1 Dr Kats onPeperine and Niacin 1 | Otter.ai

1 Dr Kats onPeperine and Niacin 1

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Dr. Dmitry Kats Phd MPH

00:00

Yeah, I mean, so they, what they do is they, they're like, oh yeah, we can make it so you don't first of all, like there's a huge dose response like niacin and it's safe. Like I would say, Piper's even safer than niacin. As long as you don't like mix. I don't know, like opioids with it or Luvox. I mean, I'm just a bunch of RX like I'm gonna make that note. If you dude like, I mean, this stuff right here is like it's gonna, if you've been seeing the insulin and the glucose research I was just

showing. I mean it basically what I think it is, it seems to reactivate GPR 1098. And that's what regulates TRPV one TRPV ones just sensing. Well, I mean, TRPV one, though. It's like downstream after GPR 109. A is reroutes the niacin gets back into the cells. It's then say not inhibited. But the Oh, I see. So the Piper in seems, and this is like through stimulating cholesterol efflux out of blood back into macrophages through the age, the HDL receptor SRB. One, that's what the ABCA one expression I believe you want to inhibit a VCA one. But you don't want to you don't want to mess with SRT be one at all, and you want to hit you want to shoot it's I can't remember if it's up regulate or down regulate ABCA on. But you want to do one of those. And both curcumin and Piper and do that same thing with ABC one. And what piperine does, it's also you don't you just want to like, express it more not mess with it's on the on the protein DNA level. But and then the SRP one, which the issue is it's upregulated based on if cholesterols. Like if HDL needs to scoop back cholesterol to prevent atherosclerosis. And I've been saying this for a while now. It's like on a thermodynamic stream. And so the spike one of its vantage points of entry, and it's the CO receptor and is probably the ES protein main viral, like binding dot a docking point for entry and uptake into our cells and, you know, inside our cells through the calcium flux pushing it in. And so what's going on is that SRP, one HDL is binding to the macrophages. And the thing is, is that it's the cholesterols not, it's not getting, like there's no force, pushing it hard enough, moving it to it from you know, from HDL coming, scooping it up to binding SRB one, and, and the collapse, there's not enough cholesterol flux power to allow enough, you know, for just the cholesterol to go in there. Like it should be what what happens in the virus, the spike will sneak into there, it's like a slower cholesterol efflux back into the macrophages rate in power and volume and force. And so it's basically like the SRB ones, like staying open. And just waiting, they're like, come on cholesterol Hurry up. And what how that happens is that SRB one becomes more and more, it's like, it's, it's becoming more and more expressed. Like it's, it's upregulated if you have, you know, more and more atherosclerosis presentation, you

Dr. Dmitry Kats Phd MPH

04:20

have more esterified cholesterol leaking out of your macrophages into the, into the, into your circulation. So then that makes HDL for more liver, I'm sorry, cholesterol transport chain, it's instead of getting developed and fortified more in the liver, it has to be like it has to be you, you know, go address all this leaking cholesterol overload. And so it's, you know, like, alright, I don't I don't have time, I gotta go deal with this, you know, getting calls all the time. And so it tries to, you know, push the cholesterol back in and bind to the macrophages that that s that's our b one is The flux back, you know, reuptake, that's, this is the main one, there's another one. But this is the this is basically just based upon if that flux leads to that level, or I'm sorry, if that cholesterol esterified cholesterol into the blood leads to that level, right? And so what that so basically this is why low HDL because that your HDL is then getting used up. And they're getting, they're getting quickly developed in the liver, and they're getting quickly, like, circulated back out and vacuum through bio, and then they don't even, it's like they're not doing proper in flux, the flux cholesterol transport, it's kind of almost recursive in a circle, but nonetheless, because so the SRB one you don't want to mess with because you need the SCR b1, you don't want to artificially that's the one like a main thing, you don't want to artificially mean that you don't really want to artificially manipulate anything, but that receptor especially is like, like, it's it's all its expression is it's not the issue, whether it's up regulate, you know, ideally you want it in equilibrium, of course, but if it's up regulated, the way to get it back to equilibrium, and everything else back to the librium is not trying to down regulate it or mess with it, which that's what curcumin does it I believe, like silence is that almost and that's that's straight atherosclerosis right there, you're asking for, you don't want that, and then development into CD. So and I can show you the literature on that. But so the, the piping, specifically doesn't mess with SRB one whatsoever. Neither does nice. But it like on a causal pathway. But I think it's the inhibition, not not inhibition downregulation of ABCA one, like on a causal level. And so this promotes, basically the AVCA one is controlling that, you know, the power of the cholesterol flux back into the macrophages from the blood. So it's like the if the HDL is if the AVCA ones going too much. And so whatever, that's our B ones doing. So if you if you then don't have an SRB one, you know, it's gonna, like curcumin will do, what's going to happen, I'm not saying it's happened, like in a week or overnight, it's this, this will be yours. Probably if you have an acute case, though, that's I don't think it's a good idea, but especially like prophylactically or after the fact but it's said that reason HDL is low, it's always getting used up this is why HDL is like the leading driver of the causal always independently causally predicting dictating governing factors single factor and not just this COVID and Sarge COVID to you and all that, but ever forever since the beginning of infectious disease it is the number is the only independent causal risk factor of in infectious disease hospitalization in the general population. Okay, so if you're if you're

Dr. Dmitry Kats Phd MPH

08:46

have low HDL say as in what this virus is evolved to, it's like a co receptor that SRB one and what it's called there's the AVCA one expression probably because the whatever this crazy stuff they're doing is making it you know, there's like a, there's some kind of energy lapse energy metabolism lapse, censoring lapse, and ABCA one, and I believe this is with the, what it does with the CYP Cyto I forget the name of that there's so many acronyms, but it's basically yeah, I mean, that's what's what I believe is like the ability of stuff to get reuptake into cells. Nonetheless, alright, so, if what you want is to stimulate the cholesterol flux back into the macrophages, and whatever SRB one is just let it be, just get that cholesterol as quickly as possible back into the macrophages because if you're gonna, if HDL is gonna be like, you know, it's gonna HDL is going to do whatever it can expecting it. I don't think it's It's It's action is really like it's it's, it's thinking that the cholesterol is going to go in and out whatever rate, but nonetheless, whatever it is exactly. The virus is what you see that it's you know, either the HDL is waiting longer as it binds to SRB one because the cholesterol is not going, you know, it has it's like, Come on hurry up, you know, it's like the bridge to get and or it's like basically just getting like, you know, it's like vapid and it's not four to five, but as it is. And then so this is, so what it does is like turns into lipid rafts and gunk and this cholesterol accumulation, the virus basically, this is a very easy vantage point for its entry and replication through cells and basically taking over us as pray for the time for you know, until as best as you can. And so the sorry, gosh, trying to think so the issue is that we need to promote the cholesterol flux, that's this is for say, you know, this is for weight loss, this is for atherosclerosis, this is for multiple sclerosis, this is for many autoimmune diseases, maybe everyone this is for cancer, this is for Neuro degeneration, this is diabetes, cardio, metabolic disorders, cardio metabolic risk factors and CVG. You know, basically, like, you know, development of chronic into chronic disease over aging. These are, you know, if this stuff's you know, dysregulated and you're ready, you know, your doctor's life, you know, you need to exercise because here, you're pre diabetic, or watch you die or take these toxins. Your it's your, you know, if the more along the path, the development of these of these risk factors and into disease, you know, phenotypes. This, this, that's why HDL, low HDL is so common among diseases, a risk factor of all diseases. But so, it's, you know, this something that is, you know, this is biochemically through an energy, it's another, you know, what's the word another way of looking at energy metabolism, you know, this this cholesterol transport chain and lipid metabolism. And you can say glucose, insulin metabolism, you can say immune response, Metallian, melatonin, it's all it's all based on an underlying thermodynamics, nonetheless, I mean, so with the ABC, the ABC one SRB, one, cholesterol, HDL, those mechanisms, right, what this leads to, is, say the, so the virus, and I believe this is also related to the TRPV. One, there's an entry into the cells through the TRPV one also. And that's like, the, like, the virus is going to be like, Haha, this guy is gonna freak out if I go by him. And it's gonna, it's gonna, you know, like, it's like, almost like a venom bite, or like, like,

Dr. Dmitry Kats Phd MPH

13:44

like a BB gun or something, but like on a, on a very small level, on a small surface area. And it's, you know, this receptor is gonna go Whoa, what the hell it's, you know, when you're ready, inflamed environments, and your whole thermodynamic, you know, regulatory mechanisms are not like, working like clockwork. What's going to happen is that your, it seems to be and it hasn't been clarified yet. But with the TRPV one, it's like, you know, you're you're very sensitive. So, the things TRPV one is sensitive to is like he talks and then comes what I would say it is free radical electrons in a sense, whatever kind of whether thermal, electrochemical or mechanical, or, you know, electromagnetic so there's essentially it's a It's a receptor of it's like a thermo regulatory receptor that's very complex, intricate. Like, basically to kind of again, like an account of what's going on thermodynamically, like, this has, like, you know, so it's so if it's sensitive to this virus, right, and it freaks out, it's like, what the virus knows, the outside exposure is that people who, like basically, it's, it's probably thermodynamically attracted in some way to be like this person's TRPV ones are really sensitive, and it's going to be really easy for us to go in there to basically just tickle it or something. And basically, and this is like, through the endothelial system, like, tickle it, and this is also with like, SRB, one and Ace, two, and GPR, 109, A, and HR and, you know, there's many, there's many kind of related receptors here that are also in there, all kinds of energy metabolism, modulating or accounting. And so, the TRPV one, the, what it does is like, if you freak out a lot, right to that acute exposure, and save saying the cold, and like winter and night, the propensity to activate, like, you know, it doesn't have to be as like sharp or harsh of a, you know, of, like, nausea, stimulation into, it can be something more minor, that's why more people get sick. So it's like, you have a higher purpose, your, your TRPV ones, they're gonna sense that, you know, things a lot more, like, you know, sensitively, they're going to be like, like, like paranoid, kind of, you know, the littlest thing will freak him out. So, that's why it will happen to cold, you know, getting sick, the viral replication or whatnot. And so, once then it basically tricks it's what it seems to be part of its route of entry. It's a very intricate route that's been engineered by them, whoever they are. And so, once it gets in there, there once you arouse sets, like the TRPV one is sensitive, everything I just said what kind of thermo, any kind of like, you know, downstream energy current into one of a free radical electrons moving, essentially moving energy, you know, from more energy to less energy at the speed of light. And so and so this isn't matter, to by the way, like a wave is matter, alright, these are real, this is his, this is, you know, a force to there's the momentum of it,

Dr. Dmitry Kats Phd MPH

18:27

you know, it's moving at a speed and it has a mass, and there's an energy of it, this is a free radical energy. This is what free radical electrons do is they, they they just go from like a lightning bolt is going from less is going down straight downstream, towards wherever the least energy is, that's where it's getting moved by the laws of thermodynamics tours. So this is what this whatever this is, that's, that's invading the tarp on Monday, you know, found a strategy to take advantage of that TRPV wanted to get in or it's like from the external environments out or subsystem world, you know, like, say, the air we breathe Earth and the space and all that, to our, you know, what protects us from that is our skin. Our skin also protects us. I think very, most importantly, it's almost as if humans or humans are just word tools that the gut microbiome evolved to, to keep their worlds in our guts and our skin and body as a way to protect them and nourish them, because they're like we're gonna die from if we don't do this and find like a skin to protect us. But we can get into that later, but nonetheless. So, the TRPV one once it gets So the thing is, it's very sensitive to say that those things I just the free radical electrons right from the exterior to our interior. And our body sensing, especially in the cold, so what the, if, you know, what I've been saying for a year and a half, but I knew and I have known that nice and standalone, maybe very earlier on, but now with reiterate being more and more deprived. And I, you guys know all about that. But God, I'm holding my finger on this stupid thing. Like, you can just press it and that's so dumb. But so for the record, like you have to hold it down, and I can't, like I feel like my thumb is really hurt like my other TRPV one receptor or channeling on my thumb is probably being expressed or activated. But so that receptor also, they believed the the guy who won the Nobel from UCSF was saying in that 97 paper that and that it's like name, the cap season, vanilla noyd, blah, blah thermoregulatory vanilloid. But there's the caspia sun, you know, that was just kind of in the timeline of the research that just happened to be that first and it was given that name in association. But qasmi isn't doesn't even it's not as effective as an agonist or like, it doesn't um, it doesn't kind of you know, activate, it doesn't bind to it and can lead to what TRPV one does downstream from its activation, keep you know, going more and more, as I say, not even close to weed there's we see synergy with and we see different binding spots with and we see. So with niacin, niacin, these sensors are extremely sensitive to niacin. And I believe it's you know, nice and actually does a binding to them upon getting into the cells from GPR 109. And I believe we're going to be able to see, I believe that the flushing should go away from the, from the beginning, I'm still trying to piece that together. But the whole paper in is essentially a way more effective. And it's basically just need, like like you'll say it'll say it's not as potent as an as an agonist. So what the whole key of the agonist is, and so there's, you don't want to be oversensitive. That's putting you at risk of, of, you know, initial exposure and progression of it. So you want to desensitize it, keep it in equilibrium, you don't want to completely antagonize it, or move it that way. You know, just keep suppressing it.

Dr. Dmitry Kats Phd MPH

23:28

Because that's going to basically like you're going to you probably will become crazy, like you won't feel pain anymore. You know, you'll probably do a lot of damage to yourself like and also cold. Like you'll be you know, you won't know where it's hot, whether it's hot or it's cold outside. You You know your sleeps probably gonna get messed up because, I mean, a lot of things. It's like, you know, like, that's, yeah, you don't want that to happen. It's not homeostatic. So what you want to do is kind of facilitate and promote. Whether it's so let's say as a as prophylaxis, first, you want to maintain it, say like you're healthy. Now, what you want to do to so what what niacin binding to it, it's very potent direct binder, it doesn't bind. So when activates, it's from the intracellular side. Niacin gets into the cells we know from GPR 109, not nine, eight extra cellularly. What it does is unclear, I believe it's what it's doing then once it gets in, is if TRPV one is what's the word there seems to be like it intracellular TRPV, one on endo lysosomes, and one on the like entering the cytoplasm. And I think what's going on is once the TRPV one words friend, that niacin, that might, that might be the TPC H well now it's not that but and you see that diagram I have word the CA two plus the cell. And it's like naessens unique processing to turn into n 80 Plus but more importantly, and ADP as the endo lysosomes form. So what that will do is like so just like any in you know, any any toxins you have any pathogens particles that you haven't you know, coming in, what's going to happen now is, so it's like, nice, and it's going to be able to clear them. Okay, and this is, let's say even with with the Piper and especially, what the Piper is doing is it seems that it's Gosh, what's the way to say it? There seems to be from the extracellular side like capsaicin in that it it's the word it says it like the you know, the it literally binds to one of the sites when the sub units and it senses something, you know, the Piper in his ear, you would you would think it's like, Oh, I'm getting hot, it's inducing, like a sweating or vasodilation that's kind of part of the flush, remember? But what I think it's, you know, however does it you know, this receptor was basically meant to be sensitive to it. Like, I don't even think curcumin or spices, right. I don't think that they're meant to be for us to feel hot from it. But say the Piper and for instance, the black peppers, corns are and the leaves that they come from and from other species, they're, they're, you know, quite mild. And, you know, effervescence, I'd say, compared to in you know, spicy hot compared to the red peppers. But this is also why, you know, so the, that's the original question. I'm trying to break you know, answer everything in the world at once. But the original question the, the bio, the bio paren it's like if you know, for it's like you just need more it just happens to be need more piping

Dr. Dmitry Kats Phd MPH

28:14

but they you know, what they do is like, ah, that's so much so let's say that they can now make a product and act like they did some fancy proprietary patented high tech health science, you know, supplement making stuff, basically. So you now buy their you know, market then and be like, you know, and it looks better like well it's only 15 milligrams that's all I need. It's more bioavailable and that's it's the Piper and and same also with curcumin that the Curcumin is not going to metabolize without the Piper and I mean, I'm not going to discuss the curriculum and that's a no go. But so the Piper and just need higher dose, it does select the caspia sim, and it's they have a little bit different and different nuances, the so what you want to do so instead of the virus are these spikes, these outside exterior exposures you know, continuing to like us being sensitive to them, like oh, god damn you got in on about to be sick and disabled more. And that's you know, so instead of that what you want is the niacin and the Piper in take advantage of those receptors, sensitive sensitivity to those two things from the extracellular side for Piper and, and which seems to facilitate then the it's It's tough to explain. But even if TRPV ones like silence, it's able to rerelease it, there's a specific binding site, that is seems to be innate, similar to niacin. And if the caspia sin is, you know, it will show similar stuff in terms of many other conditions and phenotypes as the piping. Now the pipe, and there are a few studies where they show up, you know, they're, they basically, you know, I showed this in the thread within the past hour or two, on last night, where it's basically it's like, you don't need the it's like the just go higher dose with the Piper and, um, you know, it has, it has to be this way, but that's that higher doses needed, and it's gonna be still safe. It's just this is the dose responses variabilities, you know, all the way up to like thought, you know, I'd say 500 milligram dose. Now, if they'll show like in vitro, where they do the site, they try to see like how toxic it would be just the and that's not going to happen in humans. I mean, but there's this concentrations they do in vitro to identify that what you know, the limit for toxicity, this would be something like, if you just, you know, like, probably took like, you know, 100 grams. But the achievable effects, they're safe, completely safe. They should be. I feel like for humans, and that's what Nikita was saying, I agree with him about 200 milligrams, first, you know, seeking therapy, that's a good start, if you feel really crummy, that should be a good start, especially if you're already used to Nice. Now, that's the thing is now, newcomers, and say they feel like shit, which 99% of them do, of course. And that's why it's like, it's important to go start higher, get to the higher nice, and I'm really hoping that if you do the reason people are still flushing, and I'll get into that later, I'm not gonna that's just had some Nobel shit if I figured out exactly, but I'm almost there. But the reason people are still flushing say with melatonin, Gatorade, BHB curcumin, and saving Curcumin with Piper in or bio purine, or just pipe, it's there, they're simply I believe just in this could be from the very first time or second time. Whichever way it's, it's gonna be very smooth rolling in, like, like red carpet treatment for niacin into your, into your cells and to do all this properly. With with sufficient dose amount of the Piper and like right before with it. And that's that's this, I've been challenged so many people this for a while, like,

Dr. Dmitry Kats Phd MPH

33:13

you know, if you don't have you can't go to the bar and drink two sips of beer, or Zema or something. And be like, Yeah, well, alcohol doesn't get you drunk. Those people are lying. So that's, there's no, you know, there's no illogical or unsafe, like warranted worry, or risk or harm. With going at the needed doses, I've I can show you more literature. And so I feel like once we meet, I feel like what Nikki was saying 200 Sounds cuz that sounds like a good estimate. Maybe you can start a little lower. But I feel like like around 200 milligrams. That's unlike, even in what he was saying. And I kind of agree, is like do it like three times a day? Because so and the thing is also with nice, and then I'm not sure we then even have to go to even you know, two grams per dose. I feel like we can maybe just need it because they get both potentially ated through this TRPV one and the GPR 109 80. It's quick action, whole getting an old dam writing this a lot but basically what's going on is you don't want the virus or the spikes or the external exposures to come in and rattle your homeostasis by getting into your cells, the way they get to your cells. There's like I said the SRB one a two and then there's TRPV one it seems like that's like the really worried some subconscious element you can call it and say you get like convulsions, weird feelings, whether physically or mentally, and I'm sure you know, everyone, it's, it's, it's hell, but it's basically it's a, there's a, there's, it's like you've basically now it's like, what the virus does then also tries to do? Well what happens, it's like it's such a, you know, it takes advantage, it makes it so that your TRPV ones are like, activated in and what then happens is there's a calcium release that pushes the virus into your cells. Now say what niacin will do, and say the Piper and they together have a very, it seems fall into place, like oh, like you just don't have the instruction manual. But now you got to you got to empirically move forward to figuring out how to put this together. So it seems like that the Piper in a nice and say, when they both come in, you know, they both hid the cells and in activate this, say, the Piper and does from the outside, and then the nice and then is allowed to then get in, I believe through GPR 109 A, and then the flush also won't happen. Because I again, pretty sure a lot of the GPR 109 a mechanism is that there's a side part that's a defense protected, if it knows that it can't proceed further into the cells. And so the flush part is kind of the, it's it's essentially anti thrombotic, anti septic defense and to get out, you know, inflammation, and to prevent it from getting into cells to make these like, you know, these toxic metabolites, or, say, through endothelial system, you know, film and, you know, like, LPS is and toxins, Venom's and just all sorts of gunk. And that's what happens when the TRPV one gets dysregulated I'm about to get into that now.

Dr. Dmitry Kats Phd MPH

37:26

So what you want instead of the virus then getting in, right, and then also because the virus just got in, when you didn't have niacin, you're not forming into lysosomes, and you're not able to recruit, the first fall you don't and as that happens, you don't even have an immune maintenance. And so, you lose out on T cell proliferation, the regulatory, the regulatory is you'll keep that in the regulatory T cells, which that is nice and getting in through GPR 109 A into forming an alliance lysosomes and the lysosomes is the whole purpose no lysosomes is like a biodome they're creating say over this pathogen and or toxins particles that are that are you know, you know, harmful and toxic there the endo lysosomes like the bio gem, so, each CQ tries to prevent the formation of endo lysosomes by preventing what happens it will prevent the NYAS and then to get into them and this this natural niacin was meant as medicine then well first of all, this was never meant to happen. But what niacin has the ability to do is still recruit for it. But the thing is, if you know at that time, if nice and can't get to GPR 109 A through properly it's not going to be able to and then I believe on top of that, if you're immune and it's like they're like co related like if you have this more and more G Kirwin and I suppression over butyrate depletion into you know, immune and metabolic dysregulation and the Warburg effect, cell failure, cell failure, you know lack of immune maintenance, then further further all the TRPV one's going to be more and more silence to so basically I mean niacin is not going to be able to do it's going to be impeded more and more of its of its, you know, efficiency and ability and potency to you know a mass and perform more anti inflammation and essentially auto Fuji and pathogenic endo lysosomal formation into recruitment, this is recruitment of T cells. And k cells identify target. Basically what it's doing is more and more nice is getting signaled to get into the cells by the pipe run. And then the nice and still staying on it's like the niacin and the Piper and bind when they're binded to it, there's no way the virus has no physical real realistic way of getting in or replicating it. So this again, is prophylactically. And so, what then you do then doing the nice in the paper and is you It's you, you know, like, like, the flesh goes away more. And that's something in my I'm going to prepare the flesh but what happens is you you desensitize you know, the, it's like because niacin, and Piper in our like, it's, it's used to things now it's being in a homeostasis, it's being controlled by it's the bookends that it needs to be controlled by. But especially from the beginning, they quickly especially the Piper, and it's what's gonna keep doing is that if you keep having this Piper and niacin in your body going, right, like that's why we say three times a day, what it's going to do, and I feel like, you know, we won't have to do as high a dose nice and now, especially prophylactically. I don't even think we're gonna have to do this three times a day, I'm saying like, just to, like, set ourselves straight as quickly as possible. But what we're doing then is basically like, the desensitization, is essentially us keeping the TRPV one like homeostatic Lee regulated, and in equilibrium, you know, expression in like through the cells, which is, you know, that is overlapped with the whole NADP from endo lysosomes. And it's the whole how it completely regulates

Dr. Dmitry Kats Phd MPH

42:20

the whole calcium, sodium channeling through, say, the endoplasmic reticulum and the cytoplasm, the eye, and p3, nostell, p3, all that crap, but it's all basically the immune response there. It's all like to kill pathogens, and to essentially keep them from coming in. It's what you're doing there is essentially like giving the this you know, Coronavirus, no ability or spike proteins, ability to be able to even have any word to, to where it's, you know, it's not, it's against hanging on, like, look your way, it's like you have a shield. Okay? Now say after the fact, as therapy, what you need to do, what's going on then is that your TRPV one's now being more and more suppressed. It's like not a, it's like, your thing is, is it's you don't want to be like, it'll take one time for the spikes to do this. Okay, and then after that, and as it replicates basically, it's like you're going towards, you know, you know, disk, like, this is what seratonin also and all, everything gets messed up the TRPV ones basically like they have, they have, you know, tricked, you know, the spikes like haha, we've, we took advantage of your TRPV ones being ultra sensitive because of your poor health, you know, from an early age and whatnot. And you can even still be healthy. You know, there's targeting things of this, whether, evolutionarily speaking, or no gain of function speaking, but what's going on then, you know, after the fact then if you know if you have more present inflammation, more of a gut dysbiosis your you know, your pathology you the you know, your decline is going to be more grave and accelerated from there into whether sace full cytokine storm and acute and or, like a sustained prolonged you know, accumulative suppression of immune response and maintenance, which is that goes with the butyrate deprivation accumulatively as now your diet doesn't have enough butyrate and it's getting sucked up. And so what's going on there, what's getting sucked up? What's that happens is messes up the guts, species itselves their citric acid cycle. And through those cells, and they're essentially what I'm saying is the Piper and is like, the old, it's like, Everything leads and the gut, the gut species are doing there is some really intricate biochemical, you know, pathways that they, they've mastered, like clockwork, but the whole life, the end game of all these pathways, they all kind of converge to the biosynthesis of Piper in of all things. And so one of the main kind of, you know, precursors, let's call it on the way to that, that kind of culminates, this is like after this is like, say, from glycolysis, to glucose to pyruvate to so what happens is the pyruvate, then to Acetyl Co A to start the TCA cycle, you know, the Warburg effect, because the butyrate starts going other short chain fatty acids are dysregulated they are doing, so to try to keep our energy going, you know, we're going to propria Nate, or doing some weird acetate stuff, you know, over activating those parts, because we can't keep the regular flux down from pyruvate to acetyl. Co A, because butyrate is responsible for that, and the kulana sites, and this is the cells that basically directly protect give a barrier of the gut microbial species. And so what happens and also there's the species to niacin is made from

Dr. Dmitry Kats Phd MPH

47:21

tryptophan from quinolinic acid, in quinone, in, in bacteria in single celled, bacterium. And, and so, in us humans, it's a vitamin, that our body, you know, our, our cells are meant to uptake to the GPR 109. A. And so, and there are also other, you know, non GPR 109 A mechanisms with niacin, but mainly GPR 109. A, but nonetheless, the, in the Chronos sites in the gut was, say, with the interplay of the bacterial species, the the bacteria, the prokaryotic, bacterial species themselves, are able, they don't take not it's not a vitamin from them, but they, what they do is after, so say after TCA cycle, and I believe, is it pyruvate, I can't remember pyruvate are acetyl. Co A, but that's like, then, you know, as, as it goes down TCA cycle, what also happens is that, then it goes to kind of say you're looking at the diagram, it goes to the right then also, and there are other kind of intermediate pathways there that lead to glutamate. On the bottom, and at the top is lysine, and its amino acids. And then, in the middle, the main one from I believe it's from acetyl. Co A or pyruvate, or one of the one of the species that moves it over there. And what then is niacin? nicotinic? Well, I'm sorry, I'm sorry, not the quility then and was lysine cleeland, eight, and I was right. So as glutamate Cleany and whatever aspirin I believe, and so then what happens? It's seems so then from a What's the one column of bone? Oh yeah. So from glutamate, it becomes like a linear line from POC is it called Quinlan, when a like quinoa Cass, it becomes nicotinic niacin, and from aspirate becomes a lysine. And I believe there are gut microbial species here that facilitate this forward. And then from there, it's a lot of spider webs pathways, but they all kind of then reconverge along the way of from then niacin with more nice and being made, moving it to then go up. So then it's like, what's that dye thing called? Pirate pirate dime. Pirate on. So yeah, they don't make pyridine and then it kind of like a metabolite of pyridine of all things is tobacco. There's a there's a metabolite on the, on the Elana Nene or whatever pathway that from from the glutamate like say it'll be Alon Nene, I can't move I'm pronouncing right nicotine a niacin and lysine. But so say from I believe, either from the and so the glutamate either from the glutamate then, or the aspirate one of the one of the metabolites along those little you know, side Trails is cocaine, of all things. And also caffeine is I believe around through one of the other nice and, and connecting, and I haven't charted this, but nonetheless, what through all this memorize hit the Clinton eight quinolinic acid, this is the whole with tryptophan

Dr. Dmitry Kats Phd MPH

52:16

depletion going on, and oxidation. And so what seems to be going on? What sorry, it's like the butyrate. Right, like the thing is, it's like, so if butyrate goes, which is that's what I believe is what makes it quit like first of all, there's more inflammation, but the lack of niacin to the whole body what will happen is the butyrate will have to work harder, and also eventually it'll become depleted deprived more and more. And so, what this will do is make and this is remember, I was showing you with the glutamine say what the glutamate right now I was saying earlier, through like, as a branch from the TCA cycle, what will happen is the it seems like there'll be no guts species pretty much or something, something's dysregulated something's missing, and that the passion is so hard to piece together orally. Then the basically like trip to fins, it's like the butyrate species are messed up. So this, it's like pyruvate. It's not it's like the TCA cycles not able to be made. But what I think's happening, a better explanation of what I think's happening, all those things I said, they go to the, the last main thing that's like, the, the, you know, the maze ends in these in this region of the body, with these bacterial species, like, you know, doing their thing here is the is the piping piping. And so what I think happens is there is basically, I believe, somehow that goes, there's a piece, there's a lack of its biosynthesis ultimately. And whether that comes first or save the butyrate does this a snap? And so once the butyrate goes then you're not going to want severe acreages, you're not going to have then the, you know, what, you know, for everything from there that follows into niacin, lysine and the Oh, starting one. And it's alkaloids that are being used, it's like, these are like alpha noise, that with a bacterial species, it's like, it's like, they're, it's like, they're not even really worried about much of the citric acid cycle going out, it seems like they're worrying about making this pipe ring, which is an alkaloid. And they're doing special things to try to make this pipe ring. So what so it's like, however, that happens, right? Let's say, we say it's the butyrate going. And so the butyrate goes, then it's going to be less than flocks forward into the Piper. And so then, or just say, like, well, something happens, and they can't make piping. And so that once the pipe and then goes, it's like the end of this whole reaction. What happens then is, the there aren't, then it's like, if there's the pipe rings not being made, then there's, it's like getting, it's like a basin, where the flux is moving away, where every precursor before that is becoming more and more deprived. But at the same time, the bodies, it's, it's trying to make this paper and, and I'd say also probably, you know, contains citric acid cycle, but it seems like this pipeline is some kind of, like coexisting, it's almost like any d plus or something, or AGP. It's, it's, it's a, it's like the,

Dr. Dmitry Kats Phd MPH

57:13

the gut microbial species or like soldiers working in the making. So once it goes, it's like, you know, we could have the gut microbial, well, you know, then these processes I just mentioned, there. Oh, I can on hold it sweet. So there, you know, a lot of B vitamins. Um, a lot of B vitamins crossfeed cross talk with the other bacteria would feed off them or need them to be around and need other gut bacteria species to use them and whatnot. Same with like, magnesium. Saratoga, sorry, Selenium. vitamin A, vitamin C, vitamin E, vitamin D. But so and also it's like, you know with the V vitamins and the citric acid cycle, but also say trip defend the back to the gut bacteria from tryptophan to niacin, and then remember piratey those it's like I believe, I believe pirate gene. What makes sense is that the pirating is those gut bacteria species is any d plus. But say tryptophan to niacin, this requires riboflavin and B six or B seven, I can't remember which one. And so then there's, it's like, there's just a combination, not one to one functions, by any means nothing. Nothing. Not complicated, but basically and then, you know, and other nutrients and, and the beaterator of course, and then they need to make theater aid from stuff. But so what happens if once they don't have their Piper in ability to make it, they try to make it more and more and more. And probably they try to keep the citric acid cycle going more and more through the beaterator, but they're getting used up, they don't have they can't make the beat right now. Because it's like, it's like they have to work so hard because there's not an ability to make the beat rate. And so it's like, as soon as the you know, it's like they try to come back to to become, you know, rebalance everything, but it's like, as soon as they try to come back, it's like they gotta go you know, maybe Make the blu ray. And so they get used up. And so that what you know is backup, say through the propionate as an energy source to keep even them going. But so what I'm saying is that so with glutamine, we're showing acute COVID patients adults, what separated the ones who could stay at home or how to go to emergency department setting. Was this like having like a half, like it literally half of glutamine over that, like, like, because that like that was the main thing and aspirate also, but it was the glutamine that was like most pronounced because it was so distinct. No, clinicians hadn't seen something like this. And it was so defining and asked for another amino acids probably lysine were were also lowered, but it was the gluten which has had that happens before but it was like the glue, the glutamine just like out of nowhere, just halves. It's crazy. And that's the most abundant amino acid through the human body. So there's very noteworthy, and so that's probably explained now by the the glutamate being an overload. And the glutamates an overload because there's not a gut microbial species, or it's not an there it's not there. It's not in their best advantage. To you know, what the Piper is not being made, and it's like there's species that aren't their survival.

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