Thank You Marion first lady it's a great privilege to be honest thank you for the warmth of the reception and that wonderful people have come and said thanked us for doing what we're doing I'd like to compliment Mary Ann for what she's done in Australia I seen what he's done globally and you need to understand that they are under pressure and they've they've stood up to it and they continue to stand up to it and it takes great courage because we know we're doing what's important and what ultimately will be accepted as the truth and we're here today because Ison's going to be the first country to convert to those [Laughter] [Applause] okay so because you people eat so much fish you're so clever okay I had to bring my best game today and so I apologize I'm a biologist and I want to show you the biology the time behind why we got it all wrong and you know Gary taught me I taught us all to question and he presented the evidence from the history and he's absolutely correct and people say you know Gary table since my posture is wrong but let us don't look at the history and what I want to take you today is through the biology because once you understand the biology there is only one answer and that is that we are killing ourselves through nutrition that that the chronic diseases that we see in our society are nutritional diseases they're not chronic disease of lifestyle it's nutrition is number one the lifestyle component is important but in this you get the nutrition right you can try everything else and I'm a classic example as I'll show you so I became interested in the low carbohydrate diet in 1972 although I didn't realize it at the time because we were only using a low carbohydrate diet to prove how fantastic a high carbohydrate diet was but we didn't realize it so here was the first place so that we ever published in 1980 on a low carbohydrate diet and you see mark we were we were doing this we would eat carbohydrate diets for three days we days would eat no carbohydrate whatsoever and then we just need carbohydrates and then we'd run a marathon and during that time my wife said your breath smells terrible when you're on this diet you see so my friend said ketosis hasn't been studied more recently since about 1930 and he said let's study post-exercise ketosis and so I said well if you ask my wife it's all because we eat a low carbohydrate diet so we did an experiment on these are data from myself and a friend so we ate high carbohydrate foods for two days where we did no exercise or we exercise for two hours and you'll not see our ketone bodies didn't change but when we ate the low carbohydrate diet and exercise we got quite a mild ketosis and there was the two of us but what was really interesting was what it taught me about myself forty years later when I went back to the data so so that's there are ketones increased dramatically sorry when you read the slide of this as time on the bottom and this is the concentration now Garry spoke about three fatty acids and triglycerides well that's the sort of things you like to measure and we measured incident in ourselves so he has the three fatty acid response and here's the insulin response which we'll get to remember he said when the in Sun Goes Down the fatty acids can go up and so when you on a low carbohydrate diet the fatty acids are much higher then we exercise with high carbohydrates or we didn't do any exercise and that's because you've reduced the instant suppression of free fatty acids and our glucose goes up when we've eaten the high carbohydrate diets and we exercise but stays low when we don't exercise so what really interests me when I went back to 3040 years ago was there something wrong with myself and my friend we were 27 year old each we were both lean running marathons running 70 miles hundred forty days a week minimum racing marathons but there was something wrong which we didn't see because no one pointed it out and what's wrong is that our glucose went up during exercise which it shouldn't these people have a problem with glucose regulation even though they're 28 and we need a high carbohydrate diet the glucose is out of control but it's much more important and this is the probably the whole point of this whole talk you to get this you understand is look at our insulin concentrations we we came into the exercise baths so we weren't exercising on that day and our glue ensign was city or higher these two young men have in sand resistance and it is so bad that it isn't doesn't even normalize about 4 p.m. at the end of the day these two people are walking disasters it doesn't matter that they run marathons they are instant resistant and they're going to get type 2 diabetes and so and that's exactly what happens Tim Noakes and his friend have insulin resistance hyperinsulinemia despite the use and marathon training it improved on a high-fat diet and they must develop type 2 diabetes with time if they continue eating a high carbohydrate diet and I did I develop type 2 diabetes I don't know if my friend because he went to New Zealand I haven't seen him so so so what did I learn from this well I learned and I wrote this book you see and this book tells you you must eat lots of carbohydrate because if you want to win marathons you must run carbohydrates etc and I'm very proud that the book actually has been highly rated as one of the great books in running but this is what I said all the athletes must be advised to eat high carbohydrate diets but in training especially before competition this interpretation forms a central pillar of the professional sports nutrition that is true sports nutrition that just tell you how to eat high carbohydrate diets because high carbohydrate diets are now considered ideal for both health and sport and I apologize that it's utterly completely wrong and unfortunately rewriting that book and I'm completely I've torn out the first four chapters they're gone and you know the problem was you see what we did was we reduced athletic performance to one thing how much carbohydrate was in your diet and we forgot actually brain is important and a few other things are important in trainings important so I restructured the book around that so and anyway I developed a 2 diabetes as a result of that eating this high carbohydrate diet but all to my genes and this is a picture of myself and my father and my mother in 1981 I just graduated with an MD and my father has metabolic syndrome he probably has non-alcoholic fatty liver disease he had hypertension and he'd just been diagnosed with type 2 diabetes he died 11 years later from disseminated arterial disease that's why I spoke so strongly about it this is because people didn't know how to understand how to manage type-2 diabetes and they still they do it wrongly and so here I am the genes from my father went straight to me and I was in tune resistant at that time but didn't realize it and I've been strongly influenced because I've saw my father die and you do not want to die from type 2 diabetes that is for sure uncontrolled planta diabetes it's it's the worst form of death and here's the book that my father was given through the summer hema seat and a cure the friend of the person who wrote it and I do not blame her for one moment she was telling us what the true what was understood and I haven't quoted from her book but this is the most recent book in South Africa written on what you should be eating if you're a diabetic so it's carbohydrates and diabetes and there it says carbohydrates are an important source of energy in the body and glucose which is the product of the digestion of carbohydrate is quite the only energy source for the brain that is not true it is therefore crucial for diabetics to include carbohydrate-rich foods at each meal so what that tells us is that when we prescribe diets for persons with type 2 diabetes the sole consideration is that the brain requires glucose for its function that's any reason we prescribe all you have to know about prescribing for diabetics my father did not die because his brain was getting too little glucose he died from disseminated arterial disease and what about the effects of different types and amounts of carbohydrates on blood glucose in some control and on the development of the seminary arterial disease whether Keit pathology and diabetes so all the management of diabetes is inappropriately based on the wrong science looking at the wrong measurements and so what this title should say so it says therefore effective blood sugar control is important understand that different carbohydrate rich foods have different effects on blood sugar levels because of the difference in their glycemic index well actually that's unimportant because treating the blood glucose concentration treats only a symptom it doesn't treat the cause which is a disseminated arterial disease and that's what you have to do treat and so what this should be is that for effective blood sugar control it's important to understand that carbohydrates should be removed from the diet as they are non-essential in persons with diabetes are unable safely to metabolize carbohydrates and then we start to sort the problem out because limiting carbohydrates reduces the hyperinsulinemia which is the key driver of the disseminated arterial disease which is a defining pathological feature of type 2 diabetes now we have to start talking about type 2 diabetes as disseminated arterial disease not glucose and insulin disseminated arterial disease so what saved my life was on 12th of December 2010 I know exactly the date I know exactly the time I discovered this book on the right the new Atkins for a new you and that opened my eyes within within two hours of reading that book I said never another carbohydrate in my life and it was just instantaneous and because I was type 2 diabetic without realizing it I benefited hugely the rest of my life is encapsulated we wrote this book which became a best-seller in South Africa broke all the records it was astonishing we wrote it in five weeks and it just went ballistic and we cannot explain why it did I think the reason was because it's the first book that said you're not the problem if you run the beast if you're obese it's not you're not the problem it's your food choices and just change your food choices and you'll cure yourself and that was a different than we've go of course fantastic recipes etcetera and then more recently we've written a much better book which has not sold the same way called the raising superheroes it's for children it's an astonishing book that if I can advertise a book book on what how you should raise your children that that's it we put a lot of effort into it so I saw this slide from Gary Taubes and the point I want to make is is which he made an actual made was that the dachi guidelines changed there in 1977 and in 1978 a PSD epidemic begins in the United States and no one will take responsibility for that and that's what question you have to ask why would you not take you change the guidelines why won't you take responsibility for what happened why do you ignore it instead why do you take us for asking that question so I stole this from andreas insult this lovely slide and that took millions of years to get to this guy and the point is that this guy's perfect ease how humans are designed to be and why is he like that and the answer is because you've got an epithet which Gary spoke about all he spoke about some controller which is so accurate it has to be accurate within 21 calories a day well this guy's APIs that has been accurate 221 calories per day for three million years that's why we looked like that you have to understand that so any deviation from that begins with the problem of the opposite because this is a homeostatic regulated system so the course here yeah is this guy's ever set isn't working of course as gary said all these other things could be involved the set cells and blah blah blah but ultimately the epithets failed and to understand that we have to understand that the after step by mere set has gone and we need to understand how that is and the key thing is that this guy has one characteristic he is always hungry and if you want to understand a b c that's it how why these people always hungry and once you understand that then we can reverse the obesity so i just put this together that gary spoke about the calories in calories up and the point of course is that calories in and calories out of control by the brain as he said and we just kind of forget that as if you can control it consciously and that's the point it's not consciously controlled that was the point he was making so the APIs that perhaps is what you some sort of connection between the calories in and calories out story in that santa stat function and this has to be accurate 221 calories a day as he said and as he had indicated if you reduce your physical activity you don't get fat if the homeo starts working because all you do is simply eat less that's how homeostatic it works and so if you do get fat it can't be because you've reduced your energy intake it's because the after steps wrong and since so if at home if their brain home your starts are working appropriately humans who exercise less cannot become sad they simply eat less and conversely if you increase your physical activity you don't you increase your energy intake and you don't lose weight if their brain have your starts are working approach that humans you exercise more do not lose weight they simply eat more and the problem is when you increase your energy intake because something's gone wrong with the Apple stat function which then causes you to increase your energy intake then you because there's no effect you don't go and do more exercise you become gluttonous and slothful as you indicated and so that's the key point to understand that it's adverse that is the regulator and it has to fail first for obesity to develop how it happened how the failure happens that's enough for another day but the point is that just being less physically active will not cause you to become obese unless the appstats fails so here's Gary slide again and then the point is that 20 years later the diabetes starts and is always a 20-year rule that was described by South African in in Durban South Africa he observed that when you took a population and you change the diet within 20 years of diabetes came about and I sent the classic example because II for generations you weren't eating grains I looked outside I don't see any grains growing I didn't see any bananas or apples growing so that the Icelanders people must have eaten lots of fish and other things and you will be an insulin resistant population for that reason as I'll show you and if you take that population and impose carbohydrates onto them we'll become fed much quicker than anyone else the highest rates of obesity are in the Pacific Islands the people who ate coconut and coconut oil and fish for four generations hundreds of generations and then suddenly the sugar and the flour comes and they become obese morbidly beasts very quickly so that's the challenge for Iceland you you are very likely to become fatter as soon as you introduce carbohydrates so I'm going to talk all about instant resistance because I know what exactly is this condition of insulin resistance hyperinsulinemia from which I suffer and which I'll show is the most prevalent medical condition on planet Earth and it's never taught at medical schools our betters not taught here at your university certainly not taught at my medical school but which is included in the medical curriculum taught at fear of any medical schools around the world so the father of it is not Tim Noakes it is Gerald Raven from Stanford professor of medicine at Stanford got serious gravitas and he's known as the father he could easier pedimos as the father of insulin resistance in addition to emphasizing the role of insulin resistance compensatory hyperinsulinemia in increasing the likelihood of an individual developing one or more of the consequences he first pointed out the clustering of these abnormalities called it's syndrome X it also became known as a metabolic syndrome it's also known as Raven syndrome and the two previous speakers have spoken to about that and just to remind you that Raven syndrome he was the first to put them all together under one basket in one basket and these are the conditions and I also include other chronic diseases of lifestyle his hypertension visceral obesity elevated blood triglyceride concentrations low HDL cholesterol concentrations and what axel spoke about the small LDL particles Katan B which are increased by a high carbohydrate diet but reduced by high-fat diet and and I will show you that actually the instant resistance the error he made was he didn't understand the incident wasn't the problem and I'll explain that and he will not get the Nobel Prize because he didn't understand it's not the insulin resistance it's thing else that will come to that so in the last few months evidence has come out to show us exactly how we link carbohydrates to the metabolic syndrome to arterial disease the linkage is now absolutely direct data information has come out in the last few months we now have definitive evidence that these abnormalities occur in people with insulin resistance to eat high carbohydrate diets and develop non-alcoholic fatty liver disease as a result and it's a non-alcoholic fatty liver disease into the real predictor of ill health that you can be instant resistant to be relatively healthy but once you get non-alcoholic fatty liver disease that's it your risk or disease goes up and I'll explain why so here's the macronutrient of insurance interest in chronic disease is it's called a hydrate not fat that completely got it wrong and silkies got back the wrong horse completely and I'll show you that one but this trees country understanding human metabolism not free understanding Akademi ology and I apologize that I'm going to have a few slides where we're going to look at human metabolism and the original data that Raven use and show you how it's absolutely proof that is to cover hydrates in the diet that are killing us not the fat so if you go back to Ravens earlier study I think this was may not be the earliest but it's certainly one of them 1966 and he starts looking at low as high and low carbohydrate diets and why because he was interested in the triglyceride response I have no idea I haven't fully researched enough but he became interested not in cholesterol but in triglycerides in the blood stream and he wanted to see what affected high or low carbohydrate diets have on blood triglyceride concentrations not cholesterol and that was the key to I was successful and he discovered this the majority of patients will increase their triglyceride food drive production and concentration in the blood to a variable extent as a consequence of a high carbohydrate diet so he links in 1966 the triglycerides in the bloodstream to the carbohydrate content of the diet and the more abnormal the glucose tolerance curve in other words the more insulin resistance that people that he studied in this group the higher the accompanying rises in plasma insulin the greater the subsequent triglyceride rise on ingestion of a high carbohydrate diet so now he's noticed that there's a link between insulin resistance which he might not Accord in synthesis and yet and a high carbohydrate diet and then he said hyperinsulinemia excessive production of insulin may be an important cause of the ha'n't enhanced liver triglyceride production member gary showed you that slide of how instant drives fat into the cells to produce triglycerides so he's looking at fat cells so he had liver cells so then he says endogenous heart rate triglyceride emia that's the endogenous the internal production of triglyceride is being driven by insulin so the next article he does is the role of insulin in endogenous hypertriglyceridemia i think it's a year later or 1967 and then this slide shows his data here is the blood triglyceride concentration so he goes takes a population measures their blood triglyceride concentration he once explained wise at high and he observes he checks how the liver how much triglyceride is been produced by the liver and he shows that the rate of liver triglyceride secretion it determines your blood triglyceride concentration so we now know if you have a high triglycerides because your liver is pumping out triglycerides and why is that and you could guess the higher the insulin the more the triglycerides in the bloodstream and hence the higher the triglyceride production so now he's been able to link triglycerides in the blood to live a production of liver liver production of triglycerides and to insulin and so he said in most patients the degree to which a high carbohydrate diet stimulates a patek triglyceride secretion is directly related to insulin response produced by that diet in other words the more carbohydrates the more triglyceride production and so then he develops the model over the next 40 years and he has one of his most important papers in sand resistance coronary heart disease and non-diabetic individuals where he develops his hypothesis and produced produces one very exciting diagram and so what he says is that if you're insulin resistant you're always over secreting insulin and that develops the metabolic syndrome which leads to coronary heart disease as Axl said this is the strongest predictor of coronary heart disease but also the you can get tattoo diabetes if you're instant sales or not it's inadequate you'd about type 2 diabetes which we also know is one of the best predictors of heart attack risk so that's the model but the key that he shows for the first time in any textbook of medicine is what happens when you've got too much insulin go and read your standard textbook of medicine there's no story about what happens when you've got too much insulin and this is this is what high insulin causes weight gain the Douro genic dyslipidemia adiposity and within the viscera abnormality of function of the blood vessels very important hypertension hyper you receive me a systemic inflammation mitochondrial dysfunction impaired exercise performance but he's wrong and the question is why is he wrong and he's wrong because this isn't the that's not the problem that's the problem but that doesn't come from that this comes from this that's the problem it's a high carbohydrate diet and that's why he misses the Nobel Prize because what he should have done was to spend 30 years studying high carbohydrate diets in people with infant assistance but he didn't he studied the syndrome fortunately he did something and I explained to you why he didn't study the high carbohydrate diet and more recently we know that one of the key facts about a high carbohydrate diet is you just make yourself more instant resistant so that every time you eat carbohydrates you become slightly more insulin resistant and that is why you've got this 20-year dot wake because you have to eat enough carbohydrate to for the diabetes to become apparent so the problem for for Gerald Raven was he understood that carbohydrates were involved the basic defect in syndrome X in metabolic syndrome is resistance instant mediated glucose disposal if the archie carbohydrate is increased in an either caloric diet insolent additional infant must be secreted to maintain glucose homeostasis and he showed you what the problems are was increased insulin and so his he developed the insulin eccentric model of chronic else so Raven understands that carbohydrates type in driving from secretion in the metabolic syndrome or an insulin resistance hence he had to conclude that restricting dark or dark carbohydrates should be the key therapy for this condition that that could be the only conclusion and in 1987 he was heading towards that conclusion because he published three papers in I think this 1987 1989 and 1994 all showing the benefits of low carbohydrate diets in people with insulin resistance so for example the statements I won't go through all of them but Jerry said it seems prudent to avoid to avoid the use of low-fat high-carbohydrate diets in patients with not with type 2 diabetes so that that statement is avoid carbohydrates because they're hurting you if you've got instant resistance these are all salts of this study indicated high carbohydrate diets lead to several changes in carbohydrate and lipid metabolism in patients within our DDM that could lead to an increased risk of PID it seems reasonable to suggest that the routine recommendation of low-fat high-carbohydrate diets for patients was in our DDM be reconsidered now is that a glowing support for high carbohydrate diets no and he continues this one in taught to diabetes high carbohydrate diets cause persistent deterioration of the glycemic control etc etc etc so the question is why did he stop in 1990 for doing low carbohydrate studies and the answer is because he was at Stanford which is one of the most progressive cardiovascular groups had he come out and said in 1994 you must all eat a high fat diet his career would have ended overnight his career would have ended and so wisely he chose to continue researching without drawing attention to himself and that's why that work is so fundamental but it's got lost so let's move on so here's a I think there yeah okay so now I was looking for another study which must have changed it okay so this is the paper that came up about three months ago and what it says is that non-alcoholic fatty liver disease in instant resistance is the key driver of the SLO genic dyslipidemia which we've shown is the small dense LDL particles and so I'm just going to read their conclusion patients with non-alcoholic fatty liver disease had severe insulin resistance especially at the level of the adipose tissue were compared to patients without the condition those patients had significantly higher plasma a pro-lifer protein B 2 a1 ratio to remember axial Polar's as it's a pro B which is a marker of atherogenic particles of note these differences between patients were independent of the presence of obesity worse oh sorry hello Jenna cliffs letter D Mia was best predicted by the degree of liver fat accumulation and adipose tissue and systemic insulin resistance so what they are saying for the first time is that the key driver of the atherogenic dyslipidemia is non-alcoholic fatty liver disease and how do you get non-alcoholic fatty liver disease you get it from eating a high carbohydrate diet and people insulin is listed and so they continue in the same vein conclusion non-alcoholic fatty liver disease was associated with the worst atherogenic lipid lipoprotein profile regardless of the level of obesity we speculate that this lipoprotein profile is driven mostly by liver fat content and by insulin resistance it's not worsened by obesity so that explains why some people with obesity are not at such great risk it's the instant resistance and the NASL D that causes it so taken together worsening insulin resistant and atherogenic lipid e dyslipidemia may be key mechanisms explaining increased cardiovascular risk observed in these patients in summary we have demonstrated that liver fat accumulation in the setting of insulin resistance is a draw attention to it the main factor associated with worsening atherogenic dyslipidemia and the key point is what gives you liver fat it's a high carbohydrate diet it's not the saturated fat in your diet so this finally gives us the solution to the problem and explains why it is a high carbohydrate diet that is killing all of us and so Alex so we'll go so the future understanding of how atherogenic dyslipidemia arises will come from the work of liver experts who understand insulin resistance and high carbohydrate diets not from cardiologist to protect your heart and arteries I suggest you consult a hepatologist so so now this brings me to the punchline of the talk and and that is we can now explain why medicine is completely failing us and I say that as a medical doctor and the problem in medicine is we see what is above the surface and we think that's the whole story and we ignore what's under the surface and so what we see above the surface is we see arterial disease and notice I've quoted arterial disease because there are different forms of arterial disease as actual said there's firstly there's a disseminated type which is type 2 diabetes and that's why I put arterial disease I put type 2 diabetes under arterial disease because it's the major contributor to arterial disease and then you get cardiovascular or cerebral vascular disease then you get a B City you get hypertension guards and the atherogenic this lipid emia with a focus on high Penson emia high triglycerides why high triglycerides because you've got a fatty liver pumping them out while ohd l because the fatty liver for some reason reduces its HDL production and increase small numbers of LDL particles and that is what you want to know if you want to judge whether you've got atherogenic dyslipidemia it's not cholesterol as actual indicated it's these things that you want now the point of the slide is the following these are not separate diseases they're all the same disease and they're not even diseases they are an abnormal response abnormal physiological response to an abnormal input and that's the key and it occurs in people with insulin resistance and this is the disease that's the condition so when I tell patients I say I don't tell them you have hypertension I see what insulin resistance which is fantastic because we can solve the problem so each of us sits somewhere on this curve every single person living in Iceland sits somewhere on this curve and if you all treat them the same if you treat all of them the same you're going to get it wrong for most of them you're either highly carbohydrate tolerant or you're normal or you're like me profoundly intolerant and if you're tolerant you probably an athlete and you probably normal body weight and you probably will never get these diseases you can eat pretty much what you like but if you're to a lift with me there's only one way you can go and that is expanding waste on obesity metabolic syndrome type 2 diabetes that's it there is no other way and that's the point when we talking about nutrition it's not the nutrition the issue it's who the patients and you've got to fit the diet to the patient and people just don't seem to get it that if you're in some resistant you cannot eat carbohydrates so so so I twenty five grams of carbohydrate a day maximum and I cannot eat 26 or 27 or 28 and that's that's the key people have to understand that we're dealing with margins tiny tiny margins and if you have type 2 diabetes and you want 100 grams of carbohydrate a day you do it but you're just going to kill yourself earlier the only hope is to get 225 grams or less and so and I think in time we'll find cancer and dementia also cardiac also a carbohydrate dependent diseases so briefly very briefly what happens in insulin resistance this is you know obviously a very simple explanation but I believe it's a genetic predisposition I believe we all born with a certain degree of insulin resistance and we either accelerate it or we don't accelerate it so much the youngest child ever to be diagnosed with type-2 diabetes was three years old now that person was born with high incidence and the incidence Wilson's just showed up like ramps up like that whereas for myself my rampling was like that it took me 20 or 30 years to develop a type-2 diabetes and so that's what the big difference so you born with a genetic predisposition and it just gets worse and the more carbohydrates you eat the quicker you're going to get your type 2 diabetes and but the primary abnormality is a liver that just thumps up glucose and that's really important to understand because if you're dealing with metabolic syndrome and type 2 diabetes these people are already got a liver that's pumping out glucose all the time and exits why would you want to give them more carbohydrate it doesn't make sense so that's the primary abnormality the primary abnormality is not that the muscles can't take up glucose that is an issue but it's not the key problem the key problem is a liver that is uncontrolled in the way it produces glucose then we can't store that carbohydrate that's important because if you've got athlete's to insulin resistance and you're telling to eat lots of carbohydrate they're not going to store it in the muscles they're going to store this liver fat and that's not going to help then we always got these hyperinsulinemic response to ingested carbohydrates and then this this is the key increased conversion of excess ingested carbohydrate goes to fat in the liver under the action of insulin that causes NAFLD which causes increased blood triglycerides to be stored as sat in the adipose tissue but the NAFLD then produces this atherogenic list of edenia and that's the radoo production of the good HDL and an excessive production of the small dense LDL particles and that's a very simple explanation but each of the mechanisms are documented and it explains it so now if you understand that why would you ever want anyone to give people carbohydrate unless you know whether they carbohydrate tolerance or carbohydrate resistance it's malpractice to give people in sand resistance high carbohydrate diet if you don't test them and you don't know their insulin tolerance you may not prescribe carbohydrates for them that's how I see it and if you are prescribing carbohydrates for instance distant people that's malpractice and we've got to get that message up so here are some friends from from New Zealand and here's it basically saying essentially what I'm saying and these are some of the conditions they've linked to hyperinsulinemia I didn't link all of them but here are some more and what's the turbulence of hyperinsulinemia I think it's highly prevalent California announced about two months ago that 50% of Californians who have insulin resistance because they have touched to diabetes or pre-diabetes and that means they haven't even checked for the other population the group that hasn't yet developed type-2 diabetes so a minimum of 50% of Californians are insulin resistance given its association with metabolic syndrome and and fatty liver this one site investigation could early detection careful management of - Syleena decrease decrease the need for medical interventions later in life analysis yes it doesn't take a genius to regret or not would management managing - Samim improve both quality and quantity of life and this is the picture they provide with that article so these are all the diseases and those are the diseases that are clogging up the hospitals in Iceland as they are clogging up the hospitals in every city around the world and guess what most of them maybe all of them you can explain as instant resistance and high carbohydrate diets and if that is true then we wrote a revolutionist Ellucian for our current medical problems and I spoke to one of the politicians here today and he said you guys have got to give us a standard message I said you're not going to get this message from anyone but a few of us who are independent of the industry because if you're dependent on the industry there's no way you're going to how many industries function because of these diseases just ask that question utterly dependent on these diseases are they going to cut off everything by saying just well let's just stop eating carbohydrates and then we can stop bleeding close up the pharmaceutical industry ok you get the point you're over feed somebody with that increase their cancer risk I'm so can we maybe try it again with a bit more challenge you over feed somebody with Carbaugh your over feed somebody with that you don't increase their cancer risk at all ok you over feed somebody with carbohydrates and you dramatically increase their cancer rate and protein is halfway in between and that's why we're going to have a huge debate about these carbohydrate based diets so that is could the voice of Craig Thompson is a see of the sloan-kettering Cancer Center and you heard what he said it wasn't Tim Noakes telling you carbohydrates caused or associated to cancer and because we've been told that fat causes cancer and he said the opposite it's carbohydrate based diets and it's really interesting because he believes they're the diet hot hypothesis so he sees a problem he said ok we'll save cancer but by telling people eat a high fat diet but you're caused heart disease so it's not because he is anti fat or anti carbohydrate that he said that he's a person who believes that you should be eating carbohydrates to prevent heart disease yet he can say that cancer is a carbohydrate driven disease and that's again that an important point so this is the final slide what does all this mean hypertension obesity diabetes heart disease etc are the symptoms like symptoms of the underlying physiological abnormalities are not the disease and we are treating those diseases with pharmaceutical drugs which cannot address the cause and so they must fail and ultimately that truth has to become apparent that we have to get to the cause the common pathology in all these conditions is insulin resistance instant resistance is a benign condition that is why people populations that were insulin resistant were fine they didn't have all these diseases until the carbohydrates came in a high carbohydrate diet turns into resistance into a killer I do want to make a point that there are other issues in our lifestyle but I that are killing us of course smoking and blah blah blah and not eat exercising etc but in my opinion it's the insulin resistance and the high carbohydrate diet said of the cornerstones a low carbohydrate diet is a key to the prevention and treatment of insulin resistance and hence all these conditions and and the good news is that there are some of these conditions which might we might be able to reverse freeze on some case of type 2 diabetes will reverse by that I mean they become asymptomatic they don't require insulin any further on a low carbohydrate diet so thank you very much for your attention and I hope it means something to you what I've said [Applause]