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Benjamin Bikman is an expert when it comes to all things related to insulin resistance. He became interested when he found out fat is actually an endocrine organ and that it also releases hormones. Needless to say, it shifted his interest into focusing on how the body adapts to fat tissue. He has several journal articles, book chapters, and presentations under his belt and is on course to finding out the many factors that promote insulin resistance outside of diet.

Today, Benjamin talks about his research and the results he got from his experiments, why he says what we know about insulin resistance and diabetes is outdated, and the impact he and his team’s research has on the future of healthcar

“The wonderful thing about being a scientist is I get paid to ask questions.” Dr. Benjamin Bikman

On Today’s Episode of the Low Carb Leader:

  • Certain ethnicities react differently to body fat. A mildly overweight Chinese ethnicity have similar problems to a severely overweight Caucasian.
  • Insulin resistance is when the body is not responding to insulin in a normal way.
  • Insulin will always tell the liver to not produce ketones.
  • Insulin resistance is not caused by obesity. In fact, insulin resistance precedes obesity or they occur at the same time.
  • Experiments with cells and rodents can only be so conclusive, but it allows scientist to be more mechanistic in ways you can’t do with humans.
  • Insulin changes how the mitochondria work with fat cells.
  • The difference between brown and white fat cells and how your body uses them.
  • Shivering allows your subcutaneous fat to act like brown fat.

 

Benjamin’s top health tips:

  • Change your breakfast. People are more insulin resistant in the morning than any other time of day.
  • Build your meal around healthy fat. Eating fat doesn’t have an insulin effect.
  • Look at your meal and scrutinize it.

 

The Takeaway:

  • Many physicians would agree type 2 diabetes is reversible but not curable.
  • Researchers should be skeptical of what they think they know and not believe what they are told just because they’re part of a group.
  • You can link a lot of disorders that plague the modern world to insulin resistance. The best way to fix this is improving your diet.

 

Connect with Dr. Benjamin Bikman:

 

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Read Podcast Transcript

029 – The Metabolic Advantage with Researcher and Scientist Benjamin Bikman, Ph.D.

 

DAN:

Hello, and welcome to The Low Carb Leader. You have joined us for Episode 29. On today’s episode we have Dr. Benjamin Bikman. Dr. Bikman is a Ph.D. researcher and scientist at Brigham Young University. He received his Bachelor of Science degree in exercise science from BYU, then his Master of Science in exercise physiology, also from BYU. Then he received his Doctor of Philosophy, his Ph.D., in bioenergetics from East Carolina University. And as he will talk about, he then spent three years working with Duke in Singapore doing research.

 

Benjamin focuses on the metabolic advantage and insulin resistance to a low-carb diet and why people should follow that type of lifestyle in order to maximize their metabolism. He runs a lab at the University where he focuses on this, as well as other things that he will talk about during the interview. I saw Dr. Bikman speak at Low-carb Breckenridge, and he talked about the differences and the latest research in brown and white fat. So that’s a very interesting topic that he will also discuss. All right, so on to the interview.

 

Okay, welcome, Dr. Bikman, to the show.

 

BEN:

Thank you, Dan. It’s a pleasure being here.

 

DAN:

I’m very happy to have you on the show, and I saw your presentation out in Breckenridge, Colorado, and it was an awesome presentation, and you had a lot of new research. So we’re going to cover a lot of things today, but first of all, kind of introduce yourself and go through your education and how you grew up and whatever you want to share.

 

Dr. Bikman’s Background

 

BEN:

Yeah, thank you. My name is Dr. Ben Bikman. I was born and raised actually in a very small town in Southern Alberta, Canada, called Stirling. It’s very small, about 800 people. And in fact my family of 13 kids represented a significant part of the town. And it was a wonderful place to grow up, and it was there that I began loving athletics, and that started me in my initial graduate studies as a master student looking at how the body adapts to exercise. That’s what fascinated me. But then the course of my master’s degree I had read this study from Harvard that found fat tissue was an endocrine organ, that fat tissue itself was releasing hormones. That to me was so fascinating, and that probably was the beginning of a shift from being interested in how the body adapts to exercise and then rather now being interested, which has continued to this day, how the body is adapting to fat tissue. And so my current research interests as a scientist are what are the causes and consequences of excess body fat? And much of that has had me focusing throughout my Ph.D. and my postdoctoral research, and now with my own lab, on the effects and the regulation of insulin and insulin resistance, in particular, how insulin resistance is really what I call the great mediator, linking obesity and even not so obese to virtually every chronic disease. So that’s what’s gotten me to this current point.

 

DAN:

And you have a very impressive CV. I’m looking at it. You got your bachelor’s and master’s in exercise physiology and science from BYU, a Ph.D. in bioenergetics from East Carolina University, and you did your post doctorate fellowship at Duke. And it says you went to Singapore.

 

BEN:

Yeah, isn’t that interesting? So I remember when I was in interviewing for that spot, the guy, the principal investigator I was going to work with wasn’t there yet, and I came out to the University of Utah to interview with him, and he said well, I may be – he said, Ben, I’d love to have you join the lab as a postdoc. Just so you know I may be moving my lab to Duke. And I thought at the time I was at ECU in Greenville, North Carolina, and I thought oh that’s nice. Duke’s not too far. It wouldn’t be that big of a move. And then he said, oh, but it’s in Singapore. Then I say, no it’s not; it’s in Durham. And he says no, there’s a new Singapore, a satellite, a sister campus there.

 

And it was interesting. The Singapore government, wanting to increase the panache, the status of medical research there, invited Duke to open up a campus. But they were also very interested in the unique metabolic differences that occur across ethnicities. For example, Chinese ethnicities – that’s the predominant ethnicity in Singapore – experience metabolic disorders at much lower body weights than the average European Caucasian ethnicity where in other words a mildly overweight Chinese man will have a similar degree of metabolic complications as a very overweight, indeed obese Caucasian man. And so that was part of the umbrella, understanding, or desire of the Singapore government in having a research emphasis in cardiometabolic disorders. My focus even then was insulin resistance, particularly how inflammation and insulin resistance are related.

 

DAN:

How long were you in Singapore?

 

BEN:

We were there for three years. Our middle daughter actually was born there. It was delightful. We really enjoyed it.

 

DAN:

Oh, wow. That’s a long time. So is your middle daughter a resident of Singapore and the US? How does that work?

 

BEN:

No, you can’t have dual citizenship with Singapore like I have with Canada and the US. With Singapore it’s one or the other, so we got her a US citizenship.

 

DAN:

We want to cover a couple topics today, insulin resistance and how it relates to obesity and metabolic advantage. So let’s start with insulin resistance and obesity. And just go ahead and start from the beginning. Talk about what insulin resistance is, how it relates to obesity, and we’ll go from there.

 

What is insulin resistance, and how does it relate to obesity?

 

BEN:

Yeah, so insulin resistance is a state where the body is not responding to insulin in a normal way. It wouldn’t – and I am saying that very deliberately and carefully because it’s not just a global deficiency of response. It’s tempting based on that name, insulin resistance, it’s tempting to think all right, every cell in the body is simply not responding to insulin as well as it was before. But that’s just not quite true. Whereas it’s partly true at muscle, at skeletal muscle tissue, it seems that skeletal muscle really isn’t responding to insulin very well in any way. And that’s part of the problem when someone becomes insulin resistant. They have a harder time developing or maintaining muscle mass, leading to this – potentially leading to a condition called sarcopenic obesity, or muscle wasting and too much body fat. But in another tissue, at say the liver, it’s quite split. Some effects of insulin still happen. Some effects of insulin no longer happen.

 

For example, normally insulin would signal to the liver to store glucose and not release it. But that is broken, if you will, in insulin resistance where the liver continues to release glucose when it’s not supposed to. Yet insulin still inhibits ketogenesis, for example, always. It doesn’t matter how insulin resistant the person is. Insulin will always tell the liver to not produce ketones. And then another tissue like fat tissue, insulin can continue to inhibit the ability – insulin normally will inhibit lipolysis or the breakdown of fat from a fat cell, but in this case it still does it actually. Even though the fat cell is insulin resistant, insulin can still prevent the fat cell from sharing its fat with the rest of the body, thus making it hard for the fat cell to shrink.

 

So insulin resistance, again – and maybe the most accurate yet simple explanation, it is when the body isn’t responding the same way to insulin that it was before. And it really ends up creating a perfect storm, causing virtually – well, in fact, every aspect of what we call the metabolic syndrome, the dangerous changes in lipids, the dangerous changes in blood pressure, insulin resistance has its hand in all of those things. And then you had asked – the relationship of insulin resistance to obesity is complicated where we could go on to PubMed or Google Scholar and do a search for obesity-induced insulin resistance, and we would get thousands of results, yet that’s not really – in fact I’ve even used that term before, much to my shame. But it’s not really accurate because while we do know there is a link between and indeed a direction, obesity can exacerbate insulin resistance, it wouldn’t be causing it. It’s far more likely – and indeed evidence suggests insulin resistance is preceding substantial weight gain. And that would mean that either the insulin resistance is causing the obesity – and that’s absolutely a valid paradigm – or if nothing else, that they are both occurring together. In other words, a body is becoming insulin resistant at the same time it’s becoming overweight. And the common variable there, undoubtedly, would be hyperinsulinemia. In other words, a person is living a lifestyle due to the diet they’re eating or a chronic inflammatory disorder, any of the number of chronic stress, any of the number of causes of insulin resistance. And that’s driving up their insulin. As their insulin is elevated chronically, as they’re experiencing chronic hyperinsulinemia, that is both promoting the growth of fat cells and promoting this general state of insulin resistance where – and just to emphasize then, to make that clear, insulin is a cause of insulin resistance. This is well known. I could take a cohort from campus here, some healthy young students, get them into a clinic, give them this subtle increase infusion of insulin over a couple days and they would be insulin resistant. And then you stop the hyperinsulinemia, and they would be normal in no time.

 

DAN:

A couple questions. So when you go back in time, when did insulin resistance start becoming a bigger issue? Has it always been there, or is it with the onset of more obesity – like what decade did this really start becoming a problem?

 

BEN:

That’s a great question, and hopefully – let’s see, I believe the first published article of insulin resistance was by Wilhelm Falta in – I’m going to – I think in the 1920s or so, right around there. That was the first published words of insulin resistance. We had known that diabetes, mellitus, came in sort of two forms, or at least a spectrum, you know, with two ends. And of course the most obvious had been type I diabetes, even though we didn’t call it that, which is when the patient has – and what diabetes mellitus type I and type II have in common is that they will both be hyperglycemic. So their blood sugar levels are too high. And that’s causing a great degree of urine production, so polyuria. In fact, that’s what that term, diabetes mellitus, is coming from, diabetes – the diabetes term is referring to this siphoning off of water from the body, in other words, too much urine production. And the mellitus is referring to the fact that there’s lots of glucose in the urine. And so it’s quite literally they’re saying diabetes mellitus is seeing excess of urine prod—or an excess of honeyed urine production. So that had been known for quite some time that there were two types of scrawny sort of wasting away version of this and then an overweight version of this, and then it wasn’t until the early 1900s – and again I believe it was Austrian Wilhelm Falta who identified it as insulin resistance, that it was a problem of insulin not working well with type II diabetes, and with type I of course it’s just that there’s not enough insulin.

 

DAN:

Are most of the insulin resistant experiments you do on humans or not on humans? How do you experiment?

 

BEN:

Good question. So for me personally, it is more mechanistic research. In other words, I’m – in my lab I’m using cells in rodents. That, of course, that has drawbacks, of course, significant drawbacks. We can only take our conclusions so far when we want them to be relevant to human physiology. And of course in that case you need humans, of course. But with us the benefits of using cells in rodents is that it does allow us to be more mechanistic. We can explore cellular pathways in ways that you just cannot do with humans. And so the general progression would be that we are on the front lines, if you will, among many other scientists, mind you, where we would make some finding in rodents or cells and then see whether there can be some experiments that we could then translate that to humans. In fact, that’s what’s happening now. What we’ll get to in a bit, I suspect, our initial observations in cells in rodents, that insulin was fundamentally changing the way the mitochondria, the powerhouse of the cell, was working in fat cells. That’s something we found in rodents. We found it in cell cultures working with fat cells themselves, and now we have progressed to the point that we’re doing human studies right now to look at this simple correlation. Is there some correlation between a person’s insulin levels and the degree to which their fat cell mitochondria have been altered?

 

DAN:

Is this research for knowledge, or is it to develop treatment, educate people? What’s the main purpose?

 

BEN:

Well, hopefully – I’d like to think all of the above, really. The wonderful thing about being a scientist is I get paid to ask questions. It’s really glorious to be able to just come to work and think what am I curious about today? In fact, that’s how that whole project, the insulin fat cell mitochondria, started. But absolutely, the hope is if we see similar outcomes in humans, that could start to steer the conversation with regards to application or actual clinical practice. It may give a physician pause before they give their type II diabetic patient insulin in order to control their glucose levels, perhaps. And this is maybe just my ego and my naïveté being revealed here. The physician would stop and say, wait, I’ve seen evidence that by making this patient who already has high insulin, mind you, in the type II diabetic they’re never – they never have a bottoming out of insulin, or rarely, like the type I diabetic does. We say that their insulin is insufficient, and by that it simply means they’re so insulin resistant that they can no longer make enough insulin to keep their blood glucose in control because one of insulin’s jobs is to lower glucose.

 

And so perhaps before the doctor will say here, start taking insulin, he or she would explore other options, perhaps, in fact, lifestyle options, and say well, your insulin is too high already, and that’s making you insulin resistant, which means you can’t control your blood glucose. Let’s in fact just give you a diet that will lower your blood glucose by giving you less starch and then lower your insulin because if I give you more insulin that’s going to make your fat cells more inclined to store fat and not use energy, and that will simply make you fatter. And indeed, that’s what happens. If you give a type II diabetic insulin, on average in six months they’ll gain about 20 pounds of fat.

 

DAN:

The official definition of type II diabetes it says, “occurs when the body either does not produce enough insulin or fails to use and store it properly.”

 

BEN:

Yeah, and so even there, Dan, where they say it doesn’t produce enough, so often people will look at that and say oh, well, they’re becoming kind of like type I. But that’s sort of tricky wording where it doesn’t produce enough because it can’t produce enough. They’re so insulin resistant that they’re already hyperinsulinemic. Their fasting insulin levels are already, especially at the beginning of the disease, their fasting insulin levels are already much higher, potentially several times higher than the average person. But because their glucose levels have climbed we then have that kind of vague, confusing description and say insulin is insufficient or there’s not enough insulin, even though there is in fact plenty.

 

DAN:

That’s an interesting definition, and I researched a little bit, exactly what you’re saying. And I asked this question before to someone else. Do you think that conventional physicians believe that type II is reversible or not?

 

Is type II diabetes reversible?

 

BEN:

This is semantics, but the way you described it, I believe many physicians would agree with in that they would say, “reversible” or “in remission,” but they won’t say “cure.” That’s something that you can’t get a physician to say in most cases. I don’t mean to be derogatory for any physicians that would listen. And I’m sure they’re actually nodding their heads and with – smiling. But to say that they’ve cured diabetes is very rare, and even reversing, I’ve heard more physicians use the word “reverse” or “in remission,” and maybe never heard a physician say “cure.” I will try to prompt them to say, “cure.” So you cured the diabetes? No, no, no, we reversed it. They don’t want to say that. It’s almost like they’re committing to something that I could sue them for later.

 

DAN:

I don’t have the definition in front of me, but I looked it up yesterday, and the American Dietetic Association – they have a new name now – but they talk specifically on their website about type II diabetes, and actually their official recommendation is that the diabetic should make sure they have well-balanced diet full of grains, starches –

 

BEN:

Oh, isn’t that amazing?

 

DAN:

– and plant-based oils. That is their official recommendation on their –

 

BEN:

Yeah, which I would say the evidence refutes every single one of those points, as a scientist. And again, as a scientist I have no agenda here, none. That gives me tremendous power because I can simply say show me the data. I can defend all of everything I would say, everything I’ve said so far, I can cite research for that. But what’s remarkable is that they promote that sort of diet, and yet we’ve known for decades where Gerald Reaven, in I think the 1970s or ‘80s, published a report that put people on the recommended diet of the American Diabetes Association, which the dietetics group is following quite closely. And I don’t mean for this to be derogatory. I wouldn’t want to offend someone hearing this, but I would want them to be skeptical of what they think they know and not just believe what they’re told because they’re part of some group. I am part of the American Diabetes Association, and I don’t at all buy in. But he put them on this diet, the American Diabetes Association diet, and they got worse. Their insulin resistance got worse. And so yeah, sure, put them on that diet, and all that means is they have to take more drugs and more insulin, more medications. In fact, I believe at this point, Dan, there are – just looking at body weight control, body fat improvements, I think there are 21 studies that have been published as randomized clinical trials that have put people on these two macronutrient diverse diets, a low-carb high-fat or a typical low-fat diet. And it is 21 to 0. The low-carb high-fat diet has won for better improvements in body fat losses in every single study.

 

DAN:

That’s incredible. I’m not a clinician, but I work in a hospital as a CEO, and so I know a lot of dietitians, and I know a lot of doctors, and I agree. I highly respect what they do. But from a non-clinician, non-scientist standpoint, as I learned just a little bit about this, it just makes sense. If somebody is diabetic and you feed them carbs that’s – which turns into sugar – that can’t be good.

 

BEN:

No, that’s right.

 

DAN:

It’s the simplest look at it.

 

BEN:

It’s like giving an alcoholic more alcohol and hoping it will cure them.

 

DAN:

Yeah, exactly, exactly. Well, let’s move on to the metabolic advantage because I do want to talk about the research that you’ve done around brown versus white fat and ketone wasting. I found that very interesting as a supporter of ice cold showers in the past. So kind of walk us through your research there, and then we can talk more about your presentation.

 

Metabolic Advantage, Brown vs. White Fat and Ketone Wasting

 

BEN:

Right, yeah. Thank you. It’s been a lot of fun to start to merge some of my interests. As you mentioned, my Ph.D. was bioenergetics, and that is a very deliberate, specific focus on how the body uses energy, and that is – that meant a great deal of research into mitochondrial physiology. And mitochondria represent, as I had said earlier, the so-called powerhouse of the cell. That’s where we are taking the food we’ve eaten, breaking them down to their simplest versions and then turning them into something that we can work with or that we can use to get work out of. And so you had mentioned brown and white fat. And all mammals, humans, even adults, we have brown and white fat. And it is in fact physically white-looking, if we took a little piece out – or, well, it’s kind of whitish, yellowish, or quite brown. And we don’t have a lot of brown fat. Some people have more than others, and we can sort of turn it on or turn it off. And you had mentioned cold showers. In fact that does turn on – cold exposure does turn on – when we start to shiver that does turn on the brown fat that we have, and brown fat’s job, at least as far as we know, is to keep us warm. Little babies have a lot of it, which is why they don’t shiver, and they only start to shiver as they get older. They don’t need to shiver when they’re newborns. When they’re just little infants they have enough brown fat that that keeps them warm. They’re little ovens almost.

 

And so we get older; we start to shift. We lose our brown fat, and more of our fat becomes white fat, and that’s the storage fat like we typically think of fat. That’s part of the body, the tissue in the body that’s interested in taking energy, storing it for later use, which is wonderful. We need it. It’s a tremendously lethal disorder, lipodystrophy, when you can’t make body fat. And so we have these two types of fats, each doing very different things. White fat wants to store energy. Brown fat wants to use it to produce heat. What we’ve found is that when insulin is elevated it starts to shift the profile of fat, and it makes brown fat act more like white fat. In other words, the brown fat that wanted to be wasting energy to produce heat is now not wasting energy, and it’s wanting to store it. And in contrast, ketones produced from the liver when insulin levels are really low, have a contrasting effect. They are making white fat that wants to store energy more like brown fat wanting to waste energy.

 

And I say waste energy, and I mean it, but I wouldn’t want someone to think that’s necessarily a bad thing. In our environment, indeed in this day and age, it’s a good thing. We are consuming enough. In most cases we’re consuming too much caloric – calories for what we actually are expending. The fact that we have now some fat tissue that’s actually wasting some of that energy just to create heat provides what I like to call that metabolic advantage. It allows you to change your diet in such a way where you’re eating low-carb high-fat, and you don’t have to be counting every calorie. You have some wiggle room that you don’t have on a typical low-fat high-carb diet when insulin is higher and that’s making the fat cells be more in storage mode, more in the white fat type as opposed to brown fat. So that’s the regulation of insulin and ketones with brown and white fat.

 

DAN:

How do you test for that?

 

BEN:

Excellent question. We use – we either look at protein markers – in fact, not either. We both look at protein markers. So as fat is more white or brown there will be a different expression of proteins, in particular one protein called the uncoupling protein or UCP1. That represents this protein in the mitochondria that allows it to waste energy and just create heat. And then other way is we actually explicitly just measure the degree to which the mitochondria are working. In other words, how quickly, how busy are the mitochondria? And when the mitochondria is more uncoupled like the type of mitochondria that we have in brown fat, they’re much more active. So you can see that there is this great difference in how busy the mitochondria are in white fat versus brown fat.

 

DAN:

So when your brown fat is wasting, does that mean your metabolism is higher?

 

BEN:

Yes, that’s exactly right. And David Ludwig has evidence to show the relevance of this in humans, that when you start to shift the macronutrients around, as carbs come down and fat begins to represent a bigger and bigger part of the caloric consumption, they do in fact have a demonstrably higher metabolic rate. And we’re simply filling in the gaps. So we would say Dr. Ludwig has shown this. We are potentially providing some explanation for that, and it could be that there is this shift where insulin is low, ketones are up, and that’s altering the profile or altering the behavior of fat tissue making white act more like brown.

 

DAN:

Is there a level of ketosis you need to be in? Is higher always better? I know the range for nutritional ketosis is like .5 to 3 on the scale. Is there a diminishing return at a certain point?

 

BEN:

That’s a great question. I don’t know. That is simply – I love the question. There is no answer to that yet other than I don’t know. That’s not published, and we haven’t found it.

 

DAN:

That’s interesting. When I was talking with Jason Fung about intermittent fasting he said at day five of a fast your metabolism is actually much higher. Is that because you’re in ketosis and your fat is burning at a higher rate? I’m sure there’s many factors, but it seems like that would be one of them.

 

BEN:

Oh, undoubtedly, undoubtedly. In fact, Jason and I have been in touch looking at these very mechanisms of regulation of fat tissue type in instances of intermittent fasting. Yes, that would very likely, among any other potential explanations, be an explanation for it, that we’re shifting – insulin is coming down, ketones are coming up, and that is resulting in a shift in how our fat tissue is behaving.

 

DAN:

I’m kind of laughing because I’m kind of geeking out on this stuff because me and my son, years ago we were doing this cold therapy, and we were always talking about brown fat. And so now you’re like confirming our –

 

BEN:

Yeah, good for you. I’m validating your shivering and suffering from years ago.

 

DAN:

And for those who haven’t tried ice cold showers, it’s pretty difficult, actually. It’s not an easy thing to do. My son is a lot tougher than I am, so he can tolerate it a lot longer. Yeah, it’s interesting. And most of it is around your neck and your shoulders, correct?

 

BEN:

That’s right. Exactly, yeah. The most predominant depots, if you will, or sites where the adults have brown fat is this thoracic cavity. However, there is evidence that when you are cold exposed your subcutaneous fat – and that’s all of the fat that we have beneath our skin, all the jiggly pinchable fat, there’s evidence that that shifts and starts to behave more like brown fat. So you can imagine that represents a pretty enormous source of brown fat and energy wasting and providing even greater metabolic advantage when you start to include that subcutaneous fat depot and not just those few little spots around the chest and neck.

 

DAN:

We talked about the low-carb high-fat diet. So what are some tips you would give our listeners about why they don’t want to be insulin resistant? These are obvious questions why you don’t want to be obese, but some of the damaging effects of that, and then how can you prevent this?

 

Preventing and Reversing Insulin Resistance

 

BEN:

Yeah, so why don’t you want to be insulin resistant? I would say because it is really the great mediator. It is the plague of prosperity that increases the risk, if not outright causes virtually every chronic disease. And Dan, I really mean that quite deliberately. There are certain cancers, like breast and prostate cancers, the most common cancers in men and women, respectively – or opposite. But these two most common cancers are linked. There’s evidence linking them to insulin resistance. Heart disease, absolutely linked to insulin resistance, including atherosclerosis, cardiomyopathy, heart failure, absolutely linked to insulin resistance. Dementia, Alzheimer’s disease, absolutely linked to insulin resistance. Osteoarthritis, the damage of the joints, yes, insulin resistance. Fatty liver disease, insulin resistance. You can go through the list of disorders and diseases that plague us in our modern civilized society, and insulin resistance, if it didn’t cause the problem, it’s making the problem worse. That’s why you don’t want to be insulin resistant. And if you are you want to change things around as quickly as possible.

 

And then how do you change them? It is all about diet. There are other variables. There are other causes. For example, if someone has rheumatoid arthritis, a chronic inflammatory disease of the joints, that is making the body more insulin resistant. There’s only so much you can do there. But let’s assume a person is otherwise healthy, that they don’t have some underlying inflammatory or autoimmune disease. Then it’s diet. It is absolutely what are you putting in your body? And what you’re putting in your body, what is its effect on your glucose levels? In other words is it really starchy and sugary? Appreciate that that will all be converted into glucose when it gets into your blood, and glucose will force your insulin to go high, and then the longer you’re living a life that insulin is elevated, the more insulin resistant and more quickly insulin resistant you’re becoming.

 

And to me some of the simplest strategies – in fact I would say if there was one takeaway, one thing a listener would remember, I would say change breakfast. I’m not saying skip it, although if you aren’t a breakfast eater, then don’t eat breakfast. But if you are a breakfast eater, change breakfast. Everyone in the morning is a little more insulin resistant than they are at any other point in the day, and that something called the dawn phenomenon. So of all the times of the day to eat some bagel, or eat a bowl of cereal, or eat toast, morning is the worst. The insulin effect of that very starchy meal, and sugary, as well in the case of virtually every cereal, will be higher than it would be at any other time of day because we’re all a little insulin resistant. So of all the meals of the day to shift and control your starches, let it be breakfast. Make that change immediately, and then start to decide what you can change with your other meals.

 

For me as a young – as a father and husband with little kids, I am very diligent about my breakfast and my lunch, and those are decidedly low-carb high-fat meals. And someone would say well why high-fat? It’s because fat is the one nutrient that doesn’t increase our insulin when we eat it. You eat protein, you’ll get some insulin effect. You eat carbs, you’ll get an even bigger insulin effect. You eat fat, you get no insulin effect. And so for me breakfast and lunch are the easy meals to control, and then dinner, I always sort of go in eyes wide open in that I will eat what the family is eating and then if I can make slight modifications – although my family is in fact – now that my wife is really on board – we’re fairly low-carb high-fat anyway. But the other day when my daughter, my 10-year-old daughter, for a church activity she needed to make dinner for her family, and she wanted to make grilled cheese sandwiches. I’m not going to not eat my grilled cheese sandwich – I mean the grilled cheese sandwich that my daughter makes for me, you know what I mean? I’m not going to pick the cheese out of it. And so I ate the grilled cheese sandwich, and I loved it. It was delicious. She did a wonderful job. But so for me I very pragmatically apply this low-carb high-fat all in an effort to help control my glucose levels, help control my insulin because I am a young father – well not so young anymore, older every day – but I’m a dad with young kids, and I want to be a healthy grandpa.

 

DAN:

That’s a great approach. Just do what you can. And I agree, there’s moments where you want to share a meal with your family or with friends, and I think that’s important, as long as you’re not eating grilled cheese five times a day.

 

BEN:

Yeah, exactly.

 

DAN:

On the waking up, I’ve read research, and you can confirm this or not, but where you wake up actually burning a lot of fat, and the minute you eat carbohydrates it shuts it off and it kind of shuts it off for the entire day. Is that what you’ve found?

 

BEN:

Yeah, there’s no question. No question. Overnight, depending on what the person ate for dinner that night before and how long it had been, there’s no question insulin is low. You are absolutely in a state of more fat burning than otherwise. And, indeed, the moment insulin starts to come up, as I kind of mentioned earlier, it absolutely slams the door shut. And the fat cells are no longer sharing their fat. So combining that event with the fact that your insulin is even going to be higher than normal because of other hormonal changes happening in the later part of the morning or early morning when you’re waking up, that ends up creating this scenario, particularly unhelpful when it comes to wanting your metabolic function to work with you in lowering your body weight. But it really is, Dan. You can appreciate the tragedy here of all the meals of the day that is absolutely the most high carb meal in the average home where it’s just boxes of cereal, or bagels, or toast, or pancakes or French toast. Boy, you can’t get much more starchy foods than these things I just mentioned.

 

DAN:

It’s very individualized, glucose and everything. I’m just going to share my story. I turn 50 this year. At the end of this year I will, and I think I’ve been more optimistic about my blood glucose and health. I think people are very optimistic about it, but when I really started following ketogenic, lower protein and real low carbs – and I’ve been measuring my glucose and ketones through my blood, and now I have a Ketonix, and I do it through breath. I find in myself just a little bit of carbs will completely knock me out of ketosis. If I eat carbs at night my blood glucose will go to around 100. If I don’t it’s around 70. I ate some sushi like the first carbs in like six weeks, just to help me sleep, but you know – I experiment a little bit. And I usually run about two or higher on ketones, and it actually took me down to .4. So I hear a lot of – so I’m very sensitive in that way, but I hear a lot of people say I’m in ketosis. Or my blood glucose is fine. I think they need to measure it and actually see what foods do to them as opposed to just saying oh, I’m ketogenic or my blood is fine. I think people just need to realize by facts.

 

BEN:

That’s a good point. We really can’t – you can’t tell. You need some objective marker. But I would say – to be truly ketogenic diet is daunting for some, and I wouldn’t want anyone who’s listening who’s afraid of insulin resistance – and we all should be. I’m terrified of it, and maybe just because I know so much about it. I wouldn’t want someone to think boy, I can only eat 30 g of carbs in order to be in – boy, that’s too restrictive. I’m just not going to do it. But there is something to be said for someone who is interested in this. And so I’m just such an advocate of a person who wants to sort of dip a toe in and just start to see what is this like. And so you’re very committed, which I think is spectacular. The fact that you’re measuring your glucose and ketones means that you’re in this sort of upper-level, this elite level of someone who is really committed to ketogenic, and rightly so. Tremendous evidence supports that move. There are people who won’t be but would benefit from it, and so for the average individual I would say look at your meal and really scrutinize it and say what is the relative breakdown of starches versus fat? And for me, honestly, I will look at my meal, and I will say is there enough fat in this meal? That’s my question. Is there enough fat? Am I eating enough fat that it will satisfy me, that it will fuel me and all the activities that I want to do for the day or that I have done for the day, and will it help fuel me the right way where it’s not going to be putting energy into my fat cells to be stored, but rather allowing me to use it, allowing my brain to use something other than glucose, in other words ketones, to help my brain stay healthy? All of these – you know you don’t have to be ketogenic. You don’t have to be in deep ketosis all the time to still get the benefits of a low-carb high-fat diet in keeping insulin low and helping control your risk of disease and your body weight.

 

DAN:

That’s a great point. A real-life example, there’s a lady I work with, Katie, and she’s actually been on the show before with some of our first episodes, and she’s gone to a pretty much low-carb diet. She still eats a cheat meal here and there and eats carbs sometimes, but like she’s lost 31 pounds. It is really easy to lose weight on a low-carb diet, and I know the more fat you eat, people that don’t do this – probably most of our listeners are low-carbers, but when you start eating fat your hunger goes way down. You don’t have to eat every two hours like some people do. I mean it’s easy to go hours without eating.

 

BEN:

Absolutely, I agree, and not only because of the calories you’re getting insofar as fat is more calorically dense than starches, but it’s also helping train your body to use your own fat better. We really do become fat adapted where we can have a prolonged period of time, 12 hours or 24 hours, and not be hungry because hunger isn’t just is there something in my guts? That’s a small part. That’s a very temporary part of hunger. The deeper part of hunger, feeling the need to eat, is are my cells, is my body getting fuel? And if you can use your own fat for fuel, then you are fueled. You won’t sense that hunger as acutely as someone who is really kind of glucose- or carb-dependent.

 

DAN:

That’s so cool. I don’t think people realize that you’re still getting the energy you need; it’s just through your own fat cells rather than bringing food in. Well we’re kind of running out of time, but I do want to ask you one more question. Where is the future of your research going? What do you see five, 10, 20 years down the road in your world?

 

The Future of Insulin Resistance Research

 

BEN:

Thank you for asking. We continue to explore novel causes of insulin resistance. For example, we are just preparing a publication looking at the effects of diesel exhaust. So we’re starting to look at unconventional, non-dietary origins of insulin resistance. And this is relevant as the world is becoming a dirtier place and as we have lots of societies blossoming into sort of modern day, greater degree of pollutions that we have become already somewhat familiar with. So there is causes of insulin resistance outside of diet, although I maintain diet is the most important one.

 

And then in the immediate future it’s perhaps this application of a better understanding of how our own metabolic rate is either working for us or – well, I don’t want to say metabolic rate. How our own metabolic function is working for us or against us, and hopefully it’s increasing awareness of this fact that there really is a metabolic advantage to controlling your carbohydrates. And this is part of the key, part of the lifestyle therapy that is so relevant in improving our body weight and every other cardio metabolic disease that’s related to that.

 

DAN:

That’s extremely interesting. If somebody wanted to get a hold of you, or talk more with you, or find your research to read, how do they get a hold of you?

 

Connect with Dr. Bikman

 

BEN:

Thanks, Dan. There are – the two best ways would be – I’m very active on Twitter, although I’m very new on it as well. I just started last summer because I just was increasingly passionate about spreading this gospel of insulin resistance. On Twitter they can contact me there, and that’s – my Twitter account is @BenBikmanPhD, so it’s b-e-n-b-i-k-m-a-n-p-h-d. And then I have an Insulin IQ. So Insulin IQ is a small little kind of movement that we’ve started, just promoting awareness of insulin and the relevance of insulin in health and disease. And we have a Facebook group, an Insulin IQ Facebook group. And I’m very active on that. People are making posts. And me and a physician and others, part of the team, really kind of service that, if you will, and help provide this strong sense of community there.

 

DAN:

And we’ll link the show notes to these links so people will be able to find you. Well, Ben, we are out of time. Personally this has been an awesome interview. This is the stuff I read about, and having your latest research is so interesting. And I want to congratulate you on your presentation at Low-carb Breckenridge. That was awesome. That was one of the –

 

BEN:

Oh, it was fun. It was fun to be involved. It was my first time at one of those meetings.

 

DAN:

Yeah, I think you need to go on the speaking circuit. I don’t know if your school will allow that, but I’m sure – so thank you so much for being on the show today. I really appreciate you taking the time.

 

BEN:

Thank you, Dan. I welcomed the invitation. It’s always fun talking science.

 

DAN:

Well, good luck in all your research, and definitely we’ll have you on the show, maybe a year from now, and see where you’re at with your latest findings.

 

BEN:

Sounds great. Thanks, Dan.

 

DAN:

Okay, thank you.

 

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