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Beverly Yates, ND is a licensed Doctor of Naturopathic Medicine, who used her background in MIT Electrical Engineering and work as a Systems Engineer to create the Yates Protocol, an effective program for people who have diabetes to live the life they love. Dr. Yates is on a mission to... Read More
Ari Whitten, MS is the founder of The Energy Blueprint. He is the best-selling author of The Ultimate Guide To Red Light Therapy, and Eat For Energy: How To Beat Fatigue, and Supercharge Your Mitochondria For All-Day Energy. He’s a natural health expert who takes an evidence-based approach to human... Read More
- Uncover the role of mitochondria as your body’s energy powerhouse and its critical importance in combating type 2 diabetes
- Learn how optimizing your body composition, through managing muscle mass and body fat, can significantly reduce insulin resistance
- Discover the impact of lifestyle factors, like shift work, on your metabolic health and strategies to mitigate their effects
- This video is part of the Reversing Type 2 Diabetes Summit 2.0
Beverly Yates, ND
Hi everyone. Welcome to this episode of the Reversing Type 2 Diabetes Summit 2.0. I’m your host, Dr. Beverly Yates, ND. It’s my distinct honor and privilege to interview one of our wonderful sponsors, Ari Whitten. Ari has a wonderful, extremely deep background when it comes to research and caring about how the body processes energy, where it comes from, mitochondrial function or dysfunction, insulin resistance, and things like that. We know when people struggle with glycemic regulation, diabetes, or blood sugar issues, that underneath that there is sometimes a particularly stubborn fatigue, exhaustion, and a lack of ability for the body to tap into its energy, despite ironically, often stores of energy. But they’re not functional energies. We’re going to talk to Ari about that because closing that link is often what unlocks the ability to heal and reverse type 2 diabetes. Ari, welcome to the summit.
Ari Whitten, MS
Thank you so much for having me, Dr. Yates. It’s a pleasure to be here.
Beverly Yates, ND
I’m delighted to interview you. Thank you for your time, your effort, and your consistent expertise around this, because you’ve been doing this for quite a while. With that in mind, would you please give us a thumbnail overview of your background?
Ari Whitten, MS
I could give a very long story here, but the very short version of it is health science has been my passion and obsession since I was 13 years old. We’ve been going on for about three decades now. When I was young, my interest was more, I would say, typical teenage boy interests. I wanted biceps and abs. So I was very deep into exercise, science and nutrition, exercise, physiology, and biomechanics. I was also an athlete. I was a high-level martial artist and a soccer player. I was interested in the performance enhancement side of things as well. I later went on to do a bachelor’s degree in exercise science and certifications in exercise science and as a performance enhancement specialist as a corrective exercise specialist with certifications in nutrition. I was a personal trainer for many years, both for high-level athletes and for just average Joes and Janes. Further, I spent some time in graduate school; I was in medical school for two years and decided this was not for me. I’m not into the pathology focus. I’m into health science, not disease science. I went on to get a master’s degree. I went on to a PhD program in clinical psychology. I did all three years of coursework on that and decided I didn’t want to do the internship phase of it, but fascinating education in clinical psychology as well. I’m well versed in the mental, psychological, and emotional sides of health as well. and I’ve also done a master’s degree in human nutrition and functional medicine. My interest more broadly is looking at human health through the lens of evolution, through the lens of evolutionary biology, and looking at how we can cultivate more health by providing the lifestyle for which we have evolved. Right now in the modern world, over 80% of the chronic disease burden is caused by diseases of lifestyle, sometimes called, in the literature, diseases of civilization. This means that these diseases are a result of the mismatch between the modern environment and lifestyle and what human biology has evolved to require for health. To the extent that you have a mismatch between what your biology needs to be healthy and the way that you are living in the environment you’re in, you will tend to be predisposed towards disease. Indeed, the vast majority of the chronic disease burden is caused by diseases that are directly the result of this. In my view, we cannot understand human health properly without this evolutionary lens. This is an essential ingredient for truly understanding what’s happening. Understanding things the right way is the first foundational ingredient that we need to end up approaching solutions. How to fix the problem in the right way. If we’re not understanding it correctly, then it’s pretty much all but a guarantee that we will not derive solutions that are intelligent, effective solutions. I would say, as an example, that if we don’t look at disease through an evolutionary lens, and I would argue that conventional allopathic medicine generally does not, then we might end up in a paradigm where we are trying to solve diseases of lifestyle and environment through synthetic chemicals by going into a chemistry laboratory and synthesizing new molecules that we can have somebody take in the form of pharmaceuticals, prescription drugs that we’re trying to solve diseases with. It doesn’t work very well. Less than three percent of all the drugs that have been developed over the last century are curative drugs. Most of the curative ones are anti-microbial antibiotics. This model simply doesn’t work for chronic diseases. If we want to solve these diseases effectively, we have to address them at the level of actual causation, which is lifestyle and environment. That’s my focus. I would say the last thing I’ll add is my background, my educational experience, and the way I think about health and solving health problems, which is different from most people in the sense that my background is health science rather than pathology science. This is about the science of how we build more health rather than combating disease. My background is also more of an experiential background. I’ve been a biohacker since long before there was such a term. People who are bodybuilders and high-level athletes were the original biohackers, doing self-experimentation with their physiology to figure things out. That’s what I’ve been doing since I was 13 years old. For me, health science isn’t just a set of things I learned in the classroom—in biochemistry class, anatomy class, physiology class, and pathology class. Though I took all those courses as well in graduate school, this is very experiential for me. This is years and decades of experimenting with human physiology. My own and the thousands of people that I’ve worked with.
Beverly Yates, ND
Thank you for setting up that lens for us. Much of this speaks to what I care about in my professional career, both as a licensed doctor with over 30 years of clinical experience and as naturopathic medicine, along with being an MIT electrical engineer and systems engineer, and, looking at the lens and realizing that so much of what goes on, certainly news is about disease management. It is not about caring for health or promoting health. That’s where the wheels just come right off the cart when it comes to chronic illnesses and the ones that are so sensitive to lifestyle. I’ve always thought of Type 2 diabetes as being the most sensitive to lifestyle. It’s good news. Frankly, it’s a challenge because of how we’ve got ourselves set up, and we have to be smart about what we do. When we’re talking about energy systems, mitochondria, and insulin resistance, let’s start at the beginning, or a place where I think people who are listening can engage here because we have both the general public as our audience and fellow health professionals who are part of this summit. One of the things that was super exciting to me, and this was shortly after the birth of my second child, was when the human genome was unlocked. They had figured out where it was and what it meant. We were about to have this whole new wave of thoughts, insights, and understanding. One of them that got me jazzed was some of the insights around mitochondria, whether it was specific nutrients like Ubiquinol or whatever. I was like, I think this is going to be a transformative moment because there were plenty of people that used to come to my clinic who had things like congestive heart failure, things like that, who, in the nineties, came in with buckets of supplements. They weren’t what they seemed to be taking, which might be helpful. Now I knew what was missing because I could tell it wasn’t just coenzyme Q10 as one example; it was Ubiquinol. That’s better and things like that. For what we can get accomplished here within the timeframe that we have to share, would you please give people a thumbnail overview? What do mitochondria do for them? Why should they care about its function, and how can that relate? Because you do have such depth in exercise physiology. A lot of people with diabetes struggle with consistency around their energy, feelings of fatigue and exhaustion, and being able to stick to exercise because they’re just tired. Ari, please talk to us.
Ari Whitten, MS
There’s a lot there. Let’s see how to break that down and where to start here in responding to that. First of all, let’s start by saying that mitochondria are something that we all learned about in high school and college biology courses. As everybody remembers, this is the powerhouse of the cell. That’s the one thing people know about mitochondria. Remember, on the test, if I’m asked which organelle of the cell is the powerhouse of the cell, is it the Golgi apparatus, is it the lysosomes, is it the nucleus, or is it the mitochondria? I checked the mitochondria. But beyond that, most people have been taught, including most people who go to graduate school and take grad-level courses in physiology, about mitochondria, just one of many organelles. They’re important, but so are lots of other organelles and other parts of physiology. But if we imagine a car with lots of different parts that are necessary for that car to function, if you take the wheels off, it’s not going to work very well. If you take the tires off, it won’t work very well. If you take the spark plugs out, it won’t work very well. There are lots of parts that are necessary for that car to function, but some parts might be more important than others. Like, for example, what engine it has. The mitochondria are like the engine in our body—the engine in our cells. It is what provides over 90% of the energy to all of the trillions, virtually all of the trillions of cells in your body, from your brain to your heart to your muscles and so on, to your skin cells, to your eyeballs, to just about everything. What cells do, and different cells in different parts of your body do different things. The brain does a different thing than the lungs, then the heart, then the muscles, then the thyroid gland, and so on. But to do whatever their function is, they require an abundant supply of energy. To the extent that they don’t have an abundant supply of energy, those cells tend to do their job very poorly and tend to become dysfunctional. If you understand the basic principle that cells require abundant energy to function, now we can understand why mitochondria might not just be another organelle but might be of central importance in human physiology. Indeed, we now have, especially in the last decade, an explosion of tens of thousands of studies on mitochondrial health or mitochondrial dysfunction. Something else that we’ll talk about—that’s an important distinction most people don’t talk about—is mitochondrial size. the size of your mitochondria. The robustness of your mitochondrial network is a major determinant of dozens and dozens of diseases and even the rate of aging itself. Of course, as we might logically infer from these beings, they are cellular energy generators that provide most of the energy to the trillions of cells in our body. They’re also pretty important to our energy levels. If it’s hard to feel as a whole organism energized and full of energy, if, at the cellular level, your cells are struggling to produce energy, The connection here is very logical and obvious. We don’t have to invoke a complicated, convoluted physiological explanation. Oceans of the adrenal glands are important in energy because they produce this hormone called cortisol, which impacts blood sugar regulation, and the blood sugar therefore controls your energy. Because this isn’t true, if you don’t produce a lot of energy at the cellular level, you are a collection of trillions of cells. If you don’t have lots of energy at the cellular level, you will not feel subjectively much energy. This is important again, for energy. But broader than that, it is a major determinant of your risk of many diseases and a determinant of the rate of aging itself. The reason why, if I can try to explain this very briefly, has to do with a concept, a little-known concept called the homodynamic space, and the homodynamic space is essentially your body’s capacity to deal with stress stressors of various kinds, whether they be chemical, psychological, or any other type of stressor, from a poor diet, from toxic relationships, whatever it is, poor sleep, and so on. Whenever our bodies are under stress, there is an increased energetic demand on that system. To the extent that our bodies are capable of meeting that energetic demand and it is below our body’s capacity to deal with that, we can handle it. We can maintain health and homeostasis to the extent that stressors are more than or are overwhelming our body’s capacity to deal with that bioenergy demand on the system, and our system will incur damage.
In addition, what will tend to happen is that that damage occurs as physical cellular damage, as oxidative damage, and that the physical structure of ourselves and the physical structure of mitochondria can degrade over time, hence predisposing us to many different diseases. That is essentially what aging is. It’s the accumulation of cellular damage. To the extent that that is occurring at a rapid rate, we are aging at a faster rate. The capacity of the mitochondria in the cells of our body is a direct determinant of the rate of aging. The rate of aging is itself a major risk factor for most of the chronic diseases of aging, which are most of the diseases that kill us. Age itself is the biggest risk factor for those things. You don’t see people dying in general of things like dementia and Alzheimer’s or complications of diabetes, heart disease, stroke, and things like that in their twenties and thirties. It happens at older ages, and it is precisely for this reason that biological aging itself is the biggest risk factor for getting these diseases. Now, with that said, we can understand that mitochondria have this central importance in human physiology. Now, one critical layer that I want to add to this is that most people, including in functional medicine circles and natural health circles, understand that when I started talking about mitochondria ten years ago, nobody was talking about mitochondria. This was when everybody was talking about adrenal fatigue, for example. Now mitochondria are much more in vogue. Many more people are talking about them. Mitochondria dysfunction is a buzzword. But what most people still don’t understand is that they conceptualize mitochondria as these static entities in our cells. We have these mitochondria, and they’re there, and they can either produce lots of energy or be dysfunctional. The truth is quite a bit different than that. The truth is that we have many lines of evidence showing that we on average lose about 10% of our mitochondrial capacity with each decade of life. Maybe it doesn’t sound like that much, but consider this: the average 70-year-old has lost 75% of their mitochondrial capacity. The reason why this occurs is largely a result of atrophy from a lack of stress and a lack of challenge to the mitochondria. As an analogy, I present to you the very common logical idea that if I challenge my muscles by lifting heavy objects regularly, they will adapt by growing stronger, Conversely, if I break a bone and I put my muscles in a cast and I immobilize those muscles for eight weeks, when I get that cast sawed off at the doctor eight weeks later, those muscles will be half the size as they were two months ago. This is a fundamental principle of how human physiology is designed. Use it or lose it. The body is a dynamic, malleable, adaptive machine that is intelligently trying to adapt to its environment. It has certain challenges. It says, I better adapt to these challenges to survive this environment better. If you remove those challenges, it says, I guess I don’t need all that muscle mass on that leg anymore. We’re not, and we’re not using it. Now it’s just a survival liability. Let’s get rid of it. There’s no sense in preserving all of this energetically costly tissue. That same principle applies at the subcellular level. At the mitochondrial level, it’s just less outwardly visible. We can see it the way we see muscles, but it’s the same thing. to the extent that you don’t challenge your mitochondria regularly, they shrivel up, they shrink, they atrophy, and they die off to the point where the average 70-year-old has gone from what they used to have, let’s say in their twenties was a Ferrari V8 engine, and now it’s age 70. They have a moped engine in their cells. Now, given what I explained earlier about mitochondria being central to our stress buffering capacity and our ability to prevent damage from exposures to stress, prevent cellular aging, prevent disease, and, of course, support our energy levels, Perhaps it’s clear why going from a Ferrari V8 engine in your cells to a moped engine is a big deal in terms of your health, your energy levels, your risk of disease, and your rate of aging.
Beverly Yates, ND
Along that journey, you want to optimize your health in as many ways as you can, and if you can turn back the hands of time, so to speak, with aging, and just buy yourself time so that ideally your health span equals your lifespan, to me, that’s like the magic mix because there’s a lot of people now who are living longer; they’re not living better as they age. I cannot tell you, Ari, over the last decade and a half, how many people have said to me that if I’d known I was going to live this long, I would have taken better care of myself when I was younger. But none of us know what the expiration date is.
Ari Whitten, MS
I’ll add a few layers of knowledge to that without going too deep. There is a broad misconception that humans used to live much less than they do now. This is largely a misconception that’s built around statistics more than anything else, because we measure a term called life expectancy at birth, which is the average age of death, and the rat, as opposed to the maximal age of a particular population. The problem with that is that it’s hugely affected by infant and child mortality. We have these data from 100 or 200 years ago in North America and Europe, in hunter-gatherer societies, where it says, these people used to die at age 40 or 50, and now we’re living so much longer than we ever did before. This is mostly a difference, not of living to older ages than we used to, but mostly a difference in a massive reduction of infant and child mortality, death by accidents, and death by infectious diseases. At very young ages, and by massively reducing the number of people who are dying at age zero, one, five, or 12. It used to be the case in North America and Europe 150 years ago that 50% of kids didn’t make it past the age of 12 or 15. There was a huge level of child and infant mortality, and those massively skewed the averages down. Based on that, we have this idea that people used to live only to age 40 or 50, and now we’re living so much longer. We know this is not true for several reasons. One is, for example, that we can look into ancient history, for example, the ancient Greeks, and look at famous people like Aristotle, Socrates, Hippocrates, and Democritus. Many of these ancient Greeks 2,000 years ago were living into their eighties, nineties, and even past 100. The average life expectancy at birth of people in the US right now is 73 and 79 for men and women, respectively. So as another data point, we can look at modern hunter-gatherers. For example, there’s a tribe in Bolivia called Tsimane and the Moseten tribes. There have been recent studies just in the last year or two where they take adults who are in their nineties from these tribes who have zero access to pharmaceuticals and zero access to modern medicine. These are hunter-gatherers living in the jungle, with no medical care. The idea that we modern humans are living so much longer than we used to is not true at all. We certainly have way less child mortality than we used to, but we’re not living any longer than humans did. A couple of thousand years ago or 20,000 years ago in terms of maximal lifespans.
Beverly Yates, ND
I think that there’s so much more isolation, unnecessary misery, and other things that go on now. This is why people have this idea in their heads that I’m not going to live that long. Let me say that for some people, not everyone, but then they don’t do the things that would be basic around their health care, whether it’s regular walks, doing things that require the use of muscles, use of your mind, etc. But there’s a certain level of neglect. Some people have baked into their lifestyles because they don’t think they’re going to live a long time. That’s right. The first thing is that it’s very odd.
Ari Whitten, MS
The one thing I want to add to that, in line with what you were just saying, is that you said earlier about wanting our health span to match up with our life span. The thing about these hunter-gatherer tribes, for example, the Tsimane, who have been studied in just the last few years, if people want to look this up, is that they have the lowest cardiovascular disease of any population ever studied and the lowest incidence of dementia and Alzheimer’s of any human population ever studied. Their health span matches up with their life span, as opposed to us modern humans, who have at least a decade, if not much more. Some of this has to do with semantics and how we’re defining health span, which is a whole other issue. But we have many years where we are chronically diseased and physically and cognitively disabled to one degree or another, whereas in populations like the hunter-gatherer population, their health span does match up with their life span. They live with very good physical and cognitive functionality well into old age, much more so than us modern humans. Some of these studies have shown that adults in their sixties and seventies in these tribes have a cardiovascular function that is equivalent to that of U.S., North American, and European adults in their twenties and thirties and that their brains have a rate of brain aging to the point of what I was talking about earlier with mitochondrial health: the rate of brain aging is 70% slower than for us North Americans and Europeans. That gives a sense of the power of nutrition in lifestyle, and I think there are a lot of illusions that we have about modern medicine and taking these drugs. We have 19,000 drugs that have been created in the last 100 years. How much that has boosted, how long we’re living, or how healthfully we’re living.
Beverly Yates, ND
I do think that the band-aid approach is just not effective. I think there’s a way in which people have a false sense of security and aren’t being armed with the information that they need, which is why I appreciate people like yourself and others who are experts here on the summit gathering together to help people be able to get their arms around this and understand how this can work for them. With this in mind and knowing just how functional it is around aging, around optimizing, aging, around having a mitochondrial function, about feeling energized, feeling like carpe diem, when you wake up, seize the day, and being able to do the things you have in mind throughout the day. What is the tie-in here with insulin resistance? Because again, with Type 2 diabetes, there is this irony of how much potential energy there is. If you will, not to take this into a science and engineering discussion, but there’s a lot of pent-up energy in that body. It’s just not being tapped effectively. That’s a large part of what’s going on in the resistance. Can you help us understand what it is that people might have some myths about and then bust those myths? I want people to go away from this talk with some clear action steps. Understand that this is what the issue is. Here’s my role in it. Here’s what I do.
Ari Whitten, MS
There’s so much to be said here. I’m trying to think of how I can condense this into a few-minute answer. What I talk about a lot is energy and how to have more physical energy. If we go back to mitochondria and think about what mitochondria do from the way we’re taught about them in biology and physiology courses, they take in carbs and fats, and they pump out energy in the form of ATP, Adenosine Triphosphate. On a basic level, logically, if you have that bit of information, one might say, If I have low energy, maybe I just need to add more carbs and fats to the system. Provide more fuel to those mitochondria. Maybe it’s a deficit in fuel. If I provide more fuel, then mitochondria pump out more energy. Wouldn’t it be great if the fatigue epidemic could be solved that easily just by telling people to eat more carbs and fats?
Beverly Yates, ND
Maybe by winning, we’d all be like gold, silver, and bronze on the Olympic Stadium.
Ari Whitten, MS
That’s how we know that that’s not true. We can easily disprove this basic, logical hypothesis because we can find lots and lots of people, the majority of the population, who are chronically eating fuel over their needs while simultaneously somehow struggling with low energy levels. You have an excess of energy over fuel and yet a deficiency of energy. What’s going on with the cellular engine that is causing this? There are a lot of layers to this story, but if I can simplify, one important layer is body composition and excess body fat in particular, as well as low levels of muscle mass. This story also ties into hunter-gatherers, by the way, because it turns out these exceptionally healthy hunter-gatherers generally have exceptionally good body composition relative to us modern humans. In the US right now, 30% of adults are overweight, and 30% are obese. If we look at measures where they combine blood markers of metabolic health with these body composition metrics, it’s over 90% of the US population has excess body fat. That excess body fat itself is a big problem. We have these models of insulin resistance and diabetes that are very biochemistry-centric. They are about different molecules floating around in our blood and different molecular and cellular mechanisms and biochemical cascades happening. This inflammatory cytokine does this, and it results in this. This then alters the glut for receptors, which impairs the entry of glucose into the cell. When you look at things through that paradigm, it wires your brain to look for biochemistry-centric solutions to those problems. If only I could have a molecule like a drug or maybe a natural molecule—maybe it’s metformin, maybe it’s berberine, maybe it’s alpha lipoic acid or something like that—that goes in and alters that mechanism so the cell can pull in more glucose. That would fix the problem because, as I read in the biochemistry of this problem, all these cascades are important and central to this whole story. But going back to what I said earlier about the importance of paradigm, if we want to solve problems effectively, we have to make sure we’re looking at them in the right way. What I want to encourage people to do is look at insulin resistance, Type 2 diabetes, and mitochondrial issues, which are very overlapping because obesity and insulin resistance, or being overweight, excess body fat, and insulin resistance will drive damage to mitochondria. hence they’re connected. Why someone can have an excess of energy in the form of fuel and yet have a deficit of energy in terms of the energy produced by them, by their cells? If you have a physiological environment that’s driving suppression of mitochondrial energy production, damage to your mitochondria, and atrophy and degeneration of your mitochondria, well, now you can pump all the fuel you want into the system. If I have a dysfunctional engine in my car, will adding more gasoline to the fuel tank solve that problem? No, I have to fix the engine if I want it to burn that fuel properly and make my car go fast. It’s the same principle in the human body. Now, I want to encourage people to think about what’s going on here. Less from a biochemistry frame, like, I would say, the majority, certainly within allopathic conventional medicine, think this frameless through a biochemistry-centric frame and more through the frame of the structure, structure dictates function. Going back, I’ll use my car analogy; I guess I’m fixated on that at the moment. If I have, let’s use a bicycle. I’m going to switch things up. If I have a triangle, a hexagon, a trapezoid, or a square-shaped wheel on my bicycle, will it function the same as if it’s a round shape? We’ll probably not. I’d say it’s going to function pretty poorly. Structure dictates function. This is a key principle of human physiology that is either massively unknown or underemphasized by most people. We do not. We are so fixated on the biochemistry of health problems that we do not understand. Structure, the physical structure of our physical body, is a huge, huge determinant of the problems that we have. There are lots of layers to that story I could talk about, but let’s just talk about the insulin resistance part of the story. If I have a deficit of muscle mass, if I have low muscle mass, and if that muscle mass is not being utilized frequently, but let’s just say I have low muscle mass, that muscle mass is glycogen zinc for carbohydrates entering the system. If I have a tank, you could think of it as a fuel tank, if you will. That’s a place for fuel to go. That’s a healthy place for fuel to go, as opposed to overflowing when it gets stored as fat. Now, if I have a small fuel tank, that fuel is much more likely to start overflowing and causing dysfunction and can be stored as fat. Having an abundance of muscle mass, especially highly active muscle mass, where there is a large amount of energy coming in and going out of it frequently, is a critically important piece of the story. The physical structure of your muscle mass is an important piece of the story about insulin resistance. Even more important is the excess body fat itself, which is another type of physical structure. We have fat, which is an evolutionary mechanism. Body fat is an evolutionary mechanism to pull excess energy out of the bloodstream because excess energy that’s floating around in our bloodstream—excess fuel, carbohydrates, and lipids—is itself directly toxic to our cells. We have to keep that in a narrow range—what’s in our blood—so that we’re not chronically pushing too much energy into the cells and causing damage to our cells. fat is this mechanism by which body fat is this mechanism by which we can pull excess fuel out of the bloodstream and store it in our tissues, number one, to minimize the cytotoxicity of, but also for cases where this matters a lot more in the ancestral context. Cases where we don’t have a lot of food and now we have fuel that’s stored in our body that we can pull that fuel out of and use for energy. We can go for not only hours but days and potentially even weeks without consuming any food, just based on the fuel supply that’s stored in our body fat. Now, the problem is that those are cells. This is the body fat. These are our physical cells, and we have a certain number of them. We don’t have an unlimited supply for the most part. There’s some nuance to this, but we don’t have an unlimited supply or an unlimited number of these cells. Each cell doesn’t have an unlimited capacity to expand or take in more lipids. What happens is, if you think of it like a balloon, basically each adipocyte fat cell takes in more lipids; more of this excess fuel and spans and expands. But it gets to a point where it can’t expand anymore; it can’t grow any larger. It maxes out. Once that happens, the fat cell itself becomes dysfunctional, and your fat cells more broadly become dysfunctional. They become leaky. They don’t hold in the excess energy either. and this starts an inflammatory cascade. However, the inflammatory cascade that also predisposes insulin resistance is secondary to the structural problem of the physical adipocytes. Fat cells in your body have grown and expanded to their maximum capacity. This is also called, in the literature, your fat threshold. Once you keep pouring fuel into the system, you have a physical structural problem that is driving the biochemical problem, and there is a way of simplifying this. Everything that I’ve just said is if you have good body composition, if you are lean if your body fat percentage is lower rather than higher, that doesn’t mean you have to be ripped with six-pack abs or something like that. But I’m saying, as a matter of degrees, if you’re moving in the direction of leanness as opposed to being overweight and you have more as opposed to less muscle mass and hopefully more active muscle mass, if you have good body composition in those two things if your physical structure is healthy, you’re pretty much not going to have Type 2 diabetes. You’re not going to have insulin resistance. It is almost impossible to have a good physical structure in terms of body composition and those two things and also to have large amounts of insulin resistance. You can find rare exceptions. You could point to some skinny, fat person. I would still say they have low body mass and low body muscle, and maybe they’re eating a horrific diet, and maybe they’re doing night shift work or smoking cigars, or they’re drinking alcohol or something like that. You could find some rare person who is not outwardly overweight and who is under-muscled and seems to have a lot of insulin resistance. But this is a rare exception. What I’m trying to say is that if you think about it less as a biochemistry problem and more as a physical structural problem, it reframes what you think is the solution. Maybe instead of trying to add molecules and drugs to my body to alter receptors, mechanisms, and biochemicals, what I need to do is alter the physical structure of my body by altering my body composition, my body fat level, and my muscle level. If I do that well and have good body composition, I don’t want to guarantee it because I can’t. I can’t make a 100% guarantee, but it’s pretty close to a 100% guarantee that you’re not going to have insulin resistance if you have good body composition.
Beverly Yates, ND
It certainly tips the odds in your favor, for sure. Outside of the exceptions where someone has, say, Type 2 diabetes as a viral infection result, yes, they can occur. But in general, body composition is the thing to focus on, and how you get there depends on your age and stage, your gender, and your stress levels. I love the fact you touched upon the realities of shift work, especially for people who work all night or, rotating shifts, because it is a metabolic health disaster. All the research is just lived experience; you watch people’s health unravel if they’re on shift work. It’s terrible. On the other hand, somebody has to be at the hospital in the middle of the night because sometimes people need help.
Ari Whitten, MS
For sure.
Beverly Yates, ND
It ain’t easy. Ari, thank you so much for such a wonderful session. You’re a great episode. Frans, please link arms with us. I am sincere in my effort to help three million or more people reverse type 2 diabetes. I see this as a pivotal moment in human history. We have got to work together to make this difference. Now we’ve got young children, not even in the double digits, ages eight and nine, showing up with type 2 diabetes. This can’t continue. We have people showing up, interestingly, for other reasons with Type 1 adults in their forties and fifties, something has fundamentally changed. I think we all know what it is. We each can do our part. Kindly share these episodes with others that you care about so we can give people good-quality, factual information. Ari, thank you so much for this. Where can people find out more about you and your work?
Ari Whitten, MS
My website is theenergyblueprint.com, and my newest project that I’m starting now is humanoptimization.com.
Beverly Yates, ND
Love it. Friends, make sure you go check out those websites and find out what Ari is doing and follow him because he’s a person who puts forward the effort and the sincerity around looking at the facts and how they apply so that they’re useful, not just a bunch of anecdotes or things that sound good but have no basis. Thank you so much.
Ari Whitten, MS
Thank you for having me.
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