007 GUEST SERIES | Dr. Cheryl Burdette - Clincian, Researcher and co-founder of Precision Point Diagnostics

Welcome back, everybody. This is the Functional Medicine or Funk Med Nation podcast. I'm your host, Steve Noseworthy, and today I have the pleasure of talking to Dr. Cheryl Burdett. She's a natural who wears many hats. My. My best known association with Cheryl is as a director. Director of Precision Point. Or did you. Were you one of the founders? The co founders and educational director.

Yeah.

And educational director, yeah. So, you know, to be honest, I think there's so many paths that this conversation can go down. But when I first reached out to you to see if you'd be willing to come on the podcast, it was from the perspective of talking to someone who was knee deep in the world of diagnostics. Because I think that there's functional medicine, at least in my opinion, has changed and grown so much over the last 10 to 15 years that I think there's need for a conversation about diagnostics in general and about how we can spot labs that are doing it right, labs that might be cutting corners. And so, you know, I emailed you a list of questions that I don't know if we'll get to all of them, but one of the things that I love about you is that you have a clinical background. And I think that's so valuable, your experience as a naturopath, to be able to marry what could potentially be two very separate worlds. Right. And because I think that there are a lot of companies out there that, that design diagnostic testing, that when you kind of look at the clinical utility, it's just not really there. So maybe we can start just a little bit about your transition into, like, how did you first start getting interested in research? And what led you to the point where you said, hey, I think I want to. I want to start a lab and I want to do this rather than just be a clinician?

Yeah. Well, I've always felt that our therapies need to be strongly evidence based. And as our medicine grows with evidence, so does our ability to reach more people. And just as important as ruling things in that will help people is also ruling things out. And we have a tendency in all sides of the world to become dogmatic about whatever our primary therapies are. We certainly can bump into to that in the allopathic world. But at the same time, we can get very excited about things we see in terms of natural health and how they help people, and then start to treat them all as equal. And that's just not the case. And so if we can figure out which things work and which things don't, then we can fast track getting people back to feeling better. And so I've always had a strong belief in terms of really looking at the data and deciding, is it something we think that we're seeing, or is there a larger body of evidence that supports that? And so as I was growing up in undergrad, my background was that I was double majoring in psychology and pre med. And I thought, well, surely these two things must be connected somehow. So is there a field that looks at them together? And one of my last classes in psychology was called biofeedback, self regulation and meditation. And this was a fascinating class because we dove deep into how the mind controls the body. And maybe that sounds like a statement of the obvious, but to me, to see studies about how with certain practices, people could control their blood pressure and take it up or down. And I did this. I worked with the professor and I did an experiment where we brought college students in and we put electrodes on their fingers that would measure their body temperature. And for every dot, for every degree, half degree, they could take their temperature either up or down on command, they got a dollar. And so the more you could ra. So the more you could follow this biofeedback, the more pizza money you could make or whatever. So. But I was blown away to see that people could take their body temperature up 2 degrees and then bring it back down to normal and bring it down a couple of degrees. And so I was just knocked in the face evidence and data that really supported what we, what we do. And so it always was a bright place for me that I wanted to say, yeah, let's add to this story. Let's see what we can figure out so we can help more people.

You know, I love those watershed moments where, you know, your curiosity and creativity just get piqued by something. I remember back when I first started in functional medicine, like early, early 2000, somewhere around there, and I, I had heard something, and I was never able to confirm this, but just along the lines of what we were talking about, I had heard somebody speaking and they made comment about some study that was done somewhere. And of course I can't, I haven't, I can't reproduce it, but they talked about how they, they took people in their 70s and 80s, they would measure their blood work and then they would play music that was from their youth, like their teens and their early 20s, and then a couple hours later, pull blood work again. And they would see two completely different metabolic profiles. And the only intervention was listening to music that brought them back to their, heyday, wow.

Yeah.

I wish I could find that study. I honestly don't even know where to begin to find something like that. But that was one of those, like, wow, how cool is the human frame if. If your psychology and your emotional. Emotionality is so powerful that it can actually shift your metabolic state. I mean, that was profound. It was a big picture concept for me to get my head around.

Yeah, absolutely. And how often have we had patients that when they go in and seek help and ask questions about natural therapies, they get told, well, there's no research about that. And most of the time at this point, that's not accurate. I mean, if we were having this conversation 20 years ago, it was more accurate. But the research has really grown and developed around our field, and so many times it gets used as an excuse to be dismissive, and that makes me quite sad.

Yeah, well, it's. It's, you know, difficult to change the course of a large machine. Right.

And.

And so I. I personally am grateful for, you know, people like you in our community who are. Are forward thinkers and don't just follow status quo and start to think out of the box. Like, I can't imagine that there are many practicing clinicians who would recognize the need. I guess the right term would be to say, invent a better mousetrap. And you apply that to the world of diagnostics. You know, most of us are content to be discontent. Right. Oh, well, there's just no good testing for this or no good way to do this in a clinical setting. And we just kind of live that way and we learn to adapt. So what, like, what is it about you as a person? I know we're kind of going down more of a personal story side in the conversation, but what is it about your makeup that made you go from something's not right or there's a hole and a gap that needs to be filled to the point where you said, well, I'm just going to go fill it. Because I would imagine that when you started Dunwoody, back when you were called Dunwoody, that you had something in mind. You weren't doing it just because, hey, I think this is a good business idea. And I'm going to go, you know, this is my side hustle. I'm going to start a lab. What was in your mind? Like, what were you trying to fix or what were you trying to provide? Probably first for yourself as a clinician, but also, by extension, other people.

Yeah. So I would see things in the research. I would see biomarkers that Were well validated, that were meaningful. And so oxidized LDL is a good example of this. And back in the day, we were actually the first to make that commercially available. And. But many labs do it now. But oxidized ldl, for example, many people out there listening are like, yeah, I know hdl, I know ldl, but oxidized ldl? And you then it might not be as familiar, although it should be. And the reason for that is that when you go to the literature, it talks about how that is 17 times more predictive for. For heart disease than LDL. And when you look at other biomarkers out there, a lot of the question that we're asking is just that, how easy is it for cholesterol to oxidize? And that's just a fancy way of being saying being charged by a free radical. But the reason for that is many of us are led to believe that if we. If I were to take a biopsy of a plaque in an artery, that I would find cholesterol or ldl, and I wouldn't. What I would find is oxidized ldl. That's what makes a plaque. And it's really fascinating because once it gets hit by a free radical, it changes its shape. And now the receptor on the liver that normally takes it up can't do that anymore. So the liver can take cholesterol and use it for cell membranes and use it for hormones and use it for a lot of beneficial things. This is why lowering it too much is problematic. We know less than 140 is even for a cholesterol level is even associated with an increased risk of depression and suicide. So our brain needs cholesterol, our body needs cholesterol, and the liver takes it up. Then it uses it. However, when it gets charged by that free radical, the liver can't do that anymore. And so now that's when a white blood cell called a macrophage gobbles it up, then sticks it into a plaque in the arterial wall. So if I were really trying to see what builds a plaque that would be oxidized ldl? Well, there's no lab. It was. And it was all over the literature, journal after journal. Wasn't just one article. There's this whole body of evidence. But then when I would go to a quest or a labcorp, it wasn't available. The other thing that captured my interest about it is the way that you're going to treat it. It's not just to take a medication that tells the liver not to make it. You're going to increase antioxidants, you're going to increase organic food. Because all of those things like eating a toxic food and not getting enough antioxidants and even being under too much stress, all of those things are the things that create free radicals that will eventually oxidize this ldl. So also it guides us to treatments that are meaningful, in my opinion, in terms of getting to root cause. So I'd be all over the literature and I would see these things that were well documented, but then I couldn't get them for my patients. And so I went to the person who owns the lab where I practice and I said to him, hey, we should become partners. We should found a lab together. And I've been in lab sciences before and you know, I know the, how to put the pieces together, the quality control and the Ph.D. and the, you know, all the things that we're going to need. And so we started out of a clinic and we started, like you said, with clinicians at the helm, myself and my partner, Dr. Gazagoli. And I do think you're right, that that drives the, the focus in a different direction. Because if I were trying to win a Nobel Prize for science, I wouldn't get it for oxidized ldl. It already been discovered. Somebody's already done that. You know, it's not brand new. But what I want as a clinician is something that's well documented, that's predictive, that treatments are, that align with the treatments that we want to utilize. And that's very different. So at the case of like the science, it's like being the first to publish, whereas I want the opposite. I want to see 201,000 articles on that already. And so it does. It guides you differently in terms of analytes you're going to look for. It's not necessarily, I mean, like I said, it wasn't available for our patients, but it's not necessarily the most new breakthrough. It's also what has a lot of validity behind it.

Yeah, you know, I remember back when the only place you could get oxidized LDL was like Boston Heart Labs in Cleveland. And of course they were eventually bought out by Quest and LabCorp. And I always forget which one bought which. But, you know, they're, they're kind of deep embedded that. But what I love about the last five minutes is that you just went down this, this passionate not diatribe because that has negative connotations. You should went like deep into the clinical stuff. So. So clearly, even though you're probably very busy on running the lab itself. You're still clearly a clinician at heart. Are you still seeing patients or have you completely moved over and you're in the laboratory world? And how do you navigate those two? Because I would imagine that although they go together from a clinical standpoint, you have to wear two very different hats. So how do you navigate all those influences and the responsibilities on both sides?

Yeah, so on the clinical side, I do see patients, but I'm also in an educational role. I have residents and I do. I work at Progressive Medical, and it's a larger staff, and we, of course, do grand rounds once a week where we come together and talk about cases, and we're always emailing and different treatments. And so I get the. I get to cheat. So I get to go through all of their charts and look at everything everybody else has done and kind of hopefully synthesize things and then come together and talk about them. So that gives me a lot of exposure. In addition to that, I have a clinical management practice management group, and there I teach clinicians as well. And so it's the same thing. We come together once a week and we talk about their cases and what to do. So another world of exposure. Then I'm out there lecturing a lot, so I get to hear from a lot of our colleagues what's working and what they're looking at. And then being on the lab side, I'm still also having conversations with docs. So when I see lab results that come in where something is really changed in a hugely positive direction or something's off the charts in a really abnormal way, then I have the luxury of being able to call people and rely on our community to kind of see patterns of what going on. So while, yes, it does require being kind of in different places, there is a nice synergy and overlap between.

Yeah, there's certainly. Yeah, for sure. And, you know, I think it's. Dangerous is the wrong word. I think it's disadvantageous for practitioners to live in their own silo and in their own echo chamber. Right. And so when you. When you're part of a. A larger community and you have colleagues and. And of course, nothing teaches you like teaching other people. Right. I mean, I've experienced that in the functional medicine circuit that when. When you have the responsibility of standing up in front of a room of dozens, if not 100 people and you're going to teach them about something, you better have everything in order. Right. And absolutely. Whether you're. Whether you're a kind of Teacher educator type clinician, where you're having deep, deeper educational conversations with your own clients and patients, or whether you're in more of an educational role that might be more formal, or maybe you're involved in some kind of coaching arrangement that puts a lot of onus on you to be, to be involved in the clinical stuff. I guess nobody wants to learn from the doc who doesn't practice. Right. And this kind of gets back to. Yeah, this gets back to what I was saying about. I think one of the things that makes you valuable in, in our community in terms of functional medicine in the broader sense is that clinical background that you bring to the diagnostics. And you can refuse to answer this question if you want to, but do you see other labs, don't have to name names, probably better not to. But do you see other labs that are out there that might be competitors to what you're doing at Precision Point that aren't staffed or run by clinicians? And if so, what's the downside of that from a value standpoint? Do you understand what I'm asking?

Yeah, yeah, yeah, that certainly exists. And I think a good illustration of that point is just different methodologies that are out there. So, for example, we do our food sensitivity testing with an elisa and sometimes you'll hear people say, well, and elisa, it's not sensitive enough. But while we might not be able to detect something down to parts per million, that's in some cases also not clinically relevant. Like we're not getting down to parts per million when we're looking at antibodies against certain foods. So there's a question of, well, are we just spending on fancy equipment that doesn't give us an increase in clinical data? And then the flip side of that is another methodology known as HPLC Mass spec could be seen as much more sensitive. Like that boils things down to atoms and weighs them. And you're, and you're really seeing that the tiniest part out there. But when we do something like this, let's say we on a blood specimen or a urine specimen is a good example, then it gives you all kinds of peaks and the peaks tell you the different values that are in there. And a run like this can be anywhere from 20 to 60 peaks. Well, so now think of some of those larger tests out there that you look at that are from urine. And maybe an organic acid is a good example of that. And if you have you worked with organic acids and testing, you might have said, oh, shoot, like, I don't remember this one from biochemistry and then you go to pubmed and you're looking for it and you're like, gosh, maybe I'm just not getting this. Well, no, it's not you. Not every peak that comes out is equally clinically validated at all. So some of these peaks really don't have a lot of clinical meaning. And then as the curious clinician will go looking for the data and you're thinking, what am I just missing? Everything and you're not. Some are very well validated. But what will often happen is when it's more, when we, when the peaks can be more interest sometimes in, in a, for a PhD versus for us, we're looking. Okay, but what does that mean in terms of telling me about a disease process? So that's an example of how sometimes methodology, you get this big long test and these long words, and it looks like there's a lot of information there and a lot of it is valid, but not equally.

And it's been probably a week since I went to your website and looked at the menu because I know that you do add test and change tests periodically. I, I don't remember off the top of my head, if you guys do organic acids testing.

We don't. And I'm not at all saying I wouldn't. In fact, it's one that I would love to add. So I'm just, I'm just more saying, you know, to our clinician friends out there, if you've ever picked one of those up or, or even as a patient, you picked it up and you went to look online to see what it means, don't feel like you're missing something because they don't all mean they're not all as validated as you might think.

Right. And I wanted, I wanted to dovetail off that and just, just make a comment like I, I, I personally don't run. If I've run half a dozen organic acids tests in the last 20 years, that would be a, a high estimate. Not that I haven't, but I certainly don't put it as what I call tiered one testing, which I think I should be thinking about with every single case that I work on. And it seems to me that in, in testing like that, which may have some value and some applicability when you start looking at like the interpretation guides that are generally published by the labs themselves, it seems to me that some of the commentary, and again, I'm not pointing out specific labs that do these things, and I'm not laying claim, I'm just trying to Say, okay, what's the reality of the world that you and I live in and other practitioners? It seems to me that a lot of those things are just written from the perspective of, how do I say this? Almost like folklore. Concepts and knowledge that we've inherited for people who came before us, who thought back then, this is what this means. And now we take that as gospel truth, which may or may not be true. Right. And this is one of the things that I love about the time that we're in right now in terms of functional medicine, and there's. Obviously people have been in practice a lot longer than I have, is that there seems to have been a very big shift, at least in the last 10 years, to being diagnostic focused, to being research validated focused, and to, to have more than just history and, and let's call it folklore to base your clinical decision making on. Not that history and folklore has no value, because I think it does. And there's a lot of things that I do in practice that I do because it works, not because I know scientifically how it works or why it works. I just know if I do this, this is usually the outcome. So I'm not pointing fingers and saying, you know, you're unscientific and you're, you're not, whatever. I'm just saying I agree with you. There are some labs that offer tests that are not scientifically valid or validated, at least at this point. And as a clinician, I would, I would like to have the skill and the knowledge, and I don't have it. I would like to have the skill and knowledge to be able to look at a lab, look at their certifications, look at their test menu, look at the technologies that they choose to run, and then make a decision like, that's a good lab. I think I want to work with them versus I'm not so sure about that. You know, maybe put it on the shelf and come back to them in a few years and see if they've got things in order. So one of, one of the things that I did want, and I feel like I'm jumping all over the place because as you're talking, my brain is going every direction. Like what, what kind of quality controls have you put in? And I mean, the collective you as a group, what kind of stuff have you put in to make sure that the, the services and the testing packages that you guys make available to people like me are things that I can rely on because I know that you've done your homework. Like, how do you position Yourself in. In that. In that role.

Yeah. So one of our most popular tests is a test that looks at re foods. And so it looks at four ways the immune system reacts to foods. What we're kind of more used to in terms of allergies, but which are driven by ige, but it also looks at sensitivities that are driven by IGG. Then we also tease out IGG subtype 4 because it acts very differently. I won't get too much into that right now. And then we look at complement, because it can augment all of those reactions. So basically, just like with lipids, how it's good to look at not just cholesterol, but hdl, ldl, maybe even oxidized ldl, same kind of thing. Our body reacts to foods in multiple ways. So looking at allergies, sensitivities, and amplifiers, so that can all be helpful. But we look at 88 foods. Well, in what you want for every single food is a positive and a negative control, meaning that you. So that you know that if you put something in there at a known concentration, at a very high concentration when you run that, it should come out at a high concentration if you. If you run it, and then also at a low to make sure that your reference range is working like it should. Well, there are many labs out there that will only run positive and negative controls on 6 of their foods or 13 of their foods. Because if you're already doing 88 foods, like we are now, a positive and a negative control, now that becomes 88 times three, and then we're doing four immune reactions. So 88 times three times four, so that you can see how that really adds to the workload, adds to the cost. But we do a positive and a negative control for every single food. Another kind of example of that is the way that these are done are on something called 96 well plates. So if you ever see a test that's running 96 foods, it means they're using every single well for a food, there's no controls on that plate. So it's another kind of thing to ask about. Ask in your lab, are you using positive and negative controls for everything? Are you. Will you honor split specimens? Meaning if you send in two and you blind one to me, you put a fake name on it, then you call me back up and you say, hey, I was seeing if those two specimens would look the same when I sent them in, and then we'll refund the money on the second one. So asking labs if they have practices like that or Asking them for their data, for what it looks like when they run split specimens, the same specimen, but split and run twice, because they should be keeping records of that thing or that kind of thing and doing it, you know, kind of at least every quarter. Are they monitoring batch to batch just like a supplement every time you get a new ingredient in? Are you looking at it to make sure it doesn't have things that shouldn't be there? Well, these plates, you have to coat them. Are you looking at each batch to make sure they're all consistent? So those are some things that can be done. You're a good step in the right direction when somebody is CLIA and COLA certified, because those organizations do come in every year and check all of your temperature logs and calibrations and look at your curves and your data and your methodology. So at least it's not a total buyer beware kind of market. There is some good, good heavy regulations with what's going on. And then those would be some additional steps you could look at.

So what if, you know, like, are there, are there different technologies that present more of a challenge for reproducibility where you might see split testing that doesn't work out with the same results? And, and if so, which are the technologies that tend to perform better on, on split testing and, and repeatable. Repeatability, Reproducibility?

Yeah. Well, so some published data speaks to this. And so there is a discuss that I was just looking at from the Journal of Immunology. And they talk about how the standard and this pertains to allergies. They talk about how the standard method that's used, it's called immunocap and that's used by the larger labs out there. And they talk about how it's just not very sensitive. And so they say, look at the epidemiologic data. And they go, wow, rates of allergies have skyrocketed. We know that from who presents. In practice, somebody comes in with swollen lips or hives. So we know that allergies have gone up. That data is very clear. But we're not seeing the same rates of increase on the standard testing that's out there. So they know that it's not as sensitive to pick these things up. And then along those lines, then comes a next layer of battle, which. Well, it just, it just is. It's that insurance companies, their motivation is to not pay for things because they make more money that way. So, for example, we know that, that only 50% of the time, if you react to a food Is it going to be an allergy, an IGE reaction? That means half of the time it's something else. That's why we look at four different reactions. And so generally sensitivities and these complement reactions that I mentioned. But yet insurance is still saying, oh well, we're not going to pay for that. So when labs are only working in an insurance space, which I, you know, I get it, gosh, if, if it would cover the things we would want and if our patients could use it, that'd be more than fabulous. But what tends to happen is they are very slow adopters. And so working with labs that do kind of both cash and insurance can be beneficial because they're probably utilizing services that are not just strictly insurance based services. Limits.

Yeah. Let me talk or ask questions about the food sensitivity panel because it's, you know, it's, it's a, it's an ever present potential issue with every case that walks into a funk med clinic. Are you the only lab that measures the complement as well? And I understand the, the issue with complement is it acts as a magnifier of other antibody based mechanisms. Right. It doesn't, doesn't do much just by itself other than to amplify. So for example, if someone has an IGG reaction to something, one person has this. Two people have the same IGG reaction to a given food, but one has complement involved and the other one doesn't, the one with complement is probably going to have more of a clinical issue. At least that's my understanding.

Yeah, perfect. Spot on.

So, so are, are you guys the only lab that looks at complementary as part. Because I find it very interesting that what you've done is you've, you've taken 88 foods, you run your controls, you're looking at Ige, Igg, Igg 4 and then complement as, as a, as a broader perspective. Because a lot of people, I mean you might do IGG by, or IGE by itself or IGG by itself. And half the time you're going to miss stuff. As you were saying, 50, 50. Right. So it seems to me that from a practical, trying as a clinician trying to use diagnostics to get practical and applicable information, something that I can take action on, it makes sense to limit the foods to the things that most people are consuming and take a broader look at the types of immune reactions rather than running a silo of one antibody, but doing 120, 200, 500 foods. Right. So, so give me your opinion and your perspective on that and what insight did you have that made you design your testing that way rather than the way everyone else is doing it.

Yeah. So first of all, I think food is our most important intervention. And when people come back, patients come back and say, oh, I can't swallow that, or I don't like the taste or I can't take that, then, then my response is, you know, then okay, but you've got to be even better with the diet part. And I just don't know somebody who has achieved their optimal wellness unless they're really working on the food part. That is just one of the most important things that we can do in terms of how we treat. So then the next thing is, okay, what foods? And that's going to be everybody's question. And I, I, I'm, even though I have a lab and, and I would be, I still would say that there's a lot of work that can be done without testing. Someone comes in and their diet is Diet Coke and Big Mac and that kind of thing. Yeah, I mean there's a lot of things that we can do first. We can get some vegetables in there and make those changes and then also get the macros in place and just get the junk out. Like if you're not doing that yet, then you know, let's just back up. But let's say people are at that next stage. They've been eating more cleanly. They even tried a gluten free diet and a dairy free diet and they got some improvement and they felt they were in the right direction, but they weren't able to get all the way there. Well, by being able to measure somebody's blood and look at how they react to foods really allows you to, to design the least inflammatory diet possible. And I always talk about inflammation as just being like this fire that can just slowly cook our genes and cause them to express pathology and symptoms.

So I love that, I love that mental picture. Yeah, I'm sorry to interrupt. I love that mental picture. Cooking your genes.

Yeah, yeah, yeah. So if we can remove that fire, then we can call, we can put the genie back in the bottle. We can help to reverse symptoms and pathology. And that's what we want to do. We want to limit inflammation. And, and again, if, if you are eating a lot of processed food and a lot of sugar and a lot of junk, that's first step to eliminating inflammation. And then we get more picky from there. And so testing can help take it to that next level. When people are trying and they're moving in the direction, but they're just not quite there yet. Also, I would say I will sometimes test even initially if somebody has a more debilitating chronic condition. Because my thought process is, yeah, we could do an elimination diet, or we could, you know, move them in a more of a paleo direction. But I want to calm this inflammation down as quickly as possible and go from there. So. So we just also figured out a new technology to do this by finger stick and not blood draw. So I'm very excited about that because it makes it more accessible. But the interesting thing is, like I said, we're running all those reactions. So how do you do that? When you visualize a finger stick, you think about your finger being stuck, and then you think about probably a card. Well, what we designed is something from a PhD who's watching his diabetic dad stick himself over and over. I'm like, oh, that looks terrible. Fumbling around with that. He can't get enough specimen. And so he's like, first of all, it has to be as small a prick as possible, so there's no pain. So, okay, that part. But now if you do that, how do you get enough specimen? So it's designed like a sponge on the end of a pipette or a turkey baster if you haven't used a pipette. So it pulls up through that sponge. So we're able to get specimen without even going to phlebotomist, which is nice. And then we look at those foods. And so. So now the next thing is, how do you calm down inflammation as much as possible? And getting rid of those inflammatory foods is a way to do just that. But like you were mentioning, our body reacts to foods in multiple ways. So what creates the most inflammatory reaction in the body? And so what had been noted in the research about various infectious disease, and some of the first research that noted this was in terms of polio, what they saw. So these antibodies I've been talking about are a titer. And so what they saw was the highest titer wasn't because of the worst symptoms. So there was something else that was involved in this immune reaction. And so what they found is that when this igg was also there with complement, that they were like this synergistic thing where they bind together and they amplify the reaction. And so we said, okay, is that true of foods? And so we. So we applied that same idea. As a clinician, I'm sure you've seen this hundreds of times. People come back and they. And if you're just doing that igg part they go, yeah, that high one, I don't know sometimes, but it's this medium one that I really get the migraine from or I really feel, you know, worse, more joint pain after eating. And so that's because it's one part of the reaction. So I always say it's like wonder twins activate form of a very inflammatory reaction that IgG.

And Cheryl, you're dating yourself.

I know, I know.

I have a question on that because this, this whole idea of, of complement activation is fascinating and, and I'm wondering if, if there's diagnostic applications for this because I, I quite often see people who have, you know, I, like many other people in our world, deal with a lot of autoimmune cases. Right. And so I see a lot of people with equivocal antibody levels where they may actually have no obvious signs or symptoms associated with a frankly positive result, but the ones that are equivocal or sometimes normal in a known autoimmune case or where they have problems. In fact, there was a lady I worked with several years ago up in Alberta, Canada and she was in the middle of an ulcerative colitis flare up when we ran her labs and her ASCA and ANCA antibodies were perfectly normal, but she was in the middle of a flare up. And so that was a pre existing diagnosis.

Right.

She came to me, we knew that she had that and she had many years in the history. But quite often I do see people with frankly positive antibody levels with known associated symptomatology or other confirmed diagnostics. Now we know that antibodies can be present in the system for, in some cases up to a decade before clinical manifestation and diagnosis. So there's that part. But could that be part of the reason why people have normal or equivocal antibodies and really have a problem in that tissue system because of complement? And does complement behave the same way with human tissue as it does to food protein?

Yeah, absolutely.

If so, will you develop a test?

Yeah, so that's what we look at. We look at C3D, a complement fragment that gets provoked by foods and the igg. And, and you're right that having those two together will amplify a reaction a thousand to ten thousand fold. That's pretty significant. So only looking at the igg can definitely give a confounded result. You're just, just looking at part of the picture. And so what we found is that there's much better correlation with symptom when you're looking at these kind of a lock and a key together, if you will. Rather than just one or the other part. And so, yes, I think it's moved the specificity in terms of being related to a symptom further forward. And we see it all the time. And people that are utilizing the test, they say, oh, I've done a test like I this in the past, but this time when I removed these foods, I finally felt better. And I also like to point out that the reason to do a test like this is not just to remove foods. Really the ultimate goal is to pull back in more healthy foods than you even started with, but without having symptoms from them. And so I'm not necessarily saying that I want you to get back to that Big Mac and that diet code. Those will always be inflammatory. But many times people start to have problems after the gut gets broken down and more leaky bits of food leak in the immune system becomes reactive to them. So then many times people will become, they'll have problems with things like beans or broccoli or spinach. And, you know, and, and that is a very frustrating place to be. You know, of course, gluten might be one that we want to just keep out forever or always minimize, but dairy. But even getting people back to where they can at least, at least tolerate little bits of it from time to time, but as much broccoli as you'd like, pulling those good foods in. And so the idea is limit those things that are creating inflammation, build the body back, restore the gut lining, and then bring back in the healthy foods to really expand the diet and have less symptoms.

Yeah, you, you mentioned leaky gut essentially a couple of times in that conversation. And I'm just wondering, do you guys do any internal correlations when you have clinicians who, for example, order your permeability test and a food sensitivity, how often do you find people with marked food sensitivities that don't have any appreciable permeability, at least that you're detecting less often?

You do, you're going to see a large degree of correlation there. However, what we can often think is that leaky gut, that phenomenon I described, so the wall of the lining breaks down, food begin to leak in, that looks weird and foreign to the immune system, so it starts to make this antibody response. We can get this idea that a leaky gut is the only way that occurs, and that's not accurate. It's a major contributor. But also you could have a gut lining that's, that's largely intact, but there are these immune cells that are in the gut lining part of the Galt or they're called Peyer's patches. And if in that Peyer's patch, there's a miscue as the food comes in with the immune system, you can still develop a response to that. So, absolutely, you can see people where they have food reactions, but without significant leaky gut, and so tells you you're probably not going to have to remove those foods as long. Or maybe it guides you towards certain therapies. Like if. If it's more immune confusion in those Peyer's patches, that I'm likely to use some type of immunoglobulin as a therapy, like from colostrum or eggs or serum. But when I say, like colostrum, immunoglobulins are high in breast milk. And one of the things that we know is that when we breastfeed, the kiddos that get the opportunity to do that, they're less likely to have allergies or less likely to have sensitivities. They're less likely to have autoimmunity, like you mentioned. And so. So if it looks to be more of a miscue of the immune system, then I'm reaching for immunoglobulins. But if I think it's more leaky gut, then I'm reaching for more glutamine to build the wall back. And so it can guide us in different treatment directions as well.

Yeah. My understanding is that, you know, aside from the permeability issues and the miscuing that you're talking about with the Peyer's patches, there are, you know, dendritic sampling cells that live in that mucosal surface that have one hand up into the lumen of the gut and the other ones, you know, in the bloodstream, for lack of a better way of saying it, advising the peripheral immune system. But what's happening in the gut, gut, and I know that dioxin, particularly, I suspect other things can hijack cellular transport mechanisms like the aryl hydrocarbon receptor. And so things can pass an intact gut. And I think that that's one thing that's very confusing with clinicians, like, how. Why does this person have sensitivities? Because they don't have a leaky gut with whatever test it is that they ran. What do you like about your leaky gut testing? Because you have some things in it that some other labs that do leaky gut testing don't look at. So what. What was your. What was your clinical mind telling you you should be looking at as you were looking at the research and Then trying to design a test that looks at permeability. What were your considerations?

Yeah, so we just mentioned that scenario where it's not leaky gut that causes the food reactions, but then certainly the flip could be the case as well, that the gut is leaky and that creates the food reactions. And sometimes, you know, you say, say, I'm not even going to look at food sensitivities right now, because I think you'll have so many just because your gut's more broken down. Let's work on building the gut lining first. And so that test looks at direct markers of leaky gut. And so when I was building that profile, this was when some of Alessio Fasano's work was first coming forward. And he was at Boston then, he's at Harvard now. But his research that looked at this biomarker, Zonulin, and again, and this was before other labs had it. So Zonulin tells the gut to open, it tells tight junctions to open. And his research was fascinating because what he saw was that Zonulin went up before you got an autoimmune disease. And he went on to talk about that. The whole trigger that turned on those genes, like, you're not born with rheumatoid arthritis, you're not born with lupus, There was some environmental trigger trigger. And he isolated that. The fact that the environmental trigger and many times is the gut becoming leaky because it creates all this free radicals, this oxidative burst that spurs the, the autoimmune process forward. So if we could see Zonulin going up and arrest it, we could prevent autoimmunity. But if somebody comes to us with an autoimmune condition and we see an elevation in Zonulin, we can do things to lower that level, shutting down those tight junctions protecting the immune system from everything in the world, trying to activate it and overactivate it, as in the. In the case of autoimmunity. And so, so this idea that we could actually measure this phenomenon of leaky gut, because I'm sure you and I have been talking about leaky gut for a long time, long before you could look at a biomarker that that validated the fact that it was there. And so we would have this, this, this I'm sure happened to you a billion times, too, where you work with your patient, you tell them they have leaky gut that you read, they do the things, and then their depression goes away and their joint pain goes away, and they go back to some other doc, maybe their psychiatrist, and they say, oh, I don't have depression anymore. I took gluten out of my diet and I worked on my leaky gut. And that person goes, there's no evidence of that. So here is a time again where we could measure Zonulin. Zonulin told tight junctions to open. It's a mark that validates the presence of leaky gut. And you can treat it and it can get better. It's not just academic.

And so that's, I have to ask your opinion on this because I, you know, like back when like there was talk about Zonulin being a marker that we could measure, there was a paper published in the World Journal of Gastroenterology that talked about how Zonulin varies throughout the day. So, and I, I haven't pursued that further to see like, is there, there, is there an established circadian rhythm? Does Zonulin rise as a result of other factors or variables that we can control? And if it's true, and I really want your opinion on this, if it's true that zolinin varies throughout the day, what's the clinical utility of basically a spot check, right, you do a blood draw and you measure Zonulin at that moment. And sure, maybe it's high then, but maybe it's not throughout the rest of the day. I mean, help me sort that out from your understanding of Zonulin's characteristics.

Yeah, so we checked it, we took a number of people and we drew their Zonulin at multiple points during the day and we looked to see how much difference there was and we did not see a significant amount of difference. But you always want to see more than one study. So when we go to the data, when we go to pubmed where all the peer reviewed data is, is we see many studies that show a correlation between Zonulin and autoimmunity and Zonulin and diabetes and Zonulin and even brain fog. So because of making the blood brain barrier leaky just like the gut. And so when you look at the methodology, they are using a serum level of Zonulin and finding clinical correlation with that. So the first is we check to see if there's variability. And then the second, there's a whole body of research that's predicated upon on looking at serum levels of Zonulin and, and when they are higher being associated with certain conditions. So now we do have people do our test fasting and that might not even be necessary. But to your point, we thought, well, you know, what if somebody did eat a whole bunch of Wheat right before their test, which triggers onulin. So we thought at least if they're fasting, that would control some of those dietary influences and minimize any fluctuations. Minimal fluctuations that could be there.

Yeah. Do we know of any other dietary triggers other than gluten? Gliadin.

That's the big one. So. But then of course, bacteria can, can do it. There is some emerging data looking at mold, aflatoxins that can be found in food that, that might be possible as well, and maybe even yeast too.

Is it the bacteria or is it the lipopolysaccharides that they might or might not be making?

That's probably more accurate answer. So the lipopolysaccharides that are shed from the bacteria can be more of the specific trigger.

Yeah.

Which we look at as well. On that same test, we look at how the immune system is reacting to those. And so when I first found that zonulin, it was, you know, so exciting. Here's the thing that governs the leaky gut. And if it's high, you have leaky gut, and if it's not, you don't. Well, you know, you see a patient that, that's not matching up like you would expect, and then you're like, oh, there must be something else going on. So, you know, we began to kind of think about that. And, and also, of course, your gut could just be leaky because of atrophy. NSAIDs, they atrophy the gut lining so much you ulcerate. That's a very leaky gut, but it's not zonulin mediated. So we added on diamine oxidase that looks at how thick the gut lining is. But then we also added on that lps, those lipopolysaccharides, because they can damage tight junctions. And it's another way the gut gets leaky. And I love having them on there because the LPS also binds to T regulatory cells and T regulatory or T reg cells. That name tells you what they do. They regulate the immune system. So in autoimmunity, a hallmark of autoimmune community is Treg cells are down regulated, they're dysfunctional, they're not working like they should. Well, lipopolysaccharides are one of the things that decrease their activity. So this becomes a really nice autoimmune kind of profile. We know zonulin can spur autoimmune conditions. We know LPS can downregulate that immune cell that keeps the immune system more in balance, in check. And then diamine Oxidase that degrades histamine and histamine can also push us in more of an autoimmune direction.

So you said diet, if I heard you correctly, you said diamine oxidase, which tells you about the thickness of the mucosal membrane. Like how, how does that work? How is that a correlate or an indicator?

So we make it in the fingertips of the microvilli and the microvilli are the, are the, the little, well, fingertips of the gut lining that absorb what comes into our system. And so as they get warm, worn down, we make less and less of this diamine oxidase. So for example, when you biopsy a gut lining, someone that has less diamine oxidase there has less gut lining in general. So we've come to recognize it as a marker of mucosal maturity. But the other fascinating thing about it is it's the enzyme that degrades histamine. And so when the gut lining becomes thinner and weaker, you make less of that enzyme. And so now you start reacting to kind of things just non specifically. And it's really confusing because you're going, oh my gosh, I don't know. I ate my food test says I have, I'm fine with tomatoes, but I reacted to it. Well, a tomato, even though it's a healthy food, is a food with higher histamine. Or you're sitting there going, I'm having a terrible day, what's going on? But this is the same food I had yesterday and I had no problem. Well, as a food ripens and degrades, it produces more histamine. So if you have low levels of this diamine oxidase, it tells us that your gut lining is thin and weak and atrophied. But it also tells us you can't break down histamine. You're going to just start reacting non specifically to foods that are good for you, like avocado, tomato, strawberry, that have higher levels of this. And for sure, if you drink a glass of red wine, that's giving you a headache because that's a very high histamine food.

Yeah. How often do you see people with mast cell activation, like peripheral mast cell issues and high histamine that don't have a deficiency of diamine oxidase, that can.

Happen because there are different mechanisms the, the trypsin that should be involved in terms of calming that mast cell down. That can be another reason that there's over activation of histamine. But if you have somebody who like you pull them off red wine and they don't get headaches anymore or you give them a list of high histamine foods and they do do better with that, then probably one of their issues is low diamine oxidase. And even when it's not as obvious, because, you know, histamine, we have histamine receptors in the brain. So the, we even look at histamine to decide about things like schizophrenia. But Maybe more commonly, 86% of people that have a.83% of people that have migraines have lower levels of diamine oxidate. And so it's fascinating because here's something that you could take as a supplement. It's not even bad for you, it doesn't even make you drowsy like Benadryl does. And it's very effective in terms of eradicating what can be a very, very painful quality of life consuming situation. And it's, you know, high percent, 83%.

Yeah.

And we're the only lab that measures diamine oxidase. It's done routinely in urine up.

Yeah.

But here, for some reason, yeah, it.

Seems to be, it's only like the last few years that diamine oxidase or I'm sorry, that like mass activation syndrome and histamine sensitivity has really kind of come to the, you know, the conscious mind of most practitioners. Kind of like, you know, like SIBO 12ish years ago. You know, most docs may have heard of it, but they didn't know what it was and they certainly weren't looking for it in clinical practice. And I think we tend to go through cycles every few years there's like the new kid on the block and we get all this research and then we start getting diagnostics and it's in. And there's a lag time in that process to where you get enough practitioners doing it. That makes it worthwhile for labs which are business entities to continue to offer it. Because I know sometimes there are labs that will, you know, think a test is a good idea, but nobody buys into it. And so the test goes away because nobody's going to make a product or service that they can't sell. And that's kind of a shame because I do think that there are labs offering things that are particularly insightful. But if their insight is far ahead of what the collective insight of the community of functional medicine practitioners is, you know, that's a little bit of a mismatch. Right. And so I like, I like having relationships with and talking to people like you who in many ways Are, are ahead of where the bulk of functional medicine practitioners are because you're so entrenched in the research and you've married that with your own clinical experience. Like, what am I seeing? What am I not able to figure out? And what does the research say? How do I design a test for that? Which I think is very cool to be in that position to be able to have the tools at your disposal to say, hey, I want this test. Does anybody else want this test? And then, you know, kind of goes and happens. So let me ask you this. And I know before we started recording, we said we're going to be an hour. We're like right at that. Yeah, the time has just flown by, at least for me. What is it? What is it you want? Precision Point. And for anyone who's listening, who doesn't know, they started, you started out as Dunwoody and then you rebranded a year ago, somewhere around there, two years ago, as Precision Point Diagnostics. What do you want your lab to be known for?

What we are working to do and the space that we want to fill is when there's a clinical need for that isn't being met. And so I often think in terms of, okay, yes, there's the diagnosis. So measure cholesterol. If it's high, that's hypercholesterolemia. That's the diagnosis. But the other part that exists less is, but what's the process? What's that thing that's, that's flaring that diagnosis? Why is the cholesterol high? And as you and I know, that could be because of diet and exercise, but that could also be because you absorb more. But that could be because genes in your liver make more. It could also be because of, we do it in response to various infections. And so there's all, there's many reasons. And so why is the cholesterol high? And so tests that help us to understand the process behind things. And so when I think about, okay, what is that process? I tend to think, well, inflammation's a big one and inflammation is largely gut based. So let's think about foods that could be causing inflammation, let's think about bugs that could be causing inflammation. And let's think about the state of the gut lining that could be causing inflammation. Okay, how about toxicity? And so we have testing in that arena. So are you inflamed? Are you toxic? How about mental emotional stress? And there's no singular test to really get to the heart of that, but we do do adrenal stress testing, which gives at least A piece of the puzzle of how resilient to stress are you? Then are we seeing a lot of oxidative stress, which is again, just a fancy way of saying free radicals. And so design profiles that look at at percent reduced glutathione and markers of oxidative stress. And then finally, are you nutritionally optimal? And that we're just on the precipice of. So next year in the first quarter, we'll be out with a wellness profile that's going to look at nutritional markers and some of the standard markers, CBC and chem screen, but also done through that finger stick technology.

Maybe as you're getting close to that, you can come back on and, and, and talk about it. I do. I have a question about the glutathione, because before we started recording again, I had mentioned that you and I had exchanged a few emails back, I think in the early couple years of Dunwoody, because you had initially started, somewhere along the way you had offered a glutathione test and then you stopped. And so I emailed you like, hey, where'd it go? And I, if I remember correctly, your answer to me was you, you guys weren't satisfied with your reproducibility and so you stopped doing it until you could improve it. So now you're doing glutathione testing again. So what changed in that realm? Was it, was it an issue that you just didn't have the technology or techniques available to measure something with an incredibly short half life that was maybe unstable and difficult to measure? Like, what was the issue and how did you conquer that? And should practitioners like me routinely be looking at, at glutathione, whether it's total percent reduced, et cetera?

Yeah. So the issue is that we want to know, is that we want to look at both reduce and oxidized glutathione, because the reduced is the active form, the one that hasn't been used up yet. So what we know is, for example, in autoimmunity is you could have a normal glutathione, but most of it's oxidized, not in the form that you can utilize. And so we're not really getting the clinical information that we want. So knowing both parts is useful. And again, you treat it differently. If you want to just raise a level, you, you might give glutathione or N acetylcysteine, the major building block. If you want to recycle it, get it back to the reduced form, then you're using things like ala and selenium and organic diets. And so. So it leads us in different directions in terms of treatment as well. Well as when you take it out of the body, just more of that oxidation can happen in the time it gets from the person to us. And so then. And it's not showing what was happening in live action, it's an artifact of maybe did it sit in the mail 24 hours or 72 hours and what did that difference look like? And so while originally validated the methodology, what we were seeing was when there was a certain time of year that we saw that it wasn't. We weren't seeing those same reproducibilities because we do split specimens. And so. So we weren't seeing those same reproducibility. So it's, you know, like that's it not running it if it, if the data doesn't look good. Well, what we found was a couple things, is leaving it in the white blood cell. So that preserves it and it is overnight male. But in addition to that, then when that gets to us, then we lyse it open and we immediately add the scavenger and put it in the freezer at minus 80 to make it very stable. So we had to find a new scavenger, a new way of preserving that. But. But when we did that, then again, seeing the reproducibility that we'd like to see.

Right. And I would assume that you're seeing high correlation between either a low total glutathione or a high oxidized to reduced ratio in autoimmune clientele as well as people with say, chronic infection, Lyme disease or whatever.

Yeah, yeah, yeah, absolutely. So one of the things that we know about like, well, long haul Covid, for example, is that it appears that some of this cytokine. These cytokines just continue to be upregulated. And one of the major things they do is they can deplete glutathione and that allows them to keep talking to themselves. So. Absolutely. That picture of chronic disease and glutathione has become more and more clear, especially over the past couple years.

Yeah. What are you. What have. What's been the most difficult challenge that you've had to overcome in this whole process of getting involved in the diagnostic side of functional medicine.

I guess, you know, there's a daily, daily things certainly come up when you are not using. So what. Most of the regular. What the regulatory boards are used to seeing are a lot of automated machines. So if you're getting something done like Looking at your red blood cells or white blood cells, they squirt that specimen into a machine and it prints out results. What we do in our lab is a lot of things. Well, by hand, they're actual human beings on the bench that are looking at things that are running these assays because they're not so mass produced that there are these large machines out there that do them. And many people will think, well, that sounds like a drawback, because a machine and a computer and whatnot, certainly that would be more reproducible. But that's absolutely not always the case. I liken it to a chef, for example. None of us would say, I'd rather have a meal cooked by a robot. We would want to have someone who could see it and who could smell it and who could look at it. And so, for example, some of these robotic arms that go into wells, they're so, you know, strong that they'll disrupt some of the things that are in there and create more of a reaction than should be. And so that nice kind of trained human touch can often be even more reproducible and get a better clinical result. But regulatory boards aren't used to seeing as many things done this way. Now, if you worked in academia, that would be the way things are predominantly done, because, again, you're looking for new discovery, etc. So that's probably the biggest ongoing challenge, is to make sure that they understand what we're doing well and that we're communicating well with them because it's not as automated.

Yeah, you know, that's good insight for me as a clinician to know that there are some circumstances where, where, you know, a lab tech, a microbiologist looking through a microscope, for example, is actually going to outperform a robot. As you say, what. What are you most proud of in the diagnosis?

Quickly. And add on to that, as I would say, in a similar way, whereas, you know, I'm always going to.

Think.

That your diagnosis of your patient is more meaningful than any lab test and any piece of paper. Because you spent that 45 minutes, you spent that hour, you are understanding these interconnections even more. And so then I think this is the next step back. One of the things that I think that I am most proud of is really publishing and looking to see that what we're doing is matching these clinical conditions and bringing new technology to the area as well. So, like I said, like you, you said, actually, we are the only food test that looks at those four different reactions. There are some other people that do complement but they do it all in one, well together. And so if you do that, then you don't know, are they having a reaction to igg and complement. And that's the true magic that's most inflammatory. So, so, so really taking something that was kind of always done a singular way and thinking about how do we put it together better for the clinician? And so the, the drive and precision point has always been to say, but what does the clinician need to have a better outcome with the patient? Where is the piece missing that will allow us to help them move to the next level? And so being able to develop in this, that space. Yeah, yeah. Does make me proud.

Yeah, good for you. So you said that next year you're coming out with some, like, basic chemistry stuff. What else is on the docket for 2023?

So this finger stick technology, we, we should be able to apply to all of our testing. And so I think that that is going to be hugely supportive for our patients and our community as well. So one of the things that's happening with the larger lab groups out there is they are, no, they're deciding that they're no longer going to offer clinician prices to anybody doing telemedicine or unless you see four to six patients a day that need blood work drawn and a brick and mortar. Well, so if you are a clinician like we are, and you spend an hour with a patient versus seven minutes with a patient, of course we are not going to have that volume that's going to allow for lower pricing that we often pass on to, to our patients. And, and when it's just, if you, if, if you've ever had a patient and you sent them straight to a lab or they're just said, oh, I'm going to use my, I'm just going to do it on my own without a script from you. What we know is that lab charges, you know, four and five times what would be some of that pricing otherwise? So, so this finger stick technology I'm very happy for, because if that's going to be the case, it looks like they're making phlebotomy and blood draws even harder and harder, especially for those of us who want to spend more time with patients. And so even though it's not a test in particular, I think making these things more accessible to people, doing our style of medicine is important.

Do you think there's room for, for you or anybody else to look at testing for biofilm and stool samples?

Oh, wow. Yeah, that's an amazing area. And that would be a home run.

That's number one on my wish list.

Yeah, but because it's so clinically relevant. I mean, if you just. In a dish. If they look at that. If I have a bug and a bug with a biofilm, I have to use somewhere between a hundred and I've even heard some studies, seen some studies, a thousand times the amount of antibiotics to kill that.

I've seen the thousand. I've seen the thousand number. Yes.

Yeah. A thousand times the antibiotic. And so we know that resistance is a much bigger deal. And so I'm very mindful of anytime I give an antimicrobial, an antibiotic, whether it's natural or otherwise. Usually natural because there's just less resistance to those at this point, for one. But then I'm always combining it with something for biofilm because I think otherwise you're just missing, missing the mark. A hundred that to a thousand times the amount.

Yeah. I'll tell you that when, when I first started teaching about biofilm in functional medicine seminars, I don't even know what year it was. If I asked like who, who's heard of biofilm? Nobody put up their hands. Now if two thirds of a. Of a group doesn't raise their hand, that would be unusual. Almost everyone's. They might not know what it is, is in detail or, or what how to deal with it clinically. But it's very rare for me now to ask that question to, to get less than half the group unless it's just a whole bunch of new people. Which, which kind of brings me to some, some closing questions. And, and listen, I really hope that you come on again. I, Yeah. I could sit and talk clinical stuff with you all day long.

Yeah.

All right.

Absolutely.

So let's play a little game. I'm coming to you for advice. Let's say I'm a brand new practitioner of any credential dcmd. ND do, doesn't matter. I'm just graduating. I'm coming into practice. I want to get into functional medicine. What advice do you have for me in the diagnostic part of clinical practice?

First listen to the patient and let that guide you. So I don't think that every patient needs every single test. You know, there are practices out there that will run a group of tests or something more routinely and, and that has value. But to begin to think what's the process that I think is behind this condition? And again, do I think they're nutritionally deficient? Do I think it's inflammation? Do I think it's Oxidative stress, Do I think it's mental emotional stress or do I think it's. Did I say toxic body burden? Anyway, so, and then when you kind of think of that pie now think where do they, for where do they most lie? And so if I think it's more inflammation, then that's generally gut based inflammation. So starting there, they're going to have some piece of all of that. They're going to be toxic, they're going to have inflammation, but which part of that pie applies more? And start there and do some tests in that area and then see how they respond. And then because you can't do every single test at once, you also can't give a patient every single treatment at once. So it says, so doing it all, if they're rapidly progressing, then maybe we do more in that direction. But otherwise breaking it down and realizing and explaining to them that it's, you're not going to have just like a gym, you're not going to have beautiful biceps by going one time, time. And that's how this practice is going to be. And we're going to work through these layers and these pieces of the pie and we're going to work on that gut based health and then we'll work on some detox or whatever applies to them most and keep rolling through those things. But when somebody's getting started in this area, it can be so overwhelming because the idea is that we're supposed to individualize to every single person out there. So now you don't know one thyroid treatment, you're supposed to know that's a unique thyroid treatment for everybody, everybody who walks in the door. But if we can begin to say, are you nutritionally deficient, is there toxic body burden, is it more mental emotional stress and slot them there and move in that direction, then we can begin to weave things together in a way that is manageable for us, but the patient as well.

Yeah, And I love that concept. I would call that finding the dominant driver. Right. Because you're right. I mean, especially in today's world where there's so many people with complex chronic pictures, they're going to have a little bit of everything. Right. So are you going to test everything or are you going to try to sort that out in some kind of a hierarchy? All right, so second, second question. Let's say that I am a practitioner, I have some years of experience, but nothing or not a lot with functional medicine. How do I shift my mindset from doing diagnostics one way, let's say I'm a medical doctor in the conventional side, I'm used to running labs, certain labs, looking at them a certain way. How would you help me shift my mindset so that I could understand what's available to me on the functional medicine diagnostic side? And how do I start thinking about diagnostics in a different way? That's going to help me as a clinician, help people with real health issues.

Yeah. And our patients, too, because they're very used to. A lab test is for diagnosis, and a diagnosis is. Is an ICD 10 code. It's. It's a label. It's something you look up. It's. I have irritable bowel disease. I have Crohn's, I have colitis, I have depression. So. So, so there. In certain of areas, there are tests that are diagnostically specific for that. But in the functional world, we are running tests not for merely a diagnosis. We still do that. We. I still want to know if you have hypercholesterolemia, but now we're also going to run some testing that help us to understand the process behind that. And those fall into the same categories I keep mentioning. Is your process that you're nutritionally deficient? Is it that you're inflamed? Is it that there's mental, emotional stress, toxic body burden, oxidative stress, and so now you're trying to figure out what that process is as well as the diagnosis, so that you know what to work on to help the diagnosis go into remission?

Yeah, yeah. In some ways, I think of that as a reflection of, you know, whether you're a conventional physician or some form of a functional medicine physician. Because we're not all the same, Right. We think differently, we do differently. But, you know, in general, I. I tend to look at allopathic medicine as being focused on disease management, like, you know, when. When someone comes into the healthcare community. Because healthcare to me is a continuum, right. And you might have polar opposites, but, you know, you've got a million stops in between those two ends. But when you have someone who's unwell, you can look at that problem and say, okay, I have an unwellness that I need to manage. And that to me would be more of the allopathic approach. Whereas someone like you and I and other practitioners like us would look at that and say, okay, how did you get unwell? And how do we reverse that? Like, how did you lose your wellness? How do we restore that? Those are just different ways of trying to solve the same problem. And I think diagnostics, especially the Type of diagnostics that you guys have put together is very, very helpful. All right, final scenario. I'm doing functional medicine, but I'm struggling to make it work. How would you help me? What would you tell me?

Yeah, well, I think first is make sure that you are, are shifting the patient's mindset. So when I first got started, I would have a tendency to be maybe overly optimistic. Not that I don't think that we're passing on hope because that is a big part of what we do. But saying someone, oh no, you know, you'll be better in a month or two. Now while I do think our medicine helps people feel better in a couple weeks or four weeks or a couple months, to really do the foundational work that's going to get them there.

Yeah.

Is going to be a process. And it's not one 7 minute visit once a year. And so I think setting the patient up for that, realistically that, you know what, we're going to meet at least four or five times in the next year. And so, and even, and even if you don't want to do a program or you don't want to charge, schedule them, put them on, have them pull out their, whatever their calendar and put those five appointments in there. Now this at first used to kind of offend my sensibilities because I thought, thought, well, how do I know? They might need to come back in 2 weeks, they might need to come back in 6 weeks, they might need to come BACK in 12 weeks. And guess what? I can always change that interval.

That's right.

And the patient can always change that interval. Just because you put it on your calendar does not mean that it's locked in place, but it does mean you don't schedule Bobby's soccer at that time. It does mean that you decide, oh yeah, I'll do my dental appointment at a different time. And so, so you, you start to realize that this is going to be a part of your life that creates accountability. And they also know, oh, I can't expect just to show up one time and get better. They, they understand that it is going to be a process. So just having them commit and even if they're there, even if the level of commitment is just putting it on the planner, I think that that gives the understanding that I don't get to come in once and everything's going to, to get, get better. Also my other part of me initially was like, well, what if, what if they are better after two visits? And that was really all they needed. And now I've got these other three visits on their calendar. Do you think in two visits that we have communicated everything about diet and lifestyle that needs to be said? Do you think we've communicated what you're going to do if you go into, into a flare to make you, to pull yourself out before you even get sick again? So there's preventative medicine and there's all this lifestyle part and fabulous. You feel great in two visits. Now let's talk about all the things that you need to do to keep yourself here.

That's right. How do we keep you that way? Yeah, and that just makes me think of a whole bunch of different things. Like one of them is how important it is for clinicians to be mentally flexible in one sense. That's like in the beginning when you're working up a new case. I try to advise people who seek my input. I don't jump to conclusions. Delay your decision making until you get as much data in as possible because you need to see as much of the big picture as you can. For me, diagnostics plays a big role. Of course we're going to do a good history and base a lot of our impressions on that. And like you, I use my history to drive my diagnostic choices. Right. Because I, I want to know, all right, here are the, the main drivers. Can I just assume that that's the problem and start working on it, or do I need some validation with some diagnostics? But you know, when I, and I tend to work on a programmed basis, I, I like to engage with people for a period of time, X number of visits, and, you know, space them out on some theoretical framework. But it doesn't mean we're locked into that. And I tell people, listen, this is a loose framework, it's flexible. I think we're going to be doing this. I like to try to like, map things out two, maybe three steps down the road. But when I get from step one to step two, I may do something completely different because I have to. Because I have to. And so I know that there's, you know, a lot of groups out there that, that are, you know, doing coaching and practice management and teaching a very programmatic way and they're going to help a lot of people. But I think more and more as time goes on, as people get sicker and sicker because we've messed up our food supply and our environment and that changes our phenotypic expression and all of the fancy buzzwords that we can say. Ultimately, at the end of the day, we have more complex and chronic disease that requires a different way of thinking and doing than maybe we needed 20 years ago. Things have changed and just kind of bring this to a close. Close. Doc, you know what I've. What I've heard from you in this conversation, number one, is a ton of passion. You love what you do. You love being a clinician, you love being involved in a diagnostics. That is absolutely clear. But you've said a couple of things throughout the conversation that really tells me that, that you and your group, you have a lot of integrity. You're serving yourself as well as your community. And you, you've. You've set up a business that serves others the way you want to be served. That's what I take away from this. And so I, I truly appreciate the time that you've given me today. And I, I've a wonderful conversation. I, I feel actually quite energized and enthusiastic right now because of the conversation we have, and I really hope that you do come back and we can have another acc.

Yeah, I would love to. It's been great. Yeah, absolutely. I feel very energized as well. And, yeah, I sit toe to toe with patients and look at these same results. So they better be right.

Yeah, that's right. All right, we'll close there. Well, thank you, Dr. Cheryl Burdett, precision Point Diagnostics, plus all the other things that you do that we didn't get to talk about. What I'll do is I'll include links to your lab and anything else that you want me to put in the episode description, just shoot to me an email and I'd be happy to put that there so we can promote the work that you're doing. Thank you for coming on.

Thank you very much for having me.

You're welcome.