Welcome to the architect of Resilience podcast, where we explore the secrets of overcoming life's challenges and unlocking unstoppable strength through. Deep personal conversations and expert insights. We have an entirely new series on the architect of Resilience podcast. I'm really excited about it because it's still under the same philosophy and it's about being more resilient through physiologically. And so there's been an area I've been playing in for about 20 years now, I believe with
peptides. Peptides are a very unique series of amino acids. Actually, I've got a great piece where I cover peptide fundamentals. But we're just going to go in with a deep dive today and I'm really excited to welcome Anthony Castor and also congratulate him. He's a valued member of my endless evolutionary community, but he's achieved an extraordinary achievement. He's made history as the first non physician to earn a fellowship with the Seed
Scientific Research and Performance Institute. It's a new role where he's been involved with educating physicians and members on key topics like exercise, peptides, nutrition, cellular medicine while representing the organization. So huge testament. I've known Anthony for a number of years and so he's going to be joining me on this series on
the podcast. It's really great. Successfully bridging the world of medicine and strength training, creating a path for both disciplines to grow and share their knowledge and understanding. So our first episode, we are going to dive into a controversial topic and that's GLP one agonists. These are known as semaglutide, ozempic, aretitude, liriglutide. God, there was a new one I was just looking at. Anyway, we're going to dive into those
in a bit. But I say controversial because there appears to be a whole lot of fear mongering and negativity about them in the fitness community and I'm going to propose a counter to that with the research today and so is Anthony, about their incredible value. Now if you disagree with this, please hang on and listen through because I
think you'll, you'll understand where we're coming from. If not, it will educate you on, you know, some other, other topics because a lot of the pushback is just around, well, it's just eat less, be disciplined, it's, you're going to lose muscle, you are going to have gastroparesis and die. And just, well, one, just look at the number of cases of that and you'll see that's really
a non issue. But the other does tie to, I think that there is some legitimacy to this, because when I talk to people that are in the medical side of the community, I do see a lot of people that are just pushing this as a weight loss for a bunch of people. And everybody is just taking this base standard protocol that is actually a pretty high dose, actually substantially high dose. And I think that's part of the problem. And then following this, ramping it, taking everyone to the maximal
dose. So again, there are some issues with this, but on the other side of that, like if we talk about, and we're going to go way beyond weight loss and diabetes in this piece, but when we talk about weight loss or food addiction, the simple answer of, well, it's just eat less, be more disciplined like me. That's a very fitness based, you know, approach. Food addiction is a much more complicated thing than that. Particularly, it's the only addiction where you have to face
that thing every single day. So it makes it even more complicated. So I'm not going to dive into some of those behavioral factors. But if that is your answer, I, you should not be working with, with people as a, on the dietary side like there is. It's a, it's a very complex thing. So I just want to address this controversy piece up front and say there's two sides of
the coin. I think both are right in certain aspects, but we're going to do a deep dive and also talk about some of the dosing issues as relates with this. So I didn't reorganize this, this schedule, but yeah, we're going to start off with what glp ones are. I'm going to let Anthony kind of kick that off as it relates to weight loss, insulin sensitivity
issues. I think it's interesting noting some of the history and the fact that these are actually first research as it relates to the neuroprotective effects, which we're going to get in, not the weight loss, also just the history as it relates to. We won't get into the whole Gila monster thing, but the, I find it, the history of the gastric bypass surgery quite fascinating where they were, you know, physically reducing the size of the stomach to reduce
eating because the stomach would be full. But in retrospect, they found that essentially they were cueing the mechanisms of what GLP one s do by just having a slowing of that gastric of the upper GI tract, which was then affecting, you know, the GLP in the body. And so that, in short, that's essentially what we're doing with GLP agonist at this point in time. But it's really
fascinating. We were doing a very, you know, dangerous, permanently modification surgery of people's stomachs when it was really just affecting, you know, receptors and, and peptides. So, Anthony, what are your thoughts? Absolutely. First of all, I just want to thank you again for having me on here. It's really an honor. And as you said, you know, we've known each other for a number of years. You're somebody I've looked up to and learned from. And so it's just great to be here and really
excited to talk about this subject. As he said, there's a lot of misinformation around it. And I think that when we can kind of explain to people what these are, how they work, these are things we naturally produce in our body. And you kind of get a better sense of what's happening. And even past that, all the pleiotropic benefits that come with these, I think a lot of people's minds are going to change and hopefully this will be a big step forward in health for a lot of people. So I guess kind
of good starting point. Let's just go through what the different things are. We've got like a GLP one, glucagon like peptide one, gip, a myelin comes into play and I then we've even got to think about things like glucagon itself. So when we kind of understand the role of each of these, it'll make sense what these peptides are going after, how they work and how they work together and all that cool stuff. So just give you guys a heads up. I like to use a lot of analogy
when I'm explaining things. It was explained to me that, you know, learn, learn all the depth, but try to explain it in the simplest way and kind of build up from there. So starting with a glucagon like peptide one, GLP one, I kind of think about that as like it's your body's vip bodyguard. And when you eat, what this bodyguard is going to do is it's going to show up and it's going to make sure that you're not getting out of control with your
blood sugar. And it goes right to the pancreas, kind of taps the beta cells on the shoulder and says, time to release insulin. And insulin is a hormone that's going to help get that sugar out of your bloodstream into your cells where it's needed. But the thing with the GLP, it's not just about insulin. It also stops glucagon. And we'll get to this in a little bit here, so it'll make more sense. It stops glucagon. And glucagon would kind of be
like the wild party crash. Or if we're building on this analogy and it slows down, how fast food is going to leave your stomach, so you're going to feel full for longer. Kind of like what Chris was saying with the gastric bypass and that mechanism of, like, feeling full and less drive to eat. So it's basically like the bodyguard, making sure you don't stuff yourself at the buffet. And the next one, continuing with our analogy, gastric inhibitory polypeptide. Gip, that is. It's kind of like the
hype man. So Gip is going to be the hype man of your digestive system, and it is just cheering on that pancreas to make even more insulin after you eat, especially when you've had, like, fatty or sugary foods. It'd be like standing in the back saying, come on, man, you got this. Make more insulin. And kind of like my buddies when I'm in a wing eating contest. And gip also helps store energy, and it
encourages fat cells to take in and store fat. So there's got to be this balance in there that's making sure your body has fuel for later, and that's why it helps store energy. But it's just like stashing snacks in your backpack before you go on a long trip, you know, that's not necessarily a bad thing, but you want to make sure they get eaten. And then the final player, glucagon, that's kind of like the emergency backup system, and it is
literally the opposite of insulin. So insulin, you remember, is going to kind of take this stuff out of your bloodstream, drop the blood sugar and glucagon, the emergency generator. When your blood sugar starts to get low, what it's going to do is say, hey, liver, break up backup sugar stores, and it's going to start releasing glucose
into your bloodstream, and that's going to kind of give you more energy. So just to kind of reflect on where we're at so far, we've got the GLP one that's kind of telling the pancreas how much insulin to release, modulating that blood sugar. We have the gip, the hype man, saying, keep it going, keep it going, and helping store energy, and then we have the glucagon that essentially is creating energy if that blood
sugar gets too low. And the last one, and the only reason I'm putting this in here is you guys are going to be hearing a lot more about this. They're doing some really cool stuff where it's combined with, like, the GLP ones, and we'll explain it a little bit more later. But another one to know about myelin, and we would call that the sidekick in this analogy, kind of like a Batman Robin thing. Interesting bit of trivia. When we think about a type one
diabetic, they don't release a myelin. And when we think about a type two diabetic, they release one unit of, unit of one bit of a myelin per 100 bits of insulin. So you can really kind of start to see, one, they're released hand in hand. And two, obviously it's going to be a big player. And to kind of give you guys an analogy with that, Mylan's like a friend telling you, like, if you guys go out for dinner or whatever, and if you're anything like me, pizza's in front of you, you're
tearing it up. Mylon's saying maybe we should take it slow on the pizza. You're eating pretty fast, you're going to crash afterwards. So it's kind of like that common sense in the background, a little bit more on these. And not to get too, spend too much time on this because we got a lot of material to cover.
But when you think about these working together and everything, they work in different parts of the brain and that's going to come into play when we talk about dosing instead of basically like having to go up and up and up in these things, when these signals aren't working quite right, by combining different signals. So like a GLp one and a gip or a GLP one. Gip glucagon or like a
GLP one, a myelin. We can keep doses at the bare minimum and work on different parts of the brain and really modulate that blood sugar response the way that we need to for all the benefits we'll be talking about. Yeah, there's a really great discussion on the mechanisms of action. I love the analogies, Anthony, so I. Gotta keep it simple for me. Doctor Justin, I'm going to do a quick overview of all these lesser known benefits. Now, obviously, you just covered some of the basis ones, so improved
insulin sensitivity. GLP one enhances the body's response to insulin, helping to manage blood glucose levels more effectively. Particularly beneficial for type two diabetes and appetite regulation. You know, the decrease, decrease in food intake by the slowing of the gastric emptying and acting on appetite centers in the brain, which can help with weight management, which will lead to, you know, weight loss as well, making an invaluable tool for managing diabetes. The ones that we're going to
touch on further, and I'm going to dive into those. Now, a lot of this, the research that I'm going to cite is non diabetic, so I'm going to pull this for non diabetic populations just to demonstrate the efficacy of this. And a lot of this is independent of weight loss. So everything we've talked about so far is weight loss. But a lot of these other things that we're going to talk about from cardiovascular, neuroprotective, anti inflammatory and impulse and behavior, all are independent
of this. But GLP one has been shown to have protective effects on the cardiovascular system, including improving endothelial function, reducing blood pressure, and lowering the risk of, you know, all cause cardiovascular events. Neuroprotective effects. Emerging research suggests GLP may have neuroprotective effects, potentially reducing the risk of neurodegenerative diseases
like Alzheimer's and Parkinson's. We'll dive into the research on that. A lot of this is driven by the anti inflammatory influx. So I'm going to start with that one. Even though I forgot, that's why I said I forgot to reorganize my, my presentation there slides, but the last one on impulse and behavior side. So just a quick segue into that. It does impact dopamine pathways, the reward systems affecting the central nervous system, and has been shown promising
effects in alcohol and drug treatment. And I have seen this stuff firsthand, which we will talk about. So I want to start off with, with the anti inflammatory because that is a driver of a lot of these. So the mechanisms of action for the anti inflammatory effects. So there's an inhibition of the pro inflammatory cytokines. The GLP receptors activate and suppress the release of pro inflammatory cytokines like tumor necrophosis, factor alpha interleukin one, beta
interleukin six. These cytokines are involved in systemic inflammation and contribute to the pathogenesis of several chronic diseases. By reducing their levels, we can mitigate these inflammatory processes throughout the body. They also reduce the oxidative stress, which is closely linked to inflammation. And this helped combat this by promoting the activity, the activity of anti ant.
I'm stumbling with my words. I did 3 hours of, it was actually three and a half hours of video recording before this. So I'm kind of spoken out, but antioxidant enzymes these enzymes neutralize reactive oxygen species, preventing cellular damage and further inflammatory cascades. This mechanism is especially important in conditions like atherosclerosis and cardiovascular disease. Immune system
modulation. These receptors activation influences immune cells, particularly macrophages and t cells, shifting them from pro inflammatory to anti inflammatory state. This immune modulation plays a crucial role in reducing chronic inflammation seen in diseases like rheumatoid arthritis, inflammatory bowel disease. So the benefits, we're going to talk deeper on the cardiovascular effects, but it rolls into that the neuroprotective effects and potential in
autoimmune disease. So I will cover this one because I don't cover it in the others. But emerging studies suggest that GLP may play a role in management of autoimmune conditions by regulating immune responses and reducing harmful inflammation. This opens up potential application for GLP receptor agonists in conditions like rheumatoid arthritis and multiple sclerosis. And I can tell you as someone that has autoimmune disease and rheumatoid
arthritis, that I have seen significant impact on this. And we also know that injecting directly into arthritic joints will have an impact. I'm not suggesting that anybody here does that. Listening to this, clearly, this is something that needs to have a medical intervention if you're going to pursue that, you know. So I think it's gaining a lot of recognition in broader applications beyond diabetes management, particularly in the anti inflammatory
agents. Its ability to reduce those cytokine levels through oxidative stress and modulating the immune system makes promising like therapeutic for these. And I'd love to see more research on it. The research that I have, we've got from peptide protocols, notes, receptor agonists, reducing inflammation and glp one inflammatory effect studies. Now that's a really pretty amazing job of covering everything just to fill in some spaces and build on
what you already said. It does have those amazing effects on the macrophages, specifically like pro inflammatory cytokines, tumor necrosis factor alpha, interleukin one, beta interleukin six. And what it does is it shifts these macrophages from, you have m one and m two and m one is a pro inflammatory, I lost my words too, pro inflammatory state and m two is the anti inflammatory. And they're both important. When you think about if you get an injury, there needs to be
inflammation to initiate that repair state. But then afterwards you want to be able to switch out of that and promote tissue repair. So they facilitate that switch from an m one to m two. And then when we think about our immune system in t cells. And like th one, th 17, the regulatory t cells and even neutrophils, with the t cells, it suppresses the activity of th one and th
17. And that's a kind of, I think my theory, some of the effect of what we see in terms of autoimmune suppression, and then with the neutrophils, it's going to reduce that recruitment. So you don't. And this also with the autoimmune, so you don't see, like, hyper responders to inflammation. And then what's also kind of cool in the central nervous system, it reduces microglial
activation, like the glial. You hear about glial inflammation in the brain, leading to things like Alzheimer's, Parkinson's, those sorts of things. And by reducing that inflammation in the glial cells, it helps to protect neurons
from inflammation induced damage. So another huge benefit there, and indirectly, and this is really cool, and it's going to really resonate with a lot of lifters, enhanced or not, you're probably going to have a dysregulated HPA axis if you're primarily sympathetic, really wired to go hard in the gym and normal stress of everyday life, and that HPA access, being dysregulated, can have all sorts of effects on everything from, like, sleep to whatever.
But GLP helps to modulate that HPA access and reduces the release of glucocorticoids. And that is, again, one of the ways that it helps with, like, the metabolic dysfunction that you see and regulation of blood sugar, that sort of thing. Another cool thing it does is it increases pro inflammatory adipokines like adiponectin. And those are things that improve insulin sensitivity and help to reduce fat. I think, really, I
mean, you covered pretty much everything. Vascular system, it's increasing that nitric oxide, reducing reactive oxygen species, inhibiting nuclear factor kappa beta, and it also modulates the JNK pathway, which is another inflammatory signal oftentimes associated with, like, inflammation in metabolic tissues. So, yeah, yeah, I mean, we could go on forever about all the different things. You know, that's one, that's one area I forgot to do a bullet point
was metabolic function. Right, right. So. But, yeah, I mean, let's diving a little bit towards the cardiovascular. And, you know, there's several pieces, lots of studies out there. I've got this one on 2018 study published in the British Journal of Pharmacology, emphasizing the GLP one's benefits, including effects on atherosclerosis,
largely independent of its glucose lowering or weight loss effects. The study demonstrate the GLP one receptor activation significantly reduces oxidative stress, improves endothelial function, leading to healthier blood vessels and reduced risk of plaque buildup. And several other research pieces on cardiovascular outcome trials that have shown reduced rates of mitocardial infarction, a heart attack, stroke and cardiovascular death. Again, independent of weight loss, independent of
diabetes, blood sugar, we're seeing these effects. So, you know, the main three bullets here are lowered risk of major cardiovascular events, heart failure protection and blood pressure regulation. So with the cardiovascular events, receptor agonists such as liraglutide and semaglutide have been shown to significantly reduce the risk of major cardiovascular events, including heart attacks and strokes in high risk populations, including those without
diabetes. The heart failure you touched on already, but I think the fact that actually helps repair damaged tissue is just fascinating and also enhancing the left ventricle function, which, again, not just for enhanced folks or prior enhanced folks like myself, but anyone that's a larger, like, male that has done some serious training over time, usually has some issues with left ventricle hypertrophy. And again, this is an area where microdosing could have a very
potential positive effect. Again, blood pressure regulation. Instead of taking blood pressure regulation, this increases nitric oxide, which is going to promote vasodilation and improve endothelial function. So GLP agonists contribute to lower blood pressure control, reducing the strain on the heart and lowering the risk of cardiovascular disease through that
and the way these happen. Again, some of this is straight from the anti inflammatory effects, reducing systemic inflammation, which is a major driver of these cardiovascular diseases, particularly atherosclerosis, by decreasing pro inflammatory cytokines, the oxidative stress, and it helps protect the blood vessels from damage that can lead to the plaque formation. The endolithial function I touched on to dive a little deeper into thiel cells, line the blood vessels, and help
regulate the vascular tone. Dysfunction in these cells is a precursor to atherosclerosis, and GLp one, in promoting their proper function, aids in preventing arterial stiffening and plaque buildup. Now, I'm a huge benefit of tissue quality as a whole, which is why I'm always a promoter of a lot of nitric oxide nitrate type compounds. But this is working those same pathways and improving the tissue quality of and vascular tone, the vasodilation and blood pressure
regulate pressure regulation mechanisms. I think I've hit that pretty well. But lipid metabolism. So GLP one has beneficial effects on lipid metabolism by reducing low density lipoproteins LDL cholesterol levels and improving triglyceride profiles. This contributes to a reduced accumulation within the arteries, slowering the progression of atherosclerosis. So, yeah, we're seeing less plaque buildup, less oxidative stress. And the last one is this is the inhibition of foam cell formation. So form
cells. Foam cells, which are macrophages that have large ingested large amounts of LDL cholesterol, are hallmarks of athloscrotic plaques and GLP. One receptor activation inhibits foam cell formation by promoting cholesterol efflux, reducing the amount of ldl available for deposits on the arterial walls. So, I mean, this is just absolutely fascinating. This is the driver that got me to start microdosing GLP agonists a couple times. I do a couple cycles per year.
I did run some cycles for weight loss, like back in the late, I think, 2017, 2018 era, before I built my weight back up for my big squat. But this cardiovascular impact was a driver for me to go, I need to look at this. Not for any of those other managements, and not to drive appetite suppression and shutting that down, but getting enough to start seeing these effects, seen those effects on my blood work, with my lipid profiles, with my blood pressure.
And again, you know, personally having, you know, issues with atherosclerosis from autoimmune, again, big drivers, because these are all connected. You know, one more thing I might add. In everybody's, you know, these days, it's popular functional medicine. Talk about the gut and the gut immune access. Gut brain access. And another benefit that glp ones offer is they're secreted by the enteroendocrine l cells in the gut.
And don't worry about the terminology, just think about when you hear about, like, a leaky gut and inflammation in joints. Essentially, what's happening is you have these tight cell junctions. And when we have endotoxins like lipopolysaccharides starts to kind of split those apart, and those start to accumulate and we get brain
fog. So what GLP ones do, they improve the integrity of that gut barrier and prevent that intestinal permeability and the translocation of these endotoxins and lipopolysaccharides. And to give it some context, because a lot of people hear these big words, and it's like, well, one, I don't know what that is. And two, like, what's that mean? So if a lot of people probably tried a ketogenic diet and ketogenic diet,
not exogenous ketones. But a ketogenic diet can lead to a lot of accumulation of these lipopolysaccharides. You almost see people with the ketogenic or the carnivore diet bragging about their high levels, which I think is kind of interesting. I agree. And I'm not knocking those type of diets like they're valuable as a tool for, you know, certain populations for certain goals. Right. So in acute situations, yeah, absolutely.
But it's definitely like when you think about the integrity of your gut barrier and the importance of that so that you don't get things like Sibo, so that you don't have those autoimmune reactions from food particles kind of sneaking through and getting trapped in joint spaces. Like it's really important to have that integrity of the intestinal barrier
and it's just another thing that glps help with. Yeah, it's when we start looking at this and as we continue these discussions and other peptides, you're going to see some similarities in the discussions that we have in the pathways that we talk about. I can already tell that without recording those just because my mini conversations with Anthony around these subjects. Now the next one is we're going to dive into the
neuroprotective effects and I'm going to go ahead and cite the research up front. Again, I'm choosing research independent of diabetes, weight loss type pieces. So I've got scientific reports 2020 2018 Rollins et al. 2014 only et al around these. This is so if we're going to talk about the benefits and so the
benefits. Alzheimer's Parkinson's cognitive decline in aging so Alzheimer's disease studies have shown the GLP receptors studies have shown GLP receptor agonists reduce amyloid beta plaque formation, a hallmark of Alzheimer's disease. They also improve cognitive function in animal models by decreasing these levels of neuroinflammation and oxidative stress for Parkinson's disease. Research indicates that GLP one receptor agonists protect dopa I should have grabbed something to drink. Anthony.
Research indicates the GLP one receptor agonists protect dopagenetic neuroneurons. The cell is primarily affected by Parkinson's disease. This neuroprotective action helps preserve motor function and slows the progression of the disease. With cognitive decline and aging. GLP one improves the synaptic placidity of the neurogenesis making potential therapeutic agent for age related cognitive decline. Neurogenesis is just another word for
growth of new neurons. It effects on mitochondrial function and oxidative stress further support brain health during aging. So these are the benefits, and those are powerful benefits. How does that happen again? Reduction in inflammation. GLP one has been shown to reduce neuroinflammation, contributing factor in neurogenitive disease like Alzheimer's and Parkinson's. It achieves that by inhibiting the pro inflammatory cytokines that we already talked about, which are implicated
also in neural damage. And the anti inflammatory action helps protect these from degeneration. Now, enhancement in the neurogenic generative, the enhancement of neurogenesis and synaptic plasticity. It promotes neurogenesis, particularly in the hippocampus region of the brain, crucial for memory and learning. It also supports synaptic plasticity, the ability of the brain to form new connections, which is essential for
cognitive function and memory retention. I think there's a interesting piece about, like, when you stop getting, you stick with the same haircut for the rest of your life. That, that's the point when new, you know, new brain connections quit forming. I've got a friend, he's a well known influencer. He. He started changing his haircut and it all sudden when he learned that, thinking it would work in reverse, I think.
But, you know, there's a point, you know, around that time frame, in the thirties or so, sometimes in the forties, where, you know, that's, you know, we, we quit growing the brain doesn't happen for everybody. And that's a lot of the things that we've talked about on the mental side of this architect for resilience podcast, because you can, you can help create that by challenging yourself with things that are uncomfortable. If jumping in cold water is something you're used to doing, it's not
being uncomfortable. It's truly choosing to do things that are uncomfortable. And that could be very different for a lot of people back on track. Reduction in inflammation, neurogenesis, oxidative stress and reduction. So, by reducing, again, the oxidative stress protects the neurons from damage caused by reactive oxygen species. This is critical in preventing neurodegenerative process that lead to conditions like
Alzheimer's. Mitochondrial function. We're going to do an episode specifically on mitochondrial function, possibly next week, if not in the next few weeks. But GLP one has been found to enhance mitochondrial function, promoting better energy efficiency in neurons. This contributes to overall health of the brain by preventing energy depletion that typically occurs during neurodegeneration. So, yeah, I don't know what else
to say, but that's pretty powerful stuff. And that's actually where the research on these compounds started with. Anything to add? Yeah, it's really fascinating when you look back at, like, why did they start researching these? They were actually being researched for their neuroprotective capabilities. And when they started to go through this research, they saw people's blood sugar was improving, they were
dropping weight. And when you think about those markets, there's just so much more demand for things that are going to help regulate blood sugar and weight loss than a preventative measure for the brain, so that they kind of switch gears. And one of the things, and we'll cover this more in the episode on Repurpose Pharma. But once a drug's been approved for something, so there's safety established and it goes through that pipeline, then you
can start getting it approved for other things a lot quicker. So it's kind of like, one, where can we get this through the fastest? Two, where can we generate the most funding so we can pay for the studies to have it approved for other stuff. So it kind of makes sense to unpack the kind of how it works on the cognitive function and everything, too. The only thing I'd add to that, and this is really kind of cool for all the people out there that follow that are really
into lifting. When we think about acetylcholine, it's the first thing that's going to be released from your prefrontal cortex into the neuromuscular junction to initiate that muscular contraction. And it's also crucial for memory and learning. And one of the things that GLP ones do that a lot of people don't realize, it increases acetylcholine. So a lot of benefit there. And the other thing it does is it stimulates the release of brain derived neurotrophic factor. And that's exactly
what Chris was talking about. When you're doing something that's really challenging or uncomfortable, I remember one of the tips I got when I was trying to study stuff and memorize it is do it in small chunks, and in between, like, do the stupidest balance things like stand on one leg and try to juggle, because your brain will really be generating that BDNF, and it'll make it easier to learn to. So, yep, generating that BDNF is great. I forgot about the impact of these on that.
That almost ties a little bit into maybe what's happening on the behavioral benefits, you think, Anthony? Yeah, absolutely. We have GLP receptors in the amygdala and the hippocampus in the brain, but really, they're in pretty much every cell in the body. And when we think about, like, behavioral modification and what's going on, a lot has to do with the effect on that dopamine reward pathway and what GLP is signaling in there. Dopamine's kind of our motivation, our working
towards something, and it helps to kind of modulate that. So you got that dopamine that's going to keep you engaged and doing the things that you need to be doing, but it's going to kind of turn down the signal that you get from the reward, like that dopamine hit when you're doing something that's maybe not beneficial for you. And really, the research is, I mean, it's amazing. As Chris said, I've seen it
firsthand, too. And I think the original research, if I'm remembering correctly, was done in Singapore, and I think it was, like, last May. I believe the study is probably published by now, but, yeah, just amazing. Yeah. I've got a study from 2017 in front of me. I had another one that was in an addiction related psychology publication. I lost that out
of my notes for some reason. But, yeah, I've seen this firsthand. Anthony and I talked about this a few times where, you know, we've got friends with either alcohol or opiate addictions and seeing tremendous changes in those populations, even gambling. It's really fascinating, the behavioral effects around addiction and impulse. Addiction and impulse control. Yeah. And it's.
It's easy to see it firsthand. There is, like a caveat, though, and this is where, again, like, why you don't want to taste the, the dosing too high, because those dopamine hits, if they go down all of a sudden, like, if you push that high, like, you're not going to enjoy some of the things in life that you enjoy where things just become bland. Right. It'll be the best way to put that. Right. So, you know.
Yeah, but addiction control, preclinical studies have shown that GLP one receptor agonists reduce alcohol and drug intake in animal models by decreasing rewarding effects of these substances, suggesting they could be useful in treatment for substance abuse disorders. They've seen the same thing with nicotine.
I've seen a few different other studies. Again, those are animal models. But I can tell you myself, Anthony can tell you and other clinicians that work with these populations are seeing the same thing. Obviously, you're going to see an impact on compulsive eating disorder. These agonists have been effective in reducing binge eating behaviors and aiding weight management by enhancing satiety. And reducing food cravings. But the broader implications are
massive. And this is where I think some of, like, the breakdown, well, actually. So impulse control and ADHD, I think that this is like a key. Like, we're seeing an increase in ADHD. We're seeing a increase on this, I think, brought about by our societal, again, this is doffin theory, you know, but just being connected, having technology in our face,
the shortening of attention spans, like, we're seeing more of this. And then, of course, obviously in those same countries, we're seeing the increase in the weight issues. Right. So I think that there's a lot of short circuiting of our brain through the stimulation and shortening of the attention spaniel. And so, yeah, GLP one, impulse control and
ADHD behavioral disorders. The regulation of dopamine and other neurotransmitters associated with reward seeking behaviors has led researchers to explore its role in ADHD, where simple impulse control is often impaired. Now, more research is needed, but they're starting to see an improving in attention and reducing impulsivity. And again, clinicians working with these populations are seeing those effects. And as Anthony suggested or stated already, the reward pathway
modulation is the driver here. That GLP one receptor agonist influences the mesolimbic dopamine system, which plays a critical role in the rewards and pleasure seeking behaviors. By modulating the system, GLP one helps regulate reward responses, reducing cravings and impulsive actions. Now, listen to my caveat earlier about enjoying life, too. Appetite, satiety. We already discussed
neurotransmitter regulation. GLP one reduces the release of neurotransmitters such as dopamine in response to reward stimuli, food, drugs, alcohol, lowering the propensity for negative behaviors and compulsivity actions, compulsive actions. So, yeah, I. I find this piece absolutely fascinating, and it is something that I have used with people that I work with fully outside of compulsive eating disorders.
So, yeah, I think. Did you have anything to add on that, Anthony? I mean, you kind of hit a. Lot of intuition was right on with GLP ones and potentially potentially helping with ADHD. When you think about ADHD, it's going to particularly affect that prefrontal cortex and the striatum, which are both really, really important for attention and impulse control. And those are two areas that GLP one can interact with, interacting
with that prefrontal cortex. It's going to help to kind of modulate the dysfunction in the dopamine receptors and. Yeah, exactly what you're talking about. There's, I don't want to bore people with the specifics of the part of the getting carried away, the tegmental area
and nucleus of compass. But yeah, you're exactly right. I think it can be part of a protocol that could perhaps have some benefit, probably have some benefit for people that are dealing with ADHD while also doing things like decreasing oxidative stress, improving cardiac function. I mean, it just seems like that would be so much better choice than reaching for um, like amphetamines or that sort of thing. Absolutely, absolutely. Now that's uh. I have been diagnosed with pretty
severe ADHD. If you hadn't, if I imagine most of my listeners were not surprised by that. But you maybe see why I'm a big proponent of GLP not using any now and it's been a while since I have, but like I said, I'll use a microdose a few times a year. Now we didn't cover the topic of pcos. I think the GLP ones are a tremendous choice for specific applications of pcos. Have you dealt with that at all or had any thoughts on that? It definitely makes sense that they would be
because one of the side effects from the pcO. Well, I guess a couple things. One, you're going to have a dysregulated HPA access and as we talked about previously, it's going to help modulate that. And then one of the, I guess side effects of the PCOS is going to be poor blood sugar control and it's helping with that. So it really seems like maybe a little bit on the hormonal side, but definitely in terms of controlling the blood sugar, there's going to be some
value there. One thing we did miss was talking about the muscle preservation because that is one of the fear mongering pieces of people saying. Saying it's causing massive muscle wasting. Why would you do that when the researches that they're reaching to with that is citing sedentary populations again with substantial
weight loss? So yeah, if you take somebody that is, you know, a 60 plus year old that doesn't have any physical activity, you cut their calories like massively and you don't make sure that they're having adequate protein intake in their training. Yeah, they're gonna lose muscle and fat. Now I'd like to talk about people like Doctor Spencer Ngowski, Doctor Gabrielle Lyon, Doctor Tina Moore who all work with very substantial populations using GLP one
agonists. And there's. They see the opposite of that with those because they are having those clients also do those things which is most anybody listening to this podcast is some level of physical activity and understanding protein intake. And if you do that, we think about the improvement, in instance, the improvement in anti inflammation. What are you going to have? Well, you're going to actually have an environment that is muscle preservatory, not
lost. And that's what I've seen in myself, that's what I've seen with people. And that's what those doctors are seeing in people is they're able to maintain muscle mass better than without. And not seeing that, I think that, you know, outside of that, we could also look at like how do we stave off muscle wasting with using synergistic peptides, you know, growth hormone secret dogs. I know that you've got some great ideas, Anthony. We'll talk, talk about this in synergistic stack component of
it. But I just want to, I want to drop that out there because this is just absolute hogwash when it comes to those statements. So, yeah, yeah, obviously I see why there's research showing what they're able to cite, but there's plenty, plenty of places that we can point to that are just clearly not seeing that. You talked a lot about the gut health. I didn't put that as a bullet
point. Obviously, that's a major driver of a lot of these pathways as it relates to not just the anti inflammatory being one of the background conditions driving this, but I think the gut brain barrier or the, the gut barrier and that impact on gut microbiota, systemic inflammation as a result to it digestive health function and then obviously the, you know, the gut brain connection as well, I don't know if there's anything that we want
to add on that, but I think it's important to note that. So just trying to cover all the other bases before we jump into choosing the right glps, dosage, synergistic stacks. Yeah, no, I think that covers pretty much all. But to build on what you said about the fear mongering and muscle loss, I mean, complete
hogwash. And if you think about it like, if you weren't taking a glp one and you were to reduce your calories significantly and you were to dehydrate yourself, you're gonna lose muscle exactly like you. Take, you take a sedentary person, massively reduce that, don't have protein and don't. Don'T train on top of that. Stop working out. Yeah, and the funny thing is, indirectly glp ones have positive effects on
myostatin inhibition. And that comes through what you already talked about with reducing inflammation, and they have a nutrient partitioning effect. So that actually helps to drive anabolism, and by reducing that oxidative stress, it improves the function of the mitochondria. So, yeah, I mean, it's from a. Mechanisms of action standpoint, it increases the preservation of muscle tissue 100%. That is like,
that's why I said it's absolute hogwash. Like, now, if you take something that has mechanisms of action for increasing muscle preservation and you put them in an environment without the proper nutrient intake, dehydration, and no training, yes, you're going to have muscle loss. Like, there's only so much that you can do if you don't have the right environment to begin with. I
always laugh. I mean, when people talk about, and I shouldn't laugh, but when people talk about the whole losing muscle thing, I'm like, I mean, if you work hard enough at it, you can lose some muscle, but you've basically given yourself a head start towards health. You've got a perfect environment to gain muscle, or at the very least, preserve it. All you got to do is just drink water and make sure you're getting enough protein. Go get two workouts a
week and, you know, get some steps in during the day. Your body's going to hold onto the muscle. Like, if you're losing muscle, that unfortunately usually correlates with people just kind of leaning on these for that. Appetite suppression. Yes. And that's kind of where the problem comes in with then the doctor. And this is, this is really. Both Chris and I share this vision of bridging that gap between
medical and strength training. The doctor, by no fault of their own, just doesn't have time to learn all this stuff about proper training recommendations. So it's a lot easier to follow the safety guidelines and say, well, we'll just give you more and more every two weeks.
We just add this much until we hit. In fact, as we get this bridge built and they have competent professionals they can lean on, then they can say, I've got this person that's on GLP ones, and they feel like they're kind of stalled out, I'd love for you to have a conversation with them, make sure all the basic boxes are checked. If we need to, we could go up in dose, but I think there's probably some stuff we can do, you know. There we
go. Yeah. So I'd like you to take the lead on the choosing the right glps, and I'll jump in on synergistic attacks and dosage. And protocols and interventions as well. So. Sure. Yeah. So with the GLP ones that are out there right now, we have just kind of. We'll build up. So the first one kind of think about, we've got semaglutide and semaglutide, if you're getting prescription, going to be the will gobia ozempic. And it's just a straight GLP one.
So if you remember back to the early part of the discussion, we explained what a GLP one is, what it does. Then we have terzepatide. And terzepatide is going to be a dual agonist, and it's going to modulate glp one as well as Gip. And then we have a triple agonist. Keep adding and adding and adding triple agonist retrutide. And that is going to modulate, like terzepatide, glp one, Gip, and then also glucagon. So those are kind of the three main players now to kind of branch off of that.
We also have mazuta tide, which is huge over in China. It's past their approval and everything. I imagine it'll be here soon. That is a glp one, glucagon memetic. Then we have but no gip. And then we have a shorter acting glp one, which is liraglutide. And liriglutide is basically like, semiglutide is a once a week shot, really slow releasing. And, you know, when there's that barrier of entry for people don't love giving themselves a shot.
The awesome thing about it is now we've got something that maybe they don't have to do, but once a week. So really kind of nice there. Then there's the original, the OG eggsanitide. And that's the one that when people talk about, like, the Gila monster saliva, that was the one it was formulated off of. And then there's some really cool ones in the pipeline, too. There's dunoglypripron, which is glp one receptor agonist. And it's basically, it does just like regular glp one, like a semaglutide
liriglutide. But it's being developed as an effective oral. Semaglutides available is an oral, but it's just poor bioavailability. And this one looks like they're going to be able to solve that problem. And there's
kegrocema, which is. It'll be a combination of that amyelin that we talked about earlier, myelin and GLP one and that's really cool because you're targeting, you know, more areas of the brain, and you've got two things that are at a really low dose that are sending a sufficient hunger suppression signal, and then there will probably be some more of the auxintomodulin analogs. And those are just, again, the combination of the GLP one, glucagon receptors agonists like the
Mazuta tite I talked about a minute ago. So with all these choices in front of us, you know, you start thinking like, gosh, you know, I mean, I just want to take the GLP one, like, which one's best for me? And it kind of comes down to, I think about the person that I'm talking to, you know, what one. What's their goal? So are they coming in with a skewed lipid panel? Are they coming in? They need to lose weight, but they can't put the
bottle down or they need to lose weight. They can't stop eating or they need to lose weight and they got a low energy expenditure. How adverse are they to frequency of injection? Is it somebody that you pull an insulin needle out and they hide under the couch, or is it somebody that's like, hey, hand it over, I'll do it. So those are all kind of things that are going to factor into that decision making process. So
just to give you, we'll give a couple of examples. So if somebody's starting out and they need to lose some weight, lipid panel is skewed and they do, you know, eat some of the wrong foods. But really, you know, it's just for lack of a nicer way to put it. It's like their labs look like a train wreck. Trizzepatide is a good starting point, in my opinion, because it's going to have a little bit more effect on
lipid profile. You're going to get, not generally speaking, not quite as strong of a GLP one signal. So less for most people, and there are those outliers, but for most people, less digestive distress, and you're kind of checking more boxes at once. If I've got somebody coming in that has addictive behaviors and big overeater semaglutide, terrific choice. And if that same person, like, we give them the semaglutide, you know, lowest possible starting dose, 0.25 milligrams, and they're still
having kind of a bad reaction to that. If they're not injection adverse, that might be a good opportunity to lean on liraglutide because with the daily injections, it has a faster clearance time. You can kind of pick a smaller dose and see a faster effect. So you could go down super low on that and it's going to be out of the system pretty fast. So if there is a little bit of discomfort and we'll talk about some things you can do to kind of alleviate that, then
it's an easier way to manage it. And then the retrue tide, when you have somebody that has low energy expenditure. So a lot of executives that I work with are people that just by no choice of their own, they just, you know, everybody's leaning on them. They're at their desk all day, so they're just not getting energy expenditure like they need
to. That's where I feel like something like Areta true tide can be a good tool, or even the mazuta tide that should be here in the US soon, because with the modulation of glucagon, it's going to liberate sugars and fats for energy. So that's kind of the thought process behind. With all these different tools out there. What do we reach for? So with synergistic stacks like I mentioned earlier, like CJC 1295 and
Pamamorolin, they'd be a good choice. Anything of the growth hormone releasing peptides are going to enhance those growth hormone levels, leading to better fat metabolism, muscle maintenance, and really facilitate these pathways and really facilitate these pathways
for weight loss and metabolic improvements. Tazmoralin may be another good choice in that this is really great for insulin sensitivity, enhancing insulin sensitivity, reducing appetite, improving growth hormone reduction, particularly visceral fat, it has a pretty potent impact on that in your overall metabolic health. If you want to improve the immunity,
thymosin alpha 1 may be a really good one. Really ramping up those anti inflammatory properties would be a choice for stacking with that with chronic inflammation or autoimmune disease healing. If you wanted to focus on, again, anti inflammatory effects, reducing inflammation support, gut healing, tissue repair, overall recovery. BPC 157 if you're focused on the gut impact, you would use BPC as the oral, as
an argonate salt. Tb 500 would be another one to put in there with that with systemic inflammation, tissue healing, cognitive functions. C Max would be a good one for the neuroprotective effects, enhancing cognitive function, brain repair, maybe a combination useful for people dealing with cognitive decline or neuroinflammation or brain injuries. And then epithalon. I've really loved eptathalon myself. It's been a few years since I've run it. But when combined with glp one, eptathalin can
amplify the anti aging and cognitive benefits. Both peptides can help reduce oxidative stress and inflammation, making this stack particularly beneficial for long term health and brain function. What are your thoughts? That's just my, that's my quick run through. No, it's a great run through and really covers a lot. I think if, when we think about like kind of step one, step two, step three, step four. Like what's my thought process in
building a protocol? I always try to think about what's going to check the most boxes and usually like when we, if we're starting with a GLP one or any of the ones that we mentioned, a good place to go after that is going to be the growth hormone releasing hormone. Growth hormone releasing peptides secretogogues. And the reason for that is growth hormone is going to help everything from brain function, tissue health, retaining lean muscle mass,
losing body fat. And, you know, one of the, and we'll be doing a lot more in depth stuff about growth hormone and effect on blood sugars. One of the knocks against it had always been, you know, if you take growth hormone, people would say, you know, you can make yourself diabetic, but if you've got something in there that's regulating the blood sugar, then kind of canceled out the negative side of it. Cool thing about how these ghrhs. GHRP's work is essentially there's a signal sent
from whatever part of your body needs growth hormone. There's over 100 isoforms of growth hormone we make, and when that signal is released, it signals for the pituitary to make growth hormone and then there's a signal for it to be pulsed out. It's just like having a stereo. You can crank it up to ten, but you can't crank it up to twelve, so you never have to worry about blowing the speakers.
So going back to building the protocol, if somebody's taking a GLP one for specifically for the goal of weight loss and we are going to layer something in on top of it, I would use Tessa Morellon and CJC 1295. The reason for that is because those two growth hormone releasing hormone, growth hormone releasing peptide combo, neither of those work through the ghrelin pathway. And ghrelin is one of the ways that we can signal to make growth hormone.
But at the same time, kind of double edged sword because that's one of the things that will drive appetite. So it wouldn't make a lot of sense if you're already overeating. To throw something in that's going to essentially tilt that side of the scale a little bit more just for the benefit of growth hormone, when you have two amazing options available. Yeah. So take, was it like Mk 677 or something that works on ghrelin pathways. It's
going to drive up appetite. It's going to drive, actually, blood sugar up a lot more than you want. Those would be ones to avoid. And the unique benefit, as Chris said with Tessa Marellanous, it was actually brought to market and is on market as a prescription for dyslipidemia. So with AIDS patients, what happens is sometimes they'll store fat in places that are just not conventional to store fat. And when you inject Tessa Morellin into fat or in these dyslipidemic situations, it's going
to, like, spot reduce. The other cool thing is by doing that, it decreases visceral fat. And that's the problematic one when we think about, like, heart disease and that sort of thing. And on top of that, it's going to help balance out that lipid panel by getting rid of the bad fat. So recap, it's, we've got our GLP one, and if it's weight, weight loss related, then we're going to use like a Tessa Morel and CJC.
If it's not weight loss related, then there's a lot of other ones that you can choose from, and we'll cover those in another episode. So then the next thing I think about, like, what else can we add to make this even better, more effective? And what are some of the boxes we might not have checked? Everybody's probably heard of by now? Nad and I know a lot of people are running out and getting the iv's. I don't advise that you do that and I'll explain
why. Oh, good. I don't either, but I want to hear yours. So when you think about Nad, it's got a lot of benefits. It's going to essentially, it donates electrons, so it gives your cell energy. It is going to help with synthesizing DNA, all that important stuff. We can do a whole episode on, like, NAD and all this stuff, but one of the things that happens, so if you've had an injury, you're going to have
senescent cells. If you're over the half century mark, like me, you're going to have senescent cells. You might have some cancer cells that are kind of sliding under the radar. Not problematic yet, but they're sliding under the radar. And what happens if you dump nad in the system on these senescent and cancer cells? They have upregulated cd 38. CD 38, just easy way to explain it. Think about it as a magnet that's going to grab those electrons and fuel the growth
of those cells. And there's a weaker magnet on your healthy cells. So, you know, these healthy cells that you're expecting to give energy, they're starving. And the cells that you don't want to give energy to, I mean, they're getting electron overload and replicating and replicating. So all of a sudden, you know, you've got this population of, like, really bad cells. So a better way to go about it, because Nad is absolutely important and we want to
have it for so many things. We just don't want to have too much of it. We want it to kind of trickle in at an appropriate level so that even though the good cells don't have as loud of a voice, they still have a voice and they can kind of reach out, grab the electrons and take the majority of them despite you got the bad cells yelling. So the way we do this, we would use something like, I like five amino, one mq. It's an oral peptide, and it decreases. It's called
NNMT. It's an enzyme that breaks down nad. So just to kind of think about what we have here for a second, our body makes Nad, and people say the levels decline as we get older. Usually what's happening, I mean, they do to some degree, but usually what's happening is the NNMT enzymes increasing. So if we decrease that enzyme, that means that NAD that we have is going to be active for longer. So there we got nad in our system and it's going to the right cells,
and then we still have one problem we got to solve. We got to get rid of that CD 38. We don't want anything going to cancer or senescent cells. So a simple way you can do that, you can add in apigenin you'd want to take. I take 400 milligrams in the evening hour before I go to sleep. Reduces inflammation in the brain. Downregulate CD 38. So that, again, that NAD is going to the right place and it even helps with sleep. So easy solution right there. Nice. I'm a big fan of one NQ as well.
Well, let's. Yeah, I don't want to get too far off track because these are some other episodes and we definitely need to do a piece on senescent cell reduction. I know we've got some interesting ideas on that. Let's jump into dosage protocols and interventions. Unless I'm cutting you short on this. No, it's only other thing I would say. I like to add in anytime you're using a GLP one and there's going to be synergy there both for brain health and digestion is tutca
tudca. And tudca is a protein chaperone. So it prevents protein misfolding. That could lead to like amyloid plaque, but it also increases formation or bile acid secretion. So when we think about like that gastroparesis that people talk about, that's a good kind of guard against that. And while at the same time I'm synergistically doing something to amplify the brain protecting effects, then hydration would be the other one that I think is important
to talk about. And for that, everybody's thinking, I'm drinking water, doing good, maybe even put some electrolytes in there. But there's a better way to do it. You can use something like when you think about creatine. Creatine is a neutral osmolite and it causes that cell swelling, so it's better hydration. And when the cell is better hydrated, just like a balloon, if it's blown up all the way, when it's full, it's going to have better sending signals and receiving
signals. And when you think about how a peptide works, it's cell signaling. So that's one of the things, cell volume, that's going to allow you to stay at that low dose of a peptide and get the highest rate on rate of return on the amount that you're putting in with the creatine. The other one I really like, and this has synergy for those cardiovascular benefits you were talking about, is going to be taurine.
Taurine, another neutral osmolite. And the only one that I'm aware of, the only amino acid I'm aware of, that is metabolized in cardiac tissue. So that would be kind of the gold standard status. So quite a question on that. So tutka is ursidolic acid, which is a synthetic bile duct fluid, but tudka is taurine bound to UDCA. Does that taurine become available or do you need to separately add taurine as well? If you're taking tudka, I'm assuming so.
Actually that's a really good question. I don't know when it breaks down, if the taurine stays bound. The other reason to add in the taurine is because taurine prevents oxidation of fatty acids. So, like fish oils, a lot of lifters are taking a higher dose of fish oils, as they should, to increase production of pro resolving mediators and decrease inflammation. But in doing so, there can be oxidation. So by taking Taurine, it's a real easy way to kind of safeguard against that.
So I'd still add in the taurine, but honestly, I don't know the answer to that. So that's awesome. I got, I love having stuff to research, and I will get an answer for you. So I think about this as tissue quality, and I've got a great piece on tissue quality. And so creatine, Taurine, and then I'm gonna say straight up, build fast formulas. Vaso blitz is hands down the best overall formulation for improving,
you know, cellular hydration. There's four components of this, but two different nitric oxide pathways,
betaine, basically, really shuttling this. And so anyone that's using, you know, any, you know, compounds as a whole or training as a whole, but it's going to make all of these things perform so much better by shuttling things to the tissue, getting those nutrients there, the turnover, we've got the flow of fluids and blood, and it's just absolutely, you know, a phenomenal, hands down product that is going to make everything, it's going to amplify the effects of everything that you're
doing. So use it for a month, because it's something that takes. A lot of people are not aware of this because they put a lot, some of these compounds in your pre workouts, usually not the adequate dose or not all of the products even, but it needs to be dosed on a chronic that's a daily in building your system like creatine does not an acute basis as a. You
take it once and you get the effects. Yes, you do. You're going to feel it on day one, but you're going to feel it more on day three, more on day seven, and day 21. You're gonna have the full effects of that. And so it's really important to have this in a non stimulated formula. So, sorry for the tangent and pimp of an amazing product, but it's just like a foundation piece. I recommend at Creatine, at taurine, and. Really great. I'm gonna look into the. Let's get back on the Taurine.
You're taking tudka. I believe that you would need to. I think that it's probably not going to be available, but that's a, that's a really great thought. Let's yeah, let's. Let's jump into dosage. And since we were covering so many compounds, I really like the guidelines of your approach to looking at the blood sugar levels. But as a note, like a lot of the, even the starting dosages that you're provided, it's
almost start at half of that. Right. And you're going to bump the effects not to crush your appetite, because, again, that's going to make you kind of crush your joy for life at the same time, if you push it up that much. Maybe I'm overstating that, but I'm trying to drive home a point here. But Anthony has a really great way of approaching this from also looking at your fasting blood sugar levels. So let's dive into that, because I don't think that we want to dive into the dosing
protocols for each of those individuals. Now, if you want some guidance on this, you can always reach out to Anthony or myself. Check out the endless evolution community on the school platform. There should be links wherever you're checking this out. But, yeah, dive into methodology, Anthony. Thank you. Yeah. So when we think about these compounds and why they were essentially first brought to market, blood
sugar regulation, weight loss. So blood sugar regulation kind of tips us off that there should be a favorable effect on what we're seeing when we measure our blood sugar. So what I like to have people do is, you know, we see where their blood sugars at, where their fasting blood sugars at a CGM would be ideal, but you can do the finger stick. And we really want to see somebody between like 85 to 90, 95 would be where I think people ought to be
once we kind of get them there. And, you know, for a lot of people, you know, you start them on that minimum dose and you're seeing that fasting glucose stay around where you want it to be. Once we get them in that healthy range, then if they're not losing weight and they're saying, you know, hey, I'm not losing weight, maybe we should raise my dose. I would disagree. I think that
probably indicates these are still working. I mean, we can see that by the blood sugar staying in the correct range, but there's probably something else that we need to address, and that might be as simple as hydration.
That might be taking a look at what they're doing with their training, is that driving up cortisol, which would increase sugars in the bloodstream and prevent them or increase the breakdown of muscle tissue, and then, you know, unfortunately see some muscle loss that maybe would lead to a slower metabolism and the so kind of. In summary, what I like to do is figure out kind of a target blood sugar range instead of a target
scale weight. And when we're in that target blood sugar range, and in my experience, I've found that that can be done with really like minimal dosing. Once we're in there, it's just about staying in there. And that's where we start to add in these other synergistic compounds to drive that weight loss. Keep that going, but not raise the dose.
Because anytime, no matter what it is, whether we're talking about nutrition supplement, peptide, pharmaceutical, the more you're increasing the dose, the less benefit you're going to get from it, the more likely you are if there are going to be side effects to run into. Some of those always get the max out of the minimum and only go up when
there's an actual reason to go up. That going up because the scale's not budging, in my opinion, is not, even if your goal is weight loss, is not not a reason to right away increase that dose. Awesome. I think that that is great spot to conclude this on. Do you have any additional things that you want to touch on that we didn't hit? I think we really did a pretty good job of covering everything. You did amazing research and it's so cool to see,
like, this isn't just stuff people are talking about. Like, there's really good science behind this. And I think as you pointed out to, you know, even more than just weight loss or blood sugar management, like, you can really be doing something proactive for later in life with your health. Yeah. And that's. I'm approaching the half century mark myself. And I like to think that we both not just do the research, but, you
know, demonstrate this, you know, in our lives. And it's a. It's a visible marker for those that see us, interact with us and see how we live. And I hope that this piece has hopefully, maybe changed some people's perspectives around this. We'll see if those people with differing perspectives are worth sitting down for an hour and a half and listening to us. But it's great discussion. And check out the endless evolution community if you get a chance to
learn more and interact with, with our group. Tons of great free courses on there. Anthony, myself and many, many others are on there and look forward to upcoming episodes. I think we're jumping into mitochondrial function next. We've got the senescent cell that we're going to dive into. We've got a whole series of stuff we're planning out, so hang in. It's going to be a lot of exciting research. Oh, yeah. All right.