Why Your Body Chooses Sugar Over Fat

0:00What determines whether your body burns sugar or fat? It's not just about which fuel is available. One of the biggest signals is insulin. When you eat carbohydrates, blood glucose rises and insulin rises with it. That insulin does two important things. It tells your fat cells to stop releasing stored fat, and it makes it harder for fatty acids to enter the mitochondria where they would normally be burned for energy. So as insulin rises, your body shifts toward burning more glucose and less fat. When insulin falls, that changes. Stored fat can be released again, enter the mitochondria, and be used for fuel.

0:42That's one reason lowering carbohydrate intake can dramatically increase fat oxidation. Your body already knows how to burn fat. Sometimes it just needs the hormonal signal to let it. This is Lecture 161 of the Metabolic Classroom. With no fees or minimums on checking accounts, it's no wonder the Capital One bank guy is so passionate about banking with Capital One. If he were here, he wouldn't just tell you about no fees or minimums. He'd also talk about how most Capital One cafes are open seven days a week to assist with your banking needs. Yep, even on weekends, it's pretty much all he talks about.

1:20In a good way. What's in your wallet? Terms apply. See CapitalOne.com slash bank. Capital One N.A. Member FDIC. Therapy's biggest impact doesn't show up in some dramatic breakthrough. It shows up in the smallest moments. You bite your tongue instead of escalating. You put your phone down instead of firing off that text. You say what you actually mean instead of what would hurt someone else the most. Nobody applauds those moments, but they quietly change your life. That's what growing feels like. And that's exactly what Grow Therapy is here for. Grow is therapy that works, covered by insurance.

1:59Sessions average$21 with insurance and some pay as little as$0 depending on their plan. There are no subscriptions, no long-term commitments. You just pay per session. Grow connects you with thousands of high-quality licensed therapists across the U.S. offering both virtual and in-person sessions nights and weekends. You can search by what matters, like insurance, specialty, identity, or availability. And you can book a therapy session in minutes and begin in as little as two days, not the national 48-day average. See if you could pay as little as$0 for therapy in seconds at growtherapy.com slash start now.

2:38That's growtherapy.com slash start now. growtherapy.com slash start now. Availability and coverage vary by state and insurance plan. If you felt stuck trying to lose weight, you're not alone. Enter Weight Loss by HERS. It's designed to support you in reaching your goals. And HERS now offers access to an affordable range of FDA-approved GLP-1 medications, including the WeGovi pill and the WeGovi pen. Even better, with a range of affordable GLP-1 options, HERS makes it simple to find an approach that fits your needs and your budget. If eligible, you'll get a treatment plan personalized to you and unlimited dosage changes as needed.

3:17It's weight loss designed to work with your life. Ready to reach your goals? Visit 4hers.com slash eligible to get personalized, affordable care that gets you. That's F-O-R-H-E-R-S dot com slash eligible. 4hers.com slash eligible. Weight loss by HERS is not available in all 50 states. Wegovi is the registered trademark of Novo Nordisk AS. To get started and learn more, including important safety information, Wegovi clinical study information, and restrictions, visit 4hers.com.

3:55if you've been trying to improve your health by losing weight you may have the order backwards many of the metabolic problems we struggle with today have something important in common insulin resistance i'm ben bickman and i've spent most of my career studying why we get sick and the role insulin resistance plays in that process the encouraging news is that metabolic health can improve. But knowing the science and actually applying it to your life are two very different things. That's why we created the Insulin IQ 90-Day Metabolic Health Transformation Program. You'll receive personalized coaching, a plan built around your goals and lifestyle, ongoing accountability, and access to the science and tools we use at Insulin IQ.

4:42This isn't another generic diet. It's about understanding what's happening metabolically and learning what you can do about it. If you're ready to stop guessing and take a science-based approach to your metabolic health, click below to learn more. Welcome to the Metabolic Classroom. I'm Ben Bickman, metabolic scientist and professor of cell biology. The idea that glucose and fats compete for the same oxidative or metabolic pathways is a long one. This idea that there's this competition between the two fuels in the body, whether the body's burning sugar or burning fats, is one that's become, in fact, far more popular and prominent than I ever imagined when I first learned about it in graduate school 20 years ago.

5:30But the idea of this competition between burning substrates or burning fuels originates from a paper that was published in 1963. At the time, the investigators described what they called the glucose fatty acid cycle. It was later then referred to as the Randall cycle, but I learned about it as the glucose fatty acid cycle. Their claim was that the two fuels interfere with one another. A cell oxidizing a large amount of fat will find it harder to oxidize glucose or blood sugar. Glucose breakdown happens in a sequence of steps. So there's a series of biochemical events. And the mechanism they proposed inhibits that sequence starting from the end.

6:18And so if the burning of glucose is getting disrupted, it's starting at the back end of that. Fat oxidation or fat burning actually inhibits the final step of glucose burning. That last step is controlled by an enzyme called pyruvate dehydrogenase. When that step slows, intermediates will build up and slow the steps that precede it until ultimately glucose uptake into the cell itself is reduced. So fat oxidation reduces both glucose uptake and glucose oxidation. In fact, I should say that the other way around because that's the more properly sequential series of events. Fat oxidation inhibits glucose oxidation, which starts to lead to an inhibition or reduction in glucose uptake into the cell.

7:12The original observations that led to this cycle were made in isolated rat muscle and as well as rat heart. Of course, those are not the same thing as a whole human. In humans, much of what we know about this competition comes from clamp studies, where insulin and glucose are infused and held at chosen or clamped at chosen levels while they are doing all kinds of measurements in the people. This gives the researchers precise control. Instead of feeding someone a meal and watching several things change at once, they can hold very specific variables steady and then see what the body does. In several of the studies that I'm going to review with you over the course of the mini lecture, I'm going to also introduce other studies where they also held fats or fatty acid levels constant by infusing directly into the body a particular level of fats, what's called a lipid emulsion.

8:17So the human version of the experiment that was done in rat muscle. It came decades after the first observations. One of the seminal studies in this took healthy volunteers and they went through two insulin clamps. On one occasion, fatty acids were kept elevated with a lipid infusion. So an infusion of a lipid emulsion. So there's just this liquid slurry of fats. On the other, they were allowed to fall the way insulin normally makes them fall. Now, what do I mean by that? normally if insulin is high, then fatty acids are going to be down. And this is a point we're going to come back to. So what they were able to do was keep fatty acids available, even when insulin was high and putting both of those up.

9:04So keeping fatty acids up and insulin up, it cut glucose uptake into the leg muscle by about a third. And it also changed what the leg was using for fuel With fatty acids present, glucose made up a little over half of the energy use. Without them, then the use of glucose went up over to about three quarters of total fuel use, which is no surprise. If there was more fat, the muscle was burning less glucose. Now let's go back to that enzyme that I mentioned at the last step of glucose burning, pyruvate dehydrogenase. They found that pyruvate dehydrogenase activity was significantly down. Now, remember, this is in human muscle, in whole living humans, but it complemented the work from that early initial 1963 paper.

9:54So they found the same. It supported what that 1963 paper would have predicted to happen. So the competition holds true in human muscle, and it works through the same step that the original work identified. Now, one measurement in these human studies shows up again and again, and it's called the respiratory quotient, the RQ, the respiratory quotient. That's simply the ratio of carbon dioxide that is produced compared to the oxygen that is consumed or used. So think about a working cell. The cell is pulling in oxygen and then it's breathing out or I shouldn't say breathing out, but then it's giving out carbon dioxide.

10:40When you burn carbohydrate, that ratio is about one. And when you burn fat, it drops to about 0.7 because fat has more hydrogen in it relative to carbon. It actually needs a little more oxygen. So if someone, if a muscle tissue has a respiratory quotient above, say, 0.9, it means that the tissue is running almost entirely on carbohydrate. But if the respiratory quotient is about 0.7, it means that it's running mostly on fat. Now, whether it's measured across a limb or measured at the level of the whole body breathing, which is commonly called the respiratory exchange ratio, RAR, but that's just sort of the whole body version of RQ, regardless of where it's measured, that number is how these studies can tell us which fuel is being used.

11:33but let me just reiterate a point and it is one that we're going to revisit a bit we need to pay attention to what the experiment i mentioned earlier actually created the the metabolic milieu it had high insulin and high fatty acids at the same time in a healthy person those two things don't usually happen together because insulin at high levels or even modestly elevated levels will shut down the release of fatty acids from fat tissue. So the researchers had to infuse fats in order to override what the hormone insulin was trying to do on its own. So what they created is a situation where the fat cells no longer responding to insulin.

12:15Now we're going to come back to that. As I said, when fat cells still respond normally to insulin, we would see the opposite. As I said earlier, if insulin is high, fatty acids will be down. If insulin's down, fatty acids will be high. That becomes important as we seek to understand this glucose-fatty acid cycle. Okay, so the work that I just mentioned now, the initial work, found that fat oxidation can suppress glucose oxidation. The more relevant question, I think, for how most of us eat is whether it works the other way, whether glucose oxidation suppresses fat oxidation. Now, when I say how most of us eat, that's just simply built on the fact that statistically speaking, most calories that most people consume worldwide are coming from carbohydrates.

13:05In fact, based on a nutrient database, about 70 % of all calories globally come from carbohydrates. All right, so this view was tested in healthy volunteers under a clamp that raised both insulin and blood glucose well above normal levels. fatty acid levels in the blood were held constant the whole time by continuous infusion so if fat oxidation fell it couldn't be because there was less fat available so they were putting all of these up glucose oxidation or glucose burning rose more than threefold and fat oxidation fell the investigators concluded that what mainly determines which fuel is oxidized is how much glucose is available inside the cell, not how much fat is available.

13:55Now, there was a companion or a follow-up experiment that showed us more precisely where all of this biochemistry is changing. They actually infused two labeled or tagged fatty acids. So these are fatty acids that they could measure as they were getting burned. So two fatty acids that were labeled were infused at the same time. One of them was oleate, which is a long-chain fatty acid. that has to use normal entrance into the mitochondria through this carnitine shuttle, which I'll mention again in a moment. And so just think of it as a long-chain fat that requires normal steps to enter the mitochondria.

14:34But they also infused octanoate, which is an MCT. It's a medium-chain fat. And you may recall from previous mini-lectures that as the fats get shorter, they get there's less regulation as to how readily they can enter the mitochondria. Medium chain fats are short enough and octanoate is one of those. So it can enter the mitochondria on its own. It does not go through that carnitine shuttle system that I just mentioned that the longer chain fats have to use. All right. So all this to say, they also infused these two specific fats, a long chain fat and a medium chain fat. And they held the fats constant again.

15:16So they were constantly infusing them in under the lipid, uh, under the insulin and glucose clamp. So as they were also pushing up insulin and glucose, they found that oleate oxidation, the long chain fat burning, it dropped by almost half, but the burning of the medium chain fat didn't change at all. This comparison is very helpful because it lets us understand where the regulation of the fat burning is occurring. Medium chain fats don't need carnitine as this sort of transporter to get into the mitochondria. They were unaffected. Long chain fats, and these are the fats that, of course, get released from fat to burn and the fats that we eat for the most part, they need this specific shuttle called the carnitine palmitoyl transferase one or C - and they found that the regulation CPT1 was more blocked during this by elevating glucose and insulin, and that prevented the long-chain fats from burning as well.

16:21So the fat oxidation of long-chain fats fell because transport into the mitochondria was inhibited by the glucose and the insulin signal, not because the fatty acids weren't there. Now, after a normal carbohydrate containing meal, things are pretty straightforward. Glucose will enter the blood, insulin rises in response, glucose uptake into muscle and fat tissue increases, and the release of fatty acids from the fat tissue is shut down. At the same time, rising glucose inside the muscle cell inhibits fatty acid transport into the mitochondria, like I just mentioned a moment ago with the carnitine shuttle system being turned down.

17:04More glucose is being delivered while both the supply of fatty acids and their entry into the mitochondrion are reduced. So the cell will burn glucose. Now, none of this depends on whether total calories are in deficit or surplus. It's just following a hormonal signal. And that signal is insulin. Insulin matters when you want to understand the Randall cycle. It matters enormously. Insulin regulates fat oxidation at two different points. One is the transport step into the mitochondria, and the other is further upstream at the release of the fatty acids from the fat tissue. That upstream, or we could call it the first step, is highly sensitive to insulin.

17:48Lipolysis, which is the release of the stored fat into the blood. And that fat comes out as free fatty acids or maybe what I've just called fatty acids. Sometimes it's called non-esterified fatty acids. They're all the same thing. So lipolysis is what determines whether fatty acids are available in the first place or whether they're in the blood. In a clamp that independently controlled for insulin and some other signals like growth hormone and glucagon, it took less than two micro units of insulin per milliliter to reduce fat release by half in healthy people. A healthy adult usually has somewhere between five and 10 micro units per milliliter after an overnight fast.

18:33So fat release is already substantially reduced even before breakfast. So again, they just found that if they bumped the insulin up to about two micro units, there was already, they were already seeing a reduction in fat burning. So fat release is down, even with modest increases in insulin. And so the authors, to use some of their own language, they described that the adipose tissue lipolysis is exquisitely sensitive to insulin. Yeah, you could say that again. These two control points are not equally sensitive. Remember, the control point of fat getting released from the fat cell to be burned, and then the earlier process I mentioned of that carnitine shuttle, which is the process of pulling the fat into the mitochondria.

19:16Insulin is blocking that too. In a separate study, insulin was infused at four increasing rates while both fatty acid release and fat oxidation were measured. The concentration needed to cut fat release in half was roughly one-third the concentration needed to cut fat oxidation in half. Insulin reduces the supply of fatty acids at much lower levels than those required to inhibit mitochondrial oxidation. To say all that again in a slightly different way, insulin is better at blocking the fat cell from breaking down its fats than it is from blocking the mitochondria from burning those fats. And we do see this is relevant even with ordinary meals.

20:01In one particular study, they had six active men cycled for an hour under three conditions after an overnight fast, after an hour drinking an hour after drinking a glucose solution and an hour after drinking a fructose solution. And remember, fructose is unique because, yes, it's a carbohydrate, but it doesn't increase and it doesn't increase insulin. Average insulin in the 50 minutes before exercise was 8 microunits per mil when fasted. It went to 17 after the fructose drink, so it went up a bit, no doubt, but then it went up to 38 after the glucose meal. These are very normal post-meal numbers.

20:4525 minutes into the exercise, fat release was roughly cut in half after the glucose drink compared with the fasted trial, and fat oxidation fell right along with it. They then ran a fourth trial that separated the two control points. The subjects drank the glucose again, but this time fatty acid supply was restored by infusing lipid directly throughout the rest period and the exercise period. They found that restoring the supply of fat raised fat oxidation about 30 % above the glucose-only trial, but it still didn't bring it back up to the level that they saw in the fully fasted state. Part of the reduction came from less fatty acid being released.

21:31The rest came from blocked entry into the mitochondria. So a single carbohydrate drink produced both effects. Exercise is used in these studies because it raises fuel use high enough to measure cleanly the fuel use. But the same mechanisms do still matter at rest. Someone eating several carbohydrate-containing meals across the day keeps insulin elevated for much of those waking hours. Now, you might wonder whether this is really just about the fat in the bloodstream, whether insulin is simply keeping fat locked away so the muscle can't reach it. And I've already touched on this a little bit, but there's still more evidence worth exploring.

22:12In another study, six endurance-trained subjects cycled for 40 minutes, either fasted or after a large glucose drink while labeled or tagged long chain and medium chain fats were infused. The glucose drink raised insulin and reduced total fat oxidation by 34%, so about a third. About a half of that reduction came from circulating fatty acids and half from the fat already stored inside the muscle itself. That second point is important. Intramuscular triglyceride never goes through the blood. So the fat that is within the muscle already, that muscle has its own reserve within its own fat cells. So this is fuel that's already sitting inside the muscle cell.

22:58Even still, its oxidation fell, which further points to the inhibition that insulin is able to elicit at the level of the mitochondria directly. With no fees or minimums on checking accounts, it's no wonder the Capital One bank guy is so passionate about banking with Capital One. If he were here, he wouldn't just tell you about no fees or minimums. He'd also talk about how most Capital One cafes are open seven days a week to assist with your banking needs. Yep, even on weekends, it's pretty much all he talks about in a good way. What's in your wallet? Terms apply. See CapitalOne.com slash bank.

23:39Capital One N.A. Member FDIC. Therapy's biggest impact doesn't show up in some dramatic breakthrough. It shows up in the smallest moments. You bite your tongue instead of escalating. You put your phone down instead of firing off that text. You say what you actually mean instead of what would hurt someone else the most. Nobody applauds those moments, but they quietly change your life. That's what growing feels like. And that's exactly what Grow Therapy is here for. Grow is therapy that works, covered by insurance. Sessions average$21 with insurance and some pay as little as$0 depending on their plan.

24:18There are no subscriptions, no long-term commitments. You just pay per session. Grow connects you with thousands of high-quality licensed therapists across the U.S. offering both virtual and in-person sessions nights and weekends. You can search by what matters, like insurance, specialty, identity, or availability. And you can book a therapy session in minutes and begin in as little as two days, not the national 48-day average. See if you could pay as little as$0 for therapy in seconds at growtherapy.com slash start now. That's growtherapy.com slash start now. growtherapy.com slash start now. Availability and coverage vary by state and insurance plan.

25:05All right, so a lot of this is focused on insulin appropriately. If insulin regulates fuel selection so tightly after a single meal, then sustained differences in carbohydrate intake should produce sustained differences in fat oxidation, right? In fat burning. And they do. Here's some studies. Five well-trained cyclists ate a diet that was about two-thirds of all the calories from carbohydrate for one week. then switched to a very low-carb ketogenic diet with fewer than 20 grams of carbohydrate per day for four weeks. The diets were matched for calories and matched for protein. During steady-state endurance exercise, the respiratory quotient, remember the measurement of what fuel is being burned, fell from 0.83 to 0.72.

25:54and glucose oxidation dropped roughly threefold and muscle glycogen use fell roughly fourfold. So they were burning a lot more fat. Maximal oxygen uptake. So the kind of VO2 max measurement stayed the same. So they, and the time to exhaustion was unchanged. So they still got as much work out of the workout as they did, but you know, between both, both diets. So same amount of work was being done with a very different mix of fuels. We see even larger differences in athletes who have been eating these differences, these different ways for a longer time. 20 elite ultra marathoners and Ironman distance athletes were trained or used in one study.

26:41They were matched for their age, their body size, the competition distance, and even their performance times. Half of these studies ate a conventional high-carb diet and half ate a low-carb diet. So about 10 % carbohydrate in this last study and 70 % fat in the low-carb group. And this was for an average of 20 months they found across these subjects. And some of them had been doing this for several years. Peak fat oxidation during exercise was more than twice as high in the low-carb group. and it occurred at a higher percentage of their VO2 max. There was no overlap at all. Interestingly, every single athlete on the low-carb diet had higher peak fat oxidation than every single athlete on the high-carb diet.

27:33And then they found that across three hours of running, fat provided 88 % of the energy in the low-carbohydrate athletes versus 56 % in the others. Resting muscle glycogen and how much glycogen was used during the run and restored after did not differ between the groups. So as much as people want to say, if you're on a low-carb diet, your muscle glycogen is going to get depleted. Well, it wasn't. It was the same in both groups of athletes used the same amount of muscle glycogen. All right, everything so far describes a healthy system responding to the insulin signal. as we talk about this Randall cycle or the glucose fatty acid cycle.

28:13The problem starts to show up when that response is lost. A specific scientific review examining the entire glucose fatty acid framework found that insulin-resistant muscle gets it wrong. In fact, it gets it wrong in both directions, and I'll elaborate. Between meals and overnight, when it should be burning mostly fat, the body's burning more carbohydrate. And when insulin rises and it should shift toward burning carbohydrate, that shift doesn't happen as strongly as it does in healthy people. This is what the authors call, this is the birth of the idea of metabolic inflexibility. Their verdict in this famous work based on the older framework, the Randall cycle, is that they state that the Randall cycle is a valid physiological principle, but it may not explain insulin resistance in skeletal muscle.

29:09And this is what's important, where you have a lot of people who say, if you're eating more fat, then you're developing insulin resistance. Their work suggests that it's just not true. And there is further studies to support this. Researchers sample blood going into the leg. So one of the techniques that scientists can use is sampling blood going into a set of muscle or to a leg muscle and sample the blood coming out, looking at the balance of what's going in versus what's coming out. And based on the difference, they can work out what the muscle is burning, not what the whole body burned, but just that muscle specifically.

29:47In obese study subjects, the legs respiratory quotient after an overnight fast sat almost at 0.85, which means the muscle was leaning on carbohydrate at the very time of day. When you think after an overnight fast, it should have shifted over to fat. And when they took muscle biopsies from those same people, they found lower carnitine palmitoyl transferase activity. That's the enzyme that carries the fats into the mitochondria, along with lower activity of the enzymes that do the burning of that fat. So the machinery for taking up fat and burning it is diminished on top of a hormonal environment that's already pushing the muscle toward burning more carbohydrate.

30:30chronic high insulin creates opposite problems in two tissues in fat tissue insulin is no longer effective at restraining lipolysis so again this is an insulin resistance so fatty acids keep leaving their storage site even though insulin is high this is a combination that you would never see in a healthy person, high insulin and high fatty acids. In muscle, insulin is still effective at blocking fatty acid entry into the mitochondria. So the muscle keeps oxidizing carbohydrate. Fatty acids are being delivered to the muscle, but the muscle can't burn it because insulin isn't letting it. And so they accumulate in the muscle or they accumulate in the liver or in the pancreas or any other places that were never meant for long-term storage of fat.

31:25Everything at this point that's been measured, it's looking at the fuel that's being burned. And that's not necessarily going to be the same thing as how much fat a person is burning or losing. So the next question is through the mini lectures, does the shift in fuel selection show up as differences in body composition? And this is not, there's more nuance here than most people want to admit. And I'm going to make sure you know it. The most direct test of this put 28 overweight and obese adults on two calorie restricted diets. So low, they cut calories, but they put them on two different diets in sequence.

32:08So each person served as their own control. One version of the diet dropped carbohydrate below 10 % of energy to induce ketosis. The other version of the low-calorie diet followed conventional recommendations at about carbs at 60%. The study subjects ate more on the low-carbohydrate diet. They ate almost 1900 calories a day as opposed to about 1500 calories per day, and they lost more weight, more total fat, and more truncal fat or belly visceral fat. Roughly 300 extra calories a day, and they still lost more fat. The food, now, kind of a limitation, the food wasn't provided, and intake was self-reported.

32:56And even though there was a strength that each person was acting as their own control by studying over, there's a potential for error there. Over longer periods, the advantage persists perhaps with low-carb diets, but it gets a little narrower. A meta-analysis of 13 trials running at least 12 months found greater weight loss on ketogenic than low-fat diets, but the difference was as modest as just about a kilogram.

33:23with no fees or minimums on checking accounts. It's no wonder the Capital One bank guy is so passionate about banking with Capital One. If he were here, he wouldn't just tell you about no fees or minimums. He'd also talk about how most Capital One cafes are open seven days a week to assist with your banking needs. Yep. Even on weekends, it's pretty much all he talks about in a good way. What's in your wallet? Terms apply. See CapitalOne.com slash bank. Capital One N.A. Member FDIC. Therapy's biggest impact doesn't show up in some dramatic breakthrough. It shows up in the smallest moments. You bite your tongue instead of escalating.

34:02You put your phone down instead of firing off that text. You say what you actually mean instead of what would hurt someone else the most. Nobody applauds those moments, but they quietly change your life. That's what growing feels like. And that's exactly what Grow Therapy is here for. Grow is therapy that works, covered by insurance. Sessions average$21 with insurance and some pay as little as$0 depending on their plan. There are no subscriptions, no long-term commitments. You just pay per session. Grow connects you with thousands of high-quality licensed therapists across the U.S. offering both virtual and in-person sessions nights and weekends.

34:42You can search by what matters, like insurance, specialty, identity, or availability. And you can book a therapy session in minutes and begin in as little as two days, not the national 48-day average. See if you could pay as little as$0 for therapy in seconds at growtherapy.com slash start now. That's growtherapy.com slash start now. growtherapy.com slash start now. Availability and coverage vary by state and insurance plan.

35:15now i have a problem with all of these trials everyone including those in the meta-analysis that lumped into that meta-analysis because every one of these trials that has ever been done to compare low carbohydrate versus high carbohydrate diets they all cut calories in both groups so think about this the person in the high carbohydrate arm is still eating several hundred calories less than they were before the study began, which means they're eating fewer carbohydrates. So their insulin also comes down. We aren't comparing high insulin against low insulin. We're comparing somewhat lowered insulin against more lowered insulin.

36:00So both groups end up getting kind of the benefit here where they're both having lower levels of carbohydrate relative to where they're started, to where they started, even though you'd say, one group is going lower. Yeah, but they're both going lower than where they started. So what we need to do, so what ends up happening is that the study gets designed on accident to wash out these differences. So let me, I hope I'm articulating that well, because I think it is a significant criticism of every one of these trials that's low carb versus low fat, high carb, they've all been lower calorie. So they're calorie restricted.

36:39So even the high carb group is eating fewer carbs than they did before the study started. So they also benefit. Every study that has ever looked at insulin has found that both groups experience a drop in insulin. The proper way to actually test the effect and the difference between these types of studies is to actually run it calorically in the opposite direction. We need to raise calories in both groups instead of cutting them. Then nobody is eating less than before And whatever difference that we see has to come from a strict difference in the composition of the diet. Now, there is one single study in the history of all nutrition science that's done this, but it was done on only one person.

37:24So this was a case study that was published with a single subject, Mr. Sam Felton in the UK. And he published this work with Eric Westman at Duke. he ate 5 ,800 calories a day for 21 days at a time. So three weeks at a time on three different diets. And he would give himself three months between each one to go back to baseline body weight. So he had a low carbohydrate diet where only 6 % of calories were coming from carbs. Then he shifted over after washing out and getting back to normal to a low fat diet. Then he went to a very low-fat plant-based vegan diet. Now, again, this was 5 ,800 calories, so it was hypercaloric.

38:11And what was the difference between them? On the low-carb version of eating 5 ,800 calories, he gained a little over one kilogram in the three weeks. On the low-fat version of 5 ,800 calories, he gained over seven kilograms in those three weeks. And then lastly, on the vegan plant-based version of the 5 ,800 calorie hypercaloric diet, he gained about five kilograms. Pretty interesting, isn't it? Again, it's one single study, one case study on one single person, but it is the only one that has ever been done, as far as I'm concerned, the right way. All right, so taken together, the human data support a handful of points.

38:56that carbohydrate restriction increases fat burning. It produces at least as much fat loss as fat restriction and usually more. It does this without requiring as large of a caloric deficit. And relatively more of that fat that's being lost is coming from the visceral and abdominal fat. Now, in closing, as we try to make some practical sense of this Randall cycle and the glucose fatty acid cycle, I think, is there any truth to the statement when people say, well, their body's just not burning fat? Maybe there is. Maybe they're not that far from the truth. Which fuel gets used isn't a matter of which one is more abundant in the blood.

39:39The CLAMP studies, remember, held fatty acid levels constant and fat oxidation fell anyway if glucose and insulin were up, especially insulin. Insulin decides. It controls the release of fats from fat tissue, and it controls their entry and burning into the mitochondria. That puts carbohydrate in a position that the other dietary variables don't occupy. It's alone. Carbohydrate is the main dietary driver of insulin, and insulin is the main controller of which fuel gets burned. So lowering carbohydrate acts on the control points themselves rather than somewhere else downstream. And in conclusion, lowering carbohydrate intake will lower that insulin signal that keeps the body from burning fat.

40:26So one way to interpret all of this, the complicated glucose fatty acid cycle is you burn what you eat. Class dismissed. Until next time, more knowledge, better health.

41:06Thank you.

41:23Hi, everyone. It's Katie Couric. And on my podcast, Next Question, we love stories about how women are taking control of their lives. They are increasingly leading financial decisions in their households. Yet many say they don't feel fully prepared for the long-term financial choices ahead. Real confidence comes from knowing your financial future is protected whatever happens. Pacific Life has helped generations protect what matters today and prepare for tomorrow with life insurance and lifetime income solutions. It's a promise Pacific Life has kept for nearly 160 years so its customers can keep theirs.

42:05Ask a financial professional about how Pacific Life can help you create a more confident financial future. Pacific Life Insurance Company, Omaha, Nebraska, and in New York, Pacific Life and Annuity, Phoenix, Arizona. State fair food is getting smaller and pricier. We'll have room for fried cookies. Okay, you never overspend on food. What's your deal? What's his deal? He went to Metro and got$450 in value on the new Samsung Galaxy A37 5G for free and no activation fees. free phone? Oh, sign me up. Get that more for your money feeling only on Metro by T-Mobile. Bring your number and activate$40 period plan.

42:46$450 based on device discount wage activation fee. Not available if with Metro or T-Mobile in the past 180 days.