How Low Carb Diets Work for Weight Loss and Longevity

Here's a great breakdown of low carb diets from Dr Paul Mason. We've included the transcription below the video. 

 

My name is Dr. Paul Mason, I'm a sports and exercise medicine physician and today I'd like to take you all on a journey exploring the science that underpins low carbohydrate diets and in the process, I'd like you to take away a few things. Firstly, we wanted to debunk the "calories in, calories out" low fat hypothesis of weight loss.

I want to demonstrate to you that a low carbohydrate diet is actually good for longevity. People live longer when they eat low carbohydrate. And sugar, because of fructose, has some particularly unique and toxic effects on the body. So to begin our journey, I'd like to introduce you to one of my patients. Now, this is the kind of patient that as a doctor, I loved. She was very, very compliant. So she first came to my clinic with joint pain and she was overweight and it was very clear to both of us that if she could lose some weight, that would help her condition. So we had a conversation and started talking about her existing attempts to lose weight and it seemed that she had a very conventional approach—the kind that is recommended by most doctors: eat low-fat.

So let's hear her account in her own words: “I was doing all low fat. You were to see my fridge was just full of low-fat cheese. No oil touched any frypan in my kitchen. All the meat was as lean as you could possibly get and I ate salads and I was starving all the time.”

And were you exercising? “Oh, madly. Six days a week and I was doing those classes. I was doing back-to-back classes. So an hour HIT classes followed by a pump class and six days a week. So, and then I felt really guilty on the seventh day because I wasn't exercising.”

She was following the conventional advice. She was slavishly following that advice. She was exercising, she was eating low-fat, but the trouble is it was not working. At the time she saw me, she was 30 kg overweight and gaining. So when I'm faced with this scenario as a doctor, I have to ask myself, who is responsible? Who is to blame? So the patient is following the medical advice that they've been given. So is it the patient or is it the doctor or the medical professional who gave the advice? So I would argue the blame should actually lie with the doctor or the health professional because the implication of the advice is that if you fail to lose weight, you're lazy and you're greedy, you're just not trying hard enough. But this very premise overlooks the key essence to understanding weight loss and that's hormones. The conventional "calories in, calories out" hypothesis ignores the effect of hormones, which is very strong science.

So we've got a lady here, she's 35 years old and she's got a problem with a hormone called cortisol, and she's just been gaining weight. And this is what happens when her hormone problem was treated. She didn't get given advice to exercise more. She didn't get told to eat less. We fixed the hormone problem and the weight problem goes away.

This boy here, three years old, he weighs 42 kg and he's got a problem with a hormone called leptin. Seven years old, he now weighs 10 kg lighter and a very healthy weight. See what happens when you fix the hormone problem.

Now the most common hormone in the population that causes obesity is not one of those, it's called insulin and this lady has a problem with insulin, but she's got a unique problem. She's got a tumour in her pancreas that secretes insulin and pumps it into her circulation. In this picture, she's 107 kg and she's only 152 cm tall. So she had an operation to remove the tumour which lowered the insulin levels in her body. Now these photos were taken 50 days apart. Her weight dropped to 89 kg. She lost 18 kg. And if we have a look at a graph of her weight loss, you can see that in a 10-day period she lost 14 kg. So clearly there's a problem here with insulin. It makes you fat.

Now this patient also had a problem with insulin. This was one of my patients. You can see her here, 46 years old and a size 20. This is what happened when we fixed her insulin problem, she lost 40 kg and here she is about a size 8. The big difference is she didn't have surgery to fix her insulin problem. We changed her diet.

So you're probably asking, how on God's green earth can a diet lead to such dramatic changes in your insulin level that you'll lose that much weight? So let's have a look. This is a graph here and the height of the lines there represents how much insulin your body is releasing. And each of those individual lines represents one of the three main sources of energy in our diet: carbohydrates, protein, or fat. So let's have a look at carbohydrate. Let's see what happens when you eat carbohydrates to your insulin levels. This is called the area under the curve. You get a massive and prolonged release of insulin for over two hours. Let's have a look when you have the same amount of energy contained within protein—much less. And the surprising thing for many people: fat is even less.

So think about that for a moment. High levels of insulin are associated with obesity, and carbohydrates are the most potent stimulus we have on our bodies to release insulin. So in order for us to lose weight, we need to control that insulin level, ergo, we need to control our carbohydrate intake.

Now we can broadly classify diets into one of two groups. On the left here, we have what's called low carbohydrate diets and on the right, we have low fat diets, which tend to be higher in carbohydrate because the energy has to come from somewhere. So let's have a look at an unbiased look at the evidence comparing these two types of diets in terms of weight loss. Between 2003 and 2018, there were 62 published randomized control trials comparing low carbohydrate diets (less than 130 grams a day) to low fat diets in terms of weight loss. 31 of these studies had statistically significant findings. What that means is that the results were not likely due to chance. You could probably trust them.

So what I've done here is I've graphed these 31 studies that had statistically significant findings, no cherry-picking here at all. And I've compared the average weight loss on both diets. The low carbohydrate diet is depicted in blue and the low fat diet is depicted in red. And you'll note that in every single one of these studies that we've got here, the low carbohydrate diet led to more weight loss than a low-fat diet. So the question is: which horse would you back?

Now, let's change pace a little bit and have a look at fat and see exactly how insulin makes fat tissue grow. Because if we understand this, we can understand the cause of obesity. By the time you're 2 years old, you've got every fat cell that you're ever likely to have. So if you gain weight after the age of two, it's because your fat cells have gotten bigger, not because they've multiplied. So if we can work out what makes an individual fat cell bigger, then we can determine what makes you fatter.

So what I'd like to demonstrate here is that you can see how the circulation, these blood vessels, are intimately related to each and every fat cell. Now we understand that hormone is released through the circulation and because of this relationship with the blood vessels, it can be delivered to each and every fat cell in our body and these blood vessels also contain fat called triglycerides. You can see here in these wiggly line depictions down there. So what happens to gained weight is that these triglycerides get transported into the fat cell and the fat cell gets bigger. The problem is this triglyceride molecule is very big. It's composed of four different parts. You've got this glycerol backbone, and then you've got three separate fatty acids and as a whole, this molecule cannot enter into a fat cell. It has to be snipped up first and that's where insulin comes in. So what you can see on the left-hand side, we see the triglyceride molecule and then it's being converted to glycerol and fatty acids. It is being snipped up and the LPL (lipoprotein lipase) transfer. Lipoprotein lipase is an enzyme that is stimulated to act by insulin. And then once the fatty acids have been released, they're able to cross and store fat. Without insulin to activate lipoprotein lipase, you can't store fat.

And if we have a look on the top there, you can see glucose can also enter fat cells and it does this through a little doorway or a transporter called the GLUT4 transporter. And again, insulin is what activates this transporter. Once the glucose is inside the fat cell, it gets converted to glycerol. Then the glycerol will then combine with the fatty acids, and then you'll have a complete triglyceride molecule. This is the storage form of fat.

Now, to add insult to injury, if you want to actually burn that fat, it has to be snipped up again to leave the fat cell because as you know, it can't cross the fat cell membrane and to be snipped up, it has to be activated by or cleaved by an enzyme called hormone-sensitive lipase. Insulin turns this enzyme off. So you end up with a triple whammy: you have lipoprotein lipase and the GLUT4 transporter being activated—that's stuffing fat into the cell—and then you have hormone-sensitive lipase being deactivated so that you can't burn the fat. So insulin biochemically is the cause of weight gain.

So for a final proof that insulin causes weight gain, let's have a look at what happens to people who habitually inject themselves with insulin in the same site over a long period of time. It leads to a condition we call lipohypertrophy. Hypertrophy meaning get bigger. Now, these two on the left and on the top right, these two gentlemen injected insulin habitually into these sites in their lower abdomen over a long period of time. The person on the bottom right, their preferred injection site was on the front of their thighs. About twenty to thirty percent of patients with type 1 diabetes will actually end up with this condition because they inject insulin in high enough doses for long enough.

So whatever happened to my perfect patient, you know, the one who was slavishly following the low fat exercise advice before she saw me was 30 kg overweight? Well, we had a discussion. She cut the carbs out of her diet and she increased the fat, and by doing that she fixed her insulin problem. And then this happened.

At last count, three years later, she's maintained a loss of 36 kg and she lost 28 cm off her waist and these are her actual photos.

So let's have a look at what is it about carbohydrates that can lead to this increase in insulin that causes obesity. To begin to understand, we have to have a look at what carbohydrates are. On the top here we have a molecule of glucose and across the middle there, we have a depiction of what we call a complex carbohydrate. You know, the kind of carbohydrates you're getting—brown rice and whole grain bread, the stuff that you're told is good for you. It's made of glucose, is sugar. Carbohydrates are made of sugar and when you eat them and digest them, they end up entering the bloodstream to increase your blood glucose level. When you saw Rod and he decided to have some rice, the glucose that made that rice up entered his bloodstream and in response to this increase in blood sugar, the pancreas, this organ tucked up in our abdomen here, releases something called insulin. And then the job of this insulin is to remove the sugar from our circulation. It puts it preferentially into our muscle tissue and our liver tissue and then if there's any leftover, that gets stuffed into the fat.

The problem is that if you have high insulin levels for long enough, that creates a condition called insulin resistance. So we know that when you eat carbs, you get this massive spike of insulin, and if you do that habitually six times a day, as many of you have probably been recommended to do, your body becomes insensitive to the high level of insulin. It's like when you walk into a room with a bad smell. At first, it's overpowering and after a few minutes, you don't notice it anymore. It's the same with insulin, except it only happens mainly at the muscle and the liver tissue, so they stopped taking in the sugar. Your body compensates by releasing more insulin and then the body is able to stuff that extra sugar into your fat tissue.

So this actually explains why a lot of people come in and they say, “You know what, when I was 20, I sat on the couch eating potato chips, no exercise, and I was skinny, and as I've gotten older, I've just gradually stacked on the kilograms, and this is despite becoming health-conscious. I now go to the gym three days a week. I now eat salads.” So the reason that they're gradually gaining weight is because over the years—and this happens over 10, 15, or even more years—they're becoming insulin resistant. And we can actually test for this. So in my clinic, with my patients, we do a test where patients will drink 75 grams of glucose, and then we measure their glucose levels and insulin levels over the course of a 2-hour period. And we can actually assess their level of insulin resistance based on the results.

So let's have a look. So in the red here, this represents insulin level and the blue line represents blood glucose level. So this is somebody who's metabolically healthy. We give them the load of glucose and two hours later, we're having a look. They say that blood sugar's not elevated beyond what it should be and the blood insulin is not elevated beyond what it should be. Perfectly healthy. Then in the first stage of insulin resistance or metabolic ill-health, you'll note that insulin level starts to creep up, but it's still doing a good enough job of keeping the sugar out of the bloodstream, so the blood sugar is not yet elevated. If you had a blood test, a standard oral glucose-tolerance test done at this stage, your doctor would tell you you're perfectly healthy. Don't worry, go home, you are fine. And yet you've got the first signs of insulin resistance. You've probably already gained weight at this stage as it progresses and it starts to creep up a little bit.

The insulin goes even higher and this stage is where your doctor would say, “Oh, you're pre-diabetic. You know, have you thought about doing a little bit of exercise?” Still not too worried about the whole process. And then over time, this blood sugar starts to damage the cells in the pancreas that release insulin, so even though you're becoming insulin resistant and you need more insulin, your body produces less. And then when your insulin levels start to fall, you have a precipitous increase in your blood sugar levels, and that's when diabetes is diagnosed.

So let's have a look at a couple of examples. So this patient here: low blood sugar, low insulin level. Perfectly healthy. I like this comparison. This patient here: probably putting on a little weight. You can see the blood sugar's quite low at two hours, 5.6, but you can see the insulin has now risen to 83. Okay, we're starting to see insulin resistance here. We're starting to have a problem. And here you can see that blood sugar has now come up off the floor, insulin is a bit higher again, and the blood sugar is rising to 8.3. And then what happens in the more advanced stage? Blood sugar 11.4. This is when you would be diagnosed with diabetes under standard blood tests, by the way, and the insulin level has dropped—the pancreas is starting to fail.

Now, it's all well and good to say, “Okay, you're a doctor, you can test for insulin resistance in your laboratory,” but a lot of people are curious to know if they have insulin resistance and whether they can check themselves. And you'll be interested to know that you can see a lot of signs of insulin resistance by looking at the skin. And I've got several patients here today and you know that I'll inspect your skin. These are what's called skin tags. The most common cause of skin tags is insulin resistance. If you have skin tags, you are almost certainly insulin resistant. And a lot of patients tell me, “Well, I go to my GP and ask what causes it, they say in one sentence, I don't know, but would you like me to burn them off?”

They're a warning sign. They're usually in the armpits, around the neck, in the groin region. This sign here is called acanthosis nigricans. It's pigmentation of the skin. We often see it around the neck, in the armpits, in the groin, or more interestingly on the back of the fingers. The skin creases here, and there's good research that shows that even before you start gaining an excess amount of weight, you can see the changes on the back of the fingers before anything else. I can see a few people having a look at their fingers now.

I see a lot of patients who come in with problems with their skin complexion and what we find is that when we improve the insulin resistance, that significantly improves. Have a ketogenic diet, lower your insulin levels, skin gets better. It's very nice. And that's one of the reasons why acne is very common in the state of adolescence, because the state of adolescence, puberty, is associated with insulin resistance.

Now for the good news that had to be coming. We can actually reverse this. If you go on a low carbohydrate diet and reduce your chronic elevated levels of insulin, your insulin sensitivity will improve. Have a look at the insulin levels of this patient here, and three months later, big drops. Here's another example. We can see that one hour insulin was 114 and again to 71 just in the space of a few months. And there is also a nice associated weight loss to boot.

So, I think it's pretty clear: a low carbohydrate diet is the best diet for weight loss. But some of you are probably still concerned, you're probably thinking, "Well, it's all well and good to be skinny, but what happens if it's going to kill me, all that saturated fat, right?"

So let's have a look at the biggest study that's been done to date on this topic. It was published last year and it had over 135,000 participants. They were followed for more than 7 years across 18 countries. This was a big, big study.

So what we can see is that the group that was having the least amount of fat had a mortality rate per 1000 person years of just under 7. Let's see what happens to the group that was getting more of the energy from fat—more than 3 times as much from fat. Their mortality rate dropped at 4. More fat, live longer.

And if we have a look at a graph from that same study demonstrating this, where your risk of dying is on the axis going up (the higher, the worse it is) and the effect you're having is going to the right-hand side, you can see there's no point at which having more fat becomes problematic. In actual fact, it seems the more fat you have, the total mortality continues to drop.

So now let's flip this on its head and have a look at carbohydrate intake. If you have 46.4% of your energy from carbohydrate, the mortality per 1000 person years risk was about 4. And by the way, this is not considered a particularly low carbohydrate diet, but it's low carbohydrate compared to the average diet. Let's have a look at the group of the population that was getting far more—72.2% of their energy from carbohydrate. Their risk of dying went from about 4 to over 7. With more carbohydrates. And again, we have a look at this graph—the more carbohydrates you have, your mortality just keeps on climbing. So low carbohydrate, high fat diets, you will live longer.

Now, this is not a one-size-fits-all diet. Some people might be able to have 80 grams of carbohydrates a day. Rod says his limit was 50. Some other people may only be able to have 20 grams of carbohydrates a day to be in optimal health. And we use something called the ketone meter to determine your optimal level of carbohydrate restriction. Now the only difference between a low carbohydrate diet and a ketogenic diet is the degree of restriction of carbohydrates. If you reduce your carbohydrates enough to lower your insulin levels to permit fat-burning, some of that fat, when it's metabolized, will be converted to a chemical called a ketone.

Now the thing to realize is that in the human body, the only source of ketones comes from fat metabolism—nothing else. So if you have ketones in your bloodstream, that indicates that your body is burning fat. So we can take a drop of your blood, put it on a meter, and within 10 seconds, we've got the answer. Now down the bottom, this is the scale that we generally use, and it's also useful, as well, as indicating your degree of fat metabolism for suppressing your appetite.

What we find in the clinic is over the last few years, is that people who come in with ketones hovering around 0.4 or higher, they often say, “You know what, I’ve only eaten twice a day now, I’m just not hungry.” And this is demonstrated in the research. We know when you have higher levels of ketones, that has an appetite-suppressing effect.

So not only are you burning more fat, but the whole "calories in, calories out" first law of thermodynamics equation, you put less energy into the system. So this actually dovetails in quite nicely with the conventional wisdom of "calories in, calories out," but it adds another layer. It starts to explain how you can put fewer calories in.

This is an example here of a food diary with ketones being recorded down the right-hand side, the numbers down the side, and the reason we do this is because by recording your ketones and comparing it to your food, you can actually start to understand which foods are stopping you from burning fat.

Let's zoom in a little bit so we can see down the right here. We’ve got a few ketone numbers: 1.1—that’s good; 0.7—that’s okay; 0.4—that’s still okay, and then we drop to 0.2. Why? A small piece of sponge cake, okay. Probably not the best. But it's okay because the next day they’re back up to 0.7. Piece of toast bumps it down to 0.2. This person is very, very sensitive to carbohydrates. And without doing this, they would never have known.

So now I’d like to take a closer look at sugar and the uniquely toxic effects that that has. So we’ve already seen about this glucose molecule on the left, the one in the yellow, but the one on the right is called fructose, and when you join one of each of these molecules together, it forms table sugar, sucrose, and you can see that sucrose is exactly 50% fructose. And that's important because a lot of people say, “We don’t have a problem in Australia because we don’t have high fructose corn syrup.” Well, high fructose corn syrup is only between 42% and 55% fructose, so they're very, very comparable. The table sugar we have here in Australia is every bit as bad as high fructose corn syrup.

Now, when we have a look at the sweetness of different sugars, the reason fructose is a problem is it's more than twice as sweet as glucose, and this is a problem because, as humans, we love self-gratification. We've got this pathway in the brain called the mesolimbic pathway, and this is the reinforcing pathway. It reinforces our behavior. And when we stimulate our brain with something sweet, we get a release of a chemical called dopamine, and it says, "Yes, do that again!" And fructose activates this pathway by virtue of it being more than double the sweetness of glucose. It activates this pathway more strongly.

And when we scan the brains of obese individuals and have a look at dopamine receptors, we can see there’s a reduced number of dopamine receptors in the brains of obese people. So this means to get the same level of satisfaction from a meal, obese people need to eat more. And this is where sweetness fits into it. Over time, this changes will down-regulate. But the problem is that until they down-regulate over time, you have to restrict the sweet foods in your diet.

Now, fructose has another particularly toxic effect, and that leads to insulin resistance. Fructose, far more powerfully than glucose, leads to a fatty liver. So when you eat fructose, normally about 80% of it gets taken up by the muscle, gets taken up by the liver, and then it goes to the liver and there's a capacity for storage in the liver for glucose. It has something called glycogen, so that sets up a little bit more. So the amount of energy that ends up going to the liver and going to the mitochondria within the liver is only a fraction of what you ingest. But with fructose, it doesn't go to the other tissues and it doesn't have this reservoir where it can be taken up or stored, so every gram of fructose you eat gets delivered to the mitochondria in the liver.

And when those mitochondria get overloaded, they produce fatty liver. The process is called de novo lipogenesis. This is a slide—those white globules there are globules of fat in a fatty liver, and excess fructose can do that, and this is strongly associated with insulin resistance. Another problem is that sugar can attach to protein, and you've got sugar bathing the cells of your body, and that sugar, over time, can not only attach to it, that can form these complexes called advanced glycated end products and they can affect nearly every type of cell and molecule in the body.

The problem is that fructose does this seven times more than glucose. Yet another problem with fructose. And when we have a look at the consequences of these advanced glycosylated end products, they affect a lot of the tissues that we see people with diabetes have—nerve problems. We've already talked about how the pancreas can start to fail and reduce its capacity to secrete insulin. Kidney problems, blood vessel problems, you can go blind, arthritis is really, really common.

Now just to illustrate the point that these advanced glycosylated end products are associated with aging, this is some ground-up rib cartilage on the top left. This is from 2 weeks old, and on the bottom right, from 88. And this is what normally happens across the lifespan. It's very similar to a process called the Maillard reaction or the Browning reaction—caramelisation, if you will—not quite the same, but along the same lines. And over time, the sugar in our circulation will change our tissues. And I'd have a question: why would you want to accelerate the aging process by increasing your sugar levels even more?

Now, we know that the most common sources of added sugar in our diet are sweets. Maybe some people will be surprised to know that cereals are one of the major sources of added sugars in our diets. But sugars are also hidden in a lot of foods. Not many people will realize that a squirt of tomato sauce probably, far less than what they actually habitually put on, has a good one of the health teaspoons of sugar in it.

But the real surprise is down on the bottom right here. This is a medium-sized mango juice, 12 and a half teaspoons of sugar. And there's other ways that sugar can be hidden. I've got an organic almond milk here. Perfect. You can see lactose-free, soy-free, gluten-free, no cane sugar. Okay, you're feeling pretty good right now. Let's have a look at the ingredient. Still look okay?

Show our hands, who thinks it doesn't look so bad? Organic agave syrup. You know, agave syrup is 75% fructose. It's even worse than table sugar. It's worse than cane sugar.

And this here is a list. The names that sugar is disguised in in Australian nutrition labels. Food manufacturers are allowed to use every one of these euphemisms for sugar on their label. Makes it very difficult.

Now some people say, "But fructose, it's natural, right?" Maybe it's natural, but we don't consume it in a natural way. You wouldn't know it, but this is a fruit tree on the left. It has no fruit. It's because fruit is seasonal. We don't have access to fruit year-round and if you want honey, well, you don't get to go to Cole’s. Traditionally, you had to go and ask the bee if it would lend you his honey.

So we consume fruit in a very different way. We now have 500 ml of orange juice, which contains 6 oranges, and it's had all the fiber taken out. So just as an aside, don't drink your fruit. Just do not drink your fruit.

Now I'd just like to touch on one more point before I finish, and that's artificial sweeteners. So we've already talked about them as an Olympic pathway reinforcing behaviours, and artificial sweeteners do exactly the same thing. When we have a look at the evidence, all the cohort studies, they show that consumption of artificial sweeteners is associated with weight gain, increased weight circumference, metabolic syndrome, type 2 diabetes, and heart attacks. Artificial sweeteners don't get a leave pass.

So, I'd like to leave everybody here with three key points:

1. You are not to blame for being overweight if you've been following bad advice. Critical.
2. Low carbohydrate diets are the best diet for weight loss because they lower insulin.
3. Finally, people live longer on low carbohydrate diets.

Thank you.

Try our range of Low Carb Snacks and Supplements >