Is Obesity A Muscle Problem?

21:14Jordan Feigenbaum:Muscle mass, therefore, is riding along with the things that do the work. So, sure, it correlates. So the way to settle that is to separate them, and two studies do. Let's start with the biggest one that anyone has ever run. The Sarcopenia Definitions and Outcomes Consortium grouped together 18 ,800 community-dwelling older adults, and they looked at four outcomes. Falls, fractures, mobility limitation, and death. Then they asked which body composition variables actually predicted them. Grip strength predicted all four. Gait speed predicted all four. And lean mass on a DEXA scan, which is the way that we measure changes in muscle mass, showed essentially no relationship to any of the four.

21:56Jordan Feigenbaum:Knowing how much lean mass somebody had told you nothing about whether they'd fall, break something, lose mobility, or die. So their position statement is one sentence. Lean mass measured by DEXA should not be included in the definition of sarcopenia. Now, I'll give you the caveat here before somebody in the comments tells me. That's the one statement the panel said that they were least united on. It's still the group convened to write the definition, voting on the measurement of it and what gets rolled out in clinical practice. Sarcopenia means muscle loss, and the group convened to define muscle loss just took the muscle measurement out of it.

22:32Jordan Feigenbaum:So much for calling sarcopenia age-related muscle loss, eh? And think about that for a second, because the number that the entire build more muscle prescription runs on is the one number in that analysis that didn't predict a single thing. Not falls, not fractures, not mobility, not death. The two that did predict were both measures of what that muscle can do, not how much of it is sitting there. And another interesting thing, people with obesity carry more muscle mass than lean people do on average. And they're stronger, too. That holds across the literature, adolescents through the elderly. More absolute force in the muscles that carry these folks around.

23:10Jordan Feigenbaum:Knee extension, calf extension. When you load a limb, it adapts. Now, there's a better way to measure muscle than a DEXA scan, and somebody used it as well. You swallow a dose of labeled creatine and measure what turns up in your urine a few days later. Creatine sits inside working muscle. We know that. So the size of that creatine pool tells you how much contractile tissue is actually there. Fat sitting inside a muscle holds no creatine, so this method doesn't count it where a DEXA scan usually does. We'll come back to that. 1 ,300 men in their 80s got measured that way. The ones carrying the most body fat also had the most muscle mass, which is why they're stronger in an absolute sense.

23:53Jordan Feigenbaum:But the data here is tricky because relative to their body weight, they're weaker. Now, when you put these two findings next to each other, you've got a muscle that works worse per kilo, so it takes more muscle to produce the same force. And the reason it works worse is because there's fat in the muscle. This is called myosteotosis, and the fat in the muscle actually makes force production worse per unit muscle. That said, these folks do have a lot of muscle, so they're not short on it. Now, this whole process has an end state, and it's called sarcopenic obesity. We're going to come back to that a little bit later because at that end state, these people get diagnosed with the disease of muscle loss while also carrying plenty of muscle.

24:36Jordan Feigenbaum:The point here is that the amount of muscle mass, which is elevated in this case, isn't protecting them. Now, to be clear, muscle function, improving muscle function does help. Somebody with obesity who's strong and fit is at a lower risk with respect to bad health outcomes compared to somebody with obesity who isn't fit. But it doesn't erase the risk. You take that same strong fit person with obesity and compare them to a lean person with equivalent fitness, and the risk is still higher in the person with obesity. The fat is doing something that the muscle can't cancel out, and it's the bigger or more harmful of the two signals.

25:14Jordan Feigenbaum:Now, what would happen if you designed a study that separated muscle mass from everything else? In this study, 10 men with type 2 diabetes trained one leg for six weeks three times a week and left the other leg alone. Then they did the CLAMP study, you know, catheters, both femoral veins, the same setup as the Danish study from the top. The trained leg cleared more glucose than the untrained leg, and the two legs had exactly the same amount of muscle in them. Whatever size change happened over those six weeks was too small to measure, and the authors say that the improvement was larger than size could account for anyway.

25:47Jordan Feigenbaum:What the trained leg had instead was more glucose transporters, more insulin receptors, and more of the signaling proteins in between. That's more doors and a better wiring inside the same amount of tissue. The authors said themselves that this was likely an effect not caused solely by an increase in muscle mass, which again, they couldn't pick up anyway. One-legged designs have a known problem though. If you train one leg, the untrained one improves too, mostly because the nervous system gets better at telling the muscle what to do. On average, strength improves by about 16 % when it's in the legs, which pushes the two legs towards looking more alike and works against finding any difference between them.

26:25Jordan Feigenbaum:Both studies here found a difference anyway. But it rules out the objection that this is something circulating in the blood. A hormone that's in the bloodstream can't really produce a difference between two legs attached to the same bloodstream. Now, there's a different experiment that also gives the same answer. What happens when you immobilize one leg for, say, 12 days and leave the other one active. The immobilized leg loses mitochondrial capacity and accumulates fat inside of its muscle cells while the active leg doesn't. All of this is to say that whatever's happening to a muscle gets decided in that muscle.

26:59Jordan Feigenbaum:Okay, but what happens if you train the whole body? A meta-analysis of eight resistance training studies in 360 older adults with type 2 diabetes, you get a similar result. Blood sugar control improved, but lean body mass didn't increase. at an effect size of 0.08 with the range running from slightly negative to slightly positive. Now that is a narrow null and narrow is what makes it useful because when it's wide, it really means that a study can't tell you what's going on. But a narrow one means that the effect isn't large in either direction. So the claim I'm making isn't that muscle mass doesn't matter.

27:36Jordan Feigenbaum:It's that gaining muscle mass isn't necessary because you get the glycemic effect without it and it isn't sufficient either. because you can hold muscle mass constant and still change the outcome, which in this case is how well it handles sugar. What's doing the work here is how fast the tissue handles what arrives. We call that the flux. None of which is an argument against having muscle. You need muscle tissue to produce force, and building some is a reasonable thing to want. But a measurement of how much muscle is there, like a DEXA scan, can't tell you how well it's working. And that's the part that predicts anything.

28:13Jordan Feigenbaum:Ask why the fat got into the muscle in the first place. It's there because the garage overflowed, so the muscle working worse is the storage problem showing up in one more room. The stairs, in our analogy. And the key to success here is getting the boxes moving again. Fat gets inside muscle cells. You can see it on a scan, and you can measure it in a biopsy. And for 20 years, the assumption has been that fat inside of a muscle is what makes that muscle insulin resistant. Endurance athletes break that assumption though. Cyclists and distance runners carry about as much fat inside their muscle cells as people with type 2 diabetes.

28:49Jordan Feigenbaum:And endurance athletes are among the most insulin sensitive people that anyone has ever measured. The study that showed it clamped and biopsied four different groups. Lean and sedentary, people with obesity, people with obesity and type 2 diabetes, and lean endurance athletes. Across the three sedentary groups, the more fat somebody had inside their muscle cells, the worse their insulin sensitivity was. And that correlation is the one that gets quoted. But when you put the athletes into the same study, the correlation goes away because the athletes sit at the high end for muscle fat and at the high end for insulin sensitivity at the same time.

29:25Jordan Feigenbaum:So the athletes have the fat and they don't have the problem. What do the athletes have that the sedentary groups don't? Speed. Another research group tagged a fatty acid with the tracer and followed that fatty acid into a muscle and back out again. That let them measure how fast the fat inside a muscle cell was being built up and broken down. The athletes were turning their muscle fat over about two and a half times faster than the sedentary men. The same amount of fat was sitting in both sets of muscles, but in the athletes, that fat was being burned and rebuilt continuously. In the sedentary men, it was basically sitting still.

30:00Jordan Feigenbaum:That's the difference between stairs you're storing boxes on and stairs you're carrying boxes up and down all day. That's flux. Now, you can push somebody's muscle fat up on purpose and watch their insulin sensitivity go up with it. 25 older adults with obesity trained for 16 weeks. The fat inside their muscles rose 21%, and their insulin sensitivity also rose 21%. A second research group ran the comparison the other way. 16 older adults with prediabetes were split in half. Eight of them dieted and didn't train. Eight of them trained and weren't told to diet. The dieter's muscle fat went down.

30:36Jordan Feigenbaum:The exerciser's muscle fat went up. And insulin sensitivity improved about 20 % in both halves. One group lost the fat inside their muscle cells. The other group gained some. And the two groups came out with about the same level of improvement. In both of those studies, the fat that went up with training was triglyceride, which is the inert storage form. The molecule triglyceride gets built from, diacylglycerol, or DAG as you might see it abbreviated, went down with training in both. So it seems like triglyceride is the sort of inert form which doesn't really signal anything, and then diacylglycerol is the more active, potentially more harmful form.

31:15Jordan Feigenbaum:We're going to come back to that when we talk about the liver, but what we can conclude here is that how much fat inside your muscle doesn't necessarily tell you how well your muscle handles insulin. how fast that fat is moving does. Fat that sits inside a muscle without being used is what makes that muscle weaker and more insulin resistant. Now, if the amount of fat inside the muscle didn't seem to matter that much, it was more related to how fast it was moving, what about the amount of fat in your liver? Having fat in your liver at all does tend to make people more insulin resistant. How much of it they have, past the point of having some, doesn't.

31:53Jordan Feigenbaum:In a study of 133 people who were scanned and subsequently clamped, again, that's the femoral vein and the insulin sort of infusion with the glucose, the people with liver fat were more insulin resistant than the people without liver fat. But among the people who had liver fat, whether somebody had 6 % or 25 % liver fat made no difference. Not to their liver, not to their muscle, and not to their fat tissue. The authors wrote that liver fat is neither sufficient nor necessary for the liver to become insulin resistant. So if the amount of liver fat isn't what does the damage, what does? It's what type of fat that is and what it's doing.

32:33Jordan Feigenbaum:Somebody lowered liver fat in a rat and made the rat more insulin resistant by doing so. The enzyme they blocked is called DGAT2, and the only thing that this enzyme does is the last step of building a fat molecule. A fat molecule is a backbone with fatty acids hung off of it. Hang two fatty acids on it and you've got a diacylglycerol. Di meaning two. You hang the third one on and you've got a triglyceride. Tri meaning three. Triglyceride is the word that's already on your lab report. And triglycerides, that's the inert stuff that sits in a droplet and shows up on a scan of the liver, for example.

33:10Jordan Feigenbaum:DGAT2 hangs on that third fatty acid. That's its entire job. A triglyceride doesn't really signal anything. It's pretty much inert. Diacylglycerol is a signaling molecule and it switches enzymes on. So hanging that third fatty acid does more than finish storing the fat. It takes an active signal and caps it into something inert. When you block DGAT2 in a rat liver, total liver fat is going to go down because you stopped making the finished product. But the rats become insulin resistant anyway because of the half-built diacylglycerol piled up behind the block that's now moved out to the wall of the liver cell and it's blocking the insulin receptor, which means the insulin receptor doesn't work and you get insulin resistance.

33:53Jordan Feigenbaum:Less fat in the liver, but worse insulin sensitivity. So when I told you last episode that we had to clear fat out of the liver, that is true, but we also have to talk about the type of fat. To go back to our garage analogy with the boxes kind of overflowing into the house, Well, look, if there are stacked boxes that are taped up and sealed, that can be fine in certain places. But if the boxes are open and spilling out all over the floor, that's a bigger problem. So it's not necessarily just about where the boxes are, where the fat is. It's also about what type of boxes or what type of fat is there and what those boxes are doing, whether they're moving or not.

34:35Jordan Feigenbaum:Again, that's the flux. and the way you get boxes moving is to use the muscle and to get the fat out. So that's three separate things now. And I want to name all three because we're going to come back to them at the end. The first is where the fat is, whether it's in the garage where it belongs or whether it's out on the stairs where it doesn't. That's location. The second is what form it's in, what type it is, whether it's the inert stuff that sits sealed in a droplet or if it's the reactive kind that ends up out at the wall of the cell switching things off. That's type. And the third is whether any of it is moving, which is the flux.

35:10Location, type, and flux. Those are the three things that decide whether a given person is actually in trouble, and not one of them is a number you can read off a bathroom scale, or a BMI measurement, or waist circumference. So the question becomes what changes them, and that's where exercise comes in. Liver fat behaves the same way. A recent meta-analysis found that exercise with no meaningful weight change lowered liver fat by a bit over two percentage points, and exercise with weight loss lowered it by almost five.

35:39Jordan Feigenbaum:So exercise works on liver fat without the scale moving, and it works better when the scale moves too. Now, if we're talking about fatty liver, let's really get the diagnosis down. It's actually now called metabolic dysfunction-associated steatotic liver disease, and it's defined as more than 5 % of your liver being fat, plus at least one metabolic risk factor. So when exercise reduces somebody's liver fat back under 5%, exercise has effectively reversed that diagnosis. Now, across 14 randomized controlled trials, the odds of getting a 30 % reduction in liver fat were about three and a half times higher with exercise than without.

36:1430 % is a threshold borrowed from drug trials, where a 30 % drop stands in for the liver looking better under a microscope when somebody took a biopsy. Now,

36:23Jordan Feigenbaum:that's not necessarily a clinical outcome, and as far as I can find, nobody has checked whether hitting this 30 % threshold predicts what happens to a person over the following years. Now what kills people with liver disease is the inflammation, the cell injury, and the scarring, and measuring those three things require a biopsy. In the trials that did do biopsies, the inflammation improved with exercise. As far as the scarring goes, that was more inconsistent and it seemed to move the most in people who lost weight. Now one trial biopsied the liver before and after and asked what separated the people whose liver disease resolved from people whose didn't.

36:57Jordan Feigenbaum:It wasn't their liver fat and it wasn't how well their liver responded to insulin. It was their muscle. 24 people with biopsy proven liver disease were randomized for 10 months to high intensity intervals, three days a week, plus a calorie deficit or to their usual care. Both groups lowered their liver fat. Both groups improved how well the liver itself responded to insulin. Neither of those changes tracked with the disease resolving on the second biopsy. What did track was peripheral insulin sensitivity, meaning how well the muscle pulled glucose out of the blood, and peripheral insulin sensitivity doubled in the training group.

37:31Jordan Feigenbaum:The authors think training redirected fuel into skeletal muscle so that less of it was left sitting in the liver, which means that the liver is going to produce less fat from that excess energy. So exercise moves the fat, and it changes the rate at which everything is moving. And the calorie deficit is what decides which direction the traffic runs. Those two things together are the treatment. Now, let's talk about what people are being told to do instead of that. This podcast is brought to you by Factor. We just launched Signal, and the weeks leading up to a book launch are not exactly relaxed.

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39:00Jordan Feigenbaum:Have you ever noticed that you end up wearing the same few items on repeat or is it just me? Now, I work from home most days, but I still get ready to head to the office every day, which fortunately is just down the hall. Anyway, last month I finally noticed I was wearing the same items over and over again because, well, they just work well. They make getting dressed easy. That's what Quinz does best. Their organic cotton mesh stitch sweater polo is one. I have it in almost every color. And the vintage wash camp shirts are another. That's been in heavy rotation all summer because I think it looks better than a t-shirt and it's just as comfortable.

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40:08Jordan Feigenbaum:This podcast is brought to you by FIGS. Here's a piece of medical history that we didn't learn in school. Before the 1920s, pretty much everything in the operating room was white. The attire, the walls, everything. And the logic was cleanliness. The problem is that surgeons spend hours focusing on red tissue under the bright OR lights, and then their red photoreceptors fatigued, and every time they would glance away from the white fabric, they would see a blue-green ghost of whatever they were just looking at. So surgeons were getting headaches and seeing phantom anatomy mid-operation. But the fix turned out to be pretty simple.

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41:23Jordan Feigenbaum:That's wearfigs.com, code FIGSRX for 15 % off. 220 minus your age. It's on your watch, it's on the treadmill, and almost nobody can tell you where it came from. Well, I will. It came from a review paper published in the 1970s by Fox and colleagues looking at physical activity and heart disease. Here's what 220 minus age actually is. Picture a graph with age along the bottom, max heart rate on the side, and a cloud of dots from a bunch of different studies. 220 minus age is just a straight line that the researchers laid over that cloud. It wasn't calculated, and it wasn't tested against anything.

41:56Jordan Feigenbaum:Someone just looked at the scatter plot and drew a line through the middle of it and said, yeah, that looks pretty good. That's the whole origin story. And the data in that original paper didn't even support it. The author said, and I'm quoting, no single line will adequately represent the data of the apparent decline of maximal heart rate with age. They said 220 minus age just defines a line not far off from many of the data points. That's the pedigree, and 50 years later, it's the default on every smartwatch sold. And it's not even the best formula that anyone's come up with. The better fit is 208 minus 0.7 times your age.

42:28Jordan Feigenbaum:It still carries about a 6-beat error, so what do you do? Like, if I'm going to program your conditioning, the easy runs, the cross-training, and the threshold work to make it faster for 16 weeks, I want to make sure the prescription fits you, not just a line that somebody drew through a cloud of dots. That's why I built a field test into the hybrid 5K and 10K templates, at the start and again at week 8, because fitness changes. Any heart rate estimate can be off by enough to throw off your intensity and your subsequent training load, which matters a lot when you're combining lifting and running in a way that makes you stronger and faster at the same time instead of just burning you out.

43:02Jordan Feigenbaum:So you get a 20-minute field test to make sure that you're anchored to the right intensity. The template includes three 16-week programs, 5K beginner for those who haven't done much running before, and the 5K and 10K performance versions for those who want to go fast. All of the programs include three days per week of lifting with every conditioning workout fully written out. And it's available now on our website, barbellmedicine.com, where you'll get both the desktop files and the app version of the program. The app is free, as it always is. Just search Barbell Medicine in the App Store. And like all of our other programs, it's included free for the Barbell Medicine Premium subscribers.

43:34Jordan Feigenbaum:So if you want to get better at running without giving up your strength, check out our latest template, the Hybrid 5K and 10K program. Okay, back to the show. Dr. Lyon's argument comes with a prescription attached, and the prescription is where this gets practical. If building muscle were the treatment for obesity, then somebody who's carrying too much fat should just build muscle first and worry about fat later. Some other people in the fitness space also say something like this. The argument for that rests on an intuition that many people have. Building tissue takes energy, and you're short on energy in a calorie deficit, so you should build muscle first and cut second.

44:09Let's start with the math because muscle is a little cheaper than most people think. A kilogram of muscle is about three quarters water, and water has no calories in it. The chemical energy actually stored in a kilogram of muscle is about 1 ,350 calories, and a kilogram of body fat is about 7 ,700 calories. But the stored energy isn't the whole energy bill. You have to pay to assemble the protein. You got to pay again because the assembly isn't efficient. And then you pay a little bit more to maintain the new tissue while you're still building the rest of it. Somebody added all of that up this year, and this study is a preprint, so it's not been peer-reviewed yet, but their number is about 3 ,500 calories of food to build one kilogram of muscle with a range of 3 ,200 to 3 ,700.

44:54Now, you heard the 3 ,500 and you're thinking, oh yeah, it's 3 ,500 calories to lose a pound or to gain a pound. We're talking about a kilogram. That's 2.204 pounds. So this is different math. Just wanted to make sure you're clued in on that. And then they put a rate on it. They used 12 weeks because a kilogram of muscle mass over 12 weeks is about what the resistance training literature produces on average. 3 ,500 calories spread across 12 weeks is about 40 calories a day. If you try to go faster than that, like a beginner adding a kilogram a month, which is a rate that most people don't sustain for very long, well, that's 115 calories a day that you need to build the muscle.

45:36The standard advice for a bulking phase is three to 500 calories a day over maintenance level calories. So the surplus that people are being told to eat is somewhere between three and 12 times what the tissue itself costs, depending on how fast they're actually gaining muscle mass. Over 12 weeks, 400 calories a day is about 34 ,000 extra calories against a tissue bill of 3 ,500. The rest has to go somewhere, and somebody has tested where it goes. A bigger surplus didn't just build more muscle, it also built more fat. In this study, 21 trained lifters, 17 of them who actually finished the study because this ran through COVID, well, they were randomized to either eat at maintenance, a 5 % surplus, or a 15 % surplus for eight weeks.

46:23The same training was done by all three groups, and they measured the muscle with ultrasound, which actually looks at the tissue rather than a whole body scan. Muscle thickness came back about the same in all three. What the bigger surplus produced was more skin fold thickness and a bigger bench press. I'll give them the bench. It just didn't show up in the squat and it didn't show up in the muscle. Now, the other direction, and this is where I've kind of changed my thinking. If you group the trials of resistance training together in a deficit against resistance training without a deficit, the lean mass gains do get impaired.

46:57That's the finding that everybody quotes, but you have to run the numbers out. The expected gain hits zero, so no muscle gain, at a deficit of about 500 calories a day. Now, that 500 number is certainly on a lot of PowerPoint presentations right now, and it came from a meta-analysis of seven studies where the subjects averaged 60 years of age, and almost everybody in it was untrained before they started. So it could be a ceiling for that population, but not necessarily a safe threshold, and the authors don't present it as one. Strength gains weren't impaired at all, by the way, in that same analysis.

47:31The deficit groups and the control groups came out statistically indistinguishable on strength. They both got large improvements. The deficit cost them muscle mass, but it didn't do anything to their ability to get stronger. Now, whether this applies to experienced lifters is less well-established, as only one study in that analysis used trained lifters. The authors say straight up that they don't know whether this holds in train lifters because nobody has studied them enough. But back to the muscle mass side, because the 500 calories number refers to muscle mass. 500 is where the expected gain hits zero, and it's an average, so one person's threshold is higher and another's is going to be lower.

48:08What's supposed to move that threshold is how much fat you're carrying. Carry a lot of fat, and there's not really a ceiling on the calorie deficit that's worth worrying about when it comes to gaining muscle mass. you can eat in a deficit, you lift weights, and you'll build muscle at the same rate you would have at maintenance or even at a calorie surplus. But why would that be? Now, part of the answer comes out of starvation research. Take two men and stop feeding them. A lean 70 kilo man is carrying about 99 ,000 calories of usable energy and about 20 % of that is protein. A 140 kilo man is carrying about 600 ,000 calories of usable energy and only 6 % is protein.

48:47You starve both and the lean man is running about a fifth of his energy off protein against the heavy man's 6%. By four weeks, he's lost about twice as much nitrogen for every kilo of weight that he's dropped. So the body fat is doing something. It's covering the energy gap so that protein doesn't have to. That's the whole basis for the bigger people can run bigger deficits idea. If body fat spares protein, then somebody with plenty of it should be able to sit in a large deficit and not give up muscle for it. I've made a version of that argument myself. But nobody in those studies measured muscle.

49:22When you break protein down, the nitrogen in it leaves in your urine, so urine is what most of these studies collected. That tells you how much protein came off the whole body, but it can't tell you which organ the protein came out of. But imaging can tell us that. When somebody scanned organ size during a very low-calorie diet, the gut and the liver shrank first and the muscle joined in later. The liver shrank proportionally faster than the rest of the body, and 80 % of that shrinkage happened inside the first two weeks. That often gets counted as lean mass loss because the liver mostly is lean because it's made out of protein.

49:57But body fat sparing protein and building muscle are two different outcomes and the starvation work only measured the first one. Those men were starved, given no protein and they weren't doing any training. So what that data shows is that carrying fat slows down how fast you burn your own protein. What it gets used to support is that you can add muscle while eating in a deficit, hitting your protein, and doing some lifting. Nothing in the starvation work speaks to that. Not losing muscle obviously is not the same thing as gaining muscle. And as far as I can find, nobody has run the study that closes that gap.

50:28I think it's probably true, but I can't tell you it's been shown. But here's my current thinking, and it's an update to what I've said before. Previously, I've made the point that people can get stronger in a deficit at about the same rate they would in a surplus. That's especially true in the short and medium term, and especially for people who are carrying excess body fat. But I still told leaner people to consider a small surplus, my reasoning being that gaining weight over the long run would build more muscle and therefore more potential for strength because more muscle is more force production potential.

50:59And that would happen in a surplus better than it would in a deficit or maintenance would for a lean individual. Now, the update is that until someone is relatively lean, say under around 15 % body fat, I don't think a surplus is necessary to gain muscle mass at the fastest rate. The concept here is energy availability. And until energy availability is actually constrained, which means a lean, hard-training individual, muscle mass gain potential is mostly preserved from deficit to maintenance to surplus. Behaviorally, this can be challenging to implement and tougher to test, where small changes in energy intake move somebody categorically from a deficit to maintenance to a surplus.

51:40and somebody bordering on lean may be better off just running a small surplus so as not to potentially compromise their muscle gain. Gaining muscle first, though, and worrying about losing the fat later is, for most people, a bad tradeoff. A 250-calorie deficit didn't cost any body muscle in this particular study. If you take people at about 25 % body fat with a year and a half of training behind them and you randomize them to maintenance calorie intake, a 250-calorie deficit, or their normal diet with no instructions, You have all of them lift four days a week for 10 weeks, and the two diet groups eat a lot of protein.

52:15Well, the deficit group gained about a kilogram of lean mass and lost three kilos of fat. About the same lean mass gain in the maintenance group was seen with a kilo and a half of fat lost. Now, the people who just trained and ate whatever they wanted, remember they had a lower protein intake? Well, they didn't gain any lean muscle mass, and they didn't lose any fat. So the calorie deficit didn't cost them any muscle. Both diet groups gained lean mass and lost fat. and the group that just trained didn't do either. What the study can't tell you, though, is whether the deficit beat maintenance. Because when the authors compared those two groups head-to-head, the differences didn't hold up once they corrected for the number of comparisons they ran.

52:54Now, at the extreme end, there is a trial where 40 young men who were overweight, they ran a 40 % deficit for four weeks, and they were training six days per week. The high protein group gained about a kilogram of lean mass while losing almost 5 kilos of fat. Now, this study didn't use a DEXA scan because a DEXA scan subtracts out your fat and your bone and calls whatever's left lean tissue, and then assumes that leftover is about 3 quarters water. This study went ahead and measured the water. Measuring the water fixes one problem but not the other. Lean mass still means everything that isn't fat, so glycogen and the water it pulls in alongside it are inside that number no matter how carefully you measure.

53:34Four weeks is short enough that some of that kilogram is exactly that, water weight. So don't read the whole thing as contractile tissue. But directionally, this is pretty clear. The question underneath all of this is whether baseline body fat really moves the calorie deficit threshold for gaining muscle mass. And the direct evidence on it is thin. Three groups have gone looking for it across four data sets. One found it in the Minnesota starvation trial in men in the bottom fifth of the sample sitting around 7 % body fat. Two studies found nothing at all, and both of those were run entirely on overweight people.

54:08And one found the opposite, that heavier people did worse, not better. But that one used BMI as the measure, and in that data set, the heavier people also happened to be the ones in the bigger deficits. So you can't tell whether it was the body size or the calorie deficit that was doing it. Now look at where each of those studies sit on the body fat scale. The one that found something was looking at men at 7 % body fat. The two that found nothing were looking at people who were overweight, but there wasn't a study of people between the two extremes. If a deficit only costs you muscle once you're below some level of body fat, then studies run entirely in overweight people come up empty because everybody in them was above the line, which is what happened.

54:49Jordan Feigenbaum:But it's also what you'd see if body fat has nothing to do with it and the Minnesota result was a fluke. It's the same pattern with two explanations, and I can't rule out the second one. To my knowledge, no one has published a study that would settle it because nobody has run lean people and heavier people through the same deficit in the same training study. So this is more of a theory that I'm thinking about right now, courtesy of Dr. Eric Helms, who we're going to have on a podcast addressing exactly this. But the part I'm confident about is the part that matters to most people. For somebody with obesity, which is excess body fat, which happens to be excess energy availability, well, that means that energy availability is not the constraint for building muscle.

55:28What limits them from building muscle is whether they're doing enough training and whether they're eating enough protein. Nobody in that situation is failing to build muscle because they ran out of energy. They have plenty of it. The lean end is where there's sort of this open question.

55:42Jordan Feigenbaum:How lean do you have to be, right, where you don't have enough energy on board to tolerate a energy deficit and still build the maximal amount of muscle? It's probably around 12 % body fat and probably around a 500 calorie per day deficit. I think those are fine rules of thumb, but importantly, this has nothing to do with individuals with obesity, which puts this muscle first prescription for obesity in a strange position. It's solving a problem that doesn't exist and it costs you time in the one place time actually matters, which is how long you spend over your own personal fat threshold. But see what happens when you invert the priorities.

56:21If the

56:22Jordan Feigenbaum:priority is not getting under the personal fat threshold to avoid exposure to health risk, but rather prioritize muscle mass above everything else makes you do some weird stuff. And no place is it weirder than in the GLP-1 space. Now, the worry behind this is legitimate. Losing muscle while you lose weight is a real thing that happens, and it matters more the less muscle that you have to start with. Anybody who tells you to ignore it is probably selling something or smoking something. But the problem when it comes to GLP-1s is that the concern over muscle mass loss is mostly overblown, and it's based on numbers that are inaccurate.

56:57In the Step 1 trial, people lost about 19 % of the fat they started with and about 10 % of what the scan calls lean mass. Now, those are percentages based on two different pools, and the lean pool is the bigger one because on a scan, lean means everything in you that isn't fat or bone. So 10 % off the lean side still comes out to several kilograms.

57:20Jordan Feigenbaum:And if you add the two together, you get the headline. About 40 % of the total weight loss was lean mass. 40 % is the number that everyone quotes. It's a calculation that people run off of those two percentages, but not something that the paper reports directly. You do the same math on the Surmount 1 trial with terzepatide, and you get closer to 25 % of the weight being lost is lean mass. Now those numbers are aimed at the wrong target twice over, and I want to tackle them both separately. Remember what the DEXA scan is doing. It subtracts your fat and your bone and calls the rest of it lean mass.

57:55Some of what's left over is muscle, but plenty of it isn't. For a drug that takes weight off fast, the fat that leaves first is the fat that was sitting where it shouldn't be, out of the liver, out of the muscle, out of around the heart, off of the kidneys, out from around the pancreas, and the DEXA scan counts a good share of that fat lost as lean mass loss. There are two reasons why. Your liver and your heart sit behind bone, and where bone is in the way, the machine can't work out what's underneath, so it guesses from the tissue next door. And fat tissue isn't pure fat to begin with. About 15 % of it is water and protein and structure, and that 15 % counts as lean no matter where it came from.

58:33Then there's the assumption that the machine makes. To turn the leftover into a number, it assumes that the leftover is about three quarters water. That's fine in somebody whose weight is holding steady, but in somebody who's dropping weight quickly, the water is what's leaving. So when someone loses three kilos of what the scan calls lean mass, most of it isn't muscle. Let's start with the biggest piece. Fat tissue is only about 85 % fat. The rest is water and protein and structure. So every 10 kilos of fat you lose drops about a kilo and a half straight into the lean column all on its own. Then there's glycogen and the water that goes along with it, which comes out of the liver and out of the muscle, which comes off early and comes off fast.

59:14Then the fat that was inside the liver and inside the muscle. Then the fat that was packed around the heart and the kidneys and the pancreas. And then at the bottom of the list, the smallest piece of it, two to 500 grams of actual contractile muscle tissue. Half of that list is the fat that ended up in the wrong rooms, going back to our garage analogy, which this whole episode has been about getting out of the wrong place. the scan is counting that success as a loss. Now the second problem with those numbers is the bigger one. Suppose the scan was right. Suppose all three kilos were contractile muscle tissue.

59:47Jordan Feigenbaum:Is losing that amount of muscle actually dangerous? Should people with obesity avoid losing weight because they could lose some muscle? Let's go back to that study on 18 ,000 older adults. Lean mass didn't predict falls, fractures, mobility, or death. And the consortium that ran that analysis said that the Dexan number shouldn't be in the definition of sarcopenia at all. What does predict falls and fractures and death is muscle function. And in these people, muscle function went up. In the semoline study, where people got semaglutide and they didn't exercise for a whole year, grip strength improved by about four and a half kilos.

1:00:23Let's call it 10 pounds. At the same time, the scan was saying they'd lost lean mass. So the scan says, hey, you probably should have gotten weaker, but the strength test says they got stronger. and only one of those two things predicts whether or not somebody falls. Pound for pound, these drugs don't seem to cause more muscle loss than dieting alone does.

1:00:41Jordan Feigenbaum:People do lose more weight, so the absolute numbers just look bigger. The American Association for the Study of Liver Diseases' November 2025 guidance now formally lists lean mass loss as something to monitor, which is a real acknowledgement that the concern isn't nothing. But there's a framing problem in this whole conversation that I think does real harm to real people. That argument runs like this. These drugs can cause lean mass loss. Therefore, they're dangerous. Therefore, be skeptical of them. That treats the risk of the medication as though it exists in a vacuum, as though the alternative to taking it were something other than continuing to carry the excess body fat.

1:01:17So consider the alternative, using diet and exercise alone, which we call lifestyle changes. Take everybody who sets out to lose a meaningful amount of weight and keep it off. Not trial volunteers, everybody. Roughly 1 in 10 of them are still there at 5 years. Inside a good structured program with dieticians and real follow-up, the odds get a little better than that, but they're still not great. The other nine aren't quitters and they didn't fail to try hard enough. Weight regulation is genuinely difficult to override through effort alone and suggesting otherwise is a moralizing issue that we've talked about a number of times on this podcast.

1:01:50Semaglutide, so Ozempic or Wegovi, averages around 15 % of total body weight loss at 68 weeks. Terzepatide gets to 20 to 21 at 72 weeks. Those are average outcomes, not best-case scenarios. Now, none of which makes these drugs right for everybody, and the lean mass question deserves attention in practice. But the risk-to-benefit analysis has to carry both sides, including what happens to that patient over the next 20 years if the wait stays. There are no gold stars for going through life without needing help, in this case, medicine. Now, before I tell you how to protect that muscle tissue, I really need to square two things I've said today to make sure that you don't think I'm contradicting myself.

1:02:30I told you that the lean mass number on a scale doesn't predict who falls, who breaks a hip, who loses their mobility, or who dies. And I'm about to tell you that resistance training protects that same number better than anything else we've got. Both of those are true at the same time. The number doesn't forecast your outcome, but that doesn't make the tissue worthless, and it doesn't mean you shouldn't train. What it means is that the DEXA scan is a poor tool for the question that we're asking. It's counting your organs, your water, your glycogen, and a chunk of your fat tissue right alongside your actual muscle.

1:03:00So it was never going to be a clean readout of anything. And separately, it means that adding muscle isn't the treatment for the metabolic problem. Train, because training makes you stronger and fitter, and strength and fitness are the things that actually do predict what happens to you. The lean mass number just comes along for the ride. Now, what protects that muscle tissue is exactly what you'd expect. And again, this is the Barbell Medicine Podcast. You guys already know what I'm going to say. Resistance training wins by a landslide. A meta-analysis of six trials in older adults with obesity found that resistance training prevented about 93 % of the lean mass loss the diet-only group had.

1:03:34Then there's sleep. Then there's protein. Call it a gram and a half per kilogram of body weight. The reason it's third is that without a training stimulus, the protein does comparatively little. We've written the long version of this up on our website under GLP-1s and muscle loss, and it has the full breakdown in it. The short version is that these medications are a tool for creating the deficit, and the muscle is still your problem to solve. So I don't think the number on a scan is the thing to defend. Lift, eat your protein, let the fat come off, sure. That's the same advice whether you're on one of these drugs or not.

1:04:04But if low muscle mass isn't what's hurting these people, something is. And there's a diagnosis that names it, and the name, to me, is wrong. It's called sarcopenic obesity. Sarcopenia means low muscle. Obesity means too much fat. Two conditions turning up in the same person, and the name treats those two conditions as roommates. One problem about muscle, one problem about fat, sharing the same body. The roommate's version doesn't fit what I told you earlier. People with obesity carry more muscle than lean people carry, and they're stronger in the legs for it. What they have less of is muscle that works well per kilogram.

1:04:39So how does the group with more muscle end up with a muscle deficiency diagnosis? It's because the word sarcopenia stopped meaning what its root says. The word was coined in 1989, and for about 20 years, sarcopenia meant low muscle mass and nothing else. Then strength got added alongside mass. Then strength became the thing you actually diagnose it on, and mass got demoted to confirming the strength result. And the consortium that pulled those 18 ,000 older adults together said to take the DEXA number, for measuring muscle mass, out of the definition entirely. Now, the field hasn't fully followed that recommendation.

1:05:13A separate group ran a formal consensus process, 107 experts across 29 countries, and about 9 in 10 of those experts still said that muscle mass belongs in the definition. But a consensus process is a vote on the concept, and that group says themselves that they haven't turned their vote into anything that you can measure. The consortium was answering the measurement question, with 18 ,000 people and 4 outcomes behind it. So the word still translates as muscle loss, really poverty of flesh, while the diagnosis behind the word is now mostly about what the muscle can do. I'd rather we called it dinapenia, which is at least accurate, and I'm fine with people looking at me weird.

1:05:51Which makes sarcopenic obesity a compound term where the first half doesn't mean what its root says. What sarcopenic obesity describes is people whose muscle doesn't work well, who also are carrying a lot of fat. Nothing in the diagnosis requires those people to be short of muscle, and mostly they aren't. Muscle function going down, like strength, while the tissue stays put, is what ordinary aging does on its own. Obesity didn't invent that split. Strength declines about three times faster than muscle size does, so you lose the ability, the function, before you lose the tissue. A scan is still telling you everything is fine, because your muscle mass is fine, while your function is already on the decline, because the first thing to go is the nerve supply feeding the muscle.

1:06:32The largest, fastest motor units go first, and the largest, fastest motor units are the ones you'd use to catch yourself when you fall. That's normal aging. So what does the fat add on top of it? Well, visceral fat, again, that's the fat stored in and around your internal organs. It's not inert storage. Visceral fat generates inflammation, and it puts fat inside the muscle tissue if you have to store more of it. And we already know what fat inside a muscle does, because I told you 20 minutes ago, fat inside a muscle makes that muscle weaker. It's the same amount of tissue, but you get less force out of it.

1:07:05So the sequence runs kind of like this. You run out of fat storage, which is primarily under the skin,

1:07:12Jordan Feigenbaum:subcutaneous fat, the fat you can pinch. Then fat goes where it shouldn't go, into the liver and into the muscle, for example. A muscle with fat in it gets worse at producing force. Somebody measures that person's function, finds the function low, and names the condition sarcopenia after the muscle. There's a paper that makes exactly that mistake. It's the same 1 ,300 men in their 80s that we talked about earlier with the labeled creatine. Well, they found that the men with less muscle were the ones falling down and walking slowly. Then they asked whether body fat told you anything on top of that.

1:07:46And the way you ask that question statistically is that you compare men who have the same amount of muscle to each other and see whether the ones with more body fat still do worse. They didn't. Among men matched for muscle, body fat predicted almost nothing. So the authors concluded obesity has little relevance here. Now think about what that comparison actually did. If the fat is what wrecked the muscle in the first place, then two men with the same amount of muscle have already had the same amount of damage done to them by their fat. Matching them for muscle throws away the thing the fat did.

1:08:19So of course the fat comes out looking innocent. They took its effect away before they even measured it. Let's try the same move on something more familiar. Smoking causes lung cancer, and the way it does that is by putting tar and other carcinogens into your lungs. So let's run their analysis on smoking. Let's take a group of smokers and non-smokers who all happen to have the same amount of tar in their lungs and ask whether smoking predicts cancer. It won't. Once everybody's matched for tar, smoking has nothing left to do because putting the tar there was the whole mechanism. Now, nobody would read that study and conclude that smoking is irrelevant to lung cancer.

1:08:54They'd say the researcher controlled away the thing that smoking does. That's what happened here with the fat and the muscle. The fat upstream version also explains something that the roommate's version can't. Why would the people carrying the most muscle be the ones getting a muscle deficiency diagnosis? If low muscle function and high body fat are two conditions that happen to coincide, that coincidence is something nobody has to account for. If the fat is upstream, the overlap is exactly what you'd predict. Fat being upstream also explains why the diagnosis gets missed. The screening runs on muscle mass, and in these people, the mass looks normal or better.

1:09:31The function test is the one that would catch it, and the function test usually doesn't get ordered. Now, if the fat is upstream, then treating the fat should fix the muscle problem without anybody touching the muscle. In semiline, the semaglutide study I mentioned earlier, the share of people meeting criteria for sarcopenic obesity fell from 49 % down to 33%. They didn't build any muscle and they didn't do any exercise. They just lost the fat and that was the key factor here. A third of them stopped having a muscle disorder by taking a drug that does nothing to muscle. I don't know how you look at that and keep the name sarcopenic obesity.

1:10:05That's the exact opposite of the claim here, that obesity is a disease of too little muscle. What sarcopenic obesity actually looks like when you follow it back is it's a muscle problem caused by too much fat in the wrong place. A Dr. Lyon says, we don't have a battle of the belly, we have a battle of the biceps. Sarcopenic obesity is the one diagnosis named for the biceps, and the problem is in the belly. Now, I have to be careful here because there's a way to take everything I've said today and run off a cliff in the opposite direction. If muscle mass doesn't predict anything, and lean mass on a scan doesn't predict anything, and the amount of fat sitting in a given tissue doesn't predict anything either, then somebody's going to say, well, there you go.

1:10:45Body size doesn't matter. Stop measuring people. Health at every size. But that's not really what I said. What I said is that size is a bad proxy. Bad proxy means that the measurement is imprecise. It does not mean that the thing it's pointing at is imaginary. Your waist doesn't tell me whether there's fat in your liver. It doesn't tell me how fast your muscle is handling what you ate this morning. and it doesn't tell me whether you're over your own personal fat threshold because that threshold is different for every single person and we can't measure it directly. So for any one individual in front of me, the number on the tape measure or the scale are weak about what's actually going on

1:11:24Jordan Feigenbaum:inside of them. But weak is not zero and that distinction is the whole thing. Across a population, more fat mass means more people sitting over their personal fat threshold, which means more fatty liver, more type 2 diabetes, and the risk climbs in a dose-dependent way as you go higher. That's about as consistent a finding as we have. And for the individual, if you get them back under their own threshold, a lot of that reverses. We covered that in the last episode. So that's not a moral claim about anybody's body, and it doesn't license anybody to be an asshole about it. It's a mechanism, and we've spent a lot of time on those mechanisms.

1:11:59Now, the stigma piece is real, by the way, and I don't want to wave that away.

1:12:03Jordan Feigenbaum:People with obesity get treated worse by the medical system. They get their symptoms attributed to their weight, and that does actual harm. While that's true, you can hold that and still say that the excess fat is doing something. So the two errors here are mirror images of each other. One of them says that the fat is fine, just go build more muscle. The other says that fat is fine, just stop looking at it. And both of them leave the fat sitting exactly where it is, doing exactly the same thing, which is nothing, and those are the things that make people actually sick. Everything I've told you today has been an argument against one number, which is how much muscle mass you have.

1:12:38So here's what goes in its place. We stop treating muscle mass as the target. Yes, you should lift. Yes, you should eat your protein. And yes, if you have it, you should lose the fat. The muscle is going to take care of itself, and muscle mass is not the thing that's going to fix the metabolic problem anyway. As a result, you don't have to eat at maintenance or in a surplus in order to build muscle first. The constraint is energy availability, and those with obesity have plenty of it. You also don't have to slow your fat loss down to protect muscle mass. That's mostly because individuals with obesity tend to carry more muscle mass already, and losing the fat will actually help those muscles work better.

1:13:15Now, if you're a bodybuilder trying to get on stage, sure, slower is better, but that's not really what we're talking about here. And we don't have to panic about a drug aimed to help those with obesity because of lean mass loss. Most of what's getting counted as lean mass is not actually contractile muscle tissue anyway. And I don't think you should take that you're under-muscled as a diagnosis at all, because nobody has shown that adding muscle fixes any of this. Dr. Lyon says obesity is a disease of the muscle, that people with obesity are under-muscled, and that building more muscle is the fix.

1:13:46It sounds right because muscle is where the glucose goes, and muscle is where the failure shows up first. Both of those are true, but neither one gets you to her conclusion. Muscle doesn't take up glucose by being large.

1:13:58Jordan Feigenbaum:It takes it up through transporters, the doors that sit in the wall of the cell and let glucose in. At rest, more than 9 out of 10 of the doors a cell owns are stored inside of it, not at the surface. So what limits how much sugar gets in is how many of those doors are installed, not how much tissue is standing behind them. And what installs the doors is using the muscle. Contract it and the transporters go to the surface whether insulin asks or not. So the variable is what the tissue did recently, not how much of it there is. And when we measure the muscle mass directly, it doesn't predict anything, whether it's falls, fractures, mobility, or death.

1:14:32So obesity as a disease isn't a shortage of muscle. When your fat tissue runs out of room, fat ends up in places it shouldn't be, like your liver, your pancreas, and your muscle. And what makes it dangerous there is that it sits still, and often what it's made out of. Endurance athletes carry more fat inside their muscle cells than lean and sedentary people do, but they're amongst the most insulin-sensitive people we can find. So exercise is what gets the fat moving in the liver and in the muscle both, which is one of the reasons training improves your blood sugar even when your weight doesn't change.

1:15:02But fat turnover isn't removal. Exercise means more boxes going up the stairs and more boxes coming down. Both directions speed up, but the total amount of boxes might not change. The calorie deficit decides which direction wins. And that's how the fat actually gets out. You're going to want both of them. And there's an active area of controversy here. These GLP-1 drugs cut heart attacks and strokes. They decrease kidney disease, they pull fat out of the liver, and the benefit looks like it shows up early, at three months, when people really haven't lost that much weight. Now, there's two things about that.

1:15:34The early look wasn't part of the original plan. It got done afterwards, which is the kind of analysis that turns up findings that sometimes don't hold up. But somebody sharp pointed out that the inflammation numbers and the weight numbers come down almost exactly together. So calling the benefit early might be an illusion. But here's why I'm still interested. I think there probably is something going on beyond the weight just coming off. I'm just not sure of what. The way you'd check is to ask how much of the benefit tracks with weight loss and how much is left over. But there's a real problem with that.

1:16:04In these trials, the patients who get the drug are randomized. The weight loss isn't, though. Whoever lost the most weight is different from whoever lost the least in ways that nobody has measured yet. So the moment you start asking what the weight loss explains and what it doesn't, you're really on shaky ground. You can see it in the numbers. The SELECT trial is the big semaglutide cardiovascular study. 17 ,000 people, and it cut heart attacks and strokes by 20%. Then they went back and asked what was actually causing that benefit. Waist circumference explained about a third of it. Weight loss explained nothing you could see.

1:16:36There was no relationship at all between how much weight somebody lost and whether they had a cardiovascular event. Then there's the FLOW study, the kidney trial. Semaglutide given to people with type 2 diabetes and kidney disease. it cut the odds of a bad kidney outcome by about a quarter. That means ending up on dialysis, losing half of your kidney function, or dying from your kidneys or your heart. Now, as far as I can tell, nobody has published the same kind of analysis on that one, so I can't tell you how much of the benefit is due to weight loss. So I think something else is doing part of the work,

1:17:06Jordan Feigenbaum:but I just can't tell you what. It could be less fuel going into the garage, so less boxes being packed and stored. It could be the boxes inside of the garage moving faster. It could be the removal rate, the one thing that nobody has ever managed to change. I just can't tell you which. But to me, three things move the needle here, and not one of them is the lean mass number on a DEXA scan. Train, get into a calorie deficit if you need to lose weight, and if holding the deficit is the hard part, which for many people it is, get help holding it. So let's go back to the question we started with. What is obesity?

1:17:40The Obesity Medicine Association calls it, quote, A chronic, relapsing, multifactorial, neurobehavioral disease wherein an increase in body fat promotes adipose tissue dysfunction and abnormal fat mass physical forces resulting in adverse metabolic, biomechanical, and psychosocial health consequences. Listen to that again because they got something right. They named three different kinds of harm. Metabolic, the insulin resistance and the fatty liver. Biomechanical, the load on your knees and your airway. And psychosocial, everything that comes from how the world treats a bigger body. Those are three harms with three completely different mechanisms.

1:18:16The metabolic harm runs through where the fat is, what it's doing, and its type, everything we spent the last two episodes on. The biomechanical harm really is about mass because force is force, and the psychosocial harm comes from everyone else's reaction to the tissue, not from the tissue. They wrote out three separate processes and then filed all three under the same word, and that one word describes nothing except for what the body looks like from the outside. Think about how we name other diseases. We call it hypertension because the high pressure is the thing doing the damage. The name points at the mechanism.

1:18:50You treat the pressure.

1:18:52Jordan Feigenbaum:Jaundice, on the other hand, is a color. It's the yellow that tells you something underneath the hood is wrong. Nobody treats the yellow. They treat the liver underneath it. Obesity is named like jaundice, though. It's the thing you can see. It's the mirror. And we spent decades trying to treat the mirror. Now, behind the mirror, in the people who are actually sick, is a storage system where fuel is arriving faster than it can be safely put away. Three things decide whether any one person is in trouble, and I'm going to say them in the analogy first and then in plain terms. Number one, which room the boxes ended up in.

1:19:24That's location, and it matters because the garage is built to hold boxes, but the stairs aren't. Number two, whether the boxes are taped shut. That's the type of fat, and it matters because a sealed box sits there, not bothering anyone, whereas a half-open one spills, and the spill is the thing that switches off the insulin receptor in the liver. And number three, whether or not the boxes are moving. That's flux, and it's how fast fuel is arriving, how fast it's getting packed away, and how fast it's getting burned. Location, type, and flux. And that's why exercise keeps turning out to be the answer.

1:19:57It's the only thing that improves all three at once.

1:19:59Jordan Feigenbaum:It expands the muscle's willingness to take delivery, which is location. It restores the rate you can pack fuel away, which is type, and it raises how fast everything is moving, which is flux. It's also why the drugs that only clear the liver keep disappointing. They change a number on a scan without changing where the fuel is going. If we named obesity for what actually does the damage the way we do with blood pressure, we'd call it something else. Obesity would just be one of the signs. It's how the problem usually shows up, but it isn't how it always shows up. Because you can carry the harm without the look, That's the person with fatty liver and the normal waistline.

1:20:34And you can carry the look without much harm. That's the person whose fat is doing its job. Now, that may sound like a rare case, but it's really not.

1:20:42Jordan Feigenbaum:Researchers took 40 ,000 American adults out of the National Health Survey, and they did something simple. They sorted everybody by BMI, the way a lot of medical charts do it. Then they separately checked whether each person actually had the metabolic problems associated with obesity, the high blood pressure, high blood sugar, high triglycerides, inflammation. And then they asked how often those two answers disagreed. More than 30 % of the people at a normal BMI were metabolically unhealthy. And going the other way, about 29 % of the people with obesity were metabolically fine. Even in the most severe category, class 2 and class 3 obesity, 16 % still had no abnormal marker on any of these tests.

1:21:24Jordan Feigenbaum:When you add up both directions, the paper's own estimate is that 75 million American adults are on the wrong side of the label. Lean people carrying the disease and heavy people who don't have it at all. That's 75 million. And I don't think most people appreciate how big of a gap there is here. Now, before anybody clips that and puts me on blast on the internet, being heavy and metabolically fine is real. And for most people, it's really a stage sort of that you pass through transiently. When one large study followed those people for 12 years, 48 % of them developed the metabolic syndrome anyway.

1:21:57Jordan Feigenbaum:And the people who had obesity at every single visit and never developed it, that was only 3 % of the entire group. 3%, obviously not that much. Now, one more wrinkle here. There's a study that ran this sort of comparison across five different ethnic groups. At a normal body weight, the rate of metabolic disease was 21 % in white adults, 31 % in black adults, and 39 % in Hispanic adults, 44 % in South Asian adults. And the researchers worked out what BMI produced equivalent risk. The risk that a white adult carries at a BMI of 25, a South Asian adult carries at a BMI of 20. So the same number on the same chart means a different thing depending on who's on the scale.

1:22:38Jordan Feigenbaum:But we can't rename it yet because we can't measure the thing underneath the way we measure blood pressure. There's no cuff for fat tissue. So we're stuck for now describing a mirror and calling it a disease. I don't think that holds for another decade, and I'd like to be around when it breaks. Chasing the mirror also lets you win the wrong way. You can crash diet, you can drop the weight fast, and the scale rewards you for it. The number goes down, but the fat that was sitting in your liver and inside your muscle may not have moved much, and that's the part that was making you sick. You treated the reflection and left the pathology sitting there.

1:23:09Jordan Feigenbaum:But once you can see that the word points at the wrong layer, the number on the scale stops looking like an answer. It starts looking like what it always was, just a number. I'm Dr. Jordan Feigenbaum of Barbell Medicine. Thanks for listening.