Recently I interviewed Dr. Eric Balcavage, and we talked about thyroid physiology. If you would prefer to listen to the interview you can access it by Clicking Here.
Dr. Eric Osansky:
I am very excited to chat with Dr. Eric Balcavage, as we are going to talk about thyroid physiology. I am all about talking about the thyroid, but we can’t get into everything in his book. That’s why you need to get his book The Thyroid Debacle. Let me give Dr. Eric’s background. We will dive right in after.
Dr. Eric Balcavage is the owner and founder of Rejuvagen, a functional medicine clinic in Chadds Ford, Pennsylvania. He is a nationally recognized speaker and educator on various health-related topics, including thyroid physiology, biophysiology, detoxification, oxidative stress, methylation, and chronic illness. Dr. Balcavage is a functional medicine practitioner and licensed chiropractor in PA, and he is the host of The Thyroid Answers Podcast. The podcast focuses on answering the pressing questions those suffering with chronic hypothyroid symptoms can’t get answered elsewhere. You can also find his educational Thyroid Thursday videos on Instagram and YouTube.
Dr. Balcavage has made it his mission to change the way medicine looks at hypothyroidism. He is also the co-author of the book The Thyroid Debacle. The book is also co-written by Dr. Kelly Halderman. It addresses the problems of current allopathic and functional medicine approaches to hypothyroidism as well as the solution to restoring thyroid physiology. Dr. Eric, thanks for joining us.
Dr. Eric Balcavage:
Thanks for having me on, Eric.
Dr. Eric O:
Before we talk about your book and thyroid physiology, what led you and Dr. Kelly to write the book in the first place? As you know, there is no shortage of thyroid books out there. Yours definitely takes a different perspective.
Dr. Eric B:
I got into functional medicine really by accident. I had a family member who got diagnosed with hypothyroidism, fibroids, and anemia. They were told they were going to need a hysterectomy, iron supplementation, and thyroid medication for the rest of their life. That’s just the way it goes.I was asked to help, and I said, “It’s not what I do.” When your brother asks for your help, you start figuring it out.
I went back to my roots of chemistry. I was a medical technologist before I made the decision to go off to chiropractic school. I looked into chemistry, realized what was going on there, started doing my functional training with DatisKharrazian and Apex. That was a great footing. I’m sure you did some of those courses early on because Datis was the man early in the day.
As I started working in my chiropractic base and talking about what I was learning, I realized how many of my chiropractic clients were on thyroid medication. I really didn’t pay that much attention to it early on. I was more focused on what I was doing chiropractically. As I was talking to them, most of them felt maybe a bit better, but a lot of them still had signs and symptoms. A lot of them had weight issues, most of the classic signs and symptoms. I started talking about Hashimoto’s because that was this big thing. It’s an immune issue, not just the gland doesn’t fail one day. There is an immune-driven process. I started getting more into functional medicine.
As I was doing that, we had this philosophy in functional medicine, at least for my teaching, that the immune system was out of control, and it just started damaging the thyroid gland. Our job was to look for some of those stressors and triggers. Not that there was a lot of hope. This is an autoimmune condition. Your immune system has lost control and will damage your thyroid gland.
The other piece we looked at was T4, T3, reverse T3, and these other values that weren’t traditionally being looked at in medicine and making those decisions. The thyroid gland makes both T4 and T3, so maybe we should be doing a little bit of a different job. Maybe we should be recommending T3 as well. These silly medical doctors aren’t aware that T4 is not converting to T3 well, and it’s deactivating reverse T3 and changing the treatment based on that thought process.
The challenge I had the longer I went into this was I really struggled with the idea that the immune system just lost control and woke up one day and decided it was going to destroy the thyroid gland for no apparent reason. That didn’t sound like good logic. Why would the immune system just start attacking our own tissues? I thought there had to be something else going on. I was talking to a friend of mine. It doesn’t seem quite right that the immune system would do this. I never really liked the term “autoimmune condition.” It’s an immune-driven condition, but I don’t like the idea that the body willy nilly attack ourselves.
A friend of mine, Dr. Ben Lynch, who you know, we were preparing for a conference. He sent me a paper on the cell danger response. He said, “You need to read this.” When I read that paper, I was like, oh, we operate in two modes. We are either in low stress, homeostatic regulation, or we’re in a different state, allostatic regulation, which is an excessive stress response. I said, “This makes a lot of sense.”
Dr. Naviaux showed how depending on the situation, we use micronutrients for one pathway, but in other situations, we may use micronutrients for a different pathway. Our physiology adapts to our environment, to the stressors, to what’s going on. Maybe that is really what’s going on here. The cells change their physiology, and the immune system changes its physiology based on what’s going on in the body. I thought, maybe what we were seeing was more of an adaptive change versus this systematic control because if your immune system is out of control, it doesn’t sound like you will ever recover. If it’s an adaptive physiology, then we could find out what it’s adapting to.
I got into a really deep look into the literature, papers, and research. The more I looked at it, it’s my philosophy in general that a lot of what we see with thyroid physiology is an adaptive response to some type of excessive stress response. If we can identify what those stressors are, reduce them, remove them, we can support the recovery of the physiology. In many situations, we see improved T4 to T3 conversion, reduced immune damage to the thyroid gland, and a thyroid gland recover in time. Many of my clients need less thyroid medication. The medication they take converts better, and a whole bunch of them in time don’t need it at all.
Dr. Eric O:
Makes sense. You’re not saying people with Hashimoto’s and even non-autoimmune thyroid conditions don’t need thyroid hormone. Most doctors are neglecting the physiology, so maybe some of these people don’t need to take thyroid hormone replacement. Others might not need to take as much as they are currently taking.
Dr. Eric B:
In the allopathic model, the focus has always been on TSH and free T4. Early on, we’d say, “These silly allopathic doctors and endocrinologists are only running two tests. They’re not running thyroid antibodies. They don’t know that this is an immune-driven process.” I don’t think that’s the case. I think most of them realize it’s an immune-driven problem. We pretty much know it’s either an iodine deficiency issue or an immune-driven problem. If you’re in an area where there is sufficient iodine either in the environment or in our food sources, it’s probably not an iodine deficiency. That leaves me immune. Depending on what you read, it’s thought to be that 95% of cases of thyroid, especially hypothyroidism, are immune-driven.
I would argue that whether there are antibodies or not, almost all of them are immune-driven. If you look at the immune system of people who have glandular hypothyroidism going on and negative antibodies, if you look at their T cell panels, they are Th1 dominant, which will result in lower antibody production typically anyway. It’s still an immune-driven process.
The challenge in functional medicine to some degree is- At least I think what I was taught is the antibodies are like little Pac-Men eating away at the thyroid gland. TPO and thyroglobulin gobble it up. The literature shows that thyroglobulin doesn’t create any damage to the thyroid gland. TPO antibodies create very little. If they are not creating much damage, what is causing the damage? It’s the immune cells getting to the thyroid gland and creating the damage. In that situation, the T cells are creating a lot of damage, but if you’re Th1 dominant, you may not see it.
For the most part, what we’re seeing is an immune-driven process. The allopathic world knows that, I think, but they are coming at it from a point like, “We’re not going to suppress the immune system. We know the thyroid gland will get damaged. There will be a point where it can’t make enough anymore. We have a simple solution. We give them more T4. The thyroid gland primarily makes T4, so we will give it what it can’t make, and the patient should be good. The indicator that we’re going to use that shows that we have reached euthyroidism or normalized thyroid physiology, a TSH within a preset range. If I give someone enough T4 to bring the TSH into range, everything is right in the world.”
Unfortunately, that doesn’t work for a whole bunch of people. For the listener, T4 is the pre-hormone. It does have some functionality, but most of the functionality in the thyroid world comes from T4 being converted to T3 inside your cells and tissues. T3 binding to receptors, and that’s what is turning on your metabolism. We can make the assumption that if the thyroid gland is not working, and I just give the T4, it’s going to convert to T3. That doesn’t happen; we can measure what it converts into: T3 and free T3. Or reverse T3.
In the allopathic world, they typically don’t measure those things. What you don’t see, you can’t manage. If you don’t measure it, you can’t manage it. If you don’t see it, the problem doesn’t exist. When we take a broader look at the panels, we can see that model. In a lot of patients that are taking T4-only medication, their conversion of T4 to T3 is not very good. That’s probably why they’re still symptomatic. They’re taking more T4 than they probably need, which is impacting the conversion factor.
It also misses out on one other key piece: the assumption is that thyroid physiology is regulated by just how much thyroid hormone the gland makes. That’s not true. All the cells and tissues of your body have the ability to regulate how much thyroid hormone gets into the cell and how much T3 gets to the receptors. Cells have individual control. The analogy I typically use is- Do you have kids?
Dr. Eric O:
I have two daughters.
Dr. Eric B:
Has there ever been a time where you told them to go to their room, clean it up, and they didn’t do it?
Dr. Eric O:
Dr. Eric B:
Just because we put T4 into the bloodstream doesn’t mean that those cells and tissues are going to convert it into T3, which will stimulate the metabolism and upregulate the physiology.
There is a challenge in that model that just assumes that that was going to happen. In functional medicine, I think we are aware that it doesn’t happen. Matter of fact, when you start to look at the panels, the more T4 you start to give somebody, and this happens sometimes in that allopathic model. When someone says, “I’m still tired. I still don’t feel good,” and maybe their TSH is 2, a physician might say, “Let’s drive it lower. I’ll give you more, and that must make it work.” If you look at a fuller panel and look at the T4, T3, and free T3, and maybe the reverse T3, you will see that as T4 goes up, there is a point where T3 conversion often goes down. That’s a big reason why a lot of people struggle with chronic hypothyroid symptoms, even though their TSH is either normal or maybe on the low end of the normal range or even lab low.
Dr. Eric O:
Does it all come down to addressing that cell danger response? I’m sure you’ve heard and learned that about 60% of that conversion takes place in the liver. Some of it takes place in the gut. There are other factors. Do these all tie into the cell danger response? Would you say it’s separate, where people need to do other things to optimize their liver health, gut health, adrenal health, but at the same time, also look into stressors that relate to the cell danger response?
Dr. Eric B:
I think the first part of it is some of the things we were taught about where T3 was made. The literature today is showing that those things aren’t correct. I was taught the same thing: 60% of the T3 was made in the liver by deiodinase 1. That doesn’t appear to be true in the current literature.
What it shows is that on any given day, the average person is generating about 30mcg of T3. About 5mcg, maybe 10, depending on the individual person, is coming from the thyroid gland. Another 5mcg, probably coming from the liver. Another 5mcg coming from the kidneys. The rest of the T3 is coming from the peripheral tissues that can convert T4 to T3. The vast majority of T3 that is made in the body is not deiodinase-1 driven at the liver; it’s by deiodinase-2 conversion in all the tissues that have deiodinase-2. The cell brings T4 into the cell. It has this enzyme called deiodinase-2 that converts T4 to T3. That T3 goes to the receptors and gets used. It pops back off the receptors and into the bloodstream and contributes to the circulating level of T3 that we see on a lab report.
I think that we have to keep that in mind. Some of this stuff that we learned isn’t actually correct, based on the most current science. Do I think it’s important that we address the cell danger response? I think it’s critical. In my opinion, based on everything I’ve seen and read over the years, we assume that it’s just about how much T4 to T3 is in the bloodstream. Really, the individual cells and tissues have the ability to control what happens at that cell at that tissue.
If I am a cell in low stress mode, I’m in manufacturing mode. I want to bring glucose, thyroid hormone, as much nutrition into that cell so I can make peptides into proteins. I can make hormones, generate hair, generate skin, burn tons of energy, feel and function awesome. Manufacturing mode. I need lots of T3 active inside the cell to do that. That high concentration of T3 also helps to contribute to turning off the immune inflammatory process.
If I’m a cell perceiving danger or a threat, whether it’s an organism, a toxin, hypoxia, whatever it is, what Naviaux and other people who talk about different aspects of the danger response within the cell, what a cell is typically going to do when it senses danger, is slow down the manufacturing process and ramp up the cell defense.
One of the mechanisms that it uses to regulate almost every step of the cell danger response is the amount of T3 in the cell. Cells under stress, cells in danger, cells that are hypoxic are going to decrease the conversion of T4 to T3 inside the cell.
It sounds like it’s a bad thing. It will slow down the metabolism. Actually, it’s a protective response. We are going to see that if somebody has got excessive cell stress going on, the thing that’s causing that toreduce conversion of T4 to T3 isn’t oftentimes an inability to convert T4 to T3; it’s not reverse T3 blocking receptors, but it’s the cell defense mechanisms in place that are saying, “We are going to downregulate the metabolism.” If you want to get into why that might be important, we can get into it.
For a simple standpoint, for the listener, think about your cells and tissues just like people. If I’m in low stress mode, I’m eating, sleeping, having sex, pooping, doing all these great things. If I’m perceiving danger, you can make me the best meal in the world, but I’m not eating it or digesting it well. If I’m fighting for my life, I’m not going to nap or have sex. I will be in defense mode.Our cells are like us.
Dr. Eric O:
When you say “stressor,” some people might think of emotional stressors, but you mentioned hypoxia. I’m sure there might be some people wondering what that is. “I’m probably not dealing with hypoxia.” How common is hypoxia? Can you talk more about that? Iknow on other episodes and in your book, you talk about things like mouth breathing, which a lot of people do.
Dr. Eric B:
A cell runs most efficiently when we have oxygen. We have these little engines inside the cells that are called mitochondria. The mitochondria can burn fuel, food energy, glucose, breakdown proteins into energy, or burn fats. Essentially, we take food energy, and we convert that food energy into cellular energy. We all learned about the mitochondria in 7th grade science class. We learned about the Krebs cycle, which nobody loved, because you had to memorize this thing. What that thing is doing is taking a glucose molecule and turning that thing into 36 ATP, which is your energy currency. We can use that ATP to do a whole bunch of chemistry reactions in the cell that make us feel and function good.
Thyroid hormone plays a critical role in that. But to run those mitochondrion efficiently, you need oxygen. Oxygen is a key piece. If somebody has decreased oxygen getting into a cell, the cell now becomes more anaerobic, without oxygen. It runs more in an anaerobic state, which essentially turns down the mitochondrial function. We become less efficient at getting cellular energy from our food.
If a cell is in a low oxygen state, the mitochondria downregulate. We won’t make as much energy. What does that feel like? We may not poop as well. We may be more tired or fatigued. We may feel more dehydrated. We may feel chronic thirst. There are a whole bunch of things that we may experience: more pain, more muscle tension and spasms as a result.
Getting oxygen to the cells becomes critically important. There are a number of things that can inhibit getting oxygen to the cells. One of the most common things that happens is people don’t breathe well. “I breathe a lot. Doesn’t that mean I have alot of oxygen in my system?” It’s not that simple. When we breathe out, we blow off carbon dioxide, and we bring in oxygen. Everyone thinks, “As long as I breathe in a lot of oxygen, I should have enough oxygen.”
The same thing that we were talking about with T4. It’s not important how much oxygen is in the bloodstream as it is how much oxygen gets to the tissue. If I’m a red blood cell, I’m grabbing the oxygen that is coming in from the lungs, what you just breathed in. Now I’m going around the body and blood, and I will give up oxygen to the tissues, so they can run and function optimally.
What allows that red blood cell to give up the oxygen? It won’t just give it up. The only reason that red blood cells give up oxygen is there is more of what we call carbon dioxide in the bloodstream. If there is less carbon dioxide, that red blood cell doesn’t want to give up the oxygen. It likes the oxygen, so it won’t give it up.
If someone is mouth breathing a lot, they are oftentimes blowing off too much carbon dioxide, which means there is less carbon dioxide in the body, the bloodstream. They are breathing in plenty of oxygen. If you look at their oxygen on a medical test, it may show 99% oxygen saturated. That sounds great because the red cells are saturated with oxygen. That oxygen is only helpful when the red blood cells give it up. They will only give it up if there is more carbon dioxide.
Someone who is mouth breathing a lot has a tendency to be more hypoxic. Someone who is mouth breathing especially at night is going to be more hypoxic. Just mouth breathing a lot through the day, blowing off too much carbon dioxide or mouth breathing at night is going to contribute to a downregulation of your cell physiology and an upregulation of the immune inflammatory response. That becomes a huge issue.
How big of a deal is it? Diagnosis of sleep apnea is exploding. Everybody is wearing these fighter pilot masks to go to sleep. If you are wearing one of those things, if you have cavities or gum disease or disrupted sleep, especially if you go to bed with some stuffiness or congestion, there is a good chance you’re opening your mouth at night to mouth breathe, which will create hypoxia.
The other driver of hypoxia potentially is if we have carbon dioxide in the bloodstream, that carbon dioxide plays an important role. If there is a lot of acidosis in the body, the body can pull carbon dioxide out of the bloodstream to deal with the acidity in the body. That, too, can drop carbon dioxide and trigger this hypoxic state. Without the carbon dioxide, red blood cells don’t give up oxygen.
Dr. Eric O:
If someone has normal oxygen saturation, that doesn’t rule out hypoxia. If someone does a comprehensive metabolic panel and has low carbon dioxide, they probably have hypoxia. If someone has normal carbon dioxide levels, I assume that doesn’t rule out hypoxia.
Dr. Eric B:
No, it doesn’t rule it out. There could be other factors that prevent transfer. What is normal oxygen saturation? Someone might say 99% is normal oxygen saturation. Anything under let’s say 93% is problematic.
I don’t think 99% oxygen saturation is normal. If you have your monitor on your finger, and it reads 99%, I don’t think that’s healthy. I think that’s a good indication you might not be doing a great job of transferring oxygen to the tissue.
I like to see my patients somewhere in 95-96% because that tells me that they are probably transferring oxygen to the tissues a bit better. Someone who had 99%, they feel and function awesome, everything looks great. Hey, it’s probably fine. If I have someone with chronic health issues, tiredness, fatigue, weight gain, under conversion of T4 to T3, and they have 99% oxygen saturation, to me, it’s a problem.
As far as the carbon dioxide, oftentimes I assume that if I look at the blood panel, and carbon dioxide is within the reference range, and I typically look at a reference range of 25-28 based on some of the literature as an appropriate carbon dioxide range, the lab reference range could be much lower, down to 20. I don’t think that’s appropriate. I’ll also do calculations with sodium, potassium, carbon dioxide to see from a calculation standpoint if it looks like we have an imbalance.
Dr. Eric O:
Anemia can also be a factor, which I’m sure is one of the reasons why you run a CBC in everybody.
Dr. Eric B:
Absolutely. If someone has an anemia pattern, they have less red blood cells typically to carry oxygen around the body. That can be a potential problem. The broader the panel we can run, the more important.
Anemia in itself is another can of worms. What we tell most people is they have iron deficiency. The vast majority of people don’t have iron deficiency anemia. The vast majority of people likely have anemia of chronic inflammation. Many times, we are treating that inappropriately. We assume that if iron is low and ferritin is toward the lower end, that’s iron deficiency. I don’t think it is in a lot of cases.
Dr. Eric O:
Talking more about blood tests. You mentioned reverse T3 earlier. Is that something you recommend across the board? Would you say everybody should get reverse T3?
I’ll say this:With hyperthyroidism, I stop measuring reverse T3 because everyone has elevated reverse T3. It doesn’t add value in my opinion. Again, feel free to give your opinion with that. As far as those with low thyroid or subclinical hypothyroidism, is it something you recommend for everyone?
Dr. Eric B:
I like looking at it for a couple reasons, but not the reason the vast majority of functional medicine practitioners like to look at it. I said this early on, too, because it is what I was taught. T4 is this primary hormone that is made by the thyroid gland. Then it gets to the cell, and the cell has these enzymes, deiodinase, that can either activate T4 to T3, or deactivate T4 to reverse T3. That’s Cell-driven. The cell gets to determine if I am letting T4 in to convert to T3, or if I am keeping my metabolism lower and deactivating T4 to reverse T3.
When I’m looking at the thyroid, I never look at a thyroid panel by itself. A thyroid panel without context of someone’s signs and symptoms doesn’t really tell me much. I am going to look at a thyroid panel with at least one tissue marker, but at the beginning, I look at a comprehensive panel. I’m sure you do, too.
What is the significance of it? There are some in our space who say the reason people have tiredness, fatigue when they are on T4 medication is that reverse T3. T4 gets converted to reverse T3 inside the cell. That reverse T3 goes to the nucleus and binds to receptors, the nucleus, maybe the mitochondria, and blocks T3 action.
It sounds good. People say it’s a mirror image of T3. A) It’s not a mirror image of T3. B) I haven’t seen much in the way of any true scientific data that says that reverse T3 blocks T3 from functioning at any level of significance. I just haven’t seen it. If someone says they have, I’m open to it. I like the idea that it does it, but I don’t think that’s what happens.
When I look at reverse T3, what I’m looking to see is a couple things. If I have a patient who is not on any medication, but they have signs and symptoms of hypothyroidism, and their TSH is normal, their free T4 is normal, whichever one somebody is looking at, I look at both. I want to see what their cells and tissues favor. Are they favoring the conversion of T4 to T3? Are they favoring the conversion of T4 to reverse T3?
If reverse T3 is higher, and T3 is lower, then we can start to make some assumptions that maybe the reason someone has hypothyroid signs and symptoms is because the cells aren’t converting T4 to T3 the way we want them to. They are deactivating it. Then I know that I need to look for what is driving that under conversion or over deactivation.
What does the rest of my panel tell me? Are there markers of inflammation here drivingthat process? What is the person’s story telling? Are there traumas, emotional stress, hypoxia, injuries, dysbiosis, faction, sleep disruption? I start looking for the reason why.
I just don’t think that reverse T3 is the problem. I think the reverse T3 is an indication that there is some cell defense potentially going on. Let’s say there is a normal lab TSH, and reverse T3 is low. Some people think reverse T3 should be nonexistent, and should be really low. I don’t think that’s the case either. If T4 is low, and reverse T3 is low, and T3 is low, I know that we have a person who is not making sufficient thyroid hormone. The gland is not working. Therefore, there is not enough T4 to convert to T3. There is not enough T4 to convert to reverse T3. Regardless of what my antibodies are at that moment, we have a gland problem going on. There is not enough hormone being generated.
I will go back to my labs, health history, health timeline, and say there are inflammatory mechanisms going on here that would cause thyroid hormone to be downregulated. If I have inflammation, inflammation is oftentimes going to increase conversion of T4 to T3, the hypothalamus, the pituitary early on, and can suppress TSH, even though I might need some more thyroid hormone in the system. I’ll use it from that perspective.
The third reason I want to take a look at reverse T3 is if I have somebody who is on thyroid medication, T4, and their doctor is happy they are getting enough T4 because their TSH is normal, especially if they have all the symptoms, we know T4 can easily lower TSH levels pretty quickly. The receptors in the brain are tenfold more sensitive than most of the peripheral tissues. You can normalize the brain much faster. If you have this inflammatory response going on, that can normalize it faster, too.
At the cell level, what’s happening? If they have high reverse T3, low T3, then I am probably getting an indication we still have this inflammatory mechanism going on. We need to identify what that is. They also may be taking more thyroid hormone than they need, especially if they’re struggling with some hyperthyroid symptoms: brain fog, insomnia, irritability, things like that. That’s why we might work with them to say the dose is too strong.
Again, I haven’t seen enough clear evidence that says reverse T3 blocks anything from happening. If you wanted to block anything, we would blame deiodinase-3, which is the enzyme that deactivates it. That’s how I use it.
I think the better way to assess what’s going on at the cell level is not just looking at reverse T3 because there can be things like reduced liver function that may cause reverse T3 levels to rise. If we just look at the free T3 to free T4 ratio, if that ratio is low, the cells aren’t converting T4 to T3 appropriately. There is probably some type of cell stress, cell danger mechanism going on.
If the free T3 to free T4 ratio is elevated, then we probably have a state where the cells are starving for thyroid hormone. There is not enough T4 in the system. They need to make more T3, and they are willing to do that. That’s where you will see the free T3 to free T4 ratio is high, above what we might call the optimal range of 0.31-0.34.
In a situation where reverse T3 is elevated, maybe. Really, what I want to know is is it elevated because I have too much T4 in the system? Or is it elevated if I have some other inflammatory response going on? That is where we can look at the free T3 to free T4 ratio along with the reverse T3. If it was on its own, too much medication, we should be able to back that down. Then we should be able to see a better conversion occur. If there are inflammatory mechanisms going on, it doesn’t matter if we can back it down. We won’t see as good a conversion too early too soon if we don’t identify what’s creating that inflammatory mechanism and the downregulation of conversion.
Dr. Eric O:
I have a few follow-up questions.You don’t want reverse T3 too high, but as you said, you don’t want it nonexistent or too low. If you could say what your healthy or optimal range of reverse T3 would be?
Also, I think you mentioned the optimal range of free T3 to free T4 ratio, but if you could say that again.
Also, you mentioned you test the total T4 as well as the free T4. I imagine you do the same for T3, the total and free T3. The optimal ranges for those. Why do you test both total and free hormones?
Dr. Eric B:
All right, the first question was what do I use for the range? It’s important to know there is the lab reference range, and there is what some people call the functional range. Where do we get these ranges at? It seems like a lot of practitioners have their own range. Some people may say it should be less than 9 or 10 or whatever.
For me, when I am looking at the functional range, I am more of a research geek. I am looking at stuff and saying, “Where are we finding numbers here?” I have stayed somewhere in that 9-18 range.
Every lab value has to have context. If you said to me, “Eric, my reverse T3 is 15. That’s optimal, right?” I don’t know. What’s your TSH, total T4, free T4, total T3, free T3? What are the ratios of these? I don’t know if that’s good. Is it good? Well, if your total T4 and free T4 is low, and your T3 is low, but your reverse T3 is 15, that is probably still inappropriate. You don’t have much thyroid hormone, and you’re still favoring the deactivation and not the conversion. Does that make sense?
Dr. Eric O:
Dr. Eric B:
Even though I might use a reference range of 9-18, that is a starting point. I have to interpret the rest of the labs to see is that appropriate? If someone had a reverse T3 of 15 and lower values of T4 and T3, is that important? What do I make of that? I’m also going to look at the rest of the labs. Do I have any markers of tissue hyperthyroidism going on? Do I have elevated lipids, elevated triglycerides, elevated BLDL? Do I have glucose resistance going on? If I have tissue markers of hypothyroidism going on, and I have a reverse T3 at 15, and I have lower levels of T4 and T3, I think that reverse T3, regardless of whether it’s in a functional range, is still potentially problematic.
Dr. Eric O:
Makes a lot of sense.
Dr. Eric B:
That’s sometimes the challenge, even in functional medicine. We give allopathic medicine a hard time for saying, “They just look at an H or an L outside a lab reference range. We have a better reference range.” Just because our value is in the reference range doesn’t mean it’s appropriate. A lab value could be totally within a normal, optimal range and be inappropriate. It could also be appropriate.
If you feel and function good, and you don’t have much in the way of inflammation, and your TSH is 1.2, someone might say that’s the optimal. Okay. But if you have inflammation, are tired and fatigued, have all the signs and symptoms, and your TSH is 1.2, is that appropriate? Or is the inflammation suppressing TSH, and that’s causing my T4 and T3 to be low? TSH is normal at 1.2, but my T4 and T3 is low, and reverse T3 is low. We have to interpret it. We can’t just say because it’s in an optimal range, it’s okay. Does that make sense?
Dr. Eric O:
Yes, it does. Thank you.
Dr. Eric B:
As far as the ratio of free T3 to free T4, this is a little tricky because the units of free T3 and free T4 are different when you get them on your lab report. I think you can go to Dr. Weatherby’s website. Do you know what it is?
Dr. Eric O:
I can’t think of it.
Dr. Eric B:
He has a website with calculators. You can go to his calculator and put in right off your lab report a calculation, and it will tell you if it’s in the ratio range.
What I do is convert everything to similar units, picomoles/liter, and divide free T3 by free T4. If you look at your lab report, you can say, “How do I convert picograms/ml to picomoles/l?” The calculator will convert it for you. If you convert things to picomoles/ml, you divide free T3 by free T4. Based on the literature, the optimal ratio looks like 0.31:0.34.
If that ratio is under 0.31, the cells and tissues aren’t doing a great job of converting T4 to T3. That’s where we have to find out what’s causing that reduced conversion. Is it low calories? Is it hypoxia? Is it organisms? Is it toxins? Is it emotional stress? Is it all of those things, a combination of those things? Which oftentimes it is.
If the ratio is above 0.34, then we might have a situation where even though TSH may be normal, there is still not enough T4 in the system to convert to T3. If there is no cell stress response going on, and they’re in a homeostatic state, they will take as much of that T4 and convert it to T3 as quickly as possible. A certain level of T3 is a biologic priority.
Dr. Eric O:
Gettingback to the thyroid hormone, you always test total and free hormones. Again, I have a habit of mainly testing the free hormone. What is the significance? I know you talked in your book about carrier proteins and binding globulins. If there is a discrepancy with the free hormone and the total, maybe we are looking at a problem with the carrier proteins.
Dr. Eric B:
Yeah. For the listener, in the body, we make hormones, but we don’t want those hormones all being free. They would get either deactivated, metabolized, or utilized right away, and we wouldn’t want that. Hormones are made—sex hormones, thyroid hormones, other hormones, cortisol—and they are then bound to what we call a transport molecule or protein, a binding globulin. It’s like an Uber, and it transports it around the body. When there is a cell or tissue type that needs some of that hormone, that hormone becomes free of the Uber or free of the binding globulin. Now, it’s able to get into a cell or tissue.
Why might it be important to look at both total and free, even though a lot of physicians have gone to just looking at free? “Free hormone is the only thing that matters, so we’ll just take a look at free.” But it does make a difference. If I have low free hormone because I’m not making much thyroid hormone, then I have to figure out why I’m not making as much. If I have low free hormone, but I have plenty of total, then I have to ask, why is it getting out of the Uber? Why is it not coming off a binding globulin? Is it a pH issue, a hypoxia issue? Is some other hormone I’m taking jacking up the binding globulins? We need to find that answer.
If you put more hormones into a system, the tendency is for the binding globulins to go up to manage it. Something is resulting in less hormones becoming free, and we need to figure that piece out. I want to look at both. If someone has low free, I want to know if it’s because they just aren’t making it, they have low total, or if it’s a binding globulin issue. Then I want to address that appropriately.
If they have high free hormones, I also want to know if that hormone is elevated because they don’t have much. They’re not generating much, so there is not much on the binding globulin, to where maybe something is suppressing the binding globulin and causing a lot of excessive free hormone that is either being used or metabolized too quickly.
Dr. Eric O:
Thanks for that thorough explanation. I want to circle back to the cell danger response before we wrap this up. When it comes to inflammation, I think you look at more than just CRP and sedimentation rate. You look at seven inflammatory markers?
Dr. Eric B:
When we look at labs, there are a bunch of things we can look at from an inflammatory standpoint that would be on a general blood chemistry panel. CRP, there is high sensitivity CRP, regular CRP. Homocysteine could be considered a molecule of oxidative stress. We could look at fibrinogen as a marker of oxidative stress. We could look at elevated ferritin levels.
That is another can of worms. The vast majority of people believe that ferritin levels should be somewhere in the 60-80-90 range. I think that’s absolutely insane. I start getting concerned when I see it over 25, but definitely if you have a ferritin level of 40 or 50, that is an indication of potential inflammation and oxidative stress. Again, needs to be interpreted.
For instance, “when I have low ferritin, I’m anemic.” Hold on. If your serum iron is low, and your ferritin is low, and you’re anemic, maybe you do have an iron deficiency. But we can run a soluble transferrin receptor test to find out if the cells are starving for iron or not. That’s another conversation.
I don’t think the vast majority of people are. But ferritin could be a marker of inflammation. We could look at bilirubin. Again, we have to take into consideration if it’s low because they’re anemic, or because they are using bilirubin as an antioxidant because there is inflammation and oxidative stress going on.
We can look at elevations of uric acid. We can look at alkaline phosphatase on a general chemistry panel. We can also look at elevations of 125 Vitamin D and low 25 Vitamin D. How many people today are being blasted with Vitamin D probably inappropriately because they have a low 25 Vitamin D when that’s not really the activated form? The activated form is the 125. If they have an elevated 125 Vitamin D, that’s another good indication that they probably have some type of chronic immune inflammatory response going on.
Dr. Eric O:
We’ll need you to come back to talk about the ferritin because that was a surprise to me, that you like to see it at 25 or less, and also talk about the 125 hydroxy. We don’t have time to dive into that.
I don’t know if you’re familiar with Dr. Alan Gaby. He wrote a big nutritional textbook. When going through my master’s, they were talking about how you don’t want to look at 125 hydroxy because it’s frequently elevated due to a compensation related to the parathyroid gland. This was now 10+ years ago that I went through that, so maybe the science has changed.
I know Dr. Lynch is a big advocate of testing for 125 hydroxy vitamin D. There are differences in opinion when it comes to testing for that.
Dr. Eric B:
Think of the traditional role of Vitamin D. 25 Vitamin D and 125 Vitamin D with calcium regulation in the parathyroid gland. We know way more than that now. I’d say real simply, without getting too heavy into it, if we think about Vitamin D this way. There is very little food, except for cold water fish, that has any high level of Vitamin D. Right? Where do we get most of our Vitamin D? Sun exposure.
Cold water fish have a decent amount of it. If you believe that there is intelligence in the universe, that might make sense. In the areas where we have plenty of sunshine most of the year, there is very little food that has any appreciable amount of Vitamin D in it. Most of the Vitamin D comes from sun exposure. In areas where there is less sun exposure, there are more cold water fish, where we can consume those things. I don’t think we’re designed to be taking copious amounts of Vitamin D as a supplement orally. I know it’s a $4 billion industry, but it’s just my opinion.
The other thing we don’t know too much about Vitamin D is we only measure one component of it. We don’t measure Vitamin D. We measure 25 Vitamin D. We don’t measure what happens to 25 Vitamin D. Is it being deactivated from 24 to 25? Is it going into the fat cells? That’s another discussion of how that works and what I think is going on. Is it being over converted to 125 Vitamin D? When you do have elevated 125 Vitamin D, is there an inhibitory suppression of Vitamin D to 25 Vitamin D conversion at the liver? Some of the literature seems to show that’s the case. It’s a feedback loop that turns it down.
I think we’ve taken Vitamin D, one number we can measure pretty easily, and decided that if it’s low, we just give more, more, more. Even in people that were giving 5,000-10,000 IUs per day orally, they still wind up with low Vitamin D. I don’t think we assess it right. I don’t think we look at the chemistry of what’s going on. I would make an argument that early on, it may make someone feel better, but long-term, it’s potentially problematic.
Dr. Eric O:
Definitely going to dive more into the research and have more of a conversation on this in the future.
I can’t have you leave without talking about some other things that you mention in the book about addressing that cell danger response. Obviously, a lot of it is the foundations. If you could spend the next few minutes talking about what else people can do. You mentioned hypoxia and breathing better. People know about diet, but you haven’t mentioned anything about diet. I know you’re not a fan of one specific diet;it’s all about eating whole, healthy foods. I’ll let you take over and talk more about that.
Dr. Eric B:
There is foundational principles. Kelly and I talk about them in the book. I had a couple colleagues who read the book and asked about supplement protocols. They’re not in there because I don’t have a protocol for everybody. I think that’s problematic. Even though it’s not sexy, the things that create health issues are these foundational pieces.
For the vast majority of us, better nutrition would go a long way to making us healthier, right? Whole food-based diet. One of the problems we’ve had in this industry is that we’ve circled the wagons and shot in. You and I both know that if you’re eating one diet, and you’re not feeling well, and you change to another healthy, whole-food diet, you will probably feel differently. Is there a benefit to doing a carnivore diet for a short period of time? Sure, you will change your gut biome, it will create some change in symptoms. Is a vegan or vegetarian diet potentially going to create a change in signs and symptoms? Probably. I don’t think we should be arguing about which whole food diet is the holy grail.
What we should be doing is saying, primarily, 80+% of the time, try to concentrate what you eat on healthy, whole, in season if possible, foods. As close to the way it came out of nature as possible. Limit the amount of processed food. If most people did that, they would probably start to improve their health and wellbeing. I see it every day as we start to make those changes in clients.
I think respiration is critically important. This is from a guy who has a deviated septum and should have had surgery a long time ago. Breathing is critically important. We are designed to do most of the breathwork through our nose. A lot of us, because of chronic inflammation and other factors, we do too much mouth breathing. Excessive mouth breathing creates a hypoxic state. Just changing your breathing can change your health.
Going back to food. How you eat is becoming important. Not only should you eat healthy food, but you have to take the time to chew it and help digest it well. You see a lot of people who are eating on the run. Eating healthy food, but not sitting down to eat it, not putting themselves in a situation where they can digest it well, so they still have problems.
Sleep is critically important as well. I’m guilty of this. I went for years wearing a badge of honor that four hours of sleep is all I need. I’ll sleep when I’m dead. What it does is creates-In me, it created chronic inflammation, Hashimoto’s, insulin resistance, and all kinds of stuff because four hours of sleep + running businesses+ training + everything else I was doing broke me down. That was part of my cell stress response.
We hinted about emotional stress. What goes on between the six inches of your ears makes a huge difference as to if you get well. You will be stressed or not stressed. We all have stress in our life, and you will never escape it, whether it’s physical, chemical, emotional, microbial. What we say within our mind consciously or subconsciously plays a huge role in how we heal and recover. Far too many people take in too much negative or focus on the problem and not the solution. I think that drives a lot of angst in the system, a lot of stress response in the system, so that’s hugely important.
Diet, nutrition, sleep. We talked about respiration. Physical activity and exercise. That’s critically important, too. Some people don’t like to do it, but you have to move your body. You have to do some physical strength training. You have to do some level of cardiovascular training. Slow fitness works really well for a lot of people. You want some, not excessive.If you do a lot of excessive training, you have to balance that recovery time. If you’re not, that will be a problem.
Why exercise? I have a healthy lifestyle. Well, the healthy lifestyle is if you train and recover, if you train and train and train, and don’t allow for recovery, you will have chronic health issues. I am a perfect example of that. I drove myself into doing that.
We talked about emotional and microbes. The organisms are everywhere. If they overgrow in us, then that can potentially be a problem. Then we have our environment with the toxins and things we are exposed to every day. You will never eliminate those things completely. The best we can do to have a low tox life, the less stress on the system. I think I got most of them.
Dr. Eric O:
Yeah, I think you did. Most of the foundations, if not all. Where can people find out more about you, Dr. Eric? Feel free to share your website and remind them of your book and anything else.
Dr. Eric B:
The book is called The Thyroid Debacle. It’s available wherever you get your books.
I have a podcast called The Thyroid Answers Podcast. It’s available on almost all platforms. You’ll be a guest sometime in the future. We have an interview scheduled.
I was never much of a social media person, but I got convinced to do some Instagram posts. That is primarily where I put out some content and information.
One of the things I like to do is my Thyroid Thursdays, where I am trying to educate. I know sometimes, people go on Instagram and want the three simple tips. What I am trying to do with those Thyroid Thursdays is have someone understand the free T3 to free T4 ratio. Why is that important? Why is it maybe less valid if you’re taking T3, and you can’t really use that ratio necessarily to indicate what’s going on? I want to educate people.
At the end of the day, getting well is not based on how many supplements you can take. I find far too many people are oversupplementing. Getting well and staying well is about understanding a little bit more about your overall chemistry and doing a really good job raising your level of health in all these things that we call fitness factors (your diet, nutrition, exercise, mindset, habits, behaviors). Then you will be healthy. That’s not the stuff that’s sexy.
Dr. Eric O:
Well said. It’s always a pleasure chatting with a fellow Dr. Eric. Thanks for being here and talking about thyroid physiology and blood tests. We will definitely have to have you on again in the future, and I look forward to being on your podcast. Thank you so much, Dr. Eric.
Dr. Eric B:
Thanks for having me. I appreciate it.