I’m delighted to reconnect with Dr. Eric Balcavage today! He is the owner and founder of Rejuvagen, a functional medicine clinic in Pennsylvania. He is also a nationally recognized speaker and educator on various health-related topics, including thyroid physiology, detoxification, methylation, and chronic illness.
Dr. Eric Balcavage joins me for the third time today to discuss his new book, The Thyroid Debacle, co-authored with Dr. Kelly Halderman. We dive into his motivation for writing his book, discuss cellular hypothyroidism and its triggers, and get into the impact of chronic low-grade inflammation on our mitochondrial health. We go into why hypothyroidism is a spectrum, the role of bile in thyroid functioning, and the impact of hypothyroidism on our sex hormones. We also discuss the incidence of Hashimoto’s, why iodine is so controversial, labs we want to look at more closely with thyroid issues, and supplements and nutrition.
“I think it’s helpful to change the conversation and start to consider that what we see in clients is not broken. It’s adaptive.”
-Dr. Eric Balcavage
IN THIS EPISODE YOU WILL LEARN:
- Dr. Eric explains why clinicians are failing their patients concerning thyroid management and diagnosis.
- A better clinical approach to thyroid issues.
- Dr. Eric unpacks cellular hypothyroidism.
- Why weight loss is a lot more complicated than simply counting calories and fasting.
- What bile does, apart from breaking down and emulsifying fat.
- Problems that might occur after having the gallbladder removed.
- The impact of hypothyroidism on the sex hormones.
- How a broader approach could ultimately result in more effective treatment strategies.
- Dr. Eric shares his view on what triggers the development of goiters.
- Is iodine supplementation necessary?
- Dr. Eric shares his thoughts on nutrition for thyroid health.
- The best supplements for reducing inflammation.
Connect with Cynthia Thurlow
Connect with Dr. Eric Balcavage
Dr. Balcavage’s book, The Thyroid Debacle, is available from Amazon, Barnes and Noble, Balboa Press, or online.
Cynthia Thurlow: Welcome to Everyday Wellness Podcast. I’m your host, Nurse Practitioner Cynthia Thurlow. This podcast is designed to educate, empower, and inspire you to achieve your health and wellness goals. My goal and intent are to provide you with the best content and conversations from leaders in the health and wellness industry each week and impact over a million lives.
Today, I had the joy of reconnecting with Dr. Balcavage. He’s the owner and founder of Rejuvagen, a functional medicine clinic in Pennsylvania. He’s also a recognized speaker and educator on various health topics including thyroid physiology, detoxification, methylation and chronic illness. Today, he joins me for the third time to discuss his new book, The Thyroid Debacle, co-authored with Dr. Kelly Halderman. Today, we dove deep into his impetus for writing this book right now, the role of cellular hypothyroidism, triggers for this and the net impact of chronic low-grade inflammation on the health of our mitochondria, why hypothyroidism is a spectrum? the role of bile specific to thyroid functioning, the impact on our sex hormones, the incidence of Hashimoto’s and why iodine is so controversial, labs that we want to look at more closely with thyroid health issues, the role of supplements and nutrition. I hope you will enjoy this conversation as much as I did recording it.
Welcome back, Dr. Eric. It’s good to have you back on the podcast. For listeners, this is our third podcast together on Everyday Wellness. You can check into episodes 105 and 166 and today we’re going to talk about your new book and dive into different aspects of thyroid physiology in a way that is very unique. I’m very grateful to have you back because it’s always an interesting and entertaining conversation with you.
Eric Balcavage: Well. Thanks for having me back. I appreciate it. I’m proud to be the first of the three timers, for sure. [Cynthia laughs]
Cynthia Thurlow: I’ve got another one coming up next week, so the podcast has been around long enough that now that can happen. So, it’s such a cool opportunity. Thank you for listeners for keeping the momentum going with the podcast. It has definitely been a wild ride.
Eric Balcavage: Yeah, I think it’s great that it says something when you’re having people on for multiple times, right?
Cynthia Thurlow: Yeah.
Eric Balcavage: Because you’ve been there long enough. So, congratulations to you.
Cynthia Thurlow: Thank you. Thank you, lots of alignment. Let’s start the conversation today talking about why we are failing our patients with regard to thyroid management, diagnosis, et cetera, because there seems to be this very linear and reductionistic thought process about the thyroid and I was guilty of this. I want to be very transparent and say that in my traditional allopathic training and even the way that I practiced as a NP in cardiology, we didn’t really deal with a lot of thyroid issues. We would send them back to their primaries or we would just rule out the really serious things in the hospital, like thyroid storm or myxedema coma. And beyond that we had other specialists dealing with the thyroid, but even I didn’t fully understand and appreciate the complexity of our thyroid. I can see why we are failing our patients because I’ve been one of those patients. I know we had a sidebar conversation, I believe, last year when I was like, doesn’t matter who you’re seeing sometimes we really do fail our patients, and it’s because the thyroid is so complex.
Eric Balcavage: Yeah. I think I try to be softer on how I say this stuff now, but I think the key is that I think people are doing almost often what we’re trained to do. Everybody, I think, has the patient’s best interest at heart. We want to help our clients; we want to help our patients. We do that based on our bias. We do that based on our knowledge base. We do it based on our ignorance. However, you want to say it, we have a certain way that we think that we’re helping our clients. When you look around and everybody else is doing the same thing, then whether we’re having success or failure, we just assume that I’m doing it right, because that’s what my peers do and that’s what everybody else is doing. I don’t want to beat up on anybody else saying, see, I think I’m right and you’re wrong. I think it’s more of at some point in time, we the clients, we the physicians get frustrated and start to ask better questions. Kind of go against the grain. It’s probably why you’re not doing what you were doing before and you’re doing something else because you kind of hit your wall going in and saying, “Hey, this doesn’t seem right” and for me I think this happened when we started thinking about thyroid physiology.
Physiology in general is that we’re always looking at what’s going on like somebody’s broken and we need to fix something. All I really want to do and the whole purpose of the book, whether I got that point across or not, was just to stop looking at ourselves as if we’re broken and just ask a better question, which is, maybe this isn’t broken physiology, maybe this is adaptive physiology. Maybe my body isn’t trying to kill me. Maybe my body and my physiology are really trying to help me, protect me and adapt to whatever that environmental or life stress, whatever that stress load is, so it’s not broken, at least at the onset. If we ask a better question, then oftentimes I think we’re less frustrated because I just got off the call, doing discovery calls over lunch, and the person is like, “I’m very sensitive to these things.” They’re telling them, you’re not really sensitive to B6. What you’re asking– You’re thinking that you’re in heal mode and if I give something, it’s going to help me heal. Your body is in self- defense mode. It’s using whatever that is, to more support defensive mechanisms. When we start to look at it that way, I think it really changes what we do and how we do it. When we start to say, “Oh, not broken, adapting.” I just want us to change the conversation.
Cynthia Thurlow: I think it’s such an important distinction. By no means am I ever being critical of our allopathic-trained peers. I have benefited from emergent urgent care medicine. I do, however, take great care in how I phrase, how we manage preventative and chronic disease management, which I think deserves a different lens. What you’re really begging people to do is to have a different, unique perspective. To think beyond what we’ve originally trained in, potentially to understand that we are designed to be lifelong learners, even as clinicians, and to look at things differently, I certainly have learned so much from you. If you don’t already listen to Dr. Eric’s Thyroid Thursday, it’s a treat. You are getting this incredible teaching opportunity as well as this podcast. There are so many women, which are the bulk of my listeners, that are impacted by thyroid issues, that explains why you’re such a popular guest. Because people want to learn more. They want to learn more so they can talk to their healthcare providers, so they themselves better understand their thyroid. Now, let’s unpack cellular hypothyroidism because this is unique, as you stated in the book, it’s occurring at epidemic proportions. Let’s talk about why it happens, reasons why it happens, what triggers it, as you were kind of alluding to at the beginning of our conversation. Because I think this is an important type of an underactive thyroid and we’re talking about cells, cellular level hypothyroidism, why this is unique and how it impacts us.
Eric Balcavage: Yeah. So, cells are like people. We operate from one of two modes. I try and keep it super simple. We’re either in low stress manufacturing mode or we’re in high stress cell defense mode. We operate differently whether if it’s just us in our home, if we’re in crisis mode, we’re not busy cooking and cleaning and doing all that stuff. We’re trying to protect the house or put out the fire or whatever it is, so cells are a similar way. If you’re in a low stress state, the body wants a higher state of metabolism and it needs to bring food energy into the system, convert that inside your cells and tissues into cellular energy. It can make the proteins, it can make the peptides, it can make the hormones, it can make the neurotransmitters, it can make cell membranes. You could do all this stuff, hair, skin, all the stuff that makes us feel good, move our bowels, feel good, have great libido and orgasms and all that other kind of good stuff. That’s what happens when we’re in low stress manufacturing mode. The other mode is “Oh, crap mode,” like something’s threatening me, something’s in danger. In that mode, we want to kind of slow the metabolism down to these manufacturing process because I don’t need to put a lot of time and energy towards that. What I need to do is put more time and energy to making inflammatory products, things that are going to be protective, ramping up the immune system, creating inflammatory molecules to go kill something, increasing oxidative stress.
Unfortunately, when we’re in that cell defense mechanism, most of the effect of that doesn’t make us feel good. We make the assumption that we’re sick. The reality is we’re ill, but we’re actually probably healthy, if we have the fever, if we’re nauseous, if we have diarrhea, that’s our body trying to get rid of whatever is there. We make this kind of misassumption as to what’s going on. Thermostat to determining whether we’re going to be in manufacturing mode or cell defense mode. One of the things we use to regulate that is how much thyroid hormones in the system, how much of this active hormone T3 is inside the cell. Because if you have more T3 in the cell, that turns on the manufacturing process and kind of turns off the cell defense mechanisms. If I want to turn on the cell defense and turn down manufacturing, I need less T3. What I call tissue hypothyroidism or cellular hypothyroidism is the body’s adaptive downregulation, decreased conversion of T4 to T3, reduced amount of T3 inside a cell, which allows for this immune inflammatory process to kick on, but also turns down these other things that we really want to have.
The big problem is that we don’t have a great set of tools to really, in traditional allopathic medicine, to look at it and say, “Oh, that’s what’s going on,” But it happens a lot, it probably is happening way more than we even consider. I’m sure we’ll get into it more as to the things that we can look at and say that’s going on. This is for the person who says, I’m tired, I’m fatigued, I have no libido, I’m constipated, my hair’s thinning, my skin is dry, I think I’ve got a thyroid problem, or I think I’ve got adrenal fatigue, or I think I’ve got this. Or their doctor says, you have insulin resistance or you’re putting on weight even though you’re exercising like crazy and barely eating, you’re probably already in that cell danger state. And the state of tissue or cellular hypothyroidism. This occurs long before, oftentimes, there’s thyroiditis or inflammation of the gland or long before there’s actually a diagnosis of hypothyroidism. I think the other question in that multi-question question was what causes it? And usually there’s not one thing. Sometimes that’s the sexy thing that everybody likes to do is say, “Oh, Epstein-Barr, or it’s mold, or it’s this or it’s that.” It usually isn’t one thing. It’s usually a combination of stress over time that’s unrelenting and we exceed our capacity. We all have a capacity to manage stuff, whether it’s lifting a weight, whether it’s dealing with our kids, our spouse, a poor diet, whatever. We have a certain level of tolerance level. So many of us just keep compiling and compiling stressors, physical, chemical, emotional, environmental, organisms, toxins. And eventually the body says, “Enough already, I’m shutting down manufacturing, and I’m ramping up cell defense.” Just like if there was a fire in your factory that made phones. I wouldn’t keep making phones, I would turn down and stop the manufacturing process, and I’d get everybody to put out the fire.
Cynthia Thurlow: I think it’s such an important conversation to have because on a lot of different levels we want to blame one thing when what you’re really referring to is it’s multifactorial. There are many things contributing, and my niche are middle-aged women. We know we are less stress resilient as we are transitioning into perimenopause the five to ten years preceding menopause and this is an important distinction. What you can get away with in your 20s and 30s you start becoming less stress resilient. This doesn’t mean we are incapable. We are just less stress resilient. This is a combination of loss of progesterone, additional stress on the adrenal glands, trying to effectively pick up the slack for this failing kind of ovarian reserve. And understanding that women after 40 are at greater risk for developing autoimmune issues.
We know that 90% to 95% of women that develop something called Hashimoto’s thyroiditis are women north of 40. I think many of us say, “Oh, it’s the Hashimoto’s.” Well, actually, it’s this domino effect. It can be, as you mentioned, gut microbe issues, physical stressors, chemical stressors, toxins, radiation, hypoxia, which is a decreased oxygen state that then provoke the domino that starts. You may not realize that you’re in this cellular hypothyroidism initially, but it may be two or three years down the road when all of those symptoms you alluded to really are magnified, that people say, “Okay, something’s not right.” It’s not as if the transition happens exponentially. It’s that it’s this domino effect. It’s chronic inflammation, oxidative stress, mitochondrial dysfunction that mitigates the spectrum, as you refer to it, this spectrum of hypothyroidism and I’ve never actually heard that described that way, but it makes complete sense.
Eric Balcavage: Yeah. I think one of the things we got to be careful is because people will go, I have all this going on because of the Hashimoto’s. I’m like, no, the Hashimoto’s is the result of a bunch of stressors. This Hashimoto’s is the outcome. Even in functional medicine, we still blame the disorder as the problem. Well, the reason you have this is because you have Hashimoto’s. Okay, well, why do I have Hashimoto’s? Oh, it’s an autoimmune condition. Your immune system just lost control. Really? This thing that can take two individual little cells, put them together and get this, somehow one day wakes up and just forgets, this is who I am and starts attacking me. I think that’s too simplistic of an answer. It’s the same answer when somebody says, “Oh, the reason you’re overweight is because you’re overweight.” Or if you want to get healthy, lose weight. Well, the reason I have weight is because I was unhealthy first. I didn’t get overweight and then really became unhealthy. I got unhealthy, which caused me to store calories versus burn calories. I think we just sometimes look at it from the wrong perspective and I think we’re both on the same page here. We just got to kind of change the conversation. Nobody’s right, nobody’s wrong, if we change the conversation to, I’m broken to I’m adapting. Man, that’s a much more promising thing to tell the client. Hey, why can’t I lose weight? Well, your body is trying to protect you for something. It’s saying that I’m in danger mode. I’m storing calories, I’m not burning them. Oh, you mean it’s not necessarily calories in, calories out specific. No, no, no, no. And matter of fact, if you overly restrict calories, then you’re maybe even in a bigger state of problems.
I think it’s helpful just to change that conversation and start to consider that what we see in clients is not broken, it’s adaptive, and then we can just start looking at what’s doing it. The analogy I’ve probably used on your podcast a couple of times to help people out is just imagine two cinder blocks with the board going across it and all these things we come in contact with in life are like, five-pound weights or ten-pound weights. As we go through life, we just start adding those weights to that board, and the board maybe has a capacity of 100 pound and if I overload that board, at any stage of life, the board’s going to break. If I load the board with stress, with a five-pound weight or a 50-pound weight, and then at some point I take 10 pounds off and I put five pounds back on and I take 15 off, I can still take all this stress, but I’m still able to adapt to it. For most people, what happens is they keep adding stress, not allowing for rest, recovery, and regeneration. They don’t become more resilient, they become more broken down, and eventually that board breaks. Now nothing seems to work appropriate, right. They try a strategy and it doesn’t work out anymore. Like, I tried to take the weight off. Well, the board is already broken. Taking it off that broken board doesn’t fix the broken board. That’s why that simple solution that worked for your friend may not work for you. If their board wasn’t broken, they just reduced the stress. “Oh, I feel so much more calm,” that’s great. If the board is already broken, you actually have to reduce a lot of the stress, pick up the board, rebuild it, rehab it, and then you can become more resilient in time.
Cynthia Thurlow: I think you really bring up a good point that it is never just one thing that breaks that board and understanding that we– and I’m going to borrow a phrase that Ben Azadi, uses, “We get healthy to lose weight.” It’s an important distinction. I think, for so many of us we’ve been conditioned to believe that weight loss should be effortless, and weight loss is far more complicated than counting calories and just fasting and just trying to do five minutes of meditation once a week. Once we have hit that domino effect and our bodies are perceiving there’s danger and they’re stressed, it is going to make it much more challenging. It’s not impossible and that reframe is important. It takes time. It’s like we don’t become unhealthy overnight. I don’t expect anyone to get, “Healthy overnight.” It’s a process, it’s a journey, it’s a marathon in some instances, but you can absolutely get there.
Now, one thing I really liked in your book was you were talking about the net impact of thyroid health on, for example our GI tract. I think for a lot of people, they just kind of equate hypothyroidism with constipation, and they think that’s the one thing that the thyroid does in terms of the gastrointestinal tract. I think you do a really amazing job talking about our saliva and hydrochloric acid and digestive enzymes and motility and integrity. What I really want you to talk about is bile. I think people don’t even understand the importance of bile, and yet I find bile and the net impact of healthy bile hopefully still having a gallbladder and if you don’t, we can talk separately about that. I think bile is a fascinating bodily fluid, if you will, and I think it would be really helpful for people to understand what bile does beyond just break down and emulsify fat.
Eric Balcavage: Yeah. Bile is this stuff, that’s made by the liver doesn’t get much attention unless your gallbladder is ready to explode. It’s critical to maintaining the health of the GI tract, controlling the biome, maintaining the integrity of what we call the tight junctions. I think it’s the thing that you kind of mentioned, it doesn’t get much love and attention. I think I stumbled across bile is something I think I need to take a deeper dive into when I started getting a lot of clients coming from functional medicine clinics with their third or fourth or fifth SIBO practitioner. Like, I’ve had SIBO 25 times and you’re like, “Okay, something’s wrong here.” When I’d look at their health history, I wouldn’t see much that was done from a biophysiology standpoint. I wound up taking a deep dive [chuckles] to some people that’s like, “Oh, what a geek.” I took a deep dive into biophysiology and actually, Kelly Halderman and I wound up doing a three-day seminar on biophysiology.
Cynthia Thurlow: No way.
Eric Balcavage: That’s how I roped her into helping me do the book [Cynthia laughs] because she was going to do weekend seminar. She’s like, “I need some help for you to do this.” I’m like, listen, I’ll help you with the conference, but you could come in and just help me work on the book, because I needed somebody to be the push to kind of get this thing to move. Bile is so important. Your liver brings cholesterol into the liver and converts this stuff to a couple of different processes into this stuff we call bile. It’s highly made up a ton of water. If your person doesn’t hydrate well, or you’re losing a lot of hydrations through peeing out a lot of stuff, that can create a challenge. But the bile moves from the liver, it gets dumped into this tube and goes into this thing called your gallbladder. In there, this bile, which is almost like soap, gets concentrated to be a more concentrated soap so it can do a better job. When you eat, this bile has the cholesterol, it’s got water, it’s got some other things in it that are beneficial, plus it’s got a bunch of toxins in it that were releasing into the GI tract. Bile gets released into this area of the GI tract called the duodenum, which right past after your food comes out of your stomach, it comes into this smaller area. It’s part of the small intestine and bile acid gets dumped in there, pancreatic enzymes get dumped in there, and these things start breaking down your food.
Now, the importance of bile is that at the upper end of the GI tract, it’s a direct antimicrobial. The organisms that are coming from your food, the organisms that are coming from your oral cavity, if the stomach acid hasn’t not killed some of these things, your bile is now working to kill and breakdown some of those things directly at the upper part of the small intestine. The bile is also then helping absorb fat soluble molecules, fats, as well as release some of those things. The bile, as it moves down the GI tract heads, reabsorbed by the small intestines to some degree, and the large intestine. You’re bringing this stuff back in, and as it comes back in through the GI tract, it’s actually helping to maintain something we call the tight junction. In your intestinal lining, these are one cell stacked next to each other. It’s only one cell thick. There’re the junctions in between the cells and these junctions we call them tight junctions. The bile acid helps maintain those tight junctions. If you don’t have healthy biophysiology, you may wind up with chronic, what we call leaky or increased permeability in the GI tract. As we move further down the GI tract, the bile acids are actually an indirect antimicrobial because it helps trigger the immune response to things in the GI tract. If I have bile that’s too thick, too viscous, congested, I’m going to have reduced killing capacity or reduced ability to maintain a low bacterial concentration in my small bowel, something we call SIBO or SIFO or SIMO, however you want to say it. I’m going to have a decreased absorption of fats and fat-soluble vitamins and nutrients. And I’m going to have potentially a chronic leaky gut, which then sets the stage for all kinds of immune inflammatory problems.
Cynthia Thurlow: I think it’s really important for people to understand the poor woeful gallbladder is not a sexy organ, but it’s one that’s really important. In your clinical experience, when you’re working with patients, they’ve had a cholecystectomy, they’ve had their gallbladder removed, now the bile just drips all day long. It’s been my clinical experience that these are people that either suffer with chronic constipation or they have chronic diarrhea. I’ve had people who have literally, since they’ve had their gallbladder out, they’re no longer getting attacks, but then they kind of take that symptom that they were having and it’s been replaced with digestive distress. Either to the point where they just don’t go to the bathroom or if it requires multiple interventions to get them to go, or they’re dealing with chronic loose stools, diarrhea. I’m sure for many people, they probably would not have borrowed, they probably would not have ultimately agreed had they known that they would then be suffering from additional side effects for the rest of their lives. Has that been your clinical experience as well?
Eric Balcavage: Yeah. It’s a chronic issue. It’s really bad in women. We can talk about why that might be in a second, critically tied to key, to having appropriate thyroid physiology in those tissues. Because to get cholesterol out of the bloodstream and into the liver, guess what you need? You need appropriate levels of T3 at the liver to make bile acids appropriately you need appropriate levels of thyroid hormone. Anytime there’s tissue hypothyroid impacting those tissues, you’re going to have reduced production. But cutting out the gallbladder may have to happen if it’s diseased. We still haven’t addressed the issue, which is why and now we’ve got this tube and we’re getting diluted bile. It’s not as concentrated, it’s not as effective as a cleaning agent. It’s like buying a cheap dishwashing detergent versus maybe the Dawn that you throw in there and gets rid of the grease right away. It doesn’t do as effective of a job. It sets the stage when you take that gallbladder out for chronic GI issues and chronic dysbiosis because you potentially have too much bile acids constantly being in there. They’re not really good at doing their job, but they’re also getting in the way because too much bile acids in there can create some problems with you could have loose stools as well. You could have chronic constipation [unintelligible [00:26:21] function well, you could have loose stools because there’s too much bile that’s hitting into the lower part of the GI tract, but it’s a big issue. For women, I think one of the big ties to why it might be a problem, because I don’t think women ever told, I don’t think anybody’s ever told why? It’s just like it gets diseased.
One of the most common things that I see, and I don’t know about you. I mean, this is your wheelhouse too, which is estrogen problems. So, when you have estrogen dominance for the pancreas to dump– pancreas releases digestive enzymes into a duct, into a tube. The gallbladder releases bile down a tube, and those two tubes come together, and there’s a little sphincter muscle that is closed, so it’s not always emptying into the GI tract, it opens up. That sphincter muscle is called the sphincter of Oddi. When you have too much estrogen in the system, it actually causes that valve to stay shut. So now I can’t open the valve. If I got too much estrogen in the system, now I get this tightening of the sphincter of Oddi and now I get bile that backs up. Now I can start to get more thick, more congested stone formation, get the tissue all inflamed and irritated. I also don’t have pancreatic enzymes dumping out efficiently, leads to bacterial overgrowth. Bacteria can then get up into the small bowel, up through the sphincter, and into the GI tract, get up into the gallbladder. Many times, they’re finding they’re opening up those gallstones in the gallbladder, finding there’s bacteria in the center of them. So, it’s a huge issue, I understand why people take it out if it’s diseased, because, hey, maybe we’re beyond the point of fixing it. At that point, that person now needs long term support, and we still have to address the underlying issue. Was it bacteria? Was it infection? Was it estrogen? What’s the underlying issue here? That should be what we’re all about in functional medicine. I know allopathic medicine that may be not their thing, but that should be what we’re all about in functional medicine.
Cynthia Thurlow: Absolutely. For anyone listening, you can be in a high estrogen state in your cycling years. You can be high estrogen in perimenopause, also menopause. A lot of this has to do with well, there’re a lot of things that can impact this, but it also can be impacted by our exposure to estrogen mimicking chemicals in our environment, our personal care products, our food, even our clothing. The more I learn, the more I feel like I should go live in a bubble in the middle of the world. With that being said, one thing that I thought was really interesting is that high estrogen also hinders iodine in the thyroid gland. There are a lot of questions about iodine, but it also impacts iodide in the thyroid gland. There’re multiple different ways that high estrogen can impact thyroid physiology as well as gastrointestinal physiology.
Eric Balcavage: Oh, absolutely. That’s why we can’t just look at one little window and say, “Oh, you just do this.” We have to take a broader approach on things and say, “Okay, if we have an estrogen dominance issue, we need to address it.” We also need to say what other systems could this be impacting so that we can kind of fine tune our strategy instead of being like a Pollock painting where we just throw stuff at it and hopefully, we hit the right target. In this situation, we say, “Hey, all these symptoms are tied to inflammatory stuff.” We don’t have to drill all of those, we can really just focus on the thing that’s triggering the inflammation. You’ve got estrogen dominance or you’ve got toxicity. We don’t have to address all of this stuff. We really just need to focus here, like the middle of the spider web to have the biggest impact on it. I think sometimes when we do a better analysis and we understand, how all these things incorporate. We can really streamline our treatment strategies and be much more effective.
Cynthia Thurlow: Can we touch on goiters? We got a lot of questions about goiters. And I think there’s a lot of misinformation in terms of whether they’re pathologic, whether they’re benign. Obviously, a lot of that’s based on biopsies and things like that. What is your kind of working hypothesis about the process or the physiology of when our thyroid gland will develop goiters?
Eric Balcavage: I think at the end of the day, I always look at it there’s some type of inflammatory process going on. Now in the world of allopathic medicine and functional medicine to some degree, it’s too much iodine on one end, too little iodine on the other end. I think that’s too black or white. That’s like politics, it’s either Republican or Democratic. In reality, the answer is probably somewhere in the middle. I look at it as there’s probably more of an inflammatory mechanism going on. I go back and ask the question, what’s causing the immune system, these immune cells, to come in here and create all this destruction and damage? Whether somebody says they have Hashimoto or not, that’s a whole other discussion. Now, we can argue that or talk about that point.
But I think at the end of the day, when I know somebody’s got that coming on and on, I want to make sure they’re just, A, are you taking a bunch of iodine? Yes. Okay, probably stop doing that. I’ve seen people good take a bunch of iodine because they read it on a blog or listened to a podcast, and then their neck is blown up like crazy. And you’re like, “Woof, why did you do that?” It makes sense what they’re listening to. I can see how somebody would be influenced by it, but I would say if they’re not on iodine, if they live somewhere on the coast, most of us get our fruit and vegetables and all our plants from the coast. We’re not buying locally anymore. It’s less likely that we’re in an overt iodine deficiency state. It’s probably less likely that we’re over, like it’s excessive as some people think it’s so excessive. I don’t know if it’s that. I think what makes the most sense to me when somebody’s got a goiter, they’ve got a nodule, there’s a level of inflammation. The immune system is being attracted to the thyroid gland, and instead of just trying to treat that gland or do something for the gland. We take a step back and say what else is going on in this person’s life, diet, lifestyle that might be triggering this type of damage to the gland. As we’ve talked about in the past, I think in many cases, it’s not like the immune system just woke up and went after the thyroid gland. It’s that the thyroid cells themselves are initiating that inflammation, that infiltration of the white blood cells.
Cynthia Thurlow: It’s really interesting. I certainly have had experts on that talk about a lot of thyroid issues are mediated by too much iodine, too little iodine. I know many in the functional space are not in agreement about whether or not we need more or less. I think it leaves patients and clients confused about whether or not they should eat iodine-rich foods, that they should take supplementation. It’s been my clinical experience. I always say less is more, eat some sea kelp as opposed to taking more supplementation. Unless you’ve been specifically told this is necessary. Do you find that urinary iodine testing is more accurate than serum blood testing? Has that been your clinical experience or do you hear the opposite?
Eric Balcavage: You know what? Early on, I did a lot of the testing to try and figure out what was accurate, what wasn’t accurate. I think you can get readings, but I don’t know if the testing is good enough and standardized enough that we can make a really good assessment, high or low. In all the tests I’ve run, I’ve run a bunch that have been towards the lower end or low. I haven’t run that many tests where people’s values are overly what would be considered high? In reading a bunch of stuff, I’m just not convinced that we have the best set of ways to measure it. That I can hang my hat on it, so I’m much like you. There’s the camp I grew up in functional medicine that says, “If they have TPO antibodies, no iodine.” Because iodine is going to increase TPO activity, it’s going to create the issue. You need iodine, so use iodine for so many purposes beyond the thyroid gland just for immune health and everything else.
I think I’m probably more in line with you, a mild amount of iodine getting into the system is probably not the big issue. Because I don’t believe that it’s really as simple as I take iodine, TPO antibodies go up because the activity goes up, and therefore I’m going to make more antibodies. Because what the literature seems to show is that the antibodies really don’t do much damage. If it was just that the antibodies did all the damage, then I would say, “Hey, you shouldn’t have any at all.” But I forget it’s maybe a 2019 paper said that thyroglobulin antibodies, I think they were pretty definitive on it. Thyroglobulin antibodies caused no damage, and the TPO antibodies caused very little damage if any. If that’s the case, then taking iodine shouldn’t really make a difference because it’s not the antibodies like little Pac-Man eating away the gland. It is something else that’s driving that process. I don’t really go one way or the other. I stopped doing a lot of that iodine testing. Even in the people that I see come to see me that have had a bunch of iodine testing done. I’m like, “Okay, did you take iodine?” Yeah. And what did you do? Did you feel better? No, I didn’t feel any better. I didn’t feel any different. Okay, then let’s move on. I think for the most part, it’s like the shiny object that we put a lot of attention on that probably is not the key thing that we need to put the attention on.
Cynthia Thurlow: That’s a really good point. Are you of the belief system that it’s important to chest other types of cofactors for healthy thyroid production. I’m thinking about selenium and magnesium and iron, et cetera. Because I probably got trained in the time when were very focused on– You have to make sure your cofactors are fully optimized before you start medication. Now, probably I would say a little more gray about that. I think it’s helpful to test, but it doesn’t always sway the decision making in terms of whether or not it’s a supplement versus medication as the next step.
Eric Balcavage: I think the selenium issue is one thing that gets a lot of discussion. What I’ve seen through my bias is that most people aren’t selenium deficient. Even though we say that the reason your T3 is low and your T4 is normal, it’s because your selenium deficient. You don’t have the cofactor that will convert– for the deiodinase to work, I don’t think that’s the case. I’ve run too many selenium panels; everybody seems like they’re in the normal range or really close to it. If it was selenium deficiency, then the same person wouldn’t have a high reverse T3, because all of the deiodinases, the enzymes that convert T4 to T3, T4 to reverse T3, break down T3. All the three enzymes that metabolize thyroid hormone all use selenium. If there is deficiency in selenium, you wouldn’t see low T3 and high reverse T3 because there shouldn’t be enough. Now, if you saw normal T4, high T4, low reverse T3, and low T3. Now, yeah, I’d be running selenium just to check and see. I don’t put much time and effort into the test at this point because I typically look at the labs and say, do I have a pattern? If I don’t have that pattern, I’m not running it. Because you spend another 40, 50 bucks on a test.
As far as iron, I look at iron on everybody, and I will tell you that my opinion, again, my bias is barely anybody’s iron deficient, okay. I know there’s somebody out there going, yeah, I’m, I’m, my doctor has me on iron. Unless you’ve got a massive bleed out, you’re probably not iron deficient because we have great absorptive capacity, but poor ability to get rid of it, except if you’re bleeding. We only slough off about a milligram of iron per day, but we can increase that amount that we absorb. So, where’s all the iron go? Well, the body has fantastic storage ability for iron in the body in something called ferritin. There’s also another storage molecule. Ferritin is the one that most people will see potentially if they get a blood draw done. What we see, there’re two typical patterns we see with somebody regarding iron. One is iron deficiency anemia, which used to be, I think some people are still saying is the most common thing when it happens to iron.
I would argue that is not the most common thing that causes that goes on, but it’s anemia of chronic inflammation or chronic disease is the most common. They could look very similar on a lab report for some people. Now, the easy distinguishing factor many times is that their serum iron, their iron saturation will be low. Those are things that maybe the doc will see. If they don’t run a ferritin, it may look like anemia. If they run a ferritin as well and the ferritin is high, they probably don’t have iron deficiency. If the ferritin is low though and they have low iron and low iron saturation, and high total iron binding capacity, you might think they’re iron deficient. You go look at the red blood cell panel, see if there’s an anemia pattern, and that early on there might not be anemia pattern. Early on, there may be an elevation of red blood cells to kind of compensate for it, but over time we’ll see the red blood cells start to diminish. The test that you can distinguish all of this is pretty simple, inexpensive, it’s called a soluble transferrin receptor test. If you run that test, then we’ll have a pretty good feel. Is this person truly iron deficient? Or the cells loaded with iron and they’re in this anemia of inflammation or chronic disease pattern. Do you want me to explain that test or move on?
Cynthia Thurlow: No. I would like you to because I’m not familiar with said test.
Eric Balcavage: Cells need to get iron into the cell because iron does so much stuff that helps run everything. Runs your mitochondria, it runs almost all the systems in the cell, needs some iron, but iron is like a teenage boy. If it’s not chaperoned, it’s going to get itself in trouble. I can say that because I still act like a teenage boy at times. [Cynthia laughs]. Iron gets escorted into the body, it then quickly gets escorted to a transport molecule called transferrin that’s like a little bus that drives it around the body, and then it gets escorted to the tissues. If that iron isn’t going to be used right away, then it goes into a holding storage unit inside the cell, and that storage protein is called ferritin. It gets held in there until the cell needs it and the cell can pull it back out again. If I’m a cell, how do I get the iron in the cell? Well, I put out these things called soluble transferrin receptors. It’s like a door. Like, you go through the mall, like the spinny door. The iron and transferrin docks to this soluble transferrin receptor, it surrounds it, pulls it into the cell. Now I can get the iron into the cell and do something with it. Now I can release the transferrin, it goes back out into the bloodstream. If the cells are anemic then my soluble transferrin receptor is going to be really high because the cell needs a lot of iron. It’s putting all these receptors out, these catcher’s mitts, to catch the iron as it flies by. If I’m already loaded with iron, I’m not going to have a lot of soluble transferrin receptors because I don’t need any more iron, I’m already full. So that’s the distinguishing test and nobody runs it.
Cynthia Thurlow: I’ve never actually run it. That’s why I was like, “Oh, I have to learn more about this test.” That’s really interesting. I’ll have to keep that in my mental Rolodex. Now, earlier you had talked about thyroid antibodies. There are several different kinds. You had mentioned that TPO does have destructive potential. However, not nearly as significant as those created by activated thyroid cells and invading lymphocytes. This is an important distinction, so don’t freak out about your antibodies. In your clinical experience, there are typically ranges on allopathic lab values. You get your report from your doctor, your nurse practitioner, or whomever, and you’re looking at the ranges. Sometimes it’ll say less than 9 is considered to be negative and then maybe someone’s range comes back and it’s 11,12 versus 300, 400. I’ve seen TPO antibodies that have been very high. I got this question multiple times, “How do you determine/designate the significance of those antibodies in terms of their values?” Like, do you consider to be a suboptimal amount of thyroid antibodies to be anything over what is considered to be, “Normal?” What is your threshold with your patients?
Eric Balcavage: Yeah. So, it’s a great question. The first thing that we always have to understand is not every lab measures these things the same way. Different labs have different ranges based on how they measure them and thyroglobulin is a great example of this. Even at Quest, depending on where you go, which lab they’re going through, the range may be less than 115 or it might be less than 1. So, somebody might go, well, I’m 346. Okay, well, what was it measured on? Or my value is 2, okay, but what was the range? Because what was the type of instrument it was measured on? That makes a difference, the type of instrument, it’s not always as easy as my value is 25. This lab says it’s less than 9. This lab says it should be less than 34. Which one’s right? Well, how did they measure it differently? If they measured it on something that has a range of less than 9 and you’re 25, then that’s positive finding. If it’s measured on a unit that the range is less than 34, maybe the 25 is still fine based on how they measure it. That’s a little side, just so we’re aware of that, because there’re many times that I’ve had patients say, “Oh, my gosh, look at the value.” I’m like, “Yeah, but look at the range.” It’s a different piece of equipment. Therefore, how they measure it, it’s more sensitive, they can get a bigger reading or bigger number. My take when I look at it is, I assume that everybody who’s got a thyroid gland problem has a level of thyroiditis and I don’t care really what their antibodies are per se, okay. We distinguish many times Hashimoto’s whether there’s antibodies or not antibodies.
I think that’s a waste of time discussion and a bunch of hogwash because the adaptive immune system has two primary parts, a Th1 side of the immune system and the Th2 side of immune system. When people are Th1 dominant, they really don’t make a lot of antibodies. They could still have ongoing thyroiditis, lots of immune driven damage, but not have antibodies. You think that there’s no immune issue going on because I don’t have any antibodies, not true. The other thing that happens is some people are Th2 dominant, which means they make a ton of antibodies, but if they’re shifted to Th2 dominant, they may have a lot of antibodies. If it was that the antibodies would look like little Pac-Man eating away the thyroid gland, then we might be more concerned. If they’re Th2 dominant and they have higher antibodies, it still may not mean that there’s destruction going on at the moment. They’re predictive antibodies. That means there could be damage or maybe their antibodies are being made because there’s debris, but they’re not actually eating away the gland. What I’m always looking at is, if I have antibodies, let’s say their antibodies are 200. We would consider that positive, for TPO antibodies doesn’t matter what’s going on. Is that good or not good? I don’t know. Let’s look at is this a person who’s on thyroid medication that requires thyroid medication? Well, then maybe that 200 is an issue or a problem. Is this a person who’s got indicators of tissue hypothyroidism, chronic inflammation? Then maybe that number is a problem. If the person doesn’t have, there are no thyroid hormone, they make plenty of T4, they make plenty of T3. Their reverse T3 is good, their ratios of free T3 to free T4 are good. There’re no insulin resistance markers. Their body weight is good. I don’t know if I should be concerned about it at all. I don’t have any indications that it’s an actual problem.
Let’s moderate and let’s not have a patient freaking out that, “Hey, I may have an autoimmune condition.” Because we can see numbers fluctuate pretty wildly. If somebody’s got really high numbers of antibodies, is that a problem. Same thing applies, it might be, maybe I need to look at the rest of the values. Are they making thyroid hormone? Does everything seem to be working well? If it is, everything seems to be working well and it’s really high like that, then maybe the next thing I do is go take a look at something like a Lymphocyte MAP panel and find out, “Is this a person who’s stuck in Th2 dominance?” There may not be anything that’s actually triggering the immune response at this point, but it’s kind of stuck in that pattern, and maybe I need to help shift them out of that pattern, and maybe I’ll see the antibodies improve. I don’t know if I answered your question the way you wanted it too.
Cynthia Thurlow: No. It’s fascinating because I would imagine that I’m probably Th1 dominant because I’ve never had a positive antibody. Initially, when I was diagnosed with hypothyroidism, I was told, “Oh, it’s probably because your mercury levels are high.” That’s probably what’s offsetting your thyroid receptor. That was the working hypothesis until a few years ago someone said, “Oh, you definitely have Hashimoto’s.” You just don’t have positive antibodies because you’ve been gluten free and you’ve been this and you’ve been that. How many people listening have assumed they don’t or their clinician assumes they don’t have Hashimoto’s because their antibodies are always negative. And yet, if we know 90% to 95% of people with hypothyroidism have Hashimoto’s, you have Hashimoto’s.
Eric Balcavage: Yeah. That’s why I say it doesn’t really matter. You have thyroiditis whether you want to call it Hashimoto’s, you want to call it, I just have primary– all that stuff it’s not worth the argument, right.
Cynthia Thurlow: Hmm.
Eric Balcavage: If you look at the literature, thyroiditis starts off as a Th1 dominant disorder. And in time often shifts to a Th2 dominant disorder, where we see the antibodies go up, but somebody can fluctuate back and forth. And when Dr. Vojdani came out with his Lymphocyte Map test, I said, “Here we go. I’ll run a bunch of these tests on my clients.” I took, 30 or 50 thyroid patients, and I ran these because I wanted to see what’s going on here. Maybe there’s another way we can take a look at what’s going on. I would say 80% to 90% of the patients were Th1 dominant okay. The vast majority of people are Th1 dominant and they have thyroiditis. The reason that becomes important is as sometimes we help people and we start to improve the imbalance in their immune system, they’ll go from no antibodies, so they think they just have primary hypothyroidism and no Hashimoto’s, to now starting to show some positive antibodies. They’ll make the assumption that now they’re worse because now they have these antibodies. You almost have to talk them back off the ledge and say, “Okay, wait a minute. If you were worse, would you be losing weight? If you were worse, would you be less insulin resistant? If you were worse, would you need less thyroid hormone to maintain normal values and have limited signs and symptoms?” Once you talk them back off the ledge, you say, here’s what’s happening. You were stuck in this high Th1, no antibodies, really low Th2 response.
Now that you’re getting better, we’re actually seeing kind of a balancing of the immune system and the antibodies are popping up. Not because you’re unhealthy, because those cells that should have been transferring this knowledge to the B cells can now start to transfer that knowledge and the B cells are like, “Oh my gosh. Okay, so if this happens again, we’re going to make some memory B– we’re going to make some cells, we’re going to have some antibiotics, and we kind of get this system in place.” That happens a lot, and people think where, oh, my gosh, am I getting worse. You actually even had one client whose physician said, well, working with that guy didn’t help you because you went from no antibodies, and now you’ve got antibodies, so now you’ve got Hashimoto’s. I’m like, did he look at the rest of your health history? Did he look at the fact that you’re down, like, 50 pounds. Does he pay attention to the fact that you’re almost off of your thyroid medication. I mean, let’s interpret, not just read.
Cynthia Thurlow: I think it’s important. I always say check the patient. That was the resounding thing I learned as a nurse and as an NP that the labs can look terrible and the patient feels great and that’s what you go with. I think that we would be remiss if we didn’t touch on nutrition and the role of molecular mimicry. I think that I talk about this a lot with my patients, especially about gluten and dairy and soy and things like that. Do you have any hard and fast rules about nutritional paradigms that you like to lean in for your thyroid patients. I found an interesting study talking about the impact of low carb, low grains on thyroid health. I’m curious to see what your thoughts are.
Eric Balcavage: I think it’s a general rule, maybe back up. We got too much food wars in the functional medicine industry. We have a lot of people coming up with their diet religion and something maybe that worked for them. So now it should work for everybody else. A whole bunch of people just following things and telling stories because it’s what they do. I think, for anybody and everybody, I don’t care what condition you have, 80% of your diet should be whole food. 20% of the time you’re off the reservation, eating some processed, nobody’s going to be perfect. I don’t expect anybody to be perfect. If you want to be healthy, regardless of what condition you have, eat more healthy whole food, simple. Don’t fall for the gluten free sticker nonsense. I went into the grocery store the other day and there was gluten free stickers on apples. Come on, what have we gotten to that this is just a sales pitching point, but once I know somebody’s got chronic health issues, whether it’s thyroiditis or not, then the next thing I may do, if I shift into maybe a whole food diet, then shift into anti-inflammatory protocol. Why do I do that? Because it removes a lot of the stuff that could potentially trigger more immune reactivity. If we remove the grains, remove the dairy, remove the eggs, remove the soy, remove all these processed grains, regardless of what they are, I think what it does is it takes a lot of the potential problems out of the picture, and it kind of helps us kind of focus a little bit, okay, we’ve taken all these things out and there’s still some issues here, now we got to look for some other things.
Foods all have toxins, a lot of foods have toxins in them. We’d all agree that they do. You got a carnivore community that say all plants are bad because they have toxins, they do. There’s a beneficial effect of having some toxins implants. It actually triggers some type of a stress response on our physiology that then our body immune system can kick up, the defense mechanisms kick up and then it goes away and then the body recovers. And now it’s stronger, it’s like lifting weights. Every time you eat some of that plant food, it’s like lifting weights. You stress it and it gets stronger. You stress it and it gets stronger. If you don’t eat those plants, now, it’s like not lifting weights. Well, lifting weights could be bad for you. Well, if you do it with bad form, bad technique, too heavy, yes, anything could be bad for you.
We’ve got people saying that all plants are bad because they’ve got toxins. Plants are designed to have toxins and it’s hugely beneficial for your health and well-being. But good thing to do, I think, for a lot of people who are struggling with issues is more of that anti-inflammatory protocol initially. Because as you said, some of these proteins have very similar structure when we break them down to the peptide level. It’s often not the protein itself, but the peptide structure that creates the problem. For the listener, when you eat a food, foods got protein, almost everything’s got protein in it. These are big long things made out of amino acids. These individual things called amino acids link together. If you get like 10 or 15 of them, that 10 or 15 segments group is called a peptide. We put a bunch of these peptides together and we get a protein.
Now the proteins all look a little bit different, but when I start to break the protein down into these individual peptides, the amino acid sequence within those peptides could look very similar from protein to protein. So, if its reactive to the peptides in wheat, and let’s say there are 10 amino acids in that peptide and seven of them are very similar to maybe a dairy protein that’s been broken down. Now I see the dairy peptide and six of the amino acids are the same as the seven in this wheat peptide, now the body may go, you know what, that’s close enough, I’m going to react to it.
The analogy is not probably a good analogy, but the analogy I use for my clients regarding molecular mimicry and the potential problem is if you were dating identical twins, if your husband had an identical twin and you went out to, at any given day, if they dressed the same, you would know the difference between your husband and the twin. You’d be like, oh, easy to tell. Like, I may walk up and go, they look exactly the same. You go so easy to tell the difference. Let’s say one night you go out, you go down to Jersey Shore, you go out into a bar, you drank too much, it’s so dark in there, it’s crowded, you had too much to drink. They decided for fun they were going to dress identical, same hats, same shirts, same everything. Both of them went into the bathroom and one of them came out and you kissed the wrong one. Is it really your fault? That’s how the immune system can be when there’s chaos, when it’s compromised, when it’s fighting a lot of things, when there is reduced function and chaos going on, the immune system may look at that and go you know what? That’s pretty close to the thing that I’m supposed to be going after, so I’m going to go after it. That’s why we want to remove the grains and the rice and the dairy and all these things that have similar potential structures that may cross react with something like gluten because we want to get those things out. Because it’s not that all these foods are bad, but when the immune system finds one thing as a problem and the immune system is compromised. It might start to react to these other things just because they’re so similar in this kind of chaos situation. Does that make sense?
Cynthia Thurlow: It absolutely does. I think it’s a really nice explanation with the analogy of twins for people to understand how easily that can happen. That they think of whatever it’s gluten or grains or dairy, et cetera, they’re wondering why they’re having some degree of inflammation. There was one study that I looked at that specifically looked at low carb, low grains, and it reduced antibodies by 40%, by 5%, BMI went down by 4%. Whether or not it’s vis-a-vis because someone’s a little insulin resistant and they lower their carbohydrate intake. There’re so many different factors that could impact that. Just understanding that nutrition is important, bio-individuality is certainly important. I think I’d be remiss if I didn’t at least address one more question that followers had in terms of supplementation. We kind of touched on iodine, obviously controversial, we touched on the cofactors piece. Are there any particular supplements that you have found as a generalization that have been helpful? I read a little about black cumin being particularly helpful. I know selenium can be anti-inflammatory for the thyroid or there are other things that you look at. Again, we’re talking about generalities, nothing specific. But that you have seen benefit in patients in terms of quieting inflammation, maybe giving them more energy that have turned out to be helpful.
Eric Balcavage: Yeah. I’m a big fan of sulforaphane and I know this can wrinkle some feathers, because people are like, “Well, it could be goitrogenic.” If you eat any of these kind of brassica things it can create problems with more [unintelligible [00:57:54]. That has proven to not be true in the human population based on the most current research. You don’t have to worry about that. Two, we have all these things that we can take to help with inflammation, quercetin, turmeric, all kinds of different things. Sulforaphane is the best food stimulator of something called your Nrf2 pathway. Your Nrf2 pathway is your body’s master anti-inflammatory, antioxidant and detoxifying gene. Okay, so it turns on 200 enzymes when it’s stimulated, in acute inflammation the body turns it on and it starts doing its job to allow the inflammation to go on and then calming the whole thing back down. The problem is, in chronic inflammation, something called NF-Kappa B blocks winds up not only– initially it turns it on and then it blocks its function. Now we turn off the anti-inflammatory, antioxidant and detoxifying system, so sulforaphane, highly absorbable, gets to the brain within 15 minutes of taking it and it’s hard for it to be toxic because its half-life is 24 hours, so it’s gone. I like that as a tool to help reduce the inflammatory mechanism. I work with a company called U.S. Enzymes, Master Supplements. I was trying to put together a bile formula for them and I ran across sulforaphane and that diverted the whole thing. We wound up just producing a sulforaphane supplement called SulforaXym. One of the really amazing things, as more and more physicians started using it, is the autistic community kind of picked this up. They were working on this, some of the physicians were given this stuff to their kids and they’re like, is it possible for these kids to go from nonverbal to verbal in like a really short period of time with just taking this stuff.
There’s some really awesome research out of NIH that’s been done on sulforaphane, but I haven’t seen a lot from NIH and in the autistic community, but is it a potential thing that taking that sulforaphane could have an impact like that on the brain. Yeah, if it only takes 15 minutes from the time you eat it to get it to the brain and it’s going to be anti-inflammatory and antioxidant supporting, absolutely, it could have an impact. So, I really like that. This is going to sound weird, but one of the things I think is really impactful for most people is starting with a digestive enzyme. Okay, the reason I say that is because if you have a stress response going on in your physiology, remember we talked about shifting from manufacturing to cell defense.
Well, if I shift out of manufacturing, I shift out of making a lot of stomach acid, digestive enzymes and that piece of it. Now I eat food, I bring it into the system. I don’t have great digestive capacity, now I don’t break those proteins down into amino acids. I’m breaking them down into peptides, now those peptides can cross a leaky barrier and trigger reactivity. That could be foods that are really healthy that I eat every day, that can be a process that occurs. I love people taking a digestive enzyme, especially when I do a test and confirm it. If they’ve got digestive issues, I may be talking to about stomach acid production, maybe given some Betaine HCl, some digestive bitter, or some bile, but as a base, if they’ve got digestive stuff based on the history, I always tell people before you add the multivitamin, probably the digestive enzyme is probably a better place to start. So that’s a biggie for me, so the sulforaphane, the digestive enzyme, say what you want about magnesium and how we test it.
I don’t think we have a great way to test it, but I think a lot of people are probably more magnesium deficient than we are aware of. I like magnesium as a regular supplement and then there’s a bunch of other stuff. But what I recommend directly from an inflammatory standpoint might differ based on what I saw on a blood panel. Is it fibrinogen, is it uric acid. Like, what are the things and then I might fine tune that a little bit but from just an overall inflammatory standpoint, I really like taking a look at, trying to hit with a limited amount of stuff. What can I do that’s going to have the biggest impact on the system? I really like sulforaphane.
Cynthia Thurlow: That’s awesome. Well, Dr. Eric, as always, this is an incredible conversation. Let my followers know how to purchase your book, The Thyroid Debacle. It’s an excellent resource, as well as catch you on Instagram and participate in your podcast for which I’ve been the honor of being a guest on twice myself.
Eric Balcavage: Yeah. Now I have to get you back on as a third timer. [Cynthia laughs] I don’t think I’ve had a third timer on. Now I feel guilty not having you on yet. But yeah, I have a podcast called Thyroid Answers podcast. It comes out about twice a month. I’ve got a video on Thursdays. I try to do these Thyroid Thursday videos, which is a bit educational, I don’t do a lot of– here’s the fun things, four things to do. I really try to be educational. Some people give me a hard time about it, other people enjoy it. My goal with a lot of my posts is to try and help you understand the mechanism. Why does this happen? versus, “Hey, here’s the three things to take.” I’d rather have you understand it so that way you can think through a process. That’s the goal of the Thyroid Thursdays, they’re a little bit longer, ten minutes. I have the book out. It’s called Thyroid Debacle. That’s available at Amazon, Barnes & Nobles, Balboa Press, go online and order it. What else is out there? I think that’s it. And I’m on Instagram, I guess. Yeah, Instagram. I’m not on TikTok or any of that. I think I’m on Facebook by default, but I think I’m on Instagram and that’s where I do kind of most of my posting.
Cynthia Thurlow: Awesome. Well, it’s been a pleasure as always, Eric.
Eric Balcavage: Thank you for having me on. I appreciate it. It’s always a great conversation, whether I’m leading the discussion with asking you questions or you’re asking the questions.
Cynthia Thurlow: Awesome. Have a great day.
Eric Balcavage: You too. Take care.
Cynthia Thurlow: If you love this podcast episode, please leave a rating and review, subscribe and tell a friend.