What You NEED to KNOW About MTOR | Dr. A Explains

When we age and when we have illness, we lose some of this natural balance that we have over the mTOR system. So some of the reasons, you know, if you look on social media in popular posts and things about mTOR, they're looking at. Hey, it's Dr. A. I've been involved in research and teaching in the integrative naturopathic medical community for 30 years now, and I've been seeing patients for a very long time. And I use this YouTube channel to answer lots of questions that we get about health. Health and healthcare-related topics. So today what I want to do is get into a question that kind of takes a step back from some earlier content we did on mTOR and rapamycin and mTOR inhibition. And what I want to get into here is some clarifying questions that came in about, can you explain this process? Obviously we have a drug that inhibits a process in the body, but we don't really get what that process does. So I thought I would take this one and kind of get into, okay, what is the mTOR complex in our body? What does it do? What are the primary inhibitory drugs that were discovered that do this and why do we use them? And then how does this relate to normal healthy function in a human? So let's get into that. So the first thing is mTOR stands for the mechanistic target of rapamycin kinase. That's its full official name. You could put an asterisk there because it used to be called the mammalian target of rapamycin for short. And then they changed it to mechanistic, but there was an expedition to Easter Island, also known as Rapa Nui, in 1964 by a Canadian group of scientists. And while they were collecting soil samples, they discovered a particular type of microbe. And what we know is there are certain soil microbes that have turned into antimicrobial drugs. Very common one that's used all over the world that most people have heard of is the drug nystatin. Nystatin is an antifungal drug that actually came from a soil organism. So again, in this vein, They were looking for possibly new drugs to be antimicrobials, because even back in 1964 with microbial resistance and all of those things that go on in killing bacteria and fungus and stuff, we're always looking for new drugs to be used. So that's what they were really after, and they wound up naming the compound that came from that rapamycin after Rapa Nui. Now the interesting thing is that drug was discovered in the 1960s, and the originally called mammalian target of rapamycin, now called mechanistic target of rapamycin. That pathway in the body was really not outlined for about 25 to 30 years after that. So it's sort of like, well, there's this drug and then a pathway in the human body got named after it. Well, the pathway existed long before we synthesized the drug rapamycin, but that's how it got named because it was rapamycin was able to inhibit it and that's how they found it. Now there's a long story about why it took All that time to find mTOR, but basically it's because in cell biology there are limitations in the way that you look at different subparts of the cell and pathways. And if you don't prepare the cells correctly for that pathway, you can wind up digesting the pathway. So then there's nothing much to study there. This happened a lot with other things like histamine in the nervous system and other things that we need to look at. So they figured out how to isolate mTOR without digesting it, and then they realized, oh, this is a big deal in the cell. But prior to that, It was just not there. You couldn't find it. So rapamycin is mostly nowadays called sirolimus. And if a drug ends in L-I-M-U-S, limus, it is normally in the category of an immune inhibitory drug, largely the T-cell, cell-mediated part of the immune system. And drugs that end in L-I-M-U-S are often used as organ rejection inhibitors. So they're used if you get a new kidney, your body doesn't like the new kidney because it's antigenic to it, we give anti-rejection drugs and the category that ends in -limus is often given for that. So most of the research you'll see on dosing for rapamycin, sirolimus is really looking at how do we dose it for somebody with an organ transplant so they don't reject the organ transplant. So it does that. It's an immune inhibitor, immunomodulatory, but it's also an antifungal drug. It is an antibiotic drug in the macrolide family. And so macrolides would be like erythromycin family or the macrolide family, clarithromycin, azithromycin, like Zithromax. Those are macrolides. Well, it's a relative of the macrolide family. So you have this drug that has antibacterial effect, antifungal effect, and then actually an anti-immune effect. And they're all somewhat dose dependent as well. So the other time where these drugs are used would be more like their off-label use. So you see a lot of content online now about using rapamycin or mTOR inhibiting drugs to help with your longevity or help with your inflammation, possibly help in cancer treatment, et cetera. And what you just want to keep in mind is that those things are, you know, they're being done. They're really being done and they're being researched. We're going to do a whole video on some of the research around mTOR inhibitors, but they're being researched and we know probably A little bit about how they work in these lower dose and infrequent dosing schedules, and a lot of it is sort of conjectural. So we're we're really pretty clear on how they inhibit the immune system at higher dose, but we're just learning now about how they might be immunomodulatory at lower doses and help with some types of chronic illness. So it is important to keep in mind that if you're moving forward and for some reason you you don't need organ rejection treatment, you don't need an immunosuppressive drug, and you're going to move forward with rapamycin or a related. Drug as a treatment for something that's not organ rejection, usually the dose is going to be lower. We'll do a separate video on dosing, but the dose is going to be lower and it's going to be punctuated, usually once a week or something of that nature. Quick plug here, if you're a healthcare practitioner working with patients with these issues, I have a CE website and I do webinars on this topic and others. So we're going to put a link in the description below to the CE website link and the particular webinar of interest. Thank you. Now, I did want to just make mention that There's this idea, which is true, that mTOR is a process that's already inside of our bodies. And so we don't want to shut it off because if we did that, we would actually just die because mTOR is involved in sensing the stimulating effects of eating and growth factors and other stuff. And then translating that through the mTOR system, which has 2 big arms and then a bunch of other things that it does, and translating that through the mTOR system into pro-cell growth activities. So obviously we always need cell growth. So it's great we have the mTOR system to help us with that. And we know we have to eat eventually or we'll die if we don't eat at all. So we have these pro-mTOR things, which are mostly associated with eating and the amount of amino acids and insulin and stuff like that. But then if mTOR is always turned on, we also then are blocking the cell recovery, the cell cleanup actions of autophagy, autophagy, autophagy, however you wanna say it. But autophagy is Blocked when mTOR is running. That kind of makes sense because we're building cells and helping regenerate, so we don't want to you know shut off our autophagy system you know forever. But we also don't want autophagy competing with building the cells. So this is why when we have a sort of a pro-growth process in the body, the anti-growth or cleanup processes slow down while the pro-growth speeds up. Now before this drug was discovered and before mTOR was mapped out, we had mTOR in the human. mammalian system for eons, right? So how is it normally balanced? Well, it's normally balanced in healthy people to a degree that you probably don't need to be inhibiting it, obviously, and probably not even, you know, modulating it because a super healthy body is going to modulate it naturally. And it does that basically through the ebb and flow of pro-growth factors and then resting states. So you could look at that as feeding, which is generally going to trigger most of the growth factors, and then fasting or non-feeding, which is going to shut off or shut down the mTOR activity and turn on the cell recovery, cell repair, the autophagy things that go on in the cells. So one way that the human body does this, even before we knew about mTOR or rapamycin or anything, is by limiting the amount of time we're eating during the day and then having a time like when we're asleep and around that when we're not eating. So natural inhibition Can be eating and not eating on a schedule. If you are constantly putting calories into your body, and you are constantly stimulating mTOR, and then that's going to have a negative effect on the cleanup side of maintaining your cells. If you're constantly fasting, you're going to inhibit mTOR, and at a certain point, the cleanup part of maintaining your cells will sort of overcome the growth part that mTOR does. Now, this is if you're doing either side of the equation, you know, too much, right? When we age. And when we are, have illness, we lose some of this natural balance that we have over the mTOR system. So some of the reasons, you know, if you look on social media in popular posts and things about mTOR, they're looking at, well, let's inhibit mTOR for longevity purposes or for, you know, help with chronic inflammation or something else. Well, that's true. You can slow mTOR down, modulate or inhibit mTOR, and that may help as you age. It may help if you have a chronic illness, might even help if you have cancer. Okay, so there are times then we might want to introduce some inhibition of mTOR. Now, we never really take mTOR and totally shut it down because if you totally stop mTOR, your cells would totally stop regenerating for the most part, and then you would die. So we don't want to shut it all the way off. But as we age, we lose a lot of this regulation over mTOR. As we get chronically inflamed, chronic illness, etc., we lose a lot of the regulation over mTOR. And then you might say, well, if this balance is so important, Why would we block mTOR with a drug like rapamycin or a relative as an organ rejection thing? Well, the thing is that your immune system cells also are responsive to mTOR. And so if I go in and I slow mTOR down with a drug like sirolimus, everolimus, then the immune cells that are being stimulated by the mTOR system will slow down. This is good if I have an organ I don't want to reject because it'll slow my immune response. It maybe is not so good if I wind up having having a slowdown in my immune function, and then maybe I'm more prone to or more open to infections and things that come along. So it's always a balancing act. And as I said, we're going to go into some research about that in a different video, but this is just an introduction. So when we're thinking about mTOR modulation or maybe inhibition, there's obviously the drug categories that can do that. There's diet and lifestyle things such as feeding and fasting in a cycle, which is sort of normal to humanity the whole time we've been here on Earth. It's a little less It's less common in modern times because of the availability of food, but that's one thing. And then there's a lot of plant and even amino acid constituents that can help with the modulation of mTOR. And we're going to do a whole video just on what those things are coming up. All right, I'm Dr. A. I want to thank you all for listening. Please do like, share, subscribe, hit the notifications. Really appreciate all of you new viewers. Appreciate all the people who have been with us since the beginning. We use the channel to answer questions, and we're going to put up some other content in the links there. Or you can just go on the main Consult Dr. A page on the YouTube there, and you can see all of our content. Thanks. I'll see you on the next video.