[00:00:00] hey, Hey, welcome back to another episode of super Yuma radio. Today is, uh, September 16th, 2020. We have a really important show today. Anybody who'd been watching me for any amount of time knows that we were the first to ever talk about rapid myosin senescent cells and the potential for rapid myosin to actually, uh, affect aging positively.

[00:00:23] There's always been a question about rapamycin for many of us who like to build muscle. And that is, does it interfere by it's effects on attenuating mTOR? And we're going to put that one to rest today, and it's very exciting. You won't hear this show on any of the podcasts because this kind of stuff.

[00:00:42] Doesn't interest people except deep thinkers like us, uh, before we get started. Oh, by the way, if you're watching the show live, you're on YouTube. We're not going to be streaming live on Facebook anymore. I'm going to talk about this at the end of the show. Um, but we've done with Facebook. We're really done.

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[00:02:11] Daniel ham. How you doing dr. Him? I call him. Good. Uh, I'll re I'll call you Daniel. You prefer being called Daniel. Damn well. That's fine. Yeah, no, no, no. Then he was fine. Yeah. Okay. So we're talking to you all the way from Switzerland, which is wonderful. And you were the lead author on a paper that looked at the effects of rapamycin on protein synthesis and muscle in aging, because.

[00:02:40] As we get older sarcopenia is a really big problem today. Uh, let's talk about sarcopenia. First of all, uh, for a long time, I said on this show, muscle is metabolic currency. So get into the gym and make a deposit today. Um, the gaining and losing of muscle [00:03:00] by the medical orthodoxy, let's say over the past 50 years has been looked at.

[00:03:06] As muscle really isn't essential for anything but being ambulatory. But now we know that muscle is actually a gland. It produces hormones. It helps us manage blood sugar levels and all these other wonderful things. What research preceded this that made you think rapamycin may have effect on sarcopenia?

[00:03:28] Um, yeah, well, it's good question. And, um, I mean, they're the original way we came to this work was, um, I guess, because, uh, when it comes to M tore the muscle field and the aging field, they, they seem to have completely opposite ideas, um, about, uh, you know, about whether mTOR is good or whether I'm sure is bad and.

[00:03:50] You know, in the aging field it's been, you know, accepted that suppressing M Tor is, you know, one of the best ways to extend lifespan. So. Things like rapid [00:04:00] myosin, protein restriction, calorie restriction, intermittent fasting, intermittent fasting. I'm fasting my last meal. My last meal last night was six 30.

[00:04:09] Uh, here it is one. O'clock my time. I'm fast that I won't eat my first meal until after the show today. And I will go to the gym and train later, I do that because of the anti aging benefits of it. Um, yeah. And so, and then of course the, the opposite is, um, I mean, largely within the muscle field, it's, it's long been believed that, uh, you know, the M tour's the good guy that's we we've always seen him towards the good guy, everything that activates them, or is going to lead to muscle growth.

[00:04:37] And that's a great thing. And, uh, I mean, we, we kind of, I came from the muscle field originally and originally thought that, um, you know, this is really the case. You activate mTOR, activate protein synthesis. You're gonna grow your muscles. And, uh, and to some, you know, and, and in some regards that's, that's true.

[00:04:55] I think you do still need, uh, an activation of mTOR and activation of protein synthesis [00:05:00] during these growth phases. Right. Um, But then, I mean, what we kind of wanted in the end, and it's been a thought in the muscle field for quite some time, that if you use rapamycin to extend your lifespan, this is going to come at the cost of, of muscles.

[00:05:16] Right? You can't have your muscle and live longer too. It's that old, old adage. Right. And I believe I believed that. In fact, I personally followed dr. , uh, introductory. Uh, protocol. And today is Wednesday. Every Wednesday, I take six milligrams of rep myosin, uh, two to reduce senescent cells and all the benefits that, you know, rapamycin has been shown to have pleiotropic effects.

[00:05:44] I have nothing to do with aging that have to do with enhancing immune function, so on. And so I take six milligrams, but when I take six milligrams on a Wednesday, I generally feel like my trip to the gym is wasted because I'm not going to see that, that muscle creation for the next couple of days. [00:06:00] But your research has given me new hope.

[00:06:01] I'm like, Oh my God, this may not be the case. Well, I mean, I'm not sure with in regards to muscle gain. So I mean, the, the critical thing here is that, uh, these mice were, were not being trained or they're not undergoing some kind of resistance training program. I mean, we really just sought to answer the question of if we just constantly surprised MTL with rapamycin.

[00:06:24] So we gave them, uh, quite a decent dose of rapamycin, uh, in their food. So they, you know, they essentially. Had high levels when they're eating over knives and they should have still had high levels. By the time they were ready to study myosin, have a 36 hour half life. Or am I mistaken? Yeah, I think it's something like, so, I mean, they still had signs.

[00:06:45] Yeah.  suppression when we collected this, this tissue, um, you know, the next day before they started their eating phase again. Um, so yeah, there was still, they should have been able to a suppression that the whole way through, I guess, through this throughout the day. And [00:07:00] so I guess, you know, what we were surprised to see was that this didn't didn't, um, you know, this didn't lead to muscle loss.

[00:07:07] Um, it, didn't also, it's an important point that it also didn't lead to muscle gain and we're not sure what would happen. Yeah. I mean, they were sedentary, right. They would sit in my seat. I mean, I personally, again, I'm not a scientist. I extrapolate from your research that of sedentary, rodents, or maybe people who aren't doing anything to promote muscle gains.

[00:07:34] They're halted from the natural progression of muscle loss from being sedentary by rapid myosin. Then I think that it may not help muscle gains, but it definitely isn't going to inhibit muscle gains. That's that's my takeaway. Well, I mean, this, this is, I guess not, not, not proven yet, so we didn't test it.

[00:07:55] I mean, these, these studies ends up taking quite a long time to do. And, uh, you know, we really just [00:08:00] tried to focus on. Whether it would increase losses or whether yeah. Perhaps, you know, attend any way losses of mass of mass. You know, across a long period of time during aging. So, you know, we clearly saw in the control group that they, they lost muscle mass, they lost muscle function, you know, in a variety of tests.

[00:08:17] So we tried to really test for things that, um, you also use to test for sarcopenia, right? In humans or muscle aging. So things like grip strength and their ability to just, just a, it's a rod and a treadmill, sorry, in a, in a running wheel. Uh, we looked at their metabolism, things like this. And so in all cases, in the control group, over the span span of our treatment period, all of the control groups sort of lost, um, lost mass lost function, showed signs of deteriorating, the tablets, and over the same period, uh, when we started treating with rapid myosin, there was no immediate boost, I guess, in function or in muscle mass.

[00:08:55] But yeah, rather it prevented this, this loss. Um, so [00:09:00] yeah, I mean, I think it will be still interesting to test, you know, whether with longterm rapamycin treatment, whether this would, uh, in, you know, interact with, with exercise programs. And I mean, resistance exercise is still the, you know, the gold standard for trying to avoid sarcopenia.

[00:09:18] Um, and so, you know, obviously, but also also dietary. Uh, uh, approaches to, we know that as we age, seniors tend to shy away from protein. Uh, they have a harder time digesting it. Maybe they have problems with teeth and animal protein becomes arduous to even consume. And the drop in protein consumption also contributes to sarcopenia.

[00:09:46] Uh, we actually talked about a study that was published maybe six years ago, that looked at. Uh, the dwindling proteins consumption by elderly people and whether it was contributing to, uh, muscle loss. [00:10:00] So, you know, it's, it's, it's, um, it's also interesting that, uh, protein, synthetic response, uh, from high leucine protein is, is, is an important factor in sarcopenia as well.

[00:10:12] Would you agree with that? Uh, well, I mean, this, I'm not actually sure about, um, you know, I, I agree that, uh, you know, in, in elderly populations it seems like some of them aren't getting enough protein. And I think there's really a difference here between. Not getting enough of something and whether supplemental level, most of that has, you know, additional benefits and you know what, actually, one of the reasons I, you know, I got into this area of research was during my PhD, I was interested in amino acids and you know, their effect on M sore.

[00:10:43] And this was in the days that, you know, mTOR was great in muscle. Um, and, uh, and, and, and Lucien of course is, is really, I mean, mTOR is very sensitive to Lucy levels. And so it's a, it's a great one to, to activate them two more and through starting synthesis more, [00:11:00] um, and. You know, and, and during my PhD, essentially, when I started, I started writing this review thinking loosely and is going to be good.

[00:11:08] And maybe this is a good, uh, you know, intervention to, to prevent sarcopenia or other forms of muscle atrophy. And when we, we closely looked at the literature. Doesn't seem to pan out. So I think it's, if you take, uh, things like leucine and, and amino acids, just after an exercise battle, just before, or just during this, this for sure can, can boost your, uh, your muscle gains, but just taking it alone does not seem to be sufficient to cause an increase in muscle size or even to prevent muscle loss.

[00:11:43] Um, and so, so I have a question for you. So from your research back then, did. A bolus of high leucine protein turn em tore on, but not turn protein synthesis on. That's what I'm curious about. Um, not again, not, not necessarily. So in some ways he conditions, [00:12:00] yes. This is what can happen. You can get activation without protein synthesis, but, um, you know, in most cases you would still get an increase in protein synthesis.

[00:12:09] It's just that this doesn't end up leading to muscle growth and, you know, it's, I mean, Muscle growth. If you want to measure muscle growth, you should, you should measure muscle growth, not, not protein synthesis. Right? And you can't necessarily correlate one with the other. Always. It's not a, you know, it makes complete sense that if you were, you know, wanting to grow your muscles, you would need to make more proteins, but it just doesn't always come out like this.

[00:12:34] No, that, that, that you're right. Because the Mo uh, muscle growth is the net effect. Of both stimulus and deterioration at the same time. So you're right. You're absolutely right. Um, the rodents were given, uh, rapamycin from what age on that, that would compel, that would compare to human age, for instance, like, were they given rapamycin at the age [00:13:00] of 60 on or 80 on or did they start earlier?

[00:13:05] So with the mice, with the mice, there were, um, either which we took two groups, one at 15 months and one to 20 months, and this would be around 50 to six. Okay. Um, and, and so we first characterized sort of the progression of sarcopenia in mice. And so we were able to track it to. Between 20 months and about 28 months, this is when you go from not being, you know, not losing muscle master a level, which would be consistent with sarcopenia in humans.

[00:13:33] Um, so that's why we kind of, we picked this treatment period, this and started treating just before we see signs of muscle loss and, and stopped when we knew we could detect, you know, significant loss of muscle mass. Now there are lots of different forms of mTOR, right? The C one is just one form. Right, right, right.

[00:13:55] So, um, do we know anything about all the [00:14:00] different forms of mTOR and how they are all effected by rapid myosin? So, I mean, so the, the, the main ones are, there's, this  complex one and there's antral complex two, and then they're, they still both contain the protein and store, but they can paint contained other.

[00:14:19] The proteins as part of this complex, that's sort of also the function over 10. So I mean, mTOR is the one that, that people know the most about. Um, and this one is more of a, you know, is directly inhibited by rapid myosin is quite sensitive to it. I want to also say that it's not a complete inhibitor of Anton, so, you know, need to be careful about that.

[00:14:38] It's, it's only a problem, actual inhibitors. So it only inhibits certain. Uh, certain targets of M chore, there's sort of this good targets and this bad targets and some targets can still be activated even with rapamycin. So what we're talking about here is a selective , uh, receptor agonist, if you will, like, they'd like, [00:15:00] it's not, it's not effecting all of em towards targets.

[00:15:03] That's interesting. I didn't know. That's right. That's right. So it it's so rapid myosin is binding with another protein and then they basically attached to the. The dental one complex and, and sort of, uh, partially inhibit the sites where mTOR would bind with other proteins and phosphorolate them, or activate them or any of it then.

[00:15:22] Um, and so some of these target proteins and still get around, uh, yeah, there's this rapamycin other protein complex and still get activated, whereas some Cod, so sometimes it's referred to even as, as rapamycin sensitive mentor. Uh, just because, you know, it's not, it's not the complete answer one that's inhibited.

[00:15:42] So there's the other one. The other complex is so complex too. Um, and so less is known about it. Um, and it can also be inhibited by rapamycin, uh, particularly by prolonged rapamycin treatment, although it's much less sensitive than an mTOR one, but again, this [00:16:00] is, I mean, this is really tissue sensitive, so, um, you know, Where the rapid myosin will inhibit mTOR or two, or not depends on the, you know, the levels of certain proteins that will bind to rapamycin and take it to the, the MTL complex.

[00:16:12] So, you know, it really depends on the tissue as to whether amps or two will be inhibitors, as well as insulin and so forth. So the other thing that I gathered from your study, which was kind of really counter intuitive, Was that  may contribute to sarcopenia in some way. That was shocking to me because we all think, as you said before, when you were in the whole amino acid area, turn em to Iran, muscle grow muscle grow, but it looks like  turned on too long, too often can actually contribute to suppression, uh, or muscle wasting.

[00:16:50] Talk about that. Right. So, um, I mean, in this case, we, we talk about, and I mean that we found in the old muscles, I guess, that, [00:17:00] that, uh, M Tobar is more active than in the young souls, but, uh, importantly, this wasn't immediately after feeding. So, you know, am tall would be, you know, you would expect it goes up and down during, during the day.

[00:17:11] So we'll go up after a meal, especially if there's a good amount of protein in there. Um, and then when you stop eating, particularly if you're fasting for a little bit longer or overnight, Then M torch would turn off and turning it off, then allows other processes to occur such as autophagy and you'll get damaged.

[00:17:28] Organelles damaged proteins can get cleared away, you know, and then you start F stop fresh. And then the next day you get a new meal, new proteins will be made so forth. And so we looked at these mice deliberately in the afternoon when they should. So nocturnal. So yeah, day is nighttime. So we looked at, at, at them essentially.

[00:17:49] They're resting period, uh, the equivalent of our night. Um, and so they're in the young mice  was basically turned off as it should be. Um, but these, [00:18:00] in these old mice, um, it was still active. And when we looked, when we used the dinings to look at where it was active, um, because like you said, we usually associate amateur activity with, with bigger muscles.

[00:18:12] Um, we could see that, uh, it wasn't just it's spread out around the whole muscle section. That was very. Specific fibers that were, uh, that had high levels of, of, of downstream mental target. So high interactivity in very specific fibers and the properties of these, these muscle fibers were, were actually, that was smaller than the rest.

[00:18:32] So they were atrophic. They were getting smaller. Um, So, you know, so in this case, we, you know, you count, be sure whether mentor is really, um, you know, contributing to this is empty driving the muscle wasting of these fibers, or does it bring action trying to rescue them? It may have been trying to rescue them from Acura.

[00:18:51] Yeah, exactly. So it could be trying to rescue them. I mean, it could also just be tricked into being activated. So, you know, as you mentioned, leucine, activates mTOR, [00:19:00] even if you just take leucine in high enough doses, it will activate Anton. Um, and so if you've got a fiber that's breaking down, right, you've got the proteins in the muscle fiber, they're being broken down into amino acids.

[00:19:10] This can then activate M Tor. Um, so potentially when it shouldn't be active, was it, was it like a fast Twitch, slow Twitch fibers? That seemed to be the most, uh, often recognized as the ones that were atrophying and calling for . So, I mean, so in the, in the, also we looked at that that would most, the muscle is a mostly fast muscle.

[00:19:35] So the mouse is quite a bit faster than, than a human in terms of muscle fibers. Um, so we didn't specifically stain for them, but the, because they were spread all over the muscle fiber. So, I mean, we suspect that there were a range of different muscle fiber types, but yeah, we would have to check, you know, directly, uh, whether.

[00:19:51] You know, so yeah, on this picture that's yeah. Are on the left. We have, uh, uh, a young mouse. The middle is an [00:20:00] adult mouse and then the, the, the, the right one is an adult mouse. That's been taking rapamycin, myosin. What do we see here? Yeah. So, um, these are for different mice and heavy chains, which, um, linked to the different properties of the, of the muscle fibers.

[00:20:15] So in red, we've stained for the, the very fast fibers in mouse. This is a type two B. Um, in, in, uh, in green, we've started, we've stained for, um, there's the slowest time, the slowest top of two fibers, which is two eight, and then in black, they're two X five. And so we've also stained for type one fibers. Um, but in this muscle, in the mouse, this is virtually no type one fibers there.

[00:20:39] So they're all tied to fibers, but there's, uh, you know, the green ones are the slowest and they have closest to the bone there. Um, there's two X, two X and black, and then, and then red to be the fastest type. And so what, what do we see in the young, the old and the old supplemented [00:21:00] with a rapid myosin is it is it's a fact that we have the more of the green that shows there's less muscle wasting.

[00:21:06] What do we, what does this show. Right. Yeah. So I mean, this, this end up ends up getting very complete, okay. To, to interpret. But, um, basically, I mean, when we go from young to old that that's the biggest change and we see overall a small loss of muscle fibers. So you can, you could lose the individual fibers.

[00:21:25] And this is most likely from. Uh, losing a motor neuron, um, as that's innovating a group of fibers, and then you could lose fibers in this process, but when, when this happens, um, you don't necessarily lose all of the fibers in this, uh, in this, this group of this, this murder unit unit, because, uh, some of the neighboring.

[00:21:46] Uh, axons related to other motor units and then reattach to these, these muscle fibers and then joined them up with their motor units. So some motor units that essentially get less motor units, uh, but they get bigger. [00:22:00] And, uh, and this is the master. So from the tibialis anterior, so the front of the lower leg, um, and.

[00:22:06] It's believed to be relatively good at this renovation process. So can capture a lot of the fibers that would otherwise lose. But so what we see in this age mouse is they lose a few fibers, but the actual fibers themselves get, get quite a bit smaller. And that particularly happens in the fastest of the fiber.

[00:22:23] So the two B fibers show the most dramatic, uh, atrophy. So I'm sorry, go ahead. No, go, go, go. So then when we looked at the rapamycin and mouse, what we saw was that, uh, in particular, the two way, and the two X fibers seemed to be bigger. Um, and we also saw a switch, a bit of a switch towards having more to a fibers.

[00:22:46] Um, and what you might be able to see that is this, these green fibers is that, uh, in the, in there. Control mouse. These little green fibers are quite spread out. Um, you know, there's not too many of them clump together. Whereas if you look at the rapid myosin [00:23:00] traded one, there seems to be some quiet clumps of these brain fibers.

[00:23:04] So what we think this is is that there's been a loss of the motor unit. And then the five solidation almost a consolidation. Yeah. Yeah. Right. So this would be the loss of one motor unit. And then these fives have been picked up by neighboring ones. So then they become the same as the rest of the fibers in that motor unit.

[00:23:23] So you get these, these clumps of five. I want to talk about innovation for a second. Right? So. One of the things that people take rapamycin that I take rapamycin four and then twice a year, I actually take a five day round of amoxicillin is the reduction of senescent cells. We understand that these senescent cells produce inflammatory cytokines that make everything around them, sick, uh, and slowly senescence is attributed to the cells around it.

[00:23:52] And senescent cells grow in abundance, blah, blah, blah. So. Is this the reduction of senescent cells [00:24:00] possibly playing a role in the preservation of muscle. And if so, is it through, uh, does it reduce the impairment or does it reduce the impairment of the innovation to these muscle fibers? So, so, I mean, we didn't check directly for senescent cells in the muscle.

[00:24:18] I mean, There's, there's not usually strong numbers of senescence and sales in muscle themselves. Um, but it's very possible that, I mean, we did see reductions in inflammation, you know, consistent with a reduction in the secretary, fentanyl from senescent cells. So, you know, it's very likely that this was improving or reducing the number of senescent cells in other tissues, which could have been led to an effect on, on, um, On the muscle.

[00:24:43] So, I mean, there's lots of secondary, you know, there's whole body effects there. Well, we know, we know from research done on elderly people who have taken end sets. So as you age, uh, and we couldn't get into all the mechanisms, but as you age, a whole [00:25:00] scale, inflammation goes up and as the body becomes on fire, so to speak the, uh, workout that you just did gets less attention.

[00:25:10] To repair and recover and see a greater protein synthetic response. So anything that reduces wholescale inflammation in the body makes workouts more productive. So it could very well be that that also suppresses the. The cannibalism of, uh, or anibolism cannibalism of catabolic effect. And so it preserves muscle.

[00:25:37] Could it be that simple? Could it just be inflammation here? So we definitely think that this is one aspect of it. I mean, the, I mean, Yeah. So we did see a systemically Lola of cytokines. So that's not in the paper, but we've, we've looked at it separately. Um, and within the muscle, um, the immune response within the muscle was, was clearly, uh, you know, a [00:26:00] strong, uh, strongly associated with age.

[00:26:02] And then it was also reduced by rapid mice and largely. So, I mean, for sure, I think inflammation contributes there and the anti inflammatory effect of rapamycin. Most likely also had a positive effect there. Um, but I want to go back to the, the nerves you mentioned before. Um, and I think that this one ends up being, you know, a really tricky one because, um, for sure this is probably also infected by, um, Uh, by inflammation and at some stage, you know, during the normal aging process, as you start to lose these, these motor neurons and, uh, and then the muscle can cope with this partially by this renovating.

[00:26:38] Um, but then eventually it struggles to cope with this. Um, and actually one of the really interesting things we found here was that it depended on the muscle as to whether rapid myosin was effective. So it was effective in the, in the tibialis, anterior, for example, this is the muscle you see here on the picture.

[00:26:56] Uh, but in the gas stroke, on the back of the leg, it was not at all [00:27:00] effective. Right? So. No change in muscle mass. And so we were quite, you know, we were puzzled about this, you know, why would rapamycin be effective in one muscle and not another, and largely, you know, muscles are often thought of as essentially acting the same way being largely the same, except for maybe fast, slow properties.

[00:27:18] Oh, the base muscles that are fast. Um, and, uh, you know, they both age that's for sure. And so we were quite puzzled by this. Um, we first looked at an mTOR signaling. Maybe  signaling is different between these two and that wasn't the case. Um, they both increase with age and decrease with rapid myosin. So, so that wasn't it.

[00:27:37] And then what we decided to do was extract RNA from these muscles, along with a couple of others, uh, sequence it, and then try to look for. Signals that might, you know, differentiate these muscles and are kind of our first hypothesis was well, maybe muscles age differently. And you know, this would be a fascinating way to try and understand the different mechanisms that control aging [00:28:00] in different muscles.

[00:28:00] Maybe different muscles need different interventions, you know, to be able to slow aging. Um, but what we, what we basically found was that. All the muscles express, different levels of genes to start with. I mean, they all perform different functions may need to express different genes. But in fact, the response to aging was really very similar.

[00:28:19] This was whether it was a slow Twitch muscle or fast Twitch muscle, the muscle Heartland, whatever it was all relatively the same. Um, and it only came when we started to look at the response to, uh, to wrap a mice and where we started to see a difference. And, uh, while in the, you know, in the. In the TA, there was basically only and official effects of in mice.

[00:28:39] And we had these sort of anti-aging signature where genes would change. They had went up when I went down and they were reversed by rapamycin. And this happened for not all of the aging changes, but a lot of them, whereas women, then we looked at the gap I'm struck. We saw both pro and anti aging effects.

[00:28:56] So, you know, there was still. Um, you know, [00:29:00] positive effects of rapid bison for sure. But there was also other genes that were increased with age or decrease with age and then further decreased or further increase with rapid myosin. Um, and so, yeah, it suggests that it really depends on the balance between, um, you know, that the positive effects of rapid myosin and percent, perhaps side effects of rapamycin as to, you know, whether the muscle will be beneficially affected or not.

[00:29:23] Um, and did the gastronomy. Actually re uh, reduce in size with age or did it kind of take care of itself? No, that's not. In fact it was the other way around so that the TA aged one of the less the least. So it was, it dropped about 12% between, you know, adults and very old. So the very old mouse, he is about 80 years of age.

[00:29:47] Um, whereas the gas stroke dropped almost double that amounts. So, you know, it's quite sensitive. So what we think is the TA is actually able to cope with this, this negative effect of rapamycin, [00:30:00] uh, where we've, we've kind of traced this, the side effects back. And what we think that they are, is negative effects on the nerve sexually or the.

[00:30:08] Well, the axons where we have to test this in a bit more detail, but it looks like these, these side effects are, could, could be related to the motor neurons, the axons or the nerves. Um, I, I wanted to, I want to take a quick commercial break. I've got a question about blood flow when we come back. Um, I want to understand if you looked at blood flow, uh, as well as, uh, as the, uh, nerve density, because we know now that a lot of, uh, Neuro pathologies that affect motor skills.

[00:30:43] Start with reduction in blood flow to the nerve that causes the nerve to stop doing its job. We're going to take a quick commercial break. Stay tuned. We'll be right back with more superhuman radio. When reps with the weight of the world.

[00:31:00] [00:31:00] Welcome back. We're talking with dr. Daniel ham. We're talking about rap, myosin and muscle. Very very interesting discussion because we're just learning about it. Now. In fact, I asked dr.  if I take my six Milgram's on Wednesday, but I have 350 grams of hi Lucy protein throughout the day, it was five or six meals, you know, isn't there a negative effect on turning them tore off.

[00:31:28] And he said, no, one's looked at that. No, one's looked at consuming high protein. In the face of taking a rapid myosin, but that's a different discussion. So let's talk about blood flow. Did you look at blood flow at all and its relationship to supplementation in the elderly rodents? No. In this case, unfortunately we, we never looked at it at blood flow or yeah.

[00:31:50] I mean we, yeah, so I w I wouldn't be able to speculate on what potential effects. Yeah. I mean, I mean, trying to find the pathway of [00:32:00] action. Uh, it seems fascinating to me. So, you know, there was a study published that we talked about on the show last year that showed that a single bout of intense resistance training, reduced senescence cell accumulation in muscle.

[00:32:19] So by 42%, which was significant, that's a significant reduction. Yeah. And this was in. Um, middle-aged individuals and they had, they were smart enough to do two groups, a low protein and a high protein consumption group. So we could say, Oh, you know, uh, even cause it happened in the high protein consuming groups are the same 42% reduction.

[00:32:43] So we know that turning M Tor on with protein doesn't seem to, uh, negatively affect the ability for. Uh, an exit about a resistance training to reduce senescent cells, which was positive because that, that, that, that [00:33:00] was the first time I thought, Ooh, maybe M Tor. Isn't the problem, you know, um, go ahead. I'm sorry.

[00:33:07] No, no. Well, I mean, I think, um, we ended up mixing two, two things here. I mean, exercise, uh, um, Don's active, I game chore, but it also activates autophagy. Um, and I think the danger gets here is if you're activating them or. Um, independently, perhaps through amino acid supplementation without the exercise.

[00:33:28] This is where, you know, you may have a further impact on senescence. It's, it's hard to say. Um, but you know, independently, when you exercise, you know, you already turn on autophagy and that's, I think probably one of the. You know, the big beneficial effects of exercise we're getting health anyway. So, um, one of our viewers on YouTube faith fitness guy says, does the negative nerve reaction occur in younger than 80 year old range?

[00:33:59] That this is a [00:34:00] good question. We're looking at elderly rodents here. Do we think that we see, we would see the same thing in younger rodents? So I, I doubt very much that it's having a negative effect directly on the nerves. I mean, what we think is, uh, that it might be, and I, and again, this, this requires, uh, you know, some additional studies to really show this clearly.

[00:34:21] Um, but what we think is during the normal span of aging, Um, if you are losing motor neurons then, or you're having the damage, then you need to be able to run, pay this, or you need to be able to capture these, uh, these last five years. Um, and you know, if you're impairing the ability of the nerve to remyelinate yeah.

[00:34:43] Itself. So, um, or all the cells around it to do this then, and it may, you know, in the end effects, uh, the nerve, you know, if it's already being damaged. So yeah. I don't know regarding whether you're, whether this would affect young people as well. Well, but I suspect it would [00:35:00] be rather a case of. If there's damage going on, it may impair the ability to repair this damage and you end up getting, getting worse in the nerves.

[00:35:09] So, you know, again, enter is not always good. It's not always bad. And it really depends on the tissue as to what role it plays and even the cell type. And, you know, so within the nerves, uh, MTL can be too active sometimes and then bringing it down is helpful, but it can also be, if you, if you block it, When it needs to be activated, then you can also cause problems.

[00:35:30] So, you know, it gets very tricky in the end to, to try and, you know, uh, combine all these different possible effects of a blanket's suppressing of mTOR across tissues, you know, and you really have to view each of these things as, um, you know, individual questions, whether it's during aging or during another, um, you know, pathology or in young people having said that I'm, I'm not sure that it would be.

[00:35:56] Recommended to take rapamycin as a young person, you know, [00:36:00] anyway. Wow. You don't, you don't, you don't, you don't need it. You don't need it. Uh, you know, um, an interesting discussion we had with dr.  when he was on the show last time was, uh, his conclusion is that rapid myosin was, uh, an onco drug, a chemo drug.

[00:36:19] I'm sorry. Um, because it. Reversed tissue aging. And he said, old people get cancer. Young people don't get cancer. Uh, young people have fewer senescent cells. Old people have lots more senescent cells, rapid myosin didn't directly inhibit cancer, but by making tissue younger, you, you will less likely to be able to have cancer.

[00:36:46] And I keep coming back to. Uh, the anti inflammatory effects, uh, dr. Matt, Andrew who's. Uh, my personal physician I've talked. He he's the one who prescribes a Z-Pak for [00:37:00] me twice a year. The FDA has approved a zip, the myosin, uh, to be used for anti-aging, uh, because it literally in five days reduces. All the senescent cells in your body by 97%, this has been shown in research.

[00:37:17] And we were talking about this one day and he said, said that he prescribes as if they're myosin for people who have a extreme inflammatory disorders. He said, it's amazing at reducing inflammation. And if we look back at. What senescent cells do. They basically, he turned the body on fire. You have a lot of senescence cells, you've got a ton of inflammation.

[00:37:42] It's producing all these inflammatory cytokines and chemokine and all this other stuff. That's just screwing up everything around it. And so, you know, and, and, and vasculature seems to, uh, constrict when. There's a lot of inflammation. We see [00:38:00] this in, in neuropathies, for instance. So neuropathy is now we know, start out by inflammation, which we, you know, that type two diabetes type two diabetes is usually one of the implications is, is chronic inflammation, um, inflammation, uh, starves the nerve and the nerve starts to die.

[00:38:20] And so you have. Uh, hyperalgesia or, or, or one of these conditions that is associated with the onset of neuropathy. And so it could very well be that the reason that rapamycin works as you pointed out in this study is because of the collateral effects. Of wholescale reduction in inflammation and all of the cascading effects of what that does to nerves, blood flow, and even, and possibly even a cannibalism may, maybe, maybe, uh, you know, one of the reasons that we have a harder time building muscle when we're older is because we're, we're [00:39:00] so hyper inflamed all the time.

[00:39:02] What do you think? Um, yeah, sure. I, I think, um, You know, uh, anything that can, you know, reduce the amount of senescent cells and particularly if you're not having to take this constantly, but you know, every now and then, um, to, you know, to reduce the, the burden, I mean, obviously. A cell becoming senescence is, is not, you know, it's a bad thing that they're accumulating, but it's not necessarily a bad thing that it happens.

[00:39:27] It's, you know, it's there for a reason, like, you know, like most things, um, it's there to, you know, protect against this cell eventually becoming cancerous, um, right.

[00:39:40] Cancer cells turn off, uh, you know, cell death and, and, and senescent cells also turn off cell death. So, right. But yeah, but then they become non proliferative, which is what you would want. You'd rather that version than the cancer. Um, but I completely agree that, you know, getting [00:40:00] rid of these, the cells and, you know, periodically makes perfect sense then, you know, the research supports this, I guess, at this stage, um, Yeah.

[00:40:09] I mean, with re with regards to rapamycin. So we, for sure think some of the whole body effects and, you know, potentially reducing senescent cells might be one of those, um, could be having, you know, beneficial effects on the muscle. Um, but I want to also say that, uh, we know that, um, the results direct effects within the muscles.

[00:40:29] So if you, uh, if you activate MTL constantly within the muscle, um, rather than leading to muscle hypertrophy, this actually. Uh, causes muscle atrophy eventually. Um, so, you know, it's, it's not just a case of, you know, it's, you're suppressing inflammation systemically, and then, you know, this is a, as in having beneficial effects, we think that there's, uh, you know, real damaging effects of MTL being activated within the muscle.

[00:40:56] And suppressing this probably also has beneficial effects. [00:41:00] So, so let's talk about this, uh, pulsatility that the body seems like in all areas, we talked about it before the show, you and I, dr. Don layman's lab up in, uh, university of Illinois had done some fantastic studies back in 2007, 2008. Yeah. Showed that they will look, his interest is more, uh, the protein synthetic response of dietary protein.

[00:41:26] And they discovered, and they used a wide variety of proteins, you know, soy protein and beef protein, and whey protein and egg protein were King because they have lots of leucine. They're very, very bioavailable. Um, but his lab did a study that showed that, uh, consuming protein any more often than every two or two and a half hours reduced the protein synthetic signaling.

[00:41:54] Which speaks to turning M Toronto on all the time. And all of a sudden things don't happen. So the body [00:42:00] likes M tour to turn on, and then it likes M toward a turn off and the other things autophagy. And of course when there's a there's there's autophagy, but there's baseline autophagy. This is autophagy that's going on all the time, whether you're eating or not.

[00:42:15] And the amplitude. Between baseline autophagy and a peak or tophi G a event is critical to the efficiency of autophagy, but more importantly is critical to the protein, synthetic response. People who don't have a very, very good baseline of autophagy. And then a high stimulate of autophagy. Don't see the same protein synthesis.

[00:42:44] We did an interview probably a seven, eight years ago that showed. That protein synthesis is dependent. It's efficiency is dependent on cycling M Torah turning on, uh, uh, autophagy. [00:43:00] So the body doesn't want the foot on the gas all the time or the foot on the brake all the time the body responds. And that's why it's so misguided.

[00:43:08] I have a friend that 15 years ago said no, no, 15 by seven years ago said. Um, I'm, I'm stopping. I'm not going to eat red meat anymore. I'm not gonna eat, drink dairy. Um, I'm avoiding anything that stimulates IGF one. I'm going to add anything that stimulates mTOR because he thought he was going to live forever.

[00:43:27] He's not doing well now. He's just not. And so this is idiocy to think that, Oh, just turn em tore off all the time and we're going to be great, or just turn mTOR on all the time and we're going to be super muscular. It doesn't work that way. Speak to that. Yeah, you're right. Yeah, you're exactly, uh, right there.

[00:43:45] I mean, your mTOR is for sure an important, uh, protein, um, and it controls really, uh, a lot of things. So it senses it senses whether the conditions are right to grow or the conditions rights to rejuvenate or, [00:44:00] um, or recover. And so, and it does this by the levels of amino acids that are available. The levels of energy available and the level of growth factors.

[00:44:09] Um, and so when it becomes active, it'll make new proteins. Um, and it should only do this when the conditions, the rights to do this. Um, and then it's also important that it then switches off. You know, just like it's important that we sleep. Um, you know, it's important that MTL takes a break, lets these other processes become activated and clear away the junk.

[00:44:31] Otherwise you keep making proteins, but you end up making more and more or junk. And if you build up more and more junk and uh, and, and this is also one of the theories of aging is that you. You build too many misfolded proteins and you accumulate junk essentially. And that's why autophagy works really well.

[00:44:51] Uh, and that's one of the reasons as well, why things that reduce protein synthesis or AMS or signaling can also be beneficial because you reduce the junk [00:45:00] load essentially. Um, and you know, so it's important that it really, it really important that it stays in balance. There. Um, you know, but I want to also say, I mean, M story is still important with the muscle within the muscles.

[00:45:11] Well, to be activated during growth situations. So for example, if you, and we've done this in the, in the lab, if you knock it out in March, so, you know, developing mouse, then, um, this leads to, you know, very poor muscle quality and, and the mouse, um, you know, eventually dies at five or six months, months old.

[00:45:30] Interesting. You know, too little mentor is for sure bad and particularly during important events where it's needed to be activated. Um, and then, you know, too much as well, you know, like you said, foot on the gas all the time, you know, this leaves, you know, chance to rejuvenate or recover and, and you can just cope, also causes problems.

[00:45:49] I want to take our last commercial break. When we come back, I want to talk about two things, uh, what you feel that clinicians and lay people take away from your work, but more importantly, you've devised a [00:46:00] way to. Uh, measure this kind of stuff, right. Then you guys create like this hole that other labs can use to evaluate, um, let, let's talk about that when we come back from the break.

[00:46:09] Okay, great. All right. Stay tuned. We'll be right back with more.

[00:46:17] welcome back to the super radio. So, um, before we talk about what you hope clinicians and lay people take away from this, talk about this, uh, this, um, way of. Uh, measuring gene expression in skeletal muscle that people can use to evaluate aging. This is something that all labs have access to. Right? It's a web app.

[00:46:38] Right. Right. Everyone has access to this, you know, even if you want to look up your favorite gene, you can, you can look it up. Um, so I mean, this, this was something we, we really wanted. I mean, we've, we find this, his area of research interesting. And, and, um, were quite invested in trying to understand better, you know, what's causing sarcopenia within the muscle.

[00:46:58] What's the, you know, [00:47:00] signaling events that are leading to this. And so we can try and better understand, you know, what treatments might be effective, uh, against it. And so, yeah, what we wanted to do was, I guess, give many people access to, you know, the data that we've created in a really easy to use manner.

[00:47:14] Um, so you can do your own tests. You can do your own analysis of this data, you know, within this, this, this, um, um, and so this, this was, uh, created by, um, the alcohol, right, is, um, um, we probably played a really large role in the paper and to cope with all these large data sets. So this app was created by a, by Anastasia Bush.

[00:47:37] She's um, she's a, uh, a co first author on the paper. And so this was, this was her focus, developing, um, this, and so yeah, what we really wanted to do was to, you know, to show people. Uh, easily, how, um, you know, how the genes genes were changing with, with agent this, you know, what we consider to be a well documented, well characterized study.

[00:47:59] And so they could [00:48:00] see, uh, you know, how genes might be affected by by age. Uh, but also, so then by, by rapid rapamycin and where we're slowly adding to these over time. So we have other ongoing studies where we're going to continue to, to, you know, to bring new data sets is calorie restriction is another one we'd like to include there.

[00:48:17] Um, and yeah, we hope that it will, will help advance them. Is there a URL that people can go to the average person could go to and she does? Um, yeah, it's cool to SoCo Atlas. I'm going to type it. So it's  yeah. Sarco Atlas let's yeah. Cool. Let's see. I see. O R E okay. Hold on. S yeah, say it again. So it's taco Atlas dot cycle.

[00:48:49] Oh, stock sidecar, SoCo Atlas, a T L a S dot S I C O R. C S C I C O R E. Yep. Okay. [00:49:00] Uni best still C H will you, will you, uh, email it to me after the show so that I can show him I'll post it in the final show? Cause I don't, I don't want to get it wrong and then people go that doesn't work. Um, but yeah, if you'll email that to me, I'll, I'll, I'll let people know about it.

[00:49:17] What do you hope this research does for, you know, clinicians and lay people? Uh, pointing at this aspect of rapamycin. Um, you, do you have any hopes for it? Yeah. Um, yeah, absolutely. I mean, at this stage, what we think it does is kind of paved the way for, um, for human studies. Um, and yeah, I mean, the, the. With these kinds of things, the proof is in the pudding and we've, you know, we've tested in mice and it seems like, you know, overall it's quite beneficial.

[00:49:49] There might be ways that we can, you know, we can overcome these, some of these side effects as well. Um, but I think that the, you know, the time is right to. Uh, to start a trial [00:50:00] in humans. And then the problem is, would be of how, how to do this study. Uh, and, and for me, this study would need to be, would need to be really longterm to be conclusive because, um, we're not sure yet where the rapid myosin it would be.

[00:50:14] You know, rejuvenative weather, whether you could take it already being sarcopenia and you might get improved, or whether you would need to take it over a really long period of time. You know, in which you see in the control group, significant muscle aging. Um, so we're, we're trying to answer this question as well in mice of whether we can get, you know, benefits in very, very old mice.

[00:50:35] Um, but, uh, yeah, a lot of people, not a lot of people in my audience want to beat subjects in the test. Correct. There you go. So you know where to, you know where to get humans, if you want them fantastic. Yeah. This is fascinating stuff. Like I said, you know, I'm, I I'm. I actually didn't use rapamycin for a very long time because of my fear that it would inhibit, [00:51:00] um, muscle.

[00:51:01] Okay. And the truth is that I seem to put on muscle fairly easy. And since I've been taking, I've been back on my protocol, which is just a couple months now I'm taking six milligrams, uh, every Wednesday for me. Um, and I don't seem to be losing anything in the gym either. So, um, I just makes me feel better.

[00:51:22] Cause I used to be filled with angst. I would say take it and think, Oh great. Now I'm not going to, I'm going to go to the gym for nothing for the next couple of days. And obviously it's not for nothing because all sorts of benefits of physical exercise, but this is very promising and this is, and I love that more and more people are looking at rapid myosin and doing research search on it.

[00:51:41] I mean, I really think that when. Uh, some group starts to look at rapid myosin as a better alternative to reduce, uh, chronic inflammation, uh, and reduce senescent cells. You know, [00:52:00] um, we just, I came out of COVID-19. I say we came out of it, you know, it's pretty much behind us now. Um, and I had a doctor from the UK on he's originally from Brooklyn, dr.

[00:52:12] Michael Lasante. And he published a fantastic paper showing that senescent cells were the targets, uh, of the COVID a virus. They took, uh, senescent cells hostage and turned them into replicating factories. This is why elderly people were so devastated by. The virus and young people weren't it was just the sheer volume of senescent cells that they could take advantage of.

[00:52:44] And he showed that using drugs like rapid myosin, uh Zithromycin these drugs that focus on reduction of senescent cells was the way to keep people from dying and even [00:53:00] prevent people on the front lines from, from getting infected in the first place. And right around the time I had him on the, uh, diamond princess, which was the cruise ship that had a lot of people who had COVID-19 on the ship.

[00:53:17] And there was a couple, a husband and wife, the husband was the recipient of kidney transplant and he was taking Sarah Lima's daily, which is rapamycin. And his wife was not. They both got infected. She had to stay on the ship for like a month. They sent him home. He had a mild fever for like one day and he was fine.

[00:53:44] And now I understand. This doesn't prove anything because science will say, well, this is an N equals one. We don't know anything. But then when you look at all the research that dr  has put out there, that dr. Lasantha has put out there showing that things that reduce senescent [00:54:00] cells reduce both the likelihood of being infected and the mortality rate of being infected and.

[00:54:09] I mean when you start looking at these drugs, I think, I think doctor  is right. It's a very simplistic thing to say that if you reduce the, the biological age of tissue, you're less susceptible to age related diseases. And I would lump into that sarcopenia. I would lump into that. So now how's it working? I don't know.

[00:54:32] Is it really working? You know, I don't know, but my God it's, it's it's really, I mean, I look at rapid myosin, you know, uh, individuals who takes your Lima's for kidney, uh, uh, rejection. Uh, they have far less, uh, occurrences of the seasonal flu, uh, various vital, you know, it's thought that it's thought that Sarah Lemus and rapamycin reduced immune response.

[00:54:59] Cause that's what [00:55:00] well we'll, if it causes anti-rejection, it must reduce. And now we're knowing that we know that's not dr.  has done two good studies that show that these individuals on these drugs for long time, from a far less likely to get sick in the first place, which flies in the face of, Oh, they have re reduced immune response.

[00:55:17] So it is rapid myosin. And these other rapper logs are very fascinating. And I think that you're right on the bleeding edge of what you're doing and moving forward. Cause I predict that. Time will come that every person, 45, 50 years or older will start taking a rapid log of some sort. Yeah. I mean, do you, yeah, you could, could be right.

[00:55:40] Um, yeah, there's certainly seems to be some, some, some clear advantages to it. And, um, yeah, I think that, uh, you know, a couple of things need to be worked out. Of course, the, the dosing regime. I mean, we just constantly treated, um, but. You know, in a minute, it seems to be the treatment protocol [00:56:00] generally for the humans.

[00:56:01] So I mean, some of these things will have to be tested. And, and again, the point that you made earlier about it potentially inhibiting strength gains. And I think that that's that side of the possible in my mind would still need to be, you know, thoroughly tested and, and I'd be very interested to see whether, you know, over a long term training program.

[00:56:23] You know, whether they, you, if you were taking rapid licenses at the same time, whether this impacted, you know, gains in muscle mass, I'm going to find out I'm going to find out over the next year. Because my goal, my goal is at 20, uh, 2021 to be in my best shape ever at 62 years old, uh, 63. So we're going to say, we're going to say, and I'm using a lot of other things too, but we're going to see if it inhibits a.

[00:56:46] My ability to gain muscle. Listen, I want to thank you so much for being on, we have some other questions, but I'm going to let the good doctor go because these questions are tangential. So we'll address them. Uh, but thank you so much for being on the show today, and I hope that you will come back. Well, I [00:57:00] don't want the music come on yet.

[00:57:01] Uh, thank you. And I hope that you'll come back as new research comes available. Absolutely. Thanks a lot. Take care. Uh, okay. So before we go into a break, I'm going to go ahead and just pop some of these questions up. Um, okay. So Metformin appears to only help people who have type two diabetes already. Uh, dr.

[00:57:24] we've had a conversation. And then we talked about it on the last show that he has stopped promoting Metformin, uh, as a, a cinematic. He says it only helps people who are sick already. Uh, and that sickness being typed today. Beatty's also also. It should be understood that Metformin changes the gut microbiome.

[00:57:47] And since we don't know a lot about gut microbiome right now, it is thought that those changes are not great. Okay. Again, uh, rapamycin doesn't change the gut microbiome, but Metformin does [00:58:00] Metformin works through the gut. So I would say that Metformin is only a good idea if in fact. You already have type two diabetes, uh, a better alternative is intimate and fast thing.

[00:58:14] Calorie restriction to start to get blood sugar levels under control, instead of using something like a Metformin, number one, uh, faith fitness guy says, uh, thanks to dr. Ham for your dedication and, uh, and your research. Absolutely. Uh, then we have a couple of questions up here, uh, faith that this guy also says.

[00:58:34] That he's guilty of two and a half hours getting at least 35 to 40 grams of protein. That's that's the perfect, less than that is the problem. Less than that is the problem. Doctor Don layman's results. While only looking at protein synthesis does indicate. Okay. As we said earlier, protein synthesis is, is optimized.

[00:58:57] When autophagy occurs as well, [00:59:00] fact that they saw the greatest protein, synthetic response and muscle gains at a protein pulse of no more, no more than two and a half. No less than two and a half hours. So two and a half, three, four. They're all good. But once you get below two and a half hours, you don't see the, the valuable protein synthetic response from the meal, which tells us indirectly that autophagy is working because we know that if autophagy is not in its proper pulse, you doc, you're not going to see that, that protein synthetic response.

[00:59:33] Um, as far as. Asleep, as long as you're not, you know, this idea that people have to wake up at 2:00 AM to have a protein shake in the middle of the night. Uh, it's crazy. You are really setting yourself up for disorders and diseases, because if we know anything about, um, we know anything about diseases like Alzheimer's disease from, um, [01:00:00] uh, shows that we've done in the past with dr.

[01:00:02] Dale Bredesen and others, we know that. Fragmented sleep. Almost always produces misfolded proteins that are consistently in the disorder of Alzheimer's is. And if you want waking up at two o'clock in the morning to throw a protein shake down, you're shutting off autophagy, but more importantly, if your body's busy digesting food, you are not going to go through the normal rhythmicity of sleep cycles, just because you lay still for eight hours and keep your eyes closed.

[01:00:35] Doesn't mean you're sleeping. Sleep has specific architecture that having a meal in the middle of the night, completely disrupts. So as long as you're getting your, you know, seven to nine hours of steady, good restful sleep at night and not waking up to do something stupid, like throw a protein, shake down and you're eating every two and a half to three hours.

[01:00:54] You're going to be fine. You're going to be fine. Alright. We're going to take a quick commercial break. And when we come [01:01:00] back, I want to tell you why I am moving to only streaming the show live on YouTube. And more importantly, an article that I wrote all the way back March, about the role of vitamin D three and sun, not only protecting you from getting COVID-19, but also protecting you from dying from it way before anybody else talked about it in March, it's on my website.

[01:01:25] You can check and see if I'm lying. Is now coming full circle and being recognized by many of the, uh, people, uh, including dr. Fowchee, believe it or not. Even dr. Fowchee is talking about this now. Uh, it, this may be the strongest thing you can do to protect yourself from developing. What, what do I do developing COVID-19 stay tuned.

[01:01:52] We'll be right back.

[01:02:00] [01:02:00] welcome back. I'll be real brief. I even have a little banner to put up, look at live videos. We'll only stream on YouTube. We're not promoting Facebook anymore for anything. Um, if you didn't here already, Facebook is blocked me from doing live streams because they accused me of making a post. That I didn't make.

[01:02:24] Um, you make a post on Facebook that goes against the community rules. You usually get a message that says we remove this post because it goes against our rules. And if you've done it before, then they put you in timeout for 30 days. Well, claim I made a post on September 11th that I did not. The post was something derogatory about Sama bin Laden.

[01:02:50] Could you imagine. Facebook book said that making a derogatory comment about a terrorist was against their community rules. [01:03:00] Now I did not make this post. I didn't, um, I've never seen the post before they sent me an image of it and I'm like, I didn't post that. Then I thought, well, maybe somebody hacked my account posted it.

[01:03:14] But they couldn't be because I still would've got that message that said, Hey, you broke our rules. We're removing this post. And now we're going to ban you from doing live streams for 30 days. I never got that message. So it's complete hogwash. But what it really means is that, you know, Facebook can do whatever they want.

[01:03:36] They can actually affect your income negatively. If for whatever reason they don't like you. Um, Facebook really is big brother. They really are. Mark Zuckerberg wants to his own currency. He, you know, he wants everything. He wants it all. He feels like he can make it all happen because he has Facebook and he has all these people.

[01:03:55] He controls, he controls their opinions. He controls [01:04:00] whether or not they communicate with their friends. So. I'm only going to be doing live streams on YouTube, which means that if in fact you want to participate, live, you'll have to go to YouTube. And I'm asking people to at least please subscribe to my channel so that you'll get the notifications.

[01:04:21] When a show is coming up, like this one you'll know, Oh, wow, Carl's going live. This is what he's talking about. I can't listen lie, but at least I'll listen later. The other thing is the only other place that the video will be available from now on is that supreme-a radio.net. We're redesigning the website.

[01:04:38] There's a little challenge right now, but every page. Of every podcast has this video too. So if you like videos, you just have to go to superhuman, radio.net, find the show, you like click and go to that page and you have your choices. You can listen on the player, you can download the MP3 to your phone.

[01:04:58] You can watch the [01:05:00] video or have obviously if you subscribe to one of the podcasts. Uh, aggregators like iTunes and Stitcher, uh, iHeart media, or any of those, you can go there and listen to it on their app. Replays will be available on Facebook. We're debating whether to do entire replay videos or just excerpts of the video.

[01:05:22] And I think we're going to do excerpts of the video. I really don't want to do much with Facebook anymore. In fact, I don't even want to spend any money advertising anything on Facebook anymore. I just think Facebook sucks. I really, really do. I'm not just saying that out of frustration because of what they've done, but the reality is that they really don't give a damn about anybody except themselves.

[01:05:47] So that's it. If I sound like sour grapes, I am. Uh, from now on YouTube is the place to go. If you want to participate in the, in the, in the live show. Now I have to thank, uh, Aiden Ray, [01:06:00] because he posted this and tagged me in it this morning. So hold on, let me get it.

[01:06:09] Oh, what the hell is? Why isn't it up there? Okay. Hold on, hold on. I'll bring it up. Here we go. So Aiden re posted this on Facebook this morning. And said, Carla, Nora, you've been saying automation is the new selection pressure where you get your information from. And it's true. I've been saying that for years now, the new evolutionary selection pressure of whether or not you will be healthy and thrive and live whether or not you'll be healthy enough to have children, whether or not your children will be healthy enough to live.

[01:06:38] Is no longer feast famine. It's no longer, uh, the climate, cause it's not what we're talking about. Climate change, but it's all livable, no matter what it is now, where you get your information from it's where you, because the information you get influences, the decisions you make the decisions too, eat or not eat or what to eat or sleep or not sleep.

[01:06:59] So [01:07:00] it really comes down to the information. This is why organizations like Facebook. Uh, Twitter and the media are so powerful today because they will give you information. And if you believe that information, it will dictate your decisions. And if that information was flawed, if it was biased, if it, there was an agenda behind it, and it's not accurate information, you're going to make decisions that are going to impair your health.

[01:07:25] Maybe shorten your life. So in March of this year, I wrote an article that said, um, the relationship between the sun and COVID-19, and it's still on the website. You can, you can, you can search it on Google. You can Google superhuman, right? Uh, sun COVID-19, that's all you have to do. The article come up. And I showed him that article and cited science that proves that a.

[01:07:54] The higher your 25 hydroxy levels. Your . If you're supplementing with D three or you're in the sun, [01:08:00] the least likely you are to catch the virus. That was just proved. And I did a show two, three weeks ago with an Israeli scientist who proved that a well done study has now showed that the higher your vitamin D levels, the least likely you are, it'd be infected by this virus.

[01:08:18] Think about that for a second. Do you hear anybody talking about that in the media? While everybody's waiting for a friggin vaccine that may or may not work for 50% of the population. So if you're not already taking 25. Uh, uh, vitamin D three Kohler calciferol you should be, if you're worried about this virus, how much should you take?

[01:08:39] Get your blood levels tested, go to any lab tests. Now, those places in your area have your blood levels tested results comes back at two days. You want to be up in the 50 nanogram or above, but no higher than 80 nanogram range. So the sweet spot is 50 to 80. If you're not there, [01:09:00] start supplementing, start with 5,000 or use a day and have your blood work done again in a couple of weeks and see where you are, but get into that 50 to 80 range and research has been shown now that the higher your D three levels are the least likely you are to die from this virus.

[01:09:17] Is there any reason why Fowchee isn't on TV every day, telling people to go out and buy vitamin D three? Oh, wait. That's right, because. He was the CEO of the vaccine company. That's rushing to market a potential vaccine. No, I'm not. He's making money from it, but they already said the vaccine is only going to be 50% effective.

[01:09:40] That means that one out of two people are still going to get COVID-19 even though they get the vaccine. But one thing is for sure, it's conclusively shown that vitamin D the three works at protecting you from getting the virus or dying from the virus. Yeah. Facebook wants us to all be sheep. You're right.

[01:09:58] You're absolutely right. [01:10:00] I just saw this to Allen. Uh, Gary, thank you so much. Great show and tire series on the body's response to pulse into vet. Yes. Yes. Steady state administration. Gotta get back to work. He's right. Everything from fish oil. To growth hormone likes to be pulsed, or it becomes ineffective.

[01:10:21] Getting back to this topic. If you have not read the blog post, I will post it in today's show, go to  dot net, find today's show. And in the description, I'll have a link back to the blog post, but if you don't need to be convinced by a blog post, get your D three levels tested. Keep them between 50 and 80 supplement with vitamin D three.

[01:10:43] Stop worrying about COVID-19. That's the truth. When you read the article that I wrote, it's very well sourced for research that I provide scientific studies and it's even effective at keeping you from getting it [01:11:00] HIV. Think about that for a second. Like who, why is it every, why is it every doctor in the world, auto dialing his patients and saying, I'm sending you lab, uh, re prescription.

[01:11:13] I want you to have your D three tested now. Why, why aren't they? Oh, wait, because it's not a prescription drug and big pharma doesn't make a nickel on it. I saw an article the other day that said if every diabetic in America understood that going on a low carb diet. Reducing their carbohydrates increasing their protein and fat would completely reverse their type two diabetes.

[01:11:42] Six, six major pharmaceutical companies would go out of business in a day. Think about that for a second. Think about that. Why isn't every doctor telling every one of his type two diabetes [01:12:00] patients, I'm going to reduce your medications. I want you to stop eating carbs. Why are they sinister? Do they want people to stay sick?

[01:12:09] I don't believe that. I don't think doctors do. I think doctors are worried about being sued because if they don't follow the standard of care that is accepted by the American government, they end up getting sued and lose their license. It's time for people to wake up. We are in a Renaissance right now, a thought.

[01:12:33] And it's not the thoughts, but the fact that people are starting to think, we need to question everything today, even what I'm saying, go do the research, find out for yourself. But the bottom line is we have to stop taking everything. The media, Facebook, Twitter tells us and, and forming opinions using it because they all have agendas.

[01:12:59] They [01:13:00] all have a reason, a bias. They all want us to do things. They want us to take actions and they want those actions to be what they want it to be. V3 D three D three. Keep yourself healthy. Keep your family healthy. I will going to say goodbye for today. We have a good shows the rest of the week. Thank you for those who showed up on YouTube today to parts of participant I'm sorry.

[01:13:26] Participate. Live. We're going to try to get a movement going and get more and more people to subscribe to the YouTube channel. So there'll be notified of shows. And of course you don't have to be here, live to be notified. You can always go back and watch the show later. And of course, visit supreme-a radio.net often.

[01:13:44] Okay. That's all I got for today. Thank you for being here and we'll see everybody tomorrow with more. Share the show, please share the show, share the show. [01:14:00]