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Hormones Causing Brain Fog and Fatigue? – Video Case Review – CI TV #2

Welcome to the episode #2 of CI TV!  In this episode, Dr. Clark walks you through his clinical thinking process of a 26-year-old male who is dealing with brain fog and fatigue. Hormones are the focus on this particular case review.  Would you have come to the same conclusion?  Watch below to find out!

(Scroll down to see video transcription.)

Dr. Clark is leading a 3-day program titled Mastery of Neurochemistry of Male & Female Hormones on Dec 7-9, 2018 in Cape Canaveral, FL and via internet live-stream. Click the image below to learn more!  

Hormones Causing Brain Fog and Fatigue? – Video Case Review Transcription

– Hello, and welcome to this episode of CITV. Today we’re joined by Dr. David Clark, and we’re gonna be doing a video case review. Dr. Clark, how you doing today? – Excellent. – Awesome, so what do we have going on? What’s the scoop? – Well, we’re gonna be using a case here today to demonstrate how you can use clinical neurochemistry to treat some of your patients, male patients in this case, that have hormone-related problems. So in this case we’re gonna talk about today is a 26-year-old male that I’ve just been treating recently who presented with brain fog and fatigue. All right, so here we go. Again, his chief complaint’s brain fog. Well, here’s what I like to do whenever I start looking at a case and when I’m trying to break a case down for you guys. I think brain fog, and I think, well, what does that mean? Is that telling me anything specifically about a region of the brain that might be involved or a metabolic part, a metabolic process that might be involved? I’ll just go ahead and tell you guys, that’s not specific. Brain fog, unfortunately, could be 100 different things. It could be a dysautonomia, it could be your frontal lobe. We’re talking about neurological stuff, components. It could be, I mean, you name a metabolic problem, it could manifest– – Anemia. – Yeah, it could be anemia, could be thyroid, could be neuroinflammation. Brain fog is just really nonspecific. There’s a reason why I’m making a point about it not being specific. He also has fatigue. Well, all right, fatigue. Well, if it was brain-based fatigue, primarily that’s gonna be a dysautonomia of some kind where he’s having hypoperfusion of the brain, or just for some reason, the frontal lobes primarily are not firing at the appropriate frequency, and he’s perceiving fatigue. But metabolically, again, it’s a whole laundry list of things. It could be anemia, it could be thyroid, it could be a nutrient deficiency, it could be blood sugar. Fatigue is not specific for us. Now the reason I make a point about this is when we start thinking, okay, when we’re gonna work this guy up, what are we gonna test him for? Do I need to test him for mercury toxicity? I suppose you could make a case for that because his symptoms are so nonspecific, but as I’ll explain, I don’t think we need to do that. Now he also complains of some dark circles under his eyes and that could be lack of sleep, that could just be his coloring, that could also be what we call allergic shiners. When you have immune system activation, you get these sort of global inflammatory responses, something that’ll show up. You’ll get dilatation, basically, in some of this vasculature under your eyes, and you get these dark circles. Well, that’s it, that’s his chief complaints. That’s all he’s got. When you’re a clinician and you’re coming into a case, you need to start thinking about these symptoms, do they point me in some direction that I can then be specific in my examination, or as far as my laboratory testing? What am I gonna do? Now as I’ll show you guys in a second, I like to teach the people in my classes a way of thinking about cases, a priority list, so to speak. Well, let’s just kinda go through his history. Now his fatigue, just so you guys understand the characteristics of it, and this is really important, you always wanna get people to say what they mean by fatigue. ‘Cause some people don’t mean fatigue. What they mean is weakness. What they mean is they feel muscularly weak. That’s a little different than fatigue ’cause fatigue is variable throughout the day. There’s no clear pattern relating to what he eats or how much sleep he gets. And the reason I’m mentioning that is automatically that’s ruling out for me he’s not having probably adrenal gland-related symptomatology because if it’s poor adrenal gland function, as we’re gonna talk about in the big three-day class on this stuff, there’s very particular presenting patterns to this, and he doesn’t have it. He’s not getting tired an hour and a half after he eats. He’s not crashing from one to 5:00 p.m. His fatigue is variable during different times of the day. It’s not worse in the morning. We can’t latch onto that and use that to guide us toward what we need to test or what we need to treat. Now his brain fog, again, you wanna have him clarify what you mean by brain fog, so please don’t make this mistake. A lot of people, practitioners, they just accept what the patient says at face value when they make a real generic statement like this. You have to drill down a little bit because very often, the details that are gonna pay off are if you drill down a bit. So his brain fog, now look, let me just stop there. His brain fog could be a, his brain fog could be an ocular alignment problem. It could be a hyperopia. But the thing is, that’s not what it is. He is taking a computer science coursework in school, and he finds that he has to read material over and over again. He forgets material. He forgets dates. So if we’re thinking about that, just from a brain aspect, that, to me, sounds like working memory. It sounds like some frontal lobe and perhaps even some temporal lobe, frontotemporal there. Now it doesn’t tell us why he has that, but if we’re trying to think about, hmm, what could be going on neurologically with this guy, that makes a little bit of sense. Now he forgets events in his past or finds ’em hard to recall. Now then we’re definitely getting into temporal lobe there, into hippocampus. He’s probably got some kinda axis in terms of brain fog in those areas. I’ll tell you what to do about it in just a second. Now he also notes that his mind wanders. It’s hard to focus, and becoming more difficult considering his coursework. So all of that to me sounds like a frontotemporal kind of axis. Don’t know why he has it, but that’s what it sounds like. So his fatigue is variable. It’s not really an insulin resistance pattern. It’s not really a reactive hypoglycemic pattern. If you don’t know what those are, then you need to take the classes ’cause that’s where I explain how to recognize that. Let’s just talk about his history. Where did all this stuff come from? When he was about 10, he started having frequent headaches. Well, when someone is 10 years old and they have headaches, my first thought is all headaches are autonomic to some capacity, unless there’s a tumor or something. But he began getting frequent headaches. I’ll just tell you from experience, when kids get headaches, I start thinking about adrenal gland problems, especially when they’re getting 12, 13, 14, and they start to get a lotta headaches, that’s very often when kids change their eating habits. They don’t eat enough, and they get low blood sugar, and it triggers a headache. The fatigue and brain fog basically began about the middle of high school, so roughly about 10 years ago. About 10, nine years ago was when his chief complaints began. In 2014, he had an appendectomy. He had a colonoscopy, a couple of benign polyps. No big deal there. Now he’s currently taking no over-the-counter medications, no prescription medications and no supplements, which makes my life a lot easier. When they’re not taking anything at all, it’s like, okay, I don’t have to worry about side effects of medications that could be causing this. I don’t have to worry about, so I get to start with a clean slate, which I love because if this kid’s gonna respond to my treatment, then I pretty much know it has to be from my treatment. Now when we review his system, he’s got some symptoms of erectile dysfunction. That is a big red flag for a kid who’s 26. He’s not 66 or 76, he’s 26. He has some difficulty maintaining an erection. Now you have to have something in your intake form that asks those questions. If you’re gonna treat men, you have to ask these kinda questions because, number one, the erectile dysfunction is abnormal, and possible causes could be dysautonomia, neuropathy, just problems with producing androgens. We don’t know, but right there, that piques my interest a lot, that he’s got some androgen-based symptoms for a kid who’s 26. He also complains of very cold extremities. That’s a dysautonomic presentation. We don’t know why he has it, but he’s got it. He’s normal weight. He’s not obese, he’s 5’6″, about 145 pounds. This is very important for us, as I’m gonna show you here in just a second. It’s very, very important for us to note that what his age is, what his symptoms are, what he’s weighing, what’s his constitution, what’s his physique ’cause that points us away from certain things right off the bat, metabolically speaking. Even though I haven’t given you my metabolic properties yet, if you don’t know them, I’m already trying in my mind, when I’m reading over this guy’s intake packet, I’m already making my little decision tree about what’s possible here. No family history to speak of. No family history of autoimmune conditions. I mean, just nothing there. Of course, he’s 26, he’s not a great historian about his parents’ health anyway, but nothing to go on. All right, so there’s our history. His diet history, when I had him fill out my intake packet, at the time, he was mainly just eating a raw vegetable diet in an attempt to see if that, foods, were having an impact on his symptoms. But just so you know, the methodology of what he was doing wouldn’t really tell him anything anyway. But now he’s basically eating whatever. He’s not vegetarian, he’s not vegan, he’s not carbohydrarian, he’s not on a ketogenic diet, he’s not eliminating anything. Just eating whatever he wants, which is probably part of his problem. What’s your impression? Now I’m asking Freddys because he’s the only one I can hear right now, but let me ask him. Based on what you know about things, I don’t really care if you’re right or wrong, just tell me what you think. What’s your impression of what we know about this guy, just looking at his history and his chief complaints and that kinda stuff? – I’m weaker in the hormonal aspects. I’m kinda curious about the memory. I agree with you with the frontal and temporal aspects and the working memory. And with the brain fog, it made me think if it was a brain-based mechanism, but then you said it wasn’t brain-based. Then I know the focus is hormonal, but I don’t know what hormones would cause that. I need to know. – All right, well, cool. So look, the truth is, there’s not much to go on so far. His symptoms are real vague. So we really can’t say, oh, he has insulin resistance. Oh, well, he’s got a family member with autoimmune problems. Oh, he’s been diagnosed. There’s nothing that goes, oh, yes, we know what path to go down. The brain fog really isn’t specific for anything. It could be thyroid, neuroinflammation, nutrient problems, hormones, frontal lobe, eye movement. We don’t know. Fatigue really isn’t specific for anything. Could be any of the metabolic stuff we talked about, iron, thyroid, blood sugar, testosterone. It could be any of those things. The point is we’re probably gonna have to do a little testing on this guy ’cause we don’t have anything to really go on. Where do you start? This is one thing I want people to pay attention to because it’s real easy to get thrown off on a wild goose chase and start testing for stuff that really is not gonna give you any results that you can use. Just for an example, I had a lady just yesterday that I examined and did a workup on. She said, “Well, I was seeing some other doctors “at the same time and she got, “here’s this list of tests this other “person recommended I get.” It was basically every Cyrex test that Cyrex offers. It was $3,000 worth of tests. I said, “You don’t need those, “and here’s why.” I just told her, I’m not gonna bore you guys with that, but I said, “Here’s why you don’t need this. “Here’s why you don’t need this. “Here’s why you don’t need this.” That’s someone who means well, but they don’t have any idea what they’re doing. They’re just gonna order every test, and they’re gonna treat the test. It was like, gonna order the blood-brain barrier permeability order and order a food sensitivity test and order a hidden infection test. First of all, those tests aren’t even gonna tell ya what what you think they are, so that’s my side note. Where do you start? – Hold on, hold on, can I talk about, to me, that is the difference between the novice and the more experienced doctor. One is gonna start off with the shotgun approach, as opposed to being like, “Okay, “I’m gonna start a little, based off my experience “and my exam, I’m gonna start a little deeper.” – Here’s what I’ll tell you guys, the reason I know that is I used to do the same thing. 10 years ago, I’d order every damn test you could think of. But then once you do this stuff for a while, hopefully, you start realizing, “I don’t need to do all that stuff.” Seriously, it was like $3,000 worth of tests. It was a good exercise for me to explain to her why she didn’t need those. Because most of the time, the patients are expecting you to say, “Oh, you need all these tests.” I’m saying, “No, you don’t need that.” Because a food sensitivity test at this stage is just gonna tell you you have a leaky gut. Right? – Right. – And, by the way, if you guys listening, bonus here, just because you have high IgG or high IgA antibodies to celery, for example, all that means is your immune system has seen the celery. It does not mean you’re having an inflammatory reaction to the celery. That’s a whole other thing. That’s related to dendritic cells and regulatory T-cells. You’re not testing that on a food sensitivity test. Do you follow me? Now, granted, if you’ve got four or five foods and your IgG and IgA are sky high, it’s more likely that you might have an inflammatory reaction, but it doesn’t equal sign that, just a little bonus. All right, so where do you start? Well, do you do receptor-based rehab on this guy? You could. You could do that if you wanted to. You could treat him for four or five days or whatever, and hope that it works. Because if it works, his brain fog oughta get better and his fatigue oughta get better. But I’m gonna tell ya something, I didn’t even do that with this guy because he has no trauma. He hadn’t hit his head, no concussion. He’s had this stuff for 10 years. Because of my little rule of thumb I’m gonna give you, I’m almost guaranteeing myself at the beginning of this this guy has a metabolic problem. I could just, based on his history and what I know about it and my experience, this guy has got a metabolic problem that has to be addressed first. I can almost guarantee you. Here are your four neurochemical priorities. Meaning these are the things that are most important for you to figure out if your patient has or does not have. We’re gonna start at number four. I almost feel I could do a drum roll or something. Drum roll. Number four. Is there a GI or a liver problem? Number three, is there an adrenal gland or blood sugar problem? Number two, are there any red blood cell abnormalities and why, meaning are they borderline anemic? Are the red blood cells too big, too small? And then of course, why? So we have to look at these specific nutrients that we know impact that, like B12 and iron and folate and that kinda stuff. And then number one, the absolute number one priority for these kinds of patients, in my opinion, every patient, is is there a clinically significant autoimmunity? Is there an autoimmune problem that is related directly to what’s going on with this guy? Now why are these priorities? Well, I’ll tell ya. If you look at number two, every cell in the body’s gotta have oxygen. How do they get that oxygen? They get that via hemoglobin, and they get that via red blood cells. If your red blood cells are too big or too small or not enough, you’re not gonna deliver fuel and oxygen to the body. That can manifest as 1,000 different things ’cause you don’t get to pick where it manifests. Number three, adrenal and blood sugar. Well, why is that a priority? Well, every cell’s got to have regular glucose. And the big thing in here, besides eating, the thing that really regulates your glucose levels is your adrenal glands because they make a hormone called cortisol. This is all stuff we’ll go in in depth on the three-day class. The adrenal glands secrete cortisol, and cortisol’s job, when it comes to blood sugar, is gets glycogen, which is stored glucose, gets glycogen out of storage and liberates it so you can use it. Number four, GI and liver. Why are those priorities? Well, the liver has about 1,000 functions, synthetic functions, biotransformative functions. The GI tract is pretty obvious because if you have a malabsorption problem, you don’t absorb macronutrients, you don’t absorb micronutrients. Plus, your entire GI tract is lined, just on the other side, by your immune system. So a breakdown in the GI barrier is a major source of inflammation, and inflammation is systemic. Inflammation is not confined to your knee, or not confined to your gut. Wherever you get an inflammatory reaction, that is communicated throughout your body through these things called cytokines. All right, so that’s your four priorities. We gotta figure out if this guy has got those things or not. Where do we start? Here’s my general rule of thumb when it comes to male patients. The younger the guy is, the more symptomatic he is, he’s so symptomatic he’s having to see you because most guys, most guys won’t see doctors. The younger this guy is, the more symptomatic he is, the more normal weight he is, the more you see lack of androgen symptoms, like erectile dysfunction, then you better be suspecting some kind of an autoimmune problem. It’s usually testicular autoimmunity. So I’m already suspicious of this with this guy. I’m like, well, he doesn’t have any family history of autoimmunity, et cetera, but he’s young and he’s got androgen symptoms, in addition to brain fog and fatigue. I’m like, wow, I’m suspicious of this. I’m suspicious of testicular autoimmunity. Again, there’s your priorities. I’m suspicious of this one right here. We’re gonna have to test him to get number two. He doesn’t really have a lot of adrenal symptoms. He doesn’t really have a lot of GI symptoms. We’re just gonna have to test and see if his liver enzymes are messed up, we’re gonna have to look and see what his blood sugar and HbA1c and lactic dehydrogenase look like. What tests are appropriate for this guy? $3,000 worth of Cyrex tests, ’cause I just, I don’t know where to start, so I’m just gonna do everything? Remember, guys, if you do enough tests, you’re gonna find something that’s abnormal, but it doesn’t mean that that has anything to do with that patient’s chief complaints. It just doesn’t. You can spend their life savings on tests. Easy to do. But don’t do that. Let’s think about what tests are appropriate. Now one of the things I try to teach in my classes is to teach clinicians to figure this out. Don’t just have a, “This is my standard battery of tests “that I do on everyone”, because that tells me you’re probably not very efficient, and maybe you’re a little bit lazy. So with this guy, the thing to remember is appropriate testing depends on a couple of factors. Number one, what are you gonna get by doing that test? Sorry my phone keeps ringing behind me. What are you gonna do with the information you get from that? That’s the clinical yield. Number two, logistics. This is more appropriate with kids, but logistics. And the big one, patient’s budget. The first and third ones are the big ones. What are you really gonna get from that test that you don’t already know or can’t figure out from their symptoms or history? Number three, what’s the patient’s budget? ‘Cause I’m telling ya, I would rather them spend $200 on testing, and use the rest of their budget for treatment, than to blow all their budget for treatment on testing. That’s bad patient and practice management. I’m just gonna tell ya. So for this guy, he’s got androgen symptoms, fatigue and brain fog. Most likely, the fatigue and brain fog are some kinda thyroid problem, nutrition deficiencies, could be anemias, could be blood sugar regulation, could be inflammation. Now if we order blood chemistry on this guy, which I think we should, this is where we’re gonna be able to find out a lot about nutrient deficiencies, thyroid function, is he anemic, his blood sugar. We’re just gonna have to test and see. I’m gonna do a comp metabolic, a CBC, a lipid panel, homocystine, hemoglobin A1C. Look, if you’re looking at this thing, “I don’t even know what those are”, you need to take some of the classes ’cause I’m gonna explain in detail what these tests are. Why would you do them? What do they tell you about the patient’s physiology? I wanna look at his iron and IBC, his ferritin. Ferritin, if you ever think about someone’s iron levels, guys, I’m just gonna give you this, another little bonus, look at their ferritin level because ferritin reflects 22% of your body’s iron. That test right here that you see that says iron, that’s 1% of your body’s iron. That’s essentially useless when it comes to evaluating someone’s iron. Ferritin is the one that you use. If a patient’s coming in saying, “Well, my iron was fine,” if the doctor didn’t check their ferritin, you don’t know if their iron is fine. We’re gonna look at his vitamin D, B12 and folate, his high-sensitivity CRP, which is also known as cardio CRP. Of course, I’m gonna look at his thyroid panel, a complete thyroid panel. I’ve listed that those are right there, plus looking at the thyroid antibodies. Now, just as a practical note, if he’s got health insurance and it’s a PPO plan, very often the ordering doctor doesn’t have to be in the network, just the lab you use has to be in the network. I always tell my patients, “Look, we’re just gonna do whatever’s cheaper. “If your insurance will do your blood work cheap, “great, we’ll do it, if they won’t, then we’ll use the co-op that we use.” You don’t need to blow a bunch of money on blood chemistry. Now what this little panel here is gonna tell us, guys, as I’ve highlighted in this box, it’s gonna let us know about his blood sugar stat is, relevant nutrients related to fatigue. It’s gonna tell us if he’s anemic or not. It’s gonna give us thyroid information, and it’s gonna give us a few inflammatory markers. This is valuable for us because otherwise, we would just be guessing. Here’s what I’m gonna tell you, here’s what I’m gonna tell you, I think the vast majority of practitioners just don’t test the basic stuff, or enough of the basic stuff. They don’t check ferritin, they don’t check B12 and folate, they don’t check the full thyroid panel. I mean, how many times I have people come in and say, “Oh, I just had some blood work done. “I had some complete blood work done.” And it’s a CBC and a comp metabolic. Eh, that’s not really complete. I understand why you think it is, but that’s not even close to being what you need. All right, so make sense? So the reason I’m explaining this to you is so you see why we’re ordering that. Now, to look at his hormones, ’cause he has some androgen symptoms, erectile dysfunction, can’t maintain an erection. You can guess about that if you want, but I think you should just evaluate and find out does this guy have enough androgens? So here’s how you do that. I like to use a test called a DUTCH test. That stands for dry urine testing for comprehensive hormones. That lets me evaluate the quantities of the following things. And again, if you don’t know what these are, well, I’ll be explaining all of this in the big class. DHEA-sulfate, testosterone, etiocholanolone, androsterone, 5-alpha DHT, 5-alpha androstanediol, beta androstanediol, estradiol, estriol, estrone and alpha and beta pregnanediol. So what does that tell us? It lets me look at, just so you guys know, it lets me look at the two branches that come off of pregnenolone. Pregnenolone’s a mother hormone. You go down this pathway, you’re gonna get DHEA and androgens and estrogens. And if you go this way off of pregnenolone, you’re gonna get aldosterone, cortisol and progesterone. So, I’m interested in these things because I wanna find out, does this guy have androgens that are low? And just so you guys understand, everyone talks about testosterone. Testosterone’s not even your strongest androgen. 5-alpha DHT, this guy right here, this, that’s your strongest androgen. It’s many times more powerful than testosterone. So, if you’re not looking, here’s what can be misleading. If you do a blood test, “Oh, your testosterone’s fine, “but the 5-alpha DHT’s in the toilet. “Well, that’s why you have your androgen symptoms.” The reason I like this testing is it gives me more detailed, useful information. I don’t do saliva testing for hormones at all. I did that for many years, and I’m just not happy with the data that I get from that, I guess, is the easier way to put it. I like this a lot more. This is just a little snapshot of what a DUTCH test result looks like. For example, guys, here’s pregnenolone. Now I cut off part of this. Pregnenolone is gonna turn into DHEA. Here’s your DHEA sulfate. Then these guys right here are your androgens. All this stuff right here, these are androgens. Here’s your estrogens. So if I run a DUTCH test, I can evaluate what’s happening with this guy’s quantities of his hormones. Now quantities are just one part of the picture when it comes to hormones, as I’ll kinda hit on in a second. I just wanna kinda give you a visual representation of what that is. Now that may look totally overwhelming, but that’s okay, if you’re just not experienced with it, but it’s very easy to understand once you know what enzymes are involved, et cetera. Let me just move along here. So one of the things I said I was suspicious of this guy was that he had an autoimmune problem because of my little algorithm. So what are we gonna do for that? Well, is it important that we know the specific antibody that might be involved if he has an autoimmune problem? Or is it okay for us to know there’s just some autoimmune problem involved? That’s for you to decide, but I’m gonna tell ya that it’s a whole lot cheaper to avoid a lot of antibody testing, which would be five, 600 bucks, and to just see, it is specific, but it’s expensive. But the thing is, everyone, the test I’m talking about, everyone loves that Cyrex Array 5 test, which is the multiple tissue test. That’s cool, I’ve used it, but it’s not encyclopedic. That’s not everything a person could have. So a mistake people make all the time, all the time, is they run that test, none of it’s aboral, and they tell the patient, “You don’t have an autoimmune problem.” That is wrong. That is completely false. There’s 24 antibodies on that test, great, that’s not all the antibodies a person could have. So don’t make the mistake of doing it that way. Now the cheap way to find out if someone’s got an autoimmune problem, it takes a little skill, and I’m not gonna go over it exactly here today is to do what we call a clinical challenge, where we have them ingest Th1 cytokine stimulators for a couple days, see how they feel, and then ingest Th2 cytokine stimulators, see how they feel. It’s a cheap test, it’s 20 bucks, but it’s not specific. It can’t tell us which specific autoimmune problem Jake has, but it can tell me, hey, does this guy’s immune system seem to be playing a role here, or is it not playing a role? So for 20 bucks, I can pretty much just rule that in or rule that out, and then immediately change my course of treatment. Does that make sense? – It makes a lotta sense. – I’ll go over that in detail when we get to the class. So look, here’s what happened. I did the clinical challenge with him. He had no problem with either Th1 or Th2 boosters. He had no problem with it. So what does that mean? Well, if his white blood cell count is normal when he does this challenge, and he has no reaction, no reaction’s a pretty good indicator that he does not have an autoimmune problem. It’s really that reliable. Or with his white blood cell normal and he doesn’t have a reaction to either one of those, it just means his immune system’s probably not a player in this. Go ahead. – No, I was gonna say I remember how you taught us before to always make sure that a patient has enough, what was it, IgG, IgA before you even do food sensitivity testing. – That’s right. – That’s why you mentioned the white blood cells at least being normal as a prerequisite. – This is the corollary right here. – But if somebody has low IgG, IgA, would they still possibly react to this trial? – Yeah. – They’ll still react to it? – They still could, right. They still could. – Great, that’s very useful. – It is, but again, I mean, there’s some very specific guidelines on how to do this and how not to do it, which I’m not gonna go in today, I’m just giving you this by way of explanation, to let you know that the reason I did it this way, it was a $20 way for me to find out, hey, man, is this guy’s immune system involved? And it doesn’t look like it is. So out of my number one priority list, my four priorities, he does not seem to have one with number one, which is cool. It means I don’t gotta mess with it. Now, though, if he did that challenge and he had no reaction, but his white blood cell count was less than five, not having a reaction to either one of those means his immune system is probably not even competent enough to muster a reaction. Now, also, just so you know, when the white blood cell count is less than five, that is often caused by a high cytokine load, which is very often seen in autoimmune or inflammatory conditions. This is just, some of you guys are gonna pick up on that. Look, do we think his immune system’s involved? Doesn’t look like it. Doesn’t look like it. What’s his blood work show? Well, his BUN is 10. His creatinine’s a little bit low. Eh, we’d be more worried if his creatinine was high because creatinine being high is more of a sign of renal involvement, but I’m just telling you what it was. Chloride’s a little bit low. His anion gap, which I calculated is a little bit high for my standard, which means he may be getting a little acidic. His bilirubin is a little bit high total, which ultimately doesn’t mean anything because that’s Gilbert’s Syndrome, you guys may remember from school. That’s just some people have more bilirubin than they’re supposed to. Doesn’t mean anything pathological. Now out of his thyroid panel, I’m just giving ya the highlights, his TSH, all that stuff was fine, except for his reverse T3, it was high. I’m gonna explain what it means in a second. What does it tell us? His free T4 is a little bit high. Now his TPO antibodies, for his Hashimoto’s, were 24. Now, that’s not zero, but it’s not above the lab range, so you gotta ask yourself, “Well, what do I make of that?” Now, his vitamin D’s 11. Well, let me just tell you, that’s terrible. That is terrible. That is very, very, very bad vitamin D. His MCV, which tells you how big his red blood cells are getting, that’s a little bit high for my taste, that’s why I put functionally high there. His B12 is 542. Meh, that’s okay. Not great, but it’s okay. B12 in the blood test is not a great, authentic test of your B12 levels, so that’s why I’m like, eh, 542, that’s okay. But if his MCV is getting a little bit high, that’s either gonna be caused by a folate problem or a B12 problem. And his B12 is meh. His folate’s 9.2. Let me just tell you, listeners at home, that’s not a good folate level. Now, lab low is not ’til he gets down below three, and you’re almost never gonna see people with folate that low, except for me, I just saw one this week. But at eight, nine, 10, the literature’s pretty clear, when you get folate levels that low, that’s enough to cause neuropsychiatric symptoms, such as brain fog, such as memory issues, such as mood disturbances, it absolutely can do that. Now, let me go through these a little bit in detail. Now, his reverse T3 is high, what is that? Well, reverse T3 is just the byproduct of converting T4 into T3. If you don’t know about that, we have a whole thyroid class that goes over all that stuff, but here’s the punchline. This guy’s T3 levels aren’t high, but his reverse T3 is high. Let me just tell you what it means. It means he’s got a high cytokine load, or cortisol, causing either increased production of reverse T3, or decreased disposal of reverse T3. Now, let me stop there because I just said, we did the challenge, it didn’t seem like his immune system was involved. Well, I’ll put it this way. His immune system is not involved in the sense that if we were to shake up his immune system, it doesn’t change how he feels. So this is kind of a, yeah, I’m telling you it’s a high cytokine load, but I’m not telling you what that means is oh my God, now we have to go after his immune system, I’m just explaining this to you, okay? Now, his free T4 is actually a tad high, but here’s the deal, his TSH was normal. So a high free T4 by itself in this context doesn’t mean anything. It’s just an outlier, right? So you can’t freak out, “Oh my God, he’s hyperthyroid.” No he’s not, because by definition, his TSH would have to be low, and it’s not low. So we don’t treat a single lab finding, you gotta think about the whole context. And the reason I say that’s not significant is he doesn’t have any hyperthyroidism. Now, if he was hyperthyroid, he was tachycardic, he was nervous, he was sweating all the time, I would say, well, maybe this guy, maybe we captured something here, right? But that’s not the situation. Now, his TPO antibodies, does he have Hashimoto’s? What do you think, Freddys? Does he have Hashimoto’s? – I don’t think so. – Well, even if you thought he did, you couldn’t say it because his Hashimoto’s antibodies are not above the lab range. Now, I gotta tell you, 24 makes my ears go up a little bit. Now, granted, there’s a quote unquote “normal range”, but you gotta have a cut off at some place, but 24, I don’t make a big deal of it with the patient. In my mind I’m thinking, well, probably keep an eye on that. Now, his vitamin D is terrible. Terrible, terrible, terrible. Vitamin D is anti-inflammatory, guys, and it directly affects serotonin and dopamine levels in your central nervous system. It does, okay? It’s basically a neurosteroid, it’s not really a vitamin at all, it’s more of a neurosteroid. So his MCV was a bit high, which means his RBCs are starting to get big, and the question is why is that happening? Well, because it’s either folate or B12. Well, his B-12 isn’t great, but his folate really is not great. Now, here’s the thing, as I said earlier, folate in the eight to 10 range is known to be associated with neuropsychiatric symptoms, brain dysfunction, okay? Folate is critical for energy production and it’s critical for synthesis of dopamine, serotonin, epinephrine and norepinephrine. I can tell you right now that if you gave this guy an SSRI or an SNRI medication, he might actually feel better. But the thing is, he’s, I’m just gonna tell you, I think he’s probably not making those things as well as he should, and suppose he’s getting regional brain malfunction, and he’s having this brain fog and fatigue. But also, folate in the eight to 10 range or lower should automatically make you suspicious of some kind of malabsorption problem, because this guy’s diet is not restricted, he’s eating whatever he wants, which means he’s eating a bunch of crap, and almost all of it’s fortified. Folate’s in everything, and for someone to have a folate level that’s that low, you have to be suspicious of malabsorption. Now, that could be celiac disease, or it could be some kind of gluten-related sensitivity, or it could be GI inflammation, but you have to be suspicious of that. All right, so we look at his hormone quantities. Here’s the thing. You can look at his hormone quantities, but you can’t assess how he’s using those hormones. It’s the same situation with thyroid hormones. I can look at TSH and T4 and T3 and see how much of those are floating around, but I can’t tell really how he’s using those because using them is the domain of receptors, and we don’t have tests that lets us look at the receptors. But the DUTCH test also lets look at enzymes because certain enzymes can be upregulated or down-regulated causing specific patterns of changes in quantities. Now, this can get a little bit overwhelming visually, I’m gonna hope it’s not because this is all stuff we’re gonna go over in the class, and when we go over it in the class, we’ll go over it 100 times with different cases so you can see all the different permutations of it. So here’s the thing, in general, you’re looking at hormone quantities, you can’t assess hormone receptors, and here is the basic kind of model. So you got your hypothalamus and pituitary gland, and those are gonna send signals to various glands to tell them to synthesize hormones. Those hormones then have to be transported, they have to converted peripherally, usually. And they have to be eliminated. Hormones have a half-life. You can’t just make a certain amount of testosterone and they hang out forever, it doesn’t do that. It has to be eliminated, biotransformed through your liver. The hormone has to be bound to a receptor, which means you have to have enough receptors, there’s gotta be transduction, transcription, a proteomic response, and then you have to have feedback, you have to have feedback from the periphery back to the hypothalamus that says, “Hey, we got it. “You said make testosterone, we made testosterone, “testosterone did its thing. “We’re telling you that we did it.” And here’s the problem, or the various problems, you can have a breakdown in any of these places. Any of those places. So you don’t just look at the quantities, ’cause quantities just tells you about synthesis. As much as you can, you want to try to think about these other issues, which we don’t have time to talk about today, but a little bit. So it’s real complicated, but the good thing is, you can work your way through it. The other thing I do want to mention is I could have put cerebellum up here, and obviously, there’s neural integration into all of that stuff, right? Oh, what the heck was that? All right, so here’s this guy’s DUTCH results. I kind of screwed up, so there’s his DHEA. Well, what do you think? 212, for this guy, he’s between 20 and 39, if you look right here. He’s on the lower end of that range, wouldn’t you say? – Yes. – He’s on the lower end of that range for sure. All right, let’s look at what else we got. So here’s his etiocholanolone and androsterone. Well, those are pretty normal though, right? So that going this way is a little bit low, but going this way, that’s all right. What about his testosterone? Is it low or high, or normal? – He’s high. – He’s high, and this is where everyone gets confused, right here. – I’m there, right? I’m with him. – I was with you with the DHEA because I was expecting it to be low, but why in the hell is his testosterone high? That doesn’t make any sense to me. And it should be confusing at this point. All right, so his testosterone is high, which should confuse you because he’s got low symptoms, but his quantities don’t look all that, ’cause DHEA is a pretty weak androgen, testosterone is a little bit stronger, but let’s keep going. His 5-alpha DHT, which is your strongest androgen, is that high, low, or normal, Freddys? – Also high. – It’s also high. Now, wait a second. Not only is it up, I thought this would be very simple, but it’s not. Now, his estradiol, which is your estrogen, that is high, okay? And so there’s some things going on here that I’m gonna try to make sense for you here in a second, but it’s not what you thought it was gonna be. It wasn’t like a really black and white, oh yes, testosterone’s low, we should do, it didn’t work out that way. Now, if he has low androgen symptoms, why are these quantities high? Well, I’m gonna tell you why, ’cause you probably don’t know yet, and that’s okay. So what happens if a patient like this guy has low hormone symptoms, but when you look at it, his quantities are actually high? Do you have an idea? You’re thinking about it, I can see. – Well, before, you were talking about, could it be at the receptor level? – That’s right, it could be at the receptor level. So, we could have receptor resistance. Woo hoo, good for you, right? Which means, in a nutshell, if you deluge receptors with hormones, then they tend to become less responsive. Now, that doesn’t answer why his quantities are high, but it does answer possibly why his symptoms are for low. Now, the other thing that could happen, guys, is he could have testicular autoimmunity that’s liberating high amount of hormones. – I’m just thinking– – In the thyroid gland. – Yeah, that’s what I was gonna say, I’ve seen it in thyroid before where you, they’re liberating– – As an example– – As it destroyed a tissue, they’re liberating more. – So what happens with people that have Hashimoto’s that’s not controlled is they’ll go periodically hyperthyroid because the immune system blows apart your thyroid gland and they dump hormones, right? – Mm-hmm. – Or, he could have poor clearance of these hormones via his liver. Now, these are all issues that are really, really important for me. Now, I can probably rule out number three because he didn’t have any kind of immune system weirdness with the challenge, so I’m wondering about poor clearance by hepatic function, and I’m actually wondering about whether some of these enzymes are just upregulated. Go ahead. – Is there anything in the previous CBC scan that would have indicated hepatic dysfunction to indicate poor clearance? Or, I don’t think the– – No. – I don’t think the markers are gonna, yeah. – No, no, no. All right, so obviously, you’re gonna be doing the three-day class, but here’s what’s up with this guy. So this gets a little bit confusing. I robbed this from the DUTCH Company, and they don’t pay me, by the way, I don’t have any disclosures, they don’t pay me to tell you about the labs, this is a good chart that I didn’t want to have to recreate. All right, so I like this diagram from the guys that make DUTCH because it lets you look at the different enzymes that are responsible for transforming one substrate to the next. So in this particular guy’s case, his testosterone was high, his 5-alpha DHT was high, his 5-androstenediol was a little bit high, and his estradiol was high, but his DHEA was a little bit, his DHEA sulfate, rather, was a little bit low. Now, I’ve kind of put diamonds around all the relevant enzymes that are involved in this guy’s particular presentation. And what you see is you got 3-beta hydroxysteroid dehydrogenase involved, probably 17-beta hydroxysteroid dehydrogenase involved, and aromatase. Now, what’s interesting is that I’ll go over it in the class and what they do here on the graphic is they say look, aromatase is upregulated by these things, right? 17-beta hydroxysteroid dehydrogenase is upregulated by these things. So I’m gonna show you a graph on a kind of just a text form in a second what all that means. So here’s what upregulated in this stuff, and this is the value of doing this test, we can be more specific about what’s going on with him. So here’s the mistake with this guy. The mistake is if you walk into, he walks into some practitioner’s office, whatever it is, he goes, “You know, I have erectile dysfunction. “Oh, you need testosterone.” It’s actually not the thing he needs, it’s the opposite of what he needs. So, upregulated enzymes, his 3-beta is upregulated, and look, that’s increased by insulin and obesity. I say it looks like it’s upregulated. His 5-alpha reductase, that’s increased by insulin. His 17-beta hydroxysteroid dehydrogenase, that’s increased by inflammation. Aromatase is increased by inflammation. Now, I still said earlier, right, earlier I said, well, it didn’t seem like his immune system was really involved in this. Well, maybe it is, it didn’t seem to be through the challenge. So the reason I point this out is, in terms of treatment, I’m gonna do something to try to down-regulate this guy, and the reason is this guy right here is gonna make 5-alpha DHT, which is your most potent androgen. And I think that what this guy has is he’s making too many hormones, and it’s causing receptor resistance. Which means you take these receptors and you dump a bunch of hormones on them and it exceeds their threshold, then they will start to down-regulate and prune and become less available, basically, as a self-defense mechanism. All right, so what do we know? Let’s go back to our four priorities. GI/liver? Not really. Adrenal/blood sugar? Not really. RBC abnormalities? Eh. B12, not great, folate, not good. Autoimmunity? Clinical challenge was negative. So what do you do? Well, I think you have to improve his folate, you have to improve his B12, you have to improve his vitamin D, and I think we need to improve his hormone elimination velocity, meaning I think what might be the root of this dude’s problem is he does not get rid of his androgens the way that he should. And so kind of like a back-up sewer pipe, they don’t eliminate when they’re supposed to and they get to really exert their effects on the body which causes him receptor resistance and presents with low androgen symptoms, even though he quantitatively has high androgens, right? I grant you, that is not very straightforward if you don’t know any of that stuff I just talked about, but I’m just telling you that that’s what you’re gonna see again and again and again with both men and women, you’ll see they have high levels of hormones. And when you do something to improve how fast they eliminate that stuff, their hormone symptoms get better without you giving them hormones. That’s a little gold brick I guess there. And I also want to reduce the activity of 5-alpha reductase, aromatase, and the 17-beta hydroxysteroid dehydrogenase, even if it’s just temporarily, just to give the guy some relief. So how do we do it? What are we gonna do to do those things that I just said? Well, his vitamin D, 10,000 IUs per day, sublingual is my best recommendation. Everybody makes sublingual vitamin D. Don’t waste your time with gel caps and capsules, just forget that. They don’t even absorb very well, but if you do sublingual vitamin D, in this guy’s case, 10,000 IUs per day because his vitamin D is so low, you gotta let it soak in under the tongue. And you can’t just put it in your mouth and swallow it, ’cause that’s not sublingual. You gotta let it sit on the tongue for 45 seconds or a minute before you try to swallow it. All right, methylfolate is my preferred source, or preferred form. Lots of people make methylfolate, right? Probably 1,000 micrograms per day would be enough for this guy. Hydroxocobalamin is a form of B12 I like a lot. Methylcobalamin could work as well, but there’s no data to show that it does. I like hydroxocobalamin in a sublingual lozenge, it’s just kind of a little powder thing that dissolves. About 2,000 micrograms of that per day. And you may go, “Oh my God, that’s so much B12.” B12 is water soluble, you’re not gonna OD on it, nothing to worry about, might turn his urine a little bit yellow. And now I want to down-regulate those enzymes. And I used a combo formula to do that. These are the things that work in it, I mean, I can tell you the name if you want, but it had zinc, saw palmetto, ’cause it is a known supplement that will definitely down-regulate 5-alpha reductase, without a doubt. Nettle will do the same thing. Chrysin will– – Did you say aromatase? – What’s that? – I was gonna say, I know DIM and chrysin, they’re aromatase. – So, you’re right, so exactly. And so that’s why I used this combo formula ’cause they add some stuff in it to do multiple different enzymes for him. – And I appreciate you sharing the ingredients ’cause what we don’t want is to make this a class about brands, you want the clinicians to really understand the tools they’re leveraging. – Yeah, and the thing is is there’s lots of people that make lots of stuff, right? Nobody makes bad stuff for the most part. And then it just becomes a matter of cost and does it have the combination of stuff that you want to use? Because I’m telling you, you can’t just, sometimes with these cases, you have to look for, okay well, I need something that does X and Y and Z, and this just happened that this particular formula did that for him, okay? Now, the combo formula for improving his liver biotransformation velocity, meaning improving how fast he eliminates hormones, that had a bunch of stuff in it. Glutamine, glycine, taurine, all those are important for biotransformation pathways. Milk thistle is basically something that supports hepatocytes. Curcumin, N-acetyl cysteine because that is a direct precursor to cysteine, which is the rate limiting step to make glutathione, which is the major, one of the major things you use to detoxify things. Alpha lipoic acid, grape seed, MSM, broccoli powder, yellow docks, schisandra, and green tea. Again, I could have found something that only had a couple of ingredients in there, but I know what all those things are for, and when we have the class, what I tell you, hey, here’s why I use, I’ll explain, theologically, why you want to use them. I don’t have time to do it today, but all those are to improve his biotransformation function. Now, in terms of his diet, I would say, “Look, I want you to follow an anti-inflammatory diet”, which is no gluten, dairy, grains, nuts, beans, seeds, eggs, nightshades, no melons, mangoes, bananas, pineapples, et cetera. Now that’s just a little thing on vitamin D which I’m gonna skip ’cause basically, vitamin D is an anti-inflammatory. Here’s the thing, how’d he do? That’s what we want to know, right? He did all that stuff, we talked about his folate, we talked about his hormones, but the thing is, what did he do? Now, granted, what did I give him? I gave him folate, B12, vitamin D, that enzyme down-regulated function and I gave him that liver formula to improve his transformation. So how did he do 30 days later? His brain fog is 80% improved. That’s his self-rating of it. His fatigue is 100% resolved, he has no fatigue whatsoever. He can exercise four times a week, doing 20 minutes of cardio, and then whole body lifting. So no fatigue, and essentially, no brain fog. And he never really did the Repair Diet completely anyway, that anti-inflammatory diet, he never really did it anyway. So again, it’s probably not inflammation with that guy, it’s probably not what that is, or not inflammation in a way that’s really overt, okay? So what gets the credit for him getting better? What did it? I don’t know. I mean, I don’t really care to be honest, all that much. I mean, I care and I can figure it out a little bit, but the point is, when you’re dealing with patients, you can’t do this thing with, “This month, we’ll take folate. “And next month, we’ll take vitamin D”, ’cause you don’t have time to do that. If all that stuff is wrong, just give it to him, right? The way I do things, I tell my patients, “Look, at some point, “if you respond well to the protocol”, because I do my treatment plans in 30 days chunks. 30 days is plenty of time to find out if you’re on the right path, not six months or whatever. 30 days goes by with this guy, and he’s doing better, then awesome, that’s important. Now 30 days after this, perhaps I’ll retest a couple things, perhaps I won’t. Perhaps ultimately though, what I want to do is I want him taking a few things as possible to feel good. ‘Cause I just don’t think you should take stuff forever without a really good reason. And I told one of my patients that too and that is something they are very happy to hear. I don’t know what gets the credit for him getting better yet, the point is, he got better. Now I need him to stay better. So what’s next? Well, I tell him he continues protocol. So we’re 30 days into treatment. “Keep taking what you’re taking, but 30 days from now, “we’re gonna recheck your folate, your vitamin D, “and your B12 because I’m most interested, “did those things get better?” ‘Cause check it out, what if we recheck his folate, B12 and vitamin D and they all still suck? Well, he’s still doing great though, so this must have nothing to do with how he feels, but there are important things for his health. If he’s continuing to do well 60 days in, you might retest that DUTCH test, you probably don’t need to. I mean, you could. Instead, what you could do is this, guys: You could withdraw that liver support or withdraw does enzyme influencers and see how he does. You can figure it out by eliminating things rather than by spending money on testing. Do you understand what I’m saying? Now, you’re trying to find the minimum amount of support he needs to function well long-term. That’s what you’re trying to find. Now look, if he never gets better than 80% of his brain fog, rehab him, right? I’ll definitely rehab him. Probably needs some frontal lobe, probably needs some frontal lobe help, probably needs some temporal lobe stuff, but I can tell you that trying to rehab that guy without doing what we just did there probably wouldn’t have gone very well. That’s just my clinical experience on that. But here’s the thing I want you to know. You don’t have to do it the way I did it. You could do it the way you want to. You just have to call it like it is, meaning if you had this guy walk into your office, and you think, “Man, this guy’s got a frontal lobe, “his saccades are a bit off”, whatever, and you treat him, if he gets better and stays better, awesome. But if you treat him and he gets better, but relapses, you better start considering this stuff. If you treat him but he doesn’t get better at all, start thinking about this stuff. And where I’m at now, a lot of times, I just know that this is what the guy’s gonna be, and it’d be a waste of his time and money to rehab him straight out of the bat. Okay, you can always do the rehab in conjunction, you just gotta know and have a standard and a bar to set that says, “Okay, I’m gonna treat this guy, “and how do I know if it works?” Let me just tell you something else. Don’t get happy and clap yourself on the back of someone who gets better after four, five days of rehab treatment. Be happy when they stay better for two weeks, three weeks, four weeks, that’s when you’re really happy that plasticity has kicked in. So what do we do, I don’t get super excited when someone’s better after 30 days, I want to make sure they stay better at 60 days, 90 days. And then are they staying better with less support? Make sense? All right, now, here’s the takeaways. You do need to know and own the different types of physiology, like I was talking about at the beginning in order to be efficient and effective. You need to understand that fatigue could be these 25 things. It’s the same way in neurology, right? The guy says, if the guy comes in and says, “Well, I have a brain fog.” Well, you need to be able to know the 25 things neurologically that could possibly cause brain fog. If you don’t know it, you wander lost, doing every test and every treatment that you can think of. It’s just like a roulette. And you don’t want to do that because when you could be efficient and effective, when you’re really good at what you do, then you do a really good job for the patient. You don’t order $3,000 worth of testing. You want to do testing that makes sense based on that case, like we just talked about. I mean, this guy’s symptoms were not that specific, we needed to do some testing to tell us where to go. And I tell you for sure to use those four priorities to prioritize your treatment, ’cause it’s really easy to get lost, but hopefully if you guys go back and look at this, you’ll see how we work through that. We said, okay, probably not autoimmune, he’s definitely got a little RBC thing, that’s folate. Adrenal/blood sugar? Not so much, but GI/liver, ooh, this guy’s got high testosterone but no symptoms, you have to know that one thing that can do is if he’s not eliminating those hormones the way that he should, things back up, and you get receptor resistance. So if you learn this stuff, you learn how to kind of approach it, you don’t get lost. And obviously, you gotta know which nutrients and herbs and supplements cause the desired changes you want in physiology. If you didn’t know, you might be able to figure out that, “Hey, I need to down-regulate that guy’s “5-alpha reductase”, but then you gotta know what does that. What actually does that. So there’s a lot to know, but the good thing is, it’s all stuff you can learn. It’s all stuff that you can be taught and learn. And that’s one of the things that, one of the many things we’re gonna do in that three-day class is make sure you understand all these different priorities, not priorities, all these different pathophysiologies, all these different things that can cause hormone-related symptoms and hormone-related abnormalities. And of course, the other takeaway is, integrate your brain-based treatment, your receptor-based treatment where it’s appropriate and when indicated, but just make sure you do it in a way that you can be honest with yourself and say, “This is working, or this isn’t working.” There’s no shame in that. Now as the last class we’re meeting, this is the class we’re doing in December, I don’t know what date it is, I should have put it on there, I think it’s the first weekend in December. and this is the three-day class on the Mastery of Neurochemistry and Male and Female Hormones problems. which is gonna be, that’s just a sampling, we’re gonna do another case I think probably in a few weeks where we’ll do a female hormone case. And if we have time, we’re gonna do another case after that, depending on how you guys like these things. But again, it’s a three-day class, there’s a flipped classroom, which is gonna be chock-full of stuff that you will read before the class. Am I doing what you’re supposed to be doing, Freddy? Are you supposed to be saying all this? – No, go ahead. You know what’s in the class. – I should, I’m writing it. You can certainly attend the livestream. I’m a big fan of being live in the room, that’s how I learn best, but you know, I understand you don’t necessarily have a– – We have a very, very good online learning environment though. – Oh yeah, yeah, that’s the thing, yeah, I’m just– – It’s top notch. – It’s a really good learning environment, so don’t let distance be a, I mean, I don’t care where you are in the world, you can take it and you can livestream it. And then you get a one year access to the on-demand recording, which is awesome, they don’t charge you anything extra for that, so you’re not gonna lose anything. You’re not gonna miss anything, you have plenty of time to go back and fill in the gaps. And of course, you also get Medline access upon completion of the module. So anyway, I feel like I talked for the entire time. Anything you want to say before we wrap up the day? – No, I’ll just say, I really, really enjoyed the case. I gotta tell you, I’m one of the people that would have thought more traditionally and probably made the wrong decision with this patient. So this one got me. And I, even with all my nutrition training, and I am trained, I’ve always been weaker in the hormone area. I find it very complicated, and I actually find female hormones even more complicated, to be honest with you. – Oh, yeah. – And I now you started teaching all the neurochemistry scholars that come to us from around the world about the DUTCH testing. And I see in the forums in the emails, and so we’re working very, very well for the docs that are using it. So I know, and this is, this was very cool. I just really appreciate you sharing this. We are gonna do it again in a month. Mastery of Neurochemistry of Male and Female Hormones. Dr. Clark, thank you very much for joining us for this episode of CITV, and we’ll catch you again next time. – Cool, see you guys later.
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