How To Improve Your Metabolic Health
This is a podcast episode titled "How To Improve Your Metabolic Health" recorded in March 2022. The content features a detailed discussion among multiple health experts including Ask AI Mark, Dr. Cindy Geyer, Dr. Ben Bikman, Mark Sisson, and others. They explore topics related to metabolic health, insulin resistance, the role of diet and fats, gut microbiome, environmental toxins, and diagnostic challenges in modern medicine. The conversation includes educational segments, personal anecdotes, and scientific explanations aimed at improving understanding of metabolic dysfunction and its prevention.
Coming up on this episode of the Doctor's Pharmacy.
90% of Americans with pre-diabetes are not diagnosed by their doctor. That's terrifying, especially because it is a 100% reversible, preventable, treatable condition.
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Episode of the Doctor's Pharmacy. Hi, this is Lauren Fein, one of the producers of the Doctor's Pharmacy podcast. Dysfunction in our metabolic health paves the road for chronic disease. and it deserves more time and attention than it often receives. Metabolic dysfunction is an umbrella term that includes several conditions you might be familiar with, including insulin resistance, high triglycerides, low HDL cholesterol, obesity, high blood pressure, and more. In today's episode, we feature clips from four different episodes of the Doctor's Pharmacy about why metabolic health is so important. Dr. Hyman talks to Dr. Cindy Geyer about what to look for when measuring metabolic health, and Dr. Ben Bikman about changing our metabolic health. He also discusses the importance of metabolic flexibility with Mark Sisson and cholesterol markers to be aware of with Dr. Elizabeth Boham.
Let's jump in. A recent study was looking at the NHANES data from 2009 to 2016.
To government surveys. Government survey.
Our blood tests and health records and everything, right? And trying to say, well, how many people are what we would call metabolically healthy? And if you're not familiar with it, for people who may not be familiar with that term, sort of meeting the optimal numbers for a blood pressure less than 120 over 80, HDL levels being in the high range, a good range, greater than 40 for men and 50 for women, having triglycerides that are low, having a glucose that's less than 100, and they found that 12.12% of Americans- 12.2%. 12.2%, thank you. 12.2% of Americans were metabolically healthy.
Which kind of means that almost 88% of Americans are metabolically unhealthy. And since 75% of people are overweight, there's another 13% there.
Yes.
That's like, what's going on with the skinny people?
Well, and that's the interesting piece. Fewer than one third of so-called normal weight people were metabolically healthy. So that's another really important message.
Wait, wait, wait, wait. Did you just say that two thirds of skinny people are metabolically unhealthy and have prediabetes-like syndrome.
Yes.
Two-thirds.
That's mind-boggling to me.
Okay, so that means that, what, like 95% of Americans are metabolically unhealthy?
No, no, no, it's still the 88%. But that we're looking at how strongly it correlated with weight. That's so terrible. So just having a body mass index that's less than 25 is not a.
Guarantee that you're metabolically healthy. So if you're a skinny sugar and bagel eater, Don't think it's fine because you're skinny. Exactly.
It's basically the bottom line.
Exactly.
Because foods have other impacts besides just what they do with cholesterol anyway. Foods directly impact the elasticity of the arteries, for example, which is another key player. You mean food is more than calories, Cindy?
Food is information, Mark.
You've said that for years. It talks to our genes, it talks to our systems.
Yeah. Wow. So you're talking about how the food impacts our metabolic health and we're not really good at diagnosing metabolic dysfunction. I mean, 90%, okay, one out of two Americans has prediabetes or type two diabetes. And if you look at this new study, I would argue that nine out of 10 Americans have some degree of prediabetes or type two diabetes, like 90% of Americans. So when you look at that data and you also look at the parallel data that 90% of Americans with prediabetes are not diagnosed by their doctor.
Right.
That's terrifying, especially because it's a 100% reversible, preventable, treatable condition. And it gets worse and worse over time and people just don't even know they have it and doctors miss it because there's no pill to take. Oh, tech metformin. Well, that's not going to help, right? It's like, and so what are the kinds of ways that we look at these patients differently? What are the tests that we do? What are the things that we really focus on When someone comes in with a risk of heart disease or they're concerned about heart disease, what's our approach? It's not just looking at the typical cholesterol and even CRP.
Yeah, so we would look at those, of course. We would also wanna know what is somebody's insulin? Most doctors measure glucose, but not insulin. I personally like to look at somebody's glucose trends over time, 'cause if you think about something that's preventable, you don't wanna wait till they cross that threshold to prediabetes or diabetes. So even in the range of so-called normal glucose mark, you know this, somebody who's fasting glucose runs less than 85 is in a very different metabolic place than somebody who's fasting glucose is 95 to 99, even though they're both technically normal, that it's a spectrum of risk and the farther along you march that spectrum, the higher the risk of heart disease and diabetes. So if somebody's glucose used to be 85 and then it was 91 and now it's 98, we're gonna talk to that person right off the bat about all the things they need to put into place to prevent it from progressing because they're already on that spectrum. so we also want to know insulin levels, not just a fasting insulin, but sometimes the insulin response to food, because the other thing that's emerged is insulin is a player and way before somebody's blood glucose goes up, they might be pumping out tons of insulin to try to keep it in a good place. And insulin by itself contributes to inflammation and more weight gain around the middle, that visceral adipose tissue. so we want to know their insulin, both fasting and in response to a challenge.
So wait, wait, wait. Are you saying that sugar, not fat, that's causing heart disease? And sugar, the thing that's driving the.
Insulin, because fat doesn't cause insulin spikes. Well, there is some, I mean, fat is a player. Fat by itself.
Fat by itself is a player.
If you eat fat with other food, it will. Yeah, yeah. And I would say that quality of fat does matter. And we can talk some more about that, but I think fat plays a role with artery elasticity, which is another component of vascular risk.
Yeah, so fried foods, trans fats, refined oils, those are nasty.
Absolutely.
But fat itself, if it's made from whole food sources and nuts and seeds and avocados and all that, might actually be beneficial. Actually beneficial, yeah. So what you're talking about is a set of diagnostic tests that are so important but most ignored. So the particle size and number, which nobody's doing, and the second is not just measuring your blood sugar A1C, which may be perfect and you may be in really bad trouble, but measuring also insulin in response to drinking like a couple of Cokes, right? I have a patient, Cindy, that I remember who was a super high risk for heart disease and she had, I mean, she looked like the Tasmanian devil. She was just like a round apple ball like this and her belly was like, this big thing. And I'm like, this woman is in big trouble. And she's inflamed, she's a high risk of heart disease, high blood pressure, diabetes. And I'm like, let's check her glucose tolerance test with insulin. And this is, you know, this is like 20 plus years ago and no one was like looking at this. Even today, no one's looking at this. It's like so hard. I mean, it took 50 years from the time the guy said, hey, we should wash our hands before surgery for us to wash our hands. You know, McKinley died, President McKinley, because he got shot in the belly. And the doctor, McBurney, stuck his finger in the wound to check it out without washing his hands. so that's like crazy. It took 50 years from the time the guy said, let's do a stethoscope so we don't get lice jumping into the doctor's hair. To start, you see the stethoscope because the doctor used to put their head on the patient. So it takes forever. And we've been doing this. Anyway, this woman, I did this test. I gave her this drink, and it was the most shocking thing I'd ever seen. And it taught me so much about what we miss in medicine. Her blood sugar was perfect, like 80, like. and she took the sugar drink and it was like perfect. It never went over 110 after taking the equivalent of two Coca-Colas. You know, she's fine. Her A1C was perfect. Her insulin, normally should be under five fasting and under 25 or 30 after a drink. Her insulin was like 50 fasting and 250 after a drink. So her body was just pumping out insulin which was making her hungry, slowing her tablets, putting fat in her belly cells, which were basically inflammation factories, and leading this perpetual cycle. And she was able to lose 50 pounds like that when we cut out starch and sugar. And I just feel like, you know, that showed me so much because you can even do a normal glucose tolerance test.
If you're not measuring against.
Perfect. And if you were super hyperinsulinemic, you're gonna miss that patient's real problem.
And you know, it's interesting, Mark, because that scenario is also associated with that cholesterol profile we talked about with the small dense LDL and low HDL and the sequelae that we usually link to diabetes, fatty liver, peripheral neuropathy, all these other organs that are affected. And it can happen with the high insulins alone before the sugars go up. It's a metabolic imbalance.
So that's really the take home here is that heart disease is really a hormonal issue around insulin and insulin resistance and an inflammation issue. And unless you address those two things, not with aspirin and statins, which will work to some degree or metformin, which will work to some degree, but, and by the way, high blood pressure, which just goes along with all this stuff, they're all seen as separate. High blood pressure, cholesterol, diabetes, they're seen as separate. They're the same condition. They're manifestations of the same underlying biology of insulin resistance. And unless you really know how to look at the metabolic pathways in the right way, like we talked about insulin testing or the cholesterol or the cause of inflammation, because like you said, insulin and resistance is probably the biggest cause. So probably the biggest cause of inflammation is diabetes, prediabetes, and the starch and sugar that we eat about a pound of each every day in America. That's the problem. But there are other factors that also contribute that people don't think so much about, especially cardiologists. So those are the big ones. And of course, you know, exercise, sleep, stress, all those. We've covered those on the podcast, relationships, connection, community, really important. But there's some other factors that are a little unusual that we look at in functional medicine that I'd love to dive into that have a big impact. So can you just share some of the other factors that could drive inflammation?
Well, yet another example where the gut microbiome seems to play a role. So now that we can do more sophisticated gut testing and look at these microbial patterns, there's a so-called microbial signature that strongly predicts insulin resistance, diabetes, and cardiovascular disease. And a couple of general scenarios you see is there's a loss of overall microbial diversity in the gut. There's a loss of a couple of signature species, one's called one of the phyla that produced this signature molecule called butyrate. Butyrate plays a role as fuel for colon cells to help them replenish and be healthy. And it's also an anti-inflammatory molecule and another species called Akkermansia muciniphila. And you can kind of tell from the Latin mucin base that it's a mucus loving bacteria. So that pattern of low diversity loss of butyrate and loss of Akkermansia correlates with loss of integrity of the gut lining, more absorption of unwanted things into the bloodstream, more calories and more inflammation that in turn exacerbates insulin resistance. So the question is, is it chicken or the egg? 'Cause we know that pattern also shows up in response to diet, of course, the standard American diet. Yeah, I was gonna ask you that.
Like, why do you don't have the good guys and why do you have too many bad guys? It's because of what we're eating.
It's because of what we're eating. That microbiome is influenced by the foods that we feed it. But what's really fascinating is even our thinking about how medications work. You mentioned metformin earlier, right? And we used to think that metformin helped our cells respond to insulin better, but it also has a microbiome effect. Interestingly enough, there was a study that found that people who took metformin, you saw a rebound of microbial diversity, a rebound of Akkermansia, and a rebound of those butyrate species.
With metformin.
With metformin, which I think is fascinating, right? The way we think drugs are working may actually be completely different.
We call those side effects, but they're not.
We call those side effects, right? But we also know in functional and integrative medicine that we can achieve the same thing when we encourage people to eat a diverse array of plant-based, colorful plant-based foods and foods that are really good for rebound of acromania, like polyphenolic foods, berries, deeply pigmented berries and greens and garlic and onions and cranberries, right? so of course people want a pill, but there are other things that can potentially achieve the same thing. Interesting, you know, there's a new company.
That came out with an acrylamide product. Yes. Pendulum. The Pendulum. And it's fascinating. They're not saying this is a probiotic that's healthy for your gut. This is a tool to control your blood sugar. Isn't that funny? And I think, you know, we don't even think about that, that a lot of insulin resistance can start in the gut. I've shared the story recently on a podcast, but I'll share it again. I had this patient who was diabetic, very brittle diabetic. He was kind of a type 1e2, but he wasn't on insulin, but he was just all over the place. Put him on a keto diet. Sugar's dramatically improved dramatically, but still not like going from like 250 to like, you know, 120, 130 better, but not like more where I wanted them. And then one day he called me up and said, you know, Doc, my stomach's been bothering me. I got the worst gas and I just feel so bloated and uncomfortable. I said, well, we have to get to the bottom of it and maybe have bacterial overgrowth, maybe have this, maybe have that. But like in the meantime, you're so miserable, why don't you just try some charcoal tablets, see if it gives you some relief of your symptoms. And he comes back and says, I don't know what happened to Doc, but my sugars went to normal. Like I'm in the 80s now because I took charcoal. And I'm like, oh my goodness, this is it. This is these toxic bacteria and they're producing toxic molecules and charcoal is like a sponge for toxins. So when something comes in the ER and they swat a bottle of pills, we make them drink a bottle of charcoal and they have black teeth. But it works to absorb all these other bacterial toxins. And I was like, wow. And so often the pathway to fixing heart disease might not be through the heart. It might be through the gut.
It might be through the gut or.
Other factors like toxins. We know the role, for example, pollution and the particulate matter in a lot of urban areas, huge correlation with heart disease, right?
I think part of that too is if we look upstream, even before people form plaques, they can start to have problems with the elasticity of their small arteries. And in fact, that's a more typical pattern for how cardiovascular disease shows up in women, that it's small arteries that have lost their elasticity as opposed to big arteries.
Full of plaque.
And we can think of that artery, that endothelium, as the canary in the coal mine. And they did studies of measuring people's artery elasticity as they were jogging through urban environments with high air pollution counts. And you could see the arteries lose their elasticity in response to that.
They've also shown- oh, so all my jogging and running outside in China and Beijing in the middle of winter when the skies were gray probably wasn't a good idea.
Probably wasn't a good idea. You can even show that those arteries will spasm acutely in response to stress, in response to a Burger King meal.
So- But not McDonald's.
Well, not- Let's say a Burger and Fries meal. So if we understand what keeps that endothelium healthy, that can actually clue us into how we keep ourselves cardiometabolically healthy.
Yeah. And it was interesting also heavy metals have become an interesting phenomenon. And many heavy metals are exposed to lead, mercury, arsenic, and so forth. Arsenic's been linked to diabetes and other things. but the lead story is fascinating to me because from our perspective in functional medicine, it's relatively easy to diagnose and treat, but it's been mostly ignored. And, if you look at the American Journal of Cardiology, they put out major papers that show that, for example, if your lead level is over two, which is considered normal, which is about 40% of the population has a lead level over two, which is a lot of people.
A lot of people.
That the risk of having a heart attack or stroke or dying was far greater than if your cholesterol was abnormal. And yet, what doctor is checking your lead levels? Or checking your body burden of lead? Or chelating you as a treatment for heart disease? And yet, I think it was called the TACT trial, which was a $30 million randomized control trial of chelation therapy using EDTA, which chelates lead, actually was effective in heart disease. and yet it doesn't matter what the research shows because we don't have research evidence-based medicine. We have reimbursement-based medicine. We get paid for doing angioplasty is not chelation. So that's what keeps getting done even though the data is there, which is kind of amazing. This is an NIH government study showing that it worked. I was like, okay, well, this is very slow to pick up, but we see this. So I think the take home here is if you have heart disease, Don't just assume it's high blood pressure, smoking, cholesterol, diabetes. It could be a lot of other factors. It could be your gut microbiome. It could be nutritional deficiencies. It could be environmental toxins along with.
Lack of sleep and stress and so forth. And Mark, you know my passion about sleep. I would put a sleep study very high on the radar for anybody who's got cardiometabolic imbalances because we know that two-thirds of people who are cardiometabolically unhealthy actually have sleep apnea. And our perception of how sleep deprived we are doesn't always match the reality of what we find when we screen people.
I had this guy, I remember him, he was a lawyer, came to Canyon Ranch years ago, 50 plus pounds overweight, desperate to get healthy and lose weight, trying to exercise, eat better, doing everything, nothing was working. So I'm like, tell me about your life. He says, well, I'm a lawyer, I work really hard, a lot of hours, and I work at a standup desk. I'm like, oh, that's great. I said, why do you work at a standup business? This was like, you know, before people were working at Sam's. He's, well, if I sit down, I fall asleep. I'm like, oh, no. You know, you probably have sleep apnea. And we did a sleep study, and he had sleep apnea for sure. And we got him on a CPAP machine. He lost 50 pounds and reversed his pre-diabetes his cholesterol, obviously, his weight, blood pressure. And, and most, you know, most people don't realize that, that, you know, it's a, it's a It's a bi-directional thing. So if you're overweight, it can cause sleep apnea, but if you have sleep apnea, it can cause you to gain weight. And it's very hard to lose weight. And he was able to lose 50 pounds just by getting on a sleep program with a sleep machine that helped him sleep. I was like, wow, this is interesting. Had many people like that.
Yeah.
So, you know, honestly, Cindy, I don't know about you, but like, I've learned way more from my patients than I ever learned in medical school. Absolutely. And the challenge in being a doctor is, you get trained in this paradigm and it's taught to you as if this is a monolithic truth, like this is a table and that's all it is. There's no questioning that this is a table, right? But the truth is we are just learning so much about the body and all of our old ideas are sort of breaking apart. But unfortunately, people really aren't accessing them and it just breaks my heart to see how slow medicine is to adopt the emerging science that we're talking about, whether it's around checking for lead or insulin resistance. I mean, insulin resistance is not even like a controversial thing. It's not like heavy metals or the microbiome, which seems weird. I mean, like, insulin resistance is a well-described known phenomena. It's just doctors clinically are kind of clueless because the treatments are going to be primarily lifestyle interventions. There's no drug. Oh, your cholesterol is not going to give you statin. Your insulin resistant, what do I do? Oh, we'll give you metformin, but that's not the answer. Hey everyone, it's Dr. Hyman. I'm all about using food first when it comes to nutrition, but there's certain nutrients I recommend everyone supplement with because it's simply impossible to get adequate amounts from your diet alone. One example is magnesium, which our soils, well, they're not too healthy and because there's no organic matter, they can't extract the magnesium from the soil from industrial farming, which is a drag. and that leads to 50% less of these minerals in our food than there was 50 years ago. And then of course we're doing things that cause us to lose magnesium like sugar, caffeine, fluoride, even stress, which none of us have, right? 80% of Americans are actually deficient in magnesium and that may mean insufficient, not necessarily true deficiency, but just not enough for optimal functioning because magnesium is so important. and it's a huge problem for our health. Considering the pandemic of stress along with the pandemic of COVID that we're facing, we should all really be conscious about our magnesium intake because it activates the parasympathetic nervous system, which keeps us calmer and more relaxed. Magnesium is crucial for more than 300 other chemical reactions in the body and impacts everything from metabolism to sleep, to neurologic health, energy, pain, muscle function, and Lots more. My favorite new magnesium is from a company called Bio-Optimizers. Their magnesium breakthrough formula contains seven different forms, all of which have different functions in the body. There is truly nothing like it on the market. I really noticed the difference when I started taking it, and I've tried a lot of different magnesium products out there. I also love that all their products are soy free, gluten free, lactose free, non-GMO, free of chemicals, fillers, and made with natural ingredients. Plus, they give back to their community. For every 10 bottles sold, they donate one to someone in need, and there's a lot of those. Right now, you can try Bio-Optimizers Magnesium Breakthrough for 10% off. Just go to magbreakthrough.com, that's M-A-G-B-R-E-A-K-T-H-R-O-U-G-H.com slash Hyman and use the code Hyman10 and you'll get 10% off this really great formula. I think I'm gonna like it as much as I do. And now let's get back to this week's episode of the Doctor's Pharmacy. Three quarters of the deaths globally, which is, you know, I think it's like 60-70 million a year. I mean, are actually are caused by some level of this poor metabolic health. And it's driving, you know, of course, not just weight issues and diabetes, but cancer and dementia and depression and infertility and all these other phenomena. So your research is so important to help us kind of tease apart these mechanisms. And the question I would have for you is, you know, for people listening, how do we start to think about changing? Because not everybody wants to go on a ketogenic diet, nor is it advisable, or is it good? Even though, by the way, you mentioned Jocelyn, the way they treated type 1 diabetics was a 75% fat diet, 20% protein, and 5% carbohydrates. And by the way, it was kept alive, but it also, by the way, was the way that we discovered America was through borrowing the Native American's superfood packet, which was called pemican, which was made up of, oh, yeah, yeah. Basically rendered fat from bison, you know, a few berries and the protein. And literally, a man needed a pound a day, and a woman needed a half a pound a day. And so if you had 30 pounds of stuff in your backpack, you could basically eat for a month and survive. Yeah.
Yeah.
It's, it's, there's no question that you and I, of course, are, are aligned when it comes to having a favorable view of fat. And, Mark, with, I I like what you were saying a moment ago, and you're being careful in your language, of course, as a scientist, I appreciate precision. You and I, we're not claiming that insulin resistance is the cause of every disorder, but there's little doubt that it is a key contributor. It is causing many chronic disorders, and it's contributing to virtually every other one. So my view, one of the things I hope people take away from this discussion is I can imagine someone who's opening their medicine cabinet, not that either of us is giving any medical advice here, but they're looking at their medications and they see their medication for their diabetes, or one or two or three medications for their diabetes. They may have a medication for their migraines, a medication for their fertility disorder and their blood pressure, little knowing that all of those do have a common connection with insulin resistance. When it comes to controlling insulin resistance, you are absolutely right. There are multiple inputs into this. I consider—there are various ones, and I've looked at them and consider various levels of them. To me, there are three primary causes of insulin resistance. By primary, I mean that literally I can cause insulin resistance in isolated cells in laboratory rodent and in humans with all three of these. That is elevated insulin itself, elevated stress hormones, and elevated inflammatory proteins or cytokines. All three of those things are considered primary in my definition because you can just make insulin resistance happen at the cell, in the rodents, and in humans, all three biomedical models. But as you were kind of alluding to, if we were to tell someone, all right, here—but there are others, like you said, like noxious toxins that can accumulate in fat cells and alter fat cell growth. Absolutely, that is relevant. So I'm not suggesting that there aren't others. There are. But I put these ones as the holy trinity or the unholy trinity of insulin resistance. We would tell someone, Control your stress. They would say, well, great, Doc. How am I going to do that? It's a little difficult. Stress is one of those difficult things to truly wrap your head around. You'd mentioned meditation and quiet. I wholly agree with that. Even still, it's a little difficult to fully manage stress. Same with inflammation. we would say lower your inflammation and say, well, how do I do that? You know, we'd have to find out what's the, what are the stimuli that are inducing that increase in that immune level. But if we say control your insulin, easy, easy. That is a lever we can grab with both hands and immediately start to pull down just through time restricted eating and intermittent fasting and by just managing macronutrients and, and altering that ratio, you know, focusing more on the foods that have the lower effect on insulin like fat and protein and controlling the starchiest of the carbohydrates or the most sugary. Now, neither you nor I are declaring war on carbohydrates. And, I'd hate for someone to leave this talk, leave this discussion thinking we are. We're not, you know, neither of us is advocating a carnivore diet. But, we are certainly, my view is don't get your carbohydrates from bags and boxes with barcodes.
I agree.
Yeah, good.
I love alliteration, so I'm glad you appreciate it. Bags and boxes and barcodes. All right, good. But that's where people get it wrong, right? They're thinking, I need to, they have a box of crackers or a bag of chips or a box of cereal.
No.
Go eat fruits and vegetables.
Eat them.
I'm an advocate of fruits and vegetables. Eat them.
But don't drink them and don't get them in processed foods. Yeah, bags, boxes and barcodes. My joke is I always say carbohydrates are the single most important food for health and longevity. Right? And what I mean by that is that plants are carbohydrates. Broccoli is a carbohydrate. Asparagus is a carbohydrate. Those are the ones you want to eat, not the ones that come from a factory or from some processed ingredients that you're mentioning.
Bags and boxes, barcodes.
What I'd like to sort of go into now is an understanding of some of the challenges and controversies around fat. I wrote a book called Eat Fat, Get Thin where we talked a lot about this, but there's still a sense that your cholesterol is a big problem, that saturated fat is the devil, and that we should not be eating it. Butter, cream, coconut oil, animal food, saturated fat. Talk to us about the biology of what happens when we increase fat and why it doesn't work in the same way we think. And also, if you can speak to the heterogeneity in the population because there's subsets of people who do great with high saturated fat diets and those who don't. And I'm just going to give you a quick scenario of that. And then you can kind of riff on how we start to think about it. I had a woman who was about, you know, late, late 40s woman who was struggling with her weight, inflamed, trying to do good. She exercised, she ate pretty healthy. She wasn't, you know, off the rails with her eating. her triglycerides were 3-400 or cholesterol was 300 or HDL was like 30. I mean, which is terrible numbers, you know, which is classic of pre-diabetes insulin resistance. And I said, look, you know, you've tried a lot of things. Let's just try a ketogenic diet and see what happens. You know, no harm, no foul. She did it, and it was remarkable. Her, her. Not only did she lose 20 pounds like that, but her levels of inflammation came down, her triglycerides dropped. up 2-300 points. Her HDL went up 30 points, which you never see. Her total cholesterol dropped 100 points by eating butter and coconut oil. And yet another guy was a very thin, fit, mid-50s guy who was a really aggressive bicycle rider. He rode 30-50 miles a day. And he decided he wanted to try it for performance reasons, not to lose weight. and his numbers went completely opposite. He got very high levels of cholesterol, very high levels of small particles. It just, it was just remarkable to see the difference. And I, it sort of woke me up to the fact that there isn't a one size fits all regards to this. So with that framework, take us down understanding of, you know, if we are going to be reducing our carbohydrate, starchy, sugary carbohydrates, and we're going to be increasing our fats, how do we do that? And what's the role of saturated fat and should we be worried and how does it work?
Yeah, yeah. The great question. So my post-doctoral work really was seminal in that it scrutinized the degree to which fatty acids themselves can contribute to insulin resistance. And this is a conversation that I'm passionate about because so many people start beating this drum of saturated fats and use it as evidence against animal products because animal products do contain saturated fats invariably. Now, they're never completely saturated fat, and that's important. There's a mix of saturated mono and polyunsaturated fats. And, by the way, all saturated fats aren't the same.
There's like 10 or 12 different saturated fats. So, they're not like— oh, my gosh.
Yeah, yeah. Oh, there's dozens of them. Yeah, that's right.
Yeah.
So, I'm a huge advocate of a full spectrum of fats, namely of saturated fats, even long chain, which we get a lot of medium chain and then short chain. putting that to the side, when you incubate a cell, if you have a cell culture, whether it is muscle cells, liver cells, neurons, fat cells, and if you incubate those fat cells with palmitic acid, which is the prevalent saturated fat in the human body, certainly in circulation, palmitate or the 16 carbon saturated fat, when you incubate cells with palmitate, they or stearic acid even 18 18 carbons, they will become insulin resistant. And so you treat them with the fats, then you put on some insulin a little later, and then measure it, then you take all the cells and measure what insulin did, and it is compromised. That doesn't happen when you incubate the cells with monounsaturated or polyunsaturated fats. It will not cause direct cellular insulin resistance. So I've done these studies myself. Maybe the most cited study of mine I've ever done was this exact series of studies. The same thing happens in rodents. When you infuse the rodent with fat, when you're infusing it directly IV, the saturated fat will cause insulin resistance, but the monounsaturated, like olive oil, for example, doesn't. There is a direct effect of saturated fats at the cell to cause insulin resistance. Once you actually get into the cell itself, it's because of how these fats will induce the accumulation of another molecule called ceramides. If anyone has ever heard ceramides in the audience, they might be thinking of it as in lotions or shampoos and stuff, but it is a slightly different version of it. Saturated fats will induce the accumulation of these molecules called ceramides within a cell. Then ceramides will directly prevent insulin—the insulin biochemical pathway from doing its job. It directly antagonizes what insulin is trying to do. That's the actual where the rubber meets the road molecular mediator. Now to zoom back out to the level of the whole body, some people look at those studies, even possibly my own, and will use that as evidence against saturated fat. They will say, see, saturated fat causes insulin resistance, but it doesn't work. When you actually go to the whole body and look at the consumption of fat, the paradox is the vast majority, overwhelming majority, of saturated fat in our blood is palmitate, But it's not from the diet. It comes from the liver. The liver is the primary source of saturated fats that are circulating in the blood. When we eat saturated fats, they're packaged into the chylomicron, and there can be some depositing of that throughout the body, but it goes to the liver, and then the liver will repackage all that fat. Almost always, the saturated fats will have two things happen to them. They get elongated by two carbons, so you'll take that 16 carbon, palmitate, which is the most prevalent saturated fat. We take that 60 carbon, we make it into an 18 carbon, and then we desaturate it. There are these two steps. And so we end up taking the palmitate in the diet and turning it into oleic acid or the primary olive oil. And that is the primary fat that is stored in every single person's fat cells. So 18. So basically.
So basically your liver makes olive oil. No, no, no.
So the fat cells turn it into olive oil. But the liver makes palmitate.
Yeah.
So when we eat saturated fats, the body will turn it into olive oil, basically. But when the liver is making fat, it makes saturated fats. And so, this is why you can take someone and put them on a ketogenic diet, low carb, high fat, and they could be eating three times more saturated fat than the other group than the low fat, high carb group, three times more saturated fat and yet the actual composition of fatty acids in their lipoproteins in their blood is much less saturated. The actual amount of saturated fat circulating in their blood is much lower than it is if someone is eating a diet that is spiking their insulin. Because most of the saturated fat in the blood, which is what's coming to the cells throughout the body, the phenomenon that I mentioned a moment ago, most of that saturated fat is coming from the liver and the liver makes saturated fat when insulin is up. This is a process called lipogenesis and palmitate. Yep, lipogenesis. And insulin is what turns that on. And that's the paradox here really to put a kind of point.
And, why turns on insulin.
Dr. Starchy refined carbs.
Yeah. Dr. Yes, sugar and starch. Right. Okay, well let me just recap for a second. what you're saying is that if you eat saturated fat in your diet from animal protein or dairy or coconut oil, it gets turned into olive oil in your fat cell.
That's right.
If you actually eat sugar and starch, it turns on the fat production Factory in your liver to make saturated fat.
That's right.
So you make it saturated fat that's coming from eating sugar. People don't get this connection. They think, oh, sugar is sugar. How does it turn to fat? But there's a mechanism by which these sugars cause the production of saturated fat in your blood, which is what's causing a lot of the problem.
Yeah, and it's a one-two punch. Absolutely. It ends up being a one-two punch where these starchy, sugary carbs will both act as the skeleton. The liver will take those carbons and rearrange them to create a saturated fat. and at the same time, the starchy, sugary carbs are increasing insulin, which is what's driving the signal. That's the signal to tell the liver to do that in the first place. Because the liver will not make fat out of carbs unless insulin is elevated. It is antithetical. It is impossible for the liver to do. Because like every cell in the body, insulin tells the liver what to do with the energy that it has available. And when insulin is up, one of the things it wants the liver to do is turn the carbs into, turn the glucose, those carbons into fat. And the only fat the liver is making and packaging and releasing is palmitate, that saturated fat.
That's incredible. So I wanna, I wanna drill down a little bit into the, the take homes, and I just, I sort of want to recap a little bit, and then I want to ask you what, what we can do to fix this, because 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 we, we understand that the way in which insulin resistance is controlled is through primarily diet. And, 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 stagger. 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, yeah. Well, I think— 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, they'd 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, 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 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. And, 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 kind of mushroom-like or columns, little stalks of skin. They're not like a flat kind of 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. so those are skin tags. And at the same, 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, but that's another, another one. So the, the skin, I kind of joke, the skin is the window to the metabolic soul just because like 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 of 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 going to 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, 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 have a perfectly normal cholesterol of 200 or 150, but your triglycerides, maybe 300 or 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 the 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, 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 the insulin resistance. So we look at a whole host of things and we can 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, and you mentioned the waist to hip ratio. That's important. But, you know, when you look at the data on the 88 of Americans who are metabolically unhealthy, 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 weight. 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'd 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. 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. Any pressure for the body to store more fat is primarily through hypertrophy of every individual fat.
Fat cells.
And the fat cells get to, and that's right, they get to about four or five times bigger than the normal fat cells. 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. So the fat cells will get a little big, then the body just makes more fat cells. That's a process called hyperplasia. So just multiplying the fat cells, basically. That's the difference, because if you have small fat cells, even if you have a lot of them, They're very insulin sensitive and they're anti-inflammatory, literally 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.
When you become metabolically flexible, you're able to derive all this energy from your stored body fat. And then an amazing thing happens, which is the liver, when you—when you withhold carbohydrate, which becomes glucose eventually through the digestive process. When you withhold carbohydrates-- and just to.
Be clear for people, you mean refined starchy carbs. You don't mean broccoli, right?
Okay, so we can make that distinction. I mean all carbohydrates, but I'm going to put a big asterisk by broccoli and say that when you go keto, you can eat as much vegetables as you want. That's right.
Okay, so green leafy vegetables.
And they're all carbohydrates. They're all carbohydrates. So what we're talking about is how accessible is the amount of sugar or the carbohydrate that you take in real time to the body. And if it's made less accessible because it's locked in a fibrous matrix, as in the case of broccoli.
Or a vegetable.
Any vegetable. I mean, but you know, for picking on my favorite vegetable, so you not only become good at burning fat, but then the body starts to, you create these ketones in the absence of glucose. and people would typically say, well, you know, I'm feeling woozy because my blood sugar is low. My brain isn't working because my blood sugar is low. That's why they feel like they need to have a meal. That's why they feel like they need to have a snack because they get, you know, they have these wild blood sugar swings throughout the day because they've been so dependent on a regular supply of carbohydrate to keep their glucose up. Well, when you cease doing that for some length of time, the body gets wise and the brain goes, well, look, I know how to burn ketones. I just haven't done it for a long time. So the brain becomes quite adept at deriving energy from ketones.
The whole theory that you need glucose to fuel your brain, that's a false.
That's correct. You don't need it.
One of the things that it's become kind of a- Because it's supposed to.
Use 25% of all the glucose, right?
25% of your energy. Right, that's different than what I learned in medical school.
Yeah, yeah, yeah. But you're saying that's wrong. So the brain, let me put it one way, which is that there is no dietary requirement for carbohydrate in human nutrition.
Yes. So you should just unpack that because there are essential amino acids with protein. There are essential fatty acids from fat, but there is no such thing as an essential carbohydrate and we don't need them.
Correct. We don't need them. And I'm not suggesting that we should never consume them, but the reality is we don't need them because we have this elaborate and elegant mechanism that takes stored body fat and in the absence of any food allows us to live for five, six, seven days, not just survive, but thrive and be mentally alert and to be willing and able to hunt for the source of food. Because remember, throughout most of human history, we didn't have three square meals a day. We had food and we didn't have food. And so the design of the system, and again, this elegant system, phase one of the system says the brain, when it comes across food, you got to overeat because you don't know where the next source of food is going to be. And so when you overeat, you take the excess amount of energy that is in the food and you store it as fuel that you get to carry around on your body. By the way, conveniently located right over the center of gravity. The belly, the butt, the hips, the thighs. It's such an elegant system that we would be able to carry this fuel with us for long periods of time and not worry about, oh my God, it's noon and I'm going to get hangry because there's no food around. There's no deli around.
We have the ability to use that fat for energy.
You'D use that fat for energy and that's how the system's designed. So unfortunately we get to today where we've lost the ability to, so we're very good at storing fat and we still are wired to overeat.
But because- yeah, there's like 200 genes that protect us from starvation, but none that help us deal with abundance and excess.
So it's an artifact of civilization, so we kind of have to override that with our cognition. But one way to do that, again, is to use a ketogenic way of eating for some period of time. Again, not necessarily for the rest of your life.
What is keto? Define keto.
So keto to me is cutting carbs back to 50 grams a day or less.
Which is what is 50 grams in terms of a food? For like a bagel?
Yeah, pretty much. A bagel with some jam on it and you're already over the top. or any, like if you got rid of bread, pasta, cereal, rice, cookies, candies, cakes, sweetened beverages, sweetened drinks, and all you had was, oh my gosh, real food, broccoli, Brussels sprouts, cauliflower, salads, you would be fine.
You would be within that 50.
You'd be hard pressed to get. Could you have grains and beans?
No.
So you don't have grains and beans on a keto diet. Now we'll talk about, we'll talk about what Peto looks like.
Peto.
Or paleo keto, or what are we gonna call it? Your Pegan version of keto, what's it gonna be? Keegan. Keegan.
Keegan, that's a Keegan diet. It's like a keto vegan. I have a friend who's a keto vegan.
Yeah, yeah. So you can do it for sure. It takes some adherence to this. At the end of, a couple of weeks though, you have shifted your metabolism to one of greater efficiency and-- so.
It takes like three weeks to adapt to it. You need to make sure you have enough fluids and sodium and magnesium because otherwise you feel the keto flu.
And some people still get the keto flu, but it's not like the flu.
It'S just-- you- feel achy and tired.
That's your brain going, where's my glucose, dude? And until the brain kicks in and says, wow, these ketones are amazing. The liver can make up to 750 calories a day worth of ketones.
Wow.
Like, chew on that for a second. That's unbelievable. Right. So when you, when you, when you look at how we're designed for survival, if you look at, I mean, not.
From diet, but just from your fat stores.
Correct.
Yeah. Yeah.
So because, and, and, you know, we, we have this stored body fat. and when we cut off just theoretically, if let's say you do a fast, which we can talk about what that looks like, but you do a five day fast, you become a closed loop. It's amazing that you, that you, that the body takes fat out of storage, combusts some of it in the muscles to get you through your day. And people who do five day fasts, they work out, they'll exercise, not, you know, hard, heavy, but so you combust some of that fat in the muscles, some of that fat, you know, as you take that, those triglycerides, and you strip out the glycerol becomes a backbone to make enough glucose through gluconeogenesis to supply whatever amount of brain cells do require some glucose. It's not a big number. It might be 40-50 grams a day. The liver makes ketones. The brain thrives on ketones. The brain prefers ketones.
Yeah, the brain does way better on fat than on sugar.
Well, on ketones. Yeah. the brain doesn't burn fat, but it burns ketones. Ketones are derived from fat. Are derived from fat. So you have this substrate, this fatty, this fat substance that then can become combusted by itself as fat, part of it can be used to actually make glucose if needed. That's why you don't have an external need for carbohydrate and glucose. And then you can make up to 750 calories a day worth of ketones. Now one of the best things that happens in this scenario is that, again, epigenetics at work turns on genes that cause the body to spare amino acids and spare protein. So as, whereas normally on a day-to-day basis you might eat a big meal and you might have more, you know, protein than you need and then your body has to kind of go through this work to deaminate it and pee it out because it's too much, you don't need that much. And so when you become this closed loop, this closed system, the only reason you need the amino acids are for structural, for repair, for building and repairing.
Not for making sugar.
You don't want to combust.
So people have a false idea about, you know, keto, that it's all like steak and bacon and cream and all this stuff. It's not necessarily that. No.
In fact, you can eat too much in the way of, well, I mean, a lot of people who first come to keto do so because they I heard that I can eat 4,500 calories a day and not gain weight. You know, and I'm like, well, yeah, some of the science shows that, but that's horrible because that's a bad idea because first of all, if you want to burn off your stored body fat, eating 4,500 calories a day will never tap into your stored body fat. That's just, you know, that's just trying to prime the pump with this external source of fuel that's fat that's circulating through your, through your bloodstream. and that amount of calories because you're not generating insulin, which is a nutrient storage hormone, the nutrients have nowhere to go. The body has to figure out how do I burn this stuff off? I can't store it as fat. So the body undergoes this thermogenic high heat kind of thing.
Well, that's so powerful because people don't understand that if you don't have insulin, which is only produced by eating carbohydrates or protein can also increase insulin. If you don't have insulin, you can't gain weight. So if you're a type 1 diabetic, the classic symptoms are polyphagia, meaning you eat everything in sight and you lose weight. So they could eat 10,000 calories a day and lose weight because they have no insulin, which is required to store the fat on your body. So the best way to get your insulin down is to cut out the starchy carbs and to eat more reasonable.
Amounts of protein and more fat and reasonable amounts of protein. So you don't make it up with, you know, you don't make the calories up with extra amounts of protein.
Yeah, so 20%.
Okay, I mean, I prefer to deal with hard numbers, like what's a good number for protein? Maybe it's 75 grams 100 grams a day for a man as a minimum number and maybe it doesn't exceed 120. Within a range there, you're going to be fine. And then because the body is so efficient again at conserving amino acids, protein, that it doesn't even matter meal to meal or day to day. It might be on a four-day cycle if you get 300 grams of protein in a four-day cycle, you're good because it'll just figure out. with different various protein sinks that we have in the body, how to keep it and not pee it out. So back to this closed loop that I'm talking about, so you're combusting fat in the muscles, you're making a little bit of glucose through gluconeogenesis, you're making ketones. Now we figure out that you don't really need that many calories to get through a day. We assume if we do that math that's online, you plug in your number, and your height and your weight or whatever and your activity level from one to five and you come up with some number, oh, sis, I can have 2,700 calories a day or 3,200 calories a day for maintenance. No bearing whatsoever on reality. We probably, again, if you do the math, if we, for long periods of time, if we say that protein, protein shouldn't even have a calorie a to it. It's like it's structural. You don't burn protein, so why would you even assign a value of four.
Calories per gram to protein? But it can turn into sugar.
It can. To eat excess amounts. It can. So, you know, and I guess if you burn it in a bomb, Kellor.
You know, you get some amount of thermic effect. So, how do you know if you're.
Doing a ketogenic diet properly? Well, the main thing is can you go a meal or two, skip a meal or two and just feel feel just fine.
And if you can, because it cuts hunger. So, yeah, ketones, it cuts your hunger.
The number one benefit from all of this is getting control of hunger, appetite and cravings. That's what everyone reports when they finally hit that keto zone.
So, it's not bad willpower that people want to crave and eat other food? It's just biology, right?
It's biology. It's absolutely biology. People come to this point pretty quickly where they go, Jesus, Mark, you know, three meals a day is just too damn much food. I just don't feel hungry. I feel like I'm overeating at three meals a day. And so typically what they do is they skip breakfast. They wake up in the morning, I have a cup of coffee, I go about my day, I do a hard workout. I'm like, not only do I not need to eat, I don't feel compelled to eat, I don't want to eat.
And I might have my first meal.
At one o'clock or one thirty.
Restricted eating.
It's what it is. And so then you get to the point where you're eating maybe two meals a day. And then from there, it's like even those two meals feel like if I have two regular, what would have been in the old days, regular meals, now it's like I'm gonna have lunch, kind of a smaller lunch because I want to enjoy a regular dinner. If I have a regular lunch, then I won't be hungry for dinner.
It's amazing how hunger dissipates in this context. But you don't get super skinny. You look good, right?
I mean, I work to keep my weight off.
Although I notice, Mark, is I actually have a problem. If I don't have things like sweet potatoes or some black rice, I will lose too much weight.
Do you lift weights?
I do. I started.
Lifting weights is what causes you to keep muscle on. If you don't lift weights, especially as you get older, like when you get to be 45, you'll see what I'm talking about.
I'm 60. I passed that mark long ago. I'm just messing with you. But biologically 39, because I did my telomere.
As you get older, the importance of lean tissue becomes more and more critical.
Muscle is the forgotten organ.
It's forgotten, and people think, well, if I'm jogging in my 50s and 60s and 70s, or riding a bike, that that's accomplishing what I need to accomplish, and it's not. It's actually much more important to spend some time in the gym lifting heavy weights, like the heaviest weights you can lift without getting hurt.
Without getting hurt is a key component. I don't wanna. So my trainer tells me I should do like more reps, like I do three sets. And I do, you know, it's pretty hard, but it's not like my maximum that I can do. Sometimes it is, but is that the.
Same or is it more better to do heavy weights?
How many reps do you do? Are we talking six or three and five?
10 to 12 and then I do three times. That's fine. standard. That's, that's, that hasn't changed in decades. That's still. And there's no right answer there. There's no magic.
It's like whatever you feel good. Is that building enough muscle or should.
I do more heavier weights? Sure. I'm at, you know, heavier weights and fewer reps builds more strength over time. But there's no, I can't tell you that, that that's where you need to go. But I give you an example. It's sometimes the type of weight you're doing. So if you're just doing bicep curls you know, that's, you know, for the, for the beach, but that doesn't really impact bone density, you know, muscle mass throughout. So hex bar deadlifts. You ever do those?
Yeah. Yeah.
That's the best thing you can do.
What about just a regular deadlift?
Yeah, they're good, but they're, I'm too.
Concerned with my back.
So I lift heavy with a hex bar deadlift. Oh, really? Yeah. So, but I do it once every week, and I do three sets of that.
I keep adding weights and time.
How much do you I do up to 300 pounds on a, on a, I do one, you know, to two rep Max on a, on 300.
Oh, one to two. Yeah.
I can do 335 on one, but it's too much. I, I wind up taking too long to do it. I'm afraid. Again, I don't want to hurt myself.
Yeah.
So I do. But that's like that one exercise impacts the entire body.
Yeah.
You know, it's, it's not just what you would see, obviously, from, from doing the weight of the glutes and the lower back and the hamstrings and the quads, but it's pulling on the shoulder muscles. My grip strength is sometimes the thing that gives out more than anything else. But that one exercise then has an effect on the pulse of growth hormone and testosterone through it involves so many muscles, including major muscles. Then when you go do the pull-ups and the push-ups and the dips and the squats and all the other the lunges, then you get the impact is greater. The effect, the muscle building effect is greater because you did that.
Yeah, I like that. I like that. So you do that first or last or whatever. That's amazing.
If you do it first, a lot of times you'll like, you know, you won't have the strength to complete the other stuff.
So what is the biology of doing it? You mentioned and you can burn fat, but why is that better? Like what does it do in terms of longevity? What do the signs show? Well.
As we so burning sugar is a in and of itself, it produces reactive oxygen species at a greater rate than putting combusting fat through the mitochondria. So the more energy you can drive through this metabolic pathway that uses the mitochondria, the better off you are. A lot of times people burn sugar in the cytosol of the cell, not even six.
The way I think about it is interesting. So when you eat a lot of sugar calories and starchy calories, it burns dirty in your mitochondria and releases a lot of waste products, which is these reactive oxygen species or oxidative stress or free radicals are driving aging. And when you burn ketones, it's more like hybrid.
Yeah.
Like an electric vehicle burn. burns clean, right?
Like a 93 octane.
Yeah, it burns much cleaner. Is that true?
That's true. I mean, that's the simplest way of looking at it. Then there are other nuances to this which are when you become good at burning fat, then when you skip a meal or when you have this very easy to manage compressed eating window, all the good stuff happens when you're not eating. So, the longer you can go and that's why fasting has become the rage. The longer you can go without eating, the more your body says, oh, this is a great time to do some house cleaning. And, you know, the term autophagy is thrown out probably too much now, but, you know, the body does tend to want to clean up and consume damaged proteins. Autophagy means like you're literally eating yourself.
So, eating all the waste products. Eating the waste products.
The Pac-Man goes around and cleans up the garbage. Correct. And, if you never fast, you just become this increased collection of garbage in your body.
The whole three meals, three snacks, eat late at night, night after dinner snack and wake up eating right away. That's a bad idea.
It's a bad idea. And what's ironic to me is that even going back 15 years ago in the bodybuilding, in the weight lifting, in the general health community, the mantra was don't go more than two hours without eating. You bring your Tupperware little meals with you some amount of protein, some amount of carbs, no fat, skinless chicken breast, and all that stuff. It was a horrible concept, and yet the thought process was, you don't want to cannibalize your muscle tissue, and if you go more than three hours without eating, you'll cannibalize your muscle tissue. Now, all of that was predicated on an assumption that glucose was the primary fuel that we needed, and we ran out of glucose, it would cause the brain to go into a state of, oh my god, send a signal to the adrenals to secrete cortisol so we can basically melt some muscle tissue and send some amino acids to the liver to become glucose.
Exactly.
It was a horrible, again, it was all based on the wrong, on a concept that somehow assumed that glucose was the muscle fuel that we needed and if we didn't manage glucose, all hell broke loose. Now we know that fat is the preferred fuel for human movement and human activity, and that ketones are not just a legitimate alternative energy source, they're probably a preferred energy source in many cases.
As a doctor, I see a lot of patients and I test them and I see the results. And it's humbling because you can come up with all these great theories, but then you see the individual in front of you and I've had patients I put on a ketogenic diet eating butter and coconut oil all day and they lose 20, 30 pounds, their cholesterol comes down 100 points, their triglycerides drop, their good cholesterol goes up, somebody else does that and all their numbers go terrible and they start getting really bad cholesterol numbers and I'm one of those guys, if I eat too much of saturated fat, I get in trouble and I think, how do you understand sort of how to personalize this.
Alright, so a couple things. First of all, you know, we've never had this conversation, so I don't know what your stance is currently on this, but you know, I've been pushing for 15 years to take the weight off cholesterol as a bad guy. You know, the cholesterol is not the problem.
In the blood or in the diet?
Both. But let's just talk blood cholesterol right now. I don't think cholesterol is a bad guy. Cholesterol is one of the most important molecules in the human body. It's integral to life. The body makes 1300 milligrams a day, whether or not you have any in your diet. And to vilify it and spend a trillion dollars for the last 15 years to try and eradicate it in humans is absolutely unconscionable. Through statin medications. And I shared with you before the show. So I just had some blood work done. I'm between two 245 and 290 on my total cholesterol. But my HDL is 98.
That's the good cholesterol.
That's the good cholesterol. You know, and my triglycerides are always below 75, sometimes 45 or 50. My A1C is 4.9, which you know to be.
Your average blood sugar is really low.
Really low. Fasting insulin is, you know, between six and seven. It can be as high as 45 in some people. So all my markers, are great except that if you didn't ascribe to that whole cholesterol theory, you'd go, oh my God, Mark, we gotta put you on... Everything looks great. By the way, I had a full scan of my carotids and all my blood supply to my coronary arteries, my liver. I mean, they were digging in so deep I thought, oh my God, they're looking to see if I have colon cancer. But they were trying to get at my kidney supply. And they said, you know, you're clean. You got like the blood supply of a 30-year-old, it's clean as can be. That's all that counts, Mark. I don't care what my cholesterol numbers are.
But aren't some people more at risk though?
Some are.
But again, these lean mass hyper-responder phenomena?
Yes, and it all, I think, comes down to, and I'm not a doctor, so I'm only giving you my opinion. You can opine with greater.
I guess.
You have more liability for saying it than I do. I have no liability as long as they say I'm not a doctor. But it's inflammation and oxidation that are the primary culprits here. And so if you have an otherwise inflammatory lifestyle, inflammatory diet, we can talk about sugar, we can talk about stress, we can talk about, you know, and then we can talk about some familial predisposition. Yes, but in general, so back to your two people. Some succeed wildly on the ketogenic diet and some not so much. But the not so much, if you're evaluating just on short-term blood markers, I'm not gonna say it's not working. I'm just gonna say that's, you know, if you're keto and you're good at burning fat, you got to transport the fat somehow to the muscle cells. You've got, you know, there are a lot of things going on here.
Yeah, we just don't know.
And we just don't know. And we just don't know. Now, some people having said all of that, some women in particular are not good responders to keto.
It may be-- who shouldn't be on it?
Well, so I think pregnant women probably, you know, you just work with, if you want to do this and you insist on doing this, work with somebody who knows what they're doing, right? And I wouldn't, you know, I wouldn't introduce a three-year-old kid to a ketogenic diet, right? You know?
Do you think it's something everybody should be on?
I think at some point in their lives everybody should be on it because it's the human experience.
So you think cyclical keto, that's the idea. Yeah. So do you ever go above the 50 grams of carbs?
Oh my God, I have... Last night I'm visiting here in Los Angeles. My daughter is a great chef and she made a lasagna last night. Like, I'm not gonna not eat two servings of that. I mean, you know, and it was somebody's birthday and we had some pie and, you know, I didn't sleep as well as I, as I would have had I not done that. But I also, like, I'm totally comfortable.
In, in and out.
In and out.
And that's, that's what we historically did.
That's. Exactly. So when we talk about, you know, we're humans, you know, always keto. No, we were, there were periods of time when we were, there was no access to food. You were, like, automatically, you were obligatory. sorry, keto when you didn't eat. Yeah. But because you didn't eat processed crap and industrial seed oils that would infect your, your insulin sensitivity and all these other things, even if you came across a treasure Trove of bee honey or it was late in the season and you had a bunch of fruit, you know, you'd store it as fat. But then you'd go right back to being keto when, when the food supply was cut off.
Yeah.
And you didn't go, you know, as some of these people do. well, you know, whenever I have more than 60 grams or 70 grams of carbs, I get kicked out of keto. Kicked out of keto means nothing to me.
Like, I don't even care what your keto numbers are.
So you don't think about measuring it or tracking it? I think it's a parlor trick. So what will happen is people who are new to keto will go, they'll chase the numbers, right? So they'll say, well, I didn't eat any carbs today, and I just had MCT oil, and I had my bulletproof coffee. whatever, and I'm showing 4.5 millimolar or 6 millimolar. Yeah, yeah, baby. I'm keto. Well, you're keto, you're producing ketones, but one of the things you got to look for is you're just pissing those out. So your body has not become good at using them yet. You'll get there, but right now your liver is going crazy trying to make ketones and you don't know how to burn them. So once you build the metabolic machinery to burn ketones, and once you build the the facilitation.
It doesn't go away when you have a pie and lasagna.
No, exactly. Exactly. So, let's talk about that. Once you built that, you spent three weeks, four weeks building that metabolic machinery. You've reset your metabolism to one of metabolic flexibility and metabolic efficiency. Then, if you go off the wagon one meal or eat one day of 300 grams of carbs, you might feel bad, but you just come right back to to where you were. It doesn't shift all the way back to being a sugar burner. Now, if you did it for three more weeks of just doing sugar, the body would say, well, I guess we don't need this expensive machinery lying around burning fat all the time now. I guess we're gonna just go back to burning sugar, so we'll let all of these things atrophy.
When you get your traditional cholesterol panel done, your traditional lipid panel done, They're giving you the LDL cholesterol, the HDL cholesterol, the total cholesterol. And that's one piece of information, like you said, but we're missing a lot of information there. So it's really important, I love this analogy, of the dirt and dump trucks. So dirt and dump trucks. And think of all the dump trucks that are going around carrying dirt, and we can make this analogy with cholesterol. So think of your cholesterol like the dirt, and the dump trucks are the particles carrying around your cholesterol. So what we're learning is it's not just the amount of dirt somebody has that's important. It's the amount of dump trucks that they have carrying around that dirt, and that the size of the dump trucks are actually really important. And so when you get a typical lipid panel done, you're just finding out the amount of dirt that you have and how much of it is LDL and HDL and triglycerides, and that's important and we will talk about that. But what's even more important, or at least as important, is the amount of dump trucks you have carrying around that dirt. And what we're learning is that, or what we've learned, is that if you have small dump trucks, So if you have a certain amount of dirt, you could either have a few big dump trucks carrying it around or a lot of small dump trucks carrying it around. And what we're learning is that those small dump trucks, if you have too many small dump trucks, that that's actually more concerning that they can get into the artery lining more, they can cause more plaque buildup, they can help that cholesterol get oxidized through oxidative stress. It's much more dangerous. So the size of those dump trucks you have carrying around your cholesterol, is critically important.
Yeah.
And something we look at all the time.
I mean, the way I think about it is, and I, another way I kind of look at it is, you know, the, the number you get on your test is the weight of your cholesterol. So it's milligrams per deciliter. It's just basically the weight.
Yep.
But it doesn't tell you if that cholesterol is made up of a thousand particles or 100 particles.
Right.
So you could have a cholesterol of 150, and it could be 5,000 particles or it could be 500 particles of cholesterol. And that makes a huge difference in your risk of heart disease. And you can't tell from a regular cholesterol test whether you have a lot of particles or whether they're big particles or small particles. So I think about it sort of like golf balls and beach balls. Beach balls are these big, light, fluffy balls that you can bounce and don't hurt anything. And a golf ball, small, but it hits you in the head, it'll knock you out. Right? And, the golf balls are the things that are the small particles that are dangerous that bang up against the arteries and cause the plaque to develop and cause heart attacks. So, you can't tell that from a regular test. You can have smaller, large LDL, smaller, large HDL, smaller, large triglycerides. And, the triglycerides are a little different. It's the big triglycerides that are a problem, not the small ones. But, you can really get a sense from these newer tests what's really going on. because I've seen people with a cholesterol of 300. Their HDLs, which sounds terrible, right? Because they're supposed to be under 200. Their LDL might be 150, which sounds terrible because it should be under 70. Their HDL is like 110. So they have really high cholesterol. They're skinny, they're healthy, they have diabetes, high blood pressure, they don't smoke, they're older. Often little ladies have this kind of cholesterol. There's no evidence that these people are at risk of heart disease because they have large, light, fluffy particles.
Particles.
They might have no small particles. They might have the perfect size and shape of all their cholesterol markers, and their risk is really low. And I remember talking to a colleague of, well, more of a mentor, Dr. Peter Libby, who's the chief of cardiovascular medicine at Harvard, has written the textbook, you know, on heart disease at all, cardiology study. And I said, you know, Peter, I have these patients, these little ladies, their cholesterol is 300, and they have this and that. Like, this was like 20 years ago. I'm like, Would you treat these people with a statin or a drug? Absolutely not. There's no evidence that these people are at risk, even though their cholesterol is so abnormal. So you can't just go by the cholesterol test that your doctor does. Right. Right.
So you need something called what? Particle size testing. It's telling us about those things that are carrying around your cholesterol.
Yes, LabCorp does NMR. Yep, NMR. Quest does something called Cardio IQ, which is similar. and you can ask your doctor for these. And you shouldn't stand for any other test but these tests. And then they tell you so much. So tell us, how do you get a profile that is with these small, dense, dangerous HDL and LDL?
Well, you know, it's interesting. So there's a lot of lifestyle that impacts the size of your LDL particles, right? The size of those, you know, are they small and dense and dangerous or are they big and fluffy? and not so dangerous. I mean, there's always a genetic component, right? There's a genetic component, but then there's our lifestyle. And we know that metabolic syndrome where people are insulin resistant, gaining weight around the belly, they typically have lower HDL, they typically have higher triglycerides, but they also typically have more of these small dense LDLs which are more concerning. And so lifestyle makes a huge impact on the size of those LDL particles.
And which part of your lifestyle? What's the biggest thing?
The diet.
Your diet. What diet causes you to have the dangerous kind of cholesterol?
That's a sad diet. The standard American diet, right? That's the one that, you know, that full of carbohydrates and sugar and refined and processed foods and lots of alcohol and, you know, it's the standard American diet.
That drives it. And what does that do to the body that causes these particles? And it actually leads to the high triglycerides, the low HDL, the small particles.
Right. It's that whole process of insulin resistance and it results in this really unhealthy pattern. And so, you know, we sometimes get clues of that with a standard lipid panel, right? We sometimes get clues when somebody has a low HDL, that's the one, the HDL is the one you want higher. and for men you wanted at least over 40, and for women at least over 50. And then if that triglycerides are- I'm like 50 and 60, I'm more aggressive than you.
Yeah, well that's really true.
Like what's optimal, right? What's optimal?
If your cholesterol is HDL is 40, probably not optimal.
Should be over 50. It really should, it really should. You're right, it's not optimal. I'm not a tough customer here. And then the triglycerides, you want at least under 150, or what would you say? What's optimal?
70.
There you go for triglycerides.
If your triglycerides are over 100, you're definitely flirting with danger. And there are some genetics involved. We'll talk about the genetics in a minute, but it is usually a sign of increased carbohydrate load. And I don't mean broccoli, I mean flour and sugar.
Absolutely. So, you can get some sense of if somebody is prone to metabolic syndrome, insulin resistance with that. But then the particle size testing also gives us a lot of information. The NMR, for example, gives you something called your insulin resistance score. So you can get a sense based on the analysis of the particles of cholesterol that you have, how at risk you are for insulin resistance. So it's just one more piece of the puzzle.
And I see people with a cholesterol of 150 who have like 2000 particles of LDL, which should be under 1000, who have like 900 particles of small LDL, which should be under 300, ideally probably less than 90 is perfect and you see that often. And yet their doctor, well, your cholesterol is 150, it's fine. And so you really can get duped by just looking at the total numbers. If it's 300, it might be fine. If it's 150, it might be highly dangerous to you. And it's not so easy without looking at the specific tests. So it's super important. And so what you mentioned is that insulin resistance is the driver of this, which is pre-diabetes, metabolic syndrome. And to some degree or another, 88% of Americans are metabolically unhealthy and have some degree of this. 50% have pre-diabetes or type 2 diabetes. Like every other American has diabetes or pre-diabetes. That's crazy. 75% overweight and every one of those people is some degree of poor metabolic health. So if this is true, what else does this diet do that accelerates heart disease? Because we now know that it's not just the cholesterol. Like I said, you could have cholesterol 300 and be fine. There's a special ingredient you need in order to cause the heart disease.
What is that special ingredient?
So it's inflammation and oxidative stress, right? So inflammation seems to cause everything these days, from depression to cancer to heart disease, to diabetes, to everything else. So what is the cause of the.
Inflammation in these patients with insulin resistance? So a lot of times, I mean, there's many things, right? But it's our belly fat because we know that that fat around our belly, when we get insulin resistant, we gain more weight around our belly and we know that visceral fat or weight around the belly, the apple shape is more inflammatory. It secretes all these inflammatory markers and increases inflammation in the body. And so when people, when we get them to, when they help, their weight around their belly goes down. When we get that waist-to-hip ratio better, that inflammation goes down.
So basically what you're saying is that fat around your belly is not just holding up your pants, that it's an immunologically active organ. It produces these molecules we call adipose cytokines. You've heard of the cytokine storm with COVID Yep. Well, it's that same chronic cytokine storm that's being released from these fat cells in your belly. They're not just average, I mean, you have fat in your legs or your butt, It's not gonna do that. These fat cells in your belly are super inflammatory. So then you get the inflammation, which leads to oxidative stress, which then causes what problem with the cholesterol?
Right, so when your LDL cholesterol gets oxidized- and what is that? Think of oxidative stress like excessive free radicals or rusting in the body. But, you know, we're always making free radicals. in many different cellular processes in the body, but when there's too many of them or you don't have enough antioxidants to squelch those free radicals, so if your diet's not rich enough in the polyphenols or those phytonutrients or your vegetables, then what happens is you get more oxidative stress and that oxidative stress can shift that LDL cholesterol and it's that oxidized LDL that's more damaging and more likely to cause plaque back build up and. And that will lead to heart disease.
So it's basically rancid cholesterol.
Yep.
In your bloodstream. That's the problem that gets oxidized, which is like you said, rusting or Apple turning brown or your skin wrinkling from too much Sun. These are all signs of oxidative, but this happens inside of you, and it leads to this inflammatory process, this oxidative stress, and that's what causes the heart disease. And I, you know, some of the interesting studies I've seen, like the Jupiter study, very big trial. from Harvard on heart disease. Fascinating to me that people who had high LDL but no inflammation had very low risk. People had high inflammation but kind of okay cholesterol, they were at risk. And those with high cholesterol and high inflammation had the most risk. So I think we have to be focused on inflammation, what's causing that. And it may be that the statin drugs, turns out, the benefits may not have a lot to do with cholesterol lowering.
But they're anti-inflammatory.
They're very powerful anti-inflammatory drugs, which is called a side effect. But it actually works. Now, there's a lot of better ways to get rid of inflammation besides taking statin drugs. And so when you're talking about people's cholesterol, how do you decide what to do for each patient? How do you decide from a functional medicine perspective how to work these patients up to decide whether that should go.
On a drug or whether you just do lifestyle? How do you figure that out? It is a complex process, right? Where we're taking a really detailed history and we're looking at more than just those numbers. We're looking at what are their markers of oxidative stress? We can measure those. We can measure oxidized LDL. We can measure 8-hydroxydeoxyguanosine and lipid peroxides. All of these biomarkers that give us.
A sense of is there oxidative stress? And by the way, these kinds of tests are not things you'll typically get at your regular doctor. At the Ultra Wellness Center here in Lenox, Massachusetts, Massachusetts, we do functional medicine, which takes a deeper dive into the root causes, into these diagnostic tests which are not available usually through your traditional doctor. They may not be interested in or know what to do or how to interpret even fasting insulin, which they don't even do. So we really are excited to help people figure out how to look at their risk and design a strategy that's personalized for them using functional medicine. And we see people from all over the world that the UltraWellness Center is doing like Zoom consults now. so it's pretty easy to get access.
And it's fascinating because there's so many pieces to the puzzle. And so when you find somebody with high oxidative stress, you ask that question, why? Why is there high oxidative stress? Is it their poor diet?
Is it inflammation?
Is it their microbiome? Is it their microbiome? Is it a toxin? Heavy metals.
Heavy metals, like a toxin or some other- Pollution. Yes.
All the smoke that wildfires in California, that increases risk cardiovascular disease. Absolutely, absolutely. So, you know, it's really important to think about all the different things that can lead to oxidative stress and inflammation and then try to tease out what is it for that individual person that we need to focus on. So I think that's important for some people and a lot of Americans, there's so much that's lifestyle related, right? But for some people, their lifestyle is great and it's more toxin related that we really need to work on that or or like you mentioned, the microbiome is an area that's fascinating. We're learning so much about how it influences inflammation in the body. Microbiome in your gut as well as microbiome in your mouth, right, and gingivitis and how much that we've known for years that that impacts risk of heart disease because of its inflammatory properties. So those are important things that we need to really investigate and look at.
Yeah, so true. You know, I'm just thinking about how we work with these patients. So we look at all these diagnostic tests that may not be looked at. We look at their overall cardiovascular risk, their family history. We may look at diagnostic tests. We may send them for a heart scan, look at calcium, broad ultrasound, look at particle size, look at inflammation markers, oxidative stress markers, the microbiome, heavy metals. We might look at other factors like homocysteine, which looks at B vitamin status. We look at lipoprotein A and a bunch of other factors that give us a more rounded picture. of what's going on. So we're not just focused like a laser on cholesterol. And the reason it seems to me that we are so hyper focused on cholesterol is we have a good drug to treat it. So it's all pharmaceutical driven. Whereas when you look at the data, two-thirds of all people entering into an emergency room with a heart attack have either pre-diabetes or diabetes and most of them are undiagnosed.
Right, so when you say- so two-thirds.
Of heart attacks are from sugar, not cholesterol issues. And we're just focusing on cholesterol. It seems like we're missing the mark here.
We often are. And we're saying, okay, this is high. I mean, so many people come back with high on their lab work and it doesn't necessarily, like you said, it's anything to be concerned about. And then there's so many people who come back without that H, that high level, and they do need to be concerned.
Statins have a role. But let's talk about the statins for a minute because it's very controversial. Like any drug, there are benefits, there are risks, there are side effects, and there's the right patient for the job. So how do you come to sort of decide what you should do with a patient?
Yeah, I mean, you really want to get a good detailed family history. I think that there are some people who are at very high risk of vascular disease, and for people who have a strong family history, which means that if you have a first degree relative, which would be a parent or a sibling who has had an early heart attack. So for a man less than 55 or a woman less than 65, that means they've had diagnosed heart disease because of plaque at an early age. You know, those people who have that type of family history need to be more careful.
Or were they smokers? Were they very overweight? Did they have diabetes? what are the other factors? So I always look at that as well, because you have to. I remember my grandfather, you know, everybody in his family, like, I think he had nine siblings. Everybody had heart attacks in their 50s. You know, they all had bypasses, heart attacks, and they weren't, like, significantly overweight, but they were pretty high risk as a family. And he was deaf, so he couldn't hear, so he really, he really couldn't get a, a job, like a white collar job. So he had a blue collar job, which was basically loading New York Times, big bundles of New York Times onto the trucks from the conveyor belt. So he was constantly working out all day long and was very, very strong and healthy. And every night he would go out in Queens and he would walk down the street and feed all the alley cats. So he walked every night after dinner, which we now know is a very good way to improve your health. And he, he didn't really get heart disease until his 80s. Right. Right. And they all got it in their 50s. so it's, and, and his diet wasn't the best. Right. But still, even with simple, simple lifestyle things, it can make a big difference. Absolutely.
So.
Right.
So you're, you bring up a great point that genetics and family history is just one piece of the puzzle. It's not what makes all, you know, make us, makes us make all the decisions in the world. But we take that into account as well as all their other risk factors, like you mentioned, like type 2 diabetes and are they smoker and so we really have to pay attention to all of those lifestyle factors.
High blood pressure, you know, a lot of high blood pressure is a big factor in heart disease. But again, high blood pressure is usually caused by the same thing, which is insulin resistance. So that's a big one. Yeah, it's very, very common. And I just sort of recall a patient, I'd love to hear any cases you'd like to share, but I just remembered a patient I saw, I was about 50 years old and he came to see me and he had a little bit of belly fat, maybe 20 pounds overweight, he'd had a heart attack, had a stent, and was freaked out, you know, at 50 years old to have his heart be at risk like that. And he was on a pile of medications when I saw him. He was on a statin, a beta blocker, blood thinner, you know, calcium, the whole cocktail, blood pressure pills, you know, pretty much everything. And I said, well, listen, are you willing to sort of make some changes? And so he totally revamped his diet. We got rid of all the junk out of his diet, very, very low sugar starch diet, lots of good fats, lots of fiber, got him on some basic supplements, you know, B vitamins, folate, and also fish oil, got him on an exercise program. And over the course of a year, you know, he lost, I think, I don't know, maybe he was morbid, I think he lost almost 50 pounds. He was able to normalize all of his numbers and his blood sugar was high, His insulin was high. He wasn't diabetic, but he was pre-diabetic. And they completely missed it. It's staggering to me that after 30 years that I've been doing this, that the literature has been there, that doctors don't check for pre-diabetes on a regular basis, which affects basically one out of every two Americans or more. And so you check that by measuring insulin, A1C, a glucose tolerance test with insulin. There's ways to look at it. and men look at particle number, particle size, and he lost the weight and he was able to reverse all of his numbers and he was able to get off all his medication, including statins, and his numbers were better off the statins than they were on it by fixing all these lifestyle factors. And he's been heart attack free for the last 20 years. So I just, yeah, I think we are so stuck in this paradigm of treating the symptom, the cholesterol, instead of the cause.
Absolutely. That's critical.
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