Dr Benjamin Bikman - How insulin resistance interacts with metabolic health #PHC2023

foreign [Music] good morning good morning I am delighted to be here when Sam first reached out and invited me to be a part of it I was honored because I have long respected what Sam is has been attempting to do and I'm just delighted by the not only extent of the community but the clear affection that exists here in what you've created again I'm delighted to be here I'm particularly thrilled because Sam teed this up so well and I can see why he might want a guy like me to come speak at an event like this because I have a view of chronic disease that I think has value and you'll be the judge of that in the end so what I want to present to you today is the idea that when you look at not only metabolic Health but others as I'll touch on there is a common soil from which all of these noxious weeds are springing that we call diseases and rather than continuing to trim down each individual weed only to have it grow back we can go right to the soil and address the one common root from which all the others are springing next slide so what is metabolic Health if this is the impetus for having a guy like me come give a talk as a metabolic scientist um what is it there would be multiple ways of defining it indeed as I was putting this together one version or several versions of this talk had several definitions but one definition next slide or click is the metabolic syndrome we can Define metabolic Health through what is called the metabolic syndrome next slide metabolic syndrome is defined somewhat differently depending on who is explaining it but one definition is this constellation of complications that you see here um within the UK specifically it's often defined as just the top three and the dyslipidemia sometimes isn't included but regardless this is the general consensus that if a patient comes in with dyslipidemia high blood pressure high glucose and a large waist circumference they would be defined as having the metabolic syndrome next slide um and this is a problem here where within the UK 33 so a third of all the adults um have have confirmed metabolic syndrome well that's pretty sobering and it's even more sobering when we look a little farther further abroad next slide when you look across the globe we can see that the problem in fact Nick just clicked through a few of these um the problem in South Asia in the Middle East in the Pacific Islands in Southeast Asia and then across the pond one more click there we go um we have uh issues in Mexico and the United States as much as the world wants to point the finger a chubby finger at the United States it's actually far from far from the worst and thankfully the UK is doing a little better than the US is but this helps you get an idea of the of the prevalence of the problem it's not just a problem here and one of my hopes as this message spreads and I Echo Sam's sentiments to share whatever you can and part of my motivation is to present this material in such a way that uh the idea will plant a seed in your brain and you're able to take some of what I've said and you say it in your own way if I can give you a sound bite then as a professor I will consider my job as having been done okay next slide um now within the UK the problem actually might be a little worse than we think next slide or click um because within the UK we know that 58 of adults almost 6 and 10 have confirmed hypertension and hypertension is a part of the metabolic syndrome indeed it's it's a critical part and it's often the first sign that something's gone awry because while we might not measure all the other things too often we are always measuring blood pressure click if you will so might that mean that 58 of adults within the UK have actually have insulin resistance now why would I make that connection click it's because and again the metabolic syndrome used to be referred to as click Nick if you will um the insulin resistance syndrome this is a better title while the word metabolic is certainly a little sexier feel part of me for being a little crass it has a little more of an appeal whenever we hear the word metabolic or metabolism we immediately have our interests peaked but it used to be called the insulin resistance syndrome when these when the constellation of complications was first identified by a famous metabolic scientist in the U.S decades ago who which means no one knows who he is at all um he called it the insulin resistance syndrome because all of these Pro which I prefer because when you call something the metabolic syndrome it still sounds a little vague a patient might not know what you're talking about even though they may like the sound of it or fear the sound of it if we call it the insulin resistance syndrome we are we are identifying the problem we're pointing the finger at the the cause of the complications so to make my point if 58 of adults within the UK have hypertension and then my speculation might that mean 58 have insulin resistance it's not much of a stretch because insulin resistance is generally among its first manifestations going to be identified as a hypertension or a higher blood pressure for reasons and mechanisms that I won't get into now next slide next slide um this is appropriate because Sam really teed this up well for me where he was indicating what are the top most expensive diseases within the UK this matches well with what I like to call the plagues of prosperity these disorders that were once unheard of our great-grandparents in previous generations they weren't dying from these problems that we are dying from nowadays and so insulin resistance is fundamental in contributing to heart disease it would be very uncommon not totally impossible for someone to have heart disease and hypertension plays into that without it being preceded and caused by insulin resistance and then certain forms of cancer if not caused by the insulin resistance and I wouldn't say it is it's exacerbated insulin resistance is accelerating the growth of the cancer and the most common liver problem worldwide fatty liver disease is directly caused by insulin resistance in the insulin promoting the growth or the the production of fat within the liver and then type 2 diabetes which is what I mean by diabetes here is one that we'll spend a little more time talking about I'll revisit that and then lastly body fat you cannot make fat cells grow unless unless insulin is elevated regardless of calories consumed Nick click it two times in addition to these big five Killers or problems we have some that range from similarly lethal and tragic like dementia and Alzheimer's Alzheimer's disease being the most common form and even stroke as Sam mentioned is one of the top top expenses that's contributed to here as well and then less lethal but very relevant to a population and very heartbreaking for a couple we have the most common forms of infertility the most common infertility in women polycystic ovary syndrome is more aptly called a metabolic infertility because insulin directly contributes to disrupted estrogen production from the ovaries and then in men there was a manuscript published a number of years ago that left an impression on me because the title was so compelling where they stated is erectile dysfunction the first manifestation of insulin resistance and otherwise healthy men the answer is likely yes due to what insulin resistance is doing to his blood vessels so all these across this wheel of Misfortune these plagues of prosperity um we can see that there is and I don't have the time to show you all the mechanism you'd have to take my undergraduate class at my University to get all that but there are direct mechanisms that explain how insulin resistance is contributing and causing these problems in one of my Great Hopes is imagining in my mind I imagine here in the UK a patient an individual goes home and opens their medicine cabinet every morning and they take out a pill for their hypertension a pill for their diabetes may be a pill for their migraine headaches and so on thinking that all of these problems because I have a pill for each of them must be unrelated and totally distinct little realizing that if we could shift the Paradigm somewhat to help impress upon the patient that these are not distinct problems that by changing a few core ideas which we'll get to and will be discussed aptly in this meeting and none of them will be surprising to you then we can start to put the medicine back in the medicine cabinet that one by one the pill becomes a little less relevant not that I'm giving medical advice all right next slide now I've been talking about insulin resistance and just to help you understand the scope of the problem I've already shared with you some of the statistics but I strongly suspect the problem is even worse than the data suggests they are click first one do you have high blood pressure or someone you know someone you might be thinking of click do you have a family member with any evidence or history of metabolic problems like type 2 diabetes or the pregnancy version of type 2 diabetes which is gestational diabetes next do you have PCOS for the females or erectile dysfunction for males next fatty liver disease have you ever been told that your liver enzymes were elevated not that that's proof positive you'd want some further confirmation and then next or are there some skin problems now thankfully freckles are not evidence of metabolic problems but there are some that stand out and that is skin tags and these have more complicated names and then these dark patches called acanthosis nigerkins these are often manifested on skin folds in the neck can be the most obvious example of that but these are all of these are strong evidence and with the skin in particular it's often a window to the metabolic Soul um but next if you answered yes to any one of these or the person you're thinking of they very very likely have insulin resistance each one of these are signs independently of the others of an of a metabolic problem next and this is why the problem is likely much worse because you could have someone say with skin tags and or acanthosis and agricans around the neck but they might still have a normal blood pressure and they might not have any other issues that would typically be identified as being metabolic next now what is insulin even I am a professor and I want to get back to the most basic principles next insulin is a hormone that is produced from the beta cells of the pancreas now insulin is a small hormone physically speaking the molecule is very very tiny which makes it somewhat in the past complicated for scientists to measure also complicating it is the actual amount of insulin we have in our bodies insulin is at fantastically low levels compared to other hormones and yet it is fantastically effective a little bit of insulin goes a long way it punches well above its weight class now the primary stimulus for insulin to be released next is glucose as blood sugar levels or blood glucose is going up next insulin will be released this is the most famous interaction with insulin next and insulin's primary action no surprise if its primary stimulus is high glucose no surprise that its primary mechanism or action is to lower glucose now I'm even miss speaking a little bit as I'm saying that I don't like to say that it's it's that the lowering of the glucose is insulin is its primary action it is its most famous action but that is almost part of the problem as I'll change the Paradigm in a moment people can't separate insulin from glucose whereas glucose is yes a stimulus and an effect insulin does many many more things next insulin that the effect on glucose is simply reflective of insulin's actions in nutrient metabolism it doesn't matter what the nutrient is insulin has a powerful effect on what the body is doing with it indeed one of insulin's thematic effects across the entire body is to tell cells what to do with energy which is why I made that comment earlier partly that if if you cannot you cannot lose fat if insulin is low or that body fat is directly contributed or affected by insulin it is impossible to make a fat cell grow without elevated insulin completely also it has effects on cellular growth in a very general way it has effects on electrolytes in a very important way and many many more effects but again the theme of it is telling cells what to do with energy and the fact that it lowers glucose well that's just one of its many effects um it and albeit its most famous next now what is insulin resistance we've been I've been alluding to it I've been mentioning it and now we understand what insulin is we need to understand now what happens when it breaks bad when it turns into the villain and so that's what we'll Define now next to understand insulin resistance we want to understand it from the level of the cell because when we say insulin resistance that is a cellular phenomenon and this could be any cell in the entire body it doesn't matter because every cell of the body has a little door for insulin to come and knock on called the insulin receptor literally every cell and I don't use the word literally like the kids do these days I don't use it too liberally I mean literally every cell of the body has an insulin receptor from brain cells to bone cells lung cells to liver cells and all the cells in between insulin will come and tell the cell to do something so click next and next again insulin will come and knock on the door of the cell next and in so doing will elicit the cellular action and I'm gonna I'm just going to call it action and keep it a little vague because it's no surprise what insulin does at a neuron is very different from what it does at an endothelial cell within the blood vessel so we have a cellular action next and its most famous action again next is to lower blood glucose and it does so by when insulin comes and knocks on the door it will open another door for glucose to come in now not all of the body's cells will do that but some of the biggest ones like muscle cells um will they will respond to insulin part of that response will be pulling the glucose in thereby lowering blood glucose insulin's most famous but not its most important effect next unfortunately over time due to a variety of noxious stimuli the cell can become increasingly less responsive to insulin and so what was once a robust action in response to a polite knocking on the door of the cell becomes a diminished one if not absent entirely next the consequences of this are myriad and well beyond the time that I have to share with you but suffice to say the consequences would be a lot of the plagues of prosperity that I've alluded to and Sam did too but the most famous consequence would be that blood glucose levels start to steadily climb eventually emphasis on eventually it is going to be a delayed response at the same time what is actually a less delayed response next insulin levels are elevated as well next and this is because if one polite molecule of insulin knocking on the door isn't sufficient to get the cell to do but insulin wants it to well then it will recruit an angry mob and now there is a mob of insulin pounding on the door of the cell next all in an effort to try to restore whatever action it can to whatever degree it can sometimes it can as we go across the plagues of prosperity sometimes it can't now next there are two important takeaways then in this definition it sounds like I've only been really talking about one but to understand what insulin resistance is and this becomes part of the diagnosis later that we'll talk about at the end you must appreciate the insulin resistance is a coin with two sides like every coin but the coin that I would be holding is a coin that I would say this is insulin resistance next and they're part of it one side of the coin is the whole phenomenon that I just got done talking to you about that some of the body's cells aren't responding as well to insulin as they used to but it's some cells aren't responding well next and this becomes a problem when we look at the whole body level next because if we look across the whole body insulin levels are elevated compared to where they were before next indeed there is no such thing as insulin resistance without hyperinsulinemia it cannot happen it doesn't matter what example an individual may be imagining whether it's the pathological insulin resistance that I focus on as a scientist and that contributes to the plagues of prosperity or whether it's the few instances indeed only two of physiological insulin resistance when the body has become insulin resistant in an effort to promote dramatic growth just as an aside that's the two P's of physiological insulin resistance pregnancy and puberty those are times of explosive growth in the insulin resistance and the hyperinsulinemia facilitates that explosive growth and it's not harmful it's necessary all right but in this same context whereas some of the body's cells aren't responding to the insulin and so the hyperinsulinemia isn't pathogenic or harmful we have another bunch of cells that are as responsive to insulin as they ever were like the ovaries for example they don't become typical ladies they're so sensitive all the time the ovaries never lose their sensitivity don't tell my wife I said that please um she's maybe sensitive to my joke so like for example the ovaries stay perfectly insulin sensitive and so the hyperinsulinemia is telling the ovaries to do too much whereas her male counterpart his blood vessels have become insulin resistant and so the insulin isn't telling the blood vessels to do enough the blood vessels need a lot more signal typical men right they need to be told a lot more in order to get the action that it needs all right next now in this Paradigm as I've presented it to you thus far I have described that the hyperinsulinemia is a consequence of the insulin resistance in other words the arrow going as I show you here that's not wrong I wouldn't have shown it if it were that is not a wrong perspective but it's not the whole story as we'll get to in a moment next all right now this is another Paradigm we're leaving the cell behind and now we're looking at an individual maybe a patient coming to their GP every year for an annual Wellness visit and we can see over time in the process of years that while we are obsessively measuring glucose the glucose levels are normal for decades and eventually they start to climb in perhaps even dramatically but that's not the whole story next if we were to superimpose insulin on this it would look something like this next where we can see that there are two distinct time points the first one next being a state of just what we would call insulin resistance or pre-diabetes it is so important to appreciate that the insulin is elevated in this state but not the glucose these are not the same thing and the GP you understand a clinician knows this a clinician knows that insulin and glucose are not the same thing but what they fail to appreciate so often I would say as a conventionally trained clinician and I'm not a clinician I'm a biomedical scientist but I've talked with enough and done enough versions of this talk to see the confusion in their minds so often the two can't help but go together that they are linked hand in hand in that if the glucose is high then the insulin is high or more often if the glucose is normal then insulin must be normal and it doesn't matter because what good is measuring insulin anyway to the conventionally trained clinician next it is only when the body has become so resistant to its own insulin that even though there is still an abundance of insulin and if it is type 2 diabetes it is always an abundance of insulin it does insulin never be never goes down to zero or even close in type 2 diabetes if that's happening in a patient it is not type 2. they have developed type 1 or they have some delayed version of another type called Modi it is not type two so even if the insulin levels go from their Peak which might have been 10 times higher than they used to be and start to come down which can happen it never goes down to where it was when the person was metabolically sound but even still the body is swimming in a sea of insulin and it just can't work well enough to control the blood the blood glucose levels we cannot look at these as equal numbers all the time next now we obsessively focus on glucose it has become the metric That Matters to most conventional clinicians but it shouldn't be I understand the reasons for it it's because historically the most uh prominent uh display or evidence of the disorder was the urine production which is what diabetes means producing a lot of urine and that is a direct consequence of the sugar the blood sugar levels the glute the glucose but we are more advanced than our ancestors were in some ways maybe not others but we have the ability to measure insulin next in fact two next and one more so glucose can be elevated about 10 or more years after the insulin has already been elevated this is well documented in prospective studies we can see over the person's time of getting measured and coming into their GPS that the glucose levels are staying in check thanks and the glucose but the insulin levels are higher and higher and higher so here's glucose staying normal for years here's the insulin going up and up and up and up and up just as I'm showing you here as you go from left to right we have to shift from the glucose Centric Paradigm to an insulin-centric Paradigm if we hope to really identify the problem because again it can take decades before the blood glucose levels ever start to change after the insulin next all right now we understand what insulin resistance is I've identified the villain of the story but now we need to understand its Origins how did it become the villain that it is next with insulin resistance there are what I consider to be primary causes next there are secondary and there are a myriad of them but I want to focus on the primary for the sake of time and and precision where I Define the primary causes as being causes that can independently of anything else contribute or cause insulin resistance in all three commonly used biomedical models so whether it is isolated cells growing in a Petri dish like I have in my lab back home now some fat cells are growing my students just started growing them up or whether it is in laboratory rodents or the Pinnacle the Pinnacle of all creation the humans we humans ourselves in all three of these biomedical models there are three I've identified three primary causes and I submit to you these are the primary causes so the ones that we should focus on the most not that there aren't others but they are next stress and next and one more inflammation and hyperinsulinemia which I just got done describing to you as a consequence of insulin resistance and a cause each of these are independent and and for the sake of time I'm not going to define the top two next we're going to focus on the elephant in the room the one that is the greatest contributor and the one that we can do the most about next now in this scenario hyper in too much insulin next as the body is flush with insulin it becomes increasingly less sensitive to insulin next and this is reflective of a fundamental biological principle it doesn't matter what we're talking about in life too much of something will result in a resistance to that something next now let me give you a funny little analogy this is me and my wife and our darling little children and sometimes darling sometimes demonic um but my darling wife is a full-time Homemaker which means she's full-time PTA at the school she's full-time involved in our church full-time involved in play groups with the kids very very when I say full-time I mean full-time but it means that she's around the kids quite a bit more than I am and she is used to hearing the noise of the children and this really leaves an impression on me when I'm home with all our double cherubs and when I'm with the family and I will hear the kids screaming for something and I'm amazed that my wife doesn't register it at all next she has become and one more next she's become somewhat deaf to this signal why because she hears it so much she has learned to just drown it out and if it's true crisis then she can respond next well I'm not around the children as much and so I hear everything and I react I have an action to the screaming whereas my wife is quite content to Let It Go She's become a little deaf to the children's screams I'm not I'm acutely sensitive to them because she hears it all the time I don't hear it all the time this is this analogy you can see it next now if we shift this a little bit and come back to the body and Insulin itself let me impress upon you the relevance of this issue why it is such a problem next the average in fact less than average person an uncommon person only eats three times a day a rare individual only eats three times a day and this might be what their insulin levels do they have a starchy sugary breakfast maybe a little more protein and fat for lunch and then they have a nice starchy sugary dinner this is what hap this is what their insulin levels would look like every time they spike it takes a couple hours or three hours to come down next now let's talk actually and next about the less than common person well the in fact sorry the common individual next who has been told that they should not only eat but they should snack in between their meals and so any moment where insulin might have come down it's immediately bumped back up where the average individual is spending every waking moment in a state of elevated insulin and as bad as this looks next this is what it looks like in a person with insulin resistance or sorry insulin sensitive which again is probably less common next the more common insulin resistant individual next will have an insulin level that looks like this where their insulin levels not only start higher they never go as low and they are elevated the entire time of day by the time insulin is attempting to come down they've spiked it right back up with their starchy sugary mid-morning snack or their starchy sugary afternoon snack or their evening snack next so back to this view where I described how hyperinsulinemia is a consequence of the insulin resistance next you're now understanding the idea that it's also a Cause this becomes a vicious cycle that just keeps accelerating more and more as long as the person continues their habits next now how can you correct insulin resistance next there are multiple ways actually next where it's drugs and diet are the main ones these are the ones I want to focus on because they're often the most leveraged um and and rightly so to varying degrees next now let's talk a little bit about drugs next and in so doing I cannot help but describe these what what's called anti-diabetic drugs these are drugs that are thought to be improving the metabolic health of the individual next and here is a list pretty comprehensive actually as short as it is that encompasses many of the most common or popular drugs for the sake of time I'm not going to talk about all of them for example I'm not going to talk about The glp-1 Agonist um I don't know what the trade name would be here but in the U.S bulgovianismic the world has lost its mind with these drugs and I'm certainly happy to answer any questions you have I'm very very familiar with them but I won't talk about them now because they're less used here all right next every time someone's taking a drug we must balance the consequences everything is a consequence to putting that in the body it's just a matter of are the consequences I want worth the consequences I don't want next here is my own version of it the Gospel According to Ben Vickman next let's start with metformin which is the most widely used anti-diabetic drug in the world for various reasons very very affordable and generally effective next however as effective as metformin is it has been shown to only be half as effective as even modest lifestyle changes so this big winner is still a loser when you compare it to lifestyle change which makes sense right metabolic problems are lifestyle problems next I want to introduce you to one other complication of metformin most people don't appreciate that metformin's primary mechanism of action is to act as a mitochondrial poison that's a dramatic term but of course I'm a professor and I need to keep students interested so I don't mind being a little dramatic um but it is a mitochondrial poison next it directly blocks the electron transport system the ability of the mitochondria to actually produce energetic molecules from the food that we have from from calorie molecules next and especially one of its primary sites of action is the muscle but that's a problem the muscle has a high metabolic demand and if we begin damaging the mitochondria damaging may be a strong word if we begin slowing down the function or compromising the function of the mitochondria there are consequences next in this group at a group um in in Colorado in the U.S they identified in humans this is a human study where they had individuals with insulin resistance undergo an exercise training program no surprise that when they analyze the mitochondria of the muscle the mitochondria were working better in the body was more insulin sensitive because of the exercise when they had the group exercise and take Metformin as you can see here this direct quote it undid the benefit it undid the mitochondrial adaptation to the challenge of the exercise and it even undid the insulin sensitizing effect of the exercise itself how can we in good conscience tell someone to use a drug that is literally undoing the benefits of the exercise it's difficult to Fathom next now sglt1 and two Inhibitors these are generally operated under the trade name with the suffix glyph flows in there are a lot of weird names to these drugs um but this is an interesting mechanism of action click next where sglt1 is a glucose transporter that will move glucose from the guts into the bloodstream sglt2 is a transporter that will move the glucose from the kidneys back into the blood the kidneys will pull the glucose in then sglt2 will put it all back into the bloodstream these drugs as the name suggests block that effect it closes down those transporters and that's if we are only looking at glucose next it works if you can block the glucose from coming in or push the glucose out through the kidneys into the urine you will lower glucose that will lower insulin and so if we just stopped there we would say well gosh this works let's just keep writing these prescriptions all day however there are consequences there's something within physics called an osmotic gradient to make it that sounds more complicated than it is but where there is a lot of glucose water wants to follow this is why in diabetes the person is urinating so much because the glucose that's getting filtered into the kidneys is overwhelming the kidneys ability to pull it back in and so we have a lot of glucose that stays in the urine well where there's a lot of glucose there's a lot of water and so there ends up being a lot of urine volume produced but there are consequences next if you block the intestines ability to pull glucose in you keep a lot of water in the guts as well and now anytime the person thinks they're going to politely pass gas they don't know what's going to come out and uh it's you know they're socially always on edge um or on the edge of their seat because the consequences can be quite catastrophic gastrointestinally speaking next also less maybe socially complicated but perhaps even a little more pathogenic is that the fact that you are basically creating a diabetes in the form of the polyuria the excess urine production and little bacteria eat one thing they eat glucose in the urinary tract is constantly being invaded by bacteria bacteria constantly trying to come up the urinary tract well if we are flushing the urinary tract with all the glucose that we're eating by dumping it into the kidneys it's like Aid stations on the bacteria's marathon to our bladder and then to our kidneys we're basically saying hey bacteria you look like you're getting tired here is some energy drink for you why don't and keep going and so it's no surprise that UTIs that urinary tract infections are so much more common we are feeding the little beasties helping them invade our body next but in this Paradigm if we are willing to block someone's glucose absorption and give them catastrophic diarrhea socially speaking or we are willing to block the kidneys ability and we're pushing it out forcing it out through the urinary tract I submit that there's like a little Shoulder Angel sitting on someone's side Whispering maybe just give them less glucose maybe tell them to eat less glucose if we're willing to block it from coming in or forcing it out just put Less in the system in the first place and then you've undone the necessity or the benefit of this drug class next now lastly I leave the worst for last so sulfonylureas and Insulin of course various trade names but the actions collectively of these will be to increase the insulin sulfonylureas you take the pill and it'll basically Force the beta cells to dump more insulin into the system then the insulin injection itself of course is going to increase insulin next the justification the justification for this that's not quite the next slide um is this Paradigm the the conventional clinician has a glucose Centric paradigm and so we look at the glucose and we say next we just need to lower the glucose at any cost next and ins but it's a good way to do that next is to just push the insulin up we might not even know where it is because it's so uncommon to measure insulin the clinician won't even know where the insulin is the patient won't even know where their insulin is and so who cares if we push it up even higher because we will have the patient's glucose going down but does that solve the problem next no this meta-analysis that was published a number of years ago noted that there is no clinical benefit to lowering the patient's insulin sorry lowering glucose in type 2 diabetes with elevating insulin next and in fact knowing what you know now that high insulin levels are a common cause of insulin resistance what do you think happens to the insulin resistance as you are taking the hyperinsulinemic patient and making them even more hyperinsulinemic remember it's the noise that's calling that's causing the deafness and we are simply cranking Up the Volume it's no surprise that insulin resistance gets even worse next so next again here are some quotes and mind you throughout my study throughout my presentation you might have noticed in the bottom left corner I have these little PubMed ID numbers so all of these those are all the citations if you're ever wondering so these are some direct quotes noting in type 2 diabetics that the longer or the more insulin the patient is taking the worse the insulin resistance is getting again it's no surprise if you remember that that high insulin is a cause of insulin resistance you can see how we're making the problem worse indeed giving a type 2 diabetic insulin is like giving an alcoholic another glass of wine hoping that a little extra alcohol will solve the problem it's the high insulin that caused the problem next and unfortunately it gets even more dramatic next whereas you put a patient on insulin therapy in fact Nick clicked three times if you will you look from the moment of treatment insulin dose over several months goes up and the body weight starts to climb all while based on the metrics being used the amount of food being consumed is dropping where over these few months they appear to be eating less and yet they're gaining fat now that might seem impossible if you strictly adhere to the laws of thermodynamics which I do actually um but I'm not ignorant enough to think that the human body is a closed system my body is not the universe as much as I'd like to think that I am the singular reason for the universe my body does not is not the Universe I have in your bodies as well we are open to the universe and we cannot ever totally account for all the energy that's being exchanged next case in point what few people realize is that the moment a diabetic is put on insulin therapy whether they are type 1 which I'm not really talking about or type 2 metabolic rate will slow in type 1 diabetics it's dramatic where insulin will slow the metabolic rate will slow by over 20 percent in a day once they got insulin therapy it's less dramatic in a type 2 diabetic but even still by dumping more insulin in the system metabolic rate will slow which is one of the mechanisms whereby insulin is able to tell the body to gain fat next now more lethal than just having too much body fat is the fact that substantial evidence suggests that when you are pushing the body further into hyperinsulinemia you are increasing cancer mortality in fact you're about doubling it so when the type 2 diabetic is put on insulin therapy the likelihood of dying from cancer which is modest but getting more common all the time is twice as about 90 in this study about twice as high as it should be next and then heart disease where the type 2 diabetics who have to take on the highest insulin doses even if they have perfect glucose levels they are three times more likely to die from heart disease so giving the type 2 diabetic insulin is a wonderful way to make sure their blood glucose levels are perfect but killing them faster next which is not the solution to the nhs's problems all right next now within this Grand scope to step back out and look at the plagues of prosperity again only these are only modestly affected next by elevated glucose so glucose is a modest contributor to these problems if it's a contributor at all and some of them it isn't directly next but what is directly contributing is the high insulin it is no surprise then that is if our therapy is based on increasing insulin we're killing them faster we're killing people next alright so next let's go back to the base cause if hyperinsulinemia is the primary cause next then lowering insulin needs to be the solution and we do that next through the food we eat next and that's all a matter of managing macronutrients next again so and again this is the way people eat around the world and to my great pleasure I've been able to give versions of this lecture not quite as specific as I'm giving now in countries around the world southeast Asia Asia Middle East where the problem is even worse than it is in in Europe and in the US or in America um these are the macronutrients next now let's see how these and again affect insulin click three times Nick if you would this is what happens when a person eats pure fat this is what happens when they eat pure protein and this is what happens when they eat pure carbohydrate or in the form of glucose this is a direct reproduction of data mind you I just literally made this by superimposing it on the figure you can't quite see the oh you can you can see it I can't in my view yes you see the PubMed ID number this is what happens anyone who tells you that insulin increases that fat consumption increases insulin does not know what they're talking about I've literally never seen a study that has shown that I don't know where that conclusion would come from I've done some of these studies myself and we'll be publishing some next and this is and again this is what it would look like in a different View um the effect of insulin with the various macronutrients or the effect of the macronutrients on insulin and again now it may seem like I'm just declaring war on carbohydrates and I'm not the type of carbohydrate matters enormously of course next but this is part of what plays into the justification on one side or another whether the person knows it or not for an insulin resistance scientist who acknowledges that hyperinsulinemia is the primary contributor one of these versions of the diet whether it's low fat and high carb or whether it's low carb and higher fat one of them is going to work better at removing the most offending agent here next and my earlier version of this lecture I had I was going to go through multiple studies that was just a little too burdensome indeed PhD has a wonderful um grasp some wonderful graphics and Link that actually highlights a lot of these studies themselves so I just refer you to the phd.org all right now this is one study though that took individuals and had them overeat carbohydrates which let's face it is what most people are doing right in the global diet 70 of the calories are coming from carbohydrates that's quite a majority this so this is what happened over seven days in a fasted state I'm already showing you the glucose levels now however next if we were to add on the insulin this is what happened to the patient to the subject's insulin levels over the same length of time by the end of the week in a fasted State mind you their insulin levels and a fasted state were two and a half times higher than they were at the beginning of the week just by overeating carbs for a week next this is insulin resistance normal glucose and hyperinsulinemia next and again now this is how when we eat these macronutrients there is a corresponding blood molecule with fat triglycerides would be the blood marker of fat consumption perhaps actually triglycerides is more complicated amino acids would be the blood marker of protein and then lastly glucose is the blood marker of carbohydrate next in Diabetes Type 2 diabetes which is just a prolonged insulin resistance which of these nutrients in the blood is the body struggling with actually there are it's a little more complicated than I'm mentioning but what's the one that we obsess over well of course it's the glucose and and no surprise that's the thing we're eating the most of next so I submit to you there are three pillars if lifestyle is the culprit it's also the Cure the food we eat is causing or can cure these metabolic issues and I there I could we could expand this um to add a lot more but first one click next control carbohydrates and by that I mean my suggestion is look at the amount of digestible glucose compared to the amount of fiber that would come with it um if there if it's relatively low if the fiber to everything else in there is is high then that will be a carbohydrate that's generally going to be good fiber will mitigate some of the glucose absorption and thus the subsequent insulin Spike will be about 30 or so less than it would be otherwise so control carbs my suggestion focus on whole fruits and vegetables as primary sources of carbohydrates whatever the carbohydrate desire is to eat focus on fruits and vegetables next prioritize protein this must be if you're prioritizing the best protein for the human body or any animal whatsoever it will be because even ruminant animals will digest the protein very differently but you want we humans we need it in our monogastric system we need it to come from animal sources every by every metric an animal Source will have Superior absorption and uh without the complications of a plant Source protein um not there are technologies that are improving plant Source proteins um but we are built to eat other animal and animal Source proteins prioritize the protein um whatever it's a modest insulin effect now in nature protein never comes alone in our hubris and in our fear of fat we've pulled it apart next but protein always comes with fat in nature there is there is truly no exception to this if it's a nature a natural protein fat comes with it that's how we should eat it not only do we absorb the protein better well because we digested better most people don't appreciate that that we think we have we have proteolytic enzymes in the intestines coming from the pancreas that will split up the proteins into small enough units so that we can pull it across our intestines but those proteolytic enzymes don't work as well without bile bile enhances the ability of the intestines to digest protein and we only have bile getting released into the intestines when we eat fat they should always come together do not fear the fat that comes with the protein and I would even say be liberal with adding some fat to your protein if not you know eating the fat alone perhaps okay so and Don't Fear The Fat next now as I wrap up and I just got done hopefully sharing with you some of the good news that as much as my talk has seemed a bit like a Horror Story um it's a happy ending which is that if we look through the lens through a glue an insulin-centric lens rather we appreciate that we just need to lower the insulin and we do that by managing our macronutrients controlled carbohydrates prioritize protein don't fear fat and I could have added frequently fast to keep my alliteration going um but that would be a really helpful way to lower insulin and literally cure the problem removing the medic keeping the medications tucked up in the medicine cabinet until they expire all right so how can we measure it next there are different ways to measure this and I've lumped them into two categories and for the sake of time I'm not going to talk about all of them but there are there are Dynamic measurements um and then static measurements and of course the static measurements are easier next and one more the dynamic measurement is a two hour oral glucose tolerance test with insulin being measured at the time points I'm not going to talk about it because it's so uncommon to get it done but the easiest way to interpret it in hindsight now I should have put this image in here because I have it and it's lovely but I didn't think I'd talk about it if the peak of the insulin is at 30 minutes and every subsequent point is lower that's a good sign if the peak is anywhere except anywhere outside of 30 minutes if the peak is an hour or 90 minutes that's a problem it's a warning that of insulin resistance all right now again it's not easy to get those done no matter where you live so let's talk about end with the static measurements click next and next again so there is the list and I just want to highlight the ones that I think are the most um telling the first one simply being measuring insulin I hope I got my unit conversion correctly going from the micro units in the US to the picamoles here but if fasting insulin is lower than around mid-30s Pika malls that's a very very good sign that I I believe David yes I need a GP here to kind of confirm um but that would be a good sign that insulin levels are in a healthy low range and the body is responding well to it in other words the body's insulin sensitive next but at the same time there is another molecule called C peptide that comes in the nanogram per mil range at very very low range mind you um but this sometimes I only mention this because I've seen how it gets confused with insulin levels c-peptide is not insulin but they are sister molecules that when they're born they're born as twins they come out of the beta cell into the blood one to one now hearing me say that every time the beta cell releases an insulin it releases the c-peptide that is true you may be tempted to think well then let's just measure c-peptide but you can't it has a very very different half-life see peptide sticks around in the blood much much longer so me mentioning c-peptide isn't intended to be a diagnosis a diagnostic measurement of insulin resistance but rather illustrative for the patient or the clinician to know is this a person who's making insulin on their own because if you have a type 2 diabetic patient who is on insulin therapy then measuring insulin won't work because you're just as much measuring what's coming from the syringe as you are what's coming from their beta cells but C peptide is only made from the beta cells so I cite this because if a clinician is wanting or the patient is wanting to get off their insulin therapy you need to know are the beta cells actually making insulin C peptide will be the confirmation that's the proof positive this is a person who can graduate out of their insulin treatments onto just a dietary regime and then next I have the Homa homeostatic model assessment h-o-m-a the Homa index um generally we want that number to be around 1.5 next and the value of Homa is that it takes both insulin it takes fasting insulin and fasting glucose into its equation and again if the answer if the solution to that little equation and you can find it online there are home of calculators here in the UK too then you for UK units then you know this this is a body that is insulin sensitive if the home of score is getting up to around three mid threes that's insulin resistance and then beyond that is typically just going to be full on type 2 diabetes so the homeless score is a very good one and one I recommend next now as I wrap up and I show you this wheel of Misfortune in some kind of bizarre game show um version uh there are four key things we've discussed in the time we've had together next we've talked about what is insulin resistance next where does it come from next what to do about it and lastly how to measure it with this information in all humility I believe that you are and we are all collectively well armed to not only understand this problem have the emphasis be appropriate and know how to solve it and it won't be from popping another pill next thank you all for listening and during the panel I hope you will submit a load of questions because nothing's Thrills a professor more than getting a lot of questions thank you all for listening thank you so much thank you thank you thank you [Applause] I'll say one question okay yeah yeah right well um Ben's done wonderfully on timing thank you so much found my nerves um we've got time to take one question um which I'm going to put to hey Sean good morning um and uh yes that is from Katie Whitehead where's Katie there she is excellent um so uh do you think there is a value in the suggestions of uh Jesse and chapsi the glucose goddess who's written about hacks to flatten glucose spikes um for example vinegar vegetables first and when you're eating and timing of exercise and things like that I do yeah just so I actually wrote a little blurb for her first book because I I really appreciated her sentiments yeah so she she we she and I've communicated quite readily yeah apple cider vinegar is one that I'm fascinated by um the effects of those and vinegar we don't commonly think of it as a fat but it is a short it's the shortest of the short chain fats in short chain fatty acids which we don't eat them normally it only comes from a process of fermentation but taking milk which doesn't taste sour and allowing it to ferment which now tastes a little sour if in nature or taking cabbage and then turning it into kimchi and now it's quite tart and sour those are short chain fats those hit the mouth and activate these bitter taste receptors anyway that's a long-winded way of coming back to apple cider vinegar short chain fatty acids are metabolic um very metabolically active molecules and aggressively enhance insulin sensitivity in the body so Jesse's reasons for mentioning apple cider vinegar are very very well Justified so I I really appreciate her sentiments she's a more glamorous version of a guy like me I make no claims to Divinity after all like she does excellent all right well thanks again Ben thank you thank you guys thanks so much [Applause] [Music]

Channel: Public Health Collaboration

Views: 87,591

Keywords: diabetes, diet, nutrition, health, public health, low carb, obesity

Id: KIk-uyGWnmY

Length: 55min 37sec (3337 seconds)

Published: Mon Sep 11 2023