The Insulin Doctor: This Will Strip Fat Faster Than Anything! Ozempic Is Causing Osteoporosis! ⁠The Fastest Way To Alzheimer’s! Dr Benjamin Bikman

0:00:07 When we’re looking at smoking versus vaping, vaping is probably worse in terms of the damage to the airway and the insulin resistance that comes from it.
0:00:15 But this gets worse because we know that insulin resistance is the core for most chronic diseases that are killing us when there’s a handful of other lifestyle habits that’s contributing to it.
0:00:16 That’s horrifying.
0:00:18 So tell me everything.
0:00:20 Dr. Benjamin Bickman is a leading metabolic scientist.
0:00:24 His research focuses on the hidden epidemic of insulin resistance and its devastating consequences.
0:00:28 And by regaining control of your insulin levels, he says you can regain control of your life.
0:00:32 Insulin is a hormone that affects literally every single cell of the body.
0:00:35 But if those cells become insulin resistant, you start to spread the disease.
0:00:38 For example, they call Alzheimer’s insulin resistance of the brain.
0:00:44 And even the most common forms of infertility, erectile dysfunction and PCOS, insulin resistance is a heavy contributor.
0:00:48 Now, 88% of adults in the U.S. have some degree of insulin resistance.
0:00:51 And people hear this and think America is just fat and metabolically sick.
0:00:53 But we’re not actually the worst country when it comes to this.
0:00:57 And part of it is because of how different ethnicities store fat.
0:00:58 And I’ll come back to that.
0:00:59 But there’s two roads to insulin resistance.
0:01:01 So there’s the fast lane.
0:01:04 And I could make you insulin resistant in six hours with either of these commentary things.
0:01:08 But if I removed them, your resistance would go away just as quickly.
0:01:09 Now the slow lane, that’s a problem.
0:01:15 And there’s certain lifestyle habits and problems with our diets that are massively contributing to slow insulin resistance.
0:01:18 Now, thankfully, this can be resolved through four pillars, which are very simple.
0:01:19 We’ll get into that.
0:01:21 But why don’t we just sack all this off and just take his impact?
0:01:24 Well, because people may not know about the negative side effects.
0:01:28 For example, 40% of the weight that people are losing on these drugs is coming from…
0:01:29 Holy s**t.
0:01:35 I have been forced into a bet with my team.
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0:01:54 can $1 be given to our celebration fund for the entire team?
0:01:55 And I’ve agreed to the bet.
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0:02:00 all you’ve got to do is hit the subscribe button.
0:02:03 So actually, this is the first time I’m going to tell you not to subscribe,
0:02:07 because it might end up costing me an awful lot of money.
0:02:09 (laughing)
0:02:24 Benjamin, what is the mission that you’re on?
0:02:31 My mission is to help people appreciate that much of chronic disease,
0:02:36 we look at them as the siloed individual distinct disorders with totally distinct origins,
0:02:40 and yet much of them share a common core.
0:02:43 It’s as if their branch is growing from the same tree.
0:02:48 And the conventional clinical care will look at these branches
0:02:50 and give someone a prescription for a medication,
0:02:53 which is only going to prune the branch back a little bit,
0:02:56 never actually solving the problem.
0:02:58 It can just grow right back.
0:03:04 And so we can look at most of these chronic diseases that are killing us globally
0:03:10 and then say, okay, there are in fact some simple lifestyle changes that can be implemented
0:03:13 that will help reduce the risk of not only one or two,
0:03:18 but all of the top killers from things like Alzheimer’s disease, to heart disease,
0:03:23 to type 2 diabetes, to liver failure, fatty liver disease,
0:03:26 all of them share a common metabolic core.
0:03:27 That’s my mission.
0:03:30 And what is that common metabolic core?
0:03:34 Yeah, it’s a little known problem called insulin resistance.
0:03:38 In fact, when I first started this topic,
0:03:45 I stumbled on one paper that documented how when fat tissue is growing,
0:03:47 it increases the risk of type 2 diabetes.
0:03:51 That was this concept in the early 2000s that was really getting a lot of attention.
0:03:56 Diabesity, this kind of dual epidemic of wherever we see obesity,
0:03:58 we see more type 2 diabetes.
0:04:02 In this manuscript outlined something that was to me a revelation at the time.
0:04:06 It was so fascinating where when fat tissue is growing,
0:04:09 it starts releasing pro-inflammatory proteins.
0:04:14 That inflammation caused a problem called insulin resistance.
0:04:19 And then that got me into this realm of understanding that other tissues of the body,
0:04:24 as they become insulin resistant, then you start to spread the chronic disease.
0:04:30 And essentially coming to the conclusion that something like hypertension,
0:04:34 high blood pressure, which is the most common cardiovascular problem
0:04:36 and the main contributor to heart disease.
0:04:40 Well, insulin resistance is the main cause of hypertension.
0:04:45 They call Alzheimer’s disease type 3 diabetes or more accurately,
0:04:47 insulin resistance of the brain.
0:04:51 Even the most common forms of infertility in men, it’s erectile dysfunction.
0:04:54 Well, that’s because of insulin resistance of the blood vessels.
0:05:00 In women, the most common form of infertility is polycystic ovary syndrome or PCOS.
0:05:03 That’s because of the insulin resistance affecting her ovaries
0:05:05 and the ability to produce the proper sex hormones.
0:05:10 I guess the really important question here is what is insulin resistance?
0:05:12 And can you explain this to me like I’m a 10-year-old?
0:05:13 Oh, yeah, for sure.
0:05:18 Insulin resistance is it’s kind of a it’s a disorder that has two parts.
0:05:22 It’s like a coin with two sides that as much as we think of,
0:05:26 we think of one side just because we hear the word insulin resistance.
0:05:29 But there’s another part to it that I need to that is very important.
0:05:34 So insulin, first of all, is a hormone that we make from the pancreas,
0:05:37 a long kind of gland tucked underneath the stomach.
0:05:39 And the pancreas is very busy organ.
0:05:42 It makes a lot of different hormones.
0:05:43 It makes hormones that come into the blood.
0:05:48 It also makes enzymes that go into the into the intestines to help digest food.
0:05:53 But among the hormones that are being released into the blood is insulin.
0:05:56 Now, in the person with type 1 diabetes,
0:06:01 their immune system has destroyed their beta cells so they don’t make insulin anymore.
0:06:05 That’s why for a person with type 1 diabetes, insulin is a life-saving therapy.
0:06:08 You’re giving them what they’re not making anymore.
0:06:14 But for everybody else, we have beta cells and they’re releasing insulin when they need to.
0:06:17 Now, usually the main stimulus,
0:06:22 the main reason the beta cell is releasing the insulin is because blood glucose levels go up.
0:06:23 So I eat sugar.
0:06:29 You eat sugar, or not even something as obvious as sugar, but bread or crackers.
0:06:30 White rice.
0:06:34 Oh, yes, so basically anything that falls into the family of a carbohydrate.
0:06:38 So if the earth grows it, that’s a carbohydrate.
0:06:40 If it’s a plant, it’s a carbohydrate.
0:06:42 Maybe that’s a better way of describing it.
0:06:44 And so it’s going to have starches and sugars,
0:06:48 which all is kind of falls into this family of carbohydrate.
0:06:52 Depending on how much starch or sugars that it has,
0:06:58 then that will result in a bigger or smaller blood glucose or blood sugar response.
0:07:02 But then if blood sugar is too high for too long, that becomes very harmful to the body.
0:07:06 So insulin comes in and helps lower the blood glucose.
0:07:09 And then having done its job, insulin comes back down.
0:07:17 So insulin comes out like a taxi in transports all the glucose in my blood to various places around the body to store them.
0:07:18 Perfect.
0:07:21 Yeah, in the main, yeah, that’s right, you can sit, look, it’s a shuttle.
0:07:24 It’s a taxi saying, hey, glucose, come on in.
0:07:26 I’m dropping you off at the muscle.
0:07:32 So mostly just as an interesting tangent of insulin before I finish answering insulin resistance,
0:07:41 insulin will open the doors for blood sugar to come in and drive the taxi in, mostly at the muscle and the fat.
0:07:47 Muscle and fat tissue need insulin to come and bring the sugar in via taxi.
0:07:51 However, other tissues and the brain a little bit as well,
0:07:57 other tissues will still respond to insulin, but they don’t need insulin to tell it what to do with the sugar.
0:07:59 It just takes it in.
0:08:04 But even on those, like the liver, for example, if the liver sees sugar driving by in the taxi,
0:08:06 it just opens the doors and lets it in.
0:08:10 It doesn’t need insulin to come and tell it to let the sugar in.
0:08:19 However, even at the liver and every other cell has a similar degree of this, the liver doesn’t know what to do with it.
0:08:24 So this is back to something I mentioned earlier, where insulin’s thematic effect at the entire body
0:08:31 is to tell the body what to do with energy in all of its forms as these kind of caloric, rich molecules.
0:08:38 What to do with lactate, what to do with ketones, what to do with fats or glucose, what to do with amino acids.
0:08:41 So insulin will tell the body what to do with all of those things.
0:08:46 But again, its most famous effect is to control blood sugar.
0:08:52 And that’s not wrong, because its most powerful activator is blood sugar.
0:08:58 So with all of that in mind, insulin resistance is two problems wrapped into one.
0:09:02 The one problem is the most obvious one, which is that insulin isn’t working as well as it used to.
0:09:10 So back to the analogy of the taxis dropping off sugar, if the muscle tissue has become insulin resistant,
0:09:16 insulin is coming and trying to pull the sugar-loaded taxi into the muscle, but the muscle’s not listening.
0:09:22 So say that again, so the insulin’s coming past with the glucose inside it.
0:09:26 Well, not technically, yeah, but just to sort of go with your metaphor.
0:09:30 But maybe to use another one, insulin comes and knocks on the doors.
0:09:32 It’s like the bouncer at the door.
0:09:38 It’s coming and knocking on the door of the muscle saying, “Hey muscle, I’ve got some sugar that wants to come in.”
0:09:42 And normally the muscle will say, “Oh yeah, sure, okay, open it up the doors and let the sugar come in.”
0:09:45 When the muscle is insulin resistant, the bouncer’s knocking.
0:09:54 Maybe there’s even, I’m almost getting ahead of myself, but one bouncer, maybe two or three bouncer’s pounding on the doors of the muscle cell,
0:09:57 but the muscle cell’s not listening, it’s become deaf.
0:10:05 That’s the insulin resistance of what we call insulin resistance, where some of insulin’s effects, like helping lower blood sugar,
0:10:07 it’s not working very well anymore.
0:10:11 And the muscle is just an obvious example because there’s so much of it.
0:10:14 It is the biggest tissue on the average individual.
0:10:20 Someone who’s very obese perhaps now has more fat tissue, but even people who are overweight, most of us is muscle.
0:10:22 So that’s a good tissue to look at.
0:10:30 So part of insulin resistance is that of all the things insulin’s trying to do, including lower blood sugar,
0:10:32 it doesn’t do it quite as well as it used to.
0:10:38 Some of the cells or tissues of the body have become deaf to insulin’s demands.
0:10:44 Now, however, at the same time that’s happening, insulin levels are higher.
0:10:51 And that is really important, and I’ll mention an example in just a moment that highlights the difference between the two.
0:10:58 But we have to consider, anytime we talk about insulin resistance, we think of two things happening in concert.
0:11:04 One, insulin isn’t working quite as well as it used to in various places of the body.
0:11:07 At the same time, insulin levels are higher.
0:11:16 And that kind of takes us back to the muscle cell where I’d mentioned getting a little ahead of myself that a bouncer is knocking on the door.
0:11:23 And once upon a time, the muscle cell would hear that one polite knock from that one bouncer or one molecule of insulin, if you will.
0:11:27 And it would open the door and let the glucose or the blood sugar come in.
0:11:35 But now the muscle cell, the bouncer, insulin is knocking on the door, but the muscle doesn’t listen, it’s resistant.
0:11:45 And so the body has adapted, and it learns, OK, well, if one bouncer wasn’t enough, let’s send an angry mob of bouncers.
0:11:49 And then the muscle will start to open the door, and indeed it can.
0:11:51 So those two problems go together.
0:11:54 On one hand, insulin isn’t working as well as it used to.
0:11:57 That’s what gives it the name insulin resistance.
0:12:02 But there’s another part that is equally present, which is that blood insulin levels are higher.
0:12:15 Now, earlier at the outset of the conversation, I mentioned that even infertility has an origin, has some degree of development because of insulin resistance.
0:12:23 And it’s a perfect example of both of these parts of insulin resistance, where in some instances, insulin isn’t working very well.
0:12:26 Always with insulin resistance, blood insulin levels are higher.
0:12:32 So, for example, erectile dysfunction is the most common form of male infertility.
0:12:41 In fact, its connection to insulin resistance is so strong that just a few years ago, I was so struck by a title of a paper that had just been published,
0:12:51 which stated something like, “Is erectile dysfunction the earliest manifestation of insulin resistance in otherwise young, healthy men?”
0:12:53 Now, what is the connection?
0:13:05 It’s because in a normal erectile function, in order for the man to have normal erectile function, he has to experience a pretty dramatic increase in the size of the blood vessels in his body.
0:13:09 The blood vessels expand, that increases blood flow, and then he has normal function.
0:13:16 Part of that signal that tells the blood vessels that it’s time to expand is actually insulin.
0:13:23 And so this is what I said earlier, where insulin does so many things in the body, and we only think of it as being relevant to glucose, and that’s not fair.
0:13:29 Insulin does a lot of stuff, again, including telling blood vessels to expand.
0:13:36 Now, unfortunately, in the case of this unfortunate man, his blood vessels become insulin resistant.
0:13:43 So now it’s insulin coming and knocking on the doors of the blood vessels, saying, “Hey, it’s time to expand and increase blood flow.”
0:13:53 But the blood vessels don’t respond, they don’t listen, so they stay constricted, blood flow stays insufficient, and thus he has erectile dysfunction.
0:13:55 I don’t want to be insulin resistant.
0:13:57 No, no one does, no one does.
0:13:59 So tell me how it happens.
0:14:00 Yeah, right, yeah.
0:14:07 So the origins are so important because it helps us understand why we’ve gotten into this situation we are, where it’s the most common problem worldwide.
0:14:16 There are two pathways to insulin resistance, so two roads that get to the same destination, again, the destination being insulin resistance.
0:14:23 There’s the fast lane, which I call fast insulin resistance, and it actually has three lanes, which I’ll describe in a moment.
0:14:32 Then there’s the slow insulin resistance, which is a more, it takes a little longer to get there, but at the same time, it takes a little longer to get away from it.
0:14:40 So I’ll start with fast insulin resistance because the slow one ends up getting a little excitingly complicated, but in a cool way.
0:14:51 So with fast insulin resistance, there are three things that I could take you to a clinical lab, and I could make you insulin resistant in six hours with either of these three things.
0:14:58 But as quickly as it settles in, if I remove those things, your insulin resistance would go away.
0:15:02 So these are fast causes and they’re fast resolution.
0:15:11 They are, stress is a primary cause of fast insulin resistance, so two is inflammation.
0:15:18 And then lastly, and this is going to sound somewhat paradoxical, too much insulin is also a cause.
0:15:23 And I’ll end with that one because I think it’s the most important than transition to slow insulin resistance.
0:15:29 So anytime the body is experiencing too much stress, it will very quickly become insulin resistant.
0:15:38 Now, as a professor who teaches endocrinology, no surprise, I define stress in the context of hormones.
0:15:45 And there are two primary stress hormones, cortisol and what we call in the US epinephrine or in the UK adrenaline.
0:15:47 Those are the two stress hormones.
0:15:50 Now, those hormones are very distinct.
0:15:52 They have almost nothing in common.
0:16:00 Like when you are feeling a little stressed, it’s both of those, especially adrenaline slash epinephrine that are making you feel a little jittery.
0:16:04 It’s making your heartbeat a little faster, you’re a little more alert.
0:16:08 That all starts to play into a stress response.
0:16:14 But what those two hormones have in common is that they both want blood glucose levels to climb.
0:16:20 It’s kind of their way of saying, hey, we don’t really know what’s going on right now, but we want to be ready to run away.
0:16:23 That’s the fight or flight kind of aspect to stress.
0:16:27 And so they want to push blood glucose levels up and they do very well.
0:16:37 That of course puts them at odds with the hormone insulin because these two epinephrine or adrenaline and cortisol, the two stress hormones, they’re pushing glucose up.
0:16:39 Insulin wants to push it down.
0:16:46 So the more the body has those stress hormones elevated because of, say, sleep deprivation.
0:16:49 That’s a very effective way to increase cortisol.
0:16:52 Or they are drinking too much caffeine.
0:16:55 That is a way to increase epinephrine quite strongly.
0:17:04 If both of those signals are too incessant or they continue to be present and climb, then insulin has to work harder and harder.
0:17:06 And then we have insulin resistance.
0:17:10 So stress is a cause of insulin resistance.
0:17:12 But then next is inflammation.
0:17:19 You and I were commenting earlier about how, boy, there’s a cold going around people.
0:17:20 It’s flu season.
0:17:35 Even then, if a person were wearing a continuous glucose monitor on the back of their arm measuring their glucose levels, they would see their glucose levels are much, much higher, like significantly higher during the time that they’re struggling with this infection.
0:17:38 That is a reflection of insulin resistance.
0:17:42 Insulin is having a harder time keeping the blood glucose levels in check.
0:17:47 Anytime inflammation is up, insulin resistance will be up as well.
0:17:56 Even in things like autoimmune diseases, there are reports in humans that document the degree to which someone has, say, active rheumatoid arthritis.
0:18:02 Their joints are achy because of an autoimmune attacking of the joints.
0:18:08 They will note on some days, like every autoimmune disease, there is an ebb and a flow.
0:18:11 Some days it’s good, some days it’s bad.
0:18:22 And on the bad days, if you measure their insulin resistance, it is absolutely locked with the degree to which their immune system is turned on or off or higher or lower.
0:18:24 So inflammation is another cause.
0:18:29 And then the last one of the fast lane of insulin resistance is too much insulin itself.
0:18:38 Now the astute listener will realize the kind of circular thing I’ve just presented by invoking high insulin as a cause of insulin resistance.
0:18:45 Because they will also think, but wait a minute, Ben, you just said that high insulin is also a consequence of insulin resistance.
0:18:50 That, you know, back to the bouncer knocking on the door of the muscle cell.
0:18:58 If one bouncer wasn’t enough or one molecule of insulin wasn’t enough, the body will say, okay, well, let’s send 10 molecules of insulin.
0:19:04 So high insulin is both a consequence of insulin resistance, but it’s also a cause.
0:19:19 And this is reflective of a fundamental principle in all of biology, that if there is too much of a stimulus, a cell, if it’s capable, will try to become resistant to that stimulus.
0:19:24 This would be like a funny analogy in the big man home.
0:19:27 My darling wife is home with the children.
0:19:29 That is what she wants to do.
0:19:31 She is full time mom.
0:19:38 When I’m home and I try to be home as much as I can, it’s funny for me to note the difference in how quickly we each respond to our children.
0:19:44 I will hear my child saying, mom, mom, mom, and she’s not responding.
0:19:52 Mom has heard this for so much that she’s become kind of selectively deaf to when my children are demanding her attention.
0:19:56 I’m not as around my children quite as much because I’m working during the day.
0:20:00 And so when I hear that, it’s a very fresh signal to me.
0:20:03 I’ve not heard it so much that I’ve become deaf to it.
0:20:11 And so I will respond, even though I’m in the other room, because I’m so much more sensitive to the clamoring for attention.
0:20:14 This is like the body in response to insulin.
0:20:19 If there is always insulin, it’s always going up, always going up.
0:20:25 The body will start to say, the muscle cell will start to say, boy, insulin, you are knocking on my door all the time.
0:20:26 This is getting old.
0:20:27 I’m not responding anymore.
0:20:30 I’m not going to listen as much as I was before.
0:20:35 So in that sense, insulin, too much insulin becomes a cause of insulin resistance.
0:20:42 Back to what I said earlier, I could take you into the lab, start infusing you with just a little drip of insulin to increase your insulin.
0:20:50 And over just a few hours, you would become demonstrably less sensitive to it than you were before we started.
0:20:55 But again, as I take that away, give your body a few hours and it’s back to normal.
0:21:01 In every one of those instances, it’s a fast onset and it’s also a fast solution if we can take it away.
0:21:05 If we can take it away, but if we can’t take it away, does it become sort of chronic?
0:21:12 Yeah, so especially all of these can contribute to a more lingering insulin resistance, but especially insulin.
0:21:25 Where I focus on that one the most because of not only its relevance to the slow lane, but also just how present it is where 70% of all calories globally are carbohydrates.
0:21:32 And now perhaps with the best of intentions, our experts are telling us that we should be eating six times a day.
0:21:40 And so we eat, we wake up in the morning, insulin has finally been coming down while we’ve been fasting overnight.
0:21:43 Insulin gets to take a little bit of a break, we’re fasting.
0:21:46 Then we break that fast by eating breakfast.
0:21:52 And in the UK, as it is in the US, by and large, this is going to be a very starchy, sugary breakfast.
0:21:56 It’s toast with some jam or it’s cereal or it’s bagels.
0:21:59 That is going to be, that is almost pure glucose.
0:22:05 And so what do we do? We wake up, we eat breakfast, we spike our blood sugar levels and insulin has to come up.
0:22:09 Insulin will take longer to come down than the blood sugar will.
0:22:13 It will wait in the blood to make sure that all the blood sugar has gone back to normal.
0:22:21 So depending on how much carbohydrate we ate for breakfast, it could take our insulin levels three or even four hours to come back down to normal.
0:22:26 Long before it’s had a chance to come back down to normal, we’ve had a mid-morning snack.
0:22:30 Of course, we need to go get a sugary coffee and another bagel or something.
0:22:34 And so after just a couple hours, we do it again.
0:22:43 And once again, before insulin has had a chance to come back down, we have a starchy carbohydrate heavy lunch, then an afternoon snack, and then a carbohydrate heavy dinner.
0:22:46 And then of course we have to have an evening snack before we go to bed.
0:22:52 So the average individual is spending every waking moment in a state of elevated insulin.
0:22:57 And thus the signal never really goes away because they never give themselves a break.
0:23:03 But one of the consequences of that I mentioned, which is that it directly causes insulin resistance.
0:23:08 But when insulin is high, it starts to have a signal on the fat cell.
0:23:19 And that then brings us to the slow insulin resistance, where you have something happening in the fat tissue that begins to set the stage for insulin resistance in the entire body.
0:23:23 And it takes longer to settle in, but it takes also longer to go away.
0:23:26 That’s why I call this one slow insulin resistance.
0:23:33 Now, in the case of insulin, most people– so the key with the– I’ll explain it this way first.
0:23:40 So the most relevant feature with fat tissue contributing to insulin resistance is the size of each fat cell.
0:23:48 When we typically think of fat, we would maybe say, OK, Steve has– I’ll do this in kilos for the UK audience.
0:23:52 Steve has 10 kilos of fat on your entire body. That’s probably too much for you.
0:23:55 But Ben has 20 kilos.
0:24:00 And yet it’s possible that I’m healthier metabolically than you.
0:24:05 And that’s because it’s not the mass of fat that matters most.
0:24:07 It’s the size of the fat cell that matters.
0:24:17 This is why women, despite universally being fatter than her male counterparts, are healthier with regards to insulin resistance in every single metabolic problem.
0:24:23 It’s because women, as a result of her particular sex hormones, have more fat cells, but they’re smaller.
0:24:27 So she has more fat, but smaller fat cells.
0:24:34 And small fat cells are healthy, insulin-sensitive, anti-inflammatory fat cells.
0:24:42 But the bigger the fat cell gets, the more it initiates a cascade of events or a series of events that creates insulin resistance.
0:24:46 And Amira, in thinking, we have the same amount of fat cells for our whole life, pretty much.
0:24:49 That’s a really, really safe assumption for most people.
0:24:56 Yeah, for most people, a fat cell, sometimes students will hear that fat cells are immortal. That is not true.
0:24:59 But they’re long-lived. Fat cells will live about 10 years.
0:25:10 And so typically, by the time, if you look at a newborn, during infancy, childhood, and puberty, the number of fat cells is going up, up, up, up, up.
0:25:15 Once they finish puberty, so mid to late teens for a young woman,
0:25:21 late teens or even early twenties for a young man, usually at that point, the number of fat cells they have is going to be very static.
0:25:23 This is something people don’t really understand.
0:25:27 And I actually discovered it from doing this podcast and speaking to so many experts about this,
0:25:33 that we pretty much, especially as an adult, have the same amount of fat cells, really regardless of what we eat.
0:25:34 Yes.
0:25:38 And it’s actually just the fat cells we have shrinking or expanding.
0:25:40 Exactly. That’s exactly right.
0:25:42 Now, there are differences.
0:25:45 Which, by the way, makes liposuction a pretty fucking bad idea.
0:25:49 In fact, it makes things worse. Please, let’s make sure we come back to that.
0:25:50 Okay, all right.
0:25:59 Because it really becomes, the person ends up, their vanity ends up really ruining their future metabolic outcomes.
0:26:02 But there are differences across ethnicity.
0:26:05 This is a little oversimplified, but not much.
0:26:09 On one end, you’d have Caucasians, kind of Northern European Caucasians.
0:26:16 On the other end, you’d have East Asians, like Chinese, Japanese, Korean, East Asians.
0:26:21 And then if you look at that same spectrum of people making fat cells through their life,
0:26:26 an East Asian will be making fat cells and then stop right about here.
0:26:30 So very few fat cells, relatively speaking, across all the ethnicities.
0:26:32 They have very few fat cells.
0:26:37 A Caucasian on the other end of the spectrum, they went way higher.
0:26:42 And so this guy, let’s say American Ben versus Chinese Ben, overly simplified.
0:26:44 But here we are.
0:26:50 So much of fat mass isn’t the number of fat cells, even though American Ben has more.
0:26:52 It’s the size of the fat cell.
0:26:58 So I could be the same percent body fat, really, as Chinese Ben.
0:27:02 But that would just be because my fat cells were just that much smaller.
0:27:04 But this is the problem then.
0:27:12 If you have, let’s say, American Ben and Chinese Ben both gained 10 kilos of pure fat over the next 10 years.
0:27:13 Very easily done.
0:27:15 Most people do that quite often.
0:27:21 Caucasian Ben just doesn’t look as good in his speedo, which is a pasty Caucasian.
0:27:24 He’s not going to look particularly good in that speedo anyway.
0:27:26 But I just am bulging a little more than I was before.
0:27:27 But otherwise, I’m healthy.
0:27:28 My blood pressure is fine.
0:27:29 My blood sugar is fine.
0:27:31 Everything’s normal.
0:27:40 Put that same 10 kilos of fat on Chinese Ben, hypertension, type 2 diabetes, fatty liver disease, infertility.
0:27:46 And that is because Chinese Ben had fewer fat cells to start with.
0:27:53 And so those fat cells, as the body was told to store fat, those fat cells were getting much, much bigger, much sooner.
0:27:59 And the fat fat cell promotes insulin resistance very, very readily.
0:28:04 And so that logically moves into the question of, well, what makes fat cells grow?
0:28:10 And it is two essential variables that we only ever look at calories.
0:28:20 And yet, if you take a person with type 1 diabetes and say, I want you to eat 10,000 calories, but don’t give yourself your insulin injection.
0:28:22 They cannot gain weight.
0:28:29 It is literally impossible for the type 1 diabetic to get fat if they are skipping their insulin injections.
0:28:39 In fact, this is so known that if you take, let’s imagine a young woman who would maybe have more pressure to be thin than her male counterpart, although it’s happening more in males too.
0:28:44 Imagine a young girl who gets diagnosed with type 1 diabetes at the age of 13 or 14.
0:28:50 Very impressionable time. She’s very worried about how she looks and how thin she is.
0:29:00 She learns that, wait a minute, I can eat whatever I want and all I have to do is not inject my insulin and I’ll be as skinny as I want.
0:29:05 And it works. It works so well that it’s actually a formal eating disorder called diabolemia.
0:29:14 So the fact that this exists is absolute proof that the growing and the shrinking of the fat cell is more complicated than just calories being high or low.
0:29:23 Because like I said earlier, when I talked about hormones, hormones are a way for the very tissues of the body to know what it ought to do with energy.
0:29:27 And so a fat cell will have energy all around it.
0:29:31 And if it doesn’t have insulin to tell it what to do, it won’t do anything with it.
0:29:39 Or maybe to make this more direct, back home in my lab, my students are growing fat cells in petri dishes.
0:29:50 These fat cells are swimming in a little sea of calories, lots of glucose, lots of fats, and yet they stay really small until we add insulin.
0:29:57 The moment we add insulin into that little petri dish, if we check those cells four hours later, they’re immediately fatter.
0:30:01 If we check them four hours later, they’re fatter still.
0:30:04 Now they know what to do with the energy they have.
0:30:10 So with slow insulin resistance, it develops when fat cells get really, really big.
0:30:16 It’s like a, because they have to tell insulin, insulin, you continue, you are telling me to keep growing.
0:30:19 I can’t keep growing. I’m so big that I’m going to pop.
0:30:23 I mean, literally the fat cell can get so big that it degrades its membrane.
0:30:27 It’s like a water balloon that a naughty little boy has overfilled and it’s about to burst.
0:30:29 The fat cell doesn’t want to burst.
0:30:33 And so it tells insulin, insulin, you are trying to make me grow.
0:30:36 You’re telling me to grow. I can’t listen anymore.
0:30:39 I’m becoming insulin resistant to stop growing.
0:30:41 So insulin makes you fat.
0:30:42 Oh, very much.
0:30:46 Now, if you, so a moment ago I said that the big fat cell is two variables.
0:30:48 You must have both.
0:30:52 You must have both a signal to tell the fat cell to get big, which is insulin.
0:30:54 It is the, there’s no other signal that can do it.
0:30:59 You can, in a human, just simply take away the insulin, like type one diabetes.
0:31:01 It doesn’t matter any other hormone in the body.
0:31:02 It does not matter.
0:31:04 They cannot get fat.
0:31:10 They could, again, they can eat thousand, they could eat 10,000 calories of chocolate cake.
0:31:11 They cannot get fat.
0:31:14 Not only can they not get fat, they can’t hold on to their fat.
0:31:20 Because if there’s no insulin to tell the fat cell to hold on to it or get big, it has to shrink.
0:31:21 It’s breaking down its fat.
0:31:28 So the body goes into such a dramatic fat burning state in the absence of insulin that keeping fat becomes impossible.
0:31:33 So the insulin signal is necessary to tell the fat cell what to do.
0:31:39 But the fat cell will say, okay, insulin, you’re high, you’re telling me to grow, but what am I going to grow with?
0:31:41 That’s where the calories come in.
0:31:47 Now the fat cell will say, hey, fats and glucose in the blood, insulin has told me to get big.
0:31:50 And so I need to pull you in to help me grow.
0:31:52 You’re going to give me the bulk.
0:31:55 And if you have one without the other, it is death.
0:32:01 So if I’m eating 2,000 calories and I have a different insulin sensitivity to you.
0:32:06 So we both eat 2,000 calories and I’m insulin resistant.
0:32:08 Doesn’t that mean that I will?
0:32:10 You’ll store more as fat.
0:32:11 Oh, okay.
0:32:12 Yeah.
0:32:19 So your body, now it would partly depend on, there are people where you, if all of your fat cells had reached its maximum point,
0:32:20 then you’re done.
0:32:24 You’re not going to gain more fat, you’re just going to become more and more and more insulin resistant.
0:32:25 Okay, fine.
0:32:27 So you kind of start limiting yourself.
0:32:36 But there are studies in humans to show that if you give humans isocaloric meals, so the exact same number of calories,
0:32:43 but in the same amount of protein, but you differ those meals based on the amount of carbs to the amount of fat.
0:32:50 So let’s say two meals, exact same calories, 2,000 calories or that’s in one meal, that’s too high, 1,000 calories in one meal.
0:32:57 One version of this is the conventional way of eating, which is lower fat, higher carb.
0:33:04 The other meal, same number of calories, but it’s lower carb, higher fat.
0:33:14 This lower carb, higher fat version will have a lower insulin response and they will store less fat from that meal.
0:33:17 And someone would say, well, where do the calories go?
0:33:21 You can’t, it’s the laws of thermodynamics, you can’t destroy energy.
0:33:23 The metabolic rate will go up.
0:33:31 So when insulin is low, if you have someone going a full day eating the same number of calories, but lower carb calories,
0:33:35 their metabolic rate will be almost 300 calories higher in that day.
0:33:36 And metabolic rate is the–
0:33:40 Yeah, that’s the total amount of energy that it just costs you and I to just live.
0:33:40 Okay, so–
0:33:43 We were just going through the day, but that’s a significant amount.
0:33:50 Like if you and I were to go exercise and say, let’s go burn 300 calories, we got to be on the stair stepper for an hour or something.
0:33:58 So it’s 300 calories, but at the same time, if your insulin is low, you’re burning so much fat that you start making ketones.
0:34:00 And I don’t intend to get onto that topic quite yet.
0:34:07 But suffice it to say, every molecule of a ketone has a caloric load roughly similar to glucose.
0:34:14 And what the body, when it starts making a lot of ketones, it starts eliminating the ketones.
0:34:19 So every time someone is breathing out ketones, they’re literally breathing out calories.
0:34:24 Or they’re urinating and they’re urinating out ketones if they have higher ketones in their blood.
0:34:28 They’re urinating out calories because ketones have energy.
0:34:35 And so this is the way that if insulin is low, it becomes impossible for the body to hold on to its energy.
0:34:47 It is so determined to spend energy that it will both increase metabolic rate and it will make the energy, the calories, be wasted in the breath and in the urine and in the form of ketones
0:34:50 because ketones have calories, ketones are energy.
0:34:53 Now we’re just dumping them out into the universe.
0:35:01 It’s worth, before we talk about how to keep my insulin levels low so that I can benefit from all the health benefits we’ve talked about,
0:35:07 it’s probably also worth just spending a little bit of time trying to understand the evolutionary basis of insulin resistance.
0:35:20 There are some theories that are very interesting that attempt to explain why is it that we became so fantastically different from, let’s say, our closest animal relatives, other primates like chimpanzees or apes.
0:35:24 What was the difference that had us become so different than them?
0:35:30 One of the leading theories is a theory called the expensive tissue hypothesis.
0:35:33 And it actually does have something to do with ketones.
0:35:45 In the expensive tissue hypothesis, as the theory goes, our earlier ancestors deviated in this kind of animal family line because we started eating more meat.
0:36:01 We started eating food that was so nutritious, so nutrient dense, so loaded with good calories and all of the fats and proteins that we need that it allowed two very distinct changes to occur in us compared to other primates.
0:36:05 One, our intestines became significantly shorter.
0:36:19 So if you compare the human digestive tract to any other primate animal, if we are a primate, then if you look at the intestines, they’re fantastically different, particularly the large intestine or the colon.
0:36:30 Because our ancestors, as the theory goes, began eating meat, we didn’t need the colon as much because the colon is a place for food to ferment.
0:36:36 And so if you’re eating a lot of plant matter, like other primates do, you need a much, much larger colon.
0:36:41 So we started eating food that was so nutrient dense, our colon shrunk considerably.
0:36:45 We didn’t need to waste energy on a big, busy colon.
0:36:55 At the same time, as we were eating food that was so nutrient dense and so loaded with good fat, it allowed us to have more time to be curious and explore.
0:37:00 And so at the same time, our intestines were shrinking because we didn’t need them to be so big.
0:37:06 Our brain was growing and it’s because it had so much nutrition, including ketones.
0:37:10 So ketones are an extraordinary fuel for the brain.
0:37:23 In fact, one of the reasons why a baby that is born premature will be more likely to have learning disorders later in life is because premature baby didn’t have time to get very fat.
0:37:28 And fat baby is healthy baby and fat baby gets into ketosis.
0:37:32 Let’s say you and I were to fast straight for two days.
0:37:44 If you took a six month old baby, that baby would be in a deeper state of ketosis in two hours than you and I would be in two days because the baby is burning so much of its beautiful, chubby fat.
0:37:52 And the more the body burns fat, the more it makes ketones and the tissue of the body that appears to benefit the most.
0:37:54 In response to ketones is the brain.
0:38:01 The brain, the moment ketones hit the blood stream, the brain immediately starts taking in ketones for a fuel.
0:38:14 Very often, I have students who have had a professor, perhaps with the best of intentions, but ignorant nonetheless, tell the student that the brain, the main fuel for the brain is glucose, that the brain prefers glucose.
0:38:19 And I show them just one or two papers to prove that wrong immediately.
0:38:32 And it is reflected in this idea, which if to use some convenient UK units, if blood glucose is five millimolar, that’s a concentration, a way of measuring an amount of something.
0:38:38 Blood glucose may be five millimolar or 80 milligrams per deciliter for the American audience.
0:38:46 That would be a normal glucose. And if you and I were to fast for 24 or so hours, we may get up to about one millimolar of ketones.
0:38:53 And yet even then, the brain has already switched to get the majority of its energy from the ketone.
0:38:59 And so don’t tell me that in this dynamic, the brain prefers this one because this one’s five times higher than this one.
0:39:06 And even in that scenario, the brain is already getting more than half of its energy from the ketone.
0:39:19 So all of this is my long-winded way of saying, when we look at the principles of evolution, one of the leading theories is this idea that we began eating essentially a meat-heavy diet that, again, is so nutritious that it allowed our brains to grow.
0:39:27 Maybe one final point on this, although it is a bit of a barbed comment, people may find this somewhat amusing or disappointing or frustrating.
0:39:32 The title of a book just published, which is that vegetarians have smaller brains.
0:39:40 This is seen in humans that the less a human eats meat, then the smaller the brain becomes.
0:39:49 The brain is so dependent on the nutrient density that comes from animal-sourced foods that it will suffer when it doesn’t get them.
0:39:51 Interesting. I mean, that’s a controversial thing to say.
0:40:00 It is, and you can cut it out. But it really is. It’s a real thing. And why does depression go up so much when people stop eating animal-sourced foods?
0:40:02 It’s because you are depriving the brain of what it needs.
0:40:05 What is it exactly you’re depriving the brain of in that situation?
0:40:11 Yeah. Yeah. So at least, among other things, at least it would be the essential omega-3 fats.
0:40:17 So there are three omega-3s, and we can only get one from plants, but it’s one that the humans don’t use.
0:40:21 We need the other two, and they only come from animal-sourced foods.
0:40:22 And you could supplement.
0:40:23 Absolutely.
0:40:24 Right. And the fruits.
0:40:25 Yeah, you can.
0:40:35 So the solution in that regard is the vegan must be educated enough to know what they’re deficient in, and then wealthy enough to afford the supplements to make up for it.
0:40:43 So is that the only evolutionary sort of hypothesis towards why we developed this insulin resistance?
0:40:48 Oh, yeah. In fact, it’s funny that you bring the question up again because I realized I didn’t quite answer it that way.
0:40:51 So insulin resistance, why would it exist at all?
0:40:58 It would probably be a way for the body to know when it was needed to hold on to energy a little better.
0:41:09 So now, I say that now, and someone would think, well, but you just why would I want to hold on to energy in a way where it’s causing hypertension and Alzheimer’s disease and increasing the risk of heart disease?
0:41:13 Not all versions of insulin resistance are negative.
0:41:23 So there is what all the insulin resistance that you and I have been talking about is pathological insulin resistance or harmful insulin resistance.
0:41:28 Insulin resistance that serves no good purpose, and it’s making us sick.
0:41:35 However, there is insulin resistance in human development, which is physiological or helpful.
0:41:43 It’s supposed to happen, and that is the two Ps of physiological insulin resistance, puberty and pregnancy.
0:41:49 Because in both of those instances, as we outlined earlier, when the body’s insulin resistant, insulin is high.
0:41:54 That’s not always bad because insulin wants things to grow.
0:41:56 It is like a fertilizer in the body.
0:42:02 Now, sometimes it’s misplaced and results in problems like increasing the risk of cancer, for example.
0:42:09 But in other instances, if you have a young child who needs some explosive growth during puberty, well, then that’s really helpful.
0:42:16 Insulin’s telling the body to store more energy, to build up tissues, including muscle and bone, but also including fat.
0:42:21 So in pregnancy, insulin’s playing a role in growing the placenta, the breasts.
0:42:28 Yes, so in the woman, after she’s finished puberty, the only other time of growth she’ll ever have will be pregnancy.
0:42:35 And so those are the two instances where the body has become insulin resistant to take advantage of the heightened scenario where it can grow.
0:42:37 Because the woman’s body needs more fat.
0:42:38 Oh, goodness, yes.
0:42:43 Yes, so her body not only needs to grow tissue mass, like the uterus has to get much bigger.
0:42:44 She has to grow a placenta.
0:42:53 She also needs to become a little insulin resistant to give a little more glucose to her baby because she is, after all, now living for two people.
0:42:59 And so as her body becomes insulin resistant, it actually facilitates the growth of the baby a little more rapidly.
0:43:07 But as you noted, it helps her store more fat and progesterone is another hormone that even accelerates that process.
0:43:18 But basically it’s her body’s way of saying, hey, I am committing to growing another human and it’s going to be metabolically very demanding.
0:43:33 And so I’m going to have as much extra fat or as much extra energy as I can in order to ensure that if there’s any sort of scarcity in food that happens during the course of the pregnancy, I’ll have enough energy to get through it all.
0:43:39 And then maybe I’ll even have enough to continue to feed the baby with lactation after the baby’s born.
0:43:41 What is gestational diabetes?
0:43:47 That’s a great question. Gestational diabetes is essentially type two diabetes of pregnancy.
0:44:00 So it’s perfectly timed question because if you look at the average woman who is very healthy, very insulin sensitive at the beginning of her pregnancy, so glucose is normal and insulin is normal.
0:44:09 Over the course of her pregnancy, she stays normal healthy pregnant woman, which is to say she has physiological insulin resistance.
0:44:14 She doesn’t get diagnosed with gestational diabetes though, which means her glucose is normal.
0:44:24 But to keep her glucose normal because she is insulin resistant, but for a purpose to help her body grow, her insulin levels are high and then the glucose is still in a normal range.
0:44:32 And then in some women, especially if she has a family history of type two diabetes, the insulin resistance goes too far.
0:44:39 Now she has high insulin like all pregnant women do, but she’s not able to keep her glucose levels in check.
0:44:45 So if I’m eating loads and loads of sugar throughout a pregnancy, that will compound the problem. Absolutely.
0:44:51 So then she will go from the normal insulin resistance of pregnancy into the insulin resistance of diabetes.
0:45:05 So it really is like type two diabetes, but a microcosm of it, a mini version that was really instigated or initiated because of the pregnancy, combined with a bit of a genetic predisposition, combined with her eating the worst possible way.
0:45:07 Does that then impact the future baby?
0:45:17 Oh, for sure it does. Yeah, so think about it’s almost like the baby is literally developing in a hyperglycemic, hyperinsulinemic environment.
0:45:26 So the baby gets hardwired to want to continue to exist in a state of high insulin and high glucose after the baby is born.
0:45:38 And so yes, the offspring of mothers who have gestational diabetes are significantly more likely to gain weight and be chubbier or fatter than their counterparts and to later develop type two diabetes.
0:45:39 A resounding yes.
0:45:46 I read in your book that these infants have a 40% higher chance to be obese and have metabolic complications in their teenage years and beyond.
0:45:59 Yes, I mean, a significant thing. And I say that with all of the sympathy I can for the mother who may be struggling with this, but it is certainly a motivation for mom to just be mindful of what you’re eating.
0:46:07 One of the things that I saw the other day on social media, which I wanted to ask you about was this. I’ve got a picture of it here.
0:46:16 It was someone online that hosted this photo and they said, well, this graph and they said, we need to figure out what’s going on here.
0:46:21 This is the graph. I’ll put it on screen for anybody that’s watching, but also it will be linked in the comment section below.
0:46:31 It essentially shows that over the last, let’s say 20 years, there’s been a really significant rise in cancer amongst women.
0:46:34 But when we look at cancer amongst men, it’s pretty flat.
0:46:41 And this is cancer incidents by age and gender up to 49 years old.
0:46:45 And I was wondering if you had any thoughts on why this is happening.
0:46:53 Yeah, a few thoughts come to mind. Whenever I see these kinds of reports, I always make sure I look firstly at the, what are they actually measuring?
0:47:01 So just to set the stage, this is the number of women who are being diagnosed with cancer, so not dying from cancer, but it’s going up.
0:47:09 So one simple explanation, although perhaps the most disappointing could be that more women are going in for testing younger.
0:47:20 And so we’re just seeing kind of an artifact of more women are just going in sooner and they’re detecting a problem that they wouldn’t have otherwise detected for 10 or 20 years, which is a good thing.
0:47:22 You want to detect cancer as soon as possible.
0:47:36 So that’s the boring answer that it could be a reflection of just more women going in for ultrasounds or MRIs or mammary scans, whereas men don’t ever get tested for anything, which is why we die more from everything possibly.
0:47:43 But to give a more exciting answer, this is very, very likely almost entirely driven by breast cancer.
0:47:47 Breast cancer is the main cancer for women by far.
0:47:54 And so if I had to guess, I bet almost all of this increase in cancer incidence is because of breast cancer.
0:47:56 Why might that be going up?
0:47:58 I would suggest there’s probably a couple instances.
0:48:06 One, although people might not appreciate this, is that one of the best ways for a woman to reduce her risk of breast cancer is actually having babies.
0:48:16 It’s very well known, very well documented that if a woman has babies and breast feeds, her risk of breast cancer goes down.
0:48:18 So yeah, in fact, it’s very meaningful.
0:48:21 I actually don’t know the reasons for it.
0:48:24 It could be the changes in estrogens during lactation phase.
0:48:31 I’ve just, I’ve just actually done a quick search here to, I put a picture of that graph into AI and asked him the same question.
0:48:36 And it said, pretty much what you said, it said there’s a rising breast cancer incidence according to Cancer Research UK.
0:48:39 The other one that it came up with is obesity trends.
0:48:41 Oh yeah, I promised I was going to talk about that.
0:48:42 I wouldn’t leave that.
0:48:43 Sorry for interrupting that.
0:48:44 No, no, no problem.
0:48:47 And then the other one was delayed child bearing.
0:48:48 That’s what I’m saying.
0:48:49 Which is what you were saying.
0:48:54 Yeah, so as child rates, as childbirth rates are going down, it does increase the risk of breast cancer.
0:48:56 Now, I’m a cell biologist, right?
0:48:58 I like to understand a direct mechanism.
0:49:03 And so as much as I invoke the perhaps lower rates of childbirth among women, I don’t know the mechanism.
0:49:05 So I’m sort of loathed to describe it.
0:49:15 The mechanisms I’m very familiar with are the metabolic, which is if you take a breast tissue that is tumor tissue and compare it to,
0:49:22 like if you take a breast tumor and compare it to the normal tissue right next to it, like that it would have shared its origins with,
0:49:29 the cancer from the breast will have seven times more insulin receptors than the normal breast tissue.
0:49:37 So the idea of this tracking quite nicely with obesity rates going up over the past 20 years, I wouldn’t say that it’s the obesity per se.
0:49:46 But I would say it’s the entire metabolic milieu, which is the insulin resistance, that as much as the high insulin is promoting fat cells getting bigger,
0:49:50 that high insulin is also accelerating the growth of the tumor cells.
0:49:59 Because again, one of the main mutations in breast cancer is a seven-fold, so a seven times increase in the number of insulin receptors.
0:50:01 And insulin wants to tell things to grow.
0:50:08 So it’s no surprise that almost every tumor that’s ever been measured for having insulin receptors will have a lot more.
0:50:14 It’s basically telling its neighboring cells, insulin’s going to come by and it’s going to tell us all to grow.
0:50:16 I want to grow more than you.
0:50:21 And that’s what cancer is. Cancer is growth, unregulated growth. Insulin tells things to grow.
0:50:32 So the connection between obesity with the rising incidence of breast cancer is very, very likely a consequence of the rising incidence of insulin resistance.
0:50:34 As you guys know, Whoop is one of my show sponsors.
0:50:38 It’s also a company that I have invested in and it’s one that you guys ask me about a lot.
0:50:43 The biggest question I get asked is why I use Whoop over other wearable technology options.
0:50:48 And there is a bunch of reasons, but I think it really comes down to the most overlooked yet crucial feature.
0:50:50 It’s non-invasive nature.
0:50:56 When everything in life seems to be competing for my attention, I turn to Whoop because it doesn’t have a screen.
0:51:03 And Will Armid, the CEO who came on this podcast, told me the reason that there’s no screen, because screens equal distraction.
0:51:07 So when I’m in meetings or I’m at the gym, my Whoop doesn’t demand my attention.
0:51:13 It’s there in the background, constantly pulling data and insights from my body that are ready for when I need them.
0:51:23 If you’ve been thinking about joining Whoop, you can head to join.whoop.com/CEO and try Whoop for 30 days risk-free and zero commitment.
0:51:28 That’s join.whoop.com/CEO. Let me know how you get on.
0:51:33 You know, one of the big subjects you touched on at the start was Alzheimer’s and dementia.
0:51:43 And I have heard several people on this podcast tell me that they think of Alzheimer’s as type 3 diabetes.
0:51:49 Worldwide, there is a new case of dementia every 3.2 seconds.
0:51:53 It seems like, I don’t know if this is true, but is Alzheimer’s and dementia on the rise?
0:51:59 Oh, yes. Yeah, it is. In fact, it went from not being even on the radar to being a top 10 killer.
0:52:04 Now, it’s interesting how people even die from Alzheimer’s disease. It’s a very kind of vague death.
0:52:09 But yeah, Alzheimer’s disease is one of the top 10 diseases now, certainly in the West.
0:52:12 And I would argue it’s because it has a metabolic origin.
0:52:24 Now, one of the interesting things about Alzheimer’s disease is we have spent billions of dollars on Alzheimer’s research trying to identify the plaque.
0:52:32 So just to set the stage here so that people listening can appreciate this paradigm shift that’s occurred in Alzheimer’s research.
0:52:40 Originally, and even in many people still, people thought that Alzheimer’s disease is the result of these plaques accumulating in the brain.
0:52:50 These kind of little proteinaceous, little thick things that are preventing neurons from sending the signals throughout the brain for the brain to think and have normal cognition.
0:52:58 And yet there are those of us, and I’m proud to say I have long been one of them, who has said that the plaque-based theory doesn’t make sense.
0:53:09 We have had drugs that have been available for human use for years that have effectively reduced plaques in the brain and yet did nothing to improve cognition.
0:53:13 So that is an immediate challenge of the plaque-based theory of Alzheimer’s.
0:53:28 Even further, even beyond older than that evidence, when you would look post-mortem or look at tissue donor people who’d passed away, you would look at the brains of people who died with confirmed Alzheimer’s disease at the time of death
0:53:35 and look at the brain of someone who died without any evidence of any cognitive decline or any compromised thinking whatsoever.
0:53:39 And you would be just as likely to find plaques in both brains.
0:53:44 So whether the brain had Alzheimer’s disease or not, you would still see plaques in the brain.
0:53:48 So the whole idea that plaques mattered has long been controversial.
0:54:05 And just to put a fine point on it, before transitioning to the metabolic origins, about two or three years ago, they found out that the very first published papers that implicated plaque as a cause of Alzheimer’s disease were based on fabricated data.
0:54:14 So the scientists who published those first reports that led to the entire theory that Alzheimer’s disease is plaque-based were called out as fraudulent.
0:54:17 And indeed, all of it was fabricated.
0:54:26 So the entire idea that Alzheimer’s—and we have spent billions of dollars on studies to try to determine how do plaques cause Alzheimer’s disease?
0:54:31 Why, when we reduce plaques, it doesn’t appear to help the disease?
0:54:35 Because the plaques had nothing to do with it. That’s just something that some brains have.
0:54:41 Some brains have more of these little specks than other brains, and they don’t contribute to Alzheimer’s disease at all.
0:54:57 Now, what kept rising to the top, and I would hope now as the dominant theory, is that people with Alzheimer’s disease almost always have some detectable instance of insulin resistance, if not full-on type 2 diabetes.
0:55:07 Now, I will say personally, I don’t like the term type 3 diabetes because it makes it sound like it’s a whole new version of diabetes.
0:55:13 To say it more succinctly and accurately, it is simply insulin resistance of the brain.
0:55:16 And the brain is a very hungry organ.
0:55:22 It is in what I teach as a trinity of high metabolic rate organs.
0:55:28 There are three organs in the body whose metabolic rate is so high that it just really sets it apart from everything else.
0:55:32 And the brain is one of them. The brain has a very high metabolic rate.
0:55:36 So this is a very hungry organ that needs a lot of energy all the time.
0:55:44 But the brain is unique in that it primarily will only use two fuel sources, and I’ve mentioned them, namely glucose and ketones.
0:55:52 But glucose, in that section of the brain that gets compromised with Alzheimer’s disease, the glucose can’t just come straight in.
0:56:00 It needs someone to open the door for it, and that is insulin, of course, just like we described with the muscle cell.
0:56:05 Where in order for the glucose to go into the muscle, insulin had to come and knock on the door, if you will.
0:56:10 And then the muscle being a polite, responsive host would open and allow the glucose to come in.
0:56:16 The brain is similar that in that section of the brain, it has doors that need insulin.
0:56:18 It’s locked until insulin comes and opens them.
0:56:27 So even though glucose levels may be high in the blood, like in type 2 diabetes, you would think, well, the brain can just get all the glucose it wants.
0:56:32 And yet it cannot because it has insulin regulating the entrance of the glucose.
0:56:36 And if the brain is insulin resistant, there’s not enough glucose coming in.
0:56:42 And thus the brain is forced to rely on the only other fuel that it can rely on, namely ketones.
0:56:53 But the same person who’s eating all the time to keep their blood glucose high all the time has so much insulin in their blood that they’re never making enough ketones to fill the gap.
0:56:55 Mind the gap.
0:57:01 And the brain has an energy gap now where the brain needs an amount of energy.
0:57:03 I’m kind of acting it out for those that are watching.
0:57:06 But the brain has a certain energy demand that it needs.
0:57:12 And if there’s a lot of glucose in a healthy insulin sensitive person, glucose will fill all of that need.
0:57:18 But as the brain becomes progressively insulin resistant, it cannot get all of its energy from glucose.
0:57:21 And thus there’s an energetic gap.
0:57:24 And in the absence of ketones, there’s nothing to fill that gap.
0:57:35 And the brain says, well, I don’t have enough energy to keep functioning as well as I did before, so I have to reduce my function, which manifests as a reduction in the ability to think and process.
0:57:37 In other words, cognition goes down.
0:57:51 But what’s so interesting is I just got finished describing a scenario that scientists refer to as brain glucose hypometabolism, or a reduction in the amount of glucose the brain is using.
0:57:53 There are scientists that measured this.
0:57:56 We don’t in my lab because we don’t do these kinds of techniques.
0:58:04 But you can actually infuse people with the glucose that you can take pictures of and see how much the brain is taking it in and metabolizing it.
0:58:07 In Alzheimer’s disease, the brain is not getting as much glucose.
0:58:11 So they call that a hypo or a reduction in metabolism of glucose.
0:58:20 And as much as you and I are describing that scenario as relevant for Alzheimer’s disease, you can essentially open up the book of neurological disorders and see the same thing.
0:58:25 Depression has a brain glucose hypometabolism to it.
0:58:28 Migraines have a brain glucose hypometabolism.
0:58:31 Epilepsy and Parkinson’s disease.
0:58:41 So all of these disorders of the brain, of the central nervous system, the one thing they all have in common is the brain isn’t getting enough energy from glucose.
0:58:49 And another way of saying that is the one thing all of those seemingly unrelated brain problems have in common is that they all have some degree of insulin resistance.
0:58:56 But then it’s no surprise that they all benefit when ketones can swoop in to save the day.
0:59:05 But that only can happen if the person is giving their body a break from the insulin long enough to actually start making ketones.
0:59:14 Really, really interesting on this point about Simon’s because I don’t think people have spent enough time talking about the link between insulin resistance and Alzheimer’s.
0:59:23 And one of the things I was looking at there was how many people with Alzheimer’s have meet the criteria for insulin resistance.
0:59:25 And some studies have it at 40%.
0:59:34 There’s a study I found here that has a 70 to 80%, which I wanted to say exact percentages vary.
0:59:42 But one example is a study in the Journal of Neurology in 2011 that found insulin resistance at approximately 40% of individuals with Alzheimer’s.
0:59:48 But another study in Alzheimer’s patients sometimes found it to be as high as 70% or 80%.
0:59:57 For instance, research by Dr. Suzanne De La Monte at Brown University has drawn attention to the concept of type three diabetes.
1:00:03 Yeah, again, I don’t love the term, but I appreciate the use of it, which is it does suggest a metabolic origin.
1:00:07 But even you look at those ranges, Stephen, you’d say, well, one was 41 was 80.
1:00:08 Boy, what a difference.
1:00:12 I suspect a lot of that is just how did they measure insulin resistance?
1:00:16 If they were looking at the glucose like so many do, you’re just going to miss a lot of people.
1:00:22 Yeah, it’s quite hard to think there’s different criteria for how one defines someone is insulin resistant.
1:00:24 Well, yeah, and that’s just that’s right.
1:00:28 That’s because there’s not enough training, which is at the beginning of the conversation you asked my mission.
1:00:31 One of my missions is to help people learn what to look for.
1:00:33 What do they need to be looking for?
1:00:35 Yeah, they need to be looking at insulin.
1:00:37 So is that easy to measure?
1:00:39 Well, it is technically easy to measure.
1:00:43 It’s just that we don’t have enough systems in place to enable it.
1:00:50 Like, again, if someone listening in the UK were to go to their GP and say, can you measure my insulin?
1:00:53 In many instances, they literally can’t get it done.
1:00:57 The system just isn’t in place to take it to the lab and measure it.
1:00:58 Now, some do.
1:01:03 I know some physicians in the UK who do so, and they have developed their own way of getting it done.
1:01:06 And they’re incredible advocates of this whole idea.
1:01:13 But it is harder in the UK and in Canada where the system is such that they have said out of ignorance,
1:01:19 but perhaps well placed or well intentioned, they will say, well, insulin isn’t a marker that matters.
1:01:20 It is.
1:01:25 And if you’re measuring insulin resistance just to put things back to where we had talked about it earlier,
1:01:29 many people with insulin resistance have normal blood glucose levels.
1:01:31 It’s the insulin that’s high.
1:01:35 And so I would say if a person can get their insulin measured, get it measured.
1:01:41 In US units, if it is anything above about 10 microunits per mil, that’s a warning.
1:01:46 In UK units, if it’s anything above about 40 picamoles, that’s a warning.
1:01:47 Insulin is high.
1:01:49 You could have insulin resistance.
1:01:51 It could be skinny.
1:01:52 Oh, yes.
1:01:53 And have insulin resistance.
1:01:55 Yes, especially depending on the ethnicity.
1:01:59 Like if someone listening to this is East Asian and they say, well, I’m quite thin.
1:02:01 I don’t have insulin resistance.
1:02:03 You very well could.
1:02:04 It depends.
1:02:10 Even in young women, a group out of Northern Canada, which is, of course, pretty far north,
1:02:15 they found that even in young, healthy weight women with PCOS,
1:02:20 if they compared them to their identically matched other women without PCOS,
1:02:23 they were more insulin resistant than the other group.
1:02:27 So anyway, that’s my way of saying, even if you look at yourself and think,
1:02:28 well, I’m kind of lean.
1:02:29 I’m not insulin resistant.
1:02:31 You very well could be.
1:02:32 Okay.
1:02:35 So I’ve got a friend who’s a woman who has PCOS.
1:02:36 Yeah.
1:02:41 And one of the things that she often says to me is that she gains weight easily.
1:02:42 Is this true?
1:02:43 Oh, for sure.
1:02:48 And in fact, I wouldn’t be surprised if she does because the fact that she has PCOS is
1:02:53 not absolute evidence, but very likely evidence that she has insulin resistance,
1:02:55 which would mean at any given moment,
1:03:00 her insulin is at the risk of being a little higher than her non-insulin resistant counterparts.
1:03:02 So if she goes and gets the test done,
1:03:04 I bet her insulin would be high.
1:03:07 And so all that would mean is, which is good.
1:03:09 I mean, knowledge is power.
1:03:12 And my hope would be that as someone goes and gets their insulin measured,
1:03:15 and there are a handful of other tests they could also look at,
1:03:17 but that’s the most succinct,
1:03:20 then it would be all the more impetus or encouragement to say,
1:03:23 okay, I heard, I listened to Stephen and Ben.
1:03:25 I really do need to start making some changes.
1:03:32 And even in PCOS, there are reports that document the absolute reversal of the disease
1:03:35 with nothing more than just dietary changes.
1:03:38 I was looking also a second ago because we mentioned ethnicity a few times
1:03:43 and it says, the research I was looking at says that East Asians have fewer fat cells
1:03:47 and they’re more resistant to obesity-related metabolic issues.
1:03:51 Well, that’s, second part of that statement is not true.
1:03:53 They’re more resistant to obesity.
1:03:56 But they are, it’s an interesting dichotomy.
1:03:58 Okay, I got you.
1:04:02 To find a Japanese man who’s as fat as the average American,
1:04:04 boy, you’re going to have to look, it’s hard.
1:04:09 It’s hard, but to find a Japanese man who is just as much likely to get diabetes,
1:04:12 type 2 diabetes, very easy.
1:04:15 Africans have more fat cells typically.
1:04:19 Yes, so on that ethnicity, there’s a lot of wiggle room here,
1:04:23 but on one end, we’d have Caucasians, blacks would be right nearby.
1:04:29 African ethnicities would be quite close to the kind of Northern European ethnicity.
1:04:33 And then we would move through, and I don’t mean to miss anyone here,
1:04:35 but on the other end, it would be East Asian.
1:04:40 And then sprinkled through that would be Latino.
1:04:43 Latino would be somewhere in the middle, kind of Hispanic.
1:04:47 And then other Southeast Asian and then East Asian, kind of on the worst end
1:04:51 or the least sensitive or the most sensitive to their fat,
1:04:53 the most sensitive to their fat.
1:04:58 This actually is a concept that has been presented called the personal fat threshold,
1:05:02 which is this really interesting idea born from a group in Australia,
1:05:05 suggesting that across every individual body,
1:05:08 which of course is heavily influenced by both ethnicity and sex,
1:05:10 like we’d mentioned earlier,
1:05:15 a body is going to have a rate at which it can store fat in a healthy way.
1:05:17 And then once that threshold is met,
1:05:22 any further pressure to store fat will start creating insulin resistance.
1:05:26 And that threshold is essentially how big, how many fat cells do you have
1:05:28 and how much room do they have?
1:05:31 So if you have more fat cells, you have a higher fat threshold.
1:05:34 You can get fatter before it starts to hurt you.
1:05:36 Does your fat distribution also matter here?
1:05:37 Oh, it does.
1:05:42 Different races, this research is telling me have different fat distribution.
1:05:45 It’s saying that Africans have better fat distribution,
1:05:49 lower visceral fat, and less metabolic risk because of that.
1:05:50 Yeah, yeah, yeah.
1:05:52 Caucasians moderate fat cell quantity,
1:05:55 more prone to subcontaneous fat accumulation.
1:05:56 Subcutaneous.
1:05:57 Which is that’s the fat around the organs.
1:06:00 Yeah, so Caucasians, so let’s say Northern European, African,
1:06:03 both store more of their fat subcutaneously,
1:06:05 which is the fat just beneath the skin,
1:06:07 or the fat that you can pinch and jiggle.
1:06:09 That has an ability to expand more,
1:06:11 because there’s nothing really to limit it.
1:06:14 However, the other place for people to store fat
1:06:16 is their visceral adipose,
1:06:19 which is the fat that is tucked within the abdominal cavity.
1:06:21 So tucked around the organs.
1:06:23 It’s sort of surrounding the kidneys
1:06:24 and the intestines and the liver.
1:06:27 That is an unhealthy place to gain fat,
1:06:30 but in East Asian, all things equal
1:06:33 is putting much more fat there than they are subcutaneously.
1:06:36 The advantage of subcutaneous fat is–
1:06:37 Which is the fat on the outside.
1:06:39 Yeah, yeah, so the fat beneath the skin.
1:06:41 Yeah, the loose belly fat.
1:06:43 The fat that can pinch and jiggle.
1:06:46 That fat has a greater ability to make new fat cells.
1:06:49 So as much as earlier, you and I said fat cells remain static.
1:06:50 For the most part, they do.
1:06:53 There’s a little bit of wiggle room where it can go up,
1:06:55 and that’s purely subcutaneous.
1:06:58 And Hispanics have higher fat cell quantity,
1:06:59 more visceral fat.
1:07:00 Yes.
1:07:02 And increased risk of obesity-related conditions.
1:07:04 Yes, and so the problem with visceral fat is
1:07:06 this is such a finite space.
1:07:09 There’s so little room within the core of your body
1:07:12 that if we allowed those fats to multiply,
1:07:16 it could theoretically start physically compressing on tissues.
1:07:20 And so those fat cells only grow through hypertrophy,
1:07:22 which is the thing we talked about earlier,
1:07:24 with slow insulin resistance.
1:07:27 Subcutaneous fat cells are more abundant but smaller.
1:07:31 Visceral fat cells are fewer but much larger.
1:07:34 And so any ethnicity, including Hispanic or Asian,
1:07:38 that promotes relatively more fat storage in the visceral space
1:07:41 is going to suffer from the consequences of that fat much sooner.
1:07:44 And again, it still comes back to size.
1:07:47 The bigger the fat cell, the sicker the fat cell.
1:07:49 According to Alzheimer’s Disease International,
1:07:51 the total number of people living with dementia globally
1:07:54 is expected to reach 139 million by 2050,
1:07:57 which is up from around 55 million in 2020,
1:08:02 which I imagine is in part related to people living a bit longer
1:08:04 than they once did as well.
1:08:06 Although over the past few years,
1:08:08 life expectancy actually turned down for the first time
1:08:11 in the history of modern world.
1:08:13 So who knows if it will continue to go up?
1:08:16 But yeah, it could be people are living longer.
1:08:18 One of the effects of modern medicine
1:08:23 is that people live longer with disease, Alzheimer’s included.
1:08:25 But it’s absolutely a consequence further
1:08:27 of our overall metabolic milieu
1:08:29 that we put ourselves in a position
1:08:32 where we are making our brains insulin resistant
1:08:35 and thus they’re going hungrier and hungrier.
1:08:38 There’s a study you talk about, which you’ve cited before,
1:08:42 that shows that if you move visceral fat
1:08:45 from an obese animal to a lean animal,
1:08:47 this immediately caused insulin resistance.
1:08:50 Yeah, in the animal that received it.
1:08:52 Yeah, so just to be clear,
1:08:56 if we took what they did in this study just to reflect
1:08:59 why the different depots of fat are harmful.
1:09:01 And so the human body has two distinct fat depots
1:09:02 and you and I described them.
1:09:05 Subcutaneous, which is the fat beneath the skin,
1:09:08 or visceral, which is the fat tucked within the organs
1:09:10 of the abdominal space.
1:09:13 And if you move subcutaneous fat–
1:09:15 Which is like the belly fat.
1:09:17 The belly fat, and from one animal to another,
1:09:19 you couldn’t do this in humans.
1:09:21 If you move belly fat, if you will,
1:09:23 or subcutaneous fat from one animal to the other,
1:09:25 the animal is very healthy.
1:09:27 Subcutaneous fat is inert.
1:09:29 It really is just sort of hanging out there
1:09:31 and minding its own business.
1:09:34 But in that same study, if you move the visceral adipose over,
1:09:37 now all of a sudden that animal that got that extra dose
1:09:40 of visceral fat is going to become sicker.
1:09:42 It’s going to become more insulin resistant and diabetic
1:09:45 because you’ve increased its visceral fat,
1:09:48 the amount of fat that it has in that space.
1:09:51 The body wants to limit the amount of fat that it has there
1:09:54 because if the fat, again, if the fat grows too much,
1:09:58 you can physically start compressing and squishing organs
1:10:01 that you need to be functioning, like the kidneys and the intestines.
1:10:03 Have you seen Brian Johnson?
1:10:05 I have. I don’t know him personally.
1:10:07 You’ve seen the documentaries and stuff made about him
1:10:09 and the work that he’s doing.
1:10:11 What do you make of what he’s doing to extend his age?
1:10:13 Because one of the subjects that I think is linked to this
1:10:16 is the idea of longevity in aging.
1:10:18 And he’s become a bit of a poster child
1:10:20 for the subject of longevity.
1:10:23 Well, I want to address this because this is a real person.
1:10:26 So I want to address it very politely and diplomatically.
1:10:29 I think that I want to distinguish the difference
1:10:31 between longevity research and science,
1:10:33 which is a very real living, breathing field.
1:10:37 And I’m proud to know individuals who are longevity scientists
1:10:42 and distinguish them from longevity, you said, poster child.
1:10:44 So the gurus of longevity.
1:10:46 And that’s not the same thing.
1:10:49 So what I say, I don’t mean to it to be an indictment
1:10:52 of longevity research, but I don’t mind if people hear
1:10:54 a bit of an indictment in my voice
1:10:58 of the modern longevity guru approach.
1:11:02 So these individuals, and he is certainly the most well-known,
1:11:07 they do have the advantage of never really being able to be proven wrong.
1:11:09 So there’s an inherent problem here.
1:11:16 But I will say that the application of being a longevity expert
1:11:18 or not a scientist, but a guru,
1:11:20 and I don’t mean for that to be negative,
1:11:22 but it does have a bit of a negative sound to it,
1:11:27 is that you have to rely on what I would call weak evidence.
1:11:29 Now, what do I mean by that?
1:11:32 So all of the approaches to longevity nowadays
1:11:37 rely on either correlational studies or basic research
1:11:39 or animals and insect studies.
1:11:41 And then extrapolating that results
1:11:44 or assuming those same results will apply to the human.
1:11:47 So let me briefly just mention my concerns with correlational research.
1:11:50 So the longevity guru will say,
1:11:56 “Correlational evidence suggests that people who eat meet die more.”
1:12:00 Well, a correlational study is by my estimation
1:12:03 some of the weakest evidence that you can ever generate.
1:12:06 A correlational study would just have someone come to your home
1:12:09 and say, “Steven, can you please answer this survey about what you eat?”
1:12:13 You answer the survey, you may lie, you may not remember,
1:12:16 you may have things that you don’t even think about including.
1:12:22 Like, for example, that you’re part of a very well put together religious organization
1:12:25 and I actually use that example very deliberately
1:12:29 because people who are known to be part of good tight social circles
1:12:33 like a formal religious group always live longer than people who don’t.
1:12:35 Maybe you’re really lonely.
1:12:39 Loneliness is a greater contributor to death than cigarette smoking
1:12:40 and it’s not even close.
1:12:44 So there could be things on that survey that you just cannot capture
1:12:47 and yet we end up making a conclusion.
1:12:52 And so all of that correlational evidence is deeply flawed research
1:12:56 and yet that becomes the basis for the longevity guru to determine diet.
1:13:01 So if I’m trying to extend my longevity, trying to live longer,
1:13:04 then exactly what should I be thinking about?
1:13:08 So my view on longevity is a metabolic view, no surprise.
1:13:12 I’m a metabolic scientist and I don’t mind someone sort of smirking at me
1:13:16 declaring that or admitting it, but I’m somewhat justified.
1:13:23 Just by way of setting the stage, the earliest, the birth of the modern longevity research,
1:13:29 if it didn’t start, it was heavily influenced by the work of a woman named Cynthia Kenyon,
1:13:31 K-E-N-Y-O-N.
1:13:36 Cynthia Kenyon was one of the kind of, she really did, in my mind,
1:13:40 kind of give birth to the modern longevity focus.
1:13:46 What her lab found using an insect model, and this is again a problem with the longevity gurus,
1:13:50 is that they rely on insect data, for example, but it was compelling what she found.
1:13:58 I think it was worms she found in worms that if they restricted the glucose that the worms were eating,
1:14:04 they would live 50% longer or some fantastic increase in how long the animals lived.
1:14:08 That kind of gave birth to the idea of fasting being beneficial,
1:14:14 but it also allowed her lab to start playing around with some of the genes of these little insects.
1:14:21 When they started knocking down or under-expressing some of the genes involved in insulin,
1:14:25 they didn’t have to restrict the food, the animals just lived longer.
1:14:32 That touches on this metabolic aspect and everyone nowadays is really interested in autophagy.
1:14:37 Autophagy is a term for a cell essentially cleaning itself out.
1:14:40 Which is typically associated with lung fasting.
1:14:47 Yeah, in fact, yes, so that is partly why fasting has been so embraced within the longevity community.
1:14:55 It’s because if you can promote autophagy, the cell keeping itself cleaned out,
1:15:01 that is thought to be a key contributor to longevity, so autophagy equating to longevity.
1:15:05 I don’t disagree with that. I think that probably is a very valid view.
1:15:10 Then the question comes, well, how can I control autophagy?
1:15:18 Well, there is a humble hormone that comes from the pancreas that has a very powerful effect on autophagy called insulin.
1:15:22 So as much as people are fasting, what’s the value of fasting in reducing autophagy?
1:15:24 It’s because insulin comes down.
1:15:28 Now what becomes interesting is what happens if you were to put someone,
1:15:34 allow them to eat calories, but the calories are such that their insulin is staying low
1:15:37 and they’re making ketones, in other words, a ketogenic diet.
1:15:40 You also enable autophagy.
1:15:47 There was a very well done animal study finding that they didn’t have to restrict calories and fast the animals.
1:15:52 They could let the animals eat as much as they wanted, but it was a ketogenic diet.
1:16:00 They lived significantly longer than their other littermates that were eating the normal high carb chow, similar to what humans eat nowadays.
1:16:04 And so autophagy probably does matter for longevity.
1:16:11 All the more reason to keep your insulin in check, because insulin is a powerful inhibitor of autophagy.
1:16:16 So as much as we have longevity gurus who are taking thousands of dollars worth of supplements,
1:16:23 I can’t help but look at that and think, just control your insulin, that within every cell there’s this battle.
1:16:28 There’s a yin yang of growth and death or building and breaking to say it a little more politely.
1:16:30 In fact, that is metabolism.
1:16:37 The very word metabolism encompasses anabolism, which is anabolic or building up,
1:16:40 and catabolism or catabolic, which is breaking down.
1:16:48 The key to a healthy, growing, living cell is this nice, ongoing balance of build and break, build and break.
1:16:53 You have to build something up and then modestly break it down, and then you build some things up again.
1:16:58 And autophagy is a very important part of that breaking cycle within the cell,
1:17:02 that, hey, it’s time to get rid of some old parts and now we’ll rebuild some of that again.
1:17:05 Now we’re going to break down these parts and rebuild it.
1:17:08 Insulin is the key to that process.
1:17:13 If insulin stays high for too long, you never allow the catabolic or the breakdown.
1:17:17 This is one reason why insulin is so facilitative to cancer.
1:17:20 Insulin wants things to grow. Cancer is a disease of growth.
1:17:25 We don’t ever let the cancer start to break down. Insulin won’t let it in part.
1:17:28 You’ve repeatedly talked about ketosis.
1:17:29 I have.
1:17:30 We’ll eventually get there.
1:17:32 We’re kind of teasing the audience a little bit.
1:17:33 Yeah, we are.
1:17:38 But rightly so. Ketones are a very vilified, misunderstood part of the body.
1:17:42 And to my great delight, it’s getting a sort of new appreciation.
1:17:44 Well, I’m currently on the keto diet as well.
1:17:49 So I am incredibly interested to understand, A, like what’s going on in my body,
1:17:53 but B, I’m quite compelled by both the pros and cons of doing it.
1:17:57 And I want to talk about the cons and the pros because they both exist.
1:18:04 One thing you say in your book, why we get sick is that the longest living humans are also the most insulin sensitive.
1:18:05 Yeah.
1:18:10 So you’re telling me that the longest living humans are the ones that are able to stave off that insulin resistance.
1:18:11 Yes.
1:18:12 Yes, there are.
1:18:13 Keep their insulin levels lower.
1:18:14 That’s right. Yeah.
1:18:23 In fact, most of the longevity research was sort of a final point on this is that when you look at these studies that look back in time and say,
1:18:25 okay, what is it about these people?
1:18:29 What variables tend to go along with the longest lived humans?
1:18:36 One of them is that their insulin sensitive and their blood glucose levels are, in fact, a very well done study just last year out of Sweden.
1:18:38 I think it was just one year ago.
1:18:47 They looked at all, and Sweden is meticulous in its record keeping, which is an advantage and fairly homogenous society.
1:18:50 So it kind of eliminates some confounding variables.
1:18:57 But they attempted to document what were the variables that were just the most consistent theme of people who lived very long.
1:18:59 One of them was good glucose control.
1:19:06 And this next one is very controversial because they found that they also, the longest lived people had high cholesterol levels.
1:19:08 And isn’t that funny?
1:19:14 It is one of the most consistent themes of longevity research that the longest lived people have higher cholesterol.
1:19:21 And yet we live in a world that hates cholesterol, and the moment cholesterol goes up, we put them on a cholesterol-lowering medication.
1:19:25 We could be doing the perfectly wrong thing to help these people live longer.
1:19:30 So that was, and then low uric acid, and there’s a handful of other little variables that fit into this.
1:19:34 They found that some of the longest living humans had high cholesterol levels.
1:19:35 That’s right.
1:19:37 That’s what the Sweden study found, for example.
1:19:45 The paper just published a year or so ago what were some of the most consistent themes that had good glucose control and high cholesterol.
1:19:48 I’m a great defender of cholesterol.
1:19:52 It is a molecule of life.
1:19:54 And so many, so much depends on it.
1:19:56 Mitochondria, for example.
1:20:02 Mitochondria have to have a cholesterol molecule in them in order to work, like the very powerhouse of the cell.
1:20:08 And the more you lower cholesterol through, say, drug interventions, the more you compromise the mitochondria.
1:20:10 The sex hormones.
1:20:13 All sex hormones are built on cholesterol.
1:20:18 It’s no surprise if someone takes a cholesterol-lowering medication, their sex hormones go down.
1:20:25 This is why some men experience such terrible loss of libido because he’s becoming low testosterone because of the war on cholesterol.
1:20:27 But it’s getting bad cholesterol, right?
1:20:36 Well, that’s, as the story goes, yes, and yet I think that’s overly simplified, where people will say LDL cholesterol is the bad cholesterol.
1:20:40 And yet that gets included in these studies of longevity.
1:20:44 So I think that good and bad aspect of it is not entirely fair or accurate.
1:20:45 We need LDL.
1:20:49 And LDL is just as much a component of the immune system.
1:20:51 LDL actually helps the body fight infections.
1:20:54 So it’s also an unsung hero of immunity.
1:21:00 There is research suggesting that in very old age, high cholesterol levels do not always correlate with high mortality.
1:21:04 And in some studies may even be linked to longer life.
1:21:05 Exactly.
1:21:06 Which is as well.
1:21:07 Yeah.
1:21:12 Well, you say that and yet maybe our anti-cholesterol view is the bizarre one.
1:21:20 And so as a cynic who’s very familiar with biomedical research, I sometimes will look at clinical markers and say, why are we so obsessed with glucose?
1:21:21 Why not insulin?
1:21:23 Why are we so obsessed with cholesterol?
1:21:25 Why not triglycerides?
1:21:31 Which is another lipid that can be measured that is far more predictive of who’s going to have a heart attack or not.
1:21:39 And I think it’s because we have chosen markers in modern medicine that we have well designed drugs.
1:21:42 So it’s a really, really good way to sell a lot of drugs.
1:21:45 So there’s no drug that’s going to address insulin.
1:21:46 So let’s not measure it.
1:21:49 But there are lots of drugs that will lower glucose.
1:21:55 So let’s measure glucose because then we can diagnose the problem and then we can give them a drug and make a lot of money.
1:21:58 That’s a cynical view, but I don’t think it’s unjustified.
1:21:59 Similarly with cholesterol.
1:22:05 Why look at LDL when triglycerides, another lipid marker, are a much better indicator.
1:22:09 It’s because we don’t have a drug that effectively lowers triglycerides.
1:22:14 You can with diet, but we do have drugs that very effectively lower LDL.
1:22:21 One thing that really surprised me when I was reading your work is there was a study done in Bulgaria,
1:22:32 which proved that smoking causes insulin resistance in humans by having seven healthy non smokers smoke four cigarettes over an hour for three days.
1:22:33 What did they find in that study?
1:22:38 Yeah, so they found that if you took healthy non smoking people and had them start smoking, they became insulin resistant.
1:22:46 I believe I invoked that study in the section where I was talking about inflammation where when you cigarette smoke that elicits,
1:22:52 there’s a lot of junk coming in and there’s a powerful inflammatory response and that contributes to insulin resistance.
1:22:53 Is this vaping as well?
1:22:56 Oh, so that is a very good question.
1:23:04 I have in fact published now multiple papers with a very good friend and colleague who is a lung expert at my university guided by the name of Paul Reynolds.
1:23:12 Paul and I, we have published reports together looking at cigarette smoking and the inflammatory and insulin resistance effects that come from that.
1:23:20 And now we’ve even started looking at the molecules, the hyperheated molecules from vaping and they’re terrible.
1:23:23 In fact, yes, very similar results.
1:23:31 If you were to take a comparable amount of the chemicals from normal cigarette smoke with its filter versus vaping,
1:23:35 the vaping ones are probably worse chemical for chemical.
1:23:37 In terms of their insulin.
1:23:43 Yeah, in terms of their inflammatory effect of the damage to the airway and the insulin resistance that comes from it.
1:23:45 That’s horrifying.
1:23:51 It is in part because of just how common it’s become.
1:23:53 Does smoking make us fat?
1:23:54 Oh, it’s a great question.
1:23:57 It doesn’t because it replaces other interests.
1:24:03 So if the cigarette smoker ate the way everyone else was eating, it would.
1:24:09 But because the cigarette smoke satisfies a craving, they have less of an interest in food.
1:24:17 What’s so interesting about cigarette smoking is, again, as I said, you begin to smoke, other things don’t tempt you as much like the cookies and the cakes.
1:24:23 But one of the ways the smoker helps kick the habit of cigarette smoking is actually eating candy.
1:24:26 Like they will literally start carrying around little candies in their pocket.
1:24:32 So as they feel a craving for cigarette smoking, they will take out a little candy, open it up and pop it in their mouth.
1:24:38 And so it’s no surprise that very commonly when a person quits smoking, they gain significant weight.
1:24:42 They end up trading out their addictions, if you will.
1:24:51 And unfortunately, in humans, all of the study of addictions with food, people only manifest an addiction to one type of food and that is carbohydrate.
1:24:53 There’s no evidence of addiction to fats or proteins.
1:25:06 You published a study in 2024, which found that exposure to diesel-exhaust gas was associated with increased fat mass, enlarged fat cells, insulin resistance and increased levels of inflammation.
1:25:09 That was published in the International Journal of Molecular Sciences.
1:25:14 Yeah, that was one of the studies I just was referring to with regards to my colleague Paul Reynolds.
1:25:18 Paul and I, that was one of the papers we published looking at these inhaled particulates.
1:25:26 The reason I was interested in this field of study in the first place was just to continue to kill the caloric model of obesity.
1:25:30 So this touches on an earlier part of the conversation.
1:25:34 Overwhelmingly, if you ask someone, why do we get fat?
1:25:36 Well, because you eat more calories than you burn.
1:25:37 Why do you lose fat?
1:25:39 Because you eat fewer calories.
1:25:43 And I have long just been frustrated by how naive that view is.
1:25:48 Yes, energy matters, but again, the fat cell must be told what to do with the energy that it has.
1:25:52 That, of course, points an obvious finger at insulin, which is the strongest of all signals.
1:26:01 But what we found in that study is that even something as seemingly unrelated as diesel-exhaust particles, mind you, we did not do this study in humans.
1:26:07 Full disclosure, we did the study in animals where we could perfectly control how much diesel-exhaust they’re getting.
1:26:15 So we have this mechanism in Paul’s lab where you can aerosolize these particulates and know exactly how much the animal is breathing.
1:26:29 And then at the end of the study, even though they ate the exact same amount of food, the animals that were exposed to the diesel-exhaust particulates had fatter fat cells and more insulin resistance than the animals that had just been breathing normal room air.
1:26:33 So what we’re breathing in theoretically could then be determining how fat we’re getting.
1:26:37 Yeah, in fact, this evidence would suggest that it goes beyond theory.
1:26:42 So our evidence would state conclusively that, yes, what you breathe does matter.
1:26:45 Then theoretically, we would say, well, how much does that apply to humans?
1:26:48 That is where it would get into the realm of theoretical.
1:26:52 But the evidence certainly suggests, yes, the very air we breathe matters.
1:26:54 And you see this at a population level.
1:26:57 Look in areas where there are, now there are confounding variables here.
1:27:03 Here I am invoking correlational research, and I was just criticizing it a moment ago with regards to longevity.
1:27:13 But you look in areas where they have higher pollution levels, where the particulates are higher in the atmosphere, and those same areas are always fatter and more diabetic.
1:27:15 Interesting.
1:27:18 But of course, that’s correlational.
1:27:19 Exactly.
1:27:20 Yes, thank you for pointing it out.
1:27:32 But again, as much as you and I are citing the problem with the correlational study there, we need to always cite the problem with correlational studies when it comes to informing nutrition policy, like don’t eat eggs because they cause diabetes.
1:27:35 But when you actually look at the studies, you find nothing of the sort.
1:27:40 What about other sort of environmental toxins and their impact on insulin resistance?
1:27:41 Yeah.
1:27:43 So there are the ones that you inhale.
1:27:45 A handful of inhaled particulates will matter.
1:27:56 We have shown in my lab alone, with my collaborators, diesel exhaust will do it, cigarette smoke will do it, and more, we have a funded grant right now to look at the effects of vaping.
1:28:00 So apparently, stuff we breathe will matter.
1:28:06 To some unknown degree, things that we drink will that are non-chloric.
1:28:10 So there can be, like people have heard of the microplastics.
1:28:19 Microplastics are things that you can’t, they’re so small that you drink them and they will absorb through the intestine and get into the bloodstream.
1:28:26 For reasons that are unknown to me at the moment, one of the sites where those micro particles will go is the fat cells.
1:28:30 And once there, they will directly promote the growth of the fat cells.
1:28:33 So that’s actual microscopic segments of plastic.
1:28:42 But separate from that are molecules that can come from plastics and soaps and detergents like BPA or diethylstilbestrol DES.
1:28:48 That’s actually an estrogen mimetic, kind of what we’d preferred to earlier with regards to other endocrine disruptors.
1:29:02 But there are other chemicals that a person can drink or inhale, like I mentioned earlier, but that will directly impact the growth of fat cells or promote to tell, mimic what insulin wanted to do, which is tell the fat cell to grow.
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1:31:07 So let’s talk about ketosis and ketones.
1:31:12 The diet, the keto diet is becoming increasingly popular from what I’ve seen.
1:31:15 It’s actually the diet that I’m on at the moment.
1:31:18 How does that play into everything we’ve talked about?
1:31:19 Yeah.
1:31:26 So this is an opportunity for me to do a little bit of nutrient biochemistry or a little discussion of metabolism
1:31:30 so that people appreciate what ketones even are and where they come from.
1:31:39 So the entirety of the human body is a metabolic hybrid in that the body is largely burning fuel from two sources.
1:31:44 It is burning blood glucose or sugar, blood sugar, or it’s burning fat.
1:31:47 Those are the two main fuels for the body by extension.
1:31:49 Now the brain was an exception.
1:31:53 The brain is glucose or ketones, but I’ll get to where the ketones come from.
1:32:00 The rest of the body isn’t really relying on ketones as much as fats or glucose or blood sugar.
1:32:03 Insulin is what decides which fuel is used.
1:32:10 So as much as the metabolic engine has two fuel sources, insulin will decide which one is opened and which one is closed.
1:32:13 If insulin is high, the body is sugar burning.
1:32:19 And you can measure this in the whole body level by measuring the amount of oxygen and CO2 that the body is producing
1:32:24 because different biochemistry or the burning of the fuels will produce a different amount of CO2.
1:32:27 So if I’m burning glucose, I might be producing more CO2.
1:32:35 Yes, so we could hook you up to something called an indirect calorimeter and measure that your RER, the respiratory exchange ratio,
1:32:38 the balance between CO2 and oxygen, would go higher.
1:32:40 So we increase your insulin.
1:32:46 Like if I infused you with insulin in the next few minutes, we would see that your RER would go up.
1:32:48 We would say, “Boy, you’re sugar burning.”
1:32:54 Or we allow insulin to come down and then the RER goes down, which is reflective of fat burning.
1:32:58 So it’s insulin that determines whether the body is sugar burning or fat burning.
1:33:05 Now, when insulin has been low for about 16 or so hours, something interesting starts happening at the liver.
1:33:14 So the liver with insulin being low is burning a lot of fat, including its own fat that the liver can store, the liver can store fat,
1:33:16 but also fat coming from fat cells.
1:33:22 Because if insulin is low, the fat cells are just leaking out fat to be burned by the body.
1:33:25 And because insulin is low, the liver keeps burning it.
1:33:32 And the liver essentially continues to burn so much fat that it fills its own needs.
1:33:40 It meets its own needs and says to itself, “Hey, I don’t need to keep burning fat. I have all the energy I need. I’m doing great.”
1:33:44 But it can’t stop burning fat because insulin is low.
1:33:47 And if insulin stays low, fat burning keeps going.
1:33:50 Because the body doesn’t have enough glucose.
1:33:55 Well, in this sense, it’s doing it to help replace the glucose that isn’t coming in.
1:33:57 That’s the value of the ketone.
1:34:04 So as the liver is continuing to burn fat, it essentially gets to a point of fat burning where it’s burning more fat than it needs.
1:34:08 And that excess, if you will, is what becomes ketones.
1:34:15 So ketones are kind of a metabolic release valve for the liver cell to say, “I don’t know what to do with all this fat burning.”
1:34:19 “Okay, I know what I’m going to do. There’s not a lot of glucose coming in.”
1:34:24 And so the brain may start to get hungry, so I’m going to start making ketones.
1:34:30 And so ketones are nothing more than a product of a lot of fat burning.
1:34:36 And anyone who even fasts for 24 hours, you wake up that next morning, you’re in some degree of ketosis.
1:34:42 Lest anyone think it’s an extreme thing, people are going in and out of ketosis, ideally, often.
1:34:44 Now, why do I say ideally?
1:34:49 It’s because ketones are, as we’ve already outlined, perhaps the best fuel for the brain.
1:34:51 The brain thrives on ketones.
1:35:00 You can take a person with early stage Alzheimer’s disease and have them go through a series of cognitive tests and they do horribly on them.
1:35:10 Like one example is you ask the patient with Alzheimer’s to draw the face of an analog clock, a circle with one, two, through 12, and then some hands on it.
1:35:12 And it is utter chaos.
1:35:13 This is published reports.
1:35:18 You then put them into ketosis, ask them, “Can you please draw the face of a clock?”
1:35:22 It’s still sloppy, but it is absolutely the face of a clock.
1:35:26 You ask them when they’re not in ketosis to try to tie their shoelaces.
1:35:30 They can’t think through the puzzle of tying the shoelaces.
1:35:32 Ask them to do it again when they’re in ketosis.
1:35:35 All of a sudden, they can tie their shoelaces.
1:35:37 More than that, they can get themselves dressed.
1:35:39 All of these are published case reports.
1:35:46 It’s just my long-winded way of saying the brain thrives when it has ketones as a fuel source.
1:35:48 But the benefits don’t stop there.
1:35:55 My lab published a report finding that when humans were in ketosis, which is just a term for ketones being elevated,
1:36:01 we pulled out small pieces of belly fat and measured the metabolic rate of that belly fat.
1:36:09 We found that in ketosis, the metabolic rate of that belly fat was three times higher than when the people were not in ketosis.
1:36:10 What does that mean?
1:36:15 That means that the fat was suddenly behaving in a much more energetic way.
1:36:18 That fat tissue has a very low metabolic rate.
1:36:25 All of a sudden, when the ketones came into them, they started getting much more active and they started burning more energy,
1:36:28 which is going to be very helpful for someone who wants to lose fat.
1:36:32 If your fat cells now have a three times higher metabolic rate,
1:36:36 that means that the fat cells are starting to act a little bit more like your muscle cells,
1:36:38 and they’re just burning more energy.
1:36:40 So does that mean that I’m going to lose fat faster?
1:36:43 Yes, absolutely, and that is what happens.
1:36:48 There are very well-done controlled studies to show that if you control for all calories,
1:36:51 when a human is in ketosis, their metabolic rate goes up.
1:36:54 Your whole body is just burning more.
1:36:57 It’s just, everything’s kind of been turned on a little more.
1:37:03 The furnace of the metabolism has just been, it’s have a little more fuel kind of stoking the fire.
1:37:06 So ketones will increase metabolic rate of fat tissue.
1:37:11 We found a paper that we published documenting how we took muscle cells
1:37:16 and kind of insulted the muscle cells to determine how tough the muscle cells were.
1:37:22 When we incubated the muscle cells with ketones, they were much more resistant to injury.
1:37:29 So the ketones act to protect muscle tissue, and in a way that is reflective of a function of ketones.
1:37:32 Ketones are a defender of muscle.
1:37:35 Ketones are basically the way to tell the brain, saying,
1:37:40 “Brain, you think you need a lot of glucose, and if you don’t get enough glucose,
1:37:44 you would start stripping the protein from muscle to turn it into glucose,
1:37:50 but I’m here as a ketone, so you can eat me instead and leave the muscle alone.”
1:37:56 So we published again a direct report finding that ketones actually make muscle more resistant to injury.
1:38:03 And this could be why you’re seeing more and more elite athletes using ketones as an actual ergogenic aid
1:38:06 or like a supplement to help them better, to be better.
1:38:13 So at my university at BYU, just this year, our men’s and women’s cross-country team took the national championships,
1:38:16 the best college runners in the nation, pretty impressive.
1:38:23 One of the things they do is they take these ketone drinks before they train and before they race.
1:38:30 More and more of the Tour de France teams take ketone supplements because it is just another fuel.
1:38:32 It is something that the body can burn.
1:38:38 That we always say, “Well, once you start running out of glucose, you’re going to bonk or you’re going to hit the wall.”
1:38:43 Well, what if you don’t really use glucose because you’re burning a lot of fat and a lot of ketones instead,
1:38:47 and that keeps your glucose kind of untouched or you’re not relying on the glucose.
1:38:49 And we see this in humans.
1:38:58 If there isn’t a human that is adapted to a ketogenic diet, they burn fat at a higher rate than was ever thought humanly possible.
1:39:06 That that fat is basically fueling all of their muscle movement during the exercise session rather than relying predominantly on glucose.
1:39:08 The body has adapted.
1:39:16 It’s burning fat for fuel and when available, it’s burning ketones for fuel and it’s leaving the muscle as sort of a last resort when it really needs a big kick.
1:39:18 I’ve seen these keto drinks.
1:39:19 Yes.
1:39:20 They’re almost like little shots.
1:39:22 Well, there’s a bunch of different types.
1:39:30 If you look at the spectrum of ketones, on one end you have the cheapest, most readily available, although less effective, called ketone salts,
1:39:35 where it takes a molecule of ketone and binds it to a mineral like calcium or magnesium.
1:39:40 Not as effective and it’s a lot of minerals, so people will find that they might get a lot of plaque on their teeth,
1:39:44 maybe increased risk of kidney stones, so it comes with some consequences.
1:39:47 Then you have the ketone ester, which often comes in shots.
1:39:54 Then you have the bioidentical BHB or the bioidentical ketone, one company which is original ketone.
1:39:55 They make it.
1:39:57 Now, these ones are more effective.
1:40:00 You take a little bit of these and you will get an increase in ketones.
1:40:02 They’re a little more expensive too.
1:40:05 But as the space is becoming more competitive, the price is coming down.
1:40:07 What exactly does it do?
1:40:17 If I took a shot of bioidentical ketone drink, what would go on in my body and how would that impact my cognitive performance or athletic performance?
1:40:18 Yeah.
1:40:23 It would result, so you’re drinking it in, you’re immediately absorbing it from your gut.
1:40:28 If you were not in ketosis, let’s say you had, and I’m not encouraging people to do this,
1:40:32 you had just eaten two bagels and a cup of sugary coffee.
1:40:37 You’re no ketones, undetectable, because insulin has come up, it’s inhibited ketone production.
1:40:39 Then you drink a shot of the ketone.
1:40:41 Within an hour, we would detect your ketones.
1:40:44 They would have gone up maybe to one millimolar, which is a pretty significant bump.
1:40:45 Yeah.
1:40:46 They’re capable of that kind of movement.
1:40:50 Maybe you do so because you’re thinking, “I really need to be sharp right now.”
1:40:51 Would that make me sharper?
1:40:53 Well, that’s where we have to speculate.
1:40:59 There’s no, my lab published animal evidence suggesting that, yes, indeed, it makes you sharper,
1:41:02 that we had these animals navigate mazes and recognize objects,
1:41:06 and when the animals were on a ketogenic diet, they were much sharper.
1:41:12 They were much quickly, much better at solving problems and remembering solutions to previous problems.
1:41:18 I asked this in particular because, as my team know, because I’ve said it to them a lot over the last couple of weeks
1:41:22 since I’ve been on the keto diet and I’ve been literally pricking my finger to check.
1:41:23 Confirming.
1:41:24 Yeah.
1:41:25 My keto levels.
1:41:27 The highest I’ve gotten to is like 2.5.
1:41:28 Which is high.
1:41:29 Is it high?
1:41:30 That’s not problematic.
1:41:31 Right.
1:41:36 I mean, that is just proof positive that you’re in ketosis, which itself is proof positive that you’re burning a lot of fat.
1:41:37 Yeah.
1:41:39 And three, that your insulin levels are low.
1:41:41 Fat dropped off my body like I’ve never seen in my life.
1:41:42 Exactly.
1:41:43 Yeah.
1:41:44 It’s crazy.
1:41:48 So the power there is, like, if you’ll allow me to kind of springboard off of that comment,
1:41:53 the power of, so if someone is listening to this and they’re thinking, okay, I need to shrink my fat cells.
1:41:54 Yeah.
1:41:59 Unfortunately, they don’t realize that there’s two variables to what caused their fat cells to grow in the first place.
1:42:04 They have no awareness of the value of insulin in this formula.
1:42:07 All they do is pay attention to the calories.
1:42:12 And so the average individual is looking down the road of this fat cell shrinking journey.
1:42:16 And they’re thinking, okay, what I have to do is just cut my calories.
1:42:18 And what do they do to cut their calories?
1:42:20 They do the exact wrong thing.
1:42:23 And before I even answer that, let me just present the scenario.
1:42:26 Let’s imagine that Steven and I, everyone listening is invited.
1:42:28 Steven and I are hosting a buffet.
1:42:30 We have the world’s best chefs.
1:42:34 It is going to be a table filled with the most delicious foods you can imagine.
1:42:39 You’re in our invitation, we say, come hungry, because you’re going to want to try a little bit of everything.
1:42:44 Everyone listening, ask yourselves, what would you do to come as hungry as possible?
1:42:45 You’d probably do two things.
1:42:52 Or think, how did you go to your Thanksgiving or your Christmas dinner as hungry as possible?
1:42:58 You would eat a little less in some period of time before the event, and you would exercise a little more.
1:42:59 And it would work.
1:43:01 You would be very hungry.
1:43:05 That’s why the traditional advice given for weight loss doesn’t work.
1:43:08 Because we tell people, eat less, exercise more.
1:43:12 Sure, you maybe lose a little bit of weight in the short term, but all that does,
1:43:16 you’ve given them the perfect recipe to promote hunger, and hunger always wins.
1:43:18 That’s a good example.
1:43:20 In the US, we have a game show.
1:43:23 Maybe there was some version of this in the UK called “The Biggest Loser.”
1:43:25 It was essentially, who can lose the most weight?
1:43:29 And it was through a punishing regiment of caloric restriction.
1:43:30 Eat less, exercise more.
1:43:33 That is like the perfect embodiment of that approach.
1:43:37 They were starving, and they were exercising to insane degrees.
1:43:39 And oh my goodness, did they lose a lot of weight?
1:43:41 And yet you never see them again.
1:43:46 They don’t do a reunion tour five years or ten years later because they gain it all back.
1:43:48 Do you know they gain it all back?
1:43:49 They do.
1:43:52 In fact, a paper published in the US from the National Institutes of Health
1:43:55 documented not only the degree to which they gain weight back,
1:43:59 but also how it almost literally breaks their metabolism,
1:44:03 that normally a person’s metabolic rate is connected to their body mass.
1:44:05 A bigger body has a higher metabolic rate.
1:44:08 A smaller body has a lower metabolic rate.
1:44:10 This is just human physiology.
1:44:13 And no surprise, when someone loses weight, there’s less of body,
1:44:15 and so metabolic rate goes down.
1:44:19 As they gain weight back, metabolic rate will typically go back up as well,
1:44:22 except for the contestants and The Biggest Loser.
1:44:26 They started with a high metabolic rate because of a high body fat level.
1:44:29 They lost a substantial amount of weight.
1:44:32 No surprise, metabolic rate went down substantially.
1:44:37 But if this is such a dramatic change that as they started gaining weight back,
1:44:40 metabolic rate did not come back with it.
1:44:43 It stayed lower than it should have.
1:44:45 Normally it’s connected sort of one-to-one,
1:44:49 wherever body weight is going, metabolic rate is going, except in these people.
1:44:54 That method of dramatic weight loss through such severe restriction,
1:44:57 which is based purely on the caloric theory of obesity,
1:45:00 leads to significant hunger.
1:45:05 So no surprise, if a person’s attempting to shrink their fat cells or lose weight,
1:45:10 if the first step is I’m going to cut my calories and they don’t address their high insulin,
1:45:13 they’re never going to lose weight in the long run.
1:45:15 They’re going to step right back to where they were.
1:45:19 Because if they start cutting calories but insulin is still high,
1:45:23 that’s going to make them very hungry because insulin wants to be storing energy.
1:45:26 A professor from Harvard named David Ludwig found this.
1:45:30 If you have people eating a lower calorie meal that spikes their insulin,
1:45:36 it makes them much hungrier than a lower calorie meal that doesn’t spike insulin.
1:45:37 So that’s the key.
1:45:41 Anyone listening, if you’re thinking I need to be on a fat cell shrinking journey,
1:45:46 let the first step of that journey be I’m going to lower my insulin.
1:45:49 Which means I’m going to control my carbohydrates.
1:45:54 I’m going to stop eating carbohydrates that come from bags and boxes with barcodes.
1:46:00 And while I am restricting those carbohydrates, I’m going to focus more on protein and fat.
1:46:07 So control carbs, prioritize protein, and don’t fear the fat that comes with those proteins.
1:46:14 Fat and protein together is a miraculous combination of helping you feel full.
1:46:16 And it is literally giving everything you need.
1:46:19 There are such things as essential proteins.
1:46:21 There are such things as essential fats.
1:46:23 So focus on those.
1:46:26 And that will be the key to helping insulin come down.
1:46:29 Then as you have found, you haven’t, and when you’re hungry, eat.
1:46:31 If you’re not hungry, don’t eat.
1:46:34 But what the person will find is they’re lowering their insulin.
1:46:39 All while their metabolic rate is going up, they’re learning how to burn their own fat for fuel.
1:46:45 Because remember the metabolic hybrid, that metaphor, that if you want to lose fat, you need to burn fat.
1:46:48 You’re not going to lose fat if you’re always burning glucose.
1:46:50 It’s fat that you need to burn.
1:46:55 And as you start burning more fat, you realize that it’s like the hump on a camel.
1:47:01 That hump exists because it is a big source of fat for that animal to be using its own fat for energy.
1:47:04 We have our own version of that.
1:47:07 You think about the average individual who’s chubby.
1:47:12 They have hundreds of thousands of calories waiting to be burned in those fat cells.
1:47:16 It’s just that their chronically elevated insulin is never letting them burn it.
1:47:21 And so as the person starts making these changes in their diet to lower insulin,
1:47:24 they now can finally start relying on their own fat for fuel.
1:47:28 So it’s no surprise that their hunger starts to come down.
1:47:32 Let that be the natural way in which you’re controlling your calories.
1:47:36 Don’t control your calories because you’re forcing yourself to be hungry and eat less.
1:47:40 Control your calories because you simply aren’t hungry.
1:47:44 So I have to lay this with my own sort of anecdotal experience.
1:47:48 So I every year do a keto diet for usually for about eight weeks.
1:47:51 This time it’s going to go on for a little bit longer.
1:47:56 The reason in part why it’s going to go on a little bit longer is I just learned more about what’s going on in my body.
1:48:01 And also because I podcast now and do a lot of speaking on stage and those kinds of things,
1:48:05 I see tremendous variance in my ability for my brain to articulate what I want to say.
1:48:06 I feel the same way.
1:48:08 It’s like it’s absurd.
1:48:12 I was saying this the other night to the team that with me here in Los Angeles
1:48:17 and I’ve tried to say it to so many people as someone that can spend nine hours a day
1:48:21 trying to think of the next question to ask or trying to remember the research
1:48:25 on stage in front of a thousand people trying to deliver a story or a point.
1:48:30 I get to see variance which I’ve never been able to explain.
1:48:36 Where some days I’ll go up on stage, I’ll be in a podcast and it’s like my brain and my mouth aren’t connected.
1:48:42 And then on other days specifically when I started doing ketosis or having a ketogenic diet,
1:48:44 it just flows.
1:48:45 It just flows so well.
1:48:49 And I was saying to my team, it feels like I’m looking at the world like this these days.
1:48:53 Like I’ve got this intense, for anyone that can’t see me, I just stretched my eyes.
1:48:55 Like I’ve got this intense focus on the world.
1:49:02 The other thing I’ve noticed with my diet is I get hungry but not like I used to get hungry.
1:49:07 And then very quickly after I start eating, I stop.
1:49:11 I don’t seem to be like doing like these, I used to kind of binge a little bit.
1:49:15 I used to have like longer eating sessions and my hunger goes very quickly.
1:49:20 I also found that I didn’t have these like fluctuating energy levels throughout the day.
1:49:22 I don’t crash anymore.
1:49:25 I used to get like slumps and I don’t slump anymore.
1:49:30 And then the other thing which a lot of people care mostly about is the fat, so like belly fat.
1:49:35 I have never seen anything that has stripped belly fat off me faster.
1:49:43 And I’m talking in a matter of weeks that I could, you know, count on one hand then doing the ketogenic diet.
1:49:48 And if I could literally show a picture of my scales because I have the digital scales on the screen
1:49:54 and it’s just trundling along and then there’s this cliff edge where it goes directly down.
1:49:59 And so much so actually that one of my concerns with the ketogenic diet is how the hell do I keep my muscle?
1:50:01 Oh, that’s a great question.
1:50:09 Because my girlfriend’s to her credit when I did ketosis the first time, she was like, I’ve never ever seen you look like this when I took my top off.
1:50:14 But also it was quite clear that my muscles had got smaller.
1:50:16 I was a lean as fuck, but my muscles were smaller.
1:50:22 So with caution this time, I did ketosis again and I’ve been thinking, how the fuck do I keep my muscles?
1:50:30 Yeah, yeah. Okay. So first of all, let me just add a hearty amen. I’m an advocate of a ketogenic diet, although it can be applied differently across different people.
1:50:37 But I would say anyone would benefit from having some modest period of time of elevated ketones, at least in some portion of the day.
1:50:43 Now, how do you maintain muscle mass in the midst of such obvious weight loss?
1:50:45 I can only speculate.
1:50:55 Now, there are peer-reviewed studies that I can cite which do support the idea that a human can be on a ketogenic diet and have a total maintenance of muscle and strength.
1:51:01 That is published. So we know it’s possible, although that doesn’t seem to be what happened with you.
1:51:08 I would suspect that there were two things happening, possibly.
1:51:12 Now, I’m speculating here and I’m pretending to be your coach or your expert here.
1:51:20 One could have been that you had relatively lower energy during your workouts because of a slight degree of dehydration.
1:51:24 And then the other one would be calories, which I’ll come back to in a moment. I just wanted to put it out there.
1:51:35 So when insulin comes down, one of the many effects in the body is that another hormone comes down called aldosterone, which is one we’ve never invoked yet.
1:51:46 But low insulin leads to lower aldosterone. When aldosterone comes down, the kidneys begin to eliminate salt and water much more rapidly.
1:51:53 Now, that’s not problematic, but it does mean that a person does have to focus more on hydration and salts.
1:52:05 So if someone’s going on this strategy and they exercise fairly often, you need to be much more focused on your hydration, literally drinking more because you will be urinating more,
1:52:09 which is partly why people’s blood pressure gets so good so quickly.
1:52:17 And just to pause on that point, if someone is on one or two blood pressure medications and they adopt a ketogenic diet,
1:52:25 they usually have to stop their medications within two days because their blood pressure goes to normal so quickly that if they stay on the medication, they’re going too low.
1:52:31 So one could be that you were actually working out a little less intensely because of the dehydration.
1:52:39 But then two, it’s possible that you were eating too few calories to actually maintain muscle.
1:52:45 Muscle is a hungry organ. It is metabolically expensive for the body to keep that muscle on.
1:52:51 And as you start to get leaner and leaner, it gets harder and harder for the body to defend that muscle.
1:52:55 In fact, that’s the difference between fasting and starvation.
1:53:05 The longest known evidence of a fast was a man in the UK who fasted for 384 days, literally not eating or drinking a single calorie.
1:53:13 He was under medical supervision, getting vitamins and minerals and water, and he went on to live a perfectly healthy life.
1:53:19 But what was the difference? Why was that not starvation? Starvation is when you run out of fat.
1:53:27 So you might have gotten to the point of so lean that you didn’t have enough fat to burn to make enough ketones to fuel the brain.
1:53:31 If you don’t have enough fat to burn to make enough ketones, and the brain is saying,
1:53:37 “All right, well, I wanted to switch to ketones so that I could spare the glucose, but I can’t.
1:53:46 There’s not enough ketones here, so I have to rely 100% on glucose, but if you’re not eating glucose, now the body has to start stripping the protein from muscle.
1:53:53 And it sends those amino acids to the liver, then the liver is so capable, it will turn those amino acids into glucose.
1:53:54 So it turns my muscle.
1:53:56 Into glucose to feed the brain.
1:54:02 So my comment then, finally getting to my answer is, in your version of a ketogenic diet,
1:54:10 with your level of muscle mass and your inherent metabolic rate based on your body size and your activity, you probably ought to eat more fat.
1:54:13 I wasn’t actually doing the blood test at that point.
1:54:18 I’m doing it this time around, but I wasn’t doing the blood test, so I can actually see my keto levels.
1:54:20 So maybe I wasn’t even in ketosis because I wasn’t having enough fat.
1:54:24 Well, you might have been, but it could have been that you were simply not eating enough calories.
1:54:26 So this is an instance where…
1:54:28 That’s what I’m trying to do this time.
1:54:32 So eat more fat, like every time you’re making a steak, put butter on there.
1:54:36 And when you’re drinking a cup of coffee as crazy as it sounds, I drink yerba mate every morning.
1:54:45 I will put a big dab of butter, like a big dab of butter in my tea, and I’m sipping on it while the world’s still asleep and the kids haven’t woken up yet.
1:54:54 And so I know, because I want to keep my muscle as a guy who’s almost 50, I find that during my strict ketogenic phase,
1:54:58 and I’m currently in it as well, every January I go to kind of a carnivore diet.
1:55:03 And I mostly do it to lean down, but also to check any addictions and habits.
1:55:05 I don’t like feeling addicted to things.
1:55:11 And my wife will comment, and even as an almost 50-year-old, it’s fun to see my six-pack coming.
1:55:16 I don’t want to lose my mass, my muscle mass, because you have to work so hard to get it.
1:55:21 And what I find is if I increase my fat, I always get plenty of protein.
1:55:25 But if I increase my fat content, I have an easier time maintaining my bulk.
1:55:29 Are there any downsides of following a ketogenic diet that we need to be aware of?
1:55:37 The only downside I can articulate, so in fact, I didn’t even finish, because I distracted myself, mentioning some of the benefits of ketones.
1:55:45 But ketones are further anti-inflammatory, like they directly reduce inflammation in the body by inhibiting inflammatory processes.
1:55:50 And they also improve antioxidant defenses, so it helps reduce oxidative stress.
1:55:55 So ketones do have benefits that go beyond even what we’ve taken the time to articulate.
1:56:07 If there’s any negative to a ketogenic diet, it could be that you start, you acutely or you temporarily become less metabolically flexible.
1:56:10 Now, that’s me invoking a term we haven’t brought up yet.
1:56:18 But metabolic flexibility is a term to refer to the body’s ability to, when it eats glucose, to burn glucose.
1:56:21 When it’s not eating glucose, it burns fat.
1:56:25 So you’re shifting between the two metabolic fuels that we outlined earlier.
1:56:32 When someone has been adhering to a ketogenic diet for some time, it’s almost as if their body is stuck in fat burning mode.
1:56:41 And that if you and I, being in such adapted ketogenic state as we are, if we were to go to lunch and eat two bagels and a sugary drink,
1:56:48 it would take us a very long time to clear that glucose from our blood much longer than otherwise.
1:56:52 Like let’s say we go out with the production team, they’re eating a normal higher carb diet.
1:56:59 All things equal, same body size, same activity, their glucose levels would come up and down in 90 minutes, perhaps.
1:57:03 Yours in mind may take 180 minutes to come back down.
1:57:09 So the person may say, well, gosh, Steven and Ben are no longer burning glucose very well.
1:57:10 And that’s true.
1:57:18 In that one moment, our bodies had almost forgotten what it was like to burn a bunch of glucose because we had adapted to fat burning.
1:57:20 So what about the gut microbiome?
1:57:21 Oh, yeah.
1:57:28 Because I told someone who is a nutritionist that I was doing a keto diet at the moment and they said, oh, you’re poor gut.
1:57:29 Ah, yes.
1:57:35 Well, what a naive thing to say if I may gently reprimand your friend.
1:57:38 There’s no evidence to support that there’s any harmful change in the microbiome.
1:57:48 In fact, a paper was just published that looked at a man who went from a normal omnivorous human diet with abundant plant matter to a purely carnivorous diet,
1:57:54 literally zero carb, and they documented precisely no change in his microbiome.
1:57:55 None whatsoever.
1:57:57 But is he eating plums?
1:57:58 No.
1:57:59 Well, he had been eating plants.
1:58:12 So the case study was a person eating a normal diet of plants and meat, a normal omnivore diet, and then looked at the microbiome and then adapted to a purely carnivorous diet, purely meat.
1:58:14 And the microbiome didn’t change at all.
1:58:15 What’s the time period?
1:58:16 Months, I think.
1:58:25 The problem with the microbiome, the reason I don’t take microbiome research too seriously as a scientist is that it is a big black box.
1:58:31 You came from the UK to London, to LA, to California.
1:58:37 If we took a microbiome sample analysis of your time in the UK now, it would be different now.
1:58:42 Even though you’re eating the same, but you’re drinking different water, you’re breathing different air.
1:58:46 I was just on a plane from Utah to California.
1:58:50 Give me a day or so, I would have some sort of shift in my microbiome.
1:58:53 So the microbiome can change in response to all kinds of things.
1:59:00 The idea that you somehow have decimated your microbiome because you aren’t eating fiber is absolutely false.
1:59:02 That is completely false.
1:59:08 Now, there might be a change in some of the population of your microbiome, more of one, less of another.
1:59:11 But there’s no evidence to suggest that’s problematic.
1:59:13 Your microbiome is intact.
1:59:15 Those bacteria do not die.
1:59:17 They’re just simply metabolizing other things.
1:59:19 Maybe they’re relying more on short chain fatty acids.
1:59:21 Maybe they’re relying more on amino acids.
1:59:29 They’re not eating fiber, but there’s still stuff in the meat or the eggs that the microbiome will eat.
1:59:38 But if eating lots of plants does give me a more diverse gut microbiome, then if I stop eating plants, I’m going to have a less diverse gut microbiome.
1:59:46 Yeah, but even then, there’s a bit of an assumption built into the question because it’s, do we know that the microbiome will be less diverse?
1:59:52 The case study I just mentioned found that in this one single man, it didn’t change his microbiome at all.
1:59:56 It was the exact same populations in all the same proportions.
1:59:59 Because isn’t on the plants feeding the bacteria?
2:00:02 Yeah, so the fiber is.
2:00:08 So fiber will, but again, that’s not the only thing bacteria can eat.
2:00:10 Bacteria can eat fats.
2:00:12 Bacteria can eat amino acids.
2:00:14 They can eat glutamine, for example.
2:00:16 They can even meat.
2:00:21 We’ll have a little bit of glucose in it where the muscle has something called glycogen.
2:00:25 And so there’s trace amounts of glucose and even the meat that you’re eating.
2:00:35 So I do not look at the argument that you’re destroying your microbiome that has no scientific support.
2:00:39 You may be changing your microbiome, but who’s to say that’s a bad change?
2:00:40 Maybe it’s a better change.
2:00:42 You certainly are feeling better.
2:00:43 You’re thinking better.
2:00:44 You’re thinking leaner.
2:00:45 Your insulin sensitivity is improved.
2:00:46 Cognition is improved.
2:00:53 I would argue if there is a change in your microbiome, it’s probably one that’s for the best.
2:00:55 And no one can prove that wrong.
2:01:00 As much as I just stated that comment in a speculative fashion, it’s speculative because there’s no evidence.
2:01:07 This is why I look at the microbiome and just say, yeah, it appears to matter, but in ways that we don’t know.
2:01:22 But you agree with the argument that if I sat here now and I ate a wide range of plants for the next, let’s say, six months, when you analyzed my gut microbiome, it would be much more diverse.
2:01:23 I’m not agreeing to that.
2:01:24 Really?
2:01:26 I don’t know if that’s true.
2:01:37 And again, I would cite that one case report I just mentioned now, which is a man who did this, they reported that the microbiome was identical, that there was no significant change.
2:01:38 That’s just one man, though.
2:01:39 It was one man.
2:01:44 It was a case report, which is not a randomized clinical study.
2:01:58 But even still, with my speculation heavily handed here, I would say probably more plants would result in a more diverse microbiome.
2:02:04 But I would say, but then the next step is a harder one, which is, is that good or bad?
2:02:05 I don’t know.
2:02:13 Maybe all you’re doing is promoting the growth of bacteria that make more gas because they’re fermenting the fiber and you just have more flatulence as a result of it.
2:02:18 People, dietitians will say, well, a diverse microbiome is a good microbiome.
2:02:19 We’ll prove it.
2:02:21 How do we know that?
2:02:24 How can you prove that to me as a basic scientist?
2:02:42 I want to see the hard evidence because what I can prove is that we can take humans who are overweight and diabetic and hypertensive, eating a standard American or global diet, and put them under a ketogenic diet, which is going to be a much simpler diet, and yet every clinical marker gets better.
2:02:48 And so if someone were to say, yeah, but sure, you’ve reversed your diabetes and your hypertension, but your poor microbiome.
2:02:50 I would say, well, I don’t care about my microbiome.
2:02:51 I care about the human.
2:02:59 And so if there’s less diversity, but every single clinical marker has gotten better, perhaps more diversity is not what we want in our bacteria.
2:03:03 And I’m speculating, but so is the person who states that.
2:03:17 Yes, I’m not aware of research that links the two, but I could always have a look, but I was always under the assumption that a more diverse microbiome is a healthier person.
2:03:19 Yeah, and I don’t know.
2:03:23 But do you feel healthier now?
2:03:24 Feel healthier.
2:03:32 I certainly feel, and it’s only been a short amount of time, so I don’t know what my health might look like if I’d done this for like two years.
2:03:40 Right, because then there could be a really sort of deeper change to my health composition for more than two years, and they’re great.
2:03:44 Because some of the changes that occur in our health take time.
2:03:53 Now, you show this a lot in your work with insulin resistance, that if you’re insulin resistance for 10 years, your brain, I think I read in your work is like…
2:03:54 It ages.
2:03:56 It ages by an additional two years?
2:03:58 Yeah, yeah, it accelerates the aging.
2:04:00 And I wonder the same thing with like my gut microbiome.
2:04:16 If my gut microbiome is not diverse, so I have a very sort of narrow diet or, you know, I’m not eating my plants, could it take me a couple of years to really understand the net negative impact that has on my overall health?
2:04:18 It’s entirely possible.
2:04:19 Yeah, yeah.
2:04:30 I would just ask that we be careful with the assumptions that if there is an increase in diversity with more plant matter, that’s an if.
2:04:33 Is that change beneficial?
2:04:40 Are the bacteria that we’re now promoting the growth of, are they better for us, or are they just bacteria that exist in order to handle more fiber?
2:04:45 And again, the outcome being that it perhaps is just making more gas.
2:04:49 The more plants you eat, the more gas you have to produce by fermenting more fiber.
2:04:57 What if those bacteria are only existing to just eat the fiber and not actually improve the human host at all?
2:05:07 So ketosis, possible to live in is, I think one of the important points on ketosis is when I do my blood keto test, I fluctuate wildly.
2:05:10 After I’ve gone for a run, my ketone levels are super high.
2:05:15 Sometimes later at night, I’m just on the verge of ketosis sometimes.
2:05:21 And I think that’s interesting because we don’t have to live in this necessarily deep state of ketosis the whole time.
2:05:24 We can fluctuate a little bit.
2:05:32 My thought on it is that a person would benefit from some state of ketosis on a frequent basis.
2:05:38 If for no other reason than to really give the brain a heavy dose of just straight energy.
2:05:42 Not that everyone needs to be as strict as perhaps you and I are being at the moment.
2:05:49 But I would say the more a person has a disorder or a disease that benefits from ketosis, the more than they ought to focus on it.
2:05:57 Like if someone has type two diabetes, if they adopt a ketogenic diet, they will be off all of their diabetes medications in months, all of them.
2:06:07 If someone has epilepsy or migraine headaches from 1913, I think was the first published report on this.
2:06:13 If there’s someone who suffers from migraines, as long as they’re in ketosis, they may never have another migraine again.
2:06:20 It is completely curative or preventative for the disorder, same with epilepsy, that many forms of epilepsy.
2:06:24 So depending on the person, they would benefit from being in ketosis forever.
2:06:31 For everyone else who’s just sort of a normal individual who wants to be lean and keep their brain healthy and happy, etc.
2:06:37 I would say it’s generally prudent to just control your carbs, be mindful of the type of carbohydrate you’re eating.
2:06:43 And as I said earlier, just try to focus on the carbs that don’t come from bags and boxes with barcodes.
2:06:48 I’m actually quite liberal in my view when it comes to whole fruits and vegetables.
2:06:54 I’d say eat them, enjoy them liberally, but then also make sure you’re getting some good protein and fat.
2:07:00 Because there’s no such thing as an essential carbohydrate that sounds controversial, but humans do not need.
2:07:05 We have no requirement for carbohydrate. We do have requirement for fat and protein.
2:07:18 What about artificial sweeteners? One of the things that I am tempted by when a monoketosis diet is like the soda zeroes of the world or the diet sodas of the world.
2:07:20 What impact does that have on my insulin levels, etc.?
2:07:31 Yeah, great question. There is such a breadth of diversity when it comes to sweeteners, from artificial to natural to another rare sugar more and more.
2:07:42 There’s all these random, I’m not random, but a very broad spectrum of molecules that we have developed or found that taste like sugar, but don’t have the effect of sugar.
2:07:48 So on the good end are things like that have been shown to have no insulin effect.
2:07:53 And so I appreciate everyone listening, letting me kind of stay with that as my framework.
2:07:59 Because people are going to go on and criticize all kinds of other things about other sweeteners, and that’s just too broad.
2:08:01 That’s a topic for a whole book.
2:08:07 With regards to just insulin, on the good end where they have no effect, it would be one as common as aspartame.
2:08:14 So like diet drinks, not the zero drinks, but the diet drinks will have aspartame as the sweetener.
2:08:15 Is there a difference?
2:08:18 There is a difference. And I’ll get to that other one in a moment.
2:08:20 So I should be having diet instead of zero.
2:08:31 Well, I personally go to diet rather than zero. But that’s because aspartame is the soul sweetener in the zero, in the diet, rather, and it has no effect on insulin.
2:08:37 So to erythritol, sorry, erythritol is a little right around aspartame is generally a good one.
2:08:44 But monk fruit extract, stevia, and especially allulose, those are inert when it comes to insulin.
2:08:51 You know, allulose, stevia, monk fruit extract, aspartame, no effect, erythritol, no effect.
2:08:58 But erythritol, that ending O-L is reflective of a class of sweetener called the sugar alcohol.
2:09:04 And that does not mean it’s alcoholic. That just refers to the actual chemical structure that puts it in the alcohol family.
2:09:11 Once you get into the sugar alcohols, you start to get a little problematic where erythritol is a good one.
2:09:18 And xylitol is generally a good one. But then you get to things like maltitol and mannitol, and they do have an insulin effect.
2:09:20 And what was, what kind of foods have these?
2:09:26 Yeah, so often, like, you can get mannitol in, like, artificially sweetened chocolate sometimes.
2:09:31 For reasons that I don’t know, I don’t know why the food formulator puts them in some things and not other things.
2:09:39 The problem I chuckle because it becomes so apparent with some of those artificial sweeteners, like the sugar alcohols,
2:09:43 is that as you eat them, you taste it sweet in your mouth.
2:09:48 And it doesn’t have any caloric value in the body because it stays in the intestines.
2:09:53 And this is something that is largely unique to the sugar alcohols.
2:09:58 Whereas it stays in the intestines, it starts pulling in water from the body,
2:10:03 which starts to create a fairly inconvenient degree of flatulence and diarrhea.
2:10:10 And so a person will know if they’ve eaten too many of those types of sweeteners because their intestines will tell them so.
2:10:18 So, but also on that spectrum, kind of in the middle, is the one that’s in the zero drinks, which is one called sucralose.
2:10:27 And while sucralose is generally not a problem with insulin, it is a sweetener that has been shown to cross the blood-brain barrier.
2:10:35 And so the reason I avoid the zero drinks and refer or go to the diet drinks is that aspartame does no such thing.
2:10:40 Aspartame just gets divided into amino acids. We just digest it and absorb amino acids.
2:10:47 Sucralose will go, can cross the blood-brain barrier, and I don’t know what it’s doing there, but I don’t want it there.
2:10:52 And so I avoid the zero drinks because I don’t want that sweetener.
2:11:03 But personally, when I’m adhering to this diet, diet soda is my actual indulgence, where I want something sweet and yet I don’t want the metabolic effect of it.
2:11:07 One thing you mentioned earlier, which I’ve been thinking a lot about is salt.
2:11:13 And I think a lot about salt because I went to the doctor many years ago and I think I was using this like Maggie seasoning that I put on my food.
2:11:17 And the doctor said to me that my salt levels were too high.
2:11:23 And then I’ve heard since then from other people that we’re actually probably not getting enough salt in our diet.
2:11:27 Yeah. So I’m interested to hear that your physician would have said your salt is too high.
2:11:30 That is very rare that that gets measured.
2:11:31 It’s sodium, I think.
2:11:35 Yeah, they could have measured sodium and that could have been higher. They absolutely could have. It’s just not common.
2:11:45 So salt has earned a terrible reputation because of a series of studies that implicated salt consumption as a cause of high blood pressure.
2:11:52 And really briefly, as a momentary physiology professor, that is a real effect.
2:12:03 If you and I were to go eat salt, our body for the next several hours afterwards would retain its water in order to balance out the salt so that we didn’t get too salty.
2:12:07 So we would retain water in order to keep our salt at a normal level.
2:12:12 And so that could be reflected by an elevated blood pressure.
2:12:25 However, multiple huge studies have found that if you go to a population of humans that have high blood pressure and you tell them you need to cut your salt in order to correct your blood pressure,
2:12:29 they may at most move their blood pressure by one or two points.
2:12:33 It has an absolutely negligible, irrelevant effect.
2:12:37 It’s because salt is not a key contributor to blood pressure.
2:12:42 It’s actually insulin resistance. Insulin resistance will force the body to hold on to salt.
2:12:48 Insulin resistance will force the blood vessels to be very constricted, all of which play together to make for a very high blood pressure.
2:12:57 So as much as we have been telling the world that we should be cutting back salt, no, we should have been telling them to cut back on what spikes your insulin refined starches and sugars.
2:13:03 But with regards to salt, it’s interesting for me to note where did that whole view come from?
2:13:11 Within the United States decades ago, there was a study that was published and they called it the dash diet.
2:13:16 Dietary approaches to stop hypertension, D-A-S-H, the dash diet.
2:13:23 And in the dash diet, one of the critical changes was to tell people to eat less salt.
2:13:29 And when they found that when people adopt a dash diet, it’s amazing their blood pressure goes down.
2:13:35 However, unfortunately, they also tell people to do lots of other things with the dash diet.
2:13:42 Like when they tell someone to go on the dash diet, they also tell them to eat less sugar and less refined starches and sugars.
2:13:51 Well, it’s possible, indeed I would say it’s absolutely the case, that what’s actually lowering their blood pressure isn’t that they cut their salt back.
2:13:56 It’s that they were cutting their refined starches and sugars back and it’s that that had the main effect.
2:14:00 And the cutting the salt was just some innocent bystander.
2:14:10 But to put a fine point on it, in human studies, if you have humans cut back their salt considerably, they become insulin resistant.
2:14:15 So take a healthy group of humans, say you need to eat less salt and they do so.
2:14:24 If you measure them a week later while they’re adhering to this, they will be significantly more insulin resistant than before they ever cut back their salt.
2:14:32 It’s one of the ironies of the whole scenario where a physician may be telling a patient with high blood pressure, you need to cut back your salt.
2:14:38 And they end up eating less salt and yet their blood pressure gets worse.
2:14:42 It’s because the main contributor to high blood pressure is insulin resistance.
2:14:46 And by telling them to cut back on their salt, you made them more insulin resistant.
2:14:53 And that whole mechanism is because one of insulin’s many, many effects is to want the body to hold on to salt and water.
2:14:59 And so if you start cutting your salt, all of a sudden insulin says, well, there’s little salt coming in.
2:15:02 I need to do what I can to retain whatever salt we do have.
2:15:09 And so it starts retaining salt and water more in order to try to offset the lack of salt coming in.
2:15:14 And while insulin’s going higher and higher, the body’s becoming more and more insulin resistant.
2:15:19 So salt restriction can cause insulin resistance in humans.
2:15:25 You talk about four pillars to eating in your book, Why We Get Sick.
2:15:32 You outlined these four essential pillars to develop a strategy for maintaining low insulin levels and combating insulin resistance.
2:15:34 What are the four pillars?
2:15:39 Yes, so when it comes to controlling insulin resistance, the key is to manage macronutrients.
2:15:44 And the best way to manage macronutrients is going to be a strategy that helps lower insulin.
2:15:49 Lowering insulin is the key to both slow insulin resistance and fast insulin resistance.
2:15:53 So the more the strategy lowers insulin, the more effective it’s going to be.
2:15:56 And there are four pillars.
2:15:58 So the first one, control carbohydrates.
2:16:01 Second, prioritize protein.
2:16:04 Third, don’t fear fat.
2:16:10 And then fourth, after the first three have been taken care of, four frequently fast.
2:16:18 So with the first one, very briefly, by controlled carbohydrates, I mean that it is time to focus more on whole fruits and vegetables.
2:16:20 Eat them, don’t drink them.
2:16:24 And then don’t get your carbohydrates from bags and boxes with barcodes.
2:16:29 The more you’re opening up a package and getting your chips or your crackers or your cereal or your bread,
2:16:32 the more you’re going to be spiking your glucose and your insulin.
2:16:35 Keep that on the shelves at the grocery store.
2:16:37 Focus on whole fruits and vegetables.
2:16:40 That’s going to be the key for number one, control carbs.
2:16:45 Now, while you’re eating fewer carbohydrates, you need to eat something.
2:16:47 And so prioritize protein.
2:16:54 I would say particularly animal source protein, which is the best source of all of the amino acids that humans need.
2:16:57 And then with those proteins will come fat.
2:16:59 Don’t fear that fat.
2:17:00 That’s number three.
2:17:03 Fat is very satiating when combined with protein.
2:17:07 When fat and protein come together, we digest it better.
2:17:13 Sometimes people will find that if they just have a scoop of whey protein, it can be very upsetting on their stomach.
2:17:15 It’s because we’re not supposed to eat protein alone.
2:17:17 In nature, that never happens.
2:17:20 In nature, protein always comes with fat.
2:17:21 That’s how we should eat it.
2:17:22 We digest it better.
2:17:30 And human studies have shown that when a human eats pure protein, there’s some degree of muscle growth, albeit microscopic, miniscule.
2:17:37 But when we eat protein with fat, we have significantly greater muscle growth than we do with the protein alone.
2:17:43 So that is the three pillars that encompass the macronutrients or the big parts of our diet.
2:17:52 But once a person has done that, then they are well positioned to adopt a strategy, a structured strategy of fasting.
2:17:56 And that can be, there are as many ways to fast as there are people who want to do it.
2:17:58 There’s no right way or wrong way.
2:18:03 My goal by invoking that fourth principle, and I do think it should come last.
2:18:09 Once you’ve learned how to eat better food, your body has adapted to burning its own fat for fuel.
2:18:16 But it can take intermittent fasting where it’s one meal of the day you’re fasting through.
2:18:19 It can do where people do alternate day fasting.
2:18:21 There are countless different ways to do it.
2:18:22 Even if I’m in ketosis.
2:18:25 Then you don’t need to do it as much because you’re already lowering your insulin.
2:18:36 So if a person’s already in ketosis, in fact, if a person were in ketosis and frequently fasting, depending on how lean they are, it’s going to become extremely difficult to retain muscle.
2:18:38 So those are the four pillars.
2:18:42 It will be an extraordinarily effective way to address insulin resistance.
2:18:51 But the problem, as I started, that I mentioned, is that while these concepts are simple, that does not mean they’re easy.
2:19:00 Because humans show addictive tendencies to only one macronutrient, not fats, not proteins.
2:19:05 All of the evidence of the neurobiology of addiction in humans points to carbohydrates.
2:19:09 And so as much as I lay out this simple plan, it can be difficult.
2:19:22 And this is why this self-discipline required is difficult enough that it’s why people find that they have to result in relying on drugs for these kinds of things.
2:19:24 Physical activity.
2:19:25 Exercise.
2:19:29 Useful for keeping my insulin levels in check.
2:19:30 Yeah.
2:19:32 I’m really glad you brought up exercise.
2:19:35 I’m an enormous advocate of exercise.
2:19:39 The best exercise to improve insulin sensitivity is the one you’ll do.
2:19:48 And so if someone listening to this is an 80-year-old grandma, if her form of exercise is walking around the street, around the block with her girlfriends,
2:19:53 but then if someone else has the ability to go cross-country skiing or CrossFit, do it.
2:19:55 So the best exercise is the one you’ll do.
2:20:01 Now, having said that, the better exercise is the one that you’ll do that keeps muscle.
2:20:10 Muscle building work is going to be minute-for-minute a more effective way of improving insulin sensitivity than any kind of aerobic activity.
2:20:14 And that’s because muscle is the great consumer of glucose.
2:20:23 In fact, not only does muscle eat the most glucose from the blood, but it’s also how it eats the glucose when it’s exercising.
2:20:32 So earlier, we talked about how insulin kind of comes and knocks on the door of the muscle cell, and then the muscle cell will open the door and allow the glucose to come in,
2:20:36 thereby lowering blood glucose, unless the muscle is exercising.
2:20:49 When a muscle is exercising, and I’m kind of mimicking the contraction and relaxation of a muscle, when the muscle is exercising, it has its own way of opening those doors.
2:21:00 So there’s an insulin-independent method where the muscle cell essentially tells insulin, “Insulin, I know normally I have to wait for you to come and open these doors,
2:21:04 but I’m so hungry during this exercise that I’m not going to wait.”
2:21:05 And so the doors just open.
2:21:16 So the contracting muscle has its own way to rush to pull the glucose in, which means, of course, that a person is going to have an easier time controlling their blood glucose,
2:21:24 which in turn would mean a better time controlling insulin, but the more muscle a person has, the easier it is.
2:21:35 And this could be one of the reasons why if you look at longevity and look at the markers of muscle strength versus the markers of cardiovascular aerobic fitness,
2:21:39 the aerobic fitness markers are terrible predictors of longevity.
2:21:46 It’s muscle and strength that predicts longevity for multiple reasons, including just a very active living and moving.
2:21:53 But also because if you have more muscle, you’re going to control your glucose better, which means you’re going to control your insulin better.
2:21:59 Then you’re back to these variables that people use to predict or what are the most accurate indicators of longevity.
2:22:01 It’s who has the best glucose control.
2:22:04 More muscle helps that happen.
2:22:16 There’s a big debate around whether we should be calorie restricting and low fat diet, whether we should be calorie restricting in a moderate fat diet or calorie restricting and a low carb diet.
2:22:18 What’s your take on that?
2:22:22 Yeah, I am unabashedly in favor of carbohydrate restriction.
2:22:31 I would say for two reasons that one reason I think that carbohydrates should be the macronutrient that is most scrutinized is because it’s the one we eat the most of.
2:22:35 70% of all calories consumed globally come from carbohydrates.
2:22:41 That is the one that has the biggest insulin effect, and that’s a problem for all the reasons we’ve discussed.
2:22:45 But two, carbohydrates are not essential.
2:22:53 This is controversial. People don’t like to acknowledge it, but there is literally no biological need that humans have for carbohydrate.
2:23:07 In the United States, a report decades ago from the Department of Agriculture looking at the needs of human nutrition, there’s a quote there, and I’m not going to get it exactly right, but I’ll get it pretty close.
2:23:13 It’s stated in this document that the lower limit of carbohydrate consumption in humans is zero.
2:23:17 In other words, there is no such thing as an essential carbohydrate.
2:23:29 Now, I’m not saying, well, let’s not eat any of them. No. But I am saying, why is that the one we focus the most on as 70% of all calories globally are coming from that one?
2:23:35 You’re telling me that most of what we eat comes from what we don’t need. Why not put the focus on the things we do need?
2:23:42 There are such things as essential fatty acids. Let’s eat fat. There are such things as essential amino acids.
2:23:51 So let’s eat protein and make sure we get what we need. And then on any remainder of the plate, we can get some other things that we want to nibble on like plants.
2:23:54 Why don’t we just sack all this off and just take his MPEC then?
2:24:06 Ah, yeah. Great question. So I have kept my finger on the pulse of the whole field of gut-derived hormones, which is what we talk about with these weight loss drugs, almost since their beginning.
2:24:13 My dissertation work was in a lab, one of the first funded labs to look at these drugs, although in the context of diabetes.
2:24:21 And then it’s blossomed into the context in the use of obesity. This is the class of drug, GLP1 receptor agonist.
2:24:30 First of all, what is GLP1? GLP1 is a hormone that we all make from our guts. Our small intestine will make GLP1.
2:24:38 We’re making it all the time to varying degrees. Some things we eat will result in a higher GLP1. Sometimes it’ll be a lower GLP1.
2:24:54 Like, for example, a paper just published a few months ago found that if you have people eat the exact same meal of calories, but lower carb or higher carb, the lower carb version of the meal will increase GLP1 three times higher in the blood than the high carb version of the meal.
2:24:56 Which means that they’ll feel.
2:25:03 Yeah, so then what’s the point? Who cares about GLP1? One of GLP1’s main effects is to tell the brain that we’re full.
2:25:05 Okay, so more GLP1 less hunger.
2:25:15 More satiety. Yeah, more GLP1 less hunger, which is very impactful. In fact, I would be remiss if I didn’t mention a study that was published in humans a while ago.
2:25:24 They took obese humans and lean humans and had them eat fat and found that, like, pure fat, and they found that the GLP1 response was the same.
2:25:38 Whether you were lean or obese, you had the same amount of GLP1. That would suggest that whether you’re lean or obese, both of your brains and both of these populations will have the fat and have the same sense of “I’m full.”
2:25:49 Because it was matched with GLP1. However, when they had these same groups eat pure carbohydrate, the lean group had a robust GLP1 response, big GLP1.
2:26:02 In other words, they would eat the carbohydrate and say, “I’m full,” because GLP1 would tell them so. However, in the obese group, they ate that exact same amount of carbohydrate and they had an almost negligible GLP1 effect.
2:26:03 They were still hungry.
2:26:10 In other words, they would eat the same amount of carbohydrate as their lean counterpart and then just say, “Okay, what’s next? I’m still hungry.”
2:26:19 And so it is prudent to focus on GLP1. GLP1 is a powerful hormone that does have an effect on human health.
2:26:28 What I feel inclined to comment on is the negative side effects, because the only thing we hear about is social media influencers extolling the benefits.
2:26:42 And hey, I’m on this weight loss drug and I’ve lost 50 pounds. Someone has to be the voice that says, “Yeah, but what about this?” And there are some significant “but what abouts” when it comes to these weight loss drugs.
2:26:54 One of them is the loss of muscle mass or lean mass. You’ve mentioned a couple of papers from the New England Journal of Medicine, a paper a couple years ago from what was called the step five trials looking at these drugs.
2:27:04 They found that for every six pounds of fat a person was losing on these drugs, they were losing four pounds of fat-free mass or lean mass.
2:27:13 So 40% of the weight they were losing on these drugs is coming from lean mass, like including muscle and bone.
2:27:25 So there are now case reports of young healthy women who were overweight who go on the drug for some period of time and after they get diagnosed with osteoporosis where they have eroded their bone health.
2:27:29 They’re losing lean mass. So again, they’ve eroded their bone health.
2:27:39 Yeah, so 40% of the weight that people are losing on these drugs appears at these high doses is coming from lean mass, so fat-free mass including muscle and bone.
2:27:51 The reason I find that so troubling is that in the UK at two years on the drug, 69% of people get off the drug. They don’t want to be on it anymore.
2:27:57 And now imagine this individual, imagine if you will a 60-year-old woman who’s been on the drug.
2:28:04 I take that age and that sex on purpose because it’s so hard for her to grow new muscle and bone.
2:28:09 Let’s say she’s been on this drug for a year and she’s lost 20 kilos.
2:28:16 Well, 40% of that will have come from her lean mass, and 60% of it came from her fat.
2:28:23 Then when she gets off the drug, now all of a sudden her lean mass, her muscle and bone, that’s never coming back.
2:28:32 The muscle and bone that she has lost is gone forever probably at that age because after the age of 60, good luck developing new muscle and bone.
2:28:36 But what can come back rapidly is the fat mass.
2:28:42 And so at two years, she decides to get off the drug, which again about 70% of people do.
2:28:47 They’re going to gain that fat back, but they’re not going to gain their muscle and bone back.
2:28:53 That is a significant loss that may be, depending on their age, gone forever.
2:29:02 I was scrolling on Twitter the other day and I saw a video going viral, which is now being reported in a bunch of news publications.
2:29:07 It was yesterday that I saw this video going viral and I’m going to play this video to you.
2:29:13 It’s from a singer called Avery and she talks about her experience with a Zempec.
2:29:23 I just left the doctor’s office. I went to get a checkup because I’ve been off of Ozempec for two months now and I just wanted to see if my body was in better condition.
2:29:30 If there were any permanent damages, kind of in shock right now because I wasn’t expecting this.
2:29:42 But I guess Ozempec can cause bone density loss and I didn’t think that that would happen to me because I was only on it for a year.
2:29:52 But I have significant bone loss. I have osteoporosis and osteopenias, so there’s like several of them that I have.
2:30:03 I wasn’t expecting that, but that’s what happens if you use Ozempec for weight loss and you lose too much weight.
2:30:20 Yeah, I wonder, she’s so lean. I wouldn’t be surprised if she had it even worse than normal because we see it has become, I don’t mean to suggest this is the case for her, but you do see people using these weight loss drugs who are already very lean.
2:30:24 I mean, I’ve got a picture of her here and she does look incredibly lean already.
2:30:31 But see, this is what people are doing. They’re basically using it to facilitate a needing disorder in the people who are lean.
2:30:40 This has become so common that there are complaints saying that lean healthy people are getting the prescription and people who are obese and diabetic aren’t because of shortages.
2:30:50 I’ve seen this. I know someone personally who is already a perfectly lean healthy woman and then she now looks sickly.
2:31:08 And what caused it? Well, she wasn’t lean enough. And when you take enough of that drug that you just have no more hunger because of how it’s acting at your brain, you do just stop eating and the malnutrition at least in part is going to cause a loss of lean mass.
2:31:24 But that also, it is even further exacerbated by the mental health problems where there was a paper recently published with the use of these drugs finding that people, when they begin the drug, their risk of suicidal thoughts doubles.
2:31:43 It goes up by over 100% and their risk of major depression triples. And this, so as much as we talk about these drugs and we say the drug helps you control your cravings, what it’s doing is perhaps reducing your craving for everything.
2:31:53 That while you’re eating less food, which is resulting in the weight loss, you also are not interested as much in exercise as you used to be, which is going to make it even easier for you to lose your muscle and bone.
2:32:10 You’re also less interested in hobbies like going to play pickleball with your friends or going out and drinking with the boys. So there is this kind of, what’s reflected across all of their interests is that their cravings for everything starts to decline.
2:32:26 On the case of the girl mentioned that Avery, I’ve just seen, she’s uploaded a post that says, “Thanks, my record label told me I was fat. They dropped me. I got addicted to a zempec and now as a result, I have osteoporosis and my bones are as fragile as wafer cookies.”
2:32:29 Yeah, it’s heartbreaking. So now that.
2:32:36 Obviously, you know, these are claims that she’s alleging. Now we don’t have a full picture of her health and there might be something more.
2:32:49 Yeah, but we do know based on one report that 40% of weight loss is coming from fat-free mass. And so it is in people’s best interest to be mindful of that tendency and that if they’re going to explore the use of the drug to do so responsibly.
2:33:02 And I want to mention that kind of caveat or angle to everything because I don’t want someone listening to me thinking, “All right, Ben says I should never touch this and it is uniformly evil and bad.” I’m not saying that.
2:33:11 I find that I have to speak a little more boldly about the negative consequences because nobody talks about them. What would she have done if she knew about them, for example?
2:33:23 No one knows about these kinds of negatives because people want to sweep them under the rug. Now, I believe there is a use case for these drugs, although different from how it’s being used currently.
2:33:39 In my mind, the best use of these drugs is to help someone learn how to control their carbohydrate addiction because it will help you control your addiction. Sweet cravings goes down significantly within six months of the person taking the drug.
2:33:50 So I think in addition to getting proper education, and if I may be so bold, I would say it’s those pillars I mentioned earlier, control carbohydrates, prioritize protein, and don’t fear fat.
2:33:55 All the more reason prioritize protein and fat to help preserve your muscle and bone.
2:34:01 Muscle and bone are not made of carbohydrate. They’re made of protein and fat. Eat protein and fat.
2:34:13 Lift weights to keep any of that lean mass you can, keep the integrity of your bones intact, but take advantage of the drug helping reduce your cravings for sweet things especially.
2:34:25 I would say find the lowest effective dose you can where you are able with a little bit of self-discipline, where you’re not assigning all of the self-discipline to the syringe that you’re going to inject into your tummy.
2:34:32 There is value in learning to deny yourself something you know you shouldn’t be doing. There’s life lessons to learn there.
2:34:43 So enough of the drug that makes it a little easier for you to overcome your carbohydrate addiction. At the same time, you’re learning how to eat well.
2:34:56 You’re learning how to eat properly by managing your macronutrients and lifting weights, and then over time, ideally, I would say, you find that you are able to reduce the dose of the drug and then eventually get off of it entirely.
2:35:05 It’s worth saying that I did also search to see if there was a link between a Zempec and bone density, and there was no clear link in the studies that have been done.
2:35:15 I don’t know whether there’s been a lot of studies done, but it says in the studies and reviews, some of the glutides generally shows no harmful effect on bone mineral density, although rapid weight loss itself can sometimes affect bone health.
2:35:24 Yeah, so I actually think it’s an artifact. That’s a term that we would use as a scientist to say that it’s an effect that’s happening without being a main effect.
2:35:32 So I don’t believe the GLP-1 drug is attacking the bone. I think it’s because the person has just stopped eating and stopped moving.
2:35:40 Remember what I said earlier, people find that they’re just less interested in doing stuff like going to the gym, for example.
2:35:50 And so that is probably combining where a little bit of malnutrition combined with a little less physical activity means you’re accelerating some lean mass loss.
2:35:59 One of the things that this podcast has taught me is that liposuction is dangerous. Do you agree with that statement?
2:36:10 I do, from a metabolic perspective. I absolutely do. Liposuction is not dangerous to fit into the clothes you want to wear, but it’s deeply problematic for metabolic health.
2:36:18 And that’s because, as a reminder, it’s not the mass of fat we have that matters most when it comes to metabolic health. It’s the size of our fat cells.
2:36:24 So let’s imagine an individual who has more fat than they want in some particular part of the body.
2:36:34 The best way to help reduce that fat is to shrink your fat cells. So that’s very important for people to realize when you lose weight, you’re not killing fat cells.
2:36:42 You’re not getting rid of them. You’re shrinking them. And small fat cells are very healthy fat cells. They are literally anti-inflammatory.
2:36:51 They’re releasing hormones that fight inflammation in the body, and they’re very insulin sensitive, which helps the body by extension be very insulin sensitive.
2:37:01 So very healthy. Small fat cells are healthy fat cells. The problem with liposuction is that you are going in and rather than shrinking the fat cells, you are sucking them out.
2:37:15 Now, let’s say like a study that was done in the U.S. in women, they found that when women had liposuction from their buttocks and hips area, which is where most women gain their weight, which is because of sex hormones,
2:37:23 telling her body to store that weight there, they may look at that fat on their buttocks and hips and say, “There’s more than I want. I’m going to suck it out.”
2:37:37 So they do, but they don’t change their habits. So they’re still eating the same way they were before. Essentially, now they have fewer fat cells, but the body wants to store that same amount of fat based on how they’re eating.
2:37:45 In other words, there’s enough insulin telling the body to store a certain amount of fat, and there’s enough calories to fuel that fat storage.
2:37:53 But the fat would be saying, “Hey, we don’t have all these fat cells in the buttocks and hips like we used to. Let’s go somewhere else.”
2:38:04 And so it’s no surprise that over the ensuing years after she’s had liposuction, not only does she not experience any improvement in any health marker, nothing gets better with regards to her health.
2:38:14 And that is, again, reflective of the fact that it’s the size of the fat cell that matters. Maybe she has lost 10 kilos of fat. That might be a little much for liposuction, 6 kilos.
2:38:21 And you would say, “Well, you have 6 kilos of less fat, clearly you’re healthier, and yet they’re not at all. Nothing has gotten better.”
2:38:32 And then if you follow them over the years, they cannot gain that fat back on their buttocks and hips because it was literally sucked out, and adults have a hard time making new fat cells.
2:38:39 So it’s no surprise that they start storing more fat in an area that wasn’t sucked out, namely their belly.
2:38:46 And so a woman who’s gone through liposuction, yes, she will have lost fat by liposuction at her buttocks and hips.
2:38:56 But if she doesn’t change her lifestyle habits, the body will take those 6 kilos and say, “Well, I need to store those now somewhere else because you’re eating in a way that makes me want to store that much fat.”
2:39:02 And so her remaining fat cells that are intact get bigger and store a bigger burden.
2:39:13 And so over time, it’s no surprise that health outcomes can start to get worse. By having fewer fat cells, she’s increasing the burden that the remaining fat cells have to carry.
2:39:25 Not only does that result in a change in where she’s storing fat, namely storing more on her abdomen, but all the fat cells will get bigger and thus metabolic health can get worse.
2:39:32 We have a closing tradition on this podcast where the last guest leaves the last question for the next guest, not knowing who they’re leaving it for.
2:39:40 And the question that’s been left for you, Ben, is who in your life gave you a chance or believed in you when no one else did?
2:39:45 What a fun question. Thank you.
2:39:56 Probably my wife, frankly, I just adore her. I think about, so when we were newlyweds, we got married quite young, if you’ll allow me to be a little personal for a moment.
2:40:09 We both really wanted a family. We knew that we wanted to be mom and dad, and she really wanted to be an at-home mom, just a full-time mom, which I loved.
2:40:18 I benefited. My mother, who died when I was quite young, she was a full-time mom, and most of my memories come from her being home.
2:40:30 When I would come home from lunch, or I had a tummy ache, and she would come pick me up, and I think God for my mother, of course, but also for the time I had with her because I had so little.
2:40:46 And we both really wanted Cheryl to be able to be full-time mom. Mom is just that special. That meant, as a young, newly married husband, I was anticipating a future where I would be the sole provider for the family.
2:41:05 And it was very daunting, very scary for me as a 23-year-old. That’s how old I was when we got married. And I worried how am I going to provide for my family, and I would look at the trust that my beautiful wife had in me, and I felt inadequate.
2:41:24 And I have moments where I remember young Ben in his early 20s as a newlywed and how scared I was and how my wife’s ongoing devotion put us in a position where I both make a wonderful amount of money to provide for the family and help secure our future.
2:41:38 And then at the same time, still have a schedule that lets me be really home to go home early and help one of our daughters with her homeschooling, which I do, to always not go into work until I’ve made breakfast for the kids, and we’ve had some family time.
2:41:54 So much of all of it is just the support of my wife, because at any moment, if she would have said, “No, I’m done. You’ve got to go get a job right now,” I would have. I love her and respect her enough and even rely on her insight that I would have done it.
2:42:10 But she just really believed that, “Okay, Ben, you’re not dumb. I didn’t marry you for your looks. I think you’ve got something. I’m going to trust you.” And that trust was, it was both humbling and scary, but also very empowering, and it’s given us a beautiful life.
2:42:27 Ben, thank you. That’s been truly our opening, and you’ve answered so many of the questions that I’ve had for so, so long, especially as it relates to ketosis and the broader link between insulin, infertility, pregnancy, PCOS, all of these kinds of things, which are topics of conversation amongst my friends and people that I love.
2:42:28 Ben, thank you.
2:42:29 My pleasure. Thank you.
2:42:53 Isn’t this cool? Every single conversation I have here on The Diary of a CEO, at the very end of it, you’ll know, I asked the guest to leave a question in The Diary of a CEO, and what we’ve done is we’ve turned every single question written in The Diary of a CEO into these conversation cards that you can play at home.
2:43:04 So you’ve got every guest we’ve ever had, their question, and on the back of it, if you scan that QR code, you get to watch the person who answered that question.
2:43:10 We’re finally revealing all of the questions and the people that answered the question.
2:43:26 The brand new version 2 updated conversation cards are out right now at theconversationcards.com. They’ve sold out twice instantaneously, so if you are interested in getting hold of some limited edition conversation cards, I really, really recommend acting quickly.
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