How To BURN BODY FAT, Prevent Disease & REVERSE Insulin Resistance | Ben Bikman & Mark Hyman

my view is don't get your carbohydrates from bags and boxes with barcodes you know of course not just weight issues and diabetes but cancer and dementia and depression and infertility and all these other phenomena okay so let's get into it now we're sick we're let's just face it you know 88 of americans are in poor metabolic health 6 out of 10 americans have a chronic disease it's bankrupting our health care system it's global i could go on and on about the data food is the biggest driver of death around the world period not smoking or anything else and we're dealing with all these diseases that don't seem to be getting better despite advances in medical care we have more and more we're learning more advances in every aspect of science and medicine and yet we're seeing cancer rise heart disease rise dementia rise diabetes rise obesity rise and everybody's struggling with these issues and a whole lot more things like high blood pressure weight gain fatty liver dementia low testosterone sex drive menstrual issues infertility i mean i could go on and on so we're we're down in the weeds treating all these different problems we're treating blood pressure issues we're treating hormones with the pill we're treating trying to treat dementia with a pill which doesn't work we're trying to deal with all these drugs we're doing downstream treatment but we're we're not really getting success in moving the needle in fact we're getting more and more it's like you know being in a sinking boat and bailing the boat instead of putting your finger in the hole or patching it up so what what are all these problems that i mentioned have in common and why is it such a big issue right right yeah i like that you started with one of the more sobering statistics namely the the one found a couple years ago where they noted that 88 of all u.s adults were considered metabolically unfit in fact the authors who published that paper they said an alarmingly low level of metabolic fitness that was that was their words in that scientific manuscript alarmingly low yes yeah yeah and that's sort of to put it mildly right but this uh what too many people will overlook is the fact that uh metabolic fitness or the metabolic syndrome which is how those authors were scrutinizing metabolic health is uh really a function of insulin resistance that all of these this most prevalent disorder that we're sitting on it's this deep foundation in the united states and abroad which is why i've done research at universities outside the u.s but insulin resistance really underpins not only the metabolic syndrome but every disorder you just mentioned where our focus on clinical medicine nowadays has been that we're just pruning branches from this tree and we prune the branch with with some drug and only to have the branch continue to grow back to to grow back and we have to continue to prune it well if we can get to the heart of it or to the root of it then we acknowledge that insulin resistance is a common is a root cause underlying virtually every chronic disease certainly everyone you just mentioned yeah and it's so important because you know if you go to your doctor they're not testing for insulin resistance and i've been doing this for 30 years and i learned about this insulin resistance phenomena decades ago at gerald reevan who was the pioneer in discovering syndrome x or metabolic syndrome i heard him speak and i learned a lot about this and began to understand this and seen in my practice and when you go to the doctor they check your cholesterol they check your blood pressure they check your blood sugar they took all these things but they don't actually check the thing that is at the root of all those problems which is insulin resistance they don't measure insulin they don't measure a glucose tolerance test with insulin and they don't really assess your overall metabolic health because we're not trained to do it and we don't know what to do about it except diet and maybe metformin but yeah it's a you know it's it's just striking to me that this is the central problem facing healthcare right now today and 90 of people who go to the doctor who have this problem it's not diagnosed right why is that yeah why are we like why are we just so dumb about this right right well i i think that there are two reasons one is scientific and one is historic scientifically uh it's been much easier to measure glucose glucose is something that we can measure so easily that we can put a little clamp on a patch and you and i are both familiar with levels and and we can put a little glucose monitor on someone's skin and get a continuous measurement of their insulin or sorry their glucose but we've only been able to measure insulin for a handful of decades and even then the cheapest way to do that is actually using radio like radioactive chemicals and so it's been it's now there are easier and newer ways to do it but there's the scientific hurdle in measuring a very small molecule a hormone but i've been measuring insulin for 30 years and it's not expensive it's been available yep but but my my view is that we've got it all wrong in that we had a we have a glucose-centric view of metabolic health so when we're tracking someone's metabolic health we're obsessed with the glucose because glucose is easier to measure and historically it was the most it was the cause of the most prevalent sign of diabetes which was the polyuria so someone has very high urine production because of the high glucose and you could detect the glucose in the urine and so we can kind of forgive our academic ancestors for thinking that it's all a glucose problem but uh there was an incredible an incredibly compelling paper a number of years ago talking about how one of the earlier scientists physicians who looked who studied diabetes minkowski he they noted that what if minkowski had been agusic or not had its sense of taste and that when he sampled the urine basically when you drink your urine yeah yeah the idea was it was really pretty a kind of a funny idea that the idea had been if these early physician scientists had not been able to detect the glucose in the urine they might have rather noticed the acetone on the breath because of the person have been having such high levels of ketones and rather than calling this a glucose problem they might have called it a fat a fat burning problem yeah and and that would have at least at least that would have gotten uh gotten us one step closer to looking at insulin because insulin of course dictates fuel use so yeah we have a glucose-centric paradigm i think because of scientific precedent and historical view yeah that's less it's unforgivable now it is it's important can we know like it's just that the data is there i actually reminds me of this joke which i often tell my lecturers that you know this guy looking for his keys under the lamp post and his friend comes by so what are you doing i'm looking for my keys he says where'd you lose him well i lost him down the street he says why are you looking over here he says well the light's better over here so the glucose is like where the light is it's easy to check and what what's really fascinating to me was um in a huge aha moment for me in medicine was 25 years ago so i had a patient who looked like an apple i mean she was just a classic giant belly skinny legs skinny arms looked like the tasmanian devil not a very nice thing to say but she was a very sweet woman and i'm like this woman's got problems she's got you know pre-diabetes something something and i'm like checked your blood sugar perfect checked your a1c which is the average blood sugar for six weeks perfect um something's off you know because she had high triglycerides she had low hdl she had a lot of other signs and i'm like this is weird so let me do a glucose tolerance test but also measure insulin because the truth is by the time your blood sugar goes up by the time your a1c goes up you're way down the road of metabolic disaster i mean it's a late stage phenomena to see your blood sugar go up fasting so what i did was this glucose tolerance test but instead of just giving her a test for glucose fasting at one in two hours i did also insulin and this is the key here and this is a test that is i would say almost never done except by functional medicine docs i've been doing it for 30 years on almost everybody i suspect and it's just so informative her blood sugar like fasting was probably 85 90 normal optimal at one in two hours never went over 110 which is amazing great her fasting insulin was like 50 and it should be under five and ideally under two and her one and two hour insulin i mean her one hour it was like 200 and something which is you just rarely see so her insulin was just massively being pumped out from her pancreas to try to keep her blood sugar in control that's what's happening to us so now that we understand that insulin is this driver of all these downstream consequences take us through the landscape of what high levels of insulin do to the body over time and why it ends up causing all these chronic diseases take us down that road yeah yeah yeah so i think mark by now i'm certain your audience would have i almost want it can i take a moment and just explain how i define insulin resistance really briefly sure okay oh yeah let's talk about that let's talk about that well i i have ideas about that well and i suspect i'm certain that our ideas would align but as i have kind of had to fine-tune my thinking to express this to undergraduates i i believe that in my view insulin resistance is a coin with two sides that on one side of the coin there is this phenomenon of altered insulin signaling where the hormone insulin itself isn't acting the same way that it used to at various cells in the body now that's relevant because literally every single cell in the body has insulin receptors or little doorways for insulin to come and knock on in some of those cells insulin isn't working the same way that it used to now in some of the cells insulin's working as well as it ever did but nevertheless that's the altered insulin signaling or the insulin resistance per se at the level of the cell but we're talking about the whole body so when we flip the coin over it's this other aspect that you cannot pull apart from the insulin resistance and that is hyperinsulinemia or the chronically elevated insulin and you just noticed that you'd seen that decades ago so what so one is how the insulin works on the cell and the problems of insulin actually doing its work because the cells are resistant to the effects of insulin and two is super high circulating levels of insulin in the blood dust yep and it's the confluent it's the convergence of those two things that create the insulin resistance that we're talking about and in fact now that's the perfect segue to talk about some of the disorders and you'd mentioned many just for the sake of illustrative purposes let's just kind of highlight too where if uh the liver the liver becomes insulin resistant specifically to what insulin is trying to do to glucose and insulin doesn't tell the liver to take in glucose but it tells the liver what to do with glucose and that's thematic of insulin throughout the body insulin tells the cells what to do with energy because otherwise a cell truly a cell doesn't know you know i grow fat cells in my lab all the time we have little cultured fat cells and we can have those fat cells swimming in a sea of calories glucose and fatty acids galore triglycerides galore but the fat won't know what to do with it the fat cells unless there's insulin the moment we spike in insulin into the culture now the cells know what to do so then they'll start storing the fat turning the glucose into fat which fat cells do absolutely and taking fat in and storing it as a triglyceride stored fat now back to the liver the insulin tells the liver what to do with glucose specifically it tells it to store the glucose now when the inhibit the breakdown of the glucose inhibit the glycogen breakdown and but when the liver becomes insulin resistant even though insulin is high blood glucose levels might even be high in this case but insulin is trying to tell the liver to store glucose but it doesn't get the message because it's insulin resistant now it's pumping out glucose it further amplifying the glucose which is further pushing up the insulin and the whole thing keeps moving now it's like a vicious test that that's exactly right yeah in contrast the ovaries the the fecal cells of the ovaries those are the parts of the cell of the ovary that produce all the sex hormones the estrogens and the androgens testosterone and estradiol for example those cells do not become insulin resistant so now they're swimming in this sea of insulin and insulin normally elicits this inhibitory effect on the ovaries ability to convert androgens into estrogens and you of course know this and your audience i'm sure knows it to a degree but all estrogens were once androgens they come from testosterone and there's this enzyme called aromatase that will mediate that will make this transition it'll take the testosterone and turn it into estrogens well this high level of insulin in the body that is insulin resistant actually is inhibiting aromatase's ability to convert these sex hormones so now her ovaries that are desperately trying to convert testosterone to estrogens can't so her estrogens are too little and she has an abnormal ovulatory cycle leading to polycystic ovary syndrome and her androgens her testosterone levels are too high which is which which is what can give a woman more facial hair or coarse hair acne and even male pattern baldness that's how that works i've always i was wondering how how does insulin resistance cause high testosterone women and low testosterone in men and i think you just explained it yeah well yes so that in fact the interesting thing in men to to make it one step further in men oddly when men's when when a man's fat cells when his subcutaneous fat cells are expanding and this does not happen in women he his fat cells start to express higher and higher levels of aromatase that same enzyme that the woman that has high levels of in her ovaries and so it's almost like his fat cells begin to act like ovaries converting testosterone into into estrogen so so my joke is that with too much sugar and starch in your diet by the time women are 65 and men are 65 they look about the same because the women get hair on their face and lose the hair on their head and men get breasts and lose the hair on their face women because the estrogens are coming down sex hormones tell the body where to store fat and so as her estrogens are coming down to lower levels and her androgens are relatively higher she literally starts storing her fat more where the man is storing it in the belly centrally yep in the belly so that belly fat that that so so how do you know if you have this problem right i mean you can get your insulin checked after a glucose tolerance test or fasting insulin that's really important i encourage everybody to get that checked who has any idea i mean it should be just fasting insulin should be just a part of any any any diagnosis yes that's really good and you mark you were so ahead of your time the fact that you were doing dynamic insulin tests and dynamic glucose challenges that i mean that really is the value to me continue continuous glucose monitors are valuable mostly because it gives you real-time dynamic assessments where you can challenge your body and see all right how long does it take me to get back to normal when i ate that bagel you know that's that's really so illustrative and people once they see it they never forget it but but it's more complex this woman she would have had a glucose monitor and it would be normal so i think there's a huge heterogeneity in this i think you got to watch out for that i i think um so so tell us about the the sort of ways in which the insulin is actually causing the damage so because from my perspective yeah we now know there's a whole downstream set of biological factors yes there's all the diseases we just mentioned we don't talk about those again but what are the actual mechanisms besides for example increasing uh you know the testosterone women lowering testosterone men how how what else happens the visceral fat more storage of fat in the cells what's going on biologically because it's so vast in terms of the mechanisms i want you to sort of dig into that a little bit yeah yeah so uh insulin and the reason i want you to do that is because all the hallmarks of aging almost all the harmonics of aging and chronic disease are driven by this mechanism and if you understand this it's going to help you understand how to eat and live in a way to control your insulin because yeah i i agree right yeah yeah in fact uh not to not to pull this onto a tangent but so much of the focus on longevity nowadays is focusing on a protein within every cell called mtor and everyone is everyone's going on and on about mtor and i think that there's justification to do that now because we see in in various um experimental laboratory models if we like like insects and rodents and if you inhibit mtor the animals live longer that's very very clear evidence now we don't have conclusive evidence in humans that that happens but i am comfortable assuming it's relevant we just can't do that kind of study in humans but i do think mtor is relevant to human longevity and this has had people focusing on protein because amino acids will spike mtor but i think that's unfortunate because while amino acids do spike mtor it'll turn mtor on and then it turns it off pretty quickly insulin increases mtor far more than amino acids do and it keeps it elevated longer and we're spiking insulin literally i mean mark most people as you know are spending every waking moment in the state of elevated insulin insulin has come down overnight because they've been fasting hopefully for 12 or so hours but what do we do around the world not just in the u.s we eat a starchy sugary breakfast insulin spikes and then they're hungry again two hours later they spike it again and again and again and every waking moment is spent in a state of elevated insulin which is activating mtor which is certainly i would believe promoting aging but that chronically elevated insulin also is part of one of the primary drivers of insulin resistance it's in its fundamental of a it's representative of a fundamental biological process where too much of a signal will result in a resistance to that signal so the body is inundated with insulin like the boy who cried wolf yeah that's right yeah yeah and it's that's exactly right in fact i use that i use a joke my wife raises my wife's an at-home mom you know so she's going straight to heaven someday right so she's she's at home with the kids raising the kids and when i'm home with the kids i will notice this interesting dynamic where the kids will be calling out for mom or they'll be fighting or arguing about something or calling out and my wife doesn't hear it she's become death to the kids complaints into their cries for help or whatever it may be and then when i when i'm home because i don't hear it all the time i'm exquisitely sensitive to it they're whining or they're bickering i'm immediately intervening trying to put the fire out and mom she's just kind of deaf to it anyway so so when when we when we appreciate again that insulin resistance is these these two sides of the coin we can almost go top to bottom and start to identify how insulin resistance is contributing directly causing or exacerbating virtually every disease so my lab has recently started focusing more and more on neurological physio neurophysiology and alzheimer's disease and we published a paper earlier this year where we actually had access to post-mortem hippocampus samples so the hippocampus is the part of the brain that's involved in memory and learning that's the part that's presumed to be most compromised in alzheimer's disease and we found in this was in humans that every single gene involved in glucose metabolism was significantly down compared to the in the people who died with alzheimer's disease compared to those who had died without and we compared that with the genes involved in ketone metabolism because those are the two fuels used by the brain glucose and ketones and the ketone metabolism genes were refined and so in the theory in the lab and others have been looking at this too like stephen cunning up in up in quebec up in albert and canada he's a tremendous scientist but we find that the the brain has insulin dependent glucose transporters and so this is part of what's going on in the body so in insulin resistance insulin is high and you noted this perfectly when you described that case earlier high insulin but normal glucose and then the body starts to get so resistant to the insulin that it can't keep the glucose in control anymore than 10 or 20 years later now the glucose levels start to climb and you you express that perfectly so in the brain the same phenomenon can start to happen that even though the brain may be swimming in a sea of glucose the body might be hyperglycemic but insulin has to be working sufficiently to come to the hippocampus the part of the brain knock on the door open the doors for glucose to come in and fuel the brain and that's relevant because the brain has a very high metabolic rate much higher than muscle does and because most people are always eating starchy sugary foods and they're keeping their insulin up they never have any ketones ketones are essentially below the level of detection in most people but the brain is swimming in a sea of glucose but because insulin can't work it can't get enough so the brain's energy needs are right here but now it can't get enough glucose and so you have this energetic gap and that the body just can't meet it just can't fill it up because insulin isn't getting enough glucose in and you'd say well let's just push the ketones in to fill that gap well the person doesn't have any ketones because insulin stops the production of ketones so the brain is swimming in a sea of glucose and starving in the midst of it so that that's how it's insulin resistance is relevant at the brain and maybe we'll just pick one more like blood vessels that's why they call i mean that's why they call now dementia type 3 diabetes that's right that's exactly right yep i actually i like that term in that it evokes this metabolic origin but i would i like the idea of insulin resistance of the brain um just to be eat once again just to be really precise because that is a specific disorder and then to put a visual on it literally as your belly expands your brain shrinks so yeah well that's right small brain small belly big brain better working brain yeah which affects depression alzheimer's many many biological disorders of the brain migraines yep migraine headaches and in fact one of the things that was so interesting for me mark there are there are published manuscripts from the 1930s note from physicians so these are mds noting in their clinic and publishing these case reports where they would take patients with migraine headaches there was two one in the early 30s and one in the late 30s i think or maybe early 40s but they they noted that they would take these patients with frequent migraines and put them onto low carbohydrate diets and fasting regimens to increase their ketones and the migraines went away resolved and this is very common now it's not universal there are different types of migraines of course but it's surprising to me how common it is where you can detect that even in migraine just like it is an alzheimer's disease there's this phenomenon referred to as brain glucose hypometabolism essentially the brain cannot metabolize glucose sufficient to meet its energetic needs and so you just start making some ketones and you fill in that gap it's really extraordinary we're going to talk more about how ketogenic diets and other dietary approaches can actually influence things like autism and alzheimer's and and uh and even even uh you know other neurologic disorders that we're seeing and how that works but i i want to sort of get into this study that you did with my friend david ludwig uh which was from harvard where you look at the metabolic rate from fat samples from belly fat and found that the low carb diets had a much higher increase in the metabolic rate in the fat tissue compared to the people eating high carb diets in other words if you eat a high fat diet your metabolism is faster if you eat a high carb diet your metabolism is slower how does that work what happened what was the study yeah yeah yeah so mark just people was like i have a slow metabolism you know like well yeah okay maybe they're right you know maybe they're right and how is it working yeah i just have to mention this because it's such a fascinating history so when david and i started collaborating on this it was in response to some other studies that we've been doing in my lab looking at the differential effects of insulin and ketones on fat metabolic rate fat cell metabolic rate but that whole study that whole study was born from studies in the early 1900s so just as a brief history because i know your audience is going to find this fascinating at least i hope my students sure do so i'm sure they will sure sure bring it on so this is two two early scientists um elliot joslin who is considered the godfather of endocrinology and francis benedict francis benedict really considered the godfather of metabolic rate the harrison equation yes i remember that from medical school and the jocelyn diabetes center at harvard yes absolutely that's right yes that's how well known both of these characters are and they were legends and they noted working together in the early 1900s that people with type 1 diabetes they didn't call it type 1 it was just diabetes people with diabetes had a metabolic rate that was about 20 percent higher than it was supposed to be because metabolic rate is connected to body weight essentially a bigger body has a higher metabolic rate a smaller body has a lower metabolism yes and what they found in these people metabolic rate was much higher than it was supposed to be and then decades later um this is well into the 20th century now like late 20th century um then other scientists found the same phenomenon these were studies done at the university of minnesota that meant that people with untreated type 1 diabetes and because this was before when when joslin and benedict were doing this there was no insulin yet no not discovered not used right and then decades later scientists confirmed those original findings that metabolic rate was significantly higher in type 1 diabetes higher than it was supposed to be and when they gave the people insulin to control the diabetes their metabolic rate went immediately down to normal it dropped that excess 20 went right to where you predicted it should be and so insulin so that study that as my students and i were noting this and fascinated by it we thought well let's start looking at what happens in the fat cell in these in these conditions and so sure enough we found in in fat cell cultures and in animals when we artificially increase the insulin we could take the brown fat cells so brown all all people have brown fat and white fat and white fat is the the prototypical storage fat what we pinch and jiggle and it has a very very low metabolic rate i'm very very low i don't jiggle i'm sorry i don't jiggle yeah don't jiggle yeah i'm i i won't go for jiggling yeah i got a little bit of pinch but that's it yeah but so so those are the people that metabolic if you jiggle you're in trouble that's that's what he's saying guys if you jiggle that's the problem that's that's you know i call it the i call it the mirror test for diagnosing if you have this problem you stand in the mirror with your shirt off you jump up in town if you jiggle you have this problem yeah yeah well said yeah that's called the jiggle test we got the jiggle test [Laughter] so we have that white fat with a very low metabolic rate then all people to some degree have what's called brown fat and that's typically up around this kind of a chest area and that has a very high metabolic rate as high as as high as muscle does so like 10 times higher than the white fat does well we found that when we already fish when we artificially push the insulin up the brown fat metabolic rate was depressed it went much dropped to a level that was quite close to the white metabolic rate in contrast when we increased ketones then we took the white high fat diet yeah like on a ketogenic diet or in the lab cultures it was just actually treating the fat cells with ketones it's in general and that metabolic that's exactly right and that metabolic rate went up about 10 times almost to the level about of the brown fat then in humans this is where the study comes in with david now these are unpublished data so so everyone know please these have not been formally peer reviewed and published it's in review first here folks yeah that's right yep hot hot before it's even hot off the park exactly yeah so in the printer so what david did they had access to this population of people that they'd taken a fat biopsy from the belly um at day zero and then followed it up several weeks later about anywhere between i think 12 to 15 weeks after being on three diets right humans not humans yeah that's exactly right this was something that was so important because me at a phd at a primarily undergraduate university it's difficult to do this we've done fat biopsies beforehand you're like a doctor but you're a mouse doctor yeah that's right yep i can tell you what's happening in the cells much better than i can listen to someone's heartbeat so tell us i'm so excited i'm on the edge of my see what happened i want to interrupt you so these three three groups people put on three different diets they all had the same amount of same amount of protein and same amount of calories so the caloric level between all three diets was the same so protein was clamped and then all it did was differ in the ratio of fat to carb and we found that the group that had the highest carb diet had no change in their metabolic rate on their fat cells specifically however the groups that were the low the two other groups that had the lower carbohydrate higher fat they had significant increases in their fat cell metabolic rate now this coincides what are you talking about give us the ratios is it like what's the amount of fat amount of carbs yeah yeah so david would confirm so i think i think the the moderate group was for uh about 40 carb and then the other group was 20 carb or or so i think it was right so the low carb was 20 it wasn't like ridiculously low like less than 5 grams of carbs or 50 grams a day it was that's right really it was really actually doable oh oh i would absolutely say that it's very doable that's exactly what it was it wasn't a ketogenic diet it was actually a just a lower start sugar diet yep yep that's right yep and sure enough the metabolic rate went up about two or three times in these people from the same person from their fat tissue from the same area in their body so it just goes to show that as much as folks what that means folks by the way what that focus means is if you're sitting watching netflix you're burning two three times more calories that's what that means yeah right yeah that's right yeah if you have any i would say if you're living a life where your insulin is low and there's some hint of ketones coming up then you absolutely are experiencing a higher than normal metabolic rate and this is so important because in my mind it starts to represent this convergence of what has been viewed as these two opposing ideas of human obesity on one hand we have the pure caloric thermodynamic enthusiasts that obesity is purely a matter of calories and calories out and anything else be damned on the other hand to sort of straw man each of these we have this idea that no it's purely a matter of insulin that it's purely a matter of hormones and and then the energy component is less relevant in my view the two actually go ahead and for sure that we have to account for energy of course we have to but we have to account for it through the lens of human biology we are not these perfect little thermodynamic machines we are complex biological organisms and hormones tell the body what to do with energy and when insulin is low we have these advantages one we have an actually elevated metabolic rate this has been shown in in david ludwig's group multiple times through multiple different tests and even some of his detractors have shown the same thing others have found this where when a person is it has low insulin elevated ketones their metabolic rate is higher so one metabolic rate is high so the caloric output is higher but two also if someone has low insulin then they're making ketones as we know did and when ketones are elevated the person is literally excreting ketones from their body they're breathing ketones out they're urinating ketones out and every single ketone has the caloric value comparable to a molecule of glucose so we are actually taking energetic molecules and then just dumping them from our bodies so these are calories that didn't have to be burned it didn't have to be you know stored or or burned you know eat less and you breathe them in your mouth yeah and you breathe them out because that's what ketones are imagine a long kind of string and a ketone is when we basically cut that string into pieces that's what's happening when we're burning fat we're taking a big long carbon molecule pulling off two little carbons at a time if someone is making ketones it's literally those little pieces of fat that we're splitting apart that is what a ketone is and so the person is literally breathing out these byproducts of fat burning or urinating these byproducts of fat burning that's seen really incredible you know we we now are really understanding this and what what i've seen in other studies that david has done for example this was a mouse study so i i don't like animal studies but sometimes we have to do them in medicine yeah what they did was fascinating they took these mice identical and they gave one group a very high carb low a fat diet and another a low carb high fat diet and they give them identical calories and then what happened was in the group like you're saying with the low carb high fat they started losing too much weight so they wanted to keep the weight of the animals the same so they actually had to increase the calories on the low-fat group and then at the end of the study they harvested these animals and the low-fat group that was having more calories didn't have the problems that the high carb group had which is all this belly fat inflammation poor metabolic function it was fascinating to me and and you know the other thing that's surpassing about this and i had dinner with david once he said mark you know if you look at type 1 diabetics what happens to them right they lose weight because they can't get the fuel into the cells because they have no insulin because their pancreas is basically demolished by an autoimmune disease yep and they literally come in with the classic symptom we learned in medical school which is polyphagia which means you eat and eat and eat and eat so they literally can eat 10 000 calories a day or a hundred thousand calories a day and lose weight and they're strong yep and right and and it's an exact example of this phenomena in an extreme situation where if your insulin is low it's very hard to gain weight and it's easy to lose weight and i think a lot of the keys to understanding our metabolism and by the way there are a lot of factors that drive obesity and we're just focusing on i think the biggest one but toxins play a role other hormones play a role the microbiome plays a role uh inflammation from various insults plays a role so it's not just this but i would say it's the predominant mechanism for obesity in america and i would add in type 1 diabetes like you mentioned this phenomenon is so known by type 1 diabetics that that insulin is controlling their fat growth that you have this disorder nowadays called diabolia where you have type 1 diabetics wow yep these type 1 diabetics are deliberately under dosing insulin in order to stay thin so they learn early on and imagine how tempting it is you have a young teenage usually a girl certainly who has they have more pressure than boys do but even still a young teenager who's very self-conscious of their growing bodies and they've learned i mean imagine the temptation they've learned they can eat anything they want they can eat that cake they can eat those brownies those cookies whatever that soda and they don't have to go vomit they don't have to go have go through the discomfort of throwing up all they have to do is not poke themselves with the needle and they can stop their blood sugar oh it's catastrophic they're in ketosis their glucose is 800 milligrams so they're dying they look great yeah but that's just a testament that's just the proof of how powerful insulin is in controlling this where you have type 1 diabetics who deliberately underdose insulin because they know they can eat whatever they want and they'll stay as thin as they want well what you're talking about also explains the phenomena of why ketogenic diets reverse type 2 diabetes better than any other treatment and why people who do time restricted eating and give themselves 12 14 16 hours between dinner and breakfast actually are more effective at losing weight or why people who are in calorie restriction which also does the same thing like the fasting mimicking diets also does the same thing so we are seeing from the science emerging that the key if you can keep your insulin low is that it helps to release everything and from my experience as a doctor the thing that insulin does is just catastrophic one you know it drives all the fuel into the fat cells and whether it's fats or sugars two it locks them in there it prevents them from getting out three it it turns these fat cells in your stomach into catastrophic hormone and cytokine producing machines that dysregulate your biology increasing inflammation for example why is covid ravaging the obese because their fat cells are making il-6 or interleukin-6 which is a powerful cytokine inflammatory molecule we call the cytokine storm that is what's driving all these problems and in addition it changes your hormones as you mentioned with estrogen tendonosterone it also changes your brain chemistry and makes you hungrier and it creates a catastrophic effect on your cholesterol on your blood pressure it drives oxidative stress inflammation increases your blood clotting it increases uric acid levels it causes a whole series of downstream effects that causes fatty liver it starts to affect your kidneys and increase protein in your urine so you get these massive effects that are explaining all the underlying biology of aging and and so the take home message from what you're saying in your research and david's research is that if you keep your insulin low by various mechanisms right diet exercise stress reduction i mean if you're stressed your your blood sugar is going to shoot up meditate to lose weight is that my that's my new slogan right so so this is really that's good the biggest pen pandemic to actually face humanity uh ever uh we're talking about kobe being a problem but i mean gosh you know three quarters of the deaths that globally which is you know i think it's like 60 70 million a year i mean are are actually are caused by uh some level of this poor metabolic health and and it's it's driving you know of course not just weight issues and diabetes but cancer and dementia and depression and infertility and all these other phenomena so your research is so important to help us kind of tease apart these mechanisms um and and the question i would have for you is is is you know for people listening how do we start to think about uh changing because not everybody wants to go on a ketogenic diet nor is it advisable or is it a good uh even though by the way you mentioned jocelyn the way they treated type 1 diabetics was a 75 fat diet 20 protein and 5 carbohydrates and by the way it was kept alive but it also by the way was the the way that uh we discovered america was through borrowing the native americans super food packet which was called pemmican which was made up of yeah basically rendered fat from bison um you know a few berries and the protein and literally a man needed a pound a day and a woman needed a half a pound a day and so if you had 30 pounds of stuff in your backpack you could basically eat for a month and survive yeah yeah it's there's no question that uh you and i of course are aligned when it comes to having a favorable view of fat and mark with i like what you were saying a moment ago where and you're being careful in your language of course as a scientist i appreciate precision um you and i we're not claiming that insulin resistance is the cause of every disorder but there's little doubt that it is a key contributor it is causing many chronic disorders and it's contributing to virtually every other one so my my view one of the things i hope people take away from this discussion is i can imagine someone who's opening their medicine cabinet not that either of us is giving any medical advice here but they're looking at their medications and they see their medication for their diabetes or one or two or three medications for their diabetes they may have a medication for their migraines a medication for their fertility disorder and their blood pressure little knowing that all of those have do have a common connection with insulin resistance and when it comes to controlling insulin resistance you are absolutely right there are multiple inputs into this i consider there are various ones and i i've looked at them and consider kind of various levels of them and to me there are three primary causes of insulin resistance and by primary i mean that literally i can cause insulin resistance in isolated cells in laboratory eroded and in humans with all three of these and that is elevated insulin itself elevated stressed hormones and elevated inflammatory proteins or cytokines all three of those things are considered primary in my definition because you can just make insulin resistance happen at the cell in the rodents and in humans all three biomedical models but in as you were kind of alluding to if we were to tell someone all right here but there are others like you said like noxious toxins that can accumulate in fat cells and alter fat cell growth absolutely that is relevant um so i'm not suggesting that there aren't others there are but i kind of put these ones as the kind of holy trinity or the unholy trinity of insulin resistance but we would tell someone control your stress and they would say well great doc how am i going to do that you know it's a little difficult stress is one of those difficult things to truly wrap your head around but you can still you'd mention like meditation and quiet i hope wholly agree with that um but even still it's a little difficult to fully manage stress same with inflammation we would say lower your inflammation and say well how do i do that you know we'd have to find out what's the what are the stimuli that are inducing that increase in that immune level but if we say control your insulin easy easy that is a lever we can grab with both hands and immediately start to pull down just through time restricted eating and intermittent fasting and by just managing macronutrients and altering that ratio you know focusing more on the foods that have the lower effect on insulin like in the fat and protein and controlling the starchiest of the carbohydrates or the most sugary now neither you nor i are declaring war on carbohydrates and i'd hate for someone to leave this talk leave this discussion thinking we are we're not you know neither of us is advocating a carnivore diet but we are certainly my view is don't get your carbohydrates from bags and boxes with barcodes yeah i love alliteration so i'm glad you appreciate it bags and boxes and barcodes right good yep but that's where people get it wrong right there they're they're thinking i need to they have a back a box of crackers or a bag of chips or a box of cereal no go eat fruits and vegetables eat them i'm i'm an advocate of fruits and vegetables eat them but don't drink them and don't get them in processed foods yeah bags boxes my joke is i always say carbohydrates are the single most important food for health and longevity right and what i mean by that is that plants are carbohydrates broccoli is a carbohydrate you know asparagus is a carbohydrate those are the ones you want to eat not the ones that come from a factory or or from uh you know some processed ingredients that you're mentioning bags and boxes barcodes barcodes yeah you want to know my secrets for living a long and happy and healthy life well all you have to do is check out my weekly newsletter mark's picks where i share my favorite tips for health longevity well-being and lots more check it out and link below what i i'd like to sort of go into now is understanding of some of the challenges and controversies around fat uh i wrote a book called the fact get then where we talked about this but you know there's still a sense that your cholesterol is a big problem the saturated fat is the devil and that we should not be eating it um butter cream coconut oil uh animal food saturated fat um talk to us about the biology of what happens when we increase fat and why why it doesn't work in the same way we think and also if you can speak to the heterogeneity in the population because there's subsets of people who do great with high saturated fat diets and those who don't and i'm just going to give you a quick scenario of that and and then you can kind of riff on how we start to think about it i had a woman about you know late late 40s uh woman who was struggling with her weight inflamed trying to do good she exercised she ate pretty healthy she wasn't you know off the rails with her eating and her triglycerides were 3-400 or cholesterol was 300 or hdl was like 30 i mean which is terrible numbers you know which is classic of pre-diabetes and some resistance um and i said look you know you've tried a lot of things let's just try a ketogenic diet and see what happens you know no harm no foul she did it and it was remarkable her not only did she lose 20 pounds like that but her level of inflammation came down her triglycerides dropped to 300 points her hdl went up 30 points which you never see her total cholesterol dropped 100 points by eating butter and coconut oil yeah and yet another another guy was a very thin fit mid-50s guy who was a really aggressive bicycle rider he rode 30 50 miles a day and he decided he wanted to try it for performance reasons not to lose weight and his numbers went completely the opposite he got very high levels of cholesterol very high levels of small particles it just it was just remarkable to see the difference and i it sort of woke me up to the fact that there isn't a one spice size fits all regards to this so with that framework take us down understanding of you know if we are going to be reducing our carbohydrate starchy sugary carbohydrates and we're going to be increasing our fats how do we do that and what's the role of saturated fat and should we be worried and how does it work yeah yeah the great question so my postdoctoral work um really was seminal in that it scrutinized the degree to which fatty acids themselves can contribute to insulin resistance and this is a conversation that i'm passionate about because so many people start beating this drum of saturated fats and use it as evidence against animal products because animal products do contain saturated fats invariably now they're never completely saturated fat and that's important there's a mix of saturated mono and polyunsaturated fats and now what these by the way all saturated fats aren't the same there's like 10 or 12 different saturated fats so they're not like oh my gosh yeah yeah oh there's there's there's dozens of them yeah that's right yes so set i'm a huge advocate of of a full spectrum of fats namely of saturated fats even long chain which we get a lot of medium chain and then short chain but um putting that to the side um there it when you incubate a cell if you have a cell culture whether it is muscle cells liver cells neurons um fat cells and if you incubate those fat cells with palmitic acid which is the prevalent saturated fat in the human body certainly in circulation palmitate or the 16 carbon saturated fat when you incubate cells with palmitate um they or stearic acid even 18 um 18 carbons they will become insulin resistant um and so you treat them with the fats then you put on some insulin a little later and then measure then you take all the cells and measure what insulin did and it is compromised that doesn't happen when you incubate the cells with monounsaturated or polyunsaturated fats that it will not cause direct cellular insulin resistance so so i've done these studies myself maybe the most cited study of mine i've ever done was this exact um series of studies so and the same thing happens in rodents when you infuse the rodent with fat when you're infusing it directly iv the saturated fat will cause insulin resistance but the monounsaturated like olive oil for example doesn't so there is a direct effect of saturated fats at the cell to cause insulin resistance and this is all once you actually get into the cell itself it's because of how these fats will induce the accumulation of another molecule called ceramides and if anyone has ever heard ceramides in the audience they might be thinking of it as like in lotions or shampoos and stuff but but it is a slightly different version of it but saturated fats will induce the accumulation of these molecules called ceramides within a cell then ceramides will directly prevent insulin the insulin biochemical pathway from doing its job it directly antagonizes what insulin is trying to do so that's the actual where the rubber meets the road molecular mediator so now to zoom back out to the level of the whole body some people look at those studies even possibly my own and will use that as evidence against saturated fat and they will say see saturated fat causes insulin resistance but it doesn't work when you actually go to the whole body and look at the consumption of fat this is the paradox is the vast majority overwhelming majority of saturated fat in our blood is palmitate but it's not from the diet it comes from the liver the liver is the primary source of saturated fats that are circulating in the blood that when you eat saturated fats they're packaged into the chylomicron and there can be some depositing of that throughout the body but it goes to the liver and then the liver will repackage all that fat and almost always the short the saturated fats will have two things happen to them they get elongated by two carbons so you'll take that 16 carbon palmitic which is the most prevalent saturated fat we take that 60 carbon we make it into an 18 carbon and then we desaturate it there's these two steps and so we end up taking the palmitate in the diet and turning it into oleic acid or the primary olive oil olive oil and that is the primary fat that is stored in every single person's fat cells so basically so basically your liver makes olive oil no no no so the fat cells turn it into olive oil but the liver makes palmitate yeah yes so when we eat saturated fats the body will turn it into olive oil basically but when the liver is making fat it makes saturated fats and so that this is why you can take someone and put them on a ketogenic diet low carb high fat and they could be eating three times more saturated fat than they were before than the other group than the than the low fat high carb group three times more saturated fat and yet the actual composition of fatty acids in their lipoproteins in their blood is much less saturated so the actual amount of saturated fat circulating in their blood is much lower than it is if someone is eating a diet that is spiking their insulin because most of the saturated fat in the blood which is what's coming to the cells throughout the body um you know the phenomenon that i mentioned a moment ago most of that saturated fat is coming from the liver and the liver makes saturated fat when insulin is up this is a process called lipogenesis and palmitate lipogenesis yep lipogenesis yep and insulin is what turns that on and that's the paradox here really to put a kind of point turns on insulin starchy refined carbs yeah yes sugar and starch right okay so what you're saying is that if you eat saturated fat in your diet from animal protein or dairy or coconut oil it gets turned into olive oil in your fat cells that's right if you actually eat sugar and starch it turns on the fat production factory in your liver to make saturated fat yes so you makes it's saturated fat that's coming from eating sugar people don't get this connection they think oh sugar sugar how does it turn to fat but there's a mechanism by which these sugars cause the production of saturated fat in your blood which is what's causing a lot of the problem yeah it's a one-two punch absolutely it's a it ends up being a one-two punch where these these starchy sugary carbs will both act as the skeleton you know the liver will take those carbons and rearrange them to create a saturated fat and at the same time the starchy sugary carbs are increasing insulin which is what's which is what's driving the signal that's the signal to tell the liver to do that in the first place because the liver will not make fat out of carbs unless insulin is elevated it is antithetical it is impossible for the liver to do because like every cell in the body insulin tells the liver what to do with the energy that it has available and when insulin is up one of the things it wants the liver to do is turn the carbs into turn the glucose those carbons into fat and the only fat delivers making and packaging and releasing is palmitate that saturated fat that's incredible so uh i wanna i wanna drill down a little bit into the the take homes and i just i sort of want to recap a little bit and then i want to ask you what what we can do to fix this because it seems to me that what you're saying is that this whole host of chronic diseases is is driven by or affected by this phenomena of insulin resistance and it's the biggest scourge causing 88 of americans to have poor metabolic health the second is 90 of people and 90 of people with covid to have it so bad they have to go to the hospital that's right that's right and the second thing is that we we understand that the way in which insulin resistance is controlled is through primarily diet and and i want to go through a few of the other factors too but primarily diet and it's primarily the starch in our sugar which is enormous in this country it's 60 70 percent of our diet it's usually in the form of flour and hidden sugars in our diet are added sugars about 152 pounds of sugar and 133 pounds of flour uh recently according to usda data you know that's almost a pound a day of sugar and flour per person per day it's stagger it's staggering which our human biology never never was exposed to right we see 22 teaspoons a year if we found some berries or honey now it's 22 teaspoons per day for the average adult and about 35 for a kid and and three that by changing the quality of our diet in other words reducing starchy refined carbs and increasing good fats or maybe even saturated fat we can actually stop this process which is underlying everything that goes wrong with us at least aging and that um and that there's some heterogeneity in the population but we need to figure out one how to diagnose it i want to talk about that two then how to treat it because if we understand this is the problem you know one what do what do people listening need to do to find out if they have this problem let's start there yeah yeah well i decided from the mirror jiggle test the jiggle test yeah yeah yeah well i will i will try not to be too redundant to what you said but i would say anyone who has any potential get your insulin measured and you'd mention some wonderful metrics i've always said below six i think you said below five um i think that's a brilliant way to do it now at the same time insulin like every hormone has a bit of a rhythm to it there's a diurnal or circadian rhythm so it's possible someone would go get their insulin checked and maybe it's it's 12 or 13 or so and you and i both would say oh that's a little high we need to be a little worried but it it's possible the person has measured it at a peak and that in reality that give it an hour or two later and it would have gone down to five it's possible so i think it is important to note that there are other things like challenging it in a dynamic glucose test like you'd mentioned that is absolute gold standard alternatively and another metric you mentioned is looking at lipids because insulin controls the production of fats and the regulation of lipoproteins in the body because lipoproteins are energetic molecules and so look at the triglyceride to hdl ratio and if a person has a triglyceride to hdl ratio and it's above 1.5 that's strong evidence that they're insulin resistant now that ratio doesn't hold across all ethnicities it starts to get a little loose you know from caucasians to asians to african americans or so but nevertheless that ratio of 1.5 is generally going to be a pretty good indicator that if you're lower than that if your triglyceride hdl ratio is lower that's a good sign that you're insulin sensitive um the good old-fashioned waist to hip ratio or the waist to height ratio if you measure your waist like the biggest part around your belly and if you multiply that by two if that number is higher than your height that's a very very good indicator that you have metabolic syndrome or insulin resistance to be more precise if your waist circumference times two is less than your height that's a good sign that you're generally doing okay and then one other metric among many is what's on the skin and there are two things people can look for on their skin which are it's almost proof positive of insulin resistance the first one is skin tags those are these little kind of mushroom like or columns little stalks of skin they're not like a flat kind of round mold they just sort of jut right up and they're small i bet everyone already knows what i'm talking about people can get them in their armpits or around their neck if they have a fat fold around their neck so those are skin tags and at the same in the same place especially around the neck or the armpits anywhere where skin is rubbing they can start to develop something called acanthosis nigricans or these patches of skin that are a little darker pigment and they have a kind of altered texture kind of this velvety kind of texture to it um but but that's another another one so the the skin i kind of joke the skin is the window to the metabolic soul just because like every part of the body it responds to insulin and so we start to see these little hints of it so that's really helpful you know i wrote a little description of how to look at this in great detail um called how to work with your doctor to get what you need it's available on my website dr hyman.com it's also available i think online you can just google it and i go through all the diagnostic tests to help you identify the ways in which either you have insulin resistance or the consequences of it and the things that i tend to recommend people do is like you said a fasting insulin is super important the best test is is because the fasting insulin elevation is really the second stage of the problem the first stage is elevations of insulin after you consume a sugar drink so that that's a little bit more of a pain in the ass test where you have to drink a sugar drink it's one of two coca-colas and then get your blood tested either 30 minutes after and or or one and two hours after as well as fasting uh that's really important the lipid test you mentioned are super important i'm gonna just drill down a little bit on that because there's something called an nmr or a cardio iq test from lab core quest which looked at not just the total numbers of like the weight of cholesterol which is your milligrams per deciliter it looks at the particle number and the particle size which is really important and so when you have instant resistance you have a perfectly normal cholesterol of 200 or 150 but your triglycerides may be 300 your hdl is 30. you're not so your cholesterol is fine your ldl is fine it may not be because you may actually have really dangerous small particles also we look at you know like the triglyceride hdl ratio is very important it's something not really paid attention to much by doctors but it's more more predictive than an ldl elevation more predictive the most predictive tests are you know triglyceride hdl ratio and total to hdl ratio and the hdl ratio reflects the insulin resistance so we've always been looking at it but not in the right way we also look at inflammation which can happen through a crp we look at uric acid which can be elevated which david plummer's book drop acid was all about we we look at liver function tests which can be abnormal we look at male hormones sex hormones we look at dhea and sulfate in women to look at the effect of androgens being produced from the insulin resistance we look at a whole host of things and we get a pretty good picture of where people are in that spectrum but the most important like you said is looking at the insulin fasting or after glucose tolerance test and and you mentioned the waist hip ratio that's important but you know when you look at the data on the 88 percent of americans who are metabolically unhealthy only 75 only right 75 of us are overweight three-quarters but like what about that other you know like you know eight whatever eight percent like probably about a quarter of people who are thin also have pre-diabetes they're what we call skinny fat or fin on the outside fat on the inside they're metabolically obese but normal weight um and that's just because they they may not gain weight but they actually their metabolic consequences are all the same so we start to look at all these factors and we get a pretty good sense of the problem and where you are in that spectrum so now that we've established that you know what are the top things that we should tell people to do in order to reverse this problem because we know even if you're far down the road even if you've had this going on for 30 40 50 years and you're diabetic on insulin that you can reverse this process that you can reverse the damage to your beta cells that you can increase your insulin sensitivity and you can reverse type 2 diabetes and not only just weight loss so tell us about what are the top things that people need to do from a diet lifestyle medication supplement point of view in order to actually reverse this problem of insulin resistance so one of the reasons i was invited to singapore specifically for my postdoctoral work was because of the interest in that part of the world looking at this disparity or the inequality rather with regards to metabolic predisposition and body weight changes yes so for example in singapore there's a tremendous variety of ethnicities like here in the us too frankly but they've noted that if you looked at a chinese a chinese ethnicity kind of the average singaporean and compared that with someone of european like northern european like me and you caucasian ethnicity that these were individuals who could both be gaining fat and yet the chinese ethnicity man the man the chinese guy would start to suffer insulin resistance hypertension much much earlier than the caucasian guy would he could continue to get fatter and fatter and only later would he start to experience the metabolic consequences now to varying degrees this can happen across all ethnicities where you'd noted that you have people who don't really appear to be overweight at all they have a normal body weight much of this can be attributed to how the fat cells are growing you know you and i were joking earlier that what you can pinch and jiggle is the fat that you have but you could have people who are both gaining weight and yet and they they look they're gaining weight they both gained 20 pounds since they graduated from college when they were roommates and yet how they've stored the weight i don't even mean where but how they've stored the weight is very different because fat fat tissue can grow through two different processes on one hand you can have the number of fat cells capped and that's how most people get fat across every ethnicity the number of fat cells they have is set after puberty once they get to adulthood their fat cell number is set and so any pressure for the body to store more fat is primarily through hypertrophy of every individual fat cell and the fat cells get too and that's right they get to about four or five times bigger than the normal fats in contrast there are some people and and caucasians tend to do this a little more than other ethnicities where they can continue to make more and more fat so the fat cells will get a little big then the body just makes more fat cells that's a process called hyperplasia so just multiplying the fat cells basically that's the difference because if you have small fat cells even if you have a lot of them they're very insulin sensitive and they're anti-inflammatory literally secreting proteins that are anti-inflammatory in contrast when fat cells start to hypertrophy two terrible things happen one they become insulin resistant to try to prevent their own growth they're basically telling insulin insulin you want me to keep growing i can't grow anymore so i have to become resistant to you and so the fat cell starts leaking free fatty acids into the blood at the same time as the fat cells getting so big they're pushing each other further and further away from capillaries from the blood and thus they become hypoxic or a little oxygen deficient and so they start releasing pro-inflammatory proteins a whole a whole catalog of them because some of those pro-inflammatory proteins will increase blood flow they'll try to increase the production of new capillaries so that is part of what happens across people even though their body weight may be normal they might not be in any category that would be problematic with waist-to-hip ratio or waist-to-height ratio but they have more hypertrophic fat cells than someone else does and hypertrophic fat cells are insulin resistant and pro-inflammatory yeah so thus driving driving the metabolism and we see that in you know indians uh you know from india uh chinese asians it's very something they really don't have to be very overweight and they can just have a teeny little belly bump and that little belly bump is uh kind of a hot potato so yep that's an issue um okay so let's now let's go back and go we understand the diagnostics how do we test how how do we advise people in the confusing nutrition world today about what to eat because we have the vegan community saying veganism is a cure for diabetes and we have the keto folks saying keto is the cure for diabetes and we have me somewhere in the middle saying pagan diet is good yeah you know and so we we really have to kind of go well what what's the deal how do we actually get to the end goal of reversing this and of course it's going to be personalized because some people like i said have myriad other causes like stress or inflammation or the microbiome issues or toxins that need to be addressed as well i mean i've had a woman lose 40 pounds just like that by getting rid of her mercury so there's more complexity to it but but for the predominant group of people who suffer with obesity and die and and this phenomena you know what are the top recommendations from a diet lifestyle supplement medication point of view yeah yeah so with regards to exercise and i know you're not a doctor a medical doctor but but i but i want to i want to hear what you have to say about the food and what you've learned for your research yeah yeah yeah so just purely as a scientist um to mention because you'd mention kind of three things and i agree with them kind of medications exercise and diet with regards to the exercise supplements too which yeah yeah right right thank you yes so with ex with regards to exercise my view is whatever the one is that you'll do do it so the best exercise to improve insulin resistance is the one you'll do and there could be varying degrees there but it really is a matter of just getting out and doing something and i would just say the only addition to that is whatever do something after you've eaten your most starchy insulin spiking meal of the day whatever that one is then tr that's exactly right go out and take a walk and people would be dumbfounded at how much it lowers their glucose and their insulin because the moment you start moving those muscles they don't need insulin to tell them what to do they just start pulling in their own glucose they get so greedy so demanding that they don't have to wait for insulin to open those glucose doors they open them on their own driving down the blood glucose which helps the insulin stay much lower than it would have been so movement matters 15 minute walk 10 minutes half an hour or like what yep yeah it's well the longer the better in the brisker the better but anything is better than nothing yeah okay now with regards to supplements there are certainly and you would know more about this than me so in all sincerity i would readily defer to you but some that i'm aware of supplements like berberine no question um cinnamon also has been shown to do something vitamin d as a vitamin yep yep um and and um alpha lipids alpha lipoic acid magnesium yep that's right so there are several things that people can just sprinkle in um and use judiciously to help yeah and medications um i'm not sure maybe that's too big omega-3 fats probably oh for sure that's right yep so omega-3 fats vitamin d lipoic acid berberine cinnamon that's a good start and there's more there's there's more oh yeah and you would know more about biotin and chromium and vanadium and many many other nutrients are needed b vitamins all that but basically if you take a good multivitamin and you supplement with some magnesium and lipoic acid and you know you add cinnamon in your food or maybe take berberine capsule that that that can help and there's there's more to this uh and i've written a lot about it but i think that's good next talk talk about the next piece which is yeah yes so the next piece could be medications but but maybe just for the sake of um maybe that's too much of a big black hole i would say in general maybe i'll just say this metformin is the most is the most widely used insulin sensitizing drug in the world um because it's affordable and it's effective but even metformin which is considered the best is only half as effective at improving type 2 diabetes and insulin resistance compared to even modest lifestyle changes so even if you take the very best of all the medications a study a prospective study in humans found that it was only 50 percent as effective as lifestyle changes so that then brings us you got to send me that study yeah oh yeah for sure so um now mark you would be the authority with many many other aspects to this and maybe even diet i will only focus on nutrition just because that's the one i've focused the most on despite my studies looking at stress hormones like epinephrine and and cortisol which absolutely cause insulin resistance and tremendously matter um inflammation which absolutely causes insulin resistance and i've published in in labs and papers on both of those topics but to me the elephant in the room is nutrition in in in i i like how you kind of both of us want to be diplomatic when it comes to nutrition i don't want to in all sincerity yeah i don't care i don't like yeah well well but but i think it's it's appropriate for us i want the truth yeah same same and the truth is compared to a standard american diet which is not totally fair to the us because it's really a global diet at this point so compared to the standard diet that people are eating any change is going to be a benefit yes it really to to not to at the risk of oversimplifying it this is why someone can go very strict vegan which i think is a diet that has a problem long term as a person may start to develop nutritional deficiencies but even still if you go on a vegan diet there's no question you will lose weight and your insulin sensitivity will improve at the same time there's no question i've published a clinical paper in collaboration with the local clinic here that you take people with full-blown type 2 diabetes put them on a calorie unrestricted low carbohydrate diet and the diabetes is gone so both of these clearly work and so in my mind the improvement um the steps to improve insulin resistance can start with one of two steps one controlling energy or two controlling insulin and on the controlling energy side this is why a vegan diet is on my view generally going to be successful not always because there's a lot of garbage that can be considered vegan yeah that's because people have a high carbohydrate diet that's right oh yeah for sure yeah i mean grains and beans even if they're whole are still more carbohydrates than eating protein and fat and vegetables that's right yeah very insulin spiking yep um that's true so in general if a person is eating a diet that is just overall lowering their calories calories matter and so if there's a lower calorie diet you will lower your insulin because you cannot have elevated insulin in the midst of a low caloric consumption you'll die because if calories are low but insulin stays really high then you are clearing your glucose will be too low your ketones will be too low and your brain will starve and you'll go unconscious so the two are really antithetical so if you are lowering your calories yep if you're lowering your calories and then then your insulin will come down and then you'll start to improve your insulin sensitivity that absolutely happens now however having said that i think that sets you up to failure so if your first step to improving insulin sensitivity is to cut your calories or cut your energy then you're going to be fighting a battle with hunger and usually hunger wins that's my only concern in that regard but nevertheless it absolutely will improve insulin sensitivity and by the way just to stop you the first thing that's that's what our friend david lewis book was called always hungry which explains why we're always hungry and if we are battling hunger and our lizard brain is in charge which it is which is survival we're not going to win our frontal lobe cannot match the power of our reptilian brain to search out seek and find something to eat if our blood sugar is low and our insulin and blood sugar are spiking up and down yep that's right in fact i think that to be a little crass perhaps this is why i believe you do not see reunion tours with the biggest loser tv show that game show where you have these people going through tremendous caloric restriction by following the classic advice of eat less exercise more they do it to an extreme and hunger always wins and they gain it all back and so you don't see them two years later or so because the results are not favorable much very unfortunately but nevertheless there's the low energy paradigm which which fits with veganism generally because they're by cutting so much fat typically calories are going to drop tremendously this is why fasting will work very very well but at this on the other hand you have this paradigm of just control your insulin and this is what we published a paper on where these 11 women with type 2 diabetes they were told don't count your calories if you're hungry eat eat until you're full when you're when you're not hungry don't eat but just follow these three rules and i have an affection for alliteration and it was control carbohydrates prioritize protein and don't fear fat and just to put a little nuance with each of them control carbs is something you and i have been talking about which is focus on fruits and vegetables eat them don't drink them and don't get your carbs from bags and boxes with barcodes prioritizing protein this just make sure you're getting high quality protein and you're getting plenty of it it will it will promote a greater sense of satiety protein increases metabolic rate through the process of digesting it and and you need it and then lastly don't fear fat my paradigm on that one fat has no effect on spiking insulin on its own and focus on ancestral fats which is animal fats and fruit fats we've been eating fruit fats since for millennia because our ancestors would have only needed to take that's right yep coconut and uh and olives that's exactly right because all our ancestors had to do was take the flesh of the fruit and then just press it even with their own body weight and they would have gotten that oil from it and so we've been using that for millennia and it's these modern of course refined seed oils that have only come on the line over the last century most especially the last 60 years or so when the war on saturated fat began we were desperately looking for alternatives and that took us to all these refined seed oils so don't don't be afraid of those but don't fear the insulin so my view on and i'm gonna just i'm gonna just frame this a little bit i have a very good friend who i love to pieces who happens to be the dean of tufts school of nutrition science and policy dr darshma historian who's published more studies than god and is one of the most brilliant and humane people i know and we agree on 99 of everything except for this point and his view is from the data both interventional data and observational data that high doses of refined seed bean and nut oils are actually healthful and are not a problem can you just kind of address that in the context of what you know i don't know if we're gonna get to the answer but yeah i'd love to hear your perspective so so i i do attempt to have a bit of a nuanced view on this because i'm an insulin guy i'm not a fatty acid or i'm not a seed oil guy and there are people who are seed oil guys guys and gals i i will so i'll speak to what i know which is two things one when linoleic acid so we're eating like 50 some thousand times more linoleic acid now than we were 100 years ago um and i think that matters so when when when we eat linoleic acid which is the primary polyunsaturated fat in these refined seed oils that will get that will accumulate in our fat cells and it gets metabolized into a molecule called 4-hydroxy non-enol or 4-h and e other fats do not do this they do not go down this metabolic pathway and when a fat cell is accumulating this this byproduct of linoleic acid it forces the fat cell to go down the route of hypertrophy you know kind of reminiscent of what we'd spoken about before it prevents this process of hyperplasia allowing smaller but healthier fat cells it forces the fat cells to only grow through hypertrophy which promotes inflammation because they become hypoxic and promotes insulin resistance because they can't grow anymore so that absolutely happens i can say that definitively that is one negative the other negative thing that i can speak to is similar to this although that is admittedly more my forte but um so much of the the evolution in our understanding of atherosclerosis is not just that cholesterol and fats matter something has to happen to those fats for them to be considered pathogenic or harmful oxidized for example that's exactly that's exactly right yep you can take a macrophage and and have it swimming in a little bath of of lipoproteins of various fats so one of your white blood cells floating around all your fat cells right that's right yeah or floating through the lipoproteins passing them in the blood and so you have a little macrophage which floats is floating in the blood and if you if it's bumping into lipoproteins like ldl for example it will not engulf them if the ldl is unaltered if it's fats and cholesterol esters are in in a natural native state they're not considered a problem and the macrophage ignores them this was studied by a group at ut southwestern yes a legendary group um and in fact these guys won a nobel prize not for this work but for other stuff they all they found that you could only induce a macrophage to start eating these lipoproteins if the lipoproteins had oxidized fats on them and now you start to create what's called a foam cell and that's one of the primary components of an atherosclerotic plaque like when you actually look at the blood vessel that's growing you have these these they look like little bubbles they look like they're foamy they look like they have air bubbles in them because they have these little pockets of fat but the matte and those are macrophages that start eating fats but they only eat the fats if they're oxidized and mark you cannot turn a saturated fat into what's called technically a peroxide that's what these actually are unless you heat them up to like 300 celsius lipid peroxide saturated fats yeah that's right yeah saturated fats are the most they're the most stable fats in in the in nature and the more you unsaturate the fat like a polyunsaturated fat now it can become a lipid peroxide very very readily and there are these metabolic pathways that will do that and so we take this linoleic acid that we're eating 56 000 times more now than we were a deca a century ago and now we see that as these become oxidized macrophages sense them as problematic and they will engulf them and now you have a foam cell which becomes very pro-inflammatory and you basically have the heart of an atherosclerotic plaque so basically concerns so basically those concerns just to recap is if you eat a lot of refined processed oils which is the predominant oils used in america today we used about 10 of our calories as soybean oil if you eat that that that pathway to metabolize that oil creates something called four hydroxy nanio which actually goes into the fat cells and causes them to grow and the second problem and the second problem is that these fats are very unstable they're called polyunsaturated fats but they're very unstable so they're easily oxidized and oxidation happens from lack of antioxidants in our diet basically the phytochemicals from stress from a microbiome from anything that triggers inflammation so anything that causes oxidation which is a lot radiation that causes the lipid peroxide and that is what our immune system responds to which is what causes heart disease so we now know that heart disease is an inflammatory disease and what you just described was the mechanism by which that happens white blood cells attack fat particles running around your blood if they're oxidized and then deposits them in your arteries which then cause heart disease yes the question i have for you is are those petritus studies or is this broader in its application because what dari says is that you know yes and when you look at the actual population data and interventional data we don't see this yeah it sounds good on paper but is it actually real yeah yeah so i'm admittedly a mechanistic kind of guy so i'm definitely i'm definitely citing um petri dish or you know direct cell reactions but even in human populations we see the correlation if not the causality and that and mark that's the underlying concern with all of this you you you simply cannot induce um you can't do these causality studies in in humans um that i'm aware of at least i don't know that they've been done but in humans we know that when you sample the atherosclerotic plaque the actual amount of oxidized ldl is going to be the predict or the circulating ldl that's oxidized will be a predictor um that will determine the degree of a person's atherosclerotic blocking or or prevalence so we see the correlates in humans if not the causality that we can see in the cells and in the rodents i mean look from my perspective as a doctor it's like if there's potential problems why risk it you know maybe it's okay but we do know that olive oil avocado oil for most people coconut oil fats in their original state in animal fats particularly grass-finished animals wild animals uh particularly nuts and seeds in their whole forms those are fine to eat and that's where we should be getting our fats so i think that's a really helpful point i wanna i wanna i think you just did a brilliant job of explaining what we need to do i just i i i wish we had you know hours and hours to talk about this i think that you know the dietary strategies of cutting out starch and sugar don't drink your calories avoiding boxes boxes bags and barcodes you know yeah upping your protein a little bit high quality protein eating the right good fats key exercise i think any is good you know interval training high intensity interval training and which increases vo2 max and strength training which improve mitochondrial function and muscle mass are also really critical meditation stress reduction all that stuff we talked about i want to finish by talking about this whole thing that we earlier talked about which is mtor and i i i don't know how much of you know about this but probably a lot more than i do uh and and it is it is the essential question that's running around the longevity fields and there was one large study that was done that looked at a protein intake over the years a person's life and it seemed like when they were younger if they ate less protein they did well but as they got older they they didn't they needed more protein in terms of longevity and i remember there's one story of emma morano who was a italian woman who lived to be 117 years old and walter longo who's a longevity expert has written about her talked about her and met her and apparently when she was younger her doctor told her she was anemic and she needed to eat three eggs a day which she ate for her entire life then in her 90s she was starting to dwindle and her doctor told her to eat a pound of meat a day and she lived to be 117 years old uh and and so the question i have for you is and this was a really brilliant a brilliant new understanding for me which is that the biggest driver of increases in mtor which is a regulator of aging higher mtor faster aging is too much insulin which comes from too much starch and sugar also protein and also will increase mtor right so if you're then wondering what is the best strategy for regulating mtorn aging because a lot of people are saying restrict protein restrict protein be a vegan very strict protein that's going to make you live longer and i'm not really convinced because you know i look at the data for example on the native americans the lakota who at the turn of the 1900's were the longest population they had more centenarians than any other population and all eight was basically buffalo so and a few berries and you know so so help us unpack this mtor story you know uh in like five five minutes because then we have to stop yeah so i'm i'm thrilled to circle back in fact i think you framed this perfectly and i'm kind of somewhat relieved to hear how you're framing this because i think it means that you and i see this eye so these these kinds of studies are very difficult to do in humans of course everyone listening understands that you just can't feasibly follow humans throughout their whole life and whole lives and look at and perfectly scrutinize their diet and how it influenced their longevity it's so complicated but more and more in fact the paper was just published a couple weeks ago called the in chianti study that somewhat reflected what you said again that even walter longo's own research found that the oldest um that meat consumption animal protein consumption the older we get has an inverse association with mortality in other words the older we're getting and the more animal protein we're eating the longer we're going to live and then there there appeared to be this period in walter longo's prospective kind of research or correlational studies he found that there was this kind of around middle age i think it was 50 to 60 or so and you might know this more than me they found that the people who ate the most meat did have the highest mortality but then it ended up shifting into the exact opposite at above 65 or 70. and so all of this is correlational of course so it's very difficult to state anything conclusive based on the sum of all evidence in my mind cutting protein is a wonderful way to make sure your bones and your muscles will be more frail and you will be more frail easier to kill so to speak and by the way your immune system requires protein to make the antibodies hear about antibodies and covid where do you get those from protein yeah yeah you need those amino acids yep that's right so in my view um we should not be fearing protein we should be prioritizing it in the diet in high quality sources of it especially and and the fact is although it's a little inconvenient sometimes animal protein is imminently absorbable and you at least know you have every amino acid you need i'm not saying that plant protein can't be a part of this it absolutely can but there's also no question animal protein is is fantastic and so we now i appreciate there's other issues that come into play here moral issues and ethical issues but even still whatever it may be prioritize protein because it's it's going to make you harder to kill including just disease and longevity um and then with the so that's the one the thing about just animal protein in general then so how does that how does that work with mtor then because i think that's that's what yeah i agree with them i mean the muscle building i mean you can get you know movies like game changers on the show that you can be vegan and be ripped but i i've interviewed some of these folks and one they are pounding highly processed protein powders vegan protein powders because they cannot get the muscle building effect without supplementing branched-chain amino acids and high high doses of protein powders so you cannot get i mean because otherwise you'll see a lot of vegans are relatively thin and have low muscle mass over time you know obviously they stay on it for a while but but the ones who are ripped are the ones who are actually you know kind of eating super physiologic amounts of these plant proteins that you couldn't get by eating them the whole plants no that's right that that's exactly right yeah and that's sort of reflective of my general view that the further someone's going from animal-based foods the more they need to supplement to in order um to ensure that they don't have any deficiencies um now so so mtor is relevant and and animal proteins will activate mtor more than plant proteins will and that matters if we are continuing to say that mtor is the root of all aging however that i believe it's not relevant for longevity because when we spike mtor with proteins in the diet it is very transient it comes up and it comes down and it's based wholly on the amount of amino acids that are getting pulled into a cell and of course muscle cells will pull in the bulk of those amino acids yeah because they have such a high protein demand and that's a good thing because you have to have mtor turn on and then turn off you have to have the cyclical mtor activation i have a colleague two doors down from my office right here who studies mtor and its effects on muscle and bone growth and what he's found in others that when you have mtor turned on too long you actually start to become mtor resistant and that the muscle cell is trying to grow but but mtor has been on so high for so long that its ability to promote muscle protein synthesis is compromised and now the muscle is starting to break down its protein even though mtor is elevated but that happens when mtor is elevated too much which is not the cyclical activation you get from protein consumption but rather the insulin induced mtor activation yeah insulin as i said insulin activates mtor much longer than amino acids do and importantly much more ubiquitously because if you and i were to eat a load of amino acids we would get significant mtor activation in our muscles and relatively little enter activation in our liver or our white blood cells however because they don't pull in amino acids very much it's a very modest intake of amino acids which and so that's relevant if it's protein induced mtor but insulin when we spike our insulin as i mentioned earlier literally every single cell in the body responds to insulin there's truly no exception i'm not being dramatic here there's no exception and so now we have our white blood cells that are responding to this elevated insulin and our skin cells and our bone and muscle and liver and brain and so now mtor has been spiked and it's staying on for longer and right around the time mtor is starting to turn off in response to this insulin spike what do we do we turn it on again and again and again by eating by continuing to eat and drink refined starches and sugars essentially every two or three hours from the moment we wake up to the moment we go to bed bad news yeah so if mtor matters then focus on insulin not protein that is that is a brilliant summary of something that i've struggled to understand because intuitively i i knew that that protein and also from the data that protein as we get older is really important for muscle mass and sarcopenia which we've talked about in the show the loss of muscle is the single biggest driver of age-related disease because it just accelerates everything accelerates in some resistance inflammation hormonal dysregulation high cortisol low growth hormone frailty everything else and so you need that but at the same time like well geez i don't want to i don't want to be messing up my longevity here by eating my you know grass-fed ribeye you know yeah and and the explanation of that it's actually sugar and starch that keep mtor elevated all the time as opposed to the cyclical nature which protein does is just brilliant so the take home is cut out the starch and sugar if you eat a lot of protein with a lot of starch and sugar you're a problem if you're eating a lot of fat particularly saturated fat with starch and sugar it's a big problem that's a caveat i want to make people oh saturated fats good i can eat no not if you are eating starch and sugar because then it's like putting gasoline on a fire if you loved that last video you're gonna love the next one check it out here let's just stop giving the wrong advice to people i you know somebody with diabetes telling them to eat six servings of grains a day and up to ten percent of their calories with sugar is really bad definitely bad advice

Channel: Mark Hyman, MD

Views: 213,636

Keywords: Mark Hyman, Mark Hyman interview, Mark Hyman live longer, Mark Hyman diet, how to live longer, how to age in reverse, nutrition tips, healthy foods, health tips, health theory, fasting tips, how to never get sick again, prevent disease, self help, self improvement, self development, personal development, inspiration, motivation

Id: iQZ8FD1Gwec

Length: 94min 28sec (5668 seconds)

Published: Wed Jan 05 2022