Dr. Paul Mason – 'Evidence-Based Keto: How to Lose Weight and Reverse Diabetes'. Translation and subtitles: TheNewFood. Good morning. I am Dr. Paul Mason and I am a medical sports and exercise physician from Sidney. Today we are going to explore the science of ketogenic diets and are we going to 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 are going to find out exactly what it is about vegetable oils that makes them poisonous. 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. And yet, that is the conclusion many people draw when they look 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 is not exactly the case that Dr. T. was not motivated to lose weight. It had a huge impact on the quality of her life. “It was awful every day. I can't remember a day that I didn't get up and thought, I'm just going to start a diet on Monday. Or: if I could just solve my weight problem, I could get my life back on track. " Obviously, she had also not gained dominance due to lack of exercise. “I always cycled to and from work, which was about 25 to 30 kilometers there and back. We even planned cycling holidays. I walked; I had a dog that I went for an hour in the afternoon for a walk. I went to the gym. I enrolled in weight management clinics at the university where I worked with students of 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 when I didn't have to.
" She was also not overweight because she did not follow medical advice. "I've tried all diets, I've followed eating schedules, I've tried medication, I've tried Xenical. At one point my doctor even wanted to give me Amphetamine, but I attached a little too much value to my brain for that. By the time I was 40, things had gotten so out of hand that I tried bariatric surgery. I had a gastric band placed, because I thought, frankly, I thought that at worst I wouldn't get any fatter and at best I might, as if by some miracle, go back to a normal 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 kilos. I've lost 55 kilos 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 has she done? She was clearly not following conventional medical wisdom, because following this advice has only taught her to grow fatter and sicker. No. 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 in our bloodstream, 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 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; only lower insulin levels. Anyone who has ever had to inject insulin understands that it stimulates fat storage. Injecting insulin into the same site for a long time often leads to a condition called lipohypertrophy. quite literally translated as fat gain. 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. High blood insulin levels are very predictive of future weight gain. This study initially followed slim subjects for 8 years to see who developed obesity. Those who were in the lowest 25% in insulin levels, at the beginning and end of the 8-year period, only had 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 really only good because insulin helps build lean mass, like muscle. But the story gets really interesting when we get to the carbohydrates. When we compare insulin release between carbohydrates and fat we understand why carbohydrates are fattening and fat in and of themselves.
One of the reasons insulin levels affect our weight gain is that, among other things, it regulates our involuntary use of energy, even at rest. This was elegantly shown in this recent study, in which subjects were assigned a diet consisting of a low 20%, an average 40%, or high 60% carbohydrate, respectively. And then the researchers did something really interesting. They adjusted the subjects' energy intake to prevent weight change. What they found out is that the low-carb group, in blue, even had an increase in energy consumption. Compared this to the carbohydrate-rich group, in red, where energy consumption was reduced. The difference between these 2 groups was considerable: about 278 kcal per day. This is comparable to the energy consumed in 1 hour of moderately active exercise. In fact, 278 kcal per day translates to 10 pounds of weight loss over 3 years in a 30-year-old man. This is not an isolated finding. You can even say that there is agreement between randomized controlled trials of high quality.
The definition of low-carbohydrate 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. There were 62 randomized controlled trials between 2003 and 2018 compared to a low-fat and low-carbohydrate diet on the one hand. Of these 62 studies, 31 did not yield 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, with 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 we can store some of it in our muscles and liver as glycogen. In fact, healthy people can store about 80% of the glucose as glycogen. But all of this changes when we consume too many carbohydrates. In this study, subjects were deliberately given 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 adding more carbohydrates showed no increase in how much was burned.
Part of the glucose was stored as glycogen, as we saw earlier, but this capacity diminished in the following days when stocks kept getting full, until on day 6 there was no more free storage capacity. Then what happened to the excess carbohydrates? This was converted to fat through a process called De Novo Lipogenesis. And while storage capacity continued to decline, 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. Increased blood glucose levels. 2. Increased 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: the glucose, the insulin and the triglycerides.
Let's see what happens. First, let's look at triglycerides. In its complete form it is incapable of entering a fat cell. This is where insulin comes into play. Insulin stimulates this enzyme here, lipoprotein lipase, which then cleaves the larger molecule, enabling the fatty acids to spread in the fat cell. Insulin also activates the GLUT-4 transporter, which is, as it were, 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 triglyceride. 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 get out of 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 exit 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. Encompassing we can say that insulin forces fatty acids and glucose into the fat cells and then stops them from getting out again. A threefold blow. So 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 can 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 for a moment. If you as a woman had 1 kilogram of extra visceral fat, your risk of diabetes would be 4x greater. This is because fatty liver contributes directly to something called insulin resistance. which is at the heart of type 2 diabetes. It's worth taking a moment to focus on what insulin resistance means exactly. 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 thus often be recognized by the high insulin levels resulting 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 the 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 into fat through the process of De Novo Lipogenesis. Here we see the degree 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 consequence of insulin resistance related to fatty liver disease. Fortunately, visceral fat and fatty liver are extremely sensitive to weight loss on a low-carbohydrate diet.
This is a Dexa scan on one of my patients. You can see that the visceral fat is concentrated around the liver area. After switching to a low-carbohydrate diet and losing only 9% body weight you see a big decrease in visceral fat storage. This effect can be seen even with low-carb diets, even when we deliberately overfeed people to prevent weight loss. We get this redistribution of fat. We also see 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 begin to understand why some people can be metabolically healthy and still be overweight. Of course the opposite is also true. It's possible to be lean and metabolically unhealthy. We call this 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 it has tons 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 is only 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 talk to has no idea that skin warts 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 warts and the story tells that their doctor does not know what causes them, but is still very excited 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, the back or around the neck. Acne is also associated with insulin resistance and this is a great benefit that many of my younger patients often report. There are also laboratory 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 the insulin resistance. And this differs from very mild insulin resistance, with no rise in blood sugar, to complete insulin-dependent type 2 diabetes. Let's take a look at the standard research for diabetes, which only looks at glucose levels. The problem with just looking at the glucose levels is that, even with the onset of insulin resistance, the compensatory increase in insulin levels usually keeps glucose levels within normal ranges for an extended period of time. This graph is an example of glucose levels of a typical diabetes patient in the years leading up to diagnosis. You can see that the glucose doesn't really rise until about 10 years, until the point when prediabetes may finally be diagnosed. What happens when we look at the insulin levels over the same length of time? Then we can discover the problem much sooner.
Here we see the progressive increase in insulin levels that occurs in response to the 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 the 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, at the onset of insulin resistance, insulin levels rise, but the blood sugar is still normal. So with a normal blood test, just looking at glucose, everything still looks fine, not even prediabetic, but looking at the insulin level, we begin to see a problem.
Ultimately, the elevated 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 insulin resistance started to appear. All along, the patient has probably suffered from the symptoms of high insulin levels, such as weight gain and rising blood pressure. And then when the cells in the pancreas start to fail, the secretion of insulin decreases and the combined state of decreased insulin levels and insulin resistance often leads to one 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 readings of one of my patients who took about a 2-hour test. And these are the results of the same patient 6 months later after starting a low-carbohydrate diet. You can see big decreases in insulin levels. And unsurprisingly, this was associated with 7 to 8 pounds of weight loss. I've seen this type of reaction countless times.
What about the impact of a low-carbohydrate diet on blood glucose levels, since diabetes is formally diagnosed in this way? Let's listen to Dr. T. again. “In June last year I had type 2 diabetes. In August it was the other way around. Then it was 5.8. " She's talking about HbA1c, which is a marker of mean blood sugar levels. She brought hers from 8.1 to 5.8, which is a great response. This is equivalent to reversing diabetes. This graph shows how fast the improvements can be. This chart is from a 71-year-old man, who literally cut his fasting blood sugar in half in just two weeks. And during the same period he stopped taking two medications for diabetes. This research confirms to scale that reversing diabetes is possible. The gray line shows the average blood sugar of patients receiving standard diabetes care over a two-year period. The light blue line shows the average sugar levels of diabetic patients on 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-carbohydrate 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 significant improvements overnight when starting a low-carbohydrate 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-carbohydrate diet. A few days later you see a huge improvement in the stability of the blood sugar levels.
This stability may be even more important than the absolute value, because it's the variations in the blood sugar levels which also cause significant amounts of oxidative stress which, as we'll soon see, cause problems themselves. 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 of seeing if it is being properly observed. You can't pretend something is okay. The evidence stares you in the face.
I call that real-time responsibility, and for many patients, it helps to stick to a low-carbohydrate diet. Now I would like to switch and look at processed food. Processed food now makes up more than half of the food energy consumed in most westernized, high-income countries. Despite the fact that there is often hidden behind packaging with 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 precise 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 path in our brain that triggers our limbic system is activated by sweet taste, it is a reward path. There is no doubt that a degree of addiction contributes to both cravings and overeating related to this path, in a state of obesity. Paradoxically, dopamine receptors are diminished 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 normal weight individual.
This means that for the same level of reward, an obese person should consume more or sweeter foods. This is part of that path 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 Lipogenese? 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 Lipogenese. Fructose, on the other hand, has no capacity to be stored.
All fructose you consume contributes to fat production through De Novo Lipogenese. Fructose can be hidden. These are all different names for sugars, most of them containing 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 is that they contain vegetable oils. Why? I do not know, but this poses a major problem. And that is not only due to the omega 6 fat content. Vegetable oils are high in linoleic acid, which is an omega 6 fat.
It was adopted by many, including myself, 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 thought is that arachidonic acid is only converted into these inflammatory molecules when there is some kind of inflammatory response. This means that the production of leuketrienes, thromboxanes and prostaglandins require an inflammatory stimulus. It requires activation of these enzymes that occur in inflammatory responses. With low inflammatory reactions, such as when following a low-carbohydrate diet, these enzymes are less active. Arachidonic acid on its own is therefore not necessarily inflammatory. It can even increase in a state of low inflammatory response. It is also likely that stabilizing blood glucose levels with a low-carbohydrate diet, by reducing oxidative stress, even decreases 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, comparing low-carb and high-carb diets, we see that the low-carbohydrate 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 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 compounds that are highly reactive and susceptible to oxidation.
The more double bonds fat has, the more likely it is to oxidize. Here we see the tendency for fat to oxidize 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 roughly 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 that was stored for 8 days and you can see a massive 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, absorb them. They are absorbed by the small intestine in particles called chylomicrons, whereupon they are transported in circulation to the liver. And this oxidized charge to 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 levels of oxidation and a meal with high oxidation levels.
We can absorb these oxidation products clearly. This is a picture of an electron microscope 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 disease. Here you see fibrosis, typical of fatty liver disease, 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 diseases. 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 have died of liver disease during the duration of this study. So apparently, the intake of oxidized vegetable oils is probably not good for the liver. Do you know what could be worse? The consumption of oxidized oils if you are a poorly-adjusted diabetic. This bar shows the degree 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, with well-adjusted type 2 diabetics. And if you are a poorly adjusted type 2 diabetic, it will look drastically different. That's why blood sugar control is so important. If you are a poorly-minded 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 food. As long as the food you eat isn't rancid, which is basically the definition of oxidized fat, you will 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. You may also want to discuss with your doctors melatonin, a powerful antioxidant. Predictably, studies have shown that it reliably reverses fatty liver disease. Some of you, after hearing all of this, still won't 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 in saturated fats did not consume 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 mortality rate was only 4.
There was no upper limit on saturated fat intake that proved to be problematic. As the energy intake of saturated fat increased, so did the benefits. And yes, I know that saturated fat can increase LDL cholesterol. And no, it doesn't matter. This 2016 systematic review looked at 19 cohort studies with 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 that this discovery is unlikely to be due to chance. So in conclusion: Remember that 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 would also like to express my thanks publicly 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 are a physician, please be open to the possibility that what you learned in the Medicine degree 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..