Transcription
Hello and good evening and welcome. I hope my sound works. I hope you can hear me up here. Internet is working. Um, because that's really been a problem lately. If someone could raise their hand to just make sure that you can actually hear me, I would totally appreciate that. Oh, thank you, Barbara and Anne. Pretty much all right. So we're good to go. Um, all systems running.
Topic for tonight is mitochondria in the brain and the magnesium glutathione dyad. It's a lot to take in. It's super important. You're going to see it in your practice all the time after this conference. You're going to, after this talk, you're just going to be like, wow. Tomorrow morning, I guarantee you half of you guys are gonna see this in your practice like tomorrow morning. Okay. It's one of those things that you're just hitting your head going like, why didn't somebody tell me this like 20 years ago? You know, like, what's the deal? Like, why does it take so long to learn everything? Um, it's going to make total sense, but it's probably not something you thought about. I didn't think about it. I've been in practice for 25 years until I learned about this. And it's not like I'm some brilliant person. What I do is I talk to Richard Lord twice a week, and Richard just tells me everything that he knows. And so I'm communicating that to you. So this is in, in, um, in memory of Dr. Richard Lord. He's not dead, he's still alive, but this class is all about him. He's my teacher. I work with him every Monday and every Thursday for the last four years. He's, for those of you that aren't familiar with Richard, he was this original scientist that thought about organic acid testing in the late 1960s. He had the gumption and energy to go out with Andy Brawley and start a lab company called Metametrix. And these guys ran the first amino acid profiles, the first fatty acid profiles, they did antioxidant testing, they did organic acids before anyone else in the industry even considered doing that, way, way ahead of their time. And Richard's old now, he's in his late 70s, he's almost 80. He doesn't like to wake up early and do talks like I do. I'm still in my 50s, you know, but he's really willing to talk to me a couple times a week and and tell me everything he knows. And he's still learning, as I am from him. You know, he's learning and he looks at my cases. And, you know, it's really just been the most wonderful relationship I've had professionally. And so this is 100% Richard's work. If you're wondering about anything, because I don't have time to cite all the studies, buy his book. Go to iBooks or iTunes, wherever you buy your iStuff, your Apple product. You need to either buy it on an iPad or an iPhone or a Macintosh computer. You can just type in Richard Lord Laboratory Guides to Health and you can buy his book. It's like three or four hundred bucks. Be the best money ever spent. It's a little expensive, but don't worry about it. It's 1200 pages. Each page in there is just like gold. Okay. And he explains in the book and cites over three or four thousand research studies on each topic he's talking about. Right. So the, you know, the everything I'm talking about tonight, you can go to Richard's book, you can look up the scientific studies on it. Okay.
So, um, that's all. It's all real stuff. Okay. So let's talk a little bit about me. Who I am. I'm Dan Kalish. I've been working on this for a long time. I worked with IFM for a while. I worked with Mayo Clinic for a couple years. Working with Richard Lord now. I'm still in practice. I teach a lot. And I have this institute at the Kalish Institute. We teach a lot of courses. Coming up in June, we have a Lab Interpretation Boot Camp on genomics. That's again, all of Richard's work on functional genomics. The cool stuff, like the really cool stuff, including the SNP testing. But really more focused on how to interpret these labs from a genetic perspective, how to interpret organic acids and fatty acids and amino acids from a genetic perspective. And how can we even do that? I'll talk about that a little bit more later tonight. How that's even possible. Then in August, we have, um, a repeat of our once a year Telehealth Business Essentials Boot Camp. That one's been really popular. People love it. I just talk about my business. I've been running a telehealth medicine, telemedicine, whatever I call it, a phone practice. I've been running a phone practice since 2006. It's a long time. And, you know, kind of know how it works and happy to teach you all as much as I can about the business side of things. Okay.
So, um, for night, for now, though, we really want to think about magnesium and glutathione and how are they even related? And then how oxidative stress impacts the brain and how it impacts mitochondria. And then look at the most commonly used supplement programs. We'll have some lab review at the end and questions at the end. How can you really start to restore normal function, normal physiology in these people? You know, I just had a case like this this week, which was really interesting. Major pro. All of our problems centered around the brain. Depression, brain fog. Absolutely beautiful neurotransmitter function. No problem with actual neurotransmitters. Has been on every antidepressant known to humankind. None of them helped at all. Looks like, sounds like, feels like a neurotransmitter problem, but it was all coming from her mitochondria. They were just completely shut down. And so, of course, the brain is an energy hog, right? The brain takes up huge amounts of ATP. And if your mitochondria are not up for the task of making cellular energy, you're going to have a major problem with the brain. So it's not surprising. Okay.
When we think about the major source of reactive oxygen species, the major source of free radicals, the major source of oxidative stress in the body, where does that come from? I can remember four years ago, Richard asked me that. Where is it? Where, you know, it's a straight-up question. Where does most of the oxidative stress come from? And I said, without even thinking, heavy metal and chemical toxicity. And he was like, wrong. I was like, oh, crap, really? I always thought all the oxidative stress was from all the bad stuff. And he's like, no. You know, of course, there's some of that, but most of the oxidative stress in the human body comes from our own internal production of energy. It's a crazy system. We have these mitochondria. They're not really even part of us. It's some other ancient bacteria thing that we kind of subjugated in some weird way, right? But the, and that, and they're just making huge amounts of ATP. Huge amounts. We were just talking about this. One, one of the students in the mentorship, Lars, just sent me this email from Germany, saying that the rotational speed for the ATP synthase, you know, the thing that spins around that's cranking out ATP, it rotates 14 times per second, right? And it's generating thousands of units of ATP per minute. And in general, a single brain cell, a single brain cell at rest, not even when you're stressed, but a single brain cell at rest has so many of these mitochondria cranking. It generates 4.7 billion units of ATP, not in like an hour, in a second. In one second. Okay. There's a lot of this stuff going on like so fast you can't even really comprehend. Like four billion times in a second in one brain cell. How many brain cells are there? Do the math, right? This is like, you make almost your weight in ATP every day. That's how crazy this is. Look it up. I didn't think that was possible either. I read that in one article. I was like, how could that? Yeah, it's true. You make a lot of ATP every day. Just per millisecond, you're cranking this stuff out. So there's massive amounts of free radicals being generated from that. And if this system gets a little wonky, you're in serious trouble. Too many reactive oxygen species, not healthy for brain cells. Okay. They crank up. If you crank up the free radicals too much, brain cells die. It's not like they're injured or insulted or feeling a little upset. They're dead. It's not like someone whose feelings are hurt. It's like someone who is stabbed to death. Okay. The brain cells are gone. It's not a, it's not a pretty sight, right? And what's protecting us from this is glutathione. That's the main antioxidant that we can just adjust millisecond to millisecond, up, down, up, down, protect, don't protect, protect, don't protect. Okay. And the other, the other antioxidants that we have, vitamin C, vitamin E, you can't all of a sudden crank up your vitamin C levels just because you're breathing in, but, you know, breathing in a bunch of diesel exhaust on a freeway. Right? Your glutathione levels can go up in a millisecond. Your vitamin C is kind of stuck where it is until you eat your next orange, whatever, right? So glutathione is not only the master antioxidant, it's the antioxidant that can respond to these insults moment by moment. Okay. And that's the good news. The bad news is that glutathione is in this constant battle every second of your life. And it's fighting with what? It's fighting with methylation. I know it sounds a little strange, but that's how we're set up. We'll look at some images of that. So the basic story here, B vitamins are what make everything in your body actually work, okay? If you, if you all of a sudden ran out of vitamin B1, like right now, for some weird reason, that all the B1 in your body vanished, you would be instantly dead. Okay. It's very important to have B vitamins. We often see people with genetic issues, meaning that they need a lot more B vitamins than the average person. MTHFR is just the tip of the iceberg for the SNPs, okay? There's a lot of different genetic defects that cause people to need huge amounts of B vitamins. And B vitamins are make what everything in your body is relying upon to actually work, right? That's not a mistake. That's a repeat on purpose because we're very vulnerable. And in fact, most of the patients that I do workups on have a genetic variation in their B vitamins. That's why their patients. If they were, didn't have that problem, they'd probably just eat a healthy diet and get better. Okay? These people can't eat a healthy diet and get better because they can't get enough B vitamins from their diet. It's not possible to have a genetic problem. Okay.
And so then we're going to take a step back, the, the 30,000 foot view, and think about like, why do we even have mitochondria in the first place? Why does this even exist? It's a dangerous thing. Why do we even have them? Well, because mitochondria are literally why we breathe. We consume oxygen, breathe in and breathe out. And 90% of that oxygen that the body uses is going to the mitochondria. And it's going for a very specific reason, right? Oxygen is the ultimate electron receptor. It's at the very end of that electron transport chain. And it grabs the electrons, makes water and a bunch of ATP. And that's how we survive. And if you wonder how important this process is, just try holding your breath. Take a deep breath in. I do this every day from one of my meditation exercises. Breathe all the way out. Just humor me. Breathe all the way out and hold your breath out. And I don't know how long you can do that, maybe a minute or two if you're really good. But it's not an easy thing to do because we need the oxygen to pick up the electrons. If you don't have that, then the electron transport chain or respiratory chain starts to shut down. And we don't make that ATP. And all of a sudden, you're not making 4.7 billion units of ATP every second in your brain. All of a sudden, you're not having this thing rotate at 14 times per second, every individual ATP synthase thing rotating like that. All of a sudden, the whole thing shuts down if there's not enough oxygen. Okay.
So now, this magnesium glutathione dyad. We want to understand the magnesium side and the glutathione side, both. And then this whole thing will make total sense. So let's take a look at this a little bit in depth and how this presents in terms of patients. And I see this like literally every day in my clinic. Patient comes in, they've been taking magnesium for years. I run their magnesium levels, and their magnesium levels are low. They're like, yeah, I don't know. I take magnesium all the time. Either it's a poor quality product they're buying some junky magnesium, or they have low glutathione, and they're not able to utilize the magnesium because the glutathione's low. Now, why would that happen? Well, we again, use glutathione as the master antioxidant. And glutathione is in constant competition with this methylation process up here. So every moment of the day, your body has to decide, am I going to send messages down this way, transmethylation, or am I going to send messages down this way, transsulfuration? Okay. And the more oxidative stress that you have, the more oxidative stress that you have, as oxidative stress goes up, you're going to methylate less because your body is going to preferentially go through this transsulfuration pathway to get your glutathione levels up. Okay. So the more oxidative stress you have, the more you need to produce glutathione. And if you don't produce glutathione, your cells die. So making glutathione is more important than methylating. And methylating is pretty important. DNA, you know, needs to get methylated. You need methylation to make hormones, to make neurotransmitters, to make a lot of stuff, to make creatinine or creatine, to make, choline, to make cell membranes, to make muscle energy. I mean, methylation is really important, right? We know that. But glutathione production is quite a bit more important. So your body will always preferentially produce glutathione over methylating. And so if there is a ton of oxidative stress, glutathione goes up, methylation starts to suffer. Okay. Glutathione production goes up. Now, eventually, and you can see this on the labs, glutathione production starts to drop. And that's when things are getting a little gnarly. Okay.
So let's go back here and look at some other diagrams. And I might skip around a little bit here. Uh, let's see. Yeah, let's go this one first. So here's an image of your mitochondria, right? And one of the things that's happening that's really important is that your body is using magnesium to generate all this energy. Magnesium's involved in every step of energy production. I think it's involved in like five or six hundred different enzymes. It's like mind-numbing how many things magnesium does. But a lot of the things that magnesium is acting on are directly in the mitochondria. Every step of the way, magnesium is like this key factor. So if your magnesium levels are good, you're going to make a lot of energy, which means you're going to make a lot of ATP. They have represented here. And you're going to make free radicals. Okay. If your mitochondria aren't doing well, the free radical levels are going to shoot up, and there'll be less ATP. Okay. And then the oxidative stress levels go up. And then glutathione starts to go up. And then glutathione eventually starts to drop. And if glutathione starts to drop, then what happens? It's very dangerous for your body to make more energy if glutathione is not there to protect it. So mitochondria start to slow down. They start to diminish. They start to reduce their numbers and reduce their activity. So if you take a system with damaged mitochondria and you dump in a bunch of magnesium, you gave the patient magnesium supplements, what's going to happen? Well, if they increase their energy production from the magnesium, and they're low in glutathione, that's going to be catastrophic, right? Because if you are low in glutathione and you give the patient a bunch of magnesium, maybe they need the magnesium, but that magnesium potentially is going to speed up mitochondrial function and generate even more free radicals, which is going to kill cells and then kill the person. So your body is like, no, we're not going to do that. Nice try. So if you have low glutathione and you take magnesium, your body's just like, forget about it. You know, like, no, we're not going to crank up cellular energy because you don't have enough glutathione. We're not going to go down that path. So the magnesium glutathione dyad is these two things are tied together biochemically. You can give magnesium in a supplement form, it won't stimulate mitochondrial energy production if glutathione is low. It's a protective mechanism. It's not a bad idea that your body does it. But these are the people that are on magnesium forever and it never does anything because they didn't address their glutathione.
All right. So now the reverse can be true as well. You give glutathione to somebody, or you give N-acetylcysteine, or you're doing something to try to get their glutathione levels up, but their magnesium levels are not up. Again, you're not going to get the full effect, right? These two are tied together quite intimately. And it's not that complicated. Just basically support both at the same time, and then this works really well.
All right. So let's get back here to the regular slides. So again, we talked about this, right? Glutathione and methylation are competing. That's important. They can't methylate well as well. Another question, right? So then on the testing side, you can test for lipid peroxides. And I'll show you some labs at the end, okay? And if the lipid peroxide levels are high, it implies membrane damage. And mitochondria have a lot of membranes. Remember, they have the double membrane thing. They got the outer membrane and the inner membrane. They got twice as much membrane as any other little organelle would have. And all the things that we're talking about in terms of the electron transport chain are actually happening in the membrane. It's a little wacky, but I'll show you some slides on that too. It's kind of cool how that works. So if your membranes are damaged, okay, because of lipid peroxides or lipid oxidation, there's a lot of oxidation or damage of lipids, those membranes are going to be damaged and they're not going to work very well. You got to protect the cell membranes. That's where the electron transport chain is. It's literally jammed into the cell membrane, as well as a million other structures and things, right? But just for the case we're talking about today. So you can also measure CoQ10. That in and of itself is a miracle. You can even measure that stuff. And that's really important because that's the acceptor of electrons in the electron transport chain, right? That's the thing that's pulling the electrons along. And of course, you can measure magnesium, which is involved in all these reactions. So if you see low magnesium and you see low glutathione, you fix them both simultaneously. You go along as well to fix the other things that might be involved, like lipid peroxides and CoQ10. And it's very, very important for the membranes to be healthy. You'll see why in a minute, okay? You can also do organic acid testing to check mitochondrial function, which is pretty slick and cool. You can measure all the different detox pathways, the oxidative stress markers. You can see all that stuff. So you can start to tune people up.
Let's talk a little bit about the history of this and how Dr. Lord stumbled on this, you know. So in conventional medicine, for a very long period of time, they've been doing organic acid testing to detect relatively rare genetic mutations that are fatal, right? And so it's nice to know when a baby is born if they have PKU or urea cycle disorder or a pyruvate dehydrogenase complex deficiency, because if the parents don't know about it, the kid's going to have neurological problems and potentially die soon, right? So it's very, very important. And medicine put a lot of energy into figuring out how to do organic acids, how to do amino acids, to detect these, you know, genetic disorders in newborns. In the night, late 1960s, Richard Lord was going to the University of Texas at Austin to get his PhD in biochemistry. And they were discovering B vitamins, right? They were learning all these new things at that university in his department at that time. And one of the things that they learned in the 50s and knew very well by the 1960s, well, that was that there was huge genetic, genetic variation in B vitamin needs from person to person. And so part of the organic acids testing, you know, was to determine young humans, newborns, who are at some critical level of genetic defect with B vitamins and to, you know, treat them with diet or prescription level B vitamin, you know, recommendations to keep them alive, right? And what Dr. Lord was thinking was, well, maybe we could take the same technology and apply it to adults. And in fact, if you look in the literature, you'll see there's adult onset versions of these genetic disorders. You can have adult onset PKU, you can have urea cycle disorders, you know, adult onset version that's in the scientific literature. But we're just applying it to people who are chronically ill, not people who are in hospitals and about to die, right? Whether they're newborns or adults. So Roger Williams was one of the original researchers in this area. He was born in 1893 and died in 1988. I was like, whoa, go Roger. Like, that was a long life, right? Good for him. Can you imagine? He was born before they even had cars and then he died in the 80s. Anyways, pretty cool. And he discovered folate. Like, how do you even do that? It's hard to wrap your mind around a scientist that could be that brilliant. Pantothenic acid, B6. His brother was the first person to synthesize B1. Like, figure that out. Anyways, in, in 1919, he got his PhD. This was like World War I was still going on, you know, it was a long time ago. And he was Richard Lord's inspirational teacher in the 1960s. What a legacy, you know. And so one of the things that Roger Williams espoused, and if you haven't read his books, you should go read them. I mean, I know this guy's old, I mean, he's dead now, but he was, you know, not been a scientist for a long time, obviously, but his book on Biochemical Individuality is still like a classic. So Roger Williams, Biochemical Individuality, talking about individual variation and genetic needs of B vitamins in the 1950s. This guy figured this out, okay? It's a brilliant scientist, well worth reading his stuff.
So, um, the next step is that we're thinking, okay, how does this all relate? What do these vitamins do? What is glutathione doing? Why does any of this even matter physiologically? Well, it's because of the mitochondria making energy and how that can, you know, sort of flip back on us and impact mood, okay? And mitochondrial dysfunction is a key player in the manifestation of depression. There's all kinds of research on this. You can look at, um, I was just going to read this one quote because I thought it was kind of, you know, germane. "Alterations in mitochondrial functions such as oxidative phosphorylation and membrane polarity, which increase oxidative stress, may precede the development of depressive symptoms." Okay. "In this case paper, we make the case that mitochondrial dysfunction could play an important role in the pathophysiology of depression." So this is not a really far-out idea. There's neuroscientists that are trying to figure this out as we speak, okay? Now, what we're looking at with the testing on mitochondrial patterns is organic acids, okay, in general. And then separately from that, we're looking at nutrient levels for CoQ10, magnesium, B vitamins, etc. Okay? Some of those are run from organic acids, some are run from blood work. There's, you know, a variety of ways you can test for these things. And the key nutrients that we're concerned about are CoQ10, magnesium, and B vitamins. We talked a little bit about this already. Free radicals and oxidative stress. Excessive oxidative stress is really what we want to avoid. Okay. And there's our mitochondria, kind of before and after. And after, right? Too much oxidative stress, that's going to damage them. And then this is how it actually works in your brain. If you have, I love how people depict these things. Imagine being a graphic artist and talking to like the science person and going like, how are we going to depict this? But anyways, here's your healthy mitochondria, right? Here's your severe oxidative stress. Here's your damaged mitochondria. See, it's all broken up there. And then here's your clearance of it, right? Now it's dead and gone. Now you're just breaking it up and getting rid of it. It's like, okay, dead, gone. You know, let's bring in another one, you know. And so we don't want this to happen, right? We want to keep the brain healthy, keep the mitochondria healthy to make all this stuff work. And then another kind of blow-up on this from the depression research folks. On the left-hand side, you see a normal mitochondria. And the right-hand side, you see a depressed mitochondria. Other than the fact that I don't really like their color choices, this is a pretty good diagram. So here's the mitochondria. Remember, it's got the outer membrane and the inner membrane, okay? And this inner membrane is made up of fats. These are fatty acids. They're like the consistency of olive oil or something like that, okay, in your body. And it's this, you know, dual layer phospholipid bilayer, right? This layer of phospholipids kind of facing away from each other. The point is, though, that the mitochondria have a lot of these, a lot of these membranes. It's kind of more than you would think because of the way that the actual structure is, not only the inner and outer part, but the fact that they go in and out here, looks like four, you know, fjords in Norway or something like that, right? It's a lot of them. And then there's some of these reactions that happen outside in the space in the cell, the cytosol, and then some of these reactions that happen within the mitochondria itself. And remember that, well, I'll show you in a second, but the magnesium's involved in all these things that we're talking about, okay? In the unhealthy mitochondria, you have this inflammatory activity. You have the cells potentially dying. You have damage, mutations, polymorphisms. That's what we're talking about with the variations in the vitamins that can affect all this, right? The membranes become more permeable. They're not filtering very well. There's lower ATP production. The electron transport chain is altering. That means you're increasing your free radicals, decreasing your energy production, just like that other diagram that we looked at a minute ago, right? It's the same exact scenario here. Now, so that's, and just think about that, you know, from, from a mechanistic standpoint. And now all of what we're talking about is run by a series of enzymes. And I want to show you just one example of these enzymes here. I'm going to focus on this one called Complex 2, just as an example, because we don't have time to get into all of them. But just take the Complex 2, as in, you know, a sample of one enzyme, you can kind of extrapolate to the fact that there's a whole bunch of these that are involved, right? So the basic facts on an enzyme is an enzyme is a protein that's strung together. A B vitamin then acts as a coenzyme, okay? The coenzyme is what comes along to make the enzyme work. You think of it like this, like the enzyme would be like a beautifully, beautiful, brand new Mercedes that's been built, right? The coenzyme would be like the person who comes in and starts it up and drives it. Not much happening with that car unless someone gets it and drives it, right? Now it's no useful purpose, it's just sitting there, okay? And so the coenzymes are critical. The enzyme needs to be built properly. The coenzyme needs to get in, lock in, and then get the enzyme working. So another way to think about it is these cofactors or coenzymes are the non-protein portion of the enzyme. The enzyme can't work without it. Sometimes a cofactor is a mineral, like magnesium. That's why magnesium is so important what we're talking about, because it often acts as a cofactor to get the enzyme to work, okay? And then, um, if the cofactor is an organic compound, if it has carbon, then we call it a coenzyme. If it doesn't have carbon, um, then we call it a cofactor. But they're very similar, right? They'll overlap. Sometimes people even use them kind of interchangeably, even though it's not accurate to do that scientifically accurate or whatever, right? So another way to think about is B vitamins are the non-protein portion of an enzyme. Sometimes the B vitamin actually shares electrons with the enzyme, it becomes one with the enzyme. In other cases, the B vitamin just comes in proximity with the enzyme for all this to work, okay? But the coenzymes end up being extremely important. So let's look here at all the different places where you make energy, where there's enzymes, and and dozens of them, right? So, and any of these enzymes can go bad. That's the whole problem here. So in order to take fatty acids and burn them up for energy with beta oxidation, you have to have enzymes that do that. And there's a whole series of enzymes that pull the fat into the right place, that burn it up, turn it into acetyl-CoA. Tons of enzymes that can go wrong there. You've got pyruvate dehydrogenase enzyme, lactate dehydrates enzyme, enzymes here to make that work. You've got enzymes up here, the ketoacid dehydrogenase enzymes. And then there's an enzyme in every step in here to make everything, reaction, every reaction go forward here, okay? And so what we're worried about in terms of mitochondrial function is if some of those enzymes aren't working. And then treatment-wise, in the bigger picture, for the purposes of today, we want to get the magnesium to crank up this system going along with B vitamins. And then we want to make sure that we test and correct the glutathione so the magnesium and B vitamins can work. And you have to integrate those two treatments at the same time. So you give them magnesium, B vitamins, and glutathione support all the same time as a package. And then you'll see really tremendous results.
So I'm just going to isolate down now to one enzyme, okay, just because that's like all we have time for, okay? Um, just one enzyme, but remember, there's, there's, I pointed out, there's a gazillion of them all throughout what we're talking about. So this one enzyme, I just think it's a really cool enzyme. It's called the succinate dehydrogenase complex. And it's stuck in there. Also, you guys learned this in school as Complex 2 of the electron transport chain, okay? It's stuck in there where it's stuck in the mitochondrial membrane, the inner membrane. So if the membrane's not working right, if it's being oxidized or these fats are being damaged, this whole thing is not going to work very well. So your fatty acids are really important, your membrane is really important. And it's doing all these things, but one of the things it's doing is converting succinate to fumarate. It's also helping grab electrons and chug them along the electron transport chain. And here, when they say Q, they mean CoQ10. CoQ10 is helping with all that, okay? And here's another view of the enzyme. And again, we're just looking at one enzyme as being emblematic so you can see how interesting this stuff is. The enzyme needs the vitamin to work. Remember this whole kind of lock and key kind of thing. So you've got the inactive enzyme that's like the Mercedes just sitting there. Then you've got the person that's coming in to make it work. And these things are binding together so the chemical reaction can take place. If you don't have the coenzyme or the cofactor, then the enzyme doesn't work. Now, how the actual enzymes are made is we string together amino acids to these ribbons, beta sheets, and alpha helices, all these fancy structures. The whole thing folds up into an actual physical structure, okay? And this is what the succinate dehydrogenase enzyme looks like. It's made up of hundreds of amino acids, okay? And you can see these ribbons down here, there's sort of a purpley blue and green set of ribbons. You see how long they are? They're very specific length, right? And this succinate dehydrogenase enzyme has riboflavin or vitamin B2 as a coenzyme. So what that means is if you look at the succinate dehydrogenase here, there's one enzyme out of many, right? You can see this is the, uh, cell membrane here, the inner membrane of the mitochondria, right here. That's the inner membrane. See those little ribbony things that we saw in the last picture? They're stuck into the cell membrane. So if the membrane is getting oxidized or damaged, this is not going to work very well. And that succinate dehydrogenase enzyme is just sitting there waiting to do this process here. Let me show you the process. It's taking succinate and converting it to fumarate. And in the process of doing that, it's grabbing electrons. And those electrons then are coming down. CoQ10 is grabbing them and it's taking them from Complex 2 over to Complex 3. And eventually it goes to Complex 4. And then oxygen gets involved. And then you make energy, okay? So this is the process that we're talking about. And so if you're looking carefully to try to analyze this stuff, here's your succinate converting to fumarate. We can measure all this, right? If succinate is high, it means this process is not going well. Here's your FADH2. This is your riboflavin, vitamin B2. You see that structure there? That's the B2. It's slotting right into this complicated structure in just the right way. And then here your electrons cruising down, going down, down, down to the complex. Here's your CoQ10 grabbing those electrons and going, okay, we're going to head over this way to Complex 3 with the electrons. And then eventually these electrons are going to end up unifying with hydrogen ions and what is an oxygen, right? And what does that make? Water and ATP. So this process can get screwed up in a million different ways. If this enzyme is not structured properly, then B2 can't slot in here, right? And this whole thing's going to fall apart. So you can have these genetic variations, right? If succinate dehydrogenase isn't set up quite right, one of those amino acids is out of sequence, you're going to need a ton more vitamin B2 to make this work than the average person would. And that's why some of the patients that we're working with have these, you know, systems that aren't working very well. It's probably the most common reason that I see is some kind of enzyme defect that's screwed this whole thing up.
Okay, so let's go back to the beginning here for a moment. Um, before we look at cases too, I'm just going to do my little advertisement here, which is what pays the bills so I can do this stuff. June 1st, we have a Lab Interpretation Boot Camp. We're going to talk all about enzymes, basically, for eight weeks. And we're going to look at the genetic or functional genomic interpretation of these tests, organic acids, amino acids, B vitamin markers, etc., along with lectures from SNIP about SNPs. We've got a whole bunch of hours of Richard Lord doing talks that are quite high level. We've got me doing the kind of like, this is what you do in practice stuff. And then we have Nathan Morris, who's talking on the SNPs specifically. So it's kind of a multi-speaker talk. It's eight weeks long. It's a boot camp. It's pretty intense. We got tons of material there. You get a year of access to the material. But it's eight weeks. We have a series of four live calls where you guys can ask questions. And, um, it's all case-based. So we'll have all these cases that you can review. And then it's, um, 20% off if you use that code there. And then in the summer, in August, we're going to have our Telehealth Bootcamp. Okay.
All right. So let me just go back and summarize for a moment, then we'll look at some labs, and then we can do questions. I think this is the easiest diagram. This, okay. So if you have a patient who's low in magnesium, and you start to give them magnesium, you're going to stimulate this entire process to work better. That's going to cause more ATP production, potentially, but it's also going to increase the free radicals, increase the oxidative stress. If that patient who's low in magnesium is also low in glutathione, then your body is just going to go, no way. Your body will not utilize the magnesium properly until the glutathione levels come up again. You can look in Richard Lord's book, Laboratory Guides. You have to buy it from an iPhone or an iPad. You can download it right on the device. It's 1200 pages of like hardcore material, but it's got a whole section on this, what we're talking about right now, okay? If you want to look at the research behind it. And, uh, opposite is true. If you're trying to get someone's glutathione levels to improve, you're going to need to have magnesium in the picture as well. These two are coupled together, inextricably, you can say that word right now for some reason, because they're the yin and yang kind of of energy production, right? Magnesium is what improves energy production. Magnesium is what's required for that final step of ATP turning into energy, right? And it's required for all these other steps as well. And then glutathione is required to deal with what magnesium is doing, which is making energy. And then the other thing to keep in mind is that glutathione can be low for a lot of different reasons. And make glutathione has got a lot on its mind, you know, it's got a lot to deal with. It's not like a one-trick pony. It's not just dealing with your mitochondria. And magnesium's doing a lot too, right? Magnesium's helping regulate your cardiovascular system, your blood pressure. Last time I checked, magnesium is critical for muscle contraction and relaxation. Magnesium is important for making everything in the body. Magnesium is like super important. It's doing a lot of stuff too. And glutathione is involved in a lot of other things as well. And the main sort of take home for today is that if you have a patient that's having an assertive glutathione, if you have a patient that's having trouble with methylation, then you should suspect there could be glutathione problems as well. And to maybe say the reverse is which is always true, if you test for patient, we'll look at the labs in a minute here, and they're low in glutathione participation, they're low in glutathione, they by definition must have a methylation problem because prior to the body becoming deficient in glutathione, your body would have already sacrificed the methylation process because that happens first. Okay? So I'll say that again, if your patients test low in glutathione, by definition, they must have already for quite some time had a methylation defect. And methylation is important for what? DNA, hormone production, detoxification pathways, neurotransmitter production. We, the bulk of the methylating that we do, the bulk of the methyl groups that we produce, like half of the methyl groups that we produce, you know what they actually go towards? The biggest consumer of methylation in the human body is creatine production, which makes sense. It's the energy that our muscles use, right? The second biggest sort of pull on methylation is the production of cell membranes by making choline, okay? So methylation is busy. Methylation's supplying creatine for muscle. It's supplying choline for cell membranes. That's like about 80% of what methylation is doing is making energy for the muscle tissue and making cell membranes. And then it's also doing all these other things that we typically think about in terms of methylation, okay? So anyway, super important body process, but glutathione is even more important.
So let's look at some labs here. And oh, and don't forget, you get a discount if you use these codes. I'll leave them up so you can see those, right? And let's look at a lab or two and then open for some questions. Let's see. Sorry, I'm just waiting a second here to make this all work. There. Yeah, I was teaching the boot camp last night. We're running this other boot camp right now, Lab Interpretation Boot Camp, and my computer overheated right before I was trying to teach. I just almost had a heart attack. All right, here we go. So this is an Ion Panel from Genova. You can also run NutraVal if you prefer. They're very similar tests. And let's see here. Um, well, should we do the easy stuff first? Let's do the easy part first, okay? So magnesium is low, okay? Now, right away, you're thinking, ah, you need magnesium. Will it work? I don't know. Where's your glutathione level at? So we scoot over to the glutathione section of this test. And Richard baked in three different ways of testing glutathione here. And you don't know this guy so well, right? I guess he's become, I don't even call him a friend. He's more than a friend. He's like a, I don't know, he's like a constant, he's like a force in my life now. He's like a constant force in my life, you know, in a really good way. But, you know, he doesn't do anything without thinking about it for a long time. He put three different markers on this test to check for glutathione. There's nothing else on this test that's even checked twice. This is really, really important stuff, okay? And when you have a pattern of pyroglutamate or sulfate being low, these are borderline though. But if they're a pattern of them being low, then you've got a major problem with glutathione, okay? If you've got a pattern of any one of these three markers being high, there's also glutathione issues, but not as severe perhaps as when the markers are low. So even though these are only borderline low, you still probably want to support the person with, you know, extra boosting of their glutathione. Typically, that's done using N-acetylcysteine. Some people use glycine. Some people use glutathione itself, you know, you can do your favorite thing. I usually use the N-acetylcysteine. But depending on what the lab shows, you may want to, you know, have a different way of boosting glutathione. And then what we're talking about, mitochondria, right? So we also want to look at, um, CoQ10, okay? So CoQ10 levels in this patient are quite low. So you want to give CoQ10 and give magnesium. But what's that's going to do? In the best case scenario, that's going to increase ATP production. ATP production is the number one source of oxidative stress. So you want to make sure that you're protecting, um, protecting the body, right? While you're forcing the body to make more energy with antioxidants. In this case, you can see these are the fat-soluble antioxidants here. CoQ10, alpha and gamma tocopherol, a vitamin A, and beta carotene. They're all low. All the fat-soluble antioxidants are low. So now, what's the implication of that? Well, if I was a cell membrane in this person's body, I would be a little nervous, wouldn't I? Because those cell membranes are made out of fat. And if the fat-soluble antioxidants aren't there to protect you, these cell membranes are going to take a hit. And that's going to screw up the functioning of this whole system, right? Because everything's baked into, literally stuck into the cell membrane. So that's just something to consider. And then let's see here. We've got another couple minutes and I'll go to questions. I'm just going to look at maybe we can squeeze in one more lab here. Um, here we go. And so we're not, we're not going to go through the whole test obviously, but you can go through the parts that we're talking about, okay? Magnesium testing low. So first thing you think, I want to give you magnesium. But can I? Is this going to work? Well, let's look at those three markers for glutathione. And in this case, they're okay. Wouldn't worry about it. Then it's not a crisis, right? So the glutathione markers, hydroxy alpha hydroxybutyrate, pyroglutamate, and sulfate are okay. All right. So you can give magnesium. It should work really well by itself. You could give a little bit of glutathione support if you want, but it's not going to be a sort of critical determinant, right? And then we can go back and look at CoQ10 levels. Are okay. Hey, so this person would be easy peasy. This person would be just give them magnesium, they're going to get better. Um, that's great. I was going to say, I don't get patients like this, but this is one of my patients. So obviously I get patients like this once in a while. Maybe I slightly over dramatize how hard my practice is. This kind of keeps me honest when I pull up random labs like this. Okay. Again, low magnesium. And this happens a lot, right? Almost the entire American population is low in magnesium. Why? Because nobody eats green leafy vegetables anymore. You have to eat green leafy vegetables three times a day. I see normal magnesium once in a while, 100% of the time, it's people who eat vegetables constantly and large amounts. The whole problem.
With magnesium would go away if people would eat organic vegetables with every meal, including broadleaf greens like Swiss chard, kale, collard greens, all that. And I'm telling you, I see normal magnesium once in a while. It's always people that eat a ton of vegetables.
So, CoQ10 levels are okay on this person. The omega-3s don't look that good, but that's like a different lecture, probably. And then let's look at the, um, okay, here we go. Let's look at the glutathione markers. And there's three of them again. Why are there three? Because it's super important. You want to catch this. In this case, alpha-hydroxybutyrate undetected. So, we don't really know what that means because we couldn't find it. Sulfate is looking really good. All right, that's good. But pyroglutamate is high. Bingo. Low glutathione, high pyroglutamate means low glutathione. You give them magnesium and N-acetylcysteine together. Energy production will ramp up unabated. You'll have the protection with the glutathione to deal with the free radicals coming out, and the person's going to get energized and feel better. Okay, really straightforward.
All right, so let's cut away to questions here and see what you guys have come up with. Let me go back here. Bingo, bingo, and questions. All right. Okay, so yeah, we always record these and we'll send out a link to the recording tomorrow. You can share with your friends. What are the difference between an ion panel and organic acids test? So, the ion panel includes the complete organic acids. So, back in the day, when Richard and Andy were running the lab, I think it was like the University of Georgia or something like that, someone came up to them, I think it was some college-level sports team, and they're like, "Hey, we want you to run every test that you guys have on all our football players, whatever." Right? And they're like, "Okay." And so they took, they took their fatty acid profile, their amino acid profile, their organic acids profile, their antioxidant profile. They just took everything they had at the lab, they crammed them together, and they're like, "Okay, guys, run all these." And they called it an ion panel. So, it's every test under the sun, and it's a, you know, including organic acids.
Um, how to address long-haul COVID? Yeah, so that's a big question. And I think this is a series that we're in right now. This is a mentorship mini-series, and the third one of these talks. I have a case I'm going to present where we have testing on a patient. The patient was a doctor, a medical doctor, in our class, in a mentorship class. And so, anyway, she tested herself. About six months or a year later, we retested her. She was miraculously better. The lab's gotten better. She was feeling amazing. And then she got COVID. And we have a third set of tests. So, I'm going to present that case in that, um, third mini-series. I think we're calling it like an immune system case or something like that, and talk a lot about long COVID. And we have this wonderful example of someone who was not doing well, who we got better, who then got COVID, and then what happened. And of course, what are the hallmarks of COVID? You know, damage to mitochondria because of hypoxia, right? Not enough oxygen. Okay.
Oh, yeah, I'll design a program. Someone's asking for that. I'll do that. Um, so, um, does glutathione go up in response to ROS then decrease? Yes, that's right. So, when you're getting a lot of this, a net, when you're getting a lot of oxidative stress generated from the mitochondria, your glutathione levels shoot up to deal with that. And then eventually, if you don't have the right balance, then the support starts to fall apart. Okay.
Um, let's see. So, let me, let me write out the dosages real quick. That's a good question. So, it's important to get the dosages right, or it doesn't work that well, you know. And, uh, let's just look at this for a sec. See if I can pull this up properly. All right. So, so a typical program. So, magnesium, we have to be a little bit careful of because it can cause diarrhea if you give too much. But a typical dose of magnesium is usually around 400 milligrams a day. So, it typically comes in a, um, in a capsule that's, you know, 100 milligrams. Some of them are 200, maybe the most. So, and you want to have a magnesium chelate. So, magnesium is just a mineral. It's like a rock, right? They're going to bind it to an amino acid carrier in order to get it to get absorbed. And so, you can have magnesium glycinate, magnesium malate, magnesium citrate. The glycinate form is usually pretty easy to work with because it doesn't cause diarrhea. Some people prefer 308. Each of the different forms of magnesium has slight pros and cons to it. But I would say the main thing is getting the magnesium in good quality. Usually 200 milligrams twice a day is enough. If not, you can go up higher. Just have to be careful that they're going to get loose stool. The high and low ranges for magnesium that I've experienced in my practice are somewhere around 400 milligrams. The most I've ever used is 1200 milligrams. Again, most people get diarrhea way before you get to 1200. So, that's a pretty high amount. 400 is more standard. Okay. But 1200 is not unheard of. You're trying to get someone's blood pressure down. Sometimes people use that much.
And then on the NSC, the cysteine side, usually you can get it in a 900 milligram capsule, and you want to be in the three gram to six grams a day range. Now, if for some reason N-acetyl-cysteine doesn't work, can't work, makes them sick, something like that, you can use plano glutathione in a topical form, in a spray form. It's kind of expensive, but sometimes for some people it works better. There's no, there's no problem doing that. The other ways you can get glutathione up are, glutathione is made up of glycine and glutamine. So, sometimes people use glycine or glutamine also. How much? Again, it's three grams to six grams a day range for the glycine or glutamine. And what's commonly done, and I used to do this all the time, is NAC and glycine together, three grams of each, okay, per day to crank up glutathione. Okay. So, you have all those different options.
If you want to get really fancy pants about this, okay, and I don't necessarily recommend this, but you should know about this, and because a lot of people are asking right now about the types of magnesium, you can look at an organic acid profile here. You see where it says citrate? Well, look at me, I picked a perfect example for this. So, you see how the citrate on this lab is low? Well, what do you think about giving this person magnesium citrate? Not a bad idea, right? Because you're getting two birds with one stone. Low citrate, magnesium citrate. The magnesium will help with the magnesium, the citrate will help with the low citrate. Not a bad idea. Maybe you have someone who has low malate, magnesium malate might help them, right? Most of the time, I just use a multi-chelated magnesium. But again, there's reasons why, or glycine, if their glycine is low, you could give them magnesium glycinate, and they're going to get the magnesium and the glycine together. So, if you want to get fancy pants about it, you can do that. That's maybe a little bit more bandwidth than you want to put into a typical program. Okay. And I like the multi-chelated magnesiums. They're chelated to a whole bunch of amino acids because what the person's absorbing is the amino acid, not the magnesium, right? The amino acid is what they're pulling over. And so, if you have a whole bunch of amino acids, multi-chelated to a bunch of amino acids, it seems like the absorption is more likely to be better. So, I use that. And I often use magnesium powder, so I can get the dosages up without a ton of pills. I use magnesium powder probably 20% of the time with patients. That's very helpful. Okay. People can also make a little drink out of it before they go to bed.
All right, let's see here. I'm trying to get through all these questions. I'm not going to get all the questions because there's too many. I'm going to run out of time here. I have another engagement in two minutes. Let's see. Do you ever see magnesium levels good and glutathione low? Yeah, absolutely. You're going to see that in your vegetable eaters. I swear to God, if people eat vegetables every day, all day long, you're going to have great magnesium, but they could still have messed up glutathione, for sure. Okay. So, you're absolutely going to see that.
Chronic inflammatory conditions burn through any particular component of this diet consistently? I don't know the answer to that, Elizabeth. I mean, both, both sides of this are damaged by chronic inflammation. I think it's just both. Okay. I think I got most of the questions answered. I'm sorry if I couldn't get to your question. I'm just running out of time. I have to go do an interview now. Uh, I think I got most of these done though. Okay. I'm going to wrap it up. Thank you all. And we will have another one of the series coming up very soon. I'm sure you'll be getting emails about that. Tell your friends, um, if you want to share this information. And we'll look forward to seeing you guys at our next engagement. Okay. Take care, everyone. And I look forward to catching up with you at the next one of these. And if you're interested, sign up for the bootcamps, and we'll talk to you at those as well. 20% off with those discount codes. Okay. Goodbye, everyone. You.