What You ACTUALLY Need To Know About MTOR And Aging | MTOR's Role In Aging And Longevity

In the other sections of mTOR, we'll get into the weeds of, is that a good idea? Should we always use rapamycin? Should we use certain types of rapamycin? Should we use super low dose or should we cycle it? But then also, what about these other things like— Hey, I'm Dr. A. I've been teaching and researching in the world of integrative naturopathic medicine for 30 years now. And during that time, I've been seeing patients who have cancer and chronic illness. I started this YouTube channel to answer questions people have. Today I want to start a series on mTOR and its relationship to the drug rapamycin and how that works in your body. But I want to just do an introductory here. So one of the things that we want to consider is that mTOR is a set of mediators that are biochemical pathways that help in the maintenance and production of cells, cell turnover, Et cetera. Like all pathways that are built into us, it's a good thing. You hear about things like mTOR inhibitors, like rapamycin, for example, and you think, why would that be good for me? But everyone who's doing it says it's good for you. So why would inhibiting a natural pathway that helps me maintain my cells, et cetera, be good for me? Well, that's kind of what I want to get to here today. So the The first thing is, is that mTOR is sort of little m, capital T-O-R, mTOR, and it's the mechanistic target of rapamycin. So the first thing that you might want to wonder is, why do we have a pathway mediator named after a drug? And the reason is that we humans discovered the drug rapamycin around 1964 or so, and we really didn't fully elucidate the pathways that mTOR works in until really the '90s, 1990s. So, there's about a 25, 30-year lag. Now, they knew that rapamycin did stuff. We'll get into that in a second. And, they knew that it had effect on some mediators, but why would there be this lag in cell biology between the '60s and the '90s in figuring out what mTOR does? It seemed like it should be doing a lot. The short version of the story, and there's lots of videos on this, is when they would go in and they would look and try and isolate these Pathway manipulators like mTOR1, mTOR2 that help with the pathway mediation. The process they were using to try and isolate these things would actually degrade them, and they didn't realize that. So initially they thought, oh well, these are minor effectors of the cell and cell health. But what they were looking at was that they'd burned up a lot of these mediators, so they couldn't, they couldn't really see them in their full flourish. So they found ways to take the cell apart without harming too much mTOR1, mTOR2, and that suddenly turned to Oh gee, we have a big effect. It's not a minor effector of the cell, it's a huge effector of the cell, cell maintenance, cell homeostasis, stuff like that. So what is rapamycin? If this is the target of rapamycin, that would mean that rapamycin does something to mTOR probably 1 and 2, and it turns out it inhibits or slows down mTOR 1 and 2. So what was rapamycin doing between 1960 and the '90s that we were using it for as a drug? Well, initially it was found to be an antifungal. Fungal drug, but also an antibiotic, an antibacterial drug. It is technically— it came from a soil organism that they isolated it from, and it technically is in the macrolide antibiotic family. So that's things like erythromycin, azithromycin, clarithromycin. Rapamycin is one of those. So it was being used sometimes as an antifungal, sometimes as a macrolide antibiotic, but also it was starting to be used as an immune suppressant. That seems very different from antibiotic and antifungal. Although if we know now, we look at repurposed oncology drugs, the repurposed oncology drugs, a lot of them are antifungals and antibiotics because they're also immunomodulatory. Rapamycin can be at different— at high doses, immune suppressive, can be at low doses, maybe immunomodulatory. So it fits the pattern. So it started to be used in organ rejection protocols so you wouldn't Reject your new organ that you got transplanted. So rapamycin been around a long time, and here's the thing: if you think of the pathway coming in, and then you have the mTOR complex of mTOR one and two modulating cell maintenance, cell growth, stuff like that. What rapamycin does is in a non-uniform manner, meaning it hits the two points differently. It causes what's called a steric block, which means it doesn't shut them down. If it did, you would. Die basically, but it modulates them downward. So it's an incomplete block of mTOR. So when we say rapamycin is an mTOR inhibitor, yes, but it's a steric inhibitor that hits in a nonlinear fashion at the two points and doesn't block them totally, which is great because then it doesn't wind up killing the organism or the human. Quick interruption from the regular video: If you are a healthcare practitioner and you have an interest in this topic, we're going to put a link in the description below to my CE website and specifically the webinar. That is about this topic. We'll see you over there. Thanks. So why would we want to slow mTOR down if it's helping us? Well, one of the things that can happen is although the mTOR complex has a net positive effect on cell growth and maintenance, there's a balance between growing the cell and then removing the cell when it needs to go away through programmed cell death, autophagy, autophagy, autophagy, and those. Those are normally in a homeostatic balance. But if we get processes such as precancers or cancers, or we get processes such as hyperstimulation of the growth side and diminution of the take the trash outside, essentially, then the mTOR system might need to be calmed down. Now, we're talking about rapamycin, the drug, right now. We'll talk about other things that do this, but it's sort of like the natural process that the mTOR system is supposed to be doing of maintenance is skewing towards building cells a little too much and not taking the trash out, not taking the bad old cells out. So mTOR inhibition can help with that. Now, if you're not using rapamycin, which also goes by the trade name sirolimus, that's just rapamycin. If you're not using it for organ rejection and certain other immune inhibitory things, then you're going to be using lower doses and you're going to try and hit a modulation point, not a suppressive immune So often for things like overall health, longevity, stuff like that, they'll use lower doses as they go along. Now, the next thing is, well, if this is part of the way the human evolved and the way the body works, are there natural triggers? Like what causes mTOR in a human without the drug interference to upregulate or downregulate? Well, high amounts of protein trigger mTOR to go up. High amounts of insulin trigger mTOR to go up. Fasting states trigger mTOR to go down. There's an amino structure, an amine-like acid, taurine, makes mTOR downregulate. Even though it's in the amino family, which comes with proteins, taurine actually is downregulating to it. Also, if your vitamin D metabolism is well-balanced, it regulates mTOR. Another immunomodulatory drug we like to use, low-dose naltrexone, is actually an indirect modulator of mTOR as well. So it's not just rapamycin. But then if we take a step out and we think, well, what other things that I might like eat or consume would have mTOR regulatory, mTOR inhibition things, things that you hear about a lot in the botanical medicine space, like curcumin, resveratrol, quercetin, used for all sorts of human health things. Those are mTOR modulators, mTOR inhibitors. Saccharomyces boulardii has components. We use that to help people restore their gut microbiome and stuff. Also has components that are mTOR modulatory. In the big picture, there's lots of things that do it. If we get back to just nature and how, why would I trigger mTOR? Well, why would high amounts of insulin and protein trigger mTOR? That's because insulin is going to go and do a number of things, but one thing it's gonna do is go to your cell membrane receptors and feed the cell. Glucose is gonna go inside, et cetera. Well, that turns on A cell-feeding mechanism. Amino acids come from proteins. When amino acids come in, we are also going to turn on cell-feeding mechanisms. Well, it turns out that in between the cell-feeding mechanisms, mTOR complex upregulates when it sees a lot of insulin or a lot of proteins because it thinks, oh well, we're in the business of making new cells. So it's going to go on. Well, that's great unless you happen to have cancer brewing or some other thing, in which case then you might want to modulate it. The other thing which is looked at, and this is an area I don't really talk about a ton, quote unquote longevity medicine. The idea behind this, we have this sort of one way of our body being as we're a baby and growing up, and we're very much about building on and being bigger and all that. And then we have adulthood, we're kind of, you know, at a homeostatic level, hopefully. And then as we start to age, we start to sort of lose regulation of some of these pathways. Well, what the longevity folks often look at is, well, are there things that I could do to chill out some of these processes that are pushing me into— it's sort of a net positive balance that I don't want with cell turnover and lack of old cell removal and stuff. So they look at, well, let's inhibit mTOR. So in the other sections of mTOR, we'll get into the weeds of, is that a good idea? Should we always use rapamycin? Should we use certain types of rapamycin? Should we use super low dose or should we cycle it? But then also, what about these other things like Like how we eat that modifies mTOR, how our vitamin D is metabolized that modifies mTOR, maybe using some, something real gentle like low-dose naltrexone, et cetera, et cetera. All right, well, that's the first of many on mTOR, the target of rapamycin pathway that got named after the drug rapamycin was named. I'm Dr. A. 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