187 - Energy Crisis: How Your Cell's Power Plants are Hijacked

Dr. Robert Groysman returns to discuss the mechanisms behind Long Covid, focusing on mitochondrial dysfunction and its role in symptoms like fatigue and brain fog.

• Dr. Groysman identifies six major mechanisms in Long Covid: dysautonomia, mitochondrial dysfunction, gut dysbiosis, endothelial dysfunction, mast cell activation syndrome, and hormone imbalance
• Most Long Covid patients experience multiple mechanisms simultaneously, requiring comprehensive treatment
• Mitochondria are cellular organelles responsible for energy production, with different cell types having varying densities based on energy needs
• COVID-19 not only damages mitochondria but uniquely impairs the body's ability to repair and replace them
• Post-exertional malaise occurs when damaged mitochondria burst during overexertion, triggering inflammatory processes
• Recovery requires gentle, patient approaches rather than aggressive interventions that can cause setbacks
• Dr. Groysman's two-step protocol involves daily antioxidant support followed by seven days per month of carefully managed mitophagy
• Complete recovery typically takes 3-12 months and cannot be rushed without risking relapses
• Dysautonomia often needs treatment before other mechanisms can be successfully addressed
• Pacing is critical to avoid crashes that cause additional mitochondrial damage

Check out my previous episodes with Dr. Groysman to learn more about the Stellate Ganglion block and other treatment approaches for Long Covid.

Links:

https://www.facebook.com/groups/longcovidsgb      https://www.facebook.com/profile.php?id=61553548547314   https://www.longcovidfamily.com/

For more information about Long Covid Breathing courses & workshops, please check out LongCovidBreathing.com

(music credit - Brock Hewitt, Rule of Life)

Chapters

• 0:00 Welcome and Introduction
• 4:17 Six Major Mechanisms of Long COVID
• 7:26 Understanding Recovery vs Remission
• 10:46 What Are Mitochondria and Their Function
• 19:37 How COVID Damages Mitochondria
• 29:42 Post-Exertional Malaise Explained
• 40:56 Treatment Approach for Mitochondrial Dysfunction
• 52:53 Treating Dysautonomia First for Recovery

Transcript

Jackie Baxter: 0:56

Hello and welcome to this episode of the Long Covid Podcast. I am delighted to welcome back Dr Robert Groisman, who has been a previous guest on the podcast a couple of times, and I will put links to those episodes in the show notes so you can see what we chatted about before. But today we are going to catch up on some of the more recent progress. We're going to chat through some of the mechanisms and take a bit of a deeper dive into one of them. So a very warm welcome to the podcast. It's lovely to have you back.

Robert Groysman: 1:29

Thank you so much, Jackie. I'm glad to be back.

Jackie Baxter: 1:34

It's going to be fun chatting. Before you kind of take us off into all these mechanisms, can you just say a little bit about yourself and what it is that you do for those of our listeners who haven't heard the previous episodes?

Robert Groysman: 1:51

Sure. So I am dual boarded. That means I hold diplomat status in the American Board of Anesthesiology and the American Board of Pain Medicine. Now a lot of people ask you know what is a pain doctor, anesthesiologist doing in long COVID? Well, the way I started was back in 2020.

Robert Groysman: 2:16

I was treating patients with PTSD with a stelaganglion block procedure and we started noticing a pattern that some patients were coming in with smell and taste problems only, and they seem to have recovered after the block, and occasionally we'll get other symptoms coming in, like fatigue and brain fog, and then all the other long COVID symptoms started showing up, but in the beginning it was only smell and taste.

Robert Groysman: 2:45

So people ask you know why is an anesthesiologist, pain doctor, doing long COVID? Or why isn't it an immunologist or a cardiologist or neurologist? Well, the answer is is there really isn't any specialty that's more equipped to deal with long COVID, because long COVID affects every single body system, so no specific specialty would be an expert or considered an expert in long COVID. Each one of them would be required to learn more about long COVID and be able to span multiple organ systems, which is what I've done about long COVID and be able to span multiple organ systems, which is what I've done. So this is basically how I got into long COVID and since that it's been five years I have evolved my treatment plans and diagnostics to more adequately address the multiple mechanisms that are involved with long COVID.

Jackie Baxter: 3:41

And we talked a load the first time. We talked about the stellate ganglion block, which was actually what led me to you in the first place. So, yeah, we talked a load about that there. So anyone who's like, oh, what's that? There's an episode already there that dives into what that kind of does. Now, obviously, in the last just over two years since we spoke the first time, things have evolved somewhat, and you said now that you are kind of looking at six major mechanisms in long Covid. Are you able to sort of briefly talk through what those six mechanisms are?

Robert Groysman: 4:23

Yes. So this autonomia is still a very prominent mechanism and now we split it into fight or flight POTS, which is postural orthostatic tachycardia syndrome, which is a problem with standing up and the heart rate going up, causing busyness or passing out, and vagus nerve dysfunction. Those are three subtypes under dysautonomia. It's still considered one of the most major ones. There's mitochondrial dysfunction, which is a problem with one of the energy generating organelles inside cells energy generating organelles inside cells. There is gut dysbiosis, which is a problem with the gut flora, causing problems and also includes the gut. Then we have endothelial dysfunction, which is a problem with blood vessels and the inner lining of them, and this is where clotting can come in, or microclots there. Mcas, which is mast cell activation syndrome, and histamine intolerance, another mechanism. And lastly, we have hormone imbalance, and that includes cortisol, testosterone, estrogen and thyroid hormones.

Jackie Baxter: 5:37

those are the major six yeah, and they're all quite big topics on their own, aren't they? So do you find that people have multiple mechanisms going on in their bodies, or is each individual person just got one?

Robert Groysman: 5:59

doing this for five years now, a little bit more than five years I have realized that long COVID is a multi-mechanism disease. It will always involve more than one mechanism at a time and this is what makes long COVID challenging to diagnose and treat, because sometimes the mechanisms hide and are concealed by more prominent mechanisms. But until you've treated all of the mechanisms, you will not get into the recovery phase or the remission phase. Notice I don't say cure, I don't cure long COVID. I don't think anybody should claim cures. We don't know what the future holds, but we do know that long COVID is a chronic illness.

Jackie Baxter: 6:45

So you mentioned recovery and remission. Just out of curiosity, how do you differentiate recovery from cure? So, for example, I would say I'm recovered because I am better than I was before I became unwell. Now, I didn't take a pill, that was a cure. My recovery was a big puzzle of many things, and that is true for everyone. I've spoken to who's recovered. So I'm kind of curious about the cure versus recovery. People can recover because they have, but we can't call it a cure because it's not one thing. What are your thoughts on that?

Robert Groysman: 7:28

My thoughts are there are some people that have recovered. Anywhere between 10 and 30 percent of people are considered recovered. That means that their symptoms have abated and they're pretty much back to baseline. But the way I treat this is I treat it kind of like a cancer.

Robert Groysman: 7:47

You don't never say you're cured of cancer, you say you're in remission and because you never know if it can come back and we just don't know. That's the problem. We don't know if it's able to come back. Is the damage done potentially can cause resurgence of the symptoms again If you get sick, if you have surgery, if you have anesthesia, if you're under a significant amount of emotional stress. In some people that have recovered they haven't really recovered because their symptoms come right back and they're right in the midst of long COVID yet again. So that is why I say remission more than recovery, because we really, as much as I'm just being cautious, as much as I want to call it recovery, we don't know what the future holds. So I'm more comfortable saying remission, that is, we got you better, but I just don't know if things are going to come back or not.

Jackie Baxter: 8:48

Right, and of course that is better than not being in recovery or remission at all. So you know, we will take that. I'm just curious on your perspective on that because I disagree. But that's okay, but we're allowed to disagree, um. So anyway, that was a tangent um, because what we actually were going to talk about today was we were going to dive into our second major mechanism. So when we talked about the stellate ganglion block two years ago, we talked quite a lot about dysautonomia there, and that's a topic that's been covered on the podcast quite significantly by other guests as well. So today we were going to take a bit of a deeper dive into this mitochondrial dysfunction, which you said was the second major mechanism. So maybe we talk a bit about what the mitochondria are and why they're important first.

Robert Groysman: 9:51

So just about every cell in your body has these organelles. These are kind of um, a functional part of the cell that not only generates energy. Everybody knows that mitochondria is the powerhouse of the cell, but it actually does a lot more than just generate atp, which is our currency for energy. It also controls various parts of metabolism and different ions, such as calcium, for instance. And the number of mitochondria that we have in each cell depends on what the cell needs to do. So if the cell has a high energy requirement, like a muscle cell or a cardiocyte in your heart or a neuron in your brain, it will have a lot more density of mitochondria. There'll be way more mitochondria per cell, per neuron, per myocyte in the cell. Some cells have no mitochondria, such as mature red blood cells. They have zero. They are so full packed of hemoglobin to be able to carry oxygen and carbon dioxide that they don't have any mitochondria.

Jackie Baxter: 11:46

They get energy by just absorbing and processing glucose through the bloodstream what we call anaerobic metabolism as opposed to aerobic, which is what mitochondria do when you said that there are cells that have more mitochondria and cells that have less mitochondria, and that is dependent on what their role is and whether they actually need it or not. Um, now, I don't know if we're going a bit off topic here, but you hear talk about brown fat versus white fat, and brown fat is much more mitochondria rich, so is that in areas that require it more? Is that what it is?

Robert Groysman: 12:37

So brown fat is typically used to generate heat. So one of the functions of mitochondria is, if you uncouple the energy generation from the processing of fuel molecules, you will generate heat. Okay, the muscle will, or the muscle or the fat will be used to basically heat up your body. This is what makes warm blooded animals warm blooded like ourselves, so that's one of their functions. So, instead of generating ATP, you're actually forcing the muscles to contract and relax multiple times. That's what shivering is, and you generate heat. So that's kind shivering is and you generate heat. So that that's kind of yes, so fat.

Jackie Baxter: 13:23

So brown fat is going to be very, uh, very full of mitochondria right, and that explains why the research shows that people who do things like cold water immersion have more brown fat, because they are adapting to literally warm themselves up after having been in the cold water. Um, so that that makes a lot of sense. Um, and that explains why I've heard about it as well, because that's something that I do quite a lot of. Um, so cool. So that's kind of what mitochondria are and what they do now, obviously being, you know, energy generators and controlling metabolism. That's pretty important in our bodies, and if that stops working, so if we get this mitochondrial dysfunction, so they're not working as they should, you can sort of see how this might bring the whole kind of house of cards tumbling down a little bit in the body. So maybe we talk about what can cause mitochondrial dysfunction and why. Is that something we can get into?

Robert Groysman: 14:35

We can. But before we do that, let's just talk about what mitochondria are actually used for. So Every time your cell wants to do something as in make something it needs to pay a toll. There's energy involved. You need to power the machinery for it to make it. Anytime you want to make a hormone or a protein that's going to be circulating in your bloodstream like an antibody, for instance, or a hormone, anytime a cell wants to move for instance, white blood cells they like to crawl around. They're able to move around your body and in order for them to move, they require energy. So it's just like your car or you. You need to supply energy for them to be able to do a task, including the liver, for instance, to break down a toxin or a molecule. In order for it to enzymatically break it down, it needs energy for that.

Robert Groysman: 15:34

So what happens is if mitochondria are kind of their own worst enemy sometimes because, as good of an energy generator as it is, biologically, you know that your engine in your car is not generating 100% energy from the fuel you're using, right, that's why you have a radiator there to cool it down, because a lot of the fuel is used to generate heat and you need to get that heat off that's called waste products and you have a catalytic converter and stuff comes out the tailpipe and that's also hydrocarbon and other stuff that has not been actually used to move your car along, right? So the same thing happens in the mitochondria, right? So the same thing happens in the mitochondria. They're about 40% efficient, which means that 60% of the fuel that we take in gets used for something else. One of it is for heat, which is fine, but sometimes we kick off what's called radicals or superoxides. Basically, it's fuel molecules that haven't had all their energy extracted, so they still have some energy in there and because of that they're oxidative. That is what oxidative stress is. So these own models, these own, these mitochondria that are using fuel like glucose and fatty acids to generate energy, which is ATP, occasionally, because they're not 100% efficient, will kick off these radicals and we need to neutralize them, because otherwise you increase your oxidative stress and these oxidative stress molecules or radicals can damage the mitochondria itself. So, like I said, it's kind of like its own worst enemy. It's like having the chimney plugged up and all that smoke gets into the factory and all the workers are coughing and huffing and puffing, trying to get, trying to be able to do their work. So that that's the first issue.

Robert Groysman: 17:51

Okay, so mitochondria already generate enough oxidative stress on their own, even without any help from you, any help from viruses, any help from the food or anything else. Of course that could be made worse by a poor diet. High fatty diets will increase oxidative stress. Eating a lot of processed foods will increase oxidative stress. X-rays, ultraviolet light, can increase oxidative stress. So, anyway, viral infections increase oxidative stress.

Robert Groysman: 18:23

So COVID goes above and beyond on the oxidative stress because it can damage mitochondria. Okay, it hijacks some mitochondria to be able to use its machinery to basically power itself and reproduce, and in the process it damages the mitochondria so they don't really function well. So now you're not doing 40% efficiency right, you may be 20% efficient, so now you have an increased oxidative load. That's number one. Number two, which is kind of the bad part of COVID here, is that the spike protein itself can damage the mechanism that the mitochondria are able to recycle themselves. So mitochondria, like any other part of a cell, it needs to be recycled. It gets old, it gets damaged and it needs to make new, new parts for the cell. And that whole process is damaged by COVID, by the spike protein. Okay, so that is the part that really causes the problem, because otherwise many viruses use mitochondria to reproduce and they damage the mitochondria. But then you can recycle and make new ones. It's a process called mitophagy, which is generating new mitochondria from old mitochondria. Basically, you replace the parts that are needed and replace it.

Robert Groysman: 19:58

You can't make mitochondria from scratch. That's very important to know that. All the mitochondria that you have in your body have come from the original egg that was produced during conception. So you can reuse parts, you can make some parts, but you can't make a full mitochondria from scratch, and that is because the mitochondria were originally not part of our cells. They have their own DNA, it's called mitochondrial DNA, and I guess the theory is that they were microorganisms that were incorporated into our cells at one point. And because they have their own mitochondrial DNA, you can't replace every single part of the mitochondria without having that. So you have to always make a mitochondria from something that already exists. So that's important because we can't make it from scratch. So that has implications. A lot of the mitochondrial genetic material was already incorporated into our DNA, into our genome, but it still hasn't sown little mitochondrial DNA loop that still has important components that need to come from the mitochondria itself. Okay, so now let's get into your question. Go ahead and ask it again your question.

Jackie Baxter: 22:01

Go ahead and ask it again. Yes, so I think what I was asking was what causes them to dysfunction. That was it, wasn't it, you know?

Robert Groysman: 22:04

so the virus comes along and that's the trigger, presumably well, what actually goes wrong so when, when the SARS-CoV-2 virus gets into the cell, it, like I said, it uses the mitochondria as part of its reproduction cycle and it tends to damage it. It typically happens from the spike, but the virus itself can also damage the mitochondria. But that's not the big deal. As I said, the big deal is is that the mitophagy process is turned off or severely hampered so you can't recycle those mitochondria. Now, like I said, there's many, many viruses that use mitochondria as part of their replication cycle and it doesn't really cause a problem because we could just repair or replace those mitochondria. But SARS-CoV-2 is evil. It not only damages the mitochondria but turns off the repair process to boot.

Jackie Baxter: 23:02

Right. So it sort of hampers the mitochondria that you have from doing their job, but it also kind of stops the body or slows down the process by which you would rebuild those mitochondria and and allow them to function rather than dysfunction, I suppose yes, and this is the fundamental mechanism for the chronic fatigue that we see and the brain fog that we see in long COVID.

Jackie Baxter: 23:36

Yes, and I think what blew my mind when you were talking there was the fact that mitochondria are only 40% efficient. Like 40%, isn't that much? Is it Like there's quite a lot of waste product there?

Robert Groysman: 23:52

For a biological machine actually for any machine 40% is really really good. That's quite good For any machine, biological or mechanical. I mean we really struggle to build a better machine than what's already built.

Jackie Baxter: 24:12

So all of those things that we get told when we're at school that 40% isn't very good. When you score 40% in a test, like that's all a pile of rubbish, like we should say that 40% is actually quite good, because I saw 40% and I was just like that's less than half.

Robert Groysman: 24:28

So you can tell that in my upbringing 40% would not have been acceptable 40% would not have been acceptable, sure, but for a biological machine it's actually fairly efficient, even though 40% doesn't sound like much. But it actually is very efficient at converting glucose and other carbohydrates and fatty acids into energy, and remember, into energy. And remember there's multiple processes involved in generating the energy. For instance, you probably have heard that fat is more energy dense, and the reason that it is is because it undergoes. Each of the fatty acids in fat undergoes a process called beta-oxidation, undergoes a process called beta-oxidation, which basically breaks down its carbon frame, carbon skeleton, which is typically a long line of carbons, into pairs of two carbons, and each time it does that, it generates ATP, and those two carbons now become what goes into the Krebs cycle, just like a glucose molecule would. So that's why it generates way more energy than just glucose or carbohydrates.

Robert Groysman: 25:46

And really, amino acids are not the preferred energy source for cells. Your body prefers to use amino acids for construction, for building proteins, and peptides over generating energy. If it has to. If there's no carbs, if there's no fat, it will break down muscle and use protein as a source of energy. But it's not ideal. Um, it much more prefers carbs and then fat and then amino acids. Last, right?

Jackie Baxter: 26:22

I mean that makes sense, because if you're building a house, you use different materials for different parts of your house, don't you? You don't use bricks on your roof, you use bricks for your walls. Um, so it makes sense that the body would use, you know, glucose and carbs for energy, but amino acids for building and other things for other processes in the body. It makes sense that there's a a different thing for each thing well, think about it.

Robert Groysman: 26:53

What is our dna code for? This is what we start with. We start with DNA and some organelles from the egg, from the oocyte and mitochondria right, that's what we start with. It has codons, right, it has sequences, but all it codes for are amino acids. It doesn't code for fat or fatty acids. It doesn't code for carbs or glucose, right, it only codes for amino acids. So all your DNA can do is make proteins and peptides.

Jackie Baxter: 27:33

So it can't make the other things. You have to put them in from outside.

Robert Groysman: 27:36

You have to create the machinery to make them or put them together, but you can't. We can't physically. From our DNA itself, you can't make anything but amino acids. That's all it codes for, but that's what creates the machinery and the parts to basically use the other things that we need.

Jackie Baxter: 27:57

Okay, that makes sense. So yeah, the DNA creates the machinery, but we still have to feed and maintain that machinery.

Robert Groysman: 28:06

Yes. So when you have poorly functioning mitochondria, the first thing that happens is that the oxidative stress increases inside the cell. Now there are mechanisms built in to try to reduce or neutralize these oxidative species. There's some floating around the blood, there's some that are inside your cells, inside the mitochondria, very close to the mitochondria, and the top one that everybody knows about is glutathione. It's a scavenger. It tends to reduce these oxidants chemically and hopefully prevents damage, because the longer the oxidant is present, the more it can oxidize tissue and basically deform it. So if it oxidizes a protein or a peptide, it will change shape and therefore the function is altered. And now you have a dysfunctional protein or peptide or a molecule that can cause damage or problem. And oxidative stress can also damage the mitochondria to a point where it actually bursts and is no longer functional. And bursting mitochondria is very bad because of that little mitochondrial DNA chain that I told you about.

Robert Groysman: 29:37

Now each of our cells has a defense mechanism built in. It's part of our innate immune system and it's designed to sense double-stranded DNA, and the main reason for this is viral. If a virus gets into a cell, it's designed to realize that there's something wrong and it's infected and start the inflammation process to destroy it and destroy the cell right, because it's an infected cell. But the problem is is when the mitochondria bursts it tricks the cell into thinking there's a viral infection in there, but there's not. And this mechanism it's called the C-gas sting mechanism, and this mitochondrial DNA can activate that and cause the cell to be destroyed that way and it's an inflammatory process. It's not apoptosis, where it's not, not inflammatory, where the cell can be removed without any inflammation or surrounding damage. When this happens it's inflammatory, which means there's going to be collateral damage. That means the cells nearby can also be damaged and destroyed that way as well. And this process can magnify and cause significant amount of organ damage and cause significant amount of organ damage. So we don't want mitochondria bursting inside your cells and this kind of leads into kind of what the process is going on with mitophagy. So I just told you that the process is significantly hampered or even completely shut off, so you're not able to replace your mitochondria or rebuild your mitochondria source in the cells that have been damaged by COVID and even in some people by the COVID vaccine. Okay, because the spike protein again is involved here and it's able to some extent do similar type of mitochondrial damage to the repair mechanism.

Robert Groysman: 31:42

So the issue is is people who try to rush the process or improve the process of mitophagy sometimes have a backfire and that actually causes more damage because it causes these mitochondria to burst and cause more inflammation and it sets them back. So one of the most critical symptoms that we see with mitochondrial damage is post-exertional malaise. So it's not just chronic fatigue, it's low reserves of mitochondrial energy, so that if you overdo it, even something minor whether it's a mental activity or if it's a physical activity, something that normally wouldn't tire you out or cause you problems, makes you crash. Those are what causes the long COVID crashes that we see, and for some people it's just getting up to the bathroom and getting back in their bed. For others they may be able to get a quarter or half a day of work done and then they crash.

Robert Groysman: 32:49

My point is what I teach my patients is to avoid those crashes because it's not harmless when you go beyond that limit. Some people use spoons, some people use other ways to pace, but when you go beyond that limit it will cause an inflammatory reaction because some of these mitochondria could be damaged. You're overloading the oxidative stress mechanisms that are built into your body. We talked about glutathione. The problem is, your stores will be depleted after a while.

Jackie Baxter: 33:29

Okay, because your your your body's under significant amount of oxidative stress, a lot more than it would be normally, even if you were doing everything right so if your defenses, your, your stocks of mitochondria and your energy get depleted, then it's going to take longer to build that back up again, because, as you said, you can't make a mitochondria from nothing.

Robert Groysman: 33:57

You have to make it from something, and the fewer of them that there are, the longer that is then going to take to replenish that energy, although that stock of mitochondria our goal is to prevent cell death, which um when, when there's insufficient mitochondria to maintain cellular function, the cell will die um or the cell could be destroyed by the mitochondria bursting inside the cells and that will cause an inflammatory destruction of the cell. Our goal here is to replace the mitochondria in a slow and controlled manner without causing the inflammatory destruction of cells. And it's a lot trickier than most people first realize. It took me five years to kind of come up with this and why some people get worse when they try to basically replace their mitochondria or just do mitophagy or autophagy. So a lot of people do fasting or admitting fasting. Normally that would be great, but for some people if you overdo it or do it for prolonged periods of time, you can actually cause too fast or too hard myophagy, in which case, again, like I said, it can backfire on you or in some people, not everyone. Some people maintain some function of mitophagy, some don't.

Robert Groysman: 35:38

The other thing is is I try to avoid oxidative therapies or oxidative treatments where you're basically increasing the oxidative load. So one big one comes to mind is hyperbaric oxygen therapy. I'm not saying it doesn't place in long COVID, but for mitochondria specifically, your body is already under high oxidative load, and the idea behind hyperbaric oxygen with mitochondria is that your body will basically make more antioxidants to counter the oxidative load. But the problem is that you have low energy production to begin with and your stores of antioxidants are low. So you may not get the hermetic response which is what it's called, to generate additional antioxidants where in fact, you're actually damaging the mitochondria more by increasing their oxidative load. And the worst, one of the worst oxidative agents we have is ozone. But oxygen at 100%, on high pressure Oxygen is a double-edged sword. Okay, it just is. It's something we need, but it's also something that's slowly killing us. So, yeah, it is an oxidative agents. We have some agent, we have some antioxidants obviously built in to counteract at 21 okay, at 21, um, not so much at 100 percent, not so much at 100%, not so much at 50%. So you know we've evolved to work with 21%. So our bodies are capable of dealing with it normally when you're a healthy adult, normally, but maybe not so much if you have chronic illness or if you have chronic disease going on, you may not be able to compensate for the oxidative stress. So the only thing we need oxygen for is to be the final electron acceptor.

Robert Groysman: 37:56

That's it so on the cellular level. That's all. It functions as. Yes, it also functions as a white blood cell destruction mechanism. See, oxygen is released. These radicals are actually generated and kept in the vacuole and are released to destroy pathogens by your white blood cells. It does the same thing to our body though these oxidative chemicals. Okay, so there's going to be always collateral damage. So it's always a risk, and a risk versus a reward, risk versus balance, uh, against benefit. Okay. So, um, I don't really like oxidative therapies, unless you're going to pre-treat or pre-load with antioxidants. So you should pre-load before and after and postload If you're going to do it. There is some benefit for endothelial function when it comes to oxidative therapies, but in general, I don't like to increase people's oxidative load. I'd like to decrease it and then focus on their mitophagy and generating new mitochondria, which is called biogenesis.

Jackie Baxter: 39:10

Right. So this explains why, you know, plenty of people have said that they've tried fasting and it's helped them. Plenty of people have said they've used hyperbaric oxygen and it's helped them, but equal, if not, numbers of people have said that they've tried it and it hasn't. So, again, it's this idea of, as with everything, the right person, the right treatment, the right dose and the right time, and that all of these things can help people, but only if they're done right for that person, and this kind of explains kind of why, you know, some people may be able to tolerate that and some people can't, depending on where their level of different things are, I suppose, like how their mitochondria are, how all sorts of other things are going on in their body, because mitochondria don't exist in isolation, do they?

Robert Groysman: 40:07

isolation, do they?

Robert Groysman: 40:08

Well, this goes back to the original point that we made and that there are six mechanisms involved and it may help with endothelial dysfunction, but it may be harmful in somebody who has mitochondrial dysfunction especially severe and they've lost the capacity for mitophagy and their body's already under high oxidative stress load. So, um, that's why there's this, that's why they're screening. Uh, you have to screen for the mechanisms to see which person would benefit from what before jumping into a treatment, because there is harm. Uh, by doing one of these treatments, if you have significant mitochondrial dysfunction, there's additional damage that's done, that needs to be undone, which basically makes it longer for recovery or remission. So, especially if you have huge number of treatments or prolonged treatments without preloading with, pre with antioxidants, right, cool.

Jackie Baxter: 41:12

So let's talk about what is good, and again, this is going to be, uh, probably individual, um. But you said that, okay, we want to use pacing, because what we want to do is kind of iron out those crashes so we don't get that kind of additional inflammation, that additional oxidative load. So what would you suggest to increase mitochondrial function?

Robert Groysman: 41:42

So, as I said, first is diagnosis is to link one of the mechanisms, which is the mitochondrial dysfunction, to the person's triggers. In other words, they typically are triggered with activity, either cognitive or physical. They show signs of post-exertional malaise. There's many others, but those are kind of the big ones, and the way I do it is I created a two-step model or protocol for managing. Each one is going to be slightly different or significantly different, depending on the person's needs. But step one is typically done every day and it's mainly consisting of supplements that focus on being antioxidants and support for mitochondria function or mitochondrial matrix, basically building up, being able to build the mitochondria from the components. So that's step one. That's really just a preparation stage. So that's to get your body ready for the mitophagy or the biogenesis part. Okay, if you try to do the mitophagy first, like I said, it may backfire because your body isn't ready and the cells will burst or die off and they feel worse. Feel worse, more fatigue, more PEM, more brain fog, those kind of things we kind of see, and this is something I learned from experience. If you were doing this for anti-aging, you can hit the intermittent fasting and you can hit the mitophagy and autophagy, full force, without really too much of a concern of any issues. Okay. But if we're doing this for long, covid, you have to be cognizant of the damage mechanism so you can't push it hard. It's like it's like you know, you walk up, you walk up and somebody you know somebody crawling in the desert and they haven't had food and water and they're barely able to crawl and you just make, you know, whipping them to do it faster. It's just not going to work. You need to first prepare them by you know, getting them out of that environment, right out of the heat, out of the sun, feeding them, giving them water and everything else first before you're able to do them. That's what step one does, okay. Then, seven days out of the month, I put people on step two, which is the myelophagy and the biogenesis part.

Robert Groysman: 44:19

So this, this focus, is mainly on supplements, but there are several medications that can be used. But what I realized is is that you don't want hard and fast, you want slow and gentle. Okay, and sometimes even with the ones I choose is still too much. And I follow up with patients and we need to back them off a bit because they're so far gone with their mechanism damaged, that that needs to be rebuilt first. And so it's a long process. Okay, it's done over a course of several months. It could be three months, it could be six months, it could be nine months or it can be over a year before I can get their mitochondria functioning normally again. Okay.

Robert Groysman: 45:02

And you cannot rush the process. If you feel better, if you feel like you have more energy now or you feel better brain fog, it doesn't mean you go back and doing your usual routine. Okay, it needs to be again paced and very slowly come back in. Okay, exercise is one of the greatest ways to do autophagy right, generate more mitochondria, but it's also a very oxidative process. When you exercise, you're actually causing your body to go through a lot of oxidation, okay. So, while it's a good thing, exercise normally is okay everybody should exercise and when you have mitochondrial dysfunction you need to back off.

Robert Groysman: 45:50

Okay, because exercise could be your worst enemy. Eventually you can get back into it, but in the beginning you need to give it a rest. You cannot crash. Okay, it's very important that whatever you're doing daily, you shouldn't be crashing daily. You shouldn't be crashing weekly. Okay. If it happens once in three months, I'm not going to get upset, but ideally you shouldn't be having routine crashes, okay, and a lot of my patients when I first see them. I just saw somebody yesterday or the day before and he's crashing three times a week and people don't realize that you're actually causing additional damage to your mitochondria. So there's multiple ways to initiate mitophagy, but you also want to make sure that it's very gentle. So maybe repromycin would not be a good place to start, okay, because it's a very strong metaphasia inducer. I'm just bringing it up because it may not be the best first choice or even the second or third choice when you're first starting out in rehabilitating your mitochondria.

Jackie Baxter: 47:13

Right, and this comes back to everything we talk about in long COVID and ME-CFS. It's always gentle, gentle, gentle, slowly, slowly, slowly. If you do anything too quick, then the body just says no, and I think most people have found that out the hard way. Um, you know, and often you know, what we find out to be too fast didn't seem very fast at the time. Um, so it's this whole process kind of taking that step back, allowing yourself that space, taking time and sort of sticking with the process. You know you said sometimes nine months, over a year. You know it's it's like allowing that process to happen and trusting in that.

Jackie Baxter: 47:55

Um, you know, and that's very much what I've seen with other people as well, um, so I guess finally, um, we know we've, we've taken a deep dive into this. We've talked loads about mitochondria and we've talked a bit about your protocol and what you are helping people with. Is this something that people can start the process of themselves at home, or is this something that they have to do with yourself or another professional who understands the process?

Robert Groysman: 48:24

Well, first it's always going to come down to diagnosis. Even though mitochondrial dysfunction is a highly involved mechanism in long COVID it's second to dysautonomia you still have to be able to diagnose it because every other mechanism can replicate just about every symptom that you get from mitochondria, just like gut can replicate brain fog and fatigue by a completely different mechanism and the phthalate dysfunction can do that. So many of the symptoms can be mimicked by the other mechanisms, even though brain fog and fatigue are primary to mitochondria. They don't have to be. They could be caused by others. So first it's always going to be diagnosis. I mean, if they want, they can always get my mitochondrial book, the Complete Long COVID Handbook, volume 3, which is the mitochondrial dysfunction book. I outline kind of general principles of how I do it and why I do it. The second thing they need to know is no one supplement or medication is going to be the magic pill, magic cure. Okay, it doesn't exist.

Robert Groysman: 49:38

Long COVID is complex. It's too complex to be solved with one supplement, but only if you try this one. It's going to work this time. No, it just doesn't. The point is combination of supplements in a specific pattern, a specific order, so that you use their synergistic properties to do what you want. You're not going to get there with one or two. It's just not going to work and you're just going to be disappointed, no matter how much the supplement costs or how fancy the packaging is. The point is you're just going to be disappointed, no matter how much the supplement costs or how fancy the packaging is. The point is is you're not going to get there with just one, and you have to understand that long.

Robert Groysman: 50:13

Covid is a complex, multi-mechanism disease and because most people will have more than one, some people have two, some people have four, some people have all six you have to get through all of the mechanisms in order for there to be remission. And one other thing that I didn't get the chance to say but I'm going to say now is this Anamia unfortunately has kind of a little side effect, especially if you're stuck in fight or flight effect, especially if you're stuck in fight or flight. So one of the problems with being stuck in fight or flight is it's a survival mechanism. Right, it's meant for being used in emergencies to get you out of a sticky situation.

Robert Groysman: 50:58

But a lot of people along COVID are constantly in fight or flight and your body has priorities and if you're stuck in fight or flight and your body has priorities, and if you're a stuck in fight or flight, your body's priorities and all of its resources are being forced to be focused on survival, not on maintenance and repair. You see where I'm going with this. So even if you fix the mitochondrial um repair or recycling process, if you have underlying dysautonomia, especially if you're stuck in fight or flight, you may not get too far because your body is not going to give you the resources needed to recycle those mitochondria. It's still so focused on survival because that's primary, that's primal, right. If you don't survive, nothing else matters.

Robert Groysman: 51:46

So survival always comes first and unfortunately, if you're stuck in fight or flight, treating the mechanisms may not be very successful or may not be successful at all. So that's why it's important to diagnose first, go through the triggers and diagnose each of the mechanisms involved. And then you have to treat this adenomia first okay, the triggers, and diagnose each of the mechanisms involved. And then you have to treat dysautonomia first Okay, you just have to before you before you tackle the other mechanisms. Um, maybe next time we can talk about the EAT procedure and how that comes into the dysautonomia and how it's unique and different from the stellar ganglion block and even vagus nerve stimulation. But the point is is you have to treat the dysautonomia before you can really get to the bottom of the other mechanisms. If you don't have dysautonomia, you're lucky. Then you can just go ahead and treat the other mechanisms, probably without too much of a fuss. But if you have this autonomia, then you have to treat that first. That's something I found out from a long time of experience doing this.

Jackie Baxter: 52:53

Yeah, yeah, it's like the roads in Scotland. They've got so many potholes and if you fix the potholes but you don't maintain the roads, then the roads still go to hell.

Robert Groysman: 53:06

Right, exactly.

Jackie Baxter: 53:07

Which is kind of what happens here. Thank you so much. This has been incredibly enlightening. I have learned a load about mitochondria that I didn't know before, so it's been fascinating for me and I'm sure it will be really useful for everyone listening. So I think we have decided we're going to do this again, so I look forward to that, and thank you so much for giving up your time.

Robert Groysman: 53:32

My pleasure, jackie, my pleasure.