The Insulin & Glucose Doctor: This Will Strip Your Fat Faster Than Anything!

Summary

Highlights

• Vaping may be more harmful than smoking due to its effects on insulin resistance. 😲
• Insulin affects every cell in the body and plays a central role in storing energy from carbs. 🍞
• Erectile dysfunction and PCOS are linked to insulin resistance. 🍆
• Environmental factors like pollution may contribute to insulin resistance and fat gain. 🚗
• The ketogenic diet helps improve cognitive function in Alzheimer's patients by providing the brain with ketones as an energy source. 🧠
• Different racial groups have varied thresholds for fat storage and susceptibility to diabetes. 🌎
• Four dietary pillars to combat insulin resistance: control carbs, prioritize protein, don't fear fat, and practice intermittent fasting. 📉

Key Takeaways

• Insulin resistance is a major driver of chronic diseases, including Alzheimer's and type 2 diabetes. 🧠
• There are two main pathways to insulin resistance: the "fast lane" involving stress and high levels of insulin, and the "slow lane" related to fat cell size. 🛣️
• The ketogenic diet can enhance brain function and facilitate rapid fat loss by promoting fat-burning over glucose-burning. 🥩
• Artificial sweeteners vary in their effect on insulin; some like aspartame do not spike insulin levels, making them preferable in certain diets. 💧
• Exercise, especially strength training, significantly boosts insulin sensitivity and overall metabolic health. 💪
• Dr. Bikman advises controlling carbs, prioritizing protein, and not fearing fat to manage insulin levels effectively. 📊
• While new weight-loss drugs can aid in initial craving control, they can lead to significant muscle and bone mass loss if not carefully managed. 💊

Overview

Chapters

• 00:00 - 15:00: Introduction to Insulin Resistance The chapter 'Introduction to Insulin Resistance' discusses the negative impacts of vaping compared to smoking, specifically highlighting the increased damage vaping can cause to airways and its contribution to insulin resistance. The text emphasizes that insulin resistance is central to many chronic diseases, which pose significant health threats. The chapter references Dr. Benjamin Bman, a leading metabolic scientist, who stresses the severe consequences of insulin resistance. He advocates for managing insulin levels as a means to regain control over one's health.
• 15:00 - 30:00: Understanding Insulin and Its Function Insulin is a critical hormone affecting every cell in the body, and insulin resistance is linked to various diseases, including Alzheimer's disease, infertility, erectile dysfunction, and PCOS. A staggering 88% of US adults suffer from some degree of insulin resistance. While America is notably affected, it's not the worst globally due to differences in fat storage among ethnicities. Insulin resistance can develop through two main pathways.
• 30:00 - 45:00: Causes of Insulin Resistance The chapter titled 'Causes of Insulin Resistance' discusses how insulin resistance can be induced quickly, within 6 hours, by certain common factors. However, eliminating these factors can also reverse the resistance just as rapidly. The chapter further differentiates between the 'fast lane' and the 'slow lane' of insulin resistance, with the latter being linked to chronic lifestyle and dietary habits. Nevertheless, it suggests that insulin resistance is reversible through adherence to four simple pillars. It also warns against relying solely on certain medications like EMP for weight loss, highlighting that 40% of the weight loss from these drugs might be detrimental.
• 45:00 - 60:00: Insulin Resistance in Different Populations This chapter discusses a bet made by the team behind a popular YouTube channel as they approach a milestone of 10 million subscribers. To celebrate, the host has agreed that for every new subscriber in the next 30 days, $1 will be added to a fund for the team's celebration. The host encourages viewers to subscribe to contribute to the team's celebration.
• 60:00 - 75:00: Impact of Insulin Resistance on Health The chapter discusses the impact of insulin resistance on health, highlighting it as a significant factor contributing to chronic diseases. The speaker mentions a mission to help people understand the connections between insulin resistance and health issues.
• 75:00 - 90:00: Diet and Insulin: The Ketogenic Approach The chapter 'Diet and Insulin: The Ketogenic Approach' discusses the interconnectedness of various disorders and the conventional approach to medical treatment. It suggests that many disorders, traditionally seen as distinct, actually share underlying causes, much like branches of the same tree. The conventional medical approach is criticized for only temporarily addressing symptoms (akin to pruning a branch) without addressing the root cause, implying that symptoms often return. The transcript introduces the concept of finding more holistic or root-level solutions, potentially hinting at the efficacy of the ketogenic diet in addressing some of these underlying issues.
• 90:00 - 105:00: The Role of Exercise and Lifestyle Changes The chapter titled 'The Role of Exercise and Lifestyle Changes' discusses how various chronic diseases, which are major causes of mortality worldwide, can be mitigated through simple lifestyle alterations. The emphasis is on the shared metabolic core among these diseases, including Alzheimer's, heart disease, type 2 diabetes, liver failure, and fatty liver disease. The chapter highlights the mission to address this core, suggesting that lifestyle changes can effectively reduce the risk of these diseases.
• 105:00 - 120:00: Pharmaceutical Interventions and Risks The chapter discusses the problem of insulin resistance, highlighting it as a lesser-known issue. It mentions a documented finding regarding the link between growing fat tissue and an increased risk of type two diabetes, which was gaining attention in the early 2000s under the concept of 'diabesity.' The transcript refers to a manuscript that outlines this connection, emphasizing the dual epidemic of obesity and type two diabetes.
• 120:00 - 135:00: The Importance of Monitoring and Education The chapter delves into the role of fat tissue in releasing pro-inflammatory proteins during growth, which can cause insulin resistance. This condition in various body tissues can lead to the spread of chronic diseases such as hypertension. The material highlights the critical importance of monitoring these processes and educating individuals about the potential consequences for overall health.
• 135:00 - 150:00: Alternative Treatments and Future Directions The chapter titled 'Alternative Treatments and Future Directions' discusses the role of insulin resistance in various health problems, highlighting its impact on cardiovascular diseases like hypertension, neurological conditions such as Alzheimer's disease, and reproductive health issues like erectile dysfunction in men and polycystic ovary syndrome (PCOS) in women.

The Insulin & Glucose Doctor: This Will Strip Your Fat Faster Than Anything! Transcription

• 00:00 - 00:30 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 but this gets worse because we know that insulin resistance is the core for most chronic diseases that are killing us and there's a handful of other lifestyle habits that's contributing to it that's horrifying so tell me everything Dr Benjamin bman is a leading metabolic scientist whose research focuses on the hidden epidemic of insulin resistance and its devastating consequences and by regaining control of your insulin levels he says you can regain control of your life insulin is a hormone affects
• 00:30 - 01:00 literally every single cell of the body but if those cells become insulin resistant you start to spread the disease for example they call Alzheimer's insulin resistance of the brain and even the most common forms of infertility erectile dysfunction and PCOS insulin resistance is a heavy contributor now 88% of adults in the US have some degree of insulin resistance and people hear this and think America is just fat and metabolically sick but we're not actually the worst country when it comes to this and part of it is because of how different ethnicities store fat I'll come back to that there's two roads to insulin resistance so
• 01:00 - 01:30 there's the fast lane and I could make you insulin resistant in 6 hours with either of these common three things but if I removed them your resistance would go away just as quickly now the slow lane that's a problem and there's certain lifestyle habits and problems with our diets that are massively contributing to slow insulin resistance now thankfully this can be resolved through four pillars which are very simple we'll get into that but why don't we just sack all this off and just take as EMP well because people may not know about the negative side effects for example 40% of the weight that people are losing on these drugs is coming from highly
• 01:30 - 02:00 I have been forced into a bet with my team we're about to hit 10 million subscribers on YouTube which is our biggest Milestone ever thanks to all of you and we want to have a massive party for the people that have worked on this show for years behind the scenes so they said to me Steve for every new subscriber we get in the next 30 days can $1 be given to our celebration fund for the entire team and I've agreed to the bet so if you want to say thank you to the team behind the scenes at di of all you've got to do is hit the subscribe button so actually this is the
• 02:00 - 02:30 first time I'm going to tell you not to subscribe because it might end up costing me an [Applause] [Music] awful Benjamin what is the mission that you're on my mission is to help people appreciate that much of chronic disease
• 02:30 - 03:00 we look at them as these siloed individual distinct disorders with totally distinct Origins and yet much of them share a common core it's as if their branches growing from the same tree in the conventional clinical care will look at these branches and give someone a prescription for a medication which is only going to prune the branch back a little bit never actually solving the problem it can just grow right back and so we can look at
• 03:00 - 03:30 most of these chronic diseases that are killing us globally and and then say okay there are in fact some simple lifestyle changes that can be implemented that will help reduce the risk of not only one or two but all of the top killers from things like Alzheimer's disease to uh heart disease to type two diabetes to uh liver failure fatty liver disease all of them share a common metabolic core that's my mission and what is that common metabolic core
• 03:30 - 04:00 yeah it's a little known problem called insulin resistance in fact when I first started this topic I stumbled on one paper that documented how when fat tissue is growing it increases the risk of type two diabetes that was this concept in the early 2000s that was really getting a lot of attention diabesity this kind of dual epidemic of wherever we see obesity we see more type two diabetes in this manuscript outlined
• 04:00 - 04:30 something that was to me a revelation at the time it was so fascinating where when fat tissue is growing it starts releasing pro-inflammatory proteins that inflammation caused a problem called insulin resistance and then that got me into this realm of understanding that other tissues of the body as they become insulin resistant then you start to spread the chronic disease and and essentially coming to the conclusion that something like hypertension high
• 04:30 - 05:00 blood pressure which is the most common cardiovascular problem and the main contributor to heart disease well insulin resistance is the main cause of hypertension um they call Alzheimer's disease type 3 diabetes or more accurately um insulin resistance of the brain even the most common forms of infertility in men it's erectile dysfunction well that's because of insulin resistance of the blood vessels in women the most common form of infertility is polycystic ovary syndrome or PCOS that's because of the insulin
• 05:00 - 05:30 resistance affecting her ovaries and the ability to produce the proper sex hormones I guess the really important question here is what is insulin resistance and can you explain this to me like I'm a 10-year-old oh yeah for sure insulin resistance is it's kind of a it's a disorder that has two parts it's like a coin with two sides that as much as we think of we we think of one side just because we hear the word insulin resistance but there's another part to it that I need to that is very important so insulin first of all is a
• 05:30 - 06:00 hormone that we make from the pancreas a long kind of gland tucked underneath the stomach and the pancreas is a very busy organ it makes a lot of different hormones it makes hormones that come into the blood it also makes enzymes that go into the into the intestines to help digest food but among the hormones that are being released into the blood is insulin now in the person with type one diabetes their immune system has destroyed their beta cells so they don't
• 06:00 - 06:30 make insulin anymore that's why for a person with type 1 diabetes insulin is a life-saving therapy you're giving them what they're not making anymore but for everybody else we have beta cells and they're releasing insulin when they need to now usually the main stimulus the main reason the beta cell is releasing the insulin is because blood glucose levels go up so I eat sugar you eat sugar or not even something as obvious as sugar but bread or or crackers White chips oh yes yes so
• 06:30 - 07:00 basically anything that falls into the family of a carbohydrate so if the Earth grows it that's a carbohydrate um if it's a plant it's a carbohydrate maybe that's a better way of describing it and so it's going to have starches and sugars which all is kind of falls into this family of carbohydrate depending on how much starch or sugars that it has then that will result in a bigger or smaller blood glucose or blood sugar response but then if blood sugar is too
• 07:00 - 07:30 high for too long that becomes very harmful to the body so insulin comes in um and helps lower the blood glucose and then having done its job insulin comes back down so insulin comes out like a taxi and transports all the glucose in my blood to various places around the body to St perfect yeah tax that's right that you can sit look at it's a shuttle it's a taxi saying hey glucose come on in I'm dropping you off at the muscle so mostly just as an interesting tangent of insulin before I finish answering
• 07:30 - 08:00 insulin resistance insulin will open the doors for blood sugar to come in and drive the taxi in mostly at the muscle and the fat muscle and fat tissue need insulin to come and bring the sugar in Via taxi however other tissues and and the brain a little bit as well other tissues will still respond to insulin but they don't need insulin to tell it what to do with the sugar it just takes it in but even on those like the liver
• 08:00 - 08:30 for example if the liver sees sugar driving by in the taxi it just opens the doors and lets it in it doesn't need insulin to come and tell it to let the sugar in however even at the liver and O every other cell has a similar degree of this the liver doesn't know what to do with it so this is back to something I'd mentioned earlier where insulin's thematic effect at the entire body is to tell the body what to do with energy in all of its forms as as these kind of
• 08:30 - 09:00 caloric Rich molecules what to do with lactate what to do with ketones what to do with fats or glucose what to do with Pro amino acids so insulin will tell the body what to do with all of those things but again its most famous effect is to control blood sugar and that's not wrong because its most powerful activator is blood sugar so with all of that in mind insulin resistance is two problems wrapped into one the one problem is the most obvious vious one which is that
• 09:00 - 09:30 insulin isn't working as well as it used to so back to the analogy of the taxis dropping off sugar if the muscle tissue has become insulin resistant insulin is coming and trying to pull the sugar-loaded taxi into the muscle but the muscle's not listening so say that again so the yeah insulin's coming past with the glucose inside it well not technically yeah but just to sort of go with your metaphor but maybe to use another one insulin comes and knocks on the doors it's like the bouncer yeah at
• 09:30 - 10:00 the door it's coming and knocking on the door of the muscle saying hey muscle I've got some sugar that wants to come in and normally the muscle will say oh yeah sure okay open it up the doors and let the sugar come in when the muscle is insulin resistant the bouncers is knocking maybe there's even I'm almost getting ahead of myself but one bouncer maybe two or three bouncers pounding on the doors of the muscle cell but the muscle cell is not listening it's become deaf that's the insulin resistance of what we call insulin resistance where
• 10:00 - 10:30 some of insulin's effects like helping lower blood sugar it's not working very well anymore and the muscle is just an obvious example because there's so much of it you know it is the biggest tissue on the average individual someone who's very obese perhaps now has more fat tissue but even people who are overweight most of us is muscle so that's a good it's a good tissue to look at so part of insulin resistance is that of all the things insulin is trying to do including including lower blood sugar
• 10:30 - 11:00 it doesn't do it quite as well as it used to some of the cells or tissues of the body have become deaf to insulin's demands now however at the same time that's happening insulin levels are higher and that is really important um and I'll I'll mention an example in just a moment that highlights the difference between the two but we have to consider anytime we talk about insulin resistance we think of two things happening um in concert one insulin isn't working quite
• 11:00 - 11:30 as well as it used to in various places of the body at the same time insulin levels are higher and that kind of takes us back to the um the muscle cell where I'd mentioned getting a little ahead of myself that a bouncer is knocking on the door 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 and it would open the door and let the glucose or the blood sugar come in but now the muscle cell um the the the bouncer insulin's
• 11:30 - 12:00 knocking on the door but the muscle doesn't listen it's resistant and so the body has adapted and it learns okay well if one bouncer wasn't enough let's send an angry mob of bouncers and then the glucose the muscle will start to open the door and and and indeed it can so those two problems go together on one hand insulin isn't working as well as it used to that's what gives it the name insulin resistance but there's another part that is equally present which is
• 12:00 - 12:30 that blood insulin levels are higher now there's um earlier at the outset of the conversation I mentioned that even infertility has an origin sh has some degree of um development because of insulin resistance and it's a perfect example of both of these parts of insulin resistance where in some instances insulin isn't working very well always with insulin resistance blood insulin levels are higher so for example erect stle dysfunction is the
• 12:30 - 13:00 most common form of male infertility in fact its connection to insulin resistance is so strong that just a few years ago I I was so struck by a title of a paper that had just been published which stated something like is erectile dysfunction the earliest manifestation of insulin resistance in otherwise young healthy men now what is the connection it's because in a normal erectile function in order for the man to have normal erectile function he has to
• 13:00 - 13:30 experience a pretty dramatic increase in the size of the blood vessels in his body the blood vessels expand that increases blood flow and then he has normal function part of that signal that tells the blood vessels that it's time to expand is actually insulin 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 insulin does a lot of stuff again including telling blood vessels to expand now unfortunately in the case of this un
• 13:30 - 14:00 this unfortunate man his blood vessels become insulin resistant so now it's insulin coming and knocking on the doors of the blood vessel saying hey it's time to expand and increase blood flow but the blood vessels don't respond they don't listen so they stay constricted blood flow stays insufficient and thus he has a rectile dysfunction no I don't want to be insulin resistant no no one does no one does so so tell me how it happens yeah right yeah so the origins
• 14:00 - 14:30 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 there are two Pathways to insulin resistance so uh two two roads that get to the same destination again the destination being insulin resistance there's the fast lane which I call fast insulin resistance and it actually has three lanes which I'll describe in a moment then there's the slow insulin resistance which is a more it takes a little longer get there but
• 14:30 - 15:00 at the same time it takes a little longer to get away from it so I'll start with fast insulin resistance because the slow one ends up getting a little excitingly complicated but in a cool way 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 but as quickly as it settles in if I remove those things your insulin resistance would go away so so these are fast causes and they're fast resolution they
• 15:00 - 15:30 are stress is uh is a primary cause of fast insulin resistance SO2 is inflammation and then lastly and this is going to sound somewhat paradoxical too much insulin is also a cause and I'll end with that one because I think it's the most important then transition to slow insulin resistance so anytime the body is experiencing too much stress it will very quickly become insulin resist istent now as a professor who teaches
• 15:30 - 16:00 Endocrinology no surprise I Define stress in the context of hormones and there are two primary stress hormones cortisol and what we call in the US epinephrine or in the UK adrenaline those are the two stress hormones now those hormones are very distinct they have almost nothing in common but like when you are feeling a little stressed it's both of those especially adrenaline epinephrine that are making you feel a little jittery it's making your
• 16:00 - 16:30 heartbeat a little faster you're a little more alert um that all starts to play into a stress response but what those two hormones have in common is that they both want blood glucose levels to climb 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 or to that's the fight ORF flight kind of aspect to stress and so they want to push blood glucose levels up and they do very well that of course puts them at odds with the hormone insulin cuz these two
• 16:30 - 17:00 epinephrine or adrenaline and cortisol the two stress hormones they're pushing glucose up insulin wants to push it down so the more the body is has those stress hormones elevated because of say sleep deprivation that's a very effective way to increase cortisol or they are taking too much drinking too much caffeine that is a way to increase epinephrine quite strongly if both of those signals are too incess or you know they continue to
• 17:00 - 17:30 be present and climb then insulin has to work harder and harder and then we have insulin resistance so stress is a cause of insulin resistance but then next is inflammation you you know you and I were commenting about earlier about how boy there's a cold going around people it's flu season 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
• 17:30 - 18:00 significantly higher during the time that they're struggling with this infection that is a reflection of insulin resistance insulin's having a harder time keeping the blood glucose levels in check anytime inflammation is up insulin resistance will be up as well even in things like autoimmune diseases there are reports in humans that document the degree to which someone has say active rheumatoid arthritis their their joints are achy because of of an autoimmune
• 18:00 - 18:30 attacking of the joints they will note on some days like every autoimmune disease there is an EB and a flow some days it's good some days it's bad 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 so inflammation is another cause and then the last one of the Fast Lane of insulin resistance is too much insulin itself now the astute
• 18:30 - 19:00 listener will realize the kind of circular thing I've just presented by invoking high insulin as a cause of insulin resistance because they will also think but wait a minute Ben you just said that high insulin is also a consequence of insulin resistance that you know back to the bouncer knocking on the the the door of the muscle cell 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 so High insulin is
• 19:00 - 19:30 both a consequence of insulin resistance but it's also a cause 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 this would be like a funny analogy of in in in my in the bikman home my darling wife is home with the children that is what she wants to do she she is
• 19:30 - 20:00 full-time mom 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 I will hear my child saying mom mom mom and she's not responding mom has heard this for so much that she's become kind of selectively deaf to when my children are demanding her attention I'm not as around my children quite as much because I'm working during the day and so when I hear that it's a very fresh signal to me
• 20:00 - 20:30 I've not heard it so much that I've become deaf to it 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 this is like the body in response to insulin if there is always insulin it's always going up always going up the body will start to say the muscle cell will start to say boy insulin you are knocking on my door all the time this is getting old I'm not responding anymore I'm not going to listen as much as I was before so in
• 20:30 - 21:00 that sense insulin too much insulin becomes a cause of insulin resistance and 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 and over just a few hours you would become demonstrably less sensitive to it than you were before we started but again as I take that away give your body a few hours and it's back to normal in every one of those instances it's a fast onset and it's also a fast solution if we can take
• 21:00 - 21:30 it away if we can take it away but if we can't take it away does it become sort of chronic yeah so that especially all of these can contribute to a more lingering insulin resistance but especially insulin 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 and now perhaps with the best of intentions our experts are telling us that we
• 21:30 - 22:00 should be eating six times a day and so we eat we wake up in the morning insulin has finally been coming down while we've been fasting overnight insulin gets to take a little bit of a break we're fasting then we break that fast by eating breakfast and in the UK as it is in the US by and large this is going to be a very starchy sugary breakfast it's toast with some Jam or it's cereal or it's Bagels that is going to be that is almost pure glucose and so what do we do
• 22:00 - 22:30 we wake up we eat breakfast we Spike our blood sugar levels and Insulin has to come up insulin will take longer to come down than the blood sugar will it will wait in the blood to make sure that all the blood sugar has gone back to normal 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 long before it's had a chance to come back down to normal we've had a midm morning snack of course we need to go get a sugar coffee and another Bagel or something and so
• 22:30 - 23:00 after just a couple hours we do it again 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 and then of course we have to have an evening snack before we go to bed so the average individual is spending every waking moment in a state of elevated insulin and thus the signal never really goes away because they they never give themselves a break but one of the consequences of that I mentioned
• 23:00 - 23:30 which is that it directly causes insulin resistance but when insulin is high it starts to have a signal on the fat cell 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 and it takes longer to settle in but it takes also longer to go away that's why I call this one slow insulin resistance now in the case of insulin most people so the
• 23:30 - 24:00 the the the key with the yeah I'll explain it this way first so the most relevant feature with fat tissue contributing to insulin resistance is the size of each fat cell when we typically think of fat we would maybe say okay Steve has um I'll do this in kilos for the UK audience Steve has 10 kilos of fat on your entire body that's probably too much for you Ben has 20 kilos and yet it's possible that I'm healthier metabolically than you um and
• 24:00 - 24:30 that's because it's not the mass of fat that matters most it's the size of the fat cell that matters this is why women despite universally being fatter than her male counterparts are healthier with regards to insulin resistance and every single metabolic problem it's because women as a result of her particular sex hormones have more fat cells but they're smaller so she has more fat but smaller fat cells and small fat cells are healthy insulin sensitive
• 24:30 - 25:00 anti-inflammatory fat cells but the bigger the fat cell gets the more it initiates a Cascade of events or a series of events that creates insulin resistance and am I right in thinking we have the same amount of fat cells for our whole life pretty much that's a really really safe assumption for most people yeah for most people the a fat cell um sometimes students will hear that fat cells are Immortal that is not true but they're longlived fat cells will live about 10 years and so
• 25:00 - 25:30 typically by the time if you think of if you look at a newborn during infancy childhood and puberty the number of fat cells is going up up up up up once they finish puberty so mid to late teens for a young woman late teens or even early 20s for a young man usually at that point the number of fat cells they have is going to be very static this is something people don't really understand and I actually discovered it from during this podcast and speaking to so many experts about this that that we pretty much especially as an adult have the
• 25:30 - 26:00 same amount of fat cells really regardless of what we eat yes and it's actually just the fat cells we have shrinking or grow expanding exactly that's exactly right now there are differences across which by the way makes lipos suction a pretty bad idea in fact it in fact it makes things worse please let's make sure we come back to that okay I'll write down lip because it really becomes the person ends up their vanity ends up really ruining their their their future metabolic outcomes but there are
• 26:00 - 26:30 differences across ethnicity like um this is a little oversimplified but not much on one end you'd have Caucasians kind of northern European Caucasians on the other one end you'd have East Asians like uh Chinese Japanese uh Korean East Asians and and then if you look at that same spectrum of people making fat cells through their life an East Asian will be making fat cells and then stop right about here about sort of so very few fat cells relatively speaking across all the
• 26:30 - 27:00 ethnicities they have very few fat cells a Caucasian on the other end of the spectrum they went way higher and so this guy let's say American Ben versus Chinese Ben overly simplified but but here we are um so much of fat Mass isn't the number of fat cells even though American Ben has more it's the size of the fat cell so I could be the same percent body fat really as Chinese knees Ben um but that would just be because my
• 27:00 - 27:30 fat cells were just that much smaller but this is the problem then if you have let's say American Ben and Chinese Ben both gained 10 kilos of pure fat over the next 10 years very easily done most people do that quite often Caucasian Ben just doesn't look as good in his Speedo um which is a pasty Caucasian he's not going to look particularly good in that Speedo anyway but I just am bulging a little more than I was before but otherwise I'm healthy my blood pressure is fine my blood sugar is fine everything's normal put that
• 27:30 - 28:00 same 10 kilos of fat on Chinese Ben hypertension type 2 diabetes fatty liver disease infertility um and that is because Chinese Ben had fewer fat cells to start with and so those fat cells as the body was told to store fat those fat cells were getting much much bigger much sooner and the fat fat cell promotes insulin resistance very very readily and so that logically
• 28:00 - 28:30 moves into this the question of what makes fat cells grow and it is two essential variables that we only ever look at calories 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 they cannot gain weight it is it is literally impossible for the type 1 diabetic to get fat if they are skipping their insulin injections in
• 28:30 - 29:00 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 imagine a young girl who gets diagnosed with type 1 diabetes at the age of 13 or 14 very impressionable time she's very worried about how how she looks and how thin she is she learns that wait a minute I can eat whatever I want and all I have to do is not eject my insulin and I'll be as skinny as I want and it works it works
• 29:00 - 29:30 so well that it's actually a formal eating disorder called diabulimia so this 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 because like i' said earlier when I talked about hormones hormones are a way for the B for the very tissues of the body to know what it ought to do with energy and so a fat cell will have energy all around it and if it doesn't have insulin to tell it what to do it won't do anything with
• 29:30 - 30:00 it or maybe to make this more direct back home in my lab my students my students are growing fat cells in Petri dishes 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 the moment we add insulin into that little petri dish if we check those cells four hours later they're immediately fatter if we check them 4 hours later they're fatter still
• 30:00 - 30:30 now they know what to do with the energy they have so with slow insulin resistance it develops when fat cells get really really big it's like a a because they have to tell insulin insulin you continue you you are telling me to keep growing I can't keep growing I'm so big that I'm going to pop I mean literally the fat cell can get so big that it degrades its membrane it's like a water balloon that a naughty little boy has overfilled and it's about to burst the fat cell doesn't want to burst
• 30:30 - 31:00 and so it tells insulin insulin you are trying to make me grow you're telling me to grow I can't listen anymore I'm becoming insulin resistant to stop growing so insulin makes you fat oh very much now if you so so a moment ago I said that the big fat cell is two variables you must have both you must have both a signal to tell the fat cell to get big which is insulin it is the there's no other signal that can do it you can in a human just simply take away the insulin like type 1 diabetes it
• 31:00 - 31:30 doesn't matter any other hormone in the body it does not matter they cannot get fat they could again they can eat thousand they could eat 10,000 calories of chocolate cake they cannot get fat not only can they not get fat they can't hold on to their fat because if there's no insulin to tell the Fat Self to hold on to it or get big it has to shrink it's breaking down its fat so the body goes into such a dramatic fat burning state in the absence of insulin that keeping fat fat becomes impossible so the insulin signal is necessary to tell
• 31:30 - 32:00 the fat cell what to do 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 that's where the calories come in now the fat cell will say hey fats and glucose in the blood insulin has told me to get big and so I need to pull you in to help me grow you're going to give me the bulk and if you have one without the other it is death so if I'm in 2,000 calories and I have a different
• 32:00 - 32:30 insulin sensitivity to you so we both eat 2,000 calories and I'm insulin resistant doesn't that mean that I will you'll store more as fat oh okay yeah yeah so so your body now it would partly depend on there are people where you you if your if all of your fat cells had reached its maximum point then you're done you're not going to gain more fat you're just going to become more and more and more insulin resistant okay fine so you kind of start limiting yourself but there are studies in humans to show that if you give humans
• 32:30 - 33:00 isocaloric D meals so the exact same number of calories but they in the same amount of protein but you differ those meals based on the amount of carbs to the amount of fat so let's say two meals exact same calories 2,000 calories or that's in one meal that's too high a th000 calories in one meal one version of this is the conventional way of eating which is lower fat higher carb the other meal same number of calories
• 33:00 - 33:30 but it's lower carb higher fat this lower carb higher fat version will have a lower insulin response and they they will store less fat from that meal they're met and someone would say well where do the calories go you can't this it's the laws of thermodynamics you can't destroy energy the metabolic rate will go up so when insulin is low if you have someone going a full day eating the same number of calories but
• 33:30 - 34:00 lower carb calories their metabolic rate will be almost 300 calories higher in that day a metabolic rate is the yeah that's the total amount of energy that it just costs you and I to just live okay you RIS going through the day but that's but that's a significant amount 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 so it's 300 calories but at the same time if your insulin is low you're burning so much fat that start making ketones and I I don't intend to get onto that topic quite yet
• 34:00 - 34:30 but suffice it to say every molecule of a ketone has a has a caloric load roughly similar to glucose and one of the and and what the body when it starts making a lot of ketones it starts eliminating the ketones so every time someone is breathing out ketones they're literally breathing out calories or they're urinating and they're urinating out ketones if they have higher ketones in their blood they're urinating out calories because ketones have energy and so this is the way that if insulin is
• 34:30 - 35:00 low it becomes impossible for the body to hold on to its energy 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 because ketones have calories ketones are energy now we're just dumping them out into the universe it's worth before we talk about how to keep my levels low so that I can benefit from
• 35:00 - 35:30 all the health benefits we've talked about it's probably also worth just spending a little bit of time trying to understand the evolutionary basis of insulin resistance 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 or Apes what was the difference that had us become so different than them one of the leading theories is a is a Theory called the expensive tissue hypothesis and it
• 35:30 - 36:00 actually does have something to do with ketones 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 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
• 36:00 - 36:30 one our intestines became significantly shorter so if you compare the human digestive tract to any other primate animal if we are a primate um then if you look at the intestines they're fantastically different particularly the large intestine or the colon because our ancestors as the theory goes began eating meat we didn't need the colon as much um because the colon is a place for food to ferment and so if you're eating
• 36:30 - 37:00 a lot of plant matter like other primates do you need a much much larger colon so we started eating food that was so nutrient-dense our colon shrunk considerably we didn't need to waste energy on a big busy colon 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 and so at the same time our int in were shrinking because we didn't need them to be so big
• 37:00 - 37:30 our brain was growing and it's because it had so much nutrition including ketones so ketones are an extraordinary fuel for the brain 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 and fat baby is healthy baby and fat baby gets into ketosis let's say you and I were to fast
• 37:30 - 38:00 straight for 2 days 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 and the more the body burns fat the more it makes ketones and the tissue of the body that appears to benefit the most in response to ketones is the brain the brain the moment ketones hit the blood stream the brain immediately starts taking in ketones for a fuel very
• 38:00 - 38:30 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 and I show them just one or two papers to prove that wrong immediately and it is reflected in in in this idea which if if to use some convenient UK units if blood glucose is 5 Millar that's a concentration a way of
• 38:30 - 39:00 measuring an amount of of something blood glucose may be 5 Millar or 80 milligram per deciliter for the American audience um 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 Millar of of ketones and yet even then the brain has already switched to get the majority of its energy from the Ketone 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 and even in that scenario
• 39:00 - 39:30 the brain is already getting more than half of its energy from the Ketone 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 brain brains to grow 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 the title of a book just published which is that vegetarians have
• 39:30 - 40:00 smaller brains this is seen in humans that the less a human eats meat then the smaller the brain becomes the brain is so dependent on the nutrient density that comes from animal sourced foods that it will suffer um when it doesn't get them interesting I mean that's a controversial thing to say 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
• 40:00 - 40:30 Source Foods it's because you are depriving the brain of what it needs what is it exactly you're depriving the brain of in that situation yeah yeah so at least among other things at least it would be the the essential omega-3 fats so there are three Omega-3s and you humans can only we can only get one from Plants but it's one that the humans don't use we need the other two and they only come from animal Source foods and you could supplement absolutely right and yeah you can but but that that so the the solution in that regard is the vegan must be educated enough to know
• 40:30 - 41:00 what they're deficient in and then wealthy enough to afford the supplements to make up for it so is that the the only evolutionary sort of hypothesis towards why we developed this insulin resistance 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 so insulin resistance why would it exist at all it would probably be a way for the body to know when it was needed to hold on to energy a little better so now I say that now and and
• 41:00 - 41:30 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 not all versions of insulin resistance are negative so there is um there is what all the insulin resistance that you and I have been talking about is pathological insulin resistance or harmful insulin resistance insulin resistance that serves no good purpose and it's making us sick however there is
• 41:30 - 42:00 insulin resistance in human development which is physiological or helpful it's supposed to happen and that is the two PS of physiological insulin resistance puberty and pregnancy because in both of those instances as we outlined earlier when the body's insulin resistant insulin is high that's not always bad because insulin wants things to grow it is like a fertilizer in the body now sometimes it's misplaced and results in
• 42:00 - 42:30 problems like increasing the risk of cancer for example but in other instances if you have a young child who needs some explosive growth during puberty well then that's really helpful insulin's telling the body to store more energy to build up tissues including muscle and bone but also including fat so in pregnancy insulin's playing a role in growing the placenta sure is the breasts yes so in the woman after she's finished puberty the only other time of growth she'll never have will be pregnancy and and so those are the two
• 42:30 - 43:00 instances where the body has become insulin resistant to take advantage of the heightened scenario where it can grow because the woman's body needs to more fat goodness yes yes so her body not only needs to grow tissue Mass like the uterus has to get much bigger she has to grow a placenta 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 and so as as her body becomes insulin resistant actually facilitates the growth of the baby a little more rapidly but as you noted it helps her
• 43:00 - 43:30 store more fat and progesterone is another hormone that even accelerates that process but basically it's her way of her body's way of saying hey I am committing to Growing another human and it's going to be metabolically very demanding and so I'm going to have as much extra fat or much 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
• 43:30 - 44:00 through it all and then maybe I'll even have enough to continue to feed the baby with lactation after the baby's born what is gestational diabetes yeah it's a great question gestational diabetes is essentially type 2 diabetes of pregnancy so it's perfectly timed question because if you look at the average woman um who is very healthy very insulin sensitive at the beginning of her pregnancy so glucose is normal and insulin is
• 44:00 - 44:30 normal over the course of her pregnancy she stays normal healthy pregnant woman which is to say she has physiological insulin resistance she doesn't get diagnosed with gestational diabetes though which means her glucose is normal 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 and then in some women especially if she has a family history of type two diabetes
• 44:30 - 45:00 the insulin resistance goes too far now she has high insulin like all pregnant women do but she's not able to keep her glucose levels in check so if I'm eating loads and loads of sugar throughout a pregnancy that will compound the problem absolutely so then she will go from the normal insulin resistance of pregnancy into the insulin resistance of diabetes so it really is like type 2 diabetes but a microcosm of it a mini verion that was really instigated or initiated because of the pregnancy combined with a
• 45:00 - 45:30 bit of a genetic predisposition combined with her eating the worst possible way does that then impact the future baby oh for sure it does yeah so think about it's almost like the baby is devel literally developing in a hyperglycemic hyperinsulinemic environment so the baby's get the baby gets hardwired to want to continue to exist in a state of high insulin and high glucose after the baby is born and so so yes The Offspring of mothers who have gestational diabetes are significantly
• 45:30 - 46:00 more likely to gain weight and be chubbier or fatter than their counterparts and to later develop type two diabetes yeah a resounding yes 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 yes I mean a significant thing and I 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
• 46:00 - 46:30 one of the things that that I saw the other day on social media which I wanted to ask you about was this I got a picture of it here um it was someone online that posted this photo and they said well this graph and they said we need to figure out what's going on here um this is the graph I'll put it on screen for anybody that's watching but also it'll be linked in the comment section below um it essentially shows that over the last let's say 20 20 years there's been a really significant rise in cancer amongst women but when we look
• 46:30 - 47:00 at cancer amongst men it's pretty flat MH um and this is cancer incidence by age and gender up to 49 years old and I was wondering if you had any thoughts on why this is happening yeah yeah yeah a few thoughts come to mind um whenever I see these kinds of reports I always make sure I look firstly at the what are they actually measuring 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 so
• 47:00 - 47:30 one one simple explanation although perhaps the most disappointing could be that more women are going in for testing younger 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 you know for 10 or 20 years which is a good thing you want to detect cancer as soon as possible so that's the boring answer that it could be a reflection of just more women going in for ultrasounds or MRIs or mamory
• 47:30 - 48:00 scans whereas men don't ever get tested for anything which is why we die more from everything possibly but to give a more exciting answer this is very very likely almost entirely driven by breast cancer um breast cancer is the main cancer for women um by far and so if I had to guess I bet almost all of this increase in cancer incidents is because of breast cancer why might that be going up I would suggest there's probably a couple instances one um although people
• 48:00 - 48:30 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 it's very well known um very well documented that if a woman um has a f has babies and breastfeeds her risk of um breast cancer goes down so yeah in fact it's very meaningful I actually don't know um the reasons for it it could be the changes in estrogens during lactation phase I've just I've just actually done a quick search here to I put a picture of that graph into Ai and
• 48:30 - 49:00 asked it the same question and it said pretty much what you said it said there's a rising breast cancer incidents according to cancer research UK the other one that it came up with is obesity Trends oh yeah I promised I was going to talk about that I wouldn't leave that sorry for interrupting there no no no problem and then the other one was delayed childbearing that's what I'm saying which is what you were saying yeah so as child rates as child birth rates are going down it does increase the risk of breast cancer now as I'm a cell biologist right I like to understand a direct mechanism and so as much as I invoke the perhaps lower rates
• 49:00 - 49:30 of child birth among women I don't know the mechanism so I'm sort of loathe to describe it the mechanisms I'm very familiar with are the metabolic um which is if you take a breast tissue that is tumor tissue and compare it to 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 the cancer from the breast will have seven times more insulin receptors than the normal breast tissue
• 49:30 - 50:00 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 but I would say it's the entire metabolic milu which is the insulin resistance that as much as the high insulin is promoting fat cells getting bigger that high insulin is also accelerating the growth of the tumor cells because again the main one of the main mutations in breast cancer is a Sevenfold so a seven times increase in the number of insulin receptors and
• 50:00 - 50:30 Insulin wants to tell things to grow so it's no surprise that almost every tumor that's ever been measured for having insulin receptors will have a lot more it's basically telling its neighboring cells insulin's going to come by and it's going to tell us all to grow I want to grow more than you and that's what cancer is cancer is growth unregulated growth insulin tells things to grow 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
• 50:30 - 51:00 as you guys know whoop is one of my show sponsors it's also a company that I have invested in and it's one that you guys asked me about a lot the biggest question I get asked is why I use whoop over other warable technology options and there is a bunch of reasons but I think it really comes down to the most overlooked yet crucial feature it's noninvasive nature when everything in life seems to be competing for my attention I turn to whoop because it doesn't have a screen and will armed the CEO who came on this podcast told me the
• 51:00 - 51:30 reason that there's no screen because screens equal distraction so when I'm in meetings or I'm at the gym my whoop doesn't demand my attention it's there in the background constantly pulling data and insights from my body that are ready for when I need them if you've been thinking about joining whoop you can head to join. woop.com CEO and try whoop for 30 days risk-free and zero commitment that's join. whoop.com CEO let me know how you get on you know one of the big subjects you
• 51:30 - 52:00 touched on at the start was the was Alzheimer's and Dementia yes and I have heard several people on this podcast tell me that they think of Alzheimer's as type three diabetes worldwide there is a new case of dementia every 3.2 seconds um it seems like I don't know if this is true but is Alzheimer's and Dementia On The Rise oh yes yeah it is in fact it went from not being even on the radar to being a top 10 killer um now it's interesting how people even die
• 52:00 - 52:30 from Alzheimer's disease it's a very kind of vague death but yeah Alzheimer's disease is one of the top 10 diseases now um certainly in the west um and and I would argue it's because it has a metabolic orgin 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 the plaque so so just to set the stage here so that people listening can appreciate this this paradigm shift that's occurred
• 52:30 - 53:00 in Alzheimer's research originally and even in many people still people thought that Alzheimer's disease is the result of these plaques accumulating in the brain these kind of little proteinous little thick things that are preventing neurons from sending the signals throughout the brain for the brain to think and and and have normal cognition and and yet there are those of us and I am proud to say I have long been one of them who has said that the plaque based Theory doesn't make sense we have had
• 53:00 - 53:30 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 so that is an immediate challenge of the plaque based theory of Alzheimer's even further even Beyond older than that evidence when you would look postmortem or look at tissue donor people who passed away you would look at the brains of people who died with confirmed Alzheimer's disease at the time of death and look at the brain of someone who died without
• 53:30 - 54:00 any evidence of any cognitive decline or any compromised thinking whatsoever and you would be just as likely to find plaques in both brains so the so whether the brain had Alzheimer's disease or not you would still see plaques in the brain so the whole idea that plaques mattered has long been controversial and just to put a fine point on it before transitioning to the metabolic Origins about two or 3 years ago they found out that the very first published papers
• 54:00 - 54:30 that implicated plaque as a cause of Alzheimer's disease were based on fabricated data so the scientists who published those first reports that led to the entire theory that Alzheimer's diseas is plaque based were called out as fraudulent and and indeed all of it was fabricated so the entire idea that Alzheimer and and we have spent billions of dollars on studies to try to how determine how do plaques CA cause Alzheimer's disease why when we reduce plaques it doesn't appear to help the
• 54:30 - 55:00 disease because the plaques had nothing to do with it that's just something that some brains have some brains have more of these little specks than other brains and they don't contribute to Alzheimer's disease at all now what did what kept rising to the top and I would hope now is the dominant theory is that people with Alzheimer's disease almost always have some detectable instance of insulin resistance if not full-on diabetes type two diabetes now I will say personally I don't like the term type 3 diabetes
• 55:00 - 55:30 because it makes it sound like it's a whole new version of diabetes to say it more succinctly and accurately it is simply insulin resistance of the brain and the brain is a very hungry organ it is in what I teach is is a tri a trinity of high metabolic rate organs that there are three organs in the body whose metabolic rate is so high that that just really sets it apart from everything else and the brain is one of them the
• 55:30 - 56:00 brain has a very high metabolic rate so this is a very hungry organ that needs a lot of energy all the time but the brain is unique in that it primarily will only use two fuel sources and I've mentioned them namely glucose and ketones but glucose in that section of the brain that gets compromised with Alzheimer's disease the glucose can't just come straight in it needs someone to open the door for it and that is insulin of course just like we described with the muscle cell where in order for
• 56:00 - 56:30 the glucose to go into the muscle insulin had to come and knock on the door if you will and then the muscle being a polite responsive host would open and allow the glucose to come in the brain is similar that in that section of the brain it has doors that need insulin it's locked until insulin comes and opens them 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 and yet it cannot because it has insulin regulating the
• 56:30 - 57:00 entrance of the glucose and if the brain is insulin resistant there's not enough glucose coming in and thus the brain is forced to rely on the only other fuel that it can rely on namely ketones 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 you know and mind the gap in the brain brain has an energy gap now and and where where the brain needs you know an amount of
• 57:00 - 57:30 energy I'm kind of acting it out for those that are watching but the brain has a certain energy demand that it needs and if there's a lot of glucose in a healthy insulin sensitive person glucose will fill all of that need but as the brain becomes progressively insulin resistant it cannot get all of its energy from glucose and thus there's an energetic Gap and in the absence of ketones there's nothing to fill that Gap 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
• 57:30 - 58:00 my function which manifests as a reduction in the ability to think and process in other words cognition goes down 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 there are scientists that measured this we don't in my lab because we don't do these kinds of techniques but you can actually Infuse people with the glucose that you can take pictures of and see
• 58:00 - 58:30 how much the brain is taking it in and metabolizing it in Alzheimer's disease the brain is not getting as much glucose so they call that a hypo or reduction in metabolism of glucose 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 depression has a brain glucose hypom metabolism to it my migraines have a brain glucose hypom metabolism epilepsy um and Parkinson's disease so
• 58:30 - 59:00 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 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 but then it's no surprise that they all benefit when ketones can swoop in to save the day um but that only can happen if the person is giving their body a break from
• 59:00 - 59:30 the insulin long enough to actually start making ketones really really interesting on this point of Alzheimer's because I don't think people have spent enough time talking about the link between insulin resistance and Alzheimer's um and one of the things I was I was looking at there was how many people with Alzheimer's have meet the criteria for insulin resistance and some Studies have it at 4% there's a study I found here that has it at 70 to 80% um which I wanted to site
• 59:30 - 60:00 um exact percentages vary 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 um but another study in Alzheimer's patients sometimes found it to be as high as 70 or 80% for instance research by Dr Suzanne Damon M at Brown University has drawn attention to the concept of type three free diabetes yeah again I don't love the term but I appreciate the use of it
• 60:00 - 60:30 which is it does suggest a metabolic origin but even you look at those ranges Stephen you'd say well one was 40 one was 80 boy what a difference I suspect a lot of that is just how did they measure insin resistance right if they were looking at the glucose like so many do you're just going to miss a lot of people yeah it's quite hard to I think there's different criteria right for how one defines someone as insulin resistant well yeah and that's just that's right that's because there's not enough training which is at the beginning of the conversation you asked my mission one of my missions is to help people
• 60:30 - 61:00 learn what to look for what do they need to be looking for yeah they need to be looking at insulin so is that easy to measure well it is technically easy to measure it's just that we have we don't have enough systems in place to allow to enable it like again um if if someone listening in the UK were to go to their GP and say can you measure my insulin in many instances they literally can't get it done the system just isn't in place to take it to the lab and and measure it now some do I know some physicians in the UK who do so and they have developed
• 61:00 - 61:30 their own way of getting it done and they're incredible Advocates of this whole idea but it is harder in the UK in Canada um where the system is such that they have said out of ignorance but perhaps well placed or or well intentioned they will say well insulin isn't a marker that matters it is and if you're measuring insulin resistance just to put things back to where we had talked about it earlier many people with insulin resistance have normal blood glucose levels it's the insulin that's
• 61:30 - 62:00 high and so I would say if a person can get their insulin measured get it measured in US units if it is anything above about 10 Micro units per M that's a warning in UK units if it's anything above about 40 picamoles that's a warning insulin is high you could have insulin resistance and you could be skinny oh yes and have insulin resistance yes that's especially depending on the ethnic like if someone listening to this is East Asian and they say well I'm quite thin I don't have insulin resistance you
• 62:00 - 62:30 very well could um it it depends even in in young women a a group out of Northern Canada which is of course pretty far north they found that even in young healthy weight women with PCOS they if they compared them to their identically matched other women without PCOS they were more insulin resistant than the other group so so anyway that's my way of saying even if you look at yourself and think well I'm kind of lean I'm not instant resistant you very well could be okay so
• 62:30 - 63:00 I've got a friend who's a woman MH who has PCOS yeah and one of the things that she often says to me is that she gains weight easily is this true oh for sure and in fact I wouldn't be surprised if she does because the fact that she has PCOS is not absolute evidence but very likely evidence that she has insulin resistance which would mean at any given moment her insulin is at the risk of being a little higher than her noninsulin resistant counterparts so if
• 63:00 - 63:30 she goes and gets the test done I bet her insulin would be High um and so all that would mean is which is good I mean knowledge is power and my hope would be that as someone goes and gets their insulin measured and there are a handful of other tests they could also look at but that's the most succinct then it would be all the more impetus or encouragement to say okay I heard I listened to step and Ben I really do need to start making some Chang and even in PCOS there are reports that document the
• 63:30 - 64:00 absolute reversal of the disease with nothing more than just dietary changes I was looking also a second ago because we mentioned ethnicity a few times and it says the research I was looking at says that East Asians have East Asians have fewer fat cells and they're more resistant to obesity related metabolic issues well that's second part of that statement is is not true they are more resistant to obesity but they are like if it's an interesting dichotomy I got you yeah so they're you like to find a
• 64:00 - 64:30 Japanese man who's as fat as the average American boy you're going to have to look it's hard it's hard but to find a Japanese man who has is just as much likely to get diabetes type two diabetes very easy Africans have more fat cells typically yeah so so on that ethnicity if now there's a lot of kind of wiggle room here but on one end we'd have Caucasians blacks would be right nearby African ethnicities would be quite close um to the to the kind of northern European ethnicity and then we would
• 64:30 - 65:00 move through and and I don't mean to miss anyone here but on the other end it would be East Asian and then sprinkled through that would be um uh Latino Latino would be somewhere in the middle kind Hispanic and then other Southeast Asian and then East Asian kind of on the worst end or the least sensitive or the most resp sensitive to their fat the most sensitive to their fat this actually is a concept that has been presented called the personal fat threshold which is this really interesting idea born from a group in
• 65:00 - 65:30 Australia suggesting that across every individual body which of course is heavily influenced by both ethnicity and sex like we' mentioned earlier a body is going to have a rate at which it can store fat in a healthy way and then once that threshold is met any further pressure to store fat will start creating insulin resistance and that threshold is essentially how big how how many fat cells do you have and how much room do they have so if you have more fat cells you have a higher fat
• 65:30 - 66:00 threshold you can get fatter before it starts to hurt you does your fat distribution also matter here because it does different races this research is telling me have different fat distribution it's saying that Africans have better fat distribution lower visceral fat and less metabolic risk because of that yeah yeah yeah Caucasian moderate fat cell quantity more prone to subcon Fat accumulation subcutaneous which is that's the fat around the orans yes so Caucasians so so let's say northern European African both store
• 66:00 - 66:30 more of their fat subcutaneously which is the fat just beneath the skin or the fat that you can pinch and jiggle that has an ability to expand more because there's nothing really to limit it um however the other place for people to store fat is their visceral atopos which is the fat that is tucked within the abdominal cavity so tucked around the organs it's sort of surrounding the kidneys and the intestines and the liver that is an unhealthy place to gain fat but in East Asian all things equal is
• 66:30 - 67:00 putting much more fat there than they are subcutaneously the advantage of subcutaneous fat is which is the fat on the outside yeah yeah so the the fat benath the skin yeah yeah the loose belly fat the fat that can pinch and jiggle that fat has a greater ability to make new fat cells so as much as earlier you and I said fat cells remain static for the most part they do there's a little bit of wiggle room where it can go up and that's purely subcutaneous and Hispanics have higher fat cell quantity more visceral fat yes and increased risk
• 67:00 - 67:30 of obesity related conditions and so the problem with visceral fat is this is such a finite space there's so little room within the core of your body that if we allow those fats to multiply it could theoretically start physically compressing on tissues right and so those fat cells only grow through hypertrophy which is the thing we talked about earlier with slow insulin resistance subcut cutaneous fat cells are more abundant but smaller visceral fat cells are fewer but much larger and
• 67:30 - 68:00 so any ethnicity including Hispanic or Asian that promotes relatively more fat storage in the visceral space is going to suffer from the consequences of that fat much sooner and again it still comes back to size the bigger the fat cell the sicker the fat cell according to Alzheimer's disease International the total number of people living with dementia globally is expected to reach 139 Million by 20 50 which is up from around 55 million in 2020 which I imagine is in part related to people
• 68:00 - 68:30 living a bit longer they once did as well although although the past few years life expectancy actually turned down for the first time in the history of modern world so who knows if it will continue to go up but yeah it could be people are living longer I mean one of the effects of modern medicine is that people live longer with disease um Alzheimer's included but it's absolutely a consequence further of our overall metabolic milu that we put ourselves in a position where we are
• 68:30 - 69:00 making our brains insulin resistant and thus they're going hungrier and hungrier there's a study you talk about um which you've cited before that shows that if you move visceral fat from an obese animal to a lean animal this immediately caused insulin resistance yeah in the animal that received it okay yeah so just to be clear if if if we took what they did in the study just just to reflect why or that different Depot of fat are harmful and so the the human
• 69:00 - 69:30 body has two distinct fat Depot and you and I described them subcutaneous which is the fat beneath the skin or visceral which is the fat tucked within the organs of the abdominal space and if you move subcutaneous fat which is like the belly fat the belly fat and and from one animal to another you couldn't do this in humans if you move belly fat if you will or subcutaneous fat from one animal to the other the animal is very healthy it's no problem subcutaneous fat is inert it really is just sort of hanging out there and minding its own business
• 69:30 - 70:00 but in that same study if you move the visceral atap POS over now all of a sudden that animal that got that extra dose of visceral fat is going to become sicker it's going to become more insulin resistant and diabetic because you've increased its visceral fat the amount of fat that it has in that space the body wants to limit the amount of fat that it has there because if the fat again if the fat grows too much you can physically start compressing and squishing organs that you need to be
• 70:00 - 70:30 functioning like the kidneys and the intestines have you seen Brian Johnson I have I don't know him personally but you've seen the documentaries and stuff made about him and the the work that he's doing what do you make of what he's doing to extend his age because you know one of the subjects I think is linked to this is the idea of longevity yeah and aging and he's become a bit of a poster child for the subjetive longevity right right well I want to address this because this is a real person so I want to address it very politely and diplomatically I think that I want to distinguish the difference between
• 70:30 - 71:00 longevity research and science which is a very real living breathing field and I'm proud to know individuals who are longevity scientists and distinguish them from um longevity you said poster child so the the gurus of longevity and that's not the same thing so what I say I don't mean to it to be an indictment of longevity research but I don't mind if people hear a bit of an indictment in my voice of the modern longevity Guru approach so these individuals and he is certainly
• 71:00 - 71:30 the most um wellknown they do have the advantage of never really being able to be proven wrong you know so there's an inherent problem here but I will say that the the application of being a longevity um expert or not a scientist but a guru and I don't mean for that to be negative but it does have a bit of a negative sound to it is that you have to rely on what I would call weak evidence now what do I mean by that uh so all of the approaches to
• 71:30 - 72:00 longevity nowadays rely on either correlational studies or basic research or animals and insect studies and then extrapolating that results or assuming those same results will apply to the human so let me briefly just mention my concerns with correlational research so the longevity Guru will say correlational evidence suggests that people who eat meat um die more well a correlational study
• 72:00 - 72:30 is by my estimation some of the weakest evidence that you can ever generate a correlational study would just have someone come to your home and say Stephen can you please answer this survey about what you eat you answered the survey you may lie you may not remember you may have things that you don't even think about including like for example that you're part of a very um well put together religious organization and I actually use that example very deliberately because people who are known to be part of good tight Social Circles like a formal religious
• 72:30 - 73:00 group always live longer than people who don't maybe you're really lonely loneliness is a greater contributor to death than cigarette smoking and it's not even close so there could be things on that survey that you just cannot capture and yet we end up making a conclusion and so all of that correlational evidence is deeply flawed research and yet that becomes the basis for the long longevity Guru to determine diet so if I'm trying to extend my longevity yeah trying to live longer
• 73:00 - 73:30 then exactly what should I be thinking about yeah so my view on longevity is a metabolic view no surprise I am a metabolic scientist and I don't mind someone sort of smirking at me declaring that or admitting it but I'm somewhat Justified just by way of setting the stage the earliest the birth of the modern longevity research uh at if if it didn't start it was heavily influenced by the work of a woman named Cynthia Cynthia Kenyan k n y
• 73:30 - 74:00 o n Cynthia kenion was one of the kind of she really did in my mind kind of give give birth to the modern longevity Focus what her lab found using an insect model and this is again a problem with the longevity gurus is that they rely on insect data um for example but it was compelling what she found I think it was worms she found in worms that if they restricted the glucose that the worms were eating they would live 50% longer
• 74:00 - 74:30 or some some fantastic increase in the how long the animals lived that kind of gave birth to the idea of fasting being beneficial but it also allowed her lab to start playing around with some of the genes of these little insects and when they started knocking down or underexpressing some of the genes involved in insulin they didn't have to restrict the food the animals just lived longer and so that touches on this metabolic aspect and everyone nowadays is really
• 74:30 - 75:00 interested in autophagy autophagy is a term for a cell essentially cleaning itself out which is typically associated with long fasting yeah that's yeah yeah in fact yes so that is partly why fasting has been so embraced within the F longevity Community it's because if you can promote longevity or autophagy rather if you can promote autophagy the cell keeping itself CLE cleaned out that is thought to be a key contributor to longevity so autophagy equating to
• 75:00 - 75:30 longevity I don't disagree with that I think that probably is a very valid view then the question comes well how can I control autophagy well there is a humble hormone that comes from the pancreas that has a very powerful effect on autophagy called insulin so as much as people are fasting what's the value of fasting in reducing autophagy it's because insulin comes down now what becomes interesting is what happens if you were to put someone allow them to
• 75:30 - 76:00 eat calories but the calories are such that they're insulin is staying low and they're making ketones in other words a ketogenic diet you also enable autophagy there was a very welldone animal study finding that they didn't have to restrict calories and fast the animals they could let the animals eat as much as they wanted but it was a ketogenic diet they lived significantly longer than their other litter mates that were eating the normal high carb Chow similar to what humans eat nowadays and so
• 76:00 - 76:30 autophagy probably does matter for longevity all the more reason to keep your insulin in check because insulin is a powerful inhibitor of autophagy so as much as we have longevity gurus who are taking thousands of dollars worth of supplements I can't help but look at that and think just control your insulin that within every cell there's this battle there's a yin-yang of growth and death or building and breaking to say it a little more politely in fact that is
• 76:30 - 77:00 metabolism the very word metabolism encompasses anabolism which is anabolic or building up and catabolism or catabolic which is breaking down the key to a healthy growing living cell is this nice ongoing balance of build and break build and break you have to build something up and then modestly break it down and then you build some things up again and autophagy is a very important part of that breaking cycle within the cell that hey it's time to get rid of
• 77:00 - 77:30 some old parts and now we'll rebuild some of that again now we're going to break down these parts and rebuild it insulin is the key to that process if insulin stays high for two long you never allow the catabolic or the breakdown this is one reason why insulin is so facilitative to cancer insulin wants things to grow cancer is a disease of growth we don't ever let the cancer start to break down insulin won't L it in part you've um repeatedly talked about ketosis ketones we'll eventually
• 77:30 - 78:00 get there we're kind of teasing the audience a little bit yeah we are yeah but rightly so I mean ketones are a very vilified misunderstood part of the body and to my great Delight um it's getting it's getting a sort of new appreciation well I'm currently on the keto diet as well so I am incredibly interested to understand a like what's going on in my body but be I I'm quite compelled by both the pros and cons of doing it and I want to talk about the cons and the pros um because they both exist one thing you say in your book why we get sick is that
• 78:00 - 78:30 the longest living humans are also the most insulin sensitive yeah so you're telling me that the longest living humans are the ones that are able to Stave off that insulin resistance yes yes so there are keep their insulin levels lower that's right yeah in fact most of the longevity research was sort of a final point on this um is that when you look at these studies that look back in time and say okay what is it about these people what variables tend to go along with the longest lived humans one
• 78:30 - 79:00 of them is that they're insulin sensitive and their blood glucose levels are in fact a very well done study just last year out of Sweden I think it was just one year ago they looked at all and Sweden is meticulous in its in its recordkeeping which is an advantage and and fairly homogeneous society so it kind of eliminates some confounding variables but they attempted to document what the what were the variables that were just the most consistent theme of people who lived very long one of them was good glucose control and this next
• 79:00 - 79:30 one is very controversial because they found that they also the longest lived people had high cholesterol levels and isn't that funny it is one of the most consistent themes of longevity research that the longest lived people have higher cholesterol and yet we live in a world that hates cholesterol and the moment cholesterol goes up we put them on a cholesterol lowering medication we could be doing the perfectly wrong thing to to help these people live longer so that was and and then low uric acid and there's a handful of other little
• 79:30 - 80:00 variables that fit into this sorry they found that some of the longest living humans had high cholesterol levels that's right that's what the Sweden study found for example the paper just published a year or so ago what were some of the most consistent themes they had good glucose control and high cholesterol I'm a great defender of of cholesterol it is a molecule of life and and so many so much depends on on it mitochondria for example mitochondria have to have a cholesterol molecule in them in order to work like
• 80:00 - 80:30 the very Powerhouse of the cell and the more you lower cholesterol through say drug interventions the more you compromise the mitochondria um the sex hormones all sex hormones are built on cholesterol it's no surprise if someone takes a cholesterol lowering medication their sex hormones go down this is why some men experience such terrible loss of libido because he's becoming low testosterone because of the war on cholesterol but there good and bad cholesterol right well that's as The Story Goes yes and yet I think that's
• 80:30 - 81:00 overly simplified um where people will say LDL cholesterol is the bad cholesterol and yet that gets included in these studies of longevity so I I think the good and bad aspect of it is not entirely fair or accurate we need LDL and LDL is just as much a component of the immune system LDL actually helps the body fight infections so it's also an unsung hero of immunity there is research suggesting that in very old age high cholesterol levels do not always correlate with higher
• 81:00 - 81:30 mortality and in some studies may even be linked to longer life exactly which is bizarre yeah well you say that and yet maybe our anti-cholesterol view is the bizarre one yeah 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 why not insulin why are we so obsessed with cholesterol why not triglycerides which is another lipid that can be measured that is far more predictive of who's going to have a
• 81:30 - 82:00 heart attack or not and I think it's because we have chosen markers in modern medicine that we have well-designed drugs so it's a really really good way to sell a lot of drugs so there's no drug that's going to address insulin so let's not measure it but there are lots of drugs that will lower glucose 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 that's a cynical view but I don't think it's unjustified similarly with cholesterol why look at LDL when
• 82:00 - 82:30 triglycerides another lipid marker are a much better indicator it's because we don't have a drug that effectively lowers triglycerides you can with diet but we do have drugs that very effectively lower LDL one thing that really surprised me when I was reading your work is there was a study done in Bulgaria which proved that smoking causes in insulin resistance in humans by having seven healthy nonsmokers smoke four cigarettes
• 82:30 - 83:00 over an hour for 3 days what did they find in that study yeah so they found that if you took healthy non-smoking people and had them start smoking they became insulin resistant I believe I invoked that study in the section where I was talking about inflammation um where when you cigarett smoke that elicits there's a lot of junk coming in and there's a powerful inflammatory response and that contributes to insulin resistance is this vaping as well oh so that is a very good question I have in fact published now multiple papers with a very good
• 83:00 - 83:30 friend and colleague who is a lung expert at my University a guy by the name of Paul Reynolds Paul and I we have published reports together looking at cigarette smoking and the inflamatory and insulin resistance effects that come from that and now we've even started looking at the molecules the hyper heated molecules from vaping and they're they're terrible in fact yes very similar results if you were to take a comparable amount of the chemicals from normal cigarette smoke with its filter versus vaping The
• 83:30 - 84:00 Vaping ones are probably worse chemical for chemical in terms of their insulin yeah in terms of their inflammatory effect the damage to the airway and the insulin resistance that comes from it that's horrifying it is in part because of just how common it's become does smoking make us fat Ah that's a a great question it doesn't because it replaces other interests so if the cigarette smoker ate the way
• 84:00 - 84:30 everyone else was eating it would but because the cigarette smoke satisfies a craving they have less of an interest in food 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 but one of the ways the smoker helps kick the habit of cigarette smoking is actually eating candy like will literally start carrying around little candies in their pocket so that they feel a craving for cigarette smoking they will take out a little
• 84:30 - 85:00 candy open it up and pop it in their mouth and so it's no surprise that very commonly when a person quits smoking they gain significant weight they end up trading out their addictions if you will um 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 there's no evidence of addiction to fats or proteins you published a study in 2024 which found that exposure to De diesel exhaust gas was associated with
• 85:00 - 85:30 increased fat Mass yeah enlarged fat cells insulin resistance and increased levels of inflammation and that was published in the international Journal of molecular Sciences yeah that was one of the studies I just was referring to with regards to my colleague Paul Reynolds Paul and I we that was one of the papers we published looking at these inhaled particulates the reason I was interested in this field of study in the first place was just to continue continue to kill the caloric model of obesity so our and this touches on an
• 85:30 - 86:00 earlier part of the conversation overwhelmingly if you ask someone why do we get fat well because you eat more calories than you burn why do you lose fat because you eat fewer calories and I have long just been frustrated by how naive that view is Yes Energy matters but again the fat cell must be told what to do with the energy that it has that of course points an obvious finger at insulin which is the strongest of all signals but what we found in that study is that even something as seemingly unrelated as diesel exhaust particles
• 86:00 - 86:30 mind you we did not do this study in humans full disclosure we did the study in animals where we could perfectly control how much diesel exhaust they're getting um so we have this mechanism through in Paul's lab where you can aerosolize these particulates and know exactly how much the animal is breathing and then at the end of the study after 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 so what we're breathing in
• 86:30 - 87:00 theoretically could then be determining how fat we're getting yeah yeah in fact yeah this evidence would suggest that it goes beyond Theory so our evidence would state conclusively that yes what you breathe does matter then theoretically we would say well how much does that apply to humans that is where it would get into the realm of theoretical but the evidence certainly suggests yes the very air we breathe matters and you see this at a popul level look in areas where there are now there are confounding variables here here I am invoking correlational research and I
• 87:00 - 87:30 was just criticizing at a moment ago with regards to longevity 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 interesting but but of course that's correlational so it's hard exactly yes thank you for pointing it out and 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
• 87:30 - 88:00 eat eggs because they cause diabetes but when you actually look at the studies you find nothing of the sort what about other sort of environmental toxins and their impact on insulin resistance MH yeah so there are the ones that you inhale a handful of inhaled particulates will matter we have shown in my lab alone with my with my collaborators diesel exhaust will do it cigarette smoke will do it and more we a funded Grant right now to look at the effects of vaping so apparently stuff we breathe will matter to some unknown degree
• 88:00 - 88:30 things that we drink will that are non-caloric so there can be like people have heard of the microplastics microplastics are things that you can they are so small that you drink them and they will absorb through the intestine and get into the bloodstream for reasons that are unknown to me at the moment one of the sites where those micro particles will go is the fat cells and once there they will directly promote the growth of the fat
• 88:30 - 89:00 cells so that's actual microscopic segments of plastic but separate from that are molecules that can come from Plastics and soaps and detergents like BPA or diethyl sbol Dees that's actually an estrogen mimetic kind of what we referred to earlier with regards to other endocrine disruptors but there are other chemicals that a person can drink um or inhale like mentioned earlier but that will directly impact the growth of fat cells or promote to tell mimic what
• 89:00 - 89:30 insulin wanted to do which is tell the fat cell to grow I've invested more than a million pounds into this company Perfect Ted and they're also a sponsor of this podcast I switched over to using matcha as my dominant energy source and that's where perfect Ted comes in they have the matcha powders they have the matcha drinks they have the pods and all of this keeps me focused throughout a very very long recording day no matter what's going on and their team is obsessed with quality which is why they Source their ceremonial grade matcha from Japan so when people say to me that they don't like the taste of matcha I'm guessing
• 89:30 - 90:00 that they haven't tried perfect Ted unlike lowquality matcher that has a bitter grassy taste perfect Ted is smooth and naturally sweet and without knowing it you're probably a perfect head customer already if you're getting your match at places like blank Street or Joe and the juice but now you can make it yourself at home so give it a try and we'll see if you still don't like matcha so here's what I'm going to do I'm going to give you 40% off our mat match if you try it today head to perfect ted.com and use code st40 or if you're in a supermarket you can get it
• 90:00 - 90:30 at tesos or Holland and Barett or in the Netherlands at Albert Hine and those of you in the US you can get it on Amazon as you guys know whoop is one of my show sponsors it's also a company that I have invested in and it's one that you guys asked me about a lot the biggest question I get asked is why I use whoop over other wearable technology options and there is a bunch of reasons but I think it really comes down to the most overlooked yet crucial feature it's noninvasive nature when everything in life seems to be competing for my attention I turn to whoop because it
• 90:30 - 91:00 doesn't have a screen and will armed the CEO who came on this podcast told me the reason that there's no screen because screens equal distraction so when I'm in meetings or I'm at the gym my whoop doesn't demand my attention it's there in the background constantly pulling data and insights from my body that are ready for when I need them if you've been thinking about joining whoop you can head to join. whoop.com CE and try whoop for 30 days risk-free and zero commitment that's join. whoop.com
• 91:00 - 91:30 CEO let me know how you get on so let's talk about ketosis and ketones um the diet the keto diet is becoming increasingly popular from what I've seen it's actually the diet that I'm on at the moment how does that play into everything we've talked about yeah yeah so it it this is an opportunity for me to do a little bit of um B nutrient biochemistry or a little discussion of metabolism so that people appreciate what ketones even are and where they
• 91:30 - 92:00 come from so the the entirety of the human body is a metabolic hybrid in that the body is largely burning fuel from two sources it is burning blood glucose or sugar blood sugar or it's burning fat those are the two main fuels for the body my extension now the brain was an exception the brain is glucose or ketones and but I'll get to where the ketones come from the rest of the body isn't really relying on ketones as much it's fats or glucose or blood sugar
• 92:00 - 92:30 insulin is what decides which fuel is used so as much as the metabolic engine has two fuel sources insulin will decide which one is opened and which one is closed if insulin is high the body is sugar burning and you can measure this in the whole body level by measuring the amount of O uh oxygen and CO2 that the body is producing because different biochemistry or the burning of the fuels will produce a different amount of CO2 so if I'm burning glucose I might be producing more CO2 yes yeah so we could hook you up to something called an indirect calorimeter and measure that
• 92:30 - 93:00 your reer the respiratory exchange ratio the balance between CO2 and oxygen would go higher so we we increase your insulin like if I infused you with insulin in the next few minutes we would see that your reer would go up and we' say boy you're sugar burning or we allow insulin to come down and then the re R goes down which is reflective of fat burning so it's insulin that determines whether the body is sugar burning or fat burning now when insulin has been low for about 16
• 93:00 - 93:30 or so hours something interesting starts happening at the liver 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 but also fat coming from fat cells because if insulin is low the fat cells are just leaking out fat to be burned by the body and because insulin is low the liver keeps burning it and the liver essentially Burns continues to burn so
• 93:30 - 94:00 much fat that it it fills its own needs 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 I'm doing great but it can't stop burning fat because insulin is low and if insulin stays low fat burning keeps going and so because the body doesn't have enough glucose well it's acting yes so in this sense it's doing it to help replace the glucose that isn't coming in that's the value of the Ketone so as the liver is continuing to burn fat it
• 94:00 - 94:30 essentially gets to a point of fat burning where it's burning more fat than it needs and that excess if you will is what becomes ketones so ketones are kind of a metabolic release valve for the liver cell to say I I can't I don't know what to do with all this fat burning okay I know what I'm going to do there's not a lot of glucose coming in and so the brain may start to get hungry so I'm going to start making ketones and so ketones are nothing more than a product of a lot of fat burning and
• 94:30 - 95:00 anyone who even fasts for 24 hours you wake up that next morning you're in some degree of ketosis lest anyone think it's an extreme thing people are going in and out of ketosis ideally often now why do I say ideally it's because ketones are as we've already outlined perhaps the best fuel for the brain the brain thrives on ketones 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 like one example is you ask the
• 95:00 - 95:30 patient with Alzheimer's to draw the face of an analog clock a circle with 1 two through 12 and then some hands on it and it is utter chaos this is published reports you then put them into ketosis ask them can you please draw the face of a clock it's still sloppy but it is absolutely the face of a clock you ask them when they're not in ketosis to try to tie their shoelaces they can't think through the puzzle of tying the shoelaces ask them to do it again when
• 95:30 - 96:00 they're in ketosis all of a sudden they can tie their shoelaces more than that they can get themselves dressed all of these are published case reports it's just my long-winded way of saying the brain thrives when it has ketones as a fuel source but the benefits don't stop there my lab published a report finding that when humans were in ketosis which is just a term term for ketones being elevated we pulled out small pieces of belly fat and measured the metabolic rate of that belly fat and we found that
• 96:00 - 96:30 in ketosis the metabolic rate of that belly fat was three times higher than when the people were not in ketosis what does that mean yeah so that means that the fat was suddenly behaving in a much more energetic way that fat tissue has a very low metabolic rate and then all of a sudden when the ketones came into them they started getting much more active and they started burning more energy which is going to be very helpful for someone who wants to lose fat if your fat cells now have a three times higher
• 96:30 - 97:00 metabolic rate that means that the fat cells are starting to act a little bit more like your muscle cells and they're just burning more energy so does that mean that I'm going to lose fat faster what do that mean absolutely and that is what happens there are very well done controlled studies to show that if you control for all calories when a human is in ketosis their metabolic rate goes up your body your whole body is just burn more um it it's just everything's kind of been turned on a little more the the the the furnace of the metabolism has
• 97:00 - 97:30 just been it's have a little more fuel kind of stoking the fire so ketones will increase metabolic rate of fat tissue we found a paper that we published documenting how we took muscle cells and kind of insulted the muscle cells to determine how tough the muscle cells were when we incubated the muscle cells with ketones they were much more resistant to injury so the the ketones act to protect muscle tissue and in a way that is reflective of a function of ketones ketones are a defender of muscle
• 97:30 - 98:00 ketones are basically the way to tell the brain saying brain you think you need a lot of glucose and if you don't get enough glucose you would start stripping the protein from muscle to turn it into glucose but I'm here as a ketone so you can eat me instead and not and leave the muscle alone so we published again a direct report finding that ketones actually make Muscle more resistant to injury and this could be why you're seeing more and more Elite athletes using ketones as an actual
• 98:00 - 98:30 ergogenic Aid or like a supplement to help them better be better so at my University at BYU just this year our men's and women's cross country team took the national championships the best college runners in the nation pretty impressive one of the things they do is they take these Ketone drinks before they train and before they they race some more and more of the Torrance teams take Ketone supplements because it is just another fuel it is something that
• 98:30 - 99:00 the body can burn that that we always say well if once you start running out of glucose you're going to Bonk or you're going to hit the wall well what if you don't really use glucose because you're burning a lot of fat and a lot of ketones instead and that keeps your glucose kind of untouched or you're not you're not relying on the GL and we see this in humans if there's a human that is adapted to a ketogenic diet they they burn fat at a higher rate than was ever thought humanly possible that that fat is basically fueling all of their muscle
• 99:00 - 99:30 movement during the exercise session rather than relying predominantly on glucose the body has adapted 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 I've seen these keto drinks little they're almost like little shots well there's a bunch of different types if you look at the Spectrum ketones you on one end you have the cheapest most readily available although less effective called Ketone salt where it
• 99:30 - 100:00 takes a molecule of Ketone and binds it to a mineral like calcium or magnesium um not as effective and it's a lot of mineral so people will find that they might get a lot of plaque on their teeth yeah maybe increase risk of kidney stones so comes with some consequences then you have the Ketone Ester which often comes in shots yeah then you have the bioidentical BHB or the bioidentical Ketone one company which is original Ketone um they make it now these ones are more effective you take a little bit of these and you will get an increase in
• 100:00 - 100:30 ketones they're a little more expensive too but as the space is becoming more competitive the price is coming down and what exactly does it do so if I took a shot of bi identical Ketone drink what would go on in my body and how would I how would that impact my cognitive performance or athletic performance yeah yeah so it would result so you're drinking it in you're immediately absorbing it from your gut yeah so if you were not in ketosis let's say you had and I'm not encouraging people to do this you had just eaten two bagels and a
• 100:30 - 101:00 cup of sugary coffee you're no ketones undetectable because insulin has come up it's inhibited Ketone production and then you drink a shot of the Ketone within an hour we would detect your ketones they would have gone up maybe to one Miller which is a pretty significant bump yeah and they're capable of that kind of movement and maybe you do so because you're thinking I really need to be sharp right now would that make me sharper well that's where we have to speculate there's no I my lab published animal evidence suggesting that yes indeed it makes you sharper that we had these animals navigate mazes and
• 101:00 - 101:30 recognize objects and when the animals were on a ketogenic diet they were much sharper they were much quickly much better at solving problems and remembering solutions to previous problems it's one of the I ask this in particular because as my team know because I've said it to them a lot over the last couple of weeks since I've been on the keto diet and I've been literally pricking my finger to check yeah my keto levels and the highest I've gotten to is like 2.5 which is high is it high that's not problematic right I
• 101:30 - 102:00 mean that is just proof positive that you're in ketosis which itself is proof positive that you're burning a lot of fat yeah and three that your insulin levels are low not dropped off my body like I've never seen in my life exactly yeah it's crazy so the power there is like if you'll allow me to kind of springboard off of that comment the power of so so if someone is listening to this and they're thinking okay I need to shrink my fat cells yeah unfortunately they don't realize that there's two variables to what caused their fat cells to grow in the first place they have no awareness of the
• 102:00 - 102:30 value of insulin in this in this um um formula all they do is pay attention to the calories and so the average individual is looking down the road of this fat cell shrinking journey and they're thinking okay what I have to do is just cut my calories and what do they do to cut their calories they do the exact wrong thing and before I even answer that let me just present the scenario let's imagine that step and I everyone listening is invited Steven and I are hosting a buffet we have the world's best chefs it is going to be a
• 102:30 - 103:00 table filled with the most delicious foods you can imagine you're in our invitation we say come hungry because you're going to want to try a little bit of everything everyone listening ask yourselves what would you do to come as hungry as possible you'd probably do two things or think how did you go to your Thanksgiving or your your Christmas dinner as hungry as possible you would eat a little Less in some period of time before the event and you would exercise a little more and it would work you would be very hungry that's why the
• 103:00 - 103:30 traditional advice given for weight loss doesn't work because we tell people eat less exercise more sure you may be lose a little bit of weight in the short term but all that does you've given them the perfect recipe to promote hunger and hunger always wins as a good example uh in the US we have a game show maybe there was some version of this in the UK called The Biggest Loser it was essentially who can lose the most weight and it was through a punishing Regiment of caloric restriction eat less exercise
• 103:30 - 104:00 more that is like the perfect embodiment of that approach they were starving and they were exercising to insane degrees and oh my goodness did they lose a lot of weight and yet you never see them again they don't do a reunion tour 5 years or 10 years later because they gain it all back do do you know they gain it will they do in fact a paper published in the US from the National Institutes of Health doc mented not only the degree to which they gain weight back but also how it almost literally breaks their metabolism that normally a
• 104:00 - 104:30 person's metabolic rate is connected to their body mass a bigger body has a higher metabolic rate a smaller body has a lower metabolic rate this is just human physiology and no surprise when someone loses weight there's less of body and so metabolic rate goes down as they gain weight back metabolic rate will typically go back up as well except for the contestants and The Biggest Loser they started with a high metabolic rate because of a high body fat level they lost a substantial amount of weight no surprise metabolic rate went down
• 104:30 - 105:00 substantially but it this is such a dramatic change that as they started gaining weight back metabolic rate did not come back with it it stayed lower than it should have normally it's connected sort of one to one wherever body weight is going metabolic rate is going except in these people that method of dramatic weight loss through such severe restriction which is based purely on the caloric theory of obesity leads to such it leads to significant hunger
• 105:00 - 105:30 so no surprise if a person's attempting to shrink their fat cells or lose weight if the first step is I'm going to cut my calories and they don't address their High insulin they're never going to lose weight in the long run they're going to step right back to where they were because if they start cutting calories but insulin is still high that's going to make them very hungry because insulin wants to be storing energy a do a professor from Harvard named David Ludwig found this if you have people eating a lower calorie meal that spikes their insulin it makes them much
• 105:30 - 106:00 hungrier than a lower calorie meal that doesn't Spike insulin so that's the key anyone listening if you're thinking I need to be on a fat cell shrinking Journey let the first step of that journey be I'm going to lower my insulin which means which means I'm going to control my carbohydrates I'm going to stop eating carbohydrates that come from bags and boxes with barcodes and while I am restricting those carbohydrates I'm going to focus more on protein and fat
• 106:00 - 106:30 so control carbs prioritize protein and don't fear the fat that comes with those proteins fat and protein together is a a a miraculous combination of helping you feel full and it is literally giving everything you need there are such things as essential proteins there are such things as essential fats so focus on those and that will be the key to helping insulin come down then as you have found you haven't and when you're hungry eat if you're not hungry don't
• 106:30 - 107:00 eat but what the person will find as they're lowering their insulin all while their metabolic rate is going up they're learning how to burn their own fat for fuel because remember the metabolic hybrid that metaphor that if you want to lose fat you need to burn fat you're not going to lose fat if you're always burning glucose it's fat that you need to burn and as you start burning more fat you realize that it's like the hump on a camel that hump exists because it is a big source of fat for that animal to be using its own fat for energy we
• 107:00 - 107:30 have our own version of that so where you think about the average individual who's chubby they have hundreds of thousands of calories waiting to be burned in those fat cells it's just that their chronically elevated insulin is never letting them burn it and so as the person starts making these changes in their diet to lower insulin they now can finally start relying on their own fat for fuel so it's no surprise that their hunger starts to come down let that be the natural way in which you're
• 107:30 - 108:00 controlling your calories don't control your calories because you're forcing yourself to be hungry and eat less control your calories because you simply aren't hungry so I have to I'll overlay this with my own sort of anecdotal experience so I every year do a keto diet for usually for about 8 weeks M this time it's going to go on for a little bit longer um in the reason in part why it's going to go on a little bit longer so I've just learned more about what's going on in my body and also because I podcast now and do a lot of speaking on stage and those kinds of
• 108:00 - 108:30 things I see tremendous variance in my ability for my brain to articulate what I want to say the same way it's like it's absurd yes I I was saying this the other night to the the team that with me here in Los Angeles and I've tried to say it to so many people as someone that can spend nine hours a day trying to think of the next question to ask or trying to remember the research or on stage in front of people trying to deliver a story or a point I get to see variants which I've never been able to explain yeah um where some days I'll go
• 108:30 - 109:00 up on stage I'll be in a podcast and it's like my brain and my mouth aren't connected and then on other days specifically when I started doing ketosis or having a ketogenic diet it just flows yeah it just flows so well and I was saying to my team it feels like I'm looking at the world like this these days like I've got this intense for anyone that can't see me I just stretched my thist focus on the the other thing I've noticed with my diet is I I get hungry
• 109:00 - 109:30 but not like I used to get hungry and then very quickly after I start eating I stop mhm I don't seem to be like doing like these I used to kind of binge a little bit yeah I used to have like a longer eating sessions and my Hunger goes very quickly um I also found that I didn't have these like fluctuating energy levels throughout the day I don't crash anymore I used to get like slumps oh for sure and I don't slump anymore and then the other thing which a lot of people will care mostly about is the the fat so like belly fat I
• 109:30 - 110:00 have never seen anything that has stripped belly fat off me faster and I'm talking in a matter of weeks that I could you know count on one hand yeah than doing the ketogenic diet and if I I could literally show a picture of my scales because I have the digital scales on the screen and it's just trundling along and then there's this Cliff Edge where it goes directly down and it and so much so actually that one of my concerns for the ketogenic diet is how the hell do I keep my muscle oh that's a
• 110:00 - 110:30 great question because my girlfriend 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 but also it was quite clear that my my muscles had got smaller I was lean as but my muscles were smaller yeah so with with with caution this time I did ketosis again and I've been thinking how the do I keep my muscles 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
• 110:30 - 111:00 people 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 now how do you maintain muscle mass in the midst of such obvious weight loss I can only speculate now there are peer-reviewed studies that I can cite which do support the idea that a human can be on autogenic diet and have a total maintenance of muscle and strength that is published so we know it's possible although that isn't that doesn't seem to
• 111:00 - 111:30 be what happened with you I would suspect that there were two things two things happening possibly now I'm speculating here and I'm pretending to be your coach or your expert here one could have been that you had relatively lower energy during your workouts because of a slight degree of dehydration and then the other one would be calories which which I'll come back to in a moment I just wanted to put it out there so when insulin comes down one of the other one of the many effects in the body is that another hormone comes
• 111:30 - 112:00 down called aldosterone which is one we've never invoked yet but low insulin leads to lower aldosterone when aldosterone comes down the kidneys become much uh begin to eliminate salt and water much more rapidly now that's not problematic but it does mean that a person does have to focus more on hydration and salts so if someone's going on this strategy and they exercise fairly often you need to be much more focused on your
• 112:00 - 112:30 hydration literally drinking more because you will be urinating more which is partly why people's blood pressure gets so good so quickly and just to pause on that point there if if someone is on one or two blood pressure medications and they adopt a ketogenic diet 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 so one could be that you were actually working out a little less intensely because of
• 112:30 - 113:00 the dehydration but then two it's possible that you were eating too few calories to actually maintain muscle muscle is a hungry organ it is metabolically expensive for the body to keep that muscle on and as you start to get leaner and leaner it gets harder and harder for the body to defend that muscle in fact that the difference between fasting and starvation the longest known evidence of a fast was a man in the UK who fasted for 384 days
• 113:00 - 113:30 literally not eating or drinking a single calorie he was under medical supervision getting vitamins and minerals and water and he was went to live on went on to live a perfectly healthy life um so but what was the difference why was that not starvation starvation is when you run out of fat 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 if you don't have enough fat to burn to make enough ketones and the brain is saying all right well I wanted
• 113:30 - 114:00 to switch to ketones so that I could spare the glucose but I can't 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 and it sends those amino acids to the liver then the liver is so capable it will turn those Amino acids into glucose so it turns my muscle into glucose to feed the brain so my comment then getting finally getting to my answer is in your version of a
• 114:00 - 114:30 ketogenic diet 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 I wasn't actually doing the blood test at that point I'm doing it this time around but I wasn't doing the blood test so I can actually see my keto levels yeah so maybe I wasn't even in ketosis cuz I wasn't having you might have been but it could have that you were simply not eating enough calories that I have to so this is an instance where that's what I'm trying to do this time I'm trying eat more fat like every time you're making a steak put butter on
• 114:30 - 115:00 there and when you're drinking a cup of coffee as crazy as it sounds I drink yerba mate every morning 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 and so I know because I want to keep my muscle as a guy who's almost 50 um I I find that when during my strict ketogenic phase and I'm currently in it as well every January I go to kind of a carnivore diet to and I mostly do it to one lean down
• 115:00 - 115:30 but also to check any addictions and habits I don't like feeling addicted to things and and my wife will comment and even as an almost 50-year-old it's fun to see my six-pack coming I don't want to lose my mass my muscle mass because you have to work so hard to get it yeah and what I find is if I increase my fat I always get plenty of protein but if I increase my fat content I have an easier time maintaining my bulk are there any downsides of following a ketogenic diet that we need to be aware of the only
• 115:30 - 116:00 downside I can articulate so in fact I didn't even finish because I distracted myself mentioning some of the benefits of ketones but ketones are further anti-inflammatory like they directly reduce inflammation in the body by inhibiting inflammatory processes and they also improve antioxidant defenses so it helps reduce oxidative stress so ketones do have benefits that go beyond beond even what we've taken the time to articulate if there's any negative to a ketogenic diet it could be that you
• 116:00 - 116:30 start you acutely or you temporarily become less metabolically flexible now that's me invoking a term we haven't brought up yet but metabolic flexibility is is a term to refer to the body's ability to when it eats glucose to burn glucose when it's not eating glucose it burns fat so you're shifting between the two metabolic fuels that we outlined earlier when someone has been adhering to a ketogenic diet for some time it's almost as if their body is stuck in fat
• 116:30 - 117:00 burning mode 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 it would take us a very long time to clear that glucose from our blood um much longer than otherwise like let's say we go out with the production team they're eating a normal higher carb diet all things equal same body size same activity their glucose levels would come up and down in 90 minutes for perhaps yours in mine may take 180 minutes to
• 117:00 - 117:30 come back down so the person may say well gosh Stephen and Ben are no longer burning glucose very well and that's true in that one moment um our bodies had almost forgotten what it was like to burn a bunch of glucose because we had adapted to fat burning so what about the gut microbiome oh yeah CU cuz I tell someone who is a nutritionist that I was doing a keto diet at the moment and they said oh you're poor gut ah yes well what a naive um thing to say if I may gently
• 117:30 - 118:00 reprimand your friend there's no evidence to support that there's any harmful change in the microbiome 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 literally zero carb and they documented prely no change in his microbiome none whatsoever but is he eating plants no well he had been eating plants so the case study was a person
• 118:00 - 118:30 eating a normal diet of of plants and meat a normal omnivore diet and a do and then looked at the microbiome and then adapted to a purely carnivorous diet purely meat and the microbiome didn't change at all what's the time period months I think 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 you you you came from the UK to London uh to to to LA to California if we took
• 118:30 - 119:00 a microbiome sample analysis of your time in the UK now it would be different now even though you're eating the same but you're drinking different water you're breathing different air things I was just on a plane from Utah to California give me a day or so I would have some sort of shift in my microbiome so the microbiome can change in resp response to all kinds of things the idea that you somehow have decimated your microbiome because you aren't eating fiber is absolutely false that is that
• 119:00 - 119:30 is completely false now there might be a change in some of the population of your microbiome more of one less of another but there's no evidence to suggest that's problematic your microbiome is intact those bacteria do not die they're just simply metabolizing other things maybe they're relying more on short chain fatty acids maybe they're relying more on amino acids they're not eating as they're not eating fiber but there's still stuff in the meat or the eggs that the microbiome will eat but if if if
• 119:30 - 120:00 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 yeah but but Stephen 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 the case study I just mentioned found that in this one single man it didn't change his microbiome at all it was the exact same populations in all the same proportions because isn't the aren't the plants like feeding the bacteria yeah yeah so the the fiber is
• 120:00 - 120:30 so fiber will but again it's not that's not the only thing bacteria can eat bacteria can eat fats bacteria can eat amino acids they can eat glutamine for example they um they can even meat will have a little bit of glucose in it where the muscle has something called glycogen and so there's you know Trace Amounts of glucose and even the meat that you're eating so I do not look at the argument that you know you're destroying your
• 120:30 - 121:00 microbiome that has no that has no scientific support you may be changing your microbiome but who's to say that's a bad change maybe it's a better change you certainly are feeling better you're thinking better you're getting leaner your insulin sensitivity is improved cognition is improved I would argue if there is a change in your microbiome it's probably one that's for the best and no one can prove that wrong as much as I just stated that comment in a speculative fashion it's speculative because there's no evidence this is why
• 121:00 - 121:30 I look at the microbiome and just say yeah it appears to matter but in ways that we don't know but the the 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 I'm not agreeing to that I don't know if that's true um and again I would cite that one case report I just mentioned now which is the a man who did
• 121:30 - 122:00 this they reported that the microbiome was identical that there was no significant change is that that's just one man there it was one man it was a case report which is not a randomized clinical study so um but even still I with my speculation um heavily handed here I would say probably more plants would result in a more diverse microbiome but I would say but then the
• 122:00 - 122:30 next step is a harder one which is is that good or bad I don't know 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 people dietitians will say well a diverse microbiome is a good microbiome well prove it h how do we know that how can you prove that to me as a basic scientist I want to see the hard evidence because what I can prove is that we can take humans who are
• 122:30 - 123:00 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 and so if someone were to say yeah but sure you reversed your diabetes and your hypertension but you're poor microbiome I would say well I don't care about my microbiome I care about the human 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 I'm and I'm speculating but s
• 123:00 - 123:30 is the person who states that yes I I'm not aware of um research that links the two um but I I could always have a look but um I would I I was always under the assumption that a more diverse microbiome is a healthier person yeah I don't know yeah but but do you do you feel healthier now um feel healthier I certainly feel and it's only been a short amount of time so I don't know what what my health might look like if
• 123:30 - 124:00 I'd done this for like two years right because then there could be a really sort of deeper change to um I know comp for more than two years and they're they're great because some of the some of the changes that occur in our health take time now you you show this a lot in your work with insulin resistance that if you're insulin resistance for 10 years your brain think I read in your work is like it ages it ages by an additional two years is that it accelerates the aging and I wonder the same thing with like my gut microbiome
• 124:00 - 124:30 if I'm if my gut microbiome is not diverse so I have a very sort of um narrow diet or you know I'm not getting not eating my plants could it take me a couple of years to really understand the net negative impact that that has on my overall health it it's entirely possible yeah yeah I would just I would just ask that we be careful with the assumptions that if there is an an increase in diversity with more plant matter that's an if um is that change beneficial are
• 124:30 - 125:00 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 and again the outcome being that perhaps it's just making more gas um you know the more plants you eat the more gas you have to produce by fermenting more fiber what if those bacteria are only existing to just eat the fiber and not actually improve the human host at all so ketosis possible to live in a it's I
• 125:00 - 125:30 think one of the important points on ketosis is when I do my blood keto test I fluctuate wildly after I've gone for a run my Ketone levels are super high sometimes later at night I'm just on the verge of ketosis sometimes um and I think that's interesting because we don't have to live in this necessarily deep state of ketosis the whole time we can fluctuate a little bit and maybe my thought on it is that a person would benefit from some state of ketosis on on
• 125:30 - 126:00 a frequent basis if for no other reason than to really give the brain a heavy dose of just straight energy um not that everyone needs to be as strict as perhaps you and I are being at the moment um 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 like if someone has Type 2 diabetes if they adopt a ketogenic diet they will be off all of their diabetes medications in months all of them um if someone has
• 126:00 - 126:30 epilepsy if there or migraine headaches if some of the from 19 13 I think was the first published report on this if there's someone who suffers from migraines as long as they're in ketosis they may never have another migraine again I mean it is completely Curative or preventative for the disorder same with epilepsy that many forms of epilepsy so depending on the person they would benefit from being in ketosis forever for everyone else who's just sort of a normal individual who wants to be lean and keep their brain healthy and
• 126:30 - 127:00 happy Etc I would say it's generally prudent to just control your carbs be mindful of the type of carbohydrate you're eating and as I said earlier just try to focus on the carbs that don't come from bags and boxes with barcodes I'm actually quite liberal in my view when it comes to whole fruits and vegetables I'd say eat them enjoy them liberally but then ALS make sure you're getting some good protein and fat because there's no such thing as an essential carbohydrate that sounds controversial but humans do not need we
• 127:00 - 127:30 have no requirement for carbohydrate we do have requirement for fat and protein what about artificial sweetness one of the things that I am tempted by when I'm on a ketosis diet is like the soda zeros of the world or the diet sodas of the world what impact does that have on my insulin levels Etc yeah great question question there is such a breadth of of diversity when it comes to sweeteners from artificial to Natural to another rare sugar more and more you
• 127:30 - 128:00 know these 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 effective sugar so on on the good end are things like that have been shown to have no insulin effect and so you know I appreciate everyone listening letting me kind of stay with that as my framework because people are going to go on and criticize all kinds of other things about other sweeteners and that's just too broad that's a topic for a
• 128:00 - 128:30 whole book with regards to just insulin on the good end where they have no effect it would be one as common as aspartame so like diet drinks not the zero drinks but the diet drinks will have aspartame as the sweetener is it a difference there is a difference and I'll get to that other one in a moment so I should be having D instead of zero well I personally go to diet rather than zero um but that's because Aspartame is the so sweetener in the zero in the diet rather and it has no effect on insulin so to
• 128:30 - 129:00 arrol sorry arrol is a little right around Aspartame is generally a good one but monk fruit extract Stevia and especially allulose those are inert when it comes to insulin you know alose Stevia monk fruit extract um aspartame no effect orthol no effect but ariol that ending o is reflective of a class of sweetener called a sugar alcohol and that does not mean it's alcoholic that just refers to
• 129:00 - 129:30 the actual chemical structure that puts it in the alcohol family once you get into the sugar alcohols you start to get a little problematic where ariol is a good one enyl is generally a good one but then you get to things like malol and manitol and they do have an insulin effect and what what's what kind of foods have those yeah so often like you can get manitol in like artificially sweetened chocolate sometimes for reasons that I don't know I don't know why the food formulator puts them in some things and
• 129:30 - 130:00 not other things the the problem I chuckle because it becomes so apparent with some of those artificial sweeteners like the sugar alcohols is that as you eat them you taste it sweet in your mouth and it doesn't have any caloric value in the body because it stays in the intestines uh and this is something that is largely unique to the sugar alcohols where as it stays in the intestines it starts pulling in water from the body which starts to create a fairly
• 130:00 - 130:30 inconvenient degree of flatulence and diarrhea and so a person will know if they've eaten too many of those types of sweeteners because their intestines will tell them so so but also on that Spectrum kind of in the middle is the one that's in the zero drinks which is one called sucrose and while sucrose is generally not a problem with insulin it is a sweetener that has been shown to cross the bloodb brain barrier and so the reason I avoid the zero drinks and
• 130:30 - 131:00 refer or go to the diet drinks is that aspartame does No Such Thing aspartame just gets divided into amino acids we just digest it and absorb amino acids sucralose will go can cross the bloodb brain barrier and I don't know what it's doing there but I don't want it there and so I avoid the zero drinks because I don't want that sweetener but but personally and when I'm adhering to this diet a diet soda is my actual Indulgence where I want something sweet
• 131:00 - 131:30 um and yet I don't want the Metabolic Effect of it one thing you mentioned earlier which I've been thinking a lot about is salt 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 and the doctor said to me that my salt levels were too high and I and then I've heard since then from other people that were actually probably not getting enough salt in our diet yeah so I'm interested to hear that your physician would have said your salt is too high that is very rare that that gets measured sodium I
• 131:30 - 132:00 think you yep they could have measured sodium and that could have been higher they absolutely could have it's just not common so salt has be has earned a terrible reputation because of a series of studies that implicated salt consumption as a cause of high blood pressure and and really briefly as a as a momentary physiology professor that is a real effect if you and I were to go eat salt our body for the next several hours afterwards would retain its water
• 132:00 - 132:30 in order to balance out the salt so that we didn't get too salty so we would retain water in order to keep our salt at a normal level and so that could be reflected by an elevated blood pressure um 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 they may at most move their blood pressure by one or two points it has an absolutely
• 132:30 - 133:00 negligible irrelevant effect um it's because salt is not a key contributor to blood pressure it's actually insulin resistance insulin resistance will force the body to hold on to Salt insulin resistance will force the blood vessels to be very constricted all of which play together to make for a very high blood pressure 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 but with regards to Salt it's interesting for me to note
• 133:00 - 133:30 where did that whole view come from within the United States decades ago there was a study that was published and they called it the DASH diet dietary approaches to stop hypertension Das the DASH diet and in the DASH diet one of the critical change ches was to tell people to eat less salt and when they found that when people adopt a dash diet it's amazing their blood pressure goes down However
• 133:30 - 134:00 unfortunately they also tell people to do lots of other things with the DASH diet 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 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 it's that they were cutting their refined starches and sugars back and it's that that had the main effect and the cutting the salt was just some innocent bystander but to put a fine
• 134:00 - 134:30 point on it in human studies if you have humans cut back their salt considerably they become insulin resistant so take a healthy group of humans say you need to eat less salt and they do so 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 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
• 134:30 - 135:00 and they end up eating less salt and yet their their blood pre their blood pressure gets worse it's because the main contributor to high blood pressure is insulin resistance and by telling them to cut back on their salt you made them more insulin resistant and that whole mechanism is because one of insulin's many many effects is to want the body to hold on to salt in water and so if you start cutting your salt all of a sudden insulin says well there's little salt coming in I need to do what
• 135:00 - 135:30 I can to retain whatever salt we do have and so it starts retaining salt and water more in order to try to offset the lack of salt coming in and while insulin is going higher and higher the body's becoming more and more insulin resistant so salt restriction can cause insulin resistance in humans you talk about four pillars to eating in your book while we get sick you outline these four essential pillars to develop a strategy for maintaining low insulin levels and combating insulin
• 135:30 - 136:00 resistance what are the four pillars yes so when it comes to controlling insulin resistance the key is to manage macronutrients and the best way to manage macronutrients is going to be a strategy that helps lower insulin lowering insulin is the key to both slow insulin resistance and fast insulin resistance so the more the strategy lower insulin the more effective it's going to be and there are poor there are four pillars so the first one control carbohydrates second prioritize protein
• 136:00 - 136:30 third don't fear fat and then fourth after the first three have been taken care of four frequently fast so with the first one very briefly by control carbohydrates I mean that it is time to focus more on whole fruits and vegetables eat them don't drink them and then don't get your your carbohydrates from bags and boxes with barcodes that the more you're opening up a package and getting your chips or your crackers or your cereal or your bread the more you're going to be spiking your glucose
• 136:30 - 137:00 and your insulin keep that on the shelves at the grocery store focus on whole fruits and vegetables that's going to be the key for number one control carbs now while you're eating fewer carbohydrates you need to eat something and so prioritize protein I would say particularly animal Source protein which is the best source of all of the amino acids that humans need and then with those proteins will come fat don't fear that fat that's number three fat is very
• 137:00 - 137:30 satiating when combined with protein when fat and protein come together we digest it better sometimes people will find that if they just have a scoop of whey protein it can be very upsetting on their stomach it's because we're not supposed to eat protein alone in nature that never happens in nature protein always comes with fat that's how we eat it we digest it better and human Studies have shown that when a human eats pure protein there's some degree of muscle growth albeit microscopically minuscule
• 137:30 - 138:00 but when we eat protein with fat we have significantly greater muscle growth than we do with the protein alone so that is the three pillars that Encompass the macronutrients or the big parts of our diet but once a person has done that then they are well positioned to adopt a strategy a structured strategy of fasting and that can be there are as many ways to fast as there are people who want to do it there's no right way or wrong way my goal by invoking that
• 138:00 - 138:30 fourth principle and and I do think it should come last once you've learned how to eat better food your your your body has adapted to burning its own fat for fuel but it can take the it can take uh intermittent fasting where it's one meal of the day you're fasting through um it can do where people do alternate day fasting there are countless different ways to do it even if I'm in ketosis then you don't need to do it as much because you're already lowering your insulin so if a person's already in ketosis in fact if a person were in ketosis and frequently fasting um
• 138:30 - 139:00 depending on how lean they are it's going to become extremely difficult to retain muscle yeah so those are the four pillars it will be an extraordinarily effective way to address insulin resistance but the problem as I started at when I that I mentioned is that while these concepts are simple that does not mean they're easy because humans show addiction addictive Tendencies to only one macronutrient not fats not proteins
• 139:00 - 139:30 all of the evidence of the neurobiology of addiction in humans points to carbohydrates and and so as much as I lay out this simple plan it can be difficult and this is why this self-discipline required is difficult enough that it's why people find that they have to result in you know relying on drugs for these kinds of things physical activity exercise useful for keeping my insulin levels in check yeah yeah I'm
• 139:30 - 140:00 really glad you brought up exercise I'm an enormous advocate of exercise the best exercise to improve insulin sensitivity is the one you'll do and so if someone listening to this is an 80-year-old grandma and um if she if her form of exercise is walking around the street down around the block with her girlfriends but then if someone else has the ability to go cross country skiing or CrossFit do it so the best exercise is the one you'll do now having said that the better exercise is the one that you'll do that keeps
• 140:00 - 140:30 muscle um muscle building work is going to be minute for minute a more effective way of improving insulin sensitivity than than any kind of aerobic activity and that's because muscle is the great consumer of glucose um and back to the in fact not only does muscle eat the most glucose from the blood but it's it's also how it eats the glucose when it's exercising so earlier we talked about how insulin kind of comes and knocks on the door of the muscle cell and then the muscle cell
• 140:30 - 141:00 will open the door and allow the glucose to come in thereby lowering blood glucose unless the muscle is exercising when a muscle is exercising and I'm kind of mimicking the contraction and relaxion relaxation of a muscle when the muscle is exercising it has its own way of opening those doors 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 but I'm so hungry
• 141:00 - 141:30 during this exercise that I'm not going to wait and so the doors just open so the Contracting muscle has its own way to rush to pull the glucose in which means of course that a person's going to have an easier time controlling their blood glucose which in turn would mean a better time controlling insulin but the more muscle a person has the easier it is and this could be one of the reasons why if you look at longevity and look at the markers of
• 141:30 - 142:00 muscle strength versus the markers of cardiovascular aerobic fitness the aerobic fitness markers are terrible predictors of longevity it's muscle and strength that predicts longevity for multiple reasons including just the very Act of living and moving 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 then you're back to these variables that people use to predict or what are the most accurate indicators of longevity it's who has the best glucose
• 142:00 - 142:30 control more muscle helps that happen 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 what's what's your take on that yeah I am unabashedly in favor of carb carbohydrate restriction um I I would say for two reasons um 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
• 142:30 - 143:00 of 70% of all calories consumed globally come from carbohydrates that is the one that has the biggest insulin effect for and that's a problem for all the reasons we've discussed but two carbohydrates are not essential um this is controversial people don't like to acknowledge it but there is literally no biological need that humans have for carbohydrate um the in the United States a report decades ago from the Department of Agriculture looking at the needs of
• 143:00 - 143:30 human nutrition there's a quote there and I'm not going to get it exactly right but I'll get it pretty close it's stated in this document that the lower limit of carbohydrate consumption in humans is zero in other words there is no such thing as an essential carbohydrate 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 you're telling me that we most of what we eat
• 143:30 - 144:00 comes from what we don't need why not put the focus on the things we do need there are such things as essential fatty acids let's eat fat there are such things as essential amino acids 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 why don't we just sack all this off and just take as zek then ah yeah great question so the the I have uh I have kept my finger on the pulse of the whole field
• 144:00 - 144:30 of gut derived hormones which is what we talk about with these weight loss drugs almost since their beginning my dissertation work was in a lab one of the first funded labs to look at these drugs although in the context of diabetes and then it's blossomed into the context in the use of obesity this this is the class of drug GP receptor Agonist first of all what is glp1 gp1 is a hormone that we all make from our guts our small intestine will make glp1 we're
• 144:30 - 145:00 making it all the time to varying degrees some things we eat will result in a higher glp1 sometimes it'll be a lower glp one 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 which means that they'll feel yeah so then the B what so what's the point who cares about glp1 one of glp 1's main effects is to tell
• 145:00 - 145:30 the brain that we're full okay so more glp1 more satiety yeah yeah more gp1 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 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 whether you were lean or obese you had the same amount of glp1 that would suggest that whether you're lean
• 145:30 - 146:00 or obese both of your brains and both of these populations will have the fat and have the same sense of I'm full it would 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 in other words words they would eat the carbohydrate and say I'm full cuz gp1 would tell them so however in the obese group they ate that exact same amount of carbohydrate
• 146:00 - 146:30 and they had an almost negligible glp1 effect they were still hungry 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 and so it is prudent to focus on glp1 glp1 is a powerful hormone that does have an effect on human health what I feel in to comment on is the negative side effects because the only thing we hear about is social media influencers extoling the benefits and hey I'm on this weight loss drug and
• 146:30 - 147:00 I've lost 50 pounds someone has to be the voice that says yeah but what about this and there are some significant but whatabouts when it comes to these um weight loss drugs one of them is the loss of muscle mass or lean mass you've mentioned a couple 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 they found that for every six pounds of fat a person was losing on these drugs they were losing four pounds
• 147:00 - 147:30 of fat-free mass or lean mass so 40% of the weight they were losing uh on these drugs is coming from lean mass like including muscle and bone 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 they're losing lean mass so again they've eroded their bone health yeah so 40% of the weight that
• 147:30 - 148:00 people are losing on these drugs appears to at these high doses is coming from lean mass so fat-free Mass including muscle and bone 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 and now imagine this individual imagine if you will a 60-year-old woman who's been on the drug I take that age and that sex on on purpose because it's
• 148:00 - 148:30 so hard for her to to grow new muscle and bone let's say she's been on this drug for a year and she's lost 20 kilos well 40% of that will have come from her lean mass and 60% of it came from her fat then when she gets off the drug now all of a sudden her lean mass her muscle and bone that's never coming back the muscle and bone that she has lost is gone forever probably at that age because we can't after the age of 60
• 148:30 - 149:00 good luck developing new muscle and bone but what can come back rapidly is the fat mass and so at two years she decides to get off the drug which again about 70% of people do they're going to gain that fat back but they're not going to gain their muscle and bone back that is a significant loss that may be depending on their age gone forever 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
• 149:00 - 149:30 Publications it was yesterday that I saw um this video going viral and I'm going to play this video to you it's from a singer called Avery and she talks about her experience with aenc I just L the doctor's office I went to get a checkup because I've been off of OIC for 2 months now and I just wanted to see if my body was in better condition if there were any permanent damages kind of in shock right now because I wasn't expecting this but um I guess o zumic
• 149:30 - 150:00 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 um but I have significant bone loss I have osteoporosis and um osteopenia so that AR there's like several of them that I have I wasn't expecting that but that's what happens if you um if you use OIC uh for weight loss and
• 150:00 - 150:30 you lose too much weight 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 I mean I've got a picture of her here and she does look incredibly lean already but see this is what people are doing they're basically using it to facilitating eating disorder in the people who are lean um this has become
• 150:30 - 151:00 so common that there are complaints saying that you know lean healthy people are getting the prescription and people who are obese and diabetic aren't because of shortages the more the the leaner I've seen this I know someone personally who is already a perfectly lean healthy woman and then she now looks sickly um 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
• 151:00 - 151:30 your brain you do just stop eating and the malnutrition at least in part is going to cause a loss of lean mass um but that also play 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 it goes up by over 100% and their risk of major depression triples and this so as much as we talk
• 151:30 - 152:00 about these drugs and we say the drug helps you control your cravings What It's hap what it's doing is perhaps reducing your craving for everything that while you are eating less food which is resulting in the weight loss you also are not interested as much in exerc SI as you used to be which is going to make it even easier for you to lose your muscle and bone you're also less interested in Hobbies like going to play pickle ball with your friends or going out and drinking with
• 152:00 - 152:30 the boys um so there is this kind of what's reflected across all of their interests is that their cravings for everything starts to decline on the case of that girl mentioned there 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 Zen oh my gosh I got addicted to his zek and now as a result I have osteoporosis and my bones are as fragile as wafer cookies yeah it's heartbreaking um so now that obviously you know these
• 152:30 - 153:00 are claims that she's alleging now we don't know the full picture of her health and there might be something more yeah but we do know based on that 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 and and I want to mention that um 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
• 153:00 - 153:30 that 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 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 in my mind the best use of these drugs is to help someone learn how to control their carbohydrate addiction because it will
• 153:30 - 154:00 help you control your addiction sweet Cravings goes down significantly within six months of the person taking the drug 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 Fe fat all the more reason prioritize protein and fat to help preserve your muscle and bone muscle and bone are not made of carbohydrate they're made of M of protein and fat eat protein and fat lift
• 154:00 - 154:30 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 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 there is value and learning to deny yourself something you know you
• 154:30 - 155:00 shouldn't be doing there's life lessons to learn there and 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 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 it's worth saying that I I did also search to see if there was a link between a zenek and bone density and
• 155:00 - 155:30 there was no clear Link in the studies that have been done I I don't know whether there's been a lot of studies done but it says in the studies and reviews semaglutide generally shows no harmful effect on bone mineral density although rapid weight loss itself can sometimes affect bone health 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 it's an it's an effect that's happening without being a main effect so I don't believe the glp1 drug is attacking the bone I think it's because the person has just stopped eating and stopped moving remember what
• 155:30 - 156:00 I said earlier people find that they're just less interested in doing stuff like going to the gym for example um 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 one of the things that this podcast has taught me is that liposuction is dangerous do you agree with that statement I do from a metabolic
• 156:00 - 156:30 perspective I absolutely do um liposuction is not dangerous to fit into the clothes you want to wear but it's deeply problematic for metabolic health 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 so let's imagine an individual who has more fat than they want in some particular part of the body the best way to help reduce that fat is to shrink your fat cells so that's very important for people to
• 156:30 - 157:00 realize when you lose weight you're not killing fat cells you're not 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 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 so very healthy small fat cells are healthy fat cells the problem with lipos suction is that you are going in and rather than shrinking the fat cells you are sucking
• 157:00 - 157:30 them out now let's say like a study that was done in the US in women they found that when women had lipos suction from their buttocks and hips area um which is where most women gain their weight which is because of sex hormones telling her body to store that weight there they may look at that fat on their butt and hips and say there's more than I want I'm going to suck it out 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
• 157:30 - 158:00 fat cells but the body wants to store that same amount of fat based on how they're eating 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 but the 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 and so it's no surprise that over the ensuing years after she's had lipos section not only does she not experience any Improvement in any health marker nothing gets better
• 158:00 - 158:30 with regards to her health 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 six kilos and you would say well you have six kilos of less fat clearly you're healthier and yet they're not at all nothing has gotten better and then if you follow them over the years they cannot gain that fat back on their butttocks and hips because it was literally sucked out and adults have a
• 158:30 - 159:00 hard time making new fat cells so it's no surprise that they start storing more fat in an area that wasn't sucked out namely their belly and so a woman who's gone through lipos suction yes she will have lost fat by lipos suction at her butttocks and hips but if she doesn't change her lifestyle habits the body will take those six 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 and so her remaining fat cells that are intact get bigger and store a bigger
• 159:00 - 159:30 burden 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 not only does that result in a dist 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 we have a closing tradition on this podcast where the last guest leaves the last question for the next guest not
• 159:30 - 160:00 knowing who they're leaving it for 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 what a fun question um thank you um probably my wife uh frankly I just adore her I think about so when we were newlyweds uh we got married quite young if you'll allow me to be a little El personal for a moment we both really wanted a family we knew that we wanted
• 160:00 - 160:30 to be uh mom and dad and she really wanted to be an atome mom just full-time mom which I loved I benefited my mother um who died when I was quite young she was a full-time mom and most of my memories come from her being home when I was would come home from lunch or I had a tummy ache and she would come pick me up and I I mean I thank I thank God for my for my mother of course but also for the time I had with her because I had so little um and we both really wanted
• 160:30 - 161:00 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 and it was very daunting very um 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
• 161:00 - 161:30 trust that my beautiful wife had in me and I felt inadequate and I I have moments where I remember young Ben in his early 20s as a newlywed and how scared I was in how my wife's ongoing devotion put us in a position where both make a wonderful amount of money to provide for the family and help secure our future 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
• 161:30 - 162:00 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 so um much of all of it is just this the support of my wife because at any moment if she would have said no I'm done you 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 but she just really believed that okay Ben you're not dumb I didn't marry you for your looks I think
• 162:00 - 162:30 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 Ben thank you my pleasure it's been tree ey 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 Ben thank you my pleasure thank
• 162:30 - 163:00 you 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 into these conversation cards that you can play at home 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
• 163:00 - 163:30 get to watch the person who answered that question we're finally revealing all of the questions and the people that answered the question the brand new version two updated conversation cards are out right now at thecon conversation cards.com they've sold out tce twice instantaneously so if you are interested in getting hold of some limited edition conversation cards I really really recommend acting quickly [Music]
• 163:30 - 164:00 [Music] h