Sarcopenia After 40: Dr. William Evans on Muscle and Aging

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Wow, I am clearing the rest of the day. Disney and Pixar's Hoppers Now available on Disney+. Rated PG. Most people think aging is just what happens to you. But after 40, aging actually is losing the one tissue that protects your metabolism, your brain, and your independence. And I'm talking about muscle. And today's guest, Dr. Bill Evans, is the scientist who discovered sarcopenia. That is that loss of muscle mass with aging. And what he's found lately is going to change everything that we know about aging. Literally, this episode is going to help rewire how you think about your future self and what is possible. You're going to know that you are not fragile, that your muscles are adaptable, literally in your 90s. Yes. And we'll talk about new research on natural myostatin regulators, including my favorite, Fortetropin, and why they might be the next frontier. I'll share my story with Fortetropin. This is the yogurt product, and we will make sure that we put into the show notes how you can get your hands on some too. This is a product I'm obsessed with, and so much so that I now work with the company. So I will be right back with Dr. Bill Evans, adjunct professor over at UC Berkeley in the Department of Human Nutrition and Nutritional Sciences, and also over at Duke University. He is also working there as well. And this is a massive conversation of everything you've wanted to know about muscle sarcopenia and what's on the horizon. So buckle up and I'll be right back. Hey, I'm JJ Virgin, PhD dropout— sorry, Mom— turned 4-time New York Times bestselling author. As a certified nutrition specialist, Fitness Hall of Famer and globally recognized leader in health, I'm driven to keep asking the tough questions and use my podcast to simplify the science of health into actionable strategies that help you thrive. Want an ad-free experience? You can now subscribe to my exclusive VIP podcast at SubscribeToJJ.com for just $4.99 a month or $49.99 a year. It's like your daily latte, but better for your health. I'd also love to hear your thoughts on the show. And here's the fun part. When you send me your review, I'll reply to you using my on-demand virtual me. That's right. My team and I created a virtual JJ packed with my books, speeches, and wisdom so I can personally connect with you. Here's how you do it. Subscribe and leave an honest review of the podcast. Take a screenshot of your review. Text it to 813-565-2627. That's 813-565-2627. My virtual JJ will reply directly, and trust me, this will make your day. So subscribe now at SubscribeToJJ.com and text me your review. Let's keep thriving together. Dr. William Evans, welcome to Well Beyond 40.

Good to be here.

I have been waiting for this interview for quite a while, and I have literally listened to everything I could find, all your interviews, read your research papers, because you are talking my love language of muscle. As far as I can tell, you are the guy who discovered sarcopenia. I'd love to know how that came to be.

Well, maybe DISCOVER is a little different misnomer, but my lab, which was at the time the USDA Human Nutrition Research Center at Tufts University, was a brand new 15-story building built by the Department of Agriculture to examine nutritional needs of older people. My laboratory at the time was charged with really understanding functional status and how nutrition might affect how we go about living our lives., and we studied specifically muscle. That was kind of my training. And we noticed that older people had a lower amount of muscle mass, lean mass, than, than did younger people. But we also noticed that if we exercise them, if we put them through strength training programs, we could increase the amount of muscle that they had and greatly increase their force. Sarco is flesh and penia means low amounts. So sarcopenia really refers to the lower amounts of muscle mass or the age-related loss muscle.

I hear so many women over 40 talking about things slowing down, their metabolism slowing down. Granted, they start to get into their late 40s and then they've got hormones going sideways too. But when I think of this, because I, I've heard that, oh, metabolism doesn't really slow down until after 60, but if we are losing muscle, that's got to impact your metabolism.

It is the only driver of lower metabolism. The loss of muscle is what drives the reduced metabolic rate. And you're right, it doesn't occur just at 60. It occurs throughout our lives. And that's because muscle is what we call a very expensive tissue to maintain. Takes a lot of energy, a lot of ATP to maintain the amount of muscle that we have. And so that is the reason why our metabolism slows down as we grow older. We don't need as much energy to maintain muscle because we have less of it. That's why women have a lower muscle or lower metabolism or metabolic rate than men do. It really is all a result of differences in the amount of muscle.

Now, here's the big challenge. How the heck do you know how much muscle you have? And what I've been doing is using proxies, but I recognize they're just proxies in that when I was in graduate school, we had underwater weighing and skinfold calipers. That was really unpleasant. And then we got bioimpedance. And I look at all these things, I go, I guess it's the best proxy we have. But I heard you talking on an interview, which I thought was really interesting, about I want to unpack how do we know how much muscle we have? How do we know the quality of the muscle? Because those are two different things.

Those are very, very good questions. And, and I'll preface it by saying you're right, the, the proxy measurements that we've been using for decades, whether it's underwater weighing or bioelectric impedance or the dual energy X-ray absorptiometry that we use to measure bone density and lean mass, they all measure what we call lean body mass, not specifically muscle. And it's been interesting because since we coined the term sarcopenia, all the research used lean body mass and found, interestingly, that lean body mass appears not to be closely related to function or outcomes. Because really what, what we predicted with sarcopenia is that it would be associated with age-related increases in risk of disability, risk of hip fracture, risk of diabetes, a risk of mortality. And lean body mass seems to be unrelated to these outcomes. So, um, my colleague and I at UC Berkeley invented a new method to measure the amount of muscle that we have. It's a non-invasive test. We take a small little capsule of what we call deuterated creatine. And we take a urine sample and we can tell exactly how much muscle you have. Now that we've started using this method, and we've used it now in what we call large cohort studies— these are kind of big epidemiology studies in older men and older women— we find that muscle is actually very closely related to strength and function. It's very closely related to your risk of these outcomes, like risk of disability and risk of mortality and hip fracture. So for the first time, we think we have a really good way to measure the amount of muscle that you have in your body so that we can now understand what the role is of the amount of muscle that you have. And we can begin to, to study then what changes in muscle quality may mean for some of these outcomes as well. So I think we have a new tool that's now being used. We, we've now dosed more than 4,000 people. And it's been incorporated into the Framingham study. I think that this method is, is going to be the one that we use because it's completely non-invasive. We don't need a urine sample to assess how much muscle someone has.

How expensive is, is something like this? It seems like an inexpensive test.

The creatine that we use, the dose is pretty inexpensive. It's not available clinically yet, although we've been working with the FDA to try to get this approved as a diagnostic test. But it's, you know, the analysis itself is about $150. You know, we use a, what's called a mass spectrometer to do the analysis from the urine sample. And from that we can tell how much muscle you have. So it certainly is not as expensive as other tools. Maybe bioelectric impedance is maybe a little bit less expensive, but yeah.

But the bioelectric impedance, just what you said, I want to unpack that because That's a pretty crazy statement to think, okay, fat-free mass on a bioimpedance doesn't correlate with strength. But I think it's important to understand that fat-free mass just is everything but fat. But couldn't it include— like, where is the fat in the muscle hanging out? Is it included in fat-free mass, or is it somehow included in fat mass? How does that work?

What most of these measurements are is this fat-free mass, or lean body mass, is everything but fat. And especially in older people, muscle is only about half of fat-free mass. So we start off by saying that whatever that measurement of lean mass or fat-free mass that you, you're making, muscle is only 50% of that, and it's variable, so that we, we have an inaccurate measurement of muscle. And we do know that there is fat in muscle, and it is an index of muscle quality. But as I said, unless we know how much muscle you have to start with, it's hard to correct for differences in quality. So in and of itself, the amount of muscle that you have is a powerful predictor of outcomes, kind of irrespective of anything else. And it was interesting, we were funded by the Bill and Melinda Gates Foundation to use this method and validate it in infants and children. So we've used the method in, in premature infants and healthy children. We've just completed a series of studies in boys with Duchenne muscular dystrophy. We're examining losses of muscle in patients with cancer. So we're now exploring in a wide variety of different circumstances how muscle mass contributes to strength and function. You know, as we originally thought, sarcopenia simply is the age-related loss of muscle, and that is really probably associated with almost every sort of age-related change in your health that we can imagine, perhaps even including risk of dementia.

So a couple of things here. First of all, before we get into the age-related piece of that, because I want to dig into that, you said about 50% of your fat-free mass is muscle. Does that decrease with aging or disuse? Like, And the other 50%, because I know, let's, let's say you've got someone who is morbidly obese, they need to lose some fat-free mass. Like, they just have too much mass.

They probably don't need to lose fat-free mass or muscle mass. They do need to lose fat. Right now we're at a probably a brand new age in how we treat obesity, and there is great concern among the big pharmaceutical companies that have these new, what are so-called GLP-1 drugs. That when people with obesity lose weight, they'll lose muscle, and that's probably not such a good outcome. The other half of what fat-free mass is, is water. Certainly our body has a lot of water in it. It's viscera, it's, you know, your intestines and your other organs. It's connective tissue, it's some scar tissue that we may have. So it's everything that's not muscle And that's everything that's not fat. Is that anything that's not fat? And then lean mass, as I said, only half of it is muscle. The rest of that lean mass is that other stuff, I guess, mostly water.

Got it. And then you talked about age-related sarcopenia. You know, I was looking at the stats and I think it was like 3% to 8% of people 50+. And I thought, you know, no one's looking for this. So how do we even really have those statistics, and could you predict it just from doing some of the function tests, or does it need to be combined with, say, a DEXA or something like that?

In fact, it's a very good question. We, we think that the single best measurement for sarcopenia, the way that we should measure it, is simply the amount of muscle that you have divided by your body weight, the percentage of muscle that you have in your body.. And we can do that with this test very easily and, and then measure by someone's body weight. And percent muscle mass is the thing that is highly predictive of these outcomes. And low muscle mass in older men and women is very closely associated with, for example, risk of a mobility disability. If a man or a woman is lower than 25% muscle, they have an extremely high risk of a mobility disability. That means their ability to climb stairs or to walk a couple of city blocks is severely impaired. So the percentage of your muscle as a function of the amount of weight that you are is highly predictive of these outcomes.

And any way to do that without doing the D3 test, or is there any way for everyone to get to become lab rats?

Well, as I said, we're attempting to get this approved by the FDA as a diagnostic test, so any doctor should be able to prescribe what we call the muscle assessment test to their patients. We're moving forward with that. We hope that it will be— but to be honest, the measurement of strength is pretty good. You know, as I said, what was interesting in, in those studies of sarcopenia that use lean body mass, they found that while lean body mass was not associated with these outcomes, strength was. Strength has always been associated with outcomes, and probably strength is a pretty good surrogate for the amount of muscle that you have.

So would they do it? That's like with the grip strength dynamometer, or are they using like squat test?

What? Yeah, no, no. So there are a number of ways. It's another good question. How does a doctor assess strength or function in the doctor's office? You know, grip strength is pretty good. It's related to these outcomes in large populations, whether, you know, you walking into your doctor's office and doing grip strength Tells you something about how much muscle you have. It's probably a pretty good proxy, is probably better than your bioelectric impedance, just a measurement of strength. What's interesting and what we've tried— we're lobbying for is for a doctor, especially assessing his older patients, to use standardized tools to measure functional status in their patients. And if they can get reimbursed for that, just as, you know, a doctor is reimbursed for a number of tests that they do, they can get reimbursed for measuring functional status in their patients. Then they can begin to assess whether the functional status of their patient is changing over time. Right now, very, very few physicians actually use any sort of test to measure their patient's function. And there are some very easy ones, like habitual walking speed. Just how fast does someone walk normal, or how rapidly can you stand up out of a chair 5 times. These tests are closely related to your amount of muscle, especially if you're older, and are highly predictive of outcomes. But right now, uh, doctors don't use them. So even if you don't have the equipment, a doctor could do these tests, and they would do these tests if we could convince CMS to reimburse the tests. And so, um, Right now, there's the best that a doctor can do usually is say, well, Mrs. Jones, how are you feeling? Oh, I'm feeling pretty good. And that's the end of it.

So, so that's my argument about sarcopenia at this point in the statistics I've heard. I go, but no one's looking. It's not part of any exam.

You wouldn't know. Exactly right. It's exactly right. And that's, you know, partially there are a couple of reasons for that. And I, I wrote an article a year or two ago kind of stating what's, what's going on. Part of the problem is that because we haven't had an assessment of muscle mass until recently, there are multiple different definitions of sarcopenia. Seems like every 2 years or 3 years a consensus group gets together and say, well, that last definition didn't work, so we're going to give a new definition. And the FDA, as they want, they're the ones that ultimately consider whether their sarcopenia is an indication They've said, well, we can't say what the definition of sarcopenia is until you, the field, come to some sort of consensus about what it is. That's where we are right now. I think it's one of the most important medical questions, uh, that we have. Someone should be able to go into a doctor's office and he or she should be able to tell their patients whether or not they have sarcopenia. And if they do, that should trigger therapies, you know, whatever they may be, you know, uh, changes in diet, changes in exercise and physical activity that could alleviate the problem.

The therapies require some work here, let's be honest.

Yeah, no, it's a, it's a good way, it's a circular argument, and, and I agree with you. We don't have a therapy for sarcopenia partly because we don't have an indication that the FDA agrees to. So for example, just to go back to in history, we had a definition for osteoporosis, and that was, um, bone density measured by this DEXA machine, dual energy X-ray absorptiometry. If you fell below a certain amount, then you would get this medicine. And without that, there was no way to prescribe the medicine. And I think that for sarcopenia, we're the same thing. If If drug companies could be sure that the FDA agrees to what sarcopenia is, then they would begin to develop medicines for it. I know because I was the head of the muscle discovery unit at GlaxoSmithKline for about 5 years, trying to find new medicines that would treat muscle wasting or sarcopenia. And the FDA never agreed that we could explore a medicine for sarcopenia because they, they said, we don't know what it is and you don't know what it is, and so we're Well, they know what cachexia is.

They've seen that.

Yes, they have. And that kind of fit well within kind of the way the FDA thinks about medicine because cachexia— and I was also described what cachexia is— it's associated with a disease. So cachexia is always associated with a disease, whether it's heart failure or COPD or cancer or other wasting diseases. They kind of got that through their head and it's well recognized. That there is a loss of lean mass with cachexia. And the loss in some cases is so severe that, and it occurs so rapidly that the FDA said, well, sure, you can go after medicines to treat cachexia, but sarcopenia, which obviously affects millions and millions of people worldwide, you know, there isn't any agreed-to definition of what it is. For regulators, that's a problem.

I've seen the statistics talking about starting at around age 30, how we start to lose muscle size, strength, and power. The question I always look— when I hear the statistics, I know we've had the hormonal shifts, we're having drops in testosterone, drops in growth hormone, we, we aren't using insulin like we were before with muscle protein synthesis, we're getting insulin resistant, we're getting inflamed, we're doing all these things that can make it harder for us to build muscle. But I also look at that and go, I remember what was happening to me. Now, fortunately, I've always been You know, I started exercising when I was a kid and ran gyms. So it's always been a thing. But I still think of my time in my 30s when you have little kids and you're in school and you're working and, you know, you're trying to slip in some exercise and just wonder, this age-related sarcopenia, how much of it is age-related due to hormonal shifts and how much of it is that we become more sedentary?

That's another great question. I think that early on, you know, in our 20s and 30s, as we get families and other lives, we see that physical activity begins to decrease and we begin to lose muscle. But there is another component to sarcopenia, and those are kind of neurologic changes. Around age 30, we begin to lose what are called motor units. And that's the connection between the brain and muscle. I mean, muscle is directly connected to the motor cortex through these motor nerves, and it's the motor nerves that stimulate muscle. And, and it looks like we preferentially lose what are called fast fibers and white fibers, and those are the fibers that are more associated with strength and force production. So for example, you know, in my previous life, I did a lot of work with athletes. We can see that sprinting capacity, strength and power begins to decline, you know, around age 30. And so sprinters are in the, at their best when they're 25 or 26. You know, it's interesting. We see that despite an enormous amount of talent, athletes like Michael Jordan or Jimmy Connors or other great athletes, as much as they want to exercise, they still lose some amount of speed and some amount of power. And that's also, that's almost certainly a result of this kind of small but continual loss of motor nerves. And that continues throughout life. And so that's one of the initial causes of sarcopenia and loss of strength. We also know that endurance capacity can be maintained so that marathon runners are sometimes world-class up until their, their age of 40. So there are fundamental changes in muscle that occur even early in life. And then, as you say, there are a lot of other factors that are associated with decreasing muscle— changes in hormonal status, changes in insulin resistance, certainly changes in how physically active you are. And all of those things contribute to a continued loss of muscle.

So if the majority of what we're losing as we're aging is fast twitch, yes, wouldn't we be smarter to prioritize the training that we do more in the strength and power, more in the explosive side, because those hybrid fibers that have the choice to become more type 1 or type 2, wouldn't we want to try to pull as many of those over and maintain as much type 2 fiber as we can as we age?

Yeah, that, that's absolutely true. My lab is has done some of the early seminal studies where we were able to take people in their 90s and put them through high-intensity resistance exercise training and increase the size of their fast fibers. So that it is possible. Muscle is enormously responsive to changes in physical activity. It's really quite amazing how responsive muscle is, and both with inactivity and activity, uh, muscle can increase or decrease. But I agree, you know, if someone has difficulty walking, I maintain that rather than focus on their just doing more walking, if they increase their strength, then they'll be able to walk easier, more easily, be able to climb stairs more easily. And that's kind of what we found even among our 90-year-old subjects when we made them stronger, even in a nursing home. Their spontaneous activity increased, their walking speed increased, their ability to climb stairs increased just by a simple intervention of resistance exercise training.

I love that. I like to say the more you do, the more you can do. Yeah, simple.

Yeah. But, but as you, as you suggested, focusing on those fast fibers, the ones that we lose, might be more productive. Overall. Yeah, it's missing a broad array of amounts of physical activity.

It's always made sense to me. And I was doing my PhD at USC, and it was exercise, phys nutrition, and aging. We had the master athletes. And then I was also over in Palm Springs working with like 70-year-olds and 80-year-olds. And I was working out of a gym in the Palm Springs Hospital's cardiovascular lab. And I had a woman in there, and I had her doing pull-ups and dips. She was 75, and everybody else, they had— they were on the treadmills. Like, all the other trainers kept people walking slowly on the treadmills for cardiac rehab. And I'm like, I don't get this at all. And everyone wanted to do what she was doing. And it's like, kind of started a revolt at that gym because they all thought they couldn't do that stuff because that was the common belief, right?

Well, it is crazy. In fact, there have been some very, very nice studies using resistance exercise in cardiac rehab., and with spectacular results. And there is this kind of mistaken belief, especially by many cardiologists who haven't read the literature, that somehow resistance exercise might be dangerous or might induce cardiac problems. In fact, it's just quite the opposite. Resistance exercise is extraordinarily safe, you know. So it's been a long time, and the data are very clear, but there still is somewhat of a resistance among especially cardiologists, maybe not so much other sort of physicians, on using this, this exercise as a means of rehabilitation.

I think it's starting to get there, because especially when you look at the things we should avoid at all costs— losing a high percentage of muscle when you're dieting. And that's the thing that's frustrating to me about the GLP-1s. The good news is it's made people aware that if you do a high-calorically restricted diet, you lose muscle. Whether you're on a GLP-1 or not, you're going to lose muscle. And I think people just weren't paying attention to that before. But what I'd love to look at is someone who is 30 pounds or more overweight, they're going to lose some muscle as they're losing weight. And what would be like— how do you know if this is a well-designed program and they're, they're able to minimize that amount of muscle loss? How would you be able to tell if you don't have the D3 creatine. Could you do it using a bioimpedance scale, fat-free mass, along with like qualitative tests, maybe a grip strength and a chair squat test?

We'll find that out. We just got funded by the National Institutes of Health to do a large study in older people using a GLP-1 for weight loss. And in older people with obesity, one group will be involved in exercise training and one group won't be., and we'll be measuring their muscle mass and function, and we'll be using other indices of lean mass. And so we'll see, we'll see how much muscle we lose, first of all, cuz that hasn't been measured very accurately. And second of all, whether the other measures are predictive of these changes. We already have some notion. There are a couple of very interesting studies that are in the pipeline right now using muscle active drugs, not weight loss, or not exercise necessarily. As you may know, pharma has invested an enormous amount of money now in muscle active drugs. Lilly spent more than $2 billion for a muscle pro-anabolic drug, and there are a couple of others that are in the pipeline measuring these changes with GLP-1 weight loss.

I remember hearing a company was working on like a follistatin type of drug to go along with the GLP-1. What types of things are they looking at?

The two that right now that are kind of in the pipeline, one is Lilly, which has the drug tirzepatide, which is one of the GLP-1 drugs. They've invested in, it's called bimagramab. It is an anti-myostatin, anti-actinin therapy. They've completed a number of studies showing, measuring muscle mass necessarily, but lean mass and showing somewhat of a preservation preservation of lean mass and some preservation of function and an increase in, in fat loss. And there's another company, it's called Veru, V-E-R-U, which is a small biotech that has what's called a selective androgen receptor modulator, a SARM drug. This is a small molecule, so you don't have to take an injection, and it's selective in affecting the androgen receptor in muscle specifically. And they have some very nice data showing that this upregulation of the androgen receptor during GLP-1 weight loss preserves function. They use what's called stair climbing power, how rapidly you climb upstairs, and preserves their lean mass and increases fat loss. So there'll be a couple that are out there, and we'll see which one kind of, which one makes it. And a lot of it is dependent upon how the FDA considers weight loss and what the most appropriate endpoint should be. And there's some controversy about that right now. But I think we'll be entering an age where these, these, these drugs actually will be used in combination with GLP-1.

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So good, so good, so good.

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But there's no doubt, I think the way to do it right now is to be enrolled in an exercise program and increase the amount of high-quality protein that you eat.

Yes, that's what I was just going to ask you, because if we stopped looking at it as weight loss and we started looking at it as improving quality muscle while losing fat, right, a body composition upgrade rather than a weight loss per se, and you were going to, out with everything you know, we're going to set and create a program to achieve those results, what would it look like?

Yeah, well, we had written a grant application for just that. The data that we have right now at UC Berkeley and others in the literature is that when you eat a low-calorie diet, when you decrease your caloric intake, you're obviously decreasing the protein intake as well. The result of that is a decrease in the rate of muscle protein synthesis, the, the amount of new protein that muscle is making. And that's why we lose muscle. Protein synthesis rates go down, and there are two consequences of that. One, protein synthesis is an energy-requiring process. It takes a lot of ATP, a lot of energy. When you lose weight, your metabolic rate goes down. It's almost certainly a result of this decreasing amount of protein synthesis in muscle. And we know that one of the most powerful stimulants of protein synthesis are essential amino acids, the essential amino acids that are in the protein that you eat. And so right now, perhaps a supplement of essential amino acids. I mean, as you know, that probably the best quality supplement that you can consume right now of natural products is whey protein. This is the protein that has the highest amount of essential amino acids. I would say that right now that the best that we could do is increase your consumption during your weight loss of high-quality protein. Whey protein supplements are probably a pretty good way to stimulate protein synthesis and do some resistance exercise. And it, you know, you don't even necessarily have to go to a gym. You can, you know, these rubberized tubing, you know, those things actually work pretty well.

Challenge your muscles.

Yeah, no, it's a good way to think about it. Challenge your muscles.

Well, because everything got, everyone got a little crazy on the online with the lift heavy things and go, you're just scaring people away. Stop it. Women get afraid when you say that. I go, just challenge your muscles. It's whatever you can do. Like, do 3 sets of 10 of whatever you can do that's hard, that when you get to the 10th, you feel like you can't really eke out another 1 or 2. Do that.

Just, you know, I mean, that's exactly the right advice.

Absolutely. So you'd have them— what amount of protein would you have? And what I've done with essential aminos is I took plant-based shakes and bone broth-based shakes for the people that are dairy intolerant, and I spiked the other aminos to make it mimic whey so that everything that I do has that same profile, like the whey profile. What do you think is the right amount of protein or an optimal range for someone?

Well, the thing that we know from a number of very good studies is that you, you maximally stimulate muscle protein synthesis with about 15 grams of essential amino acids.

Now, which isn't the same as protein. I think it's very important for people to understand. Oh, no.

So if you think about whey protein, for example, 15 grams of whey protein probably have about 6 grams of essential amino acids. So if you wanted to maximally stimulate your protein synthesis rate, you would probably want about 30 grams of whey protein. So that would maximally stimulate protein synthesis, I think. And so that's probably the easiest way to think about it. You know, all protein is a combination of essential amino acids and non-essential amino acids. And as you suggest, plant-based proteins often don't have all the essential amino acids. And so combining them with other plant-based proteins or some animal-based proteins is the way to get your amount that are required, I think. My concern is another one is that we know, again, from studies using lean body mass estimates, is that when older people, and by older I mean over 60, 65, lose weight, the amount of lean mass that they use is greater than younger people. So older people lose more muscle.

And is that because they lack the anabolic hormones, or what is the reason?

Well, probably two reasons. One is, is that is it could be that their growth hormone status is lower or testosterone levels are lower. But when you start to think about it, older people, number one, have a higher need for dietary protein than younger people. And that's, as you suggest, because of differences in their hormone status. So they're already consuming just to maintain their weight, even if they're obese. You know, about 2,500 kcal a day, maybe even lower than that. And so if you put them on GLP-1 or just have them decrease their energy intake by about 500 kcal, their dietary protein intake is way, way below what they actually need. And so that results in a really fantastic reduction in synthesis rates, causing a rapid loss of muscle. And the thing that we, we do know is once older people have achieved that weight loss and go back to eating a normal diet, they really don't gain muscle back again unless they purposefully try to do resistance exercise or some other change in diet. So that's the group that I'm most interested in.

What you just said right there is why I do not believe that you should ever— like, 30-plus, I do not believe that you should ever go on caloric restriction without optimal protein and resistance training. I don't think it should be like— I don't think anyone should be given a GLP-1 unless they commit to doing that. Just think of the damage you just described of someone over 60 losing that muscle. We know how hard it is to get on, and then they get down in their weight. Now their metabolism's lower. Now they're going to gain weight back. It's going to be fat. They just devastated themselves.

You're absolutely right. I mean, I couldn't have said it better. I think that that is— it's almost malpractice. And I know some very, very good obesity experts that, that do their best. To try to do that. Whether patients actually adhere to those, those sorts of things is a different story.

I just think we have to make it— help people understand how little it actually is that makes a difference. Yeah, that's what's been so amazing. When you look at the minimum effective dose of exercise to make a difference, it's not that much, you know.

No, you're absolutely right. I mean, we did a study years ago. We were interested in the effects of resistance exercise on bone bone health. And it was a year-long study. And we decided, because our lab was in downtown Boston and many of the women in the study had to come to Boston, and we didn't want them dropping out in the middle of the study, so we backed off to 2 days a week of resistance exercise. And, and I'm happy that we did, because again, the results were incredible. They increased their bone density over the course of a year, and they increased the amount of muscle that they had, and they were walking better. All of the things that you might associate with a, with a fracture were improved through just 2 days a week. So, so 2 days a week is not a lot, but it has a fantastic effect.

Yeah, I'm right there with you. That's, that's my little minimum. Do a push, a pull, a hinge. All right. So I guess it was about a year ago. It was last February. So it was this last February. I was at a conference. One of my buddies was talking about nutritional strength. I was doing exercise as medicine at a health conference, and she was doing nutritional strength training, what you needed to eat for muscles. It was like peanut butter and jelly. And I heard her talk about Fortetropin, and I was like, what is that? So I went home and tried it and put on 2.5 pounds of fat-free mass. Couldn't— I had, had no D3, didn't know you. But at 62, to be able to put on muscle after training from the age of 16 on with weights, you know, I mean, it's like 2.5 pounds of fat-free mass. So at least a pound and a half of that, I would assume, would be muscle. And it was over a 2-month test period because I did a DEXA and then I did another DEXA, and it was from Fortetropin. So I would love to talk about that. We mentioned myostatin but didn't define it for people who, who want to know what's going on as we age. So I'd love you to talk about Fortetropin and your study with it. I'm now obsessed with Yoked and use it every single day. Well, good. I hope you take it after that study.

Yes. Yeah, I, in fact, I, they were very kind. You know, one of the other products that they have is a product for dogs, for older dogs, and they were very kind to send me some for my dog who was in the last year of his life, and it really helped him as well. So it's an interesting observation. This is an extract from fertilized egg yolks. And the idea, there are some research that it seems to indicate that it suppresses what's called myostatin. And myostatin is interesting. It's a negative regulator of muscle growth. You know, is that without myostatin, muscles can get really big. In fact, there's breeds of cows and sheep that are bred to be myostatin deficient and they get a lot of muscle. The drug companies have been feverishly attempting to develop drugs that are kind of anti-myostatin drugs with moderate amounts of success. But this product, Fortetropin, in some studies appears to suppress myostatin. Now, we didn't really— we measured it in the, in the circulation, so it's impossible to say how it affects muscle. But the one thing that we did see is that compared to a very appropriate control group, given not the Fortetropin but cheese and some other factors that are calorically equivalent, we saw an upregulation in the rates of muscle protein synthesis in healthy older people. I think that that can translate to an overall increase in muscle because it's very specific. You know, I was a little skeptical, I have to say. Does this stuff really work? It may work in lab animals, but does it work in humans? And so we did the study. We were completely blinded to who was getting what. We did the analysis, and sure enough, there was an overall increase in the rates of muscle protein synthesis with, with this product, Fortetropin. And we've done some studies now for the company looking at the use of Fortetropin during weight loss in, in, during, I guess, a hypocaloric diet in mice. In rats, and we see it still upregulates protein synthesis. So it may be a really good way to help to preserve muscle mass during these GLP-1-induced weight loss with the muscle changes. So I think it's a good, safe product that is available now.

And it tastes good. Yeah. Do you think there's any application for it with bed rest?

It's another good question. So one of the other areas of research that, that I've been involved in, I had a what's called the NIH Program Project Grant, a large grant to study what happens to older people who go to bed. And when we put people, older, healthy older people to bed for 10 days, they lose an enormous amount of muscle. They lose a kilogram of muscle just from their legs. And these are healthy people. Wow. There's a 40% reduction in muscle protein synthesis rates. Now, in, in one of the studies that we did, in this case, we used, uh, just essential amino acids to see if we could slow it down. And sure enough, we could affect protein synthesis rates and losses of functional status. One of the, the key things that happens with bedrest is that muscle becomes insulin resistant. We know that sometimes people go to hospitals with normal glucose tolerance, and a week or two later they're diagnosed as being diabetic because inactivity, especially extreme inactivity, results in this profound insulin resistance. And it's a, it's a great question, you know, whether corticotropin can have this effect, you know, to counter the inactivity-induced loss of muscle. And it would, I think it would probably need to have an effect on insulin action as well as protein synthesis. But, but I think it's a great question.

I just wonder if we took people, because I had a son who had, was in a coma at 16 and, and on bed rest for 4 months and got very cachexic. He just, you know, so I had him on, I was throwing essential aminos out of there to get him to move, but I just wonder if you gave someone— if you did some electrical muscle stim, essential aminos, and some Fortetropin, if you could offset a lot of that. Probably. I know with him, the doctors, that was the least of their concerns. It just was the thing that I knew the most about.

Yes, of course. I think that there are lots of models of inactivity, and certainly bed rest is an important one, obviously. NASA has done, you know, probably hundreds of bedrest studies to just try to think about what's the best way to prevent muscle loss during spaceflight. What's interesting is that old people lose 3 times as much muscle as young people do in only a third of the period of time.

Frightening. And then how will you ever— I mean, that's, you know, I still to this day, Bill, and it just, it literally happened this past weekend, I was speaking. And I was teaching an exercise session with Fonda Wright, who's a sports orthopedic surgeon. And literally a woman said to me, because I was doing the strength part, she goes, but I don't want to get bulky. This sweet 60-year-old woman.

I know. I mean, you know better than I do. You've probably heard this 100 times of a woman who comes up and says, I don't want to get bulky.

100? Try 10,000. It's funny. They go, I want to have arms like you. I don't want to get bulky. I'm like, I don't know what to do with you. But you know, you lose what you could lose 4 to 6 pounds of muscle in the hospital and you're not going to get that back.

That's right. I mean, it's what we, what we did, you know, in the study because our IRB required that we rehab our subjects to get back to where they started. So we rehabbed often our subjects for 2 to 3 months. So it took 2 to 3 months to gain back what they had lost in just 10 days.

Wow.

So it was, uh, really quite astonishing. I'll send you, if you're interested, uh, ANOVA did a little feature on the study that we did.

Yes, please. All right, let me do a little rapid fire, a couple quickie questions. Sure. All right, here we go. One myth about aging you would love to erase permanently.

Sarcopenia is an inevitable consequence of aging because many doctors will say, well, it's just an inevitable consequence of aging. It's just normal aging. And so why should we have to treat it? It's not, you know, it, it happens to some people, not to everyone. And so if we get, get that out, that it's not a normal consequence of aging, that's a, that's a good thing.

One lab test every woman over 40 should track.

One lab test that's available obviously is their bone density. I think that's the—

and why do we wait till 65? Well, pay for it, right? They pay for it at 65. Of course, it costs your bucks.

So let's— right. It's a— I mean, it all is tied in with what doctors are going to do with that information, you know, and, and early on kind of tracking someone, it's the same sort of thing. I think every person should have some measurement of functional status. Measured at the doctor's office every time they go in. You know, many people call it the fourth vital sign. It's as important as blood pressure, measuring changes. And even if you're not using it to prescribe a drug, which is the way our medical system is now, tracking it, but kind of understanding who among the patients are getting reductions in strength or their walking speed or some other measurement lets them understand that there's maybe something going on. Maybe in the past year the patient had to go to bed for a couple of weeks without telling their doctor and suddenly lost a lot of muscle, and they show up, they still feel okay, but their functional test is way down. That way a doctor recognizes there may be something wrong here that we want to think about.

I think most people wouldn't think to tell their doctor if they were— had the flu and were in bed for a week or something. Wouldn't think about it. Yeah, I'm going to attach those tests too because we talk a lot about grip strength on this podcast and, you know, it's the $30 hand grip dynamometer. So, um, yes, these other tests are easy and free. You just need a chair, you know.

Yeah, I'll send you also a description of this SPPB, the Short Physical Performance Battery. It's very, very simple. In fact, there's a— people are doing it virtually now. Doctors can do virtual SPPB. So there are a lot of functional tests that should be incorporated into the assessment by every physician of their adult patients.

Well, they can all start. You can just become your own. Like, you do your own and monitor it. I'll tell you one. I had the littlest wake-up call. I've always been the person to open all the jars and never ask anyone. And I remember the first time I couldn't open a jar, and I was like, what is going— at first I thought it was just the jar, but when my husband opened it easily, my son opened it easily, I'm like, what is going on here? Like, what is going on? So, you know, we've got to, we've got to also just be very proactive on these. All right, most underrated exercise for lifespan and healthspan and strengthspan. How's about that?

Yeah, I mean, most under— I mean, some amount of resistance exercise, you know, whether, you know, to focus, maybe start off with with your legs. Probably the best one that includes what's called a closed chain is a squat, you know, is going down and back up again. The squat engages your calves, your thighs, and your, all of your legs. If you can do it 20 or 30 times, you can put up some weight on your back. And so that's the one that I think gets to the muscles that are most important.

I agree. It's that if I had to pick one exercise, because you load your hips, you load your spine, and in life we squat.

Yeah, you know, we do. I mean, it's— and, and for, you know, you know, if you go forward, um, the ability to get in, off, and on a toilet sometimes is the key factor where defining whether someone's going to become institutionalized or So, so squatting is really, really important.

What do you think the biggest nutrient deficiency in adults over 50 is?

High quality protein. My wife, who was pretty much a vegetarian, I, you know, she was not eating enough. And so now she eats egg whites, 3 or 4 eggs in the morning, not the yolks because she still doesn't do that. And she, she also eats tofu. So, so I've forced her into doing that. And that's particularly true of many older women who are trying Oh, I see.

Like, because I'll do consults with them. They go, "I'm getting a lot of protein." I go, "What did you eat?" They said, "I had oatmeal and an egg." I'm like, "Oh, no." Yeah, it's very— it's— I don't know why it is so difficult for women to get protein. It's why I tell people to just eat it first. That way, you know you got it in. Okay, last one. One thing that you're doing today that your 80-year-old self is going to thank you for.

I go out for long walks every day. Again, my wife, she goes almost 10 miles in the morning. Wow.

And you're not in Berkeley though. You're not in the hills, are you?

I live in, uh, actually I live in Chapel Hill, North Carolina.

Oh, I lived there too. I've, we've been to all the same places.

She, every night she says, all right, let's go. And I said, well, I'm busy. No, let's go. And so we have to go. And then for You know, when we go on vacation with our kids, we usually, we always do hiking. And so I have to increase my strength training and increase the amount of walking that I do to keep up with everybody.

So, oh, very cool. Well, Berkeley had some great hikes.

Yeah. Berkeley has some good ones.

Yep. Yep. Well, it has been an absolute pleasure. Someone, how do we support your work? If people want to learn more about what you're doing, how do they, how do they find you?

We have a website right now before our measurement of muscle mass, but it tells you a little bit about what our research is, is and what's going on. It's www.myocorps.com, myocorps.com, and get an idea of kind of what we're doing. And you can also go to my website at Cal Berkeley, the Nutritional Sciences and department, we each have a little page describing our research and you can take a look at that too.

Cool. I will put all of the stuff you send me. I'm going to put everything at jjvirgin.com/dr-evans. D-R-E-V-A-N-S. You've done some great stuff and I'll include the Florida Tropin information too. And I really, really appreciate your time and your work. And whenever that D3 test comes available, oh my gosh.

We're excited about it.

I bet. Like, that changes everything. My biggest goal for my legacy is to get people to stop using a scale to measure their health success and to start looking at what that weight's made up of. And, you know, it's, it's very crude right now, and you're changing that.

Well, I appreciate it. You asked some great questions.

It's a good one.

Thank you.

Hope what you got from this is that aging isn't passive. It isn't just something that happens to you, right? This is a negotiation between your choices and your biology, and the muscle you build today is the independence you get to keep tomorrow. So be sure to share this with your buddies 40-plus and then get them to work out with you. And again, I'm going to link to my favorite product, that is that yoked fortetropin product, at jjvirgin.com/dr-evans. D-R-E-V-A-N-S. I might even have a little special deal for you as well, and I will see you on the next episode. Be sure to join me next time for more tools, tips, and techniques you can use to look and feel your best and be built to last. Would you prefer an ad-free experience? Join my VIP podcast at subscribe2jj.com for just $4.99 a month. Or $49.99 a year to unlock uninterrupted ad-free access to all the episodes and insights you love. Also, I'd love to connect with you and hear your thoughts on the podcast. Here's how. First, subscribe to the podcast and leave an honest review. Second, take a screenshot of your review. And third, text to 2-813-565-2666. 2627. That's 813-565-2627. When you do, I'll reply using my brand new Virtual JJ Virgin. It's my on-demand virtual self built from my books, talks, and years of experience so I can interact with you directly. You'll make my day and I can't wait to hear from you. Thanks for tuning in and I'll catch you on the next episode. Hey, JJ here, and just a reminder that the Well Beyond 40 podcast offers health, wellness, fitness, and nutritional information that's designed for educational and entertainment purposes only. You should not rely on this information as a substitute for, nor does it replace professional medical advice, diagnosis, or treatment. If you have any concerns or questions about your health, you should always consult with a physician or other healthcare professional Make sure that you do not disregard, avoid, or delay obtaining medical or health-related advice from your healthcare professional because of something you may have heard on the show or read in our show notes. The use of any information provided on the show is solely at your own risk. Struggling with weight loss? Prolon's 5-Day Fasting Mimicking Diet is a clinically developed nutrition program designed to promote fat loss while protecting lean body mass. Developed at USC's Longevity Institute, It assists the body in entering a fasting-like state that helps reset metabolism and target visceral fat. In just 5 days, ProLon offers a science-backed approach to weight loss without extreme restriction or guesswork. Get 15% off plus a $40 bonus gift when you subscribe at prolonlife.com/now.