– Hello, my name’s Dr. Freddys Garcia. Today I’m joined by Dr. David Clark. We are gonna go over two video case reviews. It’s a BOGO special. It’s a BOGO special.
– It’s a BOGO, right!
– I’m excited about this. What are the two topics we’re diving into today, Dr. Clark?
– All right, so in this episode of Clinical Neurochemistry and Nutrition in Action where I show you how we utilize this with real patients from my real office where I really treat them, we have a 15-year-old male presenting with brain fog, headaches, fatigue, and joint pain, and then we have a 34-year-old woman who has brain fog, poor memory, and mood swings.
– So what’s up with brain fog? Well, when did that become so popular?
– I think it became popular the way that adrenal fatigue became popular. So when I did this seminar whenever it was, a year ago, on male and female hormone problems and also talking about adrenal stuff, one of the big points I made in that class was that adrenal fatigue doesn’t really exist, not the way everyone thinks it does. It was a term that was coined, I don’t know, 15, 20 years ago, I can’t remember, but by a guy who was a chiropractor, and everyone said, “Hey, that makes sense.” And so then it just become a mass delusion. It became a thing that people have, adrenal fatigue. But if you look at any medical endocrinology, the people who are the real experts in endocrinology, the adrenals can’t really fatigue, right? So I think without going any further to that thing, I think brain fog is the same thing. It’s just a real generic catch-all term, and that’s why, as you’re gonna find out, you never take that at face value. You have to ask, “What do you mean?” Give me an example of what you mean by brain fog, but don’t say fog.
– Oh, okay.
– What’s telling you that you have brain fog?
– Now you intrigued me. You’re , “Oh, look I’ll show later, you will undoubtedly see what I do.” All right, let’s go. Let’s go into it.
– All right. So here’s the goals for today in case you guys are not new or are new and aren’t familiar with what I’m trying to accomplish with these case reviews is we’re trying to understand physiology, okay? We wanna try to decipher the patient’s symptoms to see if it can help us develop a working hypothesis about what the heck is wrong with them so that we can then do whatever diagnostics are necessary that are relevant to help us know where to start to try to help them get better. So we’re gonna know how to do what tests are appropriate for a given patient. We’re not gonna have just a panel that we do on everybody no matter what, like we’re gonna do stool tests and candida testing and metals testing. We’re not gonna do that. I’m not gonna do that. I think I just touched the mic. Sorry about that. We’re gonna help you learn how to decipher this. Now the second thing is we wanna learn how to think, right? Not how to memorize. And of course, there’s a little bit of memorization. You have to know what is a CBC test, but it’s better to know what does it mean if a CBC says this, right? What does it mean if it says this? What if it means if it doesn’t look like a way that I think it’s gonna look? What if it’s not a textbook case, right? How do I bring everything into context? How do I develop my clinical acumen, my clinical decision making? Because look, lab tests are not a justification for abdicating your clinical thinking. We don’t just run tests and go, “Okay, I don’t have to think. The test is gonna tell me what to do.” That’s not what we’re doing. But there’s a lot information that you can get in tests, and you have to be able to prioritize this stuff ’cause look, the person could have anything. They can have anything in the world, but you know that you’re gonna go nuts trying to view every patient that. You need to look for some priorities that are probably the most important, and I’ll show you what those are. And we also gotta know how to follow up with people because one of my big criticisms, as you guys know, is a lot of people that mean well and they teach the nutrition work and et cetera, they don’t really teach you how to follow up with patients. It’s just like, “Just here’s what’s wrong. Here’s the symptom survey. Whatever the symptom survey says, here’s what you give them, and then there we go. Okay, good luck.” But that’s not really good care, in my opinion. And if you’ve only got a weekend seminar that’s two days long and you’re the supplement company that’s sponsoring it, I get it. You don’t really have a lot of time to dig deep, but we do. We got time to dig deep, so we’re gonna dig deep, and I’m gonna explain, how do you follow up with people? And our third goal is we’re not gonna memorize. This stuff I show you guys today, don’t memorize that and say, “Oh, the next person that has brain fog, this is what I give them.” That’s not what we’re doing. We’re not gonna build little robots, okay? We’re gonna get rid of the robot thinking. We’re not gonna do this for that. We’re not going to do that. Nutrition and neurochemistry just doesn’t work like that. I had somebody. Who was it just the other day I was talking to about their Ménière’s? It was a new patient, and they were talking about some doctor they were seeing who was telling them that they had some high copper, and that was probably what was causing their vertigo. No, that’s not what was doing it. The lady has Ménière’s disease, right? But that doc, I’ve seen 35 people that this guy has seen. And I know he means well, but every one of them had a copper problem, every one of ’em. Everybody’s got a copper problem. We’re not gonna do that, okay? And it’s more difficult to do it ’cause I’m not gonna lie. It is more difficult to do it the way that I’m gonna tell you, but it’s more fun. I can tell you that. It’s more fun and more rewarding, I think, and it’s just, I think you serve people at a higher level. All right, so here we go. We’re gonna start with this 15-year-old male that has brain fog, headaches, fatigue, and joint pains. Let’s go through this. Sorry for the computer sounds. Generalized muscle fatigue. Okay, well what does that mean? It means that he feels throughout his body and his muscles, he feels weak, you know what I mean? He feels a generalized muscle weakness, but he’s calling it a fatigue, okay? He feels like he can’t really exert himself very much before he feels like his muscles just are givin’ out. Now that can implicate a lot of stuff. This is a real global thing he’s saying, right? It’s probably not a discrete cerebellar lesion on the right that’s causing a generalized muscle fatigue. It’s probably something more metabolic. I think we can all agree with that. Now, if you don’t understand why I said that, then you probably wanna take the classes that we’re doing, and I’m really gonna help you understand why how you start to decipher these things when we have more time than we have today. He has generalized joint pain meaning, in most of the joints of his body, it hurts, his knees, his elbows, his ankles. Again, that is telling us there’s probably a metabolic, meaning a biochemical system wide issue, okay? Now you might say, “Well, maybe he has a parietal lobe lesion.” Maybe he does. Maybe he does. But the odds are just looking at the two camps, if you will, I would go more with a metabolic cause. He has migrainous headaches. I’m not gonna call them a migraine, necessarily, but they’re migrainous. They begin behind the ear, move over his ear to his temple, and then cover his forehead bilateral. He can become very light sensitive and sound sensitive during the episodes. The pain is pulsatile, so it hints, sounds like a migraine, and the aura he gets his pain behind the ear. Now that is an autonomic phenomenon, right? Whatever’s triggering it, it’s certainly an autonomic phenomenon ’cause migraines are basically like mini, mini, mini, mini strokes. That’s basically what they are. They’re a lack of blood flow to parts of the brain. Now he has brain fog. Now check it out how he describes brain fog. He says brain fog is pressure in his head, which sounds very autonomic, and a pushing feeling, and sometimes he becomes lightheaded. That all sounds very autonomic to me, right? ‘Cause we all realize that the brain is not pain sensitive. You can poke the white matter. You’re not gonna feel anything. but all of those blood vessels on the brain, those are all innervated. And so when someone says they have pressure in the head and a pushing feeling, they’re describing some autonomic phenomenon. It’s almost like a headache, like this migrainous thing. Now his mom says he has trouble concentrating and zones out and seems to just not be processing. Well, I can tell you if you’re not getting blood to your head, you’re gonna zone out, you are. I can speak from personal experience. I had a heart problem years ago, and when you don’t get blood to your head for whatever reason, you’re not worth much. You can’t do much. You can’t process. You stare off into space. He also has a loss of balance all the time. He tends to bump into things on the right side. Well, that certainly piques a lot of our interest, right? It’s like, “Well, what do you mean? Is this a cerebellar problem? Is it a muscle tone problem on the right side? Is it a parietal lobe problem where he can’t appreciate the right side of space?” Lot of possibilities there. And he has problems sleeping, okay? Just sometimes, that’s problem going to sleep. Sometimes he has problems staying asleep. But his big things are the brain fog, which is this autonomic phenomenon, headaches, which is another autonomic phenomenon, fatigue, that muscle fatigue, and that joint pain. All right. Now he also has numbness in his hands as well as tingling, and it gets twitching of the left upper eyelid. That could be a catecholamine issue. It could be an electrolyte disturbance. Could be he’s got some kind of a neurovascular compromise in his arm, up here in his costoclavicular space. A lot of stuff could be possible. So if we think about what is on the radar for this kid, well, I said there maybe is a parietal lobe problem. Maybe he has some sort of metabolic issue ’cause I’m curious when someone has generalized muscle fatigue and generalized joint pain. I’m thinking very metabolic. Maybe he has dysautonomia. Well, he certainly does. He’s got some autonomic presentations. Let’s see what the history. So that’s where we start, right? We start with, okay, what is this guy’s complaints? What is that telling me is in the mix, right? What does that telling me is on the chess board? Now let’s look at the history and see if there’s anything else that helps put things into more focus for us. So all of this seemed to start around, I guess it was about a year before I saw him at first. It started about March. He started feeling bad, but he didn’t tell his mom till about two months later, right? Typical boy, typical kid. Now they did some blood tests that were done that were quote unquote “normal,” but it certainly wasn’t a lot of tests. It’s like a CBC, right? It’s a CBC and a comp metabolic, and that’s cool, but not everything is gonna get screened out by a CBC and a comp metabolic, it’s just not. So a lot of times, people will tell you, “Oh, I had full blood work done.” Well, what does that mean? Usually it means I had a CBC done and a lipid panel. It usually means I didn’t have my thyroid checked. I didn’t have vitamin D check. I didn’t have B12. They didn’t have a lot of stuff that we wanna look at. So you always wanna have them submit labs that they’ve done, right? Look at ’em because the more historical sense you have of that person, I’ll just tell ya. A lot of times when someone’s had a chronic problem and they come see me and they send me labs that they’ve had done for the last couple of years, the answer is right there, usually. The answer is right there. It’s just that either A, no one saw it or B, they saw it and didn’t say anything about it ’cause they didn’t know what to do for it. Now, this kid was referred to a neurologist who gave him Nortriptylene, started at 25 milligrams, went up to 50. Initially, it seemed to help but then seemed to ’cause problems with the eye twitching and sleep, so he’s no longer taking that. Now, so what that tells you is the doctor he saw said, “I don’t see any reason why you should feel like this. I’m gonna put you on an antidepressant,” right? Well, it seemed to help a little bit, but it seemed to aggravate some other things, so he stopped taking it. He was diagnosed by somebody else with a vestibular migraine, and that’s a reasonable diagnosis. You’ve certainly got migraine symptoms, and he’s got some vestibular symptoms. The question is, and I’m not gonna get into how to diagnose vestibular migraine. That’s what you’ll see a lot though. What you’re gonna see is someone has migraine or headaches and vestibular symptoms. They just mashed the two together and say, “You’ve got vestibular migraine,” when, really, vestibular migraine is much more episodic and sporadic, and the vestibular symptoms happen at, it’s just not because you have a headache and vestibular symptoms do you now have the condition vestibular migraine. I hope that makes sense. So I’m not a huge fan of that diagnosis because a lot of people get diagnosed with it I don’t think really have it. I think there certainly is a syndrome where people get a migrainous event that affects the brainstem and affects the vestibular nuclei but not because if you just have a headache and you have vestibular symptoms, that doesn’t mean you’ve got vestibular migraine. Anyway, they did a sleep study, which was normal, but that was while he was taking Nortriptyline. He’s supposed to have another sleep study, but, due to coronavirus, he’s not able to do that, all right? So he was only taking a multivitamin, nothing weird or anything I need to worry about. His mom has Hashimoto’s. Oh, there we go. We’re interested already. Now our ears are perked up. Now the reason our ears are perked up is on the list of priorities I’m gonna give you, the number one thing I’m most interested in is whether this person has a clinically significant autoimmune problem. And the fact that his mom has Hashimoto’s really ups the odds that this kid has got something autoimmune. That’s just the way that it works. It doesn’t mean that he for sure does, but I’m really, really suspicious about it. His parents have a really bad relationship, and he has a lot of significant stress about that, and he also describes having left arm weakness in addition to the generalized muscle fatigue, lightheadedness, which we’ve already hit on, twitching in the hands and eyes, which I mentioned a minute ago, dry mouth, dry eyes, okay, which can be an autonomic phenomenon, or could be a sequelae of a rheumatological condition called Sjögren’s syndrome, which is autoimmune. It’s a variant of rheumatoid arthritis. This kid’s got joint pain, dry eyes, dry mouth. I’m super, super curious and suspicious about him having a Sjögren’s disease. And he feels cold all over his entire body, which is a sign of a generalized dysautonomia. He also has some memory loss, which really means sometimes he can’t remember things. He has a loss of coordination. He bruises easily. Now let me just tell you, when someone says they bruise easily, you’re suspicious of iron deficiency. That’s what you’re suspicious about. He also has sensitivity to some odors, perfume and smoke. All right, so that dry mouth, dry eyes thing, that could be a sign of a mixed connective tissue disease, okay? Especially that combined with the joint pain, okay? With the joint pain plus that, I’m real interested in that. The bruising easily could be low iron, okay? These are the things you’re gonna learn. When you learn how to do this stuff, these are the things that you have in your little your decoder ring, your little X-ray glasses that give you things to point at. So if you review as a system, he’s got low stomach acid symptoms, insulin resistance symptoms, low thyroid symptoms. Now what is low stomach acid symptoms? Well, belching, burping, bloating within about 45 minutes of eating. That’s a pretty good sign you don’t make enough stomach acid. The food seems to really sit heavy in your stomach like a rock. That’s a pretty good sign you don’t have enough stomach acid. If you have a sense of fullness after meals, that’s not as specific. A lot of people feel full after they eat. But somebody has a small salad and they feel really full, that could be because they have low stomach acid. So what are insulin resistance symptoms? These are all things you’re gonna have to memorize these. You have to know these. If you get sleepy, tired, drowsy about 15 to 30 minutes after eating, that’s a pretty good sign of insulin resistance meaning the glucose that you’re making from that meal is not getting into your tissues. It’s hanging out in your blood, and that stimulates a process called lipogenesis, which consumes a lot of your ATP. So basically, when someone gets sleepy, tired, drowsy 15 to 30 minutes after eating, you can pretty much guarantee they’re putting on fat, okay? Now what are some symptoms of low thyroid function? Well, there’s some classic symptoms, but these are also not super specific. He’s tired and sluggish, feels cold in the hands, feet, or all over, requires excessive amounts of sleep to function properly. Now you’ve gotta be careful, right? Because these symptoms, these thyroid symptoms, these are not that specific, and they overlap with a lot of things. It’s just like saying if you go online and say, “Lyme disease symptoms,” you’re gonna find something that you’ve got, you know what I mean? So you just gotta be careful about saying, “Oh, well these symptoms here, these mean you’ve got thyroid.” Well, not really, and those couple other things. So the low stomach acid things, those are pretty specific for low stomach acid. The insulin resistance, that’s pretty specific for insulin resistance. These, not so much, not as specific. They’re still valuable but not as much. So we did some blood work, and I can’t remember if I did this or if somebody else did it. But his vitamin D is 26. That’s lab low, right? That is below the reference range. That is not good, and here’s why. Vitamin D if you had to say anything about it, it’s anti-inflammatory, okay? It also has some impacts on serotonin chemistry and dopamine chemistry, so there’s a lot of things that vitamin D does. But if you were gonna say one thing about it, you could say it was anti-inflammatory. His ferritin is 70 which is not really where it ought to be. It really should be a little bit higher than that if he’s a guy. He’s 15, I realize, but really closer to 100 would make me happier with him. I guess that was the labs that somebody else did. So what’s our impression? Well, what could be going on with this kid? Well, he could have an autoimmune problem. I can guarantee you that, just looking at those symptoms, that history, he could certainly have an autoimmune problem. We’re gonna have to figure out if he does. Could he have dysautonomia? Sure, he does. He has dysautonomia. Could he have a cerebellar problem? Well, it sounds based on his symptoms, he certainly does. Does he have migraine? Yeah, he do, he’s got some migraine stuff. So where do we start? Now, here’s the thing. We have a lot different places we could start with this kid, right? We could start with metabolic, receptor-based rehab, I could adjust ’em, I could do whatever, crystals. I could do whatever I wanted to do with them, right? But whatever you do, you better have a standard in place that you adhere to that you can say, “Okay, I’m gonna do this intervention, this treatment, and I’m gonna give myself this amount of time to find out if it’s working or not. And if it’s not working, I gotta do something different.” I don’t have to just abandon everything, but I have to have a standard, right? Which is, you’re gonna find a lot of people that do this stuff in practice, they don’t have a standard, right? They just do the thing where the people, person comes in, they do some tests, they give them supplements, and then they just take the supplements forever. They don’t ever follow up. They never find out, “Hey, how are you doing? How is that brain fog? How is that generalized fatigue?” Which is why you find somebody a year later, they’re still taking the same supplement protocol they started a year ago, and they’re not any better. So with this kid, because of all the metabolic things I just told you about, I’m definitely starting with metabolic with this kid because I think there’s a high, high likelihood, and plus, this is right in the middle of coronavirus, right? So I can’t really do some of the in-person physical stuff I might wanna do yet, yet, okay? This kid is still a candidate for receptor-based rehab and joint manipulation. I just don’t know if I can do it yet, but I may need to do it. So what are these priorities? Let’s go through these. So number four of these neurochemical priorities is GI and liver function, why? ‘Cause the GI tract is a huge source of inflammation. If you don’t absorb things, you’re gonna have a problem. You have a malabsorption syndrome. So the GI tract is always something we wanna look at. Liver function, liver does protein synthesis, it does biotransformation. There’s a lot of things the liver does, and it is very, very important for us. He does have a little GI stuff, right? He’s got the little stomach acid thing going on. What about number three? Well, number three is cellular energy, and it’s this part of cellular energy is looking at HPA axis and glucose handling, why? Because every cell’s gotta have fuel, and every cell’s, every neuron’s gotta have fuel and activation, irrespective of your muscle cells. They’ve all gotta have fuel. Does he have a problem with that? He might have an issue with that. That’s why I put a yellow one there. He may have. We don’t know for sure, but he could. Part two to cellular energy is looking at red blood cells ’cause look, if your red blood cells are too big or too small or you don’t have enough of ’em, you’re not gonna carry oxygen to tissues, okay? We also need to look at nutrients that are specific for making ATP. Those are the big ones like B12 and folic acid and iron. We have to look at that, and we wanna think about mitochondrial function as well. So does he have any of that? I don’t know. We haven’t checked. There’s nothing that’s saying in his history that, oh, this kid’s got a B12 problem. You’re gonna have to actually test him to find that out. And then number one, which I alluded to earlier, is does he have a clinically significant auto-immune problem? Now his mom has Hashimoto’s. He’s got some rheumatological type symptoms. I’m really suspicious about that, right? So as I’ll talk about in a second, how are we gonna answer these questions? How are we gonna figure these things out? Well, we’ve gotta do the right kind of testing. So what tests are appropriate in general? Well, as I’ve said this a million times, what tests you choose depends on what are you gonna get out of that test, right? Do I need to run a metals test on this kid? No, I don’t think so. Could I run a metals test? Sure, I could do that. Why not? But I don’t really feel a clinical impetus to do that in this case. I don’t see anything that’s telling me, “Oh, I’ve got a metals problem.” Now somebody else on here watch this may go, “Oh my gosh, this kid’s got mercury symptoms!” Okay, cool. You go ahead and do it. That’s fine. You do it, right? Don’t just cast this huge trawler net at every test you can think of, hoping you’ll find something that’s wrong that you can then give them a supplement for it and it’ll work; don’t do that. Now, logistically what I mean by that is how long are you gonna have to wait to get the test results? How big of a pain in the butt is it to do the test? And then, of course, the patient’s budget. You could spend all the patient’s budget. And if you’re not thinking that your patient has got an amount of money they think they are able to spend, they don’t have a dollar amount in mind, you’re fooling yourself. Nobody comes in with just an open-ended wallet and says, “Whatever!” There’s always a limit, okay? And you should respect that. You definitely should respect that, and don’t spend more of their money than you have to ’cause I’d rather them spend their money on treatment than diagnostics if I can do that. So let’s look at this guy again. Here’s all this stuff, right? So that migrainous stuff, what is associated with that? Well, we know it’s dysautonomia. Inflammation can trigger that. Hormones are associated with migraines, especially, well, what I mean is not as much as in women. So a woman with migrainous headaches, there very well could be a hormonal influence. In guys, not quite as much. The brain fog, that could be migrainous. That could be hypotensive. That could be from an anemia or a problem with glucose regulation, a problem with catecholamine release, right? And remember his mom says he has that problem processing. That could be just poor, poor blood flow. He’s got all this cerebral dysautonomia. He has a loss of balance. That could be cerebellum vestibular cortical. So what testing would we do, okay? I’m gonna tell you what I did. I’m gonna do blood work. I’m gonna do a comp metabolic, a CBC, LDH, which is lactate dehydrogenase, lipid panel, full thyroid panel plus antibodies, ’cause guess what? His mom has Hashimoto’s. He could have it, too. Look at vitamin D, B12, folate, iron, homocysteine. Am I gonna do adrenal testing? No. I’m not doing urine testing. I’m not doing saliva testing. There’s just no need to really do adrenal testing. Now I’ve done billions of them, I feel like, and what I can tell you is that usually what the patient’s telling you is enough of an adrenal test. You don’t really have to go through all the rigmarole of testing them. You can. You’re not hurting anybody, but you probably don’t need to. Stool testing? No, there’s no indication this kid has any. He doesn’t have diarrhea, he doesn’t have significant bloating. There’s no other GI symptoms besides that, maybe a little bit of stomach acid, so I’m not gonna do any stool testing. I could do a breath test for H. pylori. I could do that. That might make a little sense. An immune system challenge. Well, I’m probably gonna do that in this kid because I need to find out, as I have done other cases, is his immune system really at play in this? I told you, I’m real suspicious about it, right? But how are we gonna find out if his immune system really is involved with it? Well, I’ll tell ya. So let’s go over this, the blood labs first. So the blood labs we did showed a BUN of 13, protein, 6.7, which is a little bit low, globulin, which is a little bit low. You put all three of those together, that supports the idea of a hypochlorhydria or low stomach acid ’cause anytime your BUN is on the low end and your protein and globulin are either low or highish, it could be a protein malabsorption. The reason you’d have a protein malabsorption, most likely, is not making enough stomach acid. Now, if that were the case, why is he not making enough stomach acid, right? Why would he not make enough stomach acid? Those are the questions we have to ask ourselves. We can’t just go, “Oh, well, we’re just gonna give him stomach acid in a capsule, and that’s great.” Well, we probably do wanna do that, but we’re not really getting to the root of why would his stomach acid be low in the first place. Could be he has poor vagal output, right? ‘Cause the vagus output is what’s gonna give you those signals to get that stomach acid flowing anyway. All right, his LDH. His LDH is 139. My cutoff for that is 140, meaning if it’s lower than that, what you’re probably dealing with is someone who’s having trouble getting glucose into tissues or they’re not eating, one of the two. So LDH, lactate dehydrogenase, is a surrogate marker for how much glucose you’re getting into tissues because there’s a difference between what’s in your blood and what you get out of your blood into your tissues. So we can use fasting glucose and hemoglobin A1C to tell us about blood glucose levels, but LDH has a way to tell us about tissue glucose levels. And his is definitely a little bit lower than I would it to be. That could explain some of his problems, maybe not everything. But his ferritin and iron saturation were normal, okay? So I don’t think he has iron deficiency, right? Remember I said earlier they did some labs a few months ago, so I wasn’t too cool with that, but they’re normal. So I’m not worried about that. His cholesterol’s 127. That’s okay. His D is now 36. That’s a little bit better, but I’m telling you, if this kid’s got an autoimmune problem, it needs to be higher than that. It needs to be in the 70s or 80s. His white blood cell count was 3.6. That’s too low, okay? I don’t know why I did it like that, but his white blood cell count is 3.6. That is almost lab low, and it’s below five. My cutoff for a good white blood cell count is five, and I’ll just tell you that if your white blood cell count is less than five, there’s some possibilities here. One is is that he could have a chronic autoimmune problem, and the reason his white blood cell count is low is because his cytokine levels are suppressing his bone marrow function, and that’s why his white blood cell counts a little bit low. It could be something else. I’ll talk about it in a second. Now his MCV is 97, which is right on the edge of being high. There’s only a couple of things that can cause that, really, and it’s either a lack of B12 or a lack of folic acid. That’s pretty much what you can hang your hat on. Now his neutrophil percent was 36, which is definitely lower than we’d like to see it. We like to see that around 60. His neutrophil absolutes where lab low. Okay, so if we go back up here, I’m gonna use my little cursor, right? So his white blood cell count total is 3.6, which is almost low. His neutrophil absolute are lab low. His neutrophil percent is pretty low. What could be causing that? There’s really only two things, big things. One is he’s got an autoimmune problem, and he’s had it for awhile and it’s messing with his bone marrow, or number two, he has our terrible, good old friends, mycotoxins, ’cause one things I can tell you about is mycotoxins love to lower your white blood cell count and love to lower your neutrophil count. Now I’ll tell you more about that in just a second. We just did a case recently about a guy who definitely had mycotoxins. So what have we got here? In looking at our priorities, ’cause we’re not gonna get lost, we’re going back to our priority list, does he have GI or liver malfunction? Well, his liver enzymes, all that junk was good, but he does still have this little protein malabsorption thing, okay? What about looking at cellular energy in terms of HPA axis and glucose handling? Well, we go back to our LDH. That could be indicative of that ’cause when people have LDH levels that are not very good, it usually means they’re not transporting glucose. That can happen for some different nutrient reasons, or it can happen because they’re just not making enough cortisol throughout the day to get stored glucose out of storage and into the system. I don’t wanna beat that up, excuse me, too bad. I don’t know why that went away. Number two, looking at the RBCs and nutrients. Well, his red blood cells were a little bit big, right? I’m not sure why I didn’t. So look, he definitely has a borderline issue with those RBCs, but his B12 and folic acid weren’t a problem, otherwise I would’ve told you. His iron was okay, so maybe he doesn’t have an issue with that. Now our big one is how do we know if he has clinically significant autoimmunity? How do we know if he has that? Well, there’s a couple ways we can try to figure that out. So how do you figure out if someone has a clinically significant autoimmune problem? Well, you can do antibody testing and try to figure out specific antibodies. I can do SSA and SSB antibodies for this kid and see if he has Sjögren’s or I could test, my God. There’s a hundred different antibodies I could test for him, and that certainly has value because it helps you be specific. But also when you do this kind of work, a lot of times, all you need to know is does the kid have any autoimmune problem, right? Just generically because, from a treatment standpoint and a management standpoint, all those different autoimmune problems, they get different names, but biochemically, they’re all very similar in what you can do to treat them, all right? So you can do antibody testing. It’s specific but expensive. It’s certainly not encyclopedic, so don’t fool yourself thinking if you do a Cyrex Array five and everything comes back normal that that patient doesn’t have any autoimmune problems. That is not what that means We can do this thing called a clinical challenge. It’s cheap, 20 bucks, 25 bucks. It’s not specific, meaning it doesn’t tell you the name of the condition, doesn’t tell you the antibodies, but it will tell you whether the person’s immune system has something to do with what they came to you for, okay? Now basically what we do, and I’m keeping this really simple, don’t think you know how to do it by just looking at this, we give them T helper 1 cytokine stimulators and see how they feel, and then we give ’em some T helper 2 cytokine stimulators and see how do they feel. And what we’re really looking for is does one or both of those things make him feel temporarily worse? So as you can imagine, you can’t just do this on anybody. You gotta do this on someone that, number one, knows what you’re expecting. We’ve gotta have full disclosure. Number two, you gotta think they could be able to handle it, and number three, you would absolutely never do that on someone that you thought had a demyelinating condition or someone that already was diagnosed with a demyelinating condition. Years ago, I had a guy take a class for me. I’ll tell you this story, and he had emailed me. God, this is like 10 years ago. He emailed me saying, “Hey, I have this patient who has been diagnosed with chronic inflammatory demyelinating polyneuropathy. Should I do this challenge with her?” “No, absolutely not. Do not do this. It’s a terrible idea. Don’t do it.” Well, guess what he did? He did it anyway, and he gave the woman permanent foot drop.
– Right? So this is not some fluffy thing. You can really have some severe effects, which is why you don’t do it right now ’cause you don’t know how to do it. I’m just showing you how I do it so that I can explain how I figure out if the immune system’s involved or not. So here’s the results of this kid’s clinical challenge. He felt bad after adjusting both T helper 1 and TH 2 cytokines stimulators. So no question to me, this kid’s joint pain and fatigue and everything else was worse after taking those. So guess what? His immune system is involved, and we’re gonna go after that, okay? Because you shouldn’t have any response to this stuff. Now can I say definitively, “Oh, he definitely has an autoimmune problem”? No, I can’t chart it that ’cause that’s not what that means cause medical legal, you gotta have antibodies, right? But I can tell you from a practical standpoint, this kid’s immune system is definitely involved, and it’s likely that he has some kind clinically significant autoimmunity, okay? So probable autoimmunity. Okay, what do the diagnostics tell us? Okay, this kid’s got probable autoimmunity, probable low HPA tone, poor glucose transport, possible probable hypochlorhydria, definitely has non-optimal vitamin D, some kind of chronic immune system challenge, which has probably that autoimmune issue, right? Or it could be mycotoxin illness. And how do we know if he has mycotoxins? Well, we do mycotoxin testing. We can do RealTime labs, Great Plains labs. A lot of people do mycotoxin testing. You can just do the test and find out if he’s got ’em or not. But I’m not gonna do ’em yet on this kid, right? I’m not gonna do ’em yet because it’s more likely that it’s this immune system stuff that’s causing his low white blood cell count and low neutrophils. So what are we gonna do for him? Well, what do we do diet wise? Because if I know this kid has got a probable autoimmune problem, he definitely is gonna have to be gluten free, dairy free. Why? Because those are the two worst things you could eat if you have an autoimmune problem. Without going into the gluten and dairy battle royal, let me just tell you the short answer is those are pretty much the two worst things you could eat. There’s significant cross reactivity between gluten antibodies and human tissues. They’re very inflammatory, and they’re just super common. They’re super common inflammatory instigators. And we don’t want to inflame this kid, right? We wanna deinflame him. Now granted his cardiac C-reactive protein wasn’t elevated, and you might say, “Well, then he’s not inflamed.” No, that’s incorrect. Just because his C-reactive protein wasn’t elevated or erythrocyte sedimentation rate wasn’t elevated, that does not mean he’s not inflamed, okay? Those are some markers. Those are all the markers. And plus, when I shake his immune system up, he feels bad. So I’m really confident that his immune system is involved, and I’m probably gonna get good results going after his immune system trying to regulate it and calm it down, all right? So there’s a really restrictive diet I could have him do, but he’s 15 and he’s probably not gonna do it. But I can probably at least get him to do this, right? Especially if it feels better. All right, what are we giving him? Well to deal with his immune system, I’m gonna give him some turmeric, some resveratrol, some sublingual vitamin D, and I go through the reasons for these in the class, but I’m just telling him giving him an adaptogen formula to try to deal with this HPA issue. I’m gonna give him a multi-nutrient formula for glucose regulation that’s got some specific vitamins and minerals and glandulars that help with that glucose transport and help with, we think, helps with cortisol production. And I’m gonna give him some mega three fatty acids. I’m gonna give him heavy EPA ’cause when I hear omega-3s, you basically got EPA and DHA, the ones that come from fish oil, and EPA is the one we want for this kid. We’re not concerned about DHA. EPA is the more relevant anti-inflammatory of those two. Now is DHA anti-inflammatory? Sure, but I wanna go with the EPA, all right? Now the amounts of all this stuff we don’t have time to go into at the moment ’cause I don’t want you guys trying to make robot your little protocol ’cause we’re not, I’m telling you physiologically, the turmeric and resveratrol downregulate NF-kappa-B and some other inflammatory pathways. We already talked about how vitamin D was anti-inflammatory. All right, so we did that. I did that with him. So 30 days later, let’s see what happens, okay? His mother says that he’s doing wonderful. He has tons of energy. He’s having a few days here and there where he feels a little bit worse, but she says she would conservatively rate him at 75 to 80% improved, okay? Sweet! Great. We were expecting that he would do pretty well with an anti-inflammatory approach. The muscle fatigue, the headaches, the brain fog, the balance, the sleep, they’re all improving. So all of that, all of that is improving significantly. So there’s a good chance that the the linchpin for most of that junk he was having was inflammatory, right? Can inflammation cause dysautonomia? Sure, absolutely. It sure can. Can dysautonomia be inflammatory? Yeah, it absolutely can. Sure. So will we know exactly what happened? Well, no, but here’s the thing. I’m also not gonna go take out a billboard and say, “Look how great I am because this kid is better after 30 days.” He’s got to stay better, right? He’s got to stay better. I’ve gotta be able to take them off some of these supplements I’m giving him and him stay better before I really start to congratulate myself and think I’ve done a pretty good job. So what’s our plan now? It’s been 30 days. What now? Well, I’m gonna have them take the same protocol for a little bit longer, but in 30 days from now, I’m gonna recheck his LDH, his D, his comp metabolic, and his CBC, and we’re gonna see if we’re making some biochemical changes ’cause I’m really interested if that white blood cell count is normalizing and if that neutrophil count is normalizing, okay? Yeah, what if the CBC is now normalized? Well, it means that that white blood cell count and that neutrophil count were low because of his immune system. If they’re not normalized, I’m gonna run a mycotoxin test and see if he’s got mycotoxins. See how we did that, right? We know what physiologically could cause the finding. We pick a treatment. We recheck the finding. It’s test, treat, and retest, right? And if it goes one way, we know what to do. If it goes another way, we know what to do, right? That’s what most people won’t teach you. Unfortunately, don’t teach you that. So what about 30 days after that, the 30 days, so 60 days now into treatment? His mom emailed and reports that this kid was complaining of some heart palpitations. Oh shit, right? Oh my God, what happened, right? Sorry for the curse word, but oh my God! You get this sinking feeling. Oh my God, did I do something wrong? But guess what? He went to a pool party, and he ate a bunch of foods containing gluten and dairy, right? Had some pizza and some ice cream, all this stuff he knows he’s not supposed to have, and he did badly with it. I’m sad that it happened to him and also glad that it happened to him because some people have gotta go down in the basement and get grinded up in the pain grinder a couple times before they go, “Oh, I probably shouldn’t eat that stuff.” So he felt very bad the next day, and the palpitations coincided with that. A week later, she reports the palpitations are gone, which is good. So we had a flare up. He stopped eating the gluten and dairy things. Things subsided. He’s been working. Now he can work. This kid’s out working physically now where he used to just be tired all the time, and his muscles just felt fatigued and weak. He’s exercising. This is what we want, right? We want this kid doing this. Occasionally he feels tired, but that just might be normal, considering the amount of physical activity that kid has. He has an occasional headache. Now one of the things I probably could’ve done was given you guys how often he was having the migraines and compared that, but I just didn’t put that in there as a marker. She says he’s doing great, which cool, awesome. Now those labs that we recheck, here’s what those showed. His white blood cell count was 4.9. It used to be 3.6. That’s good. That’s a point and a half, basically, and that’s a pretty big jump on that scale. That’s probably just not fluctuation, right? That’s probably just not chance. His MCV is 100. Well, I don’t like that, though. That gone up, so we’ve got something going on there with either B12 or folate. His neutrophil percent was 36, went to 51. That’s cool. The absolute neutrophils are now normal. They went up a full point, okay? That’s good. His LDH, nope. That ain’t changing much. Now here’s the thing. I picked the LDH as my marker, but it could be that the LDH has nothing to do with anything, you know what I mean? I don’t wanna treat the test, you know what I’m saying? There’s gotta be something that gives me a reason to make that an issue, right? You gotta be careful with that when you do this stuff because you’ll get into your mind that if the patient has this lab finding, it means it’s a problem, and I have to treat it. Not necessarily. His BUN, 13 previously that, protein the same, globulin, basically the same. We didn’t really give him anything for that, but that’s unchanged. 204 is vitamin D. Little high, a little high. So we’re gonna back him off of that. We’re gonna say, “Don’t take any vitamin D for a few weeks, and then we’ll resume at 2,000 IUs per day and we’ll see.” So obviously absorbing the crap out of the vitamin D. Now that’s also assuming he was taking it the way he was supposed to. Sometimes I give ’em these sublingual ones that are drops, and sometimes people, they just don’t measure it. They just go and just squirt it in your mouth. I’m like, “Don’t do that. You can OD on it.” So I told him, “Hey, don’t take it for two weeks, and we’ll resume at 2,000 IUs per day.” And of course I gave you the brand name of what I use, but you can use whatever. But his ionized calcium was normal. So even though his vitamin D was that high, the only real thing you have to worry about is this calcium becoming high, but it wasn’t, so that’s cool. So what’s our treatment plan? It’s the same stuff! Stay on the diet, my dude, because you probably have an autoimmune problem and you probably need to stay on that diet forever. No 15 year old wants to hear that, but the thing is, every time he deviates off it, I can almost guarantee he’s gonna have some bad consequence. And so I just have to tell him the truth, right? It’s up to him to believe me and follow and experience for himself because you can talk to someone and tell ’em something, but sometimes they need to experience it to educate themselves. So I’m giving the same stuff. Now at some point, I’m gonna pull him off of these things and start pulling some things down and find out does he really still need the turmeric? Does he really still need the resveratrol? ‘Cause that’s what I tell patients every time. And guess what? Sirens, Freddys. Every time we record something, the freaking siren comes by, and Freddy’s just like, “Why is there always sirens coming by?” Well, because it’s a major road. And there we go.
– I actually call ’em in for my own amusement, so.
– You’re, what are you calling, you’re 911ing me or whatever, SWATing me, right.
– Yeah, that’s right.
– All right. So his CBC normalized. Well, that means that it was probably the chronic immune system challenge doing that, not microtoxin, but I’m gonna retest his CBC in 30 days anyway to make sure they stay that way, okay? Now the funny thing is I did just get that kid’s labs. I’m talking to him next week. I didn’t have time to incorporate it into this. So you probably don’t want me to do a whole ‘nother thing on it, but anyway, we’re still following up. So with that kid, here’s the thing. Am I done with him? No. I need him to be doing really well for five, six, seven months, doing all the things, all the activities of daily living he’s doing. I want him to do all that, and then I want him to be able to do all that with minimal intervention, right? So that turmeric, the resveratrol, at some point I’m gonna take him off of that because it’d be great if he doesn’t have to take that. Number one, it’s less money to spend. The patients care about that. And number two, if he doesn’t need it, then he doesn’t need it, right? If he does not need that level of support to function, well, then he doesn’t need that level of support. So I always tell patients, “At some point, whatever I’m telling you to take, I’m gonna tell you to stop taking it. I just don’t think you should take something forever unless you got pretty good reason.” Now the vitamin D he could probably need to take that forever because if he doesn’t take it to some degree, he’ll probably become vitamin D deficient because that’s what happens almost all the time if you have some kind of autoimmune problem. But the adaptogens, all that stuff is fair game to get rid of, all that stuff is fair game. We’re just not to that place with him yet, okay? So what are my takeaways that I want you to know? Well, you gotta know the physiology. You gotta own the physiology so you know how to be efficient and not waste a bunch of time. You wanna do testing that makes sense based on that case. I could’ve done mycotoxin testing right out of the bat. I could have done that, but I said, “You know what? Let’s just wait ’cause based on what I’m thinking about this, if the CBC normalizes, I’m gonna have to do that, right?” And that’s what happened. Use those four priorities to prioritize, and always think of what’s next. I forget a couple of things hadn’t changed, right? The LDH hadn’t changed, and the MCV had gone up a little bit. Well, I’m not done with that because his MCV does not need to be that high, and his LDH would be theoretically better if it was better than that. But that’s what I’m thinking about next with this kid. But here’s the thing. If he’s feeling great and doing great, I’m not gonna over treat him, right? I’m not gonna over treat him. But the thing is I have longterm relationships with all these people, right? So they know it’s not just like a 30 days and you’re done. It’s not a little honeymoon. I am your doctor, right? So this is a longer term thing for us to work on. Anyway, so you gotta know those priorities. You gotta know what things, what tools are gonna do what you want ’em to do. Integrate brain-based treatment when appropriate and indicated. This kid’s just not ready for that yet. I don’t even know if he needs it yet, but it’s still on the table because I may look at him once the quarantine thing gets over with and I can actually see patients in the office. I can look at him and really assess, “Okay, what’s that cerebellum function like?” Do we need to do some rehab intervention to really get that where we want? You guys understand all that stuff. You know the longitudinal level of the legion you learn in neuroscience. You gotta learn the same thing here. You gotta be able to determine, look, is this thing this kid has, is this neurological? Is it a circuit problem, or is it a metabolic problem primarily, right? And you have to know what the symptoms are telling you about that, and you gotta know how to treat effectively and efficiently. All right, now you wanna go to the next one?
– Yeah, Dr. Clark, let’s jump right into it.
– All right. Case two. Again, we’ve got someone with brain fog, poor memory, and mood swings. So again, I’m gonna skip the goals. You guys understand those. Just save us a little bit of time here ’cause that last one was good, but it takes a little time to go through these things. All right, so we’re not gonna be robots. Everybody understands that. All right, so she’s got brain fog. What does it mean in this case? Well, she feels as if her brain is dead. That’s what she says. Her brain is dead. And really what she’s saying is it’s hard to recall words. She has poor short-term memory for what she did that morning or even the day before. It takes her a long time to say, “Hey, what’d you have for breakfast yesterday?” She’d be like, “Uh.” That’s too long. So for her, for this patient, brain fog is not a pressure in the head or a pushing. For her, brain fog is, “My memory sucks. I’m having trouble remembering words during sentences. I can’t remember what the hell I did yesterday morning for breakfast.”
– She doesn’t feel sharp.
– That doesn’t feel sharp, exactly. But specifically, she’s saying she has increased processing time and delayed reaction time. So interestingly, maybe her psy cogs look a little interesting, right? We could look and see if she has increased latencies. Who knows? She has mood swings. She feels sad but then happy, right? Now not like crying sad. She cries, and then she’ll feel happy the next day. It’s not situational depression ’cause I always ask, “Was there any reason why you would be sad? Has something happened?” You never know, man. Sometimes you hear stuff you don’t wanna hear, but sometimes you’ve gotta ask that question because maybe you’re not the best person for them, right? Over my career, I’ve had plenty of times find out about people being abused or assaulted or kids being assaulted, and you’re like, “Geez, man, I didn’t wanna hear that.” But at the same time, maybe they need to be seeing somebody else. And nothing traumatic that could have precipitated these mildly depressed feelings. She has some anxiety, too. She has some thinning hair on the top of her head anxiety. I’m not sure why I put anxiety there. I put anxiety too many times. She does actually have a little thinning of hair on the top of her head.
– That would give me anxiety.
– All right.
– You can tell it’s already done it for me. So I’m already through it. I’m just owning it. So what could it be? So if she can’t recall words, that could be a frontal temporal problem, could be some hippocampal things. The poor short-term memory is invoking those same sorts of areas. The processing time, delayed reaction time, that sounds like it could be frontal, could be cortical, could be basal ganglionic. The mood swings certainly sound they could be hormonal, but you can also have mood swings if you have limbic escape and limbic dysregulation that’s from a frontal gating mechanism, et cetera. Could she have dysautonomia? I don’t really see anything true. She could have just poor blood flow to her head, but there’s nothing classically dysautonomic about that necessarily. Let’s see what her history does for us. So in her second year of college, remember, she’s just 34, when she was 19, she developed pleurisy. Who gets pleurisy? Pleurisy’s this thing you read about that people in 1800s got. But anyway, she had pleurisy and then pneumonia. Then she noticed hair thinning, cystic acne, and brain fog. Hmm, could be that that pneumonia, which was a very inflammatory event ’cause it’s activating the immune system, that could have turned on a couple things. Now, one thing you guys gotta know is cytokines, those are immune system messengers, and they go everywhere, okay? They’re how your nervous system communicates with your endocrine system, right? That’s one of the ways that happens. So every neuron has cytokine receptors. Cytokines can stop ATP production. They can slow down hepatic biotransformation that can create blood-brain barrier compromise, gut barrier compromise. So anytime someone got sick and then a bunch of junk happened after that, you have to be very suspicious of that, okay? In her third year of college, she had pneumonia again and bronchitis, and she took steroids and Percocet. She was diagnosed at that point with my favorite, low adrenal function. Sure. What they’re really saying typically is, what they really mean physiologically is low HPA axis tone is usually what people really mean when they say low adrenal function ’cause the adrenal glands are not autonomous. They’re not pacemakers. They don’t just do whatever they want. They’re told what to do, right?
– So let me ask. So when we say low HPA tone, are we just meaning the reactivity
– of the physiology of that loop?
– Yeah, so it’s just a way of saying, “For some reason, that circuit is not responding the way that it should, right?” It’s either not recovering from hypoglycemia the way that it should, it’s not maybe sending signals to the adrenal glands to release DHEA, but you really gotta get away from this idea that there’s adrenal, like the gland is the problem. The gland is under control of super segmental things, right? So we gotta get away with that. Now it is theoretically possible for that adrenal gland to not be getting some of the raw materials and nutrients that it needs, but that’s not as common. She saw somebody who said, “I’m gonna do all the tests in the world, and guess what? You’ve got adrenal function, heavy metal problems, and high iron.” Now that’s what I’m interested in is the high iron ’cause let me just tell you. High iron is probably because someone did a ferritin test, and her ferritin was high, but here’s the thing. Ferritin is two things. Ferritin is both an iron marker and, oops, and an acute phase reactant, okay? So if you’ve got inflammation, ferritin levels can increase, and it has nothing to do with your iron levels at that point, okay? And she was put on Advair, which is an asthma medication. Now as an adult, she’s had problems with energy where she feels she could sleep all day. Energy. About five years ago, her anxiety was so severe that she had two different actual panic attacks. Currently, she’s taking B12, vitamin D, some omegas, probiotics, and Advil as needed. All right, cool, all right. What’s her family history? Oh, paternal grandmother with thyroid disease and also lung cancer. Now most of the time, thyroid disease is code for Hashimoto’s. If somebody says, “Well, my grandmother had a thyroid problem,” it’s probably Hashimoto’s ’cause it’s so common. It’s just odds are-
– What’s the percentage? It’s a crazy percentage.
– Oh yeah, like 90% of people with hypothyroidism have Hashimoto’s whether they’ve been tested or not yet. She had a paternal grandfather with Parkinson’s and dementia. I’m not really cool with that, considering her cognitive complaints about the memory stuff. Not necessarily connected, but we’re curious. She’s got a sister with anxiety, tachycardia, and an eating disorder, another sister with anxiety and depression. So now we’re wondering, “Okay, is there some sort of genetic heritable mechanism for this anxiety?” Are there some genetic snips or some other kinds of things? Oh, and she has a brother with Hashimoto’s. The brother’s also had Epstein-Barr, Lyme, and unfortunately had a TBI as well. That brother has had it bad, man. So we know she has a first degree relative with an autoimmune problem, a fully known autoimmune problem. So if you guys think about our four priorities that I teach you about, I am super interested now ’cause I’m like, “Okay. Clinically significant auto-immune is the number one thing,” because having an autoimmune problem can create so many downstream issues, okay? And just a father who has anxiety. So what’s your system review look like? Well, she has some symptoms of hypochlorhydria, some symptoms that could be from increased intestinal hyperpermeability, a few gallbladder symptoms, some low HPA axis tone, low and high thyroid symptoms, which are not very specific. They’re generic. She has heavy periods. That could be from low progesterone/high estrogen. So again, those low stomach acid symptoms, I gave you those in the last case. Intestinal permeability, increased intestinal permeability. So again, we gotta get away from the terminology of leaky gut. So let’s just get rid of that because your gut is leaky normally, physiologically normal for your gut to be leaky. What we’re really saying is hyper leaky gut or abnormal permeability. So just get away from the leaky gut thing. Just get away from that. So she feels like she has unpredictable food reactions, unpredictable abdominal swelling, frequent bloating and distension after meals. I gotta tell you something else. Those last three bullets could just be because she’s not making enough stomach acid, too. That could be what it is. Eating sugars and starches causes her abdominal symptoms. Gallbladder symptoms. This is a pretty good one. Stool color alternates from clay colored to brown, okay? Now that stomach acid, those little bullets there, those are pretty specific for stomach acid. The gallbladder symptom there, the stool changing color, that’s pretty specific. Eh, it’s not so specific for her to have whatever unpredictable food reactions mean, but getting bloating and distention after meals and getting unpredictable abdominal swelling, that starts making you think, “Well, we may have an increased permeability issue that is provoking an immune system reaction in the gut, and thus we’re getting those symptoms.” What is low HPA axis tone? Well, here’s your big clue. If she goes more than three or four hours without eating anything, she gets shaky, lightheaded, irritable, and symptomatic, okay? She’s getting that because her HPA axis is not helping her recover from hypoglycemia. And what it should be doing is releasing cortisol when necessary ’cause cortisol is pulsatile and there’s are the amount of it, but you also have to release it on demand. If it’s not gonna do that, then you can’t get glycogen out of storage, you can’t get your glucose levels back up, and you start to get flooded with catecholamines, and those catecholamines can make you all that stuff you see there. She depends on coffee to get going and stay going. That’s a generic indicator. If eating relieves your tiredness, that’s a pretty good sign your HPA axis is too low, okay? If you’re really fatigued but you eat and you feel like, “Oh, I’m so full of energy,” low HPA axis tone. Another one is a can’t stay asleep at night, and I’ll just briefly tell you the reason you probably can’t stay asleep at night if it’s caused by low HPA axis tone is because you’re having nocturnal hypoglycemia because, by the time-
– Because you get an uptick cortisol that gets some release some fuel?
– Well, what happens is they’re not releasing cortisol. So your cortisol levels are the lowest at night, but you still have to have ’em, and so your brain has gotta have glucose the entire night. And so to get that glucose, you still have to have some cortisol being released to get glycogen out of storage, ’cause look, you stopped eating at seven or 8:00 PM. Where’s the glucose coming from? Your brain’s still gotta have it. You’re supposed to get it from glycogen. But if your cortisol levels are not high enough, even though they’re supposed to be low, then you’re gonna make catecholamines, and the catacholamines, like adrenaline and noradrenaline, those are gonna get glucose out of storage, but it’s also gonna wake your butt up, all right? All right, low thyroid function. I went over these were the last case. Those aren’t super specific. High thyroid function, heart palpitations, being nervous and emotional, those aren’t super specific for hyperthyroid function. And having heavy menstrual periods, there’s certainly gotta be an issue with estrogen or progesterone. You can just bet there’s gotta be some kind of issue with that. So again, those are pretty specific. Those are not that specific, and heavy periods. You know there’s a problem with estrogen and progesterone. You don’t know which one it is, but there’s something going on with that. All right, so what’s our impression? What could be going on? Well, she could have a frontal lobe problem like we talked about, a temporal lobe, a hippocampal, hormonal problem. She could have some metabolic issue. But how do we start? We’ve got this huge forest of junk. How do we know where to start forging our way? Well, as I’ve said with every case, you have a couple options. You can do metabolic. You could do receptor-based rehab. You could adjust her. You could do gosh, anything. You could do muscle testing. No, don’t do that. You could do any of those kind of things. I’m starting with metabolic and neurochemical ’cause there’s another one of these quarantine cases. So again, from the last case, their priorities are GI and liver. She’s definitely got a little bit of that. HPA axis. Yep, she’s got that. What about RBCs and nutrients? Don’t know. We’re gonna have to test her for that. What about clinically significant autoimmunity? No, don’t know, but we’re suspicious about it, right? We’re super suspicious about it, not only because she got sick and then got a lot of other stuff that happened afterwards, but she’s got a brother with Hashimoto’s. So again, testing depends on yield and the logistics and the budget in not just casting a large net and hoping you find something that’s a red herring that you can treat ’cause you’re gonna find something that’s wrong. Trust me, you are, but it doesn’t mean that what you found has any relationship at all to their chief complaints. That’s just not guaranteed. So she has some fairly specific symptoms of GI. She’s got some pretty specific symptoms of low HPA tone. She got some hormonal symptoms. She has some vague thyroid symptoms, a family history of autoimmunity. What testing do we do? Well, yeah, I’m gonna do blood work because I can look at her red blood cells and the comp metabolic and glucose handling and glucose transport. I can look at her thyroid function and find out if she’s got Hashimoto’s with relative confidence. I can look at D and B12 and folate and find out is she absorbing that B12 she took? What about vitamin D and folate? I can look at her ferritin levels and find out if she’s iron deficient or if her ferritin’s still high and perhaps indicating a current inflammatory issue. I can look at homocysteine. I could do urinary organic acids with this patient, and now I haven’t talked to you guys about this before. So urinary organic acids is a test where it’s a urine sample, but it lets you look at several different compartments of physiology that you can’t really look at through blood. The main thing I was interested in her for this is because you can look at mitochondrial function pretty well through this test. You can look at mitochondrial Krebs cycle, intermediates and amino acid metabolites, and get a pretty good window into hey, is this person, mitochondrial speaking, making energy? And the reason I said that for her is ’cause she has fatigue all day. She’s so tired all the time, so I’m curious about it. Now I could run a urinary organic acids on everyone if I wanted to, but I don’t. I just wanted to do it on her. Hormone testing? Not yet because here’s the thing. Most hormone problems are usually secondary to one of those four priorities, typically. Adrenal testing? You know I’m not gonna order that because she’s already telling you, “I’ve got low HPA axis tone.” There’s no further value of doing some salivary cortisol test or, there’s no other value to that, in my opinion ’cause this is most likely what she has. Stool testing? Nah, no indication for that. Are we gonna do an immune system challenge? Probably am gonna do that because I wanna find out if her immune system is really involved in this, and she’s got her brother with Hashimoto’s. So let’s see what we do with the labs. So the blood work. Magnesium is a little bit lower than I’d it to be. I like it to be around two or so. Now look right there, magnesium being low. Well, that could have something to do with anxiety ’cause we think back to your module one stuff or wherever you’re at. In MDA receptors, they use magnesium ions as plugs in the calcium channel. And if you are low in magnesium, you can have a low occurrence of magnesium available, a low pool of magnesium available to be the plug in the MDA receptor, meaning those neurons can fire more often. That can manifest as anxiety, okay? That’s a possibility. Now magnesium also has a lot to do with carbohydrate metabolism and mitochondrial function, but I’m just giving you that. Albumin’s a little bit high. Albumin is one of those acute phase reactants as well. So her album being high, that could be an inflammatory marker. Her ferritin’s 46. Now that’s not high. It’s actually a little bit low. 50 is the borderline of where you want a woman who has a menstrual cycle to have her ferritin ’cause remember, ferritin is 22%, reflecting 22% of your body’s iron. And research says if you’re below 50, you’re probably gonna be tired, right? You’re probably gonna be tired. Now she could have a low ferritin because her periods are heavy. That’s the number one cause of low ferritin in cycling women is they got a heavy period. So her thyroid peroxidase antibodies were 15. That’s not zero. That’s middle of the range. Now her thyroglobulin antibodies were not out of range. Her vitamin D was 49. That’s okay. Her white blood cell count was four point, I can’t see it, but 4.5, I think; a little bit low. Her MCV 95. A little bit higher than I like it. Her folate, mid lane, I’ll call it. Her B12, okay. So what have we got from the blood work? Well, is there any GI liver stuff? The energy, the nutrients. Well, so here we go. There’s not a lot on there except for I think this ferritin might be a problem. I think the magnesium needs to be dealt with. The folate and B12 are okay. The D is not bad. So there’s not a lot on that blood work that’s screaming, “Here’s what to do,” right? There’s not a lot on that blood work that’s telling me what to do here on my four priorities. Thankfully I’ve got some other stuff I’m still doing though. So we are gonna do her urinary organic acids. What did that tell us? Well, I’m not gonna have time to go over all of this, but basically, the suberic was lab high, which is nonspecific. And here’s the thing. The urinary organic acid results basically say, “Hey, your mitochondrial function looks pretty good.” I’ll just tell you that. So I was doing it to look for that. There’s certain nutrients we could do the urine organic acid test. You can look at yeast and fungal markers with the organic acid test. Basically, there wasn’t a lot there. Now her paradoxic is a little bit low, which is your B6. Her ascorbic was definitely low, which is your vitamin C marker. So what does that tell us? Well, there’s not a lot on that. So out of our four priorities, there’s not a lot there except for that HPA tone that we talked about, maybe an iron problem, and that’s pretty much the strongest evidence so far. So how do we figure out if she has a clinically significant autoimmune problem? Like last time, I’m gonna do the immune system challenge with her. So here’s the results of her challenge. With the T helper 1 booster, she had a significant acute increase in bloating. Okay. With the TH 2 cytokine boosters, she had some headaches, but sometimes she gets headaches anyway, and she had little bit of bloating with that as well. So here’s the thing. Should she have bloating by taking some T helper 1 boosters? No she shouldn’t, okay? So I’m curious. I’m thinking I might wanna just go ahead and treat her she has an autoimmune problem and just see how she does ’cause that’s a valid way of finding out if she’s got one. So I could test her or I could treat her and make the treatment the test, right? There’s a Latin phrase for that called , and it means making an inference about the cause based on the response to the treatment, okay? So probable significant autoimmunity. She shouldn’t have any reaction at all to either one of them. All right, so she’s got all that stuff. What are we gonna do for her? Well, if I think she’s got an autoimmune issue, I’m gonna have to put on an anti-inflammatory diet. What I call there, that’s more restrictive than just gluten and dairy. I don’t do grains or nuts or seeds or eggs, but it’s also not a permanent diet, okay? You cannot do that diet permanently. It’s probably not healthy to do it that way. What about a supplement protocol? Well, I wanna get her D up to about 70 or 80, so we’re gonna do sublingual vitamin D. I’m gonna use some magnesium to correct that magnesium level; I’m gonna use some turmeric and resveratrol to help with the what I think is the probable auto-immunity; butyrate, which is a short-chain fatty acid, to help with GI tract integrity; so omega-3 fatty acids because those are anti-inflammatory; I’m gonna use an adaptogen formula because that HPA tone; and I’m gonna use a formula to help with glucose transport as well as giving her adrenal glands, theoretically, some stuff that they can use to continue to make cortisol. The thing is how does she do, all right? So we’re looking for changes in the brain fog and the word recall and the short-term memory. Three weeks in, she emailed saying that the first two weeks of the protocol, there were days she felt really good and other days not so much. All right, cool. No worries. The weekend immediately prior to emailing me, she had insane bloating and a lot of mood swings. She was waking in the middle of the night with anxiety. And again, you’re like, “Oh, right? What the heck?” But now it even out, right? So she had a little bump in the middle, but she’s doing much better. So you don’t freak out. You just gotta see what’s happening. She’s not having any headaches. That insane bloating that she was talking about is not happening. The mood swings are better. The first week of the protocol, she lost four to five pounds. That’s probably inflammation weight. And the brain fog, self-report, mind you, be the word recall and that stuff, she said that’s about 60 to 70% improved. For example, I always ask for examples. They say, “Well, I think that’s about 70% better.” Okay, well, give me an example of how that’s better. She says she’s reading a book, and she can recall what happened in the book whereas previously, like 30 days ago, she wouldn’t be able to remember what happened in the book the next day, okay? So she feels that is a concrete example of some good changes. So what’s our treatment plan? What now? Well, I’m gonna have her continue the same bit for about another 30 days. Ideally, I would think about reintroducing foods at this point because look, she had a really good response. I don’t want her to stay on that super restricted diet forever, so I wanna reintroduce some foods and use that as a test. Now, if she starts to have problems with things she starts to add back, that may tell me we have a gut issue that’s not resolved yet. Now in 30 days anyway, I’m gonna recheck her magnesium, her CBC, and her vitamin D, okay? So I don’t do labs every month. I do ’em roughly after they’ve been under care for about 60 days, typically, unless there’s other cases where you gotta do stuff earlier. That’s typically what I wanna do. All right, so this is still about 30 days later, and everything’s still going great, right? She plateaued with the brain fog issue, but still not having headaches, bloating’s not an issue, mood swings aren’t a problem, so we’re feeling pretty good. The redraw, the recheck showed her D went up to 82. That’s cool. We like that. Her magnesium went up a 10th of a point. Not super happy about that. White blood cell count went up a full point. That’s pretty cool. I like that. MCV went down a point. Eh. What do you do now? Well, I say, well, let’s just begin reintroducing foods. Now 30 days before… Well, so we do 30 days of the diet, and then, if they’re doing pretty well, we could start reintroducing foods. But sometimes, people just say, “Look, I’m feeling pretty good. I’d to just stay on this diet for a little bit longer.” All right, that’s cool. There’s there’s no ticking clock that says, “Oh my God, you’ve gotta,” there’s no deadline, right? But now, she’s 60 days into it. Let’s start to reintroduce a few foods and see how you do, right? And by the way, there’s a way to do this and a way not to do this. I’m just not gonna go through it ’cause it’s gonna take too long. But this reintroducing foods is a test, and we’re gonna have her take the same thing she’s taking. All right. So we’re 30 days later. She reintroduced eggs and those didn’t seem to be a problem. That’s cool. But then she fell off the wagon, meaning, like our kid who went to the pool party, she started adding back multiple foods at a time, and that didn’t go well, because look, when you add back foods, you can only do one at a time. If you do four or five things at a time, you don’t know what’s causing a problem or not. But that’s what she did. She had a massive increase in depression and what she called inflammation. She felt like crap, okay? So there was something and what she added back that was no good. There are a few days when she just couldn’t stop crying. This is a big deal. You’re finding out right now, “Oh, well this is an inflammatory problem.” And it’s probably related to poor gut integrity. She’s telling you what this reaction that that’s probably what’s going on with her. Now on her own accord, she went back on the anti-inflammatory diet, and the symptoms began to clear up somewhat. All right, cool ’cause the thing is people, if they do that diet, and they’re like, “Man, I feel good,” and then they veer off of it and feel crap, they are usually smart enough to go back to the diet that made them feel good and go, “Okay, I should probably stay on this and talk to the doc about this.” So what am I doing now with her? Look, she obviously wasn’t ready to open up her diet, right? Just that’s totally not what was happening. And additionally, she probably needs a slightly additional amount of support for immune system tolerance and epithelial barrier integrity. And that is gonna come in the form of sublingual vitamin A, very simple, and a probiotic ’cause she’s already using butyrate. So look, if I was gonna say, “What are three things that work really well for epithelial gut lining integrity,” butyrate, sublingual vitamin A, and probiotics. I could give you different reasons for that, but just bear with me and let me just tell you that that’s typically what we wanna do. But here’s the thing. You know that when she eats things, that causes an inflammatory problem that is systemic. It affects her brain. It affects hormones. So just remember, the gut is a huge source of inflammation in people, not everybody, but it certainly is in this patient. All right. So 30 days later, so now she’s back. We added these additional immune system things. We’re 90, 120 days in. No problems with mood. She’s pretty regular. The mood’s not going up and down. Excellent. Overall, she says, “I’m actually doing pretty good.” Her head’s not been quite as clear this time as it was the first time. Okay. That’s cool. She did do something she wasn’t supposed to do. She also says that the first time she did the protocol, really did it, her hair seemed to be not falling out at all and perhaps even maybe regrew some hair. And at this time, she feels maybe she is still losing too much hair. Well, keep in mind, she really fell off the wagon, so she stirred everything up again, so we may not be as lucky this time to have some of the same degree of positive response. Now she did say about a week before last period, she was having some mood irritability and some sadness, but it was just confined to that one time rather than throughout the month entirely. So what do we do now? So now you’re thinking, “Well, gosh, now we have do the ladies hormones. What are we gonna do?” So I’m still, hey, just stay on what you’re staying. Keep taking what you’re taking. Let’s give you another 30 days to maybe, maybe this other stuff will even out, right? Because you did fall off the wagon. Let’s let it ride for a little bit, and then we’ll determine if we wanna add any foods back or maybe titrate down to some of what you’re taking. So look, if 30 days goes by and she’s like, “You know what? My mood is actually pretty darn good. It’s stable. Even when I had my period, it seems to be fine. My hair seems to be doing okay,” cool, right? We don’t have to get super anxious ourselves and try to change a bunch of things. Now, if she has premenstrual mood stability again, then I’m probably gonna test her hormones or I’ll just empirically treat her, which is beyond the scope of what I wanna talk about in the case today. Or I might just do receptor-based rehab with her, right? If I could ever see somebody in the office again. All right, now that’s where that case stops because she’s still under care, right? But here’s the thing. What you learned from that case is she’s got these symptoms, and the labs don’t look that bad. They don’t look that bad, but on your priority list, you don’t know about that autoimmune situation, right? And what you do to try to figure that out is I did an immune system challenge ’cause he’s got a brother with Hashimoto’s. So I treat her with an anti-inflammatory protocol. She did really great with that, right? Really great with that, and then she fell off the wagon, and that made her feel really bad. She went back on the wagon, so to speak, and she does better, again, just not quite as good as the first time she was on the wagon. That’s why I say, “Well, you know what? When you added those foods back, that to me tells me that your gut was hyperpermeable. Your immune system was not tolerant. Let’s add a couple of things for that, and let’s just let that ride for a little bit and see what we get, okay?” So we’re not done with her. This is the case. Cases aren’t two weeks long. Cases aren’t 30 days long. Cases are months long. That’s how you really know if you’re doing a good job or not. And this stuff happens to real people. People will be doing well, and then, like the kid at the pool party, he goes, eats pizza and hot dogs. You gotta know what to do when that happens. So the takeaways are, you gotta know the physiology just like the last case. You gotta do the testing that makes sense. You gotta prioritize. You gotta know what’s next. So for example, when she added all that stuff back in her food and she felt like shit, pardon my French, You have to ask yourself, “What do I do? What does that tell me?” Well, it tells you that her gut wasn’t in good shape. So what are you gonna do for her gut? That’s what it tells you. That’s what’s next. And you gotta know why you would have added micellized vitamin A and why you would have added a probiotic. And then, of course, you wanna integrate brain-based treatment when appropriate ’cause look, she may still need to have some focus frontal rehab. We don’t know yet. We’re not done, okay? We are not done with her. So anyway, the point of doing all those case reviews is to show you real people, real cases. They’re still in progress. A lot of times, I’ll show you cases that are already done. The person’s got . But I also to show you cases that are still in process because that’s the real life. That’s what it’s to actually practice like this. Anyway, so we’re gonna be relaunching. I know Freddys’ gonna say some cool words about this. We’re gonna be relaunching the whole entire Clinical Neurochemistry and Nutrition program, the six module program. I think it’s been four years since we did the last one, since we started the last one. We’re gonna be launching that in October, and with that, I’ll let Freddys say some good stuff about it.
– Yeah, so the program was about three or four years ago, and it was really, really popular, helped a lot of doctors help and serve a lot of patients, and we have had it completely updated. We have updated the way we deliver it from the flip classroom all the way to the teaching methodology in the class, right? ‘Cause we keep evolving that using the latest literature in learning education and even in the way we keep the education in front of you. So in the past, you used to buy the course. You’d have a year of access. Now what we’re doing is if you purchase through the education, as long as you maintain an active learner account with us, you have all the videos. You always have access to them, and when we do the videos again in three or four years, do the courses again, you could actually go to the classroom again or get the new digital recordings added to your account as well as no additional cost. So when you buy this program, you’re buying it once. You’re getting the education, and when we get the updated education, you’re gonna get that, too, ’cause the Carrick Institute is committed to creating the best scholars and clinicians in the world, and we wanna create a model, an educational model, to deliver that. You still have to do the work, but you don’t have to worry about not having all the resources you would need to get yourself there, and when we think that’s pretty awesome.
– Oh, that’s great. I’m excited for the reasons Freddys said, which is you guys are gonna get the recordings of the class. When we start this course, since we’re doing them about, I think, about every three months, you’re gonna have the recordings of the previous class already available. You’re gonna have those before the next class starts. You’re getting a flipped classroom for every module. The way I’m teaching it is different. I’ve loaded it differently. I’m excited because of the pedagogy change, so to speak, which is I’m still gonna be me, and I’m still gonna teach it. But what I’ve decided to teach when I’m doing a little bit differently, and they’ve got some stuff that they’re gonna do with the videos, it’s gonna be really cool, that I won’t even tell him to go into, but it’s very cool to really help you guys grapple with the material and learn it and start to own it. I’m super excited. So I hope everybody that watches this is at least considering doing a course. I think you’ll get a lot out of it, so. And plus, if you buy it once, when we do the update four years from now, you get to go again, which is, who does that?
– Nobody, but we’re awesome, and you’ll be awesome if you show up in class. Dr. Clark, before I let you go, I gotta tell you, thank you for doing these cases, and the reason I like these two cases is one, for this reason, here, you got two patients, right? Different ages, right? Different sex. But they both had brain fog, but again, totally different cause. You have one cause, and then, on the second case, you go it’s not like, I get it. I guess some doctors will be tempted to be like, “Let me do all the cases that I got it right the first time, and then within 30 days they look great. And then hey, guess what? 30 days later, they were still great, and 90 days.” That’s not reality, right? These people mess up and you tell us about that. These are real cases. So I’ll leave you with this, guys. At Carrick Institute, we pick our faculty, so they’re real deal. Not only they’re brilliant in educational aspects, but they’re literally doing the works. You’re getting from their experience. So what would take you 15, 20 years to get to that level of experience, we want you to learn from the people who are actually doing this work and learn from their experience. So again, we’re sincere that we want you. We wanna make you into the best doctor we can, so that’s why we keep our guys Dr. Clark around who do a pretty good job.
– Yeah, plus I’m a pretty good painter. So when they need stuff painted around the office, they fly me down, and I paint-
– We keep him around for those two specific reasons. All right, Dr. Clark, thank you very much. We’ll keep doing these ’cause everybody keeps asking for ’em. See everybody next time. Thank you.
– See ya. Bye bye.