The Untold Truth About Insulin Resistance w. Dr Benjamin Bikman | Health Results

So this image here we see that it's called a Food Compass score. And what you can see is things like canned peaches and Cheerios cereals is ranked higher and not even by a little. It has a Food Compass score that is three or four times higher than things like eggs or beef or cheese. Any of these very protein rich sources that come from that we would have eaten naturally as humans. They are the lowest. Even something as horrible as Lucky Charms is considered healthier than eggs.

Joining me in the studio in a moment is a real hero of mine and I'm sure you've seen my tree of insulin resistance that would never have happened if it wasn't for this brilliant gentleman. Ben Bickman joins me right now. Ben, so great to have you on the show. Thank you for again taking up valuable time.

Oh, my pleasure. It's a delight to be able to talk with you right now. Steve, thank you.

Awesome. And we just saw each other at a conference in Florida the other day. I thought your speech was great. And in fact I've got to quickly say there are three things I admire about you and you don't have to blush or don't play them down because these are really important. First thing is I admire the work you do, your laboratory and what you've learned about and discovered about insulin resistance and fat cells is second to none. And I think probably as this chat develops and we start talking about all the things that insulin resistant and hyperinsulemia knocks onto, I think your research is probably some of the most important, important in the world, full stop, period. So the way I'd like to play this today, like I'll try not to interrupt the first bit at all. And then I've got probably a dozen questions I'd like to ask then afterwards, but set the scene for us about you're in the laboratory, you're mainly analyzing fat cells and insulin resistance. Take us right back. Let's just say somebody's tuning in, they've got insulin resistance type 2 and maybe they're doctor in the UK and I love doctors but you know, they have those 10 minutes and some of them don't keep up to date with all the latest research. So let's say they've gone in, they've been diagnosed type two, they've been told it's chronic progressive and you're on tablets for the rest of your life, AKA where my dad believes he is. Let's go right back to what is insulin resistance and then the knock on effect with hyperinsulaemia. Just give us a lesson for 10 or 15 minutes and then we'll get to some questions.

Yeah? Yes. So, first of all, it's very likely that the average individual, having gone to their gp, still won't even know they're insulin resistant. And it's proper, Steve, that you're mentioning type 2 diabetes. So there are really two variables that the individual and the GP, you know, the clinician would want to be taking, taking note of. One of them is glucose or blood sugar levels, and then the other is the hormone insulin. And unfortunately, the conventional clinical view is very glucose centric. In other words, the average GP is only going to be looking at the patient's glucose levels and, and not paying any attention, indeed, may have never even measured what the patient's insulin levels are. And that's because, as I noted, this glucose centric paradigm just predominates our view of metabolic health. And so over the years, what's happening is the person is, and we can talk about the stimuli or the causes of this, but they're living a lifestyle that is such that it's keeping their glucose at a normal level, but they need ever higher amounts of insulin to keep the glucose there. This state, namely normal glucose, but high insulin, is insulin resistance, also referred to as pre diabetes. This is the state where they are starting to develop all of these other chronic diseases, what I like to call the plagues of prosperity. And Steve, this is, this would be like the branches on the insulin resistance tree that you've developed. And it's a very, it's a, it's a very beautiful image. And so it's, it's, again, the trunk of the tree is the insulin resistance, and then it's all of those branches, these, all of these diseased aspects that are manifestations of the insulin resistance, not the, the glucose levels. And so you have the person seeing their GP every year and the glucose is staying normal. So the GP isn't thinking there's anything metabolically disrupted. And yet now they are on a medication for their hypertension because the insulin resistance is causing high blood pressure. They may be on a medication for their migraine headaches, because insulin resistance contributes to migraines. They may be on a medication for their infertility, because insulin resistance contributes to infertility in both men and women. And so and more and more that we could go on and listing. But again, all of those are diseases of the insulin resistance state, the normal glucose and the high insulin. And then it's gonna say, if I.

Can jump in there. My dad, right, had gout from his 20s, has always had high blood pressure, as far as when I can remember, was on Viagra, you know, three signs that he had got insulin resistance some 20 years before he was diagnosed with type 2 diabetes.

Yep, that's a perfect example. And indeed, Steve, that's one of the hopes. As I imagine the potential impact of this knowledge in people's lives. It would be someone like your father who opens up his medicine cabinet every morning and sighs and then resigns himself to the fact that he now has to take this one medication for blood pressure, this medication for his erectile dysfunction, and another medication for something else. Little realizing that each of those are simply a branch coming off of the same trunk. And rather than continuing to take a medication that attempts to kind of prune back the branches, we want this view to be so embraced that someone could simply take the axe and cut down the, the entire tree. Why do you know? Why keep feeding the tree and then insisting on trimming back, pruning back the branches when all we're doing is continuing to help this tree grow due to our lifestyle habits born from our ignorance. So back to that overall view. The patient is pre diabetic or insulin resistant. And then once the body becomes so resistant to insulin now the glucose levels start to climb and then it's on the radar, so to speak, of the clinician and the GP begins to tell the patient, hey, you're, you're really getting to pre diabetes, so now you're diabetic. And then let's just give you a whole new list of medications.

Yeah.

So having explained that whole paradigm, let's just rewind, as I say, maybe just.

One step back for those that really, this is all new to them, why we have insulin in the first place. So we have insulin because homeostasis, the body should only be suspended. And correct me if I'm wrong at any time, Ben, but my understanding is the body should only be circulating in its 60,000 miles of blood vessels. It's eight pints of blood, it can only suspend about one to two teaspoons of sugar. In fact, in the old days when we used to do the blood glucose test, rather than the hba, one C, one and a half teaspoons of sugar in that entire network, those 60,000 miles of veins and blood vessels can only suspend one and a half teaspoons. In fact, apparently, correct me if I'm wrong, three or more might kill you instantly. So you eat that subway, that 12 inches with 150 grams of bread, which turns into 15 teaspoons of sugar. Really quickly, insulin's there because if it wasn't, those 15 teaspoons of sugar would just kill it. So therefore, let's say you're supposed to suspend one. It's got to go and get those. Insulin's job is to get the extra 14 teaspoons, get it out of the bloodstream to keep you alive. But then eventually what happens is those cells become resistant to that noise. I'm sure you'll go into this a lot more detail in a minute. But it gets resistant because it's being bombarded. Bombarded, Bombarded. And then what happens is insulin goes up. And insulin goes up because it's still got to keep getting the sugar out of the blood. Is that a fair sort of simplest view of it, or.

Yep, yep, that.

That's a great view. Yeah. So let me. I'll just simply add on to that just a little bit. And, Steve, what you were describing and what everyone just heard was insulin's most famous effect. Now, there's a word here I'm deliberately not using. I'm not saying that the controlling blood sugar is insulin's most important effect, because insulin has its hand in so many different processes. From nerves conducting signals from the brain throughout the body, from the liver knowing when it's time to store energy or break it down. Insulin controls so many processes, but its control of blood sugar is the most famous, and it is very important. I just don't want to say it's the most important because there are so many things.

Things.

But as you noted, when blood sugar starts to climb very rapidly after we eat some starchy, sugary food, insulin will rush into the bloodstream, basically. Grabbing this. I'm. I'm getting a little inaccurate here for the sake of the description. It basically escorts glucose from. From the blood. It's telling all the. All of the blood sugar. Hey, there's a lot of you here. This isn't where you belong. You need to go into the cells of the body to give them energy or to allow them to store this excess glucose for later use. And so insulin will come and knock on the doorways of the muscle cells of. Of the fat cells especially, and essentially just allowing the glucose to come out of the blood, helping the glucose levels start to come down and then get back down to normal. And then insulin, having done one of its very important jobs, also retreats back into the background, waiting until it needs to be bumped up again. But that is what starts bringing us to the problem of how insulin resistance starts. And even before I mention that, let me Just say insulin resistance, to define it very, very clearly is a problem with two aspects. And I like to use the analogy of a coin, where insulin resistance is a coin and it has two sides which are always there. You cannot have a one sided coin. It will have two sides. On one side is the phenomenon that we've been alluding to, which is that insulin isn't working as well as it to at certain cells of the body. It is not a global or a universal phenomenon within. Within the body, insulin doesn't work well at some cells, but it continues to work perfectly fine at others. Now, for example, insulin's ability to control blood sugar becomes compromised due to what happens at, say, muscle cells and liver cells and fat cells. Those cells become insulin resistant. And now the body has a much harder time controlling blood sugar. And so blood sugar starts to climb up. But at other cells of the body, insulin continues to work perfectly fine. And that becomes a problem when we flip the coin over, because when the body starts to become insulin resistant, insulin levels have been getting higher and higher and higher. Now, that is actually both cause and consequence, and I'll come back to that in just a moment. But as insulin levels continue to climb, this is a condition called hyperinsulinemia. Now, the cells that are as responsive to insulin as ever, they are now too reactive insulin. Because there's so much insulin, insulin is telling them to do too much. And the perfect example to highlight this collective problem of insulin resistance in the body, namely altered insulin action and increased insulin, is most perfectly reflected in infertility in men and women. For example, in men, the most common form of infertility is erectile dysfunction. In fact, that is considered to be one of the earliest manifestations of insulin resistance in men. And what they found is that the endothelium, in other words, the blood vessels start to become insulin resistant. And that's a problem, because when insulin is working well in the blood vessels, insulin will flow to the blood vessels and tell the blood vessels to expand or to dilate. That is a very necessary process for normal erectile function. However, as those blood vessels become insulin resistant, they stay constricted. And if you can't increase blood flow, then you cannot have normal erectile function and thus the man develops erectile dysfunction. All because insulin isn't working well. In other words, the resistance part of it. In stark contrast, the most common form of infertility in females is a condition called polycystic ovary syndrome, pcos. In this condition, it's the result of the high insulin and the ovaries the cells of the ovaries are continuing to respond to the insulin, but now there's so much insulin, and so the ovaries are overstimulated. And the consequence of this is that insulin actually inhibits the ovaries ability to take testosterone or that whole family of the prototypical male hormones, what's called the androgens. And insulin inhibits the ovaries ability to convert androgens into estrogens. Now someone may be listening and hearing.

This and say, well, what does that.

Have to do with anything? The simple fact is any sex hormones that are estrogens, like estradiol or estrone, the estrogens are all converted from androgens. Basically, in order to get estrogens, you have to go through testosterone first. That's just the normal way that the ovaries and the testes work. Insulin stops that it slows it down in the ovaries. And so now her ovaries can't produce sufficient estrogens. And so her estrogens are relatively lower, her testosterone is relatively higher, and that ends up disrupting her ovulation. And she doesn't ovulate well, she doesn't have a normal menstrual cycle. And thereby we've led the woman into polycystic ovary syndrome, pcos. So all of this is simply my highlighting just how impactful insulin resistance is and how necessary it is for us to appreciate that it has two parts. It is a structure built on two pillars. Insulin resistance or the altered insulin action that is, and hyperinsulinemia. It's these, it's this two faced or two sided problem. And then we can talk about the causes. I mean, what starts to build this whole structure up. And I consider there to be three primary causes. Now when I use the word primary, I mean to say that this is, these are problems that have been validated or proven to exist in all of the commonly used models of research. So as a scientist, my lab is just across the hallway here in my building on campus. We would use three different models commonly to do. In fact, my lab only uses these three, but they're the three most commonly used, namely isolated cells, so cells growing in like a little petri dish. And then second, using laboratory rodents like mice or rats to try to test some of these theories. And then lastly, humans, you know, at the pinnacle of all creation, we have the human body. And so the primary causes of insulin resistance that have been proven in all three of those types of experiments are inflammation and stress and hyperinsulinemia itself. Now, I'LL just mention that one for another moment because I've already mentioned that word. People have heard me talk about it and I think it's the most important. It's certainly the one that people can change the most readily. Whenever the body has too much insulin, insulin will stop working as well. It's. And that is reflective of a fundamental biological principle. Whenever the body or a cell has too much of something coming at it, it will attempt to reduce the sensitivity to that something, if it can, in order to maintain normal physio, normal biology. As you noted, Steve, the homeostasis. If there's too much of a signal, then homeostasis gets disrupted. And so the cell will attempt to reduce its sensitivity to that signal. It's just like how a busy, a homemaker mom who constantly hears the kids kind of screaming, she learns to tune it out whereas dad comes home from work. Maybe this example hits a little too close to home for me and I hear all the noise of the kids and I hear it and I'm responding, I'm reacting. Whereas my wife is just sort of blissfully ignorant to it all because she hears it all the time, bless her ever deafening ears and heart. But, but that's, that's the, those are the causes and they all matter. Each of those is capable truly of, of stimulating insulin resistance on their own. For example, inflammation. If someone, as we have become all more attuned and mindful of our immunity over these last three years, if someone had become infected and even just with a cold or flu and other more modern concerns would fit into those. But they would find that if they were wearing a continuous glucose monitor or otherwise checking their glucose during that week or so when they were sick and fighting this infection, their glucose levels would absolutely have been higher. And that's because the body is slightly inflamed. And when inflammation starts to climb, or the activation of immune systems, to put it a little more precisely, the body body becomes a little more insulin resistant. It's a natural phenomenon. Second is stress. Now stress is often invoked and often discussed these days. And when I talk about stress, I mean an elevation in the two prototypical stress hormones. In other words, the poster children of stress, and that is cortisol and adrenaline, or also called epinephrine. When there is a genuine stress response, like you become startled, you're scared, or you're worried about an upcoming event, your stress hormones will be higher. And it doesn't even have to be something as dramatic as those. It could also just be getting a bad night of sleep. I Know, that's kind of discouraging, especially for parents to hear. But thankfully, a good night of sleep can correct it. But even one bad night of sleep, one bout of sleep deprivation, will increase those stress hormones that next day and you would be. Humans are demonstrably more insulin resistant following sleep deprivation. But again, it's easily, it's, it's rapidly corrected with just good sleep habits. But the problem is, as much as, as those matter, and they do, stress and inflammation, they're also harder to control and harder to really put a pin in it or to identify it. That's why I focus mostly on the hyperinsulinemia, because I could imagine someone who comes to their GP and let's say their GP says, you know what, I want to measure your insulin or some of these other markers of insulin resistance. And hey, wouldn't you know it, you are insulin resistant. Naturally, the conversation should then progress into, okay, what to do about it? Well, in a way, when we look at these three distinct causes of insulin resistance, stress, inflammation and hyperinsulinemia, it's like there are three levers on the wall. And we look at the stress lever and we would say, well, yeah, it looks like you have a little stress, your cortisol is a little high, maybe your epinephrine is a little elevated. And then the patient would say, well, what can I do about it? How can I lower my stress? And the GP may say, and justifiably, I'm not sure, it's kind of hard to know what the source of your stress is. So in other words, that's a very slippery lever if we want to try to turn it down. It's difficult to. It's difficult to know what the cause of the stress is and how to best blunt it. Not that it doesn't matter, but it can just have kind of diminishing yield or return focusing on it. And then similarly, if we move into the kind of inflammation realm, let's say that the patient comes in and the GP determines that the individual has higher than normal C reactive protein levels, and that's the most commonly measured marker of the activation of the immune system or marker of inflammation. And the GP would say, well, your CRP is a little high. And then the patient would say, well, how do I lower my crp? That's not an easy answer. We don't really know. Maybe the patient has an autoimmune disease, maybe they have a slight infection. It's difficult to know exactly how to turn that down a little bit. Now to the last point. The Hyperinsulinemia, that is the 800 pound gorilla. That is the. That is the big thing that we can really move around, where the patient said, the GP will say, wow, your insulin is really high. And then the patient would say, how can I lower that? Now, the GP has some firm solutions, but Steve, I don't want to get into that. If we're not quite ready to start talking about. GP has some firm solutions, but Steve, I don't want to get into that if we're not quite ready to start talking about solutions. That might be. We might. You know, I don't want to accelerate the conversation too far, but till this point we've certainly defined what insulin resistance is.

Yeah.

And some of the consequences of it, like moving to type 2 diabetes, migraines, infertility, and then discussed the origins of it as well, what it is, why it matters and where it comes from.

I think, I think we're almost there. I'd ask my producer, Connor. Lovely Connor. Connor just put up the. We talked about the markers because it's quite hard to get an insulin test in the uk. There are some gps that do it, there are some doctors you normally have to pay private if you want your insulin measure. But Connor, bring up the slide. It's got five stars on it. And I just want to confirm that we're talking about the same five measurements. We're talking about measuring your waist to height ratio is probably the most important or, or one of the five. We're talking about your blood pressure, your hdl, the so good cholesterol, making sure that's high enough, making sure the fat in your blood, your triglycerides is low enough, and making sure that your glucose again is within a tolerable range. Have I got that kind of right, Ben? Those are sort of five markers we can all look at very inexpensively and very quickly.

Right? Yeah, Those are the five markers. I always make a point of highlighting them because they are the stars that make up the constellation of what we call the metabolic syndrome. Each of those is a point in this constellation. And I would emphasize that as much as they have value in reflecting the overall insulin resistance state of the individual, I would emphasize that in all, probably the most sensitive marker among all of those is actually a hybrid marker, namely the triglycerides and the HDL ratio. You want to kind of formulaically put them together, stack them on top of each other, or just compare them one to one. But if the triglycerides in the HDL are roughly the same amount where it's Kind of a one to one balance of them, that's a very good sign that you're doing great. If, however, or if even the triglycerides is lower than the hdl, then that's, then you're very insulin sensitive and your metabolic health is very sound. But the higher the triglycerides are getting compared to the HDL cholesterol, if it's like a two to one kind of balance, then the further you are getting into insulin resistance and the more certain you can be that you have a problem. So if we, if we consider that constellation of metabolic, poor metabolic health, I would say really pay attention to that. What is the balance or the ratio of the triglycerides compared to the HDL cholesterol? And then similarly, if even, even more simply than that, if someone finds that they're, that they're heavier around the middle and that their waist circumference is getting to around, you know, 90 or so centimeters, or I think about, in men maybe about 85 and in women a little less than that, maybe about 80 or high 70s centimeters and they have high, high blood pressure. If blood pressure is creeping up and it's consistently in the 130s over 90s, then that's very, very likely. That's very strong evidence that the patient that you have insulin resistance, you want to pay attention to your blood pressure because that is so determined by insulin resistance. Over the years, over the decades, we've been told that it's nothing more than just how much salt you're eating, but that's a bunch of nonsense. It is very little impacted by salt consumption and it is heavily impacted by insulin resistance and overall insulin levels. When insulin levels are elevated, which they are in insulin resistance, they force the body to retain water and with that water comes a higher blood pressure. And that's one of the things that people see the most rapidly corrected. I know gps in the UK who mostly will initially pay attention to blood pressure in the patient as they start adopting lifestyle habits to correct their insulin resistance, because they know if the patient is on an anti hypertensive medication, in other words a blood blood pressure medication, they will have to very likely start lowering their dose because their blood pressure starts to drop so quickly. And I mean within 24 or 48 hours, it starts to drop so quickly that they need to be in contact with their clinical team in order to start changing their dose again, the reaction is just so, so fast. So among that constellation though, again, those are some of the things to pay attention to. If you have high blood Pressure, it's very, very likely that you have insulin resistance. And then if your triglycerides compared to your H is getting to be higher and higher and higher than around one and getting closer to two and more, that's a huge red flag. Very, very likely you have a problem with insulin resistance. And then I would just mention one final point, and that is some of the symptoms or manifestations that appear on the skin. If people particularly pay attention to the ring around the neck and around the neck, you can be looking for two symptoms. Now, not everyone will manifest with this, but if you do have these things I'm going to mention, then it is almost guaranteed that you have insulin resistance. The first is a condition called acanthosis nigricans, which is the long, complicated term for someone having rough, darkened skin around their neck. Now, my neck's covered with freckles, so it'd be, you know, but you could still, if you can't see it as well, you'd be able to feel it. It would be almost this, like, crinkled tissue paper like ring. That's not the entire neck. It is really just kind of a narrow ring around the neck. Again, it's this kind of crinkled tissue, papery type of skin. And usually it's slightly darker complected. And then the second thing again around that same area would be these little teeny mushrooms of. Of skin. It looks like a little mushroom almost, of skin bumping up and that. Those are called skin tags, the kind of informal, unofficial name for them. This is not a big kind of mound of skin. It's a distinct little, almost like a little column or a little pillar or as I said, kind of a little mushroom where it's very narrow and it can kind of bulb out a little bit on top to a very modest degree, but you can feel them. They're teeny little bumps of skin. And often you can see them, these skin tags. So once again, you look at the neck and they are almost proof positive. If a person has these, either of these things or both, you can practically be guaranteed that they have insulin resistance.

And would that be skin tags just in that area? Or could they be skin tags on arms, legs, or are we primarily looking for them just around the back of the neck?

Yeah, absolutely, Steve. They can be elsewhere, but they will almost always be where skin starts to rub on skin, in other words, a skin fold. So you can see them at the armpit as well. That's another common spot. And then you could get them elsewhere. But I've never Heard of them being anywhere other than the neck and the armpits, but suffice it to say, anywhere where the skin is sort of folding in, you can have those skin tags. And regardless of where they are, that is a manifestation of insulin resistance.

Brilliant. Thanks for that. By the way. There is a brilliant book that talks about salts and insulin resistance, and there happens to be a copy just over your right shoulder. Do you want to just quickly tell everybody about the book that you've written? It's on the shelf behind you. I can see it.

Oh, yeah. I promise this wasn't strategically placed.

It might have been one of them for me.

It's one of my favorite.

Yeah.

So, thanks, Steve. So I have such a. Yeah, well, I appreciate the mention of it. Right. So it was that, as I kind of noted early on a number of years ago, when I asked myself whether I wanted my career to be defined by the number of scientific manuscripts I published, and I answered a resounding no to that, to myself. That was the beginning of me saying, well, I want to write a book. I want to see if these ideas are cohesive enough to be put into a book to just kind of outline, well, almost everything we've been talking about. What is insulin resistance, why does it matter, and where does it come from, and then what to do about it. That was the. That's the basics of the why we get sick book. And I'm very pleased with it. Anyone could certainly get a copy. It would be available anywhere books are sold. Yeah, but. But it just takes a deeper dive than the kind of shallow water that you and I are treading in right now.

No, I love it. And it's. Again, Just like I said at the beginning of the program, it's. It's in a language that most people can understand, which is fantastic. I'll just quickly also say something about the conference. I think it was the other Dr. Ben, who said, we talk. He was talking about BMI. He said, well, I wanted to go into the army, and I couldn't get into the army because my BMI was out. And yet this guy was super, super fit. I mean, he'd got six pack, he got big shoulders. And for those who don't know, BMI is simply looking at your weight and your height, and therefore, it's a complete nonsense, Nonsense, nonsense figure. I mean, it just shouldn't be used anywhere. And doctors, sadly, still do use it. Nonsense figure. The figure we look at when we're talking about insulin resistance is your waist to height ratio. And we say, you know, any fat that you carry around is obviously more dangerous and fat around the rest of the body. But we say your waist to height ratio, you should be. If you was to get a piece of string and cut it to the length of your head, if it goes around your waist twice or more, you're probably in a good shape. The second it starts going, then you can't get it round twice. You carry fat in the wrong place. Is that, is that a good analogy?

Absolutely. That's absolutely a perfect way of describing this test.

Right.

It's basically waist circumference time. 2 times 2 should be less than your height. And that, that way you just mentioned it, we're taking, measuring out the string, taking it to the top of your head and clipping it off. And then if you can hold that in front of your belly button and wrap that around two times, well, that's, that's a warning. If, if it's rather, if it's, if, if your height can't get around two times, then it's, it's, it's a problem that your waist is more than half of what your height is. I'm kind of making it overly complicated. But again, if your waist circumference times 2 is equal to your height, that's about the limit. You want your waist circumference times 2 to be less. Or in other words, to put it your way, the string of your height should get around your belly at least two times.

Yeah. And just for complete disclosure, thanks. I've never mentioned this to you before and for everybody watching, we do have a product that it's a kit that people can use at home or go to one of our practitioners that measures those five things. Weight to height ratio, triglycerides, HDL, and the relationship of the two blood sugar levels and blood pressure. And we sell this kit to consumers at home so they can measure all five of them and they go onto App HealthResults app and they put those five measurements in and there's an algorithm that gives them a score from 0 to 100 that was partly worked on by David Unwin that you met at the conference and sat next to. And they basically written an algorithm for me that you pump in those five numbers and it looks at all the ratios, gives everybody a score from 0 to 100. And then they go to our website and we've got separate eat well plates, if you like, for the different scores. And rather than the government one, which is, you know, the same guidelines on food that my dad supposed to follow, who's diabetic and my children that are growing up, my 7 year old or my teenagers, you know, how can we have one plate that is the same for everybody? But what we've done there is we've got various plates and then we also have different plates where they then still need to lose weight or not lose weight, but just for disclosure, those are kind of the measurements that we're looking at, trying to help people realize at home, you know, how insulin resistant they are.

That's a perfect way to do that. Yeah. Good job. I applaud the effort. I think the more, the more people who know where they stand or where they're at in this journey of metabolic health, then the better it allows us to react sooner or be proactive and not wait until things are problematic. But they, they either find that they are further down the road of poor metabolic health than they want and then we need to help them create a strategy to backtrack, or they find that they're in a good spot and we want to keep them on that healthy path, moving upwards rather than descending.

That's brilliant. Right, we're going to go two different ways in a moment. Let's go to those root causes and look at them, because you've talked about stress and you've talked about inflammation, let's talk about the big elephant in the room and then we'll go to a few separate diseases and how they relate. And then I've got a few more questions for you. But, yeah, let's go now and look at those root causes and. And because so far it's all been doom and gloom. But the good thing is, and that's why I'm in this space, it is so fixable, you know, the fact that four out of five hospital beds in the UK and our NHS is completely broken at the moment, four out of five hospital beds we've calculated are as a direct result or it's been influenced by insulin resistance. So if we can get you to learn what you've discovered and covered in your laboratories, more people that get this message, the less. It's the only way to fix nhs. We can't keep throwing money at it because more and more people are getting sick. So let's look at the big root cause, if we can.

Yeah, absolutely right. So hyperinsulinemia, or chronically bumping up your insulin is the primary reason someone's developing insulin resistance. Now, what does that mean? What might that look like? Insulin is the hormone of the fed state. Basically, it's the hormone of eating. You Go and eat a typical meal, insulin comes up, and it does so on purpose. It needs to tell the body what to do with all of that energy, all of those calories that just came in. And then once all those calories have been dealt with, then insulin goes back down to normal. But the tragedy in the modern environment, whether it's the UK or the US or whether it's the Middle east or Southeast Asia or all of which are places that actually have worse metabolic health than we have in the UK or the us. So the problem, this is very much a global problem and continuing to get worse, as you noted there and here and abroad, it's that we eat the wrong foods and we eat them too frequently. Now, let's imagine the life of an average individual. They've been sleeping overnight, they've not been eating, they've been fasting a little, even if only a little. But overnight, insulin and glucose levels have been able to come down. And so by morning, they're at a nice good fasting low level. But we live in such a bizarre culture where breakfast has basically become dessert, where every common breakfast food that is certainly marketed and makes its way into our homes, it is high in starches and high in sugars, whether it is cereal or toast or juice or a bagel. All of these things are foods that will immediately take that low insulin glucose and just rocket it up. Potentially, the insulin goes to 10 times or more higher than it was just just moments earlier. And depending on the health of the person, that insulin comes up and it will take a good two to three or even more four hours before it could get back down. And so here we are, they've been kind of coming along, they rocket up their insulin levels, and then as insulin starts to come down, we live in a culture where people like to snack, and they've even been told it's good to snack in some ways. And so mid morning, two or so hours after eating breakfast, they bump it back up. Whether it's some sugary coffee or another sugary drink or something, or a snack from the break room at work, they put. They bump their insulin levels back up. And then right when insulin is kind of cresting and coming down, well, then it's time for lunch. And then they eat something starchy and sugary and they bump it back up again. And then they do that again for their afternoon snack, they do that again for supper, and then they do it again at the end of the night, at the end of the evening for their evening snack, while they are watching a show. Before they go to bed. And so the average person is spending every waking moment and several hours into their sleeping moments in a state of elevated insulin. And as I noted, elevated insulin is a primary cause of insulin resistance. I can take isolated cells growing in a little petri dish or animals or a human and just give them some insulin and keep that insulin high. And within a few hours I will start to see that the insulin is working less well and less well. In other words, they're becoming resistant to it. And so that's why I focus and why I think that's the best effort is to focus on insulin as one of the causes, because it is so correctable. Because all the GP has to do, or all the individual has to do is say, all right, I am going to either eat better foods and, or I'm going to eat less frequently. And that takes the form of basically these, these kind of dietary paradigms that I like to mention, which is the first one is control carbohydrates. Then they want to prioritize protein, don't fear fats, and fast, fast more frequently. And let's just go through those briefly. Control carbohydrates, by that I mean focus on fruits and vegetables, whole fruits and vegetables, not blended, not juiced, not in some drink box or something else. Whole fruits and vegetables. If that is the primary source of carbohydrate, then the person is doing well. That's a good way to do it. Essentially you want to avoid or restrict the carbohydrates that come from bags and boxes with barcodes. If that's where you're getting your carbohydrates, then they are very processed, starchy, sugary foods and they're going to skyrocket your, your glucose and your insulin levels and it will be very hard for you to keep them under control. So control your carbohydrates, be smart about your starches and your sugars. The second, prioritize protein. Protein is a unique macronutrient. When you eat it, it increases your metabolic rate. You need it for adequate muscle and bone mass. We always talk about it as just being relevant to muscle, but it's very relevant to bone health as well. But suffice it to say, we need protein. In fact, it is something that is essential. And although it's becoming less popular to say this with every passing day, I'm a scientist, so I don't have to care about cultural norms, but that is to focus on protein sources that come from animal. Animal sourced protein by every metric is superior for human Health than plant sourced protein. Now I'm not saying there isn't a way to get your proteins from plant sources. Well, but it becomes very, very difficult to do, especially for children where it's just, it's simple to know that if it's an animal source protein, whether it's dairy, eggs or meat, you'll get all of the amino acids, all of the kind of protein that you need, and you'll absorb it through your intestines into your body very, very well. So that's prioritize protein, make sure you're really getting protein. And then third, don't be afraid of fat. That's probably the hardest because we have such a cultural aversion born from decades of fat fear mongering where we need to appreciate that fat is not only essential, it is we need to eat a certain amount of fat and certain types of fats to be healthy. But we can't. The further we vilify fat, the more we tend to make up that difference with more and more sugar or processed starches. So don't be afraid of fat and even be liberal with it, certainly with protein. Any of these proteins I just mentioned that come from natural sources always come with fat and that's how we should eat it. So when it comes to dairy, don't get skimmed milk or zero fat yogurt. You know, let the fat be there. It's supposed to be there. When it's eggs, don't dump the yolk. It's supposed to come with those egg whites. It helps us absorb the proteins better, it helps us build muscle better. You know, a whole egg with the yolk will build muscle bigger in humans. Better in humans than just the egg whites. As much as people just focus on the egg whites, that's not how they're meant to come. We're, we should eat those proteins and fats together because in nature that's, that's how we get them.

Can I.

And then lastly it's, it's fasting.

It just pick you on a couple of things there, if I can. Fat, protein, we can't live without. We just die eventually if we don't eat them. Yeah. So we have to get those. The human requirement, correct me if I'm wrong, and you know, you're the scientist, I'm just a humble businessman trying to learn all this stuff. Correct me if I'm wrong. The human required for carbohydrates is zero. I mean you could live a real healthy, probably even healthier life with zero carbohydrates in Your diet. Is that correct?

Oh, yeah, yeah. But you're kicking a porcupine by saying that. But it's absolutely true. I mean, once again, thankfully, as a scientist, I don't have to worry about dogma, neither dogma nor cultural pressure. But you stated it perfectly accurate. As much as people don't want to admit it, even the most dogmatic dietitian has to admit, very reluctantly, that there is no such thing as an essential carbohydrate. I just recently witnessed this vigorous debate where people were describing essential dietary fiber. And I just thought, this is a. That is a. An adjective, essential. That does not belong with the rest of those words. With that noun, you know, dietary fiber or fiber is. There's nothing essential. Now, I wanted to just again emphasize that I'm not telling anyone that they should not eat any carbohydrate. I'm not saying that. That's just too polarizing. And I don't think these ideas would land. I don't think they'd be very palatable if that were my recommendation. But that is the simple reality, that there is no such thing as an essential carbohydrate. We know this. This has been borne out since time immemorial in humans. Humans can thrive on getting what they need, namely essential amino acids, proteins, and essential fats. There is. If a human gets those things, then they're good with regards to nutrients. There is nothing from a plant that a human needs is certainly not fiber. I mean, fiber is literally a waste product. Now, I'm not telling anyone they can't eat fiber, but if they do so, they do so knowing that they simply have become accustomed to the bowel habits, the bowel movements that it gives them, which, hey, that's fine. Although some people find that dietary fiber actually is quite a harmful substance in their intestines. There are many people with things like ulcerative colitis, for example, or even Crohn's disease who find that when they're tapering off their fiber, the disease symptoms improve dramatically, not even subtly. Even people with just benign constipation find that their constipation gets better as they dose down the fiber in their diet.

Wow.

And so I don't mean to declare war on fiber. I think fiber can be healthy and can be used as part of a perfectly healthy diet and even beneficially so if used judiciously, perhaps. But it is far from essential. Humans do not need it. There is no such thing as a plant that humans must eat. And indeed, the vast, vast majority of plants in the world. If a human were to eat them, it would kill them or make them very, very sick. In our wisdom, we have.

Sorry, Ben. I'll pick up on two things there. Quite interesting. We're going to quickly show for everybody at home, we just talked about breakfast, some figures from Dr. David Unwin with his brilliant work on the teaspoons of sugar. Because we can quantify that now with research and science and work from great doctors and what? There we go. So, you know, if somebody has a 200 mil, that's an average sized glass of pure apple juice. Hey, I'm guilty. I've been filled. I was feeding my kids this. There are things on there that my kids used to have for breakfast almost every single day. So if you're at home going, oh my gosh, what am I doing to my children? Well, you weren't aware of it, so that's fine. But you are aware of it now. You know, a glass of apple juice turns into over eight teaspoons of sugar. So the body's then got a battle to get rid of seven of them. But of course, you're not just having the apple juice for breakfast. You're probably having your shredded wheat because you've watched the TV advert and the TV advert. There was one recently that they had the audacity and I hate it because I go to church reasonably regularly. They said that. I think it was Moses. They said, oh, Moses must have had three Weetabix this morning. You know, it was like, terrible. So even the Weetabix is full. I mean, everything turns into sugar at breakfast. The orange juice, the bread. Oh, I'm having. Steve, I'm having brown bread, not white bread. I'm fine. I'm being good to my children. No. Yes. Brown beard bread might be slightly better than white bread, but that's only the same as saying one broken leg is better than two broken legs, you know, so get off all this junk.

It even goes further. It even goes further where? That list you just showed. It's one thing to note the actual amount of sugar.

Brown bread, not white bread. I'm fine. I'm being good to my children. No. Yes. Brown bit bread might be slightly better than white bread, but that's only the same as saying one broken leg is better than two broken legs, you know, so get off all this junk.

It even goes further. It even goes further where that list you just showed. It's one thing to note the actual amount of sugar in those. I don't know whether people are aware of a Paper that was just published in the United States. This was funded by our National Institutes of Health, sponsored by a very, very prestigious university, or performed at a very prestigious university. And it was basically this measurement of healthiest foods like kind of going down to increasingly less healthy. And they, in those, I don't know whether people are aware of a paper that was just published in the United States. This was funded by our National Institutes of Health, sponsored by a very, very prestigious university, or performed at a very prestigious university. And it was basically this, this measurement of healthiest foods like kind of going down to increasingly less healthy. And they had many wheats and things like Corn Flakes, which was just on that list. You showed having multiple teaspoons of sugar in it was healthier than eggs. It was healthier than milk. So this, this image here, we see that it's, it's called a Food Compass score. We had mini Wheats and things like Corn Flakes, which was just on that list. You showed having multiple teaspoons of sugar in it was healthier than eggs, it was healthier than milk. So this, this image here, we see that it's, it's called a Food Compass score. And what you can see is things like canned peaches and Cheerios cereals is ranked higher and not even by a little. It has a Food Compass score that is, you know, three or four times higher than things like eggs or beef or cheese. You know, any of these very protein rich sources that come from that we would have eaten naturally as humans. They are, they are the lowest. And what you can see is things like canned peaches and Cheerios cereals is ranked higher and not even by a little. It has a Food Compass score that is, you know, three or four times higher than things like eggs or beef or cheese. You know, any of these very protein rich sources that come from that we would have eaten naturally as humans. They are, they are the lowest. Even something as horrible as Lucky Charms is considered healthier than eggs, as you see on this figure. And so this just further reflects the problem. And again, this was sponsored by our National Institutes of Health in the United States. It's embarrassing to me. And it so clearly reflects either the. Even something as horrible as Lucky Charms is considered healthier than eggs, as you see on this figure. And so this just further reflects the problem. And again, this was sponsored by our National Institutes of Health in the United States. It's embarrassing to me. And it so clearly reflects either the degree to which we have food manufacturers mingling their whims and desires into the Research and enforcing outcomes almost, or we're just, our minds are broken and we can no longer truly determine what is healthy and not. But when you take David Unman's figure and then look at it in the context of this, these findings that the degree to which we have food manufacturers mingling their, their, their whims and desires into the research and enforcing outcomes almost, or we're just, our minds are broken and we can no longer truly determine what is healthy and not. But when you take David Unman's figure and then look at it in the context of these findings that were just published where someone would think that a bowl of mini wheats, which is sugar coated wheat biscuits, is healthier than an egg or a glass of milk, you can only laugh and wonder at the degree to which we really are entering into this clown world where it's a world of nothing but obesity and diabetes and an ever growing dependence. Were just published where someone would think that a bowl of mini wheats, which is sugar coated wheat biscuits, is healthier than an egg or a glass of milk. You can only laugh and wonder at the degree to which we really are entering into this clown world, you know, where it's a world of nothing but obesity and diabetes and an ever growing dependence on medications. Because if you truly believe that eating a bowl of sugary cereal is going to be healthy for you, then you will continue to eat that way. And then as you get ever sicker, the only other alternative will be to be taking more and more medication. Not only a variety of medications, but increasing the dose forever.

Yeah.

So it's a wonderful on medications. Because if you truly believe that eating a bowl of sugary cereal is going to be healthy for you, then you will continue to eat that way. And then as you get ever sicker, the only other alternative will be to be taking more and more medication. Not only a variety of medications, but increasing the dose forever.

Yeah.

So it's a wonderful way to make a lifelong patient.

Absolutely. And we learned the weekend well, I learned the weekend that a patient, the word patient comes from the word sick. So you know, we practice sick care, not healthcare. Is my take on that a way.

To make a lifelong patient?

Absolutely. And we learned the weekend well, I learned the weekend that a patient, the word patient comes from the word sick. So you know, we practice sick care, not health care is my take on that. And many people say, are you just a conspiracist theories person, Steve. But I bet that research was sponsored either by a drug company that needs you to be Sick. Or some of those big food companies. In fact, in the UK, we have two diabetes. We have one that's a charity. Diabetes.co.uk sorry, the other way around. Diabetes.org is a charity.co.uk is a commercial company. Which ones. Many people say, oh, you're just a conspiracist theory person, Steve, but I bet that research was sponsored either by a drug company that needs you to be sick or some of those big food companies. In fact, in the UK, we have two diabetes. We have one that's a charity. Diabetes.co.uk sorry, the other way around. Diabetes.org is a charity.co.uk is a commercial company. Which one do you believe? Well, actually, you believe the commercial company because the charity at their last conference was sponsored by Swept Cadbury, like they're sponsored by chocolate bars. I mean.

Yes, and the American Dietetic.

Well, actually, you believe the commercial company because the charity at their last conference was sponsored by Swept Cadbury, like they're.

Sponsored by Chocolate association. And similarly with American Diabetes. So the American Dietetics Association. So the. Well, and the American. Yes, and the American Dietetics association. And similarly with American Diabetes. So the American Dietetics association. So the entity that license licenses all of the registered dietitians in the us, they, they are funded primarily by food manufacturers, just like you mention. And then the American Diabetes association is primarily funded by insulin manufacturers. And if you have an insulin resistant type 2 diabetic who believes eating sugary cereal is the best way for them to control their disease, well, that's an incredibly efficient way to sell more and more insulin and other increasingly common diabetes drugs. So that is, that is admittedly, a little bit of a cynical take, but we can't argue with the objective reality that these things are happening. We can only speculate as to the motives behind them.

And just again, slight tangent, but I totally agree with everything. I mean, it's a very sad state of the world. And you said a minute ago, you can only laugh at it. I want to cry at it. You know, it makes me. I've got seven children, I've got a dad that's got diabetes, I've got a mum that's got Alzheimer's. You know, looking at all your research and my tree, it's the same disease manifesting in different ways. They've lived together since they were 14 years old. My mum and dad never been apart. They eat the same meal, the same amount of wine, they have to do everything the same, the same exercise. They've been together forever. They're both 82. And for my mum, she's got very bad Alzheimer's and my dad's got very bad diabetes. While we're talking about my dad and his diabetes, I'm for the first time going to be allowed to go and see his doctor this Friday and he's been on medication for three years. And I'm going to ask the doctor, why are you giving my dad insulin as a type 2 rather than medication? Because my dad has just piled on the weight. Piled on the weight and piled on the weight. In fact, we haven't talked about that yet. In fact, that if you could. If that leads nicely, segues nicely. If you could talk about why having more insulin piles on the weight than that boss hormone. And it's about putting on weight. I'm sick of trying to get through to my dad because I can't listen to you. So my doctor said it's insulin. Must be. They must be right. They must know what they're talking about. And then. And I go, well, don't listen to me, dad, listen to my doctor friends. Oh, your doctor friends must all be quacks then, because they must all be. I'll go, no, to the way around. Your doctors just must be very out of date with the latest research. He probably doesn't never heard of insulinemia. I don't know. I mean. Ben, help me, tell me.

Yeah, yep, yep, yeah, yeah, well, and I'll preface my answer by saying, I think what you said at the end there actually is quite on point, which is that neither you nor I is pointing a finger and mocking the clinician who doesn't share the same view perspective that you and I do, because we only know what we've been taught. And it is, I think, profoundly unfair of us to expect a physician, a GP or any clinician to know everything we know, because this is an individual who has been trained across such an enormous breadth of problem that how can we expect them to be an expert in this one niche area, as relevant as it is, and I believe it's very relevant of insulin resistance. If you haven't been taught this well, then you don't know it. That's one of the reasons why I so much enjoy participating in meetings like the one you and I were just at and the one we will be at with PHC in Sheffield in May, where my great hope is that there are clinicians who hear this message and they can nod their head and say, I believe this is true and I'm going to test it. I'm going to see how true this is. And so we have to be sympathetic. But I think it is unconscionable. I think it is terrible to give a type 2 diabetic insulin therapy. But that reflects this paradigm how? The very beginning of our conversation, I was talking about insulin and glucose levels and how in the insulin resistant state or pre diabetes, glucose is normal, but insulin is elevated. And then it's when insulin becomes so inefficient or incapable in the body insulin resistance, that now the glucose levels start to climb as well. The average clinician has only been trained to look at the glucose. It's the hand that's waving in their face distracting them from seeing the insulin level, which is also very, very high. They haven't even looked at that. They've only been looking at the glucose. And so to the glucose centric paradigm, as I noted earlier, the clinician feels justified in saying, well, I'm just going to give you insulin. I don't even know where your insulin levels are, but they must be too low. In reality, they're very high. It's just not working well anymore. But by pumping the insulin to what's called a super physiological level, pushing it even higher than it would have been, it is sufficient to lower the glucose. But remember that entire tree of disease, Steve, that you put together, those are not consequences of hyperglycemia. Those are consequences of hyperinsulinemia. And so it's no surprise that in the midst of improving their blood sugar levels, we actually make them fatter and sicker than they were before and ever more insulin resistant, because chronically elevated insulin is a driver of insulin resistance. And so if your dad was eating the exact same foods every day, day in and day out, he would find that he needs to steadily be increasing his insulin dose because he's becoming ever more resistant to it. And we know the more aggressively a person with type 2 diabetes needs to give themselves insulin to control their glucose, they are three times more likely to die from heart disease and twice as likely to die from cancer and twice as likely to develop Alzheimer's disease. It's because those are not problems of the glucose, they're problems of the insulin. And so that would, in a way, transition to discussing your mom, where we know that in Alzheimer's disease, the most common feature is that the brain has become insulin resistant for decades. We've spent so many billions of dollars and so many thousands tens of thousands, hundreds of thousands of man hours, science hours, focusing on this thing called plaque in the brain. And now we know that that whole paradigm was just basically fabricated and there's almost no value to scrutinizing plaque at all. Thankfully, there's another contender theory that's been waiting in the wings to become the most prominent one, and it's gaining a lot of speed very quickly, and that is to look at Alzheimer's disease as insulin resistance of the brain. The brain. And I'll just describe that briefly. The brain has a very high metabolic rate. It's constantly active. Even while we're sleeping, it's still busy, it's doing a lot of things. Even if while we're sleeping, it's cleaning itself out, which it does while we sleep, it has a high metabolic rate, it needs energy. And the brain is a hybrid engine that can run on two fuels. It can run on glucose and it can run on ketones. Now, ketones, just very briefly, ketone is simply basically a molecule, a nutrient in the blood that comes into the blood when we start burning a lot of fat. And I'll come back to that more later perhaps. But the brain can use glucose and ketones, but we only make ketones when insulin levels are low, because we can only really burn fat when insulin levels are low. In contrast, if insulin levels are high, fat burning shuts off and then the fat cells start to grow. That's why your poor father, as he's giving himself more and more insulin, is gaining more and more weight, because insulin tells the fat cells to grow by inhibiting fat burning. And if you inhibit fat burning, you don't make any ketones. That's a problem in Alzheimer's disease, because as the brain is looking at these two fuels, glucose, ketones. In order for the brain to use glucose, it needs insulin to open those doors. In contrast, the brain doesn't need insulin to open any ketone door. If ketones are in the blood, the brain will greedily pull the ketones in and burn them for energy. Indeed, the brain thrives on burning ketones. And there has been evidence to show that ketones can correct some degree of the cognitive decline that accompanies Alzheimer's disease. You can take an individual who's in the throes of full blown Alzheimer's disease, and if you can increase their ketones, they can immediately improve their cognition. Not that you've reversed the disease. No, but they will think better, they can perform better on cognitive tests. Maybe they wouldn't have been able to tie their shoelaces. Now they can. So there are known and published benefits to allowing the brain to have access to ketones. But the Particular tragedy of insulin resistance is that on one hand, you not only deprive the brain of glucose, which the brain would normally happily burn for energy, because the brain can't get it, it's insulin resistant. And so the glucose doors don't open very well anymore. And so the brain is less capable of getting glucose. That simply would increase the need for ketones. But if a person has insulin resistance, they have elevated insulin levels, which means fat burning is turned very low, and that means ketone production has turned very low. And so while the brain is. It's this bizarre kind of version of the rhyme of the Ancient Mariner, this tune of the plea of the water, water everywhere nor any drop to drink. It's basically the brain. Glucose, glucose everywhere nor not a molecule to burn it can't get it. And it's calling out for the life raft of the ketones, saying, well, I can't use all of this glucose even though the body is flush with it. Give me some ketones, because I can burn ketones. But the elevated insulin is depriving the brain of the single kind of life life raft that we're trying to toss out to it as it's drowning. And so that's the. That's the particular tragedy of Alzheimer's disease and insulin resistance.

So, first of all, I've got to talk to my dad's doctor then and get. Try and get them to change his medication. He's put on like 20 pounds. I mean, he was already overweight, hence probably the diabetes, and he's had the gout before, and he's had the erectile dysfunction and he's had the blood pressure. So all those things, now that your message getting out there, hopefully doctors in the future will start to see those are kind of early warning signs that something's wrong. But one of the things I should also tell my dad is that story about that research you did about the actual injection site. Can you just enlighten everybody with that?

Right, yeah.

One of the most common refrains that you hear when someone begins treating themselves with insulin, regardless of the disease, is that they are told, when you inject your insulin, make sure that you are rotating your injection sites throughout the body. In other words, one time give yourself.

Your insulin injection and put it in.

The back of your arm. Another time put it in one side of your belly, another time put it in the fat on your.

On your thigh, on your leg.

And we tell them to do this because insulin is such a powerful growth signal on fat cells that if. If a person who's treating themselves with insulin doesn't rotate their injection sites.

If they fail to move that around.

The body each injection, the fat cells, for example, if they, if they were only injecting on their belly, then those.

Fat cells that get all of that.

Insulin every time will get such an exaggerated growth signal that they can literally grow to become 10 times the size of a normal sized fat cell. And when you look at it from the microscopic level, that's what you can see. You can see just these incredibly exploded out fat cells. But when you look at it from the macroscopic level, in other words, just looking with your eyeballs, what happens is that those areas that are getting all of those injections become excessively, almost comically enlarged. And so the person will have a normal belly. You know, trim, trim, trim, flat, flat.

Flat, and then get down to their.

Belly button area where they've been giving themselves their injections.

And then it's just these big bubbles.

Of fat hanging down over their belly.

Or if they've only been giving themselves.

Their injections in their thighs, they have a normal shaped thigh and then these two big lumps sticking out of their thighs. It's just because the fat cells have been so stimulated with insulin. And then the same thing, to varying degrees of course, can happen throughout the body. Even if you have the diabetic who is rotating their injection sites, all that means is they're going to store that same amount of fat, it's just going to be more evened out throughout the body. It wouldn't have such a kind of bizarre appearance to it if they had gained 10 pounds of pure fat in their belly from not rotating injection sites. All that means is now they've gained that same 10 pounds, you know, or you know, six, five, six kilos throughout the entire.

I mean, this is UK, I can.

Talk pounds just throughout the body. So they've just spread it out. But regardless, this is a point worth emphasizing. You cannot stimulate a fat cell to grow unless insulin is elevated. As much as there is debate surrounding what, what's the nature of, of fat growth and obesity, it's just, it's pure calories consumed. No, it's just insulin. Well, the reality is they both matter. But a fat cell doesn't know what to do with calories unless insulin is there to tell it what to do. And for example, in my lab here at the university, we grow fat cells in little petri dishes. The fat cells are kind of incubating in this perfect bath that constitute, that gives it everything it needs to survive, including calories. Because cells need energy, but those fat cells will stay very, very small. In fact, I could even say very skinny. Until we start adding insulin into that culture.

Wow.

Into that little bath the moment we start putting in the insulin. Now, even if we don't change the amount of calories in the culture bath, it's the same amount of energy that was ever there. Now, all of a sudden, those cells.

Know what to do with all of that energy.

And in response to insulin, they know no longer are we going to be skinny fat cells, it's time to become fat fat cells. And they start storing all of those calories because insulin is telling it to. And then again, when you put this back into the type 2 diabetic who has been prescribed insulin therapy to control their glucose, what you've done is continue to push up their insulin higher and higher. And that's going to stimulate greater and greater fat cell growth, which paradoxically, makes the person hungrier and hungrier. Because as insulin is forcing any excess calories to go into the fat cells, there's less energy for the brain to eat. And then the brain starts to tell the body, hey, I'm going hungry, body, let's bring in more calories. And so, by forcing insulin to go higher, you force your fat cells to grow bigger. And in so doing, you deprive other people of energy, because the fat cells just get so hungry and greedy. And that general energy deprivation to other parts of the body, like the brain, stimulates greater hunger, which will cause the person to eat more, which will cause them to increase their glucose more, driving them to give themselves even more insulin. And then we have the vicious cycle just continuing, all with the best of intentions. It's not like the GP is trying to hurt the patient. It's not like the patient is trying to be negligible and ignore good advice. They're doing everything they've been told to do. And yet the simple reality is, the higher we push insulin, the more we force fat cells to grow, and that will drive hunger.

And, of course, the more we push insulin, I always say, people say, I want to lose weight. I said, well, first of all, you're barking up the wrong tree because you can't lose weight. Right? You've got to burn body fat. Yeah, you can't lose weight. It's impossible. Just like, oh, it's all disappeared. You've burnt it. You have to burn it as body. You have to burn the body fat as energy. And correct me if I'm wrong, when insulin's up, not only is its job to, as you said earlier, it's got many, many jobs, whereas most hormones only have one or two jobs. It's got many, many jobs. But one of those jobs, of course, is fat storage. It's there to deliberately store body fat, make more body fat for a rainy day or, you know, the next big, I don't know, ice age or whatever. And if you've got elevated insulin, and if it's. If insulin's the fat storage mode, it's kind of almost impossible to burn that body weight. So if you're carrying a little bit of body weight at the moment, avoid foods and obviously avoid stress and inflammation, but avoid foods that require insulin, because once insulin comes up, your chances of burning body fat are almost zero.

And, Steve, there is so much power in what you just said. If we could imagine someone who is standing at the beginning of a weight loss journey all for the best of intentions. They want to improve their blood pressure. They want to reverse their diabetes. They want to reduce their risk of Alzheimer's disease. They have every good reason to do this in the world. It's not like these people lack motivation. They're standing at the beginning of this long. This marathon, and they can choose to start this journey with one of two steps. One step is just reducing energy. In other words, eating less. Low calorie, low fat, low calorie.

The alternative step is low insulin.

Now, let me describe the problem. So many people with the best of intentions, they've just been told so long obesity and excess fat tissue is purely a matter of calories. You just have too much. Just eat less and exercise more. So they take that first step of, I'm eating less fats, my calories are down, and, boy, I'm working out more than ever. All that does is drive hunger, you know. So as a sort of brief aside, a brief tangent, and I'll come right back to this. Let's imagine that we had all been invited to this beautiful restaurant, and it's going to be a buffet of the world's best chefs creating for us the most delicious food we could imagine. And we've been encouraged by our host to come as hungry as possible so that we can just try some of everything and indulge. What would we do to come to that buffet as hungry as possible? We would invariably do two things. We would eat less in the days before the event, and we would exercise a little harder. And sure enough, we would be very, very hungry. Well, can we see the problem here? I just described a scenario of how can you drive hunger as much as possible. And we came to the same two conclusions that we would if we were asked, how should we lose weight in both instances, Whether it's I want to become hungry or I want to lose weight, with this classic kind of calories in, calories out idea, we would deliberately, we would, we would knowingly and exercise more. Well, that strategy is such an effective tool for driving hunger that thereby, it makes it the worst way to start.

A weight loss journey. So if that first step is built.

On eat less, exercise more, sure, we will have a little weight loss in the. In the immediate time after, but hunger will go higher and higher and higher, and hunger always wins. We can't start the weight loss journey on hunger because our body isn't metabolically adapted yet. So keep that foot behind the starting line, the low energy calorie, the low calorie foot. Let's keep that in place. Let's rather let the first step be the low insulin step, because when insulin starts to come down, as you noted and we've discussed several times now, fat burning starts to go up. And the good news of that is it finally allows us to tap into our own body fat. All of this body fat that we've been storing, it's basically little energy bars and energy drinks just waiting to be ripped open or popped open for us to use. It's just that our chronically elevated insulin won't let us use it. So if the first step is the low insulin step, we adjust our eating habits to help insulin come down and stay down naturally, namely by controlling carbohydrates. But we don't have to go hungry. We don't have to count calories. We can eat whenever we're hungry and eat as much as we want until we're full by following the next two rules, prioritizing protein and not fearing fat, particularly the fat that comes with that protein. If we nourish our body with those energy sources, again, we can delay or prevent any hunger, nourish the body, but keep insulin down. And so that allows us to burn our own fat for fuel and even start burning more fat, because when insulin is down, we burn more calories. Our metabolic rate goes up by about 300kcals per day. That's not an insignificant amount of energy. And it helps us kind of balance things out. And so that's the first step. If the first step is, I'm going to lower my insulin, then we become used to burning our own fat for fuel. And then once we've come to a plateau, which you will, you will lose weight and you will lose it quickly and you'll continue to lose weight. And then maybe you would come to a plateau where you would say, all right, I know I'm still a little heavier, I got a little more to go. Well, now you can finally move that next step forward if you want, by saying, okay, I'm going to deliberately create windows of time in my day where I'm not eating. In other words, I'm intermittent fasting. And that will allow the energy to start to come down very naturally and we're well prepared for it. We will be much less hungry because we have trained our body to use our own fat for fuel. Then again, now we have these two feet that we're using to go down the journey.

Let me get this right. This is the Ben Bitman of two step process to losing weight. Step one, reduce as much as you can foods that make insulin go up. So that's your sugars, your refined foods, your carbohydrates, your grains, all those sorts of, of things first thing, and do that till you know your weight plateaus. And then if your weight plateaus and you're still five, six pounds a stone more than you want, but you, you're still eating the right food, then maybe cut back a little bit on that food and then, you know, introduce intermittent fasting. That's the Ben Dickman sort of two stage. Is that right?

That's, that's perfect.

Right?

Yeah.

That, I believe is the most prudent way to move forward. You just have to take the right step first.

Okay, I've got loads more questions and I'm conscious of your time. I'm just going, n equals 1. I know is not the best study ever, but n equals 1. So I was obese for 25 years. I wasn't lazy. I was running most mornings. Really silly. I was getting up at four in the morning to go running because I didn't know that sleep trumps exercise. I thought exercise trumped everything. I'm obese. I'm like 32% body fat. 25 years like that. I'd got personal trainers helping me, I'd got nutritionists helping me. And I was doing everything they told me. I'd go low fat yogurt, low fat, this. I was doing everything. And I was driven by hunger. I was always, always, always hungry. And what my friends don't understand and can't get their head around is how I can now go and cycle for five days and not feel hungry once. But it's because I can just tap into my as far as I'm concerned, and correct me if I'm wrong, the body doesn't mind whether it's fat and protein coming in this way or whether it's burning its own body fat. It doesn't care where it comes from. Once you're in that fat burning mode, is that a reasonable summary?

Oh, for sure. In fact, we say that the body doesn't care. We could be even a little narrower and say the brain doesn't care because it's the brain that primarily is going to drive hunger. There's two phases to hunger. One that is quite acute and passes quite quickly, then the second, which is much deeper and more profound. The first phase of hunger is, is.

There something in my guts?

Is there something in my stomach? And if it had been distended, the intestines had been stretched with food and then they find themselves empty sometime later, that emptiness can result in a rumbling of the stomach and a sense of hunger. But that passes. We can get through that fairly well and we should be able to. If you're an adult, you should absolutely have the mental fortitude to just say, hey, tummy, you can rumble. I know that you have enough energy body because I can look and pinch all of my fat. That's what the brain really cares about and that's that next phase of hunger. And this is why you can have people who admittedly, ideally, under some clinical supervision, can fast for weeks on end. Or the story of this fellow in the UK from decades ago who fasted for an entire year.

Yep.

He literally didn't consume a calorie for a year.

Yeah.

Under clinical supervision.

This is a published, documented case study.

In the uk and he was healthier.

Than ever and went on to live.

A perfectly healthy life.

Yep.

And this.

And that's because he had gotten through.

Yep. He was a Scottish gentleman, went 360. It was over a year, a year and a few days. He was on death's door before he went into the hospital. He was morbidly obese. And they said, you know, basically you're not going to last very long. And it was his idea. He said, well, as they said to him, you actually could go a long time without eating. He said, well, let's try it. So under clinical observation, didn't leave the hospital. So there was no cheating. He lost so so much weight but didn't eat a single calorie for over a year. So makes my five day bike ride look like child's play. But here's the other thing about fasting. Isn't it and this is what most people. Well, I've tried fasting before and it didn't work. It didn't work because you were still a sugar burning machine. The second you change your diet to become a fat burning machine, it's the, I mean I'm omad, don't get me wrong, on holiday I'll have the omelettes with the kids in the morning and things like that, but the rest of the time I'll just eat once in the evening and I'll never, ever, ever hungry. I remember Tim Noakes said to me once, he said he came to realize that the thing that drives obesity is hunger itself. You know, people, they're not weak willed, they feel hungry because you know they've eaten that car breakfast instantly goes, oh my gosh, there's too much sugar, grabs it empties it puts it into the fat store and now you're hungry again. So at 11 o' clock you go, and the brain goes, well I need some energy quick because insulin's just got rid of the last meal. Oh, I'm going to have some crisps or some chips or a sandwich because it knows that that bread will turn into sugar really quickly. So now you get another insulin spike. It grabs, it gets rid of the food. Now you're hungry at lunchtime and the brain's telling you to have more carbohydrates because it knows it's going to fill you up quickly. And you're on that, what I call the carb cycle. You just, I used to call it the carbo coaster. You know, it's like you're on this coaster ride that's like this but because you're being driven by the need for food, whereas the second you can teach your body to live off more protein, you don't have to go crazy like I'm doing this month with a carnivore, but you could just be eating really nice wholesome food. Your fruit, your veg, fruit obviously a bit careful, your veg, your meats and your proteins and all that and you're never hungry.

That's right. Well and this happens very quickly. There have been very well controlled human studies to find that if someone eats, you can put people into two groups or the same person into two groups one after the other over days and they can eat the same meal, calorically speaking. So these are two meals that have.

The, the an identical number of, of.

Kcals and yet they vary based on their macronutrients. So the amount of carbohydrates, proteins Fats is different. Well, particularly carbohydrates and fats. Same amount of protein across both groups. The meal, again, the exact same amount of calories, the meal that spikes insulin the most. In other words, the higher carbohydrate, lower fat meal will result in a much faster return to hunger, as they called it. So they would eat a breakfast and then monitor their hunger scores for hours afterwards. And even though they ate the exact same amount of calories, the meal that spiked their insulin the most made them hungrier, much sooner, significantly sooner, than the meal that had the lower impact on insulin. And that is for the reasons we've mentioned. You invoked Tim Noakes, for whom I have an enormous amount of respect. We both do, but he's described it well, others have as well. A scientist here in the US named David Ludwig has really shed light on this and basically finding that when insulin is spiked, it lowers the total amount of energy that is available in the blood. And that is a unique problem for the brain because the fat cells, they store a lot of energy. They have a lot of energy on hand. They don't need to be pulling it in from the blood. Even muscle cells have a lot of energy that they've stored within themselves. The liver has lots of energy that it's stored. The brain doesn't have any. The brain doesn't have an energy storage depot built within it. It doesn't have room for that. It has to constantly be taking the energy that the blood can give it. And so if you've spiked insulin and you have lowered your total energy, which is something David Ludwig has shown very convincingly, it's no surprise then that the brain is sensing this. And then it starts to tell the body, hey, red alert, I'm going to go hungry soon. And if I go hungry, I'm going to shut off and then the brain's going to go unconscious if I can't get enough energy. And so let's eat. And like you noted, it would. It would perhaps increase the seeking, the behavior of the person to consume something that they know will spike their blood glucose levels. Again, just continuing to keep the problem propagating. The solution is, again, don't let the first step simply be low energy, especially the way most people do it, because they will go low energy by cutting out fat and usually protein and focusing on starches and sugars because they have a lower calorie little, knowing that while they are reducing their calories but spiking their insulin, energy availability in the blood is dropping more and more and more. And it's no surprise that hunger is going to invert that, that they're going to become very, very hungry. And in this world of such readily available food access, hunger always wins because you can indulge that hunger the moment it reaches the point of breaking. And then you break. And one last comment on this, Steve, if you'll allow me. Here in the US for years there.

Was this popular game show called the Biggest Loser.

And it would take individuals who were morbidly obese and put them through this boot camp of weight loss. And the weight loss would be profound, but it would be through extreme calorie restriction and extreme exercise. It worked. They lost weight. But what is so interesting is we never see a reunion tour of these game contestants.

You never see them get back together a year or so later because they.

Gain it all back and then some. A paper published sponsored by the nih. The NIH can do some good things here. They found that in these people, they basically broke their metabolic function. That normally our metabolic rate is kind of attached to our body weight, that.

If we start to lose weight, there's.

Less of our overall body here. And it's no surprise that our metabolic rate comes down. And then typically as someone is gaining weight, the metabolic rate will go back up with it. That's just the reality of metabolism. What happened in these people who entered the contest as morbidly obese with a high metabolic rate reflecting a big body, they lost an extraordinary amount of weight. Metabolic rate dropped then as they started, but through this severe starvation and calorie restriction, they started to gain their weight back as they start to indulge. And it got worse and worse. And metabolic rate didn't match. It should have matched coming back up. It didn't. Body weight started accelerating. Metabolic rate was much more sluggish and it didn't, it wasn't coupled with body weight anymore. They broke it. And now that's not to say it's irreparably broken. I would hope not. But it certainly reflects the problem with the first step of a weight loss journey being just a low calorie step with no consideration of insulin and energy availability and making sure the brain is adequately nourished so that it doesn't stimulate an ever increasing hunger.

Yeah, fascinating, fascinating. And it kind of again shows the problem that yo yo dieters like I had for that. You know, I was trying that 25, 30 years I was obese, that the yo yo diet, every time you try one with the calorie restriction and it's actually making the problem Worse and worse, because every time you lose a bit, then come back up, you always come up a bit higher. And I think you just beautifully explained probably the science why that was happening to me as well. What I'd like to do, I'd like to just go through some of the key illnesses that we know, insulin resistance and hyperinsulinemia contribute to and explain why. And on heart disease, you've kind of already said one of the reasons why it's linked to heart disease. Because when we were talking about infertility and erectile dysfunction, you were talking about the fact that, you know, it constricts the blood flow, so that we've got one there already. On heart disease, you also mentioned about the fact that these. Because when we were talking about infertility and erectile dysfunction, you were talking about the fact that, you know, it constricts the blood flow, so that we've got one there already. On heart disease, you also mentioned about the fact that insulin makes you hold on to more salt, so again, that will restrict, you know, because more salt means more water. More water. Insulin makes you hold on to more salt, so again, that will restrict, you know, because more salt means more water, more water means more volume, more volume means, you know, restriction in blood flow. There's two, but there's. There's a couple of other ones that. That relate, I know, to heart disease. And I'm just looking for something you wrote some time ago. You said almost all people with hypertension are insulin resistant. In other words, hypertension, for those don't understand, hypertension is high blood pressure. So you wrote almost more volume. More volume means, you know, restriction in blood flow. There's two, but there's. There's a couple of other ones that. That relate, I know, to heart disease. I'm just looking for something you wrote some time ago. You said almost all people with hypertension are insulin. Almost all people with hypertension are insulin resistant. And then there was another one. I can't find it here. But in your book somewhere, you quoted somebody else that said, anybody that's got hypertension that don't know they've got insulin resistance just haven't been diagnosed yet.

Right?

Yeah. Yeah.

That was a quote by insulin resistant.

In other words, hypertension, for those don't understand, hypertension is high blood pressure. So you wrote almost a scientist here.

In the US who in recent years has become quite famous, named Dr. Kraft, and he actually became famous thanks to an Irish fellow named Ivor Cummins. Ivor really contributed to Dr. Kraft's work gaining kind of mainstream attention. But yeah, he was the one who said anyone with.

Almost all people with hypertension are insulin resistant. And then there was another one, I can't find it here. But in your book somewhere you quoted somebody else that said anybody that's got hypertension that don't know they've got insulin resistance just haven't been diagnosed yet.

Heart disease, who hasn't been diagnosed with insulin resistance hasn't been diagnosed yet, but they have it. And that was his very well informed opinion, that if you remove the insulin resistance you simply remove the foundation of so much of the disease. Now heart disease itself is a very.

Right, yeah, yeah, that was a quote.

By enormous umbrella and it covers a lot of problems. But when we start talking about things like atherosclerosis or the narrow, you know, the plaque forming in the coronary arteries or hypertension, which is a key contributor to that process, I would say in the absence of insulin resistance it would be very difficult to promote either of those, certainly the ins. The hypertension. A scientist here in the US who in recent years has become quite famous, named Dr. Dr. Kraft and he actually became famous thanks to an Irish fellow named Ivor Cummins. Ivor really contributed to Dr. Kraft's work gaining kind of mainstream attention. But yeah, he was the one who said anyone with atherosclerosis could have other variables like infections in the blood vessel wall, but with elevated blood pressure it's.

Very, very uncommon that you would have.

That without insulin resistance being the primary driver. And again, that is such wonderful news because the good news of all of this, as you joked earlier, heart disease, who hasn't been diagnosed with insulin resistance, hasn't been diagnosed yet, but they have it. And that was his very well informed opinion, that if you remove the insulin resistance, you simply remove the foundation of so much of the disease. Lots of this conversation has been like we're telling a kind of scary bedtime story. But there is a happy ending and that is that in the midst of all of these years of metabolic self abuse unintentional that the good news of it is that the, that you can correct this extraordinarily quickly. Now heart disease itself is a very. There's a scientist in many, David Unwin in the UK as well and then a scientist in eastern Canada, who public who's very well documented the rate at which people with type 2 diabetes are deprescribed medications. I see this as I'm an advisor for a healthcare company. There's another physician in the US named Mark Cukozella in West Virginia who's published on this extend enormous umbrella. And it covers a lot of problems. But when we start talking about things like atherosclerosis or the narrow, you know, the plaque forming in the coronary arteries or hypertension, which is a key contributor to that process, I would say in the absence of insulin resistance, it would be very difficult to promote ivly, but it's profound. The rate at which a diabetic on multiple medications is able to start reducing the dose of almost all of them practically immediately.

So, Ben, we've covered the links with heart disease, and I know there's a few others because we can start talking about Fluffy Aldi, anyone.

They can't eat fiber, but if they.

Do so, they do so knowing that they simply have become accustomed to the bowel habits, the bowel movements that it gives them, which, hey, that's fine. Although some people find that dietary fiber actually is quite a harmful substance in their intestines. There are many people with things like ulcerative colitis, for example, or even Crohn's disease who find that when they're tasting.

Of those, certainly the ins. The hypertension, non fluffy LDL people.

Just read your book on that one. You've got a great analogy with dropping a golf ball or a bouncy ball into the river. Great analogy. Get Ben's book. It's absolutely fantastic. But there are another half a dozen reasons why insulin resistance drives heart attacks and heart disease and cbd. We've talked about Alzheimer's and the link there, in fact, many people now calling it diabetes type 3. Talk to me about the link between insulin resistant and I'm not saying all cancers. And we also know there's various reasons for causing cancer, but there is some very, very.

Sterosclerosis could have other variables like infections in the blood vessel wall, but with elevated blood pressure, it's very, very uncommon that you would have that without insulin resistance being the primary driver.

And again, strong links with certainly prostate and breast cancer. Could you sort of enlighten us a little bit there, please, Ben?

Bring off their fiber, the disease symptoms improve dramatically.

Interesting.

Not even subtly. Even people with just benign constipation find that their constipation gets better as they dose down the fiber in their diet. Wow. And so I don't mean to declare war on fiber. I think fiber can.

And that is such wonderful news because the good news of all of this.

As you joked earlier, be healthy and can be used as part of a perfectly healthy diet and even beneficially so.

Lots of this conversation has been like we're telling a kind of scary bedtime story. But there is a happy ending and that is that in the midst of all of these years of metabolic self abuse unintentional that the hap. The good news of it is that the that you can correct this if.

Used judiciously perhaps, but it is far from essential. Humans do not need it. There is no such thing as a plant that humans must eat and indeed the vast, vast majority of plants in the world, if a human were to eat them, it would kill them or make them very, very sick in our wisdom. Extraordinarily quickly we have.

Sorry Ben, I'll pick up on two things there quite interesting we're going to quickly show for everybody at home we just talked about breakfast some figures from Dr. David Unwin with his brilliant work on the teaspoons of sugar.

There's a scientist in many David Unwin in the UK as well and then a scientist in eastern Canada because we.

Can quantify that now with research and science and work from great doctors and what There we go. So you know, if somebody has a 200 mil that's an average sized graph.

Who public who's very well documented the rate at which people with type 2 diabetes are deprescribed medications. I see this as I'm an advisor for a healthcare company. There's another physician in the US named Mark Cucuzella in West Virginia who's published on this extended glass of pure apple.

Juice and hey, I'm guilty. I've been filled. I was feeding my kids this. There are things on there that my kids used to have for breakfast almost every single day. So don't if you're at home going oh.