The Peter Attia Drive - #322 - Bone health for life: building strong bones, preventing age-related loss, and reversing osteoporosis with evidence-based exercise | Belinda Beck, Ph.D.

Episode Date: October 21, 2024

View the Show Notes Page for This Episode Become a Member to Receive Exclusive Content Sign Up to Receive Peter’s Weekly Newsletter Belinda Beck, founder of The Bone Clinic and a leading authority on exercise physiology and bone health, delves into the science of osteoporosis, bone density, and the lifelong importance of maintaining skeletal health. In this episode, she explains how the foundation for strong bones is established during childhood, offering valuable advice for parents on optimizing bone health for their kids. She also explores how bone remodeling occurs throughout life, driven by activity, nutrition, and hormones. Belinda highlights the power of resistance training in improving bone strength, even for those at risk of bone loss, and emphasizes the role of essential vitamins and minerals in maintaining bone health. She shares practical strategies, backed by research, for preventing fractures and combating osteoporosis. We discuss: Belinda’s journey into bone health research and training [2:45]; The physiology of bone and how bones adapt to mechanical loading [8:15]; Bone development from birth to adulthood, why early life is a crucial period, the functions of osteoblasts and osteoclasts, and gender differences in BMD [14:00]; How parents can optimize their children’s bone health through diet (calcium and vitamin D), sunlight exposure, and physical activity [27:30]; The best sports and activities for promoting bone health, weight training for kids, and advice for parents [36:30]; The impact of corticosteroid use on bone health in children and strategies to minimize negative effects [48:30]; Advice for people in middle age to preserve bone density: physical activity and bone-loading exercises [52:00]; Bone loss during the menopause transition for women: hormone replacement therapy and other strategies to mitigate BMD losses [59:30]; Interpreting the bone mineral density results from a DEXA scan: T-score, Z-score, and more [1:03:00]; The LIFTMOR study: testing the effects of heavy weightlifting on bone health in postmenopausal women with low bone density [1:10:15]; Profound benefits of weight training outside of BMD improvements: exploring the broader impacts on patients in the LIFTMOR study [1:19:30]; Guidance for people wanting to use exercise designed to improve their bone health [1:29:30]; and More. Connect With Peter on Twitter, Instagram, Facebook and YouTube

Hey everyone, welcome to the Drive Podcast. I'm your host, Peter Attia. This podcast, my website, and my weekly newsletter all focus on the goal of translating the science of longevity into something accessible for everyone. Our goal is to provide the best content in health and wellness, and we've established a great team of analysts to make this happen. It is extremely important to me to provide all of this content without relying on paid ads. To do this, our work is made entirely possible by our members, and in return, we offer exclusive member-only content and benefits above and beyond what is available for free.

If you want to take your knowledge of this space to the next level, it's our goal to ensure members get back much more than the price of a subscription. If you want to learn more about the benefits of our premium membership, head over to PeterAtiyaMD.com forward slash subscribe. My guest this week is Professor Belinda Beck. Belinda is a professor of exercise science in the School of Health Science and Social Work at Griffith University in Queensland, Australia. Her research is primarily related to the effects of mechanical loading on bone. In 2015, she established the Bone Clinic to roll out this groundbreaking program of research,

which we discuss in a lot of detail in this podcast. She was the principal investigator of the lift more and lift more M clinical trials, which demonstrated exercise as therapy for osteoporosis and low bone mass. Something I've discussed a lot on the podcast in my conversation with Melinda, we dive into the physiology of bone. It's actually important that you understand how bone works as a tissue. It's easy to think of it as sort of a static tissue, but in fact, it's quite a reactive tissue. We talk about how the foundation is set during childhood and how the remodeling over the course of one's life takes place

based on, of course, activity, nutrition, and hormones. We then talk about what can be done to prevent bone loss as we age. And of course, this begins with what we as parents should be doing to help our kids achieve their genetic potential prior to the fusion of their growth plates. Talk about how to improve your bone health even once you're past the point of your genetic potential, i.e. once you've reached your maximum point in your late teens and early 20s,

and what we can learn from the Liftmore studies in terms of how exercise can help and even reverse bone loss in people in the throes of osteopenia and osteoporosis. So without further delay, please enjoy my very fascinating discussion with Professor Belinda Beck. Hey, Belinda.

Thank you so much for getting up so early in Australia to sit down with me. Would love to be doing this in person, but it's a bit of a hike for you. So, this will more than suffice. I've referenced your work many times before in talking with patients and talking on social media, talking on other podcasts. I've wanted to speak with you for some time because it's one thing to hear me talk about something, but it's I think far better to hear the expert talk about it as opposed to me just paraphrasing. Maybe we'll just spend a second giving folks a little bit of your background. I'll have obviously introduced you already, but tell folks a little bit about how you

came to find your interest in this. Your PhD and postdoc were both done here in the US, correct? Yeah, that's right. And my masters as well, actually. I think we can safely say a lot of people end up in research because of some personal interest and that's exactly the case for me. I was a runner and a field hockey player and I constantly suffered from short shins and nobody could help me.

They couldn't even tell me why I was getting them much less, how to prevent them or make them better. This was back in the day, mind you. So even when I was in high school, I knew that I wanted to find out what was going on. And that's actually where my research started in my master's. I was looking at two-wheel stress injuries. It became clear very, very early that this is a bone injury. This is not what everybody was saying two hours posterior, pulling on the border of that was all bunkum. That was

somebody making a supposition. And that set me down the path of trying to figure out what are the mechanical signals that stimulate bone to adapt to mechanical loading? You know, pursuit of Wolf's Law, why does a change in mechanical loading cause the bone to change shape in this amazing way? And of course, as soon as I discovered bone did that, I was hooked because it is just an incredible tissue. I did an animal study for my PhD and quickly realized that that was not

something I wanted to do for the rest of my life because it involved killing animals constantly. I went to Stanford and did a postdoc, and that's where I learned about clinical trials. Then realized, of course, that osteoporosis is the greatest burden when it comes to bone problems. Being an exercise head, that's something that I wanted to figure out exactly what was the ideal exercise program to assist people living with osteoporosis.

Yeah. Before we started the podcast, we quickly figured out that we overlapped together at Stanford for the entire three years of your postdoc. I was in medical school, which of course, I just get a kick out of knowing the fact that there was probably a day when we were literally in the same cafeteria at the VA or something. Of course, who would have predicted whatever more than 25 years later we're sitting here. I love those coincidences. Let's also talk a little bit about what you're doing today. You're obviously back home. Talk about the clinical practice that you have now and what type of patients you work with and what type of research you're still focused on.

I should clarify I'm not a clinician. I'm an exercise physiologist and I've never had a personal clinical load, although exercise physiology is one of the allied health professions in Australia. I came back to Australia to an academic position and was been teaching anatomy my whole professional career but continued my own research. I'm a professor at Griffith University on the Gold Coast in Queensland. And that's where my career sort of, I guess, triangulated onto this question of, there must be a way to load people who have osteoporosis in such a way that they can grow bone because everybody had been saying we couldn't do that because their bones were so fragile. Now when we did, and I'm sure we'll come back to the actual trials we did that showed that,

after I showed that, I did realize that the exercise, the nature of the exercise was not really safe for just anybody and it needed to be applied in a certain way and very specifically and it needed to be applied by somebody who really knew what they were doing because this is not a program that should be done unsupervised if you're at high risk of fracture. And the only way to do that was to implement it in a clinic. Now, it's hard enough to convince doctors who've been telling patients, osteoporotic patients for years that they should not lift anything heavy, but to tell somebody in a clinic to start doing this exercise, I just knew that was never going to happen. So that's what the bone clinic is.

I set up a clinical facility. It's a translational research facility where we actually implemented the program, but every patient that comes in is a research participant and they agree to share their data. We do the same testing as we did in the Liftmore trial, it's a two and a half hour appointment at baseline and then every year thereafter we test them again with the same thing so that we can see if the exercise program works in the real world. And of course, I added in other things that are really important like diet, and we take care of them.

This is not a clinical trial. We don't have a control group. Now, of course, I've got an enormous amount of data and needing to wade through all of that. Let's start the discussion with a little bit of the physiology of the bone. I think for many people, myself included, people who went to medical school,

we don't, I don't really recall getting much of an education in this. I probably did, but once you choose your specialty, unless it happens to deal with bones, as in orthopedic surgery or rheumatology perhaps, or maybe sports medicine, most of us end up getting far and far away from it. But given the ubiquity of osteopenia and osteoporosis, it really comes back to be in the fore for many physicians even if they aren't trained in it. I think it'll be helpful for everyone, myself included, to go over a little bit of bone physiology. Handle it any way you see fit, but I think we can talk about this in as much depth as you like because we have a pretty sophisticated audience.

Okay. A couple of different ways to look at types of bone, the very basic way to describe them according to their shape, which are completely related to their function, the whole basis of wolf lore, I guess. So you have long bones, like the long bones, the levers in your limbs and your feet and hands. You have short bones like the little lumpy bones in your ankles and wrist. You have irregular bones like your vertebrae and your scapula and so on. All of them are comprised of two basic kinds of bone. One is cortical bone and one is trabecular bone. There are different

words for those cortical or compact bone, trabecular, spongy or cancellous bone. Now, cortical bone is typically the shell of a bone. Every bone has cortical bone on the outside. It might be very thin in the case of vertebral bone or it might be extremely thick as in the shaft of the diaphysis of a femur. Most bones have some degree of trabeculi or trabecula bone in them. If it's a long bone, it's in the ends and if it's a short bone, it fills the whole thing. Like vertebrae of irregular bone, it also fills the whole body of irregular bone. If it's in the skull, it's called diplo and it's sandwiched in between two layers of cortical bone. It also fills the whole body of an irregular bone. If it's in the skull, it's called diplo and

it's sandwiched in between two layers of cortical bone. Ribs even have diplo, they're a flat bone as well. So the very cool thing about the bone tissue itself is the microstructure. So in cortical bone, you have a lamellar structure, so layers and layers of bone, and that occurs because of the way osteoblasts lay down bone. But the really cool thing is the fact that in each adjacent layer, the collagen is laid down almost, not perfectly, perpendicular to each other so that the lamellae combine to create a tissue that is beautifully resistant to torsion as well as the normal loading of compression and tension.

Now in trabecular bone, there are also some lamellae because of the way osteoblasts produce bone. But the really cool thing about trabecular bone, and this is I think probably what Wolf in 1882 spent most of his time trying to describe mathematically, is the arrangement of the trabeculae. So each individual strut is best aligned to the forces that are put on bone. If you look at a cross-section to the proximal femur, you'll see that there's wonderful arches that go away from the head through the neck and down past the greater trochanter. And then from the greater trochanter, there are trabeculae that come from the surface of the trochanter and arch down to the other side and over towards the lesser

trochanter. So you get this interconnection of bone that is beautifully arranged to best withstand the bending load that you will get from the opposition of the weight of the body on the head of the bone and the ground reaction force coming up, the diaphysis. That repeats itself throughout the body. If you look at any part of the body where trabeculae are, they are just aligned in response to the forces. Of course, that's one of the things that will change

if you change the nature of the loading. You've mentioned Wolf's Law a couple of times, probably worth stating it and explaining its relevance to bone. It has been paraphrased over the years, and I don't think there's any harm in that, to mean that bone will adapt to the nature of loading to which it is chronically exposed and the purpose being that it's best adapted to withstand forces to prevent fracture. In actual fact, I couldn't recount what his actual law is because he was a mathematician and he was trying to describe this mathematically. We've taken that

notion and just encapsulated it into that law of bone adaptation in response to loading. Now, is there a built-in assumption to Wolff's law that that adaptation can only happen in the setting of certain physiologic parameters being met. So for example, sufficient calcium, healthy osteoblasts, absence of certain disease pathology, or is this truly a universal law that is indeed axiomatic? I don't think anybody knows the answer to that for sure, but I would be willing to stake my first born on, don't tell her that this just occurs. This is something that happens as sand running out of your fingers falls to the ground because of gravity. This is how bone reacts to loading. It's a physical phenomenon.

Okay. You've also alluded to osteoblasts, so maybe talk a little bit about the difference between an osteoblast and an osteoclast, how this mineral makes its way to the bone. What does this look like as a child is born? Maybe even start at birth and talk about what the bones are like in that fetus and how they develop over the ensuing two decades. Well, going right back, we start as a little cartilaginous model of a skeleton and even by eight weeks, we have that model in that tiny little bean and that is progressively mineralized as it becomes skeleton. There are two different ways really of ossification, but the primary one is endochondral. Once a baby is born, they have ossified the long bones and quite a portion of their skull

bones and most of the other bones that are around organs. Just for folks listening, ossified is this process of putting mineral into the cartilage and turning it from soft into hard. That's right. I think we talk about ossification when bone cells invade the cartilage and turning it from soft into hard. That's right. I think we talk about ossification when bone cells invade the cartilage. Once there's a bone cell in there, it's considered to be ossified because they start to excrete osteoid, which then becomes mineralized. So yeah, that's right. There's a whole process of endocrine ossification. So babies are not born, obviously, fully ossified. They have still

little cartilaginous hands and feet and they have lots of cartilage to different degrees in their skull bones and those continue to ossify throughout life. And I think in fact, some of our growth plates don't even fuse until particularly in men until they're about 25 years old. But largely, most of your bones are fully formed and have bone in them by the time you're two. And that's coinciding with when you're really starting to run around and load the skeleton. The skeleton then continues to grow throughout the first two decades with the vast majority of growth happening when you're very little, little toddlers, but primarily during puberty. And that's what we all know as the

growth spurt. And that's happening because your bones are growing like crazy. That begins to slow for that growth spurt happens earlier in girls, probably about 12, probably about 13, 14 in boys. And it slows, probably is ending around about 18 in girls, can be as late as 25 in boys. And once you have reached your peak bone growth there, your epiphysis have joined to your diaphysis, so the growth plates have fused. You're not going to grow anymore. And you almost certainly have all the bone that you're ever going to have. So there's definitely a making hay while the sun shines mantra of those of us who work in the world of osteoporosis because childhood is so incredibly important. People often call osteoporosis a childhood disease. The goal is to get as much bone as you possibly can. That's limited by your genetics. We can come

back and talk about that if you want, but you do have a blueprint that you will achieve, but you want to optimize that, get as much of that genetic capacity as you have. I just want to repeat that point, Melinda, because it's actually quite profound and I want to make sure nobody missed it. He said osteoporosis is a childhood disease. Now what you meant by that, of course, is based on what you said just prior to that, which is you will reach your maximum bone potential by the time your growth plates fuse, which again, for most people is probably late teens, maybe in the case of men, early

twenties. In that sense, it's sort of like a glider. It's sort of like saying this glider will reach its maximum altitude 20 years into your 80 or 90 year life and you better get it really, really high because the best we can do is reduce the rate at which it declines, but we're not going to get it higher than it was at that point. We're going to get into a whole bunch of nuance, I'm sure later on, because I think what you're going to tell us is that actually we can maybe even change the elevation of the glider later on in these patients with osteoporosis. But I think there's no denying this idea that anybody listening to this who's thinking about

osteoporosis for themselves should also be thinking about it for their kids and asking the question, what are my 10 year olds, 12 year olds, 15 year olds doing today to reach their genetic potential? Yeah. It's one of the strongest messages. I speak mainly to older people and I say, the horse may have bolted for you, but you have children and grandchildren and this should be your mantra. Get them outside and active every single day and doing XYZ

bone-friendly activities. I should say, you know, we talk about pig bone mass being achieved and we use the word the end of the second decade because that's the average between men and women. It can creep up a little bit, but most nobody is growing anymore bone after age 30 and most people are well and truly done by then. So yes, I'm probably giving a somewhat old fashioned view of this because as you say, I do believe that there is capacity to get the glider hired later in life. But I guess the concept is you're not going to grow bone anymore.

You're not going to grow the length of bone anymore. So it becomes a lot more difficult. And the other message that is extremely important is that genes determine it's been 70 to 80 percent of the bone that you're going to have. So to a certain extent, you're working within some reasonably tight bounds. You only have to look at your parents and grandparents to get an idea of what your risk is like. If they are very osteoporotic, then your risk is also very high. I think you said 60 to 70 or did you say 70 to 80%? I know it was a high range you gave there.

It does depend on who you read, but I sort of have settled on the 70 to 80%. I think that there is certainly evidence to say that's the case, that there are twin studies and so on. Sorry, that's bone density. Obviously bone length is highly heritable, just as height is very heritable and it's determined by bone length. But you're also referring to bone density by referencing osteoporosis, correct? Yeah, I suppose. I mean, I probably prefer to use the word bone mass. The trouble is we measure it by bone density using a bone spectrometer. That is our proxy for bone mass because the only way

to measure bone mass is to actually ash the bone and you can't do that in a living person. So yeah, again, bone has been variously measured throughout the decades. BMD is the most common way to do it. And if you look at BMD plots, you'll see this very obvious, I'll do this in reverse, growth in childhood and then a flattening, pretty much a plateauing and then a gradual loss. And that flattening, plateauing or timing of loss, that is also, I believe, genetic and individual, but that's the thing that is most amenable to exercise intervention.

So somebody might have genes that allows them to get a peak bone mass of a certain amount that is the same as their neighbor, but because the rate of loss is different and their level of activity is different, they may lose more quickly. And then you throw in menopause, you know, average age about 52 to 54 or something. For women, you'll see that loss rapidly accelerate for probably five to eight years. This is because circulating estrogen almost vanishes from your blood and estrogen is an incredibly important hormone for bone because I don't think I came back to talking about bone cells. I should probably do that because of its effect on osteoclasts. It largely inhibits osteoclasts, keeps a check on them and prevents them from over absorbing. So while I'm on those cells, yes, there are a number of different

cells in bone. The two primary, well, the main one is an osteocyte. That's your standard bone cell that sits in bone tissue in its little cave and it is responsible for maintaining the tissue around it and also for sensing what's going on in the tissue environment. We can talk about that a bit more later. But osteoblasts, osteocyte precursors, and they are the ones that when they attach to a bone surface, they exude osteoid, which is the new bone tissue, which then becomes mineralized.

So they're the bone forming cells. Osteoclasts are these big multinucleated cells that also attach to bone surfaces and resorb bone in packets. And this is really important. This is not a bad thing. Bone remodeling is one of the most important ways that we maintain our skeleton, get rid of micro damage, and also adapt to mechanical loading. Resorption formation is happening throughout our life.

It is the way that we release calcium into the blood for when we need it for all those other things we need calcium for. It's extremely important. The trouble is estrogen does help to contain those osteoclasts when it disappears from the blood. Osteoclasts have a little bit of a party for a few years and resolve bone like crazy. And so that explains why in women, at menopause, we have to experience this dramatic loss of bone for a period of years. Then it levels out again and sort of matches men. But you can see why more men than women are fracturing with osteoporosis because firstly, we don't gain as much peak bone mass. Meaning more women fracture than men.

That's right. But in sort of in our 20s, we don't have as much bone as men and then we lose more throughout life. So by the end of life, there's this greater disparity and then add onto that women fall more than men in later life. And so you've got this perfect storm of this is why more women than men are affected by osteoporosis and fracture. And do we believe that women fall more because of a greater prevalence of sarcopenia? Yeah, it's a hard question.

I would say probably yes. Well, there's a reasonable amount of evidence to show that women are less active throughout their life and when they're older. Not that older men are particularly active these days either, but I suppose because men genetically have more bone and muscle to begin with, they've started from a higher place. So yes, a very frail old woman has not just not very much muscle, but not strong muscle, not very functional muscle. Their balance, the whole sort of neuromuscular package, if you like, has deteriorated to the extent that if the balance is perturbed,

they will struggle to regain their balance before they fall. Again, there's a lot there so we'll just summarize it quickly. Basically, oversimplifying a little bit, we have osteoblasts and osteoclasts that live in early in life. The balance probably favors the osteoblast. You're adding more bone than you're subtracting. We get into an equilibrium where there's a remodeling that's constantly occurring. And the bone acts in this sense as a reservoir also for something like calcium. And so, you're having rebuilding and remodeling. If there's damage to a bone, obviously if you get shin splints, there has to be some healing that goes on.

All of these things take place. Obviously if there's a need for calcium, more of it comes out of the bone, et cetera. Then we get into this state of decline where maybe the osteoclasts start winning. In women, this is really amplified in the five to eight years following menopause when the most important hormone for bone preservation, estrogen, is taken away. Estrogen being the thing that keeps osteoclasts in check is now gone. To your description, the osteoclasts have a party now. Now they really get to run amok.

Women experience a disproportionate loss of bone mass compared to men who are also in a state of decline. Because by the way, men's estrogen levels are also declining because they're tethered to their testosterone levels. So as testosterone goes down, so does aromatized estrogen and it goes down with it. And then they both sort of end up on the same parallel path again, but the women are considerably lower because they've had that accelerated loss. There's one thing I would just add in. I feel like I have to say this because I drum it into my students' heads

when I'm teaching bone growth is that the skeleton actually grows via cartilaginous proliferation and it's replaced by bone. So the osteoblasts aren't causing the growth of bone. They're just- They're just solidifying it. That's right. They're replacing the cartilaginous tissue with bone tissue, yeah.

Yeah, got it. Okay, so let's talk a little bit about the preventive medicine side of this. So before we even get into the work that you're mainly focusing on, which is on taking people who are at risk for osteoporosis and maybe holding them back from that or taking people who are in osteoporosis, let's first address the question for the parents who are listening, because contrary to popular belief, we do not have a huge teenage audience to this podcast.

For reasons I don't understand, my daughter just hasn't found this podcast interesting in her little 16-year-old self. What can I be doing to ensure that my 7-year-old, 10-year-old, and 16-year-old are set up for the best life possible when it comes to bone health? Given that I've already given them something pretty good. Fortunately, knock on wood, my wife and I both have pretty high bone density, at least as measured by a DEXA scan. I'd like to talk about how valid or how we could be misled by that if the case. From a genetic standpoint, they're not set up on the back foot, but I want to make sure that we're going above and beyond

what needs to be considered for us from a nutrition perspective, from an exercise perspective, from any other lifestyle perspective to allow our kids to reach their genetic potential. Well, let's start with the low-hanging fruit, which is diet. Anybody could argue that a balanced diet is important for everything to be healthy.

You need all the nutrients that we've known about for years. And the same can be said for bone. That means particularly, and there are some minutiae, but the most important one obviously is calcium. The amount that you need throughout your life does vary, but by the time you're a teenager, you probably need about a thousand milligrams a day of calcium and you need the vitamin D to go with that. Otherwise, you can't absorb it from your gut. So making sure dairy is by far the most abundant source of calcium, it's most bioavailable, meaning it's most readily absorbed. It's packed with calcium. You can get most of what you need each day from, well, let's say a regular glass of milk. So 250 mls, that has 300 milligrams of calcium. So if you had three of those, you'd basically be getting what you needed. Not too many people are drinking that amount of milk, although I suppose the number of bowls of cereal my son eats could possibly be approaching that number. But there are

sources, you know, cheese and yogurt. And then there's the discretionary foods. If you eat a lot of ice cream and cream and that sort of thing, you can get from there as well. But we would say yogurt and cheese and milk are the best sources. I mean, 750 ml of milk or milk equivalent is probably less than most kids are consuming. Yeah, I would say so, particularly as they move into their teenage years and probably getting more conscious about weight and are thinking that they might be drinking diet soda instead of a milk drink. And it doesn't matter what the fat content of the milk is, I assume.

I mean, for the vitamin D it probably does, but does it matter for the calcium? Well, low-fat milk actually does have more calcium in it, just by virtue of the fact that if you take the fat out, you can fit more calcium in it. You have more volume. And plus you can buy fortified milk. We have Physi-Cal in Australia, which has more calcium in it, and I'm certain you guys fortify a lot of your foods. And I believe you do put vitamin D in your milk. So it's nice to get both. But by far,

the easiest way to get vitamin D is the sun and converting it in the skin. We, in particular, Australia, we are white people living in a black people's country. We have a very high rate of skin cancer here. Sun is extremely strong. So we're quite scared of the sun. We cover up, we slather ourselves in sunscreen, hats, sunglasses, the whole bit. And to the extent that we've actually set ourselves up to have vitamin D deficiency,

and particularly in Tasmania, very south, there's a high prevalence of vitamin D deficiency. So it's important to figure out when is a safe time to be in the sun and ensure that you get a little bit of sun because it is by far the most efficient way to get your vitamin D. Never go even close to getting sunburned, but you don't have to get sunburned. In Australia, we should be able to get our vitamin D requirement before 10 a.m. and after 2, possibly a little later if you're in a really hot area. In Hobart in Tasmania in the middle of winter, you would need to stand shirtless for an hour

in the sun to get what you needed. So then you've got to start thinking possibly about supplementation. What level matters? I don't think any of my kids have ever had a vitamin D level checked, although in an adult we do this all the time. Is there a level beneath which you would say we've got to be supplementing you if you can't do better than this with sunlight? The problem with vitamin D is that nobody can agree. There are two schools of thought, there are two levels that have been published and people will

die in a ditch over those. If you've got smart people feeling that strongly about two different levels, it tells me that nobody really knows. What are the two levels that people are dying over? 30 is probably one of them, right? 30 seems to be one of the cutoffs. 30 is, I believe is the deficiency cutoff, 30 nanograms per milliliter. And 50 is considered sufficient.

So in between that you would have insufficiency, but other people say it's 75. So because this isn't really my area, I don't want to go out on limb and say which is which, they're easily searchable. There's been a lot of research done. Probably it's dropped off a little now as we've discovered that hyperdosing with vitamin D is not safe and increases falls. To get somebody's vitamin D up quickly, you have to hyperdose. So people have sort have moved away from vitamin D as a strategy to prevent osteoporosis. It's really important that you try to encourage people to be sufficient and so possibly they will need a supplement of a certain dose. That's going to depend on the person

and all manner of other things. Most people are going to require a supplement the things. Most people are going to require a supplement to be above 50. I do. I live in Texas and our sun is a lot like yours and I'm in the sun every single day. I don't even put sunscreen on anything but my face. My arms and legs, I'm not shirtless usually, but my arms and legs are constantly exposed. And I think if I'm not supplementing vitamin D, I'm lucky to be above 40. I do supplement with 5,000 IU daily and that takes me to 50 to 60, which again suggests I'm probably okay, but it's not uncommon here in the U S to see people unsupplemented easily being in the thirties. That's not uncommon here in the US to see people unsupplemented, easily being in the 30s.

That's not uncommon. Was there a reason that you started supplementing? Did you have any symptoms? Oh, none whatsoever. I literally supplement for no apparent reason other than some loosely held belief that I'm going to be better off at 55 than 35. It's more the precautionary principle. It's more that I haven't found any compelling evidence that I'm worse off at that level

and there may be benefits to it. I don't feel immensely strongly about it, but again, I'm thinking about this through the lens of children where I would worry more about supplementing a kid because it's harder to measure vitamin D levels in them. You don't want to go and poke them for blood all the time. You would hope you could get it all from milk, dairy, and sunlight. I guess would be my point. Yeah, that would be my recommendation. The other thing is too, vitamin D assays are notoriously You know, the other thing is too vitamin D assays are notoriously dodgy. So from one to the next, you may not get the same results.

So I don't know, I've never had my measured. I track my bones to make sure they're doing okay. And that's how I choose to manage it. And I think, as you say, it's just going to have to be whatever your tolerance, whatever your belief is. It's pretty much get as much education as you can and probably follow the guidelines that make the most sense to you. Oh boy. Okay. So we got calcium, which I think based on that, what you said earlier, I think most people are going to struggle to get that much in without being deliberate. So that's something we have to pay attention to. Sunlightlight. Then of course, with sunlight probably comes another very important part of it,

which is if you're getting sunlight, you're outside. If you're outside, hopefully you're playing. If you're playing, you're hopefully doing something good for the bones. Do you ever get asked the question, hey, are there certain sports that are going to be better than other sports? Is running better than swimming? Is weight training okay for teenagers or even younger? When do we start thinking about at least doing pushups and things like that that might also put a little bit more into it? Jumping sports versus non-jumping sports, how do you think through all that stuff? You've hit the nail on the head.

It absolutely is extremely important, the type of loading you're doing for bone. If we're talking about heart, lungs, mental health, metabolism, virtually anything is better than nothing. In fact, anything is better than nothing for bone too. But if you really want to make a difference, get most bang for your buck, then you absolutely are looking for high load activities. And they include things that include jumping and landing and strong muscle movements. The other thing that is probably important is variety and variety within the sport and

across sports. So, we do tend to find that runners, for example, who have only ever run less protected from bone stress injuries in their running career than people who grew up playing basketball and volleyball and tennis and running. So that variety, if we come back to Wolf's Law, has probably made the bones adapt in a more robust shape to make them more resistant to loading in all manner of ways and also to loading in one direction. So my recommendation to parents is aside from giving your kids the building blocks being enough calcium and exposure of IMD every day, then use those building blocks by getting

them outside every day. I mean, I know the guidelines don't necessarily say every day, but every day is what you're aiming for because if you tell people every day, then you may get four days a week. And of that exercise, you want it to be as vigorous as possible. Swimming isn't going to do it. Walking isn't going to do it. You need something that is just much more dynamic, varied, and will impart a high strain on bone and a strain is a measure of deformation. So you're trying to make those bones bend because it's the bending that is coming

back to my PhD and what I was trying to solve, it's the bending that is actually forming the stimulus to stimulate bone adaptation. So a couple things there. Swimming and walking, obviously both have enormous benefits, especially swimming. But again, you're in a zero, not a zero G environment, but a very low G environment that couldn't have less bone loading. The other, I think, very important takeaway there is, and it's funny because I remember seeing a study that looked at this and being a little surprised initially, but I think based on what you're saying, it makes a lot more sense. The study basically showed that runners

didn't have particularly great immunity from osteopenia and osteoporosis. And I remember at first thinking, God, how is that? They're loading so much. But your point is, if you're just running, you're just adapting to one very, not simple, but repeatable movement in one direction. Whereas if you're

playing soccer or basketball, now you're not just running, you do run, but then you move laterally, you move backwards, you jump. There's more force because you sprint. So all of those things taken together make a bigger difference in creating the variety that you talked about within the sport and then across the sports if you play more than one. Yeah, absolutely. There was a study done at Stanford in 92, well, it was published in 92 by a friend of mine actually, who looked at the Stanford varsity athletes and compared them to sedentary controls of Stanford students who weren't doing anything.

It was really interesting to see that if you compared swimmers, cyclists, runners, and gymnasts to these sedentary controls, on the scale of bone mineral density, swimmers were lowest. Then I believe cyclists were the same as sedentary controls because they're also in a weight-supported activity. Runners were slightly higher and gymnasts were off the scale. Now, this was an observational trial. It's subject to all of those selection biases, observational trials, not trial, it was a study that are subject to, for example, you're likely to have people who are lighter, so they have lighter bones who are good at swimming because they float better, so it makes them faster.

So there's that bias, they may already have had lighter bones. But on the other hand, at that time, I think they were doing about six hours of training a day in the pool and that was actually unloading their bones. So it's amazing to me because the muscle loads that are occurring during, imagine swimming 50 meters of butterfly, you know there's some big muscle forces, but it's not enough. It's weight bearing loading that is important and we know this because of how much bone people lose if they go into microgravity. So it was swimming, sedentary, runners, and gymnasts in that study? Cyclists too, I believe.

And they're the ones who were the same as the sedentary control. So I don't want anybody to take home that any of these activities are bad. They're great for virtually every other tissue. It's just that swimming and cycling and even running are not going to markedly increase your biomass. The comment about running, when we go for a run, it feels like we're pounding the pavement,

but actually the loads you're putting on your body are not that great, and particularly runners that we would consider to have good technique who are running quite lightly. Yeah, their feet are actually dissipating a lot of the load. The connective tissue in the feet and the muscles within the feet are really a big part of the shock absorption there.

Well, that's how we evolved, you know, with these amazing arches and, but also remember, when you land, your ankle is either flexion extension are weird at the ankle, but, and your knees will flex when you land and your hip as well. So you've got all this shock absorption the whole way up. So that is dissipating the load. The same thing does happen.

You do dissipate loads in gymnastics, but when you watch those Olympic gymnasts do their tumbling runs and they land from one of those crazy tumbles, boom, on the floor, they are loading their bones like crazy. So not only are they getting these enormous forces that are stimulatory to bone, but again, this cell selection effect of gymnast, the ones who had bones like iron to begin with probably were able to remain in the sport because they weren't getting injured. So there is that observational study, there are obviously caveats with the outcomes, but I do think there are lessons to be learned from it.

Yeah. There's another study I saw that expanded that and added other sports to the mix. The other sports I remember it talked about that were also very, very high were football, meaning American football, jujitsu, and powerlifting. Again, my take on that is, powerlifting is really obvious. It's the definition of literally lifting the heaviest weight imaginable. Football has the confounder that if you play football, you're also lifting weights. It's probably just as much to do with how much weight training goes into playing American football as opposed to the actual Act of playing football itself. I would argue that that has benefits from a bone perspective We could certainly talk about the disadvantages it has as well And then jujitsu is interesting in that not doing it myself

But two of my three kids do it and so certainly spend a lot of time watching it at tournaments at myself, but two of my three kids do it. And so certainly spend a lot of time watching it at tournaments, but again, a lot of force being put on bones. There is a lot of bone deformation in jujitsu just based on how hard they're tugging and contorting and stuff like that. To me, the big takeaway here is not that we should look at the sports that do the most for bone density

and say that's what we need to do. We should ask the question what is it about that sport that's doing so much for bone density and how can we replicate that because of course you could also argue that most gymnasts I assume have quite a lot of problems orthopedically later in life just based on the nature of the sport. Again the question is how do we reproduce it? Fortunately, I would say that a lot of athletes today, such as runners and cyclists and swimmers, are probably spending more time in the weight room today than they were in 1992. The early 90s was really an era when swimming was six hours in the water, everyday sport thing. I think today they're spending actually a little less time in the water and they're

probably spending more time on dry land. My guess is if that study were repeated today, I wouldn't be surprised if we found some improvements in the ultra endurance athletes. The takeaway as a parent is diversity of sport and load bearing. A hundred percent. I think because my other area of research is bone stress injuries, I do talk to coaches of swimmers and that's exactly the advice we give.

Get them out of the pool, get them cross training and get them lifting weights. You did ask just before, you mentioned what are the benefits and how early should we get kids doing weight training? And for years, people were very scared of that and they go, no, you'll stunt their growth. Yeah. And there is no evidence of that. And I don't know where that even came from. I mean, people talk about, Oh, you'll compress their growth plates. Why? That doesn't make any sense. It just takes a lot to do that.

I'm not necessarily saying that you should be loading kids up with enormous weights. There's no need for that. But there is certainly nothing to suggest that you shouldn't do resistance training when you're a kid. I would say the only reason that you wouldn't do it is if they didn't like it because the thing you don't want to do is discourage a child from being active throughout their life. So the best thing you can possibly do is whatever that child loves to do. And then if that happens to be something that doesn't include particularly bone loading, then just try and add that stuff in.

Don't force it down their throat. Otherwise it's very counterproductive as those of us with children know. I'm really glad you brought that up. I was going to ask you and I got a little distracted, but I think this is one of those myths that just drives me bananas. We've looked, I mean, we have tried and tried and tried to find the evidence that suggests that kids can't lift weights and we're coming up empty. We're just coming up empty. So hopefully folks listening to this are also

realizing and I think as a parent the easiest thing you can do, especially if you have some equipment at home that you can use to exercise is just have your kids come in the gym with you when you're lifting weights. That's what we do and never once have I said to my kids, I want you to lift weights. It's just, hey, we're going to go in the gym and I'm going to lift weights and you can do whatever you want. And look, there's not much else to do in the gym. They're going to start picking stuff up. They're going to start copying you. So anyway, I think it's helpful. It's a great opportunity to teach them technique because that's what's going to mess people up, not just kids, if they're not doing it right. You don't want a kid just going

over and trying to do a deadlift and not doing it right. So there's your opportunity. Teach them from a young age, do a beautiful deadlift. There is one of the most useful exercises they can do their entire life. Yeah. I'm glad to hear you say that because my little boys are so competitive with doing kettlebell deadlifts. Now I have to hold them back because as you know, once they start to try to go really heavy, their technique actually breaks down a little bit.

Let's talk about another sensitive area with kids that I'm sure you get asked about a lot, which is invariably some kids will have asthma or they'll have other conditions that require the use of corticosteroids either inhaled or systemic. I know that we see this in our practice when adults come in and we're surprised to see in an otherwise healthy person, astonishingly low bone density. And of course, through our history, we realize, Oh, you took prednisone for this many years of your life. So I know that nobody out there, no physician out there, no parent out there takes it lightly.

But is there any guidance you can provide as far as the minimum effective dose or maybe is there some comfort you can provide to a parent that says, hey, an inhaler for asthma used at this frequency is not going to impact the long-term bone health of a child. There's no evidence, because we haven't got long-term data, as far as I'm aware, and again, not really my area. All I can say is corticosteroids should be minimized as much as possible throughout the whole life.

If anybody, child or adult, is able to manage their asthma just with Ventolin, which doesn't seem to have any negative effect on bone, that is what I would be recommending. Try to stay off steroid inhalers if you possibly can. If you're on high doses, try to titrate them down. See if you can manage in other ways. I don't want to terrify people, but really this is abundantly clear that corticosteroids are the enemy of bone and the longer you're on them, the more damage they do. They're life-saving for some people. So you have to go on them and then

just get off them as quickly as you can once your respiratory condition has calmed down. And of course, if you are in a situation where you must take them and add high doses, then you absolutely would probably need to, absolutely probably, you would really need to consider some biomedication to counteract that. That's what I would be recommending for adults. Maybe the lesson here for parents again is if your child requires being on corticosteroids, well presumably they really require them. I don't think any doctor takes that decision lightly. But it might just mean that's all the more reason to double down on the other things we talked about, which is if your child is on corticosteroids for a medical need, then let's make sure that

that's the kid that's getting 750 ml or 24 ounces of milk a day and they're out in the sun every day and they're lifting weights and they're doing diverse sports. Because again, let's take everything else and stack it in their favor so that when they come to see their doctor in their 40s, the doctor will on the one hand realize, oh, you were on steroids as a kid, but hey, lo and behold, your bone density is actually okay. You haven't been as impacted by it as possible. Are children more susceptible to corticosteroids because they're in a developmental phase or are adults equally susceptible? In other words, does it affect

kids more because it's affecting them on the way up or does it affect adults equally because it has just as much of a down impact on them in the maintenance phase? That would be very much stepping out of my lane to answer that one. I don't know the answer to it. All I know is they're bad at any age. Okay. We've got a pretty good primer on what parents need to be thinking about with kids. So now let's turn it back over to the adults. So we're talking about men and women in their thirties and forties. So for most women, they're still on the positive side of estrogen balance. Beyond what we just said for kids,

is there anything you would add to that as important tools as a person enters middle life? It's actually exactly the same. You've got to maintain your diet and levels of exercise because your bones need those two elements to maintain. So in the old days, I'm sure you can picture in your head the trajectory of bone growth, plateauing and loss. And the mantra was, this is inevitable. That's what bone aging looks like. For years, I've been saying, that's what sedentary behavior looks like. That's what

the sedentary effect on a skeleton is. I believe that if you maintain your levels or increased your levels of physical activity, friendly bone loading from the time you were 20 until the time you died, I would be willing to bet that you could go a long way towards maintaining that plateau. The master's athletes data seems to support that. If you look at those data, you'll see that BMD is maintained in master's athletes as long as they're maintaining their activity. There may be a slight loss, yes, but that's probably because the loads that they're able

to produce in their physical performance also reduce. But this is an atrophy effect. This is not a genetically programmed aging effect. And I know that there are many people around the world who would argue with me because I don't have much data aside from the master's athletes long-term data. But it's almost impossible to collect those data because those are lifelong studies and I would be dead before the study would be finished if I started it now. This is a very provocative idea, but I'll give you an example of where there are two

arguments I would offer that suggest you could be right. The first is when you look at spontaneous activity and movement of people as they age, you see a very similar pattern, which is a relative plateau preservation of not just activity but lean mass followed by a deterioration suggesting that as lean mass goes down, movement goes down, activity goes down, and then it feeds back on itself. It becomes a vicious cycle and away you go. So again, as you said, it could be that what we see as a quote unquote physiologic decline of bone loss is not that, it's rather a proxy for muscle loss and reduced activity. The second point I would argue again in favor of this hypothesis is something that Luke Van Loon, I don't know if you know Luke, but he's a

protein scientist and I had him on the podcast recently and he shared something that I thought was fascinating. I've always taken it as a given that anabolic resistance occurs due to aging because of course we see it clearly with aging, but he discussed some studies that demonstrated that anabolic resistance was most exacerbated by inactivity. This was done on the CAST study. You take a given individual, you cast one leg, not the other leg. Before you do that, you run the amino acid isotopes through them. You do this exercise for two weeks.

You take the CAST off, so you have an atrophied leg and a normal leg. You do the same amino acid isotopes and low and behold, there's like 40% or 50% anabolic resistance on the leg that was in the cast. This is not because they got older in two weeks. It's because they were inactive and they lost muscle activity. If that's true, it really suggests that we shouldn't accept anabolic resistance as an inevitability of aging. I'm quite inclined to think your hypothesis could be correct here, which is if you just don't stop the movement, if you just don't stop the exercise, this decline of BMD might be far better than what the actuarial data predict based on sedentary behavior.

I 100% agree with you. It sounds like a village people song. Don't stop the movement. You only have to look at those beautiful studies that have shown MRIs of master's athletes' calves compared with an age matched person who's not active. This is also compared with a young person's calf. The young and the masters look identical. The muscle volume and quality, there's no fatty infiltration and the sub-Q fat is virtually

non-existent. Whereas you look at somebody the same age as the master's athlete who's not active and you've got this shrunken down little sarcopenic muscle belly, the fatty infiltration and a big wad of sub-Q fat. You could select anybody from the population and you could make the data look like what you want it to by comparison of those age groups, although the same age. But the appearance of that master's athlete muscle, essentially, it confirms what you and I are both saying.

This is a sedentary problem. This is not an age problem. And of course, this comes back to the problem with a lot of people will say, well, who cares? I know that 60% of the population will not do enough physical activity to maintain that. So we need to invent drugs or do the same thing. As far as I can tell, I never say never, but I think we will struggle to ever find a drug that will be able to replicate the action of exercise, physical loading on muscle and bone because you can't replicate the stimulus.

And, you know, any drug that is found to work probably will still need exercise for it to manifest its benefits. Yeah. And there's another deeper issue there because as you know, and maybe the listeners as well, there is an enormous interest from a pharmaceutical standpoint in antisarcopenic drugs. As it stands today, obviously we have anabolic steroids and they're very efficacious, but they require the training stimulus, as you pointed out. You can give a person all of the testosterone in the world, but if they don't

train, they have zero benefit, virtually zero benefit, you know, slight benefit. And of course, the holy grail is can we give agents that can cause muscle growth even absent the profound training stimulus that is needed in other regards? I always say, well, the answer is maybe, but will it be functional muscle? To that extent, will it be functional bone? Even if a drug like Bima or an IGF-1 agonist or some of these other drugs or molecules that are being touted potentially increase muscle size. It's not clear that they're going to increase strength, function, and bony composition. So yeah, it's just the nature I think of our species. We really love shortcuts.

We do. If we can take a pill, why would you expend any effort? And that's unfortunately the gene which is going to be our undoing in terms of healthy aging. Right. That actually got us very far when resources were scarce. That was a very, very helpful gene in a resource scarce environment. Let's talk a little bit now about this menopausal transition. It's right up there with death and taxes in terms of inevitability. It's an area that I have become intensely interested in because I view it as one of the great tragedies of the past 25 years is this very popular study done the Women's Health Initiative, which was published in the early part of this century and really came to, in my view, a very erroneous conclusion, which basically

scared an entire generation of physicians and women away from HRT. As a result of that, not only has there been an unnecessary abundance of symptoms associated with menopause, but I think the real hidden tragedy has been the larger epidemic of osteopenia and osteoporosis in a group of women who may have otherwise received estrogen as they went through menopause. I know that your area of expertise is not in the hormone side as abundantly as it is on the training side, but is there anything on the hormone side that you want to talk about beyond what we've already discussed, which is the important physiology, the important

role estrogen plays specifically in managing the role of osteoclasts in bone remodeling. I assume that most of the women and men, presumably the women of course, for the purpose of this discussion, that are coming into this clinic, are they mostly postmenopausal? Yeah, the majority would be post. We have thousands of people on the books, that number of people who are not post-menopausal is still substantial. So I think the years that we've been open and we've been open almost exactly nine years now, an awareness has grown in the community about us. People who are not post-menopausal but are aware that either they have low bone mass already or that mum or dad or granny

or grandpa had low bone mass, they want to prevent it. So, this is one of the happiest things that has happened that people are realizing that pre-menopause is the time to start taking care of this issue. So, we do have a proportion, but of course, most people don't have any idea what their bone health is like until they either have a first fracture or they go through menopause and they have a savvy enough GP who says, we need to get your baseline dexa. Let's get you started. And all of a sudden, yikes, I have either osteopenia or osteoporosis. Away you go to the bone clinic. You said something very important there, which you and I take for granted. I think it's very important to reiterate for the listeners, for the female listeners in

particular, which is you don't want to wait until you're into menopause to replace estrogen. You have to do it during the pre and perimenopausal stage to get the maximum effect. And again, this is something that I think not enough women are being educated on. As such, even if they know, oh yeah, I've heard that estrogen matters and this might be a reason for me to consider HRT as part of my decision matrix, they might think, well, let me go through these two miserable years of perimenopause, wait till I'm completely amenorrheic, my estradiol levels are unmeasurable and my FSH is through the roof and now we should start doing it. No, it turns out that there are data that suggests that they've actually lost quite

a bit of bone up until that point, which again to me is, it's so preventable. I hope that women listening to this are sitting with doctors who can help them through that transition. I'm sure many people listening to us have had a DEXA scan. When you get a DEXA scan, let's put aside the body composition part of it where you see body fat and lean mass. Sometimes when you get a DEXA scan, it shows you total bone density and it says your total bone density Z score is this and your T score is that. It doesn't give any segmental information. It doesn't tell you about the lumbar spine or the hips or the femurs or anything like

that. If you look closely, it might even give you a number in grams per centimeter squared as an actual number. Do you want to just help people make sense of what all those numbers mean? Why, for example, is it grams per centimeter squared, not grams per centimeter cubed as a density? Maybe explain to people the difference between their Z-scores and their T-scores, and if anything can be understood from the total body Z score and T score or if we must be looking at segmental.

I know there's a lot in there but have at it. Okay. So dual energy X-ray absorbed geometry is a low dose radiation tool, much lower dose than a X-ray of your chest where the name describes what it's doing. It's sending two energies through the body in a way to determine the density of the tissue it's going through. Now it is a misnomer.

It is an aerial density, which is a contradiction because it is a planar view. The x-ray source is underneath, and you lie on the bed and the detector is in the arm above and it is a projected image of this two-dimensional density. They call it aerial bone mineral density because without going into too much detail, and I may screw it up not being a medical physicist, the method of measuring is looking at what is detected according to the density of the

material. So it's not volumetric at all. If you want a volumetric density, you have to look at a three-dimensional method of measuring. So you can also get bone mineral content and area from the same scan and they derive from this density measure. So they talk about it in grams per centimeter squared because it's an aerial measure. So the answer to the question about total BMD, bone neural density, that is the amount of bone that you're observing from a whole body scan.

And normally if your doctor wants to know if you have osteopenia or osteoporosis, they will send you to the radiology clinic and they will do a standard spine and hip scan. They're the normal ones from which you would diagnose those conditions, not a whole body scan. The only reason you would do a whole body scan is if like us, we want to look at body composition because we're interested in lean mass. I wouldn't use the value, the BMD value that I get from the total scan as a marker or as any index for osteopenia or osteoporosis because the WHO definition was actually based at the hip. In fact, it was based on femoral neck. We've moved away from looking at femoral neck as the standard and we look at total hip now because it can be quite a

bit of variation of femoral neck because of the way that you analyze it. So osteoporosis should be really diagnosed from hip BMD according to the definition of the World Health Organization was that a T score of minus 2.5 is definitive osteoporosis, but the T score between minus 1 and minus 2.5 is osteopenia or low bone mass. Now that's essentially a T score is a standard deviation. So what is that compared to? Your value is compared to a reference database and the T score is actually comparing your score to what they call a young normal.

It depends on the site and that does vary, but let's just say it is roughly a 20-year-old between 20 and 30 of the same race and sex. So a 52 year old woman is going, let's say a 52 year old white woman, her value, her BMD value is going to be compared to the average BMD value of a white woman age 20. That's the T score. The Z score is comparing your value to someone the same age and sex, so

compared to the average BMD of a 52-year-old white woman. So that is if you're looking at the plot and you have the average score goes up like we were talking about in, it doesn't go up because we started at age 20, it's pretty much plateauing and then it begins to go down. So your score will be plotted on there, age 52. If you went straight up to the average value, that is what your BMD Z score is being compared to. So it's a standard deviation from there. The T score is being compared to right at the start of that plot.

The reason why they give us these two values is because it's thought that at any stage of your life, if you are two and a half stand deviations away from the amount of bone that you probably started with, then you are at increased risk of fracture. And obviously the problem with that is the fact that you could have started higher or lower than that average, and most of us did. Few of us are actually average. But the Z score gives us information about where you lie in relation to your peers, how normal that is. The Z score is normally not as scary as the T score because you will have lost some time. Yeah. The way I try to help my patients understand it is that, as you said, I always give them

an example. If your Z score is zero, you're at the 50th percentile of the population. If your Z score is one, you're a full standard deviation above the mean. So what's that? You're in the 85th percentile, if I'm doing the math correctly. And obviously, as you said, the T score is always going to be lower because we're comparing you to a perfect standard. We're comparing you to that super healthy 20 to 30 year old. So what we say to patients is, look, we want your T score. If you show up with a decent T score, your T score is zero and your Z score is plus 0.8. We say the win is keeping that T score where it is and watching the Z score go up because over time, we want you being better and better and

better than your age-matched peers because they're going down and we're going to hold you plateau. And that means we can't improve you relative to the T score, although I'd love to hear in your experience what you're finding there. But we can improve you relative to your peers. Yeah, it's a good example. And yes, you're right, we can improve the T score. Let's get right to it because this is going back to the outside of this discussion. I learned about you, I don't even know how. I think I was like literally just watching stuff on YouTube and somehow saw a clip.

It's probably many years old from local news in Australia highlighting you talking about the Lift More study. There's just something, if you look at the things that I can get sucked into on YouTube, it's car videos, F1 videos. There's this world that just sucks me in, but I'll tell you another one of the things that sucks me in. Videos of elderly people lifting weights. I can go down that rabbit hole.

I mean, it's ridiculous. You show me a 90-year-old woman deadlifting and I could watch that for days. It must be that the algorithm knows that. It's served you up to me. So let's talk about the Lift More study. I suppose around about 2013, I got to a point in my research career where I looked around and thought the exercise guidelines for osteoporosis are get your kids jumping and running and

playing as much sport as possible. Keep doing that for as long as you can. But then when you get osteoporosis, stop doing all that and just prevent falls. So you don't break. So are we done? Is this the best we can do? This is lame. All my animal research experience had told me that

even with very low bone mass animals, if you load them, they can grow bone. The only reason we hadn't been doing that in research is because we were terrified of hurting someone. And so it seemed to me we hadn't really tried. And at the risk of hurting somebody, we decided to do it. So we had three physiotherapists on that trial, including the PhD student who ran it, Steve Watson. We decided to do a brief because bone doesn't need a lot of loading. You don't need to run a marathon. You just need to do

one sprint to get those bone cells stimulated. So we had twice a week, 30 minutes, four exercises and we wanted them lifting heavy. So it was 85% 1RM. We used compound movements. This needed to be an efficient project. We wanted to involve as much muscle as possible. It needed to be weight-bearing. And we wanted something that would transfer to really useful daily activities. So clearly, a squat and a deadlift was going to be fundamental.

These are fabulous compound movements that they tick all those boxes. And these are not on machines. This is with free weights because you want to engage as much of those other systems and capacities as possible. We're trying to improve balance because we're trying to stop people falling. So away we went. Ideally, we wanted it to be 12 months because you do need a fair amount of time to be able to detect change on DExa because Dexa ionizing radiation picks up mineral. So you can't just measure new bone, which would be the osteoid, unmineralized. You need a full period of time to allow for a full remodeling cycle and mineralized bone. Because it was a PhD project, we couldn't afford a full year for each person.

So we just made it an eight month intervention, which I was confident would be enough to detect a change. We did really comprehensive bone and functional measures at baseline. We recruited about a hundred people, randomly allocated them to this high intensity resistance and impact training. Exercise research is really hard to blind to your participants and blinding is so important in clinical trials. So we had to not tell our participants

which was the intervention that we thought was gonna be effective. We just said, if you got randomized to this low intensity home program, we were trying to see whether that worked too. Of course we knew that that was not gonna work because we've got years of experience to know that that is not going to improve bone, but we gave them

things like walking, stretching, some body weight lunges and toe raises and things that would potentially improve their balance. So we weren't completely ripping them off. So then we had eight months of this intervention. It was supervised. Sorry, once again, Belinda, you said the treatment group was 20 minutes, three times a week? No, 30 minutes, two times a week. Got it.

Yeah. Maximum group size was eight and we recruited post-menopausal women. So we were looking for people, we advertised for over 60, but I think we did recruit one person who was 58 because she had been through menopause when she was young. They just needed to be well clear of menopause. We didn't want to be fighting that withdrawal of estrogen phase. They needed to have low bone mass, so they needed to be at least a T score of minus one at either the spine or the hip. So away we went. And I have to say, we were looking through our fingers for a little bit and we were so incredibly conservative to

begin with and just being very careful that we weren't hurting anybody. It became abundantly clear very quickly that we weren't hurting anybody. In fact, we were making people feel a lot better. Let me just ask you about that because the video which we'll link to in the show notes, even though it was just a local news segment, was just really inspiring. I think there were women there that were at some point basically able to pick up their body weight. Am I remembering that correctly? Literally, these women were deadlifting their body weight. How did you even train them to do this? These women show up to this study and they're probably told it's an exercise study. They think, great, I'll be doing pool jogging or something. Then you drag them into a weight room with Olympic bars.

How did you even go about getting them to do this safely? How much resistance was there on their part to the fear of weightlifting? I assume prior weightlifting experience was not an inclusion criteria? Well, they could have had it, but they couldn't have been doing anything in the past 12 months because you know bone is a use it or lose it tissue. So they needed to not be already doing this. We told them what the basic exercises were. So these had to be people who were willing to doing this. We told them what the basic exercises were, so these had to be people

who were willing to do this. We never throw somebody straight into lifting something extremely heavy and certainly nobody would have expected that we would end up with people lifting their body weight, certainly at least for us. We just did it very systematically. You start with a broomstick and you make sure that people's technique is good. I have to tell you, we had people with fractures, so they had existing kyphosis. You know what a kyphotic curvature looks like in a deadlift position. This is not a pretty thing. But as long as they had an extensor moment, it was okay. We don't want people flexing and lifting

weight because then we're putting them at risk of fracture. But it's all in the coaching. And this is the reason why it's so important that the person who is coaching somebody with osteoporosis knows what they're doing. They can't just be a strength and conditioning coach, although that really helps. They have to have some clinical training. Because people come to you in a clinic with not just osteoporosis, but pelvic floor dysfunction, frozen shoulder, spondylolisis, vertigo, knee away. You've got to be able to manage that. Many of those conditions were actually screened out of the Liftmore study because it was the first time we were doing it. We didn't want to have to manage all of that. But I just put it out there because it's something I want to remember to talk about. So it was all about just systematically training

them in the technique and then gradually increasing the load. And a lot of people think of older people and particularly older women and particularly post menopausal women who the assumption is they go completely loopy through menopause, which is not true. They think about old people as completely incapable, incapable of doing stuff and incapable of learning. But old people are you and me who just kept living longer. We have the capacity to learn and older people are perfectly capable

of learning how to do a deadlift in a squat. It might be pretty ugly to start with, but they get better and as they get stronger, they get even better. I just love it so much. I cannot, for people listening and not watching right now, just the grin on my face listening to you talk about this, it just warms my heart. I just agree with all of that. I think that one of the saddest, I think, misconceptions people have is that once they get to a certain age, it's too late

and they sort of accept their fate. And oh, I have this kyphotic spine and oh, my bones are too brittle and I guess I'm just gonna spend the next decade of my life doing nothing. Studies like this demonstrate that that's not the case. I'm looking for some of the other soft stuff as you think about the evolution of this study. What else did you notice in the subjects? What did they tell you? How did this translate into the rest of their lives? Because obviously, you as an investigator are looking for something very specific. You want to probably understand

how much muscle mass they put on, what their bone density did, how much their T-score has changed. But were there other things that you learned about these women as the study went on that spoke to their quality of life? Undoubtedly. And for them, that was the most important thing. And that is what made me want to open the clinic. This is a quality of life issue. It turns out this is not a bone issue. I'm a bonehead. I care about what their BMD scores did. But the reality is comments like, oh my God, Belinda, I can see my shoulders in the mirror

again because their posture changed. When you do a clinical trial, you measure height and weight as the standard baseline how to describe your population. Who knew that we would actually be citing height as an outcome because the control group shrank whereas the intervention group grew a little. Of course they didn't grow but their posture improved to the extent that they were taller at the end of the study and the difference between groups was significant. It was only half a centimeter, but hey. That's in eight months. Yeah. If you like

soft outcomes, people saying, my husband is hiking the Kokoda trail and I just thought I was going to be cheerleading. I can go with him now. I've got this incredible strength. I've basically got my life back. I can get into the garden and I can push the wheelbarrow full of potting mix around now. I've got this incredible strength. I've basically got my life back. I can get into the garden and I can push the wheelbarrow full of potting mix around now and I don't feel like I'm going to break. I can lift my grandchild again. I can get my own shopping out of the car. It's all about independence. Yeah. Quality of life. Major quality of life as well. And at the clinic, it's pretty obvious that that is something that is improving.

What did you find after eight months with respect to muscle mass, bone density, and the other clinical metrics? We ended up with a net benefit of a bit over 4% at the spine. That equated to about 3% improvement at the spine in BMD and about one and a half or one and a bit loss in controls. I would say that this program definitely has the biggest effect of the spine. That is a good thing because it's one of the places that fractures most frequently. At the hip, it was a real head scratcher.

When I first looked at the results, we had something like a 0.6% improvement at the femoral neck, and I'm thinking, these women deadlifting and squatting 70 kilos, how can that be? We ended up with a significant difference because the controls lost 2.5%. There was a net benefit, but I couldn't figure it out. Luckily, I have some 3D HIPS software,

which allows me to reanalyze my 2D BMD data from Dexa and look at the changes in geometry. From that, you could see things like cross-sectional area of the femoral neck, cortical thickness, and so on. When you look at cortical thickness of the total femoral neck, there was a 13% net benefit in the intervention group. And if you looked specifically at the lateral femoral neck cortex, there was a 27% improvement. So it turns out that if you were just looking at BMD from Dexar, it would look like this kind of lifting only has a maintenance effect at the hip.

But actually what's happening is it's changing the geometry. It's making it stronger by making the cortex, that cortical bone, thicker and more resistant to bending. So that was another of those fantastic moments where I had only just got this software and was just in time to show this really novel outcome. I think that's such an important point by the way. Given that most of us clinicians don't have access to that, can we in your opinion rely on the stabilization of the Z-score or the improvement of the Z-score, the stabilization

of the T-score is a win if we're in that situation. We have that patient who comes in at a minus two, you get them on a strength training program, they're putting on muscle mass, the Z-score gets better, but the T-score does not. You still say, look, you're probably winning even though you don't have the radiographic tool to document the cortical bone thickening. Yeah. If you can maintain bone mass at the hip, the bone mineral density, yes, that is absolutely a win.

Don't get me wrong, there were some people who probably the largest gain we had at the hip in the lymph more study was about 6%. So there were some people who improved BMD, but yeah, on average, it's something that you don't always see. The important thing I think for people to understand here is even if going on this type of a training program at best maintained you, let's assume even the cortical thickening was maintained, there's two important points to consider. The controls are having the floor dropped from underneath them. So that gap between what you would be doing and what you're doing is widening

even if you're not getting better. So the fact that you're even getting better slightly is mind boggling, but even if you don't, the gap between where you are and where you would be is enormous. The second point is your fall risk is going down dramatically because you're putting on muscle mass and to the very important point you made, you're using these free weights and you're improving your balance. You have more muscle, more balance, more motor control.

The likelihood of falling to get in the position that you're gonna break a bone is going down so much. So when you add to the fact that, oh, and by the way, cortical bone is increasing by 13%, this is just a win, win, win, win, win across the board. Anna, show me a bone drug that does that. If you look at our functional outcomes, we had back extensor strength, leg extensor strength,

and then we had tandem walk, timed up and go, sit to stand, vertical jump, and we also measured kyphosis. All of those things improved, but especially lower extremity strength and back extensor strength. Now, people think, oh, well, back extensor strength, yes, it's just making them stand up straighter. There's no just about it. If somebody has kyphosis and their posture is such that their vision is angled downwards, they've lost that peripheral vision for, say, when they're walking to their car at the shopping center, which is not in their comfortable environment, perhaps a little kid runs out in front of them and they haven't seen them coming.

And that's when a fall can happen on a hard supermarket floor, walking outside their own home and the neighbor's dog runs out. They don't see it coming, they get a fright and they'll fall. So posture is actually really, really important to fall risk and risk of fracture because we know pretty much half the time you fall, you're going to fracture. I would add something even more to that, which is we have a couple of folks in our practice who are really forward thinking in their understanding of the role of vision in brain health. We know this is true with auditory stimuli as well. We know that hearing loss is a risk for dementia because it's reducing sensory input to the brain.

We would argue that you see the same thing with a reduction of visual input. A reduction of visual input is a reduction of cortical stimulation, cortical meaning brain, cortical and that's also increasing problems. In addition to everything you said, which is this increased risk of falling as vision is getting narrower, you're also reducing brain input and I think you run the risk of also exacerbated or accelerated degeneration of the brain. So yeah, I agree with you completely. It's not that you just reversed kyphosis. That's a really big deal to get somebody looking up and forward.

The other things that I'm sure you saw were improvement in grip strength. There's another benefit because you can't deadlift without grip strength. If a woman's picking 70 kilos off the ground, think of how strong her hands are and think of the implication of that on mitigating fall risk. You think about that person walking down a flight of stairs. Now imagine the grip they have on the handrail as they confidently walk down the steps. You think of the devastating injuries that people can have of any age, but certainly older people when they can't hold onto a handrail and then they don't have the leg strength

to stop themselves. Just to reiterate this point that we can't make enough, which is yes, there are some really interesting and exciting drugs on the horizon for the management of this. Yes, pharmacology and endocrinology play a very important role in managing these things. I would argue estrogen more than any other drug out there. But none of these things compare or should ever be thought of as a substitute for what you're describing. No, that's right. I briefly mentioned the tandem walk and sit to stand and timed up and go and burger jump and all of those things are risk factors or predictive of your risk

of falling. So yeah, we do know that improving those things reduce your risk of falling. You're quite right about grip strength. I do as much of this lifting as I can, but I'm frequently I've just been to Europe for a month, I've been to the US for a month and my lifting falls away. So I come back to the gym and go to lift again. And whereas my muscles, my major lifting muscles may be okay, but I end up on my last set, I am just holding onto that bar with my fingertips because my grip strength goes. So it is absolutely part and parcel. This is why these Olympic lifts are so incredibly helpful because they are compound movements using virtually every muscle in your body,

including if you're frowning, like you're doing it. So Belinda, there's no chance that anybody listening to us at this point would call into question the value of this type of intervention. So now the question is for virtually everybody listening to us, they don't have access to you and they don't have access to your clinic. What would be the advice for the men and women who are coming to this discussion or people listening to this who want to send it to their parents or loved ones who really are showing up and are in the same state that the women were

in at the beginning of your study, how can we take that person, provide them with the safest environment to go forth and conquer? Because again, if you're saying all you got to do is 30 minutes twice a week of this very, very specific type of lifting protocol, which is again, very straightforward in concept, obviously in technique, it requires execution. How can they go about doing that? Who would you recommend they see? What type of individual to coach them?

So there's levels to that answer. And without turning this into an advertisement for Oniro, which is what the program is called that we deliver through the bone clinic, we get that question all the time. The minute I opened the bone clinic, everybody wanted the program. And the problem is I didn't want to initiate an avalanche of fractures for people doing the program and hurting themselves. So we decided to license it and provide that program to physiotherapists, what you guys call physical therapists, and accredited exercise physiologists, all their equivalent. We have licensed, there's probably about 60 in Australia at the moment and a growing number

overseas now. It's just starting to take on in the US. I'm an academic, so I'm not a salesperson. I don't sell this. People come to me and that's how they get it. The training for that is a very comprehensive six hours online. You must have these qualifications to do it. And then you're ready to deliver it to your patients in your clinic, as long as you have the gear. And they've always got access to me and a lot of supportive information to do that safely. And the reason I want physios and EPs to deliver it is because they have that

background information that I was telling you about that clinical training that allows them to look after the millions of different co-morbidities that are going to come into their clinic. So tell us again, Belinda, just to make sure everyone's hearing this and we'll link to it in the show notes, but what's the name of the program? Where can somebody go as an exercise physiologist or a physio to become accredited in this program? Onero is the name of the program and they just need to Google Onero Academy. O-N-E-R-O?

That's right, yeah. Okay, we'll link to it, yep. And they can read about it. This is not something that the patients go to, this is something that the trainers go to to become accredited. So if a person is listening to this and they want to be trained,

can they go to that site and find out where the accredited people are? Yeah, we'll go to the Bone Clinic site and we host a map. And if you zoom in on your area on that map, you'll see a little red tag. If you click on the tag, the contact details of that O'Neill provider will pop up. Now, as I say, at least in the US,

not a huge number of them at the moment, but the demand is so at least in the US, not a huge number of them at the moment, but the demand is so incredibly high in the US. Really, the best thing that you could do if you were in that situation and you wanted to go to an O'Neill provider is go to your local PT or kinesiologist, exercise physiologist, some equivalent and say, okay, you need this program. Here's the website, contact Belinda and I can get them licensed and away they go. For me, it's research. There is a way for them to contribute to our research program. I give them access to our database.

I'm really interested in making sure that this works, not just in our hands. And so that's part of my research. But for them, of course, it's a revenue stream. So it is a win-win for them. For the patients who cannot convince anybody to do O'Neuro, then the next best thing would still be to contact the bone clinic. We can do a telehealth appointment with them and give them our very best advice for a program that they can do either at home or at a gym. If they don't want to do that, then the next best thing they can do is just go to the gym and get some gym program. Just anything is better than nothing and start lifting weights and try to get some supervision because if you've got a T score of minus four, I'm not comfortable with

you training by yourself. So even if you're not doing onero, get somebody to look after you. So those are the sort of three levels. If you can find an onero provider, do supervised onero. If you can't, call, email the bone clinic and we'll do a telehealth appointment and get you a program that you can do, which would be the very best that we can come up with that you could do, which would be the very best that we can come up with that you could do unsupervised.

And then the next level down, just get yourself to a gym with someone supervising you and do some weights of some kind. I guess I'm going to add a fourth one, which is I've been to the Gold Coast many times. It's absolutely spectacular. I think a trip to Australia is never a bad thing. Maybe scrap the telemedicine visit and just take a two-week vacation to the Gold Coast and get some time at the clinic maybe. We'd love to see you. Actually, the clinic's in Brisbane. I live on the Gold Coast because

that's where the university is, but the clinic's just on the road. Well, Brisbane's gorgeous as well. Belinda, this has been excellent. I'm just so excited to make sure that everybody out there who's listening to us has access to this type of information. I think this is a remarkable demonstration of the power of exercise. People hear me say this all the time and I'm sure they're sick of hearing me say it. It is the most potent drug available. I am a very pro-pharma guy, but there's just no denying the evidence.

There is nothing that a pill can do to touch the benefits of exercise. This is about as pointed as an example, as you will see. And I love hearing about how in such a relatively short period of time, these women had such a dramatic improvement in their quality of life. It's such an exciting story. It's really had a greater impact on their quality of life. It's such an exciting story. It's really had a greater impact on their quality of life than I can think of any other intervention than a healthcare provider could demonstrate. So anyway, thank you for your work and thank you for, like I said, getting up early this morning to share it with us.

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