Why You Can't Lose Weight & Top Tips Proven To Burn Fat For Longevity | Mark Hyman

Let's talk about the seven simple ways that you can help your body get into more well-regulated metabolic state and lose weight. Now, your genes, like I said, do play a role, but they don't determine your destiny. Regardless of what your genes are and other health, everybody can start with these strategies. First, eat real food, right? Get rid of processed food, get rid of junk. If it ain't something that came from the ground or a farm, don't eat it, right?

I mean, if it's mildly processed, for.

Example, I had a can of mackerel today for lunch. I open it up, it's got mackerel in there, a little olive oil and some capers, salt. I mean, it's food that I recognize, right? It's a canned food, but still, it's real food. Eat lots of non-starchy veggies, lots of good quality protein, and lots of good fats. And you wanna have fruit, fruit's fine, but if you're really metabolically and healthy, you might wanna minimize the fruit. So lots of good fats are really important. That's another key principle, like avocados, nuts and seeds, extra virgin olive oil. some people tolerate more saturated fat like grass-fed butter. But fats actually, when you cut down the carbs and you eat fat, it actually helps your metabolism. With one caveat, if you're eating starch and sugar and you eat fat, it's deadly. So you can't both eat, for example, a cookie is a lot of butter and flour. That's bad news, right? And as opposed to, for example, butter on your broccoli, which is good news. really important. Also, avoid all the processed sugars or fine carbohydrates, ultra processed food. You know, you can have some grains fine, but limit your intake from bread, cereal, highly processed starches, avoid bakes, good sweets and alcohol, by the way, is not a health food. So that also is a form of carbohydrate and sugar and is not good for you. Make sure you get the right nutrients because a lot of us are, you know, starving for good nutrients because we have a very nutrient poor diet and we tend to eat more when it comes to our diet, when we are nutritionally deficient. So a good multivitamin and mineral really helps. Vitamin D, fish oil, magnesium, probiotic, maybe fiber, all these can help balance blood sugar levels. And you can get them on our online store. Any, you know, good, good quality outlet that sells good quality nutrients. Also, stress. Stress is a big factor. Stress could hugely impact your weight. Your cells are listening to your thoughts and actually your metabolism slows down. when you are stressed. You know, it wreaks havoc on your health, your hormones, your weight. So do something that's going to help calm you down. Whether it's yoga, meditation, deep breathing, you know, try all those things. And there's lots more guided imagery. The list goes on. There's all kinds of apps and devices and Sensei and Apollo. There's lots of ways to do this. So I encourage you to just practice stress reduction. Next, sleep is super important. Sleep deprivation actually makes you gain weight. It makes you hungry. It makes you depressed. It increases inflammation, increases your risk of heart disease. diabetes. So make sure you get at least seven or eight hours of sleep, good sleep. Avoid artificial light at night from your phones and tablets, from television, electronics. Keep your room really dark, keep it cool, keep it quiet. And there's lots of other sleep hacks I've written and talked about. We have a whole sleep course, which we'll connect to in the show notes. Also, exercise is a great way to activate all the pathways for longevity and health. You basically can't exercise your way out of a bad diet, but exercise is a critical step to build muscle, to build cardiovascular fitness, to regulate insulin. I mean, even just taking a 30-minute walk after dinner has a huge impact on regulating your blood sugar and reducing your risk of disease. And that helps your body become more insulin sensitive, and that means less body fat, less inflammation, less belly fat. So just start with something if you're doing nothing or do more if you're already doing something. You can do high intensity interval training, you can do strength training, but you need to do all of it basically if you want to stay healthy and live a long life. And, I've written a lot about this. I've talked about it in my book, Young Forever, but make sure that you do the right kind of exercise and that'll help speed your metabolism up. So, bottom line, stop worrying about your genes. You can actually fix the gene expression by changing the way you live and what you eat and everything from your diet to exercise, to sleep, to your thoughts, and that's what's gonna determine your health. It's not your genes. So much of what we think might be genetic is actually environmental. Our genes do predispose us to things, but they don't predestine us to things. You know, we can actually change our destiny by changing our behavior and the influence on our genes from our environment. And how this works is through the influence of everything washing over your life. like everything that you do, every bite of food you take in, every exercise you do, every stress you experience, every thought you have, every environmental chemical you're exposed to, all of these wash over your biology, wash over your genetics and affect your gene expression. Your genes are fixed, you can't change those, but with genes turned on or off, you can regulate. So the entire field of epigenetics, which we've talked about before, is so important.

Because it helps us to understand the.

Ways in which our genes are regulated. Think of epigenetics as the piano player controlling controlling the piano keys. The piano keys are your genes. They're fixed. You can't change them. There's 88 of them. Well, there's actually 20, 000 plus genes. But anyway, you get the idea. And the epigenome is like the piano player that can play all sorts of music from stuff that sounds like noise to the most beautiful song you've ever heard. Right. So how does that work? And how do epigenetics work? It works through the influence of our environment. When I mean that, our lifestyle and toxins and our thoughts, everything washing over our genes, regulating. how these are regulated. This is one of the most important breakthroughs in science and medicine. We actually use this to measure now our biological age, which I talked about in Young Forever, how we measure our epigenetic age is way we measure the rate of biological aging. I mean, chronologically, we get older every day, but biologically we can get younger. Now, I think people think, oh, you know, my dad had a heart disease or I got diabetes in my family or got cancer in my family. I'm sort of doomed. But it's really not true. You know, I think people blame their genes. Oh, you know, everybody might family was diabetic. Well, yeah, but it doesn't mean you have to be. And my grandfather was a great example. He was a laborer. He was deaf, born hearing, had spinal meningitis when he was three and was fully deaf, couldn't hear a word. And so he was a manual labor his whole life. And he exercised every day. He actually threw the, he worked for the New York Times. He would throw the newspapers onto the truck every day. So it's really strong. And he walked every night after dinner. He liked to feed the neighborhood cats in, in, in New York City. and he was a great guy. He used to handstands when he was like 80 years old. And he actually did develop heart disease later in his life. But when we look at his brothers and sisters, and he had like nine brothers and sisters, all of them had severe heart disease in their 50s. They all were educated and a little more sedentary, maybe didn't eat as well, and they ended up actually having bypasses and heart attacks and deaths in their 50s. So he lasted well into his 80s because he actually lived a very different lifestyle. So same genes, very different inputs, right? And I think, you know, what you eat, how you move, how you restore your system, how you sleep, your thoughts, your feelings, your social relationships all influence and regulate your gene expression. And those genes express who you are in this moment. It's called your phenotype. And you can regulate that and you can turn on genes for health or genes for disease. You can turn on genes for weight gain or weight loss. by what you do. Now, there are some genes that do.

Predispose you to diseases, for sure.

For example, I have genetics that make me more likely to have heart disease, but I'm good because I've done all the right things to not get that. Some genes predispose you to diabetes. We talk about some populations that are at high risk for type 2 diabetes or heart disease, but that is just a predisposition. It doesn't mean you're destined to get it. What's interesting is that 90% of our current health is controlled by the environment that washes over our genes. We call this the exposome. What our genes are exposed to, it's the food we eat, it's how we exercise, it's our resilience, it's our mindset and our thoughts, it's our exposure to environmental toxins. So you don't have to just kind of be a passive recipient of what you think is your destiny and that you're doomed to kind of be sick and be fat and whatever.

You actually have control over this.

So we're going to talk about how diet and lifestyle influence your genes and what are my top strategies for actually regulating your weight, metabolism, and creating optimal health. So, you know, they did a number of studies on genes and obesity, for example. And then let's talk about genetics and obesity. People say, oh, you know, everybody, my family's overweight. But you all know those people who are like, everybody in their family's overweight, but they're thin and healthy. Right. I've seen this over and over again because they've taken a different track in their life. But it was a comprehensive study that looked at 32 different genes that may predispose you to obesity. And they found that if you had all 32 genes, it would only account for about 22 pounds of weight gain. And that doesn't account for the massive change in obesity from when I was born, about 5% of the population to 42%. And now we have, you know, 75% of the population overweight, 93% in poor metabolic health. I mean, this is not because of our genetics, right? Some people though do have a high risk. and maybe most of the world has some degree of carbohydrate intolerance genetically, meaning they're more likely to get insulin resistant. When they have a certain amount of sugar or carbohydrate, their insulin level will go higher than the average person, right, than me for example. And that will make them more predisposed to getting type 2 diabetes or becoming overweight. So some ethic groups are really at high risk, for example, Native Americans, Samoans, Pacific Islanders, people from the Middle East. I mean, if you're from the Middle East, your risk of diabetes is one in four. In America, it's one in 10. It's actually the highest density of obesity other than I think some of the Native American populations and the Pacific Islanders. Also, if you're Asian, if you're East Indian from India, you're higher risk, even at lower weights of getting poor metabolic health and diabetes. So when they have sugar and starch, their body likes it really not very much, right? So they will produce more insulin, they'll get more weight gain, they'll get a vicious cycle of weight gain and hunger and fatigue and high blood pressure, obesity, type two diabetes. And it's actually unfortunate because they don't realize they're like Dorothy with her ruby red slippers and she can change her destiny anytime she wants, just click her heels three times. So she can get back to Kansas.

So we can all get back to.

Our metaphorical Kansas, essentially, of our, real, you know, biology's ability to regulate our, our health. So what we need to do is, is understand how to eat and how to exercise and live. That's, that's going to be in balance with our genetics.

Right.

We have to actually live in harmony with our genes. Now, we might like it, right? For example, you know, I might really like sugar, but I might, you know, be a Native American and that's like poison to me. So I really can't do that. And so we have to understand the genetics load the gun, but the environment pulls the trigger. So the Pima Indians is a great example. They, they had a metabolism was really adapted their environment. They lived in the desert in Arizona and Mexico. And by the way, you know, currently, you know, there, there, there are two populations of Pimas, one in Mexico, one in, in Arizona, the ones in Arizona. are the sickest population in America. They are 80% of them get diabetes by the time they're 30. Their life expectancy is 46. They have kids who are as young as two or three years old getting type 2 diabetes. They grew up in an environment that was perfectly set for their genes. They lived on foods that existed only in desert environments, acorns, they had jackrabbits, they grew food. They were really well adapted. they were thin and fit a hundred years ago. None of the diseases they have now, like obesity, diabetes, and heart disease. Yet in a single generation, they've become the most obese population in the world, second to the Samoans. Now, what happened, right? Their cousins in Mexico are thin, are healthy, don't have diabetes, same genetics. So what happened? Did the Pima Indians suddenly genetically mutate and get the obesity gene? No, they really ate a diet historically of squash and melons and beans and chilies and gathered foods like mesquite, acorns, cactus, chia seeds, herbs, fish. And their diet was really unprocessed, whole and unrefined. And they were fit and healthy people. But then we came along, meaning we, white people, gave them the white menace, which I call white flour, white sugar, and white fat, which is Crisco or shortening, and essentially shortened their life, which is what shortening does and all the rest of it. And they came up with these traditional Indian foods. Fry bread, for example, it's not a traditional Indian fruit. It's basically deep fried flour in trans fats and it's just deadly. So I think we have to understand that genetics play a role, but because you have a predisposition does not mean you're going to get it. Now, how is genes connected to weight gain? Well, the Pima Indians studies show that environment plays a huge role and and fat and being overweight and weight gain. But they, for example, have a thrifty gene, which means they're really great at storing food when things are bad, right? So they might have scarcity genes, which we all have. We're really well adapted to scarcity, not to abundance. So when you have these scarcity genes, you basically store fat.

And it's a good thing if you.

Came across a bunch of stuff that would make you store fat, like a honeycomb or a bunch of fruit or something, and you would berries, you would eat that. you would gain weight, which would keep you healthy through the winter. But we don't need that anymore. We just keep eating all winter, right? So the other thing that happens is, you know, there's genetics around pleasure and foods, for example, dopamine receptors and melanocortin receptors. And when you have certain of these genetic variations, you need more dopamine to.

Make you feel pleasure.

So one person can have one cookie to feel pleasure.

Another person might need 10 cookies, right?

So I think that's how we get into trouble with our genetics. But once you understand your genetics, you can personalize your diet and your lifestyle to actually match your genes. Now, sugar is really bad because sugar works on those dopamine receptors for all of us, even me, and it triggers the same response as cocaine or heroin. And when you stimulate those dopamine receptors, you need more and more over time to feel pleasure. And they set the stage for being addicted. and that's why heroin, cocaine, nicotine, alcohol, all these things work on the dopamine receptors and they make you actually want more of the stuff and need more of the stuff to feel the same amount of pleasure. Now, when you look at the science on this, it's pretty frightening around food addiction. I wrote a book about it called the Blood Sugar Solution 10-Day Detox Diet about how we deal with food addiction and sugar addiction. And it really provides a very clear roadmap on in 10 days how to completely reset your biology and get rid of the addiction to food and not crave the carbohydrates. Because if I said you use willpower, it's not gonna work. You have to use science, not willpower. Now, when you look at these foods, what they do is they stimulate the brain. They did, for example, a study where they took guys who were overweight and they fed them a milkshake one day and it was a high sugar milkshake. Now, there were the same study participants had different milkshakes on different days. When they fed them, and by the way, they were same calories, same amount.

Of carbohydrate, same amount of protein, same.

Amount of fat, same amount of fiber, identical, tasted the same. The only difference was in one of the milkshakes, the sugar, the carbohydrate was a fast-acting sugar which raised their blood sugar quickly, and then there was a slow-acting carbohydrate that raised their blood sugar slowly. When they had the fast-acting carbohydrate, they spiked their insulin more. They, their cholesterol went up higher, their blood sugar went up higher, their triglycerides went up higher, their insulin went up higher, their cortisol went up higher, their adrenaline went up higher. Remember, these are the same calories. Taste the same. They don't know they're eating something different.

Right.

What was really disturbing was when they did a functional brain Imaging, an MRI of the brain, they found the nucleus accumbens, which is the addiction center in the brain, lit up like a Christmas tree. So this area of the brain is what is the area that is, is the addiction control center, the pleasure center, the nucleus accumbens. And, and so the data this is very compelling. I mean, they've done studies with, with, with the mice, which is not very ethical, but they basically put them in an electric shock cage where they would have an electrified floor and they let them eat sugar and they would keep shocking them while they were eating sugar. And they would keep eating sugar while they were getting electric shocks. And think about, that's what's happening in America. You know, people are getting fatter and fatter and fatter and fatter. I mean, how do you get to like three, 400 pounds? It's not overnight. You, you can see it in the mirror, right? But people keep doing it, not because they want to be overweight, not because it's their fault, but because the food has hijacked their brain chemistry. so, you know, it's really important to understand, you know, how, how we need to regulate ourselves based on our biology. Now, the other thing is we're all different. So there's no one diet that works for everybody, and, and we shouldn't be trying to come up with the perfect diet. Now, people say, oh, we should all be vegan. Oh, we should all be paleo. Oh, we should be all high fat or we should be all high carb or low carb. It really is individual. So you have to figure out what works for your biology, and it's by experimentation with yourself. We call this an N of one study. So you really want to find out what works for you and how you feel. what happens to your metabolism, what happens to your energy, what happens to your digestion, what happens to your other health issues. But most people do better with a diet that's higher in good fats and lower in starchy carbohydrates and sugar. I mean, there's a one-year multi-center trial, controlled trial, randomized study, which is hard to do in nutrition, but they did. It was published in the New England Journal of Medicine. Looked at 63 obese men and women.

They were randomly assigned either a low.

Carb, high protein, high fat diet. or a low-cal, high-carb, low-fat conventional diet. So one was not restricted in calories, right? One was. The one that was restricted in calories, they didn't do as well, right? The low carbohydrate group actually lost more weight, had lower levels of triglycerides, cholesterol, blood pressure, and blood sugar, even though they weren't totally telling them to restrict their calories, right? They just ate more fat and less starchy carbs. Now, not everybody responds the same way. So we're all a bit different. For example, I know I need more carbohydrates. I have to eat sweet potatoes, for example, or things like that that actually are healthy carbohydrates but have a little more starch because otherwise I will lose too much weight. I probably shouldn't say that, but I will. So we want to actually make sure we are eating fewer starchy and refined carbohydrates. But based on whole foods, we can adjust our diet to be higher in fat or lower in fat or higher in carbs or lower in carbs. and I think we need to see how we feel. Pay attention to how you're doing. Your scale and your lab tests will help you know what's best. And there's ways to track this. I'm now co-founder of a company called Function Health. You can go to functionhealth.com and sign up for the wait list and, you know, become a member and be able to track your labs and your data on a regular basis at a very cheap price point to actually find out what's going on with you and have real time feedback. So it's important that you track what's going on. and it's important to know what's right for you. For example, if you're a type 2 diabetic, you want to reverse that. And you're not going to reverse it by eating more starch and sugar. You probably need a more of a higher fat, lower carb diet, maybe even a ketogenic diet, and that may be extreme in your mind, but actually, if you have an extreme disease like diabetes, you might need extreme interventions. Benjamin Franklin said a pound of prevention, announcement prevention is worth a pound of cure. Some people need a pound of cure, which might be a ketogenic diet. Now, once you actually fix this problem and you become more metabolically resilient, then you can actually be have a wider diet and more, more foods that may, may have been a problem in the past if you get yourself metabolically healthy and resilient. So what works for somebody else might not work for you. You have to figure out what works for you and how to personalize your.

Your approach to what you're eating. I have patients who come in and they have such significant bloating that it's stopping them from being able to eat enough nutritious food. So they've had to really restrict their diet or they don't feel like eating so much. And I have some patients and we'll talk about one later where they're getting thinner and thinner and they're losing their lean muscle mass because the amount of bloating they're having is restricting their intake of nutritious food. And that can be really significant for people. I mean, that doesn't happen to everybody, but there are people where they're dealing with it, that's significant.

No, it's a big issue.

And it's estimated that 20 to 30% of the population is dealing with bloating on a regular basis. People with irritable bowel syndrome, it's 96%. So, people who are struggling with digestive issues or irritable bowel, as we've talked about before, that is something that we really work to define greater than just putting that into a waste paper basket, right? It's even higher. It's at 96%. So bloating just means that your belly is getting bigger, right? You have this increase in abdominal girth. And it typically, when we're talking about abdominal distension from gas or bloating, what we're going to talk about today, it increases after you eat. So people will feel more bloated after they eat or they may feel more abdominal fullness or sensation of gas as the day goes on.

And.

There'S so many reasons behind the causes of bloating. And I think that's really what we want to focus on today is what we really work to get to that underlying root cause in functional medicine, right? What is that underlying cause for that person? Because there's so many different reasons for bloating. And I think that's really critical to focus on and not just saying, okay, well, take GasX or just take something to suppress the bloating. We really want to figure out why is it going on because that really then can help work on that person's symptoms that are causing them a lot of discomfort.

And I think when I was in medical school, we didn't really ever learn about what we call SIBO or SIFO. We didn't learn about that. Did you learn about that?

No, not at all.

It was kind of a new insight about irritable bowel, which is that it's really about the often, not always, and we're going to go through the causes, but it's often about the overgrowth of bacteria or fungus yeast in the small bowel. Now, you've got like 22 feet of, you know, small intestine, about 10, 12 feet of large intestine. The small intestine is generally sterile, but sometimes the poop from the large intestine kind of migrates up and we'll talk about the reasons for that and leads to the SIBO. So some conventional doctors now are treating people with antibiotics, right? What kind of things are you seeing them do?

Right, so you're talking about SIBO. So, you know, we're checking one of the major causes of bloating is SIBO, so or small intestinal bacterial overgrowth. And as you mentioned, there's a lot of other reasons that people get bloating, but one reason could be because there's the wrong bacteria that have migrated up into the small intestine as you have mentioned. And when that happens, that dysbiotic or not good bacteria, or the bacteria that shouldn't be there, consumes some foods and then produces gas. So it's consuming foods that-.

Get fermented.

Get fermented and then you produce a bunch of gas from it. And so the combination of certain foods and not always bad foods, but certain foods that cause this gas when there's the wrong bacteria in the wrong place can cause a lot of bloating. And so, SIBO is something we check for all the time. You can check for it with a breath test. Conventional doctors are checking for it as well. We check for it all the time. Yep, now they are.

And.

There'S a few ways you can work on treating that and we'll delve into that more. But one is getting rid of the bacteria that's in the wrong place and you can do that with medication like antibiotics, like you mentioned, you can do that with herbal substances that lower the bacteria in the wrong place. And, you can also change the diet for a period of time that takes away the food that's feeding this wrong bacteria that's allowing it to overgrow.

That's good.

So, conventional doctors are sort of getting the point a lot about SIBO and they're using antibiotics and then they'll use different diets to restrict the fermentation of the foods, but they really don't have a comprehensive 360 approach from my perspective. They don't deal with the overall ecosystem of the gut. they don't look at all the other food sensitivities, they don't look at how to repair and rebuild the gut after the problem is taken care with antibiotics. And these often people, they don't often treat yeast or SIFO, which is often coexisting with the SIBO, and then they end up, you know, having recurrent bloating. So that may be get better for a few weeks or a month, and then it comes back. So functional medicine is a very different perspective. And, and, and, you know, we, we we understand the problem, but then we also understand how to navigate, like, medical detectives to the cause. And, you know, what I, I think is challenging with SIBO is it's just such a, it's such a persistent and uncomfortable thing. And, and there's a lot, not a lot of insight about what, what really happens. So I would love it if you sort of take us through, you know, what are all the types of reasons people can start to develop SIBO and, and all this and, and develop this fermentation process? Because, by the way, the thing that struck me was such big insight was humans don't make gas. It's the bacteria eating the food that you eat that make the gas. So, if you have gas or bloating and you have distension and air in there, it's not you making it, it's the bugs. And it's an imbalance in your relationship with your bugs. So you got to get in harmony with your bugs, basically. So, take us through, Liz, what are the common reasons why we get this bloating and dysbiosis and imbalances in the bacteria.

I mean, one of the biggest reasons that we see that people get imbalances or dysbiosis imbalances in their gut bacteria are antibiotics. I mean, when we over-prescribe antibiotics or people have been on large courses of antibiotics for certain reasons, you know, chronic infections or they just, you know, they got on too many antibiotics when they were younger, what happens is it can result in this imbalance in the good and bad bacteria in our system. It can get rid of some of the good bacteria and fungus, yeasts and things that keep that ecosystem in better balance. So, you know, too many antibiotics, too many antibiotics in our food supply. We know that things like that stress has a huge impact because stress in our life impacts our motility and how well things move through our system. So, you know, we know that people get bloating, you know, not just that this isn't just SIBO, but bloating because of sometimes if they're, they're eating too quickly, you know, they're not digesting their food properly. So they are swallowing air or eating too fast.

Probably that's what I do. I eat too fast. I explain some of my issues. So, yeah.

And then moving on to the next thing. Right, right. So, I mean, and then there's, you know, things like lactose intolerance, which is, you know, lactose intolerance is so common, you know, that's the decrease in that lactase enzyme that's in our intestines that breaks down lactose. And when we don't have enough of that lactase enzyme, then we can't digest our lactose very well, which is in dairy, you know? And so we've done a lot of different podcasts on dairy and all of the issues, but what we, we know is that for everybody, by the time they reach 100, they become lactose intolerant, you know, so everybody in the whole world is that way. And some people become lactose intolerant at age.

So no cheese after 100.

Some people become lactose intolerant at age two. Some people at 50.

I was just in Sardinia, and I saw these little 100 year old people eating a lot of goat cheese and sheep.

And we're doing good.

Well, you know, and what do we know about when we say lactose intolerant, it's important to recognize it's a spectrum, right? So that there is, you know, when you're, you know, what does it mean to be lactose intolerant? It means you're not as tolerant to digesting as much of the lactose. And that's what gets people so confused all the time about foods and food sensitivities. They're like, well, I ate that yesterday and I was fine, but then today, I'm really struggling and it's really because of the volume, right? You can, you know, many times you can get away with a certain amount of lactose, right? And then other times if it's, if it's, you have two servings or whatever, then it pushes your body over the edge because you don't have enough of that enzyme to digest it. So it's, you know, it's a spectrum and, and, and that's what we see all of the time. You know, it's also important to recognize there's other things that can cause bloating, things like constipation can cause bloating. We know not having good motility, you know, maybe because of autoimmune processes or just a gastroparesis, like Diane, not good motility, right? Exactly. If your bloating is all the time or if it's not getting better, you really want to get evaluated because there are some cancers that can cause bloating and GYN issues, gynecological cancers, you know, so there's more things that can cause bloating. It's important that we pay attention to all of those when we're getting a really good history and timeline from our patients.

I agree. I mean, I think there's certain things, you know, we see commonly like the bacterial overgrowth. It's often because of people taking antibiotics or other drugs. You know, in fact, one of the things that people really don't realize is that the acid blocking drugs, which are the third leading class of drugs sold in America. Okay. These are like Prilosec, Protonix, Nexium, Mass Effects, all those drugs. They're given all like candy and they cause bacterial overgrowth and they cause fungal overgrowth because they change the pH, they change the environment. And so while you may not have heartburn, you end up getting irritable bowel. That's one of the side effects of these drugs. so I think it's important for people taking those to, to realize they're not lifelong drugs. There's ways to fix the underlying problem. And the other thing, you know, that I, I found often is these sugar alcohols that are now in all these healthy products that are highly fermentable, non-digestible sugar alcohols like erythritol, xylitol, sorbitol, malitol. And they, and they are in a lot of these foods. And some people do fine with them, so people don't. But I know if I have way back when, I think it was like 20 years ago when this stuff was just coming out, someone gave me this, like, sugar-free chocolate bar, which is full of maltitol. And I ate the thing at Kenyon Ranch, and I literally couldn't see patients.

The whole afternoon because my stomach just was going crazy.

You were doubled over in pain, right?

Oh, my God. And then, you know, I think you've got other things that I found clinically. You know, I wonder. You found this, too, is. I don't know how much document this, but certainly it's like tick infections, like the B and others can cause motility issues in the gut or heavy metals. So I often, you know, if we don't get better initially, I start to look for other, other factors. So I think so, so these are really common problems. And, you know, 10 of all, like, loss of productivity in corporate, corporate health care is from irritable bowel. So it's a huge economic burden on society, and it's, it's the number one reason for visits to the doctor.

For anything.

I mean, it's so important about the additives in foods. And sometimes people, you know, that's something you really have to delve in deep with people on and look about, okay, what bars are you eating? What even certain shakes that have, like you said, some of the sugar alcohols in them, chewing gum, you know, people always forget about chewing gum and how much, you know, that can cause bloating because of some of the sugar alcohols in them. and so you've got to pull those away just to help people feel better. Absolutely.

And I think, you know, it's a bit of a detective job, and a lot of processed foods has emulsifiers and thickeners that tend to cause leaky gut and other issues. So there's just so much opportunity by focusing on a very detailed history to figure out what are the culprits. And if you're not eating anything that's real food, if you're anything that's not real food, you know, it could be a thing like fructose is a big factor. A lot of high fructose corn syrup and stuff, and people have fructose intolerance. So there's a lot issues that we can really deal with. So take us now, those are the causes and those are the things we tend to think about and test for. We test for gluten, we test for food sensitivities, we test for a lot of things. What would be an approach that we would take typically to deal with these people with the food baby bloating thing? Let's just say it's kind of the typical kind of cancer, Lyme disease, right?

Right, right. I mean, exactly.

Right.

So you mentioned about the Lyme disease. That's really, I think, important when people are not getting better, when they're being treated so many times and they're not getting better. But so, yes, so we often will test for dysbiosis. So we're testing for SIBO. We also do stool testing that is fascinating, just some of the revelations we're having in improvements in stool testing. We can look at levels of good and bad bacteria and balances in good and bad bacteria. and work to shift those as well, which can be really helpful. One of the first things we always start with, of course, is dietary changes. So, you know, we'll either put somebody, depending on their history, their story, and where they are and their level of motivation, we either put them on a dairy-free diet or we put them on a gluten dairy-free diet, or we might put them on a low FODMAPs diet. So FODMAPs, you know, people have, maybe people have heard about FODMAPs and So it's important for us to just sort of delve into that a little bit.

But FODMAPs- yeah, what does that mean?

What does that mean?

Yeah, so FODMAPs foods are fermentable oligosaccharides, disaccharides, monosaccharides, and polyols. And so these are these carbohydrates that are not completely absorbed for some reason, either because of some mal digestion or just because they're harder to absorb carbohydrates. and then they get, when there's the wrong bacteria in the wrong place, they consume those carbohydrates and produce gas. So, you know, so the oligosaccharides, those are things like wheat and rye and onions and garlic and legumes, disaccharides are things like lactose and dairy. Monosaccharides are things like fructose, like high fructose corn syrup, like you mentioned. honey and apples. The polyols, those are things like sorbitol and mannitol, the artificial sweeteners, and some fruits contain some of these polyols. And so one of the first things we do is say, okay, maybe we should try a low FODMAPs diet for a period of time. So there are some foods on this list that are good, healthy foods that you don't want to stay off of forever. So it's usually with a low FODMAPs diet, it's for a period of time that you're taking people off of these carbohydrates that are fermentable and then over time working to reintroduce the healthy ones for that person. The Monash University has a really good website, lots of good resources on FODMAPs foods. But in general, you pull away things like wheat and rye and onions and leeks and cauliflower and apples and dried fruit and sugars and high fructose corn syrups and legumes. And you do that for a period of time. Not everybody needs to go to that level.

And.

For many people, it's important that they work with somebody who's a nutritionist or somebody who can help them navigate the world with this because it can be, like I was mentioning earlier, you got to figure out what you're able to eat.

So what's been, let's talk about some of the other sort of approaches besides the dietary restrictions that we would take, you know, we might get off gluten, get off grains, get off beans, get off sugars, get off all the things that you mentioned. Then, you know, what do you do for the bad bugs?

How do you reset the gut?

How do you sort of rebuild the gut?

Oh, great question. So, you know, depending on what's going on in terms of the dysbiosis, right? Dysbiosis just means imbalance in good and bad bacteria. and yeasts. And depending on what we find is going on, we will treat that. And so we can treat that with a prescription medication. So sometimes we'll use an antibiotic. I know that sounds kind of crazy because you're like, We're counterintuitive, right? Yeah, we're like, wait, we know antibiotics cause dysbiosis. True. But sometimes if people, depending on their level of symptoms, they do, you know, we can improve symptoms with a short course of a non-absorbed antibiotic. So sometimes we'll use an antibiotic for a period of time and then then we'll use an antifungal medication.

And then there are- Dr. Because you always follow the antibiotic with antifungal?

Yeah, I mean, I often do. And again, it depends on what I find with the testing we do through stool testing and breath testing and their clinical situation. So, I often will follow with an antifungal or I'll follow with an herbal medication that includes that there are many different herbs that we have, they have effect at both treating bacteria and yeasts. So we can use some herbal regimens. There's a lot of good ones out there that will treat both bacteria and yeast overgrowth. And that's one of the nice things about herbal regimens I find is that with, when you're resetting the bacteria in the gut and the yeast in the gut is, you know, they, they may be a little slower to act, but they sometimes are, are really effective long term. So there's a few herbal regimens that we use very often and some have been really well studied. We also do things that help the body with digesting your food. So whether that's something that increases acid in the stomach like betaine HCL or a digestive enzyme, there's digestive enzymes that are plant-based digestive enzymes and then there are other digestive enzymes that are, you know, they come from their porcine, their glandular digestive enzymes. Those things help with breaking down.

Your.

Food, your protein, your carbohydrates. They help with breaking them down so that they're easier to absorb into the body and less likely to feed the dysbiotic bacteria that we were talking about.

That's great.

You know, that's also really helpful.

So I think the unique thing about functional medicine is that you, you not only just sort of get rid of the bugs, but you focus on resetting the whole gut and, you know, whether it's an antibiotic and antifungal and herbs and I would love you to talk about what herbs or then you add in enzymes and other pre and probiotics and repair components for the gut. It's what really helps people get better.

Right.

So tell us about, tell us about the cases you had a 35 year old guy. quite a remarkable story.

Yeah, so, you know, there's this gentleman, he was 35, and he came in to see us, and he was really frustrated with his bloating. And, you know, what he said is that, you know, he felt fine in the morning, and then as the day went on, he became more and more distended. He became more bloated in his belly and distended. And so it's really important, as I said, that we get really detailed clues as to his history. And, you know, you know, what really helps many times is when people take that really detailed history, you know, and they think about their own timeline. When did this start? You know, how long has it been going on? You know, trying to help get the clues as to what triggered this to occur for them, right? And, you know, so we knew that as a child he had ear infections, so he was on multiple rounds of antibiotics. But then two years ago he developed a pneumonia. and he ended up the first round of antibiotics wasn't helpful getting rid of his pneumonia and he needed a second round of antibiotics. And so we can also need to delve into this, you know, this risk for pneumonia here and everything, but it was that, you know, those recurrent rounds of antibiotics at that point, since that point, he's been struggling with bloating. So, you know, he's been really, of, at that point he started saying, okay, now every time I was eating, I was getting more bloated. And prior to that, he could eat whatever he wanted. He really didn't have to be careful with his diet as at all. Now, if he noticed if he ate too much dairy, he would get bloating and diarrhea. We did do a SIBO test and it was negative. But while we were waiting for his stool test to come back, we We just decided, okay, let's pull away gluten and dairy. He wasn't really ready to go on a full low FODMAPs diet, and I didn't even know if it was really necessary for him right away. So we said, okay, let's pull away gluten and dairy. And when we did, he had significant improvement in his symptoms, but not complete improvement. He felt better, but he still was getting some bloating depending on what he ate. And so the stool test came back, and it was really interesting. it showed a dysbiosis, right? It showed an overgrowth of many different bacterias and some yeasts. And so we then treated him with an herbal regimen. So we used something that had a combination of different herbs, oregano, berberine. It was a combination product and he took it for six weeks and he found that extremely helpful. We did add in probiotics. We did wait to add in probiotics till we were done with his herbal regimen. But once we did add in like a general probiotic and there's so much to discuss with probiotics, but he found that to be really helpful and now he's back to, I mean, he really is careful with dairy and has a really good healthy diet, but he's really much more comfortable all the time now.

Well, let's talk about that. I mean, the probiotics, you know, can be problematic.

If, you know, a lot of people.

With irritable bowel, they go, oh, I'm gonna take probiotics. They go to the drugstore, they go.

To the health food store, and they.

Get the probiotics, and they take them, and often they get worse. Yes. So, you know, can you explain that there's an important order to doing things.

And that what would be beneficial at one point might be harmful at another point? I think that's absolutely true. You know, order is really important. And, you know, if, if somebody does have an overgrowth of of bacteria in the wrong place. Sometimes probiotics make that worse, you know, and you can get, if you take a probiotic and feel more bloated or your digestion doesn't feel, it feels worse, not better, then that's the wrong probiotic or could be the right probiotic, but at the wrong time. So it's really important that you're either working with somebody who knows how to recommend what order of things to do it in, or just knowing that if it doesn't feel right to you, put it on hold. There's lots of different brands of probiotics out there and quality of probiotics out there. Some probiotics have dairy in them and so for people who are dairy sensitive, they don't work, other ones don't. There are also some strains of probiotics that can in of themselves, depending on the milieu, increase the amount of bloating for certain people. So there are, it's hard to give a general recommendation. Like, it's hard for me to say, well, take this one because it doesn't work for everyone. But just know that if you try one and it makes you feel worse, put it aside. And it may be that it's just not the right one for you or it's one to try at a later date after you've gotten rid of the dysbiotic bacteria. Some people get a probiotic and they feel better right away and then that's great. Wow. Yeah, it's complicated.

So, if you're struggling with this, don't lose heart. There's a lot of things, I mean, you didn't mention histamine intolerance. There's a lot of things that cause problems, which we've covered a lot on the podcast. But, the key is that if you suffer from bloating, if you have this food baby, if you're really miserable and uncomfortable, all that, there is a way to kind of get through it and fix it. You want to know my secret for living a long, and happy and healthy life. Well, all I have to do is check out my weekly newsletter, Mark's Picks.

Where I share my favorite tips for.

Health, longevity, well-being and lots more. Check it out and link below. You also, I think you had one other case of a woman who was 25 and was also struggling.

Yeah, so yeah, I mean, she was.

Kind of classic history kind of lots.

Of antibiotics for, she had acne, so she was, she was on lots of antibiotics for, you know, between the ages of 17 and 22. And this is what we were talking about before. Her bloating was so significant at this point that it was preventing her from doing things. She wasn't, you know, getting out during the day. She wasn't seeing friends all the time. She also couldn't eat as much. So and just with her body type, if she wasn't eating enough calories or enough protein, she was starting to lose weight and she was getting underweight she was also losing lean muscle mass. And this then creates this vicious cycle because if you don't have enough nutrients coming in, then the body can't heal. I always talk to people about that. People are always restricting foods, which the elimination diets can be so helpful. But sometimes if we're eliminating, eliminating, eliminating, and then not getting in enough nutrition, then the body can't heal. And this is what was happening with her. She was eliminating so much that she.

Was.

Wasting, her lean muscle mass was decreasing, she was feeling more weak. And she-- Because if you feel bad.

When you eat, you don't want to eat.

And so you just didn't eat.

Exactly. So she was just not eating. And she was more constipated. We did a SIBO test on her. It was positive. It was positive for both methane and hydrogen SIBO, but much more positive for the methane positive SIBO.

Yeah, we'll talk about that.

So we do this testing, which is you breathe in, you breathe out, in this, you just drink this liquid that tends to cause the fermentation, right? And then you breathe into this bag and you can tell whether it's hydrogen or methane and each are different and they actually respond to different treatments. So it's important to know which type of gas you're producing because that means it's different bacteria and so you need different drugs or different herbs for different bacteria.

That's so true. That's so true. So what we know is that there's the methane producing bacteria are more likely to cause constipation, right? They're more likely to impact the motility in the digestive system and cause more constipation. And so the hydrogen producing bacteria are more likely to cause diarrhea. Now, that's not always the case. Like sometimes people have their testing looks one way and it doesn't always match up. But in general, we see the methanobacteria, the methane-producing bacteria, more likely causing a constipation picture and bloating. And so you're right. So sometimes we, the medication, there's a typical medication that is used, prescription medication that's used for SIBO called Xifaxan. But when you find the methane producing, it typically works better when you use it with neomycin together. You use both together. And she also did well when we put her on that low FODMAPs diet. We really pulled away. She needed a nutritionist on board because as we were mentioning, she was becoming underweight. So she really needed somebody to guide her through. And as you know, at the Ultra Wellness Center, we've got all our nutritionists working with all our patients, which is wonderful. And so, her nutritionist was really helpful. to guide her through the pulling away of the foods that were making her feel worse, but then getting her the nutrition she needed. And then slowly transitioning over time so she could add back in those healthy, higher FODMAP foods, right? Like the onions and cauliflower and fruits that we want to be able to add back in when possible. So after we treated her and got rid of that dysbiosis, she started to feel so much better. nutritionally she responded well, right? She was able to digest and absorb her food better, which is really important because when there's that imbalance going on, you're not digesting well, you're not absorbing well, she was getting weaker, right? So she was able to digest and absorb better and she was nutritionally getting stronger and healthier and her gut was healing and we could add back in those good healthy higher FODMAP foods.

It seems to me that what you're saying is that this whole host of chronic diseases is driven by or affected by this phenomena of insulin resistance. And it's the biggest scourge causing 88% of Americans to have poor metabolic health.

Second is- In 90% of people with COVID to have it so bad they have to go to the hospital.

That's right. That's right. And the second thing is that that we understand that the way in which insulin resistance is controlled is through primarily diet. And I want to go through a few of the other factors too, but primarily diet. And it's primarily the starch in our sugar, which is enormous in this country. It's 60, 70% of our diet. It's usually in the form of flour and hidden sugars in our diet or added sugars, about 152 pounds of sugar and 133 pounds of flour. recently, according to the USDA data, you know, that's almost a pound a day of sugar and flour per person per day. It's staggered. It's staggering, which our human biology never, never was exposed to.

Right.

We see 22 teaspoons a year. If we found some berries or honey, now it's 22 teaspoons per day for the average adult and about 35 for a kid. And, and three.

That, that by changing.

The quality of our diet, in other words, reducing starchy, refined carbs and increasing good fats or maybe even saturated fat, we can actually stop this process, which is underlying everything that goes wrong with us at least to aging. And that, and that there's some heterogeneity in the population, but we need to figure out one, how to diagnose it. I want to talk about that. Two, then how to treat it, because if we understand this is the problem, One, what do people listening need to do to find out if they have this problem? Let's start there.

Yeah.

Well, aside from the mirror jiggle test.

The jiggle test.

Yeah, yeah, yeah. Well, I will try not to be too redundant to what you said, but I would say anyone who has any potential, get your insulin measured. And, you'd mentioned some wonderful metrics. I've always said below six. I think you said below five. I think that's a brilliant way to do it. Now, at the same time, insulin, like every hormone, has a bit of a rhythm to it. There's a diurnal or circadian rhythm. So it's possible someone would go get their insulin checked and maybe it's 12 or 13 or so. And you and I both would say, oh, that's a little high. We need to be a little worried. But it's possible the person has measured it at a peak, and that in reality, give it an hour or two later, and it would have gone down to five. It's possible. I think it is important to note that there are other things like challenging it in a dynamic glucose test like you'd mentioned. That is absolute gold standard. Alternatively, and another metric you'd mentioned is looking at lipids because insulin controls the production of fats and the regulation of lipoproteins in the body because lipoproteins are energetic molecules. Look at the triglyceride to HDL ratio. If a person has a triglyceride to HDL ratio and it's above 1.5, that's strong evidence that they're insulin resistant. Now that ratio doesn't hold across all ethnicities. It starts to get a little loose, you know, from Caucasians to Asians to African-Americans or so. But nevertheless, that ratio of 1.5 is generally going to be a pretty good indicator that if you're lower than that, if your triglyceride to HDL ratio is lower, that's a good sign that you're insulin sensitive. The good old-fashioned waist to hip ratio or the waist to height ratio, if you measure your waist, like the biggest part around your belly, and if you multiply that by two, if that number is higher than your height, that's a very, very good indicator that you have metabolic syndrome or insulin resistance to be more precise. If your waist circumference times two is less than your height, that's a good sign that you're generally doing okay. And then one other metric among many is what's on the skin. There are two things people can look for on their skin, which are—it's almost proof positive of insulin resistance. The first one is skin tags. Those are these little mushroom-like or columns, little stalks of skin. They're not like a flat round mold. They just sort of jut right up and they're small. I bet everyone already knows what I'm talking about. People can get them in their armpits or around their neck if they have a fat fold around their neck. Those are skin tags. In the same place, especially around the neck, or the armpits, anywhere where skin is rubbing, they can start to develop something called acanthosis nigricans or these patches of skin that are a little darker pigment and they have a kind of altered texture, kind of this velvety kind of texture to it. But that's another one. The skin, I kind of joke, the skin is the window to the metabolic soul just because every part of the body, it responds to insulin. and so we start to see these little hints of it.

That's really helpful. You know, I wrote a little description of how to look at this in great detail called How to Work with youh Doctor to Get what yout Need. It's available on my website, drhyman.com, it's also available, I think, online. You can just Google it. And, I go through all the diagnostic tests to help you identify the ways in which either you have insulin resistance or the consequences of it. And, the things that I tend to recommend people do is, like you said, a fasting insulin, super important. the best test is, is because the fasting insulin elevation is really the second stage of the problem. The first stage is elevations of insulin after you consume a sugar drink. So that that's a little bit of.

A more of a pain in the.

Ass test where you have to drink a sugar drink. It's equivalent to two Coca-Colas and then get your blood tested either 30 minutes after and, or, or one and two hours after as well as fasting.

That's really important.

The lipid tests you mentioned are super important. I'm gonna just drill down a little bit on that because there's something called an NMR or a cardio IQ test from LabCorp Quest, which look at not just the total numbers of like the weight of cholesterol, which is your milligrams per deciliter, it looks at the particle number and the particle size, which is really important. And so when you have insulin resistance, you could have a perfectly normal cholesterol of 200 or 150, but your triglycerides maybe 300, your HDL is 30, you're like, oh, your cholesterol is fine, your LDL is fine. It may not be because you may actually have really dangerous small particles. Also, we look at you know, like triglyceride HDL ratio is very important. It's something not really paid attention to much by doctors, but it's more, more.

Predictive than an LDL elevation, more predictive.

The most predictive tests are, you know, triglyceride HDL ratio and total to HDL ratio. And the HDL ratio reflects the insulin resistance. So we've always been looking at it, but not in the right way.

We also look at inflammation, which can.

Happen through a CRP. We look at uric acid, which can be elevated, which David Palmer's book, your drop acid was all about. we look at liver function tests which can be abnormal, we look at male hormones, sex hormones, we look at DHEA.

And Sulfate in women to look at.

The effect of androgens being produced from insulin resistance. So we look at a whole host of things and we get a pretty good picture of where people are in that spectrum. But the most important, like you said, is looking at the insulin fasting or after glucose tolerance test. And you mentioned the waist to hip ratio, that's important. But, you know, so when you look at the data on the 88 of Americans who are metabolically and healthy, only 75 only, right? 75 of us are overweight, three quarters. But, like, what about that other, you know, like, you know, eight, whatever, eight percent? Like, probably about a quarter of people who are thin also have pre-diabetes they're what we call skinny fat or thin on the outside, fat on the inside. They're metabolically obese, but normal and that's just because they may not gain weight, but they actually, their metabolic consequences are all the same. So we start to look at all these factors and we get a pretty good sense of the problem and where you are in that spectrum. So now that we've established that, you know, what are the top things that we should tell people to do in order to reverse this problem? Because we know even if you're far down the road, even if you've had this going on for 30, 40, 50 years, and you're diabetic on insulin, that you can reverse this process, that you can reverse the damage to your beta cells, that you can increase your insulin sensitivity, and you can reverse type 2 diabetes and not only just weight loss. So tell us about what are the top things that people need to do from a diet, lifestyle, medication, supplement point of view in order to actually reverse this problem of insulin resistance.

So one of the reasons I was invited to Singapore, specifically for my post-doctoral work, was because of the interest in that part of the world looking at this disparity or the inequality rather with regards to metabolic predisposition and body weight changes. So for example, in Singapore there's a tremendous variety of ethnicities like here in the US too, frankly. But they've noted that if you looked at a Chinese ethnicity, kind of the average Singaporean, and compared that with someone of European, like Northern European, like me and you, Caucasian ethnicity, that these were individuals who could both be gaining fat and yet the Chinese ethnicity man, the man, the Chinese guy, would start to suffer insulin resistance, hypertension much, much earlier than the Caucasian guy would. He could continue to get fatter and fatter, and only later would he start to experience the metabolic consequences. Now, to varying degrees, this can happen across all ethnicities where you've noted that you have people who don't really appear to be overweight at all. They have a normal body weight. much of this can be attributed to how the fat cells are growing. You know, you and I were joking earlier that what you can pinch and jiggle is the fat that you have. But you could have people who are both gaining weight and yet—and they look—they're gaining weight. They both gained 20 pounds since they graduated from college when they were roommates. And yet, how they've stored the weight—I don't even mean where—but how they've stored the weight is very different because fat tissue can grow through two different processes. On one hand, you can have the number of fat cells capped. And that's how most people get fat across every ethnicity. The number of fat cells they have is set after puberty. Once they get to adulthood, their fat cell number is set. And so any pressure for the body to store more fat is primarily through hypertrophy of every individual fat cell. And the fat cells get to—. And that's right. They get to about four or five times bigger than the normal fat.

Themselves.

In contrast, there are some people—and Caucasians tend to do this a little more than other ethnicities—where they can continue to make more and more fat. The fat cells will get a little big, then the body just makes more fat cells. That's a process called hyperplasia. Just multiplying the fat cells, basically. That's the difference. If you have small fat cells, even if you have a lot of them, they're very insulin sensitive and they're anti-inflammatory. secreting proteins that are anti-inflammatory. In contrast, when fat cells start to hypertrophy, two terrible things happen. One, they become insulin resistant to try to prevent their own growth. They're basically telling insulin, insulin, you want me to keep growing? I can't grow anymore, so I have to become resistant to you. And so the fat cell starts leaking free fatty acids into the blood. At the same time, as the fat cells getting so big, they're pushing each other further and further away from capillaries, from the blood, and thus they become hypoxic or a little oxygen deficient. And so they start releasing pro-inflammatory proteins, a whole catalog of them, because some of those pro-inflammatory proteins will increase blood flow. They'll try to increase the production of new capillaries. So that is part of what happens across people, even though their body weight may be normal. they might not be in any category that would be problematic with waist to hip ratio or waist to height ratio, but they have more hypertrophic fat cells than someone else does. And hypertrophic fat cells are insulin resistant and pro-inflammatory so thus driving the metabolic problems.

And we see that in Indians from.

India, Chinese, Asians, it's very similar.

They really don't have to be very overweight and they can just have that teeny little belly bump.

Bump.

And that little belly bump is kind of a hot potato. So it's an issue. Okay, so let's.

Yeah.

Now let's go back and go. We understand the Diagnostics. How do we test? How. How do we advise people in the confusing nutrition world today about what to eat? Because we have the vegan Community saying veganism is a cure for diabetes, and we have. the keto folks saying keto is the cure for diabetes. And we have me somewhere in the middle saying Pegan diet is good.

Yeah.

You know, and so we, we really have to kind of go, well, what, what's the deal? How do we actually get to the end goal of reversing this? And of course it's going to be personalized because some people, like I said, have myriad other causes like stress or inflammation or the microbiome issues or toxins that need to be addressed as well. I mean, I've had a woman who's 40 pounds just like that by getting rid of her mercury. So there's more complexity to it. But, but for the predominant group of.

People who suffer with obesity and diet.

And, and, and this phenomena, you know, what are the top recommendations from a.

Diet lifestyle supplement medication point of view? Yeah.

Yeah.

So with regards to exercise and, and.

I know you're not a doctor, a medical doctor.

I am.

But, but, but I, but I want to, I want to hear what you.

Have to say about the food and what you've learned through your research.

Yeah.

Yeah.

Yeah.

So just purely as a scientist to mention, because you'd mentioned kind of three things and I agree with them, kind of medications, exercise, and diet. With regards to exercise, I said supplements too. Yeah.

Right.

Thank you.

Yes.

So with regards to exercise, my view is whatever the one is that you'll do, do it. So the best exercise to improve insulin resistance is the one you'll do. And, there could be varying degrees there. But it really is a matter of just getting out and doing something. I would just say the only addition to that is do something after you've eaten your most starchy, insulin-spiking meal of the day. Whatever that one is, that's exactly right. Go out and take a walk. People would be dumbfounded at how much it lowers their glucose and their insulin because the moment you start moving those muscles, they don't need insulin to tell them what to do. They just start pulling in their own glucose. They get so greedy. so demanding that they don't have to wait for insulin to open those glucose doors. They open them on their own, driving down the blood glucose, which helps the insulin stay much lower than it would have been otherwise. Movement matters.

15-Minute walk, 10-minute, half an hour, how long?

Well, the longer the better and the brisker the better, but anything is better than nothing. Now, with regards to supplements, there are certainly—and you would know more about this than me, so in all sincerity, I readily defer to you, but some that I'm aware of supplements like berberine, no question. Cinnamon also has been shown to do something. Vitamin D as a vitamin. Yep, yep. And alpha lipoic acid, magnesium. Yep, that's right. So there are several things that people can just sprinkle in and use judiciously to help. And medications, I'm not sure. Maybe that's too big.

Omega-3 fats probably.

Oh, for sure. that's right. Yep.

So Omega-3 fats, vitamin D, lipoic acid, berberine, cinnamon. That's a good start. And, there's more. There's more. Oh, yeah.

And, you would know more about this.

Biotin, chromium, vanadium, and many, many other nutrients are needed.

B vitamins, all that.

But basically, we take a good multivitamin and you supplement with some magnesium and lipoic acid and, you know, you add cinnamon in your food or maybe take berberine capsule. that can help. And there's more to this, and I've written a lot about it, but I think that's good. Next talk about the next piece, which is... Yeah, yes.

So the next piece could be medications, but maybe just for the sake of... Maybe that's too much of a big black hole. I would say in general, maybe I'll just say this, metformin is the most widely used insulin sensitizing drug in the world. It's affordable and it's effective, but even metformin, which is considered the best, is only half as effective at improving type 2 diabetes and insulin resistance compared to even modest lifestyle changes. So even if you take the very best of all the medications, a study, a prospective study in humans found that it was only 50% as effective as lifestyle changes. So that then brings us.

You guys send me that study, Ben.

Yeah.

Oh, yeah, for sure. So now, Mark, you would be the authority with many, many other aspects to this, maybe even diet. I will only focus on nutrition. just because that's the one I've focused the most on despite my studies looking at stress hormones like epinephrine and cortisol, which absolutely cause insulin resistance and tremendously matter, inflammation, which absolutely causes insulin resistance, and I've published in labs and papers on both of those topics. But to me, the elephant in the room is nutrition. I like how you kind of both of us want to be diplomatic. when it comes to nutrition. I don't want to, in all sincerity, I don't care. I don't like. Yeah, well, well, but, but I think it's, it's appropriate for us.

I want the truth.

Yeah.

Same, same. And the truth is, compared to a standard American diet, which is not totally fair to the U.S. because it's really a global diet at this point. So compared to the standard diet that people are eating, any change is going to be a benefit.

Yes.

It really to, to not to, at the risk of oversimplifying it, this is why someone can go very strict vegan, which I think is a diet that has a problem long term as a person may start to develop nutritional deficiencies. But even still, if you go on a vegan diet, there's no question you will lose weight and your insulin sensitivity will improve. At the same time, there's no question—I've published a clinical paper in collaboration with a local clinic here—that you take people with full-blown type 2 diabetes, put them on a calorie unrestricted low carbohydrate diet and the diabetes is gone. So both of these clearly work. And so in my mind, the improvement, the steps to improve insulin resistance can start with one of two steps. One, controlling energy or two, controlling insulin. And on the controlling energy side, this is why a vegan diet is, in my view, generally going to be successful. Not always because there's a lot of garbage that can be considered vegan.

Yeah.

It's because High carbohydrate diet.

That's right.

Oh yeah, for sure.

I mean, grains and beans, even if they're whole, are still more carbohydrates than.

Eating protein and fat and vegetables. That's right. Yeah, very insulin spiking. Yep. That's true. So in general, if a person is eating a diet that is just overall lowering their calories, calories matter. And so if there's a lower calorie diet, you will lower your insulin because you cannot have elevated insulin in the midst of low caloric consumption. you'll die because if calories are low but insulin stays really high, then you are clearing your glucose will be too low, your ketones will be too low, and your brain will starve and you'll go unconscious. So, the two are really antithetical. Dr. Justin:So, if you are lowering your calories—yep. Dr. Justin:If you're lowering your calories, then your insulin will come down, and then you'll start to improve your insulin sensitivity. That absolutely happens. Now, however, having said that, I think that sets you up to failure. So if your first step to improving insulin sensitivity is to cut your calories or cut your energy, then you're going to be fighting a battle with hunger and usually hunger wins. That's my only concern in that regard. But nevertheless, it absolutely will improve insulin sensitivity.

And by the way, just to stop you there for a second, that's what our friend David Ludwig's book was called, Always Hungry, which explains why we're always hungry. And if we are battling hunger, and our lizard brain is in charge, which it is, which is survival, we're not going to win. Our frontal lobe cannot match the power of our reptilian brain to search out, seek and find something to eat if our blood sugar is low and our insulin and blood sugar is spiking up and down.

Yep, that's right. In fact, I think to be a little crass perhaps, this is why I believe you do not see reunion tours with the biggest losers TV show, that game show where you have these people going through tremendous caloric restriction by following the classic advice of eat less, exercise more. They do it to an extreme and hunger always wins and they gain it all back. And so you don't see them two years later or so because the results are not favorable, much very unfortunately. But nevertheless, there's the low energy paradigm, which fits with veganism generally because by cutting so much fat Typically, calories are going to drop tremendously. This is why fasting will work very, very well. On the other hand, you have this paradigm of just control your insulin. This is what we had published a paper on where these 11 women with type 2 diabetes, they were told, Don't count your calories. If you're hungry, eat. Eat until you're full. When you're not hungry, don't eat. But just follow these three rules. I have an affection for alliteration, and it was control carbohydrates, prioritize protein, and don't fear fat. And just to put a little nuance with each of them, control carbs is something you and I have been talking about, which is focus on fruits and vegetables, eat them, don't drink them, and don't get your carbs from bags and boxes with barcodes. Prioritizing protein, this just makes sure you're getting high quality protein and you're getting plenty of it. It will promote a greater sense of satiety, protein increases metabolic rate through the process of digesting it, and you need it. And then lastly, don't fear fat. My paradigm on that one, fat has no effect on spiking insulin on its own. And focus on ancestral fats, which is animal fats and fruit fats. We've been eating fruit fats since— for millennia because our ancestors would have only needed to take— that's right. Yep.

Coconut and olives.

And olives, that's exactly right. Because all our ancestors had to do was take the flesh of the fruit. and then just press it even with their own body weight and they would have gotten that oil from it. And so we've been using that for millennia. And it's these modern, of course, refined seed oils that have only come on the line over the last century, most especially the last 60 years or so, when the war on saturated fat began, we were desperately looking for alternatives and that took us to all these refined seed oils. So don't be afraid of those, but don't fear the ancestral fat. so my view on this is- and.

I'm going to just frame this a little bit. I have a very good friend who I love to pieces, who happens to be the dean of Tufts School of Nutrition Science and Policy, Dr. Dariush Mozaffarian, who's published more studies than God and is one of the most brilliant and humane people I know. And we agree on 99% of everything except for this point. and his view is from the data, both interventional data and observational data, that high doses of refined seed, bean, and nut oils are actually healthful and are not a problem. Can you just kind of address that in the context of what you know?

I don't know if we're gonna get.

To the answer, but I'd love to hear your perspective.

So, I do attempt to have a bit of a nuanced view on this because I'm an insulin guy. I'm not a fatty acid or I'm not a seed oil guy. There are people who are seed oil guys, guys and gals. I'll speak to what I know, which is two things. One, when linoleic acid, so we're eating 50 some thousand times more linoleic acid now than we were 100 years ago. I think that matters. When we eat linoleic acid, which is the primary polyunsaturated fat in these refined seed oils, that will accumulate in our fat cells. and it gets metabolized into a molecule called 4-hydroxy nonenal or 4-HNE. Other fats do not do this. They do not go down this metabolic pathway. When a fat cell is accumulating this byproduct of linoleic acid, it forces the fat cell to go down the route of hypertrophy, kind of reminiscent of what we'd spoken about before. It prevents this process of hyperplasia, allowing smaller but healthier fat cells It forces the fat cells to only grow through hypertrophy, which promotes inflammation because they become hypoxic and promotes insulin resistance because they can't grow anymore. So that absolutely happens. I can say that definitively. That is one negative. The other negative thing that I can speak to is similar to this, although that is admittedly more my forte. But so much of the evolution and our understanding of atherosclerosis is not just that cholesterol and fats matter. Something has to happen to those fats for them to be considered pathogenic or harmful.

Oxidized.

For example, that's exactly right. You can take a macrophage and have it swimming in a little bath of lipoproteins of various fats.

So, one of your white blood cells floating around all your fat cells, right?

That's right. Yeah, or floating through the lipoproteins passing them in the and so you have a little macrophage which is floating in the blood. And if it's bumping into lipoproteins like LDL, for example, it will not engulf them. If the LDL is unaltered, if its fats and cholesterol esters are in a natural native state, they're not considered a problem and the macrophage ignores them. This was studied by a group at UT Southwestern, a legendary group. In fact, these guys won a Nobel Prize not for this work but for other stuff.

Stuff.

They found that you could only induce a macrophage to start eating these lipoproteins if the lipoproteins had oxidized fats on them. And now, you start to create what's called a foam cell. And, that's one of the primary components of an atherosclerotic plaque. When you actually look at the blood vessel that's growing, you have these, they look like little bubbles. They look like they're foamy. They look like they have air bubbles in them because they have these little pockets of fat. And, those are macrophages that start eating fats. But they only eat the fats if they're oxidized. And, Mark, you cannot turn a saturated fat into what's called technically a peroxide. That's what these actually are unless you heat them up to like 300 Celsius, a lipid peroxide. Saturated fats. Yeah, that's right. Yeah. Saturated fats are the most, they're the most stable fats in nature. And the more you unsaturate the fat, like a polyunsaturated fat, now it can become a lipid peroxide very, very readily. And there are these metabolic pathways that will do that. And so we take this linoleic acid that we're eating 56,000 times more now than we were a century ago. And now we see that as these become oxidized, macrophages sense them as problematic and they will engulf them. And now you have a foam cell which becomes very pro-inflammatory and you basically have the heart of an atherosclerotic plaque.

So, so basically those are my concerns. So basically those concerns just to recap is if you eat a lot of refined processed oils, which is the predominant oils used in America today, we used about 10% of our calories of soybean oil. If you eat that, it, it, it, that, that pathway to metabolize that oil creates something called four hydroxy noni all, which actually goes into the fat cells and causes them to grow. and the second problem is that these fats are very unstable. They're called polyunsaturated fats, but they're very unstable, so they're easily oxidized. And oxidation happens from lack of antioxidants in our diet, basically the phytochemicals, from stress, from our microbiome, from anything that triggers inflammation. So anything that causes oxidation, which is a lot of radiation, that causes the lipid peroxides. And that is what what our immune system responds to, which is what causes heart disease. So we now know that heart disease is an inflammatory disease. And what you just described was the mechanism by which that happens. White blood cells attack fat particles running around your blood if they're oxidized and then deposits them in your arteries, which then cause heart disease. Yes. The question I have for you is, are those petritis studies or is this broader in its application? Because what Dari says is that, you know, yes. And when you look at the actual population data and interventional data, we don't see this. It sounds good on paper, but is it actually real?

Yeah.

Yeah. So I'm admittedly a mechanistic kind of guy. So I'm definitely citing Petri dish or, you know, direct cell reactions. But even in human populations, we see the correlation. if not the causality. And Mark, that's the underlying concern with all of this. You simply cannot induce—you can't do these causality studies in humans that I'm aware of, at least. I don't know that they've been done. But in humans, we know that when you sample the atherosclerotic plaque, the actual amount of oxidized LDL is going to be the— or the circulating LDL that's oxidized will be a predictor that will determine the degree of a person's atherosclerotic blocking or prevalence. So, we see the correlates in humans, if not the causality that we can see in the cells and in the rodents.

I mean, look, from my perspective as a doctor, it's like if there's potential problems, why risk it? Maybe it's okay, but we do know that olive oil, avocado oil, for most people, coconut oil, fats in their original state and animal fats, particularly grass finished animals, wild animals, particularly nuts and seeds in their whole forms. Those are fine to eat, and that's where we should be getting our fats. So I think that's a really helpful point. I wanna, I wanna, I think you just did a brilliant job of explaining what we need to do. I just, I, I wish we had, you know, hours and hours to talk about this. And I think that, you know, the dietary strategies of cutting out starch and sugar, don't drink your calories, avoiding boxes, boxes, bags and barcodes, you know, upping your protein a little bit, high quality protein, eating the right good fats, key exercise. I think any is good, you know, interval training, high intensity interval training, which increases VO2 max and strength training, which improve mitochondrial function and muscle mass are also really critical. Meditation, stress reduction, all that stuff we talked about. I want to finish by talking about this whole thing that we earlier talked about, which is mTOR.

And I don't know how much of.

You know about this, but probably a lot more than I do. And it is this central question that's.

Running around the longevity fields.

And there was one large study that was done that looked at protein intake over the years of a person's life. And it seemed like when they were younger, if they ate less protein, they did well. But as they got older, they didn't. They needed more protein in terms of longevity. and I remember there's one story of Emma Morano, who was a Italian woman who lived to be 117 years old, and Walter Longo, who's a longevity expert, has written about her, talked about her, met her, and apparently when she was younger, her doctor told her she was anemic and she needed to eat three eggs a day, which she ate for her entire life. Then in her 90s, she was starting to dwindle and her doctor told her.

To eat a pound of meat a day.

And she lived to be 117 years old. and so the question I have for you is, and this was a really brilliant new understanding for me, which is that the biggest driver of increases in mTOR, which is a regulator of aging, higher mTOR, faster aging, is too much insulin, which comes from too much starch and sugar, also protein and also will increase mTOR, right? So, if you're then wondering what is the best strategy for regulating mTOR and aging, because a lot of people are saying, restrict protein, restrict protein, be a vegan, restrict protein, that's going to make you live longer. And I'm not really convinced because, you know, I look at the data, for example, on the Native Americans, the Lakota, who at the turn of the 1900s were the longest-lived population, they had more centenarians, than any other population. And all they ate was basically buffalo. So, and a few berries. So, help us unpack this mTOR story in like five minutes because then we have to stop.

Yeah, so I'm thrilled to circle back. In fact, I think you framed this perfectly and I'm somewhat relieved to hear how you're framing this because I think it means that you and I see this eye to eye. So, these kinds of studies are very difficult to do in humans, of course, everyone listening understands that you just can't feasibly follow humans throughout their whole life and whole lives and look at and perfectly scrutinize their diet and how it influenced their longevity. It's so complicated. But more and more, in fact, a paper was just published a couple weeks ago called the Inchiante study that somewhat reflected what you said again, that even Valter Longo's own research found that the oldest, that meat consumption, animal protein consumption, the older we get, has an inverse association with mortality. In other words, the older we're getting and the more animal protein we're eating, the longer we're going to live. And then there appeared to be this period in Valter Longo's prospective kind of research or correlational studies, he found that there was this kind of an around middle age, I think it was 50 to 60 or so, and you might know this more than me, they found that the people who ate the most meat did have the highest mortality, but then it ended up shifting into the exact opposite at above 65 or 70. And so all of this is correlational, of course, so it's very difficult to state anything conclusive based on the sum of all evidence in my mind. Cutting protein is a wonderful way to make sure your bones and your muscles will be more frail and you will be more frail, easier to kill, so to speak.

And by the way, your immune system requires protein to make the antibody. You hear about antibodies and COVID. where do you get those? From protein.

Yeah, yeah, you need those amino acids. Yep, that's right. So in my view, we should not be fearing protein. We should be prioritizing it in the diet and high quality sources of it, especially. And the fact is, although it's a little inconvenient sometimes, animal protein is imminently absorbable and you at least know you have every amino acid you need. I'm not saying that plant protein can't be a part of this. It absolutely can. but there's also no question animal protein is fantastic. And so we, now I appreciate there's other issues that come into play here, moral issues and ethical issues, but even still, whatever it may be, prioritize protein because it's going to make you harder to kill, including just disease and longevity. And then with the, so that's the one, the thing about just animal protein in general.

So how does that work with mTOR then? I think that's what I agree with them. I mean, the muscle building, I mean, you can get movies like Game Changers on the show that you can be.

Vegan and be ripped.

But, I've interviewed some of these folks. And, one, they are pounding highly processed protein powders, vegan protein powders, because they cannot get the muscle building effect without supplementing branched-chain amino acids and high doses of protein powders. so you cannot get, I mean, because otherwise you'll see a lot of vegans are relatively thin and have low muscle mass over time. You know, obviously they stay on it for a while, but, but the ones who are ripped are the ones who are actually, you know, kind of eating super physiologic amounts of these plant protein.

That you couldn't get by eating them, the whole plants. No, that's right. That, that's exactly right.

Yeah.

And that's sort of reflective of my general view that the further someone's going from animal-based foods, the more they need to supplement. to in order to ensure that they don't have any deficiencies. Now, so mTOR is relevant and animal proteins will activate mTOR more than plant proteins will. And that matters if we are continuing to say that mTOR is the root of all aging. However, I believe it's not relevant for longevity because when we spike mTOR with proteins in the diet, it is very transient. It comes up and it comes down and it's based wholly on the amount of amino acids that are getting pulled into a cell. and of course, muscle cells will pull in the bulk of those amino acids because they have such a high protein demand. That's a good thing because you have to have mTOR turn on and then turn off. You have to have the cyclical mTOR activation. I have a colleague two doors down from my office right here who studies mTOR and its effects on muscle and bone growth. What he's found and others that when you have mTOR turned on too long, you actually start to become mTOR resistant. and that the muscle cell is trying to grow, but mTOR has been on so high for so long that its ability to promote muscle protein synthesis is compromised. And now the muscle is starting to break down its protein, even though mTOR is elevated. But that happens when mTOR is elevated too much, which is not the cyclical activation you get from protein consumption, but rather the insulin-induced mTOR activation. Insulin, as I said, insulin activates mTOR much longer than amino acids do, and importantly, much more ubiquitously. Because if you and I were to eat a load of amino acids, we would get significant mTOR activation in our muscles and relatively little mTOR activation in our liver or our white blood cells. However, because they don't pull in amino acids very much, it's a very modest intake of amino acids. which—and so that's relevant if it's protein-induced mTOR. But insulin, when we spike our insulin, as I mentioned earlier, literally every single cell in the body responds to insulin. There's truly no exception. I'm not being dramatic here. There's no exception. And so now we have our white blood cells that are responding to this elevated insulin and our skin cells and our bone and muscle and liver and brain. And so now mTOR has been spiked and it's staying on for longer. And right around the time mTOR is starting to turn off in response to this insulin spike, what do we do? We turn it on again and again and again by continuing to eat and drink refined starches and sugars essentially every two or three hours from the moment we wake up to the moment we go to bed.

Bad news.

So, if mTOR matters, then focus on insulin, not protein.

That is a brilliant summary of something that I've struggled to understand because intuitively, I knew that protein and also from the data that protein as we get older is really important for muscle mass. And sarcopenia, which we talked about on the show, the loss of muscle is the single biggest driver of age-related disease because it just accelerates everything. Accelerates insulin resistance, inflammation, hormonal dysregulation, high cortisol, low growth hormone, frailty, everything else. and so you need that. But at the same time, I'm like, well, geez, I don't want to, I don't want to be messing up my longevity here by eating my, you know, grass-fed ribeye, you know?

Yeah.

And the explanation of that is actually sugar and starch that keep mTOR elevated all the time as opposed to the cyclical nature, which protein does, is just brilliant. So the take home is cut out the starch and sugar. If you eat a lot protein with a lot of starch and sugar, you're a problem. If you're eating a lot of fat, particularly saturated fat with starch and sugar, it's a big problem. That's a caveat I want to make people. Oh, saturated fat's good. I can eat. No, not if you are eating starch.

And sugar, because then it's like putting gasoline on a fire. We're in an interesting moment in, in society where we're fatter than ever. We keep talking about it for decades. I have been, you have been. And it just keeps getting worse and worse and worse. our government recommendations and policies don't seem to be solving the problem. And certainly the advice we're getting from our doctors and nutritionists often is not effective either, which is eat less and exercise more. It's just calories in calories out. And you've written a lot about this in the past. And recently there's been a real movement to look at radical different ways of solving some of the biggest problems we have, which is diabetes and obesity, using a ketogenic ketogenic diet. And for those who are listening, a ketogenic diet, essentially a 70% fat diet, cuts out almost all carbohydrates and has, you know, moderate amounts of protein. It's definitely not exactly an Atkins diet. It's a little bit different than that. And it's been around for a long time in medicine, but it's recently being used for all sorts of conditions from cancer to diabetes to Alzheimer's, and it's been used for decades for epilepsy by neurologists. so you really become an expert on these issues as a non-doctor scientist. You probably have read more of the scientific papers and more of the data on this than most doctors or scientists. And you've been busting a lot of the big myths that really we are facing in the world of food. And the first myth that you really took on back in 2002 with that article, what if It's All Been a Big Fat Lie? was that we should all be eating a low fat diet to lose weight because fat has more calories than carbs. So if we all eat Snackwell cookies, we lose weight except for one thing, the opposite happened. So what led you in that whole trajectory of this sort of examination of low fat movement to swing so far the other way to read, to write a book called the Case for Keto, Rethinking Weight Control and the science and practice of low carb, high fat eating. What made you go, I need to write a book about this?

Okay.

Well, when I first, by the way.

This is the book.

Everybody should get it. It's really, really awesome. It's got a nice red cover. You can't miss it. And, it's beautifully written.

It's great prose. It's just awesome. And again, thank you again. So, yeah, so that New York Times Magazine article was the third of my investigative the reports on nutrition. So I started off just by chance writing about salt and blood pressure for the journal Science, and I had no idea that it was enormous, very vitriolic controversy in the field, the basis of which was that there's surprisingly little evidence to advise us all to eat less salt. And while I was doing that work, I realized that one of the worst scientists I'd ever interviewed, and I had written a book called Bad Science, had taken credit not just for the low salt diet we were all eating in the 1990s, but the low fat diet as well. So then I did a investigative piece for science. It took me a year published. It was called the soft science of dietary fat. And it just turned out that again, the evidence, the idea that dietary fat causes heart disease was an interesting hypothesis that was launched kind of in the beginning of the 20th century and then took hold in the 1950s and never pand out. The experiment after experiment to try and test it, and the experiments, you know, sometimes they showed that people ate less fat, lived a little longer, sometimes they showed that they died a little more prematurely. And scientists fell in love with the hypotheses, as scientists often do. The public health, the establishment in this country started promoting it, and we believed that ever since, so in 2002, when I did this New York Times magazine article, initially the idea was that I just wanted to find out what started the obesity epidemic. It was relative. Our awareness of it was relatively new. Obesity rates shoot up in this country roughly in the 1980s, and it coincides with some shifts to nutritional advice. Well, we go from eating sugar to eating high fructose corn syrup. So that was one hypothesis. Michael Pollan bought into that idea and was promoting and the other was just that we started promoting this idea that a low-fat diet was a healthy diet and that carbohydrates are heart-healthy diet foods. When carbohydrates had always been perceived as kind of uniquely fattening, you know, starches, breads, and sugars, the kind of thing that, you know, people would say they go right to my hips or right to my gut. So I was reporting that story for the New York Times Magazine, and while I was doing it, it turned out I stumbled on five clinical trials, really the first five that had ever been done comparing an Atkins ketogenic diet to a low fat diet, the kind the American Heart Association was telling us to eat. And none of these studies had been published yet, but they'd all been discussed in conferences. And they all found the same thing, that if you tell someone to eat a high fat diet rich in saturated fat and animal products, but don't eat carbohydrates, and you could eat as much as you want. So, you know, the eggs and bacon for breakfast and a, you know, T-bone steak with salad for lunch and a half a roast chicken with salad. They're green vegetables for dinner and you smother in butter and oil and, you know, all the things we were supposed to not do. And if you tell someone to do that, not only do they lose weight, but they're heart disease risk factors. improve. And all five studies showed the same thing. And they were, you know, from clinical trials up and down the East Coast, basically. And it suggested, you know, this is the, the joke. It suggested that everything we know about or everything we're being told about diet and health was wrong because, you know, the Atkins diet, again, was basically was a ketogenic. It was a ketogenic diet. That's why Atkins was crucified for promoting it. He got very wealthy, but the medical establishment didn't appreciate him promoting a radical idea like ketosis.

Yeah.

So anyway, I, I wrote that article. I argued that, you know, maybe dietary fat wasn't the problem. Maybe carbs were. And I've been following that ever since. And I, I actually didn't want to call my book the Case for Keto because I didn't want to distract from the major points. I was sort of the Originally, the book was called How to Think About How to Eat. And then our mutual friend Mark Bittman came out with a book called How to Eat six weeks before mine was originally scheduled to be published. Theirs came out in mid-March of 2020, so they got swallowed up by COVID, and mine was not scheduled until late April, so we could delay it. And when we delayed it, we changed the title to so they wouldn't compete in the case for keto. I didn't fight it because I've basically been making the case for ketogenic diets since that original 2002 article.

It's a pretty profound idea. Go ahead.

Yeah, I wanted to. I just wanted to put all this in context. And the context is, you know, if carbohydrates are fattening, those of us who get fat easily can't eat them. and then the extreme version of carb restriction is, is a ketogenic diet. But for, you know, 90 years, people have been insisting we get fat because we eat too much. And, you know, I, you and I and others have been arguing when you get fat because of the carbohydrate content of the diet. And some of us just, you know, if we want to reverse that process, we basically have to restrict or abstain from them entirely, and then you replace the calories. with fat. Now you're doing a keto diet and you're fatter. Yeah. But it's the same thing that you would have been told 195 years ago. Yeah.

Well, it's true. I mean, this, this has been around for a while. In fact, you know, our, our good friend David Ludwig was a Harvard Professor, clinical trialist and obesity and insulin resistance. You know, he says, we, we, we.

Don'T get fat because we overeat.

We overeat because we're fat. And what he means by that is that when you start eating carbohydrates, you get hungry fat growing in your abdomen. And it's not just fat there holding up your pants, it's actually hungry fat that makes you hungry and eat more carbohydrates. It's a vicious cycle and it causes fat storage, slows your metabolism, increases hunger and locks the fat in the fat cells. It's literally a one-way turnstile. Once the fat gets in, which comes from the sugar, it's turned into fat, it can't get out. So it's kind of a disaster. And he said something to me once, which just blew my mind and made it all make sense to me. He says, you know, remember your training about type 1 diabetics, type 1 diabetics and autoimmune disease where the pancreas is damaged and you cannot make insulin. These people have, we call it polydipsia, polyphagia and polyuria, right? So they're constantly thirsty because they're peeing out all the sugar and salt and everything, but they're hungry. They're starving all the time, which is polyphagia. and that means that they can eat 10 or 20,000 calories a day and they will not gain a pound. In fact, they will lose weight. So why is that? It's because they have no insulin and you need insulin to gain weight. And the cold key to keto is that it shuts off that insulin. And so, you know, one of the whole issues here is that it's a whole calorie myth which you dissected in your book, Good Calories, Bad Calories. Can you take us down a little bit of why we're still so stuck on this? In fact, David Ludwig sent me a paper from the American, I think, Endocrinological Society that was relatively recent by a whole panel of experts on obesity, very renowned people. And they all came down and said, it's all about the calories. And I was like, oh, I thought we were over that one.

That's just all about the calories because they're willing to to accept that counting calories doesn't really help anyone anymore. It's this idea that it's all about energy balance. So, what David Ludwig is saying, the idea is you have the different foods have different effects on our hormonal status, and whether or not we accumulate fat is determined primarily by hormones, insulin and glucagon. So, insulin is a dominant one, and glucagon is a sort of a counter hormone. so if some foods stimulate insulin, carbohydrate rich foods and protein to a lesser extent, carbohydrates only stimulate insulin, protein stimulates glucagon, which works against insulin, the fat tissue. So it's sort of the argument is obesity is a hormonal thing. You cause your fat to your fat cells to accumulate excess fat, and that in turn steals calories from the rest of your body that you would use for fuel, and so you're constantly hungry. and when insulin's elevated, the only calories you could burn for fewer carbohydrates. So you're constantly hungry. So that's part of the vicious cycle. Back at the turn of the 20th century, when nutritionists and doctors first started thinking about what the cause of obesity is, it's funny in science and, and I, my interest even more than nutrition is, is the how science progresses and scientific thinking. And in science, the tools you have available determine what you can learn, right?

Yeah.

So in physics, you get a bigger accelerator, you can learn more about the universe and astronomy. You get telescopes that look in different wavelengths. You could learn different things about the universe, whatever you could see in that wavelength. And in nutrition, the only tool they had that seemed relevant to obesity was a device called a calorimeter, which could measure the energy be expended by a human being or could measure the energy contained in a food that the human ate. So they created this theory that obesity is caused by energy in being more than energy out. It seemed intuitively obvious because that's all they could measure. They couldn't measure a math problem.

I mean, weight loss is a math problem.

It's basically a math problem. So, you know, there are other people arguing, look, it's, it's clearly a hormonal issue. It's like you look in and women fat differently. That's hormones. You know, like boys go through puberty, they gain muscle and lose fat. That's hormones. Girls go through puberty, they gain fat in specific places. That's hormones. It's all hormones, you know? And it's just some people, they're going to get fat no matter how much they eat or the only way they're going to stop themselves from getting fat if they starve themselves. Yeah. And this was the German and Austrian clinicians who were doing the best medical science in the world. at the time argued this. It didn't matter. An American came along, a guy named Louis Newberg, University of Michigan, and claimed he had done the first experiment ever. This was 1930. And in this experiment, he proved once and for all was all about calories. It's about how much you ate. And it was always about how much you ate. And no matter what the excuse, like, you know, women, when they go through menopause, they gain fat. Now, animals, when they go through menopause, are the, if you were to remove the ovaries from animals, they'll gain fat. And that was well known even in the 1920s. So it seemed to be a hormonal thing related to estrogen. But with women, it was about eating too much. They sat down with their lady friends and played bridge and ate bonbons. I mean, incredibly sexist explanations for why it's never hormones. And it just caught on. It caught on in part because World War II came along and the German and Austrian researchers arguing the opposite vanished. They evaporated with the war.

So the Germans were the ones pushing that it's not energy balance. And so the Germans were the ones pushing that it's not energy balance. And because they were saying it's the.

Nazis, we got rid of that theory. We got rid of that. And it sounds like we're joking, but it's you, you know, nowadays, I mean, it's very easy to demonstrate in the.

History, it's people cite. And because they were saying it's the Nazis. we got rid of that theory.

They did Newberg. They didn't cite the germ. Actually, the prime guy was an Austrian. He was a Jew named Julius Bauer. He fled to the US in 1938, but the only job he could end up getting was that he was one of the founders of the sort of endocrinology research in Europe. Got rid of that. And it sounds like we're joking, but it's you, you know, nowadays, I mean, it's very easy to demonstrate in the history. People cited Newberg. They didn't cite the germ. Actually, the prime guy was an Austrian. He was a Jew named Julius Bauer. He's very well known, pioneer in the field, flees the Nazis in '38 when they attack. They move into Austria. He ends up going to Baton Rouge, Louisiana. He works at LSU for a year, and then he goes to LA. and gets a job at the hospital of medical evangelists. And he publishes papers like Julius Bauer, Hollywood, California. And nobody pays attention.

Yeah.

Yeah.

You know, he's not at Harvard. He's not at Yale.

He's not at Columbia.

He's like, who is this? We've had decades of other research since then. I mean, there's been really well-designed well-executed.

Clinical trials by David Ludwig, led to.

The US in 1938. But the only job in others looking at this whole hypothesis of the, of the carbohydrate insulin hypothesis of weight loss, which is a hormonal one. And what, what it really leads to in, in our thinking, and, and this is sort of striking to me, you know, I researching some of my books, I discovered that if you're a kid.

And you're overweight, we could end up getting was that the, I mean, he was one of the founders of the sort of endocrinology research in Europe, very well known pioneer in the field, fleas and Nazis.

It's more of a stigma than if you're a kid and you're in a wheelchair and a quadriplegic. And we basically blame the person who's overweight for being fat. It's your fault you're fat. Just eat less and exercise more. And otherwise, if you don't, it's just because you're lazy and a glutton. and that fat shaming and that underlying approach is based on this idea of the calorie myth and that weight loss is just a matter of willpower. So, why is willpower not the issue here?

Well, again, it's based on this energy balance idea. The obese 38 when they attack, they move into Austria. He ends going to Baton Rouge, Louisiana. Child, maybe he's 40 pounds overweight at age 12. That means his fat, they've been storing, you know, 50 extra calories of fat a year in his fat cells. So why can't they fix that? Why can't they just eat a little less, store a little less? And he works at LSU for a year, and then he goes to LA and gets a job at the hospital of medical evangelists, and he probably exercises a little more, store a little less, and It's the answer that lean people come to is, well, they must not care enough. If it's about energy, which is papers like Julius Bauer, Hollywood, California, and nobody pays the balance. And I make this point in the case for keto. If it's about energy balance, that absolutely, that creates the concept of fat shaming in effect, because the assumption is always, if it's about intake and expenditure, more, then you should be able to take in a little bit less or expend a little bit more. It doesn't take a world of effort. We're talking about tiny numbers every day. So why can't people do it? Then you end up assuming it's because they don't want to.

Yeah.

Or they attention.

Yeah.

Yeah.

You know, he's not at Harvard, he's not at Yale, he's not at Columbia. He's like, who is this? So we don't have willpower where you come over. And the center is by the 1960s, obesity research in the US was dominated by psychologists and psychiatrists who were trying to figure out how to get those fat people to eat less. I mean, they didn't care. The idea that they just have a fat storage disorder.

We've had decades of other research since then. I mean, there's been really well-designed, well-executed clinical trials by David Ludwig.

We have a fat storage disorder. Just like if you saw somebody walking down the street who was eight feet tall, you you wouldn't think about how much they eat and exercise. You would think he's got some kind of growth hormone dysfunction. Even if you weighed 400 pounds, which often.

And others looking at this whole hypothesis of the, of the.

And if somebody's eight feet tall, they're likely to weigh 300 or 400 pounds. You don't care about how much they're eating and exercising. You care about the growth hormone issue.

And growth hormone receptor. Carbohydrate insulin hypothesis of weight loss, which.

Is a hormonal and what it really leads to. But here they just didn't think like that. And once they didn't, and this is the danger in any sort of medical scientific process, once you assume something to be true based on an assumption, then it's going to infiltrate everything you do and it's going to affect everything you do. So David Ludwig does these terrific, you know, very well-designed experiments to suss out whether or not obesity is a carbohydrate insulin problem or a calorie problem.

And for the most part, his work.

Has sided with his, you know, his own preferred hypothesis, carbohydrate insulin. But there are other people who think the opposite, who claim to in, in our thinking.

And, and this is sort of striking to me. You know, I researching some of my books, I discovered that if you're a kid and you're overweight, it's more of a stigma than if you're a kid and you're in a wheelchair and a.

Quadriplegic, that their experiments are just as well designed. And then you end up getting- They're nameless. Yeah, they will remain. And the problem is all we can do, like you as a physician and me as a journalist, is say, look, this worked, you know?

Well, I'm a practicing doctor and I'm just humbled by seeing real patients in real time and not just looking at theory or scientific articles or textbooks, but actually seeing what works and what doesn't.

Work depending on the person.

And this is really an important piece here. And you say, and we basically blame the person who's overweight for being fat.

It's your fault.

In your introduction to your book, you say, I'm not writing this book for the lean and healthy of the world. I'm writing it for those who fatten all too easily. And I fat, just eat less and exercise more. And otherwise, if you don't think that's the key line in the book, There are some people who can eat whatever they want and they're fine because they're highly insulin sensitive. But when you look back, for example, at the Native Americans in this country, there was no obesity, there was no diabetes, there was no heart disease, and now second to Samoan, it's just because you're lazy and a glutton. And that fat shaming and that underlying approach is based on this idea of the cows, they're the fattest population.

In the world.

Why? Because their diet changed from what they were adapted to, to an extremely high carbohydrate diet. They were great at starvation. They were magnificent at managing scarcity, which 100s of generations do that.

But I don't think the Native Americans dealt with a lot of scarcity in this country.

Well, I mean, they might have had.

To deal with some scarcity. 100 gatherers, you know, they could get food, but there was food, but it was tough.

Right?

It wasn't like- It wasn't that tough. When Lewis and Clark, I hate the.

Tall-Ry myth, and that weight loss is just a matter of willpower.

When Lewis and Clark, you know, crossed the country in 1805, they had to push the buffalo out of the way on the Great Plains, literally. You know, you've got these- that's true. Herds of millions of buffaloes.

But historically, we've gone through periods where.

You know, it wasn't always easy to go. go to the grocery store and get food. So we are really well adapted. Why is willpower not the issue here? Adapted to starvation. And then there's a whole class of people that really this book is for the case.

Well, again, it's, it's based on this energy balance idea. If the, the, the obese child, maybe he's 40 pounds overweight at age 12.

That, that means is for keto, rethinking weight control in the science and practice of low carb, high fat eating. Everybody should get a you go into explaining why there's a subset of people.

Which turns out to be probably the.

Majority of people in America.

Probably the majority.

Right.

There's 75 are overweight, 88 are metabolically and healthy.

So maybe there's like, you know, one out of 10.

That's a lean, healthy person. They got lucky. But for the rest of us, carbohydrates make a difference. So what does it mean to fatten easily?

And this is fat. These he's been storing, you know, 50 extra calories of fat a year and.

His, why is this book so important for people who are overweight to really get understand and read?

Well, and this is, you know, we all, we get it. If you're one of these people who struggles with their weight, you know, again, the conventional wisdom, the assumption, the advice we get from everyone when it's a calories on fat cells. so why can't they fix the problem? And you got to eat less and exercise more. The idea is, if you're still struggling with that, why can't they just eat a little less, store a little less, or exercise a little more, store a little less? And it's the answer that lean people playing with your weight, you're not trying hard enough. Whereas the rest of us want to say, look, I tried that. I did need less exercise more. I the decade of the 1990s hungry. Okay? I gained weight anyway. This is what it means to, you know, it's like I restricted my calories. I ate in moderation. You know, Michael Pollan, I tried my best to eat not too much, and I got fat anyway. So we're different from the lean people. So a lean person comes along, come to us, well, they must not. care enough. If it's about energy and they think, okay, I eat in moderation, this is my issue with David Katz, and I hope David Katz someday reads the, you know, Yale-affiliated doctor who has become a major spokesman for the sort of mostly plant movement. And the world is full of these, you know, healthy, lean balance. And I make this point in the case for keto. If it's about energy balance, that. Absolutely. That, that creates both physical trainers and marathoners. And they think it's the concept of fat shaming in effect, because the Assumption is always, if it's about intake and expenditure, you know, I eat moderation, I'm lean, I eat moderation and I exercise. Therefore, if everyone else ate in moderation exercise, they would be lean, too, which is not true. and if they don't eat moderation and exercise, or if they're not lean, it means they're not eating in moderation and they're not exercising enough. So I have to tell them, you know, eat moderation, don't eat too much, eat a healthy diet, fruits, vegetables, whole grains, and the point is we all did that. We're not the obese and overweight, the 90, 88% of Americans who are metabolically unhealthy are not sitting in lines at McDonald's right now in the then you should be able to take in a little bit less. They're oversized SUVs with the specially wide seats waiting to get their triple cheeseburgers and super-sized fries and huge cokes. I mean, some of them are, but some of them are eating very healthy and doing their best to eat in moderation. They're still overweight or expend a little bit more. It doesn't take a world of effort. We're talking about tiny numbers. every day. So why can't people do it? And then you end up assuming it's because they don't want to.

Yeah.

Or they don't have willpower. You come over and it's interesting by the 1960s, they're getting the wrong advice. And that's what I'm trying to communicate. We've been getting lean persons diet advice for the past century. This is what I eat. Therefore, this is what you should eat. I know. What I'm arguing is that those of us who fatten easily, if we eat what they eat, we're going to be either fat or hungry. Those are our two choices. And possibly both. Yeah, that's right. That's right.

As a practicing doctor, I see this in real time by looking at people's.

You know, obesity research in the US was dominated by psychologists and psyche hormones.

And their metabolism and their insulin levels and their lipids and their inflammation. I can tell often just by looking at somebody because I had so much experience, but just looking at their lab test, which type of metabolism they have. And, and the truth is, and it's, and I often I feel bad and I apologize to my patients because I.

Say, listen, we're trying to figure out how to get those fat people to eat less. I mean, they didn't care. The idea that they just have a fat storage disorder. They, we have a fat storage disorder. Just like if you saw somebody walking down the street. it was eight feet tall. You wouldn't think about how much I.

Didn'T I didn't design this. I'm not the I'm not the creator of your biology. I'm just the interpreter. But I'm telling you, if you really want to stay healthy and avert all the diseases of aging, because they're all connected to this mechanism of high insulin, right? Heart disease, cancer, diabetes, dementia, depression.

I mean, I could go on and on.

If you don't pay attention to this, you are going to be in trouble. And the truth is, like you were saying, what are these lean people? have in common, they're insulin sensitive. I don't know if you know Jorge Plutzky. He's a cardiologist at Harvard, a preventive cardiologist. And, Mark, if you were to take a group of 100-year-old people who had.

Absolutely clean arteries, they'd have one thing in common.

I said, what's that? He said, There'd be insulin sensitive. If they eat an exercise, you would think he's got some kind of sensitive, meaning they are very good at producing very low levels of insulin that are extremely effective in the body that don't require it produces more and more to get the same benefit. And sort of like that's what insulin resistance is. Essentially when your cells become resistant to the effects of insulin, so you produce more and more and more and more.

To keep your blood sugar normal. Growth hormone dysfunction. Even if you weighed 400 pounds, which often if somebody's eight feet tall, they're likely to weigh 300 or 400 pounds.

You don't care about how much they're eating and exercising. You care about the growth hormone issue and growth hormone receptor. but eventually, you know, that burns out and you get diabetes. But even before you get diabetes, it just causes the weight to pile on and all the metabolic issues.

Yeah.

And this is, you know, those people who, I mean, you could guess if you've got a weight problem. This is right, though, the, the first symptom a doctor is supposed to look for to diagnose metabolic syndrome, which is we could call insulin resistance or hyperinsulinemia syndrome. And the first symptom you're supposed to look up for is your, your waist size is increasing, you're getting fatter. and then it's high blood pressure and low HDL cholesterol and high triglycerides and glucose intolerant, you're becoming diabetic. But here they just didn't think like that. And once they didn't, and this is the danger in any sort of medic, all those things are happening and the way you fix it is remove the cause of it. The cause is first the highly refined grains and sugars. But then for many of us, and this is where you start going into sort sort of keto diet land. For many of us, it's all carbs. All green leafy vegetables, scientific process. Once you assume something to be true based on an assumption, then it's going to infiltrate everything you do, and it's going to affect everything you do. So David Ludwig does these terrific grain, bean, starches. Yeah, it's because our bodies can't tolerate it. And this is just not the message we and it's a strange time we live in because often I feel like, you know, we were making a lot of progress getting the nutrition community to pay attention, but now we live in the age of fake news. So it's easy to write off alternative perspectives as fake news and I wander around thinking, wait, am I a purveyor?

Are you a fake news purveyor?

Am I a fake news because I disagree with the establishment. But again, the argument we're making and what you're telling telling your patients? What I'm telling readers is, look, you know, very well-designed experiments to suss out whether or not obesity is a try this. The one thing we know for sure, right, is low-carb diets are safe and benign.