Fix Your POOR DIET To Prevent Obesity, Diabetes & RISK OF COVID! | Dr. Ronesh Sinha & Mark Hyman

You treat COVID-19 kind of like a sporting event. It's like you're training for 5K or 10K. How do we get you less breathless through physical activity? How do we elevate your VO2 max? How do we get an inch or two off the waistline?

We think of COVID as an infectious disease, but actually is it a lifestyle disease and how and why?

Right. Basically with the COVID-19 pandemic, I've kind of just added a different spin to my mainstream message already just because of the data that's shown a profound link between COVID-19 and insulin resistance. So both if an individual has insulin resistance already, we know from the data that their risk of a severe COVID-19 outcome is so much higher. The obesity, even the high triglyceride, low HDL has independently been shown to be a risk factor. So we know that from that standpoint. Now what we're finding too, Mark, is individuals with a COVID-19 infection that have existing diabetes or glycemic control gets worse. but we're also seeing individuals that had no detectable signs of insulin resistance actually develop insulin resistance after COVID-19 infection. Now, most of the studies have been done in more severely hospitalized patients, but we are anecdotally now seeing that even in the outpatient less complicated cases, there are some insulin resistant features that are showing up in individuals that didn't have that before. So one of the analogies I use is it's almost kind of like gestational diabetes where pregnancy can unmask underlying hidden diabetes. COVID-19 looks like in a certain segment of the population, that stressor and inflammatory load to the body is unmasking a potential underlying tendency towards insulin resistance or possibly even causing a de novo because it can invade the beta cells of the pancreas, it can really diminish insulin production, it can affect the mitochondria, it can do so many insidious things. And that's why I use the word transmissible metabolic disorder because even after the infection is cleared, It could potentially cause some lasting metabolic changes in the body that we need to be aware of.

Yeah, fascinating. So, you talk about this whole idea of CoViDity. What is that? And how is body fat and visceral fat linked to the severity of COVID.

Yeah, I mean, basically, you know, I think the term cytokines, if one thing has happened with COVID-19, you know, I try to be as optimistic as possible, but I think People's education around the immune system has been elevated as a result of this. So a lot of people know about the term cytokines, you know, 'cause there were cytokine storms. But if we can be more specific about inflammation and limit to the cytokines, which are the inflammatory messengers from our immune system, we realize that that belly fat, that visceral fat that we talked about, it's a storehouse of chemicals, especially cytokines, which can really make our bodies more flammable. So when they get a COVID-19 infection, the risk of having a severe outcome is much worse. So with many of my patients that are worried about COVID-19, I'm like, can we get the waistline down through lifestyle changes so we can lower that total cumulative cytokine load in case you're to get a COVID-19 infection, which unfortunately the likelihood is getting higher and higher as these variants come out. But really that's a key part is.

That visceral fat is connected to that cumulative cytokine load. It's crazy. You know, what really shocked me was the data came out of Tufts from Dariush Mozaffarian, where they found that they could attribute 63% of all hospitalizations for COVID to diet. So I'm gonna say that again, 63% of all the people in the hospital from COVID is not because of COVID it's because of what they're eating. And how what they're eating has caused them to have insulin resistance, which basically lets them be pre-inflamed. And so when the COVID hits, it's like putting gas on a fire. and the inflammation goes crazy and that's what ends up putting them in the ICU or even killing them. So, you know, this is such an important moment and you talk about how you're beginning to see this as an opportunity for how we kind of have to rethink our approach to, you know, the next pandemic or even this pandemic that maybe we as a nation need to focus on how do we address this? So what are you thinking about that?

I mean, you know, Marc, I think this is my frustration. I don't think the media and public health agencies are focusing on this enough. You might see an anecdotal headline here and there, but you know, you're obviously taking this on from the food standpoint and I laud you for the work you're doing around this, but if we don't sound the alarm bells now that COVID looks like it's become more endemic than pandemic, I don't know when we're gonna do this. You know, in my patient population in the schools now that kids have been sheltered in for so long, we're seeing even worse, you know, pediatric obesity, signs of insulin resistance. So I think it's, you know, in one case, I don't wanna create a doom and gloom picture, but I also wanna create a picture of hope that there is simple things you can do through lifestyle changes that can reduce your risk of developing these severe outcomes, you know, the near term. And the good news is many of my patients that have been putting off lifestyle changes because heart disease seems so remote, now they're actually willing and accepting the fact that, yeah, I understand cytokines, I wanna get the visceral fat down, I wanna make those changes. And one way I kind of reframe it is I tell people, you treat COVID-19 kind of like a sporting event. It's like you're training for 5K or 10K. How do we get you less breathless through physical activity? How do we elevate your VO2 max? How do we get an inch or two off the waistline? These are all goals that I had even before COVID-19, but how do we accelerate those goals? And now that I'm giving talks to schools, I'm really trying to push, how do we really emphasize physical fitness more in the midst of a pandemic? 'Cause that's what all parents are thinking about. is vaccines and pandemic, but is this an opportunity to really hit the hammer a little bit harder on lifestyle changes?

Absolutely. It's such one of those moments. I have fear we'll pass us by and we'll miss the chance, but I think it really is important for us to get really serious about it. What are you seeing related to the sort of A1C and the continuous glucose monitoring in these COVID patients? You sort of touched on a little bit. Can you talk a little bit more about it?

Absolutely, since I've got a lot of techies. These patients like to develop spreadsheets and they follow their data very closely. So even though I'm not a COVID-19 frontliner, I have seen in some of my patients that had a COVID-19 infection, they share their continuous glucose monitor data with me. And some of them actually saw early elevations and markers of increased glucose in the early stages of infection, which isn't surprising to you and me, but already they were starting to see the metabolic impact of that. So I thought the CGM sensors were very powerful from that. But then the other part that I'm really starting to see is many of my patients that had a COVID-19 infection and cleared it, some of them, their A1Cs unexpectedly went up, despite their lifestyles being the same or even better. Their CGM sort of unexpectedly went up as well too, even though it was rock stable for several months or even for a year of doing CGM data. And that to me was already a marker that, wow, this is doing something that's a lasting metabolic effect. And you know, someday, Mark, I mean, five, 10 years from now, that might be part of our general history is did you have a COVID-19 infection as we're screening for heart disease risk and diabetes risk, 'cause these infections might be doing some lasting damage that we're not aware of. Now, this is very anecdotal from what I'm seeing in just small cases, but I think as we collect data and we look prospectively beyond this pandemic, we have to think about if somebody had a COVID-19 infection, let's be even more aggressive about checking their baseline numbers. Maybe they get a CGM, check your labs more regularly to see is there a trajectory that's steeper as a result of COVID-19.

So something I think we need to be aware of going forward. Amazing. So how do you help people.

Sort.

Of in the thinking about the most important lifestyle and dietary changes to reverse this? Because, you know, it's not just South Asians that are affected by this. Clearly, they have a more predisposition, they have higher risks, and they get a lower weight with lower body mass. But like I said earlier, 88% of Americans are metabolically unhealthy. that means they're insulin resistant to some degree. And what's striking with COVID was that it wasn't like, oh, well if you're obese and it's a problem, but if you're a little overweight, it's not a problem. It was a linear risk of hospital mission and death with increasing weight and poor metabolic health. So it wasn't like there was a zero risk if you were just like a little extra belly fat. You really are at risk. And I think it's important for you to understand this, that what can you do to deal with COVID you can take care of yourself. It's not just about mass or vaccines or ivermectin or whatever people are talking about. It's about your own well-being. I don't know, I don't know, I don't know why I don't have or haven't had COVID. I've been around a lot of people and I'm careful, but still, I wonder, is it just because I take my vitamins and I get enough sleep and I eat well and I exercise and I meditate and I just wonder if that's part of it. How do you advise your patients to sort of create a bulwark against COVID through lifestyle?

Totally. I mean, I think you're an example of what I explained is, you know, it's biological versus chronological age. You know, I know we put the number out there of 60, 65 and over 70 and over being high risk, but I'll tell you, I've got some patients above age 70. I'm less worried about them than some of my 30-year-olds just based on their level of fitness, their healthy lifestyle practices. I'm more worried about the outcomes in my 30-year-old patients that are sedentary and already pre-inflamed. I love that term that you used. So I think this is an understanding we have to understand is, you know, obviously we have to use things like age just for population health. These are sort of ways that we can sort of collect data, but we've got to really make people aware of these terms that, you know, the amount that you can physically act, you know, be active, not being breathless, you know, what are the elements of the diet and things. And, you know, as a healthcare system, we have to infuse this into our practitioner system too. So when physicians, again, are overwhelmed, you know, they're obviously taking on so much, but can we refer more patients to dieticians and lifestyle services consult practices as part of the COVID-19 strategy, which is just really focused right now on just vaccines and obviously social distancing. These things are important, but part of that recipe has to be how do we actually surround these people with lifestyle prevention strategies so we can again bring down that cumulative cytokine load. What you're doing through your lifestyle practices, I'm not surprised that you haven't been infected because your immune system is naturally.

So robust and that's what we have to teach our patients around this. I hope so. Maybe I've just been lucky. So why are South Asians at such risk? They make up today one third of the world's population and they have the highest prevalence of heart disease and diabetes. Like, I can't imagine that 100 or 200 years ago, that they were all suffering from diabetes and heart disease. So what is unique about South Asians? What are their dietary factors maybe that are unique to these cultures that puts them at risk? I have some ideas. I want to hear what you have to say.

Oh, yeah, totally. And yeah, you nailed them. The statistics are overwhelming. I mean, despite comprising that segment of the population, they make up 60% of the world's heart disease patients, which is pretty astounding. They've got quadruple the risk of heart disease compared to other ethnic groups. And the problem here, Mark, is they actually present 10 years earlier as well, too. So we see a lot of- They're young. I see individuals in their 20s and 30s presenting with early heart disease, which is astounding. And the way I explain it is before we sort of get into the fuel source, I like to use a lot of analogies when I teach these concepts. So I don't know much about cars, but I'm going to use a bit of a car analogy here. And before we talk about fuel sources and food, I want to explain to you sort of what the South Asian vehicle is like. If we're to think of the body of the South Asian vehicle compared to other ethnic groups, and there's a lot of rich studies out there in the UK and Canada where they have a large South Asian population. And what we first find is if you look at the body of this vehicle, there's a very high fat to muscle ratio. So lots of fat to muscle. Yeah, the fat to muscle is very high. So a lot of fat and it's localized around that abdominal area and I know you've done a lot of promotion around the dangers of visceral fat but we have a relatively much higher proportion of that. What doesn't get much attention though, Mark, is the low muscle mass. So when you look at Asian, South Asian specifically, men and females compared to other ethnic groups, we have the lowest.

Proportion of lean body mass. So that really— Justin: why is that? Why is that? Is that genetic or is it control?

You know, part of it is also lifestyle too because we place a huge emphasis on professional and academic prowess even early on in childhood. So, part of its culture as well too. But that fat to muscle ratio is really out of proportion. So, that's one part of the body vehicle. And then like we said with the fat, you're right. There are two types of fat, the visceral and the subcutaneous. And this is a tricky part because that subcutaneous surface fat that's what contributes to body weight, right? Most of our mass weight comes from that subcutaneous fat, but we have that stealth hidden visceral fat that sits in your liver and around your digestive organs. And often when we see patients in the clinic, they present with the normal to low body mass index. And a lot of doctors that know about this, they're like, Hey, you've got a free pass. You look great. And these individuals also think they got the lucky genes, so they eat whatever the heck they want because they're not overweight, but what they're doing is they're contributing to more of that hidden stealth visceral fat. So that's another part of the sort of surface issue. So the other thing is when you take this car and you look under the hood at the engine, which I know you've done a lot of work around mitochondria and really raising awareness around mitochondria, that's really the engine that gets the car going. And again, if you compare the South Asian engine, the mitochondria, it's got a lot of weaknesses. It doesn't oxidize fat very well. It produces more inflammatory byproducts when it's exposed to the wrong fuel sources. So when you look at different ethnic groups, we've got this surface body issue. And then the mitochondria are weaker at oxidizing fats and that can create a lot of different issues. So that's sort of the body habitus of the South Asian body.

So, I'll pause here for a second in case you want me to explain anything. Yeah, so there's a genetic component where certain ethnicities, even the Chinese were like this, South Asians at much lower body mass. So they look thin, but they're fat on the inside.

We call that skinny fat or tofi.

Fat on the outside, fat on the inside. right.

Exactly. Right.

As opposed to tofu, which is not what we're talking about. And, and that, and that makes them much higher risk for this. And I've seen this so much in my patients. And it's also challenging because, you know, a lot of the Indian population is vegetarian, and I've loved your thoughts on, on the challenges because I've had, you know, patients who are diabetic, type 2 diabetic, on insulin, struggling, and within, like, literally days, they're off insulin, they're off all their medications or diabetes in a few weeks is literally reversed. And that is usually by restricting every type of carbohydrate. So grains, beans, and obviously sugar. And so in the case of South Asians, a lot of the cultural preferences are for vegetarianism where there's a high amount of starch, high amount of rice, high amount of bread, high amount of sugar. How do you navigate that? Because I had a patient, it was really hard to help her because all, like, what could I have her do? I was trying to approach her shakes, nuts, and it was just, she was very resistant to it. And, I know I could have fixed her overnight, but she really struggled.

Absolutely. So, that's a big cultural part of it. And, you're right. So, the early work that I did, I highlighted that most South Asians are actually not true vegetarians. They're granitarians or they're carbatarians, right? Because the proportion of vegetables that they're consuming is- Carbohydrates, carbatarians, you mean? Carbohydrates, right? Because if you basically, if you basically use a general term vegetarian for all people that don't eat meat and fish, you miss all the nuances, right? If you look at a typical Western vegetarian diet, a healthy form of that versus a traditional Indian vegetarian diet, there's tremendous differences in that. So just to give you a quantitative approach, if you were to quantify it, and again, I think you and I both share one thing is we like to personalize diets for different individuals. So, you know, look for not right for everyone, but definitely if you take a population, and again, if we're thinking of the fact that we've got less horsepower in our engine genetically, and carbs are a high energy fuel source, we're overwhelming that engine on a regular basis. If you want to get quantitative about it, a lot of my patients, for example, they'll thrive if they can bring their carb intake down to 100 grams per carb per day. But my typical South Asians and East Asians, they're consuming 400 to 500 plus grams of carb. And I tell them the carb itself is maybe benign if it's rices and starches. If you were Michael Phelps or if you were an Olympic level athlete with a V12 engine under your hood, but you've got more like a minivan or a lawnmower engine. We can't flood it with that sort of carbohydrate. By a mix engine. Right, exactly. We don't have that sort of horsepower. We can build that up and we'll talk about that later, but we just don't have that.

So, one paradigm that I use to really- so, what you're saying is genetically or is mitochondrial function genetically less in South Asians?

So, I will tell you this. So, it's a combination. So, genetics is a part of it. But then the lifestyle is key. So when we talk about this car vehicle, I tell people the prototyping and designing happens with the parents, right? So even before conception happens, if mom and dad are both insulin resistant and they're sedentary, what happens is they're already insulin resistant and that's going to get transmitted into pregnancy. And that's why in a lot of parts of India and even the US, South Asians have 40 to 50% gestational diabetes. They're already hyperinsulinemic and they're transferring that to the placenta. And the sad thing is you mentioned skinny fat. When you look at the South Asian fetus or the newborn, they're already skinny fat. They've got less basically muscle mass and a tiny little pot belly. So they're already a version, a mini-me version of what they're gonna be later on in adulthood. So that's a big problem. That design happens early on. So part of it's genetics, but the other part is a lifestyle before and during pregnancy. So a lot of the health education I've done after tech companies in the community is how do you design a healthier pregnancy? Because I'll tell you one thing that really makes this engine much worse. So VO2 max, which is a marker for mitochondrial performance, that's something the parents can influence. So I tell parents that if you're planning to get pregnant, you gotta get fit for this pregnancy. Both of you need to be physically fit, but most South Asians are so sedentary that they come into this pregnancy unfit and they're gonna have basically an offspring that's gonna have a low VO2 max and a low horsepower engine. But my patients that take this to heart, their kids don't have that. Their mitochondria is stronger. It can withstand a little bit more carbohydrate load. But this cultural epigenetic intergenerational issue is really causing that engine to be really much less capacity. So that's a big problem.

That's huge. And it's really, it reminds me a little bit of the Pima Indians who 100 years ago, 150 years ago were thin, were fit. Their diet was about 80% carbs, but it was like acorns and nuts and things like that. They grew. and there was no diabetes, there was no obesity. And now, you know, Pima are probably the second most obese population in the world after the Samoans. And their life expectancy is 46, 80% get diabetes by the time they're 30. And we're seeing, you know, type two diabetes in three-year-olds in that population. Incredible. Is the opportunity. By the way, I want to pass on that.

I wanted to connect the Pima Indians to Indians because there's another characteristic we're seeing evolutionary that evolve in that, and that's the type of fat that South Asians and Pima Indians actually have. we have less of the brown adipose tissue. That brown adipose tissue, as you know, is the mitochondrially active fat tissue that can actually burn carbs and glucose. And Asians, populations that come from more equatorial regions, they have less brown adipose tissue. And that makes sense because if I'm out in the field, I'm out in the sun, and I'm toiling and I'm laboring, I don't want to generate extra heat, right? That's going to be a dehydrating factor. But as you take these individuals out of their equatorial climates and you put them in temperature-controlled rooms, and then all of a sudden you flood them with this diet, you see huge impact from that. And honestly, that brown fat can, it can contribute 15 to 20% to your Baseline resting metabolism. So that's a major overlap that we're seeing.

That's interesting. So there's less brown fat in these populations.

There's less brown fat. Yeah, I've got brown skin, but I've got less brown fat. Unfortunately, they don't correlate.

So amazing. And the, the, you know, the, the thing that just occurred to me Ranesh was that being South Asian and aging are very similar. And that as we age, the population loses muscle and becomes fat. And you marbleize your muscle looks like a rib eye instead of a filet mignon. And that's the source of poor metabolic health, which means pre-diabetes, diabetes, hypertension, heart disease, cancer, everything else. and it's 100% fixable, preventable. You know, I actually, as I've gotten older, I've gotten more and more muscle because I realized that muscle is the neglected organ.

Oh, so true.

It is the key to health. And it's not just about looking like Arnold Schwarzenegger. It's really about creating metabolically healthy muscle, which is the main sink for your calories and for your food. And if that's not working efficiently, you're in trouble. And what happens also to these people is they have a low VO2 max, which is basically the amount of oxygen you can burn per minute, which is the rate limiting step in your metabolism. So you can only burn as many calories per minute as you can breathe liters of oxygen or run liters of oxygen per minute through your mitochondria. And the mitochondria in these people are impaired for a number of reasons. One, the diet itself impairs the mitochondria. Two, it sounds like genetically there's some issues there. And we know even in the PCG1 receptor, there's challenges genetically even in first-degree relatives of type 2 diabetics. So, they may have 50% slower metabolism to start with. And I think this is a really prevalent condition in South Asians. And so, we see the aging phenomenon the same as the phenomenon you're seeing. So, what we're saying here applies not just to South Asians, it applies to everybody. and there's a lot of people walking around who are skinny fat. They think, oh, I'm good. I can eat my sugar and I can eat this and that. I don't gain weight. Well, that's not the key metric.

It's really a much deeper metric. I love what you brought up. You know, that age related muscle loss, which we call sarcopenia, at a molecular level, I call it myopenia, because if you lose muscles, you're losing mitochondria as well, too. And those engines, you lose horsepower, you're not going to be able to tolerate the carbohydrates. an adequate amount of that. And so one way I bargain with my patients, whether they're of Asian Indian descent or anything, is if you want to eat rice, you've got to sort of earn the right to eat that rice. You've got to squat for your rights, you've got to walk for your rice, you've got to do some physical activity to earn that. Because otherwise, if the minivan sitting in the garage and it's not doing anything, your body's not going to tolerate that. And the beauty of that, and you know this Mark firsthand, is when you get people more aerobically active, more physically exercising, they're all of a sudden they can handle a little bit more of the carbohydrates. The same root caused me to get insulin resistance. Now as a fuel source after I work out, it doesn't have the same impact. So I think that gives our patients some hope that this is not a banned food like the fructose is and the other processed foods out there.

We can reintroduce it gently to the diet as you upgrade your metabolism. It's true. I mean, honestly, I love to eat, which is why I like to exercise. I think that's true. But I'm like, I go for a two-mile bike ride.

Oh, great.

I just, I went for a 50 mile bike ride the other day and burned 2400 calories. I'm like, I can eat more food today.

Right, totally, totally.

So, you know, same way.

I don't have any willpower. Yeah, totally.

That's so great. So, Ranesh, your work is pretty remarkable in calling this out and talking about the cultural differences and health. And that's why we often see health disparities in other populations like Native Americans, African Americans, Hispanics and and of course in South Asians. So you had this problem too, right? You developed metabolic syndrome and your triglycerides were high, your HDL was low. What were you living like? What was your diet and what was the story around that?

Yeah, you know, I've been a lifelong devotee of healthy practices and even back then when I started my practice in Silicon Valley, I was following the standard dietary guidelines. I was exercising four or five days a week. But what I was doing was-- oh.

Wait, wait, that was a problem.

You were following the standard dietary guidelines. That's exactly right. You nailed it right there, right? And my standard dietary breakfast was pretty starchy with a lot of fruits and oatmeal. I'd have a whole wheat bread sandwich for lunch. So, it was a lot of those healthy carbs that were so-called healthy carbs that were really overwhelming my system. And then also my exercise was really a lot of HIIT training, a lot of high intensity interval training, and not really that steady, more long grade sort of cardio. As a result of that, I started seeing my patients developing insulin resistance. I was giving them advice, but then I was getting insulin resistant too. So I'm like, okay, so this is not going to work out. How can I be a health leader if I'm developing the same conditions as my patients? Then that really caused me to dig deep into the literature. I had the benefit also of being mentored by Jerry Reaven, who actually coined the term metabolic syndrome. Oh, really?

Yeah.

So I used to drop by his office in Stanford and he really helped highlight this triglyceride HDL, this issue. And he was really such a pioneer. He literally told me that sometimes he doesn't get invited to conferences because his metabolic syndrome criteria doesn't include LDL, right? He kind of nailed the triglyceride HDL insulin resistant axis. And so I took that learning and then really dug deep and then made changes in my body, which I basically translated to my patients. But but that was eye opening. That was over a decade ago. So when I saw that, I'm like, okay, standard dietary guidelines. the websites and resources I'm giving my patients are actually making them worse. They're making me worse as well. And that really kind of led me to really create the resources they need.

To really address this problem. That's amazing. You know, I had a lot of Indian patients in my practice and I see exactly what you see and I often wanted to create a cookbook that's like a high-fat, low-carbohydrate vegetarian Indian cookbook.

Oh, Mark, I would love it if you did that. People ask me to write a cookbook. I have no interest in that. So, if you did that, I would love to promote that. Please put that in your.

You're long to do your work. A friend of mine was an Indian woman, she was going to get her mother to do it, but she never did. But it's challenging. So what do you tell your patients? Because if they're already kind of set up with a deficit because of genetics, then it's a little bit frustrating. How do you help them?

So we do two things simultaneously. So the first thing, I have a bit of a clever mnemonic that I use with my patients called CARBS. So they can basically just identify the framework for the sources of their carbohydrates. So the C in carb stands for chapatis, which are flat Indian bread. Okay. The A is alu, which are starchy potatoes, because most of the vegetables they're consuming are a lot of starchy potatoes and samosas. The R is rice. The B is beans and lentils and the S is sugar and sweets.

So when they have that framework, I love that. It works perfectly.

I love that. Yeah. Rice, beans, and sugar sweets, right? So if you have that framework, and I'm not telling them they're going to eliminate all of those, but let's have just small portions of that with each of the meals. Maybe one meal is going to have a little bit of rice, maybe we'll have some lentils with that, but then where are our protein sources coming from? Like how do you really composed a meal so they're not like 100 to 150 grams per carb per meal, which is what I see in my vegetarians, but how do we mix proteins and healthy fats into it? And this is the hopeful part, is a lot of the fats and oils and foods that we thought should be banned in the Indian diet, they're actually now becoming healthy, right? A lot of the paleo primal movements, they're using a lot of our traditional healthy fats.

So once you put coconut oil or.

Ghee- Exactly, coconut oil, ghee for people who tolerate it. So one trick I teach them, for example, is when you have starches that are not mixed with other ingredients, that's when the problem happens. If you love rice, eat it more like biryani or fried rice style where you mix vegetables into it, nuts and seeds, healthy oils and fats, and you're gonna see that's gonna dampen the glycemic impact. A lot of people are making chapatis or flatbreads, but they're adding eggs to it like egg paratha or they might mix almond flour into the batter.

So, I teach them how to make higher protein flatbreads.

Yeah, chickpea flour, chickpea flour, almond flour. And, you get full off having one or maybe two max and your glycemic stability is much better. So, dilute out the effects of that starch by mixing the vegetable proteins and fats. And, the Indian diet has plenty of those. So, when they feel miserable about that, I really add that diversity and they feel fuller. their energy is better. And oh, by the way, their net carb intake has gone down by 30, 40%. And then simultaneously we do have to upgrade their physical activity levels and really work on the things you talked about. We gotta make up for the loss of lean, you know, body mass muscle. We gotta gently elevate that VO2 max. But I start with food first because immediately they start to feel better. And as you know, the numbers are magic, right? Within a month we see triglycerides drop and if they see that metric, we're very metrically motivated as a population. You see those numbers go down, you're.

Like, okay, what do I do next to get the numbers even better than that? So so that's one framework that I use. Yeah. That's powerful. You know, you said something that's very provocative, and I think I want to dive deep into it with you right now, which is the fact that in the criteria for metabolic syndrome, LDL doesn't matter, which seems to be the only thing that matters to traditional doctors and cardiologists. And, the thing that matters is the ratio of triglycerides to HDL, which they call it the good cholesterol, but it's just one of, you know, LDL isn't bad. It's just it's just has a different role. And the striking thing to me is that there's so much nuance to understanding lipid profiles rather than just the LDL or total or even the HDL triglycerides. And work of Dr. Ron Krauss has really sort of underscored the importance of the lipid particle number and the size. So it's not just the weight of your cholesterol, which is what we measure, but the actual number of total particles in the size. So, and you can't really look at cardiovascular disease without looking at all of the picture here. And what's unfortunate is that a lot of medicine gets practiced without ever diagnosing metabolic syndrome, 90 of the time it's not diagnosed. And yet it probably affects, I would say 88 of the population. Think about it. You've got a condition that affects 9 out of 10 Americans and doctors miss it almost every time. And they don't know how to treat it because there ain't no drug for it. I mean, metformin is something they give, but it doesn't really work that well. And so they go, oh, like the patient I had who was blood sugar was creeping up and it was like 115. I'm like, hey, to your doctor, get your stuff checked out, and she's like, well, yeah. I said, what do you say? Well, we're gonna watch it. I said, watch for what? Watch till I get diabetes, and then I'll give me a treatment. Oh, my God. So. So I want to sort of dive into this sort of framework of. Of how do we think differently about lipids? What is your approach to lipids?

And.

And what should we be thinking? and does everybody need a statin?

Yep.

Great.

A lot of topics here, but yeah, let's tackle this one together. So, so let's move from cars to boats because I think boats are the best analogy for explaining lipids. So when you think about the lipoproteins, the LDL particularly, they're literally boats that are floating through your blood vessel and they carry cholesterol and energy to your cells, which is a great thing to do, right? They've been demonized so much, but they're so essential for a body to function properly. When you look at LDL, so when I say that LDL is not part of the metabolic syndrome criteria, I'm not saying that LDL doesn't matter. LDL has to crash into the vascular wall, the blood vessel wall, and cause inflammation to cause heart disease. But on your regular blood test, we're measuring the wrong part of LDL. So if you think of these lipoprotein boats, you nailed it. You said the particle numbers and the size are more factors. But when you look at a standard lipid panel, it's not measuring those factors. It's just looking at how much cholesterol cargo is that boat carrying. And here's the part that misleads people because I don't know how many people I've seen that had an early heart attack and they were told by their doctor that their LDL looks fine. The problem is the more insulin resistant you are, the higher your triglycerides go. And when triglycerides are high, in most people they push your LDL down. Because what happens is these small particles, they carry less cargo. So that's going to make your LDL-C on the standard cholesterol panel low. So when I had triglycerides above 300, my LDL was like in the 70s or 80s. And my doctor at that time told me, Thank God your LDL is fine. But what he didn't recognize is that my LDL-C was low, but it's because I have these small particles. So anybody that's got a triglyceride, even if you don't have access, luckily these tests are accessible and they're affordable now. But even without doing that, once your triglycerides climb above 130, 140, 150, 80-90% sure that your LDL particle numbers are high. And in fact, what I started teaching doctors in my group is if you make the right lifestyle changes and you reverse insulin resistance, the LDL is actually going to go up on a standard lipid profile because now what's happening is the LDL is going to go up because you're generating larger boats and they can carry more cholesterol. But that's a good thing because you want less boats carrying more cholesterol than these tiny boats carrying small amounts.

So just to clarify what you're saying for people, the total number that you get on the cholesterol panel goes up, but the particle number goes down. Right. So, the actual problem gets better. It's not that your cholesterol is getting worse, it's actually getting better, but it's just how we look at it. I mean, I'm much more worried about someone with a cholesterol of 150, an LDL of 70, an HDL of 30 and triglycerides of 300 than I am of someone who's got a cholesterol of 300, an HDL of 100, and an LDL of 150. I got much more worried about that person who's got a cholesterol of 150.

That's something in traditional medicine just kind of misses. It doesn't. And you know, the other element of the total cholesterol, why it goes up if you're doing the right thing a lot of patients is because the HDL goes up, right? So all of a sudden LDL's going up, HDL's going up. So that's why ratios are key and we hinted on this, but I tell people just forget absolutes and just look at triglyceride to HDL ratio. That's a key number for insulin resistance. Now having said that, obviously if your total cholesterol is above 300, yeah, your.

LDL level, regardless of size, it's probably too high. But you know, for most people, if you stick to ratios, that's a far.

More powerful number to look at.

Yeah, I think that's important. And the triglyceride to HDL ratio should be ideally less than one or about one. If it's more like two or three or four, if your triglyceride, let's say 300 and your HDL is 30, that's a ratio of 10.

Double digits. Yeah, exactly.

So I think those are the challenges and we don't know often what to do with these people. How do we fix those lipid profiles? And so, what do you do in terms of statins for these patients? So good point.

So again, if they've got the insulin resistant profile, we got to focus on lifestyle first because even if you put them on a statin and they're high risk, the incremental benefit is still small relative making lifestyle changes. I mean, I've got loads of patients who are in statins that have their first MI, right? So because, you know, one of the problems with statins, we can talk about a lot of issues with statins, but when patients go on and they see their numbers magically transform, often they think it's a free pass to go back to whatever they were doing. I've seen that it does have a negative impact on lifestyle. So, I sometimes put the statin a little bit in the background and we definitely focus on lifestyle first. But having said that, the other tests I often have to do in these patients because they're so high risk is I do a coronary calcium scan. So, that's a CT scan to look at the blood vessels to see if there's early signs of plaque. And in those patients that are already developing pretty large plaque sizes, I do get concerned. These are patients where statins probably do make sense. You know, I might prescribe it in those cases. but I want a lot more data before I put patients on statins. What's her inflammation status? What's her CRP? What are the advanced lipid profiles showing before we jump into sort of putting everybody on a statin?

Yeah, it's important what you just said because in the Jupiter trial, one of the largest trials on statins, they found that the LDL, if LDL was high and the CRP was high, which is inflammation, statins helped. If the LDL was high and the CRP was normal, they didn't help. So, it's really about much more nuanced than we typically think about. And, one of the challenges of statins is that it infects insulin resistance and it impairs mitochondrial function and may affect your risk of diabetes. And, there seems to be in some studies up to 80% increased risk of diabetes. How do you reconcile that in this population so at risk for diabetes?

Yeah, good point. I mean, basically you've got to weigh both arms here. And, you're right, because you're insulin resistant, we don't want to put them on a drug that's going to make the insulin resistant worse. But at the same time, if they've already got elevated CRPs, they've got early signs of plaque, then you've got to weigh those two. I have had some patients that we did an initial trial of statins. We got their lifestyle in shape by four, six, nine months, and we often took them off the statins. That's the other, I think, misconception is a lot of doctors and patients feel like once you're on a statin, it's a lifelong sentence, right? But sometimes you can mitigate risk temporarily, make some changes, and then maybe we can I mean, just think about that. You know, I mean, it's a kind of a novel concept in traditional medicine. Can we take people off their drugs? But it's something that we should be.

Addressing every time we see our patients. It reminds me of a patient I had where his numbers after the lifestyle changes were better. He'd had a heart attack, and we. He had metabolic syndrome, and we aggressively treated him. And after his heart, after he changed his diet and lifestyle, his cholesterol numbers overall were better. than they were on the statin.

Look at that.

Right. Which is amazing. So, I think people underestimate and also it's variable depending on the person. I want to come back to something you said really that I think is really important that we just sort of brushed over, which is the change in the oils in the diet. So, traditional oils in India are ghee, which is clarified butter with the milk solids taken out, and coconut oil, right? Except, they changed to what?

Well, unfortunately, it changed to the vegetable oils, the seed-based oils, the Omega-6s, the processed oils, which are so much more pro-inflammatory. So, as you know, if you look at my grandmother, who lived to be in her mid-80s and her sisters, it was basically key. Coconut oil was a standard part of their diet, and they were making that at home, basically. That's very different than the processed oils that are out there. And, even though ghee and coconut oil are sort of back in fashion, A lot of my patients are still buying them from Indian stores or other places where they're not, you know, they're stored in jars and, you know, unstable environments. They're really not like the homemade key, homemade key. So, I wouldn't even say that all key in coconut oil is benign. It really, you know, it depends on the sourcing of that. But yeah, I mean, I'd say, yeah, the transition to these seed-based oils, major inflammatory factors. So, many of my patients, even if they've gotten the carb thing right, they're doing everything right, I still see that they're inflamed based on symptoms or ceractive proteins. But when they do the oil change methodically after a few months, you know, we start to see CRPs and a lot of inflammatory symptoms, eczema, other things start to disappear.

So really, so when you change the.

Oils out, when you give people an.

Oil change, an oil change, literally, yeah, literally change all these health symptoms.

Yeah, it's part of my, you know, initially that's not something I focused on, but I kind of call it the three C's like the carbs, the cooking oils and circadian rhythm, which we can talk about. But those are three fundamental things that we need to sort of focus on in the population to see inflammation and improved health from the dietary standpoint.

And people push back, they go, well, you know, coconut oil and ghee are saturated fat and those cause heart disease and these people are at risk for heart disease and they're caused your cholesterol to go up. How do you answer that?

So what I would say is, you know, again, you've got to go by the numbers, right? As much as you can look at all the data, a lot of my patients who want to hold hold onto those fats. I'm like, you, know what? Let's do a two or three month trial. We've got your baseline numbers. If you have a little bit of ghee and coconut oil, let's see what happens to your lipids and your insulin resistant numbers. If they're better, I don't care what the media and mainstream medicine saying. You're better, your numbers are better, so stick to whatever you're doing. Now, having said that, I would tell you, Mark, that I am seeing some of my patients that are going hog wild on ghee and coconut oil. They're on a very high sat fat keto diet and often I've seen their weight and their LDL go skyrocket. and what I tell them in that case is, again, coming back to my car analogy, is if you're not exercising, you've got a low horsepower engine, but you're putting jet fuel into it, right? I mean, even high sources of saturated fat can raise LDL and raise body weight if your mitochondrial engine is low performance. Right. So you've got to sort of upgrade the engine or downgrade that. But the other thing is I do like them to diversify fats. I don't think they should be doing all sat fats. Can we add some monounsaturateds and some omega-3s? Because as much as I find sat fat to be exactly all of fish, I mean, sat fat, I think is fairly cholesterol and neutral, but it doesn't have a lot of data unless you're aware of it that it's truly heart protective.

It doesn't compare to the monounsaturated fat, the Mediterranean trial. So, I'd want to dive into that as much as possible. Yeah. I think that's right. And one of the key things that it's important people understand is that in the context of a carbohydrate rich diet, saturated fats can be deadly. Can be deadly. Exactly right. So, if you eat them without eating all the starch and sugar and cut all the flour and sugar out of your diet, or most of it, you can tolerate it better. But if you combine them, it's really bad. Because if you're really insulin resistant, you're eating a lot of saturated fat, it can be a problem if you don't.

Change your overall diet. And that's why, Mark, I mean, you mentioned the point. This is why the studies are so misleading, right? Because the people that are consuming the saturated fats and developing heart disease in the large trials, they're consuming loads of sugars and starches.

So you don't uncouple those in the traditional trials. So people don't realize this is a starch dependent disease, but the fats really get blamed for it. So, yeah, exactly. That's right. And then the other thing is that, is that, there's a lot of heterogeneity in the population, a lot of variation in response to saturated fat or diet. So, when you just sort of alluded to the fact was that some people, you give them coconut oil and butter and their numbers drop like a stone and they get lose weight and they're healthy, other people, it's the opposite. And so how do you begin to understand that? Well, the reason is that we're all different, we're all different genetically, metabolically. and tolerate different levels of starch and fat and different kinds of fat and starch. So you have to find out what is your, what is your own approach to dealing with diet and cholesterol.

Exactly. Exactly. So true. Yeah.

So when someone comes in with a cholesterol panel and they've got, you know, problems, what do you, what do you tell them? What is your recommendations around how to fix their cholesterol? what lifestyle changes they should do and how to think differently about it.

Yeah, and again with personalization, you've got to look at the nuances of the cholesterol panel. So if it is somebody with those insulin resistant factors like the high triglycerides and or the low HDL, then you know this individual is insulin resistant, meaning they're less carbohydrate tolerant. So I'm really focused in on that CAR paradigm. How do we really dilute out the effect of the starches? How do we increase activity levels? And that's going to be nailing that Now, some patients, like I said, they might have very high LDLs or a combination of all three high triglycerides, low HDL and high LDL. And in those patients, we do have to be a little bit sensitive to the amount of sat fat in the diet. So then we'd modify that, but we also want to elevate the amount of high fiber rich foods that can bring down the LDL. I get pretty good results and maybe you see the same with even adding more fermented foods. If you improve gut microbiome health, that can actually help your body get rid of that LDL cholesterol and lower inflammation as well. And, that's a traditional part of the Indian diet and the Asian diet too. There are fermented foods that are part of it. The problem is that Indians consume, yeah, exactly, the mango pickles and things, but a lot of times they buy from the Indian grocery store and they're soaked in seed-based oils. So, then you're trading one problem for the other, but traditional fermented foods can.

Be very valuable for that. So, that's sort of how you tailor the lipid profile and do the lifestyle sort of accordingly. Right, because this problem of diabetes in Asia and in China and in India is totally changed. I mean, I, I don't know exactly the data for, for India, but in China, they went from like one in 150 people having diabetes to like one in 10.

Over such a short period of time.

Yeah.

Yeah.

Literally just over a couple of decades. So, yeah, that's just staggering. And it's, so that makes you realize it's environmental and, and lifestyle related.

So, yeah.

In, in terms of the, the patients you see and sort your framework, it just, it's like, it's like this juggernaut that's happened almost overnight. I mean, even when we graduated from, I don't know how old you are, but I'm older.

But, you know, we graduated medical school.

Last week, so. 50.

Okay, well, I'm 60 something. Oh, yeah.

Yeah, you're a good looking 60. Right. And, and the, there wasn't it, there wasn't this level of diabetes. We just didn't see it, you know? And, and what's also interesting is all this, this whole idea of comorbidities. is such a irritant for me because, oh, you have high blood pressure, you have high cholesterol, you have high blood sugar. They're all separate things. They're not. High blood pressure is one of the biggest killers, but what causes high blood pressure? Right.

I mean, insulin resistance is such a central factor to that, right? So these individuals who are overweight and insulin resistant, they're retaining more sodium fluid. They've got high uric acids, you know, that's a part of insulin resistance and that causes blood pressure to go up. You know, just putting people on a dash diet and telling them to limit salt, that's not enough. You've got to really address the insulin resistance. We now know hypertension is an inflammatory condition. So we keep coming back to this, but if you don't lower inflammation, it's.

Not going to help.

And I'll be honest in my patients, I'm actually seeing some teenagers with high blood pressure, which I'd never seen before. Yeah, yeah, for sure.

And a lot of it is related to sleep and stress too. So that circadian rhythm is a huge factor.

But yeah, I mean, you nailed it. I mean, the other thing is a.

Sign of- Just to reinforce what you're saying is that one of the biggest causes of high blood pressure is insulin resistance and it's undiagnosed. We call it essential hypertension, which means essentially we don't know what causes it. But we do actually now. Maybe when it was named we didn't know, but now we know.

And yet doctors don't address high blood pressure by addressing insulin resistance. Yeah, so true. I know. I mean, to us it seems so simple, right? It's like a fundamental process which has all these branches that link to all the typical disorders we see, but people are really not putting the pieces together. So hopefully, I think that's starting to change now with the information getting out there, but we've got to be more proactive so it just becomes mainstream.

Yeah. Do 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, wellbeing, and lots more. Check it out and the link below. So, an average day in your life, because you had metabolic syndrome, how do you stave it off? How do you create great metabolic health for yourself? What's your routine, breakfast, lunch, dinner, activity, sleep, everything?

Yeah, so one thing I would say is I put a lot of emphasis on diet so far and that's still a big foundation. But one interesting thing I've noticed in my practice, Mark, now that I've been doing this for a while, is many of my patients, when they lowered their starch and they reverse insulin resistance, they're like, wow, all I need to do is diet. Because a lot of them are reversed exercise. Culturally, we are very sedentary species. We South Asians, we like to sit in front of computers and learn a lot, but we don't like to exercise very much. But the interesting thing is those patients that reversed it, now they're coming back to me and they're like, oh my God, my A1C has gotten worse. What's happening? I'm eating the same diet that I did. And I tell them what we talked about initially is you've undergone myopia or sarcopenia because you're so sedentary. with age, you've lost mitochondrial horsepower. So, we've got to elevate that physical activity and exercise. I just want to add that in there because a lot of people feel like diet is the only way to do this. So, in my typical day, starting with that is first thing I tell a lot of my patients is many of my patients, and this is kind of a cultural thing, are evening walkers or exercisers. So, they get out of bed, they'll hop on the computer, they'll have their breakfast maybe, maybe a little fast, and then they hop on their computer and they're sitting for 10-12-14 hours. and then they'll walk the dog or do a walk with their significant other for like 30-40 minutes. And, I applaud them for doing the walk, but I tell them, if you want to rev up the mitochondrial engine, you've got to start in the morning. Like, if you start with some physical activity to get that metabolic car started, you know, a lot of us are not wasting time in cars and commutes, you've got to start there because then even when you're sitting in Zoom meetings all day, you are burning more fat and energy. So, that morning is really key window. And, you see with CGMs, when you work continuous glucose monitors, you get morning exercise. and all of a sudden your glucose is much more stable even if your dietary flexibility is not perfect. All day long. All day long, yeah, right? So it's a powerful thing. So morning, whether you're fasting or having a light breakfast, get some physical activity in there. And then throughout the day, you could probably tell right now I'm standing, right? I'm very fidgety because I'm constantly sitting, standing, moving. I'm in Zoom meetings where I'm doing what I call sort of yoga at work. So I've taught a lot of my techies how do you keep the body moving while you're actually getting your work done rather than looking for that magical hour of physical activity at the end of the day or so. And that's been a very powerful thing. I've seen people stabilize their blood sugars just by interrupting prolonged sitting and inactivity.

Just sitting is the new smoking.

Exactly right.

Right?

Yeah. So that's another key strategy. And that's from the stay-at-home workplace. Obviously a lot of us are missing out on going to the offices, but now we can be very creative in terms of how we move throughout the day. you take your dog out, you know, at lunchtime, all those little exercise snacks throughout the day can have a powerful impact on that.

And then I did exercise.

Snacker size, right? Right, exactly. And then the circadian rhythm is something I brought up. This is a big factor because, again, Asians and Indians tend to eat very late dinners. This is part of their culture, is that they might have dinner around 8 30, 9 pm plus. So just getting. So that's one piece of low hanging fruit. Really? Yeah. Oh, totally. A lot of them will eat very late. I'm like, okay. if you're not going to make any changes at all, just take that meal and just pull it back an hour or two. That's just something powerful we can all do and that can already lead to pretty significant improvements in the numbers. And then we sort of focus on how do we sort of impact each of those meals. The circadian rhythm, regular movement throughout the day, those are really low hanging pieces of fruit that we can use to really have a high impact on metabolics.

That's amazing.

I think the stress is the biggest one. By the way, so you mentioned one other thing is a cardio, right? So, The cardiovascular exercise has to be, you mentioned VO2 max. We talked about that early on. This is a key thing is many of my patients of all ethnic groups are doing too much high intensity exercise. Many of them are doing a lot of boot camps or doing a lot of CrossFit and often that doesn't have the same impact on VO2 max and insulin resistance. So really dialing in that exercise at the right dose that boosts mitochondria without triggering inflammation is sort of the magic. and a key approach that I use, I'm a big fan of Phil Maffetone. I actually did a podcast interview with him a while ago, but he's got a very simple paradigm where generally just keep your exercise 80% of it or more at 180 minus your age. So if you're 40, your target heart rate's 140. If you're insulin resistant, you might have to subtract five or 10.

That's amazing. It's your age. So I should be 120.

So if I'm 60, I should be 120. you're 120. But since you're fit and if you're not insulin resistant and if you're regular exercises, you might add five or ten to that. So maybe between I went bike riding.

Yesterday and I had my, my, my heart rate monitor on, I got up to 155 and, you know, averaging, you know, 130s, you know, 40.

Yeah. So not necessarily bad. I mean, I can already tell by talking to you that you're somebody that Fitness is a regular part of your life. right? So you might have that foundation to work on, but if you really want to upgrade like fat burning and reduce insulin resistance, you've got to do a lot of work in that 180 minus age zone. And Mafitona is trained like world-class endurance athletes and literally you're trying to build that aerobic base. So for a lot of my patients, it's fast walking instead of running. The majority of my patients should not be runners at all. I look at their Apple Watch data and they're basically 150-160 and I've had a fair number of patients, Mark, develop a heart attack while they're running or they're on the treadmill at a high heart rate because most of their workouts are very inflammatory. They're burning a lot of glucose. They're generating a lot of excessive reactive oxygen species in their mitochondria from their workouts. They've got to start with the lower heart rate foundation. As they get fitter, they'll get faster at that lower heart rate. When you look at elite athletes, they're less breathless in the fourth quarter of a game because they have such a wide aerobic base. But my patients that don't want to exercise, they want to do the 20-minute hit workout and then get the heck out of there. And, I wish that was your case because I don't want to work out for that much longer, but you got to put in at least 30 to 45 minutes of what Peter Attia calls Zone 2 or I call the MAF heart rate based on Maffetone. I know it's not the most exciting exercise, but it's absolutely fundamental to really.

Reversing a lot of these conditions. If you love that last idea, you should definitely check out the next one on food is medicine. Because you don't need a doctor's prescription for health. what you need to do is to make that part of your life in a natural way. Well, if we can get food reimbursed by healthcare, it's a game changer. I'm actually working on that at Cleveland Clinic with the food pharmacy, which is the idea of actually paying.