Collagen for Skin 'Debunked', Non-Nutritive Sweeteners on Cognitive Decline, Seed Oils, and More

Hi, welcome to the Physionic Podcast, which is now, you could say, has become the annual Physionic Podcast because the last episode was about a year ago. So, I planned on doing these every 3 months or so, but as you can see, that didn't end up panning out. Um, and I'm not putting myself under too much pressure on this podcast simply because, uh, I've got other aspects of physionic that I have to focus on. But that said, I do have a Number of topics I'd like to discuss with you today. And for those of you that

put on the podcast to fall asleep, then rejoice. You have more material to fall asleep to. Uh speaking to that, I'm going to, assuming that YouTube allows me, I'm going to turn off the ads like I usually do uh throughout the podcast. So hopefully you won't be interrupted with any sort of, you know, annoying uh advertisements throughout. But if not, then I apologize. I would YouTube makes A lot of different changes to to ad policy uh over time. So, we'll see. Anyway, at any rate, uh if you'd like to listen to the podcast, so aside

from just watching it, just to be clear, there's not nothing going to be on screen. This is a purely perfectly raw video of me just talking to the camera. I'm probably just going to be relaxing on my couch on this extremely gloomy Sunday that I have uh behind me. So, I thought it would just be the perfect Opportunity to discuss some science, get into some of your commentary. I got some really good comments uh some good push back as well as some questions that people brought up on the topics that we're going to be covering.

And speaking to that, uh, last time I think I covered every single topic that I had covered before, uh, or after the last podcast. I can't do that this time because I think I've released what, maybe 70 or 80 different investigations, different Videos, different analyses, uh, since the last podcast. So, uh, it is, well, actually probably more than that. Probably closer to well over a hundred. So, there's no way I'm going to be sitting here. Although the previous podcasts were, you know, three hours, five hours long, there's no way that I'm going to be sitting

here and talking for like three days. So, I've picked out specific topics I think are especially uh useful or interesting and things that I wanted to discuss and I think that uh you'll hopefully find interesting as well. Uh if you're one of those people that believes that a person should just get to the point, um I've probably already dragged on too long on that front. So uh first of all, I think those individuals don't understand what a podcast means. But the second thing I can say is that I will supply links uh under the video

so that you can click on the link and then go to a much shortened Version of uh what I'm going to be discussing. But you will miss out on some of the commentary that I'm going to be covering. Uh because one of the benefits is that with the comments that I can retrospectively go back and kind of highlight the top comments that people have liked a lot so they rise to the top and then I can uh discuss those uh under each topic. Okay. Well, with that uh I don't know if I mentioned it already

because I had to redo this Introduction two times already. Uh there is a link to the podcast. It's completely free. Um, you can just click on the link and, you know, sign up through Spotify or Apple Podcast or whatever you like to use. Um, just be sure to know that it's not a weekly podcast. It's not a monthly podcast. It's not even at this point a quarterly podcast. It's just really whenever I feel or have the the chance to sit down and do these extended uh stays. But that Said, let's get into it a little

bit. I've got my notes here. So, we're going to dive into I'd say maybe seven or so topics, maybe maybe a bit more. Um, and also go over your commentary. All right. So, the first topic is collagen on skin. So, this is a topic that I've covered a number of times at this point. The when I initially covered it, I had come to the conclusion that the collagen studies that had released on skin had Indicated a benefit of consuming collagen peptides on reversing skin wrinkling uh improving skin hydration, improving skin elasticity, things of that nature.

That was maybe a year ago and I think I covered that in one of the previous podcast episodes. However, then there was this new analysis that released uh this year in 2025, maybe a few months ago, wherein the researchers in their overall conclusion said uh yes, collagen peptides seem to be effective For improving uh skin and all the the different metrics that I had mentioned. However, uh what they also did, what was unique about that analysis, that meta analysis, and I think they went over maybe 20 or so studies, 28 studies, 24 studies, something along

those lines. All of them were randomized control trials. And what they did is they divided the studies based off of funding source as well as the quality of evidence. as in um for metaanalyses what They'll do is they'll go through a Cochran risk of bias assessment or a ROB scale or they'll go through a grade scale and they're very similar to one another and there's different versions of these different scales but it's essentially a standardized system by which the researchers go through question by question of you know is it are is the study double blind?

Is the study uh randomized? Is the study, you know, There's there's a bunch of different questions that they have to answer for every single study that they include into the analysis. And then they give each study a score. I think it's a three-point score. So, it they us either get a red ticker, a yellow ticker, or a green ticker. Green meaning low risk of bias, red meaning high risk of bias. And if you're thinking yellow is moderate risk of bias, you might be able to call it that, but it's really more so unknown Risk of

bias. And like I said, there's different iterations of this. So they ended up breaking up the studies based off of the funding source if it was industry funded. So funded by let's say a collagen company or a skin company and by the quality. So was it low risk of bias in all these different questions. And what they ended up showing after you got over the overall conclusion is that this analysis indicated that when you broke things up by those standards that The studies that were industry funded indicated that there was benefit of collagen peptides on

skin and the studies that were not industry funded or industry affiliated. So they had independent funding maybe by like a university or some sort of internal funding for that institution that they would show no benefit or largely no benefit of collagen peptides on skin. So On the surface of it, you'd think, okay, well then that's pretty clear. It's, you know, I've always been on this side of I'm not going to dismiss a a study simply because it's industry funded, but now that we actually have evidence at this point of, okay, well, the non-industry funded studies

indicate that there's no benefit, I'm going to side with those studies over the industry funded studies. if you actually have that comparison. However, when you Open up the analysis and go further into the details of that analysis, you look so for a lot of these meta analyses, they'll list all the studies and then they'll tell you, you know, it's basically a big table of with the studies on the left side and then a bunch of different, you know, information like the study length, the participants, the participants age, the participants weight, uh all these different factors,

you know, get put Into a table so it's just easy to read so you don't have to open up each each individual study and at the very end of this table they had put the funding source and then they had also put the outcome so what happened when collagen peptides were compared against placebo and I ended up looking at every all of the non-industry funded studies so the ones that they had said that if you pull all that data together that you don't see a Benefit of collagen peptides. And six out of seven of the

studies, there were seven studies total, six out of seven of those studies indicated a benefit of collagen peptides on skin. Only one study showed no effect. So, that's probably pretty confusing to you because you you're thinking, well, hold on. You just said that the non-industry funded studies showed no effect and the industry funded studies Showed an effect and now I'm saying the opposite. So what's with the pingponging? Well, the answer is because the researchers and what researchers do is that they speak in very scientific terms as in they use this type of language that is

uh if you're not in the field, it's difficult to interpret and it's it can be it can be misleading. We'll just put it that way. Simply because they say there was no result. I'm paraphrasing obviously. uh there was No result, but what they actually meant was that there's no statistically significant result. But then when you actually look at the data, looked at the grouped data, you notice that oh well, the reason why there's no statistically significant result is because they don't have enough power in the analysis to detect an effect, which means that they don't

have enough data included in the analysis to detect an effect. And so to break that Down further, what I mean by that is if we had 28 studies total, fund, industry funded and non-industry funded, we have 28 studies. That's a lot of data. But then once you you create this subgroup analysis where you break it up by funding, meaning we've got this group of industry funded studies. So if that's 28 minus 7, that would be 21. Hopefully I did my math right. So that's 21 studies for the industry funded and they do show an effect.

Then you have seven Studies for the non-industry funded and they don't show an effect. Now the question is well is it because there's truly no effect or is it because you don't have enough data to detect an effect? And it turns out that the answer is probably the latter. And the reason for that is because if you look at each one of those studies, six out of seven do show an effect of collagen peptides on skin. So if you were to look at the individual studies, you'd be like, "Oh Yeah, for sure collagen peptides are

effective uh for for skin." But when you group that data together and then you apply meta metaanalytical statistical analyses to it. So you know doing a bunch of mathematics to it then you have to consider the certainty of the evidence. And because you've shrunk the pool of data from 28 studies to seven studies the certainty of the data becomes a lot less certain. So that ultimately yields A situation where you have to report it in scientific speak as no statistically significant effect of collagen peptides on skin. And that's kind of that's kind of where we

landed. So you can run with that and say, "Oh, okay. Well, then there's no effect of collagen peptides in the real world on skin. Or you can say, oh, we just need more data to be input into this to really detect an effect. And if we were to just look at the individual studies, We would we would actually see an effect because you'd be six versus one indicating effectiveness. So some people didn't do that part of the study analysis and therefore in my opinion came to the wrong conclusion. Uh but I could easily see you

know an argument for a person wanting to be exactly by the letter of the law the statistical significance did not indicate you know any effect. I will Say for a lot of these subgroup analyses they do kind of like sub subgroup analyses where they look at the non-industry funded studies and then they cross examine those with the quality of the evidence. to remember the ROB scale that I was talking about, the grade scale that I was talking about. And then you're taking the seven studies that you have, which is already a small pool of studies

for in this situation, and you're cutting it down to even fewer Studies. So now you're looking at like two studies or one study and trying to make a metaanalytical uh conclusion based off of that, you know, one study or two studies. and then you're shrinking the amount of data that you have even further. So, you know, you could make an argument either way. If you're a purist and you just want to go by statistical significance, then you would say yes, there's I guess I'll say no, there's no effect of of collagen Peptides on skin. If

you are a person who's a little more flexible when looking at data, which I tend to be, I think I'm kind of in the middle between between like, oh, that's a joke to just look at statistical significance and the more strict people that are saying only look at statistical significance. I'm kind of in the middle there. But if you are more flexible in that way, then you would say, oh, okay, well, there's probably an effect here. We just don't have the data. we don't have enough data to really detect that effect and I will say

for some of the subgroup analyses it got very close even though there was very little data uh you know again relatively speaking so then there were two critiques that I addressed as well one was that collagen peptides are never compared against protein and I think that's a that's an excellent Critique That's true. That in none of the studies that I've looked at, I don't think any of the studies that were included in this analysis do they compare against protein. And that's problematic because it's possible that it's not the collagen peptides themselves, but it's once they're

hydrayed. So you you consume collagen peptides meaning that they're in these two and three amino acids that are stitched together as in they're Molecular molecularly bound to one another. So they're still together as opposed to single amino acids which is what you think of like for glycine or methionine or leucine or whatnot. But in this situation they're still stitched together as these die or tripeptides. And the argument for the protein perspective is that well if you just consume enough protein of those amino acids that make up collagen then you will no longer see an effect

of uh Collagen peptides a unique we'll call it a unique effect of collagen peptides and that's a that's a perfectly fair argument to make and I don't have a great rebuttal against that simply because we don't have that evidence except for I think one burn study. So people that were burned had like secondderee or third degree burns or something along those lines and they were they were randomized to be given Collagen peptides or they were randomized to be given protein and the collagen peptides did see an improvement in their skin recovery over the protein condition.

But that was a single study and I think I don't remember off the top of my head but there there were a few things that you know kind of like what we're talking about like I wish they had done this kind of situation. So I I I don't want to base the entire push back against the protein argument simply Based off of this single study. I think that there's a lot more that uh that we need to see. So I think that's up in the air. It's certainly a possibility. I will say that mechanistically there

has been evidence where the collagen peptides themselves have had an effect on uh cells and I even covered a study which I recently discovered on collagen peptides versus a protein in an in vitro. on cells and I covered this a little bit for the Insider version of my my analysis on uh what we're talking about here is skin but ultimately they showed that there was a unique effect of collagen peptides over protein. So you know this smidge of evidence that pushes back against this protein idea but I just don't think that it's strong enough yet

to really dismiss that idea. So from a skin perspective, yes, I think that we need comparisons to to really tease out if there's a unique effect. That's Really what the question we're trying to get to or trying to answer. Is there a unique effect of collagen peptides? is if I can do the same with just consuming more protein or a particular type of amino acid or whatever, I'd probably prefer to do that than to go with the collagen themselves simply because collagen is probably going to be an added expense on top of, you know, protein,

which is much more readily available. The other push back that I sort of thought about in my own head that I don't really hear all that often, but I still think of it as a decent push back is, well, shouldn't seven studies be enough to detect an effect? And I think I've got a twofold answer to that. One is that even though six out of seven studies show an effect, I don't think I've ever claimed that collagen peptides are going to turn you, I think in my video I said from Alpuccino now to Aluccino back

in like Scarface or The Godfather. It's not going to, you know, dial back time by 50 years or anything like that. um what it's going to do is lead to some mild improvements in skin elasticity, hydration, and uh wrinkling and whatnot and maybe has a protective effect over time as well in in mitigating some of that uh as as the aging process occurs. So, it's a mild effect. I've always said that it's a mild effect But you know for some people having that mild effect is uh is important. So you know the other aspect other

than just looking at the effect size is the overall time horizon for a lot of these studies. So, we're looking at, you know, 12 weeks, 8 weeks, maybe 16 weeks, which isn't no time, but, you know, when you're thinking about reversing some signs of aging and whatnot, it's possible that we might see greater effects. And if all The studies, if all six studies that showed an effect in the non-industry funded studies, if all six of those studies had lasted for like 3 years or a year or something along those lines, maybe the effect size would

be large enough that we would be able to tease out some of those differences. Um, I I realize I'm getting a bit technical here. I'm kind of giving myself some leeway for this podcast. Um maybe I'm banking on the people that are Going to fall asleep to this. Um helping them out by uh by getting into some of those technicalities. But the point here, the main point here to take away is that collagen peptides seem to be based on this analysis as well as others seem to be effective for improving your skin. It's a mild

effect. Don't expect anything completely transformative or anything, but it will have a mild effect on your skin. And That seems to be consistent definitely in industry funded studies, but there is even a signal in non-industry funded studies. I think that's that's where I would leave that. Okay. Actually, that's not where I'm going to leave things because I've got two more uh things to discuss. I've repeated this many times, but people will bring up, well, what about the mechanism? How does that make any sense? Why why can't I just eat more Protein? Which, by the way,

on the protein front, one more thing I will quick add is that it doesn't make a whole lot of sense to me to to try to equate the protein to collagen. So, here we are. I was thinking I was going to just give you takeaways and those takeaways are accurate, but I'm going to be talking about this for a little bit longer because I just had another few ideas. So, if in a in a study, you would typically want to equate the amount of Protein to the amount of collagen that you consume. So if you're

consuming an additional let's say 15 g of hydrayzeed collagen and then you would want in the the control condition to be consuming 15 additional grams of a protein, right? To compare because if you're consuming a 100 more grams of protein, well that's kind of unfair. Um so to to actually tease out that unique effect and in that situation it seems unlikely to me. I mean, maybe you disagree, but it Seems unlikely to me that 10 or 15 more grams of protein is suddenly going to have these lead to these positive skin effects. 10 to 15

grams of protein in the grand scheme of things isn't a whole lot. So, I find it unlikely that we would see any sort of similarity between the collagen and the protein. But the the main critique that people will say is that it's it's the components of the collagen. So like the glycine and the proline and whatnot that That are leading to these collagen producing cells, fibiberblasts, uh condraittes, but in this situation, we're talking about fiberblasts that these cells take up these amino acids and then they use them to produce more collagen. So, we might as

well just consume more proteins that have these amino acids and then they'll also still be given the requisite amino acids to then produce collagen. And that's that's Fine, but that's not actually the argument for collagen. The collagen peptides that get absorbed, and they do get absorbed, that's another question I get asked. And we have human evidence indicating that people who consume collagen peptides or not necessarily collagen peptides but peptides of dual amino acids and triple amino acids still bound together. They do end up in the bloodstream. So that for sure we know It's not just

single amino acids that get into the bloodstream. Then the second thing is well then once they're in the bloodstream are they just taken up by the cells to be then produced into collagen? And the argument by a lot of like cell biologists and people that know physiology will say well those cells will then probably take up even if they did take up the deptides and the tripeptides they would then break them up. So they Would still end up as single amino acids within the cells. And that's there's some truth to that. I mean, I'm not

disagreeing, but the real argument is that it's not actually what happens inside the cell. It's actually what happens on the surface of the cell. Because we've discovered that there are multiple collagen peptide receptors on the surface of the cell. And if that's the case, then the collagen peptides actually interact with the cell surface To the cell uh collagen receptor. And then that leads to a change in the signaling within the cell. So it's not the actual components of the collagen peptide that lead to more collagen peptide production because now you have more of the building

blocks. But it's the actual binding which convinces the cell to produce more mature collagen fibers which get deposited into the skin layer. That's kind of the idea. Now, I will admit that I don't think that we Have foolproof evidence that this is exactly how it works. Mainly because the reviews that I know of and when I opened up a lot of the studies, what they show is that these receptors bind to already present collagen fibers. Is it possible that the collagen peptides could interact with these receptors and cause similar benefits? Yeah, it is. But my

whole overall point is that there's a lot of unknowns that we're still trying to tease out, but so far the evidence Still seems to be leaning towards uh collagen peptides having a unique effect. And that may, you know, one day shift completely to the other side. So for those people that are like, well doc, you know, people say one thing one day, then they say something else for another day. It's because everything I'm explaining here, this thought process of like, here's where the evidence, what we know, here's what we're kind of speculating, but there's a

few little Gaps here that we need to figure out. Here's what we don't know anything about. This is the kind of thought process that scientists have to go through just to give an intellectually honest answer. So once we start plugging in more of that information, we once we start discovering some more of that information, it could very much shift to a more complete answer that ultimately leads to an opposite conclusion. And That's why the field grows, right? Science grows. That's why the the whole idea of things developing over time. Um it's just unfortunately social media

is not just does not lead to a environment where people can can explain a lot of those nuances. It's just everybody wants the information basically injected into their brain or transmitted. If you speak for just a second too long then you know you immediately get hit with complaints of Well this was too long. you just get to the point, all that stuff. So, you know, you get caught between these two areas of like this is the level of explanation. So, if I were to be talking with you, you know, one-on-one, this is how I'd be

explaining it to you. I'd be asking I'd first open the conversation by saying, uh, how much time do you have? Uh, and if it's an elevator pitch, I'll be like, there's a lot of holes in the research that we still need to Figure out, but so far the evidence leans to collagen peptides being a benefit for your skin. Have a great day. But then if a person's like, I want to know everything there is to know about the certainty of the evidence and just like explain the mechanisms and explain the physiology, explain the data, like

where the clinical trials, what the clinical trials show. talk to me about the funding sources. We would be here for however long it's been. I don't know The time because my camera is all the way over there. Uh but yeah, it's been about half an hour. I'm seeing by my recorder here. So, it would be that level of discussion for me to explain where we are. All right. Who's going to sit here except for you, poor soul, uh, listening to me ramble on on my couch about collagen? Very few people. So, you're just a special

person. So, yeah, the that's why I'm saying social media Is going to seem like it's flip-flopping. And another aspect is there are some people that are just grifting, bottom line. Okay, so that all said, I wanted to cover some comments like I did last few podcasts. I do enjoy this. Hopefully people feel like they're they're uh being heard. Again, I'm picking the among the top comments under some of these videos. So, Burnham's ghost, that's the name of the commenter, Said, "As a case study, I can say this. I've had five knee surgeries, two ACL reconstructions,

just as a side note. Wow, that's that's a lot. Uh speedy recovery. That's that's a lot. Uh maybe a a player of some sort. I don't know. Maybe a uh getting up there in age. Maybe a combination of the two. Anyway, continuing. Increasing knee pain over the decades, especially after military service. Okay. Well, there's your Explanation. Over this decade, over the decades, I tried everything and nothing really allowed or showed promise until I started taking collagen. I was able to start running again. And when pain does emerge, it subsides much more quickly than before. I

think I'm less likely to be a victim of the placebo effect in this case because I've tried so many things and started out as very skeptical. Yeah. So this is obviously anecdote but Um and this was highly uh you know bumped up by by people uh but that's that's certainly a possibility like I said you know and I'll say this and I've said this in the past that the scientific literature can sometimes be pretty far behind the anecdotes that come out. So people will try something and they'll experience significant benefit from that, but then when

you look in the scientific literature, there's almost no Data or no good data on that topic. So does that mean that that thing doesn't work? No, it doesn't. But that said, you're also kind of caught between a rock and a hard place because you also can't say that all anecdotes are accurate, right? And as a matter of fact, I would probably say the majority aren't simply because you know exactly what Burnham Burnham's ghost said that there's a placebo effect, but then There's also like many other things that a person might change at the same time.

Um, so there's there's it's more correlational than it is causitive. Um, there's a lot of different factors. So, kind of hard to tease out, but based on this person's experience and they're talking primarily for joint health and improving um you know, from from surgery recovery and whatnot. Um, and I do have topics I I have looked at collagen on joint health, which actually Wasn't quite as strong as it was for uh skin. But even so, this person is saying things that align their anecdote aligns with uh what some of the research indicates. I think that

the the benefits they're experiencing are probably far more than mild benefits, though. Okay. Astrolab had said, uh, one thing I noticed on these studies is that they span a short time. Okay. uh for example your joints, you notice that the benefits aren't great. But for someone Suffering with osteoarthritis, which is degenerative and with no cure, it's an awesome result to have less pain after a year rather than more pain. Same with wrinkles. Maybe the effects compound over time and after 3 years you are one year younger rather than 3 years older, which is still great.

And that's that's absolutely true. So if we had studies that lasted for longer periods of time, we'd be able to that effect slowly grows over time or at least it could. It has The potential to grow over time and we just we can try to project that outwards. We can try to estimate that outwards, but that doesn't actually mean that we've collected the data to show that that's actually the case. And yeah, so that's true. And the thing is though, you're probably not going to get studies that are going to last three years unlike collagen

and skin or collagen and even your joints simply because It's very expensive and they're going to use really sensitive metrics to try to tease out if there's an effect. And once they find an effect, they're going to cut the the the study's going to end. Um, and when they don't need a whole year or multiple years to detect an effect, why run a study and spend hundreds of thousands more dollars just to end up at the same conclusion? Although admittedly on then social media, people will say, well, you know, They've got this critique and this

critique and whatnot. And some of the those critiques are absolutely fair. It's just that researchers can't go to the NIH or they can't go to their funding agency and be like, "Hey, uh, so we could detect an effect in 12 weeks, but it's going to be a really small effect. So we'd really love to find a really big effect because uh, we want to know what happens over many years. So would you mind like floating us a couple Million dollars more uh just so we can say that there's a bigger effect than there was usually

that's not that's not going to fly. Uh that's not enough of a reason to spend millions of dollars. So uh yeah time is a huge factor when it comes to studies especially randomized control trials but uh we're unfortunately not going to get those uh those data. Okay. I think I've sufficiently rambled on enough about collagen and skin. Let's Get into another interesting topic to me. One that actually wasn't that popular, but I wanted to cover it anyway because, well, I'm just going to allow myself to be a bit selfish here. That's ketones having a relationship

with worse liver health. And the way I framed this initially was to point out that yes, there was a study that showed a relationship between higher blood ketone levels and worse liver health. So that's A relationship, that's an association, that's a correlation. But what it doesn't tell us is if the ketones are causing this poor liver health or if it's the poor liver health that the ketones are actually trying to help with or if something else is going on here. It just shows us a simple association of ketones and liver health. However, when what the

researchers ended up doing Was they generated mice that had a inability to produce ketones and then they measured their liver health when they taxed these mice to have worse liver health. And what they showed is that the mice that were still able to produce ketones had dramatically diminished liver fattiness and liver damage and liver fibrosis and just overall worse liver health. While the mice that had ketone Production blocked, known as ketogenesis, they had far worse liver health, as in they had more fatty deposits in the liver, more fibrosis, etc., etc. So, the takeaway from this

was that the excess ketone production is not a negative. It's actually quite the opposite. It's almost like a re release valve for the liver because if you're not aware, the liver is where uh ketones are produced. So the liver is producing Ketones to essentially try to tamp down any sort of fat accumulation inside of the liver. So think of like fatty liver disease. So the ketones are a way to take the fat droplets or the fat molecules that would be stored in fat droplets within the liver cells, the hpatocytes, and have them flux through the

mitochondrian and the powerhouse of the cell. And that mitochondrian will then convert those Fatty acids to ketones and then eject them back out of the cell. So, and the the m the the liver cell has a number of different ways that it can try to deal with these fat molecules that would otherwise accumulate in the liver cell. So, it can package them into LDL particles and then eject them out of the liver. It can metabolize them so it can use them for energy, but there it can only do that up to a certain amount because

the cell only needs a certain Amount of energy. and a certain point it's just not going to need anymore or because the liver has this ability it can produce ketones. So once you knock one of those systems out, the ketone production, then it has to rely on the two other systems that it has and and this is speculation on my part and that's what ultimately leads to a lot of stress that could occur in the liver if you don't have a ketogenesis Available. So ketogenesis in that scenario indicates a protective effect of the liver. Okay.

So then I took it a step further because this was all in animal models trying to figure out mechanisms of how ketones are protective and all that good stuff. And that's great. However, then I was interested in obviously the human research. And the human research pretty dramatically shows that low carb diets, fasting, whatever, However you want to improve increase your ketone levels because a very low carbohydrate diet like a ketogenic diet and fasting are two of the most potent ways of increasing your ketone production. And both of them lead to significant improvements in liver health.

So, and there's probably some nuances there that I need to get into in more depth, but you know, overall both of those were great ways of Reducing fat that's surrounded and inside of uh the liver. So, I thought that was just such a cool study to to try to figure out how ketone production and that's a key point there is it's not the ketones themselves, although maybe ketones have additional benefits, but the study was really trying to tease out what does the production of ketones, so the actual metabolic flux that has to occur for those

ketones To be produced, how does that impact liver health? And that seems to be a positive. So that association that we were talking about earlier or that I was rambling about earlier is that the the most likely as liver health is getting worse, the ketone production is increasing because it's trying to again eliminate as much of that fatty liver uh disease as as possible. However, that Doesn't necessarily mean that it can it can actually deal with that poor liver health. So, um you know, ultimately they're both going to track together as in ketone levels get

higher and higher as liver health uh gets worse and worse. But it, you know, it's like the body constantly trying to compensate and it just can't keep up with the the worsening of the the liver health. Also, I just want to be clear, just because You have high ketones doesn't mean that you have bad liver health. Um, because again, it's just an association. One may be causing the other. Uh, but it's not the ketones that are causing the the poor liver health or at least based not based on this research. So anyway, just uh a

fascinating study I thought I'd share. Now a few uh comments. Robert Stanton said, "In 2019, I was diagnosed with non-alcoholic fatty liver disease with NASH, which is Non-alcoholic steattosis steic hepatit. Nope, I'm going to struggle with that one." But it's another uh type of liver disease. Um steattoic is yeah, I think that's one of that's the S in there, but I can't remember the H. It's just fallen right out of my head. And F3 F4 fibrosis. By changing to a ketogenic diet, I completely reverse my liver uh disease. And according to The latest fibrokin report,

my liver is now normal. That's all I need to know. That's what Robert said. So, first off, Robert, I don't you're probably not listening to this, but um first of all, that's amazing. That's genuinely incredible. I mean, it's incredible at any point to have such advanced levels of uh liver disease or any sort of disease and then to be able to change your routine or change your nutrition or something along those lines and then to See such significant benefits uh that fight against this uh this disease state. So, and that takes a lot of willpower

and it takes a lot of uh I'm going to change something about myself and that in its own right just on a human level without any of this scientific uh garbage is an incredible feat. So, huge congrats to you. Um the only other thing I'll say, well actually two things. One is obviously that's again very much in line With what the research indicates. The other thing that I will say is that I I get this um I get a lot of these comments from people that say and that's all I need to know. And on

one hand I completely well I shouldn't say completely on one hand I agree but on the other hand there's a tug inside of me that's like unfortunately I think that that mentality ends up Pushing into other areas of scientific communication or nutrition and whatnot and we end up I don't know how phrase this exactly. We end up discounting scientific evidence simply because something has happened a certain way to us. So I'll give you an example using this exact situation. So if I use a low carb diet and or let's say I use fasting And I

reverse my fatty liver disease and then I say something along the lines of well that's all I need to know. I know fasting is the end all beall for me. It it almost it's not always the case, but oftentimes people will then get so focused on this one thing and they say, "Well, this is the thing that worked for me, so therefore it is the thing that will work for everyone." And that's not necessarily the case because a person Could try like a Mediterranean diet for example, so something completely different and get the same results.

And those both can be true. So you can have one thing that is really impactful and really helped you as as an individual, but that doesn't mean that other things can't help. And I'm not isolating Robert here, just to be clear. Uh but just the the overall thought process just because I see these kinds of comments all the Time, especially if people will use it as a reputation of the evidence at hand. So if you know if there's a study that says you know low carb diet is better than a Mediterranean diet for let's again

let's stick with the theme of reversing liver disease and then a person who's been using a Mediterranean diet well is like well I used a Mediterranean diet and it worked really well for me. It works I tried a low carb diet. did not work for Me, but a Mediterranean diet that did work for me. And that's all I need to know. Like, that's fine. I No, nobody's disagreeing with you on that. But it's not a reputation of the science. It it's like there many things that can be true. And it's it's it's really difficult to

communicate that stuff again in in short videos, like punchy videos that are that are trying to get to the the overall point with within a reasonable amount of Time. Very much again, I'll just crap on this podcast again, unlike what I'm doing uh right now, which I'm sure I'll get comments on. Anyway, the big point here though, Robert is really fantastic. I'm really happy for you genuinely and uh keep it up. I hope that it stays that way. Um I can't imagine that it wouldn't, but uh yeah, keep it up. The next one is from

James uh Sales Sales Sas. I I'll move on. uh in my N of one research. So anecdote again, I resolved my non-alcoholic fatty liver disease with ketogenic and carnivoreish diet and lost 48 pounds in 6 months. This is confirmed by MRI imaging and as GDT uh lab results. Thanks for the video. So first off, thanks James. Secondly, again, just like with Robert, huge congratulations. That's no easy feat. Um, especially losing 48 pounds as Well over 6 months. That's really fantastic work. Um, James is talking about for ALT and GGGT, those are enzymes that are secreted

out of the liver when it is uh being harmed. So when there's harm occurring to the liver and so if you see a reduction in them that means that the the liver is in a better uh situation and also confirmed by MRI imaging as mentioned. So again, that's that's fantastic. And Again, if if we to look at the scientific literature, you know, if you drop 48 pounds or if you just drop weight in general, you will typically see improvements in your liver markers, you will see improvements in your liver. So, it's not like a person

has to prescribe themselves to a very specific diet because that's the just because we're discussing right now we're talking about low carb diets. We're talking about fasting and whatnot And how those are beneficial for liver health. That doesn't mean that there aren't better ways or different ways or maybe not quite as effective ways but still sustain like they're they're better for you as an individual to use. There's there's a lot of different ways to attack something like that. And especially when you are pairing that with weight loss, it's a little bit different maybe when a

person is not trying to lose weight. They're trying to Maintain their weight or even gain weight but still maintain proper liver health or improve their liver health. But if you're losing weight, you that that almost necessitates improvements in your liver health. So just uh just something that I would add. um you know, if if a ketogenic or carnivore style nutrition works for you, that's that's great. There obviously, you know, certain other considerations that people have to Have to consider. Um, I'm not going to go down that rabbit hole for the time being, but the point

being and the overall point of my video and my analysis and whatnot is that low carb diets and fasting can certainly be an improvement and a significant improvement for uh, liver health. So, for both really great and I'm genuinely happy for you. All right, the next topic is to cover drowning cancer in a fatty molecule butyrate in this situation. So, I covered this fascinating study, uh, probably one of the most fascinating of the year up to now, which essentially looked at the impact that a fat, a short chain fat called butyrate, has on cancer, specifically

colon cancer. And what they showed is that butyrate can not only inhibit the growth of colon cancer but can kill colon cancer as well. And I won't go into all the details um but there's you know mass cell death to the colon cancer that While sparing healthy colon cells. So colon being uh your large intestine. And so if we were to to look at a person's colon, probably not the most desirable thing, but we're going to do it anyway. Uh so you have your intestinal tract, maybe if you if you had an image of uh

the intestines. If you were to zoom into the intestines, and then you'd notice that there are these these crypts, these kind of uh grooves that create this like snake like uh look almost. They they Look like caverns that go into the intestinal wall and then come back out and they actually make up the intestinal wall. And inside those grooves at the very bottom of that groove, you have a bunch of stem cells. And these stem cells end up multiplying and uh turning into a variety of different intestinal cells. If that's panith cells or goblet cells

or colonocytes of other, you know, general colonocytes, There's a number of different cells that they can turn into, but they ultimately give the intestine structure, right? And the intestine has a number of different functions that again we don't really need to get into. But it's at that exact site. So at the very bottom of that crypt that these stem cells if they undergo mutation burden or if uh you believe more of a metabolic environment that ultimately leads to more of a cancerous type of cell that starts Getting born and then that stem cell that is

now more cancerous starts to multiply. So you start to get a tumor or you start to get growth in in that region that is abnormal growth and that's obviously why we get colonoscopies because we start to detect some of those uh abnormal growths that start to occur and we try to catch those uh early. Okay. So why are we talking about that in relation to butyrate? Well, the reason is because as we Consume foods that ultimately get produced into butyrate, that butyrate can get into those crypts and can be taken up by the cells. And

when they're taken up by the cells, according to this research, the cells end up uh kind of freezing like they can't grow anymore. And in the worst scenarios, they end up dying. And the reason for that is because the cancer cells, at least the specific ones that were tested, the cancer cells are Using sugar or carbohydrate as energy and they are less able or less willing. less able, less willing, kind of use those interchangeably um because we're getting to the limit of my knowledge on the topic uh at this point to use fat molecules. So,

because they're using sugar, they're using carbohydrates. And I I just want to be clear here, I'm not using the word sugar As in like Pepsi or whatever, although that is also included in this definition. And I'm talking about sugar as carbohydrates, glucose specifically. And carbohydrates are made of largely glucose. So when glucose enters inside this cancer cell, it gets metabolized into cellular energy as well as many other things that again we don't need to get into. But butyrate because it's a fat can enter into the cancer cell. And Because the cancer cell is not going

to take that butyrate and produce it into energy, it starts to accumulate inside of the cancer cell. And because this butyrate is just has no destination, it's just being taken up into the cancer cell because the cancer cell would normally if it were a normal cell would be taking up butyrate for energy production. This concentration of butyrate outside the cell allows butyrate into the cell And it starts to build up inside the cancer cell. Now from there butyrate has a number of different mechanisms that it affects the cancer cell. So, one of the main ones

that was detailed was the fact that it probably, we don't know if it's direct or indirect, but it probably has some sort of interaction with key enzymes called HDAX or histone deacetylases and as well as uh histone acetal transferases. And what these two types of enzymes, these families of enzymes do is they add or remove a particular type of tag to the DNA structures within our within our nucleus within the the the cell has a nucleus where all your DNA, all your genes are kept. And there's these different structures within that nucleus that keep DNA

and genes uh we'll say organized. And the proteins that control that Organization of the DNA and the the genes are these histone deacet deacetylases and these acetylase enzymes. So they'll add what are known as acetal groups or acetal tags to these different structures and that will change the organization of the genes within the uh nucleus. Okay. So why does that matter? Well, it matters because if the cancer cell is trying to bind or close particular genes. So, if it's trying to bind and express or lead To more production of particular proteins, it has to have

access to particular genes that allow for the production of these proteins. Think of like progrowth proteins. And what butyrate does is it will close those genes so that the cancer cell can't access its own genetic information. So it cannot produce more of those progrowth proteins. The other side of it Is that it can encourage it can open up the genes that are anti-cancerous and can lead to cell death, which cancer has a number of different ways that it can stop cell death because obviously it doesn't want cell death. Why would it? It's cancer, so it's

it's trying to grow as rapidly as possible. And when I say it's trying or it's doing or all that stuff, just know that cancer cells aren't thinking about this stuff. I'm just kind of speaking in a little Bit more plain language even though it may not seem like it. So just know that the cancer is just reacting biochemically in a certain particular way. So in this situation the butyrate could be opening the genes that are anti-cancerous and a perfect example of that would be I don't know if I discussed that maybe I discussed this in

the insider uh analysis doesn't matter the they they may produce more of particular proteins Called BCL proteins these BCL proteins will uh essentially allow mitochondria to die and if you have mass mitochondrial death then the cell destabilizes and ultimately you get cell death. So butyrate encourages a lot of the anti-cancer genes to be produced into proteins and it cuts down or or shrinks closes up makes it more difficult for cancer cells to access the procancerous genes or the genes that would be more attributed to to cell Growth. So that's the mechanism by which butyrate uh

functions. Now in addition to that the concentration gradient if we go back to this crypt so again the intestinal crypt at the bottom of the crypt there's lower butyrate levels at the top of the crypt there tends to be higher butyrate concentration and the idea behind that is that the butyrate can also have a dual function in that it can also encourage the production of more healthy Colonocytes healthy uh intestinal cells while at the same time inhibiting the cancer cells that would otherwise be growing in that region. There's a lot more that especially some nuances

like the different types of cancer. I don't want to jump to the conclusion that this would apply to all cancers. We do have evidence that butyrate helps against other cancers as well, but what this study focused on was specifically colon cancer. And there's certainly more intricacies to the topic than just, oh, I'm going to up my butyrate and then therefore I'll be cured of colon cancer. I I don't want that to be the message. But there's no doubt that there is a growing body of literature which is already pretty steadfast saying that butyrate will at

least help fight against colon cancer. So I thought that that study was really remarkable. um and especially when they dove into the different mechanisms and The different concentration gradients and started getting into all those details. I thought it was uh really really incredible uh in terms of how can you increase your butyrate levels. I guess I'll quick talk quick mention. So, you can take like some people were saying, well, I'll just eat more butter uh because that has butyrate in it. And as far as I'm understanding, that is true. Uh so, there are many foods

that contain Butyrate and especially fatty foods that contain butyrate. The problem with that is that you might be I don't know what the expression is, but you're stealing from the piper to pay the popper or something along those lines. It's the point is that there are consequences. So in in some situations with particular foods like yeah you might be helping you might be increasing your butyrate concentration but then you're also in Increasing the concentration of many other molecules that you may not want. And as an example for butter you might be increasing like steeric acid

or palmitic acid which are two saturated fats. Butyrate is also a saturated fat butyrate has been consistently linked to a lot of positive effects while steic acid and definitely I'll say at least pelvic acid uh have been linked has been linked to more negative uh health outcomes. So yeah, you could get butyrate from other sources. And I kept, you know, seeing that comment, well then I'll just eat more of butter or I'll eat more of this other thing. And I mean, yes, like technically, yes, that would increase butyrate, but you also have to consider the

other consequences that come with that, the other molecules. You're not just producing butyrate or you're not just consuming butyrate plus other beneficial molecules. You're consuming Butyrate, which is beneficial, plus some potentially detrimental molecule. So, there's a lot to say there. and you know having an analysis on each single food is is completely overwhelming. So the the most direct way to get butyrate other than supplementation is to consume fibrous foods. And I've said this many times before, but fibrous foods get taken up by microbes and those get then get converted to these different short- chain fats.

And it is true that not all Of the short- chain fats that get produced are necessarily butyrate, but it doesn't really matter because many of the other short- chain fats show benefit uh on our health. So even if it's not butyrate specifically, you are going to be increasing other molecules alongside with butyrate that also have positive health effects unlike what we just talked about. So fiber and not to mention that fiber has a consistent Association I actually covered that recently as well that fiber has a consistent association with improvements in cancer. So preventing cancer across

a number of different cancers and this has been repeated across uh many many different studies. So we have a strong basis of literature indicating that fiber and we know that fiber gets converted to butyrate and we know that butyrate has these positive effects not just in this study but other studies as Well. So that's why I'm focusing on fiber as opposed to other sources of butyrate which may also come with uh undesired other molecules. Okay, let's get into some comments. And I remember I had one uh comment that strongly disagreed with uh what I presented.

So I wanted to cover that one at least to the best of my ability here. All right, the first comment is from Bill Davidson. He said, "My father always told me to eat lots of garlic and Onions. I always thought it was to attract the ladies, but now I know the real reason. Thanks." Because I'd mentioned uh high doses, not cooking doses, but uh actual like much higher doses of garlic and onion uh have been shown to increase butyrate levels. So, I will say, Bill, I'm not sure who would have said garlic and onions was

going to attract the ladies, but either way, I'm glad that uh I'm glad that the video and you know, Finding sources of butyrate is going to be an overall benefit uh to to you. Thanks for the comment. Um the another comment that I received which was quite lengthy so bear with me. um was from Wellington Amaral, PhD. So a PhD of some sort. I don't know in what field. Maybe this field. Who knows? Uh but he wrote uh a few comments. So one, legumes and roots. So this is from this uh from Wellington. I'm going

To abbreviate Wellington. Uh from Wellington. Legumes and roots like beans and potatoes when cooked and you don't want to eat them uncooked are high glycemic. So glycemic index. The glucose from these foods will overpower the effect of the fat metabolism in cancer. I'm going to come back to address these comments in just a second. I'm going to go through them um and then I'll I'll read what I responded and then I'll Maybe add a little bit more commentary. Number two, butyrate produced by bacteria is produced in fairly low amounts even among people who host ideal

gut bacteria to produce it. Plus a lot of it will be consumed by the gut cells. Number three in cancer consuming and thriving in fats. So in cancers consuming fats because there are cancers that uh take up fats. These are experiments done in a dish and usually where the cells are soaked in insulin Which is uh commonly added in in vitro cell cell culture. So in vitro meaning the cells are in a dish uh so that the cells survive in a dish. So Wellington is saying that the researchers add insulin to cancer cells. Even though

these cancer cells use fat for for energy, they're given insulin to help them survive in a dish. Enough uh insulin and the cells, even cancer cells, will feed on anything, really anything. Number four, Uh just to be clear, there's seven of these. Number four, there is another molecule that is very similar to butyrate produced by gut bacteria that doesn't depend on fiber. That's beta hydroxybutyrate produced in the liver from they wrote fast metabolism fat or fasting metabolism will produce beta hydroxybutyrate. So I'll just adapt and add a little bit to that. uh it can be

produced in much larger amounts in the Body and will reach the cancer wherever it is. Number five, beta hydroxybutyrate is also produced through dietary manipulation. So ketogenic diet. So it's a highfat, low glycemic carb, moderate protein or prolonged fasting, usually over a day or two for most people. And there are some fats that are more easily processed by the liver into beta hydroxybutyrate like MCT. to mediumchain triglycerides from coconut oil for instance. Number six, there is a concept or calculation that can be easily done at home based on the ratio of glucose to ketone as

an index. So the GKI, that's the glucose ketone index that can indicate the range or ratio where beta hydroxybutyrate is likely having a therapeutic effect on cancer in a living human body. Beta hydroxybutyrate is one of the three ketone bodies produced from fat metabolism. And finally, the Warberg effect to Explain that. Well, okay, actually he explains it. So, I'll read what he says. Uh Warberg effect explains that cells shift their metabolism into fermentation compared to regular cells because of faulty mitochondrial oxidative metabolism. I'm gonna pause right there because I'm I'm having flashbacks to when I

was 23 trying to understand some of these words. So what the Warberg effect is Describing which was discovered over 100 years ago at this point is that cancer cells many cancer cells will prefer using glucose or sugar. remember my definition of sugar uh from before for energy and for other reasons again that I won't go into for the time being because they don't or can't use fat for energy because their mitochondria are somehow defunct. So therefore they strongly prefer using glucose Sugar over fat. And that's what he's talking about. Mitochondrial oxidative metabolism is the fat

metabolism and fermentation is the glucose metabolism. Hence why cancer cells, going back to what he said, hence why cancer cells are so hungry for sugar, glucose, and why they're so good at grabbing it from the blood before healthy cells. There are amino acids from proteins that are also fermentable like glutamine among others. It is it's In every food and one can't just not eat it. Hence, there is a suggestion that blocking cancer's use of these fermentable amino acids pharmaceutically in conjunction with a generic diet may be necessary to kill cancer cells. But patient populations see

at least temporary a few years delay or regression in cancer progression just in a welldesigned mentioned diet. So, talking about ketogenic diet, Uh, there are more factors to be considered, but this is enough. Probably too much for a comment. No, I I thought that was really great, and I'm glad you're very thoughtful about it. Um, look up ketosis. Um, definitely well aware of ketosis considering I described it in the in my material. Um, and cancer research by uh Dr. Thomas Seaff freed Dominic Dagghastino um and others will come up in the in the search. Sorry

for the interruption, Doc. Uh this should render material for at least a couple more videos. That's certainly true. Uh have fun with it and nice work on the educational videos. So thank you first of all. Thank you. I really appreciate it. Um I'm very well aware of Dr. Seaff Freed's research as well as Dr. Dagustinino's research. I actually met Dr. Dagustinino uh briefly uh earlier this year uh in person at a conference, but let's uh so I'm going to go through My response and then I'm going to add in a few details um because I

thought that there were several things in the comment that were incorrect and I did double check a lot of this stuff uh just to make sure that I wasn't, you spewing BS. So, uh, my response to Wellington was, well, thanks for the comments, Wellington. I'm puzzled by some of them, though, which I was. For example, legumes are not high glycemic. They're not. Uh, I suppose you could argue that they are compared to fats, but that's not actually how the glycemic index or the glycemic load are compared. Uh, glycemic index is speaking to carbohydrates, so not

talking about fats. Um, I'm also confused on your points about low butyrate production by ideal bacteria considering that the majority of our butyrate comes from the microbiome. And then I looked up some numbers around 50 to 100 micro mole per Day. Um, mill mole mill mole per day. That's a big difference. Uh it's true that we absorb less but even so the amount consumed absorbed is consistently linked to have a biological effect especially around the liver and the portal vein because that's the first point of interaction for whatever is absorbed uh by the body from

the intestines. Uh I actually have more videos releasing on that soon. So I do have more uh I did Have another one coming out on butyrate. So that released that was on the immune system. Not sure I agree on all cancer research being done in dishes where cancer cells are soaked in insulin. Uh in fact I know that from firsthand experience considering that I worked with cancer cells and didn't use insulin. Uh here's an example of fat consuming cancer cells not exposed to insulin includes an invivo research. It even shows beta hydroxybutyrate Signaling uh cancer

growth and then I supplied a study number. Uh I agree about beta hydroxybutyrate. I have content on that too. I'm also familiar with Dr. Seaff Freed's work. I have a video on his work and plan on doing some others time permitting. Uh I definitely need to cover that more extensively. I think his uh work is intriguing and seems to have some great arguments, but it also doesn't account for many other considerations brought up By cancer re by the cancer research community. Anyway, I plan on covering more on the ketogenic diet and cancer in the future.

It's a fascinating area of research and I wish I could get uh more more into it and flesh it out more. Yeah. Again, thanks for the for the comments. Um again, I I don't actually agree with some of the the comments here. Uh and I've heard almost all of them before From other people. Um the point being that while we focus so much on cancer research and just this this idea that all cancers just use glucose and that they have a complete inability to shift to fat metabolism. Um that hasn't been what I've seen in

the lab when I was doing my PhD because actually initially I was doing some metabolism work. I ended up doing some metabolism work, but I was doing some metabolism Work where I had switched cancer cells to using more fat metabolism. And it is true that they didn't grow nearly as quickly, nearly as well, but that also doesn't mean that they ended up dying off um when switched over to fat. Now, it is true also that I did not restrict. So, part of Dr. Seaf Freed's ideas as far as I understand it is that you would

restrict glucose to the cancer cells but in addition to that you would also restrict their Glutamine which is what uh Amaral Wellington mentioned that you use a pharmaceutical to stop glutamine in the mitochondrian and you also stop the cancer cells from being able to rely on glucose and therefore it stress resses them to such a degree because they can't use fat in this instance that they end up dying and it is there is when I did do a video on this maybe two years ago a year and a half ago and I covered some of

the aspects of Dr. Seaf Freed's work. I went through multiple of his reviews and some of his papers and whatnot. And then I also presented the other counterargument and in that I brought up that there are studies looking at cancer cells that uh prefer to use fat metabolism. And I'm not sure I think Dr. Seafood may have changed his stance just slightly, just shifted it. Don't quote me on this, but my understanding is that there well I know for a fact that there are cancers That do only or I shouldn't say only uh primarily use

fat metabolism to sustain themselves. That doesn't mean that there aren't many cancers that use glucose for energy. Now the exact reason for that is I think debated from and again I just need to preface this. I need to look more into that literature. I have looked into it some. Um there's arguments that it is a mutation burden as in the cells are unable to produce the requisite enzymes Or whatever it might be to to shift over to fat metabolism. Um or that there are there's damage or morphological changes that happen within mitochondria. And Dr. Seaf

Freed offers some images when you look at some of the mitochondria. the inside of the mitochondria called the christe is either damaged like completely havoc has been wre um on the uh the inside of the mitochondrian or it just doesn't exist. Uh which speaks to the potential effect that metabolism could have in these uh cancer cells. So there's a ton to say here. I just don't think that I would boil it down to as simply as well people just need to jump on a ketogenic diet and restrict their glutamine potentially through pharmaceutical means. That would

probably be the only way and then you'll just be able to cure cancer. That seems to be an explanation that keeps being Brought up. People keep saying, "Oh, just check out Dr. Seaff's work." I don't think people understand that Dr. seafoods work. It's not just like it's not like the establishment is just like, "Oh yeah, screw that guy." Um there there are legitimate many many many many studies that show convincing evidence of the mutation burden being a causitive factor for cancer that I will say that when I looked at Dr. Seaff Freed's work, I also

found some really credible and great research indicating that he had some great points. So, in my video at the time, I kind of fell in between and I said, well, why why couldn't it be both? Why couldn't we have kind of a hybrid model that indicates that for some cancers, yeah, there's a there's defunct mitochondria and we could be be able to target those and effectively really inhibit and damage those and and and Kill those types of cancer. While on the other side, we still also have other cancers that aren't as susceptible to just metabolic

reprogramming. um that they're they're able to kind of shift from, you know, glucose to fat or maybe they're predominantly in fat metabolism or whatever it might be. So, I'm just I just don't think that it's quite as simplistic as to just say uh yeah, just eat a ketogenic diet or fast, get your beta hydroxybutyrate levels, Which is a the main ketone that we discuss, and therefore you'll be able to kill all cancer cells. I understand the point that it goes to different like you can get that those ketones to different areas of the body more

efficiently. That might be true. Um but I will say that there's other research as well that looks at butyrate that looks at butyrate outside of cancer. O looks at like endothelial cell health and they do show in vivo research Where if you increase butyrate levels that it does pass into the bloodstream and that it has an effect on the entire vasculature so your cardiovascular system and it tends to improve your cardiovascular system. So to say that we're we're not cons we can't get enough butyrate to have a biologic to create a biological difference just doesn't

really bear out in the literature. Um we have many different types of studies That indicate otherwise. Not to mention I'll also fall back on the idea that the main source of butyrate that we get so one of the main sources fiber has been consistently linked in many many many studies I'm talking hundreds and hundreds of thousands of participants uh shown to reduce cancer incidence and mortality and just has an overall positive effect. So is that necessarily through butyrate? While we can't necessarily say that I will Concede that, but I also can't imagine that that doesn't

have an effect, especially when we have so much evidence specifically pointing to butyrate having a positive effect. So, probably a more lengthy conversation to be had there. I agree with certain points. Uh I just don't agree with uh with uh certain other points. But anyway, I still appreciate the commentary and uh oh, and I will say for the cancer research for sure, uh there's Plenty of invivo research where they don't apply insulin to the cells. Uh I don't know, like I never well, I shouldn't say I never in one of my experiments that was never

published, I applied insulin just to see what would happen. And um nothing nothing crazy happened. Um, but in all of my experiments that were published and in other other experiments I did just kind of leading up uh we never used insulin in any of my uh cell research. All Right, we got uh about three more topics and then I'd like to just go over some light housekeeping like I usually keep at the end of each podcast. So for the next topic, you know, I had to discuss this because I discussed this earlier in the year.

I did some work on seed oils and their impact on our health. I mostly focused on cardiovascular health, but I also touched on other aspects of health as well. So, seed oils and health. I think the there's probably a number of different mechanisms that people discuss seed oils and how they affect our body and how they're, you know, a a negative force in our body. Um, the two that I'm aware of at least that have been discussed in the literature is or yeah, okay. discussed in the literature uh but not exactly in the context of

how it's discussed in the anti-seed oil world is the oxidation of polyunsaturated fats. So seed oils are Well examples are like soybean oil, corn oil, canola oil, safflower oil, sunflower oil. Those kinds of oils contain within them the dangerous component that a lot of people have talked about linoleic acid which is an omega-6 polyunsaturated fat. Basically what that means is it's a fat molecule that has multiple kinks in it and because of its structure it is more easily oxidized meaning that is more easily damaged in in a manner of Speaking. So that's one aspect. The

other aspect is and then of course if it's integrated into your cell. So think of like into your cell membrane uh into the the membrane of your organels like the different structures. Think like the mitochondrian, think of the endopplasmic reticulum, the GGI apparatus. Um that then you could potentially get this accumulation of these damaged fat molecules within the structure of your cells, which obviously that doesn't seem Like a very positive thing. The other thing is that omega sixes can be pro-inflammatory. Again, these are the mechanisms that have been mentioned that omega sixes can be pro-inflammatory

in that they get converted to what's known as arachidonic acid. And that arachidonic acid can have uh significant negative effects within the cell. And technically arachidonic acid is then converted or can be converted to Different uh pro-inflam other pro-inflammatory molecules I believe like prostaglandins uh icosenoids and there's a there's a bunch of other ones as well but ultimately these pro-inflammatory molecules then can get secreted out of the cell and can lead to more of an immune reaction and and damage the surrounding environment and things of that nature. So, those are some of the mechanisms that

have been brought up. I'm sure that there are others that have probably been brought up in kind of the depths of the internet that I'm not aware of. Um, and that's that's perfectly fair. I'm not here to really discuss the mechanisms uh as much as I am to discuss the clinical data because ultimately the clinical data is always going to trump any sort of mechanistic research. So, and I'm actually going to come back to that point on our final topic as well Because I think that's going to be important. Okay. So, looking at the clinical

data, I pulled together a whole lot of studies in total. I think it was I didn't necessarily open up every single one of these studies, but I opened up a lot of different analyses, including some isolated studies. And across something like 200 studies, maybe 150 studies, uh, that looked at in some capacity omega6s, again, that's these polyunsaturated fats And their impact on our primarily cardiovascular health, but again, I I did dabble in some of the other metrics outcomes as well. It showed pretty reliably that there was either a neutral effect or a slight positive effect

of consuming omega-6 fats. Now there is one research group that seems to believe differently from many other research groups especially one Research group uh headed by uh a prominent researcher known as Bill Harris. Um, this one research group, the Ramsden group, ended up doing an analysis that I thought was quite interesting where they split omega6 consumption, the studies that just looked at omega6 consumption versus a control group versus the studies that looked at omega6 plus omega-3 versus a control. And they showed that if you just looked at the Studies that gave people omega-6 fats to

consume that they tended to have more cardiovascular disease. But if you looked at the studies that used omega 6 plus omega-3, they did not show that link anymore. So then the the main point there that the omega sixs may be a negative if omega-3s are not in the conversation as well. Now I did have some negative things to say about The details of their analysis that I'm not going to rehash here. Um, I think that they missed the boat or they left out certain details and didn't do proper uh analysis on some of the data

that once you open up the studies, you realize, oh, well, I I don't know why they didn't include this or why they didn't, you know, account for that or whatever it might be. Again, for the details, check out the video. I I'll have it linked for you. Um, but there Were several things I just didn't agree with their overall interpretation based off the data that was presented. Still, that doesn't mean that they didn't have a point. And in certain respects, I did agree with them on their overall point, like omega 6's, like the relationship between

omega 6s and omega-3s. There were some other analyses that I didn't think were that great. I think that overall there just isn't a whole lot of data on from randomized Control trials that look at omega-6 consumption versus you know particular I don't know like saturated fats or some other condition. Um there are some old studies like most of them are from like the 60s7s all the way up to maybe the 80s and 90s but a lot of these studies have so many flaws within them like in certain respects they have strengths to them but in

other respects they have a lot of flaws to them. Again you know check out The video on all that. It's like a 25minute video where I go into a lot more of this stuff and there's even more to say than what what I went over in the video. But ultimately like basing any sort of strong conclusion based on just that data is not going to lead you to anywhere really. uh and my conclusion was that and it's I think largely true that the studies Showed either a neutral effect or the study and there were studies

that showed a negative effect to be clear but again if you look at some of the methodology of those studies you you start to realize oh well there's a lot wrong with these studies like the these in the modern day like if today a study was was tried to be published in a reputable journal they probably would not be able to be published. It it just the peer reviewers would be like this is insane. You you lost 80% of your participants. They how are you going to publish this? Um or at least if we publish

it, you're going to have to put in a lot of explanation for why you lost 80% of your participants or um there's in potential strong likelihood of inclusion of trans fats. uh there was a lot of mixture between the control group and the intervention group. Like there's there's all kinds of different problems. So that's why I'm saying it's really hard To sit there and look at these studies that were done such a long time ago and knowing the information that we know now try to say that those studies are a good representation of seed oils

or anti-seed oils. Um so I can't really go either way, you know, for seed oils or anti-seed oils. based on those studies and when you do meta analyses looking at all the different studies even those meta analyses I mean largely they show a neutral effect as in no Benefit no negative effects but even those there's flaws simply because of the data sets that they have to rely on to create their conclusions so then to take it a step further I decide to look at what other studies have been done so I'm looking at like huge

huge largecale uh epidemiological evidence and looking at different controls that they do different they try to control for different factors. Um they'll try to do subgroup analyses. There was one that Was really great where they not only looked at omega sixs but also looked at omega-3s. And not only did they look at the the they didn't look at the consumption, they actually looked at the blood measurements of omega sixs and omega-3s in the blood as well as um proxies for tissue. So what's actually integrated into the body? So aside from just in the blood which

is already pretty damning but then on top of that what's actually found in The tissue and there they showed a really striking graph that as the omega6 to omega3 ratio. So that means the more omega6 so omega 6 over omega3. So taking both into consideration, if you have more omega-6 or reduced levels of omega-3 that there is an increased risk of cardiovascular disease, which goes back to what the Ramston group was saying that if you just up omega sixs that you get worse Outcomes. Now again that was based on old data that had a lot

of flaws in it. But now if we look at the ep this epidemiological study that included uh tens of thousands of participants and used far more rigorous metrics of using blood measurements. They do show a kind of a similar story that if you increase omega sixs in the blood to such a degree that the ratio is is so much in favor of omega sixs over omega-3s that you start to see this Association with increased risk of cardiovascular disease. Okay. So that in itself is is pretty alarming and it's it's kind of scary. But if you

look at the numbers, so the ratio, the what they considered the ideal ratio or what they compared everything against was a ratio of four. So for four units of omega sixs, you have one unit of omega 3. Okay? And then they scaled that. So, as people had more and more and more and more omega sixs, so we're getting to 12, 15, 20 times the amount of omega sixes in the blood compared to omega-3s, they showed that the risk increased, increased, increased. Okay, so keeping that in mind, then they were like, well, what does the typical

population consume? So we've got our ideal of four to one, but what does the ideal population consume? And I think it was something like 8:1, 9:1, 10:1, something like that. So certainly more, but when you look at that same graph, it is still Squarely in reduced risk and really the best interpretation would be no reduced or no no increased risk. So right there, neutral risk as in no negative effects that are experienced from typical consumption. And keep in mind, this is typical consumption, which means that people in day-today living are consuming omega sixs and the

result is this association with no increased risk. So yes, we are talking about including people that are going for fast food. Yes, we are talking about people that are cooking at home. Yes, we're talking about people that are going out to fine dining establishments that are eating junk food that are it's it's tens of thousands of people. So, we're including all these people. We're talking about heated seed oils. We're talking about cold seed oils. We're talking about all these situations because we have such a large data pool and the result is that there is no

Relationship with increased cardiovascular disease. Now, let me take a step back from that and let I just said that we're looking at people, you know, that go fine dining that may be consuming omega sixes, that go fast food, all that stuff that may be eating heated seed oils and cold seed oils. That doesn't mean that we have the granularity through subgroup analyses to find out if one group may be getting disastrous Consequences from consuming seed oils while another group is consuming seed oils and getting benefit from seed oils and that's what's leading to a neutral

effect. Hopefully that's clear. We're looking at big data sets. So we would need to do far more analysis on these different subgroups to tease out is that neutral effect or that neutral association is that still the case when we look at these different subgroups. Is it neutral for Everyone or is it maybe slightly elevated for some people and then slightly reduced for other people? you know those answers were not provided in that study. But one other thing that they did, I mentioned this in my insider analysis that if they looked at just omega-3 consumption or

they just looked at omega6 consumption as they did a a standardized Increase in I guess I shouldn't say consumption but the blood levels as they did a standardized increase in blood levels of omega-3s and standardized increase in blood levels of omega sixes. So breaking the data apart, not looking at the ratio, but looking at just the amount found in the blood, they found that no matter what, there was either a neutral or reduced risk in the omega6 group and there was only a reduced risk in the omega-3 group. So when looking at Omega-3s or looking

at omega sixs uh separately. So that would indicate that the evidence is more leaning in the direction of omega sixes probably are not a negative to our health. Does that necessarily mean we have all the answers? No. Because of what I just explained before. We don't have different subgroups. Now, in addition to that, I did do a separate analysis on canola oil, Which isn't which is one of the the ones that people are really fearful of for some reason. I did a poll and people voted on canola oil being like the number one that they

wanted me to look into. So, I looked at canola oil and if it's inflammatory. So, I pulled together every single study I could find and I I asked the community. I used the the good old AIs uh out there to pull together every single study, every randomized control trial I could find on canola oil And inflammation. And I think I found 10. There are 10 studies currently that have been done on canola oil and looking at inflammation. I will be honest with you, most of these studies, the study quality is really bad. uh it's not

very good but based on all these studies I think nine of them showed either neutral or positive effects on inflammation and that's compared against all kinds of different things. There was one study that showed, It wasn't a very good study as well, but still there was one study that showed that it may have a pro-inflammatory risk if it was heated over and over and over again. I think it was heated something like 20 times over and led to small increases in inflammation. So based off this one kind of poor quality study, there might be a

signal there that if you constantly heat omega sixes or we'll say canola oil, we restrict it to what We looked at to canola oil. If you continuously heat it over and over like you know on on a pan or whatever it might be, you continuously use it. So think like fast food. I think that's a great example. I don't know how the fast food industry works in terms of I'm assuming they don't rotate out the oil after every single meal, right, that they make. It's probably just continuously heated over and over and over again, which

is exactly what we're Talking about here. So, in that situation, there may be a a small inflammatory risk. Keep in mind, we're not looking at cardiovascular disease in this situation anymore. So, we're looking at kind of a softer metric, but still with that softer metric, we're seeing that there may be a negative effect. So, is it possible that if you repeatedly heat these omega-6 unsaturated fats, Keep in mind that's going to massively increase the amount of oxidation that occurs to them. Could that be a negative to our health? One single study looking at this is

not enough for me to say end all beall we are for sure uh we need to cut away all seed oils or anything like that and that wouldn't be a reasonable conclusion anyway based off the other all the other data that I I told you about. But my perspective currently is that omega Sixes at the amounts that we're consuming them even at really high amounts of consumption just don't seem to be much of a risk at least for cardiovascular disease and also seems to be the case for uh inflammation based on the evidence I've seen

up to now. that could shift if you start to add in other variables like heat the heating process or we don't even know if heating, you know, if you cook with it Once, who's going to sit there and save the oil and then cook with it again and then save the oil and then cook with it again. You know, that's really only in kind of a fast food situation or a restaurant situation. So, is that applicable to how you cook? Probably not. So, I don't even know if we can extend that to one time, cooking

with it one time, and if that's going to have a negative effect. Um, I I can't even speculate. I don't know which Direction that would go. The only thing we know is if you cook with it 20 times over, then there is a potential for a negative effect. So, you can kind of see where I'm going with this. The the overall point for me is that omega sixs seem to be at least neutral for our health and likely in certain instances slightly positive for our health. Omega-3s seem to be robustly continuously positive for our health.

So, if you're Really afraid of it, just make sure just don't worry about your omega sixes as much and then increase your omega-3s a little bit and then you'll fall right in line with what the research indicates that you'll you'll be you'll see positive effects on your health. Um, and there's a lot of nuance to that as well because, you know, if you're over consuming all this stuff and you're gaining weight, well, hold on. you know, we got to back off and we can't say Then, oh, well, Nick is misleading us because omega six's uh

made me, you know, gain weight or I had a heart attack when I started consuming more omega sixs. It's like, well, hold on, you also gain 30 pounds. So, is it the omega sixes or is it the weight gain? like you know there's that's why I'm saying there's there's a lot of nuances that on an individual level you would have to figure out but on the broad strokes That's what I'm saying is that typically there's a neutral to slightly uh improvement in health from omega sixs and omega-3s there seems to be a consistent improvement in

health subgroups we still need to to look into that in more depth I'm trying to communicate this as intellectually honest as possible I'm sure I'll get called some seed oil shill by any number of different people. Um, that's fine. But that's really where I ended up uh landing based off of uh my video. And I would certainly recommend that you uh check out uh the the video because I do a far more succinct job of explaining uh everything I just went over. Okay, let's get into a few comments here. Uh, Oki Okitasuji says, "What I

find curious is why all seed oils are lumped together Considering their fatty acid composition is quite different." So, what Oki is talking about here is that I'd mentioned that there's uh soybean, corn, canola, safflower, sunflower oils, you know, etc. And it's true that each one of those has a different composition. Like canola is pretty different from the others. And yet people seem to be most fearful of canola. Uh but then if you were to look at some of these others, there's some More similarity, but there's still uh differences in the type of fat molecule that's

found. So just because we're talking about omega sixes, there are different types of omega sixs as well. I think the main one that people are afraid of is linoleic acid. So, it's true. We're lumping all seed oils together. And it kind of speaks to kind of the imprecision of how this is being, you know, talked about. And if I had it my way, I would break each seed Oil apart. I would break each fatty acid apart, the percentages of each, the absolute amounts of each. I would look at different outcomes for each inflammation, cardiovascular disease,

cancer, diabetes risk, all these different things. I would look at subgroups. I would look at which ones have been heated, which ones are cold, like all that all that information, which would, you know, it only take me about a year or two years worth of work. And in addition to that, uh we don't have some of that data. So, it's a great point. Uh it's just unfortunately again in the social media landscape people just love to oversimplify which leads to to a lot of uh I think just in general bad takes. Another question from Tropeus

or not question uh comment. My main takeaway, even if seed oils are bad, the effect size is so hard to find and easily confounded that I'm probably reducing my Lifespan just stressing about it. Yeah, that's true. Uh people are so focused on seed oils that they're kind of missing the forest for the trees. I think I nailed that one. Uh yeah, focusing on so many other things is going to have a far greater impact on your your life and your longevity, your health span, uh focusing on seed oils, especially based off the literature that we

have at this point. Another comment, water balloon Fighter. Uh thank you so much for this and for highlighting the importance of what are you replacing X nutrient with? as a dietitian, that's always something I'm keen on asking patients. Not sure if you remember uh since you have many subscribers, but I recently commented that your work was part of my inspiration to apply for a masters of science in health statistics and I just got accepted. Uh so I did I did uh comment under this one. I just want to Say again congratulations. I mean that's that's

really awesome. Um I think statistics is just such an incredible field. I've I've always hated math. Uh I've hated math. I hate math. But that said, statistics for some reason is just like conceptually is just something that I understand far better than the actual mathematical formulas. Uh and I think statistics is just such an incredible field that's I think it's often mi Misaligned uh malaligned. Maligned. There we go. Woo. got to the word eventually. English is also a struggle at the moment. Um, yeah, it's it's an area that's often maligned. Uh, people will say kind

of pathy comments like, uh, you know, you can you can massage the data however you want. Um, you know, any number of different things. I can't think of them off the top of my head. I'm not the quickest uh quickest on my feet, but um it's but to me, I think it's just an area that if you can understand it, you can have a lot of respect for it and it will help you a lot in understanding a lot of the world around you and what are the odds of something happening or or especially since

you're going into you said health uh statistics, you'll be able to learn a lot more about the epidemiology. ology you'll be able to Understand more about biostistics looking at you know when you should be using proper statistical analyses like uh tests or student t test one-way test two-way t tests looking at uh anovas bonferonia adjustments like there's there's all these different things that uh you learn about and they make a big difference because once once you start reading uh studies you're like oh And I see why they did this statistical test because if they'd used

this other more Common method, it would have given them a potentially faulty uh conclusion. Or you'll read a study and you're like, "Oh man, they really it's so like the study is so welld designed, but unfortunately they use the wrong statistical test which really makes the conclusion of the study uh basically null and void." So as you delve into that world, it it really gives you a greater appreciation for uh for study design and um and yeah, just Uh just health in general. So yeah, congrats. And you already being a dietitian and then adding health

statistics on top of that, that's going to be uh it's going to be a potent combination. I think I've taken four statistics courses. I think two in undergrad and then oh no maybe five maybe five or six even and then I've taken multiple in grad school and I still have so much more to learn. Um it's it's a it's a huge field. Uh I'm Never going to be at the level that you probably will be uh as you know getting your masters in biostatistitian being a biostistician and whatnot but um it's it's an incredible field.

Anyway, I won't uh bore people with it anymore, but I just want to say congrats. That really is a huge thing in terms of u what are you replacing X nutrient with? Yeah, that's a big thing, too. I think one point that I was trying to make in in my analysis is like we have so much Evidence implicating, for example, like saturated fats and especially trans fats as being a negative for our health. Uh saturated fat, I'm talking about an umbrella term. There's many subcategories of saturated fat that, you know, some are actually beneficial for

our health, some are negative for our health, but I'm talking about the negative ones. So, if you were to replace these seed oils with this narrative that seed oils are killing us, All this stuff, and then you replace that with like trans fats, well, regardless of what you think about seed oils, you have just va just massively increased your risk of death uh by switching over to trans fat. So what are you sub substituting a particular food for or particular type of food for? That is an incredibly important question in the real world. Uh I

mean you know this right as a dietitian. You know this better than I do as a dietician. Um that It can have massive impact on your life. So, we shouldn't get so caught up in kind of the social media sphere and world uh where people are are just scaring you with kind of nonsense. I mean like a lot of this stuff they just uh they they often don't site studies or they'll site a single study but then they if you if you go into like chat GPT or you go into like any of these AI

systems don't necessarily ask them uh are seed oils good for me because you Know they're going to come back and then if you have the mentality of like the establishment they've they've indoctrinated the the doctors and all that stuff that's fine but ask a question like list all the seed oil studies that have been done or list the ones that have been done the last five years and then look at like I'm not saying that this is the the only barometer because really you should have somebody that's like going to go through All these studies

but look at the conclusion for most of these studies and you'll be surprised I mean how many studies just consistently show positive or at least neutral effects of seed oil consumption or omega-6 consumption, linoleic acid consumption, and then you go to these fear-mongering like social media platforms, and you have to ask yourself at a certain point, why are they not covering any of these studies? Why are they They're so adamant that omega sixes and seed oils in general are so negative for our health? But then there you you will find 20 30 50 100 studies

from all these different seed oils and the vast majority of them say positive effects from all different types of labs across different countries, different funding agencies, all that stuff. It just it just kind of has to hit you and think like why are they saying that exactly? Like, can I trust these people if They're not going to address I I understand them not knowing about a particular study or even particular two or three studies. I'm not talking about that. I'm talking about the vast majority of the studies indicate no harm. So, anyway, I'm kind of

going off on a tangent there, but I just something I just wanted to point out. But again, just want to say congrats. And yes, as a listener, you should be thinking about What am I going to be substituting my omega-6 with? If I want to avoid omega sixs, what am I going to substitute that with? Is it more protein? Okay, that might be good. Uh would it be a fibrous carbohydrate? Okay, that might be good. Is it uh potentially more palmitic acid fil saturated fat or is it trans fat? that's probably not a good idea.

So, you should always think about what you're going to be substituting it for. All right, the second to last topic that I Wanted to cover is the ineffectiveness of creatine. I've done so many videos and I plan on doing so many more on creatine because there's so much research that's been done on creatine. But there was this one study that came out from some pretty reputable uh researchers that they social media I shouldn't say social media media I actually saw media covering this uh saying that Actually let me backtrack real quick. Social media largely said

that creatine was still beneficial after this study. So, this stud this study essentially says that creatine is ineffective. And I'll explain what that means in just a little bit, but social media went in on this study and said, "No, they messed all this stuff up." Which they they did mess up some things. I'm going to go over it in just a second. But I always find it funny that once We've kind of globbed on, we've attached ourselves to something, creatine is beneficial, which I am definitely in that camp. But it's almost like we have to

it's like our preconceived notion immediately when we get hit with a study that says something different, we have the only thing we focus on is what are the negatives of that study. as if there are there there's no way that we we shouldn't be like trying to integrate This study with what the broader literature has to say. The only thing we do is just go in on that study. It's like you go in angry already. It's like going into a conversation angry as opposed to going into a conversation with, okay, let me ask questions first

before I start accusing. And in social media, creatine is kind of elevated up to this point of like it's untouchable. So all the all the all the videos I saw, they weren't even necessarily critical Uh analyses of like the study design and whatnot, they were just like this study is just like BS. Like ah, you know, they're talking nonsense. You know, it's it it was like this pre again this preconceived notion of like we've accepted creatine into our ranks, therefore everything against it is just nonsense. Um, which is uh which is tough to fight against,

but it's definitely something that we all have to kind of be aware of. Definitely myself included. Um anyway, so beside that there's this this creatine study that released several months ago at this point and they were looking at lean mass. So creatine has been known that if you consume it that it increases lean mass. It's been shown across a whole host of different studies. But what this study did that was unique was they had participants load with creatine. So they took creatine and they were compared against The placebo group, but the they took their lean

mass measurements by a DEXA scan uh before they took creatine. Then they took another DEXA scan 7 days later after they'd loaded with creatine. They had been consuming creatine for 7 days. And then they underwent a resistance training program for 12 weeks after that. Um, and then they compared against the placebo group that also underwent a resistance training program for 12 weeks. And then they measured Their lean body mass again. And what they showed is that yes, their lean body mass was increased at the end of 12 weeks, but if you subtracted the initial seven

days, so after the first seven days of creatine loading, if you took that added lean mass that they they gained from the creatine supplementation because creatine leads to water weight gain, there was a nullified effect of the lean mass gain. Meaning in simple Terms that the creatine, the only thing it was doing was increasing water weight and that all the previous research was faulty because they had falsely assumed that the increases in lean mass at the end of all their studies was because creatine was leading to greater muscle growth. Okay. So in one way that's

this study was really I I liked it. It was very simple design. I really appreciated the fact that they did this style where they They didn't actually start resistance training until after the first seven days of loading with the placebo or the creatine. And then the fact that they're able to tell the difference between the creatine at the end and the creatine after the seven days to try to tease out those differences and found, oh, there's no difference. they all the the the the gain over those 12 weeks is not from anything that happened over

those 12 weeks. It's from the first seven days, The water weight. So, that is definitely on the surface it seems like a pretty damning study. And it's it's not that the other studies were like I don't know mischievous in any way or anything like that. They were just they just had an error in their methodology. But the real thing is, did they really? And here's where I came back with some critiques of the this new studies designed. One major critique that I had is that they actually clamped the Volume. Uh so from the the weight

lifted. So over those 12 weeks, the resistance training was the exact same between the placebo and the creatine. Now, if you know anything about creatine, you know the creatine mechanism of action is that it increases the energy available to continue to lift weights. So if you are clamped at the amount of weight that you can lift throughout that 12 weeks. So the volume the total amount of work done is the Same then you are and this is a major issue in epidemiology as in not not a major issue as in like many studies suffer from

this but they they're very aware of this problem. you are removing the the main benefit of creatine and then saying look creatine doesn't work. So what what would be a better design is to not keep the volume the same, but to allow the creatine group to if they were to get this benefit of added volume just because they can do more added Volume then measure if they see any improvements in in lean mass. And I think and it's not just that I think it's not this is just like some bias like because I'm a big

fan of creatine I'm going to defend creatine. There's also an aspect of there are other studies that have done that and they have shown that if you increase the volume. Sure enough creatine leads to actual muscle gain over the placebo group. Now In addition to that there are studies that have not looked at lean mass and looked at a far more specific far more targeted measure of the actual proteins within the muscle. So the problem with lean mass is that you're measuring yes muscle mass but you're also measuring bone mass and you're measuring uh cartilage

or connective tissue. And that's not to say that bone mass is going to change over you know 12 weeks 16 weeks or whatever It might be even I don't know three month well three months 12 weeks uh like 6 months it probably wouldn't change any appreciable amount um but what might change is like their cartilage or whatever it might be would it be enough to account for everything that we saw probably not but is lean mass sensitive enough to pick up small differences is between the placebo group and the creatine group especially when you clamp

the amount of volume. But even if we Take that aside, the answer is potentially not. So we don't know the answer to that. But what we do know is that there are studies that have not have just foregone the the the lean mass and looked at the actual proteins. So the actual measin and the uh actin protein. So these are the actual filamental proteins that allow your musculature to move. They actually ratchet back and forth. It's an incredible process. Um, you can look up Crossbridge cycling and you'll you'll learn how incredible it is. But anyway,

when studies look at those, they show pretty substantial increases in those proteins from just creatine supplementation. So yes, creatine has a direct effect on the musculature. Yes, it does fill it with water as well. So that is well known, no debating that. But this study, while it was illuminating in in one regard, and it kind of set off yellow flags of like, Hey, in the future, maybe when we look at lean mass, we should measure after the initial 7 days of creatine supplementation, which I think is a is a great contribution to the field. But

on the other hand, is it damnation of creatine? No. and my creatine sponsor would be pissed if I said yes. No, I'm just kidding. Um, so I still remain obviously in incredibly bullish about creatine. Again, it's a supplement. Is it going to Change a person's world? Maybe if they have some sort of creatine deficiency or something like that. But like for the vast majority of people, it's just going to be a small benefit just like any other supplement that's out there. Um, as far as I'm aware, I I like creatine simply because it has an

effect on the brain, has an effect on performance, has an effect on our musculature, has an effect on a number of different areas. Sleep, uh, and there's there's even more Research coming out that I'll get into in the future. So, is it a debunking of creatine? No, it's more of a cautionary tale, and I think it's a it's a good one to have. Um, but it doesn't negate any of the far more specific, far more nuanced research that's been done out there that people just aren't aware of. So anyway, wanted to throw that out there

just because I thought it was fascinating. Okay, so some comments. Yeah, I actually wanted to add this. This is one of my comments. I said just as a fun aside for those that uh that uh put up unending emphasis on who funded the study. So this study that showed that creatine was ineffective. One of the main researchers of the study has a sponsorship with a creatine producing company and yet they still publish a study against creatine. And this is not the first time that I've seen this. actually multiple times I've Seen when I look at

the funding source and it's by somebody who is funded by like a creatine company or there's one that was on Tongat Aliyah I think and the study was actually maybe even performed by Tongat Ali company and they published results that showed that there was no effect now is that like a is a constant thing a common thing no it's not and that's why we need uh systems like what's known as clinical trials.gov uh which forces researchers to Pre-register what they're going to measure and then to submit their data regardless of if they publish or if

they don't publish. And clinicaltrials.gov is just a fantastic website. So I thought that was it's still funny though like when you know people get so strung up on you just got to focus on funding. If the funding is wrong, then I'm just dismissing the study when there are many instances, probably not as many as there probably should be, but there Are many instances where uh the funding funding source actually would be very unhappy with the results of the study and the study still gets published because and I've had these conversations with some of my uh

my PIs in the past, my mentors in the past, but uh during my you know, grad school, But there are contracts and the university also oversees some of the at least you know the people I've spoken to they the University oversees the contracts that are that are written out and it's often written in such a language that regardless of the results I will publish the results. So you have no you once you give me the money I will conduct the study and I will publish the study as is. So regardless of if it's positive or

negative um and that happens quite often. So at least again not not necessarily something I've done but it's uh from from insight from Some of the researchers that I've spoken to. Okay. Anyway, back on topic. Pac-Man Fannibal said, "Uh, more creatine for me and anyone else who's been using it. This study is the best way to keep the cost down and the supply up. Yeah. Well, there you go. That's true. Just tell people it doesn't work and then uh just see the prices drop and then uh buy it all for yourself. Um two more two

more comments. I did add this one to Howard Davies, which did get uh Promoted near the top two, which I'm very thankful for. So, thank you. Um this next top stopping by to to commend Nick uh on the insiders program. This is kind of a self-promotion at this point, but um it I promise it did get a bunch of likes and got to the top, near the top. Um commend Nick on the insiders program and its separation from the main channel. I don't feel like I'm missing out on any on not subscribing to the insiders.

Uh that is to say, I don't Feel like I'm getting screwed into signing up. I also think that the adverts have been integrated really well into all the videos. uh the script of if you'd like more detail, you can find it here with the other benefits isn't intrusive and it gets the point across. I hope it's uh worked well and generating the revenue to support the main channel. Thanks for the quality content, Howard. Uh I really appreciate it. I know you're probably not listening To this uh but it's kind of an off chance, but uh

yeah, that was kind of the goal. I I don't I don't want uh it's I'm not a huge fan of advertising, but I have to advertise in every single video. I mean, it sounds funny because I have to advertise uh the insiders. It's just the way it is. It's the it's literally the only way that I make money other than YouTube revenue. And I promise you, YouTube revenue is not Paying in many of the bills. So yeah, it's really just the the insiders or bust. And I also don't want to get to a point where

it's like I'm not helping people uh publicly in the public videos and whatnot. So I have to I have to walk this fine line of like how much information I release. And I'm actually going to cover more on the at the end of this episode because I've got a few more things to say that I won't get into right now. But um yeah, in the end, I I Deeply appreciate it. I added this definitely as a bit of self-promotion, but also to to say thank you. Um it does mean a lot to me when I

get comments about the insiders. It means especially more to me simply because I put so much work into improving the insiders and that's why we do these live sessions and uh I do a podcast every month for the insiders as well. Um, and that's all because I'm getting feedback from people saying like, "Oh, can you can you do This? Can you do that?" And I try to do within the means of of what I have as a oneperson operation. So, um, anyway, I'll I'll get off go to the next topic, but thank you, Howard. I

deeply appreciate it. Okay. Dave Chapel, not Dave Chappelle, but Dave Chapel said, "I've been taking creatine on and off for decades. I've always known it doesn't grow muscle. However, I've always only gained muscle size when on it. The reason is that whenever on Creatine, I work out harder and longer because I had more energy. The study you talked about has them doing this exact same program. So, as in they equate the volume between the two. I don't know. But, uh, nobody ever told me creatine grew muscle mass. It was the effect on energy availability to

go harder, which is my layman experience. Yeah. So you're exactly right Dave that the primary mechanism that's brought up is that it increases The amount of phosphocreatine that's found inside your cells which ultimately leads to more uh recycling of ATP when ATP is spent. So ATP being cellular energy. Okay. Uh last topic here let me get into this. Uh non-nutritive sweeteners and cognitive decline. So, this was one that I recently covered and I wrote I think the title was like I'm starting to worry about artificial sweeteners. I use the word artificial although it was about

Non-nutritive sweeteners simply because I think people recognize the word artificial more than they recognize kind of a tongue tying non-nutritive sweeteners. So, but it did apply to a number of different non-nutritive sweeteners. And the ultimate conclusion from this study, the result of this study was that it was an associative study and they were looking at a number of I think like eight different non-nutritive sweeteners and they showed That there was an increase in cognitive decline uh more rapid cognitive decline if a person consumes more non-nutritive sweeteners as a whole uh compared to the group that

consumed very little. Now, in addition to that, what I also mentioned and they did do a bunch of uh because this is associative and I think it was over eight years or something like that. It was several thousand participants, but it was it was prospective. So, it Wasn't a retrospective study, which is a weaker study design. This is a a stronger study design, but it is still associative. And they do a bunch of adjustments for confounding variables. And among those confounding variables, they did address nutrition and they addressed uh obesity, diabetes, cardiovascular disease, and a

bunch of other uh potential reasons for why cognitive decline might uh might be a factor. Now, that said, why I came to this conclusion of I'm starting to worry a little bit about non-nutritive sweeteners is funny enough, I think I think I didn't emphasize this enough in my video, and I think pe some people, the majority of people got the idea, but some people didn't get what I was saying. They thought it was a little too extreme to say that you might worry about non-nutritive sweeteners. And the reason for that was not actually based on

this study alone. It was the fact that when I looked at randomized control trials, so I looked at uh a lot of these different sweeteners and I looked at randomized control trials looking at cognitive different cognitive uh outcomes. So looking at like yeah verbal fluency or if that was like recall or some sort of memory task or there's a a a back test which is often Used in cognitive recall uh testing and I was just stunned at how little research exists. So, I'm thinking to myself at this point, I'm like, "Wait, wait, wait, wait. So,

we are deeming non-nutritive sweeteners as safe and fine for cognitive health, but we haven't actually tested it. And now, on top of that, we now have an associative study, which easily, just like any other associative study, could be flawed in Some way that we just don't know. uh like they didn't adjust for a particular something that uh we're just not thinking of. Completely possible. I'm not saying that we should base things just on this one associative study. This is it. We're done with non-nutritive sweeteners. I still consume them. Um my point being that there's such

a lack of evidence that I think it's perfectly reasonable for a person to be like, "Wait a second. I was under the Impression that we had all this research actually proving that they were safe for my brain. But now there's I'm realizing there's almost for some of them there's zero studies, no randomized control trials indicating safety for the brain. And now I'm supposed to just be like, well, I'm just going to continue to consume them as if I have all this evidence to back it. No, that's I mean so then it becomes more of a

question of what is your risk tolerance rather than Ah yes, I have all this evidence and I'm just going to ignore it and say that they're a negative for my health. Um so and especially with so the big two that I mentioned that that had the greatest association was xylitol and arythritol. of both of these sugar alcohols. And it's funny because this isn't the only analysis. There's actually been multiple that I've covered that that have also been associative, largely associative, and they've also Identified arythritol and xylitol separately as being related to other negative health outcomes.

So, at this point now, I'm thinking like, man, is it really fair to to just keep saying that non-nutritive sweeteners are we know the the key word there, know that they are safe to consume for our brain. I don't think we can jump to that conclusion. I would challenge someone and be like, well, okay, show me then. Show me the evidence. Um it might be it Might turn out to be the case that we will get randomized control trials that do indicate a benefit. And to be clear the other outcomes that have been tested like

for example improvements in like insulin resistance or improvements in body weight, body fat thing, body composition as a whole. Yeah, no doubt. Like we have many randomized control trials and they all indicate benefits of non-nutritive sweeteners. I do have a few quibbles about sucralose because That one has a lot of mixed literature, but which I I think I covered like two years ago, but for many of the others, it's typically and even sucralose is going to lead to to more weight loss and fat loss, which is a net positive. I'm not I'm not here to

like ring the bell and say, "Oh, we're we're definitely this is doomsday, you know, stop all non-nutritive sweeteners." I I will again say I consume them. I still consume them. But when I communicate That to other people, I'm not going to sit here and say like like for example with the fat loss, I can I can point to many randomized control trials and say, "Look, we have the evidence indicating it is perfectly safe and very effective for weight loss and fat loss." And if you want to use it for that, like you're good to go.

Um, however, if a person says, "Hey, you know, I'm I'm having a tough time thinking, like I feel kind of brain fog and whatnot, and then they ask Me, "Hey, what what about non-nutritive sweeteners? Can I still take them?" and whatnot. Um, I mean, one, I'm not their physician, but like, if they just wanted my opinion, I would be like I I couldn't sit there and point to a bunch of evidence saying, "Yeah, they're just perfectly fine." Um, I would I would have to like sit down with them and have a conversation and be like,

"Look, we we don't have very many studies on that topic." Uh, we have one associative study that shows that there's a more rapid decline. There are some issues with that analysis, but, you know, they're not huge as far as I can tell, and maybe an epidemiologist might be able to correct me. They did do sizable adjustments for a lot of it. the greatest risk for was for people that are insulin resistant that have diabetes. There was far less risk uh almost no risk for people that don't Have diabetes that don't have insulin resistance. Um and

even in the the worst case scenario, I still I it's not like I'm sitting here thinking that non-nutritive sweeteners are the cause of cognitive decline. Absolutely not. I think that they're a minor factor. But you know my job is to look at the research and analyze is there an effect or is there not effect? If there is an effect how much of an effect and I think the answer is there could be an effect And the effect is probably small regardless even if there is an effect it's probably pretty small. So that was that was

really the the idea for why I'm worried. It's because I don't know about you, but I like to have actual hard evidence indicating yes, it's perfectly healthy. Like there are plenty of mechanistic studies that show cytotoxicity of cons of of applying nut non-nutritive sweeteners, a wide Variety of them to cells leading to death of those cells. And to be clear, obviously this is mechanism research and you're applying such astronomically high concentrations to the cells that unless you have proper controls there, uh it's kind of hard to say, oh yeah, this is biologically relevant. probably not

especially at those doses because the amount that's in the bloodstream is far lower than what's found in uh in in These cell studies. But now we're not just basing it on the cell studies. Now we have the first associative study looking at cognitive decline. It is a prospective study. They did a number of different adjustments that I thought were really really great. They looked at the dose consumption at that's like about the amount of one can of soda or two cans of soda which was like the highest level of consumption that they measured. Um so

And then we we have a lack of randomized control trials not for all the the non-nutritive sweeteners but for for many of them to look at something that I think is perfectly reasonable to look at like cognitive outcomes like we should be able to to just like apply it acutely you know just a single dose and then measure what happens like does a person's like memory uh get impacted somehow and then have other studies that last like 12 weeks of continuous Consumption at the dose that they were using that they were looking at for the

associative study like maybe two cans of soda or something and then measure and see and if if those came back and said hey there's nothing to worry about I would ease off a little bit more I'd still be a little uncomfortable because the the the time scale of those studies is only several months and the associative studies looking over eight years but I would still it would still Make me feel a lot better. Um, and even now, even with this information that I know now, I'd still like to see more associative studies. I'd like to

see more like it's I like to see some other labs approach this from different directions and see what they can come up with looking at different data sets. So like if we were to look at like NHANES data and and quantify, okay, do we see more cognitive decline? I don't think that they've Actually measured cognitive um like done different cognitive tasks. So I think that's probably not going to be possible. But if we were able to to find some other data sets that also looked at cognitive outcomes like memory, verbal fluency, and whatnot, executive function,

which is these different brain uh brain outcomes, I mean, I'd be fascinated to know what other uh data is going to come out to to to find this link. So initially I went From I went my position went from non-nutritive sweeteners are perfectly safe. Uh I'm not worried about them and I'll consume them at whatever quantity that I want. I went from that to non-nut non-nutritive sweeteners have not as much evidence as I would like but I still don't think and they have a little bit of evidence against them but I still don't think that

they're going to have a massive impact on your cognitive health and I will Still consume it I still consume them in small to moderate doses. Um, not that I sit here and like just mass consume them in general, but whenever I could avoid it, like here I've got water and sometimes I used to put non-nutrient sweeteners in here. Now I'll put like lemon juice or something like that, you know, something pretty simple or I'll just add nothing. And it's really just like small shifts like that. It's nothing crazy. You're Not going to see a video

from me, at least not based on this study, that's going to have me with a shocked expression and then it's going to be like, "Avoid all non-nutritive sweeteners from here on out." Uh, unless yeah, we get some randomized control trials that start saying, "Whoa, we have just detected an effect that uh we did not predict." Um, that would be a big red flag. Right now it's kind of like a went from a dark green solid Green flag to a slightly lighter green flag trying to go to yellow. It's not even at yellow yet. So that's

uh that's kind of where I stand anyway. And you may your risk tolerance may be much lower than mine and in that case maybe you'll just cut them out if it's no you know negative if it's not going to impact your life in any meaningful way. I mean, not not a big deal. Okay, let's get into uh and I guess I'll say for the other side and Other people may just need way more evidence actually showing harm. Not just a lack of evidence and this one associative study, but actual randomized control trials showing harm before

they'll even consider stopping non-nutritive sweeteners, which I think is a perfectly reasonable approach as well. Okay, number 69 said, "I was part of a PhD's research into artificial sweeteners in a rodent model, Cow, and highfat diet with uh reb. I'll just say the um one in parenthesis. Stevia is kind of the scientific name. I'm not sure if that's uh misspelled or not. Ree rebioside. Maybe that's correct. I've just haven't seen it. So anyway, stevia and asulfane K versus fructose and control. So hisytologology of fat cells was unaffected by artificial sweeteners with normal and highfat diet.

No impact on Offspring weight looking at influence in gestation and no increase in inflammation. So TNF alpha interlucan 6. Uh the literature is very mixed. The strongest potential effect might be on intestinal bacteria and the signaling pathways coming from that, but insulin and glucose tolerance was unaffected in our trials and nearly all papers. Okay, so there you go. So there's uh and that's true. I've, you know, again, I looked at some of this uh this this Mechanistic research and it's true that for some of the non-nutritive sweeteners, there doesn't seem to be much of a

signal at all. So, and I can't remember all of them off the top of my head. I don't remember if I looked at Stevia and ASEL fame K, but here uh we're hearing that there is no effect. Of course, I can't vet this comment. So, just be be aware of that, but uh based on the literature I've seen, it it has also been mixed. Some of it shows no Effect, some of it shows negative effects um when you're looking at the mechanistic research. And of course, this person is looking at fat cells, which as we

know from the impact uh that artificial sweeteners or non-nutritive sweeteners as a whole have on fat loss that it tends to be very much a net positive. So, would we expect to see anything on fat cells? I would say probably not, right? Uh but would we? That's completely different From what we're looking at for neurons right in our brain or micro ga. So if you were to look at TNF alpha and interlucan 6 at in microg ga which are the immune cells found in our brain um would we see an effect? I don't know uh

to be honest and I can tell you from some of the literature that there are studies that show that there's an increase in uh or some negative effects. So again mixed research. Uh, Thiago Zorta said, "To me this study seems low Quality, too. Just the fact that they bundle up all the sweeteners into tiers based on milligram consumption instead of typical consumption seems to be a major red flag. So instead of consum doing zero consumption, one can two cans or something like maybe zero consumption, one to two cans and then like four to six cans

or something like that of diet soda and then looked at the relationship. I think that's fair. I I that was one of my critiques that their their brackets for the amount of milligram consumption was kind of all over the place but on top of that they had lumped all the artificial sweeteners into one category. So, as in like so like aspartame you'll consume like I don't know 120 milligrams but then for like I don't remember exactly the the which one so don't quote me on this but like acceul K is like less than a milligram

to get the level Of sweetness that you would normally consume. So, if that's the case, then you're and you're lumping it all together and you're looking at uh 350 mg of artificial sweetener. That doesn't really tell you a whole lot about, you know, what composition of that is made up from asylame K versus aspartame. Now, to be clear, they did break that apart. That's in in for some of their analyses. And they did uh identify arythritol and xylitol as consistently even in Non-inssulin resistant individuals having a relationship with uh more rapid cognitive decline. Uh also

I'm skeptical of their cognitive decline being a line instead of a curve that gets much stronger towards uh the 80s. Uh where is the control? So I think that may be I mean that is a good point and typically you would expect you know as one ages that suddenly you would see a pretty rapid decline. I'm not to be honest I'm not sure if they showed it in A I think what they were showing if I had to explain it is they were showing the rate of decline although I guess that still wouldn't explain it.

Either way, the data that they that they base their conclusions off of was a rate of decline per year. So, it was a standardized measurement. It wasn't looking at the absolute change over the 8 years or whatever it might be and looking at different age categories. So, They had like 50, 60, 70, 80, and they had a line going down. It was perfectly straight. And I think that may just be the way that they were showing it. I'm not entirely sure. There might there's probably something there that I'm missing. So, I can't fully explain that

to be honest with you. Uh, and where's the control? So, the control is is the the low uh non-nutritive sweetener consumption. Um, That's very typical in a lot of epidemiological studies. You're not you're seldom going to find maybe not for non-nutritive sweeteners. Maybe you would find a group that a large enough group that don't consume any whatsoever, but the the low dose was very low. So it was like way less than a single can of soda. So they probably just from the amount they can consume from I don't know on once a week they maybe

go to 7-Eleven or something and grab like They'll have like a diet mound. I don't know like whatever it might be. Uh but in general they don't consume that much. So they're as close to zero as you can maybe get. uh in epidemiology that's it's difficult to try to tease out those groups because those groups tend to be so far outside the normal again that may not necessarily be the case for non-nutritive sweetener specifically but if you were to look at like I don't know we we'll say uh people who Don't consume people who consume

less than 10 grams of saturated fat okay saturated fat People try to reduce that in general, but like less than 10 grams or let's say even more extreme, less than five grams, you really have to work at not consuming five grams of saturated fat. Like unless maybe you're consuming a completely plant-based, but even plant-based, there are many saturated fats in like palm oil, for example, coconut oil, you know. So, and even olive oil has a little bit of saturated fat in it. So, it's primarily monounsaturated, but like it's really hard to just like completely avoid

these different fats. So, you know, finding enough people that would fit a control of like zero saturated fat or zero non-nutrient sweeteners or zero meat consumption. That one's a little little bit easier. But even then, you'd have to look at a huge population just to get enough people into that sample to Be able to compare everything against. And if you don't, if you don't, the consequence is that you have so much uncertainty in the control that it creates a lot of uncertainty in the entire analysis because everything is being compared against it. The medium, the

low non-nutritive sweeteners versus the control, high non-nutritive sweeteners versus the control, moderate non-nutritive sweeteners against the control. And if the control, the base of Your analysis is so uncertain, it renders the whole analysis extremely uncertain. So, there's arguments either way, but um that part I didn't find uh nearly as as bad. Uh also, I find it very hard to believe that all these sweeteners with completely different chemical composition all cause the same decline. Uh yes, that's true. So, that's a great point and that's why like looking at the data just all lumped together can be

Off-putting and it can be uh misleading. So that's why they broke them up and that's why I focused on specifically mentioning the the main drivers were arythrtol and xylitol also too many factors being controlled uh dilutes the confidence in the results when the results are already mixed and you already have uh another other problems. Yeah. So like controlling for different factors is always going to be a tough ask and especially how you Control it. So, is it continuous or is it categorical? Um, there's there's a lot of considerations. So, that's why again, I'm going to

go back to my point that we'd probably need more associative studies and then we'd probably also I would actually like to see the randomized control trials before I really start to wave a red flag over here, you know. But, yeah, great points, great push back. Um, some other comments and questions people ask like was Stevius uh assessed or sucralose assessed? The answer is no. Um I have done some separate stuff on sucralose and insulin resistance and blood sugar. I I think my conclusion was that the evidence was quite mixed and I would probably avoid sucralose

if you are worried about like insulin resistance. I I don't think it's going to like send you into diabetes or anything but you know maybe has a really small effect at kind of pushing you towards that. um Simply because the studies that I found all randomized control trials were uh you know some of them showed either neutral effects maybe like a few of them if I remember showed some positive effects but there were several that showed negative effects. So you know again kind of that in that like how much risk are you willing to take?

Okay, that's where I'm going to leave things. Uh we've been talking for almost three hours. I'm going to finish things off by Doing a little bit of housekeeping. I keep this till the end um simply because I don't want to bore people that don't want to listen to this. But I Yeah. So, when it comes to the videos, I want to talk about the videos a little bit because over the over this past like six months or so, I've been making subtle adjustments actually since the beginning of the year. At the at the end of

the year, I decided I'm going to start Adding a main points section at the end of the videos. And that's because I was getting this constant feedback of like, well, can you give me like the short version of this? And I'm like, yeah, that's fair. you you should be you should be able to have everything kind of like put together for you on the highlight points of what's what's kind of the most important takeaways and that's speaking of takeaways that's the other thing I Wanted to work on make things that are more applicable even if

we go over mechanism research to be able to integrate that with the clinical evidence and to say okay sure this is fascinating mechanism research but as always we can't base things off of mechanisms. So, we have to look for clinical research and is there any clinical research? So, uh I've been I've been working on Integrating both of those ideas together and I did that for about 6 months and it was working out okay except I was getting a lot of new feedback telling me that the videos were too long and that people didn't need to

hear a lot of what I was talking about. So, this one was difficult because I was thinking to myself, I'm just such a nerd. I love talking about this stuff and I know there are other people out there. Like, I also get feedback from people saying, "Hey, don't shorten the videos." So, now I'm stuck between two groups of people. But the thing is, if I don't shorten the videos and if I don't cut away some of the uh the the fat, the the juicy fat that's like I enjoy, but um the juicy fat around the

the main parts of the content, the videos tend to not perform as well. Some of them will perform really well and then the majority will perform not very well and the channel just doesn't Grow nearly as quickly as it probably should. Um, so I've been trying to strike this balance of making punchy videos that have high applicability, high takeaway value with everything summarized. Not everything, but like the main points summarized at the end while still giving a flavor, a taste of that nerdiness of the of the details. Like there's some times where it's just like

I don't I don't care what Anybody thinks. I I have to tell you about how butyrate interacts with your histone diaetylates. just like real quick. Give me like one minute to I I don't I'm not going to bore you with the data necessarily, but I am I just have to quick mention it because it's just like who wants to hear for the billionth time fasting is good for your health or eat protein to build muscle. Like who gives a damn? I I we have heard that so Many times. What's what people are here physionic physio

is phys based on physiology. It's like understanding how your body works. So being able to come to a video and not just understand what the clinical data says but also be able to understand like why did why did that happen? Why did people like for example with my FGF-21 video that I did? Why do people consume less protein and then they see this this significant metabolism boost as a Result? Like why does that happen? And it comes down to this molecule FGF-21. It's like I don't want to just say, "Oh yeah, it's this molecule FGF-21."

No, it's like well how does it work? What's it secreted from? How does it bind to our receptors? Like where is it binding? Why does it get released? like all these things like there's so many questions and so many things we can dive into and I I don't want to lose that. Like that's the heart of what makes physionic Special to me. I mean it's just what makes me tick. I'd like to be able to take a person on a journey, a physiological journey, and have them feel and feel satisfied that, wow, okay, I did

not know that that, you know, I can just tell you, oh yeah, a low protein diet will increase your metabolism, but like that's not that I guess that's somewhat novel, but beyond that, you probably want to know, well, why? And How does that relate to the high protein diets that also seem to increase metabolism because the mechanisms by which they work are completely different? That's fascinating, right? So I don't want to completely eliminate that like and that's never going to happen. I I I would just like I just refuse to do that. So what I've

done is I've tried to truncate the videos to make them punchier. Like I said, have more takeaways, but also still fill in Some of that physiological gap, some of that that the the mechanisms and whatnot without necessarily beating you over the head with the data. Um, and then when I get into the really nitty-gritty, I just save that for the insider content, which I know makes some people grown that I I'm leaving things for the insiders and whatnot, but it's just I I'm legitimately trying to make the experience as good as possible, grow the channel

as as quickly as possible within Ethical means, and also have enticing content for people that just want to learn more And I really love being able to have these discussions with the insiders, which I do in these live sessions that I do uh with the podcast. I I do a podcast every month for the insiders that goes over the month's content, all the takeaways. It lasts about an hour. It's much shorter than this dril that that I did today. But yeah, it's just like I need a Place to be able to like really nerd out.

and the other. Yeah. So, it's just it's kind of a necessity for me to to cut the video length and keep them as informative and helpful as possible um for for people while keeping the the I think some of those intricacies and whatnot for the uh for for the insiders. So, for the insider versions of of the video. So yeah, I I'm just I'm I'm just detailing you how I'm thinking about things. I'm still going to continue to Make adjustments. Certain recommendations that people give me like I I can see it in my data. Like

I go over my data analytics and whatnot on the back end. And some of the stuff that people have said for me to try, I'm like I know that's not going to work because I I can see it in the data. People don't respond to some people's suggestions. Um, I can't even think of any off the top of my head. But yeah, anyway, the point is that for you that just know That I'm constantly adapting. I'm trying to improve the content continuously. Um, it's just uh it's just slow going and I'm tinkering here and there.

I think this year was some pretty big changes. The whole main point section at the end uh I think went over pretty well. um and making sure that things are more takeaway driven instead of just this is fascinating but like this is fascinating plus this is how you apply it. Um I think I think that's uh that's Been a big thing for me too. Okay. Uh I think I think last podcast I mentioned that I was going to be doing a self-correcting podcast idea. So, the idea behind this, and I've been thinking about this this

entire time, from last podcast up until right now. The idea behind this podcast was that I was going to have a guest interview that guest at length about a topic or several topics and then I was not going to publish that Uh interview until I went into the literature, found studies to either corroborate or refute what that guest had said, and then I was gonna have that guest come back on and we were going to limit the discussion to just what we had just discussed. So filling in some of the nuances, but I was also

going to push back against some of their takes based on like literature that I had found. So I'd probably send it to them and just Let them know, hey, I'm going to be discussing this, this, and this like this is, you know, just so they're not like blindsided because they they would need an opportunity to look over that data and whatnot. So yeah, just just have this more open format so it's kind of a self-correcting. So then you would know unless you don't trust me, which is I mean if that's your thing then that's fair.

I don't know how you got to this point of the podcast. You probably Shouldn't be listening to me anyway. Um but assuming you trust me then I would be I I would make it a more a far more open format so people would know that the information that's being said is being vetted. So, the first half of the podcast, it would be more free flowing and the second half would be a lot more of this like digging deeper into the details while having all the evidence at hand. I love that idea. I really do. The

Problem is I can't do it. Uh I have thought about it a lot. As I mentioned, it takes so much manpower. I mean, just so much manpower. it would take me so long to be able to release just a single episode and I just I don't have that kind of time and I'm a This is it. This is Physionic. You're looking at it. So, I don't I'm going to be editing this video. I do have some people that I work with uh on a part-time basis that that Like edit, you know, the the physiotic videos

and whatnot, but beyond that, like I'm the ideation. I'm the one who creates like my rubrics. I do all the research. Like I I I do all that stuff. So, for me to sit there for for like a two-hour episode or even a one-hour episode and have a person talking at length and I have to scrub through the video and I have to uh like figure out what they said and then I have to find sources and then I have to bring them Back and then it would take me months just for a single video.

And honestly, I mean, it would be it would be such a drain on me from an energy perspective, but also like monetarily, I think I would lose out on so much because I and plus I would I I think I would end up resenting it just because I would feel like I couldn't pursue some of that those nerdy details. Like all I want to do is read research, distill it, and put it out there for the World for people to understand what that research says, which is the whole idea behind physionic, learn your body. Um,

from the from the uh macro to the micro, if you know that uh line from years ago um and I just don't think that it's possible if I had a team, which I don't want a team. I don't want a bunch of people. I don't want this to become like some massive company. Um, then I I would probably be able to do it. I'd be like the diary of CEO or Whoever it might be, except fact checked, you know. Um, and it would be a unique thing. I think that it's a great idea for someone

to do, somebody with with more capital, somebody with more time, somebody with a team of people that could sit there and and sift through it and and and do the research and then like, you know, get the get the guests to come back on and have this whole process uh work out. It's just it's just not feasible for me. I I'm a Oneman operation largely, mostly. So, yeah, it's just not feasible. Although I I really love the idea. Um the other thing is too like I I've been thinking about just like the podcast in general

and I I've already pulled away largely from having people on and I think I'm going to completely nyx anyone being on the podcast anymore. Not because I like to hear myself talk, but because I'm exactly afraid of that. I'm just a I'm just kind of tired of People coming on podcasts and just kind of spewing their BS just everywhere and people just lap it up and people we we just don't have enough of like a critical like a fair critical mind of like okay this person said that but is that actually true? Like there's no

evidence with podcasts, right? Like okay I'll give like Dr. Rhonda Patrick uh some credit here. like she'll put up uh the study title, like when a a guest says Something, she'll put up the study titled um on the screen, which I think is really cool. Um the same with with uh Jill Carvalo. He he does a great job because he'll put like reference number six and then you can go into the description and and click on uh reference number six and whatnot, which I I really like, but it's just it's so much work. And again,

for the vast majority of the time, it's just uh yeah, it's just impossible. So, I just don't Think I'm going to have people on for the podcast specifically. What I am probably still going to do is have people on the channel and what I'm going to do is highly edit. So, I'll have a small conversation with them in private, like a 30 minute recorded conversation on a very particular topic that they know a lot about. And then I will do I will do kind of like a mini version of what I'm talking about. This like

self-correcting thing where I will then Go and check after the references and I'll do a fully edited episode like a video that I like I usually do and feature that person. But at least then you know that I've factchecked everything they've said um because I've taken the time and it's it's a much smaller format. So, I only have to fact check maybe five to 10 minutes of them talking as opposed to a whole hour or two hours or whatever it might be. So, I think that's the direction I'm going to Go. And the podcast will

just be me ranting on this couch. Uh that it's probably going to be a negative for a lot of people, but that's just it's just the way it is. At least I know, you know, with my notes and my hopefully not demented brain that uh I will be able to just give more context and engage with the comments of what people post under some of the the most what I find the most interesting uh posts, which is what I I did uh today in this episode. Let's see. Um, I did mention the insiders, physionic insiders.

I'm going to mention it one more time. Um, it's the only way that I support myself. Uh, well, I do some consulting, but like largely this is the the primary way that I uh support myself. If you like this kind of podcast, this was way more free flowing than what I do for the insiders. For the insiders, it's it's about an hour long. Um, sometimes 45 minutes, sometimes like an hour and 15 minutes. And it's much punchier. So, I go through each every single investigation that come releases for the insiders. Um, and then I have

a takeaway section at the very end. So, I'm like, uh, you know, if this, then this, you know, then that. So, I I Yeah, like I said, it's much punchier. And the whole goal is just to go over all that month's content in one episode. So, if you're interested, check out the Physionic Insiders. It's linked in the Description. Um, no pressure, obviously. Uh, it releases once a month. You also get a private podcast link, so you can access it, uh, through Spotify or Apple Podcast or whatever, Stitcher, whatever you like to use. Um, and you'll

just get updated every month. Um, it's not the first of every month. It's like the first like seven days or so of the the month, but I have released an episode every month for the last like year and a half. Um, I'm very consistent with it. I Never miss a month. And you also get a ton of other perks like I've mentioned in all my videos. Um, if you want to engage with live sessions with me, I do those. Uh, you also get articles. You can have those sent to your email. Um, and a bunch

of other stuff. I'm not going to bore you with with all the details, but yeah. And the the last thing I want to say, which I always want to finish with this, um, look, I I always deeply appreciate anybody who's Along for the physionic journey. It's as simple as that. I I I'm a highly ambitious person, but I am also highly focused on the ethics of like the business side of physionic. and I'm constantly taking feedback and trying to improve wherever I can. There are limitations. Um, some things would just like bankrupt me if I

if I did them. Um, so and I also, like I said, I just don't want physionic to be this like That. Have you ever Okay, let me put it to you this way. Have you ever followed like a YouTuber or just like social media person? And I hate calling myself a YouTuber, but I technically am on YouTube. just like a social media person who's like they they started out small and then they grew and grew and grew and then they started growing into like oh what welcome Chad to the team and like Barry to the

team and Natalie and like And then they grow and there's nothing wrong with growing but then they grow to a point where it's like everything becomes so polished and so it I think it's almost unintentional They get into this position where they have no flexibility because they've taken on so many sponsorships or they've taken on so many uh connections with people or they've grown this thing that now they have to they've employed all these People so they can't be as free as they were before. And I really think that's just because now they have so

many people that depend on them for money that and which is a great thing. It's a beautiful thing to be able to build a business to the point where people are, you know, depend on you and you have all these employees and you can foster a great environment for for these people and a job, right? So that they can feed their families and All that good stuff. But there are downsides to that, right? And I I know of many over the many years I've been like just been watching t YouTube, I know of many examples

of people that have like grown and grown and grown and then they just kind of like lose sight of I don't want to say necessarily the ethics although sometimes it is the ethics but just this like sense of appreciation just keeping Things simple that I think that's my point just keeping things simple. And as much as I'd like to tear my like undergo mitosis and like have different versions of myself just like all working on all these different projects that I have that I would love to do. Um I think that the best course of

action is just to keep things um small. I mean obviously still grow as much as I can but like not have this pressure of having all these people depend on me. Um Because I think on the front end it allows me to be authentic. I kind of hate that word, but we'll use it anyway. To be authentic and to just have these conversations and uh not really care that much uh because I have wonderful people like you that support me and I don't and it's just me, right? So I don't have to like I don't

have to worry about like hey I need to be selling selling selling because I Have to be paying all these other people behind me that are helping me throughout this thing all these employees because that's just not the case. So yeah I mean just I realize I'm kind of like ranting and kind of thinking off the top of my head but I just again I just wanted to say thanks. It it means the world to me to physionic is my job. Like that is crazy to me. And I'm going to continue to push it as

far as I can. And it's not like it's going to stop. It's not like I'm going to suddenly be like, well, I've read all the studies done. I've got nothing else to say. That is not going to happen. There's too much. There's there's many lifetimes of content that I could produce and it and studies I could analyze and things I could learn. And I have another 30, 40, hopefully 50 years ahead of me. Uh, man, knock on wood. Uh, that I can continue to do this. And, uh, yeah, it's it's all possible simply Because people

like you actually, uh, listen or watch or engage or make funny comments like, "Zappy." Uh, yeah, I do know some of your your YouTube comment names and I do recognize them. Um, Little Voice is another one that that pops up. Cookie, definitely Cookie Cupcakes. Um, yeah, just like there there's just like so many people that I could rattle off the names and just say thank you to, but in general, just like if you're listening to this, thank you. I really do appreciate it. Um, yeah. I can't promise when the next episode will be. Uh, but

you know, it'll release at some point. Fizzyang's not going anywhere. So, until then, thanks for listening to me ramble about stuff. And, uh, yeah, have a great day. See you.