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dr. Paul Mason – ‘Evidence-Based Keto: How to Lose Weight and Reverse Diabetes’. Translation and subtitles: TheNewFood. Good morning. My name is Dr Paul Mason and I am a Medical Sports and Exercise Physician from Sydney. Today we are going to explore the science of ketogenic diets and let’s talk about the myth that low-fat diets are good for weight loss. We are going to learn how to reverse the so-called irreversible type 2 diabetes. And we’re going to find out exactly what it is about vegetable oils that makes them toxic. I would like to start by introducing a cognitive psychologist, Dr. T. This is Dr. T. Who here thinks she looks lazy? Or greedy? Of course this is a ridiculous question. It is not possible to determine this just by looking at her. Still, is that the conclusion many people draw when looking at an old photo of her. This is because we are indoctrinated that obesity is a conscious decision. That choosing to be greedy and lazy is the only reason most people become obese. Now it’s not exactly the case that Dr. T. wasn’t motivated to lose weight. It had a huge impact on the quality of her life. “Every day was horrible. I can’t remember a day when I didn’t get up and think, ‘ I’m just going to start a diet on Monday. Or: if only I could just solve my weight problem, then I could get my life back on track.” Obviously she hadn’t gained any weight from lack of exercise. I used to cycle to and from work, which was about 25 to 30 kilometers round trip. We even planned cycling holidays. I walked; I had a dog that I went for a walk for an hour in the afternoon. I went to the gym. I enrolled in weight management clinics at the university where I worked with students Movement and Physiology and with dieticians. I was the one who was always there. I never missed a session. I was always there and I even went on the days I didn’t have to go.” She was also not overweight because she did not follow medical advice. “I’ve tried all the diets, I’ve been on eating schedules, I’ve tried medication, I’ve tried Xenical. My doctor even wanted to give me amphetamine at one point, but I placed too much value on my brain for that. By the age of 40, things had gotten so out of hand that I tried bariatric surgery. I had a gastric band fitted because I thought, honestly I thought that at worst I wouldn’t get any fatter and at best maybe, miraculously, I’d go back to a regular size.” And even that failed. Despite all these failed attempts, Dr. T. eventually found a way to succeed and got her life back. At my heaviest I weighed 133 pounds. I’ve lost 55 pounds so far! My life is so much better, I feel so much healthier. Every aspect of it is better and best of all I don’t feel like my food is getting out of hand.” So the question is, what did she do? She clearly didn’t follow conventional medical wisdom, because following this advice has only taught her to get fatter and sicker. New. Her breakthrough came when she understood that obesity is not so much about calories, but about insulin. Let’s 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 woman who had an insulinoma: a tumor that produces insulin. In this photo she weighs 107 kg and she is only 152 cm tall. And then she had surgery to remove the tumor. This stopped the excessive production of insulin and in the following 50 days she lost 18 kg. Without changing her diet or exercise; just lower insulin levels. Anyone who has ever had to inject insulin understands that it stimulates fat storage. Injecting insulin into the same spot for a long time often leads to a condition called lipohypertrophy, quite literally translated as fat enlargement. Here you can see the local accumulation of adipose tissue at different injection sites for insulin. About a quarter of all patients with type 1 diabetes are affected by this. High insulin levels in the blood are highly predictive of future weight gain. This study initially followed lean subjects for 8 years to see who developed obesity. Those in the lowest 25% in insulin levels at the beginning and end of the 8-year period, had only a 2% chance of becoming obese. But what about those in the top 25%? They had a greater than 70% chance of becoming obese and were on average 50% heavier. So if high insulin levels play a big role in obesity, does it only make sense to ask the question: What makes insulin levels rise? The answer lies in our diet, or more specifically, the carbohydrate content of our diet. When we eat fat we only get a small increase in insulin. We get a slightly higher response from proteins, which is actually only good, because insulin helps to build lean mass, such as muscle. But the story only gets really interesting when we get to the carbohydrates. When we compare insulin release between carbohydrates and fat en we understand why carbohydrates are fattening and fat itself is not. One of the reasons insulin levels affect our weight gain is that, among other things, it regulates our involuntary energy use, even at rest. This was elegantly shown in this recent study, in which subjects were assigned a diet consisting of low 20%, medium 40% or high 60% carbohydrates, respectively. And then the researchers did something really interesting. They adjusted the subjects’ energy intake to prevent weight change. What they found is that the low-carb group, in blue, even had an increase in energy consumption. Compared to the carbohydrate-rich group, in red, where energy consumption was reduced. The difference between these 2 groups was significant: about 278 kcal per day. This is comparable to the energy expended in 1 hour of moderately active exercise. In fact, 278 kcal per day translates to 10 pounds of weight loss over a 3-year period in a 30-year-old male. This is not an isolated finding. You can even say that there is agreement between high quality randomized controlled trials. The definition of low carb is less than 130 grams per day and low in fat is less than 35% of the energy. Let’s take a look at the available evidence. Between 2003 and 2018, there were 62 randomized controlled trials who compared weight loss with a low-fat and low-carbohydrate diet on the one hand. Of these 62 studies, 31 had no statistically significant results, which means that this was the case at 31. Here I have graphed the results of all these 31 studies. The blue bars represent the amount of weight loss in the low-carb group and the adjacent red bars represent the amount of weight loss in the low-fat group. If you look at each pair of results, you will see that the low carb bars lost more weight, in all of them. All of them. There is no single study with statistically significant results in favor of a low-fat diet. So, which diet would you choose if you wanted to lose weight? 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 up of sugar? Just a chain of glucose molecules? Even complex carbohydrates such as brown rice and sweet potato contain this glucose. And when we digest these carbohydrates, every glucose molecule ends up in our bloodstream. This is not necessarily a problem. First, we can metabolize or burn some of the glucose. And part of it we can store in our muscles and liver as glycogen. In fact, healthy people can store about 80% of glucose as glycogen. But this all changes when we consume too many carbohydrates. In this study, subjects were intentionally fed too many carbohydrates. Just to see what would happen. Some of the carbohydrates were oxidized or burned, as you can see in the blue bars. This was fairly constant throughout the study, all the way up to Day 8. This means that administering more carbohydrates did not show an increase in how much was burned. Some of the glucose was stored as glycogen, as we saw earlier, but this capacity diminished in the following days when stocks became more and more full, until there was no more free storage capacity on day 6. What happened to the excess carbohydrates then? This was converted to fat through a process called De Novo Lipogenesis. And while storage capacity continued to decrease, this fat production continued to increase. This is an example of a fat that was produced, a triglyceride fat. And this triglyceride can be carried in our circulation. So now we have a trifecta: 3 things from eating carbohydrates. 1. Elevated blood glucose levels. 2. Elevated insulin levels. 3. Circulating Triglycerides. These are three important ingredients for fat storage. So every fat cell in the body is in contact with the blood vessels and that exposes them to these circulating factors: glucose, insulin and triglycerides. Let’s see what happens. Let’s look at triglycerides first. In its complete form, it is unable to penetrate a fat cell. This is where insulin comes in. Insulin stimulates this enzyme here, lipoprotein lipase, which then cleaves the larger molecule and thus allows the fatty acids to proliferate in the fat cell. Insulin also activates the GLUT-4 transporter, which is like a gate to allow glucose into the fat cell. And once in the fat cell, the glucose is converted into glycerol. This then binds with the fatty acids to reform into triglycerides. And this is how fat is stored, under the influence of insulin. But if you want to lose weight, the triglyceride has to be cut back into pieces in order to be able to leave the fat cell for the metabolism. This requires activity of an enzyme called hormone-sensitive lipase. This separates the glycerol from the fatty acids to allow them to leave the fat cell. Insulin blocks this enzyme, puts the brakes on it. And without this step, the fat cannot be metabolized. Insulin blocks fat burning. In summary, we can say that insulin forces fatty acids and glucose into the fat cells and then stops them from getting out again. A triple blow. Thus, insulin clearly has the capacity to stimulate fat storage. But where this fat is deposited is probably even more important than the amount of fat. In red you see what we know as visceral fat, in and around the organs. It is this pattern of fat deposition that is most commonly associated with liver disease and type 2 diabetes. In fact, for every kilogram of increase in visceral fat, the risk of diabetes in men is doubled. And quadrupled for women. Process that. If you as a woman had 1 kilogram extra visceral fat, your risk of diabetes would be 4 times greater. This is because fatty liver directly contributes to something called insulin resistance, which is at the heart of type 2 diabetes. It is worth focusing for a moment on exactly what insulin resistance means. It refers to our tissues that are resistant to the effects of insulin. In other words, the insulin we have no longer works as well. To compensate for that, our pancreas releases more. Insulin resistance can therefore often be recognized by the high insulin levels that result from this compensatory response. We know that insulin is able to stimulate the storage of glucose as glycogen in the muscles and liver, but in case of insulin resistance, this storage is compromised and we end up with higher glucose levels in the circulation. This excess glucose in the blood can be converted to fat through the process of De Novo Lipogenesis. Here we see the extent of De Novo Lipogenesis after eating a carbohydrate-rich meal, in healthy subjects, without insulin resistance. The response to the same meal in insulin resistant subjects? More than doubled. This is a direct result of insulin resistance related to fatty liver. Fortunately, visceral fat and fatty liver are extremely sensitive to weight loss with a low-carb diet. This is a Dexa scan from one of my patients. You can see that the visceral fat is concentrated around the area of the liver. After switching to a low-carb diet and losing just 9% body weight you see a large decrease in visceral fat storage. This effect can be seen even on low-carb diets, even when we deliberately overfeed people to prevent weight loss. We get this redistribution of fat. We also see it in exercise that, although it does not reliably lead to weight loss, it certainly does lead to a redistribution of fat. That’s how we’re beginning to understand why some people can be metabolically healthy and still be overweight. Of course, the opposite is also true. It is possible to be lean and metabolically unhealthy. We call that TOFI: thin on the outside, fat on the inside (thin on the outside, thick on the inside). This is clearly demonstrated in these Dexa scans. The man on the left has a BMI of only 25. And yet he has masses of visceral fat. The man on the right has a BMI of 30, technically obese. And yet it only has a third of the amount of visceral fat. This only serves to demonstrate the limitations of using BMI to assess metabolic health. It is much more accurate and very simple to simply measure the waist circumference. This gives a better reflection of visceral mass. There are also other signs, other external signs of insulin resistance that we can look at. Let’s listen to Dr. T. Everyone I speak to has no idea that skin tags are a pretty good indicator of insulin resistance. They all say, “Oh, really?!”” Unfortunately, this is not widely known. I’ve lost count of the number of patients who come in with skin tags and the story tells that their doctor doesn’t know what causes them, but is still very eager to burn them away. We also see this characteristic pattern of skin pigmentation called acanthosis nigricans, usually in the armpits or groin and sometimes on the outside of the fingers, back or around the neck. Acne is also associated with insulin resistance and this is a big benefit that many of my younger patients often report. There are also lab tests that can be done for insulin resistance. In my clinic I measure both glucose and insulin levels for 2 hours after giving a drink containing 75 grams of glucose. This allows me to estimate the severity of insulin resistance. And this is different from very mild insulin resistance, without a rise in blood sugar, to complete insulin-dependent type 2 diabetes. Let’s look at the standard diabetes research, which only looks at glucose levels. The problem with just looking at glucose levels is that, even at the onset of insulin resistance, the compensatory increase in insulin levels usually keeps glucose levels within normal ranges for a long time. This chart is an example of glucose levels of a typical diabetic patient in the years prior to diagnosis. You can see that the glucose doesn’t really rise until about 10 years, until prediabetes may finally be diagnosed. What happens if we look at insulin levels in the same amount of time? Then we can detect the problem much earlier. Here we see the progressive increase in insulin levels that occurs in response to resistance. This most often occurs as a result of excessive carbohydrates. Then, when the pancreas that secretes the insulin fails, insulin levels drop. Now let’s look at glucose and insulin levels together. This point on the vertical line shows a state where both glucose and insulin levels are normal. And after a while, with the onset of insulin resistance, insulin levels rise, but the blood sugar is still normal. So on a normal blood test, just looking at glucose, everything still looks fine, not even prediabetic but looking at the insulin level, we’re starting to see a problem. Ultimately, the increased insulin levels can no longer fully compensate for insulin resistance and blood glucose levels begin to rise. This is when prediabetes is conventionally diagnosed. Often a decade or more after the insulin resistance started to set in. All along, the patient has likely suffered from the symptoms of high insulin levels, such as weight gain and rising blood pressure. And then, when the cells in the pancreas begin to fail, decreases insulin secretion and the combined state of decreased insulin levels and insulin resistance often leads to a rapid rise in blood sugar levels. This is when diabetes is diagnosed, possibly 2 decades after it all started. Fortunately, this process is reversible with a low-carb diet. These are the insulin results of one of my patients who participated in such a 2-hour test. And these are the results from the same patient 6 months later after starting a low-carb diet. You can see big drops in insulin levels. And not surprisingly, this was associated with 7 to 8 pounds of weight loss. I’ve seen this kind of response countless times. What about the impact of a low-carbohydrate diet on blood glucose levels, since diabetes is formally diagnosed this way? Let’s listen to Dr. T. again. In June of last year I had type 2 diabetes. In August it was the other way around. Then it was 5.8.” She talks about HbA1c, which is a marker of average blood sugar levels. She brought hers up from 8.1 to 5.8, which is a great response. This is equivalent to reversing diabetes. This chart shows how fast the improvements can be. This chart is from a 71-year-old man, who quite literally halved his fasting blood sugar in just two weeks. And during that same time, he stopped taking two drugs for diabetes. This research confirms to scale that reversing diabetes is possible. The gray line shows the mean blood sugar levels of patients receiving standard diabetes care over a two-year period. The light blue line shows the average sugar levels of diabetic patients following a low-carbohydrate diet. And you can clearly see that those who received standard diabetes care had significantly higher blood sugar levels over this 2-year period. In fact, after 2 years, 53% of patients on the low-carb diet met the criteria for reverse diabetes. Since most of the glucose in our circulation comes from what we eat, it is possible, quite literally, to see substantial improvements overnight when starting a low-carb diet. This is a continuous glucose monitor sensor. It sits on the back of the upper arm and has a small, painless needle that picks up glucose levels. It communicates wirelessly with a smartphone or a special reading device and it provides 24-hour live blood sugar monitoring. This is a printout of one of my patients’ monitors the day before she started a low-carb diet. A few days later you will see a huge improvement in the stability of blood sugar levels. This stability is possibly even more important than the absolute value, because it’s the variations in blood sugar levels which also cause significant amounts of oxidative stress which, as we will soon see, cause problems of their own. I do recommend these monitors to many patients, to anyone curious about their personal blood sugar response to specific foods. It is also a good means to see if it is being followed properly. You can’t just pretend that something is okay. The evidence stares you in the face. I call that real-time responsibility and for many patients this helps to stick to a low-carb diet. Now I’d like to switch gears and start looking at processed foods. Processed foods now make up more than half of the food energy consumed in most westernized, high-income countries. Despite the fact that packaging is often hidden behind all kinds of health claims, they are really not that good for us. When I think of processed foods, I think of 2 main ingredients: sugar and vegetable oils, or rather seed oils. Let’s start with sugar. Sugar, or sucrose, is a problem because it contains fructose. 50% to be exact and that is very similar to the amount of fructose in high fructose corn syrup. So we can’t get away with that in Australia. The first problem is that fructose is very sweet, even compared to glucose. In fact, fructose is about 2.5 times sweeter than glucose. This means that fructose is more rewarding for us. This pathway in our brain that triggers our limbic system is activated by sweet taste, it’s a reward pathway. There is no doubt that a degree of addiction contributes to both cravings and overeating related to this pathway, in a state of obesity. Paradoxically, the dopamine receptors are reduced in obesity. On this brain scan you can see that there are fewer dopamine receptors in the brain of an obese individual than there are in the individual of normal weight. This means that for the same level of reward, an obese person must consume more or sweeter foods. This is part of that pathway that leads them to things like sugar and fructose. Fructose is involved in both causing this process and maintaining this cycle. Fructose consumption also leads to a much higher fat production. Do you remember De Novo Lipogenesis? As we know, in a healthy metabolic state, most of the glucose can be absorbed by the liver and muscle tissue. And only about 20% will contribute to De Novo Lipogenesis. Fructose, on the other hand, has no capacity to be stored. All the fructose you ingest contributes to fat production through De Novo Lipogenesis. Fructose can be hidden. These are all different names for sugars, most of which contain fructose, which are used on food labels. Take this almond milk for example, boldly proclaiming that it contains no cane sugar. But when we look at the ingredients, we see this: organic agave syrup. This is even worse than sucrose, as it contains 75% fructose. And typical of many processed foods, they contain vegetable oils. Why? I do not know, but this poses a major problem. And that’s not just because of the omega-6 fat content. Vegetable oils are high in linoleic acid, which is an omega-6 fat. It was adopted by many, myself included, that this linoleic acid would first be converted into arachidonic acid and then in these inflammatory molecules called eicosanoids. The problem with this line of thinking is that arachidonic acid is only converted to these inflammatory molecules when there is some kind of inflammatory response. This means that the production of leuktrienes, thromboxanes and prostaglandins requires an inflammatory stimulus. It requires activation of these enzymes that occur in inflammatory reactions. In low inflammatory responses, such as following a low-carbohydrate diet, these enzymes are less active. Arachidonic acid in itself is therefore not by definition inflammatory. It can even increase in a state of low inflammatory responses. It is also likely that stabilizing blood glucose levels with a low-carbohydrate diet, by reducing oxidative stress, even reduces the damage to the arachidonic acid in our cell membranes and that that also increases the levels. This is exactly what we see. In this recent study, in which we compared low-carbohydrate and high-carbohydrate diets, We see that the low-carb intervention had significantly higher plasma arachidonic acid levels than the high-carbohydrate diet. Furthermore, arachidonic acid is essential for good health. It is an essential component of our cell membranes and among other things, it is involved in muscle repair and muscle growth and the growth and repair of neurons. So the problem with vegetable oils is not the omega 6 content itself, but the tendency of vegetable oils to oxidize. When looking at saturated fats, they are quite resistant to oxidation, because they have no double bonds between the carbon atoms. But when we look at unsaturated fats, we do see these double bonds that are highly reactive and prone to oxidation. The more double bonds fat has, the more likely it is to oxidize. Here we see the tendency to oxidation of fat when cooking, ranging from highly saturated lard on the left to the polyunsaturated sunflower oil, with multiple double compounds, on the right. You can see that olive oil, in the third column, with a single double compound, is approximately in the middle. Even if you don’t cook vegetable oils, they are still prone to oxidation. This study measured the progressive oxidation of walnut oil stored for 8 days and you can see a huge increase in oxidation products in a matter of days. That is why antioxidants are added to vegetable oils. And even then, the oxidation is only reduced and not completely eliminated. After you ingest oxidized oils, you absorb them. They are absorbed by the small intestine in particles called chylomicrons, where they are transported in the circulation to the liver. And this oxidized load on the liver triggers an inflammatory response, which ultimately contributes to insulin resistance. It should be noted that these inflammatory effects are not limited to the liver. It also occurs in other organs, such as the kidneys and lungs. This graph compares the absorption of oxidized fats to these chylomicrons between a meal that contains low oxidation levels and a meal with high oxidation levels. We can clearly absorb these oxidation products. This is a picture of an electron microscope slide of a mouse liver, which shows that these oxidized fats can accumulate in the liver. This accumulation is associated with a pronounced inflammatory response and the development of fatty liver. Here you see fibrosis, typical of fatty liver, directly adjacent to oxidized fat. We also see clear evidence of this in humans. This is TPN, Total Parental Nutrition. This is used in people who can no longer digest food in a normal way. We try to give them their full nutritional needs, through a vein. Typical of most TPN formulations, this bag contains 20% fat, most of which is the highly oxidizable omega 6. Quite predictably, the composition of TPN, with its high content of oxidized fat, leads to liver disease. This study looked at the rate of liver disease in those who received TPN therapy over a number of years. The amount of drop in the line represents the number of people who develop liver problems. You can see that the percentage of people with biopsy-proven liver disease, after 7 years of TPN therapy, was about 60%. This trend showed no signs of stopping. In fact, several patients died of liver disease during the duration of this study. So apparently ingesting oxidized vegetable oils is probably not good for the liver. You know what could be worse? Consumption of oxidized oils if you are a diabetic. This bar shows the extent of oxidation products absorbed in chylomicrons, after a meal with oxidized corn oil, in healthy subjects. This bar, the same meal with oxidized corn oil, in well-adjusted type 2 diabetics. And if you’re a poorly set type 2 diabetic, things look drastically different. That’s why blood sugar control is so important. If you are a diabetic who consumes vegetable oils, you have no chance of success. So what to do then? First of all, keep your blood sugar low. And you get polyunsaturated fats from fresh foods. As long as the food you eat is not rancid, which is basically the definition of oxidized fat, you’ll probably be fine. This applies doubly to omega 3, which is even more susceptible to oxidation than omega 6. So you have the choice between supplements that are likely to be oxidized, or fresh food. Another thing you may want to discuss with your doctors is melatonin, a powerful antioxidant. Predictably, studies have shown that it reliably reverses fatty liver. Some of you, after hearing all this, may still not be comfortable with the idea of eating saturated fat. This perspective study looked at more than 135,000 participants, followed them for 7 years and looked at saturated fat consumption and death rates. The study found that those who usually consumed about 10% of their calories from saturated fats did not get much, had a death rate of about 7 people for every 1000 people per year. In those who consumed more than 3x as much saturated fat the equivalent death rate was only 4. There was no upper limit on saturated fat intake that proved to be problematic. As energy intake from saturated fat increased, so did the benefits. And yes, I know that saturated fat can raise LDL cholesterol. And no, it doesn’t matter. This 2016 systematic review looked at 19 cohort studies involving more than 68,000 participants. Of these 19 studies, 16 found an inverse relationship between LDL cholesterol levels and mortality risk. That means: the higher the LDL level, the lower the risk of death. And 14 of those studies rate this as statistically significant, meaning this discovery is unlikely to be due to chance. So in conclusion: Remember obesity is treatable and that diabetes is reversible. All you have to do is limit your carbohydrates, especially sugar, avoid vegetable oils and embrace saturated fat. A fairly simple recipe. I also want to publicly express my gratitude to Dr. T., who shared her journey in the hope that it might help others, suffering from the same problems as she did. If you’re a doctor, please be open to the possibility that what you’ve learned in Medicine could be wrong. And if your patients come to you and want to try keto, then support them. Their lives may depend on it. Thank you..