Your Fat Has a Storage Limit

20:33Later comes a dark, velvety thickening of the skin around the neck and the armpits, which is a visible sign of severe insulin resistance and called acanthosis nigricans. Unenlarged liver comes stuffed with fat. It's pretty close to universal in this disease, which can go on to cirrhosis, which is scarring so extensive that the liver stops working. In the largest untreated group I could find, which is 43 patients, 8 in 10 had at least one organ damaged, and the liver was the one involved most often. Now let's be clear about one thing, because the version you'll hear is that these children all get diabetes.

21:03In that group, fewer than half had blood sugar even in the pre-diabetic range. What the authors actually say is that the metabolic disease develops by late childhood and gets worse with age. That's the accurate version, and it's still devastating. So think about this for a second. These are people with no body fat, and yet they have all the disease of too much fat. They basically have no garage, and as a result, all of their boxes sit on the stairs. Which brings me to the 17-year-old, and to the part where the room that talks turns out to matter more than the room that stores. Because if these patients are missing storage, and you can't give somebody more storage, what can you actually do for them?

21:39In 2002, a research group from Yale, working with the NIH, tried something that sounds like it shouldn't work. Your fat tissue makes a hormone called leptin. Leptin is how your fat tissue tells your brain how much fat is on your body. And the direction that matters is when leptin is down. When leptin falls, your brain reads it as starvation and turns your appetite up hard. Happens in anorexia nervosa. That's the system's real job. It defends you against running out of energy. Now think about somebody with no fat tissue. No fat tissue, no hormone. Their leptin levels run near zero, permanently.

22:10So on top of everything else, their brain is receiving a starvation alarm that never stops. That's the appetite that nobody can satisfy. It's a missing signal doing exactly what it evolved to do. So the research group gave the signal back. They gave them leptin by injection for three months. Now, it's only three patients. That's the whole study. Again, six healthy women matched for age and weight. It's here because of what they measured, not because of how many people they measured. They measured how well the liver and the muscle each responded to insulin separately.

22:36Jordan Feigenbaum:I think it's worth 30 seconds on how you actually measure that because it's the same method Klein used at the top of the show. and it's the closest thing to a direct measurement that exists. You put somebody on two IV lines. One drips insulin in at a fixed rate. The other drips in how much sugar it takes to stop their blood sugar from falling. Then you read how much sugar you needed. If their tissues are listening to insulin, they pull sugar out of the blood fast and you have to pour a lot to keep up. If they've stopped listening, you barely need any. It takes four to six hours and two people to run, which is why nobody does it really outside of a research lab.

23:11And they used a scanner to measure how much fat was actually sitting inside the liver and inside of the calf muscle. Not how big the liver was, how much fat was in it. The first patient was 17 years old. She had no fat underneath her skin at all, an enormous liver, and lumps of cholesterol deposited into her skin. Her blood fats were so high that when they drew her blood, it didn't look like blood. Plasma is normally kind of straw-colored and clear. Hers came out of the needle looking like milk. Her liver was 48 % fat, and in healthy women, it's usually under 1%. Then she gets three months of leptin.

23:41Her liver fat and the other two patients' liver fat fell by more than 80%. Their muscle fat came down by about a third. Their bodies went back to responding to insulin several times better than before, and all three came off of their diabetes medication. Now, here's why the study tells you something. They didn't give these people fat, their body weight didn't change, their fat mass didn't change, so whatever was working was working because the signal came back, not because they added fat storage. And it isn't only in the liver. In the one patient where they measured food intake, leptin cut it roughly in half.

24:12So part of what you're watching is a starvation alarm getting switched off for the first time and a person eating less as a result. That's real and it's part of the mechanism. But that doesn't mean the one thing that people ask about constantly. It doesn't mean that leptin is a weight loss drug. It has been given to ordinary people with ordinary obesity and it does almost nothing because those people already have plenty of leptin. The system is powerful mostly when it's low and it has no matching break at the top. Leptin defends the floor, but it doesn't really do anything to the ceiling. So, no garage gives you the whole disease, and giving the garage's voice back fixes most of it without adding a single box, which sets up the opposite experiment.

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29:46In one study, 13 people with type 2 diabetes took this drug for four months. Their long-term blood sugar marker came down substantially, and their livers went back to handling insulin close to twice as well as before. And they gained three kilos, essentially all of it fat. Now, the reason this study is worth your time instead of just being a curiosity is that they scanned everybody. Fat under the skin went up, fat around the organs went down. The ratio between the two shifted by about a quarter. So the garage got bigger and the boxes came off the stairs. The patients got heavier and every measure of their disease improved.

30:19The result was later repeated in a larger randomized trial where people on the drug gained more weight than people on the placebo, and about half of them had their liver inflammation resolved outright. Three kilos of new fat and a better liver. I think that should have caused a much bigger fuss than it did, but why it didn't is curious. Weight gain reads as a failure to almost everybody, including doctors, no matter what the rest of the chart says.

30:40Jordan Feigenbaum:When you line those four experiments up, they all point in the same direction. Klein took 10 kilos out and the disease stayed exactly where it was. He changed how much fat somebody had and he left every room in the house full. Lipodystrophy takes how much fat down to nothing, and those patients get the whole disease anyway because with no garage, every single box goes somewhere else. Leptin didn't put a gram of fat on anybody. It pulled fat out of the liver and out of the muscle, and the disease came out with it. And pioglitazone added three kilos, and those people got better because the three kilos went into storage and came off the stairs.

31:11Jordan Feigenbaum:So across all four, the total amount of fat on the body goes whichever way you like, up, down, all the way down to zero, and the disease pays no attention to it. What disease follows every single time is which rooms the fat ended up in. That's the direction they're pointing. Okay, so you could accept all of this and say, fine, but you haven't shown me your version is right. You've shown me every other one is wrong. Okay, let's do that. I need to give you two ideas from outside of medicine because without them, the rest of this is just me saying things. The first one is why this took about 40 years to find out.

31:41You can't test an idea by itself, ever. When you test an idea, you're also testing every assumption you needed to get to it all at once in the same experiment. Here's what that means in practice. Take the question about body fat being dangerous. To study that, you need to measure body fat, and almost every study ever done measured it with BMI, which is your weight divided by your height squared. BMI doesn't know how much fat you have, and it doesn't know where any of it is. So a study that comes back showing nothing, what failed? Maybe fat isn't dangerous, or maybe fat is dangerous and BMI is too blunt to see it,

32:12Jordan Feigenbaum:or the follow-up was too short or the wrong people were enrolled. You get to pick, and whatever you pick, you can defend it. Now philosophers named this problem a long time ago, and it applies to every experiment ever run in every field. And it's not an excuse to believe whatever you want because there is a way to tell a good save from a bad one. Which brings me to the second idea, and it's a story about the same man being brilliant and wrong with the exact same strategy. In 1845, the planet Uranus was in the wrong place. Not by much, but it was measurably off from where Newton's laws said it should be.

32:41Jordan Feigenbaum:and Newton's laws were the most successful thing anybody had ever built. A French astronomer named Urbain Le Verrier did not conclude that Newton was wrong. He concluded that there had to be another planet out there, one nobody had seen, pulling on Uranus. And he calculated where it would have to be. Then he wrote to an astronomer in Berlin and told him where to point his telescope. On the 23rd of September, 1846, that astronomer found Neptune within one degree of the spot that Le Verrier had computed. That's a win. He kept the theory, he blamed an assumption instead, and the assumption really was the problem.

33:12Ten years later, the planet Mercury turned out to be off too, and Le Verrier ran the same play. Another unseen planet, this one hiding close to the sun. He named it Vulcan. Vulcan doesn't exist. That time, the anomaly really was Newton's fault, and it took Einstein, 60 years later, to explain it. Le Verrier died believing in a planet that was never there. It's the same man, doing the same move, and he was brilliant once, but wrong once,

33:35Jordan Feigenbaum:and nothing in the logic told him which was which. So here's the test that I'll hold myself to. I don't want to ask whether a theory is getting patched because they all get patched. A theory that's working right makes new predictions that then come true. A theory that's dying only explains away the things that already went wrong. So let's apply that here. Fat, if it's a poison, has spent 40 years adding a save after every null result. First, the fat was the wrong kind. Then the measurement was wrong. Then the follow-up wasn't long enough. Storage capacity keeps saying things in advance that then show up.

34:05It says that individual people should have their own personal fat thresholds, and researchers found normal weight people putting their diabetes into remission after losing about 6 % of their body weight.

34:15Jordan Feigenbaum:It also predicts that genes that build bigger garages or bigger fat storage sites should reduce disease, and they do. And it says you should be able to pull fat out of a liver without ever moving the scale, which is exactly what exercise does. Okay, so if you buy that so far, is there any additional evidence that supports this? Nature runs an enormous randomized trial at the moment of conception. When you were conceived, gene variants get dealt out at random, kind of like a deck of cards. Nobody chooses them, and they were dealt before your income, your diet, your job, or anything else in your life could really influence them.

34:47Jordan Feigenbaum:So if you compare people who got dealt one variant against people who got dealt another, you're comparing groups that differ in that one thing and are otherwise shuffled. That's a randomized trial nobody really has to run, and researchers call it a Mendelian randomization study. So somebody ran it on liver fat. They took scans from about 30 ,000 people, found the gene variants that predict how much fat sits in the liver, and asked whether people carrying those variants get more diabetes. They do. Genetically higher liver fat causes type 2 diabetes. That's a causal claim, and it holds up. And the size of it is about a quarter more risk of diabetes.

35:23Jordan Feigenbaum:That's smaller than the number you get by just looking at people who have fatty livers. And the reason why is worth 30 seconds, because it applies to almost every health statistic you'll ever hear. Fatty liver does not show up on its own. It shows up alongside low socioeconomic status, alcohol use, not exercising much, and about a dozen other things that all cause diabetes by themselves. So when you look at people, you're measuring the whole package at once. Everything, everywhere, all at once, if you will. When you look at the genes, you're measuring the liver. And I'll tell you what would change my mind, because that's the price of talking like this.

35:55Jordan Feigenbaum:Show me somebody with genuinely low fat in all of the wrong places who has full-blown insulin resistance anyway. Or show me a drug that clears the liver completely and leaves the disease of having too much body fat sitting there untouched. We may find out about the second one soon. There's a drug in development called ritatratide that drops liver fat by more than 80%. And so far, there isn't a single liver biopsy behind it. So if the liver is where the disease of excess fat shows up first, the practical question is how anybody would find out in time. And that's where the current system fails people, including people it is already marked as safe.

36:32Jordan Feigenbaum:Let me give you a patient. He's 41. His BMI is 24, which is normal, and he lifts three days per week. He comes in with a long-term blood sugar marker called hemoglobin A1c of 7.1, which is consistent with type 2 diabetes. His triglycerides, a fat that circulates in your blood, are high. His ALT is 48. ALT is a liver-associated enzyme. When liver cells are damaged, they leak this enzyme into your blood, so a high number is supposed to mean that something's wrong with the liver. His is mildly elevated, and somebody already told him that's basically normal. and a previous clinician told him that he can't possibly have fatty liver because he is an overweight.

37:06Jordan Feigenbaum:Now that conversation probably happens more often than it should and it's very very wrong and I want to show you exactly how wrong with the numbers that actually exist. Researchers took 100 people with type 2 diabetes whose liver enzymes were stone cold normal. Instead of trusting the enzymes they did a scan on everyone's liver. Three quarters of them had fatty liver. In the patients who weren't obese, the ones whose weight would have cleared them twice over, it was still at about two-thirds who had too much fat in the liver. Then they biopsied the ones whose scans looked the worst, and more than half of that group didn't just have fat sitting in the liver, they had inflammation and active damage.

37:41Jordan Feigenbaum:So normal ALT doesn't clear you, and neither does a normal body weight. Our 41-year-old patient was cleared twice by two things they can't clear anybody. So how dangerous is it really? Swedish researchers took 646 people with the fatty liver confirmed on biopsy, then they matched each one to 10 people from the general population, same age, same sex, same town, and they followed all of them for an average of 20 years. 12 % of the people with a fatty liver went on to develop severe liver disease, cirrhosis, liver failure, or liver cancer. In the matched controls, it was 2%, so more than five times as many over two decades.

38:17Jordan Feigenbaum:But that average is hiding the thing you really need to know, because when they sorted those people by how much scarring was already on that first biopsy, the risk didn't climb stepwise. It exploded. In the people with no scarring at all, the risk was about twice as high as in the healthy general population. In the people who already had cirrhosis, it ran about 100 times. And here's the finding that I think should actually change management, what you get ordered, for example, when you see the doctor. They put inflammation into the model, which is the thing that the word steatohepatitis is actually describing.

38:48Jordan Feigenbaum:And it didn't help at any stage. Once you knew how much scar somebody had, knowing whether they had inflammation on top of it added nothing. So the risk of fatty liver, or the risk from fatty liver, more accurately, covers a range. And that range of risk runs from twice normal to 100 times normal. And the only thing that tells you where somebody sits on that range is scarring, which is why the whole game is finding the scarring. The fat is just how you know to go looking. Which brings me to what's changed, and a lot of people are not aware of this yet. In 2025, the Lancet Commission on Clinical Obesity published a new definition with 58 commissioners and dozens of organizations signing on.

39:27Jordan Feigenbaum:What they wrote is that BMI should be used at a population level for research and for screening whole groups, not as a measure of any individual's health. If you want to say a specific person is carrying too much fat, you have to confirm it, either by measuring the fat directly or by adding a waist measurement. Now, to me, this was mostly a reminder because a lot of people were butchering how the BMI was either being used or communicated. It's never been a measurement for health. It's always been a screening tool for obesity since it's come into modern medicine. But people were using it wrong and also not understanding that it missed half of people who were carrying too much fat.

40:01Jordan Feigenbaum:And in fact, this definition goes on to say that, look, if a person has a BMI of 40, you can just assume and skip the confirming. So in this case, the view from the curb really does work at the far end. You know what's going on inside of the garage and inside the house without having to go inside of it. but the problem is everybody in the middle and most people are in the middle. And they also split the diagnosis in two. Clinical obesity means that you can show the organs aren't working right because of the fat tissue. Preclinical obesity means that the fat is there, but the organs are still fine.

40:32Jordan Feigenbaum:That's the storage capacity model wearing a lab coat. I think it's worth stepping back for a second because when I was putting together this episode, there's a pattern that emerged. Year after year, and really over the course of centuries, people have consistently tried to measure body fat before it becomes harmful and they keep getting it wrong. Go back to 1832. Now, in fairness, this Belgian astronomer named Adolf Ketelet wasn't trying to measure body fat, but he did create the formula that later became BMI, which is weight divided by height squared. Again, he wasn't diagnosing anybody. He was really just doing social statistics trying to describe the average man across the whole population.

41:08Jordan Feigenbaum:About 100 years later, a life insurance company built wait-for-height tables out of its own policyholder death records so it could price policies more accurately. And then in 1972, Ancel Keys compared all of the formulas that existed, he picked Ketelase, and renamed it BMI for Body Mass Index. In 1998, an NIH panel added waist circumference on top of it. In 2013, a group modeled the human body as an ellipse and produced something called the Body Roundness Index built out of your waist and your height. And running alongside all of that, for decades, we've had ways to measure body fat directly. Underwater weighing, DEXA scans.

41:46Keyes himself was using body density back in 1972. Now, here's what I want you to notice. Every one of those is a better answer to the same question, incrementally.

41:55Jordan Feigenbaum:How much fat does this person have and where is it? and they did get better. Each one was a little bit better than the one before it, but all of them are missing some important details. For example, none of them tell you how much room this particular individual had to begin with to store fat. And that's kind of the whole thing. If I tell you right now that somebody's carrying 30 kilos of fat, you still don't know whether that's a problem because you don't know how big their garage was. Two people can carry the exact same amount and one of them has room to spare while the other one is stacking boxes in the stairs.

42:27Jordan Feigenbaum:No scale, no tape measure, no ellipse, and no DEXA scan can tell those two people apart. So the tests do keep getting better, but we're still missing some key information. And it isn't that nobody noticed. In 1981, a researcher named Neil Ruderman published a paper describing what he called the metabolically obese normal weight individual. Somebody who looks lean, has a normal BMI, but has the full metabolic picture of obesity anyway. That was 1981, before I was born. 20 years later, in 2001, Ethan Sims published a paper that asked the opposite question right in the title. Are there persons who are obese but metabolically healthy?

43:04So both halves of this have been sitting in the literature for over 40 years, which I find pretty irritating because you still have a bunch of questions in the space. Meanwhile, the definitions keep getting moved underneath all of this. In 1998, an NIH panel lowered the American cutoff for overweight from a BMI of about 28 down to 25. Nobody gained a pound, but they still changed the BMI cutoff. So somewhere between 25 and 30 million Americans went to bed one night in one weight category and woke up in another the next day. And in 2013, the American Medical Association voted to call obesity a disease.

43:37But here's an interesting part. The AMA's own science council recommended against that vote. And one of their stated reasons was that BMI was too imprecise to diagnose an individual. The House of Delegates overrode their own scientists and voted yes anyway. But here's the part that bothers me the most. It's the definition problem underneath all of this. A review went looking for how researchers actually defined metabolically healthy obesity. Across 27 studies, they found 30 different definitions. And depending on which one you used, the share of people with obesity who counted as healthy went anywhere from 6 % to 75%.

44:14One group tested this directly. They took the same 638 people and applied five different published definitions to that same group. Depending on the definition, between 9 % and 41 % of them were metabolically healthy. It's the same people, the same blood tests on the same day, just a different definition. So when somebody tells you what percentage of heavy people are healthy, the first thing I'd want to know is, well, what definition did you use? Most of the time, they won't know. So why does any of this matter? We keep missing people on both sides. Remember that insulin resistance runs 10 to 15 years ahead of a diabetes diagnosis.

44:53And when researchers modeled what that delay costs, a three-year delay in starting treatment gives up about 29 % relative reduction in heart disease risk that you otherwise would have gotten if the diagnosis would have been rendered earlier. Six years gave up 38%.

45:09Jordan Feigenbaum:To me, that's not just a delay in paperwork. that is heart attacks or severe adverse cardiac events. The size of this problem is hard to believe until you go through the research. When researchers went looking for fatty liver disease in a national sample, 77 million American adults had it and about 73 million of them did not know. Awareness was around 5%, despite 90 % of those people having seen a doctor in the past year. They were in the room with the doctor, but nobody looked. and that number should be embarrassing to all of us, me included. Now, I don't want to argue with the first half of this episode and then skip this part.

45:49Weight discrimination is associated with roughly a 60 % increase in mortality risk. That showed up in two large studies,

45:57Jordan Feigenbaum:and it survived adjustment for the physical and psychological risk factors you'd expect to explain it away. And people avoid care because of it. In a study of nearly 500 women, cervical cancer screening dropped from 86 % in most of the group to 68 % in the heaviest women. Over 90 % of them had insurance. So we're not talking about access. So both of these errors have a body count. If you miss the lean patient, you can find the disease too late, over a decade later, after the damage starts. But if you label a heavy patient and never check whether their organs are actually affected, some of them stop showing up at all.

46:32Jordan Feigenbaum:So what should actually get ordered if you're concerned about this? First, a waist measurement and also a waist-to-height ratio, which is written down right next to the waist. Waste-to-height is exactly what it sounds like. It's your waist divided by your height, and you want it under a half but above 0.4. It's 15 seconds, but almost nobody does it. Second, let's take a fasted lipid panel and a fasting glucose. Those two together give you the cheapest look at insulin resistance there is, and it's called the TYG index. TYG stands for triglyceride glucose index, and that's all it is. It's your fasting triglycerides and your fasting blood sugar put together into one number with a special formula.

47:07Jordan Feigenbaum:It doesn't cost you anything extra because if somebody drew a lipid panel and a glucose, you already have both halves of the test. How good is it? Well, here's how to think about a test like this, and you can use it for the rest of your life. There's a measure called area under the curve, and it runs from half to one. A half means the test is a coin flip. One means it's perfect. against the reference standard for insulin resistance, TYG lands somewhere between about six-tenths and eight and a half-tenths, depending on which study you read. Now, that's a wide range, and I'm giving you the range on purpose because four studies is all there is, and they don't necessarily agree with each other.

47:40Jordan Feigenbaum:What TYG is good for is telling you when to look harder at somebody whose blood sugar came back fine. It doesn't really diagnose anybody, but it is better, in my opinion, than triglycerides to HDL ratio. At its usual cutoff, it's about two-thirds right in each direction, which is already unimpressive. but it really is bad in black patients who tend to have a higher rate of insulin resistance as well. The reason why is because insulin resistant black patients often don't develop the high triglycerides that the whole ratio is built on. But when you compare it to glucose, triglycerides to glucose, that is, it actually works okay.

48:12Jordan Feigenbaum:So triglycerides to HDL is an instrument that fails in about a third of the country and TYG costs about the same and doesn't do that. Third, if you have a lean patient with type 2 diabetes, at least that's what you think it is, you have to rule out that the diabetes isn't type 2. So for example, type 2 diabetes is the one that most people mean when they say diabetes. Your pancreas still makes insulin and your tissues just aren't responding to it very well. That's the disease we've been talking about the whole episode. But two other things look like it on a first blood test. One is type 1 diabetes.

48:42Jordan Feigenbaum:Now type 1 most of the time is an autoimmune disease, which means that your own immune system is attacking your body. In this case, it destroys the cells in your pancreas that make insulin, so eventually you don't make any. Most people think of this as a childhood diagnosis, but adults can get it too, and in adults, it comes on slowly enough that it sometimes gets labeled as type 2 and treated as type 2 for years, which is obviously a problem. The other one is called MODY, M-O-D-Y. You don't need the name, but this is a type of diabetes that's caused by a single broken gene passed straight down through a family.

49:14Jordan Feigenbaum:The pattern here is you have diabetes in a parent, a grandparent, and usually a sibling, almost all of them diagnosed young, and none of them usually have excess body fat. Both of those are treated differently from type 2 diabetes, and getting it wrong can be a big problem. In one study that screened lean people already carrying a type 2 diabetes diagnosis, one in six turned out to have something else. So if nobody checks, somebody can spend a long time on the wrong treatment for the wrong disease. Fourth, there's a score called the FIB4, F-I-B-4. Now this one's for the liver, and it's a formula that takes into account your age, two liver enzymes, and your platelet count.

49:51Jordan Feigenbaum:And it turns them into a single number that estimates how likely it is that you have significant scarring of your liver. Every input is on blood work you've probably already had, so it doesn't cost anything to calculate. It is recommended first step now, but it works in a pretty narrow band. If you're under 35 years old, it's barely better than a coin flip. If you're over 65, it flags almost everybody, and so there's a bunch of false alarms. Our 41-year-old patient, it sits right in the range where the number actually means something, which is worth kind of discussing a little bit further because there are lab companies selling panels straight to consumers, and they're putting Fib4 on the report for 30-year-olds.

50:26Jordan Feigenbaum:Now, you could imagine what happens when you get a scary number back and how that goes at the doctor's office. Fifth, if the Fib4 does come back high, the next step is usually an elastography, which is an ultrasound that measures liver stiffness. It sends a pulse into the liver and times how fast that pulse travels through it because a stiff liver carries the wave faster than a soft one, and stiff generally means scarred. Now, that measurement is one of the things that decides who gets treated, and it's the ones whose scan puts them in the moderate scarring range. They say to use the scan rather than a liver biopsy, which they call impractical and unnecessary for most patients.

51:02Jordan Feigenbaum:So let me put this whole thing back together. You eat, fuel shows up in your blood, insulin knocks on the door, and says put it away. And where it's supposed to go is the garage. Your garage holds what it holds. How much room you got was mostly settled before you had any say in it, and as long as the boxes fit, you can carry a lot of them and be completely fine. The trouble starts when they stop fitting. Not when you hit a certain number, not when a chart tells you to worry, when you, the individual, personally run out of room. Because a garage that's out of room doesn't just turn away the next delivery, it starts leaking.

51:34Jordan Feigenbaum:Fat cells with no space left stop hearing the signal to hold on, so they let fatty acids out into your blood all day long. Your blood goes everywhere. The liver takes some, the muscle takes some, so do the pancreas, the kidneys, and the space around your heart. Every one of those rooms starts storing what the garage couldn't keep. That's the disease. The overflow is the disease we call obesity. It's the point where somebody's storage runs out and starts spilling into organs that were never built to hold it. We'll get more precise about the definition next time, but that's the gist of it, and it's why the same weight can be a serious disease in one person and nothing at all in another.

52:09They didn't get the same garage. It's also why you can suction 10 kilos out of somebody and change nothing, because you emptied part of the garage and left every other room exactly as full as it was.

52:19Jordan Feigenbaum:And why somebody born with no garage at all gets the entire disease anyway, at a body fat percentage you would envy. And before somebody asks, because it's the obvious question, if the problem is a garage past its capacity, then anything that takes boxes out and keeps them out is the fix. That's energy balance over a long enough stretch to matter. Exercise does something extra on top of that, which is that it pulls fat out of the liver whether or not the scale moves. That's the one thing on this list that works on the rooms directly, and it's what most of the next episode is about. So here's where we're going in the next episode.

52:51Jordan Feigenbaum:If the garage is full, or if it was never built, the biggest room left in your house is your muscle, and it's the single largest place that your body can put fuel. It's not even close. And the door to that room doesn't stay open, though. Next time, what opens it, how long it stays open, and how fast it shuts? Six men in Denmark took most of what you think you know about this apart in 1989, and they did it by exercising one leg and leaving the other one alone. If you're teaching people about obesity, you can draw the diagram. Just don't point the arrow at the visceral fat. For everyone here at Barbell Medicine, I'm Dr.

53:22Jordan Feigenbaum:Jordan Feigenbaum. Thanks for listening.

53:39Thank you.