CITV: Case Review – 53yo Male with Vertigo and Dizziness

Transcription:

– Hello, my name is Dr. Freddys Garcia, today, I’m joined by Dr. David Clark. On this episode of CITV, we are doing a video case review, Dr. Clark, what’s going on?

– Well, we’re gonna be presenting, I, the royal we, are gonna be presenting a case today on using clinical neurochemistry and nutrition in action and showing you how I apply that with a 53 year old man who presented with vertigo and diplopia.

– It’s a very sexy title, I can’t wait to see what you’ve got going on. But I’m gonna dive in, let’s go right into it.

– Let’s do it, all right. So here’s the goals here. Now, the reason I’m going with goals is, any time I do a case review, any time I teach the neurochemistry classes, my goal is to try to teach people to learn how to think, how to understand and apply neurochemistry nutrition. What I don’t want people doing is memorizing protocols, meaning we’re not gonna learn, even today, we’re not gonna learn, oh, for vertigo, I give calcium, right. Or for vertigo, I give a certain couple supplements. We don’t do that because, as anybody knows for very long, somebody presenting with vertigo could have, there could be 25 different mechanisms for them or 50 different mechanisms. So you cannot and I will not allow anybody to try to learn this stuff by memorizing, oh, if somebody has a headache, this is what I give them, or if somebody has vertigo, this is what I give them. Doesn’t work like that. There’s plenty of weekend courses you can take from supplement companies who will teach you how to do it that way, and that works that way a little bit, but if you really wanna serve at a high level and be very good at this, be very efficient at this, we’re not gonna learn it that way. So that’s my ground rules for starting. So here we go, we got a 53 year old guy with vertigo and diplopia, as well as the following, these are his chief complains, he has something called an ocular migraine, you ever heard of that?

– No fun.

– Well, these are rare, it’s a rare syndrome, but basically, it’s ischemia to your retina and/or ischemia to some of the optic pathways, but it’s no fun, definitely causes–

– It’s supposed to be really painful as well, isn’t it?

– Yeah, exactly, definitely not fun. He also has really severe neck pain, he’s been told by various people that he’s got disc herniations and disc bulges, but a lot of, depending on who you talk to, that sometimes isn’t really the anatomical truth. People do X-rays, I think this guy had X-rays and someone tried to tell him he had disc bulges, and yeah, except you can’t see that on the X-ray. But he’s got a lot of very severe neck pain, has had it for several years. He also gets double vision, okay, he gets a horizontal diplopia. He gets a dizzy feeling as if he’s going to faint, and another technical term for that is what, Dr. Garcia?

– Give me the first letter.

– Pre. Presyncope.

– You got me, damn, I’m getting the next one.

– Look, presyncope is just the name for when someone’s, man, I get super light headed, I’m gonna, I’m gonna pass out. Another word for that is presyncope or presyncopal sensations. He’s also got tingling on the left side of his neck and his shoulder. That might relate to a nerve root lesion or something like that with his neck pain. He has a sensitivity to bright lights. He’s got a loss of balance to his right, meaning he tends to lose his balance to his right side. Now he has vertigo. Okay, he has rotational vertigo that can be very positional dependent if he rolls over in bed too quickly. Okay, now, first thing anybody thinks of when they hear that is they think, well, that’s probably BPPV, right. One of the classic signs, when someone rolls over in bed, they get that rotational vertigo. And in fact, this guy, as I’ll tell you, had been to several different places all around the country. Some people said, yes, you’ve got BPPV, some people said no, you don’t have BPPV, but bottom line is, he still has the vertigo, all right. Whether or not they’re telling him he has BPPV or not, he still has the symptoms. He also gets vertigo if he lays on his right side. And look at the connection between losing his balance to his right and laying on his right side. If he lays prone, he says his eyes will twitch, and what he really means is he gets nystagmus, all right. So we’ve got some cerebellar involvement, I can just tell you that, I’m cutting to the chase a little bit, because he’s got these positional things and that, to me, is seeming like we’ve got a cerebellar problem going on. If he moves his head quickly, it feels like his eyes lag behind, now, what does that sound like to you?

– VOR does inappropriate gain.

– Yeah, VOR does the wrong gain, so the gain is just the ratio of the input to the output. So when he turns his head too quickly, his eyes don’t keep up ’cause there’s some kind of delay in that vestibular signal going to his eyes. Could be a lot of different reasons, he could have a peripheral vestibular nerve lesion, he could have an MLF lesion. He could have just any number of things going on, but those are all things that are going on with this guy. All right, so that’s what he comes in with. So that’s a lot of stuff to think about. Let’s dig into it a little bit more, yeah, you have a question?

– No no no, this is an interesting presentation so far, I’m curious as to the mechanical stuff, the mechanical stuff that you see there, how much of it is caused by some sort of neurological issue, you don’t know which one came first.

– No.

– Right, but it’s fascinating. I also like to call out, point out that I got that second question right, which makes up for my first question being wrong.

– Exactly, right, you got it right. Well, one of the things I will say is people with vestibular complaints, they’ll have, a lot of those people have neck pain. Lots and lots and lots of them have neck pain. And then one of the reasons is, if you guys don’t know, is, I always explain it to my patients as if there’s this, the balance stability pyramid, if you will. So I ask them to visualize a three dimensional pyramid, right. And at the base of the pyramid, you’ve got three points. One point is the information coming from the inner ear, another point is the information coming from the visual system, and the other point is the information coming, proprioception, primarily from the muscles of the neck, okay. At the top of that pyramid is the cerebellum. And what happens is, if one of those things gets damaged or lesioned or doesn’t work right, then usually, if the system works correctly, one of the other points of the pyramid will turn up the volume and attempt to try to compensate it or recalibrate the system. So it’s extremely common, is these people with really really tight necks that also have vestibular complaints, you’ll see it all the time, and it doesn’t mean you need to go and adjust their neck, by the way. Because what you can do is accidentally decompensate them and then throw them in, I just have a guy right now that I’m seeing. And he lives in California, he came out here and he was back in California, he was like, yeah, my neck tightened up, should I go get an adjustment? I said, well, I don’t know if you should get adjustment or not, since I was talking to him on the phone, I was like, but I’m telling you, you need to watch out, because you could go get an adjustment and it could decompensate things. And that’s what happened. So now he’s gotta fly back out here for me to try to fix what the well-meaning chiropractor did, but I told him, I said, well, you can do it if you want, I said, but I don’t think you ought to do it. So anyway. All right. Also if he’s bent over and turning his head, he can have some vertiginous sensations as well. So he’s got a lot of positional evoked vestibular sorts of issues. So let’s look at the history, so those are the chief complaints, and already what we’re doing is we’re thinking to ourselves, what could be causing that, what could be causing this guy’s presyncopal sensation, right? Well, there’s orthostatic hypotension, right. Which is you stand up and your blood pressure or heart rate don’t increase appropriately and the blood falls out of your head. But then you have to ask yourself, well, why would that happen? So one of the things we’re always always always always gonna ask, I’m gonna train you to do this a million times a day is why, why is that happening? So here’s his history. In 1991, he had a bad motor vehicle accident, he required screws in both ankles. In 2004, he had a hernia surgery. He says he was really healthy until about 2015, which is just a couple years ago. One day, he bent over, and then, when he returned back to neutral, things felt very floppy and he couldn’t steady himself. Now, for a guy who seems to not have had, and we have to trust him on this, seemed to have no vestibular problems prior to that, it does seem kind of strange that one day, he bends over and all of a sudden, he has this acute onset of symptoms. I will tell you that’s probably not really what happened. He would probably been having a buildup of these things, but they were sub threshold, they were, he was having some problems and just wasn’t really aware of it. But to him, one day, he bends over and whoa, and everything goes crazy. And so that can make you think, oh, man, maybe that was a vascular event, maybe it was some, but it probably wasn’t really that acute. You know what I mean, it’s probably a process that had been building for a while. And when he finally put himself into a position where his, that was outside of this, I’m gonna use a caps term, outside of his limit of stability, so to speak, that’s when the system couldn’t recuperate and recompensate from it.

– So the systems that were compensating maybe degraded over time or he exceeded his ability to compensate.

– That’s it, he exceeded his ability to compensate. And there’s any number of reason why that can happen as we’re gonna find out. So he then developed these ocular migraines, this has only happened the last couple years. So since that time, okay, he developed his ocular migraines, which he gets these zigzag lines in his left field of vision. And actually, he had, he actually had one time when his vision went white in his right eye. Which is no good, that’s a very bad thing. A lot of ischemia is happening there. He’s had four brain MRIs all of which are negative. That’s cool, because when a guy has all these weird positional dependent nystagmus, you start wondering about tumors and things like that, but he doesn’t have any of that, which is good. He’s had a couple of chiropractic treatments, he’s had two different steroid injections in his neck. Because he’s got this real bad neck pain and neck stiffness, and that helped for about 10 to 12 days with some of his symptoms. For a steroid injection, that’s gotta tell you something, right, it’s like his problem is not inflammation in his neck, right. The problem in his neck is most likely a, as I was talking earlier, he’s got increased sensitivity and increased gain of those neck muscles to the point that it’s causing a lot of pain, because if it was a musculoskeletal source for his neck pain, you know what I mean, then steroid injections probably would’ve done something. They helped a little bit because you know, but they’re not having long lasting relief. He’s had one, check this out, he had a radio frequency ablation on the right side of his neck, he had an occipital nerve . I mean, this guy’s neck hurts a lot. And so you start thinking to yourself, this is probably not a peripheral source of this guy’s neck pain, right. It’s probably not what it is. He had some VNG testing done locally, which was diagnosed as BPPV, and then he went and had additional testing done in Florida, which said he had BPPV. This is not a guy who’s been to Plasticity, by the way, that’s not code, me saying Florida is not code for saying he went to Plasticity. So here we go, right, so that’s, so that’s his history. He had this weird thing happen in 2015. His neck’s hurting a lot, he’s got these vestibular symptoms, he’s got these lightheaded symptoms. Now, here are some additional symptoms that might help us bring a neurochemistry and nutrition perspective to this. So he very often can’t go more than about three hours without eating or his symptoms worsen. Now, let’s think about that. What is eating, what is eating, what is he doing when he eats, what is he doing for his body when he eats?

– Well, he gets some fuel, he’s gonna have, should have an increase in blood sugar and then have a reactive drop in blood sugar to an appropriate level, unless it’s a reactive hypoglycemia, which would make, can give you a lightheadedness if those mechanisms aren’t working as well as they should.

– So when he’s eating, he’s giving himself glucose, right. And what we’re seeing right here is he can’t go more than three hours without eating. Now, I’m just gonna tell you guys, what that tells you is that his HPA axis is not working correctly. ‘Cause what should happen is his hypothalamus should sense that there’s low glucose in the blood, that makes you get extra pulsatile release of cortisol, which then liberates glycogen, which should bring his glucose levels back up. All right. So I’m telling you, we know that that’s not working and we know that it also has to be related to that lightheadedness that he has, because it’s worse, right. It’s worse when it happens. Doesn’t necessarily make him have a vertigo spell, but we definitely know it affects that kind of lightheadedness presyncopal stuff that happens. He has alternating constipation and diarrhea, well, that’s not normal, he shouldn’t have that. He has afternoon fatigue, and I’m gonna tell you, that’s another sign that his HPA axis isn’t really working correctly. And he also has orthostatic hypotensive symptoms, meaning when he stands up, he gets that presyncopal stuff, right, that’s what orthostatic hypotension means. That also implicates some involvement of his HPA axis. Now, it could just be that the HPA axis is involved because of inappropriate integration through his brain stem. Like his vagus nerve and that stuff. Or it could simply be that his HPA axis just doesn’t work well. And even though his brain stem is telling it to fire, it doesn’t fire right. So there’s any number of possible influences on that, but this stuff is telling me that this guy’s HPA axis is not working very well. He often wakes up during sleep, that’s another thing that happens when people have nocturnal hypoglycemia. Meaning when their cortisol production at night is so low that they can’t keep a steady flow of glucose to the brain, the backup system comes online, which releases adrenaline. So that’s a very very common scenario as well. Now, he also has decreased–

– Dr. Clark?

– Yeah?

– Question on that, do some people sweat because of that? Have you ever heard of that, yeah, from the hypoglycemic state when they release that adrenaline to try to get some fuel out, does that–

– Sure, yeah, that can happen. Also what can happen, doesn’t have to happen at night, that can happen during the day. Some people, when they get, when their blood sugar or tissue sugar gets really really really low, that backup system comes online, which is the catecholamines. And that certainly, that can give you this, I don’t know if you guys can see that, they give you the shaky feeling, right. The little accentuated physiologic tremor that people get. And that absolutely can make you sweat for sure. Really, I mean, some people, it has to get really really bad and they start to get nauseous, right, and then they start to get diaphoretic, right, they get really close to vomiting. Just depends on the person, but it can do it. All right, so this guy’s also got decreased libido and some erectile dysfunction. What does that mean, well, I mean, that could be a sign of dysautonomia, it could be something totally unrelated, it could just be a testosterone problem, yup.

– Cardiovascular.

– Could be cardiovascular, sure. So these are all the things, see, you guys see why you can’t say, oh, someone has vertigo, I give them this. That doesn’t work. You can’t do that, you have to be a clinician, you have to think, you have to have a body of knowledge, you may not even know half the stuff I just talked about. But these are the things that we go over and make sure you know when you take the neurochemistry classes that we do. All right. So currently, he’s taking irbesartan, what is that?

– I don’t know, you tell me, I don’t know–

– It’s a blood pressure medication. He’s taking baby aspirin. He’s taken lorazepam as needed because he gets anxiety about his vertigo. He has hydrocodone as needed for his neck pain, and he also takes Protonix, which is an antacid. Okay. Now, his family history is significant for his father who died in 2000 due to progressive supranuclear palsy. That’s no joke, right. So now we’re like, okay. I don’t like that at all. Now, it doesn’t necessarily mean that what he’s having is some kind of early premonitory presentation of PSP, but you’re damn sure I’m concerned about it now, ’cause his dad died from it. So I’m like, hmm, okay, I’ve gotta be super on alert. Now, one of the things we always always always do with every patient is we do a medication review, all right. Let me ask you a question. If irbesartan is a medication for blood pressure, does it lower blood pressure or increase blood pressure? Well, that’s pretty silly. It’s gonna lower blood pressure. What kind of symptoms does he already have, I’m giving away the form here a little bit. What kind of symptoms is he already having? Is he having high blood pressure symptoms or low blood pressure symptoms?

– ‘Cause of the way he moves and he has that shift in blood flow, it seems like his blood pressure is not high enough to get blood to where it needs to be.

– Exactly. So he, I, the reason I’m telling you this, maybe he’s just overmedicated, right. Maybe he’s just taking too much medication, right, that’s certainly a possibility, I just wanna–

– He’s already on quite the cocktail.

– Oh yeah. Yeah, exactly. All right. So what’s our impression? Well, what could be going on with this guy? Well, he could have a peripheral vestibulopathy, right.

– Sure.

– He could have a centrally maintained vestibulopathy, he could have dysautonomia, which he clearly has, it just depends on how you wanna describe it. Could he have a metabolic issue, well, yeah, he’s definitely got some kind of glucose thing going on, I can tell you that. Now, what else he has? I don’t know, so I mean, there could be, god, I mean, do you just take a dart and throw it on the wall and say, okay, well, maybe he has a testosterone problem? Maybe he has yeast, maybe he has metals. But we’re not gonna do that, okay. We are gonna do our thinking about this in a much more realistic, rational way. What we’ve gotta do is we have to have a set of priorities, right. Now, fortunately, I’ve already done the work for you. I’m gonna tell you the things that you wanna look for first so that you don’t get lost in this whole vast sea of gosh, what are all these metabolic neurochemical things that it could possibly be? So where do you start, well, here’s the thing. You could start and you could do receptor based rehab on this guy, you could do that. I mean, you could say, okay, look, it’s, the gain is low here, I’m gonna do that. You could absolutely do that. What you have to be careful of is how do you know it worked, right? And what kind of a rule do you have for yourself, how are you gonna know if it worked, right? So I will tell you that, when I do rehab on people, I have a two day rule. Which means if I’m doing rehab on someone, in two days, two things should happen. I should definitely see objective change, all right. And number two, the patient ought to be able to feel enough to know that we’re on the right path. 95% of the time, okay. But here’s the thing. With some people that have these chronic conditions, it’s easy to temporarily fool yourself into thinking you did the right thing. Because you only saw them for a couple days, they got better. That’s cool. But if you’re gonna do rehab on someone, the question is, did they stay better? Right, did they stay better? So look, if you do receptor based rehab on this guy and his chief complaints clear up, et cetera, and a month later, he’s still good and two months later, he’s still good, then hey, that’s probably, you probably did a good job. What I don’t want you to do is to think, hey, I did this and that on them and I did some stuff here in the office for a couple days and he’s great and I’m done. Don’t do that, you need to follow up with people, because in about two weeks is you’re gonna find out how good is this guy really doing, all right. Just my little, now, could you start and do a metabolic/neurochemical workup? Yeah, you could do that too. The experience that I have, very often, what I’ll do is I’ll just look at the metabolic stuff first, because I have seen so many of these cases that I know that there’s a likelihood of what this guy might have metabolically, and I can just rule it in and rule it pretty quickly. All right. So where are we gonna start, well, we’ve gotta have some priorities. And these or what I’m gonna show you here are what I call the four neurochemical priorities, all right. They may be different that what you’ve seen last time if you’ve seen me talk about these before. So what’s our number four priority? I feel like it’s, number four, like a ESPN SportsCenter type thing. Number four is GI and liver function. Number three, I’m gonna call this cellular energy, specifically via HPA axis and glucose regulation, all right. Number two priority, cellular energy, but we’re talking about this in terms of RBCs, red blood cells, and the nutrients that go into RBC health, such as B12, folate, iron, that kind of stuff. As well as folate and B12 and iron as they relate to mitochondrial production of energy, all right. And then actually, the number one priority is does this patient have clinically significant autoimmunity? Now, why do I say clinically significant? Because some people have antibodies that are elevated, but it has nothing to do with anything. It really doesn’t, it’s just, they have the elevated antibodies and it just isn’t related to what they came in for. That happens. So you have to be careful again not to say, oh man, I’m gonna do $600 of antibody testing on people, and as soon as someone’s got elevated antibodies, that means that it must be related to what’s going on with them. I can tell you that that’s a trap you don’t wanna fall into. So we want, yeah?

– I was gonna say, I see a lot of clinicians falling into that, they spend a lot of money on that testing, they see the autoimmunity and they perseverate on it. And they miss the information that’s over here ’cause they go, well, this has got to be it. And then they spend month trying to work on a protocol for the autoimmunity that wasn’t gonna change their condition anyways.

– So here’s what we’re gonna do. These are the priorities, why are they priorities, well, I’ll just give you the 10 second thing. Number one is because, if you don’t have ATP, nothing’s gonna work, right, that’s pretty much it. So that’s our numbers two and three there, right. So this is all about ATP, okay. Why GI and liver, well, because if you don’t absorb the things that you need, you’re gonna be malnourished, you’re gonna have malabsorption. The GI tract is a huge source of inflammation throughout the entire body. There’s that gut-brain connection that everybody’s heard about. Why liver, well, because liver is how you bio transform and detoxify and it’s also where you make 300 different proteins. There’s lots of other stuff I could put on this list, but I’m telling you, this is the, I think this is the best way to approach these metabolic possibilities. It gives you some place to start, and you’ll see why. Oh, and why is significant autoimmunity number one, because autoimmune problems like to create numbers two, three, and four. Autoimmune problems, because of the cytokines, they love to create liver problems, GI problems, HPA axis problems, malabsorption problems. Having an autoimmune problem is like having an octopus stuck on your back, one that’s clinically significant. So that’s why, in my experience, that’s the thing that you go after to get the most bank for your buck. So what tests are appropriate, since you were just talking about that? Well, look, what testing you do always depends on what is it gonna tell me, right? If I do this test, is it really gonna change the way I treat this guy, right? The logistics of it, meaning how easy is it for this patient to get this done not necessarily financially, but logistically. And then the patient’s budget, I mean, believe me, you can spend 10-15 grand on testing like that. I mean, it’s not hard to do. But the question is, do you need to do that? People that do lots of testing, and I don’t mean to step on anybody’s toes, people that do $2000 or $3000 worth of tests, they’re doing that because they probably don’t really know what they need to know. And they’re just doing this shotgun test because it’s easier just to make everybody do these $3000 worth of tests than it is to think about it on a case by case basis. And that’s okay, I guess, but the way I look at it from just a practice standpoint is do I really need that patient to spend 2000 bucks on testing when they could spend that 2000 bucks on treatment, right? That’s the way I look at it, so what are we gonna do with this guy? Well, you know he’s got this chronic vestibulopathy. He had a VNG. What metabolic factors are associated with that kind of presentation, well, here’s what I’m gonna tell you. You can have glucose problems that can affect these chronic vestibulopathies, but here’s the thing that I see more than anything associated with chronic vestibulopathy, whether it’s peripheral or centrally maintained, is this. The patient has some kind of autoimmune problem that no one’s picked up yet. That’s what I find time and time and time again. And it’s not just that I find it, it’s just that I find it, and when I treat it, that vestibulopathy gets better. That’s how I know it.

– Clinically significant to this case, right, that’s what makes it the clinically significant one, right.

– Absolutely. Now, diplopia. That’s likely a phenomenon of the vestibulopathy, ’cause if your gain is off and you’ve got a little bit of, it’s not necessarily demyelinating per se, ’cause he’s had a bunch of MRIs. To me, that’s probably a phenomenon of the fact that his VOR is really, the gain is really messed up. What about the lightheadedness and the presyncope? Well, man, he’s hypotensive, right. We know there’s something going on with his blood pressure, but we don’t know why. Could be anemia, because look, if you don’t have enough red blood cells and you can’t get enough oxygenated blood to your head, that could be iron deficiency, could be, as I said earlier, poor HPA tone. So what testing would you do, well, I’m gonna do some blood chemistry because I can hit a lot of those bases, a lot of those questions that are right now, that we’re trying to answer about does he have significant autoimmunity, does he have RBC problems or nutrient problems? I can answer most of that through fairly inexpensive blood chemistry. So what are we gonna do? CBC, which is a complete blood count, comp metabolic, lipid panel, complete thyroid panel, D, B12, folate, ferritin, which is your iron marker. There’s lots and lots of stuff I could say about each one of these, I’m just going along so we can get to the point. His homocysteine levels. Why would I pick homocysteine, well, because homocysteine is a surrogate marker for folate and B12. And also, homocysteine, if it’s elevated, it’s incredibly inflammatory. It causes a large amount of oxidative stress, and so in your mind, you think about oxidative stress related to inflammation, because if you have oxidative stress in a cell, that can overwhelm mitochondrial mechanisms, and then what can end up getting is basically just an inflammatory cascade, so that’s why we also check homocysteine. What about adrenal testing, right, because everybody wants to do a salivary adrenal test, right. Because this guy, I said earlier, this guy looks like he’s got some kind of classic sorts of adrenal symptoms. Now, you’ll notice I didn’t call them adrenal symptoms because I don’t like to use that terminology anymore. This whole idea of adrenal fatigue, that doesn’t really exist. That’s one of the things that I talked about in a hormone class that I did, is there is no literature, none, there’s no literature to support the idea that there is adrenal fatigue the way that you probably know about it. You can have poor HPA tone, right. But you really can’t have adrenal gland fatigue. I understand it’s an incredibly seductive sort of an idea, it’s like stepping on a garden hose, right. It’s that same sort of simplicity and it resonates with people, but it’s not really true, it’s not really accurate. So do I wanna do adrenal testing on this guy, no. Here’s what I can tell you. I’ve done hundreds and hundreds of salivary adrenal tests, I’ve done a lot of the urinary adrenal type tests. And what I’m telling you is the symptoms that guy has, I can’t go more than about three hours without eating or I’m gonna start to get symptomatic. I’m waking up at night. Those are telling you he’s got a problem with HPA tone. Or he’s got a problem with getting glucose out of this bloodstream and into his tissues. So I don’t need to spend 200 or 300 bucks on doing some adrenal testing, I’m just telling, you don’t need to do it. Should I do stool testing ’cause he’s got alternating constipation and diarrhea? No, I mean, we could. But I can just tell you, the biggest, biggest, biggest probability for this guy’s alternating constipation and diarrhea, he’s got a food sensitivity of some kind, right. That’s like, 85% of people, that’s what it’s gonna be. Now, does that mean I should go and do some food sensitivity testing? No, you don’t need to do that either. ‘Cause, as I’m gonna show you, we can hit a lot of these bases of testing simply by treating him, right. So there’s a way to test as you treat rather than waiting three-four weeks and dropping hundreds of dollars on these other tests you really don’t need to do. Here’s what his labs showed. So his homocysteine, 10.3, that’s a little bit high by my standard, now, notice I’m using this term functionally high. Because I can’t say it’s high because it’s not outside the reference range. But based on my reading and the literature that I like to look at, I don’t think that’s a great level. I mean, I could live with it, probably, but I would prefer it to be a little bit lower. What about his folic acid, what do you think about that, Freddys, I don’t know if you know the ranges, what do you think about 5.2?

– I don’t have the range.

– Okay, well, that folic acid, that level right there sucks. 5.2. Now, lab low, for this lab that we did the testing, this guy is 5.9. That’s low. And here’s what I’m just gonna tell you. Any time you see low folic acid, and pretty much the literature says, there’s a paper that came out that said this. If you see a folic acid that’s under 10, you start thinking about celiac disease, just think about it. Because there’s really, it’s really hard to have low folic acid if someone’s eating the regular American diet. Because there’s folic acid in darn near everything, they fortified it. So you’re looking at probably a malabsorption problem. And the number one thing that’s gonna be malabsorption most likely is some kind of gluten sensitivity. Celiac disease or something related to it. But also, folic acid is, it’s absolutely integral to making energy, right. So if you don’t have folic acid, you’re gonna make ATP. Lactate dehydrogenase, well, what is that? Well, 64, that’s lab, that’s very very low for lactate dehydrogenase. What is that, why do we care about that? Well, this is basically a surrogate marker for telling us how much glucose is actually getting into this guy’s tissues. So you know there’s blood glucose. But then there’s also tissue glucose. And those are two different things. And the cutoff I like to use is 140 as a good cutoff for that. He’s way below that. So this makes me wonder about how much glucose this guy is actually getting into his tissues and maybe this is why we’re having some of the dysfunction that we’ve seen. Certainly, it relates to those HPA axis symptoms. That, this is what that relates to. Now, MCHC is a red blood cell marker. That’s a little bit low, not very low, but a little bit low. Come on, computer. His ferritin is 60. For a guy, that is terrible. Okay, now, the range is getting cut off over here by my face, but a guy should not have a ferritin less than 100. Just I’m telling you, I don’t care what that lab range says, that lab range, look, it’s 38 to 380. A power of 10, that’s the range that’s considered statistically normal. That’s not a healthy range. 60 is not good for this guy, and you have to ask yourself, why? Why is his ferritin so low, ferritin is your gold standard for telling you about the guy’s iron status. Well, he’s either not eating it, but he is ’cause he’s not on a vegetarian, vegan diet, or he’s not absorbing it, okay. What about vitamin D of 16? That is really bad too, that is really really bad. Lab low is 30. So what’s going on with this guy, here’s what I’m gonna tell you. You see vitamin D deficiency in a lot of people, but you also see vitamin D deficiency in almost every single person that has an autoimmune condition. Okay. You see it a lot. Okay, what’s that? Those are thyroid peroxidase antibodies, here’s our autoimmune test. So I put those on his thyroid panel just to see, because a lot of people have thyroid autoimmunity and don’t know it. And a big chunk of people with chronic vestibulopathy have got thyroid autoimmunity. In addition, they have other things as well. Now, what does this mean? Well, first of all, is it high? Yeah, it’s real high. Normal’s less than nine on this lab, so 173 is way over the mark, okay. So what does that mean for us? Well, it means, hey, we didn’t know this guy had this before. No one ever checked this. What do you call that? Well, what you call that situation right there where he has these TPO antibodies, but the rest of this thyroid panel was normal, you call it euthyroid Hashimoto’s is what this guy has. Here’s what that means. He’s got the antibodies, none of his other quantities are really abnormal yet. But he’s still got the antibodies, and the literature says all you gotta have is the antibodies for it to affect you. You don’t have to have overt hypothyroidism for these TPO antibodies to be clinically significant. Okay. Now, his reverse T3 is a little bit high, that’s an inflammation market as well, yup.

– No no no no no, I’m just nodding along because this is–

– Oh, I thought you said something, okay. So all right, what do we got with this guy? So what about our priority number four, GI and liver? Well, his Liver transaminases were normal. He does have these symptoms of constipation and diarrhea. I have to ask ourselves, why? Why does he have these symptoms? Well, here’s the thing. If someone has constipation and diarrhea, they’ve got low ferritin, low folic acid, low vitamin D, that sounds like malabsorption, that sounds a lot like malabsorption. But again, why would he have the malabsorption, let’s back up, well, I can tell you, the most common thing is he’s got some kind of food sensitivity and it’s probably gluten related, ’cause that’s the most common one. What about number three, cellular energy, the HPA axis and glucose? Well, he’s definitely got those symptoms of low HPA tone, right. His LDH is definitely too low, and that correlates with that low tissue glucose, all right. What about number two, which is our cellular energy, RBCs, and nutrients. Well, his folic acid is low. His MCHC is low. His ferritin is way too low, right. And what about clinically significant autoimmunity? Oh yeah, he has elevated TPO antibodies. So look. This guy may have all four. So where do we go, what do we start with, right, what can we do, do we just, I mean, do we just give up? Because that’s too complicated, I can’t do it. No, we don’t do that, ’cause I’m gonna show you what to do. Now, he also has vitamin D deficiency, which is related to that autoimmune problem, because if you had to say one thing about vitamin D, here’s what you could say, it’s anti-inflammatory. All right. It’s immune system regulatory. And I’m gonna tell you, you give me 100 people with an autoimmune condition that don’t take vitamin D, 90 of them are gonna have outright vitamin D deficiency, it’s that common with autoimmune problems. So what are we gonna do for this guy? Well, check this out, here’s what we’re gonna do, we’re gonna try to hit multiple bases, right. We know he’s got a malabsorption problem. We know he’s got what looks to be an autoimmune situation, but we don’t really know if his autoimmune problem is significant until we treat it, all right. If we treat it and he gets better, well, we can make some inferences about what was going on with him, right. So we gotta do some things. So here’s what we’re gonna do with his diet, we’re gonna do what’s called an anti-inflammatory diet, and I’m gonna give you this real just basically, so I don’t have to spend an hour talking about it. It’s gonna be grain-free, gluten-free. It’s gonna be dairy-free, meaning no milk products. Gonna have no beans, no seeds, no nuts, no eggs. No nightshades, which is tomatoes, potatoes, eggplants, and peppers. Why? Because we don’t wanna fiddle-fart around with eliminating one thing at a time, it’ll take two years to figure out what the guy has a sensitivity to. When you do everything at once, more or less, you have a much better chance of getting some clinical therapeutic momentum with him. ‘Cause look, if I do an anti-inflammatory diet with him and I do this little supplement protocol I’m gonna tell you guys and he gets better. Hey, we know we’re on it, right, we know we’re on it. Now it’s just, okay, what does he really need long term to stay that way, right? So what I’m not gonna do is I’m not gonna give this guy a treatment plan and then, when he’s better after 30 days, go, oh, cool, I got it. No, it’s the same kind of rule as if you were doing rehab with this guy. He’s gotta stay better, right, he’s gotta stay better. So with this diet, we’re eliminating those things. No high sugar fruits. What am I gonna give him supplement wise, well, number one, I’ve gotta go after that autoimmune problem and I’ve gotta correct those nutrient deficiencies, I’ve gotta do that to find out if they’re related or not, right. Now, you may ask yourself, well, why don’t I just say just give him folic acid for 30 days, ’cause it’s gonna take too damn long to do that. You can’t take eight or nine months, just give the guy things that look like they’re reasonable. If he responds and stays good, then you pull him away and find out what does he still need long term. But if you do one thing at a time, it’ll take forever, the guy will not hang with you long enough. He needs to get better right now, right, this is a way to do it. So we’re gonna be an anti-inflammatory protocol, we’re gonna correct those nutrient needs. So we’re gonna ask ourselves, why are we doing it this way, because that’s what he has, right. We’re gonna go after those things, and physiologically, they make sense based on what we know from the literature and my clinical experience, they make sense that they could be related to what’s going on with them. So we’re gonna give him turmeric, I’m not gonna tell you all the specifics of all of it right now but just, this is what we, this is what I gave him. Turmeric, resveratrol. Iron bisglycinate. ‘Cause he does have an iron problem. Sublingual vitamin D, sublingual folinic acid. Why would I give him sublingual vitamin D, liquid sublingual vitamin D, why would I give him that, Freddys?

– Better absorption?

– That’s right, because look, if this guy has got a malabsorption problem, what I don’t wanna do if I can help it is give this guy a capsule vitamin D or a gel cap vitamin, because I’m telling you, he’s not gonna absorb it very well. Sublingual is an excellent route of administration for this stuff, same thing with the folinic acid. Iron, there really isn’t a sublingual iron that anybody makes, but you know. We’re gonna give him a high concentration EPA fish oil of a certain level, because it’s anti-inflammatory, turmeric and resveratrol, I went through the literature with you guys. I mean, they’re probably the most powerful anti-inflammatories we have that aren’t drugs. They’re extremely good at regulating these inflammatory pathways. We’re also gonna give him sublingual reduced glutathione. Why, because glutathione, like vitamin D, like these other things, is a way to regulate the immune system, so we’re coming at this immune system issue that I think is primary with him from a couple different mechanisms. We’re using the turmeric, resveratrol, the vitamin D, the EPA, and the glutathione, okay. That’s why, that’s why we’re doing it that way. Now, let’s see what happened, I mean, how did he do, right? So he did the diet I was talking about, plus the supplement protocol, did it for 30 days. His subjective report is he’s 80% better. Over the last six days, he’s been off of his blood pressure medication entirely, okay. On August 25th, this is last year, he had a pretty significant dizzy spell, went to the ER. 8/26, he was feeling the same. They decided to reduce his blood pressure medication. He says his, excuse me, his blood pressure has been holding right around 116. That’s pretty low, right, over 71. That’s without the blood pressure medication. So think about what it was, think about what it was doing with the blood pressure medication.

– What was it before?

– Yeah, I mean, he could very easily just been overmedicated, like I said earlier, he could very easily just been overmedicated. And of course, that faint feeling has improved. In terms of the ocular migraine, he hasn’t had any since I talked to him 30 days ago. Which is good, ’cause he was having a couple of those a month. In terms of the vision changes where he’s getting those weird ocular migraine visual changes. That’s not happening. Just a few occasional little minor changes, so look, we know we’re on it. Now, you might say yeah, but that’s probably placebo. 80% improvement, that’s probably placebo. Well, we’ll find out, right, we’ll find out. But even if it was, which I don’t think it was, I mean, okay. So it is placebo, okay. Did it hurt him? We want him to stay this way though. So the people that have placebo, the people that say stuff like this, man, I took that and 10 minutes later, I felt great. That’s placebo, okay. That’s definitely placebo. Oh, and check this out. The positional vertigo hasn’t happened at all. So we know we had to have changed some of the integration of those vestibular pathways, we had to have, right. That’s cool. All right. So he seems to have done pretty well. What do we do now? Well, we’re gonna continue his current protocol for another 30 days. ‘Cause he’s not 100% yet. In three weeks, we’re gonna recheck his folate, his LDH, his vitamin D, and ferritin. See, this is what we do, we say, look, do I need to recheck everything we did, no. The four big things that were really goofed up were his folate, LDH, vitamin D, and ferritin, right. We definitely wanna recheck those and find out, is he absorbing the folate I gave him? Is he absorbing the vitamin D I gave him, is he absorbing the iron I gave him, all right? He seems to be doing well but hey, we still can’t just assume that he’s absorbing everything. Why do it that way, well, I just explained why. So here he is 60 days after starting treatment. No positional vertigo at all in two months, in two months, he’s had none. He’s had no ocular migraines in two months. He’s having now no visual disturbances at all. So yeah, that’s self-report, but that’s pretty good, you know what I mean, that’s still pretty darn good. The only thing that’s really hanging around is that hypotensive feeling when he lays down or he gets up, all right. ‘Cause his blood pressure is low, right. Why is that hanging around, well, it could be the fact that his ferritin’s still too low and he’s bordering on that. Could be his LDH is too low, it could be one of those mechanisms. He could be hypovolemic, his blood volume could be low. There’s a million reasons why it could be. So the little recheck that we did. His ferritin went down, what the hell? What the heck? Why would, his ferritin is now 38? I was giving him iron, what happened? Okay, here’s what you gotta know. And this is what no one else will tell you. Everyone else, when you take classes like this, they always just tell you the kind of, the sunshine story, which is, they never say what happens when holy shit, the guy’s ferritin went down? Well, I don’t know. Here’s the thing. Ferritin tells you two pieces of information, ferritin obviously is your iron. But it’s also an acute phase reactant. It’s an inflammatory marker as well. I personally think that what we did is this guy’s ferritin was actually that low when we first did his ferritin. It’s just that it looked like it was 60 because he was inflamed, so that’s what I think. I’ve seen that happen multiple times. So that’s still way way way way too low. I’ve just explained that. Now, his folic acid is now greater than 40. So yeah, he’s definitely absorbing the folate, okay. So he doesn’t need to take as much folate as I was giving him. So his folate is, he is absorbing now, which is great. His LDH is 64. And it was 64 previously, there’s been no change in that whatsoever, okay. Well, so he’s feeling better, probably because we deinflamed him. That’s probably what the mark, that’s probably what it was if I had to, if you forced me to say why it is. And his vitamin D is 78. Hey, he absorbed the vitamin D, right. The other thing is, guys, you can’t give people vitamin D and never recheck their vitamin D, you can’t do that, you have to recheck their vitamin D, ’cause you can make people toxic, you can do that. All right, so what do we do now? We’re 60 days in, he’s doing pretty good. A couple of these lab markers aren’t great though, do we just say, hey, man, see you later. No, we’re gonna keep working with him, number one, because he wants to get these things corrected and number two, we wanna get them corrected, because the mistake people make is quitting too early, right. ‘Cause look, he’s feeling better, that’s cool. But his LDH is way too low, his folic acid is better, his ferritin is still way too low, we need to figure out what’s going on with those. All right, so guess what? I’m gonna let him reintroduce some foods. Right, and we’re gonna find out, by doing this, what kind of shape his GI tract is in, this is our test. Okay. We’re gonna have him reintroduce those. In terms of his supplement protocol, we’re gonna keep him on those couple things right there. Why, because I’m not done yet, I need him to reintroduce these foods so I can find out what kind of shape his GI tract is in without changing any other variables. All right, that’s why we’re doing it that way. Testing, I’m gonna recheck his ferritin and LDH in about 30 days, right. It’s really relatively inexpensive to do that. So 30, three months, three months into treatment, Freddys. No positional vertigo. A couple of ocular migraines, but he thinks it’s related to his neck pain that was occurring when he was side sleeping. He’s had a few lightheaded symptoms when lying down or getting up, but that’s getting better, that seems to not be as prominent. He reintroduced eggs, pinto beans, pork and beans, potatoes with no ill effects. I gotta tell you, if he’s able to reintroduce those things, there’s a pretty good chance that his GI tract is probably doing okay in terms of the integrity as well as the mucosal tolerance of it. What do we do now? Well, now, I’m gonna have him start pulling some things away, right. ‘Cause here’s the thing, I always tell patients I want you to be stable, I want you to feel good as you wanna feel, but I want you taking as few of those things as possible to do that. Because I view all of this stuff like rehab, right. All this for me is like neurochemical nutritional rehab. That’s how I look at it. And the only way to find out if you’ve done that is to stop doing the treatment, right, and find out. So I said, hey, finish off your supply of turmeric and resveratrol, let’s see how you do for a month. So four months into treatment. He’s been without those turmeric and resveratrol for five weeks, he’s been without the glutathione for about four days. He feels totally fine. So look, if he’s off of those for a month and he’s having no recurrence of positional vertigo, no flare up of ocular migraines, he probably has gotten ahead of the inflammatory curve, so to speak, right. He’s also been recently using some protein drinks and some power bars with no ill effects. Opening his diet back up, now, what he’s not doing is he’s not gonna have gluten or dairy ever again. Because this guy has what I think is a clinically significant autoimmune problem, it’s euthyroid Hashimoto’s. And the worst thing he could do dietary wise is to eat gluten and dairy, that’s just what I can tell you, all right. What do we do now with the guy, right, we’ve pulled a couple things away. He seems to be still doing pretty well, I mean, most of his chief complaints are gone. In three weeks, I still wanna check his LDH, his ferritin, and his vitamin D, ’cause I still am not gonna let go with that, ’cause I’m giving him vitamin D, I need to recheck it at some point. I still am trying to figure out what the hell is going on with his ferritin, and what do we do about his LDH? All right. And he can try to add back tomatoes. So here’s the retest results, so now we are, what is this, five months into treatment, right. Five months. Now, for all you guys who are looking at this, this is how long, I view all these patients as long term relationships, you’re not gonna come in, make a splash, do a couple eye things and then be done. I hope everyone takes the same methodology to their rehab patients as well, where you’re following up and you’re finding out, okay, is the person still doing well, that kind of thing. So his vitamin D is 85, cool, we like that. Okay, I’m gonna reduce his vitamin D dosage. His LDH is up some more. So his LDH was creeping up, it was 64, 64, 76, and now 84, so it’s creeping up, which is good, still got a ways to go. And by the way, these results are from like a week ago. His ferritin’s 40, which is not really statistically significantly better than it was. So I’m probably, and I’m actually talking to this guy in an hour, I am probably going to change his iron to a liquid, we’re gonna try a different delivery method and see where that gets us. Because sometimes you gotta do that, ’cause look, I’ve been trying the capsule version for a while, it ain’t doing it, so we’re gonna switch to a liquid and see if that gets us. Following up with this guy today. So let me ask you, do you think this is a successful case? I’m asking you, Freddys.

– Well, you’ve had some positive changes, but I still think there’s a little bit more to be done, I think.

– Yeah. Well, I’m just saying, I’m gonna follow up with the guy today, and if he tells me, yeah, I still have no positional vertigo, it’s been five months, that’s successful, that’s for sure, right. Because we took him, we treated him, he got better, he stayed better, we took some of the treatment away and he stayed better. I mean, that’s successful, I mean, I don’t know what else I could say is not successful, now.

– I wanna figure out his ferritin now.

– Yeah, that’s what’s bugging me, is that, that’s what’s bugging me, is that. So I’m not gonna be really satisfied until I can get his ferritin to 100. And we’re just gonna have to see, I mean, his ferritin shouldn’t be that low, it should not be that low, I mean, a ferritin less than 100 in a guy is not good, less than 50 in a woman, but definitely not in a guy. So here was the goals, right, I want him to feel as good as he wants and he’s happy. I mean, he’s definitely happy. I want him to be stable that way, but I want him to take as few things as possible, so look, he’s not taking turmeric, he’s not taking resveratrol, he’s not taking glutathione. I’m gonna make him take, I’m gonna ask him to take the vitamin D and the omegas, and just a couple of things. And of course, I’ve gotta get the ferritin fixed. So that’s good, is he taking 25 supplements, no, right. Is he eating a super restrictive diet, no, because we’ve added those things back, right. Now, he of his own accord doesn’t really wanna add, he wants to try some corn and some oats and that kind of stuff, we’ll do that, there’s a programmatic way of doing that. So here’s the takeaways. You gotta know and own the physiology of this stuff in order to be efficient and effective. You gotta do testing that makes sense based on that case, right. We gotta use those four priorities to prioritize your treatment. Because you can waste a lot of time doing things that are not really relevant. You always have to think of what’s next. What am I doing next with this guy, why am I doing it? And you gotta know which nutrients, herbs, supplements cause the desired changes in the physiology that you’re looking for, right. So look, if I tell you that this guy has got an autoimmune problem, there’s a lot of different things you could do to try to affect those pathways, but then there’s things that I can tell you that are much more likely to work than other things. And you wanna integrate brain-based treatment when appropriate and indicated, and this guy hasn’t needed it yet, right. If I did this stuff with him and his positional vertigo didn’t get better, I’m only gonna give that 30 days. If I did 30 days with this guy and he didn’t get better with positional vertigo, then we’re gonna incorporate the brain-based rehab immediately, right. But he got better and he stayed better, so I haven’t had to done it. ‘Cause that’s substantially more expensive too, right. All right, so that was my takeaways. And this kind of stuff that I’m giving you guys, all the stuff that you would, all the stuff that I showed you today in terms of looking at his history and breaking it down, knowing what tests to order, knowing how to interpret those tests, knowing how to treat them, what things do you pick, what to do if it doesn’t work, that’s all the stuff that you learned in the neurochemistry classes. And I mean, that’s not all of it, I mean, that’s, you would learn all of that stuff, you would learn those, in the six module classes. And that’s what this point is we’re relaunching that whole six module neurochemistry nutrition series, we’re relaunching that in July. And again, what we’re gonna do is we’re not gonna memorize protocols, just so you can’t do that, you can’t memorize a protocol and treat somebody like that. You’re not gonna learn this this supplement for that symptom, we’re not gonna do that. You’re gonna learn how to approach these cases, just like I did here with you today, you’re gonna have the body of knowledge to do that. And we’re gonna all kinds of different cases, Freddys and I have some other case reviews planned to show you how we apply this methodology in other different types of cases, what do you wanna say about the classes coming up?

– I think one of the things that scholars who are considering this coursework should be aware of is that, when you jump into the education, you’re getting access education for your lifetime, meaning when we update it again, ’cause we’re gonna update it every couple years, you will have access to those materials again so you could either fly in or get the videos or live stream and get the updated content. So you’re gonna always have the most recent evidence-based material to work with to help your patients and that’s invaluable.

– Yeah, it’s huge. I mean, that’s huge, no one does that, no one does that, you’re the only educational institution that does, I mean, in this field that I know of, I mean, it’s huge. I hope you guys, if you plan on coming, I would encourage you to come live, because live is much more fun for me when I have a lot of people sitting there, because I can go through and talk to you and gage how people are reacting. Streaming, I understand the advantage of why people wanna stream, but I like to see you live so we can talk.

– I like live as well, actually, because you are a very interactive professor. And you are asking questions of the people in the room. And when you ask difficult questions, guess what happens? People learn. So instead of hiding behind a computer, come out there, join us in Cape Canaveral. It’s a wonderful experience, I did the program myself. And this is why you’re one of our highest rated teachers, people learn at your courses. And so I’m a big fan of your education.

– I work hard, I work hard at it.

– Do you have anything else for us today?

– I was just gonna say, so the module is gonna be spaced out one every three months. And so there’s so much information that you’re gonna have a realistic amount of time to be able to digest it and apply it. And right off module one, I’m gonna show you how to order labs, we’re gonna get labs ordered so you guys can start applying it on yourself right away. And it’s gonna be really cool, I mean, it’s gonna be really, I mean, it was a lot of fun last time, I’ve updated a little bit, I know we did a video on how we updated that, but it’s gonna be really cool, so it’s gonna be, I think it’s gonna be almost like a year and a half, you’ll have to go through all six modules, it’s gonna be awesome.

– I’ve done, so I have a master’s in nutrition, I’ve done lots of clinical nutrition education. I really admire your education that we’re doing with the Carrick Institute, because it’s neurochemistry, so we’re doing neurology and nutrition together and that’s very important. But I gotta say, the cases that you demonstrate in the classroom which are real cases with real lab markers, with real dosages, that is the most truth I have ever found in clinical nutrition work. Because I have seen other educations and they say, they do the this supplement for that symptom and they tell you these dosages and it doesn’t work in reality. It literally doesn’t. So it’s, I hope people can see the difference in regards to the truth that you’re putting out there.

– Here’s what I’ll say, it’s like, I always always always try to give people what the reality is, because I practice. I mean, this is what I do, I mean, I am not a lecturer full time, right, I don’t, so I think one of the problems with this is people try to dumb it way down so they can sell a sophomore program or sell whatever. You gotta learn how to think, there’s no substitute for knowing how to think, there’s absolutely no substitute, that’s one of the huge parts of this, is problem solving and learning and thinking and yeah, a computer program won’t rescue you, I mean, it won’t save you, I mean, I just looked at a guy’s labs the other day. And it’s like, I’m looking at it going, man, the practitioner that did these labs, they just fed it through the software program. And the stuff that it’s spitting out just isn’t right, it’s just not correct. And plus, it didn’t work anyway. And the people that sold him that software program never told him what to do if it didn’t work, it’s always just, here’s what you do with the initial labs, and then that’s it. No one ever says what do you do if it doesn’t work, how do you know when to retest? They don’t tell you that stuff, and that’s not what we do here, I’m gonna give you how to be a really good clinician.

– Yeah, you want a clinician who can think on their feet about your individual case, not just try to apply a protocol and not know what happens, not know what to do when it doesn’t go out as you expect it to go.

– The things is, so what I’m gonna teach you guys, this is not just lab analysis, it’s how do I manage this patient, right. How do I follow up with this patient long term, how do I apply that to all different types of patient populations, how do I integrate this into what I currently do? That’s all part of the program, so I’m super stoked to do it again.

– Awesome. All right, Dr. Clark, I’ll be there, thank you very much for joining us on this episode of CITV, another beautiful case review. I know we got a couple more planned throughout the next couple months. We’ll catch everybody then, have a great day, goodbye.

– See you.