markers. Do I have indications that I’m not regulating blood sugar appropriately? Is my fasting glucose high, is my fasting insulin high, is my hemoglobin A1c high? Those are like simple markers that are on almost every blood panel, or should be, in giving an indication that you are insulin resistant. So, how do we know? Maybe it’s caused by eating too much and not exercising enough. Maybe, but we all know somebody who doesn’t exercise and eat too much understand. So, what’s going on? In those situations, many times if you don’t have enough T3 in cells of tissues, you can’t transport glucose into the cell effectively. Whether it’s insulin driven or non-insulin driven, whether it’s in a fasted state or a fed state, you need T3 to operate your transporters. So, if you don’t have optimal T3, you’re going to have higher fasting glucose, you’re going to have higher levels of insulin. Even in a fasted state to try and push that excess glucose somewhere and guess where it’s going to go? It’s going to go into adipocytes. You’re going to push that all into reserve and we’re going to get our excess belly fat.

The other thing I want to look at is what other tissues. Well, renal system requires, guess what, T3. So, simple tests we can look at, BUN and creatinine, and glomerular filtration rate. Optimal glomerular filtration rate is usually over 100. But in renal disease, it’s is at less than 60. When you get a lab report done, many times a lab report just says greater than 60. What does that mean? That doesn’t tell me how healthy somebody is. That tells me that maybe they just didn’t fail yet. So, I’m seeing somebody’s creatinine levels are elevated, their BUN levels are elevated, or their GFR is starting to go from 100 to 90 to 80 to 70, I know that they’ve got something going on with the renal system, and that might help me confirm that, “Yup, I got low thyroid hormone to regulate glomerular filtration and kidney function.”

We can look at liver markers. You need T3 inside the cells for cholesterol to bind to the liver with your LDL receptor to dump off a bunch of cholesterol to make bile, to go out into poop, to help with detox. If you’re a person who’s got elevated LDL, elevated cholesterol, what you probably don’t need is a statin. What you probably need is somebody to say, “Oh my gosh, we’ve got decreased T3 impacting the liver, and now I can’t get rid of the cholesterol that’s in the physiology.” Instead, we try and suppress it but really, that’s a huge indicator that we’ve got decreased T3 in the mitochondria. We can look at triglycerides and VLDL. If we see VLDL is going up, triglycerides are going up, even if you’re on a ketogenic type diet, what’s that tell us? That tells us that we’re getting all this triglycerides spill into the bloodstream, but my liver is full. It’s pushing those triglycerides back out into the system, and then they’ve got to go back into storage. So, that’s a good indication that I don’t have enough T3. Why would T3 impact those things? Because T3 is really what drives cellular energy, your Krebs cycle, your electron transport chain. You need T3 to do those things, and if you’re in a cell stress state, actually decreased T3 is actually a protective response. We need some oxidative stress to fight the fight, but we don’t want too much to damage the cells. So, the cell decreases that T3 to cause the mitochondria to fuse together, become actually more efficient. You don’t make more ATP, but it becomes more efficient. The thing that bugs the patient is that they lose, what we call these, proton leak areas, uncoupling proteins. Typically, if you’re at healthy state, healthy mitochondria, you dissipate a lot of excess energy as heat, and when you’re in a hypothyroid state, you lose that excessive heat dump and heat production that sometimes makes us cold and chilly and always cold. But that’s an indication we can take a look at. Then we can take there’s a number of other systems we take a look at.

But as I go through the blood panel, I want to see what state of hypothyroidism and regardless of whether I’m primary or not, do I still have cellular hypothyroid state? What tissues are being impacted? Then, I want to look at the rest of the lab for like where do I need to start, are there nutrient deficiencies? If there are, many times I’m starting at the gut because everything has to go into the GI tract, everything has to come out through the GI tract. So, how can you start loading people with lots of supplements to take if they have potential malabsorption issues?

Even in some of the markers, if I’ve got an elevated bilirubin, I’ve got compromised bile flow. If I’ve got low– I may have signals or markers of hypochlorhydria. Again, T3 is needed for all those things. So, I keep looking for the patterns, then I started looking at, where do I start? And then, the last piece of that is, I’ve got to look at their health, their health timeline to look for, how did we get here? What was the path that this person took? What’s their story of how we got here? There’s a famous philosopher, I think his name is Donkey, and he’s walking through the field with Shrek and he said, “Hey, Shrek, ogres are like onions. You have to peel back the layers.” We’re the same way. Most people still associate their thyroid condition with the day of their diagnosis when in reality, you know this, you look at somebody’s health timeline, and you can see the problems just stacking up in time and then they develop hypothyroidism. No, that’s the end of it. By the time your TSH is high, your T4’s low, you’ve lost 90% of the function of your thyroid gland. That is the end stage of thyroid disease. That’s not the beginning of it. But you are slowly beginning cellular hypothyroid, cellular hyperthyroid, more tissues impacted, more tissues impacted, now, we start to see thyroiditis. Now, we start to see the destruction of the gland and eventually becomes primary hypothyroidism, but that’s the end.

When you look at labs from that perspective, and you look for the patterns, and you don’t care about H or L as the indicator, because labs could be normal and appropriate, labs could be normal and totally inappropriate, labs could be abnormal and appropriate, and labs could be abnormal and totally inappropriate. So, we have to evaluate, interpret, and I don’t think that happens enough.

Cynthia: No, and I have to agree with you that, when I am looking at lab work that’s been done on my one-on-ones or people will ask questions on social media where I always have to say, I’m a nurse practitioner, but I’m not your nurse practitioner, one of the things that comes up with some frequency is misinformation about, if they’re diagnosed with a thyroid issue, generally speaking, oftentimes hypothyroidism or Hashimoto’s, there’s a lot of misnomers and nuances about whether or not this is reversible. So, at what point is the hypothyroidism or the underactive thyroid, is it still reversible? Because you mentioned by the time you get to a point where both TSH and T4 are abnormal, you already have some destruction of the gland itself. So, where is that point? It could be that people are far blown beyond that by the time they actually get diagnosed. But for someone that’s listening who’s hopeful at some point, they don’t have to take thyroid medication, is it truly reversible in your opinion?

Eric: It really depends on the situation. If you asked me 10 years ago, I would tell you that based on the literature, the thyroid gland once it’s damaged, it doesn’t recover. I will tell you based on 27 years of doing this now that the thyroid gland can recover, and now the science is saying, “Hey, the thyroid gland can recover. It takes about five years for that thyroid gland to regenerate itself.” Now, why do most people not see it recovered? Well, because the same things that drove the hypothyroid state to begin with and the thyroiditis are still there. So, why would it get any better? But I see a large percentage of my clients that I work with have to reduce their thyroid medication dose, and many of them have to eliminate it altogether. I don’t prescribe. So, I always have to send them back to your docs. So, what’s happening? There’s a couple of options.

Option A is that they’re just absorbing more of their thyroid hormone, because their gut function’s better, and they’re converting it better because their cell stress is better. That’s part A. I definitely think that happens. But in time that they’ve been doing the right things more consistently, they’re still seeing the need for thyroid hormone to keep going down and down and down, and at some point, they become any thyroid hormone is too much, and at that point, you have to say, the thyroid gland is making sufficient thyroid hormone, it must have healthier cell function. The new literature is actually justifying that can be the case, that it can come back. I think it’s often thought of as rare, because nobody’s addressing root causes.

Cynthia: I think that’s important, because certainly, I’m a good example of this. For anyone that’s listening, I’m an open book about my own thyroid journey. I think a lot of people last fall were in full panic mode, including myself, what are my options? I would say, last September, when a lot of recalls for the desiccated products were brought about, which direction were most people heading? We’re coming to you obviously identified that you don’t prescribe. So, you’re not prescribing these medications, but where people desperately trying to stay away from the synthetics, were they more open minded to it? I know myself, I out of desperation, finally agreed and actually felt better on the synthetics, which I was shocked by because I had been the card-carrying anti-synthetic hormones person for such a long period of time, and I was actually humbled. So, I’ll be the first person to say that you can teach an old dog new tricks. You can evolve, shift, and change, and certainly, I have in terms of my own thyroid journey. But what has been your experience when you’ve got clients coming to you that you’ve either been following for a few years or new clients coming to you after the recall. Which direction do you see most of their providers heading towards?

Eric: Most of the patients that I’ve worked with aren’t on T4, T3 combinations. They’re on small doses of T4 if they’re on anything, and usually Tirosint although that’s not always the case either, even though that’s the one I prefer. But for somebody who’s had Tirosint, or they react to Synthroid or they just negatively react, one of the things you can do is you can look at all the different types of T4 medications, and even the brands, and the generics. You can see what all the other things are in it, and sometimes it’s not– Maybe Tirosint is gluten free, but it’s got corn starch, which you’re sensitive to, and that’s the issue. So, I think a lot of people who just have reactions to the different types of T4 medication, it may not be the T4 that’s in there, but really some of the excipients that are in there. Yeah, fillers.

Cynthia: I was going to say, for myself, I recall in cardiology, I would have women in particular that would tell me as we were admitting them to hospital, “I won’t be on any synthetic Synthroid.” I would take that to heart because obviously, it was something that was important to them, and what I came to find out is that when you have a generic formulation, only about 80% of what is created in a lab has to be chemically equivalent, and so you can get all these other fillers. So much to your point, I’m on trade Synthroid and trade Cytomel. Trade Cytomel is actually very hard to have covered by insurance. I actually ended up purchasing my prescriptions through a reputable pharmacy in Canada, and it was literally a third of the cost that I would have paid here in the United States. So, really being sensitive to the fact that oftentimes, it’s filler, especially, if you’re gluten free, and I know a lot of people that have hyperthyroidism are dedicated gluten free, sometimes dairy free, sometimes soy free, and really trying to be diligent with your diet, you can unknowingly be exposed to some of these fillers and perhaps not realize it.

Eric: Yeah, and many times I think that’s the bigger part of the problem. The amount of gluten that’s probably in the medication is probably for most people not as big a factor. But it’s available. It’s gluten free. If I know somebody gluten intolerant or gluten sensitive, definitely put them on it, but I’ve had a number of patients are like, “I can’t take it.” Then you say, “Okay.” Let’s look, compare and contrast which ones these have cornstarch in them, which is a common thing that people are sensitive to. These are the two or three that you can try. These are the ones that you should probably shy away from. Let’s see how you tolerate,” and they do better with a different form, even though it might not be a certified gluten-free form of it.

But most of the patients I reach out to me like, “I have a thyroid problem. I can’t get NP-Thyroid. What can I do? What should I do?” My advice to most of them was, if you’re we’re going to work with somebody to figure out why you have this tissue hypothyroidism to begin with, then my suggestion is switch to T4 only, and then get working on what the root cause issues are. If they don’t want to go through that process, then it was, “Hey, try one of the other combination T4, T3 medications and see if you tolerate that, or you’re going to have to take the T4 and the T3 and see,” and do it that way. But I think by the time most people come to see me or call me, they are will hit that point where they’re like, “I need help. I know T3 is not the solution,” and they’re frustrated, and they’re looking for an answer. A lot of the people that I see have failed on T4, because it’s not converting. They started T3, and they felt good, but then, the honeymoon period was over, and then it went a lot more and more–

I’ve had patients taking more than 200 micrograms a T4 more than 25, 30 micrograms of T3 in a day and still feeling hypothyroid. I understand why their allopathic physician has thrown their hands up like, “Hey, I’m dumping as much stuff as I can put into the system, and you’re not responding.” Patient gets looked at sometimes like they’re crazy, but it’s like, we’ve totally forgot about the tissue response. For those patients who are willing to, then I’m like, “Okay, let’s get busy and figure out what’s going on here.” There’s definitely a transition period if you are on T3, and now you’re coming off T3. You’re going to go through a divorce period where you’re not going to feel so good, and then everything starts to stabilize. What I hear from a lot of people is, “Hey, I’m a little bit more fatigued and tired, but my brain fog is gone, my anxiousness is gone, I can sleep again,” because what happens, when you have a stress response going on the body, the brain is upregulated. So, you can increase conversion of T4, T3, and the peripheral tissues get downregulated. They’re still hypothyroid, but the brain is racing, and it’d be like sitting in your parking lot or in your driveway with your foot on the gas but in park. You’re not going anywhere, but you’re just killing that engine. Same thing in our bodies. We’re revving this fight or flight system, but nothing else is working. That’s not a good place to be.

Cynthia: Is that what happens when– I know for myself personally, when I first got started on nature thyroid, anytime there was an adjustment in dosing, I would have two weeks of insomnia, where I would be laying in bed, eyes were closed, and I would just be awake. I’m curious if is it the sympathetic overdrive as your body’s acquiescing to more hormone. I would assume that that’s probably what’s driving it, and that was one of the questions I also got, is insomnia with medication changes. What’s normal, what’s not normal?

Eric: Well, I think when you increase your thyroid medication, you get insomnia. You just created a hypothyroid state in the hypothalamus. What happens is that hypothalamus converts T4 to T3, and then when there’s lots of T3 in the hypothalamus, that activates the sympathetic nervous system. That’s good. Your sympathetic nervous system says, “Hey, let’s get rid of some of this extra stuff, burn off some calories. Let’s do some stuff,” if everything is working downstream, but instead what happens many times, somebody in this stress, their bodies in the stress state, so they get this sympathetic upregulation and they don’t have the ability to calm that system back down. In time, if their body starts to increase the deactivating portion, I think they can start some of those people get to actually balance it out, but a lot of people still continue to have problems.

We talked right before we got started that if you are in a hypo or a hyperthyroid state, you can up regulate mast cells in the brain, then those mast cells are like immune cells, and they dump out histamine, which a lot of people are familiar with. But also, mast cells hold on to T3. So, in a hypothyroid state, mast cells can degranulate, and provide T3 if needed. Unfortunately, you get the negative side effects of the histamine. But when there’s high T3, the high T3 actually stimulates the mast cells to degranulate. So, it is this balance, but I think sometimes when somebody gets anxious, anxiety, is it normal? It’s common. I don’t think it’s normal. I think when you have those anxious, anxiety, and insomnia, that’s a really good thing to acknowledge, and then make sure you’re talking to your practitioner who’s ever providing that and say, “Hey, listen, this is the signs and symptoms I’m experiencing,” and they should be aware enough to say, “Okay, those are more hyperthyroid symptoms. Let’s back this down a little bit.” You as the individual have to be aware that, “Okay, cranking my thyroid hormone cranked up my anxiousness, anxiety, insomnia. Maybe more hyperthyroid in the brain is probably not the right strategy to increase weight loss, and grow my hair, grow my nails, because it’s still probably not the right environment to do that.”

Cynthia: Right, and it’s important for listeners to understand that there’s this autonomic nervous system, and so you’ve got fight or flight and rest and repose. So, if you can’t sleep, and you’re stuck in sympathetic dominance, there a lot of other things that don’t happen accordingly as well. So, we want to find balance between these two aspects of our central nervous system, and unfortunately, most if not all of us are sympathetic dominant. Because we’re constantly on the go multitasking, not getting enough sleep, not getting enough exercise.

One of the things I found fascinating when I was doing a little bit of research prior to our recording was, you were talking a lot about fat malabsorption. So, now, we’re pivoting a bit and talking about the gut. What I found particularly interesting was your discussion about high HDL. So, this beneficial aspect of our cholesterol panel. Most people were talking about total cholesterol, LDL, HDL, triglycerides. As someone who has always existed in the high HDL, low triglycerides realm, I found your discussion, and I think this would be really interesting to listeners, I was like, “Oh, I’ve got high HDL. So, I don’t even worry about what the other values are,” especially with low triglycerides. You actually feel, and this makes sense, that a high HDL can sometimes be an indicator of poor liver function or this decreased conversion of T3 in the liver. Can you talk a little bit about that?

Eric: Yeah, high T3 and what’s high, what’s normal? If you look at a lab report, I think if it’s over 45, it’s considered good. But I think the optimal range for female is 65 to 85. For male, I think it’s somewhere like 45 to 65. I think that’s the range. I don’t remember offhand, but those are the optimal ranges. But what is HDL? HDL, is it good, is it bad? I think we have to get rid of those good/bad things because HDL, and LDL, and VLDL, these are just boats that carries cholesterol, and free fatty acids, and other proteins around the body. They’re not bad or good. The body produces these things based on what it needs. HDL is always considered good because it’s carrying this emptier molecule back to the liver, and there’s less bad stuff in it, so it can pick up more stuff if it wants. But I think low HDL is probably not a great thing, but HDL is probably not a great thing either. What the literature seems to show is that when you have a high level of HDL, it’s probably more indicative of immune or autoimmune issues than it is like, “Whoo, whoo. I just have high HDL,” that it’s like a badge to be worn.

Cynthia: All these years, mine’s been in the 90s, and I just thought I was a total badass, and this is completely blowing my mind right now. Go ahead.

Eric: Yeah. I think we often make the assumption that because we call it the good one, that the high rate is the better, but in reality, it probably means we have an issue with the unloading and offloading of free fatty acids. We’re not really doing what we’re supposed to be doing, and we have probably an immune or autoimmune condition going on. T3 physiology plays a huge role in how we regulate our lipids from triglycerides to cholesterol, to LDL, to VLDL, HDL. When we see a change in lipid status, it does not mean that you probably ate just too much fat in your diet. That’s probably not the case. It’s probably an indication that there’s breakdown in cell physiology at the liver. We’re not using ATP to burn our free fatty acids, we’re not able to transport these things as effectively, and we’re not able to get them into our liver, get them into bile so we can have proper detoxification pathways.

So, HDL may be good if it’s elevated, but not high. If you’re female, 65 to 85, I think if you’re a man, somewhere in that 50 to 65 range is probably good. If you’re walking around with something over 85, and you’re not aggressively trying to ratchet that up with maybe with high-dose oils or fish oils or something like that, it’s probably worth investigating and taking a deeper look at why would it be elevated. Especially, I would be interested if there’s some type of immune or autoimmune issue going on.

Cynthia: Well, it’s interesting. When I was diagnosed with hypothyroidism, now it was four years ago, my antibodies have always been negative and I was taught, “You’re one of those very small percentage of people, maybe 10% to 15% that have nonautoimmune hypothyroidism, whereas 80% to 85% of people have Hashimoto’s, which is an autoimmune component.” Interestingly enough, when I interviewed Dr. Alan Christianson, he said, nonautoimmune hypothyroidism is really rare, and you probably do/did have Hashimoto’s, and you can have Hashimoto’s and have negative antibodies, and that completely blew my mind. The reason why I wanted to make sure we touched on this is that, I was always taught that, “Oh, if your antibodies are negative, you don’t have Hashimoto’s.” What I’ve come to realize is that there are, again, nuances to the thyroid, and it could very well– maybe six months before my antibodies weren’t normal. By the time I finally figured out something was amiss, and I had them tested, they were within normal limits. So, I’m curious if that’s a pattern that you’ve seen or do you agree with Dr. Christiansen in terms of, there’s a lot more Hashimoto’s than what we actually realize is out there.

Eric: Yeah. I think it comes down to how we’re going to classify what’s going on. My intake on it, to some degree, I agree with a lot of Alan’s thoughts. Sometimes, some of the things I think he says, is “Yeah, I’m not quite sure, but that’s okay.” I think it’s great to get bunch of us in a room and hash out some of these things, because none of us know all the right answers or have all the right answers, and we’re just working off experience and what we learn to research. But my take on what’s happening at the thyroid gland is it’s all thyroiditis. So, the differentiation between thyroiditis and Hashimoto’s is TPO and thyroglobulin antibodies, TPO antibodies specifically. But we know that TPO, thyroglobulin, TSH antibodies can be made when you have Graves, whether you have thyroiditis, or you have Hashimoto’s. They can be produced in any one of those states.

Now, when is it thyroiditis and when is it Hashimoto’s? The differentiator is, if there’s no antibodies, it’s thyroiditis. If we see antibodies, it’s Hashimoto’s. Sometimes, we make too big of a deal about that, because people believe and have been told that the antibodies damaged– They’re like little Pac-Man eating away at the thyroid gland and that creates all the damage. The reality is the science doesn’t seem to show that that’s the case. What happens often with thyroiditis is that thyroid cells have danger centers on the cells. When thyroid cells perceive danger, whether it’s from peripheral sources or damage to the thyroid gland itself, these damaged particles can bind to receptors on the thyroid cell, and the thyroid cell initiates its own self-destruct. As a matter of fact, the thyroid cells have centers for lipopolysaccharides, which are LPS, lipopolysaccharides, is something [crosstalk] to find out with leaky gut.

Cynthia: Terrified of it.

Eric: LTA, which is the coating of gram-positive bacteria. But these things from the lymph system, the GI tract and go right into the lymph system of the thyroid gland, soon as those dangerous signals are recognized, the thyroid gland itself, doesn’t even need the immune system, actually initiate its own self-destruct mode. So, it self-destructs and it actually spews out signaling molecules that invite the lymphocytes into the thyroid gland. There’s our thyroiditis, these infiltrating lymphocytes. What the literature shows is that thyroglobulin antibodies cause no damage to the thyroid gland at all. None. That TPO antibodies, while they can cause damage, cause a very small amount if any damage to the thyroid gland cells, maybe less than 5% of the damage to the gland is caused by the antibodies. The vast majority of is just caused by the infiltrating lymphocytes. So, if that’s the case based on the literature, TPO antibodies are gobbling up your thyroid gland. So, you have thyroiditis, whether you want to call it Hashimoto’s thyroid or thyroiditis. I don’t care, but you have thyroiditis that’s causing the damage.

Now, some people say, what’s the immune system out of control, there’s nothing you can do about it. The allopathic medicine’s approach is it’s idiopathic, it’s out of control, there’s nothing you can do, it is just going to either away. In functional medicine, we hear people say, “Hey, it’s an autoimmune condition. There’s not much you can do. We’re going to try and do some things, maybe that can trigger it, but it’s immune system out of control.” I don’t believe in most situations, it’s an immune system out of control. I don’t think the immune system just loses it somewhere along the way, and somehow forgets cell from non-cell. Now there’s lots of theories about autoimmunity. I think at the last count, I think there was 13, and I get it, and I think molecular mimicry, I understand all those things as well. I’m a bigger believer that the body does things for a reason, and if it was just an immune system out of control, then you’re doomed. You’re screwed. You’re never going to get rid of it. But what do we spend all our time doing in functional medicine is reducing an excessive stress response. I’m getting rid of gluten, I’m getting sleep, I’m trying to breathe better, I’m getting rid of bacteria and viruses in my gut, and eating better food. We’re trying to reduce the stress load.

When you going to reduce the stress load, we see the thyroiditis starts to subside. We see antibodies go down. So, if you think about it from my perspective, if I’m a cell and I’m in danger, I can decrease thyroid hormone in one cell, that’s easy. If I have to do in one tissue, maybe that’s easy. But if I can do it globally, shut down the source. It makes sense because we see that in cases of famine and starvation, and other factors where the body’s in a global distress, and we see the deactivation of thyroid hormone. So, what I think is going on in most cases, isn’t that immune system’s out of control and the antibodies are just gobbling up, the antibodies are like the cleanup crew. Would you really yell at the cleanup crew after New Year’s Eve party for making all the mess in Time Square? They’re cleaning it up. They’re doing all the– Sure, they break a couple of things on the way but they’re doing most of the cleanup, which is where I think we’re seeing when we see thyroid antibodies. So, to me, I think everybody has thyroiditis to some degree whether we see antibodies or not. I don’t put as much attention. If you want to call it Hashimoto’s, great. I think they’re probably all Hashimoto’s. The only reason we call it Hashimoto’s because Dr. Hashimoto saw the thyroid antibodies but it’s thyroiditis.

The key is in functional medicine that we see sometimes is that people are focused on, and I was too, when I learned that– Because when I originally heard that thyroid antibodies would cause– TPO antibodies are causing all the damage, the goal was to suppress antibodies. How do I lower the antibodies? And I did Thyroid Thursday, well how do you lower your antibodies? Now I could kick myself, because I don’t know if that’s necessarily what you want to do. If the thyroid antibodies aren’t causing most of the damage, artificially suppressing antibodies doesn’t make a ton of sense. Yes, it masks the issue, but the thyroiditis could still be going on. That’s when you see somebody who’s taking high-dose vitamin D because it suppresses my antibodies. It does. It suppresses the Th2 side, your adaptive immune system. But is that what you want?

If the antibodies truly aren’t causing the damage to the gland, do you really need to blast vitamin D to suppress it? I don’t know if that’s the right strategy. We know we have Th1 and Th2, and some people have talked about Hashimoto’s as Th1 dominant disorder or Th2 dominant disorder. The literature seems to show that it’s both, that it starts as T1, transitions to T2, and you can flip flop back and forth. But if you think alike about it, similar to I think about, the immune system is not doing the wrong thing. It’s saying, “Hey, we’ve got a danger mode, slow down metabolism. Let’s find what this thing is and get rid of it. We don’t need a lot of metabolism.” Somebody may say, “Well, why would the cell do that?” Well, if I’m a cell and I’ve got a bacteria or virus inside of me, and I keep bringing glucose in, I’m going to feed the organism. If I keep making proteins, I’m going to support that organism. If I keep bringing iron in and start having this iron available, now those organisms can replicate. If I make more energy, the organism can still use it.

So, there’s this constant battle when an organism in the cell with for resources. The cells are pretty smart. “Hey, there’s a threat in here. Wall the cell off, stiffen the membranes, make it hypoxic, increase oxidative stress, but not too much. And don’t make glucose, don’t make building blocks. We’re going to do autophagy and mitophagy instead. We’ll live off the debris in the cell and in the process of cleaning up the cell, we’ll actually probably find those organisms, kill them, eat them up, and get rid of them.” So, I don’t think this thing is all broken. I think that’s good for the person. You’re not broken. Your body is adapting to some type of excessive stress. The most problematic part of the whole thing is, it’s not the same stress for everybody. Everybody wants to know, what’s the one thing? What’s the one thing that fixes my T4 to T3 conversion? You got to reduce yourself excess of cell stress. People get angry all the time, like, “Well just tell me what I need to do.” Well, you need to eat better, sleep better, rest, better, less trauma, emotional improvement, change your gut, good diet. Nobody wants to hear that stuff. They want the easy stuff, like give me the next capsule to do, and it’s different. There’s 10 people, hypothyroidism, all got there for different reasons. So, the solution is only going to be the same if your goal is to normalize TSH with T4. If your goal is to normalize or restore normal homeostatic thyroid physiology, the solution is different because 10 people got there for 10 different reasons.

Cynthia: Well, I think it’s so important to honor bio-individuality. But certainly, your explanation is far more positive and supportive than any other explanation I have actually listened to. Because I think for so many, there’s this doom and gloom. If you have an autoimmune issue, then it’s all bad. Oftentimes, what you’re really saying, the crux of the issue is, we’ve conditioned our patients, and this is part of allopathic medicine. I was part of that for many, many years. Every symptom requires a pill, instead of really doing the hard work, which will probably yield better results than masking or band-aiding a problem.

Now, I want to be mindful of your time, but I just have a couple more questions. A comment that came up quite a bit is, I know that iodine is particularly controversial as it pertains to thyroid function. There are some pro-iodine camps, there are some anti-iodine camps. Where do you fall on the continuum of iodine?

Eric: Well, I would say I’m more neutral. I’ve read Alan’s information, and I don’t know that I agree with all of what he has to say. I’ve seen the other camp and I’ve seen people taking iodine and blow out their thyroids.

Cynthia: Yep.

Eric: I think for the general population, loud amounts of iodine are not going to be the be all, end all. I think we live in a time where, A, there is in most of the areas where we’re advanced, we’ve got food, we have iodine. There’s arguments in some areas there aren’t. But most of the food, if you’re eating processed food, there’s usually iodine added in there in some form or another. I think it’s critical for many functions. I think the biggest challenge is that there isn’t a clear-cut answer. We don’t have a clear-cut way to really assess it, manage it, because they’ll always say, it’s by the population. Well, [makes a raspberry sound] have you seen this population? Our population isn’t super healthy. So, I don’t think you can go by that because everybody’s not the same set of health, and we’ve got different things going on, and people eat different foods within that same population. Some people eat a lot of processed foods, some people don’t eat any processed food. But I think trace amounts of iodine for the vast majority of people is fine.

But I rarely find that I’m treating somebody specifically with any iodine. I’ve done a bunch of the tests on iodine testing in people that are struggling with thyroid issues, and I’ve done most of the tests that are out there. I’m just not convinced one way or the other that iodine is the under– iodine deficiency or iodine excess is the primary driver, especially in places like the US, as the underlying reason.

I know Alan is kind of, “It’s iodine excess in everybody.” I know the other camp is, “Everybody’s deficient.” I just don’t think it’s that black and white. So, for most of my patients, when they asked me, “Do I need to be on the iodine?”, I usually tell them, probably not at the moment. If you really want to know, we can do some tests. I can’t confirm, actually, but probably need to do it a couple times in a row to get a base, and then see how things differentiate with eating the same type of stuff. But for the vast majority people, having just focus on eating whole food, real food, and let’s address all the other things, and if things still don’t improve, and we don’t see the thyroid gland improving in output, then maybe it’s something we take a look at. But I think most things, they’re not black and white.

Cynthia: I think that’s certainly a fair response. My practice, I was using the Hakala, which is this iodine test and had some good results, but I’ve always been cautious. I would just tell people if they were low, I’m like, “Go eat some sea vegetables,” which no one– unless they like seaweed, that was always an interesting self-flagellation by my part.

Now, I’ve got a couple questions about, why do I get cold when I’m hypothyroid, and I have some ideas, but I thought you probably would have a more eloquent explanation for why that actually occurs. What is actually going on with thermogenesis in the body that’s driving that sensation of feeling cold with an underactive thyroid?

Eric: Well, one of those we already talked about, is you lose some of the uncoupling protein in the mitochondria to actually dissipate heat as– When you have healthy mitochondria, they make a lot of ATP, so we don’t have too much oxidative stress can dissipate heat. Well, if you don’t have a lot of thyroid hormone in the cells, your mitochondria don’t have that heat pump leak and can dissipate heat real well. But on more of a macro level, your brown adipose tissue primarily is the big heat generator of the body. So, you do need T3. You need two things. You need sympathetic stimulation and you need T3 inside your brown adipose tissue to generate heat. If you have tissue hypothyroidism at your brown adipose tissue, you’re going to have a hard time generating heat.

The other thing is a lot of us, as we get older, don’t have that much brown adipose tissue. We got fats, but we don’t have brown adipose tissue. Brown adipose tissue is really the more metabolically active at generating heat. White adipose tissue is more active at generating inflammation. Most of us have more white adipose tissue. The nice thing is that if you do the right things, diet lifestyle wise, and you have a nice enough T3 actually getting to the cells and tissues, you can beige your white adipose tissue. So, make it more brown like and they call that beige adipose tissue. But if you’re cold all the time, despite a normal TSH and T4, it’s lack of T3 getting to those brown adipose tissues to degenerate heat, reduced mitochondrial function, which you should expect if you are in a hypothyroid state. You’re going to make less ATP, it’s going to be maybe more efficient with the resources it has, but you’re going to generate less and you’d probably have a higher level of white adipose tissue. So, there’s a bunch of things diet, lifestyle wise that somebody can do to help that along if they’re feeling function enough to do it. Exercise is one of those things. It’s a really good inducer of browning your adipose tissue.

Cynthia: Yeah, I also like to suggest things like cryotherapy, which has become my geeky thing that I do– not with my husband per se. We do it separately, but at the same time in the same location, really enjoy that quite a bit.

Last two questions. I know your opinion of fasting, but the caveat is, what are your thoughts on women– and I got this question five separate times. What are your thoughts on intermittent fasting for women of middle age, so perimenopause, menopause that have an underactive thyroid? It’s like add in all those variables and my standard response, it’s all about bio-individuality but I’m curious to get your take on it. Because one of the things about fasting that not necessarily everyone talks a lot about is that fasting can improve mitochondrial efficiency, and perhaps for these individuals that have got an underactive thyroid, it can be beneficial, but I think there are a lot of caveats. It’s all those nuances again, a saying, “Well, if you’ve got your sleep dialed in, if your stress management’s under control, if your blood sugar,” and it’s like all these variables that can impact that answer, but I figured I would ask you anyway.

Eric: When you’re perimenopausal or menopausal, typically, one should have a reduction of estrogen. So, estrogen and thyroid hormone, both drive mitochondrial function. If you’re hypothyroid, whether it’s glandular, and if you’re glandular, and you’re remediated with thyroid hormone, and it’s all good, not an issue. But if you still have tissue hypothyroidism despite that, and you have lower levels of estrogen because you’re going through that change, you don’t have the hormones that are really going to drive mitochondrial function. The challenge then becomes, people are concerned that fasting is going to be problematic, and I get it. It sounds like that would be the state, like if I don’t eat calories, if I don’t have food in, that’s going to trigger my thyroid hormone to slow down. However, if you already have slow mitochondria, they aren’t burning much energy in the first place. They’ve reduced the amount of food energy they’re converting into cellular energy already. So, if you put more food calories into a system that already has downregulated mitochondria, it’s not going to work or make it work any better. Matter of fact, it’s going to have to dissipate, and go out, and make other things. More cholesterol. It’s going to go into creating more of the fat that they don’t want.

This conversation that fasting creates a problem, I think in short term, it does create a change in our physiology, but it’s temporary. The body also has a backup system to take T3, deactivate to T2, but that T2 is actually functional, and actually maybe has more of a mitochondrial function. So, even though, we might see with fasting in some of the science that there’s an elevation of reverse T3 in a fasted state and lower level of T3, what we’re not measuring is T2 and T3 when it’s converted or metabolized to T2, T2 and T3 metabolites may have, if not more, as much to do with the function of the mitochondria. So, the body always has a backup plan. I think the bigger issue for people isn’t whether you’re fasting. It’s about signaling. If you are eating small amounts of calories and not getting satiety signals to the brain, I think that’s more problematic. Because you’re not giving the brain the signal that I’m feeding on a regular basis. It’s not enough of the signal to say, “I’m good, Increase metabolism.”

When you eat a bunch of food, what should happen is, you should get signals to brain that says, “Hey, I’m good.” One of those things that goes to your brain, when you get food in and we start having some spillover, like, “Hey, I’ve got to start storing some of this stuff,” your adipose cells produce leptin. Leptin is that thing that says, “Hey, we’re good. Don’t need to eat anymore, and shut it down.” Shut down satiety. If you’re getting satiety signals in a 12-hour period, 24-hour period, or even a 48-hour period, your body’s going to get that signal that, “Hey, I’m not starving. I’ve got stuff in.” But when you graze, you eat little bits of stuff, and not a lot of calories and never enough to really get a satiety signal, I think that’s the bigger problem. I don’t think there’s a problem with somebody fasting. I think actually, the opposite is true for a lot of people. I don’t want anybody to starve themselves, and matter of fact, I use time-restricted eating quite a bit with my patients, but you have to see how do they adapt to it, and it’s not necessarily something you need to do every day. Be flexible about it and see how you do, see how you respond. But most people do really good with it. I don’t see a problem with my base of patients for the most part. I see a lot of people struggle in the beginning as they transition to it, because they’re used to having some type of snack every hour, two hours, or three hours, and are constantly small grazing through the day, because they’re living on carbohydrates.

But I think the problem becomes is that they’re not getting the satiety signals, and if they’re not getting satiety signals, that’s when the body may have more of a danger response, which could be the problem. I don’t think that’s usually the issue. I think the cases for most people is, which is the opposite, is there’s combination of factors going on. This is ugly. But you’ve got cellular hypothyroidism because they’ve got decreased T3. Because they have decreased T3, they’re storing excess calories as adipose tissue. As they’re storing excess calories as adipose tissue, they’re increasing their leptin, and they’re increasing their inflammation. The inflammation is going to then downregulate their metabolism a bit, and that leptin should signal to the brain that, “Hey, we’ve got plenty of food on board, ramp up thyroid hormone production, let’s kick this thing into gear, increase that sympathetic nervous system, let’s just sweat, let’s get active,” and that’s how it should work. But the problem is that as we start to have slower metabolism in stored calories, and especially, if we’re doing that low, eating small amounts of five, six small meals per day, we wind up not being able to get satiety signals, but we also wind up storing some of that extra caloric load. We start having more body fat, we start having more circulating leptin, and then leptin resistance kicks in where the brain says, “Hey, I’m not going to listen to that anymore.”

Now, your brain doesn’t turn off. It doesn’t get the satiety signal even though, there’s tons of leptin in the system. It doesn’t listen to that signals anymore and now, you’re constantly hungry. That’s not a good sign. Then you eat more, which you can’t use, and then you store it, and then it creates inflammation, which creates problems, and then it can increase more leptin, and it keeps going. Then what happens is, we get diagnosed with hypothyroidism over time and somebody comes in and says, “Hey, I’m just going to blast you with some thyroid hormone.” Is that good? Well, I don’t know, because now you’re giving somebody a bunch of thyroid hormone that we would hope is going to help improve metabolism. It’s going to increase maybe that fight or flight response, but it probably is not going to have the intended impact, especially if that person is already in leptin resistance, because they’re already hungry. Now, we just flooded a brain or hypothyroidism T4, which said, “Hey, brain, I’ve got lots of T4 converted to T3 up here. We’ve got to increase metabolites.” We got to increase eating, because now, I’ve got all this thyroid hormone on board because when you have in a hypothyroid state that increases your demand for more calories.

It’s really problematic for the person who’s been leptin resistant for a period of time, and then you give them thyroid hormone, you may actually make them even hungrier than they were before, and that high level of thyroid hormone that you’ve put in there, you saturate the hypothalamus, you drop their TSH, you increase their sympathetic nervous system, decrease their vagal response rates, and now they’re not digesting well, and then the last piece of that is, when the brain has that signal that it’s flooded with thyroid hormone, it ubiquitinates something called deiodinase 2 which is the deactivating enzyme of deiodinase 2. When you ubiquitinate deiodinase 2, it turns it off. So, now you have a brain saying, “I’m hungry, I’m hungry. I got all this thyroid hormone. We’ve got to eat, got to eat, got to eat. You’ve got reduced satiety signals because of your leptin resistance, and now you just deactivated the converting enzyme in your peripheral tissues, and now your TSH is low, T4 is high, you’re hungry, and you’re gaining weight. Your doctor’s looking at you’re like, “This can’t be your TSH is like 0.00. There’s no way you’re gaining weight.” They can absolutely gain weight because of this ugly hormonal web of dysfunction that’s going on. Sorry about that, I think I got a little off.

Cynthia: No, no, no, I think it’s also fascinating. As I said, the last time we connected for the podcast, I’ll have to have you back because you do such a beautiful job explaining some pretty complicated subjects, but distilling it so that the listener can literally digest the information, and feel empowered and inspired. Now, how can listeners connect with you on social media? If you don’t follow Dr. Eric on Instagram, you need to, because he does so much teaching, there’s a lot of great information. Whether you’re a clinician or the lay public, I highly recommend following him on Instagram, and I’m not usually plugging people on Instagram, but that’s where you have a lot of fantastic resources. How can listeners connect with you? What’s the easiest way to find you on social media or your website?

Eric: My website’s rejuvagencenter.com, and anybody who wants to reach out to me, they can go to rejuvagencenter.com and they can schedule a complimentary discovery call. I do a few every day to talk to people about their thyroid issues and give them some insight. If they’re interested in working with me, it’s a good interview process to find out if we’re compatible and what they want is what I provide or what I provide is what they want to do. But if they’re looking for some of the stuff that I talk about, do definitely Instagram. It’s funny. I think a year ago, I didn’t even have an Instagram account, and somebody convinced me to have an Instagram account. But I find it it’s the best platform. So, I’m on Facebook, but I’m not really on Facebook. I’m really post everything, I guess, on Instagram, then it goes to Facebook somehow. But that’s where I post most of my stuff. I have Thyroid Thursday videos, I have a YouTube channel that most of the stuff is on. But I’d say Instagram is the place, @drericbalcavage is where I put most of my stuff. Really, my goal there is just to take the stuff that I learned or read, or that I see in clinical practice and try and help explain it so that people can understand why they don’t feel good.

Then, I have a podcast as well. I think we’ve had you on the podcast. We’d have you back on soon. It’s called Thyroid Answers Podcast. On that podcast, we have people come in and we talk about–answer the questions that people have about thyroid physiology. We talk about gut, we talk about cellular hypothyroidism, we talked about cell danger response, we talked about fasting, we talked about all different aspects of health that actually are the cause of cell stress and hypothyroidism, and when we address those other things, thyroid physiology, because it’s not broken, it’s adapting, can actually come back into normal range most times and normal physiology.

Cynthia: Awesome. Well, thank you again for your time today, and I look forward to connecting again as always.

Eric: Hey, thanks for having me on.

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