Cancer. Alzheimer’s. Heart disease. Diabetes. Infertility. While these prevalent and dreaded diseases are caused by multiple factors, my guest says they also all share a common thread: a ubiquitous and too-little-understood condition called insulin resistance.
His name is Dr. Benjamin Bikman and he’s a professor of biology and physiology, an expert in obesity and metabolic disorders, and the author of Why We Get Sick: The Hidden Epidemic at the Root of Most Chronic Disease — and How to Fight It. Ben begins our conversation by explaining insulin’s role in the body, how it goes awry when it comes to Type I and II diabetes, and how giving Type II diabetics insulin to treat their disease actually makes them “fatter and sicker, and kills them faster.” We then turn to the fact that even if you don’t have diabetes, you very likely still have insulin resistance (something helpful to keep in mind during this conversation is that “insulin resistance” is bad and “insulin sensitivity” is good), and the condition’s three primary causes. Benjamin then unpacks how insulin resistance correlates with cancer, obesity, cardiovascular disease, and reproductive health problems, including the fact that erectile dysfunction isn’t a function of low testosterone, but insulin resistance. We then talk about the role of insulin resistance in someone’s susceptibility to COVID-19. We end our conversation with the four pillars of reversing insulin resistance, including the role of diet and physical activity, and how these lifestyle changes can work to help relatively healthy people get healthier, all the way up to allowing diabetics to get off their medication.
I can’t tell you how motivating this conversation was for me to start a habit of walking more during the day, as well as after dinner. I bet it will have the same effect on you.
Resources Related to the Podcast
- Insulin resistance
- Connection between high blood pressure and insulin resistance
- Erectile dysfunction and insulin resistance
- Connection between cancer and insulin resistance
- COVID-19 severity and insulin resistance
- AoM’s series on testosterone
- AoM’s fitness articles
- AoM’s article on the benefits of cold showers
- AoM podcast on intermittent fasting
- AoM article on intermittent fasting
- HLTHCode (We’re not affiliated with this company and they’re not a sponsor, but we tried it, and love it, and have been consuming it daily.)
Connect With Benjamin Bikman
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Read the Transcript!
Brett McKay: Brett McKay here and welcome to another edition of The Art of Manliness podcast. Cancer, Alzheimer’s, heart disease, diabetes, infertility, while these prevalent and dreaded diseases are caused by multiple factors, my guest says they also all share a common thread, a ubiquitous and too-little-understood condition called insulin resistance. His name is Dr. Benjamin Bikman, he’s a professor of biology and physiology, an expert in obesity and metabolic disorders, and the author of “Why We Get Sick: The Hidden Epidemic at the Root of Most Chronic Disease and How to Fight It.” Ben begins our conversation by explaining insulin’s role in the body, how it goes awry when it comes to type 1 and type 2 diabetes, and how giving type 2 diabetics insulin to treat their disease actually makes them, in Ben’s words, “fatter and sicker and kills them faster.” We then turn to the fact that even if you don’t have diabetes, you very likely still have insulin resistance. Now something helpful to keep in mind during this conversation is that insulin resistance is bad and insulin sensitivity is good.
We also talk about the condition’s three primary causes. Ben then unpacks how insulin resistance correlates with cancer, obesity, cardiovascular disease, reproductive health problems, including the fact that erectile dysfunction isn’t a function of low testosterone, but insulin resistance. We then talk about the role of insulin resistance in someone’s susceptibility to COVID-19. We end our conversation with the four pillars of reversing insulin resistance, including the role of diet and physical activity, and how these lifestyle changes can work to help relatively healthy people get healthier, all the way up to allowing type 2 diabetics to get off their medication. I can’t tell you how motivating this conversation was for me to start walking more during the day, especially after dinner. I bet it’ll have the same effect on you. After the show’s over, check at our show notes at aom.is/sick. Ben joins me now via ClearCast.io.
Alright, here we go. Benjamin Bikman, welcome to the show.
Benjamin Bikman: Thanks so much, Brett. I’m delighted to be able to chat with you about all things metabolism.
Brett McKay: Yeah. You are a professor, a scientist of diabetes and obesity, and you wrote a book called “Why We Get Sick,” which you discuss a disease that’s connected to both diabetes and obesity, and we’ll see here in a bit a lot of other diseases as well. Problem with this disease is it’s extremely prevalent, but doesn’t get much attention, and it’s called insulin resistance. So I think to understand what insulin resistance is, you gotta understand what insulin is. So I’ll start off there, what is insulin? What does it do in our body? Where does our body make it?
Benjamin Bikman: Yeah, it’s a great place to start. Yeah, insulin is a hormone that is flowing through the blood all the time. It’s made from these little cells in the pancreas, and unless a person is a type 1 diabetic, then they have beta cells in their pancreas that are producing insulin all the time. And I do mean all the time, whether you’re eating or whether you’re fasting, there’s some amount of insulin always coming out. Of course, it’s higher when you’re eating and much lower when you’re fasting. But insulin’s effect is quite robust, it literally will affect every single cell in the body. Every cell in the body has these things called insulin receptors, which are kind of like doors on the cell that only insulin can knock on. And because every cell has insulin receptors and every cell has a different function in the body, it’s no surprise then that insulin does a lot of different things at different cells.
But if we were to create a theme of insulin’s effects throughout the body, I think it would be best described as insulin tells a cell what to do with energy. And then relevant to that is its effects or is its most famous effect, namely what it does with glucose levels in the blood, where when blood sugar levels or glucose levels are going up, insulin will come in and save the day. Because if glucose levels stay elevated for too long, that’s lethal, and so insulin saves the body by essentially knocking on the doors of certain cells that will then open to allow the glucose to come rushing in. Now, not all cells need insulin to tell them to take in glucose, but some of the big ones do, like muscle cells and fat cells. And so that’s insulin’s most famous effect, and unfortunately that’s partly why insulin resistance itself has become such a problem, though I won’t get ahead of myself.
Brett McKay: Alright. So insulin is a hormone that knocks on doors of cells and say, “Hey, let this energy in.” You mentioned people with type 1 diabetes, their pancreas doesn’t produce insulin, and so they have to take artificial insulin, so what would happen… Maybe this will help understand the importance of insulin, what happens when your body doesn’t make insulin?
Benjamin Bikman: Yeah, yeah. So that is very lethal, which is why a diagnosis of type 1 diabetes 100 years ago… Well, a little more than 100 years ago, before insulin was used or discovered as a therapy, it was lethal within weeks to months, very… Usually, it’d be very rare to live a couple of years with it. And that’s just because the cell… The body essentially doesn’t know what to do with energy, and this is very powerfully affected where you can have a person with type 1 diabetes. And in the absence of insulin, because they’re not making any, they will have a voracious appetite. They are eating thousands and thousands of calories, 4000 or 5000 or 6000 calories a day, and yet their body doesn’t know what to do with the energy, and so the person is wasting away. They look like they are an emaciated prisoner of war. And yet again, they’re eating several times what their actual caloric needs are, they should have ample fat, they should have robust muscles and bones because there’s all that energy, but in the absence of insulin, the cells don’t know what to do with it.
Brett McKay: What do the… Okay. If they’re eating a lot, 5000 calories, 6000, but they’re not storing it or it’s not going to the cells, where does it go?
Benjamin Bikman: Yeah. Yeah, yeah. So, this is… We’re really diving in, this is actually now touching on a bigger debate and a bigger topic, which is what is the root of obesity? We’re kind of alluding to this, although maybe not explicitly, where there’s this idea that obesity is purely a metric or purely determined by caloric balance. And based on the caloric balance, these people should be gaining weight, or at least maintaining body weight. But it introduces the complexity of obesity and weight management, which is that, yes, energy matters, calories matter, but so too do hormones and specifically insulin. So, to reconcile the thermodynamics of the untreated type 1 diabetic or, in other words, the body with no insulin, we have to appreciate that there are inherent wasting mechanisms that start to take care of this.
I just can think of three, and hopefully I can elaborate these as I come through them. One is that metabolic rate itself is going to be much higher than it should be. And this is very well-documented, and we’ve known this for well over 100 years now, some of the most legendary physiologists in the early 1900s, and they really were legends in their field, they identified that the metabolic rate in diabetes was about 20-30% higher than it should be. And so this touches on even studies that my own lab has contributed to in recent years, finding that insulin has a depressing effect on metabolic rate. It will literally slow the action or the rate at which cells are doing their work, which is in some metabolic rate as we define it. So they have a much higher metabolic rate than they should, so they’re burning several hundred more calories than they should.
They also have a wasting mechanism built in with regards to the excess glucose, that when glucose levels are chronically elevated, and this touches on what I said a moment ago with regards to chronically high glucose being lethal, you overwhelm the kidney’s ability to keep all of that glucose in the blood. And now you start spilling glucose into the urine, and that starts pulling water with it, which is why the untreated type 1 diabetic has such a high urine production. But it’s that loss, the person’s losing a few hundred calories or so of glucose in the urine.
And then the last part is what’s happening, too, with fat metabolism and the production of ketones. When insulin is absent or low, the body is in an exaggerated state of fat-burning. And that sounds kind of like pop culture language in a way, and I don’t mean for it to, fat-burning versus sugar-burning. But glucose or sugar and fat are the two primary fuels for the body, and insulin is what dictates which fuel is primarily being used by the body. If insulin is elevated, the body is primarily using glucose or, as I like to say, sugar-burning. If insulin is low, the body is primarily burning fat or fat-burning, of course. When the body is in that fat-burning state for a prolonged period, but roughly what could happen within the span of a day, it’s burning so much fat, it’s burning more than it needs. And this excess, if you will, start… Is converted into ketones. So ketones are essentially the byproduct of fat-burning.
But they do have a caloric value roughly comparable to that of glucose. And in ketosis… Or in the state, it’s gone beyond just mild ketosis, this is ketoacidosis, where there is 10 times more ketones being produced than the average person could ever get to, because the average person will always have some insulin. But be that as it may, the untreated type 1 diabetic has an incredibly elevated rate of ketone production or ketogenesis, and when it gets to a point, now they are once again wasting this energy. Again, ketones have a caloric value that we would say, “Well, do you have to store the calories or you have to burn them?” Well, in this case, you’re just dumping them from the body, like the person is with their glucose, and the person is excreting ketones in the urine at a very high rate, and excreting ketones in their breath. And again, that means every time the person is exhaling, they are literally exhaling molecules that had a caloric value.
And so there are these built-in mechanisms to sum it all up. There’s the changes in metabolic rate, the changes in ketone production and ketone wasting, and the changes in glucose wasting through the kidneys. All of these allow us to appreciate the absolute necessity of insulin in storing energy. And I don’t just mean fat cells. You could say that we’re storing energy by helping muscle cells form protein and bones form protein, and helping the liver know what to do with energy, creating lipids to be stored, for example. The liver can’t do that if insulin is not there to tell it to. So, this is, as I mentioned, of course, touching on the bigger topic of obesity and weight management, but if we just bring it back to the diabetic, it certainly, once again, is proof positive that while calories certainly matter when it comes to having a body that can store energy and be healthy, it needs a signal to tell it what to do with the energy.
Brett McKay: Okay. So, type 1 diabetics, if your body doesn’t have insulin, your body basically isn’t gonna use that energy you give it through food. It’s just gonna expel it, ’cause it doesn’t know what to do with it, ’cause there’s no insulin to knock on the doors of cells. Let’s talk about insulin resistance, so these are people who their body is making insulin, but for whatever reason, the insulin is no longer… The knocks aren’t working as effectively. So explain in simple terms what happens. How does insulin resistance happen?
Benjamin Bikman: Yeah. Yeah, yeah. Awesome, wonderful. Yes. It’s an interesting kind of paradox, because if we were just comparing now the untreated type 1 diabetic where there’s no insulin, it would be tempting to conclude, well, if insulin isn’t working, which it isn’t in insulin resistance, then they should have the exact same symptoms or same consequences. Right? It should be the same. No insulin should be comparable to insulin not working. But, in fact, it doesn’t play out that way at all, because insulin resistance is just a little more complicated than that. So, insulin resistance, to define it, is… I think the best analogy is like a coin that I’m holding in my hand between my thumb and my index finger. A coin, and I call this coin insulin resistance, the coin itself. Now, this coin has two sides, and there are two aspects to insulin resistance. One is, as the name suggests, insulin isn’t working the same way that it used to. Now, the complexity there, the nuance is that that is not to say that every cell is failing to respond to insulin. If that were the case, then insulin resistance really would just be another… It would be identical to the untreated type 1 diabetic. That is not the case.
And so, by insulin resistance at the level of the cells, we have to more accurately say insulin isn’t working the same way at some cells. And that’s important, because while some cells are insulin-resistant, like some fat cell effect or some muscle cell effect, it’s not even global within the cell itself. It’s some of insulin’s effects may be compromised in some cells, but in those very same cells, some of what insulin is telling the cell to do can continue to operate just fine. And, in fact, the liver represents a tremendous example of that. The liver… Insulin will normally tell the liver to inhibit ketogenesis, in other words, block the production of ketones. Well, insulin can tell the liver to do that always. Whether the liver is insulin-sensitive or insulin-resistant, insulin always is able to inhibit ketogenesis.
In contrast, on the insulin-sensitive liver, insulin would tell the liver to store glucose as a molecule called glycogen. It basically is telling the liver, “Hey, we got a lot of glucose in the blood, I need you to pull it in and store it for later use.” But when the liver is insulin-resistant, that doesn’t happen anymore. And now, in contrast to the liver storing glucose as glycogen, it’s breaking down the glycogen, releasing that stored glucose into the bloodstream, increasing the glucose even more, which makes insulin have to work harder, and now we’re just self-perpetuating the problem, or it becomes a vicious cycle. So that was the one side of the coin, that some cells are failing to respond to insulin like they should.
The other side of the coin, and this is very important, is that blood insulin levels are elevated. This is a condition that we call hyperinsulinemia. But this matters especially because of the cells that still respond to insulin, because remember only some of the cells have become insulin-resistant. Many of them still have a normal sensitivity to insulin, they’ve never become insulin-resistant. Now they are simply suffering because there’s too much insulin telling them to do too much, and the best example of that, among many, is what happens in the ovaries of women. Insulin will normally inhibit the production of estrogens from testosterone, so it’s a little known fact that all estrogens in men and women come from androgens, and testosterone being the prototypical androgen.
So there’s this conversion from androgens to estrogens, that’s how it always happens. In the ovaries, it happens more than it does in the testes. But insulin inhibits that process, and so now the ovary, who has perfect insulin sensitivity, is flooded with the insulin that is rising in this condition called insulin resistance, and so there’s too much insulin inhibiting the production of estrogens too much. And thus her ovaries are releasing too few estrogens to maintain a normal ovulatory cycle, and unfortunately, too many androgens for her body, giving her, say, the acne or the excess body growth that comes along with polycystic ovary syndrome or PCOS.
Brett McKay: Okay. So just to summarize here what’s going on. Insulin resistance, some cells… Is whenever there’s too much insulin, some cells become basically desensitized to it, not all cells, some cells.
Benjamin Bikman: Yep.
Brett McKay: And then as a consequence, the body makes more insulin to compensate for that. And that can become another problem, like you said, the other side of the coin, because some cells that have no problem with insulin insensitivity get flooded with insulin, and that can cause cascading problems.
Benjamin Bikman: Yeah, perfect.
Brett McKay: Okay. So, I think when people I’ve heard talk about insulin, they typically see it connected with blood glucose, and that maybe they are a type 2 diabetic or they’re told by the doctor, “You have pre-diabetes ’cause your blood glucose level is too high.” You make the case in your book that blood glucose is a useful marker, but you make the case that it’s probably more useful to focus on insulin levels as opposed to blood glucose levels. Why is that?
Benjamin Bikman: Yeah, yeah. I’m so glad you’re allowing me to elaborate on this ’cause it’s something… It’s sort of one of my missions in… My professional mission in life. My main mission, of course, is to be a good husband/father, my professional mission is to spread the word of insulin. So, yeah, glucose has become the focus in any conversation of metabolic health, in any invocation of insulin almost always still will do so with a primary focus on glucose. And I think that is what has led us down the problematic path that we find ourselves on. As you and I both said now, one of insulin’s… Well, insulin’s most famous effect is what it does to blood glucose, but that paradigm, that glucose-centric paradigm is what has, again, put us on this problematic path. And it’s best viewed temporally.
So if we look at an individual who’s living their lives and living his or her life through… Over the years, let’s say this fellow is progressing towards type 2 diabetes, and the fact is most of us are, and over these years, he’s becoming more and more insulin-resistant. And so if we had these two variables that we were tracking, we have glucose that we can track, and we have insulin that we can track. What’s been happening over these years, and this is a process that can go on for decades the insulin is climbing, it’s getting ever higher, higher and higher and higher, but it’s working well enough to keep the glucose in check.
And so every year, the patient is coming in for a visit, and they’re gaining weight, they may have hypertension, high blood pressure, they may have infertility. And because the glucose is staying normal, the physician is simply prescribing an anti-hypertensive medication, or “Here’s a fertility medication,” not knowing, because our paradigm doesn’t allow a focus on insulin, that insulin has been waging this silent war behind the scenes for 10 or 20 years. And then it’s only when the body becomes so resistant to its own insulin, even though it’s swimming in a sea of it, that now the glucose starts to climb. Insulin simply can’t keep the glucose in check anymore, reflective of this growing insulin resistance. And now the glucose starts to climb, and then 10 or 20 years later, we finally detect the problem.
And again, you can see the tragedy here, we’ve detected the problem much, much later than we should have, if we had been looking at it through an insulin-centric paradigm. And so, in other words, insulin is a much more sensitive marker, a much earlier indicator of metabolic disarray. But the tragedy in that paradigm persists when it comes to treatment, because now the patient who has this mounting blood glucose level, very often they are given insulin as a therapy. And already, I’m sure the listeners can see the problem with this. I just described this person’s situation, which is that they’re swimming in a sea of insulin, and now the glucose starts to climb. This is not a disease of insufficient insulin.
It’s a disease of too much insulin, we’ve become too resistant to it. But the traditional paradigm is that it’s a glucose disease, so they will, the average clinician, look at the mounting… The rising glucose and say, “Well, you know what? Here’s insulin, just take some insulin, and this will push the glucose down.” And it will, it does, by putting the Type 2 diabetic or the person who’s moving towards type 2 diabetes on insulin as a therapy, it will help lower their glucose, but the tragedy is not a single clinical outcome improves once we put a Type 2 diabetic on insulin. And in fact, the more aggressively we give them insulin to lower their glucose, they become three times more likely to die from heart disease and twice as likely to develop Alzheimer’s Disease, twice as likely to die from cancer. And they gain a significant amount of weight, they gain about 20 pounds in six months. So when we do this, when we ignore the insulin, and we give them even more of what they already have too much of, then we make them fatter and sicker, and we kill them faster. Because this is not… It’s not a glucose disease, it’s an insulin disease.
Brett McKay: Okay. And so just to clarify, there is a distinction there, Type 1 diabetes, the problem is not enough insulin, they’re no insulin, so you have to give insulin?
Benjamin Bikman: Yes.
Brett McKay: Type 2 diabetes, the problem is too much insulin?
Benjamin Bikman: That’s exactly right, yeah. Brett, so that… Allow me just to elaborate just for one second. This is… I think it’s tragic that we’ve ever put those two diseases together. That we call them diabetes, both of them, Type 1 and Type 2, I think is a tragedy, because it suggests that they’re similar diseases when in fact they’re opposites. As you just said, Type 1 diabetes is a disease of deficient insulin, type 2 diabetes is a disease of too much. And so giving… We haven’t… I haven’t elaborated the paradigm this way, but we’ve already elaborated on the fact that insulin resistance is a state of too much insulin, but the fact is too much insulin is a driver of insulin resistance, not that we’ve really dived into the causes of insulin resistance yet. But elevated insulin is what I consider a primary cause of insulin resistance. And so by giving the Type 2 diabetic insulin, we’re making the problem worse, in part in the kind of harsh analogy, but that’s like treating an alcoholic with another glass of wine, or treating someone with hyperthyroidism by giving them more thyroid hormone.
Brett McKay: Okay. Let’s talk about what’s going on, what causes insulin resistance. And you… In the book you say that this… The number of people in our population, particularly in Western industrialized countries, and it’s expanding beyond the West, you’re seeing it increase all over the world, the number of people with insulin resistance is on the rise. Do we have a figure how many people have or perhaps have insulin resistance? ‘Cause as you said, it’s usually you don’t know till it’s too late, till the blood glucose is measured, ’cause those people aren’t measuring their insulin levels. So do we have an estimate about how many people have insulin resistance or what percentage of the population?
Benjamin Bikman: Yeah, yeah, so we do have an estimate. In the United States, this shouldn’t be a surprise, we actually have a pretty good idea. Now, I understand a lot of people like to criticize the United States, it seems. And I’m born and raised in Canada, and I’ve lived in multiple countries and traveled to dozens and dozens of them. No one likes to insult the United States like Americans do, unfortunately, so we tend to be our own most harsh critics. But the problem is bad here in part because we’ve documented it so well, but evidence suggests that in other countries it’s worse in some of them. So some of our best numbers… And I believe this is an accurate assessment, a paper published a couple years ago from University of North Carolina, Chapel Hill, they suggested that 88% of US adults are considered metabolically unfit. Not surprisingly, in their manuscript, they consider that a, “alarmingly low level of fit individuals.” And I agree, that is alarmingly low. They base that assessment on whether or not the people had some markers of the Metabolic Syndrome. I’m sure everyone’s heard of this, this is the constellation of problems that encompasses waist circumference, high blood pressure, high glucose, and dyslipidemia, in other words low HDL or high triglycerides. Mind you, no mention of LDL importantly. But this… They found only 12% of US adults were good in all five of those metrics.
That’s a problem. And I think it’s relevant to this conversation simply because while they were doing this with the stated objective of determining the Metabolic Syndrome prevalence, the Metabolic Syndrome used to be called the Insulin Resistance Syndrome. And so to me and to others who are scrutinizing this, these are markers of insulin resistance. So potentially almost nine in 10 adults in the United States have some degree of insulin resistance. Now, as I alluded to, this is not a local problem, and I appreciate you mentioning that too, the problem actually might be worse in Mexico, it could be worse in several countries in the Middle East. In fact, the most diabetic countries, type 2 diabetes, on the planet, I think eight of the top 10 are in the Middle East. It’s a tremendous problem. And then I think the 10th was a country in South East Asia, a country that I love and I’ve studied… Done research there in the country called Singapore. But even throughout some countries in Southeast Asia we have a problem. So the United States, yes, it’s an enormous issue here, but we don’t… We’re not in the number one spot of this dreaded list. And again, we’ve not talked on the consequences, but it’s part of the problem is we simply don’t detect it soon enough, we don’t talk about insulin enough, we just talk about the glucose.
Brett McKay: And as we said, that’s… The glucose is just a marker of insulin resistance.
Benjamin Bikman: That’s right.
Brett McKay: Okay. So well… Okay, it’s been increasing among… Across the population, nine in 10 adults, 90% of the adult population probably has insulin resistance. I imagine was this a problem 20, 30, 40, 50 years ago, or has it been getting worse? And if so, do we know why it’s getting worse?
Benjamin Bikman: Yeah, yeah. So there’s no question this is getting worse. All of these diseases we have nowadays are disorders that our ancestors couldn’t have even dreamed of, and partly because they were more worried about infections than we are. Our… That really is the single most telling difference, is the presence of antibiotics that we have now and the breadth of them, and the efficacy of them as a testament to science, but these diseases that we all think are distinct things like cancers and Alzheimer’s disease, heart disease, fatty liver disease, infertility, they all share a common core of insulin resistance. Now, I’m not silly enough to claim the insulin resistance is the only input or the only cause of these diseases. No, they’re all multi-factorial, but fact is, insulin resistance is a common and prominent thread woven through all of them, and the general premise of my book is that if our ongoing reluctance to acknowledge the relevance of insulin is partly what’s putting us in this position and it is wholly a function of the environment we live in and almost totally a function of the food we eat.
Brett McKay: Okay, so yeah, I wanna dig deeper into like some of the problems that are related to insulin resistance, so you… Okay the environment, so what is it about our food today that basically causes the body to have to create too much insulin, which will cause insulin resistance?
Benjamin Bikman: Yeah, so I consider there to be three primary causes of insulin resistance; two of them, I have nothing to do with food, and I’ll start with them just because they’re so simple, but they are real. And I consider these to be primary causes because you can cause insulin resistance with all three of these that I’ll elaborate on in a moment, in every bio-medical model that scientists will use to study insulin resistance, and that includes isolated cells like cells that are grown in little petri dishes in the lab, or it includes laboratory rodents like mice and rats that we will sometimes use in our studies, and then humans the pinacle of all life on the planet, even in humans, who can cause insulin resistance with these three stimuli each on their own. So they are independent. One of them is stress. And so the prototypical stress hormones, cortisol and epinephrine, will cause insulin resistance in all three biomedical models, and this is relevant to humans, of course, it’s mostly relevant to our sleep habits because bad sleep leads to elevated stress hormones, and that will in fact cause insulin resistance, even after one bad night of sleep, now thankfully, one good night of sleep can correct it, but it just touches on the relevance of the stress hormones, so stress is a primary cause.
Another one is inflammation. Now, inflammation is a term that it’s almost cliche, it’s thrown around so often these days, and I’m using it quite carefully. So the activation of these, what we could call inflammatory pathways within cells or these, the biochemical process of activating these immune-related pathways will cause insulin resistance in cells in rodents and humans. And so it’s a primary cause, and this is most obvious in conditions of autoimmune diseases, where if someone has an autoimmune disease and the autoimmune disease is very active or aggressive for a period of time, ’cause it tends to ebb and flow, then the insulin resistance will be quite pronounced.
Then as the autoimmune disease subsides for a time, so to does the insulin resistance and they’re insulin sensitive again. Now, I don’t elaborate on those too much because it’s hard to control them. If you’re talking to someone and you say, “Well, lower your stress and lower your inflammation,” they say, “Well, thanks.” Easier said than done. The thing that is very potent now is the elephant in the room, and that’s the food we eat. Essentially, the problem is we have created a diet and a way of eating that is spiking our insulin all day, so the average individual wakes up in the morning and overnight insulin has been coming down and helping the body be a little more insulin-sensitive and frankly get into a higher state of fat-burning, which is why some people may be in a very mild state of ketosis upon waking.
And tragically what do we do? Well, breakfast has become basically a dessert, and we eat a starchy sugary breakfast; it’s some starchy sugary cereal or a starchy bagel, or starchy toast or sugary orange juice or something, or a sugar-loaded coffee. We then spike her insulin rapidly. And we know that an insulin spiking breakfast, and by that, I mean there’s clinical studies to prove this in humans by spiking insulin for breakfast, we have quicker return to hunger. So we get hungry or sooner, and so then two or three hours later, what do they do? They spike their insulin again, right as in the Sun was cresting and about to come down, we spike it again with a starchy mid-morning snack, and right when insulin is about to come down, we bump it up again with our lunch, and we do it again in the afternoon, again for dinner and again throughout the evening with our snacking. So the average person is living every moment of their waking life in a state of elevated insulin and frankly into maybe half of their sleeping time too, because insulin will take a few hours to come back down. And that chronically elevated insulin is a primary driver of insulin resistance, and of course that I think really does point the finger at our excessive consumption of refined carbohydrates.
Brett McKay: We’re gonna take a quick break for words from our sponsors. And now back to the show. Okay, so yeah, the world is increasingly eating more, just pounding away, processed carbs, sugar, and we’ll talk a little more later on the end about what we can do to become more insulin-sensitive, but besides food, the other thing you talk about is we’ve become more sedentary. What role does movement play or the lack of movement play in insulin resistance?
Benjamin Bikman: Yeah, yeah, one of the nice things about the way the muscles are built is that the moment the muscle starts well, moving, contracting and relaxing, it becomes able to pull in glucose without the need of insulin. In other words, it opens those glucose doors even though insulin isn’t there knocking on them. And so it’s an insulin independent mechanism of glucose uptake. And this is very relevant; you can take a person who eats a starchy sugary snack or meal, and if they just get up and go on even a modest walk of 10 to 20 minutes, their glucose levels will not get as high as they would have; it’ll only go to about half as high it would have, and it comes down much, much faster. The same goes with insulin, because yeah, you’re flushing your body, your blood with all that glucose you just ate, but the moment you start moving those muscles, well by mass, muscle represents the primary tissue in the body, and it is overwhelmingly the main consumer of glucose. Roughly 80% of the glucose that gets cleared from our blood goes into the muscle. And so if we just get up and start moving our muscles around, we start just pulling in the muscles, begin greedily consuming all of that glucose.
And so insulin right when the beta cells of the pancreas, we’re about to load the system with all that insulin, they sense that the glucose is dropping rapidly on its own, and so what would have been enormous insulin release becomes a very modest insulin release because the muscles have essentially saved the day. So that’s at least some part of the power of exercise used in that acute moment after eating a starchy or sugary meal, but the implications are broader, where if someone is exercising frequently, especially if it’s a higher intensity exercise, then they have the potential to gain or at least retain muscle mass, and as I mentioned, muscle is the main consumer of glucose. So if you have more muscle, you simply have more little mouths that are gonna eat up all that glucose from the blood, and this certainly plays out; people with higher muscle mass can clear glucose much, much faster from the blood than people with less muscle mass, even if they weigh the same.
Brett McKay: Okay, so I think we have a good idea of what insulin resistance is, what causes it, and as we’ve said before, when people think about insulin resistance, they typically connect it to metabolic conditions like pre-diabetes or type 2 diabetes, but in your book, Why We Get Sick, you talk about, well, no insulin or too much insulin, not only contributes to diabetes, but it’s contributing to other sicknesses as well, and you’ve kind of mentioned it throughout our conversation, the first one is heart and cardiovascular disease. What role does insulin resistance play in those?
Benjamin Bikman: Yeah, in fact, that’s an enormously intimate association. Heart disease is a very broad term that applies to a lot of specific cardiovascular issues. The most common is hypertension or elevated blood pressure, and so maybe I’ll just focus on that one for the sake of time, but with insulin resistance, insulin has a direct effect on controlling blood pressure. The most obvious one is that insulin, when it’s elevated, will force the kidneys to hold on to salt. Normally the kidneys, as salt goes up, if you and I were to eat a load of salt, our kidneys would just excrete it all very easily without any complication and our blood pressure wouldn’t really change a blip, but when insulin is elevated, let’s say you eat that salty food with an insulin spiking starch or sugar, and let’s face it, a lot of people do, salty and crunchy is one of the vices of most people’s eating, then now the kidneys can’t excrete that salt, and so they have to hold on to that salt and where salt goes water follows.
And so as the blood is holding onto the salt, now it’s holding on to all that water that it wanted to excrete, and more water means higher volume of blood, and as physics demands, more volume means more pressure. And so we have an increased blood pressure. At the same time as the blood vessels themselves are becoming insulin resistant, they can’t dilate as well as they used to, and if naturally, if a blood vessel can dilate, it’s expanding, and that would mean the volume of the space there has gotten bigger and so the pressure will go down.
But it can’t happen. When the blood vessels themself becoming insulin resistant, now they stay in a more constricted or narrowed state, and naturally that keeps blood pressure or it keeps it high, but it pushes it even higher. And then maybe one last example, ’cause there are even more than I could mention, when insulin levels are chronically elevated, it activates something called the sympathetic nervous system, and I’m sure your audience has heard of this, but this is the infamous fight-or flight response. And so when insulin is high, the heart rate starts beating harder, or higher and harder, and the blood vessels once again constrict; that’s part of the normal response. Like if we needed to run away from danger, for example, or react very quickly, it’s a pronounced benefit in that circumstance, but in this case of this kind of artificial sympathetic response, because of the chronically elevated insulin, it becomes purely pathological or pathogenic; it starts to hurt the blood vessels in the cardiovascular system.
Brett McKay: Okay, so insulin, too much insulin, insulin resistance is not good for our heart or cardiovascular system. You also talk about the effect of insulin on our reproductive system, and you mentioned a female reproductive issue, which is PCOS. What about men? Does too much insulin or insulin resistance affect male reproductive health?
Benjamin Bikman: Yes, it sure does. I’m thrilled you mentioned that because I’m always reluctant to just mention PCOS and think the girls are… Have the girls just think I’m coming after them. No, it’s certainly relevant to the guys as well. So while PCOS is the most common form of infertility in females, the counterpart in males, the most common infertility is erectile dysfunction, and that is entirely a problem of blood vessels, and in fact, I actually alluded to it or explain the problem just now, where when the blood vessels become insulin resistant, they can’t dilate or open as well as they used to, and that of course is an essential physiological change in a fellow in order to have normal fertility. And so if he suddenly has blood vessels that cannot dilate, well, then he is, then he has erectile dysfunction, and it’s entirely a consequence of the insulin resistance at the blood vessels. A lot of people misunderstand erectile dysfunction, and they will claim that it’s a result of low testosterone. That is just not true.
More and more individuals that study this, in fact, there was a paper published just a couple of years ago, and the title reveals everything you need to know, and it was something like, Is Erectile Function The Earliest Manifestation of Insulin Resistance in Men? So the title of the manuscript was kind of posed as that question. And the answer throughout the manuscript was, yes, it is. And again, it’s simply a matter of insulin resistance affecting the blood vessels. And once affected, they can’t dilate, and the lack of dilation means erectile dysfunction.
Brett McKay: One thing my sort of rudimentary understanding of endocrinology is that hormones affect hormones. Do we know if insulin affects testosterone in any way?
Benjamin Bikman: Yeah, that’s a great question. It does through the reaction of converting androgens to estrogens, and so you’d think, well, if the same thing is happening in a guy’s testes, then he should have more androgens being released. Because that’s what’s happening in the woman with her ovaries; higher insulin is resulting in higher testosterone. But that does not happen in the testes, there’s not that same effect. And unfortunate… So there’s not a direct effect of insulin on testosterone, but there’s an indirect effect through the fat cell. As insulin is promoting the growth of the fat cell, which it does very readily, fat cells end up acting kind of like ovaries. And so the fat cells that are growing on the man actually will pull in testosterone and pump out estrogens as a result. It’ll convert the androgens to estrogens just like the woman’s ovaries are doing.
Brett McKay: Okay, so we’ve talked about reproductive health. The chapter that’s kind of scary when I read it is Insulin Resistance’s Potential Role in Cancer. Are there particular cancers where there’s a strong connection with insulin resistance?
Benjamin Bikman: Yes, yes, there sure is. I share that kind of sobering sentiment that you do, that sobering view of cancer. I have a very hardy respect for it and a fear of it, because it seems like one of those things that you can’t do much about. Well, in some instances, that’s undoubtedly the case, because cancer is such an unknown beast of unknown origins. But the most common cancers, breast and prostate cancers, have very strong evidence linking them to insulin resistance. For example, breast tumors will… One of the many mutations that they’ll manifest with is a mutation in the insulin receptor. And breast tumors will have about seven times more insulin receptors than even neighboring breast tissue that’s not cancerous will have. And at the broader level, independent of any other variable like obesity for example that is a risk factor for breast and prostate cancers, you can control for obesity and insulin resistance still persists as a more relevant risk factor. So the evidence is…
There’s some direct evidence of insulin receptor mutations enhancing the effect of insulin on the cancer cells, and then there’s that more indirect finding just these correlations. But the relevance also has one other aspect to it, which is glucose. Cancer cells eat glucose, that is their primary fuel. They eat about 200 times more glucose than the normal cell does. And so the tragedy, of course, in the average individual who has rising insulin and rising glucose is that you have all that insulin signaling the growth or stimulating the growth of the cancer cell, and you have all that glucose fueling all of that explosive growth.
Brett McKay: Okay, so here’s the one… You didn’t talk about this in your book, because the book came out before this hit, but I imagine as a scientist who researches insulin resistance, the COVID pandemic provided an opportunity to study the connection between insulin resistance and COVID. Has there been any research done in that area?
Benjamin Bikman: Yes, there has been, but very, very little. Now, there’s no question that there’s a metabolic aspect to COVID. And at the risk of offending some, while many wanna claim that this is a pandemic of the unvaccinated, I just don’t think that’s fair. I don’t think that’s accurate. I think it is more accurate to say it’s a pandemic of pre-existing conditions, because that just continue… Every single study continues to confirm that if a person has these relevant or underlying metabolic pre-existing conditions, they are much, much more susceptible to having a serious infection. And they carry a much higher load, so there’s higher potential for transmission. And we know, even further, that the vaccines are less effective in these individuals. And I hate for that to sound incriminating in any way, and I really do, I don’t intend for it to sound like that, but as a scientist, I do want to be precise, and I don’t think there’s any value in ignoring data, even if it’s a little inconvenient. I think nobody benefits in that regard.
So the connection between insulin resistance and COVID-19, there’s one study that I know of that has looked at insulin levels versus glucose levels, and the general finding was that they both appear to be predictive, but I will maybe more focus on the glucose aspect, and at the risk of diminishing insulin resistance, the relevance of insulin resistance. But when a cell has become infected with a virus, it tends to start using glucose at a higher rate. So once again, in this metabolically unhealthy individual, we have the potential where we’re fueling this growth, and not to… I’ll be very brief on this, ’cause I fear that it would be getting off topic, but fat cells are a very welcoming host for COVID-19. A virus is very distinct from a bacterium where the bacteria is its own self-contained cell. A virus is simply a particle of peptides, and it needs a cell to infect, and then that cell begins producing more of the virus. And in order to get in a cell, a virus needs a co-receptor, it basically needs… It’s a doorway that allows it to come in. And fat cells tend to have more of those doorways than almost any other cell in the body. And so naturally, if you have more fat cells, you have more potential homes for the virus to come into, and then it turns the home into a factory producing ever more of itself.
Brett McKay: Okay, so let’s talk about another problem or disease that we associate insulin or insulin resistance with, and that’s obesity. So just as insulin resistance has been increasing across populations, so has obesity. So the question is, is it the insulin resistance that’s causing obesity, or is it the obesity increasing body weight causing insulin resistance?
Benjamin Bikman: Yeah, yeah, so the answer to that two-sided question is yes, Brett. I hate to…
Brett McKay: Okay, alright. [chuckle]
Benjamin Bikman: Hate to take a… But I’ll elaborate very briefly. So there’s no question that when fat cells are growing that they start to promote insulin resistance. There’s no question that happens. So fat tissue can grow through different ways, but if it’s growing through a process called hypertrophy, or each individual fat cell is growing rather than we are pulling in new fat cells and have an increased number of fat cells, but if it’s through hypertrophy or each individual fat cell getting bigger and bigger, then they start to become increasingly insulin-resistant. And they do that to try to control its own growth, because the fat cell’s essentially signaling to insulin, “Insulin, you want me to continue to grow, but I’m reaching a point of maximum dimension, and I can’t grow beyond this, so I need to become a little insulin-resistant.”
And that’s why most people have a limit to how fat they can get. The individuals that are on these documentaries where they’re super, super morbidly obese, the average person can’t get that fat. Those are the few individuals who are getting fat through a process called hyperplasia, which is when the fat cells themselves are pretty modestly sized, they just start making new fat cells all the time. So there’s almost this limitless potential for fat growth. And paradoxically, Brett, while these people become remarkably overweight and obese, they actually maintain a pretty high level of insulin sensitivity, and that’s because the fat cells are always happily storing more energy and they’re never getting too big because any time they start to get a little big, well, then they just have a new fat cell get created. So anyway, back to the discussion.
There’s no question that fat tissue, if it’s growing through hypertrophy, will contribute to insulin resistance. But there’s also evidence to suggest the opposite, that as the body has higher and higher levels of insulin, which is happening with insulin resistance, that that precedes weight gain. And evidence from a guy named Jim Johnson, who’s at the University of British Columbia, he finds that in these animal studies that he’s done, that has to happen, that you can’t promote the fat growth without the elevated insulin. I’m certainly suggesting the relevance of insulin at the fat cells, so there’s… I think the view that excess weight or the growing fat cells will cause insulin resistance is absolute consensus. Everyone would nod their heads to that. There’s less of a consensus that insulin resistance can proceed and even contribute to weight gain. There’s evidence to support it, and I just cited it, but it’s a much less prominent view, but I think it’s a valuable one.
Brett McKay: And I imagine that it goes back and forth, so as you… As insulin resistance causes an increase in fat cell size, that fat cell size is gonna cause more insulin resistance. So it’s sort of like this vicious cycle that’s going on.
Benjamin Bikman: Yeah, that’s right. And my view is a fat-first perspective, which is the fat cell is generally the first to become insulin-resistant through the process I just mentioned of hypertrophy, and then that starts to spread the insulin resistance through other mechanisms, basically through the rest of the body.
Brett McKay: So, okay, let’s talk about… We talked about all these problems that can be caused by insulin resistance. What do you do about it? So the first question is, how do you even know if you’re insulin resistant? Is there a test you can take to see if your insulin levels are elevated? ‘Cause usually you go to the CVS and buy a blood glucose test, but I haven’t seen an insulin test there.
Benjamin Bikman: No, no, there isn’t one, and that’s certainly an ongoing hurdle and why glucose continues to occupy the primary position in this discussion, because it’s just so much easier to measure. But yeah, you can get insulin measured, and that is kind of the least thing you can do, or you ought to do, in order to determine your insulin-resistant status. So next time a person’s going in for a blood test, just kind of beg, plead, cajole, pay off your clinician to check the box and say measure the insulin. That’s something that every lab can do nowadays, a clinical lab, it’s just whether or not the physician will do it. And sometimes whether or not the insurance will pay for it, but more and more it will. Even if it won’t, a person can get it done usually for 20 bucks or something. So yeah, get your insulin measured to know where your insulin levels are; that’s a great, great way to get a feel for where you’re at. Now, there are some surrogates here, like a poor man’s method of measuring insulin-resistant status can be done just by looking at a ratio of your lipid levels in your blood. And so if a person… Every blood test, thankfully, will measure triglycerides, and every blood test will measure HDL cholesterol.
Well, those are the two ones you need. So take the triglycerides number and divide it by HDL, so triglycerides over HDL cholesterol. If that answer is less than 1.5, then that’s a very good sign that you are insulin sensitive. If that answer is above 1.5 and getting higher into the twos or the threes, the higher it’s getting the more insulin-resistant you are. So that’s a very reliable indicator. So if you can’t get your insulin measured, then at least look at your lipids, which again are always measured, and that’ll give you a pretty good idea of where you’re at.
Brett McKay: When you do measure insulin levels, what’s the level where you’re like, “Okay, insulin resistance is probably happening right now”?
Benjamin Bikman: Right, right. Yeah, I should have said that. It’s around 10 micro units per ml. So here in the US, those are the units that we’ll use with insulin, micro units per ml. In other countries, it may be picomoles. We don’t do that here. So if your fasting insulin is around 10 micro units per ml or less, that’s a great sign.
Brett McKay: Okay, let’s say someone has insulin resistance, and chances are the person listening to this right now probably does, ’cause about 9 in 10 Americans have insulin resistance, is insulin resistance reversible? And if so, what are some things you can do to reverse insulin resistance?
Benjamin Bikman: Yeah, yeah, the good news is, it is almost immediately reversible and really within weeks. You can take someone with profound insulin resistance, they’re really type 2 diabetic, deep into type 2 diabetes, they’re that insulin-resistant, and within just weeks they become so insulin-sensitive that they can get off all their medications, of course, under clinical supervision. So in my view, there are four steps, or four pillars rather, because it doesn’t need to be sequential, so I shouldn’t say steps, four pillars that can be used to build the proper foundation of an insulin-sensitizing diet. And the first one is control carbohydrates. I’m not saying don’t eat any, but those are the biggest offenders, so control them. Don’t eat your carbohydrates from a bag or a box with a bar code. Focus on raw carbohydrates, or mildly cooked or processed, fruits and vegetables. Those are the main ones to eat. Be very careful with grains, they always have much more starch, and will have a higher glucose and insulin effect. And then of course, the more processed it is, like even juicing the fruits and vegetables, you wanna avoid. Eat your fruits and vegetables. Don’t drink them.
So that’s what I mean by control carbohydrates. And then next, prioritize protein. Protein has a modest effect on insulin, but it’s fine. It’s a very modest effect. And proteins are essential, and most people aren’t getting enough to sustain their lean mass, namely muscle and bone. And so focus on protein, eat it frequently, and get it from animal sources. It’s a very uncomfortable thing for some these days, but there’s no question, animal protein is superior to any plant protein. Every conceivable metric… And I know this is upsetting, a lot of people truly are offended by me saying this, but I’m not going to deny human physiology just to be politically correct. Every animal protein is superior to any plant protein, full stop. So make sure you’re getting the animal protein. Now, the third one is don’t fear fat. Fat has no effect on insulin, and we’ve been eating it for millennia, well, since the beginning of who we are. However humans came to be, we’ve been eating fat since the beginning, and that includes animal fat most especially. So focus on animal fats and fruit fats. The fruit fats are coconuts, avocados, olives. And as much as you can, studiously avoid the seed, the refined seed oils, or what some people will call through an act of clever marketing vegetable oil.
There’s nothing vegetable about it. These are seed oils, refined from soy beans, cotton seed, or corn seeds, etcetera. Avoid them like the plague. And unfortunately… Well, fortunately, if you’re avoiding… If you’re not getting your carbs from a bag or a box or with a barcode, then you’re doing a good job already because it’s those processed carbs, and the main fat in them will be from these seed oils. So as you’re eating, be very liberal with fats from animals and fruits. We’re well-adapted to those. And then the last one, the fourth pillar, is take a break from eating all the time. You don’t need to eat three meals a day all the time. You especially don’t need to eat six meals a day all the time. If you want to improve your insulin sensitivity, give your body a break from eating and engage in some form of intermittent fasting. There are so many ways to do this, but just give your body a break from eating all the time. Occasionally, maybe even do a 24-hour food fast where you’re just drinking water, no calories during that time. And then, on occasion skip a breakfast or eat a very, very modest dinner in order to just help insulin get down a little faster or stay low longer.
Brett McKay: Besides diet, what role does movement play in preventing insulin resistance or…
Benjamin Bikman: Yeah, yeah, yeah. Excellent question. I’m often asked what’s the best exercise, and my kind of witty response is the one you’ll do. But I do mean it, any form of movement is going to be beneficial, so just get up and move. You can strategically you do that. If you know you’ve only got 30 minutes a day to exercise, well, you can do a hell of a lot in 30 minutes. But maybe if you’re older and less capable physically, then couple that with the meal in which you eat the most starches, just like I explained earlier. Do a brisk walk at the end of that. But for those of us that are more capable physically, then the more aggressive we can be, the better. Have a high-intensity workout as often as you can. It doesn’t need to be long. Mine are only around 30 minutes, and I’m in my mid-40s, and it’s been sufficient to keep my muscle. I just do very, very brief rests, basically to failure every set. But whatever you’re doing, do what you can to move the muscles, and especially do what you can to increase your muscle mass.
Brett McKay: Yeah, and strength training, you’re getting free pumping of glucose into your body without insulin, which is…
Benjamin Bikman: That’s right. And by helping increase your muscle mass, you’re walking around every moment of the day with a better glucose sink, so to speak.
Brett McKay: And there’s some other weird things you can do. I wouldn’t bank on these little things to do to increase insulin sensitivity, but they’re interesting. We’ve talked about and read about cold showers on the website and the podcast before, and there’s actually research to say that cold showers can help increase insulin sensitivity.
Benjamin Bikman: Yeah, yeah, there’s two distinct mechanisms. One is just through shivering, and when you’re shivering your muscles are spasming, and that’s a muscle contraction, so they start pulling in the glucose just like they would if you were exercising. And then the second thing during cold exposure is you’re activating this unique type of fat called brown fat. And brown fat, oddly, has a very high metabolic rate. It’s not designed to store fat like your white fat cells are. This is designed to burn energy, glucose and fat, to produce heat. And so cold therapy will activate brown fat very aggressively, and then you’re just chewing through your glucose that much faster.
Brett McKay: Alright, so these are all simple lifestyle changes that people can make. What if someone does all these things, the insulin is still staying high, is there a certain point where you feel like, “Well, I’m… ” There’s other medications you take or there are medical interventions you might have to do?
Benjamin Bikman: Yeah, so frankly, Brett, usually they won’t. But just for the sake of argument, let’s say that maybe they would, just to introduce the drugs. But again, they’re not nearly as effective. Even the most effective drugs, and that’ll be the first one I mention in a moment, is only half as effective as even modest lifestyle changes. So if the lifestyle changes don’t work, then you’re hosed pretty much. So usually, it’s people go to lifestyle changes once the drugs stop working. That’s usually the way it goes, because drugs do have heavy diminishing returns. But the most common that is prescribed because of its efficacy and the minimal side effects, because every drug has a side effect, it is one called metformin. That’s the most widely prescribed anti-diabetic drug in the world, and for good reason, it’s very affordable, ’cause it’s off patent now. And it’s very effective with generally minimal side effects, so that’s typically the first one. And that’s one that I give the highest grade too of all the available drugs, but there are so many more that would take too much time for me to get into, so I’ll just end it there.
Brett McKay: Sure.
Benjamin Bikman: Usually metformin will be the first one. And thankfully, it works pretty well with minimal side effects.
Brett McKay: But the point, your take-home point, is that you’re better off doing these lifestyle changes, ’cause one, they’re free, and there’s no side effects. And they work.
Benjamin Bikman: And the only… Yep, that’s exactly right. Yeah, so you could imagine someone whose physician says, “Alright, you have type 2 diabetes, or you’re really pre-diabetic, you’re on the doorstep of type 2 diabetes”, you have two options; one, is to go and do a lifestyle change, and then… And you’ll probably reverse the disease if you’re smart about it. Alternatively, you can leave my office with a prescription for, say, metformin. If this is the only path you take, the drug path, you will never get off the drugs. All that will happen… And this sounds like I’m being hyperbolic here, but this is exactly how it goes, where the person will be given a prescription. The only outcome is that they increase the dose of that drug, and then as that becomes increasingly ineffective, then they have a different drug that they add on to it, and then a different one. And that puts them on this path of never reversing the disease. That is why conventional medicine will say type 2 diabetes is irreversible, because if you treat it in a conventional way with drugs it is. The drugs will never solve the problem. If, however, you acknowledge that type 2 diabetes is a disease of the food we eat, essentially, that the food is the culprit or the cure, then you can let it be the cure and start making changes accordingly.
Brett McKay: Well, Benjamin, this has been a great conversation. Is there some place people can go to learn more about the book and your work?
Benjamin Bikman: Yeah, thanks so much, Brett. The book is available anywhere books are sold. And again, the title is Why We Get Sick. And notice, I didn’t say in the title, Why Insulin Resistance Matters, for the very reasons we’ve spent an hour elaborating on. It’s ’cause most people don’t know the value of insulin, and so they wouldn’t have ever… They would’ve never pulled it off the shelf. So yeah, anyway, go buy the book, Why We Get Sick. And I’m moderately active on social media, mostly Instagram where I usually put out a few videos a week just about insight into human metabolism. And then one shameless plug. I have a little business with a couple of my brothers, a little family business, where we make low-carb meal replacement shakes, and people can learn more about that by going to the website, GetHlth.com. And health, health is spelled H-L-T-H. GetHLTH.com.
Brett McKay: Fantastic. Well, Benjamin Bikman, thanks for your time. It’s been a pleasure.
Benjamin Bikman: My pleasure. Thanks so much, Brett.
Brett McKay: My guest here was Dr. Benjamin Bikman. He’s the author of the book, Why We Get Sick. It’s available on Amazon.com and book stores everywhere. You can find out more information about his research and work at his website, BikmanLab.byu.edu. And if you wanna learn more about his supplement health code, you can go to GetHLTH, that’s health, just H-L-T-H. Check it out if you wanna learn more information about that. Also check out our show notes at AOM.IS/sick where you can find links to resources where you can delve deeper into this topic.
Well, that wraps up another edition of the AOM podcast. Make sure to check out our Art of Manliness website at ArtofManliness.com, where you can find our podcast archives as well as thousands of articles written over the years about pretty much anything you can think of. And if you’d like to enjoy ad free episodes of the AOM podcast, you can do so on Stitcher Premium. Head over to StitcherPremium.com. To sign up use code “manliness” at check out for a free month trial. Once you’re signed up, download the Stitcher app on Android or iOS, and you can start enjoying ad free episodes of the AOM podcast. And if you haven’t done so already, I’d appreciate if you’d take one minute to give us a review on Apple podcasts or Stitcher. It helps out a lot. If you’ve done that already, thank you. Please consider sharing the show with a friend or a family member who you think will get something out of it. As always, thank you for the continued support. Until next time, this is Brett McKay reminding to anyone listening to the AOM podcast, put what you’ve heard into action.