[00:00:00] Carl Lanore: [00:00:00] welcome back to another episode of super human radio. Today is May 4th, 2020 we're 47 days into. A quarantine, self-imposed lockdown, keeping people safe. You see, I've got my, this is my covert mask. This is it. I walked into Kroger's today. I don't know why everybody put their hands up. I had to take it off like that.

[00:00:21] I don't want to scare people. Anyway, we have a great show. Uh, this is a topic that we've talked about for years, but we keep learning more and more. We're going to talk about, uh, the aging brain. And just a moment before we get started, we have to pay homage to our title sponsor, legendary foods, the makers of fine.

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[00:01:50] All the things you buy there, including the ridiculously amazing tasty pastry. And we're going to hide some things here. I'm going to bring my guest on [00:02:00] now. Make things look pretty here. Let's get rid of that. I produce my own shows, you know, welcome to the show, dr Lily Mojica. Herati how are you?

[00:02:11] Dr. Lilianne Mujica-Parodi, PhD: [00:02:11] Thank you so much for the invitation and so happy to be here.

[00:02:14] Carl Lanore: [00:02:14] You've got good information that we love to talk about on this show. Uh, and, and we've been talking about the ketogenic diet in specific since 2000 and. Five believe it or not, before it became involved. Dr Morell DePasquale wrote a book 35 years ago for athletes using a phase shift diet, as he called it, which was a high fat, moderate protein during the week in a car brief feed on the weekend.

[00:02:39] And a lot of people saw great results from that, both in performance and, and, uh, body fat, Redis distribution. So. Um, your study is called diet modulator, brain networks stability, and a biomarker of brain aging and young adults. Why this study? What preceded this study that [00:03:00] required you to take a deeper look?

[00:03:03] Dr. Lilianne Mujica-Parodi, PhD: [00:03:03] Um, well, so one of the things that I think, um, makes my lab a little bit unique is that we tend to be very, um, question driven rather than technique driven. Which is to say that, um, usually people kind of work in some particular area and they focus on that area for most of their careers, and they become sort of the domain experts in that area, um, over many, many decades.

[00:03:31] And in my lab, we seem to be sort of drawn to questions very much at the edge of what's known. And then we follow the questions, and that sometimes takes us across many different, uh. Areas of a field or even across fields. Um, so initially the question that I was grappling with, um, 10 years ago, 20 years ago even was about [00:04:00] stress resilience.

[00:04:01] Um, originally. In the context of psychiatric illness, trying to understand why some individuals were more vulnerable to psychiatric illness than others. And if we could understand the circuits that are responsible for one type of psychiatric illness versus another, if we can diagnose them based on this regulation with those circuits.

[00:04:20] Um, but gradually that work then led me, um, to stress resilience, thinking mechanistically about the way the circuit works. And one of the things that is very well known. In stress research is that the brain, um, becomes temporarily brain damaged under stress. That is to say there are parts of the brain, specifically parts of the prefrontal cortex and hippocampus that behave as if you were actually, um.

[00:04:52] You become brain damage and over short periods of time, that could be temporary. So often you probably have experienced this [00:05:00] phenomenon of, you know, when you're stressed, you start losing things, right? Or if for people who are, um, afraid of public speaking, they'll give a talk and then they'll sort of forget what they wanted to say.

[00:05:10] Um, but over long periods of time, so particularly when you're dealing with people who've been in chronic stressors like combat, um, that kind of damage can become permanent. And it turns out that. The mechanism behind this, and this was something that even though I've been working in that space for awhile, only became really clear a couple of years ago, that the mechanism behind that brain damage is actually that the neurons become insulin resistant.

[00:05:38] So if you, if you think about it so that the rest of the rest of the body could be absolutely not insulin resistant, but there's something about glucocorticoids that. Disabled neurons by making them insulin resistant. And specifically what that seems to do is to impair the ability of neurons to [00:06:00] effectively utilize fuels, specifically glucose.

[00:06:03] And as a result, they don't function properly and the circuits become disrupted. Cognition is disrupted. And so I remember looking at this, so remember, this is in the context purely of stress research. This was reported initially, to my knowledge. Um, by, I mean the people kind of working in that space for Bruce McEwen and Robert Sapolsky, um, who are the dominant people, um, who were doing the animal research mechanistically on trying to understand us.

[00:06:33] But I remember reading one of the popsicles, these, uh, articles, and this was back in 1986 was the article and seeing that he had this little footnote to this mechanism, which was that. When he said his animals, he tones, the neurons recovered. And so here's a mechanism where on the one hand, I was pretty shocked to find out that [00:07:00] the mechanism for how glucocorticoids actually impair neurons is through their ability to utilize glucose.

[00:07:05] So here's evidence of insulin resistance of neurons, which I have to say like in a neuroscience space, it was pretty controversial because until recently people didn't even think that neurons utilize insulin. The assumption was that neurons were not insulin dependent. Um,

[00:07:23] Carl Lanore: [00:07:23] but then we went, I have to stop you there.

[00:07:25] But that is, is really, uh, in direct opposition to the discovery about eight or nine years ago that the brain makes its own insulin, which tells us that insulin is so important for the brain, that it doesn't even want to depend on the pancreas.

[00:07:43] Dr. Lilianne Mujica-Parodi, PhD: [00:07:43] So, so interestingly enough, you know, once you start searching, you see that there were clues all along, there are all sorts of clues.

[00:07:50] And one of them was that there are, you know, there's this insulin degrading enzyme. And the prob, the purpose of the insulin degrading enzyme, as you might imagine, is to degrade [00:08:00] insulin, insulin in the brain, which doesn't make sense if the brain doesn't have insulin. Um. But, and you know, and, and there are receptors for insulin in the breakfast.

[00:08:09] But what I'm saying is that one of the interesting things, so, you know, I came from a background in mathematical logic, you know, initially, and then moved into theoretical physics and whatnot. And these fields are very much about integrating, um, many different areas, but biology tends not to work that way.

[00:08:27] People tend to focus on their own specific cottage areas. And as a result. Um, it was very possible even two years ago to find very high ranking neuroscientists who would argue very strenuously that the brain does not utilize insulin. And in fact, to find this in medical textbooks at the same time, that if you actually dug, dug things out a little bit, you would actually find that there were papers in nature and NAS that actually were reporting.

[00:08:59] The [00:09:00] effects of insulin on the brain. So, I mean, there's this, there's, there's an advantage in specializing in the sense that you can have a very deep knowledge about what it is you're doing. But the disadvantage is sec, because become somewhat closeted in terms of your understanding of the larger context.

[00:09:16] Right. Right? And so, so my point is that on the one hand, like, okay, so here's this amazing piece of information from my perspective of the stress researcher is that the mechanism is insulin dependent, but even more amazing piece of research that was just sort of thrown in there. What is that ketones for able to bypass this insulin resistance so well.

[00:09:40] Well, okay, so

[00:09:42] Carl Lanore: [00:09:42] I've got, I've got, I've got two more questions. So from an evolutionary perspective, does it make sense why when you're under great deals of stress, the brain, the brain wants to not access those stressful events any longer? You know, in modernity, stress is [00:10:00] synthesized. By watching the news and so on.

[00:10:03] But, but one of our evolutionary edicts is to be aware of the danger in our environment. But unfortunately now, because of the internet and everything, it goes way beyond our environment. Is there some evolutionary connection to why that would have been a good thing to be able to have stress disrupt certain neurons to where certain memories may have been stored.

[00:10:27] Dr. Lilianne Mujica-Parodi, PhD: [00:10:27] So the important thing to understand about these evolutionary explanations is that you want to be careful that you don't lapse into what's known as just so stories, right? Where we say that again, you want to be careful, not you particularly. I mean, one wants to be careful that one doesn't lapse into with, you know, just so stories.

[00:10:49] So it's possible to come up with a potential explanation. That is very reasonable. But the issue is, what often happens in evolution is that an [00:11:00] optimizing over one parameter, you optimize over another. And so if your top priority as an animal is avoiding predation, Mmm. They could be that your top priority is mobilizing glucose into the muscles.

[00:11:14] Mmm. And they eat, you run as fast as possible. Okay. But the areas of the brain that. Suffer for. It may not be, you know, that those may not be the, like

[00:11:27] Carl Lanore: [00:11:27] in other words,

[00:11:28] Dr. Lilianne Mujica-Parodi, PhD: [00:11:28] there's a trade off. There's a trade off in, in getting away from the animal you may have to take from somewhere else. And so what often happens is that not every biological solution is optimal overall overall possible parameters.

[00:11:41] There are trade offs in biology, and very often what happens in biology, we see this, we think an aging is that the body actually protects itself by. Mmm. By reducing its consumption because it has less access to it. So it kind of re optimizes so that it can do [00:12:00] with less. But what happens as a result is that cognition takes a hit.

[00:12:05] So, you know, um, it's, it's good to sort of keep the wider context in mind.

[00:12:11] Carl Lanore: [00:12:11] Okay. So, so talk about this study. How was the study designed?

[00:12:18] Dr. Lilianne Mujica-Parodi, PhD: [00:12:18] Mmm. So starting from this place that I described this, this initial study by Robert supposed to be 1986. Um, and I'm not that old. So I was, you know, I was a kid. It's not like I was reading this when it came out, but at the same time, I, you know, that's the beauty of having this historical record of articles that are available.

[00:12:36] Sometimes you go back and there's something very surprising that you can learn from us as if it were new. And, um. It occurred to me that this was potentially an extraordinary thing, because as people age, their, their brains become hypermetabolic. And what I mean by that is it's a little bit deceiving to say they become [00:13:00] hypermetabolic because what people mean by hypometabolic is hypometabolic with respect to a particular fuel, which is glucose.

[00:13:06] So the way this is typically measured is with FTG pats. Um, so you have a. Radioactive tag to glucose, and you inject it, and then you see where it goes to the brain, and then how quickly it gets utilized. And what happens as people grow older is that, um, the brain stops utilizing glucose as effectively. Um, and I should back up and say, initially this was seen for dementia, right?

[00:13:35] So in dementia, you see very pronounced hypometabolism. Um, and Alzheimer's disease, you see very pronounced type of metabolism. In fact, that's one of the ways you diagnose dementia is with FTG Pat. But here's the rub. You would, you know, it's not an all or nothing thing. It's not as if you're fine, fine, fine, fine, fine.

[00:13:54] And then one day you wake up and you're hypermetabolic and you can't declare. It's actually a pretty, [00:14:00] um, gradual process. And if you go back and you look at, for example, what happens with mild cognitive impairment. You see some hypometabolism. So it's, it's, it seemed on the one hand that there was sort of a more gradual process of hyper metabolism.

[00:14:16] And then on the other, you know, Bob, suppose these papers suggested that in fact the brain couldn't utilize glucose and if in fact there were this back door to feed these neurons that maybe just maybe we might have sort of a trick. To reverse this, you know, this really critical factors in aging, which is the brain's inability to utilize glucose.

[00:14:42] So if we can give it an alternate fuel source, the idea is we can rejuvenate the brain. So that was the thought process. So in the study, the study really have three components, um, and this study isn't over and it has kind of ongoing directions, and I'm happy to talk about, but the [00:15:00] first one was to first establish.

[00:15:02] What hypometabolism looks like in a way that is kind of nonspecific for fuel type. So if you look at FTG hat, you are only looking at how the brain is utilizing one type of fuel, which is glucose. But what we care about ultimately from a functional standpoint is how is the brain utilizing any type of fuel?

[00:15:24] Is it, it doesn't rain half the fuel at eats, does it not? And what we found is that. There was a particular signature for aging, um, that had to do with communication between brain regions. So, you know, whenever you are doing anything, even doing nothing, your brain is operating as a series of circuits and networks of different brain regions that are communicating with one another.

[00:15:49] And the degree to which you are able to function depends upon those networks actually being stable. They actually need to be able to continue to talk to one another without sort of fading out or stacking [00:16:00] or reorganizing and so forth. On the other hand, by the way, I should mention, you don't want written networks that are so static that they can't adjust.

[00:16:07] So you want to be able to switch from doing one thing to doing another thing, and so a healthy brain. It's not purely static. It is able to stabilize sufficiently to be functional, but then is able to adjust into, move on to other things as needed. But what we found is that as people were older, um, the brain networks started to destabilize.

[00:16:27] That is to say they're sort of connected to one another. But if you look at the same network over time, it starts to disintegrate. And what it was doing was not just. Fading out. It was actually turning into a different network. It was actually switching from one network to a different one, which is kind of interesting behavior.

[00:16:48] You might imagine, for example, like with your, with a light bulb, you know that as the light bulb is kind of running out of energy, it might start flickering, but that's not what was happening. It was actually a [00:17:00] network is running out of fuel and it starts actually reorganizing into different configuration.

[00:17:07] The second piece of information though that was very important was that again, it did not happen all at once. There was actually a very kind of longterm degenerative process that started. In the late forties. Um, so you know, around the age of 47, you start to see the degeneration of these networks. It became very sharply accelerated around the age of 60, and then became kind of to the point where it didn't change that much after around the age of 72.

[00:17:37] And, um, the third piece of information that was important was that this process became, um, accelerated. In type two diabetics. So if you happen to be a diabetic, a type two diabetic, this curve shifted to the left. So in other words, the process of aging versus we at [00:18:00] 65 became more like what we were a type two diabetic would be in his fifties per se.

[00:18:06] So it's, you know, it's an acceleration of the brain aging process, which was also accompanied by lower cognition. We then, once we had a pretty clear cut signature for what brain aging look like, we wanted to find out could we manipulate it? So is this just a fact of aging? Is this just something that is becomes things?

[00:18:31] So for example, you could imagine a situation where your brain structurally reorganizes and it is what it is and you can't do anything about it. So we put people on a. Several different dietary routines. Uh, one was, um, just their normal standard American diet, which as you know, tends to be rather, um, high-glycemic.

[00:18:53] The second was fasting and the third was one week on a ketogenic diet. Now, [00:19:00] when week isn't a very long time, and to be honest, we were, you know, to remove age out of the equation, we were only testing individuals who were younger. Um, because we wanted to see what is the effect of the diet without confounding that with the age effects right away.

[00:19:18] And what was actually quite striking is that the same individuals, I remember we're talking about young individuals, their networks stabilized during fasting and also during the ketogenic diet. So at this point, you might ask yourself, well, what these people were insulin resistant. So what's the mechanism for that?

[00:19:41] If they weren't missing glucose, if they weren't hypermetabolic, how come changing their diet then provided a backdoor for additional fuel? So there are many ways to think about what might've happened. And part of what we're trying to figure out now is really what the mechanism is. Um, but [00:20:00] one possibility came from Richard beaches work.

[00:20:04] Um, and what have you found with, uh, his colleagues? Sado was that actually ketones? Even if people who are non hypermetabolic and here he was really wanting to say people, and he was working with animals, actually produces about 27% more available energy, biologically available energy and glucose and the organ that he was focusing on with the heart.

[00:20:28] So he showed that there was more cardiac output. Um. And of course people like your Clark, we're looking at other muscles. She was working with elite athletes. What she found is that even again, in healthy young people who were not in a deficit state, ketones, produce, and here, I mean by ketones, ketones, beta hydroxy Peter, it produced more.

[00:20:49] Uh, energy, more available energy, and then the same amount of calorically matched glucose. So, so now we've got sort of an interesting, um, [00:21:00] neuroscience finding, which is that the brain, even in a non deficit state, seems to benefit from more energy. And here's what it looks like, right? So, um, but you know.

[00:21:14] Here we moved on because here's the problem. When you put people on diets, lots of things change, you know, as you know, I mean, a ketogenic diet, um, because of the fat content might produce more satiety and therefore you might eat less and that might affect your floor, you know, content or it might affect other macronutrients that kind of go along for the ride.

[00:21:38] And so we then followed up by isolating the fuel source as a very precise variable. Um, we had people coming in on two days in a fasting state, um, one day while we stand in first, and we gave them a bolus of glucose and then scan them again on the other day. We scanned [00:22:00] them and then gave them a Polis of beta hydroxybutyrate and scan them

[00:22:04] Carl Lanore: [00:22:04] again.

[00:22:05] Was that, was that beta hydroxy butyrate? That the beach. A ketone Ester.

[00:22:10] Dr. Lilianne Mujica-Parodi, PhD: [00:22:10] Okay. Okay. So here's the thing. I mean that the glucose and the beta hydroxybutyrate were, um, two fuels horses with, um, exactly the same amount of caloric, um, you know, the same number of killer calories in them. So it wasn't the number of calories.

[00:22:28] Um, it was the type of fuel and, and it was weight dose. So everybody had, you know, the same amount, uh, based on their particular waves, three 95 milligrams per kilogram. And so, um, we actually saw the same results, um, the same stabilization of networks in response to both the fasting and the ketone condition.

[00:22:57] So. We [00:23:00] didn't did one more, which was to ask if we put someone on a high glycemic index diet, is it, is it what we're taking away or is it what we're adding? So in other words, what's happening that we're taking away the glucose, or is what's happening that we're adding the ketone? So what we did is we then have people on a hypoglycemic diet.

[00:23:27] Consuming a bolus of sugar, which would be sort of the equivalent of eating a piece of chocolate cake or donuts, whatever. And that gave them the ketone and the ketone, again, stabilized. So that risk that established essentially that it was the ketone itself. And how does that work? Well, interestingly enough, what that showed is that the brain, when it has the choice between glucose and ketones, it goes from ketones.

[00:23:54] And the reason for that. Um, probably again, here we're getting [00:24:00] into one of those evolutionary, just so stories that I'm a little suspicious of, but he tones the ball within a context of starvation. Right, right,

[00:24:09] Carl Lanore: [00:24:09] right. And so we had, when we had to have all of our senses working, because we have a short window of time to straighten things out.

[00:24:17] Dr. Lilianne Mujica-Parodi, PhD: [00:24:17] So the way the biology works is there are ketones there. Grab it. Because there's not a whole lot of school like he can't be choosing. So if there's glucose, um, it actually gets pushed into the side, sorry. If there's ketones, it gets pushed into the cell. Whereas with glucose it gets pulled in only as required.

[00:24:38] So if your, if your, if your cells don't have sufficient glucose and there's a mechanism to look at to actually push them in as hard through insulin, push them in. But. With ketones. It doesn't matter if you have ketones, they get pushed into the cell. And so when you have access to both, what seemed to be happening was that the brain was going for the ketones and then [00:25:00] suppressing the, the glucose.

[00:25:02] Um, and actually, um, was actually quite striking because we have people's glucose levels going from like. One 82 70 within 10 minutes, it was working like a drug for type two diabetes. So

[00:25:20] Carl Lanore: [00:25:20] that's very fascinating. In fact, uh, we've been, you know, we've had shows specifically about the effects of the ketogenic diet and also beta hydroxybutyrate with dr Dominic, Doug casino's lab and lots of people now.

[00:25:32] And it's just phenomenal to me because, um, I will use. Uh, the beach ketone esters. I get them from a company called ketone aid and, uh, and they, they don't pay me anything for, for the plugs. I loved their product. Um, but it's amazing because I'll take some ketones even though I'm, and I eat a very low glycemic diet, low carb guy.

[00:25:56] Um, but I'll, I'll take those and I'll still feel them, even though [00:26:00] I'm in a phase of fed state, which, which speaks to your, your observations. So, um, I've OHSU, who watches the show from very, very far away, he said that some people get an elevated heart rate from the ketogenic diet. Do you think it's because the ketones, uh, uh, more efficient and they, and they increased cardiac output?

[00:26:23] Dr. Lilianne Mujica-Parodi, PhD: [00:26:23] Uh, yeah. So, um, here at Clark's work with  and Richard Veech work would suggest that in fact, they do increase cardiac output, but I have also seeing that they increase up epinephrine effort. So, at least in the beginnings, um, you know, there seems to be this adrenaline response to ketones that I think also may interfere with sleep.

[00:26:44] So lots of people have observed that, but you get this very clear, like a rush of energy when you consume ketones. I run and I definitely seal it, you know, if I have just consumed ketones before I run, I definitely feel. [00:27:00] A change in performance. Um, but I'm not sure if we know if that's because of the, you know, 27% more, you know, ATP that's available, or if it's actually because of, um, this adrenaline

[00:27:13] Carl Lanore: [00:27:13] response.

[00:27:14] Well, it's funny because when I do, I generally fast anywhere from 12 to 16 hours a day, just because I like a time restricted feeding. It works for me, but if I, if I fast for 24 hours. I literally feel euphoric. So much so that the idea of eating is discouraging. I think, ah, do I want to eat? And this is going to go away.

[00:27:37] And I've, I've fasted regularly for three days and I've trained intensely, and I've had some of my best lifting days on a 72 hour fast. Um, it is, it is a euphoric sensation that you get, uh, from, from the ketones. And, and it's, uh, again, I, you know, I like to look at everything from [00:28:00] an evolutionary standpoint.

[00:28:01] I feel like evolution is smarter than us and we have to try to understand why these things have happened, or are they benefits or, or, or, or in the context. And I think, well, you know, if you're starving you, you can't be down on your luck. You gotta be motivated. Like, Hey, you know, around the next corner, I may find something to eat.

[00:28:18] And I kind of feel like that's part of the reason. And again,

[00:28:23] Dr. Lilianne Mujica-Parodi, PhD: [00:28:23] fasting does seem to trigger neurogenesis in the hippocampus, for example. I mean, people have observed that, in fact, it does trigger the sort of compensatory hair, Janis to the skin areas of the brain that would be associated with spatial reasoning, which would be necessary if you were foraging.

[00:28:40] Um, but I would also point out, and here's something that we also tested, which I didn't mention. So when you start an experiment. If you are careful about it, you don't just jump into doing an experiment. You often do some piloting beforehand to establish some key parameters. Um, because at [00:29:00] least what I do is, is neuro imaging, and it's a very expensive technology.

[00:29:04] So we're, we're often talking about the $1,200, $2,000 at the data point. Um, you don't want to screw up. So one of the things that we didn't know was exactly what the time course was a beta hydroxybutyrate in the brain. Um. Nobody had really done neuro imaging, functional imaging. Um, and by that I mean as MRI, a functional magnetic resonance imaging update, the hydroxy computerate.

[00:29:30] So imagine, you know, you do this experiment and you give someone beta hydroxybutyrate, but at some point you have to put them in the scanner and like, when do you do that? Do you wait half an hour or do you wait 10 minutes? How long does it take? Um, and so the first thing we did once we did, um, a time for study.

[00:29:47] And we gave people, um, glucose. Again on one day he tones on the other and scan them for, you know, like an hour, an hour and a half to see what is [00:30:00] the time course of how it hits the brain. Cause you know, people have studied what, how, how his blood that we were interested in the brain. And what was very interesting, um, and this is in that paper as well, and it's in the appendix, is that if you look at the time force, which measured with magnetic resonance spectroscopy, somebody presents spectroscopy is a way actually to look at the chemistry of the brain.

[00:30:23] Um, so what is the substances in the brain and how is it changing over time? And one of the things that was very striking was that, uh, okay, so we establish the time force. That's fine. But what was really striking to me was that if you look at the type of person, glucose is like all over the place, it's up and down, up and down, up and down, up and down.

[00:30:41] You know, it's incredibly variable. And the reason for that is that, again, you've got this Lucas insulin, you know, going back and forth. So insulin

[00:30:49] Carl Lanore: [00:30:49] oscillates. What people don't realize is that insulin is on demand and, and

[00:30:54] Dr. Lilianne Mujica-Parodi, PhD: [00:30:54] exactly. Yeah. So. So, so you've got these control circuits that are making this going up and down, up and [00:31:00] down, up and down.

[00:31:00] It's a very unstable fuel source, whereas the ketone goes up, stays up, you know, so it's a much more stable, slow burning fuel stores, which means that you're not going to get as hungry because you're not going to get into a state of hyperglycemia. It's very possible to have, you know, a bunch of donuts.

[00:31:19] And then what happens is that you have this. You know, indogenous release of insulin, which then plummets you into a state of post prandial hypoglycemia. And at this point you become ravenous again. Right? So what happens with ketones is that because they are a more slow burning and stable fuel source, I think that mitigates some of that hunger right away.

[00:31:44] That's

[00:31:44] Carl Lanore: [00:31:44] fascinating. We have to take a break. Um, I've got lots more questions. This is, this is a great discussion because you, you know, we've always suspected a lot of the things that you're telling me what validated in a lot of this research. So it really helps a lot of people who have [00:32:00] been saying that the brain prefers ketones, but really no one has ever actually looked at some of the parameters that would indicate that that's true.

[00:32:10] So this, this is great. I'm so excited. We're going to take one quick commercial break. We'll be right back with more super human rater if you're watching live. Then why don't you share the show, start a watch party, and get more people to listen. We'll be right back. We're brawn and brains finally meet

[00:32:34] So many of you know, I had to give up coffee because coffee was jacking up my gut really bad, and since I've given up coffee. I don't snore anymore. I don't have GERD anymore. I knew it was the coffee and I've tried every type of coffee. I know that gets, Oh, Carly got to use this coffee and that coffee and no coffee today for me.

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[00:33:30] I've been drinking. Organifi pure. Ever since I gave up coffee, I don't miss coffee anymore. And the other thing that happened when I started, I stopped drinking coffee was I felt it. I couldn't think, I couldn't remember things I had. I had a struggle with those of you who've been watching this show or listening to me for the past 14 years, Nope.

[00:33:48] My stock and trade is my memory. I can remember interviews and discussions I had from 10 years ago, like they were yesterday, but when I stopped drinking coffee, that was it. I couldn't remember anything anymore. [00:34:00] Organifi pure saved me and it saved my gut too. Uh. First of all, it ships right to your door, which is convenient, especially today because you can't go out to stores half the time.

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[00:34:36] So check them out and we'll get right back to the discussion here. Now we'll bring, Oh, I got to get rid of something here. I produce my own shows. So you know, I don't have a producer here. I got to do it all. So we're talking. Uh, right now with, uh, dr Lily Mojica Perotti, we're talking about her recent research on brain aging [00:35:00] and the effects of dietary regimens.

[00:35:02] And so, uh, I think it was end of last year, I read a study that showed that, uh, a low carbohydrate diet can reverse, uh, the markers of brain aging. Now I'm starting to suspect it's because people have. Higher levels of ketones maybe, you know, because, because I've checked my ketone levels just after a 12 hour fast, I stopped eating at 6:00 PM I go to bed at nine I'm a very boring person, and when I wake up in the morning, if I check my, my blood glucose levels, I'm already at one millimole just from that short period of time.

[00:35:35] Do you think that the reason that the low dose low carb diet showed the reversal of brain aging is because intrinsically it's producing more ketones.

[00:35:45] Dr. Lilianne Mujica-Parodi, PhD: [00:35:45] Yes. So the fact that we saw the same effects with fasting and administering ketones is pretty clearly showing that the two are, are doing essentially the same thing.

[00:35:57] When you go into fascinating you and [00:36:00] indogenous with previous content, what do you take? Becomes your stockings. So you're taking a few times. Um, but the brain doesn't seem to care, uh, one way or the other. And as I said that the way to the. Narrow physiology seems to work. Is it up? So

[00:36:18] Carl Lanore: [00:36:18] one of the things, because I'm 62 years old now and I don't like aging, I don't like it at all.

[00:36:24] I could tell you that. And so, you know, one of the things that I strive to do is try to understand what is it really that's going on in my body when it ages. I mean, surely my cells don't have, I know they have clocks, but. They don't know that I'm 62 years old, but something happens when I had Dr. Dale Bredesen on a couple of times over the course of the past five or six years after he wrote his book and did his initial studies on a reversing Alzheimer's disease with a multifaceted protocol.

[00:36:54] Uh, I became fascinated in 2010 with iron accumulation for a variety of [00:37:00] reasons and his discussion and research. Shows that brain accumulation of iron contributes to the onset of what we consider dementia or Alzheimer's disease. A recent study that I talked about on the show showed that senescent cells have six to 10 fold more iron than quiescent acid cells.

[00:37:23] And now I've studied, I, I read, uh, last quarter shows that the more iron you store. The more insulin resistant you become, is it possible that it's not chronological aging at all, but since we're on the planet longer and we're eating more things with iron, we're accumulating more iron, and this could be the reason that we see these changes in our brain.

[00:37:50] Dr. Lilianne Mujica-Parodi, PhD: [00:37:50] I don't think I can answer that question. Um, you know, I think if I had. Tested this specifically. I could, I'm not familiar with the [00:38:00] research that you're describing. Um, so I wouldn't feel comfortable commenting. Um, I think that w what I mean, one thing that does make, um, this kind of research complex, complicated, particularly when you're looking at naturalistic studies where you have like large groups of people and you look at what happens during Egypt is that a lot of things happen during the day.

[00:38:22] Um, you know, and, and. You know, one of the things that happens is that, uh, there are immune factors that change with aging. And even with diet, um, there's this, uh, insulin degrading enzyme and accumulation of beta L, Adelaide flack and all those things. And, you know, certainly you can, uh, you can create a, a narrative for how all of those things are related to one another.

[00:38:48] So, for example, you could imagine. That, you know, people who are becoming insulin resistant, they are accumulating more glucose. And therefore, because an insulin degrading enzyme has to do two jobs, it has to remove [00:39:00] insulin. But it also needs to clear the brain of beta. I'm like, fuck. What happens is that if it's spending all of its time pairing insulin because someone's insulin resistance and it doesn't do as effective a job clearing out the plaque, and then, you know, so ultimately, um, as I started off talking about, I mean, I think that.

[00:39:19] What's going to have to be required is gradually moving to work. Interpretive understanding of how all of these pieces of the puzzle fit together. Because I think what often happens is that, um, you know, because people work on particular things, one person says, Oh, I studied this. It must be this. And another person says, well, I said, you know, I do this experiment.

[00:39:40] It must be that. But the reality is that, you know. Like that very old cliche about the, the elephant and the blind man trying to understand the elephant. You're only seeing the part that you look at. And so ultimately there's going to be, uh, an effort, um, as the data accumulate to start [00:40:00] trying to come up with a picture that incorporates all of these different pieces of the puzzle.

[00:40:05] For me, what was necessary was to kind of go back and think about this from first principles and say, you know what? I'm a little bit scared to. Try to identify a mechanism in old people because old people have so many things that look different. If I, if I, if I go back and look at young people and I look at how in fact this particular one variable of fuel affects the brain, um, then I can take that information and then moved from an older population or to a counselor resistant population.

[00:40:38] Right. And at least I'm just kind of taking one step at a time, isolating variables, one at a time, so that, for example, I can exclude inflammatory markers or a beta insulin, you know, the, the, um, insulin degrading and assign, because these are factors that wouldn't operate on the timescale that I was measuring.

[00:40:57] Um, these are effects that we saw, [00:41:00] um, with the beta hydroxybutyrate on the order of 10 minutes, you know, two to 30 minutes, right? So these are effects that are too fast. To be, um, lots of the other mechanisms that we think might be relevant, but this is something that happened too fast to be able to incorporate those mechanisms.

[00:41:21] Carl Lanore: [00:41:21] Do we do, we're all, Oh, I'm sorry. I'm sorry.

[00:41:24] Dr. Lilianne Mujica-Parodi, PhD: [00:41:24] Good. Um, the, the other thing I wanted to mention a propos of your comments about, you know, measuring your blood in the morning. Um, you know, for a long time people were measuring. Their urine and the move, the move to move, you know, to, to measure blood seems like it's a step forward to measuring urine.

[00:41:49] What happens, of course, is that over time, so what you excrete through urine is the overproduction of ketones, right? So what happens is that when you switched from. Burning glucose to [00:42:00] burning ketones. You have to produce ketones and your body doesn't know in the beginning how many eights you produce. And so it, it produces an overabundance in the beginning, and that's why you excrete the ones you don't need.

[00:42:10] But what happens is that the longer you're on a ketogenic diet, the more your body downregulates and produces only the ketones that you require, which means that if you're asking were the effects of a ketogenic diet with urine over time, do they think that you're not in ketosis anymore? Isn't helping, but, but there are problems also with measuring blood, um, and specifically to address the issue that you raised.

[00:42:36] So one thing that a lot of people don't know, and in fact, I didn't know until I started measuring it, is that the brain runs out of glucose a lot faster than the rest of the body does. And so, um, typically when you go on a ketogenic diet or you're fasting. The rest of your body requires about 30 to 36 hours to transition to Burnie.

[00:43:00] [00:42:59] You're on fat in the form of ketones, but your brain has a much smaller storage container. Um, and as a result, it actually switches to burning ketones after, you know, five to 10 hours, which means that you could be measuring your blood in the morning. And not be in a ketogenic state in terms of the rest of your body, but your brain is in a ketogenic state.

[00:43:28] So a lot of people say, well, I don't, I wouldn't naturally burn ketones because I'm not fasting. Um, but everyone's fasting. I mean, unless you're getting up every two hours to eat while you're sleeping, everyone goes through a fasting period. And one of the reasons that ketosis has evolved is to allow you to do things like sleep because you don't have to eat as regularly.

[00:43:51] So anyway, I just wanted to make that point because one thing that we often try to do when we study these things in ourselves is to [00:44:00] try to adapt measurements that we see in laboratory to, um, to our own metrics. But, but this is something to consider. This is one reason that we had to measure in the brain.

[00:44:10] Carl Lanore: [00:44:10] I want to take our last commercial break and when we come back, I want to ask you specifically, is there a way to determine how long the brain needs to be exposed to. Ketones to start to reverse some of the, let's say, stress, stress induced changes or age related changes, and do we know how high ketone levels need to be or, or is there any way to measure that?

[00:44:36] When we come back, we're going to take one quick commercial break. Stay tuned. We shall return later in the show. I'm going to give you a little virology one-on-one. We're going to talk about. The Corona virus a little bit. I know a lot of people have been asking me to do some stuff on that, so we have an interesting discussion later in the show.

[00:44:50] Stay tuned. You are listening to this superhuman channel. We're ripped and we're ready.

[00:45:00] [00:45:00] Welcome back. We're talking with dr Lilly Mojica Perotti. This is a fascinating discussion cause I love discussions that shed light into actionable steps that we can take to. Protect our brain because so many people in our population today, uh, developing, uh, issues related to dementia and, uh, and, and Alzheimer's disease at younger and younger ages.

[00:45:24] It's a very, very sad situation. So, uh. Do you think? Is there a way to give us any type of a quantification of how long it takes for exp, for the brain to be exposed to ketones, let's say, with great regularity, to start to see some of these mechanistic changes, uh, away from aging, the aging brain phenomenon.

[00:45:47] Dr. Lilianne Mujica-Parodi, PhD: [00:45:47] Uh, one of the things that was very surprising and very striking about this study, um, was how short a time it took to see effects. And again, here we're talking about healthy young individuals. Right now [00:46:00] we are. Doing experiments in older individuals up to the age of 80, as well as individuals with insulin resistance, and also looking at animal studies to better understand mechanistically what going on.

[00:46:13] But I will say with the healthy young individuals, we saw an effect after one week on a ketogenic diet, which is not a long time at all. Um, and after 30 minutes on, after consuming beta hydroxy theatre, right.

[00:46:30] Carl Lanore: [00:46:30] That's so exciting.

[00:46:32] Dr. Lilianne Mujica-Parodi, PhD: [00:46:32] Yeah. It means you don't have to do this for years to see an effect

[00:46:36] Carl Lanore: [00:46:36] when, when the, uh, subject will on the ketogenic diet, did you measure blood levels or how did you determine if they were actually in ketosis and how deep

[00:46:46] Dr. Lilianne Mujica-Parodi, PhD: [00:46:46] they were?

[00:46:47] So we did measure blood levels probably similarly to how you were measuring them. Um, Sam. It seems to be a switch. Either you're burning ketones [00:47:00] or you're not. Um, we did not find that being more ketogenic was better. Uh, so for example, one pilot experiment we did involved, uh, fasting, having people be on a ketogenic diet and then also giving them the ketone or not.

[00:47:18] And what we found is that. Once you're in ketosis, the word ketosis doesn't make your brain behave better. It's either it's burning ketones or it's burning glucose and the dose. There is no dose response effect that we could notice. We did notice that, um, and here we didn't do these experiments ourselves, but we relied on our collaborator here in Clark.

[00:47:40] We had done experiments with the dose response study. And what happens is that at least when you take exogenous ketones. Um, past a certain point, you start seeing some gastrointestinal side effects. Um, and so what we found was a three 95 milligrams per kilogram was sort of the sweet spot in terms of [00:48:00] reliably getting people to the point where they were definitely in ketosis.

[00:48:05] Um, but not to the point where they started feeling nauseous. Fascinating.

[00:48:10] Carl Lanore: [00:48:10] Um, so. Well, I just, I have too many questions in my head, so I'm just going to stick with this one here. So in the reality is, if you're at, because there's a phenomenon called Quito license, which is the utilization of ketones by the body, and then there's ketosis, which is the production of ketones by the body.

[00:48:33] And so from what you just said, is it safe to say that if you are producing ketones, even if it's just one millimole. That your body, your brain most likely is using them since the brain seems to prefer them.

[00:48:47] Dr. Lilianne Mujica-Parodi, PhD: [00:48:47] Uh, this is what we found. So when we, when we looked at people who were indogenous like producing more, or

[00:48:55] Carl Lanore: [00:48:55] we're less

[00:48:56] Dr. Lilianne Mujica-Parodi, PhD: [00:48:56] details, if we were not seeing a dose response [00:49:00] effect, basically either they were in ketosis or they were not, either.

[00:49:05] Stability was stabilized or it was not.

[00:49:08] Carl Lanore: [00:49:08] I know you can't talk about, or you have to be cautious about talking about future research. Um, but I have to believe you're working on other projects as a result of this project. Will you come back on the show and talk about your findings?

[00:49:22] Dr. Lilianne Mujica-Parodi, PhD: [00:49:22] Sure, sure. I would love to.

[00:49:24] I mean, I think one of the most exciting things is that, um. Well, and again, this kind of makes our lab maybe a little bit unusual in the field in that typically people, when they think about translational research, they first start with animals and then then they take it from the animal experiments up to the human scale.

[00:49:44] Um, as a matter of kind of a practical philosophy, we always work in the opposite direction. We first see some effect at the human scale and then go to the animals to understand the mechanism. And the reasons for that is that if there's no effect on the human [00:50:00] scale, it doesn't make sense to look at it.

[00:50:02] Carl Lanore: [00:50:02] Oh, darn it. I can't believe we lost her. Oh, Oh man. Well, we were lucky to have. Her for as long as we did given the internet challenges today. Um, I'm going to see if I can get her back here. Oh, I hate it. I hate technology. I gotta be honest with you. This is why I prefer to do shows. Hold on. Let me just see if I can reach her.

[00:50:29] Dr. Lilianne Mujica-Parodi, PhD: [00:50:29] Hey,

[00:50:29] Carl Lanore: [00:50:29] I'm so, Oh darn it. Oh darn it. Oh, he's on it. Well, let's see if she reconnects cause we did talk about this possibly happening. No, no. We talked about this possibly happening, but I think we got all the really good details from the interview. Um, I have to take my last commercial break, and when we come back, we're either going to be rejoined by dr Mojica karate, or I'm going to talk about the absurdity of continuing to be locked down [00:51:00] in light of what viruses actually do.

[00:51:05] Uh, in human populations. And I think that when we connect these dots, people are going to get really, really interested. Well, let's take our last commercial break. Stay tuned. We'll be right back. The superhuman channel.

[00:51:35] okay. Welcome back. Unfortunately, we're having some technical difficulty, but I. Have the good doctor on my phone, and we literally dropped you at the last second. Let's see if my audience can hear you do so. So you were wrapping things up. Do you remember where we dropped you? I, yeah. So, um,

[00:51:51] Dr. Lilianne Mujica-Parodi, PhD: [00:51:51] what I was saying is that typically the way we, um, envision, uh, translational research is that you, you start from [00:52:00] some animal experiments and then ask, Oh, could this also be true in the human?

[00:52:04] Um, but, um, that can lead

[00:52:07] Carl Lanore: [00:52:07] to.

[00:52:08] Dr. Lilianne Mujica-Parodi, PhD: [00:52:08] Situations where you do a great job of curing rat cancer, but, um, it doesn't work in the human. There are many examples actually where, uh, animal results do not translate to the human because of, um,

[00:52:20] Carl Lanore: [00:52:20] lack of

[00:52:21] Dr. Lilianne Mujica-Parodi, PhD: [00:52:21] homology. But in, in any case, um, what we're doing now is having established this, uh, network stability measure in humans and knowing that it can be.

[00:52:31] Uh, it can be adjusted through changing fuel sources and through changing the amount of energy available, we're now doing, um, animal experiments in collaboration with a very talented electrophysiologist, uh, Nathan Smith at children's national in Washington DC in his laboratory. He's actually taking mice and making them insulin resistant and then looking at the neurons.

[00:52:56] And how they change, how they communicate with one another, how they [00:53:00] changed their firing dynamics so that we can try to understand the mechanism. For the effects that we're seeing in humans. And so that's kind of where we're at right now, and it's very exciting and we're seeing actually very profound effects in terms of how neurons communicate with one another and how even they fire in the presence of insulin resistance.

[00:53:19] So definitely stay tuned.

[00:53:21] Carl Lanore: [00:53:21] This is very exciting to me and I appreciate you dealing with this last moment of a technical difficulty. I want to have you back on. I think the work that you're doing is profoundly important as well for the population. Uh, so this is, this is fantastic. Thank you so much for being here today.

[00:53:39] Dr. Lilianne Mujica-Parodi, PhD: [00:53:39] My pleasure. Thanks so much for the invitation.

[00:53:41] Carl Lanore: [00:53:41] Take care. Bye. Bye. Well, there you go. Manipulating technology to get the complete interview done. Uh, as always, always trying to deliver. I'm always trying to deliver. So, um, the last thing I want to talk about is, uh, a brief. Intro to [00:54:00] virology, one Oh one about the covert 19 epidemic.

[00:54:03] I'm going to put my mask back on for this just in case dr Tony vouches is watching. I want him to see that I'm abiding. So, uh, I look more like Antifa now than somebody who's worried about catching the virus. Right? So, okay. So there's this, um, there's this really bad notion that if we could lock the population down, let's say it was possible.

[00:54:29] To completely lock the population down for the next six months. Let's say the government had enough money to give us money and give businesses money and keep everybody in gear, and we were like, okay, this is great for six months. I'm just going to social distance. Just do what I have to do, stay home, not work.

[00:54:47] And then when we all come out in six months, everybody will be safe. No one will get the virus. This is exactly. Uh, a profound untruth. [00:55:00] No one's talking about this in the media at all. What I'm about to say, quite frankly, no one talked about vitamin D in the media and sun exposure. No one's talked about how this, uh, virus has ceded and spread.

[00:55:16] Uh, no one's talking about a lot of the things I talk about, but because my audience is this niche. Boutique audience and I don't reach millions and millions of people like let's say a dr Oz or somebody like that. I talk about things on this show, and then two weeks later somebody is on CNN talking about it.

[00:55:32] I go to Alyssa. I just talked about that. Like I talked about the sex differences between co contracting this virus before anybody did. So anyway, I know I'm patting my own back right now. Um. My friend Jeffrey, we would say, never let the hand print on your back be your own. Um, he says, I know what you're going to say.

[00:55:57] I've discussed this with friends. Fred [00:56:00] Shora says, okay, Fred, stick with me brother. So there's this notion that if we just lock the country down long enough, everybody will come out of this just alive. And that's not true. That's not how viruses work. So. Let's say we did lock the country down for six months and we're actually able to do that, and six months from now we will like, okay, flip a switch.

[00:56:22] Because of course there's no new cases. Nobody's dying, nobody's getting sick. As soon as we started going out again, people who had started getting sick and dying again, why. Because once you're exposed to the virus and you build up antigens to deal with it, you are still a carrier. So we can't delay this virus from running through the human population.

[00:56:44] This is idiocy. And it's why people are predicting, well, if we open the country back up, we're going to see a spike again. Of course we are. If we kept the country close for the next six years and then reopened it, we'd see a spike again. This is how [00:57:00] viruses transmute and survive the only way tenfold.

[00:57:06] Thank you, Fred. I'm glad you're here listening live today. The only way for us to beat this virus is to start going back to normal. Now, granted, elderly people take precautions during the normal seasonal flu period. They should take precautions and sadly, all U M efforts who didn't give a damn about your health for the past 20 years and became insulin resistant and and have all sorts of comorbidities as a result of your insulin resistance, you're stuck.

[00:57:36] You're going to have to stay in doors more often. Because you are going to be susceptible, but you're also more susceptible to dying from the regular seasonal flu. Who we kidding. The only difference between this virus and the seasonal flu is this virus is so much more transmittable. It's two to three times more transmittable than the seasonal flu.

[00:57:59] If the [00:58:00] seasonal flu was this transmittable, we'd have the same predicament. That's the only difference. So the sooner we get back, I can't keep doing this. I feel like I'm smothering. The sooner we get out there and start mingling and people get sick and don't die from it, and people get sick and unfortunately die from it.

[00:58:21] I know that people think call you crazy. No, those people are the ones that need to self quarantine. Those people need to take precautions. Those people need to start thinking about their health now. Now they're going to think about the health. Oh, I got to think about my health, but. We can't freeze this virus in place and beat it.

[00:58:39] The only way to beat this virus is to get out there. No one in the media is discussing this. This is the God's honest truth. Ask a viral logist. Just ask one, say, Hey, if we lie, if we literally froze the country for the next two years when we came out, two years with this virus, be gone. They go, no, of course not.

[00:58:59] Oh [00:59:00] really? So why the F are we doing this? Then why aren't we just telling the people most likely to die from this virus? Stay home, self quarantine, let everybody else get back to life and governors. I'm sorry. I used to say, well, they're well meaning, but misguided, but they're not well-meaning and misguided.

[00:59:20] They have no idea what they're doing except they love the power to tell people you can't travel. You got to wear a mask when you go into a store, you got, those things are not laws. They're voluntary. All these things that governors are telling us we have to do. They're voluntary. They can send the police out to our house and, and while we're writing your name down, we know you exist, but show me the law.

[00:59:44] Take me to court and let, let's see if a judge puts me in jail for this. It's all voluntary. When people realize this, they can tell these governors to F off. Man. My question is where do they think [01:00:00] the virus is going to go? We are play. We play hide and seek with the virus. Ha. Exactly. Patrick. We need to get back out there so it works its way through the population because then what happens is we actually develop immunity that can be passed on to others because the virus mutates in us.

[01:00:19] Man, I am tired of being directed by stupid effing people. They're stupid. It's almost like if you're a stupid person, you rise to the top in politics. If you're stupid and easily corrupted, you can be a politician. It's why I'll never be a politician. I would have to be a complete sellout to be a politician, to agree with what going on right now.

[01:00:43] I'm tired of it, so this virus will not go away. If people like governor Andy Bashir locked the population up for the next 10 months, it's going to come back and if anything, it's going to kill more people. Thank you. Thank you. I've also. My [01:01:00] good friend. I got to come and visit you someday. I cause I know you live in the sun.

[01:01:04] I want to be where you are. I that's it. You know, start, start talking about this with your friends. Start explaining to them that we cannot hide from this virus. We must meet it head on. And if you are sick and one of the people that they're saying you're going to have a comorbidity, stay the F home. But let the rest of us get back to our lives.

[01:01:22] All right. That's it for today. We have great shows planned all week long. Thanks to the lovely and talented Elisa Profumo share this show. Please share the shows. I ask people to do this all the time. Start a watch party. Just click start a watch party. Next time you watch a live show, Fred shore a one more comment before we go.

[01:01:39] Or they have stakes and pharmaceuticals like Doocy and AC. Yes, of course. Of course. And they do. When people, when you say this stuff all your conspiracy. No, no, they do. Listen, I am been trying for three days now to find the budget line. In the federal government's budget [01:02:00] of the money that the CDC makes on the now 30 patents it holds on vaccines.

[01:02:09] Remember, they hold those patents for a reason. They hold those patents because they can then license those vaccines out. So it's making our government money now. Is it going right into Fowchee pot pocket? Probably not, but it's why they made him bizarre of science. It's why he's been there through like five presidential, uh, administrations now.

[01:02:35] I mean, he just keeps licensing vaccines and, and then, and then there's a invest invested interest for them to promote vaccines because the government makes money. It's just like tobacco. I've said it before. You can kill people in this country as long as the government gets their VIG. For those of you don't know what Vegas, it's the vigorous.

[01:02:52] If you borrow money from a loan shock shock, it's not interest. It's called VIG. And if you don't pay it, you get [01:03:00] killed. So the reality is that you can kill people in the United States. I mean, look. Vioxx killed 50,000 people. No one from Vioxx, from the makers of Vioxx ever went to jail. Why? Because they paid big fines.

[01:03:14] The government got big money like, okay, you kill 50,000 people. Write us a check for 60 million or whatever it was. I don't know. You can kill people in United States and probably in other governments as well. As long as the government gets a cut of it. Proof of that is tobacco. People really gave a damn about human life in America.

[01:03:31] Politicians would be thinking about how to get people off of tobacco products and outlaw them once and for all 1.5 million a year die from tobacco. Everybody's wringing their hands about, well, we lost 28,000 or 60,000 yeah, it's a horrible number, but why don't you think about that number when people are starting to smoke cigarettes.

[01:03:50] 1.5 million every year. The CDC knows that that's the CDC number, so let's stop the BS and let's get back [01:04:00] to life so this virus can work its way through and we can build up immunity and not be afraid of it any longer. That's it for today. My rant. People are going to, I know on a couple of websites they say, well, he yells too much.

[01:04:11] I don't yell too much, but I do get spirited when I feel something strongly, so there you go. I see you tomorrow. Thanks for listening. Share the show. Please share the show. Please share the show. Please. [01:05:00] .