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Prevent Muscle Loss and Improve Mitochondrial Health | Nicolas Verhoeven

Episode 83, duration 1 hr 23 mins
Episode 83

Prevent Muscle Loss and Improve Mitochondrial Health | Nicolas Verhoeven

Nicolas Verhoeven is a PhD Candidate in Molecular Medicine who works in a mitochondria and autophagy laboratory; he also holds a Masters in Exercise Physiology. Verhoeven runs Physionic, a brand that bridges the gap between scientific studies and the public’s understanding by opening studies, showing and explaining the data, and explaining the physiology that underlies that data. One of his missions is to improve the public’s understanding of the scientific literature without sacrificing the details (or the fun!).

Prevent Muscle Loss and Improve Mitochondrial Health - Nicolas Verhoeven

In this episode we discuss:
– How to improve your mitochondrial health.
– The best skin supplements.
– Common misconceptions about Autophagy and how to trigger it.
– Which forms of training increase muscular power?

00:00:00 – Introduction

00:04:58 – Molecular Medicine

00:10:19 – The Relationship Between Aging and Power

00:15:57 – The Role of Muscle Denervation in Power Decline

00:21:19 – The Impairment of Mitochondria in Sarcopenia

00:26:30 – Exercise for Mitochondrial Health

00:32:00 – The Importance of Healthy Mitochondria

00:37:01 – Autophagy and Mitophagy

00:42:16 – Autophagy and Cancer

00:47:18 – Blood Work for Overall Health

00:52:25 – Effects of Exercise on Fiber Types

00:57:30 – The Neuromuscular Junction and Power Output

01:02:29 – Creatine for Brain Health

01:07:33 – Improved Insulin Resistance in Older Individuals

01:12:37 – Collagen Peptides

01:17:31 – Inexhaustible Curiosity in Science

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Dr. Gabrielle Lyon[0:00:02]

Welcome to the Dr.Gabrielle Lyon Show where I believe a healthy world is based on transparentconversations.

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Nic Verhoeven, soon to be PhD, welcome to the Dr. Gabrielle Lyon Show. I have to say, I am a huge fan of yours. I am so impressed by your translational ability to take studies and science and really break it down in a way that is incredibly easy to understand, and probably most importantly—well, they’re equally important—accurate. There’s a lot of accuracy and intellectual integrity in what you do. Thank you for everything that you’re doing.

Nic Verhoeven[0:03:54]

Well, thank you. I’m incredibly humbled.Thank you very much. I appreciate it.

Dr. Gabrielle Lyon[0:03:59]

You are a PhD candidate, and you’re going to be finishing up your PhD in molecular medicine. This is work in mitochondria, autophagy. You also, quite interestingly, hold a Master’s in exercise physiology, and you run Physionic, which, everybody listening, you have got to check this out. I am a regular tuner inner of Physionic. It is fantastic. I would love to hear a little bit about the research that you’re doing, how you got to where you are, and for the listener to get to know you.

Nic Verhoeven  [0:04:38]

I think most scientists’ origin stories, I guess, go back to the very beginning of what inspired them to get into science in the first place. But for me, I was actually initially pursuing a psychology degree and actually ended up graduating with a psychology degree. You know how people go through college. For those listeners that have gone through college, they’ll go through the first two or three years, and then they’ll maybe switch their major to something else because they think they’re actually more interested in this. Then maybe they’ll switch it again and again. Well, I stuck to psychology for the full four years. It was literally right after graduation that I realized I should not be doing psychology. I spent a lot of money to do that and ended up not pursuing that degree. But I ended up switching gears to science because, ultimately, I got really into fitness during my psychology degree. I couldn’t stop thinking about it. I’m sure you, Dr. Lyon, have gone through that yourself. I mean, that’s why you’ve got your MD, and the reason you’ve done so much work in the field is because you just can’t stop thinking about it. It overwhelms you; it takes over.

I decided to go back to school. I ended up, as you mentioned, getting my master’s degree in exercise physiology. But then I was still unsatisfied. I felt like I wanted to know so much more than just exercise, Although exercise is a fascinating field. I ended up going for, as you mentioned, my PhD in Molecular Medicine, so I could actually delve into looking at Alzheimer’s, looking at cancer, looking at all these different areas of health. That’s where I am now. In terms of my research, the lab that I work in, does a lot of mitochondrial work and autophagy work. Actually, the paper that I’m going to be published in is actually quite different. it’s going to be in peroxisomes, which is not something that most people talk about because they’re the ugly sibling of mitochondria.

Dr. Gabrielle Lyon[0:06:51]

That is very funny. I would love to hear a little bit about what molecular medicine is and just some of the details of that, because I don’t think a lot of the listeners or the viewers understand what that is.

Nic Verhoeven  [0:07:10]

You and I both actually learned about it when I first learned about it. I was extremely focused on getting a degree in exactly what I wanted to do. I was actually offered a PhD in physical therapy. I didn’t know that existed, but apparently it does. I ended up looking into molecular medicine. It turns out that molecular medicine is essentially a degree in which, if you think of research into drugs or any sort of disease, these researchers are multifaceted. They specialize in that particular degree and then start doing research just in that field. They would do anything from cell biology to molecular biology; they might do some biochemistry; they might also go all the way up to physiology, which is kind of between physiology and molecular biology, between those two. molecular medicine extends from the real bottom, maybe not quite chemistry level, but a step above that all the way up to physiology, understanding how the heart works, understanding how the liver works, and the inter-organ relationships and things of that nature.

Dr. Gabrielle Lyon[0:08:26]

It is really fascinating, and exactly what you are mentioning is this interface. I know that you are very interested in this concept of sarcopenia. Certainly, sarcopenia affects mitochondria, or, who knows, it’s possibly bi-directional. Please tell us a little bit about some of these core concepts as they relate to significant health concerns, particularly for an aging population, which arguably we all are.

Nic Verhoeven[0:08:58]

Yeah, I feel like I’m describing something that you know more than I do about the topic, but I have delved into sarcopenia quite a lot. During my master’s degree, my research was actually related to atrophy. For the listener, atrophy is essentially the breakdown of your musculature. It’s the diminution of your musculature. Sarcopenia is an issue. I know that you’ve discussed it in the past, but sarcopenia is essentially a disease or a condition wherein a person will experience a significant decrease in their muscle mass, but not only in their muscle mass but also in their ability to develop strength. On top of that, something that’s not as often discussed is the decrease in power output, so three things: muscle mass, strength, and power output.

That can have dramatic effects on a person’s health span and even on their lifespan, because as an individual, if you—I’m sure you’ve discussed this as well—end up, let’s say, breaking a hip or whatnot, the studies really show that if you end up in a hospital because of a broken bone, especially if you’re in your 70s, 80s, and 90s, the ability to recover from that is extremely small. A lot of that is due to this massive drop in muscle mass, strength, and power that is already on a strong downward trend from just the aging process. That’s why it’s incredibly important for both of those, healthspan being, to define that as just the ability to function within what you want to do. If you want to go for a walk, if you want to be able to cut wood, if you want to make coffee, whatever it is, you should be able to do that in the body that you have, so you should have the ability to live a fulfilled life within the life that you have. Lifetime is essentially just the extension of that life; how long are you actually alive?, and sarcopenia affects both of those.

Dr. Gabrielle Lyon[0:11:19]

Yeah, I couldn’t agree more. I saw that certainly as a geriatric fellow. doing obesity medicine research, there’s this increase in obesogenic sarcopenia. Your statement about power and the change in power as we age is critical. How would you define power? When do you think that we see it from an aging perspective versus a disused perspective? That might be somewhat of a splitting hairs question, but the reason I ask this is because oftentimes, when people think about aging, there’s this idea that there’s an inevitable decline, which is potentially true. But the idea that power suddenly drops off may or may not be true, and in fact, when you’re young, establishing that and then taking that forward to aging.

Nic Verhoeven[0:12:16]

The way I would define power is that you’ve got a time component when it comes to being able to develop strength. If you are trying to move from point A to point B, the ability of your body, your musculature, to recruit itself to actually be able to accomplish that movement is how I would define power. There is a time component to how quickly you can move from point A to point B. They do these tests. I for sure know that you know this as well: they have all kinds of different tests where they do that. It can be a sit-to-stand test. They might measure how quickly a person can get up from a chair, for example, or the ability, or what’s known as, I believe, a six-minute walk test. Researchers will be able to determine how many steps a person can take within a certain amount of time. All those are proxy measures of power output. We can also do direct measures, which we usually do in animal studies.

It’s this incredibly important aspect that, when we think about it on the surface of things, we think of muscle mass and strength, which are, of course, incredibly important, especially strength. But we don’t often think about the impact that power has on our overall health. I think that’s something that, in general, I think that’s an area where, when we talk about people, especially around age 50 or so and going onwards, it starts to really decrease. But then it really falls off the proverbial peak where it should be—I’d say around 70 or 80 years old. It really just drops off massively. You see these gigantic drops in power. A person might still be able to be relatively functional, but it really gives you an indication of something that really needs to be fought against to try to bump that back up to at least reasonable levels.

That’s an area, at least in terms of sarcopenia, that I think is often overlooked. I think it’s something that there are ways of combating, which is of course why I think your podcast is so fantastic because you do a lot of focus in that realm, focusing on muscle strength, and obviously, it’s going to have an impact on muscle power as well.

Dr. Gabrielle Lyon[0:15:06]

It’s certainly an underrepresented organ. Where I think that skeletal muscle is highlighted is really in athletic performance and body composition. But from a medical perspective and improving quality of life, it is not packaged well and discussed in an appropriate body where it’s usable and comprehensive. Thank you, and that’s one of the reasons why I do talk about it. Is this idea of power impacted from a mitochondrial perspective or a molecular perspective? Do you see changes from proteostasis or mitophagy? Are there things that happen that you think directly affect the power from an aging or hallmarks of aging perspective?

Nic Verhoeven[0:15:58]

Yeah, there’s one huge one, actually, which is one that I’ve always been really fascinated by but haven’t talked about to a great degree yet. I certainly plan on discussing it more in the future. But it’s a consequence of what’s known as muscle denervation that comes with aging. For the listener, let’s say you’ve got a grouping of muscle cells. That grouping of muscle cells may be, let’s just say, 10 muscle cells. That grouping of muscle cells is being controlled, in a manner of speaking, by a neuron, so a nerve cell that extends from a part of your body, let’s say your spine. That nerve cell will then control or activate your muscle cells, which usually contract. You’ve got a single neuron, a single nerve cell, that’s forcing these muscle cells to contract. That’s how we generate strength. That’s how we generate power.

However, with the aging process, as we’ve talked about, you could see this decrease in muscle size and muscle function. But what’s not as readily discussed, and there’s more and more research coming out, is the disconnect between that neuron and your brain’s ability or your spinal cord’s ability to activate those muscle cells, which starts to dissipate as the neuron starts to pull away from the muscle cells. That one neuron has control over 10 muscle cells—I’m just throwing out a number. Usually, it can be a lot more or a lot less, depending on the neuron. That alone, if you think about it, means you’re essentially removing your ability to activate 10 or 100 or 1,000 muscle cells, even though the muscle cells themselves may be perfectly fine. But because that connection is no longer there, those muscle cells atrophy, which is going back to what I defined earlier: this rapid diminution of these muscle cells incredibly quickly simply because their activator has disappeared.

That symbiotic relationship between these two cells, the nerve cell and the muscle cell, is an area that, without even going into the muscle cell, can have this tremendous effect. As a matter of fact, there’s this review that talks about mitochondrial health and how mitochondria can affect this process because there’s this constant crosstalk between the nerve cell and the muscle cell. The muscle cell is constantly—you want to put it in simplistic terms—convincing the nerve cell to stick around, to stay in close proximity. The nerve cell is constantly sending chemicals back to the muscle cell to indicate, okay, I’m activating. I’m nearby. I’m the support system. With mitochondrial dysfunction, which would be damage to mitochondria, that could again be the diminution of mitochondria. That may be just an overall mitochondrial inability to generate the correct signals for the rest of the cell; they may not be able to generate ATP, which is the cellular energy of the cell.

With mitochondrial dysfunction, what can happen is that you see a drop in the ATP levels or the energy state of the muscle cell, which can thereby lead to a change in the types of molecules that are released to the neuron. If that happens over time, you start to accumulate insults between those two systems, between the nerve cell and the muscle cell. The nerve cell starts to separate itself slowly from the muscle cell, and therefore, the muscle cell starts to decrease. Now, on top of that, if that happens, let’s say, to a single muscle cell in that population of, let’s say, 10 muscle cells that the neuron activates, it can actually start to influence nearby cells a little bit like—I’m sure you’ve discussed this before as well—senescence. If you have a senescent cell, which is this dormant cell, which is an incredibly simplistic way to look at senescence, but I’ll put that aside for a second, you have this zombie-like or dormant cell that can start to secrete these different factors that also affect all the nearby cells. The exact same thing can happen with muscle cells and neurons. Mitochondria can have a direct effect, and there are many other different pathways that have this tremendous effect on denervation of the musculature.

Dr. Gabrielle Lyon[0:20:58]

It’s really fascinating.Is the review the Mitochondrial Impairment in Sarcopenia?Is that the review that you’re referring to?

Nic Verhoeven[0:21:05]

That’s the one.

Dr. Gabrielle Lyon[0:21:06]

Okay, wonderful. We will link that, and we’ve put together a quick summary for the viewer and listener, and of course, I’m sure that it’s covered in Physionic. Listen, I didn’t want to tell you guys about Physionic because if I do, you’re no longer going to watch my podcast, and you’re going to be binge-watching Nic and his very funny jokes. He’s extremely funny. Just to recap, and not to get off track talking about your funny jokes, are you talking about the neuromuscular junction? Are you talking about components of the neuromuscular junction, essentially?

Nic Verhoeven[0:21:43]

Yes, that’s exactly it.That separation between the neuron and the muscle is extremely small, and that starts to widen as the denervation process occurs.

Dr. Gabrielle Lyon[0:21:54]

What I’m hearing you say is that there is this lack of stimulus and signals, which ultimately, and again, these are very complex processes that then affect the mitochondria. The mitochondria become a bit dysregulated. They are not utilizing ATP and the chemical signals that they should in an appropriate way. Ultimately, the major end product of this combination of issues is atrophy, which is, obviously, the change in tissue, the loss in tissue, and can also affect and have a cascade effect on nearby muscles. Does it also affect, I’m assuming, muscle satellite cells and just even the metabolism of skeletal muscle in and of itself?

Nic Verhoeven[0:22:49]

Satellite cells—to be honest, they didn’t discuss it in the review to any great degree, and I haven’t looked at the effect that it has on satellite cells. I guess I can speculate a little bit here, but if you were to lose the connection between the neuron and the musculature, you would no longer have the ability for the musculature to be activated by its chemical components. The release of neurotransmitters, which would then have an effect on calcium within the musculature—I’m not going to go into that because I don’t want to get too into the weeds. But the point is that you have this chemical crosstalk between the neurons and the musculature. If you remove that and no longer allow the musculature to have the potential for growth, then the satellite cells are not going to be able to actually integrate with the musculature or have that drive to integrate with the musculature. My speculation is that yes, at least by indirect means, it would have an effect on the muscle cells.

Now, from a metabolism standpoint, oh, absolutely. If you have mitochondrial dysfunction, there are a number of problems that occur with the musculature. You usually see a decrease in what’s known as fat oxidation. To define that for the audience, when you consume the nutrient fat or the molecule fat, not to be confused with the cell, the adipocyte, the actual fat cell, the molecule fat will enter into any cell—but let’s stick to the muscle cell—so it’ll enter into the muscle cell using these transporters, which are conveniently called FAT, fatty acid transporters. Those fat molecules will then enter the mitochondria, and through some other transporters that get activated, they get sent into the mitochondria, where they get chopped up. Think of cutting up an onion. They just get chopped up, and you have these little components that then go through this whole what’s known as an oxidation process, which then ultimately spits out ATP, which is what we were talking about earlier, so the cellular energy.

The ability to do that goes hand in hand with overall health. If our metabolism is unable to go through this fatty oxidation process, then you start to have some serious problems across the board, like insulin resistance, for example. With mitochondrial dysfunction, it’s not only just affecting this denervation process; it’s also affecting the actual health of the musculature because, again, the drive—again, I’ll say it for the fifth time; I’m sure you’ve covered this before as well—for the muscle cells to be healthy and to function and whatnot is by creating essentially a sink. When you exercise, you’re moving, and you’re using a ton of ATP. It is cellular energy for a reason, so it gets sucked up and used up to such a tremendous degree that if you were to never exercise or if you were to actually remove the ability for the muscle cell to reap the benefits of exercise with this denervation process, for example, then you’re effectively lowering the ability for your muscle cells to actually continuously suck up these fat molecules. That can have tremendous effects on our metabolism.

When you think about it, muscle is such a common tissue in our entire body that if that were to happen over and over and over again, and you see again this precipitous drop in power and muscle and muscle strength and all that stuff, it’s going to have a tremendous effect on your metabolism. Absolutely.

Dr. Gabrielle Lyon[0:26:55]

I think that number one, people oftentimes don’t appreciate that the primary fuel for skeletal muscle at rest is fatty acids. People always think about glucose; it is the primary site for glucose disposal. But at rest, the requirement is to have healthy mitochondria to be able to utilize these fatty acids. What do you believe can be done? What are some of the things that can help with mitochondrial health from a preventative perspective?

Nic Verhoeven[0:27:29]

I’m going to shock people here.

Dr. Gabrielle Lyon[0:27:31]

I love it when you shock people.

Nic Verhoeven  [0:27:35]

Oh, yeah, I’m definitely going to shock people by screaming the word exercise for the billionth time. But I mean, honestly, there’s just nothing nearly as powerful as exercise. That can go for any type of exercise, but certainly aerobic training because it specifically affects mitochondria through a number of mechanisms, which I’d be happy to go into as well. But exercise is such a massive way of improving your mitochondria in so many different ways, from the mitochondrial number to the mitochondrial quality from each mitochondria being able to oxidize more fat. You literally have a shift.

There’s another condition with sarcopenia where you have this intramuscular fat. Fat will actually accumulate inside the muscle cell itself. The proportion of where that fat is located in the muscle cell can actually have an effect on the health of the muscle cell. If you exercise, you can also shift, which is wild. It’s actually called the athlete’s paradox because it actually happens in athletes as well that you can have this shift of these lipid droplets, so these just sacks of fat that get placed actually closer to mitochondria in a healthy individual. They get placed in other areas of the cell in sarcopenic or obese individuals. There’s all kinds of different ways that exercise can have these tremendous effects on mitochondria, both in terms of quality and number, but also in terms of the placement of the nutrients and much more. That’s certainly the number-one thing. I struggle sometimes to think of nutrition interventions, but generally, just exercise—aerobic certainly—but lifting weights is also a fantastic way to go.

Dr. Gabrielle Lyon[0:29:39]

I really appreciate that. The idea of intramuscular adipose tissue, the athlete’s paradox, is really important, and eventually, there is a change in tissue for an individual who is not healthy and aging in this way where they’re not creating flux. They’re not exercising. These lipid droplets remain. Eventually, you do see connective tissue changes; fibrosis happens. It’s not a good situation.

This is going to be an obvious question, but I think talking about some of the basic stuff—basic information for the listener who’s perhaps just turning this on—why would one care about the number of mitochondria? Why would they even care about the health of the mitochondria? Is it something that requires a particular amount of stimulus? Do we know that the input should be 150 minutes a week? Do we know that it’ll take roughly 60 minutes to begin to mobilize intramuscular adipose tissue? How can we think about this in an action-oriented way that provides a specific benefit?

Nic Verhoeven[0:30:48]

Yeah, that’s a really great question. People often have these flashbacks to biology class about the powerhouse of the cell, which is absolutely true. I don’t want to deny that. It’s not like I want to get on here and say that your biology teacher was lying to you all these years. That’s certainly all true. Mitochondria are definitely the main areas of our cells that actually generate cellular energy. That’s one aspect that has a tremendous effect. I don’t even think the word tremendous—I don’t think the adjective tremendous speaks to exactly how important this is. I mean, we’re talking about life-changing If you have these dips, even small dips in ATP levels, again, just to remind everyone, that’s the cellular energy of the cell, it can have profound effects on the entire cell, just can slow down. It’s like it barely functions anymore. Having these mitochondria that are healthy, that are full, and that are generating optimal amounts of ATP is critical to literally every single cell of your body, with the exception of very few cells, like red blood cells, which don’t have mitochondria.

That’s one way that mitochondria are incredibly helpful, or critical, I should say. But on top of that, they also are huge generators of reactive oxygen species. When we think of oxidative stress, so for the listener, oxidative stress is just you have this generation of these chemicals, these molecules that are in, I usually describe it as unsatisfied. I mean, a chemist would probably scream, but let’s just let’s run with it. They are these unsatisfied molecules that rip away at other molecules. Your cells are made up of millions of functional molecules, they all serve a particular function. When you start to rip away at those, then obviously, you’re going to have a less functional cell.

Mitochondria generate those molecules. You’d be thinking, Well, why? Why would you do that to us? But the reality is that these reactive oxygen species also serve a purpose. They actually serve a positive purpose, as they can act as a signaling molecule. They can affect cells that they’re supposed to affect and, therefore, propagate a signal within the cell. However, if you have too many of them, if you’re producing too many, which tends to rise as we age, we start to produce more and more of these reactive oxygen species, and on top of that, we also have a decrease in our ability to eliminate them, so through what are known as antioxidant means, you start to damage the cell more than you’re able to repair the cell. This, of course, occurs in mitochondria as well. You start to damage the mitochondria.

Having healthy mitochondria can have an effect on your cellular energy state, which has tremendous effects. I mean, it’s a whole field in its own right. Then, on top of that, it can have an effect on oxidation, so the oxidative stress that builds up in your cells On top of that, let’s add one more: it can also have an effect on your cell signaling. Your mitochondria are also very much in tune with cell signaling. I’ll give you an example. Your mitochondria are actually one of the two ways that your cells either decide to kill themselves or to remain alive. You want that cell signaling process to work extremely well because it’s one way that we’re able to prevent cancer. If your mitochondria are in tune with the ability to be okay, we need to release particular factors that ultimately lead the cell to die, and that’s a positive thing. They’re not going to do it willy-nilly; they’re going to do it specifically and exactly when they’re primed to. But when you want the cell to essentially succumb to, in a word, it’s tough to anthropomorphize the cell, but let’s say that the cell decides or needs to essentially eliminate itself because it sees itself turning into a senescent cell or it sees itself going down a cancerous path, then you want mitochondria to be able to release these factors and essentially tell the rest of the cell, okay, we’ve decided, we’re now going to go through what’s known as mitochondrial-dependent apoptosis or cell death.

That’s three, and there are many other factors that lead to mitochondria having or a person wanting healthy, functioning mitochondria, and you could go into mitophagy, autophagy, and all that stuff. Now, in terms of the amount of exercise, usually whenever I talk about that, I usually talk about recommendations based on what the ACSM says, so the American College of Sports Medicine. I don’t know if we’ve ever gotten granular enough to say exactly. I know that the ACSM, at least the last time I checked their guidelines was a number of years ago, so this may be slightly outdated, they said that the minimum was 10 minutes of physical activity, which is really low to just start to see some benefits. Now, obviously, more is going to be better up to a point. Now exactly what that point is, I think, if I remember correctly, I think you actually said it yourself: 150 minutes per week, something along those lines, or it may be a little bit more. But also, that depends on the intensity of the exercise, whether it’s moderate intensity or vigorous intensity, which is usually based on what’s known as a heart rate reserve calculator, which is a proxy of VO2, and I’m sure you’ve discussed VO2 as well in the past.

Dr. Gabrielle Lyon[0:37:03]

It’s really interesting, especially because I believe that mitochondria is this hot word: mitochondria, autophagy, mitophagy. There’s potentially a lot of confusion in this space surrounding the things that actually influenced it. What does it mean? What does it mean for the health of an individual? Could an individual fast for, I don’t know, a day and then improve autophagy? Or is that not true? What are some of the misconceptions about this idea of autophagy or mitophagy that you would correct for us? I think hearing it from you, someone who studies this, would be really helpful.

Nic Verhoeven[0:37:45]

Yeah, that’s a fantastic question.

Dr. Gabrielle Lyon[0:37:48]

We definitely can tell by your excitement.

Nic Verhoeven[0:37:51]

Well, if you ask me any question about science, I’m going to get excited. Okay, so autophagy, just to define it for everyone, is when your cells need to break down something inside of themselves; your cells can’t constantly be building and building and building. Think of a room; you just can’t keep adding and adding and adding. Eventually, you need to start taking stuff out, and usually you try to take out the stuff that you’re no longer using or that’s broken for whatever reason. Your cells do the exact same thing. You even mentioned the word before, proteostasis. You have more protein synthesis, or you have protein degradation; protein synthesis is the buildup of any particular protein.

But we’re talking about the other side, we’re talking about protein degradation, which falls into three major camps. You have the proteolysis through the cleavage enzymes. You have the proteasome, which is a particular funky-looking little molecule that essentially grabs on to tagged proteins and funnels them through what literally looks like a funnel and then just spits out the broken pieces out the other end. Then you have autophagy, which is typically considered macroautophagy, where you have something like this sack, almost like a garbage bag. It’s almost like floating in water, which is what our cells are primarily made of. It will engulf these large swaths, these swaths of the cell where you may have mitochondria, you may have parts of the endoplasmic reticulum or the peroxisomes that I mentioned earlier that nobody talks about, or just anything, any number of different proteins.

I think a great analogy for that is that if you’ve ever seen a whale eating krill, it opens its mouth, and it’s just this massive thing that just sucks up all this krill. Once it’s trapped in the sack, it’ll close the sack, and then another vessel, another sack, will come in and bind with the previous one, which ultimately leads to the production of what’s known as the autolysosome. Now the autolysosome drops the pH of the autophagy machinery in these sacks. It also introduces a bunch of degradation enzymes.Whatever’s inside, whatever’s trapped inside that sack gets bombarded with a bunch of, quote, unquote, toxic materials that are specifically designed to just eliminate those sections of the cell.

That’s a background on autophagy, and that’s a good thing to have in general. As a healthy individual, you’re going to have certain levels of autophagy. It’s going to go from high levels at certain points to low levels at other points. That’s fine, and that’s typically how people think about it. Exercise is a potent stimulator of autophagy in a beneficial way. Certain levels of fasting can increase autophagy. There are all kinds of different ways that you can increase autophagy. But does that necessarily mean that it’s always a good thing? The answer is absolutely not.

I’ve been doing some reading on autophagy and some weird things that autophagy does that are unexplained in fat tissue, but I’ll leave those for another time. But a great example of that is cancer. Cancer cells can actually use autophagy for their own benefit. The one question that I get, or I guess two questions that I get, related to this is, okay, what cancers? Is it this particular cancer? Does that mean that autophagy is at a negative level? The answer is no. That doesn’t mean that autophagy is always negative, just because in certain cancers, you can get an upregulation of autophagy. It just means that certain cancers can hijack the system, in a manner of speaking, and use it to their own benefit.

There was this study that was done where there was this particular cancer that was being studied. They found that when they used a, let’s say, chemotherapy drug or some sort of drug against that cancer, it had some effect for a while, and then it stopped having that effect anymore. What they posited was okay. Well, let’s see what happens when we block autophagy. Suddenly, it became far more effective. The reason for that is because the cancer cell was using autophagy to trap the chemotherapy drug, degrade it, and then eliminate it.

The answer is that autophagy is always, just like anything in the body, an incredibly nuanced conversation. But by and large, I think the way that people should consider autophagy in their day-to-day lives is that if you’re generally healthy and you’re not suffering from any major issues, then autophagy is generally seen as a positive.

Dr. Gabrielle Lyon[0:43:20]

Would you say that it’s happening no matter what, that exercise is likely the greatest stimulus? Would it be fair to say that if you are going on an overnight fast, you are generating some type of autophagy, and it’s not necessarily measured in a particular way? Just to clear up some of the discussions around autophagy.

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Nic Verhoeven[0:46:08]

Yes, definitely. Our body is constantly in flux. That’s true for really any situation. Proteostasis is another example if we were to go one layer higher than autophagy. That’s certainly true for autophagy. If you’re just existing, you’re going to have periods where autophagy is more upregulated, and sometimes it has nothing to do with nutrient consumption. It’s just increased because maybe you got sick. Your cells have to increase what’s known as xenophagy. They try to eliminate viruses and bacteria by increasing autophagy. It doesn’t matter if you’ve been eating protein, if you’ve been fasting for three days, or if you’ve been exercising; it’s just going to force autophagy because it has to. But that’s why it’s generally best to try to look at averages and look at a healthy individual as a whole because they are going to see increases and decreases in autophagy that may be beyond their control, even though some elements are in our control.

Dr. Gabrielle Lyon[0:47:08]

For you, when you’re thinking about your overall musculature, health and wellness, and mitochondria, is that something that is on your mind, or are you just executing the day-to-day activities like making sure you’re creating flux and exercising? I do want to talk about the impact that exercise has versus resistance training, endurance, or cardiovascular. You’d mentioned Zone 2 as opposed to high-intensity interval training. Are there multiple ways to get to one result?

Nic Verhoeven[0:47:46]

In the last part of that question, the answer is definitely yes. Especially if you’re talking about autophagy, there isn’t a whole lot of data on exercise and autophagy yet, mainly because autophagy was just discovered, and really, there’s been a lot more research just recently. The research really hasn’t caught up to that. But my educated guess would be that absolutely, yes, any form of exercise is going to increase autophagy. We may end up figuring out that resistance training may be better in certain circumstances. For example, resistance training is a good example of proteostasis; again, taking that one level higher, autophagy is under the label of proteostasis. Resistance training can increase degradation for a short period of time when it tries to clear out particular broken pieces of the musculature, whatever they might be. For that, autophagy is probably going to be upregulated exactly for that process. But at this point, I probably wouldn’t worry about exactly which exercise is going to be superior to another exercise simply because, at least, there’s no research yet on that. In five years, the answer is probably going to end up changing. To be honest with you, I forgot the first part of your question.

Dr. Gabrielle Lyon[0:49:12]

I’m sorry, I’m just so interested in what you’re saying, so if I bunch the questions, I can just listen to you. The first part of the question is: is there a particular influence, depending on the activity, if someone is doing high-intensity interval training, on the outcome of having healthy mitochondria? Obviously, there’s different fiber types in skeletal muscle, but the influence on the health of mitochondria is important because, again, we hear a lot about Zone 2 training. We hear a lot about resistance. We’re beginning to hear more and more about high-intensity interval training and what effect that has on, I suppose you could say, even the fiber type and then the subsequent mitochondria, but the influences on those things.

Nic Verhoeven[0:50:01]

Once you start to extend the scope beyond autophagy, because I just went over autophagy, we don’t have enough data on exactly which exercise modalities, but we do know exercise definitely increases autophagy. If we start to extend the scope to fiber type, when we’re talking about fiber type, for the listener, we’re talking about muscle cells. Muscle cells can also be considered fibers, so they’re synonymous; they go back and forth. Some people say fibers, some people say muscle cells, and some people say myocytes. When you’re talking about fiber type, it does matter what type of exercise you do. You would do cardiovascular exercise, so cardio of some sort, so that would be like long-distance exercise, something that you can do for long periods of time.

Admittedly, I haven’t done much research into Zone 2 specifically, so I can’t speak to that yet. But what we do know is that it tends to have a tremendous effect on really all fiber types, but especially type I, which is the red oxidative fiber type. If we go back to the very beginning of our conversation, talking about how mitochondria, if they have the sink, are able to take up these fatty acids, these fat molecules, and oxidize them and generate ATP for the cell, well, that’s where cardiovascular exercise is incredibly helpful in that it does specifically affect mitochondria in that it increases a protein called PGC-1 alpha. Now PGC-1 alpha is a coactivator, so it will enter the nucleus of our cells and coactivate a host of other proteins that are specifically related to mitochondria. It will also have an effect on autophagy, but it’s most well known for its effects on mitochondria. Once you have more PGC-1 alpha, you have more activity of PGC-1 alpha, and you tend to have more mitochondria generation, so you get mitochondrial biogenesis, which is the creation of new mitochondria.

On top of that, you tend to have more mitophagy, which is the autophagy of mitochondria. The reason why you would want to do that, or your cell would want to do that, is because, again, your mitochondria are generating reactive oxygen species. They’re causing so much damage to themselves that you do have times when, and this is a really cool process, your mitochondria will actually combine, so you’ll have really damaged mitochondria and really healthy mitochondria. Sometimes, they’ll actually combine. They’ll go through a process called fusion. That’s to essentially mix up everything, and then they’ll separate out all the negative components into one section of the mitochondria and essentially eject those back out. That’s through a process called fission. Then you’ll have this small mitochondria that’s completely dysfunctional, and that’s when the autophagy machinery comes in because it’ll be tagged for degradation. The autophagy machinery will come in and remove it. Cardiovascular exercise has a tremendous effect on that.

Now, in terms of resistance training, that tends to be more type II, although again, it’s not like they’re these hard cutoffs where fiber types march down the aisle, and they get designated, you’re type I, you’re type II, and you can only get a benefit from one thing or another. Ultimately, it’s going to have an effect on the entire scope of the different fiber types and whatnot. But resistance training has an effect on the size of the musculature. It can have an effect on the different contractile componentslike myosin and actin.It can have an effect on how much glycogen is stored in our musculature, which is stored glucose, for those that are listening.Actin and myosin are contractile components of the cell. It’s definitely going to lean one way or another with cardiovascular exercise or resistance training, but they’re going to have a ton of crossover.

There’s such a thing as fiber type switching, which isn’t a completely permanent process, but you can have it, which is usually defined. The fiber types are usually defined, and at least one of the ways that they’re defined is by the type of myosin that’s found within the muscle cell, myosin again being one of those contractile components that allows the muscle cell to squeeze together to elongate. Resistance training can have an effect on fiber type switching as well. If we go back to sarcopenia, we typically see, especially with diabetes, obesity, and sarcopenia, a loss in type II fibers. The ability to fight that and encourage the muscle cells to maintain those muscle fibers can be absolutely invaluable.

Dr. Gabrielle Lyon[0:55:13]

Yeah, we certainly do see a change in fiber types.You guys can witness that when you see an older individual get skinnier. We’ve all seen our parents—sorry, Dad—our grandparents get skinnier, and it’s thought to be due to a change in fiber type. What about high intensity interval training, and what about power generation? How do we train for power?

Nic Verhoeven[0:55:41]

High-intensity interval training is a great middle ground between the two. You can reap some of the benefits from cardiovascular exercise, and you can reap some of the benefits from resistance training. It is, as you’re alluding to, a fantastic way to also increase your power output, mainly because it’s burst. I mean, when you think of power, you should be thinking about bursts. Again, it’s that time component. It’s not just, can you do it, which would be like strength, but can you do it extremely quickly, as quickly as you possibly can? High-intensity interval training is a great way to figure out and try to push your body to adapt back to increasing that power output again, because you’re massively telling the nerves, the neurons, to constantly engage with the musculature as quickly as possible.

For example, we’re talking about the neuromuscular junction; we’ll call it a connection even though they’re not physical connections, but a very close proximity connection between the nerve cell and the muscle that can actually widen and deepen as well. You have these trenches in the muscle cell, in the muscle membrane, and those can actually widen or become much deeper, and that tends to be because this connection is strengthening. I would imagine that probably has quite an effect on power output. I think that high-intensity interval training probably has a pretty significant effect on those kinds of metrics. So yeah, I think that it’s a great way to go. I’m not going to do it because I can’t stand it. But I mean, for anybody else who wants to do it, I stick to resistance training myself. But yeah, it is a great way to go.

Dr. Gabrielle Lyon[0:57:37]

Basically, what you’re saying is that if you don’t use it, you lose it. I personally recommend people do high-intensity interval training because it’s exactly for the reasons that you’re speaking about and being able to generate that power quickly.

You mentioned reactive oxygen species. There’s a lot of information on supplementation. Are there particular supplements that you find valuable? One of the things that you do in your work is look at a large body of literature. You’re very clear as to where the literature is coming from and the quality of the studies. Are there certain supplements that you have found valuable?

Nic Verhoeven[0:58:19]

Yes. I’m incredibly conservative when it comes to supplement recommendations simply because there’s a lot of different criteria that supplements, supplement companies, and supplement research in general have to fit. I look at things like effect size, the duration of an effect, or what it specifically affects, like if it affects mitochondria, that’s great. But then, does it actually affect the whole cell? If it affects the whole cell, can we actually measure that in terms of clinical outcomes? I tend to be really conservative.

I’ll mention two. One of them, which I feel certain you’ve discussed in the past, is creatine. Creatine has hundreds of studies behind it. There’s some evidence that it actually specifically affects mitochondria as well, so it can help in the health of mitochondria mainly because there’s this enzyme called creatine kinase that it binds with. Creatine kinase is actually also found in a particular section of the mitochondria. I think they’re still trying to figure out exactly why it’s located there, but it seems to have a positive impact, and it may potentially be in that it allows for the energy transfer from inside the mitochondria to back outside of the mitochondria, where it actually gets used, the ATP. That’s one that’s really huge.

Another one, and that has an effect on the brain musculature. There’s a lot of data coming out.

Dr. Gabrielle Lyon[0:59:52]

I want to stop you for a second because you did point out something that I thought was really great: creatine’s impact on the brain. I think there are still questions out there. But certainly if you’re older, if you are an older individual, there seems to be even more evidence to support creatine use in an aging individual.

Nic Verhoeven[1:00:15]

Yeah, that’s such a fantastic point. I’m glad you mentioned that because it’s so true. The research I’ve looked at on creatine in the brain has been really specific to older individuals. The benefit has been far greater for older individuals. Taking creatine has helped with different indices of memory, but I’ve also looked at some research on other neurological outputs, and it seems like it has an impact there as well. The effect is far stronger for older individuals. That may be because there’s a drop in creatine concentration.

Our body actually has two different creatine systems. It has a creatine system in the brain, and it has one for the rest of the body. They aren’t synonymous. If you supplement with creatine, typically your endogenous or your body’s production of creatine decreases, and people get really worried. They think, Well, then, am I shutting that down? Will I not be able to have my creatine synthesis come back? The moment you stop it, it pumps back up. I wouldn’t worry about that.

But the brain is far less sensitive. That’s why there were some questions on whether creatine supplementation will actually have an effect, and now there’s more and more data coming out that it does seem to have an effect, a positive effect, almost solely a positive effect. I should also add athletes, especially people who experience head trauma. Traumatic brain injury seems to be helped. This is all mainly from animal models; I should mention that. But the data has been just incredible in relation to how creatine can actually save neurons from cell death when you don’t want them to die. That’s definitely a big one.

Dr. Gabrielle Lyon[1:02:06]

It’s fascinating that an oral dose, so the oral absorption, can be measured in isolation, but the fact that the oral dosing is utilized and effective is pretty tremendous.

Nic Verhoeven[1:02:25]

Absolutely. It’s a remarkable molecule. It’s been a fascinating discovery.

Dr. Gabrielle Lyon[1:02:31]

Do we know the dosing? Is it a standard of 3 to 5 grams for brain health?

Nic Verhoeven[1:02:39]

I think that’s still being figured out. When I went over the research, I have to admit, I think I have a bias in that I do think, and I don’t think I’m alone in this because there have been multiple studies that have used higher doses; they’ve used 15 or 20 grams of creatine, and some even go beyond that, like 40 grams. Usually, you just end up excreting a lot more creatine, which is the degradation product of creatine. My bias is that I think that as more research comes out, there’s a potential that we’ll discover that maybe higher doses can have a greater impact on the brain. But the current literature does not support that. As it stands, most of those studies still use 5 grams, and they do still find an effect. Exactly teasing that out is going to depend on the amount of data input that we’re able to put in, and right now, it’s just too low.

Dr. Gabrielle Lyon[1:03:37]

That’s a very valuable insight. Thank you.

Nic Verhoeven[1:03:42]

The second supplement that is really taking things by storm as of actually around this time last year was this grouping of studies that came out of Baylor University, the medical school there. They were looking at–

Dr. Gabrielle Lyon[1:04:00]

Which we’re here, just so you know.My husband is a surgical resident at Baylor.

Nic Verhoeven[1:04:08]

Okay, well, perfect. Hey, I mean, perfect podcast to talk about it then. A group of researchers looked at the combination of glycine and N-acetylcysteine for the abbreviation of GlyNAC. Now, to get the results that they found, they first started with animal models. They found some really tremendous results. I know that you mentioned reactive oxygen species; that’s why I’m specifically mentioning this one. Then they came out with a pilot study, and then they decided to do a full-fledged study because the results just translated from animals to this pilot study, and then they did a larger study. In every single study that they did, GlyNAC had incredible results. I mean, you have effects on mental ability; the cognition had an effect on muscle function. They didn’t measure any power outputs, but they did measure strength output, so from sit to stand tests and things of that nature.

They looked at some blood pressure and some heart metrics. Those results weren’t quite as astounding, but there were some slight improvements. They looked at DNA damage. There are different molecules that get secreted by ourselves when we experience DNA damage, so they looked at some of those proxy measures, and they found that they were reduced. There were just all kinds of different areas. Insulin resistance was, for sure, significantly improved. That was done specifically for individuals who were in their 70s.

While the sample or the number of individuals in the study was still pretty small, the effects were just so tremendous that it was an incredibly exciting study. Now, I am still incredibly conservative about it simply because, while Baylor is a fantastic university and I have no reason to doubt these results, I typically don’t really jump on a bandwagon until I’ve seen another independent group of researchers also show the exact same results. That’s one thing. The other thing is that for the third study, so the larger study, they did add another group of younger individuals—I don’t remember exactly how many it was, maybe eight or 10 or maybe 20 individuals that were in their 20s—and gave them GlyNAC as well, which is again, Glycine and N-acetylcysteine. They only measured for two weeks, but they found no effect. From the zero-week mark to the two-week mark, there was a zero difference. I really think that makes a lot of sense. I would actually like to see that extended to the full 16 weeks or 24 weeks because the older individuals ended up consuming GlyNAC for at least 24 weeks, or something along those lines.

The effect takes a while to develop. But once it’s there, it seems to be pretty profound, again, if the study results end up holding true. But the way I would interpret that is that it really only applies to older individuals. People, I would say, who are like 60 years and older or individuals who may not be dealing with a particular health condition, it could potentially be beneficial. But there’s not a lot of data on that, based on some anecdotes that have been sent my way. I get flooded with people telling me that they’ve been taking GlyNAC, and it’s been life-changing for them, which is fantastic. But I tend to be, again, very conservative and very stringent about what the data shows, even though anecdotes tend to jump many years ahead of the data in certain circumstances.

Dr. Gabrielle Lyon[1:08:02]

I really like how you point that out. You said something here that everybody should listen to: there have to be multiple groups. It can’t just be one study at one university. It has to be replicated. The data has to be replicated, and that’s an important point. Thank you for that. Selfishly, completely off topic, hyaluronic acid, which I know you did a video on. I have not gotten to that video. Is it a yes, or is it a no? It’s all I want to know. Yes or no? Ladies, listen up. Was it topical or oral?

Nic Verhoeven[1:08:45]

I can say it was oral that was the most effective.

Dr. Gabrielle Lyon[1:08:50]

But did you look at topical? Again, ladies, listen up. This guy, if you want to know good skin products, I have an idea. We should all send him our favorite products, have him review the literature, test it out, and tell us collectively, let’s do this if it is going to work. We can all save money. Are you up for it?

Nic Verhoeven[1:09:11]

That’s what I’m trying to do.I would definitely be up for it, sure.

Dr. Gabrielle Lyon[1:09:16]

Forskin, oral hyaluronic acid. Yes?

Nic Verhoeven  [1:09:22]

Leaning towards yes.

Dr. Gabrielle Lyon[1:09:24]

Wait, everyone wants to know. He’s a scientist, and scientists, when you ask them yes or no, are very challenging. When you put them on the spot, it is very challenging because, as an expert, things are very nuanced. That’s just the reality of it. For example, if you were to tell me about plant or animal protein, you would guess I would say animal, but again, well, it depends on whether they need fiber. What is it that we’re talking about? But Nick is much more of a scientific expert than I am, so yes or no?

Nic Verhoeven[1:09:57]

Back to the question: again, I’m leaning towards yes. I think that in the topical studies, I found some glaring issues in their methodology. I was not impressed; I’ll just put it very mildly. I was not impressed by the topical studies. The oral studies were a little more consistent and did show that it seemed to be pretty effective at reducing wrinkling. Another one that I take for skin products, which I’ve been taking for a number of years as well as a preventative, is collagen peptides. There’s a good amount of evidence now that collagen peptides seem to be quite effective, and usually the pushback that I get for that is, Well, why don’t you just take protein because protein is typically a more complete source of the amino acids that make up collagen peptides? That’s a fair point. When it comes to muscle mass, absolutely. There’s no competition.

But when it comes to skin health, it’s not actually the amino acids themselves; it’s the stitching of how they’re put together, and those can actually get absorbed by the intestines. Usually, people think that it’s just single amino acids. Amino acids, for those listening, is the component that makes up protein. When you consume protein, you’re actually consuming amino acids. The collagen peptides come in these di- and tripeptides that can be absorbed in the intestines. Those can actually bind to what are known as fibroblasts, which are these collagen-producing cells. They can use the components of the collagen peptides for the production of collagen. But what the collagen peptides can also do is bind to actual receptors on the cells and actually change the cellular media or the cellular signaling within the cell to convince it to start to secrete more collagen in the skin. That’s where the evidence is currently leaning, so I just wanted to throw that out there.

Dr. Gabrielle Lyon[1:11:57]

I love that. It’s an important point because I’ve had a lot of conversations with Don regarding collagen, and the one thing that we kept coming back to is its absorption capacity. What I’m hearing you say is that the di- and tripeptides are absorbed, and they do have a subsequent impact on skin wrinkling. I’m all about it. Do you know the dosage? Would it be 20 grams? Where’s the dosing?

Nic Verhoeven[1:12:24]

Yeah, 10 to 20 grams is a goodplace for most people.

Dr. Gabrielle Lyon[1:12:27]

Easy. I love that. There are a whole bunch of companies that make amazing collagen, whether it’s 1st Phorm or BUBS. They’re amazing. I will say oral hyaluronic acid. There is a new product out; it’s called Glōci. Have you heard of this? I will get you some. My dear friend, Lori Harder, made this product. It’s amazing. She gifted us; we have a little girls group. We all got it early, and now I know her secret because it is evidence-based for her oral hyaluronic acid.

We talked about a lot of stuff, Nic, and you’re not off the hook yet. We talked about sarcopenia. We talked about mitochondria. We talked about exercise; we talked about their influence. We talked about your top two supplements that you feel are worth the cash, which are creatine and GlyNAC potentially. Do we have any more? Otherwise, I want to talk to you about why you do what you do. This is your last chance to throw out what else you really like.

Nic Verhoeven[1:13:35]

For individuals that are struggling, let’s say, with insulin resistance, which again tends to increase with age, curcumin. Curcumin, however a person wants to pronounce it, I’ve heard it in a thousand different ways. I didn’t know much about it at all, and I ended up looking at maybe 15 studies on the topic. The evidence was overwhelmingly positive in its effects on preventing insulin resistance from going from a pre-diabetic state to a diabetic state. There’s this one study where they gave—it was a pretty large study, like 200 individuals that were given curcumin over nine months. They also had a placebo group, and the placebo group was like 16% or 18% of individuals who ended up going from a pre-diabetic state to a diabetic state over the year that the study was running. Meanwhile, among the people in the curcumin group, there wasn’t a single person who went from a pre-diabetic state to a diabetic state, which is a pretty profound protective effect of just one compound.

Dr. Gabrielle Lyon[1:14:53]

And there was no change in nutrition or training? I mean, it’s probably pretty hard to control for those things, but no change.

Nic Verhoeven[1:15:02]

I can’t say training. There’s a potential that there were differences between the two because they didn’t measure it. However, I would say that once you get up to larger and larger sample sizes, a lot of that gets diluted, so that, let’s say, maybe three people or 10 people are avid trainers, and they’re only in one group, those will tend to get diluted by the 90 other people in the group. But it’s certainly possible that there were differences in that regard because they simply didn’t measure it. In terms of nutrition, I don’t think there were any differences between the groups.

Dr. Gabrielle Lyon[1:15:36]

Very interesting. Any other last words?

Nic Verhoeven[1:15:44]

No, I think that’s it. I think, like I said, I could talk about science for hours and hours and hours and days.

Dr. Gabrielle Lyon[1:15:53]

Now we’re going to talk about you, which is always a scientist’s favorite subject. I will tell you, I am friends with a lot of scientists; they avoid the topic of themselves nearly at all costs. Aside from a handful, right, and I’m not talking about absolutes, the majority don’t want to talk about themselves. Why do you do what you do? How did you go from psychology to being very interested in exercise to then being very deeply involved in basic science, which is not regular medical science—no offense, when we say basic, it’s different; it’s molecular—to becoming an internet sensation? How? Are you embarrassed? If I am, I’m doing a fantastic job because, okay, how and why?

Nic Verhoeven[1:16:48]

I’ll go and correct you with the internet sensation. I don’t think we’ll go to that extent. But thank you; I appreciate the kind words. I think it just stems from one thing: you end up. I’m sure people who are listening have found that thing that they just can’t stop thinking about, like we were talking about earlier. You just get to a point where you just succumb to it. This is what my brain keeps coming back to, and that’s exactly what happened to me. I always allude to this, like when you’re five years old and someone just keeps asking you why. Okay, why does this happen? Why? It’s just nonstop, and that’s exactly how my brain works. I’m not satisfied with how the muscles are connected to the nerve. I need to know exactly. If I were to keep zooming in, why not just continuously zoom in and understand on a molecular level why these things are happening? That’s what continues to fuel me: this inexhaustible curiosity. Physionic, what I started, was completely selfish at first. I just thought to myself, I’m annoying my professors, so I might as well just start learning on my own and then start putting things out for people to also reap the benefit. If I’m going to reap the benefit, I might as well put my notes up online and have other people enjoy them as well or suffer with me.

Dr. Gabrielle Lyon[1:18:26]

You did it selfishly for yourself at first and then realized that there was a massive need to get good information. It’s fascinating. The amount of scientific information out there now is greater than ever before. When I was doing it, we had to go to the library, go to the card catalog, and pull out these—I mean, maybe I’m not that old—journals. It wasn’t as accessible as it is now. With accessibility, you can appreciate this; good studies take a long time. We’re seeing whether it’s because of the influx of data accessibility; there’s a lot more studies coming out, and it does become challenging to be able to sift through what is good, what is valuable, and how do we even understand it? How many hours a week are you spending doing what you’re doing—reading literature?

Nic Verhoeven[1:19:28]

I think I usually lock myself up for maybe 10 hours a day just by constantly reading literature. I even work on the weekends sometimes. But again, I mean, when you find that thing that makes you—you just can’t stop thinking about it. It’s not a sacrifice. It’s just a part of who you are, so you just end up doing it. You can’t help it.

Dr. Gabrielle Lyon[1:19:54]

I just love it. Again, I found your information and then the way you do it so valuable. I know that my audience is going to find you, and the information and the work that you’re doing are incredibly valuable. You have a ton of free content. Not only that, you have a ton of free content; you also have paid content. You’re probably so busy with inquiries, but there’s a whole host of ways someone could essentially pick your brain and help you understand science better. I just wanted to say thank you. I believe that you are an absolute superstar, and you are going to change—here’s what I think. I think that you’re providing a service that is so articulate that you’re going to change the expectation and the standard for what is provided to the general public. You’re hearing it here first, people. Follow this guy, and you will see exactly what I’m talking about. Nic, thank you so much.

Nic Verhoeven[1:20:54]

I deeply appreciate you having me on. It was so much fun, and I have so much respect for you, and I thank you. I can’t say it enough.

Dr. Gabrielle Lyon[1:21:03]

The Dr. Gabrielle Lyon podcast and YouTube are for general information purposes only and do not constitute the practice of medicine, nursing, or other professional health care services, including the giving of medical advice. No patient-doctor relationship is formed. The use of information on this podcast, YouTube, or materials linked from the podcast or YouTube is at the user’s own risk. The content of this podcast is not intended to substitute for professional medical advice, diagnosis, or treatment. Users should not disregard or delay in obtaining medical advice for any medical condition they may have and should seek the assistance of their health care professional for any such conditions. This is purely for entertainment and educational purposes only.