The Dylan Gemelli Podcast - Episode #42 Featuring Dr. Elizabeth Yurth Part 2! The TRUTH about the NAD craze, Jardiance and SGLT2 inhibitors, AMPK vs mTOR, CLEERLY and other hear...

Episode Date: August 7, 2025

Episode #42 Featuring Dr. Elizabeth Yurth Part 2! Episode 1 was a major hit and with the amount of requests for part 2, it was now time! This episode starts with a highly impactful discussion on the TRUTH about the NAD craze which will shed light on the many misconceptions associated with it's misuse! The discussion shifts to a discussion on Jardiance and SGLT2 inhibitors, what they are, how they function and the major health benefits they have. Dr. Yurth then provides an in depth breakdown of AMPK vs mTOR explaining what they are and the importance of the proper balance between them. There is an extremely detailed discussion about different heart scans and tests with an explanation on the CLEERLY test. Dylan and Dr. Yurth discuss their top 5 most essential supplements and Dr. Yurth calls out bcaa and amino acid supplements shedding light on why they are not necessary and can be harmful instead of helpful. Dylan looks at Dr. Yurth as a mentor and it is easy to see why as you listen and learn from her in this impactful and highly requested part 2!! STAY TUNED for PART 3, coming for the Holidays!!   Check out The Boulder Longevity Institute https://boulderlongevity.com/   Follow Dr.. Yurth on Instagram https://www.instagram.com/dryurth/     _______________________________________________________________________________ Today's episode is sponsored by Apollo Neuro!   Get the Apollo Neuro for $90 OFF!! USE CODE GEMELLI to save https://apolloneuro.com/gemelli _______________________________________________________________________________ To PURCHASE MITOPURE visit Dylan's landing page and use code DYLAN to save 20% OFF!! https://shop.timeline.com/DYLAN     TONUM supplements for the MIND AND BODY!   USE CODE "DYLAN" to save!!  https://www.tonum.com/DYLAN     THE BREAKTHROUGH MIMIO HEALTH FASTING MIMETIC SUPPLEMENT!  20% OFF with code Gemelli  https://mimiohealth.sjv.io/c/6588260/3323599/30611     TRULY Increase Your NAD LEVELS with WONDERFEEL NMN: https://getwonderfeel.com/?utm_source=DylanGemelli&utm_medium=podcast     MESCREEN: The world's first and only at home mitochondrial efficiency test Save $100 with CODE   DYLAN   https://mescreen.com/cart/47561239626013:1?discount=&ref=DYLAN       HIRE DYLAN ON THE MINNECT APP HERE: expert.minnect.com/@DylanGemelli     Follow Dylan on Instagram, Facebook, Twitter and Tiktok @dylangemelli and PLEASE SUBSCRIBE and leave reviews!!   MAKE SURE TO GO TO DYLAN'S YOUTUBE CHANNEL for MORE video content!!    https://www.youtube.com/@DylanGemelliBiohacking Email Dylan for booking, collaborations and/or to apply for the Dylan Gemelli Podcast [e-mail] Visit Dylan's Homepage https://dylangemelli.com

Today's episode is sponsored by Apollo Neuro. Apollo is the leading doctor recommended wearable technology. Apollo's award-winning smart vibes AI works effortlessly behind the scenes, automatically integrating into your life to deliver gentle, personalized vibrations that activate your vagus nerve, helping you fall asleep faster, stay asleep longer, and wake up balanced, focused, and ready each day. Not only that, but the Apollo Neuro is the first and only wearable that improves your HRV. Apollo is effortless. Simply wear it throughout the day and night and let it do the work

for you. It's safe for anyone and everyone with no side effects and is the only wearable that can be worn anywhere on your body. Optimal health requires both the mind and body to be in line and Apollo is the key to establishing that connection. Check the description below to save $90 with my special discount. Take control over your health today with Apollo Neuro. Welcome back to the Dylan Jameli podcast, everybody. So my guest today, I gave her a really nice rundown the first time I had her, but I have a little bit different intro that I want to give today. So sometimes teachers will have an ego about them with having the knowledge base that we have. I've been through that many, many years. And it took me a while to understand that I am smart because of the people I surround myself with,

and that's what makes me smarter. And I, am very, very, very careful to this day about who I go to for information, who I would even possibly refer to as a mentor to me or somebody that I know I can trust no matter what. And so it's a list that I can count on my hand and really not even all five fingers. And my guest today happens to be one of those people. She is one of my go-to resources of information. And I will tell you this right now, she was one of the reasons where I realized maybe I don't know as much as I think that I know in a humble way and a very, very appreciative way.

So I can give her all the rundown in the world, but I think the, at least coming for me, the best thing I could say is that I look up to her and I find her to be one of the most valuable assets in our community. So my friends, without further ado, Dr. Elizabeth Yourth. Dylan, such gratitude to you for that. And, you know, I'm going to put in a plug for you because guys, I, you know, Dylan and I met, I think we met first Olympia, right? That was probably the first place we met and then we subsequently kind of become friends and, you know, and done some work together. And Dylan recently joined, we started sort of a whole new training program where we're actually

trying to train people who are just passionate about help, how to be more like doctors. So the doctors have these people that they can turn to that can deal with clients when doctors sort of ran out of time. And so we're training sort of a force. And we actually take these people, we put them through pretty rigorous training. We teach them how to read all the labs. We teach them out of read labs that all the doctors don't know how to read. I taught them how to read clearly scans and prodrome scans is tough. And we chose a very small cohort of people who we knew had at least some base knowledge to do the first beta course with. And Dylan's a lot of people we chose because you have to have some background to kind of get there. And so, and you know, honestly,

It was an honor to have you there. And, you know, I just want to speak to. It's not a lot of people, I think, who are in your position who take the time to really learn as much as you do. There's a few. And so I just, for all you guys who are fans of Dillans, I just really want to put out there that he's a little more even though what you think on the surface, see on the surface. Because he is really down there doing the deep dive school stuff that a lot of people aren't doing. That means so much to me because I've always been like a face to an influencer and that's not what I want to be known as or recognized as and you gave me that opportunity that I can't stress

enough how valuable everything I learned from that was and that's going to be a lot of the inspiration on what we talk about today is because I learned so much that I mean if I actually printed everything out and it's I mean people that aren't watching on video it's it's way bigger than any college textbook but it's invaluable and the things that I learned and So I want to give that back to people, at least in some pieces today on what we learned. And then just some other things that I've learned that I've talked to you about personally that I would like to talk about and bring to light. And that's where I'm going to kind of lead with this because several, several months ago now I sent you a stack of things that I wanted to run. And one of the things in there that was extremely popular still is at the time that there's a craze on is NAD.

And you said to me, you're not going to like my answer on this about NAD. and I chuckle because it's like I always come to you because I want that direct answer. And I showed Queenie and we had a laugh and I said, I love this. But anyway, to the point, you said in there that NAD may not be the best option. Here's the reasons why. And we never really got into it. And what I've found is the people that really know a lot that aren't trying to sell a bunch of crap are going to be honest about this and get into it. So first, can you kind of get into this NAD craze?

what it's about and then the misconceptions that are going along with it. Yeah, I think that, you know, really we started learning about NAD not that long ago in the scheme of what we know about medicine, really back in the early 2000s. And we realized that NAD was this critical molecule to life. It absolutely is. Nobody will doubt that, right? And we absolutely know that levels seem to decline in all organisms as we age. So the belief was sort of, okay, well, obviously, NAD is important.

it declines when we age, let's give back NAD and life will be better. The problem is that when you give NAD, yes, our cells like NAD, your healthy cells like NAD, your unhealthy cells love NAD. Your cancer cells love NAD. And when you actually look at the literature, they really could not support that the decline in NAD was truly the problem. So if you had a mouse that was just bred to have low NAD levels, they were not less healthy than a mouse who had normal NAD levels.

What happens when we age is we upregulate two bad enzymes. And those bad enzymes are draining our NAD. So by filling this bucket, we're like, okay, all is good, we're filling this bucket. Well, what's actually happening is on the other end of the bucket as a whole. and these enzymes are just taking this NAD and they're spilling it out. Two big enzymes, one called CD-38, and one called NNMT. And those enzymes are actually doing a lot of bad things. They're screening up methylation.

They're feeding cancer cells. All bad cells have higher levels of these enzymes. So when you give NAD, they're like, great. I'm going to use this for myself. So it's not the drop in NAD. That's the problem. It's the increase in these bad enzymes. So all you're doing when you're giving an AD, and this was well shown in a big niacin

study that came out the end of last year where they gave high dose niacin, and they found up they had an increase in cardiovascular risk. When you give high dose on isin, you do increase NAD, but it also increased cardiovascular risk. It's because of the downstream effects. It's because of this NMT enzyme draining the NAD. So what we should be focusing on is not just filling the bucket, but patching the hole. If you patch the hole, then occasionally you might want to fill the bucket. Maybe you had COVID or you ran a marathon or you did something really stressful or a really stressful virus,

but at the same time, you better block the hole in the bucket. So periodically using a little bit of NAD if you want or a precursor like NR or NMN is okay. You don't want to be doing that continuously. And well shown that your bad cells, your senescent cells thrive on that. So people will get this like flushed kind of kind of good accelerated feeling when they give NAD. It's actually not a good thing. It's actually a spill out of a bunch of synestate proteins that are spilled out your blood. When you give an AD because of these senescent cells that are fed.

And so it's actually that sort of like high that we get is actually not really a good thing, even though people are like, I love it. I feel all hyped up and all this stuff. That's actually not a positive thing. So I think it's something we're still on the brink of understanding and people who are doing a whole lot of this, getting their weekly NAD infusions, taking their NMNNNR every day, are probably going to be nice test organisms to see what happens 10 years from now and those people. So when we actually start filling that bucket, this CD-38 and NMNT kind of thrives on

the more NAD that we're bringing in, correct? And then that's what's causing the problem. Right. So these enzymes accelerate as we age, so that older we are, the higher levels of CD-38 and NMT we have. If we have cancer, we have very high levels of both of those enzymes. Google NMT and any disease you want. The bad diseases have high levels of enzyme. Same things through CD-38. So all these bad diseases are linked to higher levels of enzyme, including aging, right? Aging is a bad disease. So basically, what's happening is, you know, that all we're doing is we're, you know, so if you're super young, like you're 20 years old, you probably don't need NAD. If you're 20 years old and you don't have really any diseases or bad cells or anything wrong going around with you.

Maybe given NAD is not going to be a bad thing periodically. But in me, who's old, giving NAD is going to be spilling right down. It's going to be stealing my methyl groups. I'm going to be creating bad metabolites and it's going to be a bad thing. So that's really, guys, you have to focus on why these things are happening in our body. And then not just looking and going, oh, this is low. I'm going to put back in. It doesn't make sense.

It's not the way our cells work. So two part question then, um, from what you said because it's so interesting. When we're talking about, you said, stopping, patching the draining going on, what are the best options to do that? And how do we know if that is occurring? Is there telltale signs? Is there a blood test?

Is there anything like that that we would know where, hey, we got an issue here? So it's interesting because the only really thing we know right now to block N&MT is the same way the body does. So NMT, when it's accelerated, one of the things it produces, besides going on and screwed up methylation, it produces something called one methyl nicotinamide. One methyl nicotinamide, then when it accelerates, goes off and turns off this bad enzyme so we can refill the NAD bucket. So it's our body's attempt to say, let's refill the bucket, there's too much bad stuff going on. So we can actually give one methyl nicotinamide exogenously to turn off that enzyme. Now, the way to measure that whether that enzyme's high or low would be to measure. measure one methyl nicotidymide level. So for instance, like True Age does a, in the

metabolomic testing, does a one MNA. And what they'll say is, if this is high, it's a bad thing. And that's true. Because if it's high, then I mean I've got high levels of this NMT enzyme. But if it's high because I'm taking exogenously, it's actually a good thing because I'm actually turning off the enzyme. So when my body's making a whole lot of one methyl nicotidymide, that means it's trying to keep up with these high levels of this enzyme that's draining my NAD. So my body is trying to keep up. So it's getting more and more 1M&A. So basically we can give it exogenously turn off the enzyme and that's going to have a good effect.

So we know that if you're naive to any medications that you're taking, if you measure one methyl nicotimide levels, 1MNA levels, you know that your MTA levels are high. So there is a way to do that in the true age testing. It's kind of an expensive way to do it. So I think that in general, what I tell people is if you're older, if you've been sick, if you've just been through a traumatic event, if you've just been through a virus, viral illness, probably a good time to be taking more of the one methyl nicotomy. I, because I'm in my 60s, take a couple every day because obviously everybody, as they get to be over 50,

is going to have higher levels of the M.MT. So I'm going to just presumptively block it without doing a whole bunch of testing on it. CD38's a little bit harder to block. the best thing we know right now is apigenin. I was talking to Eric Verdon, who runs Buck Institute recently. Eric's lab is doing a lot of research on CD-38, and he said he's not particularly compelled

with how effective apigenin is to block CD-38, which was news to me, disappointing news. So I said, well, what is a good way? And he said, well, we're trying to work on that. So I think epigenins, there is research to support it from what Eric said, they're not finding it to be great in their lab setting at Buck Institute. But I think it's the best we have right now until they come out with something better.

So they are trying to actually come up with a drug, which may be also distorting his input a little bit. But they're trying to come up with a drug with a CD-38 inhibitor, which will be a good thing, but not available yet. And for now, Apigenogen is the best thing I have on my list to do that. What about rospheratrol? Does that have any benefit there at all? It doesn't really work on CD-38. So Vesveretal really has some antioxidant effects. I'm not a big fan of antioxidants, nor I'm a big fan of resveratrol.

So it's not wanted, you know, Resverichael got its fame from David Sinclair, right? And then we found out most of that research was not reproducible. Resveratrol probably has some benefits at a very low dose for cell metabol. But at a much lower dose than what most people are taking it. I feel like resveratrol is one of those things where people, People want a good excuse to drink wine, so they use that as theirs. Okay.

So with NAD levels then, aside from aging, which we know, you brought up, you mentioned like a virus like COVID or a marathon. Do those drop NAD level? The thing that's a stress to our body, remember, NAD is producing our energy. It's the NAD to NAD to NAD. And that's what's going in the electron transport change to make ATP, right? Right. So that's an NAD, NADH ratio is what matters.

So that's, that's really, it's not really just NAD. It's the NAD, NADH ratio. That's the important thing. When we've just gone through a really energy exhausting event like COVID or, which is, COVID's really damaging to mitochondrial function. So we get damage to mitochondria or you just ran a marathon or you just, you know, we're up for four days straight. So those are all things that we know were energy drains, meaning my NAD, NAD, NAD, NADH ratio reduced. So that should tell my body. to turn up, you know, to turn off this enzyme and start to make more.

But the problem is, if there's been mitochondrial damage, if I'm older, things like that, then those events will actually sort of cascade and move, you know, keep going on. And somebody who's super young and healthy, that's where you can probably say, okay, those enzymes went up for a little bit. I'll use something for a brief period of time. I'll give a little NAD with a little NNNNNNNNNN inhibitor, and that's probably going to be a fine thing to do. But most people, it's going to be blocking that enzyme.

And then you can do a little restorative NAD now and then. So I'm not going to ban the NAD is always bad. I think he can use it appropriately judiciously like everything. Just not able to being used. Okay. Well, I appreciate you clearing that up there. I'm not going to get a better explanation than that. And I've had so many different explanations, but a lot of it are from people selling it.

Yeah, that's a hard thing, right? There's a huge market. I was lecturing in Portugal recently. And I was in between one guy who owns a company that has NAD infusion centers all over. entire, you know, Europe, you know, like 500 NAD centers across here. So I was sandwiched between him and another person who sell it, who has a company who sells an, you know, an NR kind of supplement. And I was sandwiched between them and, you know, and fortunately neither were very good

speakers. So I was still able to do okay. But it was like, you know, here I am slammy, this guy who, and they were actually a big funder of the conference. It was actually really awkward. I'm like, you know, telling me how great NAD was and how race to go get there and confusions every day. And I was like, maybe not. Well, I mean, you got to keep your credibility. Right. But it is where we have to look at things. Guys, you always have to look at science.

It's where you have to be careful on who you're learning from, right? Are you learning for somebody who has a vested interest in something? Because unfortunately, that's where a lot of the literature comes from. So if you read a study, a lot of times, you'll have to go, look, who was this fun to buy? What were they? Or they're bowls? You have to look at that. Thank you for that breakdown and for the honest integrity that you bring. It's appreciated. I'm going to shift to something now. that I really wasn't planning on talking about before, but you and I got to talking about before and I was telling you about how I had started to take Jardians. And I want to get into this class of drugs, these SGLT2 inhibitors. I've never talked about them. And to be to be honest with you,

I didn't have the understanding about it being used for heart failure as opposed to just being a diabetes medication. And so I guess what I'd like to do is get a breakdown. of what these are and how they're multifaceted in use. Why can it be used for diabetes? Why can it be used for heart failure? What are the things that it's prescribed for? And I kind of want to take a deep dive into that because I want to focus on these a little bit more than I have in the past. Yeah, these are actually cool drugs. And I think much like the GLP-1s, which started out for obesity, and now we've realized they may be just one of the most prominent drugs for longevity in general. you know, the GOP1 inhibitors.

Now we know improved cardiac function, improved kidney function, improved liver function, improved brain function. And the SGLT inhibitors, and I think these two actually work very nicely in concert with each other, quite frankly, but sodium glucose-like transport inhibitors.

And what they actually do is they actually take glucose and instead of being absorbed, the kidney just puts it into the bladder and eliminates it. So really, instead of absorbing backs, So when you eat a high glucose load meal or high carb meal, instead of glucose going back into your bloodstream causing a big spike in insulin, it just spills out, right? So great for diabetes. The one downside is if you have somebody who's a diabetic who has very high glucose levels

and is eating a lot of crap, well, what happens if you're always taking a lot of glucose out of the bloodstream and putting it in the bladder is you can see bladder infections. And that's the one risk of this drug. Now, people like you and I who are eating healthy and aren't diabetics, that risk is pretty nil. But you have to be careful on people who are eating super high carb meals, things like that, because you will see it increase. You know, if glucose is sitting in the bladder, it's a greatitis for bacteria. You'll get bacterial infections in the bladder. They can sometimes be severe.

So it's just the one caution I have about these drugs. Otherwise, they are super safe drugs. And a huge advantage is beyond their metabolic benefits. And it's really because when you look at anything that really, that's why the GLP1, so when you look at these transport mechanisms, they're not just involved in one thing. So if I can actually modify this little transport of sodium glucose, I can actually start changing cardiac function. So I'll actually increase cardiac output. So they've been now utilized a lot in congestive heart failure just by changing that sodium pump, you actually will improve cardiac output in patients. So you can actually improve, you know, in congestive heart failure, patients.

So people that say we've had a heart attack and now their ejection fracture, the heart just can't pump as much because it's been damaged the muscle. You'll start to increase the pumping ability of the heart. And I've seen injection fractures improve from like 25% back up to normal, like 60% in people who are on these. It's also really good for kidney function. So when you improve metabolic health, kidneys are just naturally improved. But even in people who are relatively healthy, you'll see improvements in kidney function. As we're looking, much like the GLPs, they may fall into one of the best drugs that we have for longevity in general. Because whenever you're, if you look at most of the drugs that are truly are helpful for longevity, most of them are focusing on really metabolic stringent control. Right.

And that's one of the things that this works out. Now, because the GLP1 inhibitors or the GV1 agis are working on a very different pathway than the estrogen. GLT2 inhibitors, you can actually merge them together and take a low dose of each of them. And that's what I do for my longevity, because I use Jardians. And I do use Jardians at, because for me, getting my glucose into a really stringent range, I really do need a little bit more. So I take Jardians at a pretty typical dosy and then just a very loss of a GLP1. But you and I were both talking before the show that one of the things you and I were both thin.

And one of the things you do find is when you're, you know, just sort of spilling out your glucose. is a little bit harder to keep weight on. So if they are classified as weight loss drugs, you do see weight loss in people, not so much in people who are obese. You don't see it that much, probably because they're just eating through it. But in people who are eating pretty stringent diets, you do sometimes see a little bit of weight loss. I'm telling you, I've gone from like, I went from 1,500 calories to 2,600 calories,

now 2,800 calories, and I'm adding a little more. And I'm like, looking at Queenie, and I'm going, am I dying? Like, is Cynthia wrong with me? Because, like, yeah, I keep losing weight. And I'm like, I've even lessened the cardio load. And I'm like, okay, I was over-training. It makes sense. And it's anyway.

You have to go down on the dose. You know, if you just get your weight on. You know, I kind of found a point now where my weight can stay stable on these drugs. But they do, you know, so if it is something where somebody is just a little bit overweight, it can be nice adjuncts there too. The GLP ones are still better from that realm. But I think these drugs, you know, and we could, you know, we should do a whole other podcast just talking about these because it would be a whole podcast.

Pakistan itself to talk about the universe. My Abid Hussein, who's our cardiologist here in the practice as functional medicine, but also cardiology, he uses these drugs a lot for his cardiac patients, people with atrial abnormalities, congestive heart failure patients, just cardio protection and arthroscopic protection for people who have arthroscopic disease. So they're really hugely beneficial drugs. And I really like them a lot for my people who have sort of declining kidney function. Do you think that these pair well then with like a PCSK9 inhibitor too if you're using that? Definitely. And then you know, in PCSK 9 inhibitors are going to work primarily on getting that lipids perfect, right?

You're going to get that perfect lipid balance with PCSK and 9 inhibitors. But the SGLTs are working in that whole different pathway to work more on the inflammatory changes in the endothelial wall that lead to plaque, right? Because it's not all lipids. So now you're going to be targeting different. approaches for atherosclerotic disease. Okay, so I have a couple part question then on the Jardian side of things, diet related. If you are having not even necessarily a ketogenic diet, but on the lower carbs. So let's say 100 grams of carbs or less per day.

And you know you're getting rid of these, you know, at a rapid rate. Is that dangerous in any ways? Do you have to, should you eat more carbs? Like, how should you eat more ketogenic, right? Now there's people who eat no carbs and are fine. I need some carbs, right? So if you're a super low carb, like you're somebody who's eating 20 grams of carbs a day, then you might find, you know, that you feel a little less energy,

that you don't have the endurance, you know, that you may have to up that carb intake a little bit more. Because, you know, I don't have that issue with too many of my patients. But if you're somebody who truly is, you're a carnivore, you're eating really, you know, like I said, 20, 40 grams a carbs a day, you may run into problems on these where you're feeling. I've never seen anybody get really frankly hypoglyceal. but I think they feel more fatigue, their energy levels can go down.

Okay. You know, it's a lot like putting somebody who's not used to ketosis into a catotic state. You are going to put people into more of a catotic state here. One of the things that I've noticed is because I do the breath checks in the morning to see how I'm metabolizing fatter carbs. And you taught me, too, if you're waking up in the morning extra hungry, you're probably in the carb state of burning. And I'm generally at a one or two level of fat burning.

And as I've gotten on the Jardians a little bit, I've been like, nothing's changed, but I'm at a three or four. And I'm wondering if that's due to. to the fact that I'm running through them so fast. Right. Yeah. You're running that glucose through faster without being absorbed. Okay.

You're not seeing the insulin changes, right? So you're going to be more, you know, when we're not getting those spikes in insulin, we don't go into as much fat storage mode, right? Right. That's the nice thing about it. This is insulin levels are going to stay much more stable. So, you know, every time we eat, we see insulin level spike. You're going to see insulin level spike a lot less on the majority.

Like for me, for instance, like rice is a big group. It's a big insulin. spike to me. If I eat rice, my insulin or my glucose will go up to 170 and then I'll drop down. I've got a big insulin surge, right? When I'm on Jardians or Paglphos and I don't get that. It'll maybe go up to like 120 my glucose levels, you know, so still bumped up a little, but then they'll kind of gradually come down much less of this sort of big surge and big jump in insulin. Wow. Okay. Well, one more question on the Jardians before I move on then, because we were talking about ejection fraction and you said that you've seen it improve it drastically.

what would one expect in the amount, like the duration of time it takes to take effect to make that improvement? I guess that would depend on how much the damage is and how long it's been going on, right? I think it's going to be slow, but I think even at 12 weeks you're going to start to see some changes, probably six months to see more dramatic changes. Got it.

For me, that changes, it was probably closer to like a nine month period of time. But I had one guy who had a more acute injury, developed acute myocarditis. from COVID and he dropped his ejection fracture. He's a young guy in his 30s, dropped his ejection fraction dramatically. He came back really fast, you know, within like 12 weeks.

Yeah, because I think I've had COVID seven, eight times, something like that. So I'm certain that has had a back. Robith is a big player, unfortunately. And even if you don't get a myocarditis, we know that the spike protein from COVID and the vaccine, unfortunately, can really cause dysfunction in all the little blood vessels, right, in the endothelial of the blood vessels. And that's probably the biggest, we're doing a big long COVID summit. I'm not calling it a long COVID summit.

It's a post-viral summit that in October with New BioAge. And, you know, it's funny because I'm talking immune system. And Dr. Hussein's talking about endothelial function and somebody else's talking to gut. We're in this argument about what's the most important thing here that COVID's affected. And, you know, the endothelial lining, the glyco-Kylics lining of our endothelium is probably the one of the big hits. So that's why the cardiac function can so declines, this endothel damage that COVID has created. And that's something you can't measure very easily. We don't have a great measurement of endothelial function.

There's a lot of people who say, you can look at a camera under the tongue. We don't really have anything that measures it well. So that's people like you, where also you see these changes in cardiac function, you're like, but there's nothing on my MRIs game. there's nothing on this. It's really the microscopic changes that we don't know how to define yet. Yeah, and that's my, I'm certain that's got to be what it is. Because I, it's somebody that COVID that many times, especially people who have had vaccine and COVID seem to be the worst hit. I haven't had that, but about half of that. But yeah, the multiple COVID hits, yeah, not great.

I ported out COVID once and that was it. So, oh, man, I don't know why I'm so susceptible, but I don't know. Yeah, I mean, there's a lot of genetic factors that play a role your susceptibility there. Yeah, it seems like every time I go to a big event or something, I just, yeah, I'm limiting the events that I go to anymore because it's just not working. You keep getting hit, right? That's a bad thing. No.

Yeah. Okay, so I have a couple routes I want to go with you and I want to make sure I utilize the time. So the first one that I would like to talk about, we discussed this in class. And another thing that I'm going to admit, I didn't know a ton about that you fascinated me so much with the breakdown of understanding AMP and EMTOR, what they were, because it's especially so important in bodybuilding, but it is in general.

And I never really focused on it enough. Could you do a nice little breakdown of what these two things are and the importance of and possibly the detriment of being an MTOR too long and why we want to be in, you know, the other state and just kind of get into that a little bit? This is such an important thing for everybody to understand, because this is sort of the, you know, the balance between longevity and muscle is this understanding of these two competing pathways.

MPK stands for AMP-activated protein kinase. M-Tor stands for mechanistic target of rapamycin, right? So when people take rapamycin, so those people who are, you know, big rapamycin fans, and they're taking it for longevity, what they're doing is blocking mTOR. And we'll talk about, you know, is that good, is that bad? So if you look at, you know, what that all means. So AMPK activation occurs when our body senses we don't have enough energy, right? So when we don't have enough energy, we're in an energy depended state, we've fasted or we exercise.

And we've utilized a lot of our energy source. Then AMP is this kind of catabolic switch. It tells the cells stop making new proteins. instead focus on breaking down damaged and recycling damaged parts, which is really important, right? We know getting rid of the damage is as important as building back up, if not more important, right? So it's not really just energy conservation. So the goal is stop using energy. You don't have enough energy.

Stop using it. So MPK, you exercise, you fasted. AMPK turns on. It says stop using energy. So it's conserving energy. But it's also playing cellular housekeeping. Now it's stimulating. Okay, I need a little bit more.

of this, I'm going to break down these bad cells, take the good parts away, reprimodment. It's going to promote fatty acid oxidation. It's going to shut down the really energy expensive anabolic process, right? That's really important for longevity, all of those things. Conserving energy, recycling, breaking down damage things. Those are the big pieces of longevity. So everybody's like, okay, then you just want to be in an AMP case state.

But MTOR is the opposite, right? So MTOR is the C-Saw. So mTOR, when nutrients are abundant, like you've just eaten a whole big steak or, you know, or you, you know, so you're really well fed or you've stressed your body a little bit, but not to the point of extreme stress, right? So doing some, you know, PR type weightlifting kinds of things. Then mTOR could accelerate. You have to be fed to be an mTOR stay. So mTOR is not going to be activated when you're fasting. That's why feeding is important because we do need some mTOR. So here's what kind of the fascinating thing is, right? So mTOR is going to drive protein synthesis, lipid synthesis.

That's important. It's important for brain. It's important for muscle. Right. If we don't have mTOR, we're going to be frail. Our brains aren't going to work as well. So at the same time, it stops autophagy. It says, okay, we don't need to break anything down.

We've got plenty here. And it's going to promote cell growth and proliferation, right? So if you think cancer is the ultimate mTOR state, lots of growth, lots of proliferation, which is why cancer does better if you are more fasted, less glucose, things like that. But for most of us, unless you have cancer, the balance has to be there. So if basically I'm always in AMPK activated state, I'm always doing an endurance exercise, I'm always fasting, right? So I'm one of the people who loves fasting.

I fast every single day for 20 hours, right? I only eat one meal a day for two hours. I'm exercising a lot. I'm taking rapamycin all the time. or metformin, that form is also a blocker of mTOR. So if I'm always AMPK activated, that might be good for longevity. What it's not good for is being muscular, having great brain function, being robust, right, feeling like, you know, like you could take on the world.

So the key is that we have to be able to kind of transition back and forth. So we have to be able to go into AMPK, turn off MTOR for a while, and then turn on MTOR. So that's where it becomes a tricky challenge. And that's why things like maybe periodically doing a fast, right? Now, if you're people like us who are fitter, that might not even be the best thing for us because we may be a little bit too, you know, too much in that autophagy state all the time a bit. But, you know, for some people, that's why the 16 sort of nine eating pattern

became sort of the rage is that, okay, I'm going to, I'm at 16 hours, at least I'll be more of an AMPK state, but then I'll refeed, right? So basically what we want to do, if you think about this more therapeutic target approach, it's selectively activating mTOR, so going and doing heavy weight training while you're eating a good amount of protein, 170 grams of protein a day, doing your heavy weight training, and then backing off at periods of time, so you're going to do that, and then periods of time backing it off. I'm going to eat less. I'm going to go more into my cardio training phase so I can turn these things on and off.

And we've tried to do that with drugs as well, right? So that's where it's taking periodically taking rapamycin. Well, rapamycin is going to be an mTOR inhibitor. Now, I think that maybe the problem with rapamycin is, we have no idea what the right dose is for that process. So people kind of hang their head on the six milligrams once a week dosing. And that's sort of just been formulated for Matt Cabellon and some of his dog studies and things like that.

But we don't really know is that the right dose to be doing. anything. Mikhail Blagoslani, who's a Russian who recently died, he had done the most research on rapamycin, and he really felt like we needed much higher doses. He thought you needed like, you know, two weeks of a 12 milligram daily dose, and then off, so we don't know. So I think instead, this is where things like the GLP1 agonists may be really beneficial. The GLP1 agonists seem to be able to do is sort of up and down AMPK and MTOR. So they seem to really regulate turning on AMPK just enough, but still allowing you to push up to mTOR when we're eating when we're fed when we're exercising when we're doing heavy weight training and things like that so i think that's where these

g lp1 agnes are going to be really a nice benefit to play the seesaw game because if you really want that's what you got to do is up and down up and down so i want big muscles but i want to live forever how i'm going to do that i have to go into you know and that's too where maybe protein restriction periodically is a good thing right i don't i i'm eating you know i try and eat 100 i'm I'm about 128 pounds, so I try to need 120 grams of protein every day, 130 grams of protein every day. And, you know, but going to periods where now I shift, where I drop that down to maybe only 60 grams of protein for four days, right?

So I get myself off of this. And during that period of time, I'm going to do less hardcore, heavier weight training and more of my hated cardio that you love, but I hate. So that's what people really need to know, because that is going to be the key to longevity, is being able to see saw these appropriately so that I have enough AMP, K to last forever, but enough mTOR to be muscular and have robust brain function. Right. It's balanced like everything else. It can be hard. And then here's a question based

upon what you said that I maybe is just theoretical, but see if this hits with you. So when you do a protein restrictive day and let's say that's like a nonlifting day, non-training day, and maybe it's a cardio day, and maybe it's a rest day, would you then counteract that with maybe a little bit of a higher carb day or no? Probably, I mean, the higher carb is, you know, at least you're not feeding so much into the MTOR with a higher carb diet, but you don't want to be in nutrient excess either. Right, right. Or not necessarily.

It's probably a day where I just eat a little less. Eat less. I lower my caloric intake of it, right? I don't do, I mean, I fast for, I make sure I'm fasted from, you know, for a good period of time overnight, but I don't do long fast. I don't tolerate them well. I think that depends. Of course, I think there's people who do really well.

well on longer fast or fasting mimicking diets or things like that. I think that's very personal on what works for what person. If you, you know, if you do have some extra weight, things like that, probably being in a fasted state for a longer period of time, like up to 24 hours is probably a good thing.

Yeah. I didn't, you know, I've always been the way you are because of all the training and everything with the longer fast. Now, I have found during this whole entire moving process that I am able to fast 18 hours if I need to.

Or think about it. Right. You just, you know, right. You just don't think about it. Yeah. Yeah.

when forced and it's a little bit of benefit there. And I do believe, and I'm wondering your thoughts on this and eating in a maybe a smaller window. So like a eight hour window, all of your calories in a day. The big thing is we should stop eating, you know, a few hours before I go to bed. We don't, you know, so you really, that's why I think that it's easy. If you're actually sleeping eight hours, right, and you stop eating two hours before you go to bed, you know, you got 10 hours there and then maybe, you know, I mean, I tend to eat after I work out in the mornings. I work out early, so I probably am getting at least because I do a protein shape within an hour after I work out. So I'm probably getting, but I'm probably going a good 14 hours without

food then. Yeah, I agree with that. The other day I did a thousand calorie meal and it was like gone like this and I didn't even realize I'd eaten because I had, you know, it had been 24 hours since I had even eaten anything. Right. I'm everything and so yeah, definitely. Okay. So, all right, Next question then. You and I, in our class, especially, we talked about a clearly exam. And I actually talked to Dave Asprey about it last week. He brought it up and he was like, you know what it clearly is. Of course, I know what it clearly is.

Probably more than I should. So can you, okay, so like when we're looking at standards of testing on the heart, looking at things, I'm going to give you some examples and you tell me where it clearly ranks among these. So we've got your calcium score, your echocardiogram, your EKG, your stress test, your CT angio, and then your cardiac MRI. I think those are probably the main, you know, ones. And then the catheter, the other angiogram that they do, and it's more evasive. So I guess now it's kind of said that the MRI is more of the gold standard of testing as from what I understand. Now, MRI scan's not going to find atherosclerosis.

Right. So MRI scan's great for looking for myocardial damage, myocarditis, you know, inflammatory changes the heart muscle itself, but it can't look at the small blood vessels, which are going to be what potentially drops you down on the golf course. So remember we're looking at different things. We're just doing an EKG,

unless you're having an active heart attack, The EKG is, unless you're either in arrhythmia or I've had an active heart attack or having a heart attack, your EKG is going to be normal, even if you have horrendous atherosclerotic disease, right? That won't typically reflect in your EKG. Now, it might reflect when you're doing a stress test because you'll get chest pain, but a lot of people don't, right? A lot of people don't have plaque to the point where it's inhibiting low in the blood vessels, so they're not going to get chest pain.

They're completely asymptomatic. So that's the population that's been missed. Because if our standard testing was doing, and then you're talking about the coronary calcium score, so I said, okay, I'll do a coronary calcium score. So I've got my EKG, it looks normal. I do my stress test, you know, or you're just a high level athlete. So you're stress testing yourself every day. I don't ever get chest pain, so you think you're fine. You do a calcium score and you're like, oh, my calcium score is zero.

I'm golden, right? And that's what a lot of doctors still believe. The problem is what a calcium score looks at. is calcified plaque. Calcified plaque is low-risk plaque. Think about calcified plaque. It is cemented there. It is going nowhere.

The plaque that is going to break off, kill you while you're out running, and it goes, oh, my God, he had perfect heart problems. I don't know why he dropped dead running. That's soft plaque. It cannot be seen on a calcium score. So you have a calcium score of zero

and have horrible soft plaque. and be at a very high likelihood to have a cardiac event. In fact, a much higher likelihood than somebody who has a calcium score of, you know, that's mid-range. Because that calcified plaque is no longer risky to them. Right. So what a clearly can do. And so a coronary CT scan where a coronary angio CT, which you write, they run the basic, and you have to do a coronary CT angio when you do it clearly.

But basically, you run die through the blood vessels and you do a CT scan of the heart. But what clearly does is it takes that information and it can quantify the type of plaque. So basically it can look and say, is this plaque with a whole lot of fat in it? So it's basically a very low density plaque. That's a very high-risk plaque. Is it just a low-density plaque, a soft plaque? That's a little less risky. And how much that is calcify?

My goal, if I'm treating somebody, is actually to calcify the plaque. I want that plaque to become stable. The other thing that clearly allows us to do is it actually looks at what's called a remodeling score. So remodeling score is basically how much the vessel's expanding outward. So if I have plaque forming, and this is why you might not get chest pain, right? So my plaque is forming inside the artery. But instead the artery getting narrower, what happens is the artery just expands outward. it. So there's no restriction in flow, so I never get any chest pain. But that's called

positive remodeling. That weakens that blood vessel. And it creates it a plaque that's much more likely to rupture, break off, go down a small artery, and drop you dead. So basically, that's the test. What clearly does that it can quantify the type of plaque and your actual risk factors, right? Otherwise, we don't find people unless. you have, you know, unless you have a, you're having chest pain, right? And then we know something's wrong. So honestly, but clearly is my only way. I think everybody should get clearly, especially if you have any high risk disease in your family, but I think everybody over 50 should be getting a clearly scan because you should know this, right? I have people who I would have thought were the

most perfect cardiac people in the world. There's great athletes, they're working hard, they're doing all stuff. And they do it clearly scan. You're like, oh, my God, this person's at high risk. And once you see that and you know what the risk is, so, you know, do they have this high risk morphology, this positive remodeling of the plaque, unstable plaque, then I actually can work to stabilize it, right? So I can actually use things like colchicine or, you know, PCSK inhibitors, things that will actually help me to turn this plaque into stable plaque. And then once the plaque stable, you can actually use things. At calcified plaque, you can't eliminate. The goal is first calcify it and then you can eliminate it. Make it safe. Make this person not vulnerable. But this is the

only way we're going to ever catch people who are those people who, you know, one of my patients just told me a sister with playing golf. She's like 60 years old, drop dead, you know, never a problem in her life. It's actually sitting there talking. You know, so those are people we have to catch because those are scary people that just are outrunning and drop dead of a heart attack. Most of the people are developing chest pain, they get caught and they, you stent them or whatever, you know, and then they get treated. But how do they, you know, people like you or I who are walking along our lives being fine and are like, oh, I'm good. Look at my lipid panel looks good. Everything looks good. You're not going to find them. So honestly, this is to me a really important test that

everybody gets. Now the question is, what age should you get? I have people who I'm ordering it in their 20s because they have a bad cardiac industry in their family and their lipid levels are crappy and I really want to know. And also is a great way for those of you guys who have really crappy lipids, like, you know, your doctor's like, you need to be out of statin drug. Well, let's say you have horrendous looking lipid panel, but I get your clearly, you've got zero plaque, nothing. No soft plaque, no calcify plaque, no, you know, negative remodeling index on everything. And then I'm really not that worried about you. I'm not going to jump to saying, let's get you on three different drugs, right? We can cheat you more conservatively and work with other less

aggressive methods. So it does also help you to decide how you're going to treat yourself. So you talked about kind of it's showing like the smaller vessels, right? So what if you have plaque and a smaller vessel that they can't stent? Like then what is the protocol or how do you get around that or fix it or are you kind of screwed? So basically the small vessels are not going to be typically the ones that that need the stents. It's going to be the larger ones because the smaller vessels aren't so important. What happens with the smaller vessels, vessels, however, is that the plaque breaks off and sits in them. So they're unstentable vessels, right? But it's not that there's plaque forming the smaller vessels as much, but clearly is looking

at all your vessels, all the cardiac vessels, from top to bottom. So basically, you want to catch the people to stent, who have actually the plaque forming inward to the point where it's creating stenosis, creating narrowing in the blood vessel, and those are the people you could consider stenting on. Really, it's not until you have about 80 percent. loss of flow in the blood vessel that you would even think about stenting. So really those people are the small, and again, most of those people get caught way earlier by things. They have abnormal EKGs.

They had heart attacks, things like that. So, but yeah, the small blood vessels, that's why we've got to prevent the plaque from breaking off because you can't stent them. You can't, in fact, it's not where the plaque really forms. It's that breaking off of soft plaque going to the small vessels that becomes a problem. So that's really what we see is that, you know, and the clothing matter clearly too, as you can see, you get to see pictures of your plaque, which comes really kind of this dramatic feeling when you see this like, oh my God, you know, look at this plaques and it's in. You can see where it is in the blood vessel. So it's much more impactful. When you can see a picture of your heart and you see this stuff, it's much more impactful to you. Right. So it's a, it's a super fun and interesting test to do. It's not a fun test to do because when they do an angiogram, it's uncomfortable. You got to put dye in. You have to lower the heart. You have to lower the heart. You have to lower the heart. You have to do. You have to lower the heart. You have. It's a. It's a lot. You have to do it. heart rate to around 50, 55. So you've got to use beta blockers, things like that, to lower the heart rate. So it can be a little bit of a difficult test to go through, but it's so critical. And so

most of my patients get clearly scan. So when you go to sign up for the clearly scan, you have to have a CT angiote there? Is that how it works? It has to be a facility that knows the clearly protocol. Because for a CT angiogram, you don't need to slow the heart rate down to the degree you do for clearly. So it has to be a center that works with clearly and knows how to do the protocol that they can send it off to clearly with the AI or with the data that the AI can interpret. So it's really the way the test is done, the imaging quality and the rate of the heart, pace of the heart that allows that data to be sent to clearly technology. So clearly it's outside technology, but you need a facility that knows the protocol.

Got it. The catheter that I had put in, I mean, I was sitting right there and he just looked at me and said, I don't see any blockage. I don't see any plaque anywhere, really, but they can't really see in detail what kind of plaque you have, right, with the catheter that's in there and there looks. If they did an angiogram, right, so if they did a CT angiogram on you, you know,

where they did they ran diet and they did CT singing in images, they will see plaque. And they will, you can to some degrees see soft plaque, not as well, but you can see soft plaque. It just tends to be underestimated. and you can't quantify the type.

But if you had a completely normal coronary CT angio, so they did a CCTV, a coronary CT angiogram, and it was completely clear, do I think you need it clearly? Probably not. Yeah, because I had a CT angio done two years ago, and it said 38%. But then when I was in, when I had that episode, now recently, I had the full-blown catheter up my wrist,

the uncomfortable shit, you know, and I mean, he told me I don't see any blockage and I barely see any plaque in there at all. What he told me? And that's where it was like... So you'd have to follow that, make sure that he's followed it with a CT because you can see the blood flow.

All that's telling you is flow, right? So if they're following the die pattern, you could tell if the blood vessels narrowed or not, right? But remember that positive remodeling, the blood vessel's not narrowed. So remodeling, if I do an angiogram and I'm just looking at pictures, I can't see it. So that's the problem is the positive remodeling

makes the flow fine. And yet that's still vulnerable, dangerous plaque. That's what you put things like that. Okay, cool. So, okay, let's talk about some of your personal preferences or protocols. I want to know because there's so many damn supplements and things that you got to take this, you've got to take that.

You know, I want to know if you had a breakdown of things that you were staples for you that you say you should generally take, like for me, creatines one, right? Everybody's creatine. Yes. If you could give me your top five that are just that you feel are essential, what would they be? Yeah, I think that we have gotten way overboard in the supplement realm, right? And, and you know, and you just keep going, oh, I need this and I need this and I need this and I need this. And you end up with, you know, a billion supplements.

And I won't say that I'm, I refined my supplements down. Great. I mean, here's my like, you know, supplements for the day. It's like, but, um. worse but if I want to say okay what does everybody absolutely need

I will tell you I get that from a lot of patients I will take five things that's it right I get that a lot of people my staff says it I will take five things

that's it because these younger people they're not going to do this right so so we've kind of had to say okay we've got to work with people where they're at and I do think if you're going to say

I'm going to take five things number one D3 K2 that combination of D3 with K2 at a high enough dose so you really want to make sure that your D3 levels are 80 to 110. You really want that in that range.

You need K2 along with the D3, both for vascular health, but also because D3 and K2 works synergistically to transport the D3 into the cell. So you need a combination of D3 with K2. So I encourage you can buy that supplement, you know, all over the place. I think everybody needs some magnesium. I think magnesium has to be deficient in most of us, particularly because our diets, even if you're eating a really healthy organic food diet, the soil has been depleted magnesium. So almost every would test, if you get a red blood cell magnesium test,

you'll see it's most people are low. You really want to get that in the 6.5 range and above. So most people need D3K2 magnesium. I think that you're right on the creatine. Everyone needs creatine for their brain as an age. I think he needs something for detox. So if you look at the things that really were getting killed with glyphosates, environmental toxins, one of the main ways to get rid of those is having higher glutathione levels. So I think nesedal cystine becomes a pretty critical player in there. If you look at most of the cancers, the neurodegenergid diseases, a lot of them are played by the crap that we're in our environment that we can't get away from. I don't care how pristine you live. I don't care what kind of perfect house you live in.

You will get environmental toxins. You will get glyphosates, you know, so you don't have to protect yourself. And I think NAC is a simple way to do that. NACA, NACETAL cystine is what will raise glutathione levels. You can go get your IV glutathione, but really gluteothium gets broken down into cysteine to get into the cells. So taking nesedal cystin is a simpler way of getting glutathione levels up. So I have everybody particularly people who live in cities, things like that, be taking nesedal cysting or, you know, or if you're drinking. I don't care if you're just the person is drinking twice a week. If you're drinking, you need more glutathione. So, so any single cystin, I think should be added to that list. I think if we look at, um,

most people need a little more B vitamins, so a good B complex is really useful. And then if we, you know, one of you and I's favorite supplements, if I look at the other thing that declines with longevity, it's going to be mitochondrial function. And so, you know, what you can do there, Coenzyme Q10 or things like uralithinae, one of your favorites, is huge there. So, you know, something that's supporting mitochondrial function. Coenzyme Q10 may not be as good as something called gerinal gerinial, Gigi. because that's higher up in the chain. So everybody's replacing coenzym Q10. Those of you guys want to statin should really be aware of this

because even if you're taking close to 10 with your statin, you need GERNio-GNiol and just look up Gigi. It's a little higher in the pathway. It's why you'll still get statin problems and people who are taking Coenzyme Q10 is because you have to hit higher the chain. So I think something from mitochondrial function, using a combination is something like ulythine,

which is working in a different mechanism, right on that intermitondyl membrane. So something that's going to be really important. So if I have sort of go after my sort of top realm, it's hard because certainly, you know, you need carnitine. You need lots of things. But so much you can still do if you're eating a really good diet. And you can meet. You have to make sure you're eating meat because that's got more of the nutrients that you need.

You know, you're not going to, I don't think you can do it with a vegan or a vegetarian diet as, you know, as much without taking a lot more supplements. If you're eating a really healthy diet where you're eating a good complex of vegetables and fruits and meats. more of a Mediterranean-type diet, then you're getting a lot of other nutrients. So, you know, so obviously if you want to be a vegetarian or vegan because you have moral ethical reasons for that, then you've got to take a lot more supplementation.

Yeah. I don't know what would you add to that list. You know what? I really like what you put on there. I was going to ask you about ubiquinol versus Coke-Q-10. So I think if you're taking Coke-Q-10, it should be in the ubiquinol, not the ubiquitone form. Okay.

Or mital Q, which is sort of a... sort of gets into the mitochondrial a little bit better. But I think if you use just ubiquinol with something like your urolithin A, you're going to get pretty good mitochondrial function help there. And I do think vitamin C is very important for a variety of reasons, but we get it. I don't think that it necessarily needs. Yeah, if it's going to be my top five, then I'm going to say, I'm going to try and get it with my diet and C, right?

Especially if you have collagen dysfunction, things like that, a lot of orthopedic issues. More vitamin C really helpful. Cancer than more vitamin C. Remember, your collagen, your vitamin C are really helpful for bone and joint functions. So, you know, if you're taking collagen, make sure you're taking vitamin C with it, those two works that are just over. One of the things I think is important that I want to retouch on that you covered was the

importance of taking K2 with D3. A lot of people try to slam D3, don't take K2, don't understand the correlation of the importance. And then one other thing, I don't necessarily think this is a top five, but one thing that I think is so important that people don't get enough is selenium. And, you know what? So we test micronutrient levels in people. So we do a full micronutrient panel. I will tell you selenium is low in a lot of people.

And it's not all that available in our diet. So you and I know, you and I talked about this is like Brazil nuts, you know, are great selenium source. So eating like five Brazil nuts a day, but who does that? Yeah. But I see selenium low a lot. And remember, selenium is absolutely critical to your thyroid function. Yes. So, you know, these micronutrients are so, so critical.

and that is one I see low in a lot of people. I overeat fish. I've tried to cut back a little bit, but that's helped my levels. I'm just doing seven days a week. I know that's my fish is my staple and not great on our mercury levels. No, no. It is my, you know, salmon's sort of my staple food. I've cut it back now.

I was doing seven days a week. I've found some good pasture chicken to mix in and take out those days because I have beef every day. I don't care. I mean, like that's literally a thing now. So, okay, I have to ask you this as the last question because you made me laugh. I think I had the thing on mute that day in class, but you said, I'm going to tell you why these are bullshit. And I know Dylan, and I can't remember who else it was, Likes him, but it was the BCAA and EAA. And I laugh because it's, I use EAAs to a point, but I don't, I honestly know like what you said.

I just like it after I work out anyway. But talk about why you said that or why there may be. Not necessary. I mean, there is some detriment to doing them, actually. So our amino acids are really designed to be in this sort of specific complex. Yeah. Of amino acids. Really the perfect complex that comes in like a weight protein or a beef protein.

You know, so if you, and so if you're just taking four different amino acids, for instance, and you're pounding a whole bunch of those after you work out, it actually changes the metabolism of some of the other amino acids that you're, you actually need for muscle building. So Bill Campbell did some great work with this where they actually looked at whether people did better, you know, if they just loaded amino acids, like taking a BCAA after workout versus just eating a really good protein load after workout,

it's dramatically different for muscle building to actually just eat protein. So to me, it's like, I know it's easy to pop a bunch of BCAs. They've also shown some dysfunctioning neurotransmitter function probably because, again, this changing the balance, our body doesn't like it. It doesn't like when we throw a whole, bunch of one thing in. So, you know, if you look at the way our bias were designed, it was designed to get this full complex of amino acids in one source, which would have been a, you know, sort of a meat

source. And so when you're trying to screw around with that and take, okay, well, I know these four amino acids are the most important for muscle building. They're not. It's the complex working together that become much more critical. So I think that there's very little evidence that they support muscle building the way that people say it. If you start looking at gut health, should the fan levels, things like that, they start to get skewed and people who are taking a whole bunch of EAs or BCAAs. So, yeah, I'm not a fan. I think that they can actually kind of some disruption in gut metabolism and brain metabolism.

And, you know, when you look at gut microbiome health and people who are taking a lot of you'll see changes. So you think then stick with the protein patterns. You just have a nice little protein shake after you, you know, you know, I don't know. There's, there's, there's, there's, also did some research to show that there was no reason to have that protein load within two hours after workout, which you and I have all learned, right? I still do it. I still, I don't know. I mean, he said it doesn't matter as long as you get your protein in throughout the day. It doesn't really matter if it, you know,

but somehow that still seems right to be is to replenish a little faster. So I still am stuck on that robe. I think I was taught it too long for me to change my mind on. So I just, you know, I get home from the gym. I do a little protein shake. I go get ready, you know, for work and everything and then, you know, anything else for a while. If you're working out and you're working out any sort of hard. You're going to be hungry when you're done. Yeah. And it's better than eating a bunch of garbage or a hell. Right. Just, you know. Yeah. I don't like that part. A little protein shake and, you know, and, you know, and then I add things like some myosmd, those guys aren't familiar with that.

Myosemd is pretty cool. It's got fortitropin in it, which is a myostatin inhibitor. So you can add a scoop of that. So basically, I want to turn off myostatin so I can keep building muscle for a while for my workouts. So if I do my protein shape with a little of this forotropin, this myos md, this fortitropin, it's good. Inhertotin, it's good, and inhibit myostatin. It's going to encourage muscle building from this full, all the amino acids put together to help encourage my muscles grow. So that's, I think, my perfect realm.

If you want to have a few ketones and there might be helpful too. Yeah. That's kind of my perfect realm for really, you know, maximizing muscle after you work out. So lay off the EAAs, add some protein pattern, stop wasting your mind. Yeah, and I know that, you know, I always hear Nat Nat Nat Nat and I'm talking about the BCAs and, you know. Now. And I go argue with her. But so, so if you love your brand.

you know amino acids, I think maybe just be a little careful what you might be screwing up. Yeah, I would say cut it down. They're just so intricately designed. And so when we slam a whole bunch of one thing in, you know, that's why you sort of have to do what kind of makes sense with what our bodies were designed for. And they weren't really designed to do that, right? We never, did our muscles say, oh, I just want this amino acid. And we know Lucene is really important for muscle building. But it without taking with other things is not going to do it.

I think on my end it's because I sweat so much and work so hard. I'm just trying to replenish a little bit, but I also know what you're saying is so accurate about don't try to overload and replenish something you're not even losing or go. Right. You're not rapidly using the knee glasses, right? No, and we tend to always go a little overboard on things, especially when it comes to replenishing.

So I think it's good to be cognizant and understand that. Yeah, but what? Yeah, just creating these disruptions. Yes. Oh, yeah. No, I've gotten the brain that can to be most affected by that. Yes. These really like things in a really delicate ballot.

Well, I can't believe how fast an hour goes with you. It's ridiculous. It's... Yeah, an hour too. That's how'd that happen. No, I know. I could go 20 more. I'm going to hold you to it.

I want to do another one just kind of... Let's do podcasts on the SGLT's because I think people don't know about it. I think they're a really cool topic to really deep dive down and explain how they're working in all these different realm. Because I think you guys are going to start seeing these, just like the GLP ones. Yep. You know, became the huge rates. I think we're going to start seeing more of these in longevity, biohastrofenes. or wool is coming more of the forefront.

Yeah, I think that that's where people get really gigged down on all the peptides and things like that. But we have some really cool things that are FDA approved and, you know, and well-established and safe that we can utilize very easily. And I think that's YLT inhibitors are one of those ones that we need to learn more about. Yes, we're going to do that. We didn't even talk about peptides today as much as we've talked about them before because there was so many other great things. So and then, you know, everybody to make sure. In October now, we're both going to be speaking at the Mr. Olympia initiative. So all of you guys who are into, you know, bodybuilding, weight trading, just health in general, honestly, I love Olympia for a whole lot of reasons.

If nothing else, the exhibit hall is just fascinating. But Olympia University, you know, we've been doing it for a few years now. And it never gets the turnout as should. I mean, we just get these panels together of people just talking about topics. it is, I think, one of the most interesting, fun little conferences I go to, and people aren't really coming to it as much as they should. So put it on your radar, guys. It's not expensive. You know, it's, in fact, you might not be able to do it free with your ticket, I think. Yeah. And, and, and, and, and, and, and, and, and, and, and, and, and, you know, there's, you know,

Rick Collins, who's a, you know, attorney there, Dylan and I, Jay Campbell's always there. And it was just talking muscle and, you know, and everything under the sun. And it's really, I think, so valuable. And we need to get bigger turnout there. So put it on your radar. It's fun. Yes. I swear the first time that I went and I wasn't speaking and I said, things like this exist.

Like I was shocked. And no one. You don't know about it. It just doesn't get marketed enough. No. Well, we're going to make sure this year because we have a really tight panel this year. And I think as many things as you and I speak at or that we go to or that we see, I swear this is the most impactful of all.

Talking, someone, you get a group of people, not all of us agree with each other, but just talking. So to watch a panel, it can just sort of converse. There's a lot of time for questions. It's just, it's not like somebody's up there just lecturing to you, right? Yeah. Their opinion, you gain all these different, like six different people talking about a topic. You know, everything from training practices to diet to hormones to, you know, peptides,

just across the board. And, you know, in a place where it's, you know, clinically relevant but not, you know, pushing the envelope a little bit more, right? Which is fun. And nobody's selling anything. And they're all trying to sell anything, right. No. And no matter what we do or where we're at, it's just a just a discussion.

And I, I mean, I come home learning a ton, probably. I know. I always love it. I always learn, God, why can't, why are people not coming to this? Plus, the whole event is just a kick, right? It's just, I know. We're going to work on that this year. We got, we're definitely ahead of schedule on that.

So tell you, anybody's listening to tell your friends. and, you know, hopefully this will get out there before you'll live here. Well, as usual, I value every moment that I have with you, and I appreciate your time. I know you've been all over the place talking, recording, and doing everything. So anytime you give me and my audience, we really appreciate it. I appreciate you, Dawn. I'm so happy you're out there teaching because, you know, again, this is the guy who's doing it right, guys. He's learning the science, teaching the science, and that's what you need to be listening to.

Yes. I went from 10 years of bro science to actual real, I, or name. and I appreciate everything. You have no idea how much. I can't express it into words, and I know everybody else does. So tell everybody where they can follow you, and of course I'll link everything down here for everybody as well.

Hey guys, I'm about the falls on at Dr. Ureth on Instagram. join my YouTube channel. I'll do a lot of education on that. At Boulder Longevity also has an Instagram. And then, you know, we have a whole training academy, BLI.acad Academy. So you can join that training academy. me with monthly Q&As that people ask amazing questions.

We talk a lot about peptides, we talk hormones, we talk everything in the Q&As. It's kind of no holes bar. And so go to BLIDOTA Academy for that. Our clinic is boulder longevity.com. Any of you guys who want consultations, we're licensed in every state so we can see people virtually. So anybody who's interested in consultations can contact us there. So everybody, you always hear people say, so and so deserves more followers and deserves this and deserves that. There's not one person on the planet that I can find.

find that deserves more following than Dr. Yertha. So make sure that you go follow her, please. You don't have any idea what you're missing out on and you're going to gain a world if you do. So go follow her. All right. Everybody, of course, always. Everybody, stay tuned for plenty more to come. Dylan Jemeli and Dr. Elizabeth Yerth, signing off.