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Speaker 2blood pressure migraines infertility they are all manifestations of the same problem
Speaker 3dr ben bickman is a metabolic scientist revealing why insulin resistance may be the root cause of nearly every chronic disease and the simple ways you can reverse it so many people are addicted to
Speaker 2refined starches and sugars only 12 of american adults have optimal metabolic health our carb crazed culture is the main driver of insulin resistance it sounds so controversial i don't mean to declare war on carbs but i mean to declare war on carbs but the more metabolically unhealthy you are the more that is the macronutrient that is problematic moderation doesn't work if you're an addict and if you have insulin resistance you're gonna very very likely be a person who within a few years starts to really notice the cognitive decline gosh it's frightening the good news of all of this when we recognize that what we're eating and how frequently we're eating it is a primary driver of so many problems all right you can change that protein is a friend a human can eat fat and there will be no effect on insulin whatsoever none within weeks person can totally reverse type 2 diabetes there are four critical pillars that improve insulin resistance control carbs prioritize protein don't fear fat and that's going to shock
Speaker 4people can you do one quick thing to help this channel grow just tap the follow button it's completely free and helps us bring these types of episodes to more people now let's get into it dr benjamin bickman it is so wonderful to have you here today oh kristen my pleasure thank you you have done groundbreaking work in the area of insulin metabolism and have really i think led the way in bringing quite a crisis to the consciousness of americans so i just first want to say thank you for all the good work that you do for our listeners who
Speaker 2are new to your work you have done a great job and i'm very grateful to have you here today and i'm very grateful to have you here today and i'm very grateful to have you here today and i'm very grateful to have you here today to as a scientist appreciate the answers that we find after all that's what a scientist is a guy who's a person who's just trying to answer questions i asked a question a number of years ago at least to myself what is the relevance of metabolic health in chronic disease so is there a metabolic foundation to much of chronic disease and the answer just continued to be a resounding yes as a scientist academic i don't want to be content finding an answer publishing it no one ever sees anything i'm not going to be content finding an answer publishing it no one ever sees anything i'm not going to be content finding an answer publishing it no one ever sees anything about it so the professor part of me kind of came out and told i said to myself i need to find a way to share the information because that's what a professor wants to do and as much as i was incorporating some of these metabolic ideas into my classroom i still thought having a few students every semester isn't going to cut it and that then was a lot of my motivation to find ways to take these very relevant i believed ideas and move them from the ivory halls of academia into the real world where things actually will be tested and proven and we determine whether they
Speaker 4matter or not so you had kind of a breakthrough moment that i think anyone who's worn a cgm might might realize that food does really interesting things to my blood sugar right so we've got you know i think your first one had to do with cereal so um i don't know if you're triggering loops i know don't you
Speaker 2just want as a cereal holic it's like you've put the drug in front
Speaker 4of the added literally have like a box of frosted flakes when i was in high school like this is why
Speaker 2higher yes this is why if you'll allow me to say this is why i rail against this this mantra that you hear so often in the realm of dietetics and nutrition of moderation and all things most people it's designed to to to go around moderation it's designed to hijack us and so many people as inconvenient as it may be to say are addicted to refined starches and sugars and moderation doesn't work if you're an addict and so yeah i mean you noting the cgm and then waving a bowl of my drug of choice in front of me yeah it certainly makes me think about my own habits and and particularly what the cgm revealed where i would find after imbibbing in my my drug of choice i would have glucose levels that would not only be elevated for 24 straight hours it would take even me a lean healthy physically active guy i would indulge because i'm an addict in overindulge to be more precise in in cold cereal in the evening and my glucose in the absence of any other food for the next about 20 hours would be above 100 100 into the 100 teens for me a lean healthy non-diabetic guy and then at the same time with wearable devices finding that my chronically poor sleep might less be a matter of anxiety and just i'm wired to sleep badly and more actually a consequence of wrecking my sleep and i'm not going to sleep badly and i'm not going to sleep badly and i'm not going to metabolic state right before I'm going to bed, and most people don't appreciate it. We have wild data. We're going to talk about how much you can eat in goatee. Just the combination between what you do to your metabolic state prior to what you're trying to do with your nervous system state in order to get into sleep. I don't want to get ahead of the
Speaker 4conversation, but yeah, that's my drug. That was your moment. So to break this down for folks who aren't familiar with what this means to have these blood sugar spikes, what it means to have 110 sustained over the course of a 24-hour, what does a normal cadence look like? And maybe this is a good segue to kind of talk about to introduce insulin and glucose, and what is the difference, and why does that difference matter?
Speaker 2Yeah. Yeah. That's a really good point. So let me touch on that last point first. Why does the difference matter? We need to appreciate that glucose and insulin are separate. Sure, we look at them as they're married. They're a couple in this relationship, if you will, but they are separated. They're married. They're married. They're married. They are distinct. And by treating them as distinct, we are enabled to have a more precise view of the individual. In other words, to say all that another way, we have a glucose-centric paradigm of modern metabolic medicine. As much as we have all of these other markers that we look at with the blood test, when it comes to metabolism, the conventional clinician will look no further than glucose or A1C, some surrogate of glucose. And I'm not saying glucose doesn't matter, but the problem with insulin-resistant glucose is that it doesn't matter. It doesn't matter if you're on an insulin-resistant diet. It's affected more by insulin directly than the glucose, as much as glucose has an effect on insulin. It's the insulin that's driving the insulin resistance. And when we look at these two variables, if you're monitoring the health of an individual over years, insulin resistance is a state where glucose is staying normal, albeit with some variations that a CGM and monitoring can reveal is where something might be going off. But in a static, you come in for a fasted blood test, glucose may be hovering at normal, but insulin is getting progressively higher. And so my contention is we need to treat the two separately. And indeed, we need to put them in their proper place, which is that insulin ought to be the primary metabolic marker. And then glucose ought to be looked at as a sidekick, or rather assimilation. And so we need to treat the two separately. There's a symptom of insulin going wrong, but one of many symptoms. I know within your own interests and MOOP, one of the big outcomes you guys look at is cardiovascular outcomes, including blood pressure. Blood pressure is a much more sensitive indicator of insulin resistance than glucose levels are, because glucose can stay normal. Although insulin's waging a silent war to keep it there, it's working well enough. But then as insulin's climbing, it's affecting other things like salt and water handling in a way that's not good for your health. That is going to be an earlier indicator than the glucose problem. So you can have normal glucose levels, but be insulin resistant. Absolutely, yes. Resistant. Yeah, resounding yes. And that's why we have to shift from the glucocentric paradigm. Not that glucose doesn't matter, but maybe rather than shift, we need to expand it to say, well, we have to include the insulin component to this.
Speaker 4So is it fair to say for someone who, for example, maybe hasn't gone to get a blood test, they don't know what their insulin levels are. But they're monitoring their glucose levels, and those appear normal. But perhaps their blood pressure is a little high. So maybe they go and they do a cuff, or they have a device that is able to measure their blood pressure. And maybe their HRV is on the low side, and resting heart rate maybe is on the high side. Is that kind of a window into what might be happening metabolically?
Speaker 2Oh, absolutely. Right. Yeah. So insulin, one of the reasons, I wanted to put these thoughts into the book or other, this kind of all-encompassing view of as much as we have all these chronic diseases, they share a common core. I'm kind of acting out almost a tree where we have all these branches. And one of the branches is going to be cardiovascular health. Well, that's coming off the same trunk of insulin resistance that things like infertility and cognitive decline are coming from. But with cardiovascular health specifically, we know that insulin, as it is elevated, will activate the sympathetic nervous system. And if you have a chronically elevated sympathetic tone, well, good luck having a normal HRV. You are going to constantly be up in that narrower range. You are narrowing down the ability of the heart to be slowing and accelerating in a normal kind of dynamic pattern, which would give you a good heart rate. good HRV. So autonomic
Speaker 4nervous system dysfunction is a marker.
Speaker 2You could say you have an autonomic dysfunction. At the same time, you could say you are not allowing the sympathetic to turn into the autonomic or to give way to the autonomic. Because insulin and glucose, when they're elevated back to my bad sleep habits, it forces the system into a nervous state and dampening the autonomic state. And you want autonomic to dominate if you want not only vasodilation and a reduced systemic blood pressure, but even for the HRV to be as dynamic as we want it to be, which is a strong indication of just good health and even, to your point, metabolic health.
Speaker 4And insulin resistance is going to impair that vasodilation. It does. That's right.
Speaker 2Yeah. So not only does that explain the incredibly intimate connection between hypertension and insulin resistance, but even in men, it is. It is considered to be one of the earliest instances of how insulin resistance is driving erectile dysfunction. So the most common form of infertility in men is directly attributable to some degree to this metabolic problem that is insulin resistance.
Speaker 4Jeez. It's like it's the root. It's the foundation.
Speaker 2Amen. Of pretty much everything. So it brings meaning to my career. Why would I devote a career. You're so important. Yeah. But that's also why, when I started putting these thoughts together, you know. In the form of my book, Why We Get Sick, which you've been nice enough to put here.
Speaker 4I know. It's so good.
Speaker 2I actually had to go through several versions of the title. So good. The first version of the book was insulin resistance, you know, why it matters or something. Yeah. But I knew no one would care. Most people hear the word insulin and think of it no further than the context of, well, it's a drug for diabetes. They just think of it as a medic. Some people don't even know we make insulin. That's a normal hormone. They think of it purely as just a drug therapy for. A hormone therapy. for diabetes. No. And so I needed to have a way to make it a little more provocative and go outside just the normal restrictions that people place on insulin, which is to think that it has no more relevance than just controlling blood sugar.
Speaker 4Right. If you don't. You don't need to worry about it unless you have diabetes. Yeah, that's right. Yeah. And that. What a mistake. So for folks who aren't familiar with all these terms, we've been thrown around a lot of terms. So define the peptide hormone, insulin, glucose, blood sugar. Just help people understand that signaling pathway. Yeah, sure. Yeah, that's a good.
Speaker 2That's a good question, just to help us really have a common kind of framework and map. Yeah, so insulin is a peptide hormone, a little petite peptide that is made. Produced from the beta cells of the pancreas. Now, the main stimulus of telling the beta cells to release insulin is blood glucose, blood sugar. So now that then is a separate thing, not a hormone. It's a nutrient or an energy source or calorie source.
Speaker 4So we ingest the Apple Jacks.
Speaker 2Yep. And then what happens? Yep. That's. Yeah, great. So we eat a starch or a sugar, and then to some degree, that's going to be digested. But every carbohydrate to some degree is going to get broken down into blood sugar, a lot or little, rapidly or very slowly. But as blood glucose levels start to climb, that will stimulate the beta cell to release insulin. And in this context, insulin is acting as a hero. If glucose levels are too high for too long, it is acutely lethal. We need to correct it. And there's no other nutrient that does this, by the way. If you eat. If you and I were to eat a load of fat, fat would have a very slow. Like we ate a stick of butter. We would notice this very slow creeping increase in our triglycerides, and it would come back down. If we ate a load of protein, we'd see amino acids go up and then come back down. Glucose, nothing changes like glucose does.
Speaker 4Carbohydrates are non-essential.
Speaker 2They are not essential. That is controversial. And most people will hear us say this, and they will think, well, but the body needs glucose. Blood glucose is not the same as dietary carbohydrate. The liver has the ability to create all the glucose the body needs. So back to the glucose exchange or excursion, glucose goes up a really high. Insulin acts as the hero saying, hey, you're too high. I'm going to bring you back down. And so among its many effects from top to bottom, it will go to the biggest tissues of the body by mass, fat mass and muscle mass. And so insulin will come to the doors of the muscle, knock on the doors. Open the doors when insulin's working well, and then allow the glucose acting like a gatekeeper to come from the blood into the muscle, thereby lowering blood glucose, ideally quite quickly. And then we've returned to homeostasis.
Speaker 4And a person who can do that would be
Speaker 2considered to have good insulin sensitivity. That's right. Glucose levels can come up and down. Ideally, with monitoring devices, we'd want to see glucose levels get back down to around 100 milligrams per deciliter by about two hours. That's a good sign. So there is value in the dynamic testing of glucose that we don't get with just a one single. Which you can do with a continuous glucose monitor. That's right. Rather than like one time a year, we fast to get our blood drawn.
Speaker 4Right. And there's so many confounders that can influence that one moment in time.
Speaker 2That's right. But insulin doesn't come down as quickly. It sort of lingers in order to determine, all right, is everything back to normal here? Okay, it is. Now I'll go away. And so insulin, even in an insulin sensitive person, can stay elevated for up to three hours just with even a modest amount of carbohydrate consumed. And unfortunately, in our modern environment, not only do we have that three hour window of insulin, but if you're an insulin resistant person, you could eat that same carbohydrate load. And now insulin might be elevated for five or six hours. Well, long before insulin has even had a chance to come back down, we've spiked it again because we have this culture of chronic carbohydrate consumption. So we start the morning off with a bowl of starchy sugar, sugary foods, and then we have a mid-morning snack or sugary drink. And then we do the same thing for lunch and throughout the day. So we're spending every waking moment in a state of elevated insulin. So hard. Yep. And like happens so often, too much of a signal results in a deafening to that signal.
Speaker 4So insulin no longer becomes responsive, insulin resistance.
Speaker 2That's right. Yep. So too much insulin is the main driver of insulin resistance. And our carb crazed culture is what's driven it.
Speaker 4So for that person who's having the Apple Jacks at 9 PM, a couple hours before they go to bed or whatever, they do it once, not a big deal, two times, not a big deal. But I think what you're saying is that the more you do that, the more stress you're putting your body under. And how long does it take for that kind of chronic carbohydrate consumption throughout the day to put you in a situation where you're maybe pre-diabetic, pre-diabetic,
Speaker 2and then diabetic? Right. Well, it's actually faster than most people would think. And I can cite specific studies to support it. There was a paper published on young, healthy college-aged individuals. So these are the most metabolically bulletproof people you can find, right? Think about the average college student. They're doing all kinds of horrible things to their bodies, and yet they're still reasonably fine. So that just helps us put this in perspective. So even the most metabolically immune among us still had this happen. So over a six-day period, they had these individuals just simply overeat carbohydrates more than they needed, which, as we noted, is essentially zero. But they took the average what they were eating and then just said, all right, stack on some extra carbs. In just six days, their insulin levels in a fasted state had, if I recall correctly, gone up by about three times. So their fasted insulin had gone up by about three times, but their fasting glucose was still normal. Again, back to this original point that if we had a metabolic review, which was just glucose-built, we would miss this. So in as little as a week of a little bit of carb-induced self-abuse, you can have demonstrable insulin resistance settle in.
Speaker 4For the layperson who might be hearing some of this for the first time or is trying to maybe talk to a loved one, knowing that, hey, maybe this person is eating over the course of 15, 16 hours primarily carbohydrates, how do you have that discussion with the mom or the dad or the brother and just be like, all right, I'm going to take this. I'm going to take this. I need to tell you what's going on here.
Speaker 2Yeah. Yeah. I actually always start these conversations with insulin. And that enables a conversation because most people are just familiar enough to kind of think they know what it means, but unfamiliar enough that they're going to want to be a little curious. And so I would, I try to take this kind of holistic view where I say, hey, you are taking a blood pressure medication. You are taking a migraine medication. You are taking maybe a fertility medication. Imagine, if rather than, and that almost enables this view where we look at them all as utterly siloed, unrelated problems, because there's a medication for this one, a medication for that one and for that one. But the reality is all of these are back to my earlier metaphor, branches coming off the same tree. And the medication is simply clipping at the branches only for them to grow back because it's an ineffective approach. So to put that another way, all of these medications that we take are only treating symptoms in this instance of the three I mentioned. What was it? Blood pressure, migraines, and I don't know, maybe it was, I don't remember the other one I mentioned. Infertility. They're all, they are all to varying degrees manifestations of the same problem. And so to me, that is sobering, but it's also encouraging because as much as a person who's, say, taking these three drugs for these three problems, they're looking at this as almost hopeless. I'm on this drug for the rest of my life. And indeed, if you are taking a drug to try to solve this, what is a metabolic problem, you will be on it for life. It will never actually solve the problem. Until we shift the paradigm around, acknowledge that we just keep pruning the branches only for them to grow back, let's just cut the tree down. And that, I think, is what's encouraging, that if we can acknowledge all of these problems share a core, then it gives us one single point of attack. And moreover, perhaps the most encouraging of all is that that doesn't require medications, that that just requires lifestyle changes, which is, of course, easier said than
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Speaker 4Reproductive health. And specifically, you know, for men and women, their sexual health and how that is tied to insulin resistance. Because I think that that's also, you know, someone, you know, their sexual health is tied to insulin resistance. And I think that's also, you know, someone, you know, their sexual health is tied to insulin resistance. And I think that's also, They're feeling more anxious. You know, they're not sleeping as well. Obviously, this has like a compound effect. They're getting weight. Tie that back to sexual health.
Speaker 2Oh, yeah. Yeah. The metabolic connection to fertility and sexual health is robust. Like every problem is people listening may think they're rolling their eyes by now thinking how many things can Ben connect insulin resistance to? Oh, a lot. And this is another.
Speaker 4there's more, but yeah.
Speaker 2So let's start with men just because male fertility is so much simpler, but it's still critical. So I would say two things. One, we've already mentioned the connection between insulin resistance and erectile dysfunction because of the challenges of a dynamic blood flow change. And if you have a blood vessel that stays insulin resistant, it stays constricted. And if you can't vasodilate, you don't have normal erectile function. So You've gained weight because you're low T. And testosterone is a fat-burning hormone. It doesn't want the body to burn fat. It is, in fact, the other way that if you look at the person who's overweight, the man who's overweight and low testosterone, that's probably a consequence of actually having fat cells that are too big. So one of the quirks of male physiology is that as fat expands, it increases the expression of an enzyme called aromatase. And aromatase is an enzyme that will take testosterone and convert it into estrogen. Most people don't appreciate that all estrogen in men and women was once testosterone. Then the ovaries and the testes will just convert a certain amount of that via this enzyme aromatase. Now, ovaries convert a lot more. So in the female, her testosterone levels are here and her estrogen levels might be about here. Still, testosterone is higher, importantly, gals. In men, it will be like this. Because aromatase isn't quite as active. But in the man, his fat cells start to act like her ovaries, where it is now taking the testosterone that the testes are producing, literally pulling it in, having the aromatase rearrange it, clip it apart, and send it back out as estrogen. So he has this one-two effect, this two-part punch, which is, one, depriving him of his testosterone and all the metabolic magic that comes with it, but at the same time, increasing his estradiol, which may be telling his body to store. But at the same time, increasing his estradiol, which may be telling his body to store. In ways that are awkward for the male physique to store. And just not feeling like the testosterone wants him to feel, like this big, strong, capable man. Now, so low T, compromising erectile function and fertility, there's a huge metabolic component to both erectile dysfunction and then the testosterone reduction itself. In women, polycystic ovary syndrome is the most common form of infertility in women, increasingly common worldwide. There is an effort, actually, among fertility specialists to change the name and call it some form of metabolic infertility, which is a much more accurate term. So this comes back to insulins. One of its many effects is to affect the actions of that enzyme aromatase. And so in a person who is insulin-resistant, in this woman, her insulin levels are high, which always accompanies insulin resistance. That enzyme aromatase, which is attempting to convert testosterone into estrogen, gets inhibited by insulin. So when insulin. When insulin comes to the ovaries, one of its many effects will be to tell aromatase to work less. Now, her ovaries are releasing too much testosterone, which will cause the woman with PCOS to have some of the symptoms like acne or male pattern baldness, which are both testosterone effects. But at the same time, she's not getting sufficient estrogen to promote, to work with the LH surge, both of which are necessary for ovulation itself.
Speaker 4Luteinizing hormone. Yeah, yeah.
Speaker 2So you have luteinizing hormone, LH, from the anterior pituitary, which is interacting in a really dynamic way with the ovaries to really over-activate aromatase to release a lot of estradiol or the main estrogen. Both of those are essential for ovulation.
Speaker 4The compensatory mechanisms in the body are just wild.
Speaker 2Oh, yeah, yeah. Well, especially with endocrinology, which is why I love it so much as a science, and especially in the female fertility cycle. It is just this beautiful mass of organization, which looks like. It's not chaos, but it's, of course, intricately well-organized. But suffice it to say, when insulin's too high, it disrupts that surge, and as the surge is disrupted, ovulation does not happen. Now, all of these follicles, which had been growing throughout the normal follicular phase, the follicles developed during the follicular phase, one becomes dominant because of the estradiol, the estrogen, and the LH surge, and then that is the one that will ovulate. And then once that ovulates and you enter into the luteal phase, which is defined by the. corpus luteum, the remnant structure, which released the egg, the ovary has this remnant structure on it. It dictates the signal change to all the other follicles, which had been thinking they might be the winner, to go away. And so as the ovary was literally expanding in volume, now it shrinks back to normal, as all these follicles would have been developing. But if she doesn't ovulate, all of those follicles stick around, and now they become cysts. And now her ovaries are getting bigger, and she starts going through another cycle. And they get even bigger, and that can be exceptionally painful. And that explains the physical pain that a woman may experience with PCOS and her disrupted cycles. But once again, as discouraging as this all is, the good news is that this is something you can grab and change when you acknowledge the metabolic underpinning of this somewhat ambiguously seeming form of infertility.
Speaker 4Maybe just go into a little bit what the data say on insulin.
Speaker 2Yeah, that's one of the greater shifts in the realm of chronic disease study that's pleased me the most is this evolving view of Alzheimer's disease. What was once viewed as a disease of these plaques and who knows where they come from and who knows exactly what they're doing has now become a kind of metabolic view. Like type 3 diabetes.
Speaker 4Yeah, that's right.
Speaker 2In fact, I starkly remember I was literally attending a conference of the American. Diabetes Association. I was a postdoctoral fellow at the time coming all the way from Singapore, and I met up with a colleague of mine, a good friend, Dan Cain, who's a wonderful mitochondrial scientist in his own right. And he mentioned to me as we were going on a morning jog, he said, hey, are you going to go to this session I saw, which is as I was studying diabetes more, he said it was Alzheimer's study section. And it's all they call it type 3 diabetes. And I thought that is the craziest thing I've ever heard. I literally remember that moment at this conference. And that is. That was maybe the beginning of my book, Why We Get Sick. That was the first time I realized in stark clarity that insulin resistance has more relevance than just type 2 diabetes. I didn't know. I was studying insulin resistance and thinking it's only relevant to type 2 diabetes because insulin doesn't work well, glucose goes up, and now you have type 2 diabetes. So that was the first time I had become aware of this metabolic problem seeping into other areas. So with the brain, the brain is very sensitive to metabolic changes because it has such a high metabolic rate. It is such an energy hog. We demand so much of it, no surprise that it demands fuel in turn. insulin is the master metabolic hormone. So it's no surprise that insulin has an effect on this master metabolic organ. Part of the brain, and indeed the neurons involved in cognition, require insulin to open the glucose doors. So that provides an immediate relevance to insulin and an explanation for how insulin resistance compromises the brain. If these sections of the brain are not responding to insulin, they're not able to get sufficient glucose, now they go hungry, and like an engine that's running out of fuel, it starts to chug along and perform more poorly. But all the more reason to let it be the hybrid and give it ketones. But even then, the ketones become a problem in their absence, because if a person is insulin resistant, insulin levels are elevated. That is a core feature of insulin resistance. Insulin levels are high, so not only is it not working well at the brain to allow the glucose in, that high insulin is, at the same time, compromising the liver's ability to make ketones, which would circumvent that roadblock in glucose metabolism. But I think it's sort of a metabolic version of the rhyme of the ancient mariner. This is an old piece of poetry, and this is this sailor who's stranded at sea and bemoaning the irony of him dying of dehydration while being surrounded by water. And so he bemoans his fate. Water, water, everywhere, he says, nor any drop to drink. There's a metabolic analog with the brain and metabolism where the person may ironically be hyperglycemic, but because they're insulin resistant, that glucose isn't getting into the brain. So the brain is bemoaning its metabolic fate and saying, glucose, glucose, everywhere, but none for me. Hyperglycemic, elevated blood sugar. Yeah, glucose is elevated. I can see it there in the blood. Just give me enough to meet my energetic needs. Not only is it not getting enough, despite the body swimming in a sea of it, the fuel that it's calling out for, you know, give it a life preserver, give it a bottle of fresh water in the case of the dying sailor. The ketones, namely, are unavailable because the high insulin is driven by the high glucose is preventing the ketones from being made. So the brain is starving in the midst of plenty.
Speaker 4Gosh. So the starving brain or the brain that is less good at using glucose as fuel. Let's call it the starving brain.
Speaker 2The starving brain. It's not inaccurate because it can't get enough fuel from glucose. Dr. Stephen Cunane, the gentleman scientist I invoked earlier, he has shown in humans, even in women with metabolic, with insulin resistance, as early as their 20s, in their 20s, he has found that if they have insulin resistance, he detects a demonstrable reduction in her, in their brains to take in and metabolize glucose. So this is something you can start to see as early as people in their 20s.
Speaker 4And this is going to manifest as brain fog, you know, fractured memory or inability to remember things. Even irritability. Yeah.
Speaker 2So the person just may feel a bit anxious. They would certainly start to have some degree of, oh, gosh, I just can't remember. What was that phone number again? Or what was that address again? Yeah. So at that earliest stage, it's difficult to kind of really put a pin in what the symptoms would be. But what is so sobering is realizing that that is as early as you can start to detect some of these problems. What would be interesting is then to follow up with them 30 years later, when a woman loses the protective effects of estradiol, which is tremendously and directly beneficial to the brain, that it's no surprise that now these metabolic problems start to come to the fore because there's not enough estradiol to kind of make up for it. Because estradiol is a powerful neuroprotective signal. As it goes down to these kind of male-like levels, she's lost that protection. And if she comes into that with already compromised brain metabolism. It is just a triple whammy. Good luck. Yeah. Yeah. You're going to. We're going to very, very likely be a person who, within a few years, starts to really notice the cognitive decline. Gosh.
Speaker 4It's frightening. Yeah.
Speaker 2It's sobering. But again, the good news of all of this, the gospel message here of these chronic diseases is that the empowerment that when we say, yeah, but they all have a metabolic problem. And that same metabolic. Like the same young woman now who's worried about Alzheimer's disease may, in fact, be dealing with PCOS, the most common form of infertility in females. Well, what wonderful news that the same interventions you would make right now to help enhance your fertility and normal menstrual cycles and getting rid of your PCOS are the very same steps to help make your brain as resilient as possible to avoid that cognitive decline that we see in grandma at the moment and help your brain and your cognition maintain its function until the point of death. It's the good news. Yeah. So as sobering as it all is, I like to joke that my book, the first part portion of my book reads like a horror story, that we're all going to die and it's all because of this metabolic mayhem. But it ends with, there's a happy ending, that as sobering as this messaging is and as sobering as our conversation might have sounded to some, there's still this lingering kind of good news, this hope that this is something we can start to control and control it really well to the point of reversing all of it.
Speaker 4Right. And you can reverse a pre-diabetic state as quickly as four weeks.
Speaker 2Yes. So my lab published a report, finding that we took 11 women with full-blown type 2 diabetes and in just 90 days with just these simple but not always easy interventions, these four pillars, protein, fat, and family fasting. Yes. We took those four pillars and in just 90 days, every single one of them had reversed their type 2 diabetes. No drug injected, no pill popped. It was simply by changing what was going in their mouth and how frequently it was going in. So yeah, within weeks, to just a few months, a person can totally reverse all of this. In fact, it's so fast that if a person listening to this is a type 2 diabetic on multiple drugs, like you're taking a drug for your glucose, you're taking a drug for your blood pressure, you actually need medical supervision because you may need to start getting off those drugs within as little as a few days. It's that quick.
Speaker 4So all of these chronic diseases that we're all familiar with, cardiovascular, metabolic, if you can. You can stabilize. If you can become more insulin sensitive, you will improve your situation to the point of reversing whatever that disease is.
Speaker 2Yeah. Yeah. Yes. Yeah. Now, I don't want to. It's hard for me to make a perfect exclamation mark claim to that, but to some degree, so I'll soften it a little bit. To some degree, you are either going to fully reverse the problem or substantially improve it. Like, for example, type 2 diabetes, it'll be gone based on multiple reports, my own included. You can remove that disease without even a hint of it. Alzheimer's disease, if we're talking about our kind of 80-year-old grandma with significant Alzheimer's, no. You've done some irreparable damage to those neurons and they're not going to come back. However, the evidence is also clear that you can still improve it. So maybe, grandma, you're not going to perfectly correct the memory and some of the deficits, but now maybe she can get up and dress herself, which was something that was reported on in some of these case studies that I referred to earlier. So to some degree, you can remove that disease without even a hint of it. So to some degree, you can reverse it. If not all the way, even any reversing is better than just slowing the decline.
Speaker 4So there's a laundry list of symptoms that would make me believe, okay, I might be insulin resistant here, resistance here, and I need to go to the doctor. What would be that kind of those warning signs or that laundry list?
Speaker 2Yeah. Yeah. We've already mentioned high blood pressure. That is a really consistent, reliable marker. So if someone has high blood pressure, it's likely that you have insulin resistance. So if you have high blood pressure, it's likely that you have insulin resistance. There are other causes, but that's the most common one. Actually, we don't even need to look too far. The skin can be a window to the metabolic soul, if you will, where as a result of insulin resistance, a person can start to manifest with two distinct skin disorders, coincidentally, both around the neck. And this can happen anywhere skin is just folded and kind of rubbing. So it can happen on the armpits or the groin area as well. But two distinct disorders. One is called acanthosis which is a term to describe a darkening of the skin. Now, depending on someone's natural pigment, it can be harder to detect this or not. If you're a pasty, freckled guy like me, it would be pretty obvious. We're right around that kind of collar line of my neck. I would see this darkened pigment, kind of a coppery on my skin tone, a coppery section of skin. But that's not the only one because you also, with that disorder though, mind you, even still within that same problem, you can also have a kind of. It's. It's often referred to as a tissue paper texture where it's like you've taken a nice sheet of tissue paper, crumpled it up, and then opened it back up. And so the skin is really just crinkled, I guess, for lack of a better word. Like crepey? Yeah, yeah. Yeah, yeah. Like a crepe kind of ish paper. So again, right along that same area. And that's helpful because if a person has a darker pigmented skin, you might not see the pigment change, but you will see the texture change, that crinkled skin. That's one problem. The second, and people will know this probably, as I describe it, skin tags. These are not like a mole or a mound of skin. They're like small little mushrooms, like microscopic little mushrooms that you will also see along the neck or the armpits. And those are also these little teeny columns of skin, a secondary sign. So if someone has acanthosis nigricans, the crinkled, darkened skin around the neck and or skin tags, those are almost proof positive of insulin resistance. Now the nice. So you should be sprinting to your doctor. If you notice this, and I bet someone listening, if they don't see it on themselves, I bet they have a loved one where they are hearing me describe this and they think, my mom has this or my older brother has this.
Speaker 4How early should we be testing for insulin resistance? Yeah, I would say.
Speaker 2And how do we do it? What are the best tests? When the person has come out of puberty, now you can start to rely more on some of these best tests. You can't rely on blood glucose. We need to measure insulin. So if insulin levels are around seven or so microunits per mil in U.S. units and in the U.K., in other metric countries, it'll be kind of around 40 picomole. That's a good sign. That means insulin is low in a fasted state, which is evidence of insulin sensitivity. As it gets beyond into the teens, kind of mid-teens, I'll say around 16, 17, that's a kind of warning stage where it might be a problem, but it might be fine. The reason I have to use squishy language here, which is painful for a scientist, is that insulin has a rhythm to it, and it's possible that you're catching it at a bit of a high point, whereas if we would have measured it two hours later or two hours prior, maybe it would have been a five microunits per mil. And so there is that wiggle room, which we need to account for maybe some other markers, but then anything getting into high teens and 20s, that's too high. But then in the midst of all this, we can look at another marker, which is a really good surrogate, and that is the triglyceride to HDL ratio. So someone listening, take your triglycerides as they would come in milligrams per deciliter and then divide it by the HDL cholesterol number. And if that number is below 1.5 and the lower, the better generally, that's a good sign that you have good insulin sensitivity. So it's a surrogate, but very good marker for insulin sensitivity.
Speaker 4And blood pressure, is that like how we
Speaker 2triangulate? Blood pressure is another one.
Speaker 4Are clinicians triangulating like this? No, not at all.
Speaker 2But I do think, yeah, you and I, I know what you and I have in common is the hope that the message is definitely spreading. I mean, the fact that I'm even here, a metabolic scientist talking with you and your platform, this is evidence of things moving in the right direction. My hope is that part of the shake-up will be to ask.
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Speaker 2How are we missing so much of these metabolic problems? And then the follow-up question would be, well, how can we be monitoring it, measuring it better? My great hope is that we start to get not only some of these, what's called a post-hoc, but also some of these, what's called a post-hoc, like someone's getting their triglycerides and someone's getting their HDL, but we're never looking at them together. And there is a powerful synergy to taking these two parts and getting something greater, which is the triglyceride to HDL ratio. So at a minimum, having a separate metric that's taking those for the individual already, and having a clinician who's trained enough to point a finger at it, but then including fasting insulin. And I would even want to see fasting free fatty acids, the marker that we mentioned earlier, that's a sign of coming from the fats. And I think that's a good thing. I think that's a good thing. One of the coolest metabolic markers is one called the Adipo Insulin Resistance Index, which takes fasted insulin and multiplies it by fasting free fatty acids. And it allows us to look at the insulin resistance right at the level of the fat cell, which is the first tissue that really falls. That is the earliest tissue of all the dominoes that are going to start to begin. Well, you have to beg your physician and say, hey, can you please not only check the insulin box, but can you please check the free fatty acid box? And in the United States, love or hate our healthcare system, it does allow a person to have a little more power over what gets measured than other more centralized healthcare systems. You just have to know what to ask. And have a clinician who's hopefully open-minded and maybe humble enough to think that the patient may know something they don't know. Yeah. Which is a big ask. The more degrees you put after someone's name, the more the ego becomes settled in stone.
Speaker 4How can we increase our insulin sensitivity or reduce our insulin resistance?
Speaker 2Yeah, yeah. Those meaning the same thing, we just lower insulin. The most powerful lever we can grasp and pull down is lowering insulin. And the best way to do that is by managing macronutrients optimally. In my view, there are four critical pillars that improve insulin resistance. The three based on macronutrients, one on when to not eat the macronutrients, control carbs, prioritize protein, don't fear fat, and frequently fast. So controlling carbohydrates, I put that first. because it's the one that simply matters most. So the more a person can be consuming carbs that are from whole fruits and vegetables and less from carbs that are coming from bags and boxes with barcodes, the better. Now, in the midst of that restriction comes the abundance, which is fill the rest of your plate and stomach space by prioritizing protein. So high quality, ideally animal source protein. And then don't fear the fat that comes with that protein. In nature, all protein comes with fat. I love sausage. And I would say enjoy it liberally. When humans eat, as much as you and I both have a very favorable view of dietary protein, if we just eat protein alone, we do not digest it as well. And it's not as anabolic. Human studies have shown if protein is consumed with fat, we digest the protein better and we have a greater anabolic response for muscle protein.
Speaker 4So if you're eating like really lean turkey, you're really lean. If you're eating like lean beef, like bison, you're probably not getting the fat in conjunction with it. So you're not going to be able to utilize that protein as well.
Speaker 2Yeah, I would say be liberal with the fat. Even sometimes adding a little to it. In nature, protein comes with fat. That's how we should eat it. And then in the midst of those macros is that fourth pillar, which is just engage in some form of structured fasting. Whether it is a very deliberate time-restricted eating with what we could call mini fasts in a structured 24-hour window or some degree. 12 on, 12 off. Yeah, absolutely. There are so many ways to do the time-restricted eating and the intermittent fasting. My only reminder and encouragement would be the more a person looks at longer window fasts, keep in mind this idea that how you end your fast matters much more than how long you fast. And with that in mind, just when you think about, well, how do I end my fast, go back to the pillars of managing your macros. Protein, fat, control carbs,
Speaker 4and reduce carbs. Yep. Amazing. All right. So we're on the hopeful side of this conversation right now. So insulin resistance, chronic disease, you have kind of these four pillars that can put us in a better situation. Now, what if we layer exercise on top of that?
Speaker 2Yeah, right. Exercise is a great buffer because the muscles, as we've noted, are not only the majority of the human body by mass, but the ability of them to increase their metabolic rate and consume more glucose, especially, is unlike any other exercise.
Speaker 4So resistance training is just like one of the
Speaker 2best ways to get. I'm an enormous advocate of resistance training. Yeah. So I'm a huge advocate of muscle mass. And unfortunately, so maybe I'll start this little rant another way. If someone were to ask me, what is the best exercise to do? My answer is just going to be the one you'll do. So if there's a kind of a little old grandma listening to this and she just likes to go out walking with her girlfriends, you keep doing it. And the more you can incorporate any modest changes, great. But minute for minute, the best thing is going to be resistance training. Build muscle any way you can. And there are lots of ways to do that, as modest as little air squats and pushups to doing something as high intense as CrossFit. Any way you can increase your muscle mass, not only the exercise itself is, of course, promoting an enormous amount of glucose uptake. Independent of insulin, just as an aside, when the muscle is exercising, it becomes so hungry. That it uncouples itself from insulin. It essentially doesn't need insulin to open those glucose doors. It opens them on its own. So you have an insulin independent method for the muscle, the working muscle, to just be pulling in glucose as much as it wants. So during the exercise that's building the muscle, you're pulling in a tremendous amount of glucose, which is going to help your blood glucose settle down after you're done exercising. But then the act of increasing your muscle mass means you have more mouths to feed at any given moment of the day. Day and night. So more muscle mass will mean, at every moment, better glucose control. Better glucose control will suggest improved fasted normal insulin baseline. insulin and dynamics, which is then going to lead to more stable and low insulin, thereby improving insulin sensitivity. So minute for minute, resistance training is the way to go. And I would encourage anyone to incorporate any amount of resistance training, whether it's body weight based or kettlebells or high velocity swinging barbells around, whatever it looks like for you, just do something repetitively until it gets uncomfortable and you can't do more and then you've done it.
Speaker 4Yeah, wonderful. Is there anything that you'd add to these four pillars? It's hard to get humans to do things, but let's say they're willing to do all five of those things. What's even like another intervention they can layer on top?
Speaker 2I want to answer it maybe in an unexpected way, because as much as I'm talking about these habits, I look at my own life and my own motivations and the success of other people I know, and I would say try to have a reason for wanting to make these changes, whether it is family or community. Or other goals in life that you want to accomplish in a healthy grandpa. Yes. In fact, indeed, that one lingers in my mind because the moment my first daughter was born, my first born baby, an incredible moment for me. I, I saw in that flash of a moment, if you'll pardon me to lean into the soul part of this, I saw my I saw her life and I saw my life. It was almost like I was looking, I was standing in between two mirrors and there was like, eternity bouncing between our two faces as she was squealing beside me as I'm holding her and in with my darling wife, of course, right there. I saw my future and I saw her someday being a mother and giving me grandbabies, which is now my kids don't cuddle me anymore. It's my greatest hope of having little babies. I have
Speaker 4teenagers, too, so I
Speaker 2can't wait for it. But I think I want to be, yes, a very involved dad. I want to be a very healthy grandpa. That goes into this idea. If my only motivation were to look good, that wouldn't get me very far of all people. So my motivation needs to be something outside of Ben. And for me, it's my family. It's my community. And so as much as someone's looking at these principles, knowing they need to change, I think there is a little extra oomph. There's a little more fuel on the fire if you have a motivation that's beyond. Yeah, that's right. A good way of saying it. If your why is more than I want to look and feel, beyond your ego, beyond yourself. I love that.
Speaker 4I am not going to romanticize the experience of cold plunging. It's uncomfortable and it's intense, but it's supposed to be. That's the whole point. Getting in cold water is a deliberate choice to lean into stress, then practice staying composed while you're in it. That ability to regulate your nervous system under pressure is foundational. It's how we become more adaptable, more focused, and more steady for all the moments that matter to us the most. I've been using the Vigor, Cold Plunge from our sponsor, Hot Spring Spas. And what I love is how seamlessly it supports my habit of cold plunging. It's a plug-in tub and it's always ready to use. So I just step in, do my work, and get on with my day. And believe me, it's cold. It goes all the way down to 40 degrees Fahrenheit or four degrees Celsius, but three minutes in Vigor can elevate your energy levels, your mood, sharpen focus, and ease muscle soreness. Hot Spring has put nearly 50 years in water care and energy efficiency experience into this design. And it shows. If you're ready to make cold exposure part of your practice, head to hotspring.com slash soul. Again, hotspring.com slash soul. I'm an individual who believes in living my core values, but it can be a challenge sometimes when there are a lot of demands on my time. Life lately has felt especially busy between meetings and research, book writing, live talks, self-care, and family time. My days are already really busy. Then I added a podcast and things started to feel, well, a little out of balance, which is why you're hearing me talk about my new show sponsor. Viver is a virtual assistant who's legitimately helped me reclaim my time and my peace. Viver is the marketplace where thousands of skilled freelancers are ready to meet your business or personal needs. Browse portfolios to find someone whose expertise, skills, and budget aligns with yours. It's free. You can find me on Twitter at Viver. I'm Viver. I'll see you next time. Literally that simple. If you're looking to free up time in your life, head to Viver.com or click the link in the description and use code Kristen, K-R-I-S-T-E-N, at checkout for 10% off your first hire. That's F-I-V-E-R-R.com. So here's a plate of food. I'd love for you to just evaluate the composition, okay, as it relates to just kind of this idea that we're trying to eat in a way that's put us in the best possible position for optimal blood sugar levels and just kind of a path to insulin sensitivity. And then also, which one should we eat first? Does that matter?
Speaker 2Great. No, it does. In fact, that was a point I was absolutely going to make. So again, first and foremost, just to frame this, this is not a common meal. Most people would not be eating this. Most people would be getting something out of a bag in a box with a barcode, which I've stated repeatedly. So as much as we sort of frame this plate as a common meal, it is not common. This is much healthier than the average person would be eating. But also to put all this in proper framework, we're talking about the person who's worried about their metabolic health and is attempting to lose weight and reverse diabetes and all those metabolic problems, not the lean athlete who can do whatever he or she wants. So here we have the protein, the fat, and then carbs. So that just composition of the plate, the fat and the protein, back to the managing macros, I'm such an advocate of them. One, because they're essential. Both of these would have the essential, some degree of essential fats I need and essential amino acids that we need, whereas there's no such thing as essential carbs. And I love that there is fat and protein together. Chicken is a bit on the lean side. I'm such an advocate of fat with protein. Avocado would check that box in a really good, healthy way. Carbohydrates, if it's plant, it's carbohydrate. And we have a view of plants, which is I think a little rosier than it ought to be. Fruits and vegetables, you can enjoy, this would do nothing to insulin. This amount, especially this amount, but you could eat an entire bowl of this salad here and it would have no effect on your glucose or insulin. There's so little digestible starch offset by so much soluble fiber. Now, grains are the are the others. And the other side of that spectrum of carbohydrate at the other end, where the rice is absolutely going to elicit a glucose and insulin effect, although that's a modest amount. Now, you'd mentioned the timing. Carbs come last. So this would be a reflective, a plate that could reflect a human study that's been done, indeed at this point, multiple studies, which took the exact same foods consumed by the same people, but in different orders. One order was eat the carbs first and then eat the rest. And their glycemic balance would be the same. And so, if you're eating the carbs first and then eating the carbs last, it would be the same. And so, if you're significant, when they shifted the order around, eating the exact same foods, but the fat and protein were first and the carbs came last, it brought it down to about 60% of what the curve, the spike was when it was consumed first. So one, this is an uncommon plate. Two, we want to appropriately appreciate the macros that some matter more than others by way of what's essential and what has the strongest insulin effect. But then even then, we could take a meal like this and then balance that or time it, structure it in a way to minimize or mitigate some of the metabolic impact. And the simple reminder there is carbs come last.
Speaker 4Amazing. And how does diet soda factor into all of this?
Speaker 2Yeah, right. So this is a diet soda, which is a majority of Americans,
Speaker 4of course, are drinking some sort of diet soda regularly.
Speaker 2Yeah. And I come from Utah, which is like the soda drinking capital of the world, ironically. So with diet soda, of course, the critical difference being the absence of sugar and then the presence of a non-sugar sweetener. I am actually very, as a metabolic scientist, have a very favorable view of sweeteners. Now, other people will make other claims. Like, for example, this soda here is sweetened with aspartame. Some people want to get very worried about the scare of cancer. Well, I'm a metabolic scientist. I'm not a cancer biologist. So I can't really speak to that other than to say there's no evidence in humans to support that. That worry that you see in rodents that are not only genetically inclined to get cancer, but you're giving them super physiological doses of the aspartame. Like you would have to drink an impossible amount of aspartame. And again, even then, to find the corollary from the animals, the animals are genetically prone to get cancer. They're literally bred for that. So you're kind of priming the pump in a way that is not really fair to humans. But just to make sure that's clear, though.
Speaker 4So to be really clear, aspartame is not a carcinogen.
Speaker 2Well, the evidence in humans, certainly there's no causal evidence. Some people will cite correlational evidence, but there's just as much correlational evidence to refute it that for me, an honest assessment would have us conclude that we can't make a claim. But having said that, in the realm of sweeteners, I look at them all as a metabolic scientist through the lens of what's it going to do to my insulin. Some sweeteners actually do have an effect. Others don't. And so on the good end, it would be sweeteners like allulose, Mm-hmm. Aspartame even. Stevia is probably the most studied and still standing sweetener that we've ever seen. And monk fruit extract. Erythritol doesn't have an insulin effect. And that's about the extent on that good end. And then as we start to slide down the spectrum to the other end where the sweetener does have an insulin effect, that's where you start to see all of the other sugar alcohols. The sweeteners that end with an OL. So xylitol is pretty good. It's still down at that kind of modest end, but it has been shown to have a little effect. Then you have other ones like mannitol or maltitol, which do have an insulin effect, although less than sugar. But to me, those would be the ones to be more careful with. Now, coincidentally, and somewhat here's a crazy adverb, scatologically. So talking about like bowel habits, the more of those types of sweeteners you're eating, you'll know when you've eaten too much because your intestines are going to tell you. Right. And it's because you don't absorb it and it stays in your guts and creates a lot of GI distress, to put it politely.
Speaker 4People get habituated to that, though.
Speaker 2Yeah, that's right. Yep. You can adjust and the intestines will adjust. So those are the sweeteners to be a little more careful with. But generally, I have a pretty rosy view of sweeteners because all of them are going to have less of a glucose and insulin effect than sugar will. And so as a metabolic scientist and a guy who kind of defines or sees all habits through that lens, my view on these sorts of things is generally pretty fair. But maybe I'll give some little piece of action for a person who is curious about it. There was an animal study finding that differing populations of the microbiome actually could influence a person's response to the to the sweetener. And they tested multiple sweeteners in this study. And I can't I couldn't list them all. But they did find that different microbiome populations tended to dictate whether the animals would eat more or not. So to me, someone who's listening to this study, I think it's a good idea to do a little bit of research. I think it's a good idea to do a little bit of research. I think it's a good If they want to know perhaps the degree to which their diet soda habit is a good thing or a bad thing, I would say, what does it make you want after you're done? And if you drink that can of a diet soda and you start craving something else, that's probably something to be more careful with. If you can drink it and you feel perfectly satisfied and it scratched your sweet itch, then I'd say then you're good. And I think there's no reason to be worried about that as a habit.
Speaker 4When I'm talking to, you know, a loved one or whatever, and who's kind of struggling with, you know, just intaking too many carbohydrates or just, you know, poor eating generally, eating over long periods of time, my recommendation always is, all right, don't change what you're eating. Just try to eat more protein in the morning, more protein generally, but consolidate all of your calories inside a 10-hour window. So talk about what you've seen in the literature, what you've studied personally related to time-restricted eating as really, I think, the lowest. barrier to entry in terms of moving metabolic health in a positive direction.
Speaker 2Yeah, great. That's a great point. Yeah, as much as the conversation so far has been focusing on kind of managing macros, you know, changing the carbohydrate consumption, which of course has a huge impact, but it can be difficult.
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Speaker 2VELUX Skylights. There is clarity in simply saying, this is when I eat. And then when I'm eating, I'm simply enjoying what I'm eating. But the power in time-restricted eating is that it gives, it forces you to have a better life. It forces you to have a better life. It forces you to have a longer period of time to allow insulin to come down. And that is the great essential step in reversing insulin resistance and becoming more insulin sensitive and then enjoying all the benefits that come from it. So the evidence is quite clear that when you, it's actually appropriate and good that you've mentioned breakfast. The evidence is clear that if you were to kind of stack your time-restricted eating in a way that says, okay, I'm either going to eat in the morning or I'm going to eat it all in the afternoon or kind of stack my calories or my food on one part of the day or the other. The evidence is very clear. You want to stack it early. So there's this old maxim, which goes something like breakfast like a king, lunch like a prince, and then supper like a pauper. And so this idea of stacking everything towards the front, that is the best way to do it.
Speaker 4Ancient wisdom right there.
Speaker 2Yeah. Yeah. So, so if you get everything earlier in the day, it helps you settle in through the evening, which is when we are at our weakest. It is human nature. Yes. We're not only metabolically, but our habits. And maybe we would say the metabolic shifts are what's driving the habits. It's people experiencing changes in ghrelin or GLP-1 or even blood sugar potentially coming down because in the morning blood sugar is elevated, which would give perhaps the brain a sense of plenty and not be, you know, think about the average person listening to this. I can almost guarantee they could walk by a plate of cookies in the morning and be indifferent. To it. And yet 4 p.m. Yeah. Yeah. Yeah. In the evening, they're walking by that plate of cookies. Oh, no. I mean, they are. And so back to your point, if we stack things earlier in the day, it's easier. Not only are we eating it at a healthier time, the evidence is clear. The metabolic outcomes are better in someone who's stacking their meals earlier in the day rather than later. But you also allow yourself the clarity of just getting through the evening without being tempted, because if you have a framework which allows you to eat whatever you want in the evening, you're going to start craving stuff you should not be eating. Yeah. But if your framework says, I'm done. Yes, that's right.
Speaker 4You know, just mentally, emotionally.
Speaker 2The siren call of these seductive little sweets start
Speaker 4just screaming at us. Seventy four percent of Americans are eating something sugary within an hour of bed.
Speaker 2Yeah. And that's terrible. And you go to bed hyperglycemic. And back to our earlier point, if you go to bed hyperglycemic, you are forcing your nervous system into the sympathetic state, which sounds sweet because sympathetic. It's a nice term. But when it comes to the nervous system, that is your fight or flight. You are going to go to bed. Yeah. Your heart rate is up. It is pounding. You're physically hotter. You're warm. Your body temperature's higher. And you're laying there wondering, why am I having such a hard time going to sleep? Why am I so anxious? You're not anxious. You just had your metabolic system hijack your nervous system. So good luck falling asleep.
Speaker 4In our data, you know, looking at millions and millions of data assessments, huge hundreds of thousands of folks. Yeah. The third, so basically a high fever is going to impact sleep and recovery. And then it's altitude and then late night meals or then alcohol and then late night meals is fourth.
Speaker 2Yeah. I'm not surprised.
Speaker 4You know, it's just when people are reporting eating meals within two hours of bedtime, you know, their sleep and markers of recovery
Speaker 2are worse by a lot. Yep. Yeah, that's right. Yeah. So that's a good indicator. If someone finds they're chronically sleep deprived and are feeling what we just, some of these symptoms, I would strongly encourage you to just look at what you're eating. And that is, I really, again, as I said earlier, it's an, when you have a metabolic view of poor health, it is empowering because if you have a view, which is, no, I'm just an anxious person. Well, there are a lot of things that can drive anxiety. And so you feeling like you can grab it and change it. Like it's a lever on the wall that you can firmly grasp and pull down. You don't feel like you can, but if it is something as obvious and actionable as, oh, wait, I just don't eat that. Those three bowls of cereal every night. Oh, I can change that tonight. Yeah. That's why it's empowering that when we recognize that what we're eating and how frequently we're eating, it is a primary driver of so many problems. It is empowering because if, if we say, well, it's stress or it's inflammation or it's things, whatever, those are hard. Yeah. You don't, you might not know what's causing stress. Yeah. That's right. A lot of things that you don't know what's driving your inflammation. So it's harder to grab it. But if you know, no, it's what I'm eating and when I'm eating it. All right. You can change that
Speaker 4from my perspective. TRE is the number one intervention that you should, you know, if you're going to do, if you're not going to do anything else, time restrict your eating.
Speaker 2Yeah. No, I agree. You know, like I just feel like it's a very simple structured clarity that you can start implementing now and rely on monitors, devices to help you and anyone who's listening and tempted to do it, get help. Yeah. You know, like recruit a friend or family to say, Hey, can you kind of just follow up on me? This is when I'm eating and this is when I'm not.
Speaker 4So I always like to distinguish intermittent fasting so intermittent fasting has this kind of caloric restriction component to it, whereas time-restricted eating is just merely not changing your caloric load, but just consolidating your eating window to a specific timeframe during the daylight hour. So there's a circadian component to time-restricted eating, whereas intermittent fasting, there's no circadian component. It's more of just restricting calories during windows of time. Mindy Peltz, for example, a huge proponent in terms of intermittent fasting. Someone like Stacey Sims said that women should never intermittent fast, right? So what's your take on this landscape from a metabolic perspective?
Speaker 2Right. So there are, first of all, the problem with intermittent fasting, so time-restricted eating naturally limits itself to 24-hour windows. And Mindy, you can play around with it. Yeah, yeah. You can do six, you can do eight. That's right. So there's still some variability there, but just by nature of limiting it to 24 hours narrows down the number of options you're going to have. With intermittent fasting, one, not problem, but quirk, is that it can mean as many things as there are people who are invoking the term, that there's lots of different ways to engage in intermittent fasting. In general, I am an unabashed advocate of fasting. I think fasting is a tremendously effective tool. It is the fastest way to lower insulin, which is my main concern as a metabolic scientist. You'd mentioned some individuals. Now, I sometimes get a little heat for talking about female physiology because I clearly am not one. But as a professor who teaches graduate classes in endocrinology, I'm extraordinarily familiar with the differences in hormones between males and females, and the differences are substantial. However, that doesn't mean there aren't some consistent rules across both sexes, and in other words, applying to all humans. So what I've appreciated very much about Mindy's messaging is noting the remarkable dynamics of the menstrual cycle. Or specifically, I would narrow it down to a specific component of the ovarian cycle, where when you look at in a menstruating woman, there is nothing comparable in men. The changes you see in sex hormones are unlike anything that I joke with my students that female fertility is like a 200-piece orchestra. Male fertility is a barbershop quartet. It's very, very simple, and it gets the job done, and it sounds nice, but it's nothing compared to what you see in women. And during that luteal phase, after ovulation, that increase in progesterone is a game changer, which needs to be acknowledged because progesterone has a central effect, literally telling the brain, we need to eat more. And that's not surprising because progesterone's job is to promote an environment of gestation. And so if you suddenly are growing another little human.
Speaker 4Whether you want to get pregnant or not. Yeah, yeah. So it's sort of this
Speaker 2little warning phase, this kind of early trigger phase of saying, we might be pregnant. But regardless, progesterone promotes hunger. And so if a woman is wanting to sort of force a fasted state, and I shouldn't use such strong language, if she was wanting to fast during the luteal phase, it may be harder. Progesterone is going to make her body. Progesterone not only promotes hunger, it also promotes insulin resistance, which is why during pregnancy, you have one of the very few instances of insulin resistance that's supposed to be happening, what we call physiological insulin resistance, because it promotes a metabolic environment that wants everything to grow, which is great, because mom needs to grow.
Speaker 3And that's a feature of a healthy cycle.
Speaker 2That's right. It is. That's right. So to Mindy's credit, she's really been on the front end, the front lines of kind of saying, hey, look, women are not the same as men, and they're not. And one of the big differences among many is that menstrual cycle, and specifically the dynamics of the ovary during these phases, and especially the luteal phase. Now, sometimes, though, I feel like that gets pushed a little too far, where you have a message perhaps, where the individuals may say, well, women shouldn't fast. And I don't think that's productive. And I don't think it's justified, because the evidence suggests that there is a short-term difference in women, where women will see an increase in cortisol that men don't. And often, that gets turned into. Translated. Yeah, translated into saying, well, it's a unique stress. Well, cortisol, sure, we call it a stress hormone, but we could also just call it a metabolic hormone or an immune hormone or any other number of things, that cortisol, one of its main effects is to increase blood glucose. And so it's no surprise that cortisol may go up and does go up during a fast. It's just, and so does glucagon, so does epinephrine, which is why, oddly enough, in a short-term fast, but I mean, like, even to the point of 24 to 48 hours, in humans, metabolic rate actually goes up.
Speaker 4Where do we see a point of diminishing returns on our platform? It seems that there's like a, 24 hours, they seem to get better. And then there's kind of a sharp decline after 24, I'm sorry, after 48 hours.
Speaker 2Yeah. So actually, that's probably a pretty good window. Although, I think there's probably going to be tremendous variance. For sure. So within the massive variety of humans, metabolically speaking, there'd be a couple of ways to define them or to put them into categories with regards to the efficacy of fasting. One would be the degree of body fat on the individual. And then the other would be the degree to which they are already familiar with the body fat. And then the other would be the degree to which they are already familiar with the state of ketosis. So if a person is, for lack of a better term, keto adapted, they make ketones very readily and they burn ketones readily, a fasted state is going to be something they transition into very, very easily. Because that's a difference where, especially at the brain, the moment, in fact, there's probably no tissue more sensitive to these dynamics and glucose and ketones than the brain, because those are the two main fuels for the brain. And so, you know, I think that's a good way to put it. I think that's a good way to put it. Unlike any other tissue, which will very readily burn fat as a fuel, the brain doesn't. It primarily just relies on glucose and ketones. So the more a person is letting the brain burn ketones and has sufficient mitochondria to use the ketones, the more fasting is going to be pretty benign and smooth. The more they, the degree to which they do not have ketones and they are not used to ketones in their blood, or it takes them longer to make them because their insulin is chronically elevated, then fasting is going to be very difficult. They're going to be very lethargic, very hungry, and it might be consequential to the point that they shouldn't do it or should ease into it. Intermittent fasting can mean any number of things, but when it comes to multi-day fasting, I confess that I get a little uncomfortable in part because to me, when it comes to intermittent fasting, how you end your fast matters much more than how long you fast. So I worry about an individual who just looks at the fasting craze and says, I'm going to do a three-day fast without any plan on how to end it. And let's admit, if we're being honest, the average individual is going to end that three-day fast by binging on all sorts of junk. It would be bowls and bowls of cereal, perhaps. And that can actually create a lethal situation called refeeding syndrome. And I won't get into the physiology of that, but suffice it to say, if you've been bringing down your insulin and your glucose over this multi-day fast, you're going to end that three-day fast. And that's a lot of metabolic harm. So as much as I'm an advocate of intermittent fasting, I'll just say it again, how you end your fast matters more than how long you fast. So I would suggest starting modest, maybe just a single 24-hour period. But what matters even more than that is that you know exactly what you're eating when you're done. And if you need to, again, I encourage people to recruit help. Get outside influences to make sure that you only eat what you've laid out. And then you have a plan. Maybe one hour later or two hours, you feel like you need a little more. Okay, then this is what I eat for round two. And you stick to the plan. So to say all that another way, you do not want to end a fast with a high-glucose, high-insulin spiking food. So protein, primarily fat. Protein, fat. Absolutely.
Speaker 4All the way. Yep. So that's your refeeding kind of protocol after post-fast. And you would recommend for men, for women, 24 hours is a good kind of sweet spot.
Speaker 2Certainly a good starting spot. And when it gets to, 48 and beyond, not that people can't do it. You sure can. But I just start to get a little.
Speaker 4You just don't have the energy to work out. You can't lift weights. You maybe can, but not at the intensity levels where you're getting returned for those workouts.
Speaker 2Yeah. And I think too often with intermittent fasting, it becomes its own version of a binge purge cycle, as indelicate as that sounds, where the person, they jump into a fast, and then they get hungry, hungry, hungry, hungry, hungry. And then they just binge. They eat themselves to a point of regret and remorse and shame. And they say, oh my gosh, I can't believe I did this. I'm going to do better tomorrow. And they do the same thing again. Then they feel like they have to fast again to purge all of the binging and the discomfort. So intermittent fasting is incredibly effective, but like most things effective, there can be a downside to it. Yeah. I want to talk
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Speaker 2Yeah, protein is a friend. But I look at what is the effect on insulin and what do I need? And thankfully, those two priorities coincide perfectly with regards to how we ought to structure a diet. So there are such things in the human diet called essential fats, fats that a human must eat in order to survive. Okay, so let's make sure we get them. All natural sources of fats will have these in them. So animal fats, there are animal fats and fruit fats, lesser sown fruits. But all animal fats will have the essential fats that we need. And thankfully, interesting. A human can eat fat and there will be no effect on insulin whatsoever. None. If someday we get to the point of having a continuous insulin monitor, and we are a long way from that. So far. So far, because of so many hurdles. But insulin would be a flat line. This has been studied in humans. My lab has done this work as well. Now let's go to the next macro, protein. There are such things as essential amino acids. Amino acids that a human must eat to ensure survival. And there are nine. Yeah. And animal. Animals give you all of them. And you can sort of find them in various plant sources, but why complicate it? Yeah. And thankfully, protein will have little to no effect on insulin. But that's, you know, people will notice I'm using a little bit softer language there. Because in people with type 2 diabetes, protein can result in a bigger glucose spike, which will give an insulin spike. So some people can eat a load of protein and have no insulin effect. Some people may see it. But it will still be relatively. It's relatively modest compared to the third and final macronutrient, namely carbohydrates. So not only do carbohydrates, which is a big variety of foods, you know, broccoli will have a different effect compared to pure glucose will, or a piece of bread, and yet they're all considered part of the one class of carbohydrate. But taking something like the more refined end, which if we're being honest is what most people eat, you will have a huge increase in blood glucose. And then, of course, a huge increase. Insulin can eat. It can easily go up by 10 times and stay elevated for 2 to 3 hours, even in an insulin-sensitive person. It's a very normal response with insulin to a pretty normal carbohydrate load nowadays. So that's one automatically that suggests, okay, well, that's the macro we should be cautious with because it has the biggest insulin effect. And I'm claiming very much that chronically elevated insulin is the main driver of insulin resistance. All right. So it behooves us to be cautious with that one. But thankfully, it's also the one macronutrient, as we've said, that humans need. It sounds so controversial, and yet all rigorous, honest assessment of human biology admits, including even the slow-moving entity of the U.S. government in the USDA report from decades ago, notes that the lower limit, I'm almost quoting it verbatim, the lower limit of dietary carbohydrate is essentially zero. In other words, humans do not need carbohydrates. And so when it's the one we don't need, it's the one that has the biggest effect on glucose. Okay, well, that's the one I'm just going to eat the least amount of. I'm going to focus on the ones I need and the ones that will keep my metabolic health in the best state. Now, I don't want someone to think I'm saying we can never eat carbs. I'm not saying that. But I am very much unapologetically saying that is the one we should be the most cautious with. That if you're laying out your plate, let the fat and the protein be the majority of it. And then let the carbohydrate be the complement to it. And even then, I would. I would say, because there's such a variety of carbohydrate, focus on the carbohydrates that do not come from bags and boxes with barcodes. Those are the ones to be cautious with. If it's whole fruits and vegetables. So anything processed. Yes, that's exactly right. is what we want to avoid. Whole fruits and vegetables, eat them. Don't drink them, I would say. Yeah. But then if it's processed, keep it on the shelf as much as you can. A raw apple, a carrot.
Speaker 4That's absolutely right.
Speaker 2You know, sweet potato. And those are going to have a modest effect on insulin and glucose as it is. But the more you've refined it. Mm-hmm. which makes it more and more delicious. Yeah. that is what we start to crave or even have an addiction for. It's the sweet and the gooey or the salty and the crunchy. Mm-hmm. And that's going to be based on the carbohydrate backbone.
Speaker 4Damn. Mm-hmm. Are there any different considerations for elite-level athletes? Yes. You know, they're eating a lot of carbohydrates. Yeah, yeah. And they burn a lot of carbohydrate. They burn a lot of glucose. And Lane Norton is going to come at you with daggers.
Speaker 2Yeah, yeah. So there are people who. And I just want to make sure everyone appreciates that as a metabolic scientist, I'm not an exercise physiologist. Now, as much as I do, in fact, have a graduate degree in exercise physiology, my main focus as a bioenergetics student and a postdoctoral fellow in metabolic disorders and all of my getting close to 100 papers published on metabolism, they're not exercise-focused. And so I really am happy to have an opportunity to create a big line between these two populations that I have in mind. Throughout this conversation, and indeed the focus for my book and much of my work, is focusing on the overweight person struggling with chronic disease. Right. That is not the person who's training and is already lean. I think it's important to. It is. It really is. And so the more a person finds themselves on that end of the spectrum. The more the carbohydrate consumption can go up. So I am good friends with. You have more muscle. You do. And you have more muscle. Explaining why your muscle matters. You're demanding the muscle eat more. And muscle is hungry. I'm good friends with a guy who at one point was training for an Ironman. And he was wanting to be able to capitalize on the extra fuel of ketones. Ketones are. There are more and more, especially endurance athletes, who are making sure that they have ketones available as this extra fuel. And the evidence supports it very readily. So he was wanting to make sure he was in a metabolic state to have ketones and to be making them and using them well. He could eat over 300 grams of carbs a day and still be in a deep state of ketosis every morning that next day. That's wild. He was just using it. And so the more a person's using carbs, the more I would say, because of physical activity, the more they're able to eat them and have no dent in their metabolic health. Negative consequences. Yeah. And I think it's just important. But to note these differences, that I don't mean to declare war on carbs, but I think if we're being honest, and the evidence certainly suggests this, the more metabolically unhealthy you are, the more that is the macronutrient that is problematic. Right. So just again, to state it clearly, carbs are not a villain. I think they are an enemy to most people, but they're also an ally to others. And it depends on the metabolic state of the individual. But with carbohydrates and why I say that some people struggle with them, there was a fascinating paper published in 1996, one group in Scandinavia, they published a report looking at two groups of people in their GLP-1 response to certain foods. And so to set the stage, these popular weight loss drugs, the main mechanism of action is to mimic this hormone that we all make from our intestines called GLP-1. And GLP-1 has myriad metabolic effects throughout the body. The two that are most relevant to the modern weight loss craze are an effect on the guts to slow the guts down, so we feel fuller longer. There's just more bulk there longer. And to activate central satiety centers in the brain. So the brain is telling us we're full. The intestines are making us feel full. That's a wicked combination that works well. So it's slowing motility. Yeah. And basically- Promoting, reducing hunger. Right. Yeah. So that's a great combination that makes us think GLP-1 is our friend. And justifiably, it is our metabolic ally in this war of healthy body weight. Right. So in that 1990s- 1996 report, they noticed a difference in lean versus obese individuals. So when they both ate a high-fat meal, lean and the obese group, they found that GLP-1 levels were roughly the same in both groups, suggesting that satiety in response to fat would be roughly similar between the two groups. Very relevant. So imagine two individuals, an obese one and a lean one, or back to how I was acting, lean and obese. They eat something very fatty. They're both going to have a roughly equal degree of saying, I'm full, and push the plate away from them. However, when they ate, both groups ate a high-carbohydrate meal, the difference in GLP-1 was enormous. The lean group had a huge increase in GLP-1 that persisted for about two hours, and it came down around the two-hour mark. In stark contrast, the obese group ate that same amount of a high-carb meal and found that not only did the GLP-1 not rise at all, at around that 90-minute to two-hour mark, it actually went below baseline. So not only did it not rise, it actually hovered around baseline with a little bit of physiological noise and then went down. And that's where the error bars tightened, on the drop of it. So now back to them sitting at a table, now they eat, rather than a fatty meal, they eat a pasta-rich garlic bread meal. The lean group, with this huge GLP-1 response, would eat that amount of carbohydrate and say, I'm full, I'm done, I don't need any more, because their guts are feeling full and their brain is, they're telling them they're full. But now, with all empathy, we look at the obese individual, in an almost total absence of GLP-1, they've eaten these carbs, and now they just, not only are they not pushing the plate away, they're saying, can I have more? Because around that 90-minute, 120-minute mark, it actually goes down. Now, GLP-1's not the singular satiety signal in the body, but if we claim GLP-1 matters, to me, this represents the best use. So rather than looking at these GLP-1, agonists, and just calling them weight-loss drugs, here's your weight-loss drug, continue to engage in any habit you currently are, and you're just going to lose weight. No, we should tell them, this is a drug, well, in fact, even before we give them the drug, we should talk about the dynamics of fat loss, and how if you help, if you lower your insulin, you increase metabolic rate, and you will burn more fat more easily. That should be the first conversation. And so we say, here's your fats, your proteins, your carbs, really start trying to control your carbs. Some people will be able to, and they don't even need to have a conversation about the drug. Some people will try to control their carbs, but they will continue to go back to their bad habits like an addict, because food addiction is real, and no one's addicted to proteins and fats. It's only ever cravings for carbohydrates, and some people can't kick the habit. So now to that person, we say, this is a drug that's going to help you change your habits. Let's not talk about them as weight-loss drugs.
Speaker 4I love that.
Speaker 2Let's talk about them as habit-changing drugs. And so we're going to put you on a low dose, what we could call a micro-dose, and we're going to be on it for 90 days. And 90 days has been shown long enough to control addictions and habits. So let's see how you're doing over this 90-day period. Change your habits, and then we can talk. Change your habits. And they'll notice, hey, I'm not craving the cereal in the evening to confess my own sins again. They'll find that they're having a little easier time, that the food noise, as people call it, is just a little quieter. So let's leverage that and aim it at the proper enemy, which is going to be the constant consumption of refined carbs. Then the person's losing weight. At that 90-day period, we say, how are you doing? They're saying, I'm doing great. Okay, let's now cycle you off the drugs. So that's the second component that I believe is the best use case of these drugs. A low dose with the intention of controlling habits, and then finally you cycle off and see whether the habits have stuck. In some people, they will have, and they have a new baseline, a new normal. Other people, they may find the cravings coming back. Okay, let's cycle you on again. Now we're going to cycle you off again. Remember, you're being mindful of your habits. That's how we ought to
Speaker 4use them. Do you consider that a dietary strategy?
Speaker 2Yeah, I do, I guess. It would be a dietary strategy with some assistance. Throughout this conversation, I hope I've been articulating the relevance of changing diet and how simple it is. It is simple in principle, but that does not mean it's easy in implementation because human habits and addictions are their own thing entirely. And so this is a way to, I guess, make it a little easier to implement. The ideas are simple. Control your carbs, prioritize protein, don't fear fat, and frequently fast. Those are the four pillars to improving insulin resistance. But they can be, number one, control carbs can be a real killer. It's hard for some people to do. So this is where we say, here is, I guess, a crutch. It's going to help you limp through some of these changes until you're strong enough to stand on your own two legs.
Speaker 4Do you think keto is a good dietary strategy to control carbs? And kind of as a, you know, hey, let's try this intervention before we go into a GLP-1?
Speaker 2Yeah, oh, I do. Absolutely. I think, in fact. We've talked a little bit about.
Speaker 4Yeah, yeah. I wanted to try to
Speaker 2frame this in a way to suggest that before we should ever get to these carb-controlling drugs, to call them maybe a better term, I think we ought to have the Can you control your carbs? And at the lower level of carb consumption, as insulin comes down, the body shifts into a fat-burning state, and the more you're burning fat, the more you're making ketones. A good friend. That's ketosis. That's ketosis. That's right. But people aren't leveraging this. No, no, they're not. And even worse than that, they're told by these well-trained and certified dieticians that they should avoid it at all costs. I mean, the number of myths I have heard from educated people within the nutrition realm, about ketosis, are almost too many to count.
Speaker 4What's the number one myth that you've heard?
Speaker 2The number one myth is that ketosis will burn your brain. That's one I've heard. And the irony to that is that humans. In fact, one of the leading theories of evolution by a scientist named Stephen Cunane, who's just a wonderful individual as well, brilliant scientist, wonderful gentleman, he actually has a theory of human evolution that suggests the reason we even became what we are with our big, hungry brains that are unlike any other animal on the planet is because of our ability to get into ketosis. Especially as newborns. So the time. So the irony in this statement, which makes it so false that ketones are burning your brain, is that during the state of the most accelerated, massive brain growth, which is a newborn baby, is a state that is almost defined by ketosis. So a newborn, if we and I were talking, we have a six-month baby here, a darling little chubby cherub, and that baby doesn't eat for two hours, it would be in a deeper state of ketosis than you, then you and I would be in two days. What? It'll get to one to two to three millimolar of ketone, which would take me almost three days of fasting to get there. Yeah. And so how can we say that ketosis is burning a brain? And indeed, studies that have used non-human models find that in the fetus, if the mother has ketones in her blood, that baby is using. The brain of the baby is using more ketones than any other single tissue in the entire two-person organism. That's wild. I've never heard that. So yeah, the brain, far from burning the brain, ketones are the preferred fuel. Just to put a fine point on that, people will often say glucose is the fuel or it's the preferred fuel. No, we know Dr. George Cahill decades ago found in humans that if you have glucose and ketones that are even disparate to the point of two times, if glucose is, say, five millimolar and ketones are two and a half millimolar, which is a very reasonable metabolic state, the brain is already getting about 70%. So if the brain has a preference for any fuel, it's for the ketones. The moment ketones come into the blood, the brain starts using them. And this is probably why almost across the board, if you take a brain disorder, a neurological problem, it gets better with ketones, whether it's migraines or bipolar disorder or schizophrenia or cognitive decline, Alzheimer's disease, Parkinson's disease, literally every one I just rattled off and more, epilepsy, that have been shown to improve to the point of absolute curing the individual, depending on the problem. Migraines and epilepsy will often stop entirely as long as a person's in ketosis. The brain loves ketones. So of all the myths, that's probably the one that's the most egregious.
Speaker 4How do you get into ketosis?
Speaker 2Yeah. So the key of getting into ketosis is lowering insulin. And that is a reflection of insulin being the master metabolic hormone, that at a broad level, the human body is a hybrid. At this broad level, we're burning fats or glucose, and some mix of them at any point. We're sugar burning or fat burning. And it's insulin that dictates the fuel. If insulin is up, the body is sugar burning. If insulin is down, the body is fat burning. In fact, that whole phenomenon is metabolic flexibility. A lot of people invoke that term nowadays and might not really know what it means. It's used incorrectly. It's the ability to shift between them. All the time. It is. It is. So there you have it, everybody. That is the definition. It is, are you sugar burning when you eat carbs or are you fat burning when you're not eating? That's the difference. And metabolic inflexibility, as it was first identified by David Kelly and Brett Goodpaster 30-ish years ago, it really was known to be a state of insulin resistance. If you are metabolically inflexible, when you eat, you burn sugar. And when you don't eat, you're still burning sugar. It's because their chronically elevated insulin won't allow the metabolic hybrid to shift over to fat burning. And then back to ketones, that shift must happen. When insulin is low, it immediately shifts the cells of the body that are capable into fat burning mode, the liver included. And the liver is important to understand when it comes to ketones. Because the liver is the ultimate nexus of all nutrients, whether it's lactate or ketones or amino acids or fats or glucose, the liver handles all of them. And there's no other tissue like the liver. I say that the liver is the soccer mom of nutrient metabolism. It knows just what to do with everything around it. It is monitoring and organizing the metabolic chaos. So. the liver is using its own fuel or storing fuel. When insulin is low, like so many cells of the body, the liver shifts to fat burning. And in the early stage of the fat burning, the liver's burning fat in order to meet its own needs and its own cells, creating energy for the liver cells. But then as insulin stays down for a period of about 16 to 20 hours, once you reach that point, the liver has run out of glycogen. So its own stored glucose has run out right around that time. Which is not harmful. It's perfectly natural.
Speaker 4So basically there's no more kind of carbohydrate
Speaker 2or glucose in the blood. That's right. It's gone. That's exactly. Yeah. From the liver. Yep. So of what it has stored on hand, it's run out of its own glucose. And at that point, you have potential to get into ketosis. That's exactly right. Yep. So now the liver is continuing to burn fat, burn fat, burn fat, and it starts burning more fat than it needs for its own needs. So its own kind of energetic well becomes full. It's energetic cup. It's full. It's burning fat, burning fat, burning fat, and it's meeting its own needs, but it can't stop burning fat. I mean, it literally can't stop burning fat even because insulin is low. Even though it's met its own needs, it keeps going. And now this excess is what starts shunting into the ketones. So it's spilling over the fat burning cup is what's becoming ketones. And that's the liver's way of telling the body, hey, I know glucose has stopped coming in. And it knows that because the low insulin is telling it. We've stopped eating glucose. Now I'm still going to make glucose, which it does. It continues to make glucose. This is why a person can fast for 384 days and a perfectly normal blood glucose levels. And mind you, the main source of that is lactate. So the liver will say, hey, there's less glucose coming in. I'm still going to make it, but I'm also going to start making this replacement fuel, especially for you brain, because you're so big and hungry. I want to make sure that you have this other fuel as well. And so as much as it's still making the glucose, it's the body's a little more miserly. And so it's going to start making glucose. And so to account for that, it's now, if you will, creating this replacement fuel in the form of ketones. So that is what ketones are. And again, the number of myths surrounding ketones and ketosis, which is a state of just when ketones are elevated, are innumerable. And they are all based on this old mistaken view that ketones are, at best, metabolic garbage. And at worst, at worst, they're a toxic metabolite. They're a fuel for the brain. Further. It could not be further from the truth.
Speaker 4Let's just say I go into sleep and I've got, over the course of the day, I had 100 grams of carbohydrate. Would it take 12 hours to kind of get through all of that glucose? Then in the morning, I would be in ketosis?
Speaker 2Yeah. So unfortunately, you'd have to go back in time and say, well, were you already kind of carb loaded before you ate those 100 grams? And so that would come back to the liver. So let's assume you went into it with a liver that was already void of its glycogen. You'd gone and fasted, let's say. Fasted for 16 hours, and then you ate 100 grams. You would be in ketosis the next morning, probably. You would be. You're fit. You're active. You would be an insulin sensitive. You're insulin sensitive enough, your insulin would come up, clear the glucose, come down, and within a couple hours, you're back to fat burning. And then you're back into ketosis. So 100 grams in you, you'd be all right. So a lean, healthy adult who's moderately active, maybe to take it away from Kristen and apply it generally, you'll be in ketosis probably, if not in the morning. when you wake up by about noon or early afternoon. Now, a type 2 diabetic who's overweight, that 100 grams may take till the end of the day before they get into ketosis, or maybe even the following morning. Now, I don't mean for that to sound dramatic. It's just all a function of how high did your insulin go, and how high did it stay, and how long did it stay elevated. The longer insulin is up, the more it is inhibiting fat burning, and literally inhibiting the production of ketones, a process called ketone. And so you'd be in ketosis, and you'd be in ketosis, and you'd be in ketogenesis. At every single one of the steps, when you take the fat molecule and break it apart, and then start taking those individual pieces to make ketones from it, that's about four or five steps. Insulin inhibits every single one. And so that's why to understand ketogenesis and ketosis, you really need to appreciate the master metabolic hormone, insulin. But the degree to which that stops ketosis really depends on the person, what they did before they consumed it, and what they're natural. The natural metabolic state is in that moment. So it can vary widely. Like that lean triathlete buddy of mine, it wouldn't even dent him. He'd be in ketosis. He might not even get out of it.
Speaker 4Yeah, that's why.
Speaker 2He might stay in it the whole time.
Speaker 4So if I were to wake up in this state of ketosis and the conditions you described, and I had a few eggs and some avocado, I stay in ketosis, right? Because there's no carbohydrates there. That's right. Okay. How long do I need to be in ketosis? To really get the benefits.
Speaker 2Yeah. So I would submit that the benefits start immediately. And so that's because of its signaling effects. So there is human evidence to show, take someone with cognitive decline, have them conduct. So early stage Alzheimer's, this has been done in humans. Have them conduct a series of cognitive tests. And of course, they do terribly on these because they're cognitively compromised. You give them a ketone supplement.
Speaker 4So this is the fastest way.
Speaker 2But. We can do with it. This is why we can speak to how rapidly these things can work. Because you can immediately spike the ketones up by drinking them in or consuming them in some way. And so now you can determine within just hours, the cognition has improved. If they repeat those cognitive tests, they do better on all of them. And the same thing can be said for a host of other neurological problems that we've mentioned. So with the rise of ketone supplements and exogenous ketones, that's allowed us to kind of put a stopwatch. Yeah. So
Speaker 4that's a good
Speaker 2question.
Speaker 4Every. Are there instances where some people shouldn't?
Speaker 2Yeah. There could be an instance where if a person's already very, very strictly adhering to a ketogenic diet, like little to no carbs, then I would say the value of the exogenous ketone might not be worth the cost, whether it's extreme or modest. It's just not as needed, I would say. But for all the rest of us, I think there could be a case. I know more and more athletes, as I noted. At BYU, my university, we had this remarkable distinction of both the men's and women's cross-country teams winning national championships this year. A feat, I don't think has ever been done before. I don't think it's a coincidence that while we have some awesome strength training coaches, they also take exogenous ketones. More and more Tour de France teams are doing the same. So ketones are a good fuel. That, of course, is some evidence, albeit anecdotal. The more a person. The more a person is eating carbs, the more I think exogenous ketones are therapeutic and warranted and helpful. Maybe that's the nicest way to say it.
Speaker 4If they're not necessary, I'd say they're helpful. Thank you for that. That was so. I mean, I've never tried exogenous ketones. It's encouraging, isn't it? I'm like, can you get them at CVS, like your local pharmacy?
Speaker 2No, not yet, but I'm sure we're getting there. As the benefits of ketones are getting so well documented, naturally, we're going to start to see more of a shift, which is the beauty of capitalism. The market will return. There's a need. The invisible hand is going to escort more and more people into that realm.
Speaker 4So where does one get exogenous ketones?
Speaker 2Yeah. So there are a lot of supplements that'll come in various forms, where on one end of the spectrum, you can get ketone precursors called 1,3-butanediol, where the liver will convert that molecule into beta-hydroxybutyrate. But then there's also direct sources where the person can just get, like GoBHB, the person just can directly get beta-hydroxybutyrate. In the form of electrolytes or other liquids that they can just drink easily. So the technologies are expanding the offerings.
Speaker 4Yeah. And you can just like at a GNC or.
Speaker 2Online. Online. Yeah.
Speaker 4And would you recommend a precursor for someone who's just getting into using these ketones? I will. Asking for a friend?
Speaker 2Yeah, yeah, yeah. So I think, I actually think just the direct source of BHB is, you are literally just getting straight ketone. There's no conversion required.
Speaker 4So. Benjamin, final question. What does it mean to be human?
Speaker 2Oh my gosh, that's a great question. Earlier in the conversation, I mentioned having a reason for making a change and wanting to be healthier that would go beyond just the self or the ego. I think one thing that would set us apart, if we look at the variety of life on this beautiful planet, is that we're not just going to be healthy. We're going to be Why are we so different? A part of perhaps of that among many differences would be our community. So one, maybe one definition of human would be to think beyond your immediate needs and think about what others may need. I think one of the ills of society where we have such a mental health crisis, I think it is because we are denying what ought to be a human concern for our brothers and sisters on this planet. So I think one of the cures for poor mental health to some degree is thinking about someone else. So maybe perhaps just to sum that up in as tidy a way as I can. To me, being human. Being human means to seek connection with other humans in a meaningful way that wants you, that forces you to think about someone else. Family is a great test kitchen for that, immediate family, having immediate needs, having a little baby who demands more of you than you think you can give, but it also brings out more of you than you ever knew you could give. But then even going beyond your immediate household, find community, whether it is finding people with common interests that you can go and enjoy those common interests with, whether it is gathering for something as formal as organized religion, whatever that community is, seek it, be a part of it, and make it better. And I think you are, to a degree, realizing your potential as a human. That's beautiful. Thank you. Thanks for your time today. My pleasure. Thanks.
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