Insulin Resistance Scientist on How to Reduce Abdominal Fat & Lower Insulin Resistance | Dr. Koutnik

but we have to largely look at these on two ends of the spectrum right you have high carb low fat over here you have very low carb high fat they both seem to produce some pretty powerful health benefits the second you start mixing both of them at high levels in this Western diet I mean that is what a western diet is it doesn't go well almost ever all right so Andrew kutnik you are a researcher at Sanson Diabetes Research Institute so you study nutrition you study diabetes you study abolic Health all day every day tell

me what is going on why is it that people that typically have insulin resistance or overweight yeah that that story is is quite interesting I don't think it's a straight for forward as a lot of people assume you know we know that people with type 2 diabetes tend to be overweight Andor obese and that uh body elevation and and adapost tissue or fat tissue can be strongly linked to insulin resistance and so that's a lot of where that story comes from but we also know that there are many scenarios where someone isn't obese and can

also develop insulin resistance uh in the context of something like uh type 1 diabetes and so there is is it's very complex story but I we know that increased atopos uh being obese uh uh is a strong predictor developing type 2 diabetes um largely through this well-known phenomenon most characteristic of something like type 2 diabetes which is insulin resistance so we we know that fat tissue can lead to insulin resistance it is it is tightly coupled um but it's not always the case where someone has to be obese and they develop insulin resistance so is

it not real cut and dry on which came first the chicken or the egg I think that there's strong evidence very strong evidence that as people become more and more over weight and or obese uh that they develop higher and higher insulin resistance that is very tightly coupled but there's all these other factors so uh exercise is a very strong factor in that where someone can you know uh exercise and we see these robust elevations and insulin sensitivity or a reduction in insulin resistance immediately post exercise that can linger for hours maybe even a day

um or days in some scenarios so there are other factors that play into why someone may or may not be insulin resistant uh that is not always related to how much fat tissue someone has on their total body composition but body composition is absolutely predictive uh in most data for someone developing insulin resistance what is happening even surface level mechanistically sort of a just a basic 500 foot aerial view uh of someone that is how atopos tissue or just osity in general is affecting insulin resistance like what's happening top down there I think uh a

lot of one of the big themes that comes up a lot of times in this discussion is is of course you know like subtle inflammation so as someone develops more and more out a out aost tissue there can be signs of uh subtle but elevated levels of inflammation in the body we know that inflammation uh can ultimately facilitate insulin resistance there's data um in a lot of studies be it you know preclinical models or Nitro models where people are looking at cells or animal models where they can pull tissue and and and ulate experimentally what's

going on and see that uh many inflammatory biom biomolecules actually can block uh the signaling pathway of insulin actually getting to the insulin receptor and ultimately facilitating uh a a glucose uptake effect so uh that's ultimately what we're talking about insulin sensitivity right is when uh you know molecule gets the receptor and ultimately facilitates this this glucose uptake into tissue the biggest tissue we have that's kind of this glucose sink is obviously muscle so a lot of times when we speak about insulin resistance we're often talking about insulin resistance of the muscle uh tissue predominantly

although there's obviously other tissues of high relevance insulin resistance or in insulin insulin in general like the hepatic tissue uh as well where um outside of context uh of type 1 diabetes which is his own unique physiology which we can learn a lot from uh where you can actually have insulin uh initially when it's released and and to back up for a second to tell tell people the full story of what's going on so let's say you go and eat food right so let's say you went to uh you know it's you getting close to

lunchtime you have lunch that that lunch has the typical breakdown of a mixed meal for the average American let's say 45 to 50% of that's carbohydrates you know anywhere from 15 to 25% of that might be protein um and then about a similar ratio for fat and depending on you know how you make up that total uh caloric composition someone eats that food that those carbohydrates uh that fat that protein gets into the stomach that that acid starts to in the stomach actually starts to break down these these macro molecules into individual let's say uh

polym mono and ultimately uh saccharides and ultimately individual sugars in the context of protein protein could actually upon ingestion some of those amino acids might be converted to Sugar but also can cause a glucagon response which also releases sugar so all these foods have different degrees of glycemic impact and the reason we're focusing on glycemia here for a second is because ultimately the magnitude of glucose response to that meal there's supposed to be in a healthy normal scenario a dose dependent response on the amount of insulin that's going to be released from the uh beta

cells of the pancreas and so the higher that glucose level these beta cells have this fine-tune Machinery that would detects elevations in glucose in the beta cells and releases a dose dependent and appropriate amount of insulin to handle that glucose response but what we know over time is that in the context of type 2 diabetes where someone is probably becoming more obese they start developing signs of things like pre-diabetes they probably don't know 80% of people who have pre-diabetes don't know it and they start developing this dis glycemia but what's actually happening when this dis

glycemia is starting to emerge is these subtle signs of insulin resistance early on and and ultimately when that glucose is released from these pre-stored granas from the beta cells into the hepatic C uh hepatic portal vein that insulin usually goes straight to the liver a huge chunk of that insulin is is eaten up by the liver and glucose is brought into the liver to be stored as glycogen you know in case you were in a fam in or running away from a dinosaur historically speaking right to ultimately release that glucose in times of stress or

in times of low glucose environments to maintain uh blood glucose homeostasis in a 70 to 120 normal glycemic range but as glucose gets higher and higher insulins release more and more and then it starts to store it in other tissues such as the muscle tissue and as your body develops things like increased osity inflammation being a a part of that you start to develop things like insulin resistance the insulin stops working as well you start needing more insulin to compensate for the insulin not working as well at the receptor level and actually the excess insulin

in the periphery starts to then also develop things like insulin resistance and that's actually what we see in the context of a disease like type 1 diabetes where patients lose complete beta cell function or almost complete beta cell function they have to start taking exogenous insulin uh and when they take EX exogenous insulin because it goes predominantly to the periphery at higher levels than someone who doesn't have exogenous insulin or doesn't have to take it in the peripheral tissue they also develop insulin resistance so this is a very similar model of why ins excess insulin

in the periphery causes insulin resistance but all the way back to your original question one of the fundamental reasons someone develops insulin resistance for most people is because they develop excess autocity that's one of the mechanisms by which can lead to things like inflammation and things like inflammation are tightly linked with things like uh more and more resistance to insulin so it's not the only thing that's going on of course there it's many many complex things are happening in biology and and no seems to happen in isolation but that certainly seems to be an important

component to the story does muscle size versus function dictate the ability for it to be a glucose snc and what I mean by that is obviously muscle is trending for metabolic Health right everywhere you turn you hear like build more muscle it's a metabolic sink yes okay but there's also a lot of people that don't necessarily want to put on a lot of muscle and I I can't help but wonder is like healthy mus muscle tissue muscle tissue that has healthy mitochondria like what is more important having more sheer mass that can be a snc

for more glucose or better metabolic Health mitochondrial health of that muscle tissue so after today's video our sponsor is seed I put put a link down below for 25% off their daily symbiotic so it's a probiotic and a Prebiotic in one so it has a really unique delivery system so I am a fan of probiotics when you're making a change to like your diet or a lifestyle because it can kind of help remodel that gut microbiome to help you make that shift a little bit sooner now full disclaimer they're a sponsor on this channel that's

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I'm actually going to simplify that or dumb it down even a bit more and say the most important thing is that someone actually engages in physical activity there is so much evidence that if someone just engages in meaningful purposeful physical activity you know obviously being physically active in a daily setting where you're standing up and moving around that's obviously great very important we know that let's say stepping doing like 8 to 10,000 steps has all this metabolic health benefits but purposeful exercise someone showing the gym I'm purposely working very hard moderate to Vis phys moderate

to vigorous physical activity is incredibly important for acute insulin sensitivity and we know that the benefits of exercise obviously have long-term impact but there's a lot of evidence that suggest especially in the context of something like type two diabetes where there is notorious insulin resistance I mean that's what characterizes this disease that it's it's a it's a short short benefit meaning that you have to keep it up so if you do an acute exercise bout that can immediately induce insulin sensitivity reduce insulin resistance and you can maintain that benefit for hours sometimes days maybe a

couple days but you have to do it again you have to you have to maintain that regular exercise pattern uh routine and that is much the probably the most important thing not so much the size of the muscle not so much the function of muscles but that you're actively engaging it on a regular basis to induce a lot of the the sensitivity to insulin the glucose uptake into those tissues more than let's say size more than let's say function in and of itself so if someone wanted to take an actual step and say I want

to improve my overall metabolic Health reduce my insulin resistance maybe my glycemic control showing up to the gym being purposeful with your exercise routine is frankly one of the most powerful things you can do right here right now to improve your insulin sensitivity that is well known uh but that also tells us a little bit more of an answer to your more Nuance question uh and that seems to be that engaging that muscle and utilizing it and keeping it active and all the things that come along with it you mentioned the mitochondria just there's so

many mechanisms underlying that that clearly seem to be important for facilitating this instant sensitivity so yes I I I I think there's there's importance to your question but a general theme for people to take home and actually acally walk away with today they can go do is go engage in physical activity because that is the one thing that reliably increases in sensitivity right now yeah I think there's a uh there's a I don't want to say it's a misconception but I think sometimes an overemphasis on sheer muscle mass you know where it's once I have

this muscle mass like I have this magical sink that's going to just collect my glucose and I do think that that's true to a certain degree but that muscle in motion is what matters more than anything and it's you know you can be a brick house bodybuilder and have you know but if you're dormant you know it's not really doing that much for you and burns a couple additional calories per day too it's nothing crazy but when it's in motion it's an entirely different ball game and to Tom to that point think think about this

someone with that type of muscle you you know you mentioned the bodybuilder fenal type right there's no way they're maintaining that level muscle mass without being he highly Physically Active engaging in probably huge volumes of physical activity so one usually is is happening with the other very few people are sitting around like we're sitting here today you know we did exercise today and and we engaged in a lot of uh things that would be beneficial for everything we're talking about insensitivity glucose control all those things but those people you know who have have huge muscle

mass they're not sitting around on their their butt all the time they're they're usually doing quite a lot to maintain that so that that's it's you're kind of getting two for one there you can't really have that without having the other uh and so yeah why do you think there is such a I don't want to say a demonization of sugar right I mean you and I both come from uh probably similar camps that we've been in in terms of like our viewpoints I know you and I have both kind of been in the low

carb space and we've both been in and out of it and we both have looked at that we're both big into fasting we both kind of we look at metabolic Health probably through a very similar lens um why is it and where did it come from that there's such a massive demonization of carbohydrates because even as someone that's still a low carb person I'm still am low carb on the grand scheme of things but I'm not anti-carbohydrate so where did this come from and where can we give a thoughtful acknowledgement to the fact that hey

like maybe they're not wrong but some of this is just been blown out of proportion in different ways I think that comes because we know that there's a lot of scenarios where excess carbohydrates leading to excess blood glucose causes all these detrimental acute and chronic complications and and most notorious of that is in the context of diabetes and we know that in those context that if you reduce carbohydrates it has this often times very potent therapeutic response and so the easy thing to jump to is that well obviously sugar might be causing that effect it's

it's in and of the same as how the story on type 2 diabetes has occurred where we know that you can improve type 2 diabetes and or obesity by being physically active and improving your nutrition but actually we know the story is much more complex than that and how someone may get there doesn't mean that because you didn't do those things you got type 2 diabetes or obesity it just means that those are beneficial tools so then people jump to the other side of the coin W is obviously if you have type 2 diabetes you're

physically inactive and you must be having a poor diet often times it is the case but it's not always the case and it doesn't mean it's the cause and I think that's often how this story has occurred in that we know that in athletic context you know uh carbohydrates can reliably in the literature so let's just stay away from any you know conversation we just stay very evidence-based and data driven and just say in the literature we know that carbohydrates are important for things like performance are they essential no that's a whole different conversation we've

done a lot of research in the lab actually looking at that conversation uh uh there's a lot to unfold into that category but I do think that because reducing carbohydrates has such a potential powerful response in context where dis glycemia in the context of insulin resistance are present that people look at it being sugar in the context of carbohydrates because sugar comes from carbohydrates that is a problem and that it must be the cause of the problem and certainly if you change it you can improve outcomes in many of these scenarios but it doesn't mean

that in all scenarios in all context is bad that makes a lot of sense and if you look at and we were talking offline a little bit and uh you know you've held this close to your chest for this conversation but you're type 1 diabetic Y A lot of these discussions surrounding glucose you mentioned something you know it was interesting they kind of stem from what we experience in a type 1 diabetic realm right see these things is in isolation and all that you kind of describe that you know you've got a phenotype that's generally

pretty healthy and then the only difference is the fact that they don't produce insulin right so you all of a sudden you see so let you kind of describe that because I mean what do you see in the lab from a type 1 diabetic standpoint and how that translates into the discussions that we have in the mainstream yeah it's I I so I have you mentioned I have type one I've had type one for 17 years now and I have played around a lot with different dietary strategies to your question before in the context of

type 1 diabetes for those who aren't familiar with this this is this very unique phenotype we can learn quite a lot about as you mentioned the average patient with type 1 diabetes is usually normal or low body weight at least historically speaking that was the case uh for a lot of reasons they're actually looking a lot more like the general population but that's a different discussion but historically speaking they were normal body weight they don't have excess osity levels uh they don't have excess lipids they don't have all these things that happen in type 2

diabetes they just lose the function of their beta cells which produce insulin and regulate blood glucose and you can think about this as almost like a thermostat your beta cells almost acts like a thermostat for glycemic control in the body and your and your body keeps this really tight glycemic control 70 to 120 milligrams per deciliter very very tight uh That's essential for maintaining overall uh Health if you you go too low you can uh on the extreme end die uh you go too high it can cause these chronic complications so in type 1 diabetes

we've learned that these often very normal perceivably very healthy individuals they just lose their ability to normally regulate glucose levels so most patients live not in this tight range but this very high and variable glucose levels all day every day and what we see is we're able to largely isolate out the impact of glycemia on acute and chronic complications and one of the the first things we see in this context is when you see these high and variable glucose levels with without all these other negative metabolic health problems that this can lead to very early

signs of microvascular complications that means retinopathy the small vasculature in the eye uh nephropathy the small vasculature in the kidneys it can damage uh your your nerves these are very vulnerable tissues to high glucose level a lot of people use a analogy it's a lot like sandpaper to these small vasculature and that's definitely true people with type one because of their high and variable glucose levels can have much higher complications of microvascular disease but in the context of macrovascular disease is what most people think about when they think of cardiovascular or or blood vessels like

based diseases and we see that patients with type 1 diabetes who are largely normal but just have these high invariable glucose levels have tenfold higher risk for cardiovascular disease and so it's actually the number one cause of death in type 1 diabetes what that tells us is that glucose plays a very very important role in the context of obviously microvascular disease but also macrovascular disease in fact when we look at some of the largest studies ever conducted over 30 years over a thousand patients with type 1 diabetes we see that the number one modifiable risk

factor for reducing or increasing the risk of macrovascular again heart disease vascular disease is glycemic control in the context of a biomarker carard hba1c hemoglobin A1c which is this average of your glucose over a 2 to three month period of time and so we can learn a tremendous amount on the impact of glucose to tissue-based organ Health uh macrovascular complications and also cardiovascular disease when looking at this very unique phenotype question not to Pivot too much but you know with your hba1c yeah if someone has a normally healthy person not type one not type two

but they are stressed a lot and active a lot can that influence their hba1c or is there like a natural sort of um you know barometer that kind of or I shouldn't say barometer is there sort of a natural thermostat with that that wouldn't affect the hba1c or if you're looking at hba1c is that a very clear indicator that this is hey no this is almost entirely metabolic hb1c because it's a chronic capture of the amount of glucose that sticks to the red blood cell what is hb1c has largely been viewed as this biomarker that

it has more glucose sits around in your blood so this tight range of glucose as in your vasculature as more glucose is sitting in that blood it will stick to tissues so it's very sticky so it stick to tissues like hba1 or your hemoglobin uh but also sticks to other tissues like your Li uh your tendons ligaments um other tissues in fact that's actually why if you've ever seen a analogy for people if you've ever seen a caramelized onion it's before you take an onion you actually cook it before you cook it it it's this

you know white color and you cook at it starts to turn brown well that's actually a lot of the same Pathways where and it tastes sweeter right um that's actually because of similar processes in the body to someone let's say with type two diabetes you there's it's pretty there's some evidence that people with type two diabetes you actually look at cavers you can actually see almost a a Browning of their their ligaments and and T tendons and it's largely believed to be due to this the sticking of glucose to tissues um but there's a lot

of reasons why hb1c may be that influen hb1c so why would something stick to a red blood cell more or less or tissue more or less well obviously having more of it around is the most strongest predictor of glucose sticking to uh a tissue like a red blood cell and and then you measure your hp1c and it's higher so that's the most important factor but we also know variable levels of glucose so so uh having these big spikes in glucose let's say you have you know you just down a old school Coca-Cola or Pepsi or

something like that you do that every single day that the variable Peak uh and trough and Valley that the higher that variability also is a predictor of higher hba1c um and there's a few other variables that that play into that but hp1c is a is a hard and fast strong predictor of chronic glucose exposure in the blood and with a pretty reliable predictive value for that north of 70% but it's not 100% And the reason it's not 100% is because it's it's it's a biological process of a glucose molecule sticking to a tissue was it

it its own process in and of itself it's not just total glucose exposure there's a there's a process that is leading to that that stickiness um that isn't the same for me and you Tom or or or say someone else right so there's always individual variability and that but those are the key variables in chronic glucose exposures the most important of all those and why hb1c would be higher so if someone is stressed on a regular basis and they see their hb1c go higher and higher that is probably a pretty good predictor that they're seeing

higher and more variable glucose levels in their daily life which would often not be a good thing uh you wouldn't expect it higher and higher glucose levels is a good thing in fact most of the data to date says that as you see higher and higher levels of glucose in an average person uh that this is predictive of things like all cause mortality and cardiovascular disease early mortality uh and all these things and this is a very predictive dose response so um that that's so glucose has a important impact in in our overall health it's

very clear that that's the case we've learned a lot of that predominately historically from patients with type 1 diabetes where it's the main thing that goes wrong um and everything else seems to be pretty good if not a really healthy phenotype and uh as a result we we can learn how and why glucose might be very important for people what about in the case of you know a metabolically healthy person that is a level of peripheral insulin resistance as a result of let's say low carb fasting I mean it it can happen right it's it's

I noticed my hba1c was actually higher on a low carb diet than it is not on a low carb diet interesting and I would have my fasting glucose was significantly higher on a low carb diet whereas obviously I am a a healthy active person whereas in a lot of people that go on say a low carb diet that are overweight they see an improvement right um and I know I'm not the only one that's experienced that you know I went up to a 5.4 which is not high but you know 5.7 being the outer range

before you kind of start looking at things I was up as high as a 5.4 with all my other biomarkers looking great yeah and the only thing that was different was okay that was a very very low carb diet and you would think okay well that would modulate your glucose but generally speaking my glucose was higher so um can you explain sort of the difference between pathological insulin resistance and peripheral insulin resistance in that case you know because people hear peripheral insulin resistance or you know my blood sugar's higher when I go low carb uh

or when I'm fasting or anything like that what's what's happening there specifically like is it a preservation thing is it a yeah so pathological vers this physiological insulin resistance so pathological insulin resistance is this resistance at the the receptor to insulin often due to let's say excess autocity inflammation excess insulin floating around the blood because it's not working as well in the context of type two diabetes typically associated with obesity and it doesn't work as well doesn't bring in glucose into these large glucose in like muscle but in physiologic instrument resistance this is a term

often given to when someone may be normal healthy and they go onto a low carbohydrate diet and they notice that when they consume things like carbohydrates they don't seem to have uh or maybe some maybe higher or glucose tolerance test or uh they this appears to illustrate this insulin resistance because if you take glucose and you need more insulin um or glucose goes higher it there must be insulin resistance going on there's there's this is a very complex scenario so let's once your body starts adapting to utilizing fat we've done a number of studies in

the lab looking at you know total body carb and fat oxidation and when you go on a long-term ketogenic diet go through the multi-week adaptation period which we have done many studies like this where we see someone come into the lab they go onto a very low carbohydrate diet they go through this multi-week metabolic uh adaptation ultimately reach what we think is you know this metabolic homeostatic stage typically around 4 weeks for a normal glycemic person let say you you continue on that pathway you we assess these individuals at this time point right after they've

done this diet they see this change in in metabolism what what is that change that change is if you look at whole body metabolite oxidation or fuel oxidation you see lower carbohydrate oxidation and higher fat oxidation so if you were to dump a bunch of glucose in your system do something like oral glucose tolerance test would you use as much of it no you because you've shifted your fuel use towards things like fat so you're not per se so much resistant but you have shifted your body's Machinery to be better at what you were giving

it in this context fat and all of a sudden when you reintroduce something that it's not using on a regular basis like sugar you you may be less inclined to oxidize it as quickly doesn't mean it's a bad thing it's just someone chose that dietary strategy for a purpose and they've shifted their metabolism and your body gets good at utilizing what it has so when we think about insulin resistance in in in a physiological context it's always in the backdrop of these standard carbohydrate diets and so it's a it's a different conversation when we start

talking about low carb because you are changing so much about your metabolism that the same rules don't always apply and there's a lot less research on what it means to be low carb and have this physiologic insulin resistance is it even insulin resistance this these are open-ended questions that aren't really answered but what a lot of people jump to immediately is well if I have carbohydrates my glucose might go higher or my hb1c might be climbing up a little bit and there's so much under that hood that may be explaining that that we don't fully

understand and so what often people might want to do when they think about this is why'd you do it do you feel better did it move most of your health metrics in the right direction and that probably was a good decision for you but if everything's static and all of a sudden you just have these much higher more variable glucose levels H maybe it's time to reevaluate what you're doing you know um because if the the only one thing got worse and everything else stay the same that's that's not a good trade-off but in the

context of say like I have type 1 diabetes and and we know that there's a lot of emergent evidence from our research team looking at these low carbohydrate based strategies um and how powerful they they can be for a patient uh on that Journey but you know we know that low carbohydrate diets may not be the end all be all may not be optimal for everyone and everyone has to kind of go their own path figure out what works for them and ultimately uh uh find a strategy that optimizes their own health so if we

flip that whole situation on its head though like we've got you know physiologic insulin resistance which is the body preferentially utilizing fats and glucose therefore going higher if you take someone that's the opposite that's primarily a carb oxidizer and they're eating the standard American diet does that mean that they have a surplus of fatty acids circulating and don't those theoretically not even theoretically in reality store significantly easier they don't have to go through denova lipogenesis and go through the process that xcess glucose does so if someone is a poor fat oxidizer and much more geared

towards carbo oxidation and this is sounds like I'm leading this up for a specific answer but I'm genuinely curious like does that mean that when they were to eat a mixed their body's going to take in most of those carbohydrates and oxidize them because it's a preferential fuel source and then it's going to leave them with free fatty acids and don't those have to go somewhere yeah they have to go somewhere usually not just being dumped out of your system um yeah so actually it hearkens back to some of the early parts of this conversation

where one of the on a standard dietary strategy okay meaning not low carb you know uh you know these 45 to 65% carbohydrates you know again is 15 to 25% fat and/or lipids on a dietary strategy like that there are a ton of experiments that have been done where you do lipid infusion on that dietary backdrop that Foundation that environment of a high carbohydrate based diet that most people are consuming and you infuse lipids we know that that's one of the most reliable physiologic environments to induce insulin resistance and so uh it's actually a model

of insulin resistance to infuse fatty acids on the back of a high carb diet to induce insulin resistance so to your your original question um having higher fat levels or shifting from what is a standard diet to a standard American diet which frankly what that means is you're lowering little bit of carbs but you're upping the fat you're predominantly upping the fat in this environment would it cause insulin resistance yes it does and the largest or the the one strong belief as to why that actually is is from these lipid infusion experiments where high levels

of fat lead to insulin resistance in that context which is why fat has been looked at at least in part why fat has been looked at as such a bad thing for people but again most of the evidence looking at our understanding of lipids and its role in overall health and carbs and fat and all these other contexts has largely been an experimental designs where someone is high carb we have done so many experiments with athletes patients with diabetes on these different dietary strategies and the physiology of high carb is the physiology of low carb

are completely different than and we know a lot less about the physiology of low carb on the acute sense but definitely on The Chronic sense and so there's a lot to be learned there but we do know some core principles and that one metabolism fundamentally changes you shift your fuel demands towards fat and lower on carbohydrates uh it typically means less insulin although not always and you you are shifting a lot of your metabolism uh towards just a fat dominant metabolism and over here you're your carb dominant and when on your high carb diet you

add more fat can you cause more insulin resistance yeah I mean that that's all the evidence seems to point that that is in fact the case over here it's a high fat diet you know and is high fat diet inherently insulin resistant no it's not for a lot of people it actually reduces the amount of insulin and ultimately biomarkers of insulin resistance for these people so these are two different scenarios that have to be looked at in not simple context but in in in in a more complex Nuance way that these are different physiologies from

one of the most potent stimulus of changing metabolism which is nutrition nutrition is one of the most powerful ways to shift our metabolism we know this and have known this for a long period of time oftentimes more than any medication can replicate and so yes to answer your question we know that fat seems to induce insulin resistance to a number of uh wellone experimental physiology environments but a lot of that's on a high carb diet so we have to contextualize it in that context without getting too far into the weeds I mean you're a good

person to ask this the Randle cycle I mean is that something in general independent of being in a surplus mixtures of high fat and high carb and again Surplus an asterisk this because I always get hung up on this to find a surplus is it in the moment is over 24 hours is it over days it's so you know like if I if I eat a you know two peanuts right now technically for a nan I'm in a surplus right I mean I don't know so it's it's difficult to answer but is the Randle cycle

something that people should at least it should at least be on their radar or is it something that is so and you can describe what it is but I mean I'm I'm genuinely curious because I've always found from a fat loss perspective I can speak from my own my own that when I I tend to go through phases of either if I'm higher carb I'm typically lower fat and I know that's just a displacement thing too but I also am conscious of that and if I'm higher fat I Am lower carb I tend to not

I just don't respond well from a body composition standpoint or cognitively when I'm like high on both and actually to that's a very important point to address first is that this middle ground and so you can kind of look at this as the Spectrum right so over here you have these high carb lowfat diets that have been promoted for many years to be very health promoting and then on the other end of this there's all this emerging evidence that these ketogenic diets can have all these health benefits in various context but we have to largely

look at these on two ends of the spectrum right you have high carb low fat over here you have very low carb high fat they both seem to produce some pretty powerful health benefits the second you start mixing both of them at high levels in this Western diet I mean that is what a western diet is it doesn't go well almost ever you know um maybe the only scenario where it seems to be seemingly okay so to speak is in very high volume athletes who do a ton of physical activity who are essentially almost pushing

as much into their system as they can to maintain caloric needs for the physical activity that's a very unique scenario 99% of people do not apply for this and so you know that's a whole different conversation how people should not look at literature on like the elite athletes and say you should do this because Elite athlet is its own pheny type okay its own scenario but most of the benefits we see are on these two ends of the spectrum and so it's it's just on a big picture level we see that just loading the system

with more fat and or carbs simultaneously doesn't seem to go very well your body seems to do very well when you are on one end of the spectrum so high levels of fat and high levels of carb it it seems that that usually on the context of a high carb diet you start adding more fat more insulin resistance higher glucose levels over time over here you're on a low carb diet you have very low carbs you start reintroducing carbs things don't also go well as we're talking about this physiologic in resistance you add more carbohydrates

to someone who's reduced their carbohydrate oxidation it probably you're going to lead to higher and higher glucose levels in the blood so those are scenarios where that's not ideal and this or sorry where you add it's not ideal to kind of take from these two ends of the spectrum where it seems like there a health a lot of health benefits and start shifting closer towards the center and that is a western diet and we know that a western diet is an obesogenic diet um Beyond this the physiology of the body seemingly have a harder time

when these are both High oftentimes eating a dietary paradom like that is also obesogenic so people tend to overeat those diets and uh that obviously can lead to osity insulin resistance and all the metabolic Soliloquy that comes along with that uh which is often not good yeah now that's a very interesting way to look at it because I mean it's I think way back when it was like even Charles Paquin talked about that right his theory behind it was flawed in the sense that like I think he used to talk about how insulin would essentially

allow fat into storage which is not exactly how it works specifically but I mean his concept of it back in the day it made a lot of sense to a lot of people right and you coming from somewhat of a bodybuilding background I think you probably can appreciate some some of his principles made some sense even though some of them were seemed like they were pulled out of thin air but it was also um it just seems and even from an athletic perspective like looking at that it's like hm okay like yeah you could probably

influence a certain level of metabolic flexibility sheerly just by the volume of training and the type of training that you do but that can also be accelerated by sort of this nutritional Catalyst and when you look like think okay well if I if I need to get fat adapted sure I can do that by doing lots of endurance work but it's an accelerator to obviously deprive myself of carbohydrates and get myself there faster so I'm looking at these I'm like okay if these SE are big levers that we want to pull for Optimal Performance in

different Avenues it would make sense that you're like blunting some of that by standing in the way of it right so like why would I if I was try hypothetical why would I if I was training for maximum endurance yeah like why would I want to muddy the water with both substrates when I could really just pick one and double down on that uh it seems like it'd be counterproductive absent of the fact that I probably just have a high caloric and the most important thing at that rate is probably being adequately fueled so it's

interesting because a lot of the exercise physiology mindset was the opposite of that which was push as many calories into the system as possible from diverse sources so that all of them can be used simultaneously to give as much fuel substrate to the tissues as possible this is also why back in the 1970s there was a ton of research on MCTS because the idea is we know that Medium train triglycerides when consumed rapidly convert to Ketone bodies so if we can push GL glucose we can push fat we can push ketones get every substrate we

can in there to utilize as many of these metabolic pathways to push as much HP um uh out so that you can utilize it during exercise so that was actually the philosophy for a long period of time it's also the same philosophy by why a lot of people who consume these very high carbohydrate based fuels um and and do it intermittently during exercise like long duration prolonged exercise we'll often use multiple types of glucose um um or or uh things that will ultimately convert to blood glucose because it can use different Transporters push as much

into the system so that's actually a common theme in exercise physiology get as much in that system so you have as much available fuel substrate but it's a totally different scenario outside of exercise where what you're talking about is what's Peak Performance what can we do to achieve Peak Performance and push as many fuels in the system it is so important and people often don't talk about this that the average person does not fit in that category okay and so should not be taking that type of philosophy towards their overall metabolic Health more than like

I mean do whatever you want right do whatever you want but logic dictates that if you start doing what a lead athlete does and pushing all the calories into the system as much as you can outside and during exercise probably not a good move for you but um uh the average person it seems like you know the idea of finding a new nutritional strategy that not only complements something you can comply with and fits with your life but also allows you to hit some of the key pillars of Health right can can it help you

maintain normal body weight um Can it help you not feel ravenously hungry all the time you know for a lot of people low carb or getting away from highly pable carbohydrates is like a is life-changing to them so they're they're not constantly feeling like they need to feed all the time um so that person might do really well on a low carb diet and then you know some people who uh are more prone to let's say uh having high fat and they they notice that they may flip into this physiologic insulin resistance maybe that we

don't know completely maybe that is or isn't a good thing we don't know um at least I would argue we don't completely understand uh if that's a good or a bad thing in this context if someone were to go up within the normal range of hp1c um by booing low car but it's still normal does it really matter it's all very complex and not completely answered but most people can tell when they go on a dietary St if they're feeling better if they're sleeping better if they feel more physically active they don't feel more lethargic

um and I I think it's I many people are going to lose their mind when I say something like this but I don't think everyone should be on the same diet and I think that goes back and hearkens back to a number of factors genetic what have you been doing what lifestyle do you have that leads you to be more successful on one strategy or another I have type 1 diabetes and so these two diets are not the the same thing for me you know a high carb diet versus a low carb diet or like

see a difference between the impact it will have on my overall health so you know disease context also matters and then maybe also the type of activity you do may have an impact we've done a lot of research recently looking at highlevel athletes and their ability to utilize high carb versus low carb Andor ketogenic diets and his performance or metabolic but also subsequent performance impact on these very short duration High intensity exercise but also these very prolonged exercise bout and I think what comes out of that tells us a lot but in a general theme

you have to find what works for you and if it works or try it right and you know if a lot of times in science there's this bar graph right that you're looking at in these Publications and you're like okay that study says this but what often people lose is in that bar graph is 10 different dots that fit above and below that line what if you're the dot way up here or you're the dot way down here maybe you should be doing something different than the person way up here and what these studies often

tell us is what is the best idea what is the what is science telling this on average in these individuals in which it was studied but it may not tell you how Tom should optimize his life or Andrew should optimize his life because maybe Tom is this guy way up here and Andrew might be down here or maybe the opposite you know and so you have to consider that and try it and see if it works I that's solid man well Dr cnck where can everyone find you man so I honored to be here I

appreciate the opportunity to speak with you guys uh on Twitter at ack a k u TN i k uh I'm also a researcher at Sansung Diabetes Research Institute so you can check Sansung dorg out for a lot of the research we're doing um on the context of people at risk or who have diabetes and I am on Instagram although you know a total novice I don't really I just put things out randomly it's Andrew kudick PhD and and I do have a website andrut nick.com where I try and put out free information and materials for

people uh who have or at risk for diabetes and and maybe some strategies they may have uh to utilize or or have resources available to them right on well thanks for being here brother honor thanks