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The Truth About Visceral Fat: Critical Insights | Benjamin Bikman DSH #787
00:40:11
Discover the truth about visceral fat in this captivating episode of Digital Social Hour with Sean Kelly! 🎥 Join Sean and expert Benjamin Bikman as they dive into how visceral fat impacts different ethnicities, focusing on why Asians are more prone to
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- [00:01]
A
And you've done studies on visceral fat. We were talking off camera about how Asians actually are more prone to getting it right. Is it certain foods or diets that are more causing of it?
- [00:10]
B
This is something that has become so apparent globally that some ethnicities have a lower tolerance, if you will, to fat. It's because they've. They're seeing this in real time. So there's this idea of a. Of a fat threshold. Basically, how much fat can your body hold before it becomes pathogenic or harmful?
- [00:29]
A
Foreign Guys, Benjamin Bakeman here, professor at byu. Thanks for coming on today, man. We're going to talk some health.
- [00:37]
B
Yeah, my pleasure. Yeah. My favorite topic.
- [00:39]
A
Yeah. And you do a lot of research on it. So you can actually speak from data and numbers, which I like.
- [00:43]
B
I do, yeah. I mean, as a scientist, I'm the director of the metabolism research lab at byu and this is. I live and breathe.
- [00:48]
A
Yeah. And you've done studies on visceral fat. We were talking off camera about how Asians actually are more prone to getting it right.
- [00:53]
B
That's exactly right. Yeah, let's. I'll be happy to get into it.
- [00:56]
A
Yeah. So what is it? Certain foods or diets that are more causing of it.
- [01:01]
B
Yeah, that's a great question. So just by way of background, this is something that has become so apparent globally that some ethnicities have a lower tolerance, if you will, to fat that, that. I did my postdoctoral fellowship work in Singapore, of all places. You know, beautiful country in Southeast Asia. We loved living there, every minute of it. But why would Singapore invest so much in metabolism and diabetes research? It's because they're seeing this in real time across the various ethnicities that live in Singapore. And it's a beautiful, multicultural kind of melting pot. You can take on one end of the spectrum, kind of European, Caucasian guy, slap 10 extra pounds of fat on his body, and he's just a little chubbier. Everything else is fine. Every clinical marker is totally normal. You take a guy who has the exact same body type, but now he's a Chinese, Singaporean ethnicity. Put those ten pounds on him. Now he's got fatty liver disease, he's got high blood pressure, he has got pre diabetes. And so there's this idea of a fat threshold. Basically, how much fat can your body hold before it becomes pathogenic or harmful? And that Asian body type just has a lower tolerance or capacity to store fat. And it's pure, it's heavy, heavy genetic. Which is to say that the healthiest plant place to store fat Is subcutaneous fat, the fat that you can pinch and jiggle. The most problematic place to store fat is visceral fat, the fat that's tucked within that abdominal space. And that's where more Asians tend to store fat. It's very, very well documented. You can take people, there are studies in men and women. Look at the same percent body fat and the Asian will have more fat centrally, even in the liver.
- [02:47]
A
Wow.
- [02:48]
B
And that ends up being a gateway to bigger liver problems. Fatty liver disease can become what was once a fatty liver becomes a fatty and scarred liver. So you start moving into cirrhosis. So while nutrition plays is a problem globally, and we always used to say the American diet, then it was the Western diet, now it's the global diet. Doesn't matter where you go. From Singapore to the US and everywhere in between, it's high fat, high sugar. So everyone has that pressure to store more fat. And it's more complicated than just calories in, calories out. But different body types have a lower threshold for that fat. And that Asian body type with South Asian, Indian, those are the bodies that have the least tolerance or the lowest threshold that they can handle a little fat. And anything that goes beyond that begins to be problematic.
- [03:37]
A
Crazy. So when you're measuring your body fat percentage, does visceral fat pop up on that?
- [03:40]
B
Well, it depends on how you're doing it. Yeah. So if you're measuring body fat through what is commonly the most common method of doing it, the poor man's method is just these skin calipers. We were doing pinching with these little kind of a pincher device, a caliper that will not in any way account for visceral fat. Then it needs to be like a deeper scan, like an MRI or a DEXA scan. But for everyone listening, they're not going to go do that. Most people don't have the ability to go do that.
- [04:08]
A
It's expensive.
- [04:09]
B
It's expensive. Simple test you can do at home. Get a measuring tape, measure the biggest part around your belly, and then times that by two. And if that number times two ends up being less than your height, it suggests you're okay.
- [04:24]
A
Wow.
- [04:25]
B
It suggests you're okay. Now, it's a little more complicated than that, but by and large, that very, very simple metric waist circumference times 2. If it's greater than your height, that's a huge red flag. If it's less than your height, you got you. You could be okay.
- [04:39]
A
Yeah. I wish more insurance providers covered MRIs, honestly, because, oh, I Totally agree. Yeah, we were talking about mine and I'm 27, just to give people context. And I'm pretty skinny. Yeah, I was a distance runner my whole life. So my body fat was usually in the single digits. And I got an MRI last month. Visceral fat everywhere.
- [04:55]
B
Do you know, was it visceral fat alone, like. So visceral fat sometimes includes fatty liver. You know, today was. Did that include liver?
- [05:04]
A
Yeah, they did all my organs. I did an abdominal scan.
- [05:08]
B
Yeah.
- [05:08]
A
So it was all over my heart, liver, everywhere. I even had a cyst on one of my organs, which, I don't know, maybe kidney. Yeah, I think kidney.
- [05:15]
B
Yeah. So fatty liver disease is a, is a pretty big spectrum where. And that, once again, is a place where Asians just put fat. Fat goes to the liver. That's heavily, heavily dietary influenced as well as a little genetic predisposition. But the things that make the liver get the fattest is alcohol and fructose. So sugar or anything sweet, so fruit juice, even anything that is loaded with fructose. What alcohol and fructose have in common is that they're both almost entirely metabolized by the liver. So the liver has to take all this energy in and it overwhelms the liver's ability to burn. And so if the liver is overwhelmed with burning, it says, well, I'm going to divert this into fat. I'm going to hold on to this for later. And thus the liver starts accumulating fat.
- [05:59]
A
Yeah. So I get a blood test every year as well. And I've always had liver issues. I don't drink, so I don't know what that's from.
- [06:05]
B
Watch your sugar.
- [06:06]
A
Sugar. Even sugar from fruit.
- [06:08]
B
Absolutely.
- [06:09]
A
I eat a lot of fruit.
- [06:10]
B
Yeah. So if it's. Eat. I always say if you're eating fruit, you're generally okay. But be most mindful of the. The most sugary of the fruits, like pineapples, mangoes. But don't drink it. Don't be drinking fruit juice or even smoothies if it's, if it's a concern for fatty liver disease. A paper was just published on this top, just last, literally just last week, one of many papers that looked at the rate at which fatty liver disease was resolved in across two different diets. Exact same number of calories, and they just varied in the sugar content, low carb or high carb. And so protein was kept the same and then just shifted the macros of carbs versus fats, identical calories. But the lower carb diet, which is going to be lower in fructose and sugars had a significantly greater reduction in liver fat. So not all calories are created equal. My worry would be that you would have gone to the doctor and they say, hey, you have a sign of fatty liver disease. You need to eat less, exercise more. That's the same old dumb advice we've been giving people for 70 years. It's not just a matter of calories. You have to consider the hormones that are affected too. But that's a whole other topic.
- [07:18]
A
Yeah. You can't be getting preventative advice from western doctors, in my opinion.
- [07:21]
B
No, no, you can't. No. If this advice worked, we wouldn't be in the midst of the obesity epidemic that we are. And it is global. As much as we want to think this is just a western, even US problem, Far, far from it. The rates of diabetes and obesity related pathologies are. Even the US isn't even in the top 20 when it comes to type two.
- [07:40]
A
Oh, wow.
- [07:41]
B
Look across Southeast Asia. Look across even North Asia. Look across the Middle East. Almost all of those countries are higher than the U.S. dang.
- [07:48]
A
I didn't know that. I thought we were one of the worst.
- [07:50]
B
I know it's a uniquely sort of American thing to think that the US is the worst, but we're not.
- [07:54]
A
Yeah. Just because of fast food and.
- [07:56]
B
I know, I know, but like I said, it's global.
- [07:58]
A
Yeah.
- [07:58]
B
You know, my beloved Singapore, one of my kids was born there. We love Singapore. Talk about fast food. Oh my gosh, it's everywhere. Everywhere.
- [08:07]
A
So they're doing studies on obesity and by 2030 they're saying 1 in 2 people will be obese. That is crazy.
- [08:13]
B
Oh, well, it even gets worse. So my, my most clear area of expertise is a problem called insulin resistance, sometimes referred to as pre diabetes. I've. Most people have never heard of insulin resistance, but it is the single most common health problem worldwide in. And it contributes to all of what I refer to as the plagues of prosperity. All of these chronic diseases that were once unheard of. You know, people dying from heart disease, breast and prostate cancers, Alzheimer's disease, type 2 diabetes. What they all have in common, even forms of infertility, low testosterone, erectile dysfunction, polycystic ovary syndrome. What they all have in common is that insulin resistance contributes or directly causes every problem.
- [08:52]
A
Wow.
- [08:52]
B
So the reason I beat that drum so loudly is if we could focus all of our energy on one single thing, we can start to reduce the risk of literally every chronic disease. And in this case, the focus on insulin resistance is important. Because it precedes the obesity epidemic. So as someone is on that spectrum where they're getting chubby or now they're fat or now they're obese, long before that ever started happening, they were insulin resistant. And so before they ever became obese, they were told they had fatty liver disease or they had high, you know, dyslipidemia. You know, all of these problems that are sort of precursor warnings to a more chronic problem. But the main reason it's overlooked is that we look at metabolic health on lab tests purely through the lens of glucose. We have a very glucose centric paradigm to metabolic health. And so you'd be going in, or you'd mentioned that your grandpa had type 2 diabetes despite being fairly lean, super lean. Of course, he's Chinese ethnicity, which automatically brings a higher risk at a lower body fat. But I bet he would have been going in year after year for his checkups and his glucose levels would have been normal, his blood sugar normal. Normal, normal. Slightly higher. Slightly higher. Now really high. Even when the glucose levels were normal, the insulin levels would not have been. Insulin is the canary in the coal mine. Metabolically, it is the earliest signal that, that metabolic. That we're headed down into this metabolic disarray. And. And so as much as we've had a glucose centric paradigm and glucose has value, but not on its own, it is the Robin to Batman in the story, it's the sidekick.
- [10:28]
A
Wow.
- [10:29]
B
Insulin is the main character we need to be focused on. So if we could shift the metabolic, the clinical paradigm away from a glucose centric perspective to an insulin centric perspective. Insulin can be elevated up to 20 years before the glucose has ever risen. Just imagine if we can start detecting the problems years in advance and then start to make some changes and then get them off that path and keep them on a healthy path.
- [10:53]
A
Yeah, that's an important message. Oh, you hear about people going gluten free but never talking about insulin problems.
- [10:58]
B
No, no, no, that's right. Yeah. So as much as people want to be monitoring their blood sugar, and again, that has value, we have to include insulin in the conversation. Because insulin's main job, its most famous job, because it does all kinds of things, its most famous job is to control blood sugar. Blood sugar levels go up. If that stays up, it becomes lethal. Insulin comes up to basically open doors into cells to allow the blood sugar to come back down, pushing that sugar into the cells, and then insulin, having done its job, will retreat back into the background. But in this case, the more the body has to Fight to keep that blood sugar under control the higher and higher the insulin gets. That is insulin resistance, where the insulin is elevated, but the glucose is still normal. And so our paradigm focused on the glucose has no regard for the insulin. We're just waiting for this to go up.
- [11:47]
A
How could people monitor their insulin? And what are some recommended ranges you recommend to be?
- [11:51]
B
Yeah, yeah, great question. In fact, I'm very grateful we can focus on this because it is the drum I beat the loudest that we have to include insulin in these clinical conversations. Yeah. Unfortunately, insulin is not easy to measure. No hormones are. There is no way to simply, you know, like where you and I could do it on our own, like in our, in our own home, like with glucose. We could prick a finger or slap on a continuous glucose monitor, and we could be monitoring our glucose every moment, literally every minute. Any, any hormone is. It's. We're years away from that type of technology. So there are some at home tests that people can do. And I get, I have no vested interest in saying this. There's companies where they'll send you a little kit and you just prick your finger and then send it in. That's a company called Cifox S I P H O X. But most commonly it's you going into a clinic and just telling your doctor, look, I know you're not going to measure my insulin because no one does. Please check that box because it is. Every lab can do it.
- [12:50]
A
Yeah.
- [12:50]
B
It's just a matter of insisting that it get done.
- [12:52]
A
Is it on a blood test?
- [12:54]
B
Okay, so next time someone goes in, just say, hey, please, physician, please check that insulin box. Because it's that easy. Yeah, every laboratory, every clinic can do this test. It's just not on. They, they're not thinking about it either.
- [13:07]
A
Yeah, I just had a blood test at Nex Health. I think they measured it there.
- [13:10]
B
They could have. So what you want to do is you want, you look at your insulin, your fasted insulin, and ideally in, in US units, you want it to be six micro units per mil or less. Anyone for international audience, you want it to be under about 30 picomoles. That's the cutoff as we look across the different units. Um, but even then, if you have your fasted insulin and you have your fasted glucose, which you probably do from that test, you can put that into a little equation called the homa. H O M A, the HOMA score. And you want your HOMA score to be less than 1.5, and if so, then you're doing fine.
- [13:46]
A
That's good to know. So if your score is way more than that, are there ways to lower it?
- [13:49]
B
Oh, absolutely. That's the good news. That's the good news of the kind of metabolic message here that you can take people who are so insulin resistant, high insulin, and the insulin isn't working well that now their glucose has gone to the range of type 2 diabetes. We published a report, a clinical report a couple years ago, finding we'd taken 11 people who had just been diagnosed with type 2 diabetes, which again is just extreme insulin resistance, and within 90 days, without ever having popped a single pill, no injection, like all these GLP1 drugs, which you know are all the rave these days and I know all about them, never no drug taken. And within 90 days the disease was completely gone.
- [14:29]
A
Wow.
- [14:30]
B
Type 2 diabetes is a disease of diet. The food we eat is the culprit or the cure. We've just been giving all, we've been given all of the worst possible advice when it comes to diet.
- [14:39]
A
Yeah.
- [14:40]
B
The diet that we eat globally and the advice we've been given globally is a perfect way to promote type 2 diabetes.
- [14:47]
A
Absolutely. I used to really fear diseases growing up, but the more I talk to people like you, the more I get hope that it's really preventable.
- [14:53]
B
Oh, yeah, completely. But even then, like your grandpa, when he was diagnosed with type 2 diabetes, the clinical team would have told him in some way, shape or form this is an irreversible disease because the standard of care is to give him drugs. The problem with so many of these so called anti diabetic drugs is that they are focused on the glucose.
- [15:13]
A
Right.
- [15:14]
B
And so they're just saying this is a disease of glucose, that even the clinician has no awareness of the insulin. They might not have even measured the insulin in your grandpa or any other type 2 diabetic. They say glucose is the only thing that matters. Even if we have to push the insulin up, which many of the drugs do, then we'll push the glucose down. And if the, if glucose were the main variable that mattered most, you would think they're going to live a better, longer life. And it doesn't happen. There's no clinical evidence to support that if you push glucose down by bringing insulin further up, that they live longer. In fact, the more you have to push the insulin up in order to control the glucose, this is human evidence. They're three times more likely to die from heart disease, twice as likely to get Alzheimer's disease, twice as likely to die from cancer.
- [15:58]
A
Jeez.
- [15:58]
B
When you give a type 2 diabetic insulin. You are literally giving them more of the very thing that's killing them. They have too much insulin in their body already and too much insulin is the main cause of insulin resistance. And now you're pushing it up even higher. That's like giving an alcoholic another glass of wine and hoping it's going to solve their alcoholism. You are literally killing them faster. By putting them on an insulin based therapy, you're pushing the insulin up even higher and that's what's making them fat and sick. It's not the glucose.
- [16:29]
A
That's so ironic because there's millions of people on these.
- [16:31]
B
Oh, it's a hell of a way to make a lot of money depending on where you're coming from.
- [16:34]
A
Right. Because they, they got to take them every day. Right?
- [16:37]
B
Every day. But that's why they say the disease is irreversible. Because if you go the standard of care, which is drug based, you'll never get off the drug.
- [16:43]
A
Right.
- [16:44]
B
You'll only need more and more dose and more and more medications. Before you know it, you're on seven medications to treat one problem.
- [16:49]
A
So that being said, you think diabetes can be reversed?
- [16:51]
B
Oh, I've literally published papers on it. Wow. So absolutely 100% type 2 diabetes. Mind you, I'm talking, we're talking type 2, not type 1, which is an autoimmune disease. There's no way to reverse that. Type 2, absolutely reversible. Anyone who tells you otherwise is so steeped in the clinical dogma that they can't get their head out.
- [17:11]
A
Wow.
- [17:12]
B
We've literally published papers and there are entire clinics and practices that are based on doing just this.
- [17:19]
A
I think people have been so conditioned, so programmed hearing that it's non reversible. Even myself, I had no idea that you could.
- [17:25]
B
Well, Sean, I'm glad to give you even more good news.
- [17:27]
A
Yeah, that's great news because there's a lot of people getting diabetes right now and again globally.
- [17:32]
B
This is a global problem. I will give talks on this topic. I'm going to be in Oman in a couple weeks, then Dubai a couple weeks after that. I'll be in Southeast Asia in a couple months giving this very message.
- [17:43]
A
And it's bad in Asia, you said it is.
- [17:45]
B
Yeah. And it's part because of this sort of fat threshold. But the mistaken view that a lot of people have is there's a clear link between body fat and metabolic problems. Clear link. However, it's not the mass of the fat that matters most. It's not that we have 10 pounds of fat or 20 or 30. It's the size of each individual fat cell. And that begins to help people understand why. You could have a relatively lean Chinese guy and you have an obese Caucasian guy. And the obese Caucasian guy is metabolically, all his markers look normal. It's because Caucasian people tend to have a greater ability to make new fat cells. And there's a bit of a paradox here, but if you can make new fat cells, that means all of the fat cells are generally smaller and small fat cells are very healthy, happy fat cells. They're very insulin sensitive and they're anti inflammatory. However, if you have fewer fat cells, then as the fat cells get bigger and bigger, they become very insulin resistant and literally begin dumping out these pro inflammatory proteins into the body.
- [18:47]
A
Wow.
- [18:47]
B
Which starts promoting insulin resistance everywhere.
- [18:50]
A
Damn. So that's causing fat.
- [18:51]
B
So it's not the mass of fat, it's the size of the fat cells that matter most.
- [18:54]
A
So that's what causes inflammation then?
- [18:55]
B
Well, yes. That's what causes what we often refer to as subclinical chronic inflammation. And this was my postdoctoral work when I was in Singapore. My biggest, most cited scientific papers are on this exact topic. That when we often think of inflammation, we think of I'm infected or I have an infected wound or an illness or something, or even an autoimmune disease. But when it comes to metabolic health and inflammation is one of the pivotal causes of insulin resistance, this is the kind of subtle creeping inflammation that's coming from these overstuffed fat cells. When the fat cell gets too big, it starts releasing, it's belching out these pro inflammatory molecules called cytokines. And that starts promoting, it starts turning on this subtle inflammation throughout the body. Not like an inflammation like we think of when we have like an infection or an angry wound, you know, but rather this. You measure their blood sample and you say, hey, your C reactive protein is a little too high. In fact, when you would have had your test, I strongly suspect, Sean, if you look at it, you'll probably see something called HSCRP or high sensitivity C reactive protein or something like that. That's also a marker. Now that is, it's actually a better predictor of heart disease risk than LDL cholesterol is.
- [20:08]
A
Whoa.
- [20:08]
B
And it's almost entirely a product of big fat cells.
- [20:11]
A
I need to look into that. My LDL was high also.
- [20:13]
B
Yeah. And you know, the irony once again, sort of this, this dogmatic thinking, LDL is a terrible predictor of heart disease risk. Terrible in Fact, some of the most compelling data suggesting that LDL is beneficial comes out of China where they find that if people have if all other cardiometabolic markers are good, like insulin and C reactive protein, and the LDL is high, it's actually one of the best predictors of longevity.
- [20:41]
A
Wow.
- [20:42]
B
Yeah. People with the lowest LDL have the highest risk of not only serious infections, but also developing Alzheimer's disease.
- [20:48]
A
Disease.
- [20:49]
B
LDL is very protective to the body. It's anti inflammatory. It literally scavenges inflammatory bacteria from your blood and dumps it from the body through the liver into the intestines.
- [20:59]
A
Wow.
- [20:59]
B
LDL is not the villain we've been told.
- [21:01]
A
That's crazy. There's a study for and against everything. So how do you personally vet out the studies you listen to?
- [21:06]
B
Yeah, and I actually really appreciate that you, you state it that way. It's one of the things that I find very frustrating as a scientist where. And I also find it very concerning when people just have these ardent declarations of, you know, I believe the science or we believe science, that's, that's inherently anti scientific. The scientific process is a rigorous pursuit of proving yourself wrong. And when people are making that claim, you know, I believe the science. You shouldn't ever say that. What you should say is, I have a hypothesis and I adhere to that until I prove it wrong. That is science at its core. It is. How can I, can I set up a set of experiments to prove my theory wrong? Okay, it did not prove it wrong. Okay. Then the theory stands.
- [21:53]
A
Right.
- [21:54]
B
Then we continue to pursue this. So how do I cut through all of the nonsense? I look at the quality of the study. Unfortunately, like with ldl, it's a perfect example. Every line of evidence that suggests LDL is a problem is based on what's called correlational data. Now, that stands in stark contrast to causal cause, causal data, or causality data, or clinical data, where in that case, the correlational data is purely coincidence. You look at a full population of people, you. You have them fill out a questionnaire of trying to recall what they'd eaten for the last two years, which is of course horrifically flawed in the process. No one can really remember and no one wants to be honest about those kinds of things. And then you happen to look at what their LDL levels are and look at medical records of who's dying from what. Those are the data that suggest LDL is a problem. But when you actually start to. Even then, however, there's as much data of these correlational studies suggesting LDL is not a problem. Like that study out of China. That's a correlational study. It's prospective where it's following people. Over time, they suggest LDL is beneficial. How do we counter it? It's hard to know. I mean, at the end of it all, I, as a basic scientist, look at the most simple, direct line of evidence I can, which is if I do something to a person or to a model, a rodent model. We sometimes use rodents in our research just because we can get tissue from rodents that we couldn't from humans. You know, it's hard to get a brain sample donor from a human if we want to study brain metabolism, which we have. So we will do rodent work and human experiments. Some what we see is that when people are reversing their type 2 diabetes, they're losing weight. Every metabolic marker is getting healthier. They can have an increase in their ldl.
- [23:36]
A
Wow.
- [23:37]
B
Should we be have them stop losing weight? Should we have them stop improving their type 2 diabetes? No, it would be crazy. And so I look at this, what is obviously an improvement in their cardiometabolic profile, and think, how do we square this if LDL truly is killing them? Well, it's not.
- [23:55]
A
I know a lot of scientists do tests on rodents. Have you seen the results translate pretty well from rodents to humans?
- [24:00]
B
That's a great question, Sean. It really is something that we. That I am always challenging myself with. I'm mindful of the limitations. So the closer you get. So you go from a, you know, I do mammal work. So we'll use mice, which are a good model for genetic knockouts. Like, if we want to try to understand how one particular protein influences metabolic processes, then we use mice. Otherwise, whenever I'm doing typical just kind of diet work where we want to get the animal fat and diabetic, the rat is a great model and does appear to have a very similar response, including a hormone response that we see in humans based on human work. And again, I understand the ethics, I truly, truly do. But the pursuit of knowledge and truth and helping humans live longer, better lives. Like I just mentioned the brain. We've done a lot of papers looking at how Alzheimer's disease is really a metabolic problem. That's not a problem of plaques in the brain. It really is just the brain is becoming more and more insulin resistant. And as it becomes more insulin resistant, it can't get enough glucose from the blood to fuel itself. And so with insufficient fuel, brain function just turns down and dementia begins to result. Mind you, it's not just dementia. It's depression, it's bipolar disorders, it's migraine headaches.
- [25:19]
A
Wow.
- [25:19]
B
All of those have in common this phenomenon of brain glucose hypometabolism, where the brain just isn't metabolizing glucose well. Because they can't get it. But back to the rodents. We couldn't do that in humans. You couldn't get brain samples from a human to measure the mitochondrial bioenergetics and the insulin signaling. So to answer the question explicitly, there are limitations because they're clearly not humans, but it still gives us insight into how the human would respond. And it fits with some of the broader correlational data that we see with humans.
- [25:49]
A
Now, you could clone animals, so the ethics might be shifting your way too.
- [25:52]
B
Yeah, it could. It could. But, man, once upon a time, it was easy. Literally, it was as easy as going down to the pet store and buying animals and doing this.
- [25:58]
A
Yeah, you probably need crazy approvals now.
- [26:00]
B
You do. It's frankly pretty exhausting.
- [26:02]
A
Yeah, that animal movement was. Was a strong one.
- [26:04]
B
Yeah. And look, I mean, I know it's a sensitive topic and. And I really try to be sympathetic to it, but suffice to say, we always, you know, go through every needed approval process, and it is rigorous.
- [26:15]
A
Yeah, well, I think the greater good, you know, because eventually could save lives of humans.
- [26:20]
B
Yep. And. And as far as I'm concerned, a human life is the most precious to me. That's an easy decision.
- [26:26]
A
Yeah. Human over. Yeah. Some people would argue otherwise.
- [26:29]
B
Absolutely. Yeah. And I know they do, and that's why I defend it the way I do.
- [26:32]
A
Yeah, I love that. Have you seen any correlation with sleep and insulin?
- [26:37]
B
Oh, great question. Yeah. So, yes, it's a huge, huge connection. So when I talk about insulin resistance, after I sort of define it and tee it up, which is, again, relevant because it's the most common health disorder worldwide, I then always transition into where does it come from? And there are three primary causes of insulin resistance, and I've mentioned two of them already. One is chronically elevated insulin. The more we are spiking our insulin up by eating or drinking refined starches and sugars, the more the body just starts to become resistant to the insulin. So too much insulin causes insulin resistance. The second is inflammation. When inflammation is dialed up, it begins to directly promote insulin resistance. And then sleep brings us to the third primary independent cause, which is stress. Now, most people don't think about stress when they think about poor sleep, but it is absolutely a stressor. One bad night of sleep, you wake up that next day. And you are markedly, demonstrably more insulin resistant than you were the day before. Wow. And it's entirely because of the stress hormones. Now, when I talk about stress, I talk about it as a professor who teaches graduate endocrinology, which is stress is when the stress hormones are elevated. And the two primary stress hormones are cortisol and adrenaline. Both of those are increased after a poor night of sleep, especially cortisol. If you sleep poorly, your cortisol is substantially elevated that next day, and then the cortisol directly causes insulin resistance. But, Sean, to make it all the more tragic, most people who then have a bad night of sleep try to correct how they feel that next day by taking a lot of caffeine. Caffeine increases adrenaline, and so now they're having a further contributor to their insulin resistance, further just kind of compounding this problem. Whereas one bad night of sleep, the metabolic consequences can be corrected by one good night. The more this starts to spiral out of control where it's a bad night, now my cortisol is up, now I'm drinking a lot of caffeine. Now also my adrenaline is up. All of these things start spiraling together into a bit of a metabolic storm. Now the insulin resistance becomes much more insidious, and one good night is not going to wipe it out.
- [28:47]
A
Crazy.
- [28:47]
B
That's when you really have to start changing these habits.
- [28:50]
A
And as a college professor, you see a lot of students that live like that.
- [28:52]
B
Oh, my gosh. Oh, my gosh, yes, I sure do. Yeah. It's. In fact, I shudder when I look at them and think, did I. Was I ever this stupid?
- [29:00]
A
I have no idea.
- [29:01]
B
No, they don't. No. And mind you, when you're young, you do. You are a little bulletproof. You know, these kids really can shrug off a lot of these metabolic shots pretty well. You know, for me, as I'm nearing 50, I can't shrug them off as well as I used to. But that brings me to my point, which is when you're going through, after you've come out of puberty, which these kids are, the girls already have for a couple years by the time they start college. Some of these boys are not done puberty yet. When they start college, they still got another year or two to go. But typically that's going to set your habits right. So get out and break those habits, you college kids listening as from a college professor. Go to bed early, wake up early. That's the key. And don't mess with alcohol. It screws up your sleep. Even Worse. There's a myth that alcohol helps you sleep better. The reality is you fall asleep faster, but then the rest of the night is horrible. Alcohol is terrible for sleep.
- [29:55]
A
BYU is a dry campus.
- [29:57]
B
Oh, it sure is. And I love every minute of it.
- [29:58]
A
Yeah.
- [29:58]
B
And I joke whenever I go speak at science meetings. I show all the data that we've been generating, all the paper we've published, all the papers we publish. And I always show a little picture of the student who did the majority of the work. And it's always undergrads. And I joke, but I say it with purely affection. When you're at a school where you can't have premarital sex and you can't do drugs and drink, these students are really productive.
- [30:22]
A
I bet.
- [30:22]
B
You know, like it's a Saturday night, they go on a date and they go bowling and go get ice cream. Then they go into the lab and get work done.
- [30:28]
A
I love it.
- [30:29]
B
I mean, these kids are super motivated.
- [30:30]
A
I don't know any other college like that.
- [30:32]
B
No, it's. It's very, very unique. And. And just to be clear, I love every minute of it.
- [30:35]
A
Yeah. I'm a fan, too. These days. I'm a fan. But when you asked me that in college, I would say.
- [30:39]
B
I know, I know, it's hard. It's hard to imagine.
- [30:41]
A
Yeah. Where do you stand on the Ozempic debate? Because that's a hot one.
- [30:43]
B
Oh, it is. I'm so grateful you're bringing this up. Yeah. So all of these Ozempic and McGovy, and it's in their ilk, there's a huge, huge. That's a huge class of drug. Now, they all fall within a drug class called GLP1 receptor agonists. And let me just give a brief break. Background on that. GLP1 is a hormone that we all make from our small intestine. So when food starts coming down the small intestine, certain carbohydrates, certain proteins, certain fats, they will stimulate this increase in GLP1. Other things like yerba mate as a tea, that will increase GLP1. Allulose, a rare sugar. It's not an artificial sweetener, but it doesn't have calories. It has a greater effect than, like, sugar does. So there's. There's a handful of molecules that will increase GLP1. But when GLP1 is up, its main. It has two main mechanisms of action. Firstly, it will inhibit a hormone called glucagon, which is kind of insulin's opposite. Whereas insulin is trying to bring glucose down at any moment in the blood, glucagon wants to push blood glucose levels up. And so when you take these things, GLP1 comes up, it inhibits GLP1's up, it inhibits glucagon, which helps blood sugar levels come under control. But the second effect of GLP1 is that it induces a sense of satiety by really slowing down the intestines. Now let's bring that back to the drugs. When these drugs were first used, they were used at a very relatively low dose. And at that relatively lower dose, its primary effect was to inhibit glucagon. Thus the primary observation was that blood sugar levels would be down. And so it was used as an antidiabetic medication because it helped control blood sugar. However, they noticed that these people tended to eat a little less, that they just weren't as hungry as often. And that is, but is, is what's been really leveraged with these other drugs now, like WeGovy now, where you've just basically all you've literally done is multiplied the dose of the drug.
- [32:42]
A
Right.
- [32:42]
B
And now in addition to inhibiting glucagon, you are really slowing down the intestines. And I mean, really. So, you know, if you and I were to go out and get some lunch after this, food would sit in our stomach for about four to five hours. And then it starts moving out of the stomach through the small intestine and ultimately out through this process called peristalsis, which is just kind of this slow rhythmic contraction along the intestines, moving the food out of the body. However, with these drugs and what GLP1 is doing, when it's up dialed up to an 11 out of 10 now, it's slowing down the intestines so much that food can be sitting in the stomach for up to 24 hours.
- [33:20]
A
Wow.
- [33:21]
B
So people will experience something called ozempic burps.
- [33:24]
A
Yeah.
- [33:24]
B
Where the food is like putrefying in their stomach, creating noxious gas.
- [33:28]
A
Jeez.
- [33:29]
B
Now they're burping up this horrific scent stench because of the food. In addition, people who appear to be somewhat sensitive to it or take a double dose because it's not working as well as it used to, they can freeze, they can paralyze their intestines, which is acutely very lethal. So these drugs, they, yes, they will, they will cause weight loss, but it comes at a substantial risk. Including a paper published in one of the most preeminent biomedical journals, the New England Journal of Medicine, they found that for every, for every 10 pounds of weight lost 6 pounds is fat mass, 4 pounds is lean mass. So 40% of the weight loss is coming from tissues like muscle and bone.
- [34:13]
A
Geez.
- [34:13]
B
Now when you imagine, let's imagine a middle aged or older woman who has a very difficult time making muscle and bone, let's say that she's overweight, as most people are these days. They get on this drug two years in. A paper was published recently finding that 70% of people in the US at 24 months get off the drugs because they get sick of feeling sick. So the patient themselves decide, I don't want to be on this drug anymore. And weight rebounds immediately and within a year or so they've often gone within just a few pounds of where they started.
- [34:46]
A
Wow.
- [34:46]
B
But imagine, think, let's go back to the paradigm I just presented which is for every 10 pounds, 6 pounds is fat mass, 4 pounds is lean mass. Now they get off the drug and they start gaining it all back. One of these weights is one of these masses is going to come back very quickly. One is not, especially depending on your age. If you were a young college aged male, no problem, you can gain that muscle and bone mass back. But if you're a 60 year old woman or even a 60 year old guy, no, good luck, you're not getting that back. You're going to gain that fat back very easily, but you're not going to gain that muscle and that bone back. So you want to try to take it. And all of this isn't to say GLP1 isn't beneficial, it is. So let's find a way to take advantage of it on our own by eating a little better, you know, avoiding the refined sugars and starches, focusing more on whole proteins and fats and other things like yerba mate and allulose that can help take advantage of it on our own, at our own level, at a physiological level, we are not going to get any of those consequences.
- [35:47]
A
Right. Do you eat any carbs and sugar right now?
- [35:49]
B
Yeah, that's a great question. Yeah, I do. I, I generally say that I'm kind of low carb light because I'm a dad, I'm a, you know, I'm a husband father and I eat with my family. So the way I eat, as a kind of middle aged guy who wants to stay lean, I generally for breakfast and lunch eat little to no carbs, sometimes even fasting through one of those meals but drinking, so, so I'm taking in water and electrolytes. But then dinner, I'll have dinner with my family because that's, that's special to me. Family matters most, you know, nothing else should get in the way of me spending time with my family. And it's weird if we're sitting around the dinner table and they're all eating, staring at them all, you know, awkwardly. So I generally am kind of low carb light, but it very much. My dietary pattern is very much informed by my focus on insulin resistance. I want to control my insulin, most importantly, to stay lean, to keep my brain sharp and to keep my body running well. And I want ketones from time to time, too, especially for the sake of my brain. My brain is my money maker, professionally speaking. And ketones are the preferred fuel for the brain. And there are other ways to help with brain health. Things like creatine and other supplements can help with brain health.
- [37:03]
A
Really? Creatine?
- [37:04]
B
Yeah, they can? Yeah, it can. You have very clear evidence on that. But anyway, yeah, so I'm kind of low carb light. I want to keep my insulin under control.
- [37:10]
A
That's interesting to me. I just got a brain scan, so I need to look into that.
- [37:13]
B
Yeah. So creatine is a supplement that most guys think of taking just with regards to muscle performance or athletic performance. And that's absolutely well established. It can reduce the period required to rest and fully recharge the muscle, if you will. But that's not why I take it because I'm not a college athlete. I take it because my brain is my money maker. And there is clear evidence, multiple clinical studies published. You give people with a little bit of cognitive decline, a little bit of early stage dementia, give them creatine, and it's significant improvements in cognition. But that's because cognitive decline is not a plaque problem. It's an energy problem. And when you look at the brain problems as energy problems and anything you can do to enhance the brain's ability to get energy, even through the creatine phosphate cycle, by creatine loading, it makes sense that it would help with cognition and thinking. And it does. The evidence is very clear.
- [38:06]
A
Yeah, I love that way of thinking because growing up, they taught us outside plaque problem.
- [38:09]
B
Yeah. And that's absolutely false. And literally. In fact, Sean, you'll get a kick out of this. Those papers have had to be retracted because the data were literally falsified.
- [38:18]
A
Wow.
- [38:18]
B
Speaking of faults, it was literally falsified data that gave birth to the entire plaque based paradigm of Alzheimer's disease. It's literally built on a lie, and there's never been any good evidence to support it. For those of Us who've long been critical of that view. I'm one of them. Much to my pride. We've. This was very validating when. When this came out that the data had been falsified.
- [38:40]
A
Yeah.
- [38:41]
B
It was a tremendous win for those of us who have been saying this is not working. Alzheimer's and related pathologies are energy, they're metabolic problems, they're not plaque problems.
- [38:50]
A
I can't believe I didn't see that anywhere in the news. When did they publish that?
- [38:53]
B
Yeah, about a year, year and a half ago.
- [38:54]
A
Wow. That should have been everywhere.
- [38:55]
B
It should have been. Yeah. But it's really awkward, right? It's really uncomfortable because we have so many vested interests, so much invested in that paradigm that it's plaque. So many drugs have been developed, so many drugs were skirted through FDA approval while people were covering their eyes and plugging their noses knowing that the data was not good. So we had an ant. There was an anti plaque based drug that was approved by the FDA despite the clinical data suggesting that it had no benefit. And the reason the FDA admitted they gave approval even while admitting that the efficacy was not there, because they said they don't want to discourage further drug development. And so they approved this drug that had no clinical benefit to be used for Alzheimer's and people were taking it even though they knew it didn't work.
- [39:38]
A
Yeah. I'm not sure how I feel about the fda.
- [39:41]
B
We should be deeply conflicted and deeply concerned.
- [39:43]
A
Yeah.
- [39:44]
B
Yeah.
- [39:44]
A
Benjamin, where can people find your work and what you're up to next?
- [39:47]
B
Yeah. Listen, I appreciate you and appreciate your platform. Yeah. I try to put a lot of my stuff on@insuliniq.com so everyone, I got a lot of stuff I'm always doing just to try to preach the metabolic message, but insuliniq.com is the best place.
- [39:59]
A
Perfect. We'll link below. Thanks for coming on, man.
- [40:00]
B
My pleasure.
- [40:01]
A
Yep. Thanks for watching, guys. Hopefully you learned something. I definitely did. Stay tuned for more episodes. I'll see you guys next time.