David Ludwig - Which Comes First, Overeating or Obesity?

you usually when I you know when an academic gives a talk in front of peers you know even if they agree with you they won't let you know in the audience's you know you get points for making zing questions and you know so it really is a pleasure to speak to a friendly audience for a change and my work will be really easy because this question which comes first overeating or obesity was beautifully answered by Gary Taubes yesterday so many of these concepts are going to be very familiar at this point so my job will be just to dig down a little bit deeper into the research data and build a broader case and these are my disclosures well the first law of thermodynamics holds that all that energy can neither be created or destroyed and applied to living systems we have the familiar equation calorie intake - expenditure equals calories stored and since in humans most of our excess calories are stored in fat we can change the right side of the equation - fat mass or adiposity according to the conventional interpretation of this law obesity is a personal failure to control their energy balance so in our modern food environment with ubiquitous tasty foods it's easy easy to over consume taken too many calories but because of the absence of opportunities for physical activity recreational and lifestyle those calories build up in the bloodstream they don't get burned off they build up as calorie rich substances like glucose and lipids and they get forced into fat cells making them anabolic or making them grow so the simple solution of course is eat less and move more the conventional view places the responsibility squarely on the individual to control energy balance this is from the USDA MyPlate website reaching a healthier weight is a balancing act the secret is learning how to balance your energy in and energy out and if you like the energy balanced approach to obesity you're gonna love a low fat diet fat has twice the calories per gram of carbohydrate and protein and it this notion was one of the main design principles for creation of our first USDA food guide period of a pyramid of 1992 we were told to eat all fat sparingly no avocados nuts fatty fish or full fat dairy they should all be consumed sparingly and instead we were supposed to load up on those mostly processed grains remember how many servings 6 to 11 servings and if you add in those little potato that potato you know you could get up to 13 servings a day of starchy foods and be in full compliance with recommendations now this notion of low fat diet was inspired specifically out of considerations of energy density the Surgeon General's report in the 1990s placed specific primary emphasis on reducing dietary fat because of its high calorie content whereas sugar was really just a consecutive concern for groups like children who were at risk for dental caries now we you know colleagues nutrition establishment doesn't like to it has a remarkable amnesia about this just 20 years ago extreme statements were made in favor of carbohydrates and against fat these are quotes from society leaders published in leading medical journals one team said when people are allowed to eat from ranges of high fat or high sugar foods passive overconsumption only occurs with fat it follows that fat promotes over consumption while sugar probably prevents it another team said the evidence intriguingly suggests that it is specifically an increased intake of sugars rather than complex carbohydrates that dilutes fat energy and a third group said by decreasing the ratio of fat to carbohydrate eating less fat in more carbohydrate carbohydrate you can get balanced with less emphasis on the carbohydrate so you don't have to worry about the quality of the carbohydrates you're eating just eat more of them all of them and the problem will be taken care of the government joined in on this quest this is the healthy to people 2000 goals that called on the food industry specifically to market thousands of new processed foods that were low in fat and saturated fat so if you're gonna take out the fat what are you gonna replace it with if it's a processed food sugar and refined starches and we got an invasion of the food supply with these foods with these products now the apologists of the conventional view like to say there was no problem with nutrition recommendations there was no problem with the government's advice it was the public they misunderstood our approach we meant that they should be eating more fruits and vegetables and instead they took this as license to eat junk food but that's a selective amnesia you know I'm know I've never been a big defender of the food industry but the food industry responded to calls from the putt from the government and from nutrition experts and the public was doing what they were told you know and I think it's important not to forget this history because if we forget it you know we're gonna be doomed to reproduce it to relive it so as a result proportion of calories went up as carbohydrate down as fat just as intended and the obesity epidemic developed over that time period now this doesn't prove cause and effect but these randomized these meta analyses of clinical trials suggests that our recommendations to reduce dietary fat actually was not just misguided they actually importantly caused the trout in each of these cases whether the comparative group was a medium fat Mediterranean diet high fat low carb diet or a ketogenic diet in each of these cases the low fat diet was inferior to the higher fat diet opposite to what was predicted we know that very few people can lose weight and keep it off for the long term in adults and children the situation is just as bleak very few you know the situation is marked by small changes in weight and substantial relapse so we have to ask why is this paradigm it's so simple right just eat less move more why is it failed well one obvious problem is that completely neglects virtually a century of research to indicate that body weight is importantly controlled by biology a complex interaction of crosstalk among key body organs hormones metabolic signals neurological influences that serve to control weight we know for example that when a person whatever their weight is lighter for a lean person heavier for someone with obesity whatever that baseline weight is when you put that person on a low-calorie diet cut back calories at first they lose weight that's just a law of physics but what happens hunger increases and if you ignore hunger and try to keep eating less your metabolisms going to slow down your body is gonna fight back against calorie restriction and that's inevitably for most people going to push them right back to where they started but the opposite is also true when individuals are overfed you know in these classic force-feeding studies you know the volunteers to these studies would think this is great I'm gonna get paid I'm gonna get paid to eat a thousand extra delicious calories a day but they quickly realize it's not such a great bargain after a few days of overeating they lose all interest in food and their metabolism speeds up in their bodies attempt to get rid of those calories and so they to come right back down to baseline giving rise to this notion of a body weight set point which we intuitively sense must have something to do with our genes but if we do have a set point we have to ask why is this defended level of body weight crept up year after year why did a typical man of 5 foot 9 inches have happily maintained a body weight of 160 pounds in the 1960s if you force-fed him to gain weight you would have come back down to 160 but today that same typical man is defending a weight of 185 or 190 pounds so why is that what can we do about it well we're not going to get any answers from the conventional calorie balanced view this conventional view may acknowledge that body weight is controlled by biology but it lacks any kind of compelling biological explanation for the for the obesity epidemic beyond saying that you know it's difficult for people to control their behavior in the modern food environment there are no testable hypotheses for why the setpoint is going up and with this insistence that all calories are alike treatment inevitably devolves back to what eat less and move more well we know that this relationship between energy and take expenditure and fat storage can't be wrong that's a law of physics but maybe as Gary Taubes suggested yesterday our assumptions of calls of direction were the problem maybe the arrows don't flow from left to right they flow from right to left now this also doesn't violate the law of thermodynamics but it has a fundamentally different implication to obesity treatment according to the carbohydrate insulin model something has triggered fat cells to take in and hoard too many calories leaving too few for the rest of the body the brain perceives that and that's why we get hungry and if we neglect that if we keep trying to restrict calories energy expenditure declines we get fatigued were less likely to be active more likely to collapse on the couch are resting energy expenditure decreases muscles work at different efficiencies so from this perspective the recommendation to eat less and move more misses the point and can actually make the problem worse if the problem is there aren't enough calories remaining in the bloodstream to nurture the brain which we heard so much about yesterday and the body organs then further attempts to establish a negative calorie balance are going to make people feel worse and that's why people fall off diets and feel terrible on diets long before their weight loss goal is in sight you know somebody 250 pounds loses 20 pounds their body is going to be fighting back even though they still have plenty of calories on their body too many calories but their body's fighting back because those calories are locked away in the cupboard you know like what is it the calories check in but they don't check out and they're not doing any good if they're stuck in the fat cells the brain thinks it's a question of starvation so what could be triggering fat cells well the obvious player is too much insulin and I call insulin the miracle-gro for your fat cells just not the sort of miracle you want happening in your body insulin regulates the availability of all of the metabolic fuels it stimulates fat synthesis of deposition it limits release of fat from fat cells we know that states of excessive insulin action know not levels because there can be also insulin resistance so you have to think of insulin action states of excessive insulin action consistently lead to weight gain such as starting someone with type 2 diabetes on insulin or an insulin secreted that's going to cause weight gain but the opposite is also true without enough insulin you can't gain weight a child with type 1 diabetes which is an autoimmune condition which lowers makes the body unable to make enough insulin when that child first comes to attention she will have inevitably I lost weight that's one of the key presenting features of type 1 diabetes she might be eating three five or seven thousand calories a day weight loss is inevitable with new onset diabetes until insulin treatment is starting give the right amount of insulin weight trajectory returns to normal give the child too much insulin and excessive weight gain occurs now if you and some studies by Robert Lustig on insulin blocking drugs are also part of this story if you don't have diabetes the quickest way to change your insulin levels you know without just eating less is based on the amount and type of carbohydrate you consume and in terms of the type glycemic index is relevant it's not the whole story we really need the two together glycemic index takes him to account how food with the same amounts of carbohydrate influence blood sugar so it's going to distinguish white bread from beans or berries you can have the same grams from those two foods and most people although there's going to be variation as we know from the Israeli studies but most people are going to have markedly different on average glycemic responses to those kinds of differences so when you put them together you have glycemic load and that means you know you've heard it the grant process grains potatoes and added sugar verses depending on your capacity to handle it and we'll come back to this minimally processed whole grains whole kernel grains whole fruits beans and dairy and so this concept of glycemic load takes into account most of the variation in blood sugar and thus insulin levels after the meal so what happens after meals differing and glycemic load in this study we looked at three meals with identical calories in adolescents with obesity one was instant oatmeal with a little milk and sugar that was actually a whole-grain meal and low-fat just as recommended but instant instant oatmeal digests very quickly versus steel cutouts that's an old-fashioned preparatory method the kernel is intact I think it's tastier nobody has time for it these days but those two comparisons had the same protein fat and carbohydrate and then we also had a vegetable omelet with fruit that had no starch or added sugar at all and so this is what happened during the five hours after the meal to two key hormones insulin which we've talked about is of course higher after the high glycemic instant oatmeal then after the other two meals but glucagon now that's a key hormone we don't think a lot about but it's the yin to insulin is young or beiong to insulins Yin I'm not sure which but it does the opposite glucagon pulls calories out of storage and so if you have too much anabolic hormone too much storage from insulin and your glucagon is suppressed which a high glycemic load meal will do that's a metabolic double whammy those calories are going to get locked away very avidly and so you can see that after the meal blood sugar initially surges after the high glycemic index meal but then comes down into a relative hypoglycemic range and that's not all free fatty acids which are a key metabolic fuel are suppressed to a greater degree after the high glycemic index field so that the time period of interest isn't one hour one hour after the bagel fat-free cream cheese and orange juice you're feeling great your blood sugar surging and you know you're happy it's what happens three or four hours later so these show very short-term studies miss the miss the boat here and that's the time when you're going to either eat an extra snack or an extra large meal or your metabolism is going to be affected and was this just a laboratory curiosity look what happened to epinephrine adrenaline an emergency stress hormone same calories at baseline but in one case epinephrine was surging in the other two cases the body was hormonal II happy if your blood sugar and free fatty acids are low enough to trigger this stress hormone response what's that going to do to hunger it's gonna increase it and when subjects were given when we gave them free access to food after in a second meal they ate six or seven hundred calories more after the instant oatmeal now a small fraction of that difference were maintained meal after meal day after day it would explain much of the obesity epidemic that arose as these processed carbohydrates entered our diet so what's happening in the brain as blood Sugar's crashing well to do to look at this we used a new technique called functional MRI specifically arterial spin labeling we did this in a double-blind fashion in this case with 12 men with overweight who were given one of two milkshakes on they both they got both on different days masked so they nor the investigator that day knew which was which and the milkshakes had the same protein fat and carbohydrate one was low glycemic index with uncooked corn starch that's a very slow digesting carbohydrate that's used for some metabolic diseases and the other had corn syrup so it's both glucose polymer glucose no fructose in any of this so this is we're just focusing on glucose either slow digesting glucose or fast or fast absorbing high glycemic glucose so as expected the fast-acting milkshake with the corn syrup caused a rapid rise of blood sugar and then down at four hours the pre-specified time point of interest people so they were hungrier after the fast-acting milkshake and at that time one area of the brain lit up like a laser this is the nucleus accumbens nucleus accumbens and this occurred in every subject I've never seen I've never done a nutrition study in which every subject responded the same way we had very high statistical power to take into account comparisons throughout the brain nucleus accumbens is considered ground zero for the classic addictions of cocaine heroin abuse alcoholism it's the center of the dopamine striatal pleasure and reward system raising a provocative concept of food addiction now of course we need food to live but it suggests that these highly processed foods but specifically the highly processed carbohydrates are driving cravings and the potentially addictive behaviors not because of their tastes I should say these two milkshakes were designed to have the same sweetness and it was four hours earlier it's not because of the tastes I mean think about it playing you know baked potato chips plain popcorn bagels you know these binge foods nobody binges on butter right you binge on the processed carbs aren't they really that tasty I mean most people would say that butter is tastier than white bread but given the but they would binge on the white bread not the butter so it's suggesting that there that food addiction might be a real thing but not because the food is so tasty it's because of the biological impact of the food on our metabolism potentially hours later because of how it's affecting our or hormones alright let's turn to an animal model where we can control things a little bit more completely and this is sprog dolly rats that we were giving them again low or high glycemic index diets same carbohydrate yeah so we're going to come back to low carbohydrate but this is effects even at higher amounts of carbohydrates just controlling carbohydrate quality so we gave them we pair fed them to keep their weight the same and you can see on the panel on the Left that over the 18 weeks of the study which is like 7 rat years the animals maintained the same average weight but to do that had to begin to restrict calories in the high glycemic load group at about seven weeks what does that mean well you know the hydrolase lima group started gaining weight faster on the same calories and so what does that imply that metabolism is slowing down just as predicted but so we did what you're supposed to do we put the animals on a diet and prevented excessive weight and despite the fact that we were able to prevent excessive weight gain which is something that's rarely accomplished in humans they had 70 percent more fat same weight 70 percent more fat so they're gonna have less lean tissue now I'm glad that we're not talking right after lunch this is my one graphic slide these two animals weighed the same the animal on the Left had a low glycemic index diet and was metabolically healthy the one on the right belly filled up with the highest risk fat Depot and it's diabetes and heart disease risk factors were sky-high there's no way this finding can be explained by the conventional calorie and calorie out model of obesity you know that animal on the right was gaining weight excessively so we did what you're supposed to do and despite that it was a metabolic mess does this finding apply to humans we looked at 21 young adults with obesity and what we did was we gave them we monitored them and we put them on a weight loss diet to lose 10 percent of their weight at least and then we stabilized them and then put them on one of three diets either low-fat high-carb or the other extreme Atkins very low carb or sort of a Mediterranean diet forty forty and we saw as expected that the low-fat diet in the late postprandial period three four hours after the meal caused this drop-off in total metabolic fuels total if you add up all the calories in the blood you know you're fine at one hour thirty minutes in an hour but at three four or five hours there's that drop-off and then when we measured total energy expenditure with doubly labeled water remember this is a crossover study so everybody got all three diets when they were eating the low-fat diet their calorie burn had dropped by more than 400 a day on the low-carb Atkins diet it didn't drop statistically at all it's like the body didn't know it had lost weight and so wasn't adapting and that's a really good thing this difference is 325 calories is pretty much the whole obesity epidemic and I just want to play out we saw something else that was interesting that that the beta cells calm down when they were on the low-carb diet when they when we gave a oral glucose tolerance test the time to peak insulin and the peak of insulin were all lower and we saw also that if people got the low carb diet first then they didn't react badly to the low fat diet to the high carb diet it's as if and so in it implied that there is persistent benefit of a low carb diet even after you stop eating it that may help you tolerate a higher carbohydrate diet so maybe if you just get off of all processed carbs you know go really low carb for a few months you may be able to add back some more carbohydrate and tolerate it in ways that you couldn't before don't know how long it will last but it's just you know it's an interesting finding so why aren't we using this approach in weight loss clinics across the country why aren't public health recommendations focused on this well two reasons one is the metabolic studies and the second is the behavioural studies metabolic studies such as this by a group at the NIH that took nineteen adults with obesity and on a crossover fashion put them on a lowest carb diet 30% carbs versus a ultra low fat diet eight percent fat nobody there's no there's plenty of historically populations that ate very little that ate five percent or less carbohydrate I don't think you could find any natural populations that would have beating eight percent fat but that's what they did and note that the study was six days long and they found that there was no difference in energy expended we didn't get at this metabolic benefit on the low-carb diet and if anything fat oxidation was worse on the low-carb diet so these studies flood the literature and are dominating the mindset of nutrition research today but there's an obvious limitation which is that the physiological adaptations to a low-carb diet don't happen immediately we've heard about this already fasting which is a very potent stimulus to ketogenesis even during complete fasting such as the classic studies of Cahill and Owens ketones take a couple of weeks to reach steady state and there may be ongoing changes after that six days you're only halfway there the same is true for ketogenic versus non ketogenic diets takes a couple of weeks you know after six days you know your body is still adapting and yeah so there's the many many studies are demonstrating this and so if you cut down carbohydrate your brains depended upon glucose and you quickly eliminate carbohydrate from your diet what happens as your body is rich you know before your body reaches steady-state ketones what do you do how do you feed your brain well you have to borrow from your muscle through gluconeogenesis of amino acids you produce enough glucose to get your brain by during that time but your nitrogen balance is going to be negative you're gonna be you know in a not great metabolic state maybe exogenous ketones could be useful to help this transition but look what happens to nitrogen balance on a ketogenic diet people are in more nitrogen balance but it's temporary they come back to to balance after about a month in two or three months who knows what happens it may go in the other direction and so even one of the chief critics of the carbohydrate insulin model published if you look carefully at a figure in one of their studies you can see that first minus 15 to 0 was the time on a standard diet and fat was decreasing and then they put them on a ketogenic diet and the rate of fat loss decreased they make a big deal about that but they kind of ignore what happens during the second two weeks which is the rate of fat loss picks up what happens after thirty days it might get even faster we know there are dozens of studies in animals and in humans demonstrating that the process of adapting to a ketogenic diet takes a while takes two to three weeks at least thanks to Steve Finney found this great quote we've known about this for 150 years at least Schwab because did an Arctic voyage to search for the Lost Royal Navy Franklin expedition and he said look us up in the Arctic you're not gonna be eating bagels said when first thrown wholly upon a diet of Ranger mate you know this we're talking basically a you know very low carbohydrate if not a ketogenic diet it seems inadequate to properly nourish the system and there is an apparent weakness and inability to perform severe exertive fatiguing journeys but this soon passes away in the course of two to three weeks what do we call it today the keto flu so these very short-term studies really provide no information about the long-term relationships between macronutrients and metabolism and I know it's sort of like my favorite analogy is like suppose though researchers wanted to look at the benefits of intensive physical fitness training they took sedentary middle-aged adults and they put them into a boot camp with calisthenics and running and contact sports six hours a day three days later they measured them what would they say well they're tired their muscles are sore they're weak their physical abilities actually declined so do we conclude that fitness training is bad for your physical abilities no we just say we need longer studies but this is a mistake that's consistently made in nutrition we have just finished a 20 week study so ten times as long and it had 164 people who's funded it's a 12 million dollar study funded by new C I'm not at liberty to present the results today but we will be presenting the results at the obesity Society meetings November 14th and I encourage any of you to come and come join us there and we will hopefully have the results in press around that time so that we we we hope that the study will inform longer-term understanding of these macronutrient relationships okay so what's the other criticism it's the behavioural studies these are long-term you know what do you do you take people and you assign them to one diet or another diet and you give them some behavioral accountant counseling and you say go off eat this way such as I think the poster child for this kind of study is the pounds lost studying 800 people that's a lot for a nutrition study put on diets ranging from 35 to 65 percent carbohydrate 20 to 40 percent fat 15 to 25% protein this isn't as broad a difference as you can get it's certainly not a very low carbohydrate diet but if you don't see anything through this range maybe you could fairly say well what's the public health relevance and again so this is individual and group counseling and they report no difference in weight in any group the off stated conclusion of this study is that it diet doesn't matter the only thing that matters is compliance choose any diet you'll stick to it that's a that's an erroneous conclusion for a simple reason that these behavioral studies consistently have a major flaw they don't achieve the targeted dietary goals in pounds loss studying the reported self-reported maximum difference in the nutrients was less than half the intended difference even these small differences are likely to be overstated due to what's called social desirability bias let's say I recruit you to be on a low-fat diet study and I pay your financial compensation I select you for your ability to comply and then I ask you what are you eating what are you gonna say a low-fat diet regardless of what you're actually eating the biomarkers in this study suggested little if any significant persistent difference triglycerides are a sensitive marker of carbohydrate intake no difference at any point in the study nitrogen excretion for protein no significant difference at any point of this study so the obvious limitations of these studies are that they really are not sufficiently intensive to fairly test a dietary hypothesis there are a few studies that tend to do this right such as the direct study you've already seen the results so I'm not going to belabor this but this was conducted at a nuclear power facility in Israel where they could people would check in in the morning and stay there all day because you probably had a big procedure screening in and out and so they could control lunch at least one meal and they got significant you know reasonably a meaningful differences not huge differences but then they didn't control all of their meals and the diogenes study which I won't take the time to discuss now so I've argued that the dietary carbohydrate that's flooded the food supply during the low-fat years has increased insulin secretion triggered fat cells to hoard too many calories that causes too few now too many circulating fuels in the bloodstream and that's why we get hungry that's why metabolism slows down but this isn't just a single nutrient single hormone hypothesis there were many component it provides an intellectual infrastructure for understanding how multiple components of our diet fatty acid types mounts prebiotics probiotics micronutrients you know the gut my mic microbiome protein a mountain type and non dietary factors which all directly influence adipocyte behavior could determine our risk for obesity could influence our ability to you know gain or lose weight and also of concern our endocrine just these these environmental pollutants that our endocrine disrupters which have frightening effects on fat cells specifically on fat cells differentiation and behavior outcomes be hot beyond body weight diabetes this study by Laura Saslow was recently mentioned I think this morning so I won't belabor that we did a you know type 2 diabetes of course is our condition of carbohydrate intolerance and so it you know it doesn't seem that big of a stretch the reducing carbohydrate would be helpful but the concern of the type 1 diabetes has always been ketoacidosis because in that you we all heard you know you don't go into ketoacidosis if you're healthy on a low-carb diet except in extreme very rare situations but there's no protection there in type 1 because you don't make enough insulin to turn off ketosis ketones feedback on insulin and create a negative homeostatic loop but in type 1 there's a big concern of ketoacidosis people die of ketoacidosis so there's been a big fear of it but there's a large mostly underground community this particular facebook group following dr. Bernstein's approach we got rights we got permission to survey the community do a scientific study and we found that they're mean and this is about half children and half adults the adults the children were represented by the parents in the survey mean carbohydrate intake was reported was very consistent with ketogenic diet a very low carb diet although their protein intake was higher than a classic ketogenic diet they focused more on protein their insulin insulin dose was very low for type one diabetes they had the classic lipid panel high LDL but also high HDL and low triglyceride look at that one-to-one ratio of HDL to drag let's ride for tot for type 1 diabetes that's impressive low not high rates of hypoglycemia and decay they were not they did not seem to be an increased risk for decay high satisfaction and look at this this was our primary endpoint hemoglobin a1c average was in the normal range that's unheard of for type one diabetes you know if you come into the doctor as many of these families do with and they find out you've got a hemoglobin of 5.5 you know if it's a parent of a child the parent gets a lecture that they're running them too tight and they're at risk for severe complications you know these people know not to listen but we but it sets up a problem and the problem is that the patients are doing one thing and not talking to the doctors directly and the doctors are you know thinking something else and lecturing their patients and that's actually assess setup for for catastrophe because you know these patients no matter how sophisticated they are they're still not physicians and there are still things they don't know about management of type 1 in disease and so I think that we hope that the study we published in Pediatrics will help start a dialogue so that these patients don't feel like they have to be stigmatized and have to hide and ultimately we need randomized control trials we don't know from this observational study long term safety you know I'm gonna just skip over heart disease well I'll just mention that the big another concern is alright maybe a low carb diet will help you lose weight but you'll be a good-looking corpse you know your arteries are gonna fill up with fat plaque well the two major studies of low fat diets were flops from cardiovascular disease perspective the Women's Health Initiative and the looker head study in fact the look at head study had to close early for futility if you know you never want to hear that term if you're an investigator your study is futile resistance is futile why haven't we why isn't the government funded a single big multi standard low carb diet study we don't have any but we do have epi now I know to some people in the low-carb community observational research has a it's quite a dirty name but there are limitations to clinical trials as I've shown I mean those behavioral diet studies have major limitations and while there's a lot of problems with epi I think it there there's a way to do epi right that can really minimize concerns for confounding and in this particular study I would say this is a study that said low risk for confounding at least because the confounding would go in the other direction healthy people were consistently eating a low-carb low-fat diet so the health halo effect would tend to bias the low-fat people to longer life span and in fact the opposite was seen that the lower the fat you were eating the higher their risk for premature death so that gives you pause we've heard about ketones having a variety of biological effects through other pathways not specifically insulin so in summary and conclusion the conventional approach to weight loss the low-calorie diet has poor efficacy in an environment with unlimited food availability yes if you're an impoverished Chinese peasant working 12 hours a day you're not going to get obese on you're not going to develop obesity on a high carbohydrate white rice diet but that's not what's what that's not what's happening here and in China as the peasants are moving to the city bringing their high carbohydrate diet but leaving behind their physical activity levels you know we have a massive epidemic of obesity and specifically type 2 diabetes an alternative approach aims to reduce anabolic Drive leading to reduced at a paucity ad libitum now that's got to be appealing and this can be achieved by lowering total carbohydrate or glycemic index or both and other qualitative aspects of diet it's not just carbohydrate the findings from the feeding study have to be the short-term feeding studies I think you just got a Chuck them and you know we need longer studies to see what really the effects of these macronutrients on metabolism the behavioral studies have to be interpreted cautiously - but we can do them better with intensive support to help people really change behaviors give them cooking classes if they're financially stressed help them you know deliver parts of their diet you could deliver olive oil and avocados and make it easy and or even send a personal counselor or personal chef to the home these are not expensive interventions in in the context of the costs of obesity diabetes and heart disease so we've got to do these behavioral studies better and you know we want to also look at whether ketogenic diets have unique benefits above and beyond more less restrictive regimens so in I'm Gary Taubes offered a quote from 1942 and I'm going to best him with this and here's the quote the editors of a leading journal wrote when we read that the fat woman has the remedy in her own hands or while they're between her own teeth so this is the editors citing some other article that was written that had it clearly had a an element of snark there is the implication that obesity is merely the result of unsatisfactory dietary bookkeeping well the logic suggests that body fat may be decreased by altering the balance sheet through diminished intake or increased output or both the problem is not really so simple and uncomplicated as it is pictured so Gary's quote was from in the 1940s this was from 1924 by the editors of JAMA so follow follow me on social media and thank you for your attention on time so we have plenty of time again for questions and we can get started right down here hydrophobic what advice would you give to primary care you might just saying who you are and where you're from just Jeff capitan I'm a nurse practitioner working nice you but my wife is a primary care physician works at Kaiser and frequently gives people advice to eat low carb diets but has endocrinologists and cardiologists that don't follow that advice that she refers patients to that would probably think she's crazy and organizations like the ABA that recommends 50% of calories from carbohydrates to diabetics so what advice would you give to primary care physicians they have these obstacles in front of them well actually just to modify the last thing the a da was recommending the American Diabetes Association was recommending diets as high as 60% carbohydrate in the 80s and 90s but that's changed now they're they've retracted any specific macronutrient recommendation although there still is a bit of a schizophrenic mindset because they say you individualize it there's no 1 ratio but they say start with I think it's you know 45 grams of carbohydrate per meal and work from there and if you add in snacks and so forth you know you're talking about a significantly high carbohydrate diet you know I think we're living in a field with emerging science and we didn't talk today about individual differences I think there's clearly individual differences I'm very interested by groups very interested in how insulin secretion people who are high insulin screeners they look more like apples and pears are uniquely sensitive to carbohydrate whereas the low insulin secretest may do reasonably well on a broader range as long as you focus on nutrient quality we don't know if there's downsides to some for some people with very low carbohydrate or ketogenic diets I think you know I certainly agree with the other speakers that you know when you're talking about type 2 diabetes or severe insulin resistance the likely benefits are likely going to far exceed any theoretical risks but I think we're you know we have to just keep doing research get the findings out there and let clinicians use their best judgment also we're also seeing patients and the public jumping over the clinicians because before you know I'm not going to be jealous about this but the for Best Leading best-selling Amazon diet books or all ketogenic diets right now so the word is getting out we just want my goal is to pursue the science so that we can all start moving in the same direction and not have this polarization with different sides not talking to each other that does not serve science hi I'm Elizabeth Walton an internist in Atlanta my question is are there any adverse effects scene with the ketogenic diets in people with mental health problems particularly depression anxiety bipolar disorder I'm seeing in my practice tremendous improvement and anxiety and improved mood and decreased medication use for that kind of stuff but I've heard some mental health providers caution about it especially the beginning phase when the keto flu yeah you know I think that's a fair like so ketogenic diet is again the most extreme version of this there are ways down there that don't or aren't going to get you into so phase 1 and our diet program is 25% carbohydrate we wanted to go as low as you can without getting people in and out of that keto range I mean I kind of think you have to either if you're going to go below 25% you just got to go for it and deal with it and get through it so yeah that could be an issue but the conventional diet is producing an or monel storm with every meal you know you have this massive we're supposed to have a little anabolic fact after we eat and then a little catabolic effect later you know instead we have this massive anabolic effect when we eat processed carbohydrates that for many people lead to a massive catabolic effect of stress hormones and so the body's being yanked in every direction and that can't be good for the brain you know we know that chronic inflammation can set in we've gotten hundreds of reports you know even on the 25 to 40% carbohydrate diet that we provide in our program focus on unprocessed cover but I get we get hundreds of reports of people who are giving up their depression medications they are feeling less anxious more socially confident you know I guess it's it's the selection bias because if people are doing poorly we might not hear about them but but it does sound a reason and I would say the bottom line is if somebody's got a major psychiatric issue and you're considering a ketogenic diet you want to just be mindful of potential complications hello I'm Catherine price I'm a science journalist knife type 1 diabetes so I appreciate your work greatly but I had a comment and a question on the journalistic side of things as a number of people been asking about how to interpret study head sorry headlines that seem to directly contradict what we're hearing here and the comment is just from a journalistic perspective it's interesting some pointed this out to me that if you're someone who knows what you're talking about and you look at a study and you see it's bad and then you might say it's not worth covering and so that you don't actually write a critical article about it but if you don't fully understand it and it says that keto is killing people or whatever you're more likely to write about it so there's this weird amplification that happens we're responsible writers are not writing the stories and as a result you get these inaccurate messages so that's that's my comment but my question to you we've kind of danced around numerous times what the major limitations of some studies are to look out for but I was hoping you and perhaps the next questioner could outline some bullet points from a consumers perspective of things that you should immediately look at when you're reading an article about a nutritional study let's say a low carb diet study that can help you evaluate whether or not that message is actually worth believing as so that all of us can become better ambassadors of being able to explain or answer a friends-and-family when they're like well what about that it's a great question I don't think I could do it anywhere near justice I mean that would be a whole conference how to interpret science you know properly and that's why ideally you have science journalists who actually knows something about science beyond just regurgitating the press release which is oftentimes hyperbole but we've covered but just to summarize the two issues that we talked about today if it's a feeding study and it's short and it's making claims about long-term macronutrients chuck it if it's a behavioral study and it's a long-term but they don't show that the two groups are eating any differently you know chuck it but I shouldn't say chuck it because there's no perfect study and we can learn from failure you know failure can be very instructive if we get our egos out of the way as scientists unfortunately that's not always the case but if we do a study and we put it out there and somebody comes with a really good criticism rather than going into denial about it or setting up camps you know we say all right I think maybe your criticism is a little overstated but here's the points that are correct about it here's how I could now better design a study let's work together as friendly opponents and do it right that's what science should be it's disappointing that it's not so often the case David I'm surprised you didn't bring up the fact that the study you did with Lenny lessers showed that the odds ratio for a study being favorable to the food industry was 7.6 one if the food industry paid for it so that's the first thing you do is look at the as look look at the funding and if the funding is from a food industry chuck it I actually have two comments so David you had you mentioned the pounds lost study and the pounds lost study was kind of interesting because if you look at the data it looked like it didn't matter what diet you were on which so the the the shall we say the ethos of that was well then if it doesn't matter about the diet it's out the calories but if you look at the standard deviation from the mean in any of the diets it was greater than the mean itself and what that saying is that there are some patients who did well on that diet and there's some patients who did not do well on that diet and you yourself just said that we need to take into account these personal issues and we had an entire talk from Erin Siegel yesterday about those personal issues and let me give you an example because David did this study as well and I did it as well in a different way he did it with diet I did it with drugs there's a group of québécois written up 2008 first authors Chapu and what they what David and he showed was that they have an enormous insulin primary insulin response early insulin response to glucose and the higher that insulin response went on a glucose tolerance test the more likely they were going to gain weight on a low-fat diet and the reason is because they're putting out insulin to beat the band presumably because they have a vaguely driven insulin hyper secretion so the point I'm trying to make we did that with children with brain tumors we gave them a drug called octreotide which is suppressed early onset insulin hypersecretion and demonstrated that we could get them to lose weight and feel better and improve their resting energy expenditure in other words it's not just how high your blood insulin is it's how high your insulin goes in response to a glucose load there's a secretion component there's a resistance component I believe in measuring both of those you can do that often or look tolerance test but you can only measure resistance off baseline testing the point point is and David I want your you know your your feedback question yeah this is question yes there's a question not that not that I mind you talking the question is can we can we as a society as a as a group of you know non what he called non takin you know not non you know we're not taking money okay we're not taking money okay we're independent scientists can we come up with a flowchart that can help people figure out who's who parse this there's so much ad hominem in the world of research nutrition research I'm really loath to say these investigators are on the take and therefore don't trust them because it's never black and white and there are people who do take money from the food industry who are doing you know very good research name one I'm not gonna be at hominem one way or the other right now but I I think the first place we have to start is before we can ask nutrition researchers to give up industry funding we have to provide an alternative legitimate source of funding to them we are presently spending a fraction of a cent in research nutrition research for every dollar of diet-related disease it's a terrible policy we need the government to be properly investing in nutrition research and then once that research is in place we can then say alright we're gonna come in with much stricter stipulations for who can and cannot take research if you want to be part of the this ha this prestigious hospital or this prestigious academic community I mean anybody can take money and go do what they want but that's gotta come first until we improve the supply I don't think we can choke off industry funding that's my view last question yes hi I'm Michael Kunz and I'm an intelligently person I am sorry you're what an intelligent layperson with with no medical training I am wondering if the carbohydrate insulin model that you've kind of walked us through as well as what really undergirds some of the interventions like what they're doing at Verta health and jumpstart md is perhaps an incomplete model from a scientific perspective meaning there are important may be things that you could add to it for example the effects of adiponectin you know in terms of you know folks that are obese have low levels of adiponectin there are interventions that you can use to target that for example exercise you know glucagon as well as perhaps taking the fact that you know as an apple-shaped person as well I probably do have higher levels of baseline insulin I've been you know anecdotally working with you know a weight trainer and seeing very good results there and I think possibly you could try to incorporate this into an effective behavioral intervention to say well you know you're gonna be predisposed to anabolism why not use this to put on something that will raise your resting energy expenditure and possibly in the long run help you create that deficit in addition to like an ED concil or keogh-style dive thank you yeah great you know I I do want to say that the carbohydrate insulin model is not right well it's not a hundred percent right there's inevitably going to be complexities it needs to evolve you know obesity is far too complicated to be a model is just a model you know it's just one view of reality and it's only useful if it guides hypothesis generation and advance the science and then the model changes so you know it's not up but I did try to emphasize that it's not about just one hormone or one nutrient there are many factors that are environmental factors that feed in on our biology now you mentioned adiponectin and yeah that could be an issue Karelin pyy GOP but we haven't suddenly evolved to have inborn defects in our at a connecting regulation those are secondary the point is that environmental factors or acquired dysfunction dis regulate the system and how can we without resorting to bariatric surgery you know reverse this and there's a plausible case can be made that for many people greatly reducing the processed carbohydrates is going to set into action hormonal and metabolic changes that will make many of these missing pieces fall into place now it may not always be the case you know there people who are have hypothyroidism you know just they develop an autoimmune condition maybe some autoimmune disease as influenced by diet but some isn't and you know in that case nothing you're going to do is really going to solve the problem until you get on the right dose of thyroid replacement hormones and you know there are other issues but I what I think is appealing about the carbohydrate insulin model is it offers a holistic approach to understanding why fat cells may be expanding in ways that don't have to blame just poor self-control in our modern food environment and it again it's a basis for informing new studies and potentially new treatments in the clinic

Channel: JumpstartMD

Views: 35,378

Rating: 4.7647057 out of 5

Keywords: jumpstartmd, weight of the nation, wotn

Id: P0o_Wdsv-j8

Length: 62min 28sec (3748 seconds)

Published: Wed Jan 30 2019