Prof. Jeff Volek - 'The Art and Science of Low Carb Living: Cardio-Metabolic Benefits and Beyond'

well thank you very much that was really an awesome talk grant and I'm happy that our message is very similar a lot of overlap perhaps set in a slightly different way not as eloquent as as grant was but a lot of really great points were made especially related to personalization and individual variation that I think is lost amongst many scientists and so I want to echo many of those comments in my talk today but let me just first thank Rod Taylor I think most of you know organize this event glad to call rod a friend and gracious host really a outstanding human being who's doing a lot of great things in promoting low carb here so rod thank you so I'm going to get right to it got full disclosure I I tend to view nutrition through a metabolism lens and also you know very grounded in biochemistry so I'm constantly thinking about the way nutrients affect our metabolism and our biochemistry and how it's impacting our processing of nutrients from that perspective and you know despite being taught metabolism in different disciplines whether you're a dietician or physician or an exercise scientist you learn about glycolysis you learn about beta oxidation you learn about the Krebs cycle and so forth but what is often overlooked or neglected is this idea that carbohydrate has a profound effect on how our body processes nutrients how our body regulates lipid metabolism and so this this graph somewhat depicts that at a fundamental level a low-carbohydrate diet shifts metabolism over to burning fat it is by far the most profound stimulus to do that more profound than exercise more profound than any other drug so this idea that you know burning glucose as a fuel is ideal is clearly not consistent with the literature in fact we're now have a much greater understanding that when cells are utilizing ketones and fatty acids that's associated with profound effects on health very robust effects on a variety of different cardio metabolic risk factors most especially type 2 diabetes you know that's the no-brainer as you as you heard just a few minutes ago I mean insulin resistance is a form of carbohydrate intolerance so that's a no-brainer but we're actually seeing now increasing reliance on fat is beneficial for athletes who are insulin sensitive so there's a whole spectrum of potential benefits here ranging from different clinical applications to generally people who we think as being very healthy who are more interested in optimizing performance and recovery in addition to health so we in the United States have been advocating low-fat high-carbohydrate diets for almost 40 years with our dietary guidelines and all the other promotional materials around that but really the last year I've been at this for almost two decades there has been a really an uprising and debate that has reached a level that is much higher than I've ever experienced and that's just depicted by a few events here I think grant you had this particular paper on one of your slides there are a lot of people upset with guidelines unfortunately our expert scientific report released a month ago was a lot of the same old same old so it didn't really embrace a lot of the new science but there was a lot of debate around that a lot of people really very openly upset with those guidelines so I think we're on the verge of something changing quickly the you know in the background what we have going on is in obesity and diabetes epidemic that's sweeping across the planet like us like a slow-moving plague really I don't have the figures here for Australia but I get the sense you're following a similar trajectory as as we are in the United States we're looking at about 10% of the population in the u.s. having type 2 diabetes and what's more concerning is we have at least three to fourfold more individuals who have pre-diabetes so they're on the pipeline you know to develop to likely develop type 2 diabetes and that's why you see this upward trajectory so by 2020 we're looking at well over 40 million individuals with type 2 diabetes and you know beyond the personal suffering that goes along with these diseases there's an enormous economic impact here we spend in the u.s. today 200 billion dollars managing diabetes alone and that's expected to go to half a trillion dollars by 2020 so you know there's a huge burden here you know we're hemorrhaging money into our healthcare system to manage these diseases and that could bankrupt us so you know you heard about this continuum and it is a continuum the insulin resistance continuum on the far end you have the type 2 diabetics who at the core of their disease their insulin resistant they don't respond to insulin like they should in our current treatment paradigm for managing type 2 diabetes is low-fat high-carbohydrate diet plus drugs and more drugs and more drugs and it's it's insanity what other condition do we advocate a diet that requires you take more medication and it's not working the insulin is not without side effects it causes weight gain for example so that's the price you pay it to normalize your blood sugar is weight gain and so it's it's a progressive disease despite the fact that you're taking more medication but this idea that you know there is no one-size-fits-all again it's very important as a population now two-thirds of Americans are overweight so if you think about it the average person is not healthy anymore the average person probably has some degree of insulin resistance so we're not talking about a small number of individuals who would be better suited to a diet restricted in carbs versus one restricted in fact so you know I've mentioned this term carbohydrate intolerance and so you know insulin resistance manifests itself many different ways but we tend to really focus in on the impairment and glucose uptake so just think about that when your insulin resistant you're not able to take up blood sugar and utilize it normally you're you have an impairment so that is a form of intolerance if you're intolerant to gluten lactose or you're intolerant to gluten it's pre obvious what you do to manage that condition so what why that escapes us when you're carb intolerant I don't know but it makes perfect sense if your insulin resistant and carbon tolerant that you would restrict cars but if you look at what Americans have been consuming over the last several decades we have in fact done what we've been told we've been told to restrict fat and to some extent we've been successful at that proteins been pretty stable over the decades clearly the most salient change here has been an increase in carbohydrate and it's not spinach and broccoli it's accounting for that extra 50 grams of 200 kcals per day it's a lot of sugar and and unprocessed I'm sorry processed carbohydrate and that's not benign we're really struggling to metabolize that extra carbohydrate we're consuming so if you sort of track how does the body metabolize just a single meal of carbohydrate if you had a muffin and a banana this morning you had ten times as much sugar in that meal than you have in your bloodstream and that's a stress on the body so how does the body respond well normally if if you're if you're healthy the majority of that incoming carbohydrate gets absorbed as glucose and has taken up my skeletal muscle and it's oxidized or hopefully it's oxidized it may be temporarily stored as glycogen we have a finite capacity to store glycogen but eventually it's oxidized and that would be okay like your fourteen-year-old son probably manages that that pretty well but we now have very good evidence if you have insulin resistance you process that carbohydrate a little differently a greater proportion of it is diverted to the liver where it's converted to lipid it's converted to a fat process is called de novo lipogenesis and that's a you know an early sign that you're miss managing your current carbohydrate load in it's sort of the canary in the mine shaft that hey bad things are going to start to happen you're converting this cart to fat and we make our the fat that's made as a saturated fat palmitic acid that gets packaged up into a VLDL particle that gets secreted by the liver and that's what we measure as triglyceride in the blood and it's not you know it's not just any VLDL particle it happens to be packaged with a lot of saturated fat and I'll come back to this issue of plasma levels of Sacher FAT another fatty acids a little later but this is associated with a lot of collateral damage it's you know it's the starting point here for inflammation oxidative stress this lipid emia etc and it's in a fundamental to this is this diversion of carbohydrate to an alternative pathway so I've been very interested in studying ketogenic diets and I'd like to just depict here how that difference is different from other popular diets even different from paleo which is you know very popular in the United States I suspect it also has some traction here but that diet tends to be a little higher in carbs as well as a little higher in protein so for most people to be in a state of ketosis which I'll define in a minute that requires that you know the the diets probably less than 10% carbohydrate or less than 50 grams a day it also has to be somewhat restricted in protein which is fairly anti ketogenic and that's very different than paleo very different than Mediterranean and clearly different than you know the Ornish diet or the standard American diet so ketones are widely misunderstood even among healthcare professionals and physicians and dietitians so so I'll go through a quick definitions here first of all ketones are metabolites secreted from our liver their archaic molecules I mean they've been around throughout human history they were very important part of human history for Homo sapiens for that allowed us for you know to develop big brains you know even when we were going through long periods without food so they're very natural we're all producing ketones even if you're eating carbohydrate you're producing some level of ketone bodies in the liver and the primary one is beta hydroxy butyrate we also make a little bit of acetyl acetate these are really important molecules the term nutritional ketosis generally refers to an elevated level of ketones in the blood arbitrarily you know that level is about maybe 0.5 milli molar I'll talk about levels in a second but this is very different and this is the key point that is often lost this is a very different metabolic state than ketoacidosis yes ketones are acid very incredibly weak acids but the state of nutritional ketosis does not create any acid stress on the body whereas ketoacidosis is a very serious dangerous condition that is life-threatening then it and it is primarily a concern in type 1 diabetics who are insulin insufficient it is not a concern in anyone who's not insulin insufficient so the if you even if you have a basal level of insulin you will not have any concerns with developing ketoacidosis and then keto adaptation is a closely related term but that's more in regards to the process of adapting to being in a sustained level of nutritional ketosis and we don't fully understand the time course of these adaptations but the there is this important aspect of time it does take you know weeks perhaps months in some cases for the cells to get used to utilizing ketones so the level of ketones is important to understand because this is a differential factor between the nutritional or starvation or ketosis and ketoacidosis so in a carb fed state if you're eating more than 50 grams per day you're probably at a level of ketosis around 0.1 milli molar if you have fast overnight that may double but that's well below the levels you see when you consistently restrict carbs below 50 grams for most people where you'll see an order of magnitude increase so now you're up words of 1 millimolar or higher but to contrast that to ketoacidosis that's a whole other order of magnitude height now you're above 10 millimolar or in many cases with uncontrolled diabetes above 20 milli molar and that again is dangerous but you never get there it's not physiologically possible to get there if if you're not a type 1 diabetic so it's a matter of of concentration here that really differentiates us from ketoacidosis so a lot of the pioneering work and understanding ketone metabolism was done back 4050 years ago in the 60s by George Cahill and others and what they discovered was that the primary role of ketones was to serve as an alternative fuel for the brain and we often hear or read in textbooks that the brain is a glucose dependent organ and you know I guess that's true to some extent if you're constantly eating carbohydrate then you're inhibiting ketosis that the brain does rely on glucose as a fuel and it's not a small amount of glucose I mean our brains burn about 600 kcals per day just being a brain so they're very energetically expensive you know per program of tissue so that's about 120 hundred 50 grams per day required to fuel that brain and it likes to have a steady source of glucose otherwise bad things happen so in you know some of the work Kano did they they were looking at starvation ketosis so they had people that were without food for 3-4 weeks with ketone levels four or five millimolar and what they showed was that the brain could extract over half closer to two-thirds of its energy supply from ketones substantially reducing the need for glucose and there is no obligate need for dietary glucose because of course we can meet that small amount of glucose required for the brain through gluconeogenesis or the formation of glucose from non carbohydrate sources now one of the really important adaptations that occurs in ketosis is you know is this protection from low blood sugar I guess that should be Kido adaptation on the top there typo but this was an experiment dr. Cahill did in the 60s which I doubt we'll ever be replicated because of IRB boards and etc but they took a group of healthy individuals that had been starved for four weeks and you can see their ketone levels were elevated as you'd expect around five millimolar there glucoses were very normal at 70 milligrams per deciliter sorry if you're thinking in millimole I guess that's what for roughly so normal level they then proceeded to intentionally drive their blood sugars down by intravenously infusing insulin and of course being healthy the insulin drove their blood sugars down to an levels that were on average around 20 milligrams per deciliter and they talked about in one of these papers one individual getting down to nine milligrams per deciliter so that's what point 5 milli molar and you know for the non clinicians in the room that level would cause coma and most people and you'd be very close to death in these individuals who had been starved and in ketosis and notice that insulin infusion lowered ketones but they're still well in the millimolar range they had absolutely no signs or symptoms of hypoglycemia or low blood sugar felt completely fine and you know this is a dramatic example of protection from up low blood sugar but we're seeing this all the time in athletes for example who are becoming bomb-proof or they don't hit the wall now after two hours of exercise when their glycogen levels are depleted and their glucose supply to the brain is is impaired but even the average non-athlete often you get these mini bonks during the day when you get tired after you eat a high carb meal at lunch and you're ready for a nap that's a you know that's related to decreased blood sugar supply those are gone when your key to adapted and it's part of this this mechanism here this profound protection from low blood sugar so we've known about these metabolic benefits of ketosis at what it's what allows us to survive in the absence of food but it also has a lot of benefit when you're eating fat and protein but continually restricting carbs and in a state of ketosis so there are these well-known and important metabolic roles of ketones what has also emerged really in the last two years and it really broadened my perspective on ketosis is information about ketones and their non metabolic roles so their role as signals and regulators of gene expression so without going into too much detail there was a paper published in science in December of 2012 which i think is really a you know watershed paper that laid out in a very elegant series of experiments the mechanism by which beta-hydroxybutyrate increases gene expression in particular antioxidant genes that protect against oxidative stress and of course it was a science paper so there was a little science in I mean they they showed it was a potent histone deacetylase inhibitor which is a really hot drug target right now for anti-aging in longevity and insulin sensitivity and so forth so you know if you think about it a minute we have a diet now that produces a metabolite that is well known to have potent drug like effects I mean if we could bottle beta hydroxy butyrate as a drug I mean we'd have a blockbuster drug really and we can do this just by manipulating our diet and elevate this particular metabolite so you know this is just kind of a diagram to depict some of the new rules of beta hydroxy so I guess I didn't mention explicitly the substrates for ketones or fatty acids so we have a huge reservoir of fatty acids in our adipose tissue or we can get those fatty acids from our diet and they're converted to ketones and that provides an important fuel for the brain that's our traditional understanding now we're really broadening the perspective of ketones in terms of other metabolic effects we also have known for some time that when ketones are eventually oxidized I mean they are alternative fuels so they do eventually get into the mitochondria and generate ATP but they seem to have some unique features that for example work by Richard Veatch has shown when mitochondria are utilizing ketones as fuel they're throwing off less reactive oxygen species less free radicals compared to glucose or pyruvate or even fatty acids so in that regard you can kind of view them as clean burning fuel not not as much exhaust being generated that the body has to then deal with combined with this fact that they're up regulating anti oxidant genes it's kind of a dual protective effect you're generating less reactive oxygen species if you're burning ketones plus you're enhancing your body's ability to defend against those reactive oxygen species so the science of ketones is really fascinating now but just to kind of take a step back and look at the the body of work that's been done on low carbohydrate diets over the last decades really been quite a remarkable decade the majority of its focused on weight loss and you know look at these meta-analysis now that we know pretty recent published in the last couple years there's not a lot of controversy here all these meta-analysis are more or less agreeing with the idea that low-carb diets result in greater weight loss than low-fat diets and even cardiovascular risk factors are improved more so the science is really compelling and most of you know that so speaking to the choir but in my mind you know weight loss is sort of a side benefit it's really the one you know one benefit of a low-carb diet that represents sort of the tip of the iceberg there are so many other metabolic effects of low carb diets that are being explored now so just to give you a sense of current areas or emerging areas of interest around ketogenic diets it's not just adult obesity now there's pediatric obesity is a huge problem not just type-2 diabetes which I'll talk a little bit more about but there's pretty good evidence now type 1 diabetics have a lot of benefit from following a ketogenic diet polycystic ovary syndrome which is highly related to insulin resistance we've known for a long time that ketogenic diets were nothing short of a miracle for for kids with intractable epilepsy and and that continues to be looked at in terms of understanding mechanisms and just awareness of that but what I've been fascinated with and I've spoke a couple times that the neurology meetings is that this is expanding into other areas of Neurology so there is very strong interest in therapeutic roles of ketogenic diets and Parkinson's disease and Alzheimer's disease and autism even migraines etc so so that's all looking very promising we have a long ways to go in terms of clinical studies and so forth but we're seeing a lot of interest in a lot of basic science all pointing in the right direction and perhaps the most exciting area I think is in answer where we have a really good understanding of some of the basic aspects of tumors it's incredibly complex because every cancer is different but the majority of cancers seem to you know be associated with mutations in the insulin signaling cascade and they seem to be associated with an increased reliance on glucose metabolism so it makes an enormous amount of common sense that these types of tumors would be amendable to a ketogenic diet and that's in fact with a lot of the basic science the animal studies and even now we're starting to see some human data showing remarkable benefits of ketogenic diets so that's really exciting area that I'm sure is going to continue to see a lot of attention so I think grant showed you this slide this was one of our studies that shows pre broad spectrum improvements in all sorts of different biomarkers in response to a ketogenic diet versus a low-fat diet this was in pre diabetic patients that were both consuming low calorie diets so we have really tried to take a broad perspective and measure all sorts of different biomarkers and there's hardly any they respond in a negative way I will instead of going through each of these just point you to one that I'll maybe talk more about if you'd like but you know the one area that does get some attention and does create some anxiety even in low-carb supporters is this it's not even on here but the increase in total cholesterol and LDL cholesterol which is quite variable from person to person unlike the triglyceride response which goes down in almost everyone so we see in a subset of individuals maybe 15 to 20 percent a rather sharp increase in total and LDL cholesterol and the question is should we be concerned with that sometimes it's quite dramatic and I'm not sure I have you know the the end the total answer to that question because we don't have the long-term studies with hard outcomes but in the context of an isolated increase in cholesterol when every other biomarkers improving it's hard to imagine that's associated with an increase in ethyl cirrhosis or plaque development and and contributes to this pathogenesis of heart disease but we don't have that hard data but we do know that cholesterol is disconnected from atherosclerosis in many studies and it's very much a byproduct of pharmaceutical marketing in my mind even the statins that lower LDL in almost everyone don't do a great job at decreasing heart outcomes but we've looked at more than just biomarkers we've looked at vascular function you know looking at brachial artery reactivity which is kind of taking us a little step further rather than just looking at intermediates we're actually looking at how the blood vessels are functioning and that improves in part because I think we're decreasing the light payment response the triglyceride response to a meal as Grant showed earlier is dramatically decreased by 50% and we know that the either high glucose or high triglycerides is associated with vascular impairment but when you're adapted to the diet you you see both those metabolites go down in the blood so it's not surprising we see improvements in vascular function and of course blood pressure that's a very consistent response as well both systolic diastolic blood pressure improve we also very consistently see a range of pro-inflammatory biomarkers decrease on the diet so when you get the diet right you often see a lot of signs and symptoms of inflammatory diseases improve so that kind of ties in with the decreased oxidative stress and inflammation they kind of go hand-in-hand so the I think just coming back to that isolated increase in LDL cholesterol that we see in some individuals that is a little bit unpredictable so we don't know you know which individuals those are going to be what's not so variable is the qualitative changes in LDL cholesterol so we now have a really good understanding that you know the the LDL particle is not a homogeneous particle it's made up of different sizes and compositions and it's really the smaller denser LDL particles that are most problematic these are the guys that get into the arterial wall they're more prone to oxidation they have a longer half-life etc so there's many good studies now that show if you if you have a lot of these around then you're at higher risk for heart disease there is no stimulus that increases the size of these particles more than a low-carb diet statins don't do it none of the other lifestyle even exercise or fish oil or smoking cessation do it so if you want large fluffy buoyant LDL particles restricting carbs is definitely the most effective way to do that so that's very a very consistent response even if your cholesterol total cholesterol LDL cholesterol concentration went up your small LDL particles will likely decrease and that's not just work we've done we've probably published to half a dozen studies showing that but Ron Krause was really the pioneer in in you know developing a lot of the methodologies for measuring these particle sizes as well as publishing many studies these dots are all studies from his lab group and they all represent different levels of carbohydrate and on the left or on the y-axis rather what you have is the percent of the cohort who has pattern B pattern me being the unhealthy profile or phenotype where you have a lot of the small dense LDL particles so you see a very tight fit here you know it's almost too too good to believe that you have this tight correlation between carbohydrate and a diet and the prevalence of this pattern B to eat more carbs you have more that this atherogenic pattern B profile and we see people all the time convert from pattern B to pattern a when they go on a little carb diet so I want to I want to switch gears a little bit and move away from cholesterol because I've never put a lot of weight in cholesterol in the first place I tend to think it's the fatty acid composition that's a much better indicator of disease risk and this ties into the saturated fat story which you know could kind of take another step back has been the cornerstone of our dietary guidelines and which continues to be in this latest report we're continuing to tell Americans to restrict saturated fat and it's really backfired but hey we're sticking to our guns you know we didn't do it hard enough right so so here's the latest evidence though around saturated fat that apparently our expert scientists all ignored but this is pretty settled in my mind I mean these are three really large meta-analysis there's been a couple others even more recently that all ask the question is there an association between dietary saturated fat and heart disease of course the result as you can see here is no and these are pretty comprehensive examinations of all the evidence and if you take it a step further you can also look at risk for diabetes risk for cancer not nothing so why are we concerned about saturated fat I don't know but and it's not without consequence either because by telling people to restrict saturated fat we in turn replaced those calories and more with carbohydrate and in one of these meta-analysis they actually showed that dietary flip-flop increased your relative risk of having a heart attack and that's not some bizarre flip either that's exactly what Americans have done but it gets a little more complex because if you look at studies that have measured saturated fat levels in our body so this is typically done by measuring blood levels but you could measure tissue levels as well if you can get access to tissue you do see a consistent increased risk for heart disease if you accumulate saturated fatty acids in your lipoproteins or in your membranes that's not a good thing and so here's just four I could present another dozen studies that have all shown higher levels of Kemetic acid or total saturated fatty acids does increase your risk not just for heart disease but also diabetes or metabolic syndrome even some forms of cancer you know it's it's consistently associated with a lot of bad things so then the question is well what's contributing to storing saturated fat and a lot of us just over simplify this and think you know we are what we eat so if we eat saturated fat we're going to have more in our body and of course we we know that's not true what's really happening and we've talked a little bit about this earlier is the conversion of carbs to fat when you're over consuming carbs relative to your tolerance you're making more saturated fat and so that saturated fat is what gets packaged up into the LDL particles and ends up in our blood and that's what measuring and we know from many studies that's associated with insulin resistance so we've now done three feeding studies to address this issue or and this is data from our first study where we randomized individuals to a low-carb or low-fat diet what's important here is that the ketogenic diet had three times the level of saturated fat as the low-fat diet when we measured saturated fat in the blood it actually went down more in that group so you're eating more fat but you have less in your body and then I'm going to come back to this as well a little bit later but we also see very consistent changes in this particular fatty acid called palmitoleic acid or 16-1 which we know without going into too much depth here increases when your body is converting a lot of carbs to fat so it's a good surrogate for de novo lipogenesis which otherwise is not really easy to measure so here's sort of a cartoon to represent the what I would say the current understanding of the interaction of carbs and fat and and the main point here I'll just say up front is that any discussion about saturated fat has to also talk about the background level of carbohydrate because that you know going back to my very first slide is what controls fat metabolism it's the carbs in your diet if you're eating carbs and you're secreting a lot of insulin you're constantly inhibiting your ability to burn fat so you're more likely to accumulate and store it so if you kind of play this out with the typical meal if you have a nice marbled steak here for dinner but you also indulge in the starch with that that saturated fat you're likely to be in a metabolic state where you're more prone to accumulate the saturated fat and that's what's happening you know the average diet is high in saturated fat and sugar and carbohydrate but if you have that exact same steak and even lather it with some some butter but you forego the rice or the potato and instead have extra vegetables even a glass of wine maybe some cheese perfectly enjoyable pleasurable meal you don't have the insulin response you have a very different metabolism of that that's the same saturated fat you're not going to accumulate it you're going to burn it for fuel and it's really hard to imagine that saturated fat that you're eating is going to have any harmful effect if you're promptly converting it to co2 and water and that's what happens you know when you become really efficient at burning fat you're converting saturated fat into fuel and those are the byproducts so what happens when you're over consuming cards and I apologize if fatty acid composition and nomenclature makes you nauseated because it even makes me a little nauseated but this is kind of important because I I thought for some people this would be interesting in that it's really in my mind moving us toward developing some biomarkers to help people personalize a low-carb diet because again everyone's a little different but if you intentionally over feed carbs to people and that's what they did in this experiment it was short-term but they were stuffing people with carbohydrate and they were even infusing glucose into these people just to intentionally induced de novo lipogenesis you do see that saturated fat levels go up in the blood after three days of carb overfeeding it's a pretty big increase but proportionally the greatest increase was in this particular biomarker this palm palmitoleic acid which is the one I was telling you that goes down most consistently on a ketogenic diet so that's some of the evidence that suggests it's a good marker of carbs converting to fat but those are overfeeding studies what about if you're eating a low calorie diet canary if your carbon tolerant can you still be converting carbs to fat even though you're in a negative energy balance and that was sort of the question we wanted to ask in this feeding study where we took people through six different diets that were increasingly higher in cards and lower in saturated fat but low calories so there was actually continuous weight loss over this about five and a half month period where we had them in a ketogenic diet initially and then we took them out of ketosis and added more carbs and we published this paper a few months back and plows won but I just want to show you the changes in palmitoleic acid under conditions of vince's hypocaloric conditions but high carb moderate carb very low carb you see every single person here you know goes up in this biomarker as they increase carbs but at any given level of carb these people were all eating the exact same food yet look at you know there's a two full difference in their level of this marker and that's probably because of their genetic propensity for insulin resistance so this again speaks to the need to individualize the diet but we're moving closer to potentially using a marker like this that's surveying our body so to speak in terms of how were processing carbs on an ongoing basis and whether or not we're disposing of too much of it into alternative pathways and converting it to fat and we kind of knew this this was from old study that Steve Finney had done and we combined it with some newer data we had and kind of came up with this this graph which shows the same concept that you see a uniform change in this biomarker as a function of carbohydrate or fat in the diet but at any given level there's quite a bit of variability with it with a group of people so what do we know about this biomarker palmitoleic acid well it's a monounsaturated fat and has one double bond it's made as the desaturation product of this saturated fat palmitic acid that's the most common saturated fat in our diet and the most common saturated fat in our membranes but when we when we have a lot of that it gets D saturated by this enzyme into this monounsaturated fat so proportionately that's why it goes up more than this this is confounded by diet too we don't get a lot of this in our diet we don't know let's eat a lot of macadamia nuts or avocados which some of you may do I'd certainly do those are the only really rich sources of this so it's not confounded a lot by diet which is another reason it's a good biomarker but more than that we have a vast amount of research on this particular fatty acid correlating with a wide range of negative health outcomes so higher proportions are associated with obesity insulin resistance type-2 diabetes heart disease cancer a lot of bad things so in it of itself this is an independent risk factor for a lot of diseases and we know that higher levels are predictive of developing type 2 diabetes even before you see big increases in blood sugar so I'm almost done here I want to sort of summarize in a minute here but just one of the questions I get a lot we could because a lot of people are moved by the science now it's pretty overwhelming if people are willing to listen for a little while but even even so there there still seems to be a lot of skepticism on whether people can sustain this diet and so there's a you know multiple ways to sort of address that but in the literature anyway I think one of the best studies and this gets ignored a lot because it wasn't a randomized controlled study was done in Kuwait by a doctor dasht-e and I like this work too because he's one of the few people who I think really got the diet right I mean they used a well formulated ketogenic diet can kind of see the their principles of the diet they used they didn't over consume protein they encouraged fat and they really kept these individuals who were primarily type 2 diabetic low-carb through the entire duration of the study so this is basically the weight loss trajectory in individuals with high glucose and normal glucose you see sustained weight loss over a year period and you see rapid improvements in their blood sugar that again were sustained over a year period they were also reported sustained improvements in blood lipids and other other biomarkers so this can be done if it's if it's taught appropriately and people are given support it can be sustainable and clearly as there's many examples in this room I'm sure that you know are able to also sustain this type of diet and I'm going to skip past this because grant you covered the A to Z study but just to sort of summarize here and sometimes cartoons are and analogies are good to understand complex metabolic concepts so if you think about over consuming carbs relative to your tolerance it's it's a bit like filling up your gas tank it you know you need to have gas in your tank but if you just kept the tank on and gas is squirting all over the place that's not a good situation especially if you have a spark somewhere and that's what's happening with a lot of individuals they're already tapped their carbon tank is full and they're continuing to eat more carbs and there's nowhere else for carbs to go if we can't store it you can't burn it you can't store it as glycogen rather and you can't burn it the only other alternative pathway is to convert it to fat and that really set you up for a lot of about problems so in summary that's that's kind of my main point its the overconsumption of carbohydrate that exceeds an individual's tolerance so it's not some magical number it's different for everybody and even within a person it changes over the lifespan as as grant very appropriately stated so so it is individual but that inability to oxidize the incoming level of carbohydrate is the fundamental problem that underlies obesity and insulin resistance and all its secondary manifestations so that's why low-carb works we don't understand exactly all the details of how low-carb works but it's really that simple I mean it's it's it's correcting that a overconsumption of carbs and when you do that a lot of these bad things get better especially for individuals with insulin resistance so I'm just going to leave you with this slide because this really my point here is that this is it's just how important this is because in the United States for example again as I said earlier we have two thirds of Americans overweight so it's likely most of those individuals are insulin resistant at some level so we're talking about not even tens of millions of people that's incredibly conservative more like hundreds of millions of people in the US and this is worldwide there's no continent that's really escaped this you know this this problem so worldwide we're talking about hundreds of millions of people who would be much better suited for a low-carb diet I was just reading in China that they have over a hundred million people with type two diabetes and just under a half a trillion people with pre-diabetes in China alone so the numbers are staggering here so in terms of the good that can be done and people that we can help just by manipulating diet so thank you for your time I hope there was some new information in there that you were able to to absorb and carry forward thank you very much

Channel: Low Carb Down Under

Views: 319,516

Keywords: Professor Jeff Volek, Professor Stephen Phinney, The Art and Science of Low Carb Living, Low Carb Down Under, www.lowcarbdownunder.com.au, LCHF, LCDU, The Art and Science of Low Carb Performance, Low-Carbohydrate Diet, Metabolic Syndrome (Disease Or Medical Condition), Carbohydrate (Nutrient), Metabolism (Literature Subject), Nutrition (Medical Specialty)

Id: tC_qBC1EEvw

Length: 48min 16sec (2896 seconds)

Published: Sat Jun 20 2015