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In this episode, you will learn about the thyroid and how thyroid conditions may be the result of a Cell Danger Response.
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About My Guest
My guests for this episode are Dr. Eric Balcavage and Dr. Kelly Halderman.
Eric Balcavage, DC, CNS, CFMP, BCIM is the owner and founder of Rejuvagen, a functional medicine clinic in Chadds Ford, PA. He is a nationally recognized speaker and educator on various health related topics including thyroid physiology, bile physiology, detoxification, oxidative stress, methylation, and chronic illness. Dr. Balcavage is a Certified Nutrition Specialist (CNS), 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. The podcast 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. Balcavage has made it his mission to change the way medicine looks at hypothyroidism.
Kelly Halderman, DCN completed a Family Practice Medicine internship with the University of Minnesota. She has a Naturopathic Medical Degree from Kingdom College of Natural Health. She holds certification in MethylGenetic 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 Physician’s Committee for Responsible Medicine. Dr. Halderman 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 bile physiology. She serves as Weo Foundation’s Chief Health Officer; the global leader in water research and its application to living systems. Dr. Eric and Dr. Kelly are the 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.
- What symptoms might lead one to explore thyroid physiology?
- Why are thyroid issues broader, systemic issues?
- What is the best way to evaluate thyroid conditions?
- How does the Cell Danger Response (CDR) play a role in thyroid conditions?
- What are the primary triggers of the CDR that lead to issues with thyroid physiology?
- How might an autoimmune attack on the thyroid itself be an intelligent response?
- Is it more important to kill the bug or to modulate the host response?
- Could an elevated rT3 be an indicator of a Cell Danger Response
- Is iodine appropriate to use in Hashimoto's?
- What is the role of the mitochondria, compared to the thyroid and adrenals, in chronic illness?
- How might supporting sulfation and glucuronidation make the thyroid problem worse?
- What is "Multisystem Adaptive Disorder"?
- How might SIBO be associated with the thyroid?
- Is hypercholesterolaemia associated with the Cell Danger Response and issues with thyroid physiology?
- Is blood sugar metabolism associated with cellular hypothyroidism?
- What is the "Strategic Thyroid Solution Protocol"?
- What are the fitness factors that comprise the wellness wheel?
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October 7, 2022
Transcript Disclaimer: Transcripts are intended to provide optimized access to information contained in the podcast. They are not a full replacement for the discussion. Timestamps are provided to facilitate finding portions of the conversation. Errors and omissions may be present as the transcript is not created by someone familiar with the topics being discussed. Please Contact Me with any corrections.
[0:00:01] ANNOUNCER: Welcome to BetterHealthGuy Blogcasts, empowering your better health. Now, here’s Scott, your BetterHealthGuy.
[0:00:15] ANNOUNCER: The content of the 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.
[0:00:34] SCOTT: Hello, everyone. Welcome to episode number 173 of the BetterHealthGuy Blogcasts series. Today's guests are Dr. Eric Balcavage and Dr. Kelly Halderman. The topic of the show is The Thyroid Debacle.
Dr. Eric Balcavage is the owner and founder of Rejuvagen, a functional medicine clinic in Chadds Ford, Pennsylvania. He is a nationally recognized speaker and educator on various health related topics, including thyroid physiology, bile physiology, 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. Balcavage 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 Methylgenetic 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 bile physiology. She serves as Weo Foundation's Chief Health Officer, the global leader in water research and its application to living systems.
Dr. Eric and Dr. Kelly are the 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 Balcavage and Dr. Kelly Halderman.
[0:03:02] SCOTT: 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?
[0:03:21] DR. ERIC: Well, initially, I had no interest in thyroid physiology, to be honest. But I had a family member, my brother had one day they had a conversation with me about what was happening with his wife. She had fibroids, so they were going to do hysterectomy. She had hypothyroidism, she had iron deficiency, so they're going to take out her hysterectomy, thyroid meds and iron. That was going to be the solution. I said, “That's not what I do. I'm a chiropractor. Why are you reaching out to me?” He's like, “Because you're going to fix it.” I was like, “Oh, okay.” When your big brother tells you, this is what you're going to do, you kind of do. He's done this to me multiple times, by the way, just as a side note.
I started digging in and getting back to my roots and blood chemistry. Then as I'm helping her, I'm having conversations with my chiropractic patients. I was floored by how many people were on thyroid medication, and how most of them didn't feel well. That fueled the fire. I did a lot of work with Datis Kharrazian, Apex, and all that early education. Did my functional medicine training. Then I just thought something was missing from the big picture. That really had me just digging and digging into the literature and eventually, a friend of mine, 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.
[0:04:46] SCOTT: 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 you to create a larger toolbox for yourself and for your patients? What was it that drove you to shift to the new paradigm?
[0:05:06] DR. KELLY: Right. Just like you explained, I was practicing allopathic medicine. 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 to the root cause. We were taught to address with medications and lifestyle innovations, epigenetics, which we're going to get into, were definitely not something that we had grand rounds about.
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 have a white coat on. I'm going to get the best care ever. I got shipped off to the Mayo Clinic, best neurologists 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. I was left with a lot of medical educational debt, but no tools in my toolkit that could actually help me.
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. I use those tools to help, really reverse my health. Meeting Dr. Eric, one of the diagnoses is that I have was Hashimoto’s, that along the way. A lot of people struggling with Lyme and mold, and those were part of my root causes. The Hashimoto’s, I really felt like in medical school and in training and doing even the residency, rounding with really great endocrinologists, I'm like, this just doesn't make sense, you guys. Why are these people were putting on medication? Why are they still not feeling well? What are we missing here? You just don't really bring up those kinds of things, until you are the patient.
I was treated by a wonderful Lyme literate doctor. She put me on a bit of thyroid hormone replacement. I did not feel better. That actually made me feel good for about two weeks, and Eric will go into that mechanism. Then I really crashed. It wasn't until I started really digging into Dr. Eric. I became 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 your idol. I was like, “Can I get your autograph?” Because he's just someone who I respect so much, because he digs into this literature. On average, a published paper gets read by seven people in the medical literature. Eric's one of those seven people. I guarantee you that, is that he went in and he dug in and to help us all understand better, give us a model to get people better.
I applied what Dr. Eric told me to do, basically, through his teaching. I call myself recovered. I mean, I'm constantly doing things to help my health. That's why I wanted to come help with writing this Thyroid Debacle, is because I have the perspective of sitting in the chair of the prescriber. I had to use the guidelines to help with the people in my care and your hands are tied, when you have those guidelines. That's it. That's really my story of the thyroid journey.
[0:08:34] SCOTT: Since you want his autograph, maybe you can get him to sign a copy of the book, The Thyroid Debacle.
[0:08:39] DR. KELLY: Maybe. We’ll see.
[0:08:42] SCOTT: 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?
[0:08:53] DR. KELLY: Yeah, so absolutely. Symptoms are very, very important. Because as we will talk about, you can have normal, completely normal labs. But in the labs, they look good, but there's not enough thyroid hormone inside the cell. What are we looking for? Chronic fatigue, weight gain, hair thinning, dry skin, constipation and reduced libido. I checked off all those boxes, even when I went on thyroid replacement.
[0:09:20] SCOTT: 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? Then why are those not the same thing?
[0:09:43] DR. KELLY: I think, most allopathic physicians are taught that hypothyroidism is a condition where the thyroid gland doesn't make sufficient T4. The allopathic mantra in my mind is as long as there's enough thyroid hormone in the blood, there's enough inside the cells. Okay, that’s flag number one. Red flag number one. The problem is that 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. They don't have a tool to address it other than medication.
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. Because most of the production thyroid hormone is by the thyroid gland. The thyroid hormone is most active inside of your cells. 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, it's tissue specific.
[0:11:01] DR. ERIC: I think, what we see 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. Based on the scientific literature, it's about 90% of the thyroid gland is damaged by the time somebody gets diagnosed. You've lost about 90% of the function. That's not the beginning of a disorder, any more than cardiovascular disease starts when you have your fatal heart attack. What we don't have is great tools for assessing what's going on in the cell. From an allopathic standpoint, we don't have guidelines to dig in and address. 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.
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 and a free T4. I think, for the vast majority of people we see who get told, “Hey, your TSH is normal. 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.
[0:12:16] SCOTT: In the book, you go into great detail about a number of the tests that can be explored. Are there a few tests that you find important evaluating thyroid function? Then, are there any tests for the exploration of this more cellular hypothyroid condition that happens as well?
[0:12:32] DR. ERIC: I think, when we're looking at thyroid gland function and production, obviously, you can do an ultrasound, see if there's thyroiditis. You can do a biopsy to see what's going on there. Just from a standard assessing the thyroid gland, traditionally, there's just – TSH is used as a screening test to determine is there too much or too little thyroid hormone production? Then there's what they call a reflex to free T4. If free T4 is within the reference range, then it may be considered sub-clinical hypo, or hyperthyroidism.
Those things, I think the assumption is, 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. It really doesn't. I mean, really, what TSH oftentimes is evaluating is what's going on with the hypothalamus and the pituitary, and not at the peripheral tissues. 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 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 that gets regulated.
I just think when we're thinking about assessing from a medical standpoint, those are the two tools that are looked at. Rarely will I see a medical physician run a T3 or free T3. Rarely will I see a physician run thyroid antibodies. I think, the reason for that is that they pretty much assume that if there's the person who’s got hypothyroidism already has thyroiditis, that is it's an immune-driven problem primarily, so there's no need to run those things. They're not medically necessary to diagnose.
From a functional perspective, every test in a thyroid panel that's available is, I think, important assessing tissue status. 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.
[0:15:04] SCOTT: 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?
[0:15:20] DR. ERIC: Absolutely. Because the tissues have the ability to self-regulate based on what's going on at their level, at their tissue. If we didn't have that ability to do that, we'd be in trouble. Because if I was 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, right? I don't want all the tissues upregulating their metabolism at the same time. It could be a disaster, right?
What we have the ability to do is if the GI tract needs to upregulate its metabolism, we can turn it up there and turn it down somewhere else. 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.
[0:16:17] SCOTT: Many of our listeners will be familiar with the Cell Danger Response model from Dr. Bob Naviaux. I did a podcast with Dr. Neil Nathan on that as well. 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, hypo-metabolic adaptation, or a protective state? Then should the focus be on the thyroid? Or should it be more on the broader triggers of that Cell Danger Response?
[0:16:49] DR. KELLY: Sure. I am a very big fan of both Dr. Naviaux and Dr. Nathan. If your listeners have not listened to your podcast with Dr. Nathan, just run and go listen to those. Absolutely excellent. Cell Danger Response, you did a wonderful job, and you did, too, Scott of really going through this and digging in. Really simply, it's an evolutionary conserved metabolic process that's designed to protect us, ourselves from harm. It can be triggered by chemical, physical, biological threats. Those threats exceed the cellular capacity for homeostasis.
It's like, we get a threat and it's just beyond what we can just shrug off, I guess, in layman's terms.
This paper changed everything for me. This paper changed everything for Dr. Eric, because we realized that cells and tissues respond differently to homeostasis, versus allostasis, like that load that's pushing down. What we're realizing with thyroid is that the dysfunction is more likely better term in adaptation, and adaptation as part of a Cell Danger Response. 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. Just like Eric said, we hope your body's going to act differently.
When we think of, okay, we have to – it's almost like when we have to 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. We talked about in the book, it's usually not one thing, one magical, “Oh, I killed all the Lyme and ow I’m good.” It’s gut function and brain function. I mean, all of our respiratory function, and all of that, which we call fitness factors.
Again, it's that adaptation, which is not a dysfunction, because when I was taught as allopathic medicine is that, oh, your body's just turned against you. It's like, how disempowering, or what a message of hopelessness. My body turned against me? No, no, guys. No. It actually is really, really helping, again, that model of laying on a beach versus running from a tiger. You want your body to be responding this way. Our job as practitioners and clinicians, health coaches is to figure out what's weighing you down. Figure out what set it off. Again, I think, again, to answer that last part of that question, Scott, we believe that it is protective. Protective state.
[0:19:36] DR. ERIC: When I read that paper, it was eye-opening. It was the piece I was missing. 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. I read that paper. It was interesting. There was not much of a discussion about thyroid physiology in that paper.
I reached out to Dr. Naviaux 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. He said, “Listen, Eric, I don’t know much about thyroid physiology.” I was like, “Wow, I got to dig in here.” I've done the research and looked at whether this is a broken physiology, or adaptive physiology. But the downregulation of cell metabolism in 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 down-regulate the metabolism, you need a lower T3 state. I think it's the one step that's missing on that paper is the adaptive changes in thyroid hormone in those cells perceiving danger. Critically, critically important.
[0:21:06] SCOTT: 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, so that they're even in a Cell Danger Response. 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?
[0:21:29] DR. ERIC: Yeah. I think, you have to take everything into context, right? What's the person's timeline? What does their story tell me? What are their signs? What are their symptoms? What did the labs show? You're absolutely correct. We don't have a definitive task to say, is this person in homeostasis, or allostasis? There's not something we run in. It's like, “Bing, bing, bing. Allostasis.” We have to look at the factors. Do they have multiple markers of inflammation? Do they have 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? Do we have patterns that we would associate with a cell that's in allostasis? If they have that, then I think we have a pretty good indication that, hey, this is the person – this person is not operating from a homeostatic standpoint.
[0:22:19] SCOTT: 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? Are we talking about mold, or Lyme disease, or viruses, or heavy metals, environmental toxicants, maybe EMFs? What are the things that you think are likely the bigger triggers of Cell Danger Response?
[0:22:41] DR. ERIC: I think, all of those have the potential in everyone. Is it mold? I think we get stuck, as Kelly alluded to, we get this stuck on the one thing. It's this. It's mold. It's EBV. It's this one thing. I shy away from that model. I think, it's more the load over time. 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, the capacity of that plank is a 100 pounds, and I have one acute stress. Boom. Dropped it on that board, it could break.
Really, that's not what often happens to us. We think it is, because it's the last piece. Really, what happens for most of us, we go through life, we stack a 5-pound weight. We keep going through life, we stack another pound of weight, we stack another 5-pound weight, and another and another and another. Eventually, we stack the fifth-pound weight and we get to a 105 pounds and the board breaks. Which one of them caused the problem?
In our model, we have to look at all these things. We talk about them as fitness factors. Hypoxia. Poor breathing. Of course, 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 diet, nutrition, toxins, all of these have play a role and we're only going to be as healthy as the weakest link. What I try and get people to understand what that analogy with the board and the cinderblocks is, once the board breaks, if I just pull the last 5 pounds on, the gluten that you think triggered it, or the virus that you think triggered it, if I just take that away, is the board fixed? 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 may be have adapted to and seem to be pretty good at adapting to in the past. 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. Then we can set it back up there. Then what you realize is 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.
[0:25:15] SCOTT: I love that. It's the super smart person's bucket analogy, the cinder blocks and the boards and all that stuff. Very cool.
When the body is in an intelligent protective adaptation, essentially, putting on the brakes, would 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?
[0:25:44] DR. ERIC: I'd say, the answer to that is, it could be. 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. 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.
We also get reduced peripheral conversion, because TSH, higher TSH is a driver of T4 to T3 conversion. It helps that conversion process. By saturating the hypothalamus and dropping the TSH, and some docs, like to be having it as low as possible, we actually prevent the thyroid gland 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. People feel good initially, and then all of a sudden, they hit their plateau, and then they start to regress. I think, it can be a problem.
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 nongenomic effect of T4 on cells is not discussed very often, except in the cancer literature and research. In those circles, hypothyroidism is considered a protective mechanism against cancer growth, okay. I said, it would be great to see a paper of 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.
Lo and behold, in 2019, the paper came out. I said that to Kelly. No way. Somebody actually took all these different types of cancer, and the incidence of a whole bunch of different cancers is greater in people that have been on longer term T4 therapy. Isn't that crazy? 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.
For some people, that may sound scary. “Oh, my gosh. Is my T4 going to cause me to have cancer?” We can't say yes, for any one particular person. When you look at the literature, there is increased potential of a number of different cancers.
[0:28:41] SCOTT: 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. 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 hadn't really heard before. As I understood, your perspective, was that auto-immune response would itself be intelligent? Talk to us about how that autoimmune attack on the thyroid gland could also be an intelligent response. Then, how do we fix the damage to the thyroid gland once that attack is no longer needed?
[0:29:25] DR. ERIC: I learned that when you have antibodies, the immune system makes these antibodies that are little PacMan, eating away at your thyroid gland. It senses it's no longer self-tissue for some reason, and it starts to attack. There's lots of mechanisms for, I think, there's seven or eight listed hypotheses for autoimmunity. I just thought that was – that can't be the case for everyone.
As I was digging through the literature, you find out that the thyroid cells actually have sensors for danger particles. When a when a cell is being impacted by a bacteria, a virus, it can release signaling molecules. We call those things PAMPs, that can release parts of its structure. We call those DAMPs, danger associated molecular proteins. 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. I'm the tissue that's in danger. Come help me.” Those are signaling molecules. Those particles in some of the other things warn the other tissues that hey, somebody's trying to break in.
The other surrounding cells can initiate their own Cell Danger Response. It'd be like me sounding the alarm like, the troops are coming. Hide, block your doors. The thyroid cells themselves have danger sensing receptors, which is really interesting. 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. The cells almost initiate 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.
When you think about it like that, you go, “Wait a minute, 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. If this becomes a chronic, persistent danger physiology, what's the best way to slow down and globally slow down the metabolism? That is to slow down the production of thyroid hormone right at the source. We see this in cases where there's famine and starvation. There tends to be some increased incidences of thyroiditis Hashimoto’s.
It changes the idea that the antibodies are the thing that are just gobbling up. Your immune system lost control, and it's gobbling up. Matter of fact, that paper, I think it was 2020, stated that the thyroglobulin antibodies produced no damage to the thyroid gland, and that the TPO antibodies caused very little, if any direct damage to the thyroid gland. 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.
[0:32:35] SCOTT: 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 repair phase that we necessarily have to think about. Am I understanding correctly?
[0:32:55] DR. ERIC: There has to be a time for repair and regeneration. 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. I'm doing things to help the physiology overall. What we see in time, as we address these triggers, these stressors, there can be a lot of destruction that occurs in 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.
What I see in my practice is that, hey, I need as they're getting better, they need less and less thyroid hormone, and they have better and better conversion. 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 and it can't repair itself, the literature seems to show, no, the thyroid gland can redevelop. It can regrow.
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 triggered the thyroiditis to begin with. Why would it ever get better? I understand that perspective. 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 recover all the time.
[0:34:28] SCOTT: 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? Would you then use something to support immune modulation to calm that hyper-vigilant immune response? Or is that even a bad idea, because you're suggesting that that auto-immune response itself might be part of the protective mechanism?
[0:35:00] DR. KELLY: Yeah. I think in some situations, we need to directly address the infection, but not always. Again, it's a spectrum. I think, we always need to consider what's allowing the organism. Let's say, if it's Lyme, or co-infections, what's allowing that organism to thrive? Considering the physical terrain, chemicals, environmental toxicants, like our emotional health. Considering that entire entirety of what could be causing, again, that organism to not be dealt with appropriately? Because we have an immune system. We have thaT4 protection. It just maybe overwhelmed.
Regarding the tools, Scott, I think it depends on the shift in the immune system. Dr. Eric and I, he's much more down the road in this, but we started using the Lympho MAP from –
[0:35:56] SCOTT: Lymphocyte MAP. Yeah.
[0:35:58] DR. KELLY: From Cyrex. I think, that can provide a lot of insight on which products in which way you want to try to help shift the immune system, because we really look at it pretty antiquated. This test is very revolutionary. I know Dr. Eric, on his podcast try the right answers. He interviewed Dr. Vojdani.
[0:36:19] SCOTT: Aristo Vojdani.
[0:36:21] DR. KELLY: Thank you. Yes. They had a wonderful conversation about that. I think that the listeners might want to listen to that as well. Overall, with the immune system modulating, I think he made a good point, is that we – you don't want to shut everything off, or suppress everything. We're trying to offload the allostatic load, but I always think gut healing, breathing exercises, meditation, cold exposure, looks like it has some balancing of the immune system early. Right now, we're still learning a lot about that.
Plant sterols. If you look at the science on some of the studies on the plant sterols, I find that those are really important, because they can go both ways. They can balance the two active immune system. They can modulate that down, underactive, pull it up. I really am a fan of plant sterols.
Then lastly, I'll just say in my toolkit has three years of peptides, like TA1, TB4. Some of those are very nice complements. Again, per specific person. I really encourage everyone to just work with someone who knows what they're doing here. Not everything's good for everyone, right?
[0:37:32] DR. ERIC: Yeah. I'll jump in there, too. I think something Kelly often says is, is principles over protocols. 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? I think, that gets us in trouble sometimes. Sometimes, if we have organisms, we maybe like, okay, this might be excessive. We need to tamp in this load a little bit. I often think, at least initially, the immune system is adapting to try and help.
Suppressing the immune system when there's a chronic infection, 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. We'll look at the immune system. I'll look at that Lymphocyte Map. You can say, some of the things that you might have been doing were probably working against the immune system. Maybe those were the wrong strategies.
Even when we look at that Lymphocyte Map and 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. The people feel worse, because there is some type of active issue going on that we should back off and let the immune system do what it's doing, and address all the things around that, we give the immune system the best chance to heal and recover.
[0:39:07] SCOTT: I love that you mentioned, Dr. Kelly, the plant sterols. I was just talking with a mentor yesterday. We were talking about the Moducare product from Thorne, which is one, that can be very helpful and it's 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? Could we be hyperthyroid based on some of the conventional tests and still have hypothyroidism at a cellular level?
[0:39:38] DR. ERIC: Yeah. When we think about hyperthyroidism, without somebody on – 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 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 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 few others.
The mechanisms is 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 drove the thyroiditis to begin with, or the immune 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. I see that all the time.
People, often when I'm talking, or 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 plan.” If 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. I think, that gets missed many times in hyperthyroid treatment. 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 radiate it, and then everything will be good.”
No. That was the effect. It wasn't the cause. We still have to address the same factor. Everything we talked 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? Absolutely, we can. We often see people, especially as their dosage goes up, and they have this allostatic physiology going on, the brain, the pituitary gland get upregulated, because there's different receptors there, that different sensitivity in a lot of the peripheral tissues, so we quickly saturate the hypothalamus. We activate the sympathetic nervous system. We drop TSH. Now the person is struggling with brain fog and fatigue and even histamine related problems as a result of creating hyperthyroidism in the brain, and hypothyroidism in the peripheral tissues. I think, they go to their physicians and have both signs and symptoms, and their physician is like, “Okay, we need to get you on an antidepressant,” because this can happen.
[0:42:39] SCOTT: Integrative doctors will often look at reverse T3, which I think of as the brake pedal. What are some of the common causes that reverse T3 would be elevated? 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?
[0:43:02] DR. ERIC: Yeah. I think, we can sometimes use reverse T3 as an indication that we've got a problem, okay. If we have a person who's on no thyroid medication, if we just do a general comprehensive thyroid panel, and a 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.
We always have to take the context into perspective, right? Somebody could have problems with their liver, 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 T3 as well as well. There are a number of factors. When I see a T3 that's starting to elevate, we have to take into consideration, is there physiology that matches this from a signs and symptoms perspective? 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 – there's this discussion that reverse T3 blocks T3 from binding to receptors. Reverse T3 does not, based on the literature, block T3 receptors at the nucleus, okay. 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.
I don't look at it as a functional problem. I look at that as an adaptive change. 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 plasma membrane, of what we call the integrand receptors, but that's a whole another in-depth conversation. I think, we look at as an indicator that there's potentially tissue hypothyroidism.
The other thing we always have to keep in mind is, where am I starting with T4, free T4? Because if I have a lower T4, or free T4, then I'm going to potentially have a lower T3, 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? How much free T4 do I have in the system? I don't have much T4, free T4, then reverse T3 three could be normal and I could still have tissue hypothyroidism going on. We have to look at T3, free T3. We look at the ratios of T3 to reverse T3, free T3 to reverse T3 free T3 to free T4 to get an indication of what's happening inside the cells and tissues.
[0:45:59] SCOTT: 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. What are some of the key things that impact the conversion of T4 to T3?
[0:46:19] DR. ERIC: Yeah. Inflammation, hypoxia, any of those danger physiology things happening in the cell will cause a down regulation of T4 to T3, and an increased conversion of T4 to reverse T3. The discussion about, hey, people do – I hear this all the time. I see people coming in with the same merry go round with T3 that they do on T4. “Hey, initially, I felt better.” Okay. 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. So then, I had to take more and take more and take more.”
About two weeks ago, I had a 140-pound female who's taking a 150 micrograms of T4 and 80 micrograms of T3. This is somebody who kept trying to fix the T4, T3 values in the blood and didn't understand the impact. They were frustrated, because T3 levels just didn't seem to stay upregulated. We have to remember, 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. When you deactivate that T3 to T2, that some of those metabolites can almost act like 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 physiologic mechanisms. 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.
[0:48:16] SCOTT: Is part of the reason that people feel better initially, and then that wears off because there's essentially a feedback loop that then as you're taking T4 or T3 that that then suppresses your body's own production of those hormones. Does that happen as well?
[0:48:32] DR. ERIC: Yeah, there's a bunch of loops. We learned one loop in school. If you read papers, like Hoermann’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 transport mechanisms potentially. T3 at physiologic doses doesn't have the potential negative consequences that T4 might have. 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, okay.
[0:49:18] SCOTT: Where do you stand on the use of supplemental iodine and people with Hashimoto’s? I know many people suggest it's contraindicated. Other suggestion is completely fine. Any thoughts on that debate?
[0:49:29] DR. KELLY: Yeah. It is definitely all over the place with recommendations. I have noticed that quite polarized. Or can I really agree on this is that just like everything in reality, we're probably somewhere in the middle. There's a lot of people who are probably a little deficient and not so much probably in this country, because we have, salt has iodine in it. I feel like, we're not necessarily – the number one cause over in our civilization, like it was for third-world countries, first-world countries versus third is Iodine deficiency. Ours is Hashimoto’s, that's the cause of most hypothyroidism.
Then, I think that a lot of people may be overloaded. They may be eating too many foods high in iodine salt. I rarely tell people, get some iodine. It'll fix your thyroid problems. I will tell you this is that I saw a video on Instagram, on the weekend, where you put a couple drops of Lugol’s on your arm. This doctor was saying, after an hour, if these dots are gone, you're very deficient in iodine. Well, my dots weren't gone. I'll tell you what, I did not feel well at all the next day. I think I set off a mini-flare. I'm careful. I'm really careful. I'm not on the polarizing, no iodine. Never, never, never. Nor am I telling people to take it. My mantra is be careful.
[0:50:59] SCOTT: 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. I'm wondering, where do you place mitochondria support in terms of comparing that to supporting the thyroid, or adrenals? 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? 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?
[0:51:41] DR. KELLY: I mean, people think that they're going to fix their fatigue, their Cell Danger Response symptoms with ribose and CoQ10. I shake my head, because I feel it's like using high-octane gasoline in a car that's clunky and old and needs a lot of work first. That's how we look at what we're doing. I've said over and over again, you can't medicate yourself to health. That's how I feel. I feel, you have to put in a lot more work than just put pills in your body.
Eric has then noticed that you can't really supplement yourself to help, correct me if I'm wrong Eric, but what we're saying is that all three of us have seen the clients come in with suitcases full of supplements. It just didn't fix any of their problems. We feel like, there's a great place for supplementation. Some of those nutrients I just mentioned are absolutely wonderful. 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.
[0:52:48] DR. ERIC: I think, it's a nice protocol. Oh, the mitochondrial doesn't have the nutrients. We could try it. Sure. Give it a shot. See if it improves. I would ask them the next question like, if it's just nutrient deficiencies, why do I have nutrient deficiencies? 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. 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.
Downregulation of the mitochondria is a protective mechanism. One of the things you need to do to down regulate that is reduce the amount of T3 in the cell. Now, why would we do that? I think that becomes important. One of the reasons that we actively downregulate that mitochondria, we have this cell danger physiology going on, is when we rev up the mitochondria and we have high efficiency, or high function, I should say, better say not efficiency. I'll talk about why I say that in a second. When 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 of the body, it makes antioxidants inside the cell. One of those is something called glutathione. 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. If we ramp up the mitochondria during that process, we can – the cell is already increasing oxidative stress, or free radicals to deal with whatever that threat is.
If I increase the free radicals, the oxidants as 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. Now I get excessive oxidative stress, which does what? It destroys the cell and I'd lose cell function. I don't want to lose the cells. This is beautiful design, that we have this downregulation of the metabolism, downregulation of the mitochondria. 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.
I've done it. I've given people mitochondrial support, and it doesn't work. 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. 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. 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 the efficiency of the mitochondria. In the cell danger physiology, the mitochondria actually becomes more efficient at pushing energy, food energy through to make cellular energy. That doesn't sound like it makes sense, because I'm not making a lot of ATP. I don't feel. I don't have energy. It becomes more efficient, when we have a really robust cell function, where we're in homeostasis, we're pushing a lot of stuff through. Thyroid hormone helps regulate these things called UCP proteins. These are disbursement channels for excess energy.
That helps us blow out some of the extra energy, and we can use that, like in the fat cells to generate heat. One of the reasons why with people always chronically cold when they have hypothyroidism is because they lose that electron leak that helps generate heat as a source. We push more food energy through the electron transport chain, more cellular energy through there. It's more efficient, because we don't have to waste, but it also means we don't need as much food energy to drive that system.
[0:57:37] SCOTT: If the thyroid gland is producing adequate thyroid hormone, but the peripheral cells are still hypothyroid, is that always a Cell Danger Response? Or are there cases where there are things that you can do at the level of the cell to optimize thyroid physiology?
[0:57:53] DR. ERIC: I think, in acute situations, if I saw normal thyroid physiology, a person had symptoms, I'd have to take into consideration what they did in the last couple of days. 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 chronic changes in let's say, lipid physiology. They have insulin resistance. That's when we say, okay, there's something bigger going on here. If somebody came in and I'll always ask the person, what did you take yesterday? What did you do yesterday? 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 bloodwork and whether somebody is on a fast, whether somebody just worked out, whether they were hydrated, not hydrated, all those things can play a role in what their labs look like.
[0:58:49] SCOTT: Many people think of low thyroid as a problem with the thyroid gland. In the book, you say that hypothyroidism is a spectrum. 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. Where's the majority of T3 in the body produced?
[0:59:13] DR. ERIC: Any cell that has the deiodinases, deiodinase 1, deiodinase 2 can help with that production of T3, okay. We talk about the liver plays a big role. We talk about the kidneys play a big role. We talk about the GI tract. Any cell that has deiodinase 2, which is the primary converter of T4 to T3. Deiodinase 1 is another one that people talk about. 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 deiodinase 1 often upregulate. Definitely, the liver produces some with deiodinase 1 in the renal system.
When a cell takes in T4, it converts it via deiodinase 2 to deiodinase 3. Deiodinase 3 binds to the receptor, hangs out for a while. Then T3 can go right back out into the bloodstream and become part of that circulating pool. Any cell, or tissue that has the ability to convert T4 to T3 contributes to the blood level of T3. That's really important, because there are some tissues, some cells and some tissues that cannot generate their own T3. That's considered a biologic priority to have – thyroid gland makes some, but all these peripheral cells make quite a bit of T3.
[1:00:48] SCOTT: 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. 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 2 detox interplays from a thyroid perspective?
[1:01:22] DR. ERIC: I think again, this depends on the extent that we're trying to push pathways. Is the person already in a hypothyroid state? If we push those pathways harder, could we deplete some of the available thyroid hormone? That's a possibility and that's been discussed in the literature. I think at physiologic levels, that the person is not hypothyroid is probably 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. That's been talked about in the literature and the research.
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, 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. Then I guess, I would have one other comment on that. That is, why are these pathways not working to begin with? I think that's the other question we have to ask.
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. I don't want to be like, hey, more as 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.
[1:03:03] SCOTT: You coined the term Multi-System 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. Talk to us a little more about multi-system adaptive disorder. Is it the case that similar to the Cell Danger Response, leading to cellular hypothyroidism, that the same model, essentially, is applying much more broadly, much more systemically throughout the body?
[1:03:29] DR. ERIC: Yeah. I think what happens is for physicians, for clients, our patients, they want to know what is wrong. “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 allopathic thinking, in my opinion. That it's just an individual system or tissue. 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 downregulated. 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? If somebody broke in and attacked her child, Kelly's not going to – right Kelly? You're not going to continue to cook.
[1:04:33] DR. KELLY: Correct.
[1:04:34] DR. ERIC: You're not going to probably take the time to turn the burners off, put everything in nice glass, glassware, put it in the fridge. You're not going to probably try and slide an extra load of wash and finish that up. I'll be with you as soon as I finish the vacuuming. You're not going to go take a nap. You're not going to go have sex. All the systems, and we see this in 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? You're not stopping to take a nap. You're not stopping to have sex. You're not doing that stuff.
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, bile, those things don't – they lose their importance. I needed to come up with something to tell my patients, because they wanted to know what is wrong with me. Do I have an adrenal? Yes, you have a multi-system adaptive disorder. You're not broken. You're adapting to get some type of an excessive stress response. It's physical, its chemical, it's emotional, it's microbial, it's environmental. It's respiratory. It's sleep oriented. Trauma. These are the things that are causing you to be in this danger physiology.
When I explain it to them, the intruder, they start to have that aha moment. “Oh, I get it.” I say, from an allopathic approach, we'd say, we'd walk into Kelly's house and go, “Kelly is a terrible cook. All the food is 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. But the problem isn't solved. Kelly's not eating the meal. She's still fighting to 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. We need to go find it.” Not how do we clean this up?
[1:06:40] SCOTT: SIBO is such a common issue these days. We know that hypothyroidism can impact GI motility. When and how often do you suspect some degree of cellular hypothyroidism in people with SIBO? What is motilin? How does impaired bile flow come into the discussion around cellular hypothyroidism and SIBO as well?
[1:07:01] DR. KELLY: Sure. SIBO is just so common. 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. Certainly, 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 bile flow specifically. That motilin, that hormone that's released by the duodenum and the jejunum, that stimulates the contraction. The T3 and the T4 that they'll have influence over that. Again, go back to what Eric is saying. Everything is connected. Also, those bile salts, they're actually very modulatory to the gut flora, the microbiome. When that's off, you have to suspect that that has something to do with what's going on with the SIBO and the recurring, revolving door of SIBO. If you're not addressing the cellular hypothyroidism, we're just going to be going around in circles.
[1:08:14] SCOTT: You hinted at this one earlier about hypercholesterolemia is a common issue. When high cholesterol in some cases, that may not be a huge problem. But I'm wondering, is there a connection between high cholesterol and cellular hypothyroidism? 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?
[1:08:39] DR. ERIC: Yes. 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 help with a 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. Cholesterol level can go up.
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. 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 proteins to dock to the cells and release the cholesterol. 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.
Now, that LDL receptor doesn't talk 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 bile physiology, because cholesterol is a huge piece of it. It's also going to impact other tissues. Almost every hormone has cholesterol as the base. If we're talking about, I hear people say, “Well, I don't have a thyroid problem. I've got an adrenal problem.” Okay. Well, you have high cholesterol. Cholesterol is in an acute state, the adrenal gland can make its own, what they call De novo cholesterol.
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. 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. All my hormone metabolism gets down regulated.
When we see the elevation of cholesterol, we have this 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 on that. 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. Then I can't get the cholesterol into the tissues out of the bloodstream, and so it builds up. T3 plays a critical role at the hyperlipidemia we typically see.
[1:11:54] SCOTT: So many people these days dealing with glucose dysregulation, insulin resistance, diabetes. What's the connection between those conditions and cellular hypothyroidism?
[1:12:05] DR. ERIC: There's these things called GLUT transporters, that help get glucose into a cell. There's a whole bunch of them. Guess what? T3 helps regulate all of them. 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 GLUT 2, with the least amount of T3. What's the impact there? Well, GLUT 2 is what transports glucose out of the liver into the bloodstream, and it's what helps transports glucose into the fat cells. We can make more glucose and get fat, even though we have a lower T3 state.
When we think about insulin resistance, we blame glucose. We blame insulin as the problem. Oftentimes, we see people who don't eat much carbohydrates. 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 reduces glucose. He said, “All your patients are probably over-consuming glucose.” I'm like, “That's not true. That's not true.”
Why is glucose not getting into a cell? Why are the cells not listening to insulin? Well, if I'm a cell and I'm in danger, 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. To get glucose in the cell, you need these glucose transporters. In a fasted state, depending on the tissue type, maybe use GLUT 1, maybe using GLUT 3. In a fed state, primarily you're using – that's when we start to use GLUT 4, which is an insulin dependent receptor.
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, so now blood sugar goes up. 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. Increased insulin goes up to try and activate more of those receptors. Then we have this back-and-forth yo-yo effect, where I need more and more and more, because the cell is 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, a danger physiology, versus it's just the cells are full, you eat too much carbs, you don't exercise enough.
[1:14:31] SCOTT: 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. 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?
[1:15:11] DR. ERIC: 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. I don't think the solution is always suppressing. What's interesting about histamine, we talk about mast cells producing histamine, almost every cell can produce histamine, right? What's interesting in the literature about the mast cells is the mast cells, I think there's – We're not clear on it, but that they can generate their own thyroid hormone, or they can store thyroid hormone. What's the significance of that? Maybe thyroid hormone is actually stored in the granules. If a cell is perceiving a hypothyroid state, the mast cells can come in and release their vesicle, and provide some thyroid hormone for the support, maybe for the immune system, maybe for the cells in general.
[1:16:05] DR. KELLY: Especially in the brain. That would make sense in the brain.
[1:16:09] DR. ERIC: Right. Now, the problem with that is now we get an excessive histamine response. We have to tailor these things. Another interesting point on that is too much thyroid hormone will also initiate the release of histamine from cells. We've got to be really careful. If we provide too much thyroid hormone, we can actually generate excessive histamine response. In a hypothyroid state, the release of histamine may still be a protective mechanism to provide thyroid hormone to the immune cells, or the surrounding tissue.
I think, this is one of those things where we have to see, okay, how's my patients struggling? What are the issues I'm dealing with? Is there something I can do from a crisis standpoint to just take the edge off, while I started addressing the issue? I don't want to say that, “Hey, you can't – Stay out of the way. Let the body do it.” We have to manage where our patients are in reality.
[1:17:06] DR. KELLY: Right. That support and definitely, detoxification support and binders, artichoke, things that help move the physiology appropriately. Not too fast, not suppressing, and not pushing, but just really – That's nuanced, extremely nuanced. You get better at it as you practice more on people, unfortunately. Really, that's again, something where 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.
[1:17:40] SCOTT: From Trevor Marshall’s work, we know that vitamin D, the 1,25 vitamin D can be a potential indicator of intracellular pathogen burden, particularly when it's significantly higher than the 25 Vitamin D. I'm wondering, how often do you suggest supplemental vitamin D? Are there people that are taking vitamin D where you might suggest that they discontinue it?
[1:18:02] DR. ERIC: It's not very often that I provide vitamin D. That goes against the main talking point everybody's doing. More vitamin D, more vitamin D, more vitamin D. You have Trevor Marshall, you have Megan Manchin, you have Douglas Kell, these are some bright minds who are talking about what's going on. We have to consider that it's not just, we just pound away. I mean, we look at vitamin 20 – The only thing that's typically measured is 25 OHD. It's rare that you see somebody measuring a 1,25, because it's small, it doesn't matter.
25 OHD is like T4. It's the circulating hormone. 1,25 Vitamin D tells us what's happening to it. 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. We don't know, do I have low 25 Vitamin D, because I can't make it? Because I have a cholesterol issue maybe?
Do I have a 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 25 OHD, because I'm quickly deactivating it? Do I have a low 25 OHD, because I have high 1,25 Vitamin D that's then reciprocally inhibiting the production? Because the immune system is pretty smart and says, “Whoa, we want to start shutting this stuff down, but we don't want too much, right?” Then, where else is it going? Well, it's going into the fat cells. For a while we thought that that 25 Vitamin D, or 25 OHD, if it went to the fat cells, it was just getting stored.
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. It can actually help expand the cells to create more room for more calories. An interesting study, it's a rat study, but when they took rats and got rid of their vitamin D receptor, the VDR receptor, which 125 binds to date could not get fat.
[1:20:09] SCOTT: Wow.
[1:20:10] DR. KELLY: Wow.
[1:20:11] DR. ERIC: Interesting, right? If I have an overweight patient, and they're taking 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 1,25? What's that ratio? Oftentimes, I'm taking it off. If 25 OHD drops too low, then I might say, “Okay, now we have some considerations.” I'm also taking in consideration what's going on with calcium status.
Here's the other thing I caution people about, too, is what is 1,25 job’s role? It plays a role in calcium homeostasis. If I'm constantly taking a whole bunch of vitamin D, and I'm over-converting that to 1,25 vitamin D, is there potential to bring more calcium into the bloodstream from the GI tract? Yup. 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. If they're pounding away vitamin D, am I actually contributing to the demineralization of the bone? 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 master problem. I think some is good. I tell most people to go outside and get some sun exposure. 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 just pound away.
I have an issue. I'm a contrarian on a number of those things, which I think aggravates some people. I just like to ask the question, are we all deficient? Or are we just assessing things wrong?
[1:22:14] SCOTT: 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?
[1:22:22] DR. ERIC: Yeah. Initially, we want to take a look at what's going on with thyroid markers. Do I have a state, where I have a true glandular hypothyroidism going on? If I do, we got to get that person safe. Then we want to start to look at the rest of the panel. 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. A lot of production, but under-conversion. Things that would indicate that yes, this is a person who potentially has some tissue hypothyroidism. Of course, context matters. Does my patient have signs and symptoms?
Once we look at that, then we want to look at okay, are there things in the blood chemistry that we can look at that may be driving this process? Look for the inflammatory markers. Does the person have elevated CRP, homocysteine, uric acid, fibrinogen, elevated ferritin. There's a lot of inflammatory markers that might indicate or drive the reduced conversion in this tissue hypothyroid state.
Then we want to look at the rest of the panel to say, okay, what tissues are potentially being impacted here? Is blood sugar regulation potentially being impacted? Is cholesterol physiology being impacted? Is liver physiology being impacted? Is renal physiology? Adrenal physiology? What tissues are being impacted by this? So we have a good idea of, okay, where do we need to put our attention? What's the order? What's the hierarchy of what we need to do here? If I missed the part, one of those parts is to make sure we're also not being overmedicated, our client is not being over-medicated in an effort 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, were just way too low, and we need to get that modified early on. I think it's also important to say that it is very rare that I'm directly trying to manipulate T4, or T3. I'm going to give this to do this. 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 really critical, too high, or too low, that can have an impact on thyroid physiology.
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. I got to be able to put it into something. That process of looking at labs for me has really been the way – 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 of criteria. Are the values normal and appropriate given the person I'm working with?
If I have a 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 everything's good. Is the lab value may be normal, totally inappropriate, right? I have a patient sitting in front of me, no eyebrows, the hair spinning, 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 up the street, “That person's got thyroid problem.”
If their TSH is normal or low, the value, somebody might say, “Well, they don't have hypothyroid, because TSH is normal.” Well, that value is inappropriate. Or, you don't have hypothyroidism, because your TSH is low. You're more hyperthyroidism. Look at your patient. It's a normal value, but it's totally inappropriate for the person sitting in front of me. Then I have to be as a good clinician interpreting labs, have to 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, TSH is high, T4 is low, T3 is low, and the patient's got hypothyroidism. Totally abnormal, but totally appropriate. 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? These are the cases where you look at the labs and go, “This is not good. Hey, my patient’s CRP is 68. They're telling me they feel fantastic.” You're going, “Ooh, this is not good.” You see things and you'll – that's not a good scenario.
[1:26:54] SCOTT: 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. 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. 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. I'm wondering why might that be a helpful diet for people with cellular hypothyroidism?
[1:27:27] DR. ERIC: Well, in this case, I think, he had already done a bunch of different things. He had chronic GI issues going on, blood sugar regulation issues. We did the carnivore diet as a way to just make a hard change in his GI tract. 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. We're doing a disservice to the community when we do that. 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. 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? 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 those things today. Getting them off of those foods that are creating a potential problem, not because we're sensitive, or intolerant to it, but we don't have the flora, the enzymes to actually break those things down appropriately. In that situation, it was just a – I think, the big thing was it made a significant change in his biome. Dysbiosis, again, another potential trigger for cell stress.
[1:28:49] SCOTT: Or sleep fitness. How often is EMF and blue light mitigation a big winner for your patients?
[1:28:55] DR. ERIC: I'd say, it's 50-50. I mean, a lot of people are like, it didn't move the needle at all. Some people, they're like, “Oh, my gosh. 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 5 pound weights off the plank, so we can fix it. You reduce the load the best you can, because that'll get us on that healing path that Naviaux talks about. He talks about the CDR 1, 2, and 3. I changed that to make it easier for some of the people I talk to, from the Cell Danger Response to the cell healing response. We need that cell to start to say, okay, crisis over. Time to start getting back to normal.
[1:29:44] SCOTT: Or respiratory fitness. Are there particular air filtration devices that you recommend in the home? Then I'm curious, too, also in the respiratory realm, are you a fan of mouth taping?
[1:29:56] DR. KELLY: Respiratory fitness is I think one of the fitness factors that I know I under-appreciated. Then when you read through that chapter, you too will be very shocked at how important it is and how again, under-appreciated it is. That being said, our air quality is super important. I don't have a brand in particular that I endorse, but I am a fan of home filtration for your air. Your air quality's very, very important. I also think that opening your windows even when it's colder climate and getting some airflow in. I mean, I live in Minnesota, and we keep our windows and doors shut for nine months out of the year. Just think about unhealthy that is.
Just trying to get some airflow in. Avoiding toxicants. Put the hairspray down, or the aerosols and the breezes, the candles all contribute to your environmental fitness and your respiratory fitness. It goes without saying, 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. Fixing that is really important. All that information is in part three of our book.
Finally, I am a fan of mouth taping. I think it's, there we go. It's person by person. My son was just asking me the other day, he's like, “Do you still put that funny tape on your mouth at night?” I thought, I should probably start doing that again. Looking at my Oura Ring. I think that any intervention that can move the needle, again, and I like objective data. That's really my gold standard, is that objective data, I'm a fan of.
[1:31:45] DR. ERIC: The funny thing is patients ultimately will always say, I don't mouth breathe. 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? 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 your mouth breathing, it has an impact on vasopressin. You wind up making too much urine. Now you're up multiple times at night. Your bladder is not too weak. You're just making more urine than you should. It's probably because of mouth breathing.
Put this thing, 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. 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. Just go to sleep.
[1:32:42] SCOTT: I'm a huge fan. I like the SomniFix strips. I've worn them for a long time. Those are great.
Wanted to touch a little bit on the emotional conversation. In the chronic illness community, I think there is sometimes resistance to exploring items in this emotional fitness realm, because it triggers that PTSD that the conventional medical communities said, “Well, it's all in your head. Your illness isn't real.” Yet, it's probably one of the more important areas to work on. 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. Talk to us a little bit about that connection. Then, what are some of the things we can do to optimize, or increase heart rate variability?
[1:33:30] DR. KELLY: 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 with external things, supplements and other things. That one is something where we got to ease into that one, but extremely important. Measuring your HRV. Again, in the book, we talked about how that can be really nice reflection of your autonomics, the automatic 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.”
I was just thinking of HeartMath and how using that 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. 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 what may they be appropriate. 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.
[1:34:52] SCOTT: 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?
[1:35:04] DR. ERIC: Yeah. I mean, I got an infrared sauna. I have, what's the little neuro thing that I wear on my wrist? I forget the name of that.
[1:35:11] SCOTT: Apollo maybe?
[1:35:13] DR. ERIC: Apollo Neuro. Yeah. I mean, I’ve got BrainTap glasses at home. All those things are tools. I think, the important thing is that the tools can help us. We shouldn't be purchasing all the things to hack our physiology without addressing the foundational things. I think what I see is, a lot of people have spent a lot of money on tools. Then you ask, are you doing – just you're working on your breathing exercises. Do you tape your mouth shut at night? No. 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. I think that tools can be really helpful.
I'm a person who buys them and says, “How does this work? Is it changes, it moves the needle?” Hey, let me do this for a month and then let me check my chemistry. Let's see what's different. Do I feel better? Do I sleep better? Is my HRV better? I think that can be beneficial. 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. The dollar bills being the things that are free that you need to do on a daily basis.
[1:36:18] SCOTT: Perfect.
[1:36:19] DR. KELLY: That's what I want to highlight from our book. Part 3. Part 3 is, it just feels so overwhelming. I know, I was I was so ill. So are you, Scott. It’s just like, where do you begin? Where do you even start? I feel like, part 3 in our book is all about putting it in simple steps, that some are completely free, but can be just so important. You have this guide, and each of these fitness factors to help you not buy another $10,000 tool. Although again, we all like those tools. I do like red light therapy. I like laser therapy. All of it. Again, it's very just helpful to have almost a manual on optimizing it all.
[1:37:02] SCOTT: My last question is the same for every guest. That is, what are some of the key things that you do on a daily basis in support of your own health?
[1:37:09] DR. ERIC: Yeah. It's essentially, live the life of that part 3. Every day, it doesn't matter if I'm in Arizona, like I am today. Up in the morning, exercise in the morning, hydrate, make sure I get a good sleep, mouth taping. All the things we talked about in the book, I do them on a consistent basis. Good diet, good nutrition. I want to make sure, too, that I say that I don't have a perfect life. I don't do everything perfect. It's not my goal. I think, we talked about, 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, to be perfect on everything. I try 80% of the time, 85% of time I try to have really good habits as my stable. Exercise, fitness, everything on that wheel, I try and address. Then 15% of the time, I divert from that just to make sure, hey, everybody's eating maybe some crappy stuff. Do you put them at a party with people? All right, what's the big deal, right? I'm not a big drinker. Hey, if I'm at an event, I'm having – maybe I'll have some cocktails. Because I don't want to have this life where I'm afraid of everything. 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. If you're a person who's got mostly bad habits and a few good behaviors, you're in trouble.
[1:38:34] DR. KELLY: 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. A dynamometer. It’s really 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. First week, and wake up in the morning and go, “I feel good. I don't feel good.” I will tell you this, that I changed my exercise program a little bit. Just a couple little tweaks. My grip strength skyrocketed, which is a reflection of your mitochondrial ability, like a stretch. 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. I mean, it was terrible. Easily. Now I'm getting myself back up and I'm watching to go up and I feel it's just a cheap, easy way of a reflection of overall health. There's my nugget.
[1:39:25] SCOTT: 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. Thank you both for the work that you're doing and for being so generous with your time and sharing with us today.
[1:39:49] DR. ERIC: Hey, Scott. I just want to thank you for bringing us on the podcast. Really appreciate it. 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 are helpful in getting started with the finding the publisher, getting involved. 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.
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 just put a bunch of ideas on paper. We really appreciate your role in the production of The Thyroid Debacle.
[1:40:36] SCOTT: Thank you. Whatever small part I had in it, it turned out to be incredible. I think it'll help a lot of people. Thank you for that.
[1:40:42] DR. KELLY: All right. Thank you, Scott.
[1:40:44] SCOTT: To learn more about today's guests, visit Dr. Eric at RejuvagenCenter.com. That's RejuvagenCenter.com. RejuvagenCenter.com. Dr. Kelly at DrKellyHalderman.com. That's DrKellyHalderman.com. DrKellyHalderman.com.
[END OF EPISODE]
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