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Guest Bio:

Michael Ruscio, DC, is a naturopathic practitioner, researcher, and adjunct professor at the University of Bridgeport. He has published numerous papers in scientific journals rigorously researching complex gastrointestinal disorders as well as their relationship to thyroid health. Dr. Ruscio founded the Ruscio Institute for Functional Health, a consulting practice and research clinic that helps patients heal a wide range of GI conditions. From his clinical research and experience, Dr. Ruscio authored the book Healthy Gut, Healthy You, created a Thyroid Self-Management Course, and developed the first ever over-the-counter fully elemental diet formula on the market.

Transcript

Kalea Wattles, ND, IFMCP:
Dysfunction of thyroid hormone activity is quite common, caused by conditions such as thyroiditis and often accompanied by symptoms of fatigue, weight gain, GI distress, and even mood disorders. Research continues to reveal the complexity of the thyroid’s hormonal interplay with other biological systems, including the gut microbiome. How can improving gut health improve overall thyroid function?

Michael Ruscio, DC
And so, what can happen in some cases is TSH is normal, free T4 is normal, but free T3 is low. So the provider says, this is hypothyroid. And they really missed the thing that needs to be addressed, which might be, why is this patient so reactive to, let’s say, FODMAPs or starches, thinking maybe SIBO or Candida. And that would rectify the metabolic stress that’s causing the low T3.

Kalea Wattles
On this episode of Pathways to Well-Being, we welcome clinical researcher and thyroid expert Dr. Michael Ruscio to discuss functional medicine approaches to optimizing and balancing thyroid hormone levels. From evaluation of subclinical hypothyroidism to personalized treatment strategies, we’ll dive into the functional medicine approach to thyroid health. Welcome to the show, Dr. Ruscio.

Michael Ruscio
Hi, thanks for having me. Well, it’s a great thing that we’re talking because…

Kalea Wattles
According to the American Thyroid Association, 20 million Americans have a thyroid disease, and up to 60% of them don’t even know it. What’s your reaction to that statistic as we kick off our episode? Are you surprised by that? Is it something that you see in clinical practice all the time?

Michael Ruscio
Yeah. So I’ll maybe take a little bit of a party pooper perspective on this. There was a very important meta-analysis published in the journal Thyroid in 2021. And surprisingly, they found that 37.2% of people who are on thyroid hormone medication could discontinue the medication, maintain normal thyroid levels, and have no change in their symptoms. So said more simply, about one in three people at current are on thyroid hormone that they don’t need. And I think this is really important because the perspective I take is not that there’s a lack of diagnosis but rather there’s over and incorrect diagnosis. And to bring in the ATA, as you cited, we had a very insightful conversation with the former president of the ATA, Antonio Bianco, and I feel the reason why that podcast has had over 112,000 views to date is because people, patients, and providers are starved for this information, which is nuanced. It’s going to borrow some from conventional perspective, some from alternative perspective, but it’s really going to put the patient first rather than the philosophy. So what I would say to that again is I think the bigger problem is too quickly rendering a diagnosis of hypothyroidism that’s not correct. And this is part of what we’ve published in 2022 in that there’s a subset of people who are suffering in some cases for years with trying different perturbations of thyroid hormone all the while they’re treating the wrong thing. There’s a lot that we can do to prevent hypothyroidism and to help with inflammation and the like. There’s a lot to do, but part of what to do is also knowing what not to do. And I think that’s a really important piece maybe to lead with.

Kalea Wattles
Yeah. Well, I would love to talk about all of these things. I’m sure any healthcare providers who are listening are thinking, gosh, I have a lot of patients who are on levothyroxine right now. And maybe there’s a subset of this population that doesn’t really need that medication. Are there some features of these patients, biological features, lifestyle factors, something that is indicating to you that maybe we can do some experimenting, maybe this patient doesn’t need that medication?

Michael Ruscio
Yes. People, providers can get so much done if they do a few simple things. Firstly, put a little clause in your paperwork with the following questions. Who diagnosed your hypothyroidism? Was it a conventional endocrinologist? Was it some sort of integrative or naturally minded provider? That right there rouses suspicion. And I say that as someone in the alternative camp, but the prevalence of misdiagnosis seems to be higher in the alternative camp. So that’s one. Two, is there a family history? And then three, do you have the lab work that diagnosed you as hypothyroid? And if you go back and look at that, the lab work, that is, you will oftentimes shockingly see a TSH, let’s say of 4.75, sometimes even normal TSHs, according to the lab corporate request ranges of about 0.5 to 4.5. So even within the normative ranges being used to quote unquote diagnose hypothyroid. So that right there gives you a really important starting screening for, well, maybe this person has been incorrectly diagnosed. And again, looking at that meta-analysis from thyroid, it’s one in three. And in our office, we’re seeing a case of this per week. So it’s not something that you’ll infrequently see, and it’s pretty easy to suss this out.

Kalea Wattles
You’ve mentioned TSH, which is obviously such an important part of any conversation about thyroid monitoring and prescribing, but there’s some controversies about TSH and what’s considered normal and what is our threshold for treatment. In case that controversy is new to any of our listeners, will you just recap why TSH might not be the best measurement of overall thyroid function?

Michael Ruscio
Yeah. Part of the controversy in my view and my examination comes from hypotheses from five, ten years ago where there were patients who were suffering with symptoms, and the healthcare community was looking for additional answers. But we now have a number of studies that have really looked at this because researchers have said, well, maybe, right? Maybe the TSH needs to be re-examined. So to frame the controversy, right now the upper cutoff for TSH in most labs is 4.5. It might be a few points higher or lower, but you’re essentially going to clock in at 4.5. So above 4.5 is abnormally high. Now, where the problems come is at what level of elevation of TSH will this predict if people will benefit from thyroid hormone? Because ultimately what we want, patients and providers alike, is if you give a hormone, you want the person to say, yeah, I feel better. And what you don’t want is a person to say, well, I don’t really think that I’m better. And right then you go down this, I think, rabbit hole in some cases of forcing more thyroid hormone upon the individual. And there’s nuance that we can get into with the balance of T4 and T3, but just really high level. What level of TSH elevation will predict if someone’s going to benefit from hormone? And that seems to be somewhere between seven to ten. And this is the really important nuance that I think the functional medicine field is missing and is doing wrong. There have been a number of studies now, I believe it’s over 10 randomized control trials, that have asked this question. Well, what happens when patients have sluggish or subclinical hypothyroid? That’s the mild elevation of TSH. What happens when we give some of them hormone, the other half placebo, because we always want to evaluate against placebo, a placebo group. And consistently across all these trials, they’ve demonstrated that patients with sluggish or subclinical hypothyroidism do not see improvements in either their thyroid-related symptoms or in their general quality of life. So while it is controversial, I think we do have data that answers this question that unless someone’s TSH is somewhere in the seven to ten range, they’re not going to benefit from thyroid hormone. And I understand that sounds contentious, and some people vehemently disagree with me. But this is one area, thankfully, where studies have been done to answer this question, and that’s what they clock in regarding.

Kalea Wattles
Yeah. I’m sitting with this information. I’m letting it soak in and processing. How do the measurement of free thyroid hormones, free T3 and free T4, play into your decision-making, if at all?

Michael Ruscio
Well, the most accurate, I guess, diagnosis for hypothyroid will be a pairing of high TSH with low free T4. But usually they’re going to inversely correspond with one another, right? The higher TSH goes, the lower T4 goes. But again, what you’ll see in some cases is the TSH might be, let’s say, six, yet the free T4 is normal. So that doesn’t mean that the person is deficient in thyroid hormone. In fact, and this is where things get really murky. One analysis found that, and many have found like results, that 60% of people with subclinical elevations of their TSH revert to normal with time, with no other intervention, which is wonderful, which means those people don’t need lifelong thyroid hormone. Now we can improve those odds even further with vitamin D, selenium, myo-inositol, and there’s even been a few studies finding impressive results with photobiomodulation with the red light directly to the thyroid gland itself. But that’s a really important point. Now, the other component of this is low T3, I think the other point that you’re sort of intonating to. But that is more so a measure, if we’re talking about screening for hypothyroid or not, the T3 is more so a measure of metabolic and inflammatory stress. If people, and this is very relevant, I think, to the functional medicine community. If people are too low calorie or too low carb, so let’s say you’re, like we are in my clinic, looking at and serving a cohort that has a lot of digestive dysfunction, IBS, IBD, SIBO, Candida, what have you. These individuals are oftentimes highly avoidant of food. So what can happen is they’re either too low calorie or too low carb or both, and this causes low T3. And so what can happen in some cases is TSH is normal, free T4 is normal, but free T3 is low. So the provider says, this is hypothyroid. And they really miss the thing that needs to be addressed, which might be why is this patient so reactive to, let’s say, FODMAPs or starches, thinking maybe SIBO or Candida. And that would rectify the metabolic stress that’s causing the low T3. But low T3 in and of itself is not diagnostic of function of the gland. That’s really looking at TSH and T4. Now, and sorry to go too far afield here, but if you’re treating the hypothyroidism with hormone, then you can look at the T3 to see if the person has either adequate conversion or adequate absorption. So it does have relevancy when treating people, but when we’re talking about screening for hypothyroidism, yes or no, the T3, at least in my view, doesn’t really have a lot of relevance.

Kalea Wattles
Will you walk us through how this conversation with the patient goes? Let’s say they come in, they have that TSH that’s maybe six, but their free thyroid hormones are normal. They have done their reading, and they have read, if you have an elevated TSH, you should be on thyroid hormone replacement. How do you have that conversation to ease their mind or help set healthy expectations?

Michael Ruscio
Yeah, great question. I do think it depends on where they’re reading because there’s kind of a bifurcation of two camps here. One camp, which would be the camp that I agree with, which would say the first thing you should do is selenium, myo-inositol, vitamin D, and monitor. And this is the same thing, the conversation you can have with a patient, which is maybe, right? If you have elevations of TSH, there is a slight increased chance that you’re going to become hypothyroid in the future. But the odds, coming back to my earlier comment about 60% of those people reverting back to normal in time, the odds are that your thyroid is going to be able to normalize. And I think it’s important to paint this perspective because sometimes the things people read or the podcast I listen to say, if you’re not feeling well, get on thyroid hormone, and all your problems are going to be solved. That’s actually not the way this tends to play out. And I think people would rather not be on hormone lifelong if they don’t have to. So the way, again, I would frame this is there are probably other systems of the body that are driving your symptoms. We’ll watch your TSH, we’ll support your TSH with natural agents, but I’m hoping that you don’t have to go on lifelong thyroid hormone. So I think if you frame it like that, people kind of buy in and say, okay, yeah, I mean, the prospect of having to be on this hormone forever isn’t super attractive. And if you’re offering me another path to symptomatic resolution, that’s ultimately what I want, that’s really attractive.

Kalea Wattles
Very attractive. And how often are you monitoring TSH while you’re doing that more holistic systems approach to healing?

Michael Ruscio
It depends on the background of the individual. So if there’s a family history, then…that’s one point to rouse suspicion. Their age and their TSH also matter. The older you are, the more we’re expecting a little bit of a drift upward of the TSH. For every decade of life, you can add a point to the normal reference range. So that’s helpful. So if someone is 30 with a TSH of six, I’m a little bit more perked up than if someone is 70 with a TSH of six, right? And then also to sort of build more of a composite scoring, you can look at their TPO, not their TG. And this is something that was surprising to me when we recently did a review of the evidence on this. Thyroglobulin does not correlate with thyroid gland health or ultrasound-confirmed destruction of the gland, but TPO does. So the most predictive and the most tracking with treatment is TPO. Thyroglobulin is more of a red herring because it can have false positives for other reasons. But looking at their TPO, the higher the level of their TPO, the more attentive you want to be to follow up. And there was one prospective study, I believe this was the analysis out of Tehran. They found that a TPO above 500 correlated with a moderate risk of progression to hypothyroid. But if it was below 500, TPO was below 500, there was a minimal risk. I don’t want to go too into the nerdy details, but the details here really do matter. So when looking at TPO and predicting, well, what does that mean in terms of risk over time of development of hypothyroid? Because TPO is a marker for thyroid autoimmunity. Autoimmunity and hypothyroid are two different things, as I’m sure most of the audience knows, but just to sort of repaint that distinction. If you look at population level data, about 20% of the US population has elevations of TPO, but only 5% are hypothyroid. Not to say only, but right, but it’s relatively a smaller percent, right? So for that 5%, we want to do everything that we can. But nevertheless, comparatively, 20% have Hashimoto’s, 5% are hypothyroid, which tells you, I think, a really empowering and important thing, which is 75% of people with TPO will not become hypothyroid. And I just mentioned that because what happens in some cases is people come in with a positive TPO convinced that they’re essentially hypothyroid.

Kalea Wattles
Yeah. I mean, that makes great sense. I think something I’ve seen, a theme that I’ve seen over and over, is that patients have elevated TPO antibodies, and they have been told this is a ticking time bomb. It’s only a matter of time before you become frankly hypothyroid. But you’re saying you haven’t seen that play out.

Michael Ruscio
Well, it’s not that I haven’t seen that. I mean, I haven’t. Well, in some cases it does, but this is where we really have to look at good evidence to guide the decision-making and taking a step back because if I’m being a little bit candid, sometimes there is a clinician, a thought leader, a researcher who’s really dismissive of everything and it’s kind of this arrogant, well, if there’s not a really huge RCT or meta-analysis, then I’m not going to look at it. So that’s not what I’m talking about. There are some areas where we don’t have adequate research, and we have to be open-minded. I think mold, Lyme, these are areas where there’s less research and we’re really sort of piecing together smaller observational trials because it’s the best data that we have. But thankfully, we have decent studies that have looked at and tracked hundreds or in some cases thousands or even tens of thousands of people to help us understand how this all looks. And to your point, the ticking time bomb analogy, I think it’s good. The functional medicine field has brought to the forefront of the conversation that antibodies can be predictive. That’s a win, right? And that’s where I think conventional medicine oftentimes doesn’t do an awesome job. But the functional field in my view has gone too far telling people it’s a ticking time bomb. And we can have the conversation of this gives you a risk of about 25% and give people the straight talk, quantify it for people, right? Using these loose languages, which I know some thought leaders use, it just inculcates unnecessary fear with patients, and it doesn’t allow people to make sort of a, you know, I guess a risk-awaited decision, which is 25%. You know, that’s actually not as alarming as maybe I was reading about, so I’m less stressed now. And it’s even more likely that I’ll maintain normal levels if I use some simple supplements, vitamin D, selenium, myo-inositol, and maybe use a red light on my thyroid gland.

Kalea Wattles
And now that we’re on a mission of reducing fear, reducing stress, there’s one other clinical scenario that I have to ask you about. It’s the patients who their TPO antibodies are within the reference range, but they’re not zero. And people will ask like, well, is it normal to have any amount of antibodies? Shouldn’t this be zero? And I’d love your perspective on that.

Michael Ruscio
Yeah. And this again is where some of these studies have been really helpful in that 75% of people will have elevations, even frank elevations, right, outside of the normal ranges and maintain normal thyroid function for their entire lives. That’s the most important bottom line. That’s what we can say with a margin of confidence. Now we can speculate or theorize as to why that is. Maybe there’s some inflammation, maybe the thyroid blood barrier is a little bit porous and you have some particles leaking into the bloodstream and now there’s this immune upregulation to clean up some of that debris. Autoimmunity isn’t all bad. Some of it is a housekeeping function. So this is a scenario where I would just talk people off the ledge, so to speak, and let them know that not every lab finding has significance.

Kalea Wattles
Right. Yeah. You mentioned that as you’re treating someone who might have that elevated TSH, normal thyroid hormone, that it’s really a multi-system approach. And I know you’ve done a lot of work looking at the gut/thyroid connection. Are there some other systems we should be aware of? Of course, in functional medicine, we’re thinking systems biology. So what systems are popping up for you the most?

Michael Ruscio
Yeah, I’m so glad that you mentioned this. And it was very reassuring for me when I had the conversation with Dr. Antonio Bianco where we both had found that female hormone imbalances were one of the most common factors that sometimes looks like hypothyroid but obviously is not. And part of this might be as clinicians, if our intake systems are incomplete, we may miss half of the symptomatic picture, meaning someone may have the complaints of dry skin, depression, fatigue, and thinning hair. But they didn’t mention that they also have PMS, irregular periods, and heavy menstruation. And so when you put those things together, now it creates a little bit of a different picture wherein, maybe those symptoms that you’re complaining about are part of this female hormone imbalance syndrome and not from hypothyroidism. Coming back to some of your other questions in terms of what do we do for these people, if they’re having symptoms, we want to get the symptomatic resolution as quickly as we can, obviously. If they’re not frankly hypothyroid, the top two things I would look at is gastrointestinal function and female hormones. And that can save so many people. And this is what we published in the IMCJ, a six patient case series of patients who before coming to our office, it may have been months or even years where they bopped around from the thyroid specialist to the thyroid specialist. One person was the tyrosine person, the other person was a desiccated person, right? And they were all trying to help. But what was disheartening about those case studies was in some cases between one and three months, there was near or complete symptomatic resolution by either female hormone support or gastrointestinal support. So this is what we’re really trying to bring to the forefront of the conversation, which is not shoehorning people into the thyroid diagnosis and why those criteria of the labs, the more conventional criteria are so important because it helps you determine, where do I go at that fork in the road: do I use thyroid hormone in someone who doesn’t have frank hypothyroidism? Or do I maybe look for another system in the body and at least start there and maybe come back to a compassionate trial on thyroid hormone after I’ve looked into these other systems?

Kalea Wattles
Right. Okay. I’m going to put a pin in hormones and gut health because I’m going to come right back to it, but I have to clarify before we move on. Is it safe to say someone who has an elevated TSH and low free thyroid hormones, we’re giving them thyroid hormone replacement, or that part’s not controversial? Is that correct?

Michael Ruscio
I mean, I think it would partially depend on the levels. So if their TSH was five and their free T4 was 0.7, I might retest. There is some fluctuation. Sorry, this is overly rudimentary, but the larger the disparity in the hormones, the more likely the person is truly hypothyroid. And there was one study, I might have the numbers here slightly off, but I think the average TSH of diagnosis of someone who was frankly hypothyroid was like 50. So when someone’s frankly hypothyroid, it’s fairly obvious. And I guess maybe the bigger point is just to take a moment of pause when you’re seeing some thyroid signal before you go rushing in with thyroid hormone because A, a lot of these cases may rectify with doing nothing. B, we can use natural therapies to help preserve their thyroid function. And then C, the symptoms might be coming from somewhere else.

Kalea Wattles
Okay. All right. The picture’s all starting to come together. So let’s loop back to some of these systems that we can support to prevent that destruction or slow it down. Let’s talk hormones first because I’m very interested in this connection with female hormones. And I think many of us were trained that if someone has female hormone disorders like low estrogen or low progesterone in the luteal phase, that we have to correct the thyroid first. I think many of us were trained that way. Is that your understanding or are we saying that actually repleting those hormones will help to restore thyroid function?

Michael Ruscio
Yeah, and I understand where that comes from because there is a bidirectional relationship between thyroid hormones and female hormones. But I think it’s important to ask the question when we’re talking about supporting the hormone, the thyroid hormones, if that’s someone who’s frankly hypothyroid, I would agree, right? If someone has frank hypothyroid, I would treat that first before many other things, really before anything else. But that’s really the issue at discussion here, right? It’s, well, how do we determine who is frankly hypothyroid and who’s not? So if they don’t meet those criteria of the TSH above somewhere in the range of seven to ten paired with low free T4, if that’s not the case, then I would treat the female hormones first.

Kalea Wattles
Yep. Okay. That makes great sense. Let’s shift to talk about how the gut interacts with all of this. So if you’re working up a patient, they maybe have an elevated TSH, regardless of whether their free thyroid hormones are high or low. What type of investigation are you doing into their gut? Are you doing stool testing? Is there some other type of testing? What does your evaluation look like to understand if there is a relationship here?

Michael Ruscio
Sure. And let me just take a step back and paint an important perspective, which is if someone is on thyroid hormone and they’re complaining of symptoms, fatigue, brain fog, poor sleep, thinning hair, dry skin, these thyroid-like symptoms, and they have any digestive symptoms, constipation, bloating, fatigue, reflux, abdominal pain, then it’s possible that they’re not consistently absorbing their thyroid hormone medication, which is really important because in some people, their symptoms and their levels are in flux, and that could directly be because of inconsistent absorption of the medication. The second point is regarding conversion. So to convert from T4 to T3, if there’s inflammation in the body, that can be thwarted. And obviously the gastrointestinal tract is a decent source for inflammation in the body. So it really is important to get to the bottom of any GI issues. In terms of workup, a SIBO breath test, I think, has some clinical utility as we’ve been watching the literature on this, I think the case for a SIBO breath test is partially diminishing and maybe taking a big step back. One of my hopes is that the functional medicine field will move to a place where we don’t have to do thousands of dollars of lab testing on every patient and we get better at using our clinical skills and maybe even something like a validated symptom inventory. As an example, the FRDQ7, the fungal-related disease questionnaire, seven questions that have been correlated or they’ve been documented to be predictive of response to antifungal treatment. So instead of having someone do a Candida or fungal workup, which to do a good one, you’re probably looking at a saliva, or I’m sorry, a serum antibody plus a stool test plus a D-arabinitol, that could be $600. It’s three different tests. It’s a lot of rigmarole, and you also want to test SIBO and you also want to test leaky gut. I mean, before you know it, you know, the patient is spending weeks doing testing and a lot of money wherein you could use an inventory to predict, well, you know, from these seven questions, are you fatigued? Do you have watery eyes? Do you have any sort of vaginal discharge? Have you used antibiotics in the past for longer than a month? Do you notice your symptoms are worse on rainy days or in damp places, just to give a few, then you may say, well, let’s try a Candida diet, something like garlic extract at 1,500 milligrams per day. And that might be enough between that visit and the next time you see them to resolve a ton of symptoms instead of having the person go do labs for a month and burn all that time just waiting for your quantification to come back. But there’s the Candida workup, a SIBO workup. But those are things that we’re using much more sparingly now, and we’re using much more either questionnaires or just conversations with a patient that try to figure out what to do. As another example, maybe you notice that lots of vegetables flare you. Well, that might be more of your IBS, SIBO, and that enough could be a prompt to say, let’s try a low FODMAP diet. So the thyroid testing, I think, is really important because symptoms are not a good predictor of thyroid function. But in gastrointestinal care, it’s kind of the opposite, where I think we can get a lot done just by looking at their history and their symptoms.

Kalea Wattles
I love the idea of the careful history collection. Asking those targeted and specific questions help you to discern between SIBO or just dysbiosis in general versus someone who has hypochlorhydria versus someone who needs digestive enzymes. There’s so many different avenues we could explore. Are you able to get that information through this careful history collection?

Michael Ruscio
Yes. And we’re getting there, and we’re getting better, and we’re collecting data on this as we speak. The way that we’ve broken this down is into one of three gut types, a bacterial type, this is your SIBO, IBS types, a fungal type, or an immune type. Now the bacterial types tend to not do well on high fiber, high vegetable, high prebiotic, and they notice that too much of those foods bloat them. Now conversely, the fungal types, these are usually the people that get flared by carbs, starches, and sugars. And they might have things like toenail fungus, thrush, rashing, recurring vaginal yeast, watery eyes, and be fatigued all the time. What’s so helpful about making the determination is the fungal types can’t do starch. But the bacterial types oftentimes thrive on high starch, low vegetable. Whereas the fungal types need to be on low starch, kind of low carb, if that makes sense, right? So as an example, if you have an individual do a SIBO breath test, that’s essentially white rice and meat for the prep and diet for the SIBO breath test. A bacterial-type patient will say, gosh, I felt great eating rice and meat, but a fungal type, they will not do well on that at all because it’s high starch. Just thinking about the foods that feed or push or pull you in either direction can give you a lot. And we have a short series of questions, kind of like I just outlined, in our intake paperwork that group those together. So before we even see someone, we’re saying, okay, here’s your symptoms, and here’s the foods that trigger you and don’t trigger you. So I’m already thinking you’re a bacterial type or a fungal type. And then with the immune types, that’s more of your histamine intolerant. These are the people who may notice they don’t do well on fermented foods especially. And that’s where a low histamine diet might be helpful.

Kalea Wattles
Those who are doing the anti-Candida food plan or the low-histamine food plan, what’s your timeline? Is the ultimate goal to be able to bring back as many of these foods as possible? Is it long-term? What’s that timeline?

Michael Ruscio
Yeah, it’s a great question. I’m so glad that you asked that. The analogy that we like to use at the clinic is if someone hurts their back, it would be very logical to assume, okay, a month, maybe two, reducing activity, doing rehab, and then you gradually resume and you can go back to running, weightlifting, whatever it is with time. That’s the exact analogy that we use, and people get it like, yeah, that makes sense with the diet, right? If we’re doing the right diet, if we’re healing, if we’re reducing inflammation in the leaky gut and also restoring enzyme production, then we should be able to tolerate more foods over time. So that’s generally how we frame it. And we make one other caveat, which is we may discover that you lean in a certain direction. So you may never be someone who thrives on a high carb, high starch diet, but at least we know, okay, like, you know, here’s my core diet. And then sure, on the weekends I can have pizza or whatever and have a little bit of an excursion, but this is sort of the general core I’m going to be aiming for. And, you know, at least people have the knowledge to be able to elect where their deviations are and be able to have clarity. Meaning their symptoms are reduced and stable enough to where they can now test against that new healthy baseline. Because in some situations, I’m sure you can identify with this, if someone is so symptomatic, you can’t make heads or tails out of anything. But once you get them more stable, then they say, I brought back in this food, and I got really bloated or I had loose bowel. So now it’s clear for me to be able to see what my triggers are and what they are.

Kalea Wattles
Yeah. This is really fun to talk about. And I want to focus on the microbiome because of course in functional medicine, we love to talk about the microbiome, and you’ve done some compelling work that highlights this connection between the gut microbiome and thyroid health. And you’ve dubbed this term nutrient-GI-thyroid axis. Can you unpack that for us a little bit? Tell us what that connection looks like.

Michael Ruscio
Yeah. I mean, some of the broad strokes there are in those who do have Hashimoto’s, estimates vary, but it’s between 20 to 40% of those individuals will have a deficiency of either an intrinsic factor, HCl, or both. So they’re at risk to be iron anemic or B vitamin, B12, not the only one, but they may be a number of B vitamin insufficient due to low ionization of the minerals and the vitamins. So that’s one in terms of someone might be fatigued because of low ferritin or low B12. Maybe a lot of the people that we work with aren’t because I’m assuming they’re on multivitamins and B vitamins because they’re just so proactive, but it’s certainly something to be attentive to, especially depending on your population. Our population is just so well-read and so proactive that they’re usually on a number of vitamins already, but that is one important factor. Another, in regards to thyroid conversion and autoimmunity like we discussed earlier, vitamin D, selenium, and myo-inositol. And those aren’t necessarily broadly deficient, but they have been documented to help lower antibodies and improve conversion of T4 to T3. The other is iodine. There was one study, and I think this has been replicated by others, that found long-term adherence to a paleo diet actually did pose a risk of iodine insufficiency. So it’s not something that I think is on the population level. But if someone’s been on a restrictive diet for a long period of time, thinking about the Paleo diet cutting out some of the main foods that are fortified with iodine, which would be iodized salt, dairy, and grains, then inadvertently, these people might be eating their way into iodine insufficiency. So it’s just something to maybe have them use an iodized salt. And there’s even, I believe, an iodized sea salt out there where the iodine has been added back. And then gastrointestinal absorption. The other thing that happens in some of these cases is they’re not absorbing nutrients well. So wrapped in with the IBS, SIBO, whatever it is, especially if it’s chronic diarrheal type, they’re just not able to extract adequate nutrition from their food. And that’s where some of the, let’s say, fatigue, depression, thinning hair, and dry skin is coming from. It’s not thyroid, but it’s nutrient deficiency.

Kalea Wattles
You mentioned iodine. I think there’s a lot of interest in this because so many, you just go look at the thyroid support supplement blends, many of them will have iodine. And what we know is that perhaps that’s not always appropriate for someone who has hypothyroidism. Will you talk us through your strategy for evaluating iodine? Are you testing this? Are you doing a dietary recall? How do we assess someone’s iodine status?

Michael Ruscio
Yeah. I used to look at this more closely with, if we could get it, a 24-hour urinary iodine. Some people don’t do that because it’s like carrying around a gallon of pee with you all day. It’s sometimes easier said than done. But to be honest, I didn’t see a whole lot of signal there. So what we’ll do in some cases, especially if we’re seeing a high TSH without any antibodies, and this wouldn’t be a frankly high TSH, this would be like a subclinical hypothyroid, no antibodies, no family history of hypothyroidism, we’re thinking, well, maybe the gland doesn’t have enough substrate to produce the thyroid hormone. And we’ll try something like a low dose iodine repletion. I have a little bit of tenuousness with the multi-milligram doses of iodine because as the audience probably knows, there is some evidence showing that high iodine intake can flare autoimmunity, but you also see problems with too low of intake. So the Goldilocks sort of principle here resonates anywhere, but maybe you could do a gram to five of iodine per day along with some selenium if you suspect it. In terms of working it up, there might be something here that I’m missing, it just never, at least from our purview, seemed to really move the needle. And again, there may have been something that we missed because we really turned our focus to where there was a much more consistent benefit to patients, which was their gut health. It is possible within our sampling, there was a subset who had problems with iodine that we just didn’t fully pick out. So there may be something that we’ve missed, but those are my two cents.

Kalea Wattles
Yeah, the gut health seems to be pretty high yield. And my last question about it is, let’s say someone is, they’re already on thyroid hormone replacement. They come to see you. You start doing some of this gut restoration. Are you able to lower their dose or take them off their medication at some point once the gut health has been restored?

Michael Ruscio
Absolutely. Yeah. And for some people, actually, they will express signs of being over-medicated because their absorption improves. So definitely. And it’s an important thing to just keep an eye on. If someone does have frank gastrointestinal symptoms and they’re on hormones, they may start having palpitations, insomnia, feeling hot, which could indicate that, again, they’re overly absorbed. I guess they’re correctly absorbing the thyroid hormone. And coming back to that meta-analysis, because this is a common patient question, well, I’ve been on hormone for five years, ten years. Does that mean my gland is kind of wrecked and I can never get off of it? This study looked at these factors, and length of time someone was on hormone did not predict their ability to come off. So it was really reassuring, but what did was at time of diagnosis, TPO levels and TSH levels. So that’s something else you can do if you can get that data from before they started on hormone, what diagnosed them, then that can be used as a prognostic indicator of if they’ll be able to come off the thyroid hormone or not, or at least reduce their dose.

Kalea Wattles
Yeah, wow, that’s so fascinating. And I think many of us have been told once you measure TPO and it’s positive once, you never have to measure it again. I know many of us have been told that. What’s your approach? Are you monitoring those TPO antibodies over time to make sure that they’re coming down, knowing that they don’t necessarily correlate with symptoms.

Michael Ruscio
We used to look at them much more closely, and now we’ll only retest if they were above 500. Now if they are above 500, you know, then we want to monitor that, right? Because again, I think a reasonable goal is trying to get them sub 500. And if they’re not, then I mean, if someone wanted to repeat a TPO every six months to a year, especially if there’s a family history, then maybe. It also depends on the person. Let’s say you support their female hormones and a month later they go, wow, I’m sleeping better. My mood is better. Okay, I’ll take the win, right? And I won’t go into such fastidious monitoring if the person is doing really well.

Kalea Wattles
Yeah, that makes great sense to me. What’s the future of thyroid hormone research? I know that you’ll keep your eye on the frontier. What are you feeling excited about? What do you think will develop over the next few years in terms of our insight into thyroid function?

Michael Ruscio
Yeah, you know, what I found fascinating, we reviewed a study on this just recently. It’s one of a few, but this one study in particular found that red light therapy on the thyroid gland led to a 400-point reduction of TPO. Now for context, most of the studies looking at vitamin D, selenium, myo-inositol are averaging around a 200-point reduction. So pretty fascinating that an inexpensive red light, I mean, if you get a full body panel, that can be like $1,000 to $3,000, but in this case, you only need something maybe the size of like a computer mouse to light therapy the thyroid gland. So that’s pretty impressive. The study that I would love to see done is using any of these interventions that lower TPO, right? The photobiomodulation, the vitamin D, the selenium, the myo-inositol, and then seeing if that reduces the conversion to hypothyroid over time because we don’t have that data. All we have is the studies that have shown the ability to lower the antibodies, which will probably correlate, but there are examples, as an example, lowering homocysteine with B vitamins doesn’t seem to reduce cardiovascular events. Treating a marker doesn’t always lead to the outcome that you want. So that’s a study that I’d love to see published. But otherwise, in terms of thyroid care, the biggest thing that I think needs to be done is the functional medicine field to start updating some of the paradigm that we use, which I think, again, coming back to that meta-analysis from the journal Thyroid, if one in three are on hormone that they don’t need, then that’s really disturbing patients, and it may be distracting from where the actual cause of their disease and dysfunction is coming from. So as a field, I think we’ve done so much to help patients with diet, nutritional support, lifestyle factors, and prevention of Hashimoto’s. But where I think we’re really missing the mark is being too quick—compassionately, but too quick nonetheless—to give people hormone and not making enough of a case before we do so.

Kalea Wattles
And if the solution is supporting gut restoration, repleting female hormones, reducing chronic inflammation, improving nutrient status, we are well suited to meet that.

Michael Ruscio
Yes. Yes, thankfully. Totally.

Kalea Wattles
Dr. Ruscio, I wanted to thank you so much for your time today and sharing all these insights. We will definitely keep our eye on your work as you’re always giving us the latest and greatest in thyroid health. And thank you so much for being with us today. It’s been a pleasure to chat with you.

Michael Ruscio
Same here. Thank you again.

Kalea Wattles
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