Episode #173: The Thyroid Debacle with Dr. Eric Balcavage, DC and Dr. Kelly Halderman, DCN

Welcome to Better Health Guy Blogcasts Empowering your better health and now here's Scott, your Better Health Guy. The content of this show is for informational purposes only and is not intended to diagnose, treat or cure any illness or medical condition. Nothing in today's discussion is meant to serve as medical advice or as information to facilitate self treatment. As always, please discuss any potential health related decisions with your own personal medical authority.

Hello everyone and welcome to episode number 173 of the Better Health Guy Blogcast series. Today's guests are Dr. Eric Balkavic and Dr. Kelly Halderman and the topic of the show is the thyroid debacle. Dr. Eric Balkavich 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. He is a Certified Nutrition Specialist, a Certified Functional Medicine Practitioner, Board Certified in Integrative Medicine. Along with being a licensed Chiropractor, he is the co host of the Thyroid Answers Podcast which focuses on answering the pressing questions those suffering with chronic hypothyroid symptoms can't get answered elsewhere. You can find his educational Thyroid Thursday videos on Vimeo and YouTube. Dr. Balkavich has made it his mission to change the way medicine looks at hypothyroidism. Dr. Kelly Halderman completed a family practice medicine internship with the University of Minnesota. She holds a naturopathic medical degree from Kingdom College of Natural Health. She holds certification in Methyl Genetic Nutrition by the Nutrigenetic Research Institute and certification from the American Functional Neurology Institute in Functional Neurology and Neurofeedback. She is an active member of the American Academy of Anti Aging Medicine, President and founder of the American association of Nutraceutical Formulators, as well as a member of the Physicians Committee for responsible medicine. Dr. Kelly is also Board Certified in Clinical Nutrition by the Clinical Nutrition Certification Board. She coined the term Phase 2.5 detoxification which involves properly restoring biophysiology. She serves as WIO Foundation's Chief Health Officer, the global leader in water research and its application to living systems. Dr. Eric and Dr. Kelly RV Co authors of the book the Thyroid Debacle, which addresses the problems with current allopathic and functional medicine approaches to hypothyroidism as well as the solutions to restoring thyroid physiology. And now my interview with Dr. Eric Balkavich and Dr. Kelly Halderman.

I am super excited today to have Dr. Eric and Dr. Kelly on the show to talk about the thyroid in a way that most of us probably have not heard before. I appreciate both of them being here today. Dr. Eric, what was your personal journey that led you to becoming so passionate about thyroid physiology?

Well, initially, I had no interest in physiology, to be honest. But I had a family member. You know, my brother had one day had a conversation with me about what was happening with his wife, and she was gonna. She had fibroids, so they were gonna do a hysterectomy. She had hypothyroidism. She had iron deficiencies, so they're gonna take out her hysterectomy, thyroid meds and iron, that was gonna be the solution. And I said, that's not what I do. I'm a chiropractor. Why are you reaching out to me? And he's like, because you're going to fix it. And I was like, oh, okay. When your big brother kind of tells you this is what you're going to do, you kind of do. And he's done this to me multiple times, by the way, just as a side note. And so I started digging in and getting back to my roots in blood chemistry. And then as I'm helping her, I'm having conversations with my chiropractic patients. And I was floored by how many people were on thyroid medication and how most of them didn't feel well. And so that kind of fueled the fire. I did a lot of work with the TS, Karazia and Apex and all that early education, did my functional medicine training. And then I just thought something was missing from the big picture. And that really had me just digging and digging into the literature. And eventually, a friend of mine, Dr. Ben lynch, sent me a paper on the cell danger response, and that was my aha moment. Like, hey, we've got to change the conversation here about what's going on.

Nice. Dr. Kelly, I know some of our listeners have been familiar with your journey from our prior podcast, but why don't you tell us a little about your personal health journey, your diagnosis with Ms. And Lyme, and how that was the catalyst for you to create a larger toolbox for yourself and for your patients. What was it that drove you to shift to the new paradigm?

Right. So just like you explained, I was practicing allopathic medicine. You know, really was very happy in my practice. Although I was noticing, because I was a young physician, I was noticing that we weren't really getting to the root cause of diseases, but we weren't Taught to get through the root cause we were told to. Taught to address, you know, with medications and lifestyle innovations. Epigenetics, which we're going to get into, were definitely not something that we had grand rounds about.

So.

So when it came to my own health, when I started to have these just very strange symptoms, neurological symptoms, I thought, I am in the best place in the world. I am. You know, I have a white coat on. I'm going to get the best care ever. So I got shipped off to the Mayo Clinic, best neurologist around, and I was handed a death sentence with not a lot of hope. The medications to treat Ms. For me at that point, that was something where that wasn't sufficient. And so I was left with a lot of medical educational debt, but no tools in my toolkit that could actually help me. And so I had to step away and go get a naturopathic medical degree and learn about detoxification and other things that are very, very important right now foundationally to me. And, and I use those tools to help really reverse my health. And meeting Dr. Eric, one of the diagnoses that I had was Hashimoto's along the way, like a lot of the people struggling with Lyme and mold, and those were part of my root causes and the Hashimoto's, you know, I really felt like in medical school and in training and you know, doing even residency surrounding with really great endocrinologists, I'm like, this just, this just doesn't make sense. You guys, like, why are these people we're putting on medication? Why are they still not feeling well? Like, what are we missing here? But, you know, you just don't really bring up those kind of things until you are the patient. And I was treated by a wonderful Lyme literate doctor, and she put me on a bit of thyroid hormone replacement, but I did not feel better. That actually made me feel good for about two weeks. And Eric will go into that mechanism. But then I really crashed. And it wasn't until I started really digging into Dr. Eric. I became like his number one fan. I was listening to everything because everything he said made sense. The first time I met him, it was like meeting like, you know, your idol. I was like, can I get your autograph? Because he's, he's just someone who I respect so much because he digs into this literature. You know, on average, a published paper gets read by seven people in the medical literature. And Eric's one of those seven people, I'll guarantee you that is that he went in and he dug in to help us all understand better, give us a model to get people better. And I applied what Dr. Eric told me to do, basically through his teachings. And I call myself recovered. I mean, I'm constantly doing things to help my health. But that's why I wanted to come help with. With writing this thyroid debacle, because I have the perspective of sitting in the chair of the prescriber. I had to use the guidelines with the people in my care. And your hands are tied when you have those guidelines. So that's really my story of the thyroid journey.

So since you want his autograph, maybe you can get him to sign a copy of the book, the Thyroid Debacle. Maybe.

We'll see.

So let's talk then about what are some of the symptoms that would clue you in as practitioners to consider exploration of a patient's thyroid physiology?

Yeah, so, absolutely. Symptoms are very, very important because as we will talk about, you can have completely normal labs, but in the labs, they look good, but there's not enough thyroid hormone inside the cell. So what are we looking for? Chronic fatigue, weight gain, hair thinning, dry skin, constipation, and reduced libido. And I checked off all those boxes, even when I went on thyroid replacement.

So let's talk then about why is it that most people that talk about thyroid issues are really focused on the thyroid gland and not thyroid physiology? What happens at a more systemic cellular level? Is the problem always at the thyroid and not producing enough thyroid hormone? Or can it be an issue that really is far away from the thyroid itself? And then why are. Why are those not the same thing?

I think most allopathic physicians are taught that hypothyroidism is a condition where thyroid gland, the thyroid gland doesn't make sufficient T4. So, like, the allopathic mantra in my mind is, as long as there's enough thyroid hormone in the blood, there's enough in that inside the cells. Okay, that. That. That's flag number one, right? Red flag number one. But the problem is, is that, you know, physicians, they may realize that there could be a reduced T3 at those tissues and cells, but they don't have a tool to evaluate it, and they don't have a tool to address it other than medication. So, you know, again, you can have the normal tsh, the normal thyroid gland function, normal levels of thyroid in your blood, but the thyroid hormone in your cells is creating the symptoms. That's what we call cellular hypothyroidism, you know, because most of the production of thyroid Thyroid hormone is by the thyroid gland. But the thyroid hormone is most active inside of your cells. So tissues and cells have the ability they can increase the metabolism converting T4 into T3, or they can deactivate it. And we're going to talk about that. When we talk about the cell danger response, they have the ability, tissue specific, to just deactivate that thyroid hormone again. So it's, it's tissue specific.

I think what, what we see is, is pretty clear that a lot of people start to have signs and symptoms long before a TSH and T4 go out of the reference range. And based on the scientific literature, it's about 90% of the thyroid gland is damaged by the time somebody gets diagnosed. So they've. You've lost about 90% of the function. So that's not the beginning of a disorder any more than cardiovascular disease starts when you have your fatal heart attack. Right. And so what we don't have is great tools for assessing what's going on the cell. From a allopathic standpoint, we don't have guidelines to dig in and address it. Even though there's assumptions like, hey, if your cholesterol is high, that could be a good sign that there's tissue hypothyroidism going on. We just. If the only tool you have is T4 primarily in that model, then the only thing you really need to evaluate and assess is TSH in a free T4. But the. I think for the vast majority of people we see who get told, hey, your TSH is normal, so you're, you eat too much, you don't exercise enough, and you're just depressed. Those are the people that are probably struggling with chronic cellular tissue hypothyroidism as a result of what's happening in individual cells and tissues.

In the book, you go into great detail about a number of the tests that can be explored. But are there a few tests that you find important for evaluating thyroid function? And then are there any tests for the exploration of this more cellular hypothyroid condition that happens as well?

I think when we're looking at thyroid gland function and production, obviously there's. You can do an ultrasound, see as. See if there's thyroiditis. We can do some more. You can do a biopsy to see what's going on there. But just from a standard assessing the thyroid gland, you know, traditionally there's just. TSH is used as a screening test to determine is there too much or too little thyroid hormone production. And then there's what they call a reflex to free T4. If free T4 is within the reference range, then it may be considered subclinical hypo or hyperthyroidism. But those things. I think the assumption is that as long as there's enough production at the gland that it's ultimately going to mean that there's sufficient thyroid hormone getting into the tissues.

That.

But it really doesn't. I mean really what TSH oftentimes is evaluating is what's going on at the hypothalamus in the, in the pituitary and not at the peripheral tissues. And that's not always the case either that they're sufficient. Just because there's sufficient getting there. Things like inflammation can suppress tsh, hiding a systemic thyroid problem, low production, because when there's inflammatory mechanisms going on, there's an increased conversion of T4 to T3 at the hypothalamus specifically to kind of at least early on to make sure that, hey, this is an important thing when we're in danger, right? We need our brain to work, so we, that gets regulated. So I just think when we're thinking about assessing from a medical standpoint, those are kind of the two tools that are looked at. It rarely will I see a medical physician run a T3 or free T3. Rarely will I see a physician run thyroid antibodies. And I think the reason for that is that they pretty much assume that if there's, that the person who, they're, who's got hypothyroidism already has thyroiditis. It's an immune driven problem primarily. So there's no need to run those things. They're not medically necessary to diagnose. But from functional perspective, every test in a thyroid panel that's available is I think important for assessing tissue status. And we have to even go beyond that and look at the rest of the metabolic panel, Blood sugar regulation, cholesterol regulation, renal function. We want to look at what's happening at the other tissues to get verification that we do have a potential tissue hypothyroid situation going on.

So am I understanding correctly that we could have a normal TSH, maybe even a high normal T4? T3 looks good. Everything looks good from a thyroid testing perspective. But we could still be cellularly hypothyroid. Can that occur?

Absolutely. Because the tissues have the ability to self regulate based on what's going on at their level, right at their tissue. If we didn't have that ability to do that, we'd be in trouble. Because if I needed to go for a run And I needed to increase my physiology, increase my metabolism to go run, to get out of danger. I don't want my bowels moving at the same time. I don't want all the tissues upregulating their metabolism at the same time. It could be a disaster. What we have the ability to do is if the, if the GI tract needs to upregulate its metabolism, we can turn it up there and turn it down somewhere else. So we have, in tissues have the individual ability to self regulate to some degree independent of what the thyroid gland is producing and to some degree independent of what's in the bloodstream.

Many of our listeners will be familiar with the cell danger response model from Dr. Bob Naviau. I did a podcast with Dr. Neil Nathan on that as well. So we. Let's talk a little about the overlap between the cell danger response and how you view thyroid physiology. Could we think that maybe a hypothyroid state could be a wise, intelligent, hypometabolic adaptation or a protective state? And then should the focus be on the thyroid or should it be more on the broader triggers of that cell danger response?

Sure. So I am a very big fan of both Dr. Navio and Dr. Nathan. And if your listeners have not listened to your podcast with Dr. Nathan, just, just run and go listen to those. Absolutely. Excellent. So the cell danger response, you did a wonderful job. And you did too, Scott, of really going through this and digging in. But really simply, it's the evolutionary conserved metabolic process that's designed to protect us, ourselves from harm. And it can be triggered by chemical, physical, biological threats. And those threats exceed the cellular capacity for homeostasis. So it's kind of like we get a threat and it's just beyond what we, what we can just kind of shrug off, I guess, in layman's terms. So this paper changed everything for me. This paper changed everything for Dr. Eric because we realize that cells and tissues respond differently to homeostasis versus allostasis, like that load that's pushing down. So what we were realizing with thyroid is that the dysfunction is more likely better termed an adaptation. Right, an adaptation as part of a cell danger response. And I think of it as this. It's laying on a beach versus running from a tiger. Wouldn't you expect your body, just like Dr. Eric said, wouldn't you expect your body to act differently? I mean, we hope so. Right? Just like Eric said, we hope your body's going to act differently. And so when we think of, okay, we have to, you know, it's almost like when we have to like kill the bug, kill the bug without thinking about the terrain. It's like we have to step back. Look at why. I mean, the root cause. I mean, why is our body doing this? What set off the cell danger response? Because that's how you're going to get your health back. You're going to get it one step at a time, pulling off the allostatic load. And we talk about in the book, it's usually not one thing, one magical, oh, I killed all the Lyme and now I'm good. Like gut function, brain function, I mean, all of, all of our respiratory function and all of that, which we call fitness factors. So again, it's that adaptation which is not a dysfunction. Because what I was taught is allopathic medicine is that, oh, your body's just turned against you. And it's like, how disempowering or you know, what a message of hopelessness my body turned against me. No, no, guys, let's. No, it actually is really, really helping you. Again, that model of laying on a beach versus running from a tiger, you want your body to be responding this way. And so our job as practitioners and clinicians, health coaches is to figure out what's weighing you down, Figure out what, what set it off. So again, I think, again, to answer that last part of that question, Scott, we believe that it is, it's protective, Protective state.

When I read that paper, it was like eye opening. It was the piece I was missing. And I think the person who sent that to me, Ben lynch, knew that was going to be a big factor for me trying to understand where I had confusion from what I was being taught in allopathic and functional training about thyroid physiology. And I read that paper, it was interesting. There was not much of a discussion about thyroid physiology in that paper. And I reached out to Dr. Navio and said, hey, we missed thyroid physiology in here. It was interesting. I mean, I totally respect him and the work he's been doing. But he said, listen, Eric, I don't know much about thyroid physiology. And so I was like, wow, I got to dig in here. So I've done the research and looked at whether this is a broken physiology or adaptive physiology, but the downregulation of cell metabolism and all. Every step of the cell danger response requires a change in thyroid physiology within the cell. When you talk about every step, thyroid physiology is an integral part in that. When we talk about down regulation of the metabolism, why is that important? Well, to downregulate the metabolism, you need a lower T3 state. And so it was like, I think it's the ne. The one step that's missing on that paper is the adaptive changes in thyroid hormone in those cells perceiving danger. Critically. Critically important.

So in the cell danger response, we have the CDR1, CDR2, CDR3. My understanding is that there is not currently any test that we can run to determine that someone is in a particular part of the cell danger response or that they're even in a cell danger response. So how do you. When you're working with that patient in front of you, how do you determine whether they're lying on the beach or running from the tiger?

Yeah, I. I think you took it. You have to take everything into context. Right? What's the. What's the person's timeline? What does their story tell me? What are their signs? What are their symptoms? What did the lab show? Right. You're. You're absolutely correct. We don't have a definitive test to say, is this person in homeostasis or allostasis? There's not something we run and it's like, bing, bing, bing. Right, Allostasis. Right. So we have to look at the factors. Do they have marker, multiple markers of inflammation? Do they have marker, multiple markers of oxidative stress? Do they have multiple markers of malabsorption? Do they have multiple markers of tissue hypothyroidism? Do they have insulin resistance? Right. Do they have patterns that we would associate with a cell that's in allostasis? And if. If they have that, then I think we have a pretty good indication that, hey, this is the person. This person's not operating from a homeostatic.

Standpoint in your patient population, what would you say are the primary or more common triggers of the cell danger response that can then lead to thyroid physiology issues? So are we talking about mold or Lyme disease or viruses or heavy metals, environmental toxicants, maybe EMFs? Like, what are the things that you think are likely the bigger triggers of cell danger response?

I think all of those have the potential in everyone. Right. So is it mold? I think we get stuck. As Kelly kind of alluded to, we get this stuck on the one thing, right? It's this. It's mold. It's ebv. It's this one thing. And I kind of shy away from that model. I think it's more the load over time. And the analogy I use for my patients is, imagine the stress on your life. Almost like stacking weights on a plank.

Right.

If I had two cinder blocks with a board on top of it, as we go through life, that the capacity of that plank is £100 and I have one acute stress, right?

Boom.

And dropped it on that board, it could break, right? But really that's not what often happens to us, right? We think it is because it's the last piece. But really what happens for most of us, we go through life, we stack a five pound weight, we keep going through life, we stack another pound weight, we stack another five pound weight and another, and another and another. And eventually we stack the fifth pound weight and we get to 105 pounds and the board breaks. Which one of them caused the problem? Right. So in our model, we have to look at all these things. We talk about them as fitness factors. Hypoxia, right? Poor breathing, horse, disrupted sleep patterns, organisms for sure. But don't get caught up that it's just one, right? We have to consider the fact that that diet, nutrition, toxins, all of these have play a role and we're only going to be as healthy as the weakest link. And what I try and get people to understand with that analogy with the board and the cinder blocks is once the board breaks, if I just pull the last 5 pounds on the gluten that you think triggered it, or the, or the virus that you think triggered it, if I just take that away, is the board fixed? And they're like, no, I'm like, right, what do we need to do? We need to get out of that danger physiology. We actually have to take really reduce all of those things, things that you maybe have adapted to and seem to be pretty good at adapting to in the past, but now we have to get all of those things off the board, all the weight off the board, so we can actually rebuild the board and reinforce it and then we can set it back up there. And then what you realize is now I can, now I have. As we pull all those things off and support the healing, the rebuilding of the board, not only can I manage the stressors I had before, but actually can adapt and manage more stress more effectively.

I love that. It's kind of the super smart person's bucket analogy with the cinder blocks and the boards and all of that kind of stuff. So very cool. When the body is in an intelligent protective adaptation, essentially putting on the brakes, could we view pharmaceutical thyroid hormone as essentially trying to press on the gas pedal when the body is essentially working against the body's own intelligent design?

I'd say the answer to that is it could be right. I think sometimes when people hear Me talk for sure. They think that I'm anti thyroid medication. I am not anti thyroid medication. What I am is do we have more in the system than we should have? Because what we know from the literature is that especially under stress conditions, you can quickly saturate the hypothalamus, the pituitary gland, and yet the peripheral tissues aren't getting the thyroid hormone they need. And that can create a problem because as TSH goes down then we get less stimulation of the thyroid gland for T4 and some T3 production. But we also get reduced peripheral conversion because TSH higher. TSH is a driver of T4 to T3 conversion. So it helps that conversion process. So by saturating the hypothalamus and dropping the TSH into, and some docs like to be have it as low as possible, we actually prevent the thyroid gland from doing, from producing T4. So we become more dependent. We essentially eliminated much of the T3 that might be produced by the gland and we reduce the peripheral conversion. And so people feel good initially and then all of a sudden they hit their plateau and then they start to regress. And so I think we can, it can be a problem. And to add to that, if we look at the literature, I joked with Kelly, this was maybe four years ago or five years ago. I said the impact non genomic effect of T4 on cells is not discussed very often except in the cancer literature and research. And in those circles, hypothyroidism is considered a protective mechanism against cancer growth. I said it would be great to see a paper of the is there an increased incidence of cancer in people who are taking thyroid hormone replacement therapy, especially T4? I said, but that paper will never get done. And lo and behold, in 2019, a paper came out. I sent that to Ken. I'm like, no way. Somebody actually took all these different types of cancer and the incidence of all whole bunch of different cancers is greater in people that have been on longer term T4 therapy. Isn't that crazy? So maybe we have to consider that maybe this intelligence was pretty smart. Whoa. We've got abnormal cell development, abnormal cell growth, let's slow down the metabolism, let's limit the reproduction of these cells. And so for, for some people, that may sound scary. Oh my Gosh, is my T4 going to cause me to have cancer? We, we can't say yes for any one particular person. But there is, when you look at the literature, there is increased potential of number, a number of different cancers.

I want to talk a little bit about Autoimmunity. When we think about Hashimoto's and we have the presence of these thyroglobulin or thyroid peroxidase or TPO elevations, and commonly people then think about things like Epstein Barr virus or Borrelia or heavy metals. You actually in the book had a very interesting perspective that at first I kind of hadn't really heard before. And as I understood, your perspective was that that kind of autoimmune response would itself be intelligent. So talk to us about how that autoimmune attack on the thyroid gland could also be an intelligent response. And then how do we fix the damage to the thyroid gland once that attack is no longer needed?

I kind of learned that when you have antibodies, the immune system makes these antibodies that are like little pac men, right. Eating away at your thyroid gland. Right. It senses it's no longer self tissue for some reason and it starts to attack. And there's lots of mechanisms for, I think there's seven or eight listed hypotheses for autoimmunity, but I just thought that was kind of, that can't be the case for everyone. So as I was digging through the literature, you find out that the thyroid cells actually have sensors for danger particles. So when, when a cell is being impacted by a bacteria, a virus, it can release signaling molecules. We call those things pamps. They can release parts of its structure. We call those damps, dangerous ocean molecular proteins. And so these damps and pamps go out into the bloodstream to alert the immune system to say, hey, here's the thing that's causing the problem. Find it and get rid of it. And here's I'm the tissue that's in danger. Come help me. So it's a sick, those are signaling molecules and those particles and some of the other things warn the other tissues that, hey, there's somebody's trying to break in. And the other surrounding cells can initiate their own cell danger response. Right? It'd be like me sounding the alarm like, the troops are coming, Hide, lock your doors. But the thyroid cells themselves have danger sensing receptors, which is really interesting. And so what the literature seems to show is that when these danger particles, these damps, these pamps bind to those danger receptors on the thyroid cells, the thyroid cells become immune. Like it's the cells almost initiate like a self destruct mechanism where they're then throwing out danger signaling particles to attract the lymphocytes to come in and start to cause some of that damage. And so when you think about it like that, you go, wait, A minute. If, if the thyroid cells themselves are initiating the thyroiditis, maybe this is part of that protective response. If I have one cell or one tissue that's perceiving danger, hey, let's just handle that locally. But if this becomes a chronic, persistent danger physiology, what's the best way to, to slow down globally slow down the metabolism, and that is to slow down the production of thyroid hormone right at the source. And we see this in, like, in cases where there's famine and starvation, there's, there tends to be some increased incidences of thyroiditis. Hashimoto's. So it changes the idea that the antibodies are the thing that are just gobbling up, like your immune system lost control and it's gobbling up. Matter of fact, a paper, I think it was 2020 stated that the thyroglobulin antibodies produce no damage to the thyroid gland and that the TPO antibodies cause very little if any direct damage to the thyroid gland. So I, I try and get my patients to understand, think of the thyroglobulin antibodies, TPO antibodies, more like the cleanup crew after Mardi Gras than the actual people that are actually creating all the trash and damage.

So if I'm understanding correctly, it's not that there then is significant damage to the thyroid gland that we have to then do something to potentially repair after the triggers of the cell danger response, the triggers of the autoimmunity have been addressed. It sounds like there's not a, not a repair phase that we necessarily have to think about. Am I understanding correctly?

No. I think there has to be a time for repair and regeneration. And in my client base, what I see in the last 20 plus 25 years of helping people is that I'm not directly trying to do things to the thyroid gland. Right? I'm doing things to help the physiology overall. And what we see in time, as we address these triggers, these stressors, there can be a lot of destruction that occurs the gland as a result of the thyroiditis, the inflammatory damage that's going on. But the thyroid cells and the thyroid tissue itself can start to rebuild and regenerate. And so what I see in my practice is, is that, hey, I need. As they're getting better, they need less and less thyroid hormone and they have better and better conversion. And many of my clients over time wind up not needing thyroid hormone replacement therapy because the gland has become dysfunctional thing again. I think we thought that, hey, once the gland is damaged, it can't repair itself. The literature seems to show no, the thyroid gland can redevelop it can regrow. And why does it not happen many times? And why would people come to that conclusion is especially in the allopathic model, we're not doing anything to stop the stressors that trigger the thyroiditis to begin with, so why would it ever get better? So I understand that perspective, but in a functional model where we're actually reducing the stressors, the triggers, and we're reducing this inflammatory, immune driven attack, I see people's thyroid glands recovery all the time.

So when we think about infections and molecular mimicry as a potential reason that we then have this immune response, is it more important that we address or kill the bug? Is it more important that we create integration and tolerance and support immune modulation? And would you then use something to support immune modulation to kind of calm that hypervigilant immune response? Or is that even a bad idea? Because you're suggesting that that autoimmune response itself might be part of the protective mechanism.

Yeah, so I think in some situations we need to directly address the infection, but not always. So, you know, there, it's just again, it's like a spectrum. But I think we always need to consider what's allowing the organism, let's say, like if it's Lyme or co infections, what's allowing that organism to thrive. So considering the physical terrain, chemicals, you know, environmental toxicants, like our emotional health, considering that entire entirety of, you know, what could be causing, again, like that organism to not be dealt with appropriate. Because we have immune system. Right. We have, we have that for protection. It just might be overwhelmed. Regarding the tools, Scott. I think it depends on the shift in the immune system. And so Dr. Eric and I, he's much more down the road in this, but we started using the lympho. Lymphomap from lymphocyte map. Yeah, yeah, from Xyrex. And so I think that can provide a lot of insight on which products and which way, you know, you, you want to try to help shift the immune system. Because really we really look at it pretty antiquated. So this test is very revolutionary. I know Dr. Eric on his podcast Thry the Right answers, he interviewed Dr. Viejo Aristo Bostoni.

Thank you.

Yes. And they had a wonderful conversation about that. So I think that your listeners might want to listen to that as well. But overall, you know, with the immune system modulating, I think made a good point, is that we, you know, you don't want to shut everything off or suppress everything. We're trying to offload the allostatic Load, but I always think like gut healing, breathing exercises, meditation, cold exposure. Looks like it has some balancing of the immune system early. You know, right now we're still learning a lot about that. But plant sterols, if you look at the, the, the science on the, some of the studies on the plant sterols, I find that those are really important because they can kind of go both ways. They can balance to. To active immune system. They can modulate that down underactive, pull it up. So I really am a fan of plant sterols. And then lastly, I'll just say in my toolkit, past three years, peptides like TA1TB for some of those are, are very nice compliments and again, per specific person. So I really encourage everyone to just, you know, work with someone who knows what they're doing here. And, you know, not everything's good for everyone. Right?

Yeah. And I'll jump in there too. I think something Kelly. Kelly often says is, is principles over protocols.

Right.

And so we want to have this. Hey, you have this. What's the protocol for treating Lyme? What's the protocol for treating mold? What's the protocol for suppressing the immune system? And I think that gets us in trouble sometimes. Sometimes we have. If we have organisms, we may, okay, this might be excessive. We need to tampen this load a little bit. But I often think, at least initially, the immune system is adapting to try and help. So suppressing the immune system when there's a chronic infection, I don't think that's a great. I don't think that's a great scenario. I've run a lot of lymphocyte maps on patients because usually by the time people get to me, they've seen a number of practitioners, they've done their mold treatment, they've done their Lyme treatment, they've done all these things and still don't feel well. And so we'll look at the immune system. I'll look at that lymphocyte map, and you can say some of the things that you might have been doing were probably working against the immune system. And maybe those were the wrong strategies. And even when we look at that lymphocyte map, say on paper, it looks like the thing that will help balance this, we should give those. It doesn't often work out that way. And the people feel worse because there isn't. There is some type of active issue going on that we don't, that we should kind of back off and let the immune system do what it's do what it's doing and address all the things around that we give the immune system the best chance to heal and recover.

I love that you mentioned, Dr. Kelly, the plant sterols. I was just talking with a mentor yesterday. We were talking about the module care product from Thorn, which is one that can be very helpful and is a plant sterol based product as well. I'm wondering if some of the concepts that we're talking about today also apply in hyperthyroidism or Graves disease. How is that the same or different? And could we be hyperthyroid based on some of the conventional tests and still have hypothyroidism at a cellular level?

Yeah. When we're thinking about hyperthyroidism, you know, without somebody on medic, just on medication, they just get diagnosed as hyperthyroidism. It's still an immune driven issue. The mechanisms are a little bit different as to what's going on in that situation. We want to be, we've got to be very cautious because hyperthyroidism can quickly turn into bigger challenges and bigger problems. There are some things that we can do to help kind of mitigate that with nutritional products. L. Carnitine is one of those things. Milk thistle is another one that can have an impact as well. And there's a. There's a few others, but the mechanism's the same. We've got an immune system that's creating some abnormal physiology. We still need to ask the same questions.

Why?

Because what's the driving source if we just remove a thyroid gland and don't address what maybe it drove the thyroiditis to begin with, or the immune system production of the things that are binding to these TSH receptors and causing the excessive stimulation. We're going to have a person who gets diagnosed with hyperthyroidism, gets treated, becomes hypothyroidism as a result of medication, and then fails when they're given thyroid medication for hypothyroidism. And I see that all the time. And people often when I'm talking are saying, well, what about, I've had my thyroid gland removed. What about me? I don't feel good on thyroid medication. I don't have a gland. Once the gland is gone, we know that we can run the physiology without the gland. We have enough T4 in the system and maybe a little bit of T3, but all the downstream physiology works. We can function fairly well without that thyroid gland. The issue is we still have to address what's triggered this immune upregulation to begin with. And I think that gets Missed many times in hyperthyroid treatment. And what happens is we just kick the can down the road by saying, hey, let's just kill the thyroid gland, let's just take it out, let's irradiate it and then everything will be good. No, that was the effect, it wasn't the cause. So we still haven't, we still have to address the same factors. So everything we talk about from a hypothyroid cell, danger, physiology, improve the fitness factors, all that pertains to the hyperthyroid patient as well. Now, the second part of that was, can we see problems with people having hyperthyroidism, maybe with medication, treatment? And absolutely we can. And we often see people, especially as their dosage goes up and they have this kind of allostatic physiology going on. The brain, the pituitary gland, get upregulated because of there's different receptors there that have different sensitivity than a lot of the peripheral tissues. So we quickly saturate the hypothalamus, we, we activate the sympathetic nervous system, we drop tsh. And now the person struggling with brain fog and fatigue and, and even histamine related problems as a result of creating hyperthyroidism in the brain and hypothyroidism in the peripheral tissues. And I think they go to their physicians and have both signs and both sides and symptoms. And their physician's like, okay, we need to get you on an antidepressant. This can't happen.

Integrative doctors will often look at reverse T3, which I kind of think of as the brake pedal. What are some of the common causes that reverse T3 would be elevated? And can we to some extent use elevated reverse T3 as maybe an indicator of whether we're in a cell danger response or have some cellular hypothyroidism? Potentially, yeah.

So I think we can sometimes use reverse T3 as an indication that we've got a problem. Okay. So if we have a person who's on no thyroid medication, if we just do a general comprehensive thyroid panel and their reverse T3 is up and everything else is normal and the rest of their labs are normal and they feel good, that reverse T3 could be up for a number of reasons that don't indicate that we've got a problem. So we always have to take the context into perspective. Right. Somebody could have problems with their liver. Right. And so then they can't process that reverse T3. Somebody could have inflammation that could cause increased reverse T3 as well. Somebody could be taking excessive amounts of T4 and that could increase reverse T3As, as well. So there are a number of factors, but when I see T3, that's, that's starting to elevate. We have to take into consideration the, is there physiology that matches this from a signs and symptoms perspective and is there physiology from a blood chemistry perspective that also would indicate that maybe we do have this tissue hypothyroid state going on? Now, there's a problem with reverse T3, especially in the functional medicine and integrative space where we've been kind of, there's this kind of discussion that reverse T3 blocks T3 from blind binding to receptors and reverse T3 does not, based on the literature, block T3 receptors at the nucleus. Okay, So I think we can look at it as a break, but that's again, not broken. Physiology. That's blocking the function. If you want to blame anything for the blocking function, blame deiodinase 3, which is the enzyme that converts T4 to reverse T3. But it's not. I don't look at it as a functional problem. I look at that as an adaptive change. So if I see it high, then I would say, hey, there's a potential. We got to investigate this a little bit more. Reverse T3 does have an impact on the, on the plasma membrane, what we call the integrin receptors. But that's a whole nother in depth conversation. So I think we look at it as an indicator that there's potentially tissue hypothyroidism on. The other thing we always have to keep in mind is where am I starting? With T4 and free T4. Because if I, if I have a lower T4 or free T4, then I'm going to potentially have a lower T3 or even, or reverse T3 or a normal reverse T3 when somebody might say, hey, that's normal. Okay, well, what's the context? Where's my starting point with T4? How much T4 do I have in the system? Right. How much free T4 do I have in the system? If I don't have much T4 or free T4, then reverse T3 could be normal and I could still have tissue hypothyroidism going on. Right? So we have to look at T3, free T3. We look at the ratios of T3 to reverse T3, free T3 to reverse T3 and free T3 to free T4 to get an indication of what's happening inside the cells and tissues in the.

Chronic Lyme disease community. And people that are taking pharmaceutical thyroid, my observation over many years and my personal experience as well was that people tend to do better with T3 rather than taking T4, that it's not always converted efficiently. So what are some of the key things that impact the conversion of T4 to T?

Yeah, so inflammation, hypoxia, any of those danger physiology things happening in the cell will cause a downregulation of T4 to T3 and an increased conversion of T4 to reverse T3. So the discussion about, hey people, do I hear this all the time, this. I see people coming in with the same merry go round with T3 that they do on T4. Hey, initially I felt better. Okay, what you're on, you're on 50 micrograms of T3. Now, did you start at a lower dose? Yeah, I started at 5 micrograms and I felt better. But then it plateaued and so then I had to take more and take more and take more. Right. So I think I have a. About two weeks ago I had a 140 pound female who's taking 150 micrograms of T4 and 80 micrograms of T3. And this is somebody who kept trying to fix the T4 T3 values in the blood and didn't understand the impact and they were frustrated because T3 levels just didn't seem to stay upregulated. We have to remember that the T. If T4 is being deactivated to reverse T3. The same enzymes deactivate T3 to its metabolites, different forms of T2. I think the beauty of the cell physiology is when there's different forms of T2 and when you deactivate that T3 to T2, that some of those metabolites can almost act like the, the backup battery or the backup generator when the power goes out. We still have to have some level of cellular physiology going on. So the body's got backup physiology mechanisms. But I don't think we're going to solve the problem oftentimes with just saying, well, if I can't convert T4 to T3, I'll just give T3. I think it becomes problematic on many.

Fronts and is part of the reason that people feel better initially and then that kind of wears off because there's essentially a feedback loop that then as you're taking T4, T3, that that then suppresses your body's own production of those hormones as that happen as well.

Yeah, there's a bunch of loops like we learned one loop in school. But if you read papers like Heuerman's thyroid allostasis paper. He shows all the loops in there and you go, oh, a lot of things have some feedback. The other factor is T3 can get into the cell maybe a little bit more efficiently. It's got a lower energy point to get in more, more transport mechanisms potentially. And T3 at physiologic doses doesn't have the potential negative consequences that T4 might have. So as long as the T3 is in the physiologic dose in the bloodstream, it's not going to have maybe the significant impact that too much T4 in the system might.

Where do you stand on the use of supplemental iodine in people with Hashimoto's? I know many people suggest it's contraindicated. Others suggest it's completely fine. Any thoughts on that debate?

Yeah, it is definitely all over the place with recommendations. I have noticed that quite polarized. Eric and I really agree on this is that just like everything in reality, you know, we're, we're probably somewhere in the middle, right? There's a lot of people who are probably a little deficient and not so much probably in this country because, you know, we have salt has iodine in it. And so I, I feel like we're not necessarily, you know, the number one cause over, you know, in, in our civilization like in was it for third world countries, first world countries versus third is iodine deficiency. Ours is Hashimoto's. That's the cause of post hypothyroidism. But then I think that a lot of people may be overloaded, right? They may be eating too many foods, high iodine. So, you know, I, I rarely tell people, get some iodine, it'll fix your thyroid problems. I, I will tell you this is that I saw a video on Instagram over the weekend where you put a couple dot drops of Lugols on your arm and if after this doctor was saying after an hour, if these dots are gone, you're very deficient in iodine. Well, my dots weren't gone. But I'll tell you what, I did not feel well at all the next day. I think I set off a mini flare. And so I'm careful. I'm really careful. I would, you know, I'm not on the polarizing. No iodine, Never, never, never. Nor am I telling people to take it. I'm just. My mantra is be careful.

I would say recently I've heard some of my mentors talking about thyroid and adrenals more as the pebbles rather than the boulders and that supporting mitochondria may be more important than either the thyroid or the adrenals. And so I'm wondering, where do you place mitochondria support in terms of, you know, comparing that to supporting the thyroid or adrenals? And then when we look at the whole cell danger response and the idea that this extracellular ATP is the danger signal, do we need to be careful with introducing mitochondrial support? And then related. Can a lack of energy or a lack of ATP at the cellular level itself be a potential trigger for the cell danger response?

When people think that they're going to fix their fatigue, their cell danger response symptoms with Ribose and Coq10, I kind of shake my head because I feel like it's like using high octane gasoline in a car that's clunky and old and needs a lot of work first. And that's how we look at what we're doing. I said over and over again, you can't medicate yourself to health. That's kind of how I feel. I feel like you have to put in a lot more work than just put pills in your body. And Eric's been noticed that you can't really supplement yourself to help. Correct me if I'm wrong, Eric, but what we're saying is, is that we, all three of us, have seen the clients come in with suitcases full of supplements, and it just didn't fix any of their, their problems. Right. And so we feel like there's a. There's a great place for supplementation. Some of those nutrients I just mentioned are absolutely wonderful, but again, some of them may be going against what the body is inherently trying to do. We don't want to speed up a mitochondria that's trying to slow down to protect us.

I think it's a nice protocol. Right. Oh, the mitochondrial doesn't have the nutrients. Well, I think we have to. We could try it. Sure. Give it a shot, see if it improves. I would ask the next question, like, if it's just nutrient deficiencies, why do I have nutrient deficiencies? Right. Maybe I've got a gut issue. Maybe I got a poor diet, maybe I've got absorption issues. Maybe I've got another issue versus I just don't take enough bottles of supplements. Right. If you look at the literature on something like, let's say, CoQ10, which is a common thing that we give people who have mitochondrial problems, hypothyroid patients have high levels of serum CoQ10, not low levels because they're not utilizing and so downregulation of the mitochondria is a protective mechanism. And one of the things you need to do to downregulate that is reduce the amount of T3 in the cell. Now why would we do that? And I think that becomes important. One of the reasons that we actively downregulate that, that mitochondria. When we have this cell danger physiology going on is when we rev up the mitochondria and we have high efficiency of or high function. I should say better. Better say not efficiency. I'll talk about why I say that in a second. But when we're mitochondria is working at a high level, we can put a lot of energy, food energy through that to make cellular energy. And there's exhaust that's created as a result of that. Now for the listener, that's oxidants like these things that can create damage. The cool thing is with the innate intelligence in the body, it makes an antioxidants inside the cell. And one of those is something called glutathione. So we typically have produced this exhaust from our mitochondria, our energy producing proper or organelle inside the cell. And we have an antioxidant system that's designed to manage that. Right. If we ramp up the mitochondria during that process, the cell is already increasing oxidative stress or oxygen free radicals to deal with whatever that threat is. If I increase the free radicals, the oxidants to deal with the threat, and I'm increasing the oxidation because I'm trying to ramp up the mitochondria. Now I overwhelm the amount of antioxidant I have in the cell to deal with the oxidative free radicals that are occurring, these oxidants. And now I get excessive oxidative stress, which does what? It destroys the cell and I lose cell function. I don't want to lose the cells. So this is like beautiful design, right? That we have this downregulation of the metabolism, downregulation of the mitochondria. And so we should expect that mitochondria is going to be downregulated in these states because it's a protective mechanism. So we can make enough free radicals to deal with the threat, but not so much to kill and destroy the cell. So I've done it, I've given people mitochondrial support and it doesn't work, right? I'm like, okay, some people it works, some people didn't. What's the difference? I think the people that I gave it to and it seemed to have a benefit we probably already dealt with the cell danger physiology, and now we're supporting the recovery. And it worked. It was awesome. But when we start to give that to somebody and they don't feel well and it doesn't change, then we have to ask the better question, which is maybe this is part of the process. I'm still in that cell danger physiology, and I probably trying to give more stuff that the tissue doesn't want or need or can't use effectively is a problem. I do want to say I touched on efficiency of the mitochondria, Right. And so in the cell danger physiology, the mitochondria actually becomes more efficient at pushing energy, food energy through to make cellular energy. And that doesn't sound like it makes sense because I've got, I'm not, I'm not making a lot of ATP, right. I don't, I'm not. I don't feel well, I don't have energy. But it becomes more efficient when we have a really robust cell function. When we're in homeostasis, we're pushing a lot of stuff through. And thyroid hormone helps regulate these things called UCP proteins. Right. And these are disbursement channels for excess energy. And that helps us kind of, kind of blow out some of the extra energy and we can use that, like in the fat cells, to generate heat. Right. One of the reasons why people are always chronic, chronically cold when they have hypothyroidism is because they lose that, that electron leak that helps generate heat as a source. So we push more food energy through the electron transport chain. Right. More cellular energy through there. It's more efficient because we don't have the waste. But it also means we don't need as much food energy to drive that system.

If the thyroid gland is producing adequate thyroid hormone, but the peripheral cells are still hypothyroid, is that always a cell danger response? Cases where there are things that you can do at the level of the cell to optimize thyroid physiology?

I think in acute situations, right. If I saw normal thyroid physiology, person had symptoms, I'd have to take into consideration what they did in the last couple days, right. Did they exercise? Are they fasting? What's going on? It's when we see it chronically that they have chronic signs and symptoms. They have, they have chronic changes in, let's say, lipid physiology, they have insulin resistance, then we have. That's when we say, okay, there's something bigger going on here. But if somebody came in and, you know, I'll always ask the person, like, what did you take yesterday? What did you do yesterday? Like, what did you do the day before this blood draw? Which may be having an impact on what we see. Because let's face it, we all look at blood work and whether somebody is on a fast, whether somebody just worked out, whether somebody that, you know, whether they were hydrated, not hydrated, all those things can play a role in what their labs look like.

Many people think of low thyroid as a problem with the thyroid gland. But in the book, you say that hypothyroidism is a spectrum, and by the time the gland can no longer produce thyroid hormone, that that's really end stage. You also say that only 20% of T3 or active thyroid hormone circulating in the blood is produced in the thyroid. So where's the majority of T3 in the body produced?

Any cell that has the deiodinases, Dionase 1, Dionase 2 can help with that production of T3. Okay, so, you know, we think about, we talk about the liver, it plays a big role. We talk about the. The kidneys play a big role, we talk about the GI tract. But any cell that has deiodinase 2, which is the primary converter of T4 to T3, deiodinase 1 is another one that people talk about. It's. Its primary function isn't really to make T4 into T3. Its primary function is to get rid of reverse T3. It's only in cases where we either have hyperthyroidism, we have excessive thyroid hormone replacement therapy where we see Dionase 1 often upregulated, but definitely the liver produces some with Dionase 1 and the renal system. So when a cell takes nt 4, it converts it via Diademase 2 to Diadenase 3. Diademase 3 binds to the receptor, hangs out for a while, and then diademase, then T3 can go right back out into the bloodstream, become part of that circulating pool. So any cell or tissue that has the ability to convert T4 to T3 contributes to the blood level of T3. And that's really important because there are some T tissue, some cells in some tissues that cannot generate their own T3. So that's considered a biologic priority. To have thyroid gland makes some. But all these peripheral cells make quite a bit of T3.

In the mold illness arena, we talk about phase two detoxification, particularly glucuronidation, and how important it is to optimize glucuronidation to help with excretion of mycotoxins in the book, you made it sound like supporting sulfation and glucuronidation could create more problems for the thyroid discussion. So I'm wondering if that's true and does better glucuronidation lead to hypothyroidism, or is the body also intelligent about how it manages those phase two detox interplays from a thyroid perspective?

I think again, this depends, right, on the extent that we're trying to push pathways. Is the person already in a hypothyroid state? And if we push those pathways harder, could we deplete some of the available thyroid hormone? And that's a possibility, and that's been discussed in the literature. So I think at physiologic levels that the person's not hypothyroid is probably not not an issue. The issue becomes when we really try and push these detoxification pathways hard, could it become a problem? It could increase the metabolism of those thyroid hormones and reduce the amount of available hormone to do. And that's been talked about in the literature and the research. But I think in general, it's probably not an issue. I think there's some intelligence there that, hey, we can regulate that. Matter of fact, those. If we glucuronidating those thyroid hormones, I mean, that's a reserve, right? That's where we talk about the gut and the gut bacteria helping to actually recycle those things. I think it's when we get into heavy, extended periods of trying to push pathways. And then I guess I would have one other comment on that, and that is, why are these pathways not working to begin with? Right? So I think that's the other question we have to ask. And it's not that I don't support sulfation and glucuronidation and methylation at times with my detoxification pathways. But I just don't want to push those systems excessively, right. I don't want to be like, hey, more is better. I want to provide. If I see that there is some challenges there, if I see there's micronutrients that aren't maybe a deficient in supporting detoxification, I may want to provide those, but I don't want to just hit it as hard as possible and try and force detoxification in a system that may not be in a great position to detoxify.

You coined the term multisystem adaptive disorder. You mentioned that earlier to describe the changes you see in those that are in this cell. Danger response that are dealing with cellular hypothyroidism. So talk to us a little more about multisystem adaptive disorder. Is it the case that similar to the cell danger response leading to cellular hypothyroidism, that the same model essentially is more broadly, much more systemically throughout the body?

Yeah. So I, I think what happens is for physicians, for clients, you know, our patients, they want to know what is wrong. Right. I need, I have an adrenal problem. I need to see an adrenal specialist. I have a thyroid problem, I need to see a thyroid specialist. That's kind of allopathic thinking in my opinion.

Right.

That it's just an individual system or tissue. And I think that anytime there's a chronic cell stress response, cell danger response going on, we should expect multiple systems to start to become compromised and down regulated. Because the analogy I make for my clients to try and make it simple is let's assume that Kelly is home. She has got a big party going on this weekend for the Minnesota football game. She's cooking lots of food, all the burners are on. She's cleaning the house, she's doing wash, she's feeding her kids. It's like every day. Right. And so if somebody broke in and attacked her child, Right. Kelly's not going to. Right. Kelly, you're not going to continue to cook.

Correct.

You're not going to probably take the time to turn the burners off, put everything in nice glass Tupperware, you know, glassware, put it in the fridge. You're not going to probably try and slide an extra load of wash in. Finish the, I'll be with you. And as soon as I finish the, you know, the vacuuming, right. You're not going to go take a nap, you're not going to go have sex. Right. So all the systems, and we see this in the individual cell, but we should also look at the bigger issue globally. Like what systems in the body don't really matter when I'm in that danger physiology, when I'm being chased by the proverbial tiger, right. You're not stopping to take a nap, you're not stopping to have sex, you're not doing that stuff. So we should expect adrenal physiology to change. We should expect GI physiology to change. If I'm not stopping to have a meal, my body's saying, hey, I need to put more energy towards inflammation and cell defense. I'm not putting as much attention towards my digestive production. HCl, pancreatic enzyme production. Bio. Those things don't they Lose their importance. So I needed to come up with something to tell my patients because they wanted to know what is wrong with me. Like, do I have an adrenaline? Yes, you have a multi system adaptive disorder. You don't. You're not broken. You're adapting to some type of excessive stress response. It's physical, it's chemical, it's emotional, it's microbial, it's environmental, it's, it's, it's respiratory, it's sleep oriented, you know, trauma. These are the things that are causing you to be in this danger. Physiology. And when I explain it to them, like the intruder, they start to have that aha moment. Oh, I get it. Right? And I said from an allopathic approach, we'd say we'd walk into Kelly's house and go, Kelly is a terrible cook. All the food's burning. She's a terrible housekeeper. The place is a mess. Let's hire her a cook and a chef and a house cleaner. Problem solved. Right? But the problem isn't solved. Kelly's not eating the meal. She's still fighting protect her child. And the house may look clean, but we haven't still addressed the real issue from a functional medicine perspective. We should walk into that home and go, something's wrong here and we need to go find it. Not, how do we clean this up really quick?

Sibo is such a common issue these days, and we know that hypothyroidism can impact GI motility. Wondering how often do you suspect some degree of cellular hypothyroidism in people with sibo? What is modalin? And how does impaired bile flow come into the discussion around cellular hypothyroidism and SIBO as well?

Sure. So SIBO is just so common. And I feel like if someone walks in the door with sibo, I'm always going to be looking for cellular hypothyroidism. I want to look for those patterns as well. But certainly, you know, hypothyroidism can definitely be the part of the cause because thyroid hormone helps regulate stomach acid, bile flow, and some degree of pancreatic output. Now, if you want to get into the weeds on this, go back and listen to my episode with Scott, episode 79, when we really go into the weeds on the bioflow specifically. But you know that model and that hormone that's released by the duodenum and the jejunum that stimulates the contraction. And so the, the T3 and the T4, they all have influence over that. And again, go back to what Eric saying. Everything is connected. And also, you know, those bile salts, they are actually very modulatory to the gut flora, the microbiome. And so when that's off, you have to suspect that that has something to do with what's going on with the, with the SIBO and the recurring revolving door of sibo. If you' not addressing the cellular hypothyroidism, you're just going to be going around in circles.

You hinted at this one earlier, but hypercholesterolemia is a common issue. And when high cholesterol, in some cases, it may not be a huge problem. But I'm wondering, is there a connection between high cholesterol and cellular hypothyroidism? And then when you address the factors that are triggering the cell danger response, and thus the cellular hypothyroidism, does that often lead to reductions in people's cholesterol?

Yes. Yeah. So what's like, what's the mechanism? Well, thyroid hormone regulates every part of the lipid metabolism process, the hormones. Thyroid hormone regulates all these hormones that are like, help with the conversion through the process. When we have optimal thyroid hormone in the cell, then we can take food energy, drive it through the mitochondria to make ATP. When we have reduced cellular physiology, then one of the things that we can do is we can divert that food energy out to make cholesterol. Okay, so cholesterol level can go up.

Okay.

So in a hypothyroid state, we can see high or low lipid levels based on the phase they're in, how early on in the process it is. But the big thing, when we take a look at why is cholesterol elevated in patients with hypothyroidism? To get cholesterol out of the cell, I mean, out of the bloodstream, we need ldl, hdl, we need these, these proteins to dock to the cells and release the cholesterol. So if we talk about the liver, which is the biggest, maybe place that we dispense cholesterol, if you don't have functional high levels of T3 in the cell, the LDL receptor does not work appropriately. And so now that LDL receptor doesn't dock. Well, I can't dump cholesterol in. That's going to impact what's happening at the liver. It's going to impact what's going on with bile flow and biophysiology, because cholesterol is a huge piece of it, but it's also going to impact other tissues. Almost every hormone has cholesterol as the base. Right? So if we're talking about. You know, I hear people say, well, I don't have a thyroid problem. I've got an adrenal problem. Okay, well, you have high cholesterol, and cholesterol is in a. In the acute state, the adrenal gland can make its own de novo. They call de novo cholesterol. But in a chronic and just in general, where is the adrenal gland getting the cholesterol to make into the hormones? It's getting it from the LDL receptor, maybe the HDL receptor, maybe some of the other lipoproteins docking to the gland, binding to the receptors and being pulled in. And what, what do we need for those receptors to work? Well, we need T3 at the tissue level. Also to take cholesterol and convert it into those hormones. We have to do a big step of that occurs in the mitochondria. Well, if I have decreased T3 in the mitochondria, guess what? I can't bring the cholesterol in and I can't make the pregnenolone that I need to make at the mitochondrial level. So all my hormone metabolism gets down, regulated. So when we see the elevation of cholesterol, we have to consider a. It can be upregulated by decreased T3 at some tissues where, hey, I can't use this food energy. I got cell stress, so I'm not. I can't use that food energy. So let's divert it to make cholesterol. That makes sense. Let's make hormones because I don't need the energy. And then I can't get the cholesterol into the tissues out of the bloodstream. And so it builds up. And so T3 plays a critical role in the hyperlipidemia.

We typically see so many people these days dealing with glucose dysregulation, insulin resistance, diabetes. What's the connection between those conditions and cellular hypothyroidism?

There's these things called glute transporters that help get glucose into a cell. There's a whole bunch of them. And guess what? T3 helps regulate all of them. And to different degrees, these things can start to fail. Based on the tissue and the amount of thyroid hormone, one of the ones that hangs on the longest is glut2 with the. With the least amount of t3. And what's the impact there? Well, glut2 is what transports glucose out of the liver into the bloodstream, and it's what transports glucose into the fat cells so we can make more glucose and get fat, even though we have a lower T3 state, but when we think about insulin resistance, we blame glucose, right? We blame insulin as the problem. But oftentimes we see people who don't eat much carbohydrates, like we always blame it on the nutrition. Well, you must be eating too much carbohydrates. And that's why it is. I just had somebody wanted to come on my podcast and saying the solution to insulin resistance is this thing that, that reduces glucose. And, and he said all your patients are probably over consuming glucose. I'm like, that's not true, that's not true. And so why is glucose not getting into the cell? Why are the cells not listening to insulin? Well, if I'm a cell and I'm in danger, what I, one of the things I want to do is I want to stiffen my cell membrane and I want to reduce the things coming into the cell that might support the threat that's inside the cell. And so to get glucose in the cell, you need these glucose transporters in a fasted state. Depending on the tissue type, maybe you use glute one, maybe you're using glute three. In a fed state, primarily you're using that's when we start to use GLUT4, which is an insulin dependent receptor. So if I have cell stress and I downregulate T3 inside the cell now I decrease the amount of glucose transporters that are going to the plasma membrane, I'm going to get less glucose into the cell. And so now blood sugar goes up. So what does the body do even in a fasted state? Hey, there's still too much glucose hanging around. I'm going to increase insulin to try and get it in. So increase insulin goes up to try and activate more of those receptors. And then we have this kind of back and forth yo yo effect where I need more and more and more because the cells resisting, resisting, resisting. I think at the root of almost every case of insulin resistance and diabetes and prediabetes, however you want to say it is a tissue physiology problem, a cellular physiology problem, like a danger physiology versus it's just the cells are full, you eat too much carbs, you don't exercise enough.

You've said that replacing medications with supplements isn't the answer. If we think of mast cell activation syndrome and histamine issues, oftentimes we will support stabilizing the mast cells, reducing histamine, those types of things with nutraceuticals, while also working on the triggers of the mast cell activation or the trigger for the cell danger response. So is there a place in thyroid physiology for intelligent use of supplements to improve cellular thyroid physiology to improve someone's symptoms while you're simultaneously working on those cell danger response triggers, or is that also working against the body's intelligent design?

I think this comes down to the individual, right? I mean, you're working with the client. You got to see how they respond to things. But I don't. I don't think the solution is always suppressing. What's interesting about histamine, like, we talk about mast cells producing histamine. Almost every cell can produce histamine, right? But what's interesting in the literature about, like, the mast cells is the mast cells. And I think there's. There's. We're not clear on it, but either they can generate their own thyroid hormone or they can store thyroid hormone. And so what's the significance of that? Maybe that thyroid hormone is actually stored in the granules. And so if a cell is perceiving a hypothyroid state, the mast cells can come in and release their vesicle, right. And provide some thyroid hormone for the support, maybe for the immune system, maybe.

For the cells, especially in the brain. That would make sense. In the brain, right?

So now the problem with that is now we get an excessive histamine response, right? So we have to kind of tailor these things. Another interesting point on that is too much thyroid hormone will also initiate the release of histamine from cells. So we've got to be really, really careful. If we provide too much thyroid hormone, we can actually generate an excessive histamine response. But in a hypothyroid state, the release of histamine may still be a protective mechanism and to provide thyroid hormone to the immune cells or the surrounding tissue. So I think this is one of those things where we have to see, okay, where's. How's my patient? Struggling. What are the issues I'm dealing with? Is there something I can do from a crisis standpoint to just kind of take the edge off while I start addressing the issue? So I don't want to say that, hey, you can't stay out of the way, like, the body, dude. We have to have to manage where our patients are in reality.

Right? Like gut support and definitely detoxification support binders, you know, artichoke things that help move the physiology appropriately. Not too fast, not, you know, not suppressing and not pushing, but just really. And that's nuanced. Extremely nuanced. And you get better at it as you, you know, Practice more on people, unfortunately. But really that's again, something where just, we just. It's a delicate balance. It's not a yes or no, no supplements, yes, no medication. It's just like Eric said.

Individual from Trevor Marshall's work, we know that vitamin D, the 125 vitamin D, can be a potential indicator of intracellular pathogen burden, particularly when it's significantly higher than the 25 vitamin D. So I'm wondering, how often do you suggest supplemental vitamin D and are there people that are taking vitamin D where you might suggest that they discontinue it?

It's not very often that I provide vitamin D. And that goes kind of against the kind of the main talking point. Everybody's doing more vitamin D, more vitamin D, more vitamin D. And I, you have Trevor Marshall, you have Megan Manchin, you have Douglas Cal. These are some bright minds who are talking about what's going on. And so we have to kind of consider that it's not just, we just pound away. I mean, we look at vitamin. The only thing that's typically measured is 25oHD. It's rare that you see somebody measuring a 125 because it's, it's small, it doesn't matter. But 25oHg is like T4, right? It's the kind of circulating hormone. But 125 vitamin D tells us what's happening to it, right? So shouldn't we know what's happening to it? I mean, this is the thing that drives me crazy sometimes in allopathic and functional medicine is we look at one marker out of context of everything else and assume that because it's low, we need to provide it. But we don't know is, do I have low 25 vitamin D because I can't make it right, Because I have a cholesterol issue? Maybe do I have it? Do I have low 25 vitamin D because I got problems at the liver? Do I have low levels because I have magnesium deficiency because the transport and transport mechanisms, conversion mechanisms aren't working? Do I have low 25oHD because I'm quickly deactivating it? Do I have it low 25oHD because I have high 125 vitamin D? That's then reciprocally inhibiting the production because the immune system is pretty smart, says, whoa, we want to, we want to start shutting this stuff down. So we. But we don't want too much, right? And then where else is it going? Well, it's going into the fat cells. And for a while we thought that that 25, that vitamin D or 25 D, if it went to the fat cells, it was just getting stored. But what some of the literature is showing is it's not going there and just being stored. It's trying to help maybe potentially make the fat cells a better storage area for more stuff, which is interesting. So it can actually help expand the cells to create more room for more calories. In an interesting study, it's a rat study. But when they took rats and got rid of their, their vitamin D receptor, the VDR receptor, which 125 binds to, they could not get fat. Wow. Wow. Interesting, right? So if I have an overweight patient, I and they're taking like high levels of vitamin D for sure. I'm saying, hey, let's downregulate, let's get that down. What is your 25? What's your 125? What's that ratio? Oftentimes I'm taking it off. If, if 25oHD drops too low, then I might say, okay, now we have some considerations, but I'm also taking into consideration what's going on with calcium status. Right. And here's the other thing I caution people about too is what is 125 jobs role? Right. It plays a role in calcium homeostasis. Right. And so if I'm constantly taking a whole bunch of vitamin D and I'm over converting that to 125 vitamin D, is there a potential to bring more calcium into the bloodstream from the GI tract? Yep. Is there a potential to increase calcium being pulled out of the bone? Yup. Why are most people taking calcium? Because they want to increase their bone density. But if they're pounding away vitamin D, am I actually contributing to, to the demineralization of the bone? And then the other question we have to ask is if that's the case and I have normal levels of calcium in the bloodstream, where's the calcium going? Well, we know via the literature the calcium can go into the cell and vitamin D binding to the VDR can also accelerate that calcium into the cell. Which then does what? That excessive calcium can create increased oxidative stress, making the tissue issue worse and creating this kind of, this master problem. So I, I think some is good. I tell most people to go outside, get some sun exposure and then the other times of the year, hey, maybe a low level, but not taking vitamin D on its own. Taking vitamin D with vitamin A so we have good balance. It's not, it's not like just pound away. And I Have an issue. I'm a contrarian on a number of those things, which I think aggravates some people. But I just like to ask the question, are we all deficient or we are we just assessing things wrong?

In the book, you have your five step strategic thyroid solution protocol, Wondering at a very high level if you can talk to us about what the steps consist of.

Yeah, so initially we want to take a look at what's going on with thyroid. With thyroid markers, right? Do I have a state where I have a true glandular hypothyroidism going on? If I do, we got to get some. We got to get that person safe. Then we want to start to look at the, look at the rest of the panel, right? Am I getting good conversion? Do I have indications of tissue hypothyroidism? Do I have this pattern? Just looking at the thyroid panel of under or overproduction of thyroid hormone on a lot of production, but under conversion things that would indicate that, yes, this is a person who potentially has some tissue hypothyroidism. And of course, context matters. So does my patient have signs and symptoms? But once we look at that, then we want to look at, okay, are there mechanism, are there things in the blood chemistry that we can look at that may be driving this process? So look for the inflammatory markers. Does the person have elevated crp, homocysteine, uric acid, fibrinogen, elevated ferritin? Right. There's a lot of inflammatory markers that might indicate or drive the reduced T, reduced conversion in this tissue hypothyroid state. And then we want to look at the rest of the panel to say, okay, what tissues are potentially being impacted here? Right. Is. Is blood sugar regulation potentially being impacted? Is cholesterol physiology being impacted? Is liver physiology being impacted? Is renal physiology, adrenal physiog? What tissues are being impacted by this? So we have a good idea. Okay, where do we need to put our attention? What's the order? What's the hierarchy of what we need to do here? And if I missed the part, the other one of those parts is to make sure we're also not being over medicated, our clients not being over medicated in an effort to net to try and manage symptoms like, hey, more is better. Many times I'll see people come in and they're just overloaded in thyroid medication. TSH is driven. We're just way too low and we need to get that modified early on. But I think it's also important to say it is very rare that I'm directly trying to manipulate T4 or T3. Like, I'm going to give this to do this, right? I'm going to give this to make more T3. I'm going to give this. I don't think it's a selenium deficiency. The literature is not clear on this. There's a lot of micronutrients and peptides and amino acids that are. That are really critical, too high or too low that can have an impact on thyroid physiology. But if I. If I know I've got deficiencies specifically, then I know I probably have a gut issue that I need to address before I start trying to dump more stuff in or to try and detox stuff. I got to have a healthy vessel to put it into, right? I got to be able to put it into something. So that process of looking at labs for me has really been the way, or a really organized way to look at and interpret the labs. Not just read them for high or low, but interpret them based on a couple criteria. Are the values normal and appropriate given the person I'm working with? Right. If I have the person, they feel good, they function good, and all their labs are within whatever range you want to use. Optimal range, functional range, lab reference range. If they feel good and the labs are in range, maybe that everything's good. But is the lab value may be normal. It totally inappropriate, right? I have a patient sitting in front of me, no eyebrows, hair's thinning, they're overweight, they're tired, fatigued, they got no libido, they look hypothyroid. Anybody first day of med school would say, that's a hypothyroid person, right? Somebody upstream, that person's got a thyroid problem. If their TSH is normal or low, the value, somebody might say, well, they don't have hypothyroidism because TSH is normal. Well, that value is inappropriate. Or you don't have hypothyroidism because your TSH is low, you're more hyperthyroid. Look at your patient, right? It's a normal value, but it's totally inappropriate for the person sitting in front of me. And then I have to be, as a good clinician, interpreting labs, have to know, go now, go figure out why that value is normal even though it's not appropriate for my client. The other two is, is the value abnormal and totally appropriate? Right? Hey, Tshsi. T4 is low, T3 is low, and the patient's got hypothyroidism. Totally abnormal, but totally appropriate and Then the last category is, the one that's most concerning to me is, is the lab value abnormal and totally inappropriate for the way my patient feels. And I've, you know, these are the cases where you look at the labs and go, this is not good. Hey, my patient's CRP is 68 and they're telling me they feel fantastic. You're going, this is not good. You see things and that's not a good scenario.

In the book, you have a wellness wheel that talks about genetic fitness, physical fitness, dietary fitness, respiratory, sleep, emotional, environmental, habitual, microbial and metabolic fitness. So I want to talk in our last few minutes together, just do a little bit of rapid fire on these wellness wheels, talk a little bit about some of them. So in the book, you talk about the case of Chad and how he benefited from a carnivore diet. I'm hearing a lot of debate on both sides of the carnivore conversation. And I'm wondering, why might that be a helpful diet for people with cellular hypothyroidism?

Well, in this case, I think what he had already done a bunch of different things. He had chronic GI issues going on, blood sugar regulation issues. And so we did the carnivore diet as a way to just make a hard change in his GI tract. And I think by changing the gut flora, that's what allowed some of that stress response to calm down. I don't adhere to any one particular diet religion. I think that's a. We're doing a disservice to the community when we do that. We Paleo is better than carnivore, Carnivore is better than vegan. The paleos don't know what they're talking about. I think what we've done is circled the wagons and shot in. And really what we need to be doing is focused on what's the right diet for my person, my patient right now, that's whole food based and low processed. And I think we can change our gut flora pretty quickly with changing our diet nutrition. Not that vegetables are bad, but a lot of people, depending on what's going on in their GI tract, may not be able to process things today. And so getting them off of those foods that are creating a potential problem, not because we're sensitive or intolerant to them, but we don't have the floor, the enzymes to actually break those things down appropriately. So in that situation, it was just a. I think the big thing was it made a significant change in his biome and dysbiosis again. Another potential trigger or cell stress or sleep fitness.

How often is EMF and blue light mitigation a big winner for your patients?

I think it's. I'd say it's kind of like 50, 50. I mean, a lot of people are like, it didn't make. It didn't move the needle at all. And some people, they're like, oh my gosh, it's a huge difference to me. I don't care whether they think it's going to be a thing to move the needle or not. If they're already getting a lot of exposure, it's part of that piece. Like, hey, we've got to get all the five pound weights off the plank so we can fix it. So reduce the load the best you can because that'll give us the. Get us on that healing path that Navio talks about. And he talks about the CDR 1, 2 and 3. I kind of changed that to make it easier for some of the people I talk to from the cell danger response to the cell healing response. Right. We need that cell to start to say, okay, crisis over time to start.

Getting back to normal or respiratory fitness. Are there particular air filtration devices that you recommend in the home? And then I'm curious too, also in the respiratory realm, are you a fan of mouth taping?

So respiratory fitness is, I think, one of the fitness factors that I know I underappreciated. And then when you read through that chapter, you too will be very shocked at how important it is and how again, underappreciated it is. That being said, our air quality is super important. I. I don't have a brand in particular that, that I endorse, but I am a fan of home filtration for your air. Your air quality is very, very important. I also think that opening your windows, even when it's, you know, colder climate and getting some airflow in. I mean, I live in Minnesota and we keep our windows and doors shut for like nine months out of the year. And just think about unhealthy. That is so just trying to get some airflow in, avoiding toxicants. So, you know, like, put that hairspray down or, you know, like the aerosols and the Febrezes and the candles all, all contribute to your environmental fitness and your respiratory fitness. It goes without saying, like, you know, don't smoke, don't vape, any of those things. I think that sleep apnea, you mentioned that, Scott. I think that is a very underappreciated trigger for the cdr. Just think of Your body's in hypoxic state for that many hours, it's going to be thinking it's running from a tiger. So fixing that is really important. And all that information is in part three of our book. And finally, I am a fan of mouth taping. I think it's. There you go. It's person by person. But, you know, my son was just asking me the other day, he's like, do you still put that funny tape on your mouth at night? And I thought, I should probably start doing that again. Like, right. And, you know, looking at my oura ring. But I think that any intervention that can move the needle again, like, and I like objective data. That's really my gold standard, is that objective data I'm a fan of.

The funny thing is, patients ultimately will always say, I don't mouth breathe.

All right?

I know.

I don't mouth breathe at night. Okay. How do you know? Well, because I know. I think my partner would tell me, well, do they snore? Yeah. Well, then how would they know? Right. And two, the easy question that I will ask somebody is, do you get up often at night to pee? I do. Okay, then you're probably mouth breathing, because when you're mouth breathing has an impact on vasopressin, you wind up making too much urine. And now you're up multiple times a night. Your bladder is not too weak. You're just making more urine than you should, and it's probably because of mouth breathing. So put this stink, a piece of tape on your mouth. It's not a big deal. People think they'll be weird. How many people are staring at you while you're sleeping. That's your bigger issue, Right? It's not. It's not that you have tape on your mouth. Besides that, by the time you're ready to go to bed, all the things that are going to go on are over. Right. So just go to sleep.

I'm a huge fan. I like the Somnifix strips, and I've worn them for a long time, so those are great. I wanted to touch a little bit on the emotional conversation. So in the chronic illness community, I think there is sometimes resistance to exploring items in this emotional fitness realm because it kind of triggers that PTSD that the conventional medical communities kind of said, well, it's all in your head, your illness isn't real. And yet it's pretty probably one of the more important areas to work on. So in the book, you talk about heart rate variability as an indicator of emotional health and also the autonomic nervous system. The autonomic nervous system part made complete sense to me, but I hadn't made the connection between emotional health and hrv. So talk to us a little bit about that connection and then what are some of the things we can do to optimize or increase heart rate variability?

Okay, so number one, I do think emotional fitness is something we'd rather not talk about as a human species. We'd rather talk about things that we can fix, you know, with external things, supplements and other things. So that one is something where gotta ease into that one, but extremely important. So measuring your HRV again, I, I, in the book we talk about how that can be a really nice reflection of your autonomics, your autonomic nervous system. I don't think it's the best indicator for emotional health. However, we don't have a whole lot of good tools to look at someone and go, oh, I think emotional fitness is something you need to really work on. So I was just thinking of heart math and how using that device and optimizing that heart rate variability, using that, that can really help with some of the emotional pieces sometimes. I mean, there's a lot of different things. There's emdr. I had a lot of success with the MAP method for neural retrainment. Scott, you talk about Annie Hopper's extraordinary program, and I heard she's coming out with a new and improved one. But I just think in this chapter in the book, we just introduced you to things that you can just start to think about, start to think about may they be appropriate, and then dabble on the side. A lot of these things are free, EFT is free, that's tapping. They're just completely free and they can really help with your health.

Are there any biohacking tools that can be helpful for metabolism, for thyroid physiology? Are you supportive of photobiomodulation devices, red light therapy, anything like that?

Yeah, I mean, I got infrared sauna, I have. What's the little neuro thing that I wear on my wrist? I forget the name of that.

Apollo maybe.

Apollo. Apollo, Neuro, Yeah. I mean, got braintap glasses at home. All those things are tools. I think the important thing is that the tools can help us. Right, but we shouldn't be purchasing all the things to hack our physiology without addressing the foundational things. Right. So I think what I see is a lot of people have spent a lot of money on tools. And then you ask them, are you doing just, you're working on your breathing exercises, do you tape your mouth Shut at night. Do you do the. No. Do you. Are you on your phone to all hours of the night? Yeah. Okay, let's do the things that are simple, easy, and free before we spend a bunch of money on tools. But I think the tools can be really helpful. I mean, I've got them. I'm a person who buys them and says, how does this work? Is it change? Does it move the needle? Right? Like, hey, let me do this for a month. And then let me check my. Let me check my chemistries. Let's see what's different, right? Do I feel better? Do I sleep better? Does my HRV better? I think they can be beneficial, but especially when you're tight on dollars. People in this chronic illness space have spent a ton of money. Be careful not to jump over dollar bills to pick up the pennies. Right. And the dollar bills being the things that are free that you need to do on a daily basis.

And that's what I want to highlight from our book, Part three. Part three is. It just feels so overwhelming. I know I was. I was so ill, you know, so are you, Scott. It's just like, where do you begin? Where do you even start? And so I feel like part three in our book is all about putting it in simple steps, that some are completely free but can be just so important. So you have this, this, like, this guide to each of these fitness factors to help you not buy another $10,000 tool. Although, again, we all like those, those tools. And I do like red light therapy. I like laser there, all of it. So. But again, it's just like, it's very. Just hopeful to have almost a manual on, like, optimizing it all.

My last question is the same for every guest, and that is what are some of the key things that you do on a daily basis in support of your own health?

Yeah, it's essentially live the life of that part three. So, you know, every day, doesn't matter if I'm in Arizona like I am today, you know, up in the morning, exercise in the morning, hydrate, make sure I get a good sleep, you know, mouth taping. All the things we talk about in the book, I do them on a consistent basis. Good diet, good nutrition. And I wanted to make sure too, that I say that I don't have a perfect life. Right. I don't do everything perfect. That's not my goal. And I think we talk about the touch on this in the book, that you need to have more good habits and a few bad behaviors, I think to be happy. Some People can be perfect and meticulous with everything. I think that creates its own level of stress, right. To be perfect on everything. So I try. 80% of the time, 85% of the time, I try to have really good habits as my stable exercise, fitness, everything on that wheel, I try and address. And then 15% of the time, I kind of divert from that just to make sure, hey, everybody's eating, maybe some crappy stuff, but I'm at a party with people. E. All right, what's the big deal, right? I'm not a big drinker. But, hey, if I'm at an event I'm having, you know, maybe I'll. I'll have some cocktails because I don't want to have this life where I'm like, I'm afraid of everything, right? I can't do anything because I'm afraid I won't be healthy. If you're a little bit of stress on the system has a hormetic effect, right? But if you're a person who's got mostly bad habits and a few good behaviors, you're in trouble.

The only thing I would add to that, that's pretty much the way I roll as well, is that I implemented in doing my RIP test, so a dynomometer. And it's really. There's some really great science, because I want to know if the stuff I'm doing is working and the more objective, cheap data that I can get, of course we can wake up in the morning, go, I feel good. I don't feel good. But I will tell you this, that I changed my exercise program a little bit. Just a couple little tweaks, and my grip strength skyrocketed, which is a reflection of your mitochondrial ability, like a kind of a stretch. But again, it gives you an idea of where you're at. Because I'll have bad days, like when I took too much iodine. Couldn't even squeeze that. I mean, it was. It was terrible. So easily. And now I'm getting myself back up, and I'm watching it go up, and I feel like it's just a cheap, easy way of a reflection of overall health. So there's my nugget.

Nice. Another cool tool. I want to thank you both for being here today and really enlightening us and opening our mind to the thyroid debacle. I think there's so much great information in here that really lots of people need to hear about. It's a totally different way of looking at the whole thyroid conversation. It opened my mind, and so thank you both for the work that you're doing and for being so generous with your time and sharing with us today.

Hey, Scott, I just want to thank you for bringing us on the podcast. Really appreciate it. And I do should say that whether you know it or don't know, you played a big role in this version of the book because you were kind of helpful in getting us started with the finding the publisher, getting involved and then your work. To go through that book the first time and have so many questions about things really helped us change the book. If you didn't notice, this is a totally different book than the first version that you read. It's a softer version. It's got more. A lot of the questions you had asked, we answered in there. So I want to thank you for putting the time in to read the original draft from two people that didn't know how to write a book and kind of just kind of put a bunch of ideas on paper. So we want to appreciate, we really appreciate your role in the production.

Thank you. Yeah, whatever small part I had in it, it turned out to be be incredible. And I think it'll help a lot of people. So thank you for that. All right.

Thank you, Scott.

To learn more about Today's guests, visit Dr. Eric@rejuvencenter.com that's Rejuven R E J U V A g e n center.com rejuvencenter.com and Dr. Kelly@drkellyhalderman.com that's Dr. Kellyhalderman.com drkellyhalderman.com thanks for listening to today's episode. If you're enjoying the show, please leave a positive rating or review as doing so will help the show reach a broader audience. To follow me on Facebook, Instagram, Twitter or MEWI, you can find me there as BetterHealthGuy. To support the show, please visit BetterHealthGuy.com donate to be added to my newsletter, please visit BetterHealthGuy.Com newsletters. This and other shows can be found on YouTube, Apple Podcasts, Google Podcasts, Stitcher, and Spotify.

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