so good morning I'm dr. Paul Mason and I'm a sports and exercise medicine physician from Sydney and today we're going to explore the science of ketogenic diets and address the myth that low-fat diets are good for weight loss and we're going to learn how to reverse the supposedly irreversible type 2 diabetes and discover exactly what it is about vegetable oils that makes them toxic and I'd like to start by introducing a cognitive psychologist dr. T this is dr. T now who here thinks she looks lazy or greedy of course this is a ridiculous question you can't possibly tell just by looking at her and yet that is a conclusion that many people would come to when they looked at an old photo of her and this is because we've been indoctrinated that obesity is a conscious decision that choosing to be greedy and lazy is the sole reason that most people become abby's now it's not exactly as if dr.
T wasn't motivated to lose weight it was having a massive impact on the quality of her life it was miserable every day I can't remember a day I didn't wake up and think I'll just start a diet on Monday or if I could just fix my weight problem I could get my life together clearly she also wasn't overweight because she didn't exercise well I always rode to and from work which was about 25 to 30 K roundtrip we would plan holidays that were cycling holidays I would walk I had a dog I would walk my dog for an hour in the afternoon I would go to the gym I signed up with weight management clinics at the University I worked with where I work with exercise physiology students and dieticians so I would be going and I was the one who always showed up I never missed a session I was there all the time and then I would go on the days I didn't have to go and nor was she overweight because she didn't follow medical advice I've tried all the diets I've tried the eating plans I've tried drugs I tried xenical my doctor at one stage wanted to put me on amphetamines but I kind of value my brain a bit too much for that and by my forties things were so out of control that I actually tried bariatric surgery I went in and had a lap band because I thought honestly I thought the worst case I won't get any fatter and the best case by some miracle I may actually get back to a normal size and even that failed and despite all of these failed attempts dr.
T eventually found a way to succeed and got her life back at my heaviest I was a hundred and thirty three kilos I've lost 55 kilos to date my life is so much better I feel so much healthier every aspect of it is better and the best part about it is I don't feel like my eating is out of control so the question is what did she do well clearly it wasn't following conventional medical wisdom because following this advice had only led her to get fatter and sicker no her breakthrough came when she understood that obesity is not so much about calories as it is about insulin and let's take a look at the evidence that insulin a hormone secreted into our blood can make us fat this is a picture of a 34 year old female who had an insulinoma a tumor producing insulin in this picture she's 107 kilograms and she's only 152 centimeters tall and then she had surgery to remove the tumor this stopped the excess insulin production and over the next 50 days she lost 18 kilograms without any change in diet or exercise just reduced insulin levels and anyone who's ever had to inject insulin understands that it simulates that storage continued injection of insulin into the same site over a period of time often leads to a condition called WIPO hypertrophy quite literally fat enlargement here you can see the localized accumulation of fat tissue at different insulin injection sites and about a quarter of every type one diabetic patient will develop this and high insulin levels in the blood is highly predictive of future weight gain this study followed initially lean subjects for eight years to see who developed obesity those who were in the lowest 25% for their insulin levels at the start and end of the eight-year period had only a 2% chance of becoming obese what about those in the highest 25% they had a risk of becoming a base of over 70% and on average they were 50% heavier so if high insulin levels plays an important role in obesity it's only logical to ask what raises insulin levels and the answer is found in our diet or more precisely the carbohydrate content of our diet when we eat fat we only get a small rise in insulin levels we get somewhat of a larger response of protein which is actually a good thing because insulin helps build our lean tissues like muscle but it's when we get to carbohydrates that the story starts getting really interesting when we directly compare the insulin release by carbohydrates and fat we understand why carbohydrates are fattening and fat itself is not and one of the reasons why insulin levels impact our weight gain is that because amongst other things it helps regulate our involuntary energy expenditure even at rest and this was elegantly shown in this recent study where subjects were allocated to either a low 20% moderate 40% or a high 60% carbohydrate diet and then the investigators did something really interesting they adjusted the energy intake of the subjects to prevent any weight change and what they found was that the low carbohydrate group in blue actually had an increased energy expenditure and this compared to the high carbohydrate group in red which had a reduced energy expenditure and the difference between these two groups was very significant about 278 kilocalories a day and this is basically equivalent to the amount of energy expended in one hour of moderate intensity exercise in fact 278 kilocalories a day would translate into a 10 kilogram weight loss over three years in a thirty year old man and this is not an isolated finding in fact amongst high-quality randomized control trials you could even say there's a consensus using the definitions of low-carb is less than 130 grams a day and low-fat is less than 35 percent energy let's have a look at the available evidence so between 2003 and 2008 eeen there were 62 randomized control trials that compared weight loss on either a low-carb or a low-fat diet and of these 62 studies 31 of the did not find statistically significant results which means 31 did and here I've graphed the results of all of these 31 studies the blue bars represent the amount of weight lost in the low-carb group and the adjacent red bar represents the amount of weight lost in the low-fat group and if you look at each pair of results you'll see that the low-carb arms lost more weight in all of them all of them not one single study with statistically significant results found in favor of low-fat diets for weight loss so if you were wanting to lose weight which diet would you choose now let's take a closer look at carbohydrates most of us instinctively know that sugar can be bad for us but did you realize that carbohydrates are literally made of sugar just a string of glucose molecules even complex carbs such as brown rice and sweet potato contain this glucose and when we digest these carbs each and every one of these glucose molecules will end up in our bloodstream now this may not necessarily pose a problem first of all we can actually metabolize or burn some of the glucose and we can also store some in a muscle and liver as glycogen in fact healthy people can store about 80 percent of the glucose as glycogen but this all changes if we have too much carbohydrate and in this study subjects were deliberately fed too much carbohydrate just to see what would happen well some of the carbohydrate was oxidized or burnt as you can see in the blue bars but this was relatively constant right through the duration of the study right through today a meaning that putting more carbohydrates into the system did not increase how much was burnt and some of the glucose that wasn't burnt was stored as glycogen as we've already seen but this capacity was reduced over subsequent days as the stores progressively filled up until by day six there was no spare storage capacity at all what then happened with the leftover carbohydrate well that was turned into fat via this process called de novo lipogenesis and as the storage capacity continued to reduce this fat production continued to increase and this is an example of the fact that was produced a triglyceride fat and this triglyceride can be carried around in our circulation so now we have a trifecta three things from eating carbs increased blood glucose levels increased insulin levels and circulating triglycerides and these are three key ingredients for the storage of fat so each and every fat cell in the body is in contact with blood vessels and that exposes them to these circulating factors the glucose the insulin the triglycerides let's see what happens let's look at triglycerides first in its complete form it's unable to enter the fat cell and this is where insulin comes in insulin stimulates this enzyme here lipoprotein lipase which then cleaves the larger molecule and allows these fatty acids to then diffuse across into the fat cell insulin also activates this glute for transporter which is like a gate that allows glue to enter the fat cell and once inside the fat cell the glucose is converted into glycerol this then combines with the fatty acids to reform our triglyceride and this is how fat is stored under the influence of insulin but if you want to lose weight then the triglyceride must be sliced up again to allow to exit the fat cell for metabolism and this requires activity of an enzyme called hormone sensitive lipase and this separates the glycerol from the fatty acids allowing them to leave the fat cell insulin blocks this enzyme puts the brakes on it and without this step the fat can't be metabolized insulin blocks fat burning so putting it all together we can see that insulin pushes fatty acids and glucose into fat cells and then for extra insult it prevents them from leaving a triple whammy so clearly insulin has the capacity to stimulate fat storage but where this fat is deposited is probably even more important than the amount of fat shown in red here is what is known as visceral fat in and around the organs and it's this pattern of fat deposition most strongly associated with liver disease and type 2 diabetes in fact for every one kilogram increase in visceral fat the risk of diabetes in males is doubled and for females quadrupled process that for a second as a female if you were to have one extra kilogram of visceral fat your risk of diabetes would be increased by four times and this is because hatty liver disease directly contributes to something called insulin resistance which is at the heart of type 2 diabetes now it's worth focusing for a moment on just what exactly insulin resistance means so it refers to our tissues being resistant to the effects of insulin in other words the insulin that we have just doesn't work as well and to compensate pancreas releases more so insulin resistance can often be identified by the high levels of insulin that result from this compensator e response now we know that insulin is able to stimulate the storage of glucose in muscle and liver as glycogen but in the case of insulin resistance this storage is impaired and we end up with higher levels of glucose in the circulation and this excess blood glucose can be turned into fat through the process of de novo lipogenesis and here we see the degree of de novo like a genesis following a high carbohydrate meal in healthy subjects without insulin resistance and the response for the same meal in insulin resistant subjects more than doubled and this is a direct consequence of the insulin resistance associated with fatty liver fortunately visceral fat and fatty liver is extremely sensitive to weight loss on a low carbohydrate diet this is a DEXA scan of one of my patients and you can see the visceral fat concentrated around the region of the liver now after going on a low-carb diet and losing only 9% body weight you can see a big reduction in the visceral fat stores and this effect is even seen on low-carb diets even when we deliberately overfed to prevent weight loss we get this redistribution of fat we also see it with exercise which while it doesn't reliably lead to weight loss certainly leads to this redistribution of fuss and that's how we're beginning to understand why some people can be metabolically healthy and still be overweight and of course the reverse is also true as possible to be skinny and metabolically unwell what we call tophi thin on the outside fat on the inside and this is clearly demonstrated on these DEXA scans the man on the Left has a BMI of only 25 and yet he's got masses of visceral fat the man on the right has a BMI 30 technically obese and yet he's only got one-third of the amount of visceral fat and this only serves to illustrate the limitations of using BMI to assess metabolic health much more accurate and very simple is to simply take measure around the waist abdominal circumference this better reflects visceral mass and there's also other signs other external signs of insulin resistance we can have a look at let's hear from dr.
T again and everybody else speaks you has no idea that skin tags are a pretty good indicator of insulin resistance they all go oh really unfortunately this is not common knowledge I've lost count at the number of patients who come in with skin tags who tell me the story that their doctor doesn't know what causes them but is still very very keen to burn them off we can also see this characteristic pattern of skin pigmentation called a can ptosis nova concerts usually in the armpits from the groin sometimes it's on the back of the fingers around the neck acne is also associated with insulin resistance and this is a major benefit that many of my younger patients often report there's also laboratory testing we can do for insulin resistance and in my clinic I measured both glucose and insulin levels over two hours after giving them a drink of glucose seventy five grams and this allows me to grade the severity of insulin resistance and it falls on a continuum from very mild insulin resistance without a rise in blood sugar all the way up to full-blown insulin dependent type two diabetes so let's look at the standard testing for diabetes and that only looks at glucose levels and the problem with only looking at glucose levels is that even with the onset of insulin resistance the compensator increase in insulin levels usually keeps glucose levels within the normal range for quite some time and this graph is an example of glucose levels in a typical diabetic patient in the years leading up to their diagnosis you can see that the glucose doesn't really rise until about 10 years at which point pre-diabetes may finally be diagnosed what happens if we look at insulin levels over the same period of time we can detect the problem much earlier here we see that progressive increase in insulin levels which occurs in response to the resistance and this most commonly occurs as a result of excess carbohydrate then as a pancreas which secretes the insulin begins to fail some levels fall let's now look at glucose and insulin levels together this vertical dash line represents a state where both glucose and insulin levels are normal and over time with the onset of insulin resistance insulin levels rise but blood sugar is still normal so on a standard blood test only looking at glucose everything still looks hunky-dory not even pre-diabetic but looking at the insulin level we can begin to see a problem finally the increase in insulin levels can't complete the compensate for the insulin resistance and blood glucose levels begin to rise and this is when pre-diabetes is conventionally diagnosed often a decade or more after insulin resistance has began to occur all the while the patient has probably been suffering the effects of high insulin levels such as weight gain and increasing blood pressure then as the cells in the pancreas begin to fail insulin secretion Falls and the combined state of reduced insulin levels and insulin resistance often leads to a precipitous rise in blood sugar levels and this is where diabetes is diagnosed possibly two decades after it all began fortunately this process is reversible on a low-carb diet and these are the insulin results of one of my patients on one of these two hour tests and this is the results in the same patient six months later after commencing a low carb diet you can see big reductions in insulin levels and unsurprisingly this was associated with seventeen killers of weight loss and I've seen this type of response countless times and what about the impact over low carb diet on blood sugar levels given this is how diabetes is formally diagnosed let's hear from dr.
T again I had type 2 diabetes in June last year it was August so she's talking about her hba1c which is a marker of average blood sugar levels and she took hers from eight point one to five point eight which is an excellent response and this is consistent with diabetes reversal and this graph here shows how rapid the improvements can this graft was reported by a 71 year old gentleman who dropped his morning fasting blood glucose levels quite literally in half in only two weeks and all the while he stopped to diabetic medications over the same period and this study here confirms the reversal of diabetes is possible on scale the grey line shows the average blood sugar level in patients receiving standard diabetic care over a two-year period the light blue line shows the average sugar levels of diabetic patients on a low-carb diet and you can clearly see that those receiving standard diabetic care had significantly higher blood sugar levels over the two-year period in fact at two years 53% of the patients on the low-carb diets met the criteria for diabetes reversal now given that most of the glucose in our circulation comes from what we eat it's possible to see major improvements quite literally overnight when we start a low coke diet and this is a continuous glucose monitor sensor it sits on the back of the upper arm and has a small painless needle which senses glucose levels and it communicates wirelessly with a smartphone or a dedicated reader device and provides 24-hour real-time blood sugar monitoring and this is a readout from a continuous glucose monitor from one of my patients the day before starting a low carb diet and a couple of days later you can see the vast improvements in the stability of sugar levels and this kind of stability is perhaps even more important than the absolute level because it's a variations in the blood sugar levels which also generates significant amounts of oxidative stress which has we'll soon see causes problems in and of itself and I do recommend these monitors to a lot of patients to anybody who's curious about their personal blood sugar response to specific foods and it's also a great compliance tool you can't pretend that something is okay the evidence there is staring you in the face and it's what I call real-time accountability and many patients this helps them stick to a low-carb diet I'd like to now shift gears and have a look at processed foods and processed foods actually now make up more than half of the consumed dietary energy in most westernized countries high-income countries now despite often being disguised behind packaging making various health claims they're really not that good for us and when I think about processed foods I think of two key ingredients sugar and vegetable oils or more correctly seed oils let's start with sugar no sugar or sucrose is a problem because it contains fructose exactly 50 percent in fact which is very comparable to the amount of fructose in high fructose corn syrup so we don't get away with it in Australia and the first problem is that fructose is very sweet even compared to glucose so fructose is actually about two and a half times sweeter than glucose and this means that fructose is more rewarding to us this pathway in the brain the meanso limbic pathway is activated by sweet taste it's a reward pathway and there's no doubt that a degree of addiction contributes to both cravings and overeating related to this pathway in the state of obesity and almost paradoxically in obesity the dopamine receptors are reduced so you can see on this brain scan there's less dopamine receptors in the brain of the obese individual than there is in the normal weight individual this means that for the same level of reward and abby's person needs to consume either more or sweeter foods and this is part of the pathway that drives them to things like sugar and fructose and fructose is involved in both causing this process and continuing this cycle fructose consumption also leads to much more fat production remember that de novo lipogenesis well as we know in a metabolically healthy state most of the glucose can be taken up by a liver and by muscle tissues and only about 20% will actually contribute to the novo lipogenesis fructose on the other hand has no capacity to be stored all the fructose you ingest will contribute to fat production via this de novo lipogenesis and fructose can be hidden these are all different names for sugars most of them containing fructose that are used in food labeling take for example this almond milk boldly proclaiming that it contains no cane sugar but when we look at the ingredients we find this organic agave syrup and this is actually even worse than sucrose because it contains 75% fructose and typical of many processed foods it also contains vegetable oil why I don't know but this poses a significant issue and it's not solely due to the omega-6 fat content so vegetable oils are high in linoleic acid which is an omega-6 fat and it was assumed by many including myself that this linoleic acid would be converted first to arachidonic acid and then to these inflammatory molecules down the bottom called eicosanoids the problem with this line of thinking though is that a rakha Datuk acid is only converted to these inflammatory molecules if there's an inflammatory trigger of sorts that is the production of leukotrienes thromboxanes and prostaglandins needs an inflammatory stimuli it requires activation of these enzymes that occur in inflammatory States and in a low inflammatory State such as on a low carbohydrate diet these enzymes are less active so a record onok acid in and of itself is not inherently inflammatory and it can actually increase in low inflammatory State it's also likely that stabilization and blood glucose levels on a low-carb diet by reducing the oxidative stress actually reduces the damage to the arachidonic acid in our cell membranes also increasing the levels and this is exactly what we see so in the recent study comparing low carbon high carbohydrate diets we can see the low-carb intervention actually had significantly higher levels of plasma arachidonic acid than the high carb diet and furthermore arachidonic acid is essential for good health it's an essential component of a cell membranes and among other things that's involved in muscle repair and growth and the growth and repair of neurons so the problem with vegetable oils is not the omega-6 content itself but the tendency for vegetable oils to become oxidized so when we have a look at saturated fats they're quite resistant to oxidation because they lack double bonds between the carbon atoms but when we have a look at unsaturated fats they do have these double bonds which are very reactive and prone to oxidation and the more double bonds our fat has the more likely it is to be oxidized here we can see the tendency of fats to oxidize with cooking ranging from the largely saturated fat lard on the left through to the polyunsaturated sunflower oil with multiple double bonds on the right and you can see that olive oil in the third column with it's single double bond sits somewhere in the middle and even if you don't cook vegetable oils they're still prone to oxidation this study measured progressive oxidation in walnut oil stored over eight days and you can see a massive increase in oxidation products in a matter of days and this is why vegetable oils have antioxidants added to them even then though the oxidation is only reduced and it's not completely eliminated and after you ingest oxidized oils you absorb them they get absorbed through the small intestine in particles called chylomicrons whereupon they get transported in the circulation to the liver and this oxidized load to the liver activates an inflammatory response and ultimately it leads to it contributes to insulin resistance and it should be noted that these inflammatory effects are not isolated to the liver it also occurs in other organs such as the kidneys in the lungs and this graph here compares the absorption of oxidized fats to these Carly microns between and containing low oxidation levels and a meal with higher oxidized levels and clearly we can absorb these oxidation products and this is an electron microscope picture of a mouse liver showing how these oxidized fats can accumulate in the liver and this accumulation is associated with a pronounced inflammatory response and the development of fatty liver and here you can see fibrosis typical a fatty liver immediately adjacent to oxidized fats and we also see clear evidence of this in humans this is t pian total parenteral nutrition and this is used for people who can't digest food in normal ways and we try and give them their complete nutritional requirements through them now typical of most TPN infusions this bag contains 20% fat most of which is the highly oxidized Abul omega-6 and quite predictably infusion of TPN with its rich content of oxidized fats leaves deliver disease this study looked at rates of liver disease in those on t pian therapy over a few years and the amount that the lime drops by represents the number of people developing liver problems and you can see that the percentage of people with biopsy proven liver disease after seven years of TP and therapy was about sixty percent and this trend showed no signs of stopping and in fact several patients died of liver disease over the course of this study so clearly the ingestion of oxidized vegetable oils is probably not good for the liver do you know what could be worse though the consumption of oxidized oils if you're a poorly controlled diabetic this bar represents the degree of oxidation products absorbed into chylomicrons following a meal of oxidized corn oil in a healthy in healthy subjects this bar here the same meal of oxidized corn oil in well controlled type 2 diabetics and rafi wrap or lis controlled type 2 diabetic then all bets are off and this is why control of blood sugar is so important if you're a poorly controlled diabetic consuming vegetable oils your honor hiding to nothing so then what to do well first of all keep your blood sugar level low and get your polyunsaturated fats from fresh food so long as the food you're eating is not rancid which is actually the definition of rancidity is oxidized fats you're probably going to be okay and this doubly applies to omega-3s which are even more prone to oxidation than Omega 6s so you've got a choice between supplements which are probably oxidized or fresh food and you might also want to discuss with your doctor something like melatonin which is a potent antioxidant and predictably it's actually been shown in research to reliably reverse fatty liver disease now some of you will have heard all of this and you'll still be uncomfortable with the idea of eating saturated fat well this prospective study looked at more than 135,000 participants and followed them for seven years and looked at saturated fat consumption and mortality rates and it found that those habitually consuming about 10 percent of their calories from saturated fat not much had a death rate of about 7 people for every 1000 person years but in those who were consuming more than three times as much saturated fat the equivalent death rate was only four and there was no upper level of saturated fat intake which appeared problematic as energy from saturated fat increased so too did the benefits and yes I know that saturated fat can increase LDL cholesterol and no that doesn't matter either this systematic review from 2016 looked at 19 cohort studies with over 68,000 participants and of those 19 studies 16 of them found an inverse relationship between the level of LDL cholesterol and risk of mortality that is the higher the LDL level the lower the risk of dying and 14 of those studies reach statistical significance meeting this finding was very unlikely to be due to chance so close remember that obesity is treatable and diabetes is reversible all you have to do is limit your carbohydrates especially sugar avoid vegetable oils and embrace saturated fat a pretty simple recipe and I'd also like to offer a public thanks to dr.
T who shared her journey in the hope that it might help others suffering from the same problems and issues that she did if you're a doctor please be open to the possibility that what you learnt in medical school may be wrong and if your patients come to you wanting to try Aikido support them their lives might depend on it thank you [Applause].