40: How to Measure and Fix Insulin Resistance with Dr. Ben Bikman

Good day everybody, who is joining me today for the Metabolic Classroom. The discussion that we have today is continuing, and indeed, it's the final part of our discussion about insulin resistance. Uh, to this point, in the previous episodes, which you definitely need to listen to or watch if you haven't yet, we introduced, uh, uh, this topic, and you are now more familiar, having watched them or listened to them, on what insulin resistance is, and, and where it comes from, and, uh, why it matters, namely all of the diseases that it contributes to. And we did a kind of overview of some of the big ones. And then, as sobering as all of that is, we end with a bit of a happy, uh, ending, which is today's discussion on what to do about it. So, as much as we've been discussing the problems with insulin resistance, the scope, the, the prevalence and relevance, if you will, uh, now it really is the resolution, which is, um, comforting because, because it is something that is so solvable or even so preventable now.

So, the focus of today's class is really, um, how to, how to fix insulin resistance. But before I discussed that, I thought I would take a few minutes to share with you ways that you could just know where you're at with regards to your insulin resistance. Um, just a generally kind of helpful overview where you may be listening to this and not know, um, your own insulin resistance, or the insulin resistance, um, state of the loved one that you have in mind as you've been listening to these discussions.

So, firstly, let me just, um, revisit a topic, um, that we discussed earlier, namely the problem with the traditional view of insulin resistance. The traditional view of insulin resistance is very glucose-centric, um, because we have assigned the hormone insulin to having no more relevance than, than diabetes. We purely look at it through the lens of glucose. And so, most conventional clinical tests that are attempting or speculating on the nature of insulin resistance or pre-diabetes, which is the same thing, are only looking at the glucose.

The problem with that view is that, remember, insulin's most famous job, but not its most important. Insulin does all kinds of important things and many critical things. Insulin's most famous effect is to correct what is a steady increase in insulin, sorry, glucose. So, if glucose is going up, insulin will sense this, it will be mobilized, it will come up, and then open the doors of cells throughout the body, allowing the glucose to come down, which then, uh, allows the insulin to come back down. Uh, but they're not the same thing. Glucose is not insulin. Insulin is not glucose. That seems very obvious, um, but even still, there's this weird, uh, inability to disconnect the two ideas where it's important for you to remember that insulin resistance is a state where insulin is elevated. That says nothing about the glucose. We don't know what the glucose is. In fact, glucose can be normal. And therein lies the rub. That's the problem, right? If we have a glucose-centric paradigm of insulin resistance, it's possible that the individual that we may be moving through the years, get an annual blood test, and we are measuring our only ever our glucose, and the glucose is staying normal. All the while, insulin is getting higher and higher and higher, working harder and harder in an effort to keep the glucose in check, but it is doing it. And then it's only once the body becomes so resistant to its insulin that even though insulin is still multiples higher than it should be, now the glucose starts to climb, and now we detect the problem 10 or even 20 years after the insulin had already been fighting. So, insulin is the more sensitive signal. It's the canary in the coal mine, if you will. It gives us the earlier warning.

Now, that brings us back to measuring, uh, what are the actual tests now that we can measure, uh, to determine your insulin resistance state. One of them is fasting insulin. Insulin is a marker of insulin resistance. Ideally, that number is less than six in a fasted state. So, if you're doing a 12-ish hour fast, you would love for that number to be six micro units per mill. I'm, of course, in the US, so I'm giving us units. You can convert to pmol/L as needed, and I believe the conversion would be around 30-ish or, or high 20s, maybe 27 pmol/L, um, for those outside the US. Um, so six micro units per mill.

Now, however, what if it's a little higher than that? What if it is up to the mid-teens, for example? So, I kind of have this other cutoff, which is a little, you can be a little loose with this, but if someone has a fasted insulin between, say, 7 to 17 or so, that doesn't necessarily mean they're insulin resistant. Now, why do you ask? Um, elevated insulin is a sign of insulin resistance. It's because insulin has a rhythm to it, like so many hormones do, not all hormones, but many. Insulin will, it will, it'll ebb and it'll flow throughout the day, and it's entirely possible that you get your insulin, your blood drawn at a moment when insulin was starting to climb up a little bit. For example, insulin will climb in the morning, and then it may do so again in the mid-afternoon, just as a, even in a purely fasted state, it's just part of its rhythm.

Now, that I mentioned that second kind of category, if insulin is six or below, that's a really good sign that you're insulin sensitive. If it's in that intermediate realm, 7 to 17, that suggests there's a problem, but not absolute. And then, if it's high teens, 18 and above, it's very likely that you are, in fact, insulin resistant, and you've detected a true problem there.

Now, what if it is in that middle range? In fact, even if it isn't, we don't need to stop with just fasting insulin. Insulin is volatile, it changes. So, are there markers that are a little more stable? There are, albeit now we get into the realm of a little indirect with this one, but it is surprisingly accurate, and that is the triglyceride to HDL ratio. The triglyceride divided by HDL number. So, you take your fasted triglycerides, which you get at every blood test. That's the benefit of this. It's not common to get insulin measured at a blood test, whereas we always will get our lipids measured. So, you look at your blood test and you see your triglycerides, and then you divide triglycerides by the HDL number, and you always get HDL cholesterol. That will give you this ratio. And if it is less than 1.5, that's a really good sign. If it's above 1.5, that starts to get into the realm of being troublesome. It's a little problematic. Um, so you'd want to be a little more cautious and assume that you have some degree of insulin resistance. So, that's the triglyceride to HDL ratio.

Now, the last test that I want to mention, remember, and we're all just sort of kind of framing the conversation of how to fix insulin resistance, but again, my purpose in having this bit of a pre-quill tangent is to help you understand where you're at. The last one is my favorite one, which is called the ATPO IR score. ATPO just for adipose. So, it's the adipose insulin resistance score. This is a test that is looking at the insulin resistance at the fat cells. Now, why does that matter? Do you recall from our earlier conversation of the tissue that I said likely starts insulin resistance throughout the body when you have this progressive and, uh, steady insulin resistance that's creeping into the person's life throughout the years? I submit that it's the fat tissue that becomes insulin resistant first. And thus, if you have a way of determining insulin resistance at the fat tissue, then you are detecting it potentially at its earliest possible stages. That's what the ATPO IR score will tell us.

Now, something that's so interesting about this is just the elegance of the biochemistry of what's happening. The fat cell, or the, the biology of the fat cell. Now, we know that the fat houses, fat cells house this big droplet, I mean, relatively big, microscopically big, but big by cell standards, a big bubble of fat, if you will. And insulin is largely the signal, not the only one, but is a primary signal that's influencing the growing or the shrinking of that, what's called a lipid droplet, that big bubble of fat within the fat cell. If insulin is elevated, it is preventing the fat cell from breaking down its fat through a process called lipolysis. Insulin inhibits lipolysis. Now, the product of lipolysis, or the evidence of lipolysis in the blood, is something called free fatty acids, also sometimes referred to as non-esterified fatty acids. They're the same thing. FFAs or NEFAs, it's the same. I'm just going to call them free fatty acids to cut out a couple of syllables for the sake of the discussion. So, if insulin is elevated, free fatty acids should be down because insulin's inhibiting lipolysis. In contrast, if insulin is down, through say, a fasted state or low-carb diet, then you'd expect free fatty acids to be higher because insulin is not present to inhibit lipolysis. And that's indeed what you'd get. Uh, so high insulin should be leading to reduced free fatty acids. Low insulin would lead to elevated free fatty acids. That's what this test is attempting to determine. The two parts of this formula is fasted insulin and fasted free fatty acids.

Now, measuring free fatty acids is not common. It can be done, but it is not a common test. So, you'd have to either go in and pay for it directly at Labcorp or Quest or something, um, or convince your clinician to check that box and hope, hope your insurance will cover it. But it's a fascinating test. Um, one of the reasons I'm so fascinated in it is its sensitivity of actually indicating metabolic problems. Now, I'm going to come back. I'm not done with this, but as an example, one of the very first papers I ever saw that used this study was looking at the degree of insulin resistance in healthy, in otherwise healthy women who had PCOS. So, they had women with, in without, with and without polycystic ovary syndrome, the most common infertility and its metabolic, go to the previous lecture, Metabolic Classroom, and listen for more details on that. We talked about it in more detail. So, two groups of ladies, controlled for age and even body weight and body fat, so they were the same overall body type, and yet, and, and in the women with PCOS, in this particular study, they did not detect, they did not see signs of whole-body insulin resistance. But when they looked at the fasted insulin in combination with the fasted free fatty acids, then, or in other words, the ATPO IR score, they detect a significant increase in these, in these women with PCOS. So, the insulin resistance wasn't even manifesting at the level of the whole body, but it was evident at the level of the first tissue that becomes insulin resistant, namely the fat tissue.

So, if you've gotten those numbers, fasted insulin in micro units per mill, and the, the, the units are important here, so micro units per mill, and you multiply that number, fasted insulin in micro units per mill, times free fatty acids in mmol/L. Now, thankfully, that's going to be mmol/L anywhere in the world, so that's going to be a pretty consistent unit. And you want that number to be below a certain cutoff, but it's different for men and women. Now, another little tangent here to explain why, at any given moment, women will have a free fatty acid level in her blood that can be up to 40 or even 50% higher than it is in a man. So, if a man is manifesting with, um, a free fatty acid of one mmol/L, his healthy female counterpart is very likely going to be one and a half mmol/L free fatty acids. Women are constantly mobilizing fat from her fat cells much more than her male counterparts, and that's entirely a product of sex hormones, particularly the estradiols, um, or sorry, estrogens, estradiol being the main one. The estrogens, estrogens are promoting this higher rate of turnover of the fat cells. So, at any moment, there's more fat coming out of the fat cell, and indeed, at any moment, a female is burning more fat. This will be the topic of another, of a future Metabolic Classroom, um, but suffice it to say, women are fat-burning machines relative to her male counterparts. Now, of course, the woman is rolling her eyes thinking, well, why do I have more fat? Because you're also putting more in to those fat cells, but again, you're taking more out. So, there's, that's where I, what I meant by the higher turnover, more going in, but more coming out, and that's evidenced as the higher free fatty acids.

So, what are the cutoffs? In a man, that ATPO IR score is ideally less than five. If his ATPO IR score is less than five, that suggests that his fat tissue is insulin sensitive. In a woman, that cutoff is eight. It's higher. She has a little more room there because her free fatty acids are naturally higher. Men and women will have generally similar levels of insulin, um, but when it comes to free fatty acids, no, not similar. Females will be higher because they're fat-burning machines because of the estrogens, and so her ATPO IR score has to account for that, and thus the cutoff is higher. So, women, if it's less than eight, thumbs up, your fat tissue is insulin sensitive. Men, if it's less than five, thumbs up, high five, you're doing well. Okay.

So, those are some tests. Maybe a final one, if you don't want to wait for, um, getting any kind of blood draw, because all of these are dependent on a blood draw, and maybe don't have access to that, or you don't have the data on hand. There's a bit of a quick and dirty way as well, but emphasis on dirty because it's going to be very, very indirect. But one is simply, do you have high blood pressure? If you have high blood pressure, it's very likely you have insulin resistance. I know that's a very kind of dramatic statement for what's a fairly common problem, but it really holds true. Um, or you can do some circumference measurements. Measure the biggest part around your belly, and if you multiply, literally, that number by two, and if that number is higher than your height, that's a problem. Let me say that again in a slightly different way. Measure your height, and measure your waist circumference times two. If your waist circumference times two is a bigger number than your height, that suggests you're storing fat in a healthy way, and you, like, and it would likely be contributing to insulin resistance. If your height is a bigger number than your waist circumference times two, that suggests that you're likely doing fine. All right.

Now, let's really dive into the solutions here. Um, firstly, let me just remind you of the three primary causes of insulin resistance: stress, inflammation, and hyperinsulinemia. When I introduced those three in an earlier classroom, I emphasized how the problem with stress and inflammation is that it can be difficult to change those numbers because you don't know what's causing them. Let's say you measured your epinephrine or adrenaline, and, or your cortisol, a stress hormone markers, and you had a marker of inflammation like C-reactive protein, and it was high, you might not necessarily know how to lower them. It's not clear what's contributing to them. So, just for the sake of time, I'm not going to spend too much time on those, um, other than perhaps to say, when it comes to stress, very, very often poor sleep is going to be the main aggravator. If it's not sleep, then it's likely going to be excessive caffeine consumption can increase your epinephrine or adrenaline numbers. So, perhaps a reason to focus on sleep, um, and better sleep habits, and be mindful of your caffeine consumption.

All right, now, the elevated insulin. This is the one to focus on because it can, it can yield such immediate results. Now, in talking about the elevated insulin, I wanted to frame this in a bit of a, a bit of a metaphor where if we think of an insulin-sensitizing lifestyle change, we can think of it as a journey. And as we stand at the beginning of this journey, with the end result being, I want to reduce my insulin, um, or, or, or to say that another way, the end result being, I want to shrink my fat cells. Because remember, progressive, um, pathogenic insulin resistance is usually starting at the fat cell, because the fat cells are growing too big, they're undergoing hypertrophy. So, the solution then, simply, well, simple in concept, if not practice, is to shrink those fat cells. So, there we are at the beginning of this fat cell shrinking journey. We have two feet. We can take one of two steps. First, each of these steps could be reflected in two different ideas, namely calories and insulin. The traditional view of improving insulin sensitivity through shrinking fat cells or weight loss is the caloric view, namely, eat less, exercise more. So, that's the first step. Step that most people take with no regard on insulin. But let's say the person is going into this journey with elevated insulin, as virtually all of them would be. And if, if you take a first step, reducing the calories coming in is the first step, and insulin is not dropping quickly, that creates a bit of an energetic crisis for the following reasons. If less energy is coming in, and insulin is still elevated, then insulin is pushing whatever energy is available in your blood out of your blood, pushing it to be stored in tissues throughout the body, like fat tissue, like muscle tissue, like liver, etc. All of these tissues that are now being told to store the energy. Unfortunately, the brain doesn't store energy. It really needs to rely almost constantly on any energy that's being provided from the blood. What, in other words, what are the calories in the blood that can feed the brain? And if less calories are coming in, but insulin is a little sticky, and it's staying elevated because you're just dropping your fat consumption to lower calories, but you're still eating plenty of carbs because they're lower calorie, which is what everybody does on a low-calorie diet. It's always cut the fat, which, uh, won't affect, um, insulin at all, and focus on the carbs, which will increase insulin. So, they are restricting calories coming in, but in the presence of high insulin, the limited calories that are available in the blood are being pushed into cells. And so, the brain, who must constantly rely on the blood, blood for its energy, is looking at the reduced energy in the blood and it panics, and it starts to tell the body, you need to eat. In other words, it stimulates hunger.

Now, let me just, I, in the midst of this metaphor of a fat cell shrinking journey, in which step is first, let me introduce another metaphor. So, we're going one level deeper, um, or just an example here. Let's imagine that I am inviting all of you listening, um, to a dinner. We're going to meet, and we are going to be fed by the world's most famous chefs preparing the most delicious foods. And as I'm inviting you to this dinner, I want you to be able to try all of it. And so I say to one and all, come hungry because you're going to want to eat some of everything. What would you do to come as hungry as possible to this grand and beautiful buffet? I submit you do two things. In the days before this beautiful buffet, you would eat a little less, and you would exercise a little more. And it would work. You would come hungry. Eating a little less, exercising a little more, would be the perfect recipe to come to my grand buffet as hungry as possible. But do you see the problem? That's also the two pillars. That's the two, um, pillars of strategy that has existed since, uh, for 50 or 60 years on how to lose weight or how to shrink fat cells. Every professional will tell this person who's trying to shrink their fat cells, you need to eat less and exercise more. The problem is, is because the consequence will be the same thing as is, as would happen in the example I'm presenting, which is you coming and meeting me to eat as much as we can. You're going to be as hungry as possible. It's going to stimulate ever more hunger, and thus you will fail.

Last part of that, how many times have you guys seen a reunion tour for the contestants on that morbid game show, The Biggest Loser? You don't. These people don't, they don't put them back on screen. You don't see them again because they gain it all back. Um, that can be a topic for another time. The metabolic consequences of the severe restriction that they go through actually have lasting effects, and they're negative. Unfortunately, they're negative consequences to that. So, back to the fat cell shrinking journey. If the first step is immediately pushing down the calories without addressing the insulin, it's going to be a very short journey. You'll get, you'll get a little down the road, you'll lose some weight, shrink some fat cells, but inevitably, you're going to find yourselves back at the beginning, and maybe even 10 yards further back than you were at the start. So, keep that foot firmly planted. Don't worry about calories. Let the first step be, I'm going to lower my insulin.

Now, if you lower insulin, why don't you have to focus on calories? You, well, you have some adaptations that begin to occur as insulin comes down. Your body is now a little looser with all of its stored energy. It is now, in fact, mobilizing more energy to be burned. So, the brain has an abundance of energy. It has sufficient glucose because the liver is providing everything else that you're not getting from your diet. And now, all of a sudden, it has access to all these beautiful ketones. Remember, ketones are simply products of fat burning. And if insulin, the very first, a metabolic classroom in this sort of re-released version, we spoke about metabolic flexibility and how it's insulin that dictates whether your body is sugar-burning or fat-burning. If insulin is low and you're fat-burning, you may start, you may get to a point where you're burning so much fat that you start creating ketones from that fat. And again, the brain loves ketones. If the brain has any preferred fuel, it is, in fact, ketones, not glucose. So, the, we have this state where the brain is very adequately fed. Um, no, no panic signal, no signal to try to increase the energy of the blood, and thus reduced sense of hunger. So, the person has greater satiety. But at the same time, when insulin is down, you not only are you have an elevated metabolic rate, so low insulin means higher metabolic rate. Insulin suppresses the metabolic rate. It wants to reduce the idle of your metabolic engine. So, when insulin is down, the engine just starts revving up a bit. It's like you're starting to press the metabolic accelerator of that metabolic engine. So, uh, that's one.

And then the final part of it is when you start creating ketones. Remember, remember ketones have a caloric value, um, and you start excreting them from your breath and from your urine. So, every breath, as you're breathing out ketones, every urination, when you're urinating out ketones, those are caloric, were once caloric molecules that would have otherwise had to be burned or stored. Not anymore. Now you're just wasting energy, which is good if you're trying to shrink fat cells that are overfilled with energy.

Now, how can you lower insulin if that is the step you want to take? That's a little easier said than done. You've heard me give these three pillars before, and they're always worth emphasizing if for no other reason than they just roll off the tongue so well. First, control carbs. This is, I put it first because I deem it the most important. You, you want to make sure you're, whatever carbs you're getting, uh, that you're focusing on sources that are not coming from bags and boxes with barcodes. Whole fruits and vegetables, eat them, don't drink them, are generally going to all be good. There's different levels we could, could go with different depths and, and defining that a little more clearly depending on the beginning, but just at its simplest form, just control carbs, eat fruits and vegetables, and enjoy them liberally. Next, prioritize protein. Make sure you're getting abundant, high-quality, which means, and preferably animal-source protein, every day. Third, don't fear fat. In particular, don't fear the fat that comes with the protein. In nature, there is no exception to this. Every protein comes with fat. Don't be afraid of it. We, I understand we have a fat-phobic culture now. You need to reject it. Fat is not only essential, we need it. There are some fats that are necessary for human survival, but they also have no effect on blood sugar or blood insulin. So, it's a nice nourishing option. You have to get over the fear of fat, especially the fat that comes with protein. So, those are the three steps: control carbs, prioritize protein, don't fear fat. That will really help you lower insulin. So, that is that insulin step that really moves you down the journey very, very far indeed. That step alone, only focusing on lowering insulin, never worrying about calories, may be sufficient for anyone listening to shrink their fat cells as much as they need to and as much as they want to. And some people, they may plateau a little earlier than they'd like by focusing only on the insulin. They'll get some benefit, indeed, maybe a lot, but they know they got a little further to go. Now, you are ready to take that other step, that other foot that's been so firmly planted, and you just had one really big step that got you farther down the road with the insulin, uh, lowering. Now you can take that next step, which is addressing the energy explicitly. Usually, the energy corrects itself for reasons I mentioned earlier, that when insulin's low, your body is using its own stored energy. All of those energy bars, if you will, that you've had stashed away in your fat cells are finally being opened up to be used, which is what they're there for. So, sometimes people will begin restricting their, they'll have greater satiety and start eating less just on their own without even doing it deliberately. Indeed, that is what usually happens. But if you need to, now you can explicitly address the energy part of it, but don't do so by counting calories. Do so rather by structured fasting. So, that's that fourth part of the three parts I gave earlier. The fourth could be frequently fasting, and that can take any form. Um, we'll have more discussion in the future about specific versions of fasts, but suffice it to say, a period of structured fasting and then eating can be a very, very good way to overall restrict energy in a, in a healthy way. Um, now, one comment on that, though, uh, is that, um, fat, uh, with, with fasting, how you end a fast is more important than how long you fast. So, the temptation is to obsess over a 48-hour fast or something like that, and then you get so hungry that you just binge, and then you stuff yourself full of food that came from likely bags and boxes with barcodes, and you feel miserable mentally and physically. Uh, and that basically leads into a disordered eating pattern of, of almost kind of a binge-purge, um, cycle. You don't want that. So, how you end your fast matters more than how long you fast. Have a very specific meal plan in mind for when you are, um, ending your fast.

Now, let's talk a little bit about exercise, um, to kind of wrap it up. Exercise is very important at improving insulin sensitivity. One primary reason for this is it really lowers insulin. When you exercise, insulin is antithetical to what the body's trying to do metabolically. When you're exercising, you want to be moving or mobilizing and burning energy. Insulin, uh, up, mobilizing and burning energy. It only wants to store energy. And thus, it's no surprise as the body starts to demand exercise, insulin will retreat into the background, knowing that it's not its turn to be active. The body needs to use the energy. Insulin retreats, and so it will lower insulin. Also, remember the main stimulus for insulin is elevated blood glucose, and the nice thing about exercise is that muscle is the main consumer of glucose. So, muscle is, in other words, the, the most hungry tissue that up to 80% of the clearance of glucose from the blood after a meal is glucose that's going into the muscle. So, the muscle eats the lion's share of glucose from the blood. And so, when you're exercising, the muscles are eating a lot of it, and that lasts for several hours after exercise. And then, if you happen to be engaging beyond the acute benefit over a day or so of improving insulin sensitivity with exercise, if you are increasing your muscle mass, now at any given moment, you have more of these mouths to feed, and, and the muscle will greedily pull in and use glucose every time you're moving them. And the nice thing is, when you move the muscle, it doesn't need to rely on insulin to eat the glucose. In a rested state, if you're sitting down, now any glucose that would be going into your muscles would be doing so because insulin comes and knocks on the door, most especially if you're listening to this in a postprandial state or a state after you just ate, then insulin goes up, it then knocks on the door of the muscle cells in particular, and, and a few others, and opens those doors to allow the glucose to come in. When you're exercising, remember, insulin cannot tolerate that. It can't be elevated, but the muscle is so hungry that it has an insulin-independent mechanism. In other words, it can open those glucose doors without insulin, without needing to wait for insulin to come and knock. There is, if you will, a back door. Exercise opens the back door, allowing the glucose to come in through an unconventional route, thereby helping lower blood glucose, which helps lower insulin in the long term, which then improves insulin sensitivity directly and by shrinking fat cells.

Now, with that in mind, you may be thinking, well, then Ben, what's the most important or best exercise I can do? My answer, and I hope it's not too pithy, is the one you'll do. Whatever you can do to just get out and be mobile, that's what you should stick with. Now, if you have options and sufficient motivation, my strong recommendation is resistance training over endurance training. Endurance training is not going to do too much to help maintain muscle mass. Indeed, it may start to work against you maintaining muscle mass. Um, you want resistance training as much as you can. Anything you can do to fatigue your muscles, even something as simple as push-ups and chair squats until you start to feel a little bit of burn, and do that just a few times a day, is going to be, depending on where you're at, is going to be a stimulus to help you increase your muscle mass. And remember, more muscle means greater insulin sensitivity, usually.

Now, the great big elephant in the room on ways to improve insulin sensitivity are drugs. But here you're going to be disappointed because that's the topic starting next month. That's going to be February's Metabolic Classrooms all about the cardiometabolic drugs and the options for, and we're going to go across a few different cardiometabolic complications, including weight loss, including diabetes, and a handful of others, high blood pressure, and we're going to just look at the, um, generally do a bit of an overview, but also focus, um, a little directly on the, on the cardiometabolic ones. All right.

That is it for today's Metabolic Classroom. Um, and now let's move on to the Q and A. And you guys, as usual, thank you so much for joining and listening and for your support. Um, it is something that I really enjoy doing. I love the idea of having a bit of a bigger classroom, if you will, than just what I may get, um, at, at my university. Okay. All right. Let's start with the first one, Carly, sharing a question from Tracy. Can a young active person develop insulin resistance? And she continues, could they develop insulin resistance and have the numerous health consequences including insulin resistance in the muscle and limit their energy storage and release? That would be unlikely. Um, uh, Tracy and Carly, that would be unlikely if a, if a young active person is generally going to be insulin sensitive. Now, let me clarify, um, a topic for another time, um, is going to be discussing the differences between physiological and pathological insulin resistance. And depending on the age of the person, if this person is, um, an adolescent still, so up to mid-teens in girls, up to late teens or even early 20s in boys, um, that's the adolescent phase, and there's a natural insulin resistance there, which is the insulin resistance that accompanies growth, um, interestingly. Um, but no, if a person is young and active in their healthy body weight, they're not going to have insulin resistance, um, in, in a pathological sense. But let's just go a little further because the question addresses very specifically the muscle. If you did have a person whose muscle was insulin resistant, they would, they would have a potential problem with energy storage, um, particularly, um, they may have a problem with glycogen. Uh, the muscle is very greedy, and it will store its own glucose and its own fat. Both of that is dependent on, on insulin, mind you. It stores those nutrients to burn them. It doesn't share them with the body. If these, if these energy depots are in the muscle, they're going to stay in the muscle and feed only the muscle. If the muscle becomes insulin resistant, its ability, particularly to make glycogen, could absolutely become compromised. And if muscle glycogen is down, that could limit intensity. Interestingly, um, one of a study from a couple of years ago found that even very staunch ketogenic adherents that are trained athletes, they have as normal muscle glycogen as a, a non-ketogenic athlete, as a conventional high-carb athlete. That's how greedy the muscle is that even if you're not eating carbs, it's still going to pull in all the glucose it needs to from the, from the blood, which came from the liver in this case, and have its own storage of glycogen. Okay.

Another one from Carly. If someone is active and eats poorly but a normal BMI, could they still be living with all the issues? Um, yeah, with all the metabolic problems and the plagues of prosperity. It depends on how active they are, but in general, um, and they have a normal BMI, um, in general, diet is going to dictate disease state that exercise can only make up for so much. Now, age can also make up for a fair amount, but I have seen it now multiple times that even in people who are normal weight, and this becomes particularly problematic across various ethnicities, um, like for example, Hispanic and Asian ethnicities, who can be very normal weight but have fatty liver disease or elevated, um, visceral adipose tissue, which is much more pro-inflammatory, and we'll talk all about fat tissue more explicitly later in a future episode, a lot of future episodes, but we got a lot to talk about. Um, but even in Caucasians and in Blacks, who are a little more healthy with their fat storage, some, I've seen it now too many times where someone is generally lean, um, but they're just not storing their weight in a healthy way, either through adipose hypertrophy or through liver fattening, they begin to experience metabolic disruption. So, exercise can only make up for so much. Diet dictates disease state. All right.

Carol. What if a person is on a statin? Does that make the triglyceride to HDL ratio a little less reliable, or is it still informative? It is still informative because, uh, statins don't really influence those. Statins certainly don't influence triglycerides, and they have a very modest effect on HDL. Um, so, you know, I have pretty strong feelings about statins, and I'm not really an advocate, but we'll talk more about that next month. Um, uh, but it is certainly not, it's not going to move it too much, Carol. I mean, statins do have other consequences, particularly mitochondrial. All right.

Lindsay shares an anecdote. Her Standard American Diet patients all have high adipose IR scores, and low-carb fasting patients have normal scores. I assume this leads one to believe it is quick to reverse adipose with diet. It is indeed. Yep. And this is why I focus on insulin so much rather than stress and inflammation because you can move that lever. You know, I've, I've used this analogy before, but it's like these levers on the wall that contribute to insulin resistance, and stress and inflammation are really slippery. You just can't really get a good grip on them. Insulin, you can grip it and pull it down. You just change your diet. All right.

From Tony. I swim, but have tried doing it fasted the last two times. I've come out of the pool, it's as if I'm drunk. I'm unable to walk straight. That's not good, uh, Tony. Now, it could be that, have you, well, I mean, it may be a low blood sugar phenomenon, but I would suspect that's a little unlikely. Um, usually, if people fast, what they may have found is that their blood pressure has dropped. So, um, now I'm not, of course, giving any kind of medical advice, but one recommendation could be to try drinking a little more and load it with electrolytes. Um, that might be an option that you could use in order to see if you feel a little better. Typically, that lightheadedness, um, it could be low glucose, but that's not too common, um, especially for swimming, unless you're really sprinting swimming. Um, uh, I suspect you may have a better benefit by focusing on the water and electrolytes. Rich, what impact does fructose have on insulin? That's a great question. Fructose does not directly have an impact. Fructose does not induce an insulin release. The problem with fructose, why you, you could someone have, they could drink pure fruit juice, which is just fructose, and then have a spike in glucose, is because the body can convert the fructose to glucose very, very well. And indeed, the liver does that very well. And so, pure fructose will, in fact, give a high glucose rise, um, usually, which is why a type 1 diabetic will say, give me some, give me some juice, because it will correct blood sugar. Yeah, so Rich, we do want to be strict on fruit juice in particular. Okay.

Evette. Exercise with some dang good music is winning. It sure is. In fact, my world lately is filled with Taylor Swift because I have teenage girls, um, even though I don't listen to her while I'm working out. Actually, I listen to podcasts and books, if, um, but music is a good way to do it. All right.

Marsha has a question. Been keto for two years and lost a lot of weight. Blood pressure has gone through the roof. It is 170 over 80, and nothing helps. Is there anything you can suggest that is surprising? Mara, that is not common. Um, not to make you feel, I hope you feel special, um, usually blood pressure pressure drops, and it drops so quickly that a person has to change their medication. I can't, um, I have to speculate here because I'm not familiar with any papers, Mara, that have identified a mechanism. One mechanism could be that when we restrict carbs or fast, epinephrine goes up, um, or adrenaline. That's because it wants to start telling the liver to release more glucose in order to make up for the glucose that's no longer coming in through the mouth. Um, the, another effect of adrenaline or epinephrine is that it will increase blood pressure. Now, that's a high blood pressure in this case, um, and then alternatively, then it might just be excessive caffeine, although that would be a lot of caffeine to increase blood pressure that high. But Mara, that is a high number, and it may be worth you just having a visit with your clinician because that is pretty high, 170 over 80, especially if you're in a fasted state, when fasting usually will lower that. Um, but yeah, I mean, you, that, that's that's awfully high.

Carol. If I need more insulin as a type 1 diabetic when I lift weights, is that a problem? I guess resistance training leads to glycogen release. Yeah, any kind of training, any movement will stimulate the liver, the muscle to start, oh, well, breaking down its own glycogen, but also the liver breaking down its glycogen, especially if you aren't eating. If you're not eating during the workout, then the liver is going to be releasing glycogen into the blood. Um, but yeah, and remember, Carol, of course, you are constantly struggling with your elevated glucagon, um, and in that case, an insulin dose would be absolutely appropriate for type 1 diabetes. All right.

Dave. Can you possibly give a good animal-based protein to use? I have one occasionally, two protein shakes daily, and you've been using Z-Works, thanks. Um, yeah, I mean, there are some good options indeed. Um, Health Code Complete Meal is a good option, although that's more of a full meal replacement than just protein. Um, in general, if you can be getting your protein, if you're not going to get it from that, I mean, whey protein is a good source. That's an animal. So, so basically, Dave, I mean, the, the short and skinny of it is, if it's meat or eggs or dairy, that's an animal protein. Now, it doesn't have to be a shake, of course. It can be a full meal of, of say, hamburger or chicken or eggs or, you know, whatever. But the animal-source proteins are any of the above: meat, eggs, dairy. Dairy is the easiest because it's been powdered into so many different types of whey, and whey is a very, very good source of protein that you can get from all kinds of sources. All right.

Last question. Amanda. UA. What is the best practice for type 1 to regulate glucose insulin? Yeah, Amanda, of course, remember guys, I'm not giving medical advice, but now I can cite studies. There are now multiple papers finding phenomenally good glucose control in type 1 diabetics with the use of a low-carb diet. So, as everyone with type 1 diabetes knows, or the loved one you're thinking of, often they suffer from this just massive variability in their glucose levels throughout the day, which is an enormous source of not feeling well and being anxious. As the person adopts a low-carb diet, and any of the type 1 diabetics listening can attest to this, it just starts to flatline, which is much more comforting. And at the same time, you dose with significantly less insulin. So, the insulin needs drop dramatically as carbs are restricted. And remember, that used to be the standard of care in type 1 diabetes. We call type 1, it wasn't called, it was just called severe diabetes at the time. It used to be that you would put them on a carbohydrate-restricted diet, and they would feel better, um, until we discovered insulin. And once insulin became a therapy, thankfully, thank goodness, it is life-saving, then all of a sudden it became the mantra of, eat whatever you want and just inject yourself with insulin. And that is not a good way to have stable blood sugars in anyone, let alone a type 1 diabetic. All right.

Now, speaking of insulin and medications, join me next time. Um, and then all of next month's episodes will be all about diet. Sorry, drugs. All of the episodes will be about drugs, and that'll be the focus. Uh, the focus looking across various cardiometabolic disorders. You guys, thanks again for joining, um, and I will see you next week. Be smart and stay healthy.