Transcription
Hey, we're here to talk about the brain and ADD/ADHD and all that kind of stuff. So, this is me. Uh, if you are new to this, this is our summer series. We're just rolling through the summer here, talking about different clinical topics that hopefully are of interest and importance to you. And, um, I'm Dan Kalish. I've been doing this for a long time, 28 years, which is hard for me to believe that that's actually possible. I'm working really closely with IFM these past three or four years. I'm working with Richard Lord every day now, practically. And a lot of what we're going to talk about tonight is his work, basically, that I'm presenting to you. I'm also in practice. I had a ton of patients today. I don't know why today was a busy day doing complex lab interpretation. So, kind of fresh off of that whole experience, and, you know, want to try to make sure that we carry on this tradition in functional medicine of lab interpretation.
And so, a couple of resources for you that I would highly suggest that you purchase if you're interested in lab interpretation. And here is one of them. This is Richard Lord's new book. So, I think it's $279 bucks, something like that. It's 1200 pages long, which, if you think about it, per page is not a bad price. It's called "Laboratory Guides to Health" by Richard S. Lord. It's 200 pages of everything you need to know about labs. And you can buy it from iTunes, wherever you buy your iBook, iTunes type stuff. You have to download it onto a Macintosh or an iPad, and it's an interactive book. And you can, apropos of today, type in something like catecholamine, catecholamines, and find out everything you need to know about catecholamines and the lab testing and all these kinds of things. And it's pretty dense. It's a reference book. It's not the kind of thing you sit down and read after dinner, but it's a very important reference book. And he is the leader in our field in terms of lab interpretation. In fact, he's a scientist that developed most of these labs that we're going to be talking about. And it's kind of a precious resource here and well worth it.
If you don't have the book already, the original book. Let me grab my copy. This book has been out of print for a long time. This was Richard's original book, "Laboratory Evaluations for Integrative and Functional Medicine." That's been out of print for years. And this is a pretty much new but improved version of that book. Quite new and quite improved. And I want to talk about some of these things and that they're going to tie in today. We want to tie in, uh, Richard's work on methylation and how that we're, you know, kind of blends over and relates to neurotransmitter production and detoxification. That's kind of tonight's talk. There's this interface or interaction between neurotoxins, things that are toxic, that are bad for the brain, that damage the brain chemicals, and heavy metals, and methylation, and the neurotransmitters themselves. So, we get these weird behavioral problems like focus, concentration, memory, ADD, ADHD when we are not making the neurotransmitters properly, when we're not methylating properly, and when we're neurotoxic, that, you know, have a lot of neurotoxins. And in most of these patients, that's why I want to talk about tonight, all three of these things are happening simultaneously. They have a lot of neurotoxins, which you can see on the lab. They're not making enough dopamine or epinephrine or norepinephrine, which you can see on the lab. And they're not methylating, which you can see on the lab. These three things together are a perfect storm of bad stuff. And we'll show some lab examples and then talk about some treatment protocols.
So, if you're interested in this, you think it's kind of cool, there's a neurotransmitter master class, a mitochondria master class that I built a few months ago, which is available. And if you can remember this URL, it's like a brain test, right? Here: https://bit. You don't have to remember that because we're going to email this out to you. Okay? And, uh, you'll get the email, I'm sure, you know, today or tomorrow. If you want to check out the master class, you can check that out. And it talks about mitochondria also, a little more detail than we're going to have time to go over right now.
So, always thinking about the highest level when you're trying to explain this to patients. "Doctor, why do I have this problem? Why do I have ADD, ADHD, brain fog, memory problems?" Well, it could be a deficiency. Could be damage to the neurons. Could be genetic. Could be any one of these, maybe all three. I think where we're all heading right now in terms of, um, next-level understanding, right, is how much of this is really, you know, nutritional deficiency and how much of this is really genetic. And in my experience, in my practice, if I look back on it, knowing what I know now, the vast majority of patients that I see have a long history of toxins in their body, neurotoxins or endocrine disruptors. So, they either have hormone imbalances or brain imbalances. And they have some pretty heavy-duty genetic disorders in, in terms of B vitamins, in terms of methylation, in terms of the ability to get rid of these toxins. So, it's a combination of exposure and then clearance problems. And that equals a functional medicine patient. In fact, I think people who are really good at clearing toxins and don't have a lot of exposure don't come into our practices.
So, if we can understand this connection between nutritional deficiency states and genetic factors, you really got it made. These are completely unrelated problems, right? One is that you've got genes that don't clear toxins very well, or genes that don't make neurotransmitters very well. And the other is that you have nutrient deficits. Very different problems. And I think a lot of the confusion in my mind all these last 28 years is that the lab tests, and they're not really pointing out like, "Okay, this is purely genetic. This is nutritional." How can you tell the difference? And that's a lot of the work that I'm doing right now with Dr. Lord is trying to tease those things out.
So, when these chemicals get messed up, we have, of course, weight gain, fatigue, depression, ADD, ADHD. Some extreme levels, you can have even something like Parkinson's. We're not talking about that tonight. And, um, last time we talked about tryptophan a lot. If you want to listen to the last recording, um, I don't know where that is, actually. Um, we'll probably repeat it sometime next year. But we don't, I just want to just mention that this is an integrated system. You need to address both the serotonin side, which we're not talking about tonight, as well as the, um, slash, uh, catecholamine, slash, myconocyte. So, one of the, the take-home message here is that you should be able to use tyrosine and mucuna properly to get the neurotransmitter levels to improve. You should be able to assess neurotoxins and get how to use glutathione precursors or glutathione itself to assess glutathione and fix glutathione issues. And we'll look at some of those labs too. Okay?
And then, you know, there's one more thing you need to kind of understand: methylation and how it relates to both neurotransmitter production and toxin removal. So, if you got a methylation defect, you're not going to make neurotransmitters real well, and you're not going to detox real well. And so that sort of sits in the middle of all this. And we hear a lot about methylation, but what is it really? Like, I don't really even know. Do you know? I don't know. Nobody really knows. So, complicated. I'm going to show you a diagram about what I think. There's just like different ways that you can think about it, you know. And here's one way to think about it. I don't know if this, this may be like not a good idea. So, you may want to close your eyes. This may be like, I don't know, when you're in an action movie and they're about to cut, cut the guy's finger off or something, you know, they're going to cut his finger off. I always close my eyes because I don't like to see like horrible stuff like that happening. You may not want to see this diagram on methylation, or you may be like intrigued now that I said that this is kind of like a dangerous and not great thing. Here we go. So, and, and this is just to get an impression, not to memorize anything. But, uh, let's see here. Oh, I don't know. I'll come back to it later. Maybe I can't even find it right now. It's so confusing. Let's not, let's just skip that. Let's just look at the actual slides here. Okay.
So, you've got, I'll come back to that at the end. So, glycine protects the brain, right? Glutamine protects the brain. N-acetylcysteine protects the brain, okay? And we can measure for all these things. So, I'm putting glycine on here because everybody always forgets about glycine. But glycine, N-acetylcysteine, or cysteine, glutathione, these are all measured and these are all important for protecting the brain. So, we have, again, think about glycine, glutamine, cysteine, or N-acetylcysteine. Those are the sulfur-containing amino acids that help protect the brain. And then together, they make glutathione, which protects this whole system that we're looking at right now. And then on the production side for the neurotransmitters themselves, you need to learn how to use tyrosine and herbal form of L-dopa, that's called mucuna. And if you can figure those things out, you're going to be in pretty good shape. And the way we measure all this is by measuring tyrosine levels themselves, measuring phenylalanine levels by measuring the amino acid. And there's an interaction here is that we should freely convert phenylalanine into tyrosine. And there's a ratio or a balance that should exist between phenylalanine and tyrosine. If that ratio is not being maintained, you're going to potentially have problems with dopamine, norepinephrine, and epinephrine, which is going to be problems with ADD and ADHD and memory problems and focus and concentration and obsessive eating and all that. So, we're going to look in depth tonight at the ratio or balance between phenylalanine and tyrosine. And if the patient can't maintain that, then you're going to have a pretty big problem.
Okay. So, there's a disease in newborns that we all learned about in school called PKU. PKU, you know, when babies are born, they do a heel stick, they take a little bit of blood, and they would let the mom know, "Oh, your child has PKU," because it's a really severe genetic disorder. And if you don't know that by the time you leave the hospital, you're feeding your kid wrong, you could have some serious, you know, neurological damage or other really big health problems, or your baby could die. So, when babies can die, we take it really seriously. We do these genetic tests. And again, if you have PKU, it means that you cannot convert, the baby cannot convert phenylalanine to tyrosine properly. And that's a genetic condition. It's relatively rare. And, you know, people learn about it the day they're born, right? Their mom tells them as soon as they can figure it out because you have to eat in a special way. What you're going to find is that there's a certain percentage of the patients that we work with that have a snip or a genetic defect in their ability to process phenylalanine and turn it into tyrosine. Obviously, they don't have PKU, or they would have died, you know, either been identified in childhood or died in early childhood. So, not having PKU, but they have a very, very mild form of PKU. It's the same thing with all the diseases that we treat. You could have a heart attack and drop dead. You could have high blood pressure. There's a spectrum in there. Yeah. You could have, you know, blood sugar instability. You could have diabetes. There's a spectrum in there. So, you can have PKU in the newborn baby, but you can also have a variant of that, which is inability to convert phenylalanine into tyrosine. And that shows up on these labs. And I'll show you how to find that.
So, if that's happening, it means this person has a genetic problem with getting enough tyrosine. And they're probably going to need some tyrosine off and on throughout the rest of their life. And if they have that problem, they're highly prone to thyroid imbalances because the tyrosine converts into thyroid hormones, and to what we're talking about tonight, which are the catecholamine imbalances that cause ADD, ADHD, and are behind a lot of the attention and memory problems. Okay. So, we'll look at these in a moment. But what we're concerned about is, can this person convert phenylalanine into tyrosine? What's that ratio like? And if there's a block there and that can't happen because of a genetic defect, then guess what? Phenylalanine will be high and tyrosine will be low. It's that simple. So, if you ever see phenylalanine up a little bit and tyrosine down a little bit, that shouldn't happen. That means that there's very likely a genetic block in their ability to convert phenylalanine to tyrosine. Solution? Obviously, you can't use phenylalanine. That's going to work, right? That's not going to work at all because the enzyme defect is right here. So, you give tyrosine to make up for that. And again, I'll show you in a few minutes when we did the lab review how that works. So, that's item number one. You should just memorize and understand how to diagnose that because that happens. I see that in my practice a couple times a month. And if you miss that one, you know, people are going to just kind of skate by, and it's not a good thing.
So, item number two would be that we're going to look at homovanillate and vanillylmandelate, how these two get produced. These are the urinary byproducts of dopamine and norepinephrine and epinephrine, right? So, I don't know if I can blow this up a little bigger. Oh, yeah, look at me, I can. All right. So, I don't know, this goes back to like high school chemistry. But remember, Cu means copper. So, you'll have some patients that have no problem making dopamine, and you will see that their homovanillate level is normal, maybe even it's a little high. But they don't have enough copper. They don't have enough copper. They don't have enough copper in their body. And so they can't make epinephrine and norepinephrine. So, they get spacey and tired and they can't focus. And you'll see that their vanillylmandelate levels are on the lower side, whereas their homovanillate is kind of up there. So, if there's a differentiation, if homovanillate is normal or high and vanillylmandelate is low, it means they have a problem with copper. In which case, the block is right here. This is a nutritional deficiency, right? They have a nutritional deficiency and there's a block right here. So, they're okay with dopamine, but they're not okay with norepinephrine and epinephrine. And those people need copper. Copper is not the kind of nutrient you usually just wake up in the morning and think you're going to prescribe all day. But you should know how to use copper because if you don't give these people copper, they're just going to get stuck. And if you give them thousands of milligrams of tyrosine every day, and they don't have the copper, and they have the copper problem, then they're not going to get better, right? So, copper can be super important. How do you know? Because homovanillate will be good, vanillylmandelate won't be, it'll be low because they're not coming down to this extra pathway. And that could be anything from ADD to ADHD to asthma, right? Because epinephrine and norepinephrine are important for a lot of different things. Okay.
So, those are kind of random factoids to keep in mind. We're going to look at this variation of PKU where you can't convert phenylalanine to tyrosine. Be on the lookout for those folks. And then this problem where people have a copper deficiency, they don't have enough copper. And then we're going to cover all the basic stuff as well. Okay. So, again, same thing we're looking at here, talking about tyrosine converting to thyroid hormones, all these metabolites. And here we have the cofactors again, written out, make it a little clearer for you. You need vitamin B6, you need copper, and vitamin C. Remember, there's a big problem with a block right here. Not enough copper means you can't make enough norepinephrine and epinephrine. And then how do you know that that's a problem? Because vanillylmandelate will be low. It's the same thing, but same diagram, but sort of represents slightly differently. Homovanillate will be okay, vanillylmandelate will be low in people that have a copper deficiency. And if someone's been walking around their whole life with a copper deficiency, they're going to care that you give them copper. If they don't have the problem, then don't give it because copper can be toxic. All these nutrients can be toxic. You just want to hand out, don't want to hand out copper. But if you know they need copper, then it can be a game changer. And again, we're going to look at phenylalanine converting into tyrosine. If that's not happening and phenylalanine is normal and tyrosine is low, then you know that they have a variant of the genetic disorder that we call PKU. Then.
So, let's see. Let me kind of summarize. We talked a little bit about the neurotransmitter production side. Do they have enough copper? Do they have enough tyrosine? Do they have the phenylalanine and tyrosine problem? All that. Then we want to consider the toxin side, the detoxification, which is going to center around glutathione. That's your glycine, glutamine, N-acetylcysteine. And you want to have that protection from glutathione to protect the brain and to protect these catecholamine systems. And, and this is really confusing, and you just see this written in different ways. So, I'll just mention it. Glutathione is made up of three amino acids. And you should just know this. This is like something you should measure with. Sometimes people call it glutamate, sometimes they call it glutamine in the supplement form. It's glutamine. Glutamate is scientifically accurate as well. So, that always kind of confused me. But those are used interchangeably. And the things that we read all the time. So, glutamate or glutamine, cysteine, and cysteine is usually the supplement that we use, and glycine. So, let me say it in two different languages. It's like the science guys will say glutamate, cysteine, and glycine. If you're talking about supplements, usually we're talking about glutamine as a supplement, N-acetylcysteine as a supplement, and glycine as a supplement. And those are really critical because those are how we make our glutathione. And you have to have these amino acids present for the production of, um, of the neurotransmitters too. And then there's folate, B12, B6, all the things that we kind of associate with methylation. So, those are important too.
Oh, here's the diagram I was looking for. This is a methylation thing. Okay. So, remember, again, review. Dopamine sitting on one side. Do they have enough copper? Do they have enough tyrosine? Do they have that weird PKU thing? What's going on? I'm going to correct their dopamine. Sitting on the other side, you got, are they, are they neurotoxic? Do they need glutathione? Do they need N-acetylcysteine? Do they need glycine? Do they need something to get toxins out, right? And then remembering that these sulfur compounds are required to make the neurotransmitters, which is weird. And then right in the middle of this sits methylation. Methylation's controlling both sides. Methylation is controlling the ability to make the neurotransmitters, and methylation's controlling detoxification. So, if you've got a problem here, then everything's blown out. And it kind of says that right here. Methylation products, epinephrine. See that? But now we're not going to have too much time for methylation. But let's just briefly talk about the single carbon pool. We all know that to methylate, you need B12, right? B12 is the link here. You need folate and you need B6. And that's in every supplement catalog, in ev, from every company. But what's kind of interesting and kind of cool is that right up here, I'm going to blow these up because these are things you may not have thought about a lot. Part of a very important part of methylation is happening up here. And this has to do with the conversion. And honestly, I mean, I'm still trying to understand this myself after 20 years, but the conversion of methionine to homocysteine. So, your body takes methionine, it makes homocysteine. Your body takes homocysteine and makes methionine. So, when we look at these labs, if you see low methionine, big, big problem. If you see low methionine, big, big problem for everything that we're talking about, brain, detox, everything. If you see low homocysteine, not high, but low homocysteine, big, big problem. Why? Because that means that you can't run these methylation pathways. So, high homocysteine, we are not talking about that. That would be a cardiovascular disease lecture. We're talking about extraordinarily low homocysteine or extraordinarily low methionine, meaning that you can't run this part of methylation. And then the link between this higher part of methylation, the lower part down here, is vitamin B12. So, you've got to have that pulley. That's just everywhere throughout this. You can't even count the number of folate things, right? THF, anyway. You see that? That's that folate, really a thing. And then what's, and of course, B2, B6. But then what's a little strange is that in order to get the single carbon pool going, in order to methylate properly, you need to have amino acids. And not all the amino acids, just a few: serine, glycine, histidine, glutamate, glutamine, right? And tryptophan. Weird, right? Did you know that? I didn't know that. I think that's kind of cool. You need amino acids to provide these single carbons in order for the single carbon pool to exist, in order for you to be even talking about methylation. So, you also need good amino acids. And when you're looking at the labs, it's going to matter because remember, just to keep it simple, you have to memorize everything. Low methionine is disastrous. Low homocysteine is disastrous. And then low amino acids over here, serine, glycine, serine, glycine, histidine, glutamate, can be converted over there, but tryptophan, any of those being low, also disastrous. So, amino acids, glycine, serine, histidine, tryptophan, dose being low means you can't methylate because you don't have the single carbon pool. Weird, right?
And then you can think about this is easy-peasy stuff. We're going to give tyrosine. If it's not strong enough, then we're going to give mucuna also. And there's a bunch of enzymes that are involved in that. We probably don't care too much about. Okay. And then I was a self-promotional thing for my master class. And the thing you got to be a little bit careful about is tyrosine has a regulatory control thing where you can only make a certain amount of catecholamines from tyrosine. Mucuna doesn't have any regulatory control. So, the more mucuna you give, the more dopamine, epinephrine, and norepinephrine they're going to make. So, just be a little careful when you have mucuna products in your hand because they're strong and there's no like shut-off valve on them. Okay. When you're talking about the, um, tyrosine conversion, and we use tyrosine a lot, I do, talking about tyrosine. Tyrosine converts to L-dopa, then dopamine, norepinephrine, and epinephrine. But if at some point, if you give enough tyrosine, there's an enzyme that shuts this whole thing down. So, you won't, it's not so easy to make people, to give people too much of the catecholamines using tyrosine. But mucuna, not so much, you know, has no safety valve in that sense. There's no enzyme that helps shut things off.
All right. So, let's talk about a common clinical protocol situation. I want to show you some labs and then I want to talk about, I guess, a little bit about, um, just the practical aspects of doing this. So, you know, the, I don't know, I mean, we have, we're wearing so many hats in functional medicine. We're learning how to be clinically competent, you know, and that's where I put most of my energy, my whole career. At the same time, you got to run a business. You got to hire people. You got to fire people. You know, it's a merciless thing to run a business. You gotta really pay taxes if you don't want to go to jail, you know. There's a lot of stuff that's involved. And I think one of the key ways to make this whole thing work, and from a business perspective, is to have clinical competence. But to also, you know, spend two, five, six, seven, eight hours a week on your practice, on the business side, right? And a lot of clinicians are kind of spaced out, talk about brain fog and memory problems and stuff like that. So, as you get crisper and crisper with your own brain chemistry, maybe run, run one of these tests on yourself and tune yourself up, then you make sure that you focus some of your time on your business so that you're not stressed out of your mind. Because there's lots of successful clinicians who are stressed out of their minds and really don't help patients very much because they don't have the business part figured out. So, I think we just need to put an adequate amount of time, I don't know, like at least two to five hours a week, you know, just pure administration and working on the business.
Okay. Let's talk about common clinical scenarios. Some kind of thing that we walk into my clinic all the time. Detox pathways aren't working well. Lack of glutathione. High stress. Completing the catecholamines. Methylation's not working. So, now the toxins are building up even more. And now they can't make, make the catecholamines either because the methylation's off. And then all of a sudden, you know, they're wondering why they have a problem. Okay. So, toxins induce neuron, neuron damage. Like these toxins actually physically damage the neurons. And this is a problem. Now, let's go here and, um, let's look at some labs real quick. You can see some real cases. Now, this is an Ion Panel from Genova. It includes organic acids and a bunch of other stuff. I just want to show you a few of the key markers related to what we're talking about tonight. So, we're skipping a lot of stuff, kind of focus on the important part. So, here you will see phenylalanine and tyrosine, both measured. Now, from just already what we talked about, if phenylalanine and tyrosine are both low, that's a pretty bad sign, right? That, you know, the person's brain is not going to be getting the nutrients it needs to make the catecholamines. You can't make these chemicals out of thin air. You need to have the actual stuff you need to make them.
I'm going to skip around a little bit and we'll show you. Oh, wait a minute. Oops. Remember we said that in homocysteine levels, we're always thinking about high homocysteine, bad. High homocysteine, bad. Give homocysteine blocker, com supplement, give B6, B12, folate. Every integrative doctor gets it drilled into their head. High homocysteine is bad. The regular cardiologists don't understand that. So, you get B vitamins and you knock it down. But nobody ever talks about low homocysteine. Is it a lower the better situation? Absolutely not. That's why there's a little red zone down here because low homocysteine. Let's do a little flashback here. I'll flashback to my other diagram. Not so easy, is it? There we go. Remember low homocysteine? Remember, you can't methylate. Homocysteine high, not good. Not what we're talking about. Low homocysteine, low methionine, cannot methylate, can't detox, can't make brain chemicals. Game over. Low homocysteine, bad. Low homocysteine, bad. So, high homocysteine, bad. Low homocysteine, I don't know. You, if it's even worse? Maybe. Yeah, probably. It's even worse. But anyways, equally, let's say at least as bad. How are you going to fix that? Well, look at the diagram. Methionine. Yep. How hard was that? All right. Let's go back. Low homocysteine. Oh, and just for kicks, we could go back up and say, where's their methionine? Low. Normal. Okay. All right. Oh, and just to open your eyes to this other stuff because this is so cool. Remember we're thinking about methylation and we're like, wait a minute, these are, there's amino acids related to methylation. Yeah, they were. And here they are. Glycine, serine. Remember those? Those are related to methylation too. So, methylation is a little more complicated than we usually think about. So, we talked about that. Oh, and then this test also measures copper. Copper levels were good, so you're not worried about copper. But we could be worried about copper. We should be worried about it. Not in this case.
And then let's scoot on down to the neurotransmitter metabolites, which are way down here. And oops, vanillylmandelate and homovanillate are quite low. That's not good. That is ADD and ADHD on a lab report. If you can bring these up here, I guarantee you this person's brain will be a whole new and fresh and better brain. Okay. These are both low. What do they need? Tyrosine, methionine, right? You can kind of see phenylalanine maybe if you want to give them because they're low in phenylalanine. So, you can see the precursors like phenylalanine and tyrosine low. The result is these metabolites are low. The result is that they can't make enough brain chemicals. There's no one can feel good. If you run a lab like this, and both these levels are low like this, guarantee you the person is going to have some pretty serious cognitive problems. They're going to be complaining about, "Just doesn't feel good."
All right. So, let's go look at one more example here. See, we're okay on time. Yeah, a few more minutes, then we'll stop. Um, it's a whole new case. Yeah, I think it is. Let's see. Oh, here we go. Remember I said that the ratio can be off? Phenylalanine and tyrosine ratio is high. That means there's a fair amount of phenylalanine and not enough tyrosine. When this ratio goes high, that means they have that snip, that's a distant cousin of PKU. They can't take phenylalanine and turn it into tyrosine. So, they can't, in turn, have a, they don't, in turn, have enough tyrosine to do all the things that tyrosine's supposed to do. Okay. So, be on the lookout for that ratio. That would invite a neurotransmitter problem because they don't have enough tyrosine. Kind of makes sense, right? This person's homocysteine is normal. Well, that's good. Their copper is normal. That's good. Then we'll just skip on down to the neurotransmitter markers, way down here. And now homovanillate is quite low, and vanillylmandelate is fine. So, they have extraordinarily low dopamine, but epinephrine and norepinephrine are fine. That's interesting. Very specific. Get that dopamine level up, they are going to feel like a million bucks.
And let's look at one more, and then we'll wrap it up, and I'll answer some questions. So, here's another one. You can kind of scoot down through here. Well, let's just look. We can see, we kind of see glycine is low. Remember that's one of the amino acids you use to make glutamine. Hmm. Just thinking. Hmm. Is that bad? I don't know. Probably. That's not a good thing. Arginine is low. Tyrosine and tryptophan seem to be fine. These other ones seem to be fine. So, let's see what the heck else is happening here. As we go on down, now you're kind of getting used to this, right? You can look and you see, I'm also seen as normal. Copper is normal, so you don't have problems there. And then let's look at the actual brain markers themselves. Oh, they're both normal. I don't know. That one's a little on the high side, but it's, yeah, it's still within the normal range. Yeah. And then this person has, remember they had a glycine problem. So, when pyroglutamate goes high, that is a glutathione marker. In fact, all three of these markers here, alpha-hydroxybutyrate, pyroglutamate, and sulfate, they're all glutathione markers. So, this person has a glutathione problem, but not such a huge problem with the brain.
And let me just go back and I'll show you. Wrapping this up. Oh, that didn't work, did it? Sorry. What I did there. That was weird. There we go. So, uh, program design. Thinking about the supplements: tyrosine, mucuna, and N-acetylcysteine. You should learn how to use glutathione, B6, folate, glycine. It's a lot. You know, it may take you a few months to really figure this out. It's probably not going to happen all at the same time. But you get the conceptual framework. Methylation in the middle, neurotransmitters on one side, detox on the other side. That'll get you going. And that you balance both dopamine, epinephrine, norepinephrine, all of those by also looking at methylation and detox. And you will find, as I have, I'm sure, that a very large percentage of people that are low in glutathione are going to have low dopamine. And a large percentage of people that can't methylate are going to have both of these problems. And you start to see the genetic underpinnings of a lot of this stuff. And then if you guys are just deathly curious about more, you can buy the master class. And we're right on schedule here. I'm going to open it up for some questions for the last couple of minutes.
Uh, what areas of the Ion Panel do you need to focus on treating patients with Parkinson's? So, for sure, detox and methylation probably would be the places that we would start. That's a good question. All right. What we're talking about today, uh, Nyman suggests some supplements for tyrosine and mucuna. So, all the companies that we work with have tyrosine. It's just sold as L-tyrosine, either usually in a 500-milligram capsule, sometimes maybe 600 milligrams. That's pretty generic. Any of the companies that we work with have that. For mucuna, the two companies I use are Pure Encapsulations, and they have a product called Dopa Plus that has mucuna in it, which is very effective. And then Designs for Health, and they have a product called Dopa Boost, which has mucuna in it, which is equally effective. So, you have, depending on if you prefer one company or another, Designs for Health or Pure Encapsulations, both have mucuna products.
Uh, do you find patients who have been on medications are often depleted? Yeah, absolutely. The more medication that you're on, and it could be anything from antidepressants, which deplete neurotransmitters, to drugs like cocaine, which deplete neurotransmitters, the ADD meds, all deplete neurotransmitters. So, the longer the person's been on a medication like an ADD med or an antidepressant or something like cocaine or speed, the more depleted their brain will be. And of course, some are more dramatic than others. Like, obviously, if you're on methamphetamine every day for a long time, you're going to be really severely depleted. But, you know, Wellbutrin and the ADD meds are going to cause problems over time. That's part of what their effect is, is they deplete things over time. Yeah. You can do, you can get some of this information from organic acids only. It's not quite as complete, but you can do that.
So, then Stephanie's asking, what if I see high phenylalanine and tyrosine? That's weird. I don't know. I'd have to see the rest of the lab. Not sure. Most of the time, when amino acid levels are high, it means they're not being broken down properly and they're circulating in the blood. And so you have to look at what nutrient breaks that amino acid down. And more often than not, it's a B vitamin. Okay. Low PQQ mean low tryptophan? Not necessarily. No. Can you take coaching training? Did I take coaching and training courses? Uh, yeah, constantly. Um, I've been through all the IFM classes like three times. I worked one-on-one with Dr. Timmons and Dr. Freder. Dr. Timmons for six years, Freder for five years. I pathologically took almost every course that was out there. Now, this is in the '90s, okay? I'm a little old. But I took every weekend conference and daily conference and class that was available from like 1995 for the next 15 years. Then my son was born, and I took a break, and I was like, "Okay, enough of the conferences." And then I got back to it. So, I would just go out, you know, you got to take them all, basically. My classes are just the beginning, really. See, hi MMA. Now, I'm kind of confused. Stephanie's trying to ask questions, but I don't really understand. Oh, here we go. High ammonia but low orotic acid? Erotica orotate? Basically, I think of orotate. Well, that's a confusing question. I'm not sure that's, I don't know. That's too specific. I'm not sure. But I can tell you one thing, um, is general for Stephanie's question, which is that, um, yeah, one minute here. Yeah. So, let me just mention this. So, when with a lot of these labs, this is something Richard talks a lot about in his new books. There's a, um, phenomena called hypo, well, they're compensatory states. Compensatory states. This column, this is a horrible example of it. That's not a good one. Let me find a better example. And compensatory states are confusing. So, by definition, a compensatory state means you're compensating for something. And so I'll show you, like, it's easier to see it on organic acids, probably. But in a compensatory state, you're going to have low homocysteine, low orotate, you might have low amino acids. You're going to definitely have low organic acids. Everything's low, low, low. You might have low fatty acids. The person's just decompensating, really, and starting to fall apart. And so if you see these patterns, like here's, this is a pretty good example here. Let me just, I'm going to zoom out, and you see low, low. Let's see, low, undetected, which means very low, low, undetected, undetected, right? This person's not making a lot or not making enough of these organic acids. Why? You go on, you look at some of these other markers, low with the brain markers that we're just looking at. And then you look at orotate and glucorate and pyroglutamate, low, low, low. So, in many of these compensatory states, you're going to see low detox markers, low mitochondrial markers, low neurotransmitter markers. The person just doesn't have the basic nutrients and substance and sustenance they need to make these chemical pathways work. Okay. And those people, they need pretty large dosages of amino acids and other nutrients to bring things back. Let me just point out one last thing because this is a perfect example. Remember how we said high dopamine marker? This is the homovanillate and low vanillylmandelate. Look, I just stumbled on this one. This is your classic copper deficiency. Ding! High homovanillate, low vanillylmandelate. That means that they're making plenty of dopamine, but they can't make epinephrine, norepinephrine. And that means they need and adrenaline. And that means they need copper and tyrosine together and vitamin C to make all that work. So, again, that's a classic example of what I was just trying to talk about. There's that and that. And when there's a huge differential there, that ratio is off. Copper, vitamin C, and tyrosine will work really, really well. And don't give copper unless you have to, right? Because it's kind of a weird nutrient to give.
And a few more questions that will wrap up. So, Elena asks, is Genova test appropriate for someone who would like to go off SSRIs? Absolutely, yes. Do that a lot. I think that's a great thing to do. Low H, low HVA, and VMA, and a high ratio of the two, but feels fine. Yeah, if people feel fine, you don't have to do all this. If there's absolutely no complaints, I mean, you might want to do it just for fun and just see what happens, you know. Sometimes people are depressed but they don't realize it, or they're not aware of it. Sometimes they, you know, have been anxious their whole life and they don't know what it's like to not be anxious. So, I basically fix anything I find on labs and then wait and see, you know, what are the potential symptoms that start to relieve. I see more questions about coaching certification courses. I didn't do any coaching certification outside the doctor stuff. I'm not really like a joiner. I don't do well in groups. I'm just kind of like a lone wolf person. So, I haven't really been certified. Well, I was certified by IFM, but that's because I went to their classes like three times and I took the test. Let's see. Uh, why did I take IFM classes? Because they're, I don't know, just go meet the IFM faculty. Bob Brown, Tree, Michael Stone, Patrick Hanaway. You know, they're legends. They're all just legends. Each of those human beings. It's just, you know, Phil Amanna, Christy Hughes. I mean, every single one of their faculty. You sit down and talk to them for an evening, you'll learn more than you ever learned in your life. It's just, and it's a very spiritually connected group of faculty as well. Um, David Hassi. You want to have a good time and learn? Like, these are mind-numbingly bright people. They're all actively in practice. They really know what they're doing. And their backgrounds are amazing. And so, you know, I've been able to hang out with them for the last three years and learn so much from each of those people on every level, emotional, you know, spiritual, as well as, you know, all the biochemistry and functional medicine stuff. So, yeah, the, the IFM faculty is like, I don't know, I don't think you get a better group of people in our industry anywhere, really, to be honest. But you got to go to the conferences and not just sit in the back. You got to engage with people. Ask people if you can take them out for lunch, or at least kind of corner them for 10 or 15 minutes and talk. Ask them if they want to go out for a drink or something after. And, you know, kind of interact and network with the people that are there. And you really learn a lot. Okay. All right. And the Neuroval and Ion Panel tests for MEG are basically interchangeable. You know, there's some pros and cons to each one. You know, I just like the Ion Panels because I'm old and I've been using them for a while. But they're almost interchangeable with Neuroval. Okay. They're basically the same test. All right. I'm going to wrap it up for tonight. We'll be doing another one of these soon, and I hope to see you guys there. Okay. Bye for now.