29-10-2021
EPISODE 34: DR BEN BIKMAN
RELEASING THE HOT FAVOURITES FROM THE HEALTH EVOLUTION PODCAST! TRANSCRIPT BELOW What a treat getting to chat to this man! In this podcast you will learn where things are going wrong with our health today, and what we can do about it. When we can understand the lever that is insulin - and thus insulin resistance - we gain back a lot of control over our own health. In terms of the lipid values we talked about: In the US, values are expressed as mg/dl: Ben was talking that the ratio of triglycerides to HDL should be less than 1.5. In Australia, values are expressed as mmol/L, the ratio of trigs to HDL should be less than 0.87. I encourage you to buy Ben's book: Why We Get Sick. It is an an excellent read, and while he is a Professor, he puts things in really easy to understand terms. A true gentleman and a lovely man in every way. Benjamin Bikman earned his Ph.D. in Bioenergetics and was a postdoctoral fellow with the Duke-National University of Singapore in metabolic disorders. Currently, his professional focus as a scientist and associate professor (Brigham Young University) is to better understand the role of elevated insulin in regulating obesity and diabetes, including the relevance of ketones in mitochondrial function. You can find Ben on all channels of social media, and here on his website: BIKMANLAB.BYU.EDU. ******** http://www.traceymcbeath.com.au tracey@traceymcbeath.com.au Instagram: @tracey_mcbeath_healthcoach Facebook: Tracey McBeath Health Coach To purchase the Summit Replay: http://bit.ly/longweekendreplay If you are a health practitioner and are interested in learning how to bring low carb in to your practice and reverse insulin resistance in your patients, the Nutrition Network has a number of programs to help. For GP's; Dietitians; Nurses and Health Coaches. The Nutrition Network is run by the Noakes Foundation. To learn more, click here: http://bit.ly/nutritionnetwork Dr Ben Bikman (00:00): It's suffice it to say, virtually every chronic disease has some connection to insulin resistance where the insulin resistance is either explicitly causing the problem, or it's exacerbating it, or accelerating the problem. Tracey (00:13): Hello everyone, and welcome to the health evolution podcast. This is episode 66 and you are so in for a treat today. What an amazing chat I had with the incredible Dr. Ben Bickman, who has so much knowledge. Not only that, he puts this knowledge into such easy to understand terms. So this whole podcast, is talking about why we get sick. It's the title of the new book he has recently produced, and I highly recommend that you buy this book. It is amazing, and there's so much information in here. So that's really what we're going to be talking about. And of course, looking at the fundamental cause of many modern diseases today, which is the fact that our insulin isn't working the way it should. And that's due to lifestyle, genetics, a whole range of conditions that we also talk about. So these are things like type two diabetes, some cancers, heart disease; a lot of stuff that in today's modern world, we attribute to other causes and we just treat the symptoms. Tracey (01:19): But when you look at the reasons and the causes of these diseases - insulin resistance being the number one, and you know that it's actually possible to reverse and turn that around with lifestyle changes, then this podcast holds so much hope. So enjoy it. And I'd like to say a huge thank you to my friend, Carmel, who was kind enough to reach out and offer to do the transcribing for these podcasts. So I will release the podcasts as I get them done. And then when Carmel has the time to do the transcript, she will do that. And I will add it in as soon as it's done. So thank you, Carmel. I love the community I'm involved in. Thank you to you for listening to the podcast. Please, you can do me a favor by rating, by making a nice comment and by sharing this podcast so we can help as many people as possible see the potential that is a health evolution . Tracey McBeath (02:37): Today on the health evolution collective I'm here with Dr. Ben, big Ben, what an honor to have you here on my show. Thank you so much. Ben (02:45): Oh, Tracey. It is my pleasure. Thanks for the thanks for the invitation. Tracey :50): Oh, absolutely. So I have been following you for quite some time now. I absolutely love the work you do, and the way you present it to people. It just is so easy to understand, and you give people so much; so much information to help them with their health. Before we get into your talking about your awesome book, 'Why We Get Sick', can you just share a little bit about, I guess, you know, you're a scientist and professor, but what's led you to writing this book, 'Why We Get Sick'. Ben (03:20): Yeah, again, thanks for the invitation and for the introduction. My focus as a scientist is in general terms, metabolic health, but it was a bit of an unexpected route. Although it didn't take me long to get on it, but my initial graduate work was focused on muscle cells. And I was curious about the process whereby a muscle cell, well, muscles would get bigger and better. But by the end of my masters degree, I was actually far more interested in fat cells. Around that time, a few years prior to me doing a masters degree, I had stumbled across this study that explored the endocrine features of fat cells. Basically it was this to me, a discovery that fat cells actually release hormones, release proteins, and that some of these proteins are pro-inflammatory proteins. And that at the time , was thought to be really the single variable in how someone could be obese, and that would start spilling into type two diabetes. Ben (04:23): It was this obesity induced insulin resistance, which started as a research interest in muscle cells that quickly shifted to a research focus on fat cells. And now I'd say that it's really the tissue or the cells that I focus on most as a cell biologist, namely the fat cells. My focus now is, what are the variables that are stimulating growth of fate cells, the shrinking of fat cells, and fat cells behaving entirely differently; you know the metabolic rate difference. That means I focus a lot on the hormone, insulin, because you really can't understand a fat cell without looking at it, at least partially through the lens of insulin. Tracey (05:11): Now we are going to really understand what insulin is and the term insulin resistance. This is talked about a lot, but I think a lot of people don't really understand this. But before we do, can I ask you, people also talk about metabolic health and I've been guilty of that; you know, I had someone say to me the other day, what do you mean by metabolic health? What does that actually mean? Can you explain that a little bit? Ben (05:33): Right. I suppose metabolic health probably has a different definition according to every kind of biomedical scientist or clinician. To me, I suppose the simplest definition of metabolic health would be that the person is insulin sensitive. But if that's still a little too vague, then I would say metabolic health would be someone having an OK grade, if you will, on the five variables that are conventionally used to indicate the metabolic syndrome. And so in other words, the metabolic health would be someone who has a normal waist circumference (so if they measured their fatness around their waist,) and then second, they have a normal blood glucose, and normal blood pressure. Then the last two are basically just normal lipid levels - normal triglycerides and HDL cholesterol. Those five variables constitute the constellation of what's called the metabolic syndrome. And so I suppose if we use that as a foundation, we could say in turn, well metabolic health then is being OK in all of those categories. But the truth of the matter is back to my original answer. All of those things are very much related to; insulin resistance when they go poorly, or if they're working well, then it's an insulin sensitive person. Tracey (06:54): Makes a lot of sense. So obviously when we're talking about metabolic health, i.e. how our body can make energy, and how it functions, then when we can have those conditions (our body is not functioning optimally); we're tired, we don't have a lot of energy because our body is basically struggling to keep us well . Ben (07:10): That's right. But something you said also prompted another thought, one other perhaps definition of metabolic health would be based on this idea of fuel or energy that you mentioned. So for example, well specifically that would be someone who has metabolic flexibility. At its simplest, it's just this idea that the human metabolism or our energy needs, can shift between the two primary metabolic fuels; that when we've eaten a meal, we go to a glucose burning or sugar burning, you know, blood sugar, that being the primary fuel that the body is using. And then several hours after eating, in other words, getting into this at least mild state of fasting, then we shift to predominantly obtaining most of our energy from fat. So we go to fat burning if you will. So this ability to shift from glucose burning to fat burning very readily when we eat and when we aren't eating, that is a good, also a good definition of metabolic health. But again, that idea is metabolic flexibility. But once again, even that can be seen through the lens of insulin in so far as insulin dictates what fuel we're using. Tracey (08:19): Okay. So let's learn about insulin. So I think firstly, what is its role? I know in the book you go into a lot of detail and I definitely encourage people listening to get the book and really understand it. But just in terms of a brief summary on this amazing hormone. Ben (08:38): Yes, it is amazing. And I think it really is unappreciated given how relevant it is in so much health and disease. Ben (08:46): The most obvious effect or role of insulin is to control blood glucose. And that's how most people understand it. And that's okay. That's fine, because it is a very powerful influence. It is really the single hormone that will lower blood glucose. Whereas, there are multiple other hormones that will increase blood glucose. So it does its job well. Now it's helped with other processes in the body that can also act to lower blood glucose, but that is the most sort of poster child example of what insulin does, it lowers blood glucose. But the truth is far more complicated and that's because insulin affects every cell in the body. Literally every cell in our bodies has insulin receptors. So these little sites where the hormone insulin can come in and dock and bind and then tell the cell to do something. Ben (09:39): And because every cell in the body has these insulin receptors and the various cells in the body play different roles, they do different things. It's not surprising that insulin will do different things at different cells. But the theme of it, the general theme across all of the cells of the body is that insulin tells the cells what to do with energy. It can not only stimulate the uptake of energy in most cells, but it will also then tell that cell what to do with it. And once again, the theme of that is, storage. Insulin wants to store energy and even to the point that it will lower metabolic rate in the body to help the body store more energy. So insulin abhors wasting it abhors breaking things down. It just wants to build things up, including fat in our fat cells and have it get locked away untouched by the body. Tracey (10:34): So without insulin, then obviously we wouldn't be here. If we think about our evolution in times of when food we had to hunt for it, today we don't have to do anything for it, apart from a walk to the supermarket. Without insulin, we wouldn't have got through winter. Ben (10:50): Absolutely. We would have no kind of metabolic insurance, if you will. We would have no energy storage, if it weren't for insulin. It is impossible, to my knowledge. For any organism, from fruit flies to humans, and every other less complicated organisms and humans, and more complicated organisms than fruit flies; insulin must be present and indeed elevated in order for that organism to store any energy. I don't believe it is possible in any other, without insulin. You take away the insulin and immediately this is an organism that loses its ability to store energy in any way, including energy in the liver. And very obviously, loses the ability to store any energy in fat cells. Tracey (11:40): Where has it gone wrong. So you talk in the book, well Jason Fung talks about how, you know, how this has changed so much over probably only really a few generations. I mean, it used to be, you know, we got sick, from dysentery and diseases and things like that. So how has it changed, and why has it changed and what does it have to do with insulin? Ben (12:02): Right. We see obesity strictly through this calorie centric paradigm or perspective. So we look at the fat cell regulation only in the context of, is energy being used or stored, as if the fat cell is just the simple kind of bank account idea. It's just these deposits and withdrawals that are just happening passively. Almost as if the energy we eat it, just comes into the fat cell and comes out when we need it. But that is just not true. We are far more complicated organisms. In order to understand human obesity, I strongly believe we need to consider, yes energy, calories, but also hormones. If we take hormones out of this equation we are doomed, because then we just fall into this cycle of failure of trying to starve ourselves to weight loss. And to your point a moment ago, in this environment in today's world, hunger will always win. Ben (13:05): I stole this analogy from Gary Taubes, a very wonderful author. I'd recommend anyone ,after they read my book, go read some of Gary's books. They're wonderful, but he once shared this and then I stole it and I share it with my students. When I discuss obesity in my patho-physiology class, I present this caloric paradigm and then we start poking holes in it. I show them some of the data that challenges that it is just purely a caloric imbalance. I present this analogy, which is, that I'm having the best chefs in the world come to my home. Everyone's invited. I want you to come as hungry as possible. What would you do to make sure you came to this glorious buffet as hungry as possible? And invariably my hundred and 30 clever young undergraduates come to these two ideas. Ben (13:57): And that is that they would exercise more in the time preceding the dinner and they would eat less. Exercise, more, eat less; these are the two pillars of the current dietary advice that we give people when we need them to lose weight, but hunger always wins. In this environment of readily accessible food, hunger will win. Now, I'm not saying there's no role for discipline and denial of indulgence. I do think that's very important, but I think we can help the person through that, by not forcing hunger on them all the time. And when someone realizes that, they can start leveraging, changing their insulin levels in order to favour this process. They don't have to be hungry; they can be eating in such a way that keeps their insulin down. You are then allowing the fat cells to share their energy, their fat ,with the body to be used and you also shift into that highest rate of fat burning and your metabolic rate, actual accounting for calories, which a caloric purist wants to do. The metabolic rate goes up even to the point where it can raise by almost 300 calories per day, if someone's eating meals that are keeping insulin low. So addressing the endocrine aspect of obesity, namely insulin, I think that the person really has a very effective tool that they now can use that they wouldn't have had otherwise, if they're were just focusing purely on calorie number. Tracey (15:26): Well, you've just really given us all a great reason to drop the belief that we have to be hungry in order to lose weight, because I see it every day. It's one of the biggest challenges with most of my clients, you know, getting them to see that we actually can lose weight. And in fact, we do it so much easier when we are not hungry. And it does come from manipulating insulin if you like, understanding it, working with it, working with those hormones in our body. It's a huge thing because I know certainly until I was 40, that's how I thought. And I was a personal trainer then, and I was continuing to spread that myth that it is about calories in calories out. And if you're not feeling hungry, you're not going to be losing weight. What a revelation to see, we don't have to do that. Ben (16:13): The nuances with insulin and obesity, I certainly touch on that in my book, but there are some other wonderful books, including Jason Fung and Gary Tobbs that I would recommend anyone read to just get more of a well rounded idea of obesity.Because while I certainly touch on that, and I'm a fat cell scientist, I look at it more in the context of overall disease in the book. Tracey (16:34): Absolutely. So then what happens when things go wrong with insulin? And one of the scariest things I read, was that most people are actually walking around, not even realizing that insulin isn't working, that they have insulin resistance. Ben (16:50): It is, I consider it the most common or widespread disorder in the world. And so we are not only, not diagnosing it correctly, but we're also not appreciating its role in other diseases, which means we're missing the potential to treat a patient much, much better. And so basically with insulin resistance, the simplest definition, and you kind of mentioned this, it's just when insulin isn't working the right way at various cells in the body. Now at some cells , insulin's working perfectly fine, but at other cells it is not. And that imbalance actually becomes a problem. And we appreciate the fact that in a body that is insulin resistant, insulin levels themselves are much, much higher than before. So those two features come together; insulin isn't working the right way throughout the body, and insulin levels themselves or itself is much higher. So some cells that are continuing to respond to insulin normally now are hyperactive with their insulin. Ben (17:54): Insulin is now telling the cell to do too much, and the cell is sensitive to that signal, so it keeps doing too much. Then there other cells that aren't really getting the signal very well at all. So those two variables are what comes into play, making insulin resistance, the problem that it is. And in this, we could almost, as you know, from going through the book, it is shocking how many diseases, chronic diseases that we think would have no metabolic origins actually have at their core, an unavoidable metabolic origin. For example, the hyperinsulinemia that comes with the high insulin levels that someone has an insulin resistance. If we look at what that does to the ovaries in a woman, it's profound. The most common form of infertility in women, is a disease called polycystic ovarian syndrome. Ben (18:45): The woman is going through the menstrual cycle. The ovaries are developing a lot of little eggs every month, but in order for all the rest of the eggs to go away, one of them must ovulate. And with that one egg ovulating from one of the ovaries, then all the other kind of budding little eggs will go away. But in the absence of one ovulating, all of those little eggs stick around and they become these big cysts in the ovaries. That problem happens because the woman doesn't get this big estrogen spike, which she needs immediately proceeding ovulation, this big estrogen spike, and one other hormone. Well, many hormones come into play, but estrogen spike is a big one. Too much insulin blocks the ovaries from making that big estrogen spike. Insulin inhibits the process whereby, in fact this is fascinating, but all estrogen hormones were once testosterone, the ovaries convert the testosterone into the estrogens. Ben (19:43): And this happens in men and women. Of course, in women, it happens more in women, thus having higher estrogen levels than men. But that one enzyme that mediates that conversion from testosterone to estrogens is inhibited by insulin. And so the woman who has insulin resistance and high insulin levels at her ovaries, the insulin is directly preventing that big estrogen surge, preventing ovulation. And as a background problem, when she has too much testosterone she'll start to have other problems like more coarse body hair, for example, or acne like you might have in an adolescent boy, who's going through a big testosterone surge. So that's a problem with the ovaries. When we look at the brain, some of the brain's energy comes from glucose from the blood, and insulin mediates some of that movement of the glucose into the brain. Ben (20:36): And so when the brain becomes insulin resistant, it can't get enough of its energy from glucose anymore. And so there's this kind of gap of energy. You know, the brain's energetic need is up here. Glucose used to give all of it to the brain, but now the brains become insulin resistant. And now we have this gap where the glucose can't meet the need, and the person starts to develop brain disorders, including Alzheimer's disease and including migraines, frankly, even migraines are looked at as a bit of an energetic deficit in the brain. So I could keep going. We can talk about muscles, bones, joints, liver, kidneys, eyes; it's suffice it to say virtually every chronic disease has some connection to insulin resistance where the insulin resistance is either explicitly causing the problem or it's exacerbating it or accelerating the problem. Tracey (21:26): So what I find interesting with what you're saying there, that there isn't a neat and homogenous condition. You know, it's not that you're either insulin resistant or you're not, it is a spectrum. And as you said, clearly it affects the body in different parts and in different ways. I just wanted to ask, is that kind of potluck. So if I was insulin resistant in the brain versus somebody else in their ovaries, is that a genetic thing? Is it just pot-luck? How does that work? Ben (21:54): Yeah. That's a great question. There could certainly be some instances of that happening, but that would be very uncommon. The common process would be that the fat cells become insulin resistant first. So there is no total consensus on this. So I'd want anyone to sort of take this with a grain of salt where I'm speculating a bit, but at the risk of sounding smug, it's informed speculation. So I think the fat cells become insulin resistant first, that's the first domino to fall, but then it starts bumping into the other dominoes or basically spreading that insulin resistance around throughout the body. And then what would cause someone to then have say, the ovaries get affected before the liver would, for example, if we take two organs that are just right around the same area; I don't know. Ben (22:46): I'm not sure what would predispose one, what the next issue would be versus the other. But in general, I think it would be safe to assume that the fat cells are the first to become insulin resistant. And as they become insulin resistant, they start leaking fat throughout the body and they start leaking those pro-inflammatory proteins that I mentioned earlier, these what's called cytokines. And those two things are really the key variables, the key parts of the equation that equals insulin resistance; the leaking of fat, the free fatty acids from fat cells and the fat cells leaking these pro-inflammatory proteins. As these start to spread through the body, they cause other tissues to become insulin resistant. Tracey (23:27): So that leaking of fat is that triglyceride marker, is it? Ben (23:31): So actually these fats would be the free fatty acids. So when the the fat cells are breaking down their fats, they are leaked as free fatty acids. The triglycerides are predominantly coming from the fat we make in the liver, which is again, another insulin signal telling the liver to make triglycerides. Tracey (23:52): Okay. All right. So what I'm hearing from you here is that insulin resistance, isn't just a risk factor for type two diabetes. We haven't actually really even touched on that yet. You've talked about all of these other conditions that insulin resistance is the precursor for be it, most people will tend to think that it's type two diabetes that is the biggest risk factor, or the only thing we're likely to get if we're insulin resistance, but that's clearly not the case. Ben (24:22): No, that's right. Yeah. In fact, it's far from a guarantee that the person would progress to full on type two diabetes. What is far more likely is that they would have hypertension, so high blood pressure, fatty liver disease. Then a woman would have polycystic ovarian syndrome; a man would have erectile dysfunction that's also a common early symptom or sign of insulin resistance. Yes. So waiting and that's part of the problem. And I do emphasize the word waiting. When we look at insulin resistance strictly through the lens of type two diabetes, it is unfair to the hormone insulin, which I believe is the more relevant one. And we shift our focus to glucose. But the tragedy of that perspective, if we look at all metabolic health, just through the lens of glucose, as if it's like a progression just towards type two diabetes; then we're only looking at the glucose and we fail to acknowledge the reality that behind the scenes underlying that normal glucose is this ever increasing insulin level where the body has to work harder and harder. Ben (25:28): The insulin has to work harder and harder in order to keep that glucose in check. That is the insulin resistance. In other words, if we looked at the insulin, we would have detected the problem potentially decades, 10 or 20 years before the glucose would have changed, but we don't look at insulin. It has not made its way into just the common clinical diagnostic. When someone comes in for a conventional or just routine lab visit, we always measure glucose. We always measure the lipids. And I think those are fine. They certainly have value, but if we really want to detect insulin resistance, we've got to bring in insulin. We have to allow it into the discussion Tracey (26:10): We do. But as you say, it's not a standard test. In fact, just yesterday, a client told me that a doctor refused to check it, because I give a recommended list of what are their blood tests to go and ask for from your doctor, and one of them is fasting insulin. No, doctor wouldn't do it. When you understand what you're saying, that this is going to tell us what's going on with our metabolic health, 10 to 20 years prior to being diagnosed with type two diabetes. We know PCO for females that usually teenagers are getting that. And then of course, breast cancer is another one I know you've spoken about and being mostly women, listening to these podcasts, that's something I'd love to talk about as well but why is this happening? Ben (26:52): I know isn't it. Well, I often say that it was forgivable. It was forgivable that the focus was exclusively on glucose because of two reasons. One, traditionally the most obvious sign of diabetes was the excessive urine production, what we call polyuria. The person was just urinating gallons and gallons of urine every day. And that was because of the high glucose. And we knew that even early physicians hundred thousands of years ago, because the urine was enriched with the glucose. They'd see animals, dogs would want to come and lick up that glucose and the flies with just swarm to it, to eat all those sugars from the urine. And so the most obvious symptom, polyuria, was directly a result of the high glucose levels. And then the second reason why it was forgivable is that scientifically we were able to measure glucose from the blood far, far earlier than we could ever measure insulin. Ben (27:51): So we had the technology to measure this molecule when we did not have the technology to measure insulin. And even nowadays, as you just mentioned, it's getting the insulin measure is not a simple test. It is a full on blood test at the lab. It often incurs a cost that depending on the healthcare model or in the U S the insurance that a person has, it might not get covered. And so the physician may be reluctant. Even if the physician appreciates the value of insulin, they may be reluctant simply because they know the insurance won't pay for this. I can't bill it and the patient doesn't want to pay for it. Then I have to get in a fight with the patient. So it's unfortunate, but given how it is getting easier and easier to measure insulin, these costs are coming down. It's getting less forgivable to not measure insulin. Ben (28:43): Now I will say there is a poor man's method where if someone has gone into their physician and gotten, or the clinic and gotten a blood test, if they can measure their triglyceride, they will almost always get a triglyceride number and an HDL cholesterol number. And they can take at
