Speaker 1:
Welcome to The Dr. Gundry Podcast, the weekly podcast where Dr. G gives you the tools you need to boost your health and live your healthiest life.
Dr. Gundry:
Welcome to The Dr. Gundry Podcast. Obesity, heart disease, neurodegeneration, the list of modern diseases goes on and on, and although they all seem unrelated, research shows that the cause of many of these serious illnesses may actually be driven by just one thing. I’m talking about insulin resistance, and it’s a lot more common than you may think. In fact, insulin resistance is the most common health disorder worldwide, yet very few people are familiar with it. That’s why today I brought on Dr. Ben Bikman, a renowned metabolic research scientist, professor at Brigham Young University, and author of the book Why We Get Sick: The Hidden Epidemic at the Root of Most Chronic Disease―and How to Fight It.
After a quick break, Dr. Bikman and I will unpack insulin resistance and how it affects virtually every system in the body. We’ll also share why there’s no better time than right now to take control of your health and give you the tools to do just that. Whether you’re interested in losing excess body fat, optimizing brain function, supporting your heart health, or simply feeling your best, this is an episode you don’t want to miss. We’ll be right back.
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It’s actually been, I think, 20 years now when the concept of insulin resistance was proposed. I know Garrod Wearden was a big proponent of this about 20 years ago. The concept of insulin resistance is a culprit in our health issues. So I thought we could do a deep dive into the subject and give kind of a refresher course to the audience because I’ve been writing about this for a long time and I tend to forget, like you say in your book, that most people haven’t even heard of this even though it’s been around. So when it comes to insulin, most people think about insulin as a medication for people with diabetes. So let’s start off by defining insulin and how it works in the body. Go ahead, take it away.
Dr. Ben Bikman:
Yeah, yeah, yeah, sure. Thank you so much. Right. In fact, it’s funny you mentioned how most people aren’t familiar with this. That’s why I didn’t name the book Insulin Resistance: Why You Should Care because I knew no one would. They would only read it if they thought they had diabetes. Yeah, so this is the most common problem, and it all starts with that humble little hormone insulin. It is very little on the grand scale of hormones and what their sizes are, but insulin has an effect at literally every single cell of the body. Now, I don’t use the word literally too liberally like the kids do these days. Literally, every cell will respond to insulin. From brain cells to bone cells, or lung cells to liver cells, insulin will come to a cell, knock on a door, if you will, that’s specifically designed for insulin, and then tell the cell to do something.
And it does a lot of things, of course, because it does things differently at different cells. But insulin’s most famous effect, and I’m not saying it’s most important, but its most famous effect is to control blood sugar or blood glucose levels. And that’s why people typically only think of insulin as being relevant to, say, diabetes, which is they look at diabetes as a disease of glucose. Now, I have my own issues with that definition, but nevertheless, that’s its most famous effect and that’s how people see it. The problem that we live in is that the average individual is eating the wrong foods and eating them so frequently that their body is flushed with insulin all the time. And right by the time in the morning, overnight that insulin’s starting to come down, what do they do? They immediately bump it right back up for the next 20 or so hours.
So we’re living in a state of chronically elevated insulin, and this is, I would say, the primary driver of insulin not working as well as it used to. And as you noted, this is the most common problem potentially affecting up to 88% of US adults. What we call the metabolic syndrome, what used to be called the insulin resistance syndrome is the most common disorder that we deal with.
Dr. Gundry:
Yeah. Now, you made a good point. I tell my patients that insulin literally is a salesperson that knocks on the door and says, “Hey, I want to sell you something.” And as I tell my patients, right now the home is full that they’re not interested in buying what insulin is selling anymore and they’re resistant to the sales pitch that insulin is making. Besides the fact that we eat 20 hours a day almost constantly, why has this happened? Why is this a modern disease?
Dr. Ben Bikman:
Yeah. Yes. This is the modern disease, and in my mind it’s certainly the case I make, is that insular resistance is the foundation of all of the so-called plagues of prosperity. These diseases that our ancestors never heard of that are just eliminating and wiping us out, they are diseases of lifestyle and it is absolutely the food we eat and the frequency with which we eat it. Now, unfortunately, to make matters even worse, so much of what we do is at the behest or the encouragement of people who we trust. We’ve been told that we should avoid fat, and we’ve been told that we should eat just low fat foods and we should eat six times a day. And I look at that as a metabolic scientist and I think, boy, that is a perfect recipe to create a perfect metabolic storm of ensuring that insulin is chronically elevated and then every chronic disease will start to follow in some order.
Dr. Gundry:
How do we get this so wrong? You’re right, everybody has been told, “Eat six small meals a day. You got to keep your metabolism revving. You can’t have a fall in your blood sugar that’ll sap you of energy.” I mean, where did we go wrong?
Dr. Ben Bikman:
Yeah. Well, there’s certainly a lot of myths that need to be busted. And you’ve noted some of the biggest ones. I believe the origins of this all started with the anti-fat crusades of the 1950s and ’60s, which was built on this idea that eating saturated fat will cause heart disease, and then in short order, that became a concern of eating fat in general is going to make you fat. That was not the prevailing paradigm at the time. What we take as the gospel of metabolism nowadays, which it’s just accepted as dogma, was absolutely not accepted broadly in the earlier part of the 1900s. This really came to life in the mid 1900s. And of course, it’s only grown and it was institutionalized, which is where I think it really became a problem.
I don’t mean to be perceived as an individual who is opposed to political power, but it’s just particularly tragic that, as far as I know, with the issuance of the initial dietary guidelines in the US, that became the first time that a government told its people what to eat. And wouldn’t you know they got it all wrong, in my mind. The pyramid ought to have been flipped or at least ought to have been more balanced and not vilified fat. I’m a great defender of fat, and I know that’s something you and I are aligned with. That idea then started getting mingled with other ideas, like you need to eat to keep up your metabolism. What a remarkably amusing statement.
One of the realities of fasting is that on a short order fast, 24 to 36 hours, metabolic rate actually increases. Most people don’t appreciate this due to… And in contrast, eating frequently where you’re bumping up your insulin. We just published a paper looking at how insulin slows down metabolic rate in fat cells. We published that last year, from human fat samples. We took fat biopsies from humans. So the whole idea of how we look at food and how we need to be eating all these calories to accelerate our metabolic rate, while there has always been an ounce of truth to some of those ideas, it has increasingly ignored the fact that at the end of the day, it’s not calories that dictate metabolic health, it’s hormones. Because on its own, a cell doesn’t know what to do with the energy that it has around it. Hormones tell the cell what to do.
Case in point, and then I’ll be done, right across the hallway here on campus is my lab, the Metabolism Research Lab. Now, we grow fat cells in little Petri dishes. These little fat cells are swimming in a sea of calories. They have abundant fats, abundant glucose, all of which a fat cell is eager to take in and turn it into stored fat, but it can’t do it until we start sprinkling in the insulin. And I’m not saying calories don’t matter. Energy matters. Of course, it does. But hormones tell a cell, especially a fat cell, what to do with the energy that it has.
With your metaphor of the salesperson, insulin will knock on the door, and what it’s attempting to sell to every cell of the body is this message of, “I have something here for you to store. Don’t let it go. Take it into the house of the cell and store it and hoard it and hoard it. Don’t break it down. Don’t give it away.” Now, as you noted, some cells stop responding to that with numerous consequences, but some cells don’t. Some cells continue to be responsive to that sales message that insulin is trying to pitch.
Dr. Gundry:
And you mentioned a very important point there that I want everybody to realize, and I spend a lot of time in my more recent books trying to make this point. Let’s assume that elevated insulin is bad, and we’ll get into why that’s bad. But one of the consequences of having a high insulin level, you’re right, insulin is trying to get fat cells, “Take this stuff, store it as fat,” but you said, “and don’t release it.” And one of the, I think, most important concepts for people who are trying a ketogenic diet or trying even fasting, is that most Americans, most westerners are metabolically inflexible, and they have such high insulin levels that insulin prevents the fat cell from releasing the fat. It blocks hormone sensitive lipase to get to-
Dr. Ben Bikman:
Yep.
Dr. Gundry:
And without hormone sensitive lipase, you can’t release that fat. I mean, it’s a really damned if you do and damned if you don’t with insulin. So many people just kind of fall flat on their face when they attempt time-restricted eating or intermittent fasting. Can you get into that?
Dr. Ben Bikman:
Oh, yeah.
Dr. Gundry:
I think that’s a really important part of what you mentioned in your book.
Dr. Ben Bikman:
Yeah. Right. Well, I very much appreciate you bringing this up. From the way I’m looking at what you’re describing, you’re touching on this idea of, well, the relevance of the fat cell, which is enormous, and then how the fat cell kind of gets it wrong or gets it right for improving metabolic health. The fat cell is one of the cells that my lab studies most heavily in recent years. We are sort of split between the fat cell projects and neuron projects with regards to the brain and brain metabolism. But with the fat cell, the mistake that many people will make is assuming that… Well, one, we assume fat is bad, which is just not true. We are designed to have fat on the body and we need it. The absence of fat completely is utterly catastrophic.
To the species, for example, there’s no reproduction without fat mass on the body, just as an example of one of many consequences. But of course, too much is a problem. And that’s the problem that we have nowadays. But it’s not a problem of mass. The mass of fat we have isn’t important. What is important is the size of the fat cells themselves. So if you could imagine two individuals that each is gaining weight and they meet up again as college roommates 20 years later and they’ve both gained 50 pounds, which is not too hard to believe at all.
Dr. Gundry:
No.
Dr. Ben Bikman:
But one fellow, he has normal blood pressure, he doesn’t have any migraine headaches, he has normal fertility, but even though, he’s gained the same 50 pounds. The other guy has migraines, he has fatty liver disease, he has erectile dysfunction, hypertension, but they have the same amount of fat. But one fellow has gained his fat through a process called hyperplasia, which is when the fat cells are multiplying to store more fat and to respond to insulins storage signal, but they never get very big. The moment the fat cell starts to get big, we simply recruit a new fat cell. So while there are a lot of fat cells, they’re all metabolically sound and happy and healthy.
On the other hand, we have the individual, and this is where the vast majority of people fall, most people are this fellow, where the number of fat cells they have is set. This is typical. After puberty, when we’ve gone through adolescence and we’re adults, whatever number of fat cells we have is done. And thereafter, any growth of fat mass is due to hypertrophy. Each individual fat cell starts to get very, very big. That is the fat cell that becomes very insulin resistant because it gets so big. And it can get 10 times the size of the other fat cells it has to start to tell insulin, “Insulin, you are continuing to force me to take in what you’re selling and you’re not allowing me to let it go, but too bad, I have to start letting it go.” So it starts leaking these free fatty acids that will get stored elsewhere in the body where the body shouldn’t be storing fat, like muscle and a liver especially.
But at the same time, the hypertrophic fat cell gets very inflamed. It starts releasing a lot of pro-inflammatory cytokines, all in an effort to try to survive. It actually is doing so to try to increase blood flow to itself. It’s starting to run out of blood. As it gets so big, it can’t get enough blood. But unfortunately, while the hypertrophic or really fat fat cell is doing these two things in order to ensure its own survival, it’s starting to damage the rest of the body.
But then, to kind of bring it back to what you mentioned, as I quickly wrap up, most people would say immediately, “Well, I’m going to shrink my fat cells.” Even if they don’t say it that way, they’ll think, “I’m going to lose weight,” and I would say, “You want to shrink your fat cells.” “I’m going to do it by cutting energy and I’m going to go fast really quickly and immediately.” But that’s not the best way, in my mind, to shrink a fat cell because if someone, as you noted, has metabolic inflexibility and they kind of have chronically elevated insulin, if they just jump into a fast, they’re going to be stuck in sugar burning mode because insulin determines sugar burning mode and turns off fat burning mode. Because of what you noted with the change in lipase activity at fat cells, you literally can’t access your own stored fat. So the person’s glucose starts to come down and they start to get really hungry, and more and more hunger climbs and then hunger wins, and then they break and they end up binging and going back to old habits.
So in my mind, while energy matters to shrink fat cells, don’t start with that. Start with cutting back insulin. And when you start cutting back your insulin through dietary changes, then you can allow the fat cell to shrink as you start using your own fat, then later you transition into some degree of fasting where now you’re scrutinizing energy a little more.
Dr. Gundry:
So the answer is, for years, well-meaning physicians, since insulin seems to be the “cure” for type 2 diabetes, that we should give our type 2 diabetes more insulin.
Dr. Ben Bikman:
Yeah.
Dr. Gundry:
That’s fine. We’ll just pound the cells with more and more insulin. And as you know and I know, we’ve seen people gain 10, 20, 30, 40 pounds once they’re put on insulin. How did we get that so wrong?
Dr. Ben Bikman:
Yeah. Oh, I love that you’re bringing this up because it touches on what I believe is a fundamental misunderstanding of type 2 diabetes and even type 1. So just very, very quick background: Diabetes means a lot of urine production, just for everyone listening. What type 1 and type 2 have in common is that they can get high glucose levels, and when glucose goes too high, it starts spilling into the urine, making a lot of urine. That’s where the term diabetes comes from. But unfortunately, because they both have that in common, we’ve diagnosed or determined both of these diseases based on glucose problem. It’s a blood sugar problem. To me, it is not. To me, it’s an insulin problem. And if we look at type 1 and type 2 diabetes as insulin problems, then they’re exact opposites. Because while type 1 diabetes is a disease of no insulin, type 2 is a disease of too much.
As we’ve kind of been discussing, there’s too much insulin and the body starts to become resistant to it. So now when insulin’s coming to the muscle cells, which is the main consumer of blood glucose, and it’s trying to sell the glucose to the muscle, the muscle says, “I’m not buying it.” So the glucose stays in the blood and keeps climbing, and then we call it type 2 diabetes. So I believe that the whole problem is that we have a glucose-centric paradigm of type 2 diabetes when we should have an insulin-centric paradigm because it’s the high insulin and the insulin resistance that’s killing the person. That’s what’s causing the heart disease and the increased Alzheimer’s risk and the hypertension and the fatty liver disease. It’s not the glucose being high, it’s the high insulin.
If we look at this through the lens of insulin, then we can see just how catastrophic it is to give a type 2 diabetic more insulin. It’s the high insulin that caused it. It’s as if we are trying to cure someone’s alcoholism by giving them another glass of wine. We’re giving them more of the very thing that caused the problem.
Dr. Gundry:
I’m reminded, and I wrote about this in one of my early books, the New York Public Health Department tracked diabetes beginning actually in the 1920s. Every year, diabetes really wasn’t even known until after the turn of the last century. And what they found surprised people because we’ve been told that say, Blacks and Hispanics have a very high risk of developing diabetes, that it’s part of their genetic makeup. And yet, when in New York City, they found that, in fact, when they started tracking this, diabetics in Hispanics had virtually no diabetes, and the people who had diabetes were the bankers and the merchants. They were the ones who were not working, they were desk jobs, and the Blacks and Hispanics were workers. It gets back to your point that the workers, the muscles, were hungry and happy to take in what insulin was selling, but the merchants and the bankers, their muscles weren’t hungry. We should have realized way back then that we had this kind of all backwards, that the family history, “Oh, well, Blacks are predisposed to that.” No, that’s not it at all. It’s whether the muscles are hungry.
Dr. Ben Bikman:
Yep. Yeah, well said. I couldn’t agree more. That’s a great metaphor again. Yeah. That’s why exercise and moving the muscle is such an immediate benefit. Exercise is antithetical to high insulin. The moment the muscles start moving… Most people don’t appreciate this. While muscle does need insulin to open up those glucose doors and bring it in, it only needs it when it’s not exercising. The moment the muscle starts contracting, it’s dynamic, it becomes so hungry for energy, it opens those glucose doors on its own. It no longer needs insulin. This is one of the many reasons I’m such an advocate of exercise, and indeed, any exercise. The best exercise is the one a person will do, is just get up and move those muscles and it will force those glucose doors open, thereby lowering blood glucose, thereby lowering insulin, helping the body be a little better with insulin.
Dr. Gundry:
I think this is very important for anybody listening who says, “Well, exercise is difficult for me because I’m carrying a lot of weight and it hurts me to exercise and I don’t like to exercise.” How do you break this cycle?
Dr. Ben Bikman:
Yeah. Oh, yeah. Well, I think it’s very important for people to adhere to the simple, even silly maxim which is, the best exercise is the one you’ll do. If it is just get up and go walking. One of the activities my wife and I enjoy doing here in the mountains in the winter is cross-country skiing. It’s crazy, it’s a challenge, but boy, minute for minute, oh my gosh, you are really going to work your body. In this podcast, if I said, everyone should go cross country skiing or even crazier, if I said everyone should go do CrossFit, no, almost every single person listening would just say, “Well, I’m not going to go CrossFit,” or, “I can’t cross-country ski, so I’ll just do nothing.” Don’t worry about that, just do anything.
Even if it’s just taking a walk or doing some air squats or just being up and busy and roaming around the house, just get up and move. Particularly, get up and move when you’ve eaten whatever starchy or sugary intake might have been. And if you just get up and move, you can lower that glycemic load and insulin spike by up to 50% just by getting up and doing something for about 15 minutes. Because you basically recruit the muscle. You say, “Muscle, I got a big load of sugar coming, or whatever it may be, a big load of glucose. I need you to take it in so that my body doesn’t have to really bear this metabolic burden.”
Dr. Gundry:
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We spent a lot of time in Europe, particularly in France and Italy and Spain. One of the things that’s really interesting is that so many of these cultures have a habit of strolling after dinner. Strolling, walking, not exercising. It’s ingrained in these cultures. Years ago, I found a paper that looked at people, they were asked to walk for 10 minutes before the meal versus walking 10 minutes after the meal, and they looked at actually weight gain. It turns out, just like you said, and they ate the same calories, the people who walked after the meal actually lost weight and the people who walked before the meal didn’t lose weight. And I think it gets down to exactly what you’re saying. It’s those little things that can make a big difference when we’re trying to turn this around.
Dr. Ben Bikman:
Yeah, yeah. By getting up and doing something, basically, the body is saying, “Hey, all the energy that just came in, you don’t get to go to the fat cells. I need you to go to the muscle because the muscle’s demanding it. It’s the squeaky wheel that gets the oil here.” So go to the muscle cells instead of the fat cells. But if you haven’t coupled it with some movement, well then insulin will go up and insulin will just store it where it wants, including fat cells.
Dr. Gundry:
That’s why, as people who follow me, I actually write prescriptions for people to get a dog.
Dr. Ben Bikman:
Yeah.
Dr. Gundry:
Dogs make you move. Whether you want to or not and whether it’s 20 degrees in Provo, Utah, the dog says, “I don’t care. Come on, we’re going.”
Dr. Ben Bikman:
In fact, case in point, that was me at 5:30 this morning, literally.
Dr. Gundry:
You and me both, actually. The dog said, “Come on, I know it’s dark outside. Grab a flashlight, let’s go.” Yeah, it’s amazing. I have so many of my patients say that this was the only prescription that a doctor ever wrote that was useful. Some of them bring in their prescription framed and they’ll actually bring in the dog and say, “Here’s your prescription. Thank you.”
But you’re right, they seem inconsequential. And I think let’s shift gears. Okay, most of us in this, including you, know that an elevated insulin is really behind so much of what’s going to happen to us. Let’s talk about the brain and insulin. When I was in training back in the dark ages, we thought that somehow the brain was privileged and that insulin had nothing to do with the brain and sugar. Number one, how did we get that wrong? And number two, why is insulin so important and insulin resistance in brain health and brain deterioration?
Dr. Ben Bikman:
Yeah. So I can speak to this with a fairly high degree of authority. We’ve just published two papers within the last year, and one more in review right now on this very topic. All of the brain is important, of course, it’s the hippocampus that we’re primarily interested in and what we’ve been studying because that’s the part of the brain that becomes compromised with cognition and memory. In other words, Alzheimer’s disease or classic dementia. We know now that the brain is able to… Well, multiple things we know. One is that the brain is a hybrid in that it is at any moment relying on both blood sugar or glucose and ketones. Ketones are the other primary fuel for the brain. Second, we know that much of the brain’s glucose is dependent on those doors that insulin comes and knocks on. This was something we did not know even 20 years ago, where a portion of the doors that allow glucose to come in need insulin to come and knock on them first. If the knock doesn’t get heard, those doors don’t open.
So what we’ve similarly discovered in the ensuing years is that many of the neurological diseases that we look at as distinct have one thing in common. And I’ll back up briefly then come back forward. If we look at epilepsy and migraines and Alzheimer’s disease and depression, we would say they have nothing in common. And indeed, they have a lot that is very, very distinct. But in every one of those brain disorders or neurological problems, every one of them has a confirmed phenomenon known as brain glucose hypometabolism. In every one of those disorders, we’ve been able to measure, not me in my lab, but other scientists, we’ve been able to confirm that the brain isn’t getting an optimal amount of energy, it can’t get glucose in very well. And that is very, very likely because the brain becomes insulin resistant. That’s absolutely the case in Alzheimer’s disease.
So there are two interventions here. One is to say, “All right, I’m going to improve my insulin sensitivity.” And this is why insulin resistance in particular is so predictive of Alzheimer’s disease. In fact, a study published in Finland, what was called a prospective study, where they looked at people that went back in time of people who had Alzheimer’s disease or didn’t, and they found that someone’s markers of insulin resistance ended up being more predictive of developing Alzheimer’s disease than their age. I mean, it was what a mind-boggling concept. And it certainly added a little cement to this growing foundation that this is a metabolic problem.
So on one hand, again, it would be this effort to improve insulin sensitivity and allow the insulin to come and knock on those glucose doors and then open and return, and then allow the glucose to come in and feed the brain. And that is important. It’s important to note that the brain is part of this trinity of very high metabolic rate organs. By mass, the brain has one of the highest metabolic rates in the body, at any moment, including sleep. So it’s constantly demanding energy. And importantly, unlike other cells, like muscle cells, the brain can’t store its own energy. Muscle has a little reserve of glucose and a reserve of fat. The brain has no such reserve. It has to constantly be getting its energy from the blood. So if it can’t get blood sugar, of course it starts to go hungry, then the person has migraines or they have depression or they have an increased risk of Alzheimer’s.
Now, in addition to improving the insulin sensitivity, a person could give the brain a break and let it eat ketones from time to time. The brain is desperate for ketones. One of the myths that I was certainly taught was that the brain prefers glucose. People will say that. They will say that glucose is the brain’s preferred fuel, or they might not even say preferred and just say it’s only fuel. That is categorically false. We know that the moment ketone levels start to climb in the blood, even if the ketones are only a fifth or a third, let alone a half of what glucose is, the brain has already shifted to be getting more than twice the amount of its energy from ketones compared to glucose. And this is even in a healthy person where the insulin’s working.
So if the brain prefers any fuel, in my mind, it clearly prefers the ketones because the moment the ketones start to climb, the brain immediately starts pulling them in. And that is something we studied. We actually had brain tissue, hippocampal tissue from human donors who had died with Alzheimer’s disease and without. And it was the glucose pathways, it was the glucose biochemistry that was compromised at every step, not the ketones. So when it comes to Alzheimer’s disease, certainly there is this inability to get its energy from glucose. So all the more reason to give the brain a break and let it have some ketones. And you’ve kind of fill that gap. I just was in London giving a talk a couple weeks ago. Mind the gap, they say, as I’m going into the tube.
Dr. Gundry:
Yep.
Dr. Ben Bikman:
Well, we got to mind the energetic gap. We need to fill that gap. The brain’s energy demand is right here. Glucose can only feed it up to here. Well, ketones can fill the rest.
Dr. Gundry:
All right, so how do we do that? That’s the $64,000 question. My last book, Unlocking the Keto Code, gives my impressions on how to do this, but I want to hear it from you since you’re researching this. You and I both agree that we’ve got to give the brain some ketones.
Dr. Ben Bikman:
Yeah.
Dr. Gundry:
Most people can’t give the brain ketones because of the insulin resistance.
Dr. Ben Bikman:
Yep. Indeed, that touches on just the scope of the problem. Because the average individual nowadays who is insulin resistant, not only is the brain crying out for the glucose that it can’t get, but because they’re insulin resistant and they have high insulin levels, they can’t make any ketones. So the fuel, it’s swimming in a sea of one of the fuels and it can’t get enough of it, and the other one that it can pull in isn’t even there to help it anyway. So yeah, in my mind, we have to address the insulin. And this touches on the fundamental biochemistry of metabolism and ketone metabolism certainly.
Ketones are products of fat burning. When the body is burning a lot of fat, it starts to essentially burn more fat than it needs for its own energetic demand, especially this is in the liver. When insulin is low, the liver starts burning more and more fat, and a lot of that energy in the fat burning will feed the liver cells. The liver will use that energy. But eventually, if insulin stays low, the liver can’t stop burning fat and the fat cells can’t stop giving fat to the liver to burn. So the liver just keeps burning more and more fat to the point that even after it’s met its own needs, it keeps going. And that excess, if you will, is what becomes ketones. It’s basically the liver’s way of saying to the body, “Hey, body, I can’t stop burning fat, but I don’t need it, so I’m going to share these ketones with you, and now you guys use it.” So the brain starts burning the ketones. Fat cells start burning the ketones, which is work we’ve published in how the ketones actually accelerate metabolic rate in the fat cells.
Muscles burn ketones. Every cell with mitochondria, which is practically every cell of the body, will gladly use ketones for fuel. So again, to kind of bring it back to the question, the key is lowering insulin. Whether it is by managing your macronutrients or whether it is by time-restricted eating or intermittent fasting, the moment insulin starts to come down, ketones will start to go up because the body has shifted to fat burning. And if insulin stays low for about 16 to 20 hours, the body has been burning so much fat that in a way is burning more fat than it knows what to do with, and then starts to become the ketones.
Dr. Gundry:
And from an evolutionary standpoint, free fatty acids are very difficult to get into the brain. They’re too big to get past the blood-brain barrier. But the brilliance of the design, as far as I can tell, is that ketones are very small fat bodies that easily penetrate the blood-brain barrier.
Dr. Ben Bikman:
Yep, I agree completely. It’s interesting to note the metabolism of the brain, where the brain doesn’t burn fat, it uses fat for structure. The brain itself is a very fatty.
Dr. Gundry:
Yeah.
Dr. Ben Bikman:
There’s a lot of lipids, there’s a lot of fats in the brain. It doesn’t burn the fat, it uses the fat for structure. And instead, as you note, relies on these products of fat burning, namely the ketones.
Dr. Gundry:
Yeah. In fact, it is interesting. Neurons are perfectly capable of actually burning free fatty acids in their mitochondria, but they just can’t get in through the blood brain barrier normally.
Dr. Ben Bikman:
Yeah.
Dr. Gundry:
All right, so we’re talking or dancing around the essential problem that we started talking about, and that is, our current diet is the perfect storm for insulin resistance. So what’s the perfect solution? Number one, you’ve already said it, make muscles hungry. And however we can do that, you’re right, is whatever you’ll do and do consistently is the correct answer. What else can we do?
Dr. Ben Bikman:
Yeah. Right. Yeah. So to me, it is all about managing macronutrients. We’ve already touched on exercise and we’ve mentioned intermittent fasting, so I won’t mention those again. But at the same time, as important as those are, to me, they are supplemental because if we aren’t managing our macronutrients, carbohydrates, proteins, and fats, then those are going to have a limited benefit. Particularly with regards to intermittent fasting, as much as I’m an advocate of it, I’m always quick to say how an individual ends a fast is more important than how long they fast. And I think too many people fall into that trap of just shrugging their shoulders and saying, “I’m going to fast for 24 hours.” Getting hungrier and hungrier and hungrier with no plan, and then they binge and then they just do the whole thing again the next day.
So to me, the key is lowering insulin, and that is best achieved with three, I believe, hopefully to remember rules. The first one is control carbohydrates. And that doesn’t mean we don’t eat any carbohydrates, but we just appreciate the fact that carbohydrates that come in a bag or a box with a barcode are going to be carbohydrates that are going to spike blood sugar, which is going to spike insulin. The amount of starch and sugar compared to the amount of any kind of soluble fiber is going to be so problematic that it’s just going to be a rush of glucose. So control carbohydrates, that would be, in my mind, the first rule.
And then rules two and three kind of come together because in nature they do. But the next one is prioritize protein. In my mind, getting adequate protein, which really promotes a sense of satiety. And don’t be afraid of fat. Don’t fear fat. Generally, by that I mean, in nature, protein comes with fat. There’s no exception to that, in nature. All of the best proteins that exist in nature that humans would’ve been eating since time immemorial come with fat. That’s how we should get it. Don’t try to cut that fat out. When we just eat pure protein, we don’t digest it as well. Most people don’t appreciate the fact that bile, which is typically only thought of as being involved in fat digestion, actually enhances protein digestion. Fat and protein together are more anabolic to muscle growth than just protein is. That’s how we should get it. So control carbohydrates, prioritize protein, don’t fear fat.
Dr. Gundry:
Rather than needing six small meals a day, and you and I, I think, are both obviously proponents of intermittent fasting done correctly, is there any recommendations or your research that says, “Well…” Okay, I love your description. If it comes in a bag or a box and it’s got a barcode, probably that’s not what you want to eat. I’ll even go farther. The idea that I want a protein drink or a protein shake that’s got protein isolates where everything has been broken down already strikes me as equally as big a problem.
Dr. Ben Bikman:
Yeah, yeah. We don’t want to… Yeah. So we need to be careful when it comes to a food being processed, no doubt. Not that it can’t be done well, it can, but it has to be smart. And I do think there’s something to be said for foods that are convenient but allow an individual to adhere to their rules. If someone were to say, “All right, Ben, I’m going to do control carbs, prioritize protein, don’t fear fat, but how do I do it?” Well, the best way we would both agree is eating real food and planning meals, but it is difficult to plan and prepare perfectly packaged meals.
So there’s something to be said for the convenience of meals and something that’s ready to go. But you certainly need to be smart about what you pick. Because the easy way, as you note, the easy thing for a manufacturer to do is to just pick pure dextrose as a filler and it’s pure glucose. They’re going to pick the cheapest fats or oils, and it’s going to be sunflower oil or it’s going to be soybean oil. And they’re going to pick the cheapest proteins, and that’s going to be, I don’t know, pea protein or something.
Dr. Gundry:
Pea protein, yeah.
Dr. Ben Bikman:
They’re going to pick which is, you and I both know, is deeply problematic for many reasons, not to mention the compromised amino acid absorption and the anti-nutrients that are there, that people think they’re doing their bodies such a favor with by eating. So that’s the problem, is that the manufacturer is too tempted to pick the cheapest version. And then the macronutrient ratio might look good, but those are macronutrients that you just don’t want.
Dr. Gundry:
Yeah, that’s very well said. You’re right. Manufacturers, unfortunately, because of price constraints and profit margin, will usually always find the cheapest available ingredient. That sounds good when you look at the macronutrients, and yet each one of them is a health bomb in so many ways.
Dr. Ben Bikman:
Yeah, yeah.
Dr. Gundry:
All right. So where do people find out about you, your research? Of course, you got your new book Why We Get Sick, which is-
Dr. Ben Bikman:
Yeah. Well, thanks again. What a fun opportunity to talk about these things. So I’m fairly active on social media, and the nice thing about my social media, I hope it’s nice, is that it’s never about me doing something. It’s just a little lesson. I try to create, one or two times a week, a brief little one-minute kind of primer on all things metabolism, whether it’s talking about brown fat versus white fat or the effects of estrogens on fat storage. That’s what I aim to do. And I’m mostly active there on Instagram, but also on Twitter and LinkedIn. But people can find me on any of those platforms, @BenBikmanPhD. And I’m also a co-founder of Meal Replacement Shake, and I do blog posts there. People can find out more about that at a website, gethlht, H-L-T-H, gethlth.com.
Dr. Gundry:
Great. Well, before I let you go, I have an audience question that I answer, but I’m going to ask you to answer this one before I come in because it’s exactly what we’ve been talking about. Are you ready?
Dr. Ben Bikman:
I am.
Dr. Gundry:
Okay. The user is @HannahLee. “I need to do intermittent fasting for health benefits, but I do not need to lose weight. I am already too thin. Do you have any advice for me to do intermittent fasting while not losing weight, please? Thank you.” That’s a great question.
Dr. Ben Bikman:
It is. I don’t want to answer a question with a question, but I just can’t help but start it. I would say, what would be the benefit to intermittent fasting? But let’s say that Hannah Lee is saying, “Yep, I just have to do it. No way around this.” Then I would say you need to make sure that when you eat, you are eating the most nutrient dense foods you can put in your dainty mouth. Don’t waste time on empty nutrients or low calorie. If you already struggle with maintaining weight, one, I would say heavily scrutinize how long you need to fast because I think that is important.
But when you do eat, pick the most nutrient dense foods and ensure that you’re getting an abundance of natural fats and proteins because the combination of those is going to help the body maintain mass. Just fat alone won’t maintain mass that well, just protein alone won’t, but protein and fat together, both essential, make sure you focus on those. And then the least refined starches, whatever the best fruits and vegetables are, and of course, Dr. Gundry talked amply abundantly about that in a context that I don’t, but focus on the protein and the fat because that’s literally what you’re made of and that’s the mass that you want to keep.
Dr. Gundry:
Yeah, that’s a great answer. I see people who are often so successful on my program that they literally want to stop losing weight. What I do is my favorite go-to, is to have them eat a lot of macadamia nuts. In my humble opinion, and certainly I’ve done the experiment of myself, an over consumption of nuts, particularly macadamia nuts, is a really good way to add, I think, healthy weight onto people.
Dr. Ben Bikman:
Mm-hmm.
Dr. Gundry:
The other thing that can work, but I think you and I would both agree, starches do have a place in weight gain, but you got to be really careful because there’s a very slippery slope in starches beginning to pop up insulin.
Dr. Ben Bikman:
Well said.
Dr. Gundry:
I see it all the time. I know my friend Dale Bredesen, because of insulin resistance of the brain, is now very skeptical that even “good starches” like a sweet potato probably in his program has no place in an Alzheimer’s prevention program. Because you’re right, we all agree that so much of Alzheimer’s is driven by insulin resistance and high insulin levels. So yeah, it’s just going on a healthy organic carbohydrate diet to gain weight. Boy, I see it in the blood work and I go, “Oh, no, this is not what we’re looking for.”
Dr. Ben Bikman:
Yep. Well, all the more reason to. In particular, with Hannah Lee, if she’s determined to fast, you don’t want to be spiking your insulin right after a fast. That’s just not a great way to do it. So I strongly recommend anyone who fast frequently start with the protein in the fat and then let the starches, whatever form they may take, let them come after, let the nutrients get in and get nourish throughout the body, and then when insulin comes up a little later, then it will feed fat cells. Make sure that everything else has been fed first to a degree. Because the moment the insulin spikes, the fat cells are going to start taking a lot of it, and that might be the last tissue you want to feed.
Dr. Gundry:
All right. Great answer. And that’s great question, Hannah Lee, because I get that with my own patients as well.
Speaker 4:
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Dr. Drew:
Hey, this is Dr. Drew, and I’d like to invite all of you to subscribe to The Dr. Drew Podcast. We are very proud of what we’re doing there at that podcast. I am interviewing some of the most interesting, well, people you could ever want to talk to. Just whatever I find fascinating, whether there’s a smart person or an expert in a field that I’m interested in, or maybe I’m not even interested in, I’ve only interested because I’ve heard them speak and become intrigued. I think you’ll be intrigued as well. We get deep into topics that are quite important to the current age, things like cognitive dissonance, cognitive distortions, how does our mind work? We talk about everything at The Dr. Drew Podcast. It is of real relevance. We get all the way into deep physics and all sorts of stuff, but trust me, it’s all very accessible. It’s very interesting. Headaches, if you’re even interested learning about headaches, we get there. We go to the interesting topics of the day. Please join us at The Dr. Drew Podcast.
Dr. Gundry:
All right. It’s time for the review of the week from Flex Dog 17 on YouTube, “Dr. Gundry, thank you so much for all that you do. My blood pressure is below normal for the first time in three years, and I’ve been losing weight and feeling great.” Well, thank you, Flex Dog 17. That’s actually kind of what we were talking about on this podcast. The things that we often assume are just kind of the part of getting older or a part of, “Oh, you’re in your 40s or 50s, you’re supposed to have high blood pressure.” In fact, we used to call it essential hypertension, and I used to joke with patients, “Well, if you have essential hypertension, then why is your doctor giving you a blood pressure pill to bring it down?” The point of all this is, these are diseases of modern eating. Thank you for telling me that this is working, and I’m going to keep doing this because I’m Dr. Gundry and I’m always looking out for you.
I hope you enjoyed this episode of The Dr. Gundry Podcast. To stay updated on the latest news and episode drops, don’t forget to follow The Dr. Gundry Podcast on your favorite platform and sign up for my free newsletter at drgundry.com. If you like what you hear, be sure to leave me a review so I can feature it on an upcoming episode.
