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

00:00:00.000 Hey, everyone. Welcome to the Drive podcast. I'm your host, Peter Atiyah. This podcast,

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00:01:04.220 My guest this week is Professor Belinda Beck. Belinda is a professor of exercise science in

00:01:09.900 the School of Health Science and Social Work at Griffith University in Queensland, Australia.

00:01:14.260 Her research is primarily related to the effects of mechanical loading on bone. In 2015, she

00:01:20.080 established the Bone Clinic to roll out this groundbreaking program of research, which we

00:01:24.820 discuss in a lot of detail in this podcast. She was the principal investigator of the Liftmore and

00:01:30.040 Liftmore M clinical trials, which demonstrated exercise as therapy for osteoporosis and low bone

00:01:36.780 mass, something I've discussed a lot on the podcast. In my conversation with Belinda, we dive into the

00:01:42.040 physiology of bone. It's actually important that you understand how bone works as a tissue. It's easy to

00:01:49.160 think of it as sort of a static tissue, but in fact, it's quite a reactive tissue. We talk about

00:01:53.980 how the foundation is set during childhood and how the remodeling over the course of one's life

00:01:59.620 takes place based on, of course, activity, nutrition, and hormones. We then talk about what can be done

00:02:05.700 to prevent bone loss as we age. And of course, this begins with what we as parents should be doing

00:02:11.720 to help our kids achieve their genetic potential prior to the fusion of their growth plates.

00:02:17.340 Talk about how to improve your bone health, even once you're past the point of your genetic

00:02:23.640 potential, i.e. once you've reached your maximum point in your late teens and early 20s,

00:02:27.880 and what we can learn from the Liftmore studies in terms of how exercise can help and even reverse

00:02:35.660 bone loss in people in the throes of osteopenia and osteoporosis. So without further delay,

00:02:42.640 please enjoy my very fascinating discussion with Professor Belinda Beck.

00:02:47.340 Hey, Belinda, thank you so much for getting up so early in Australia to sit down with me. Would

00:02:59.040 love to be doing this in person, but it's a bit of a hike for you. So this will more than suffice.

00:03:04.520 I've referenced your work many times before in talking with patients and talking on social media,

00:03:11.800 talking to other podcasts. And so I've wanted to speak with you for some time because it's one thing

00:03:16.340 to hear me talk about something, but it's, I think, far better to hear the expert talk about it as

00:03:21.620 opposed to me just sort of paraphrasing. But maybe we'll just spend a second giving folks a little

00:03:26.220 bit of your background. I'll have obviously introduced you already, but tell folks a little

00:03:31.480 bit about how you came to find your interest in this. Your PhD and postdoc were both done here in

00:03:36.940 the US, correct? Yeah, that's right. And my master's as well, actually. I think we can safely

00:03:43.780 say a lot of people end up in research because of some personal interest. And that's exactly the

00:03:48.560 case for me. I was a runner and a field hockey player, and I constantly suffered from sore shins.

00:03:54.720 Nobody could help me. They couldn't even tell me why I was getting them, much less how to prevent

00:03:59.900 them or make them better. This was back in the day, mind you. And so even when I was in high school,

00:04:06.380 I knew that I wanted to find out what was going on. And that's actually where my research started

00:04:11.900 in my master's. I was looking at trivial stress injuries. It became clear very, very early that

00:04:17.260 this is a bone injury. This is not what everybody was saying, two hours posterior, pulling on the

00:04:22.160 border of that was all bunkum. That was somebody making a supposition. And that set me down the path

00:04:27.860 of trying to figure out what are the mechanical signals that stimulate bone to adapt to mechanical

00:04:36.140 loading. You know, pursuit of Wolf's law, why does a change in mechanical loading cause the bone to

00:04:42.640 change shape in this amazing way? And of course, as soon as I discovered bone did that, I was hooked

00:04:46.620 because it is just an incredible tissue. I did an animal study for my PhD and quickly realized that

00:04:52.760 that was not something I wanted to do for the rest of my life because it involved killing animals

00:04:56.760 constantly. So I went to Stanford and did a postdoc and that's where I learned about clinical trials.

00:05:03.420 Then realized, of course, that osteoporosis is the greatest burden when it comes to bone problems.

00:05:09.820 And so being an exercise head, that's something that I wanted to figure out exactly what was the

00:05:16.400 ideal exercise program to assist people living with osteoporosis.

00:05:21.000 Yeah. And before we started the podcast, we quickly figured out that

00:05:24.260 we overlapped together at Stanford for the entire three years of your postdoc. I was in medical

00:05:30.200 school, which of course, I just get a kick out of knowing the fact that there was probably a day

00:05:34.380 when we were literally in the same cafeteria at the VA or something. And of course, who would have

00:05:39.980 predicted whatever more than 25 years later? We're sitting here. I love those coincidences.

00:05:44.320 So let's also talk a little bit about what you're doing today. So you're obviously back home. Talk

00:05:51.560 about the clinical practice that you have now and what type of patients you work with and what type

00:05:56.460 of research you're still focused on. I should clarify, I'm not a clinician. I'm an exercise

00:06:01.240 physiologist and I've never had a personal clinical load. Although exercise physiology is one of the

00:06:08.960 allied health professions in Australia, I came back to Australia to an academic position and was

00:06:14.840 been teaching anatomy my whole professional career, but continued my own research. I'm a professor at

00:06:22.220 Griffith University on the Gold Coast in Queensland. And that's where my career sort of, I guess,

00:06:30.780 triangulated onto this question of, there must be a way to load people who have osteoporosis,

00:06:38.840 in such a way that they can grow bone because everybody had been saying we couldn't do that

00:06:44.100 because their bones were so fragile. Now, when we did, and I'm sure we'll come back to the actual

00:06:49.420 trials we did that showed that, after I showed that, I did realize that the exercise, the nature

00:06:55.580 of the exercise was not really safe for just anybody. And it needed to be applied in a certain way and

00:07:04.080 very specifically, and it needed to be applied by somebody who really knew what they were doing,

00:07:08.400 because this is not a program that should be done unsupervised if you're at high risk of fracture.

00:07:14.360 And the only way to do that was to implement it in a clinic. Now, it's hard enough to convince

00:07:19.860 doctors who've been telling patients, osteoporotic patients for years that they should not lift

00:07:23.920 anything heavy. But to tell somebody in a clinic to start doing this exercise, I just knew that was

00:07:29.600 never going to happen. So that's what the bone clinic is. I set up a clinical facility. It's a

00:07:35.900 translational research facility where we actually implemented the program. But every patient that

00:07:42.780 comes in is a research participant and they agree to share their data. We do the same testing as we

00:07:50.580 did in the Liftmore trials, two and a half hour appointment at baseline. And then every year

00:07:55.200 thereafter, we test them again with the same thing so that we can see if the exercise program works in

00:08:00.880 the real world. And of course, I added in other things that are really important, like diet,

00:08:06.300 and we take care of them. This is not a clinical trial. We don't have a control group. Now, of course,

00:08:11.700 I've got an enormous amount of data and needing to wade through all of that.

00:08:16.620 Let's start the discussion with a little bit of the physiology of the bone. I think for many people,

00:08:22.640 myself included, people who went to medical school, I don't really recall getting much of an education

00:08:28.000 in this. I probably did. But once you choose your specialty, unless it happens to deal with bones,

00:08:34.420 as in orthopedic surgery or rheumatology, perhaps, or maybe sports medicine, most of us end up getting

00:08:41.380 far and far away from it. But given the ubiquity of osteopenia and osteoporosis, it really comes back

00:08:48.640 to be in the fore for many physicians, even if they aren't trained in it. So I think it'll be helpful

00:08:55.440 for everyone, myself included, to go over a little bit of bone physiology. Handle it any way you see

00:09:01.400 fit. But I think we can talk about this in as much depth as you like, because we have a pretty

00:09:06.160 sophisticated audience. Okay. A couple of different ways to look at types of bone, the very basic way

00:09:12.700 to describe them according to their shape, which are completely related to their function,

00:09:18.780 the whole basis of Wolf's Law, I guess. So you have long bones, like the long bones,

00:09:23.360 the levers in your limbs and your feet and hands. You have short bones, like the little lumpy bones

00:09:30.360 in your ankles and wrist. You have irregular bones, like your vertebrae and your scapula and so on.

00:09:37.900 All of them are comprised of two basic kinds of bone. One is cortical bone and one is trabecular

00:09:45.420 bone. And there are different words for those, cortical or compact bone, trabecular, spongy,

00:09:50.580 or cancellous bone. Now, cortical bone is typically the shell of a bone. Every bone has cortical bone

00:09:58.700 on the outside. It might be very thin in the case of vertebral bone, or it might be extremely thick,

00:10:03.980 as in the shaft of the diaphysis or the femur. Most bones have some degree of trabecular bone in them.

00:10:12.780 If it's a long bone, it's in the ends. And if it's a short bone, it fills the whole thing. Like a

00:10:19.020 vertebrae, a regular bone, it also fills the whole body of an regular bone. If it's in the skull,

00:10:24.200 it's called diplo and it's sandwiched in between two layers of cortical bone. Ribs even have diplo,

00:10:29.780 they're a flat bone as well. So the very cool thing about the bone tissue itself is the microstructure.

00:10:40.280 So in cortical bone, you have a lamella structure, so layers and layers of bone. And that occurs

00:10:47.300 because of the way osteoblasts lay down bone. But the really cool thing is the fact that in each

00:10:53.280 adjacent layer, the collagen is laid down almost, not perfectly, perpendicular to each other so that

00:11:01.020 the lamellae combine to create a tissue that is beautifully resistant to torsion as well as

00:11:08.600 the normal loading of compression and tension. Now in trabecular bone, there are also some

00:11:15.420 lamellae because of the way osteoblasts produce bone. But the really cool thing about trabecular

00:11:21.740 bone, and this is I think probably what Wolf in 1882 spent most of his time trying to describe

00:11:27.220 mathematically, is the arrangement of the trabeculae. So each individual strut is best aligned to the

00:11:35.420 forces that are put on bone. If you look at a cross section through the proximal femur,

00:11:40.140 you'll see that there's wonderful arches that go away from the head, through the neck and down past

00:11:45.200 the greater trochanter. And then from the greater trochanter, there are trabeculae that come from

00:11:50.720 the surface of the trochanter and arch down to the other side and over towards the lesser trochanter.

00:11:57.100 So you get this interconnection of bone that is beautifully arranged to best withstand the

00:12:05.100 bending load that you will get from the opposition of the weight of the body on the head of the bone

00:12:09.680 and the ground reaction force coming up, the diaphysis. And that repeats itself throughout the

00:12:14.920 body. If you look at any part of the body where trabeculae are, they are just aligned in response to the

00:12:22.200 forces. And of course, that's one of the things that will change if you change the nature of the

00:12:27.240 loading. You've mentioned Wolf's Law a couple of times, probably worth stating it and explaining its

00:12:33.240 relevance to bone. It has been paraphrased over the years, and I don't think there's any harm

00:12:38.640 in that, to mean that bone will adapt to the nature of loading to which it is chronically exposed.

00:12:47.700 And the purpose being that it's best adapted to withstand forces to prevent fracture. In actual

00:12:55.300 fact, I couldn't recount what his actual law is because he was a mathematician and he was trying

00:13:02.000 to describe this mathematically. We've taken that notion and just encapsulated it into that law of

00:13:09.380 bone adaptation in response to loading. Now, is there a built-in assumption to Wolf's Law

00:13:15.620 that that adaptation can only happen in the setting of certain physiologic parameters being

00:13:23.140 met? So, for example, sufficient calcium, healthy osteoblasts, absence of certain disease pathology,

00:13:31.980 or is this truly a universal law that is indeed axiomatic?

00:13:37.360 I don't think anybody knows the answer to that for sure, but I would be willing to stake my firstborn on,

00:13:42.540 don't tell her, that this just occurs. This is something that happens as sand running out of

00:13:49.640 your fingers falls to the ground because of gravity. This is how bone reacts to loading.

00:13:56.520 It's a physical phenomenon.

00:13:59.540 Okay. You've also alluded to osteoblasts, so maybe talk a little bit about the difference between an

00:14:05.060 osteoblast and an osteoclast, how this mineral makes its way to the bone. What does this look

00:14:12.880 like as a child is born? Like maybe even start at birth and talk about what the bones are like in

00:14:17.820 that fetus and how they develop over the ensuing two decades.

00:14:22.560 Well, going right back, we start as a little cartilaginous model of a skeleton. And even by

00:14:28.160 eight weeks, we have that model in that tiny little bean, and that is progressively mineralized

00:14:37.560 as it becomes skeleton. There are two different ways really of ossification, but the primary one

00:14:43.360 is endochondral. Once a baby is born, they have ossified the long bones and quite a portion of their

00:14:52.300 skull bones and most of the other bones that are around organs.

00:14:55.680 And just for folks listening, ossified is this process of putting mineral into the cartilage

00:15:00.860 and turning it from soft into hard.

00:15:03.160 That's right. I think we talk about ossification when bone cells invade the cartilage. Once there's

00:15:09.000 a bone cell in there, it's considered to be ossified because they start to excrete osteoid,

00:15:15.180 which then becomes mineralized. So yeah, that's right. There's a whole process of endochrondral

00:15:20.340 ossification. So babies are not born, obviously, fully ossified. They have still little cartilaginous

00:15:28.240 hands and feet, and they have lots of cartilage to different degrees in their skull bones, and those

00:15:34.560 continue to ossify throughout life. And I think, in fact, some of our growth plates don't even fuse

00:15:40.620 until, particularly in men, until they're about 25 years old. But largely, most of your bones are fully

00:15:46.880 formed and have bone in them by the time you're two. And that's coinciding with when you're really

00:15:53.940 starting to run around and load the skeleton. The skeleton then continues to grow throughout

00:16:00.700 the first two decades, with the vast majority of growth happening when you're very little,

00:16:07.460 little toddlers, but primarily during puberty. And that's what we all know as the growth spurt.

00:16:13.240 And that's happening because your bones are growing like crazy. That begins to slow. That growth spurt

00:16:18.960 happens earlier in girls, probably about 12, probably about 13, 14 in boys. And it slows,

00:16:27.080 probably is ending around about 18 in girls, can be as late as 25 in boys. And once you have reached

00:16:37.900 your peak bone growth there, your epiphyses have joined to your diaphyses, so the growth plates

00:16:44.800 have fused, you're not going to grow anymore. And you almost certainly have all the bone that you're

00:16:49.900 ever going to have. So there's definitely a making hay while the sun shines mantra of those of us who

00:16:57.220 work in the world of osteoporosis, because childhood is so incredibly important. People often call

00:17:02.600 osteoporosis a childhood disease. The goal is to get as much bone as you possibly can.

00:17:07.920 That's limited by your genetics. And we can come back and talk about that if you want,

00:17:11.260 but you do have a blueprint that you will achieve, but you want to optimize that, get as much of that

00:17:17.040 genetic capacity as you have.

00:17:19.940 I just want to repeat that point, Melinda, because it's actually quite profound.

00:17:23.340 And I want to make sure nobody missed it. You said osteoporosis is a childhood disease.

00:17:27.840 Now, what you meant by that, of course, is based on what you said just prior to that, which is

00:17:33.300 you will reach your maximum bone potential by the time your growth plates fuse, which again,

00:17:42.100 for most people is probably late teens, maybe in the case of men, early twenties. And in that sense,

00:17:50.000 it's sort of like a glider. It's sort of like saying this glider will reach its maximum altitude

00:17:56.160 20 years into your 80 or 90 year life. And you better get it really, really high because the

00:18:04.700 best we can do is reduce the rate at which it declines, but we're not going to get it higher

00:18:11.860 than it was at that point. We're going to get into a whole bunch of nuance. I'm sure later on,

00:18:16.620 because I think what you're going to tell us is that actually we can maybe even change the

00:18:21.460 elevation of the glider later on in these patients with osteoporosis. But I think there's no denying

00:18:28.680 this idea that anybody listening to this, who's thinking about osteoporosis for themselves should

00:18:36.540 also be thinking about it for their kids and asking the question, what are my 10 year olds, 12 year olds,

00:18:44.060 15 year olds doing today to reach their genetic potential?

00:18:49.580 Yeah. It's one of the strongest messages. I speak mainly to older people and I say,

00:18:54.720 the horse may have bolted for you, but you have children and grandchildren, and this should be

00:19:00.680 your mantra, get them outside and active every single day and doing X, Y, Z bone friendly activities.

00:19:08.220 I should say, we talk about pig bone mass being achieved and we use the word end of the second

00:19:15.220 decade because that's the average between men and women. It can creep up a little bit, but nobody is

00:19:22.860 growing any more bone after age 30 and most people are well and truly done by then. So yes, I'm probably

00:19:29.640 giving a somewhat old fashioned view of this because as you say, I do believe that there is capacity to

00:19:37.400 get the glider higher later in life. But I guess the concept is you're not going to

00:19:43.420 grow bone anymore. You're not going to grow the length of bone anymore. So it becomes a lot more

00:19:49.780 difficult. And the other message that is extremely important is that genes determine it's been 70 to 80

00:19:58.500 percent of the bone that you're going to have. So to a certain extent, you're working within

00:20:03.120 some reasonably tight bounds. You only have to look at your parents and grandparents to get an idea of

00:20:12.240 what your risk is like. If they are very osteoporotic, then your risk is also very high.

00:20:19.260 So I think you said 60 to 70, or did you say 70 to 80 percent? I know it was a high range you gave there.

00:20:25.140 It does depend on who you read, but I sort of have settled on the 70 to 80 percent.

00:20:30.300 I think that there is certainly evidence to say that's the case, that there are twin studies and

00:20:35.800 so on. And sorry, that's bone density. Obviously, bone length is highly heritable,

00:20:41.520 just as height is very heritable and it's determined by bone length. But you're also

00:20:46.060 referring to bone density by referencing osteoporosis, correct? Yeah, I suppose. I mean,

00:20:51.320 I probably prefer to use the word bone mass. The trouble is we measure it by bone density using a

00:20:57.740 bone thermometer. That is our proxy for bone mass because the only way to measure bone mass is to

00:21:03.580 actually ash the bone and you can't do that in a living person. So yeah, again, bone has been

00:21:09.560 variously measured throughout the decades. BMD is the most common way to do it. And if you look at BMD

00:21:16.560 plots, you'll see this very obvious, I'll do this in reverse, growth in childhood and then a flattening,

00:21:23.680 pretty much a plateauing and then a gradual loss. And that flattening, plateauing or timing of loss,

00:21:32.700 that is also, I believe, genetic and individual, but that's the thing that is most amenable to

00:21:40.460 exercise intervention. So somebody might have genes that allows them to get a peak bone mass of a

00:21:47.500 certain amount that is the same as their neighbor, but because the rate of loss is different and their

00:21:53.260 level of activity is different, they may lose more quickly. And then you throw in menopause,

00:21:58.320 you know, average age about 52 to 54 or something. And for women, you'll see that loss rapidly accelerate

00:22:06.980 for probably five to eight years. This is because circulating estrogen almost vanishes from your blood and

00:22:15.120 estrogen is an incredibly important hormone for bone because I don't think I came back to talking

00:22:21.560 about bone cells. I should probably do that because of its effect on osteoclasts. It largely

00:22:26.760 inhibits osteoclasts, keeps a check on them and prevents them from over-absorbing. So while I'm on

00:22:34.100 those cells, yes, there are a number of different cells in bone. The two primary, well, the main one is

00:22:40.640 an osteocyte. That's your standard bone cell that sits in bone tissue in its little cave and it is

00:22:47.180 responsible for maintaining the tissue around it and also for sensing what's going on in the tissue

00:22:53.320 environment. We can talk about that a bit more later, but osteoblasts, osteocyte precursors, and

00:23:00.360 they are the ones that when they attach to a bone surface, they exude osteoid, which is the new bone tissue,

00:23:07.280 which then becomes mineralized. So they're the bone forming cells. Osteoclasts are these big

00:23:13.720 multi-nucleated cells that also attach to bone surfaces and resorb bone in packets. And this is

00:23:23.200 really important. This is not a bad thing. Bone remodeling is one of the most important ways that we

00:23:28.240 maintain our skeleton, get rid of micro damage, and also adapt to mechanical loading. So resorption

00:23:35.380 formation is happening throughout our life. It is the way that we release calcium into the blood for

00:23:40.560 when we need it for all those other things we need calcium for. So it's extremely important. The

00:23:45.120 trouble is estrogen does help to contain those osteoclasts when it disappears from the blood.

00:23:52.420 Osteoclasts have a little bit of a party for a few years and resolve bone like crazy. And so that

00:23:57.600 explains why in women at menopause, we have experienced this dramatic loss of bone

00:24:03.680 for a period of years. Then it levels out again and sort of matches men. But you can see

00:24:07.660 why more men than women are fracturing with osteoporosis because firstly, we don't gain as much

00:24:15.120 peak bone mass. Meaning more women fracture than men.

00:24:19.180 That's right. But in sort of in our 20s, we don't have as much bone as men, and then we lose more

00:24:26.200 throughout life. So by the end of life, there's this greater disparity. And then add on to that,

00:24:31.040 women fall more than men in later life. And so you've got this perfect storm of this is why more

00:24:36.880 women than men are affected by osteoporosis and fracture. And do we believe that women fall more

00:24:42.540 because of a greater prevalence of sarcopenia? Yeah, it's a hard question. I would say probably

00:24:49.440 yes. Well, there's a reasonable amount of evidence to show that women are less active throughout their

00:24:56.540 life and when they're older. Not that older men are particularly active these days either, but

00:25:01.840 I suppose because men genetically have more bone and muscle to begin with, they've started from a

00:25:07.640 higher place. So yes, a very frail old woman has not just not very much muscle, but not strong muscle,

00:25:16.380 not very functional muscle. Their balance, the whole sort of neuromuscular package, if you like,

00:25:22.200 has deteriorated to the extent that if their balance is perturbed, they will struggle to

00:25:27.760 regain their balance before they fall. Again, there's a lot there, so we'll just sort of

00:25:31.980 summarize it quickly. But basically, oversimplifying a little bit, we have osteoblasts and osteoclasts

00:25:38.020 that live in early in life. The balance probably favors the osteoblast. You're adding more bone than

00:25:46.280 you're subtracting. We get into an equilibrium where there's a remodeling that's constantly

00:25:52.360 occurring. And the bone acts in this sense as a reservoir also for something like calcium. And so

00:26:00.200 you're having rebuilding and remodeling. If there's damage to a bone, obviously, if you get shin

00:26:06.800 splints, there has to be some healing that goes on. All of these things take place. Obviously, if there's

00:26:11.220 need for calcium, more of it comes out of the bone, et cetera. And then we get into this state of

00:26:16.260 decline where maybe the osteoclasts start winning. And in women, this is really amplified in the five

00:26:23.780 to eight years following menopause when the most important hormone for bone preservation, estrogen,

00:26:30.500 is taken away. And estrogen being the thing that keeps osteoclasts in check is now gone. And to your

00:26:38.180 description, the osteoclasts kind of have a party now. Now they really get to run amok

00:26:42.420 and women experience a disproportionate loss of bone mass compared to men who are also in a state

00:26:49.700 of decline. Because by the way, men's estrogen levels are also declining because they're tethered

00:26:53.940 to their testosterone levels. So as testosterone goes down, so does aromatized estrogen and it goes

00:26:59.140 down with it. And then they both sort of end up on the same parallel path again, but the women are

00:27:04.900 considerably lower because they've had that accelerated loss.

00:27:08.500 There's one thing I would just add in, I feel like I have to say this because I

00:27:13.400 drum it into my students' heads when I'm teaching bone growth, is that the skeleton actually grows via

00:27:20.400 cartilaginous proliferation and it's replaced by bone. So the osteoblasts aren't causing the growth

00:27:26.860 of bone. They're just- They're just solidifying it.

00:27:29.400 That's right. They're replacing the cartilaginous tissue with bone tissue. Yeah.

00:27:32.840 Yeah. Got it. Okay. So let's talk a little bit about the preventive medicine side of this. So

00:27:41.120 before we even get into the work that you're mainly focusing on, which is on taking people who are at

00:27:48.280 risk for osteoporosis and maybe holding them back from that or taking people who are in osteoporosis,

00:27:54.320 let's first address the question for the parents who are listening. Because contrary to popular belief,

00:27:59.380 we do not have a huge teenage audience to this podcast. For reasons I don't understand. My

00:28:05.060 daughter just hasn't found this podcast interesting in her little 16-year-old self.

00:28:11.480 So what can I be doing to ensure that my seven-year-old, 10-year-old, and 16-year-old

00:28:18.860 are set up for the best life possible when it comes to bone health, given that I've already given

00:28:25.100 them something pretty good. Fortunately, knock on wood, my wife and I both have pretty high bone

00:28:30.440 density, at least as measured by a DEXA scan. I'd like to talk about how valid or how we could be

00:28:36.960 misled by that if the case. So from a genetic standpoint, they're not set up on the back foot.

00:28:43.480 But I want to make sure that we're going above and beyond what needs to be considered for us

00:28:48.740 from a nutrition perspective, from an exercise perspective, from any other lifestyle perspective,

00:28:53.680 to allow our kids to reach their genetic potential.

00:28:57.840 Well, let's start with the low-hanging fruit, which is diet. Anybody could argue that a balanced diet

00:29:04.420 is important for everything. To be healthy, you need all the nutrients that we've known about for

00:29:09.980 years. And the same can be said for bone. That means particularly, and there are some minutiae,

00:29:15.660 but the most important one, obviously, is calcium. The amount that you need throughout your life

00:29:21.000 does vary. But by the time you're a teenager, you probably need about 1,000 milligrams a day

00:29:26.480 of calcium. And you need the vitamin D to go with that. Otherwise, you can't absorb it from your gut.

00:29:34.640 So making sure dairy is by far the most abundant source of calcium. It's most bioavailable,

00:29:40.860 meaning it's most readily absorbed. It's packed with calcium. You can get most of what you need

00:29:48.460 each day from, well, let's say a regular glass of milk. So 250 mils, that has 300 milligrams of

00:29:57.340 calcium. So if you had three of those, you'd basically be getting what you needed. Not too

00:30:01.280 many people are drinking that amount of milk, although I suppose the number of bowls of cereal

00:30:05.800 my son eats could possibly be approaching that number. But there are sources, you know,

00:30:10.920 cheese and yogurt. And then there's the discretionary foods. If you eat a lot of ice

00:30:14.560 cream and cream and that sort of thing, you can get from there as well. But we would say yogurt and

00:30:18.440 cheese and milk are the best sources. I mean, 750 ml of milk or milk equivalent is probably less than

00:30:26.860 most kids are consuming. Yeah, I would say so, particularly as they move into their teenage years

00:30:33.720 and probably getting more conscious about weight and are thinking that they might be drinking diet

00:30:39.280 soda instead of a milk drink. And it doesn't matter what the fat content of the milk is,

00:30:44.680 I assume. I mean, for the vitamin D, it probably does. But does it matter for the calcium?

00:30:49.580 Well, low fat milk actually does have more calcium in it just by virtue of the fact if you take the fat

00:30:55.120 out, you can fit more calcium. Give more volume. And plus you can buy fortified milk. We have

00:30:59.860 physical in Australia, which has more calcium in it. And I'm certain you guys fortify a lot of your

00:31:05.500 foods. And I believe you do put vitamin D in your milk. So it's nice to get both. But by far the

00:31:12.420 easiest way to get vitamin D is the sun and converting it in the skin. We in particular, Australia is,

00:31:20.660 we are white people living in a black people's country. We have a very high rate of skin cancer here.

00:31:25.320 Sun is extremely strong. So we're quite scared of the sun. We cover up, we slather ourselves in

00:31:32.660 sunscreen, hats, sunglasses, the whole bit. And to the extent that we've actually set ourselves up to

00:31:38.380 have vitamin D deficiency, and particularly in Tasmania, very south, there's a high prevalence

00:31:44.120 of vitamin D deficiency. So it's important to figure out when is a safe time to be in the sun

00:31:50.860 and ensure that you get a little bit of sun, because it is by far the most efficient way to

00:31:56.080 get your vitamin D. Never go even close to getting sunburned, but you don't have to get sunburned. In

00:32:02.600 Australia, we should be able to get our vitamin D requirement before 10am and after two, possibly a

00:32:08.580 little later if you're in a really hot area. In Hobart, in Tasmania, in the middle of winter, you would

00:32:13.300 need to stand shirtless for an hour in the sun to get what you needed. So then you've got to start

00:32:18.400 thinking possibly about supplementation. What level matters? I don't think any of my kids have

00:32:24.340 ever had a vitamin D level checked, although in an adult, we do this all the time. Is there a level

00:32:30.900 beneath which you would say we've got to be supplementing you if you can't do better than

00:32:36.160 this with sunlight? The problem with vitamin D is that nobody can agree. There are two schools of

00:32:44.140 thought. There are two levels that have been published and people will die in a ditch over

00:32:48.740 those. If you've got smart people feeling that strongly about two different levels, it tells me

00:32:55.520 that nobody really knows. What are the two levels that people are dying over? 30 is probably one of

00:33:01.560 them, right? 30 seems to be one of the cutoffs. 30 is, I believe, is the deficiency cutoff, 30 nanograms

00:33:09.280 per milliliter. And 50 is considered sufficient. So in between that, you would have insufficiency.

00:33:16.320 But other people say it's 75. So because this isn't really my area, I don't want to go out on a limb

00:33:22.860 and say which is which. They're easily searchable. There's been a lot of research done. Probably

00:33:28.320 it's dropped off a little now as we've discovered that hyperdosing with vitamin D is not safe and

00:33:35.280 increases falls. To get somebody's vitamin D up quickly, you have to hyperdose. So people have

00:33:42.700 sort of moved away from vitamin D as a strategy to prevent osteoporosis. It's really important that

00:33:49.080 you try to encourage people to be sufficient. And so possibly they will need a supplement of a certain

00:33:55.440 dose. That's going to depend on the person and all manner of other things.

00:34:00.700 I mean, most people are going to require a supplement to be above 50. I do. I mean, I live

00:34:07.040 in Texas and our sun is a lot like yours and I'm in the sun every single day. And I don't even put

00:34:15.360 sunscreen on anything but my face. So my arms and legs, I'm not shirtless usually, but my arms and legs

00:34:22.320 are constantly exposed. And I think if I'm not supplementing vitamin D, I'm lucky to be above 40.

00:34:29.400 I do supplement with 5,000 IU daily. And that takes me to 50 to 60, which again suggests I'm

00:34:39.040 probably okay, but it's not uncommon here in the U S to see people unsupplemented easily being in the

00:34:47.460 thirties. That's not uncommon. Was there a reason that you started supplementing? Did you have any

00:34:53.040 symptoms? None whatsoever. I literally supplement for no apparent reason.

00:34:59.080 Other than some loosely held belief that I'm going to be better off at 55 than 35. It's more the

00:35:08.220 precautionary principle. It's more that I haven't found any compelling evidence that I'm worse off

00:35:13.280 at that level. And there may be benefits to it. I don't feel immensely strongly about it, but again,

00:35:20.000 I'm thinking about this through the lens of children where I would worry more about supplementing

00:35:24.880 a kid because it's harder to measure vitamin D levels in them. You don't want to go and

00:35:29.460 poke them for blood all the time. You would hope you could get it all from milk, dairy,

00:35:35.020 and sunlight. I guess would be my point. Yeah, that would be my recommendation.

00:35:40.880 You know, the other thing is two vitamin D assays are notoriously

00:35:44.520 dodgy. So from one to the next, you may not get the same results. So I don't know. I've never had

00:35:53.060 mine measured. I track my bones to make sure they're doing okay. And that's how I choose to

00:35:59.540 manage it. And I think, as you say, it's just going to have to be whatever your tolerance,

00:36:04.620 whatever your belief is, that's pretty much get as much education as you can and probably follow

00:36:10.060 the guidelines that make the most sense to you. Oh boy. Okay. So we got calcium, which I think

00:36:16.780 based on that, what you said earlier, I think most people are going to struggle to get that much in

00:36:20.880 without being deliberate. So that's something we have to pay attention to. Sunlight. And then of

00:36:25.200 course, with sunlight probably comes another very important part of it, which is if you're getting

00:36:28.980 sunlight, you're outside. And if you're outside, hopefully you're playing. And if you're playing,

00:36:31.980 you're hopefully doing something good for the bones. So do you ever get asked the question,

00:36:35.820 hey, are there certain sports that are going to be better than other sports? Is running better

00:36:41.420 than swimming? Is weight training okay for teenagers or even younger? When do we start

00:36:48.300 thinking about at least doing pushups and things like that, that might also put a little bit more

00:36:53.040 into it? Jumping sports versus non-jumping sports. How do you think through all that stuff?

00:36:57.300 You've hit the nail on the head. It absolutely is extremely important, the type of loading you're

00:37:02.660 doing for bone. So if we're talking about heart, lungs, mental health, metabolism, virtually anything

00:37:08.320 is better than nothing. In fact, anything is better than nothing for bone too. But if you really want

00:37:12.660 to make a difference, get most bang for your buck, then you absolutely are looking for high load

00:37:18.160 activities. And they include things that include jumping and landing and strong muscle movements.

00:37:26.100 The other thing that is probably important is variety and variety within the sport and across

00:37:34.800 sports. So we do tend to find that runners, for example, who have only ever run less protected from

00:37:42.260 bone stress injuries in their running career than people who grew up playing basketball and volleyball

00:37:48.480 and tennis and running. So that variety, if we come back to Wolf's Law, has probably made the bones

00:37:56.060 adapt in a more robust shape to make them more resistant to loading in all manner of ways and

00:38:03.720 also to loading in one direction. So my recommendation to parents is aside from giving your kids the

00:38:11.780 building blocks being enough calcium and exposure to vitamin D every day, then use those building

00:38:17.620 blocks by getting them outside every day. I mean, I know the guidelines don't necessarily say every

00:38:23.680 day, but every day is what you're aiming for because if you tell people every day, then you may get four

00:38:29.360 days a week. And of that exercise, you want it to be as vigorous as possible. Swimming isn't going to do

00:38:36.360 it. Walking isn't going to do it. You need something that is just much more dynamic, varied, and will impart

00:38:44.680 a high strain on bone. And a strain is a measure of deformation. So you're trying to make those bones bend

00:38:50.380 because it's the bending that is coming back to my PhD and what I was trying to solve. It's the bending

00:38:56.960 that is actually forming the stimulus to stimulate bone adaptation.

00:39:03.160 So a couple interesting things there. Swimming and walking, obviously, both have enormous benefits,

00:39:08.320 especially swimming. But again, you're in a zero, not a zero G environment, but a very low G environment

00:39:13.560 that couldn't have less bone loading. The other, I think, very important takeaway there is,

00:39:17.920 and it's funny because I remember seeing a study that looked at this and being a little surprised

00:39:22.180 initially, but I think based on what you're saying, it makes a lot more sense. The study

00:39:26.820 basically showed that runners didn't have particularly great immunity from osteopenia and

00:39:31.940 osteoporosis. And I remember at first thinking, God, how is that? They're loading so much. But your

00:39:36.860 point is, if you're just running, you're just adapting to one very, not simple, but repeatable

00:39:43.880 movement in one direction. Whereas if you're playing soccer or basketball, now you're not just

00:39:49.560 running. You do run, but then you move laterally. You move backwards. You jump. There's more force

00:39:56.040 because you sprint. So all of those things taken together make a bigger difference in creating the

00:40:01.760 variety that you talked about within the sport and then across the sports if you play more than one.

00:40:06.600 Yeah, absolutely. There was a study done at Stanford in 92, well, it was published in 92 by a friend of

00:40:15.260 mine, actually, who looked at the Stanford varsity athletes and compared them to sedentary controls of

00:40:23.920 Stanford students who weren't doing anything. It was really interesting to see that if you compared

00:40:30.880 swimmers, cyclists, runners, and gymnasts to these sedentary controls on the scale of bone mineral

00:40:38.980 density, swimmers were lowest. Then I believe cyclists were the same as sedentary controls because

00:40:47.240 they're also in a weight-supported activity. Runners were slightly higher and gymnasts were, you know,

00:40:53.180 off the scale. Now, this was an observational trial. It's subject to all of those selection biases

00:40:58.920 that observational trials, not trial, it was a study, that are subject to, for example, you're

00:41:05.240 likely to have people who are lighter. So they have lighter bones who are good at swimming because

00:41:10.120 they float better. So it makes them faster. So there's that bias. They may already have had lighter

00:41:15.100 bones. But on the other hand, at that time, I think they were doing about six hours of training a day

00:41:21.080 in the pool and that was actually unloading their bones. So it's amazing to me because the muscle

00:41:28.580 loads that are occurring during, imagine swimming 50 meters of butterfly, you know, there's some big

00:41:34.300 muscle forces, but it's not enough. It's weight bearing loading that is important. And we know

00:41:40.200 this because of how much bone people lose if they go into microgravity. So it was swimming, sedentary

00:41:46.740 runners, and gymnasts in that study? Cyclists too, I believe. And they're the ones who were the same as

00:41:52.460 the sedentary control. So I don't want anybody to take home that any of these activities are bad.

00:41:59.020 They're great for virtually every other tissue. It's just that swimming and cycling and even running

00:42:05.340 are not going to markedly increase your biomass. And the comment about running, when we go for a run,

00:42:11.440 it feels like we're pounding the pavement, but actually the loads you're putting on your body are

00:42:16.160 not that great. And particularly runners that we would consider to have good technique who are running

00:42:21.560 quite lightly. Yeah. Their feet are actually dissipating a lot of the load. The connective

00:42:27.140 tissue in the feet and the muscles within the feet are really a big part of the shock absorption there.

00:42:32.180 Well, that's how we evolved with these amazing arches. But also remember when you land, your ankle

00:42:39.420 is either flexion and extension are weird at the ankle, but your knees will flex when you land and

00:42:44.800 your hip as well. So you've got all this shock absorption the whole way up. So that is dissipating the

00:42:49.260 load. The same thing does happen. You do dissipate loads in gymnastics, but when you watch those

00:42:55.440 Olympic gymnasts do their tumbling runs and they land from one of those crazy tumbles, boom on the

00:43:01.860 floor, they are loading their bones like crazy. So not only are they getting these enormous forces

00:43:07.960 that are stimulatory to bone, but again, this self-selection effect of gymnasts, the ones who had

00:43:15.520 bones like iron to begin with probably were able to remain in the sport because they weren't getting

00:43:21.820 injured. So there is that observational study, you know, there are obviously caveats with the outcomes,

00:43:27.860 but I do think there are lessons to be learned from it. Yeah. And there's another study I saw that

00:43:32.940 expanded that and added other sports to the mix. And the other sports I remember it talked about that

00:43:39.900 were also very, very high were football, meaning American football, jujitsu, and powerlifting.

00:43:47.980 Now, again, my take on that is, I mean, powerlifting is really obvious, right? It's the definition of

00:43:53.420 literally lifting the heaviest weight imaginable. Football has the confounder that if you play

00:43:58.640 football, you're also lifting weights. So it's probably just as much to do with how much weight

00:44:03.360 training goes into playing American football as opposed to the actual act of playing football itself.

00:44:09.900 I would argue that that has benefits from a bone perspective. We could certainly talk about the

00:44:14.380 disadvantages it has as well. And then jujitsu is interesting in that not doing it myself,

00:44:20.520 but two of my three kids do it. And so certainly spend a lot of time watching it at tournaments.

00:44:25.000 But again, a lot of force being put on bones. There is a lot of bone deformation in jujitsu

00:44:31.080 just based on how hard they're tugging and contorting and stuff like that. To me, the big takeaway here is

00:44:39.220 not that we should look at the sports that do the most for bone density and say, that's what we need

00:44:44.920 to do. We should ask the question, what is it about that sport that's doing so much for bone density

00:44:49.840 and how can we replicate that? Because of course, you could also argue that most gymnasts, I assume,

00:44:55.700 have quite a lot of problems orthopedically later in life just based on the nature of the sport.

00:45:01.540 Again, the question is, how do we reproduce it?

00:45:03.880 But fortunately, I would say that a lot of athletes today, such as runners and cyclists

00:45:08.960 and swimmers, are probably spending more time in the weight room today than they were in 1992.

00:45:15.200 The early 90s was really an era when swimming was kind of a six hours in the water, everyday

00:45:21.500 sport thing. And I think today they're spending actually a little less time in the water and

00:45:26.060 they're probably spending more time on dry land. And my guess is if that study were repeated today,

00:45:31.700 I wouldn't be surprised if we found some improvements in the ultra endurance athletes.

00:45:37.440 The takeaway as a parent is diversity of sport and load bearing.

00:45:42.900 A hundred percent. And I think because my other area of research is bone stress injuries,

00:45:47.980 I do talk to coaches of swimmers and that's exactly the advice we give. Get them out of the pool,

00:45:53.760 get them cross training and get them lifting weights. You did ask just before,

00:45:58.580 you mentioned what are the benefits and how early should we get kids doing weight training? And for

00:46:06.180 years, people were very scared of that and thinking, oh no.

00:46:10.000 You'll stunt their growth. Yeah.

00:46:11.340 And there is no evidence of that. And I don't know where that even came from. I mean,

00:46:15.580 people talk about, oh, you'll compress their growth plates. Why? That doesn't make any sense.

00:46:20.440 It just takes a lot to do that. I'm not necessarily saying that you should be loading

00:46:25.900 kids up with enormous weights. There's no need for that, but there is certainly nothing to suggest

00:46:32.400 that you shouldn't do resistance training when you're a kid. I would say the only reason that

00:46:37.700 you wouldn't do it is if they didn't like it, because the thing you don't want to do is

00:46:41.940 discourage a child from being active throughout their life. So the best thing you can possibly do

00:46:47.800 is whatever that child loves to do. And then if that happens to be something that doesn't include,

00:46:54.220 particularly bone loading, then just try and add that stuff in. Don't force it down their throat.

00:46:59.920 Otherwise, it's very counterproductive as those of us with children know.

00:47:04.080 I'm really glad you brought that up. I was going to ask you and I got a little distracted, but

00:47:07.680 I think this is one of those myths that just drives me bananas. And we've looked, I mean,

00:47:13.860 we have tried and tried and tried to find the evidence that suggests that kids can't lift weights

00:47:19.840 and we're coming up empty. We're just coming up empty. And so hopefully folks listening to this

00:47:26.320 are also realizing, and I think as a parent, the easiest thing you can do, especially if you have

00:47:31.260 some equipment at home that you can use to exercise is just have your kids come in the gym with you when

00:47:36.760 you're lifting weights. That's what we do. And never once have I said to my kids, I want you to lift

00:47:42.360 weights. It's just, Hey, we're going to go in the gym and I'm going to lift weights and you can do

00:47:46.600 whatever you want. And look, there's not much else to do in the gym. They're going to start picking

00:47:51.760 stuff up. They're going to start copying you. So anyway, I think it's helpful.

00:47:56.540 It's a great opportunity to teach them technique because that's, what's going to mess people up,

00:48:01.340 not just kids. If they're not doing it right, you don't want a kid just going over and trying to do

00:48:05.540 a deadlift and not doing it right. So there's your opportunity to teach them from a young age,

00:48:09.600 do a beautiful deadlift. There is one of the most useful exercises they can do their entire life.

00:48:15.900 Yeah. I'm glad to hear you say that because my little boys are so competitive with doing

00:48:21.180 kettlebell deadlifts. Now I have to hold them back because as you know, once they start to try to go

00:48:26.220 really heavy, their technique actually kind of breaks down a little bit. I want to talk about

00:48:29.660 another kind of sensitive area with kids that I'm sure you get asked about a lot, which is

00:48:33.760 invariably some kids will have asthma or they'll have other conditions that require the use of

00:48:38.980 corticosteroids, either inhaled or systemic. And I know that we see this in our practice when adults come

00:48:45.720 in and we're surprised to see in an otherwise healthy person, astonishingly low bone density.

00:48:54.520 And of course, through our history, we realize, oh, you took prednisone for this many years of your

00:48:59.720 life. So I know that nobody out there, no physician out there, no parent out there takes it lightly,

00:49:05.520 but is there any guidance you can provide as far as the minimum effective dose? Or maybe is there some

00:49:14.340 comfort you can provide to a parent that says, hey, an inhaler for asthma used at this frequency

00:49:20.760 is not going to impact the long-term bone health of a child?

00:49:24.380 There's no evidence because we haven't got long-term data as far as I'm aware. And again,

00:49:30.580 not really my area. All I can say is corticosteroids should be minimized as much

00:49:39.380 as possible throughout the whole life. If anybody, child or adult, is able to manage their asthma just

00:49:47.540 with ventolin, which doesn't seem to have any negative effect on bone. That is what I would

00:49:53.260 be recommending. Try to stay off steroid inhalers if you possibly can. If you're on high doses,

00:49:59.800 try to titrate them down. See if you can manage in other ways. I don't want to terrify people,

00:50:07.440 but really it is abundantly clear that corticosteroids are the enemy of bone. And the longer you're on

00:50:14.380 them, the more damage they do, they're life-saving for some people. So you have to go on them and

00:50:20.280 then just get off them as quickly as you can once your respiratory condition has calmed down.

00:50:26.840 And of course, if you are in a situation where you must take them and at high doses, then you

00:50:31.940 absolutely would probably need to, absolutely probably, you would really need to consider

00:50:38.500 some biomedication to counteract that. That's what I would be recommending for adults.

00:50:42.840 Maybe the lesson here for parents again is if your child requires being on corticosteroids,

00:50:50.020 well, presumably they really require them. I don't think any doctor takes that decision lightly,

00:50:54.220 but it might just mean that's all the more reason to double down on the other things we talked about,

00:50:59.720 which is if your child is on corticosteroids for a medical need, then let's make sure that that's

00:51:06.140 the kid that's getting 750 ml or 24 ounces of milk a day. And they're out in the sun every day and

00:51:13.800 they're lifting weights and they're doing diverse sports. Because again, let's take everything else

00:51:20.680 and stack it in their favor so that when they come to see their doctor in their forties, the doctor

00:51:27.220 will on the one hand realize, oh, you were on steroids as a kid, but hey, lo and behold,

00:51:31.100 your bone density is actually okay. You haven't been as impacted by it as possible. Are children

00:51:36.880 more susceptible to corticosteroids because they're in a developmental phase or are adults

00:51:44.000 equally susceptible? In other words, does it affect kids more because it's affecting them on the way up

00:51:49.340 or does it affect adults equally because it has just as much of a down impact on them in the

00:51:54.460 maintenance phase? That would be very much stepping out of my lane to answer that one. I don't know the

00:51:59.640 answer to it. All I know is they're bad at any age. Okay. We've got a pretty good primer on what

00:52:06.780 parents need to be thinking about with kids. So now let's turn it back over to the adults. So

00:52:11.140 we're talking about men and women in their thirties and forties. So for most women, they're still on the

00:52:17.820 positive side of estrogen balance. Beyond what we just said for kids, is there anything you would

00:52:23.520 add to that as important tools as a person enters middle life?

00:52:30.060 It's actually exactly the same. You've got to maintain your diet and levels of exercise because

00:52:37.640 your bones need those two elements to maintain. And so in the old days, I'm sure you can picture in

00:52:44.360 your head the trajectory of bone growth, plateauing and loss. And the mantra was, this is inevitable.

00:52:51.100 That's what bone aging looks like. For years, I've been saying, that's what sedentary behavior looks

00:52:58.720 like. And that's what the sedentary effect on a skeleton is. I believe that if you maintain your

00:53:05.120 levels or increased your levels of physical activity, friendly bone loading from the time you

00:53:11.120 were 20 until the time you died, I would be willing to bet that you could go a long way towards

00:53:17.880 maintaining that plateau. And the Masters Athletes data seems to support that. So if you look at those

00:53:25.820 data, you'll see that BMD is maintained in Masters Athletes as long as they're maintaining their

00:53:30.940 activity. There may be a slight loss, yes, but that's probably because the loads that they're able to

00:53:36.580 produce in their physical performance also reduce. But this is an atrophy effect. This is not

00:53:44.000 a genetically programmed aging effect. And I know that there are many people around the world who

00:53:50.100 would argue with me because I don't have much data aside from the Masters Athletes long-term data.

00:53:57.640 But it's almost impossible to collect those data because those are lifelong studies and

00:54:02.060 I would be dead before the study would be finished if I started it now.

00:54:05.880 This is a very provocative idea, but I'll give you an example of where

00:54:10.120 there are two arguments I would offer that suggest you could be right. The first is when you look at

00:54:17.120 spontaneous activity and movement of people as they age, you see a very similar pattern, which is a

00:54:26.500 relative plateau preservation of not just activity, but lean mass followed by a deterioration suggesting

00:54:34.260 that as lean mass goes down, movement goes down, activity goes down, and then it feeds back on

00:54:41.960 itself. It becomes a vicious cycle and away you go. So again, as you said, it could be that what we see

00:54:48.240 as a quote-unquote physiologic decline of bone loss is not that, it's rather a proxy for muscle loss and

00:54:55.960 reduced activity. The second point I would argue, again in favor of this hypothesis, is something that

00:55:02.900 Luke Van Loon, I don't know if you know Luke, but he's a protein scientist and I had him on the

00:55:08.060 podcast recently and he shared something that I thought was fascinating. I've always taken it as

00:55:11.960 a given that anabolic resistance occurs due to aging because, of course, we see it clearly with

00:55:18.480 aging. But he discussed some studies that demonstrated that anabolic resistance was most

00:55:24.040 exacerbated by inactivity and this was done on the CAST study. So you take a given individual,

00:55:29.400 you cast one leg, not the other leg. Before you do that, you run the amino acid isotopes through

00:55:35.220 them. You do this exercise for two weeks. You take the CAST off. So you have an atrophied leg and a

00:55:40.700 normal leg. You do the same amino acid isotopes and lo and behold, there's like 40% or 50% anabolic

00:55:47.680 resistance on the leg that was in the CAST. This is not because they got older in two weeks. It's

00:55:53.620 because they were inactive and they lost muscle activity. If that's true, it really suggests that

00:55:59.520 we shouldn't accept anabolic resistance as an inevitability of aging. And I'm quite inclined to

00:56:05.620 think your hypothesis could be correct here, which is if you just don't stop the movement, if you just

00:56:11.460 don't stop the exercise, this decline of BMD might be far better than what the actuarial data predict

00:56:19.400 based on sedentary behavior. I 100% agree with you. It sounds like a village people's song.

00:56:26.740 Don't stop the movement. You only have to look at those beautiful studies that have shown MRIs of

00:56:33.500 masters athletes' calves compared with an age-matched person who's not active. This is

00:56:39.960 also compared with a young person's calf. The young and the masters look identical.

00:56:45.760 The muscle volume and quality, there's no fatty infiltration and the sub-Q fat is virtually

00:56:52.180 non-existent. Whereas you look at somebody the same age as the masters athlete who's not active

00:56:56.500 and you've got this shrunken down little sarcopenic muscle belly, the fatty infiltration and a big

00:57:02.380 wad of sub-Q fat. You could select anybody from the population and you can make the data look like

00:57:08.520 what you want it to by comparison of those age groups, all those the same age.

00:57:12.820 But the appearance of that masters athlete muscle, essentially, it confirms what you and

00:57:19.460 I are both saying. This is a sedentary problem. This is not an age problem. And of course, this

00:57:25.300 comes back to the problem with a lot of people will say, well, who cares? I know that 60% of the

00:57:30.380 population will not do enough physical activity to maintain that. So we need to invent drugs or do the

00:57:37.260 same thing. As far as I can tell, I never say never, but I think we will struggle to ever find

00:57:43.260 a drug that will be able to replicate the action of exercise, physical loading on muscle and bone,

00:57:50.020 because you can't replicate the stimulus. And any drug that is found to work probably will still need

00:57:57.820 exercise for it to manifest its benefits.

00:58:00.240 Yeah. And there's another deeper issue there because as you know, and maybe the listeners

00:58:05.800 as well, there is an enormous interest from a pharmaceutical standpoint in anti-sarcopenic

00:58:11.880 drugs. You know, as it stands today, obviously we have anabolic steroids and they're very efficacious,

00:58:18.540 but they require the training stimulus. As you pointed out, you can give a person all of the

00:58:23.540 testosterone in the world, but if they don't train, they have zero benefit, virtually zero benefit,

00:58:29.720 slight benefit. And of course the Holy grail is, can we give agents that can cause muscle growth,

00:58:39.040 even absent the profound training stimulus that is needed in other regards? I always say, well,

00:58:45.320 the answer is maybe, but will it be functional muscle? And to that extent, will it be functional

00:58:50.900 bone? So even if a drug like BEMA or an IGF-1 agonist or some of these other drugs,

00:58:59.720 molecules that are being touted potentially increase muscle size, it's not clear that they're going to

00:59:06.080 increase strength function and bony composition. So yeah, it's just the nature, I think, of our

00:59:11.880 species. We really love shortcuts. We do. If we can take a pill, why would you expend any effort?

00:59:17.880 And that's unfortunately the gene, which is going to be our undoing in terms of healthy aging.

00:59:23.680 Right. That actually got us very far when resources were scarce. That was a very,

00:59:28.200 very helpful gene in a resource scarce environment. Let's talk a little bit now about

00:59:33.840 this menopausal transition. It's right up there with death and taxes in terms of inevitability.

00:59:38.900 It's an area that I have become intensely interested in because I view it as one of the great tragedies of

00:59:47.320 the past 25 years is this very popular study done the Women's Health Initiative, which was published in

00:59:53.880 the early part of this century and really came to, in my view, a very erroneous conclusion, which

00:59:59.740 basically scared an entire generation of physicians and women away from HRT. And as a result of that,

01:00:08.280 not only has there been an unnecessary abundance of symptoms associated with menopause,

01:00:14.700 but I think the real hidden tragedy has been the larger epidemic of osteopenia and osteoporosis in

01:00:22.040 a group of women who may have otherwise received estrogen as they went through menopause.

01:00:27.400 So I know that your area of expertise is not in the hormone side as abundantly as it is on the

01:00:33.420 training side, but is there anything on the hormone side that you want to talk about beyond

01:00:37.020 what we've already discussed, which is the important physiology, the important role estrogen plays

01:00:42.820 specifically in managing the role of osteoclasts in bone remodeling? And I assume that most of the

01:00:49.420 women and men, presumably the women, of course, for the purpose of this discussion that are coming

01:00:53.280 into this clinic, are they mostly post-menopausal?

01:00:57.380 Yeah, the majority would be post. We have thousands of people on the books. That number of people who are

01:01:03.780 not post-menopausal is still substantial. So I think the years that we've been open, and we've

01:01:11.020 been open almost exactly nine years now, and awareness has grown in the community about us.

01:01:17.720 People who are not post-menopausal, but are aware that either they have low bone mass already,

01:01:24.480 or that mum or dad or granny or grandpa had low bone mass, they want to prevent it. So it's one of the

01:01:32.720 happiest things that has happened that people are realising that pre-menopause is the time to start

01:01:38.920 taking care of this issue. So we do have a proportion. But of course, most people don't

01:01:43.780 have any idea what their bone health is like until they either have a first fracture, or they go through

01:01:49.760 menopause and they have a savvy enough GP who says, we need to get your baseline, Dexa, let's get you

01:01:55.740 started. And all of a sudden, yikes, I have either osteopenia or osteoporosis, away you go to the bone clinic.

01:02:01.680 You said something very important there, which you and I take for granted. I think it's very

01:02:07.080 important to reiterate for the listeners, for the female listeners in particular, which is you don't

01:02:12.240 want to wait until you're into menopause to replace estrogen. You have to do it during the pre and

01:02:19.100 perimenopausal stage to get the maximum effect. And again, this is something that I think not enough

01:02:26.780 women are being educated on. And as such, even if they know, oh, yeah, I've kind of heard that

01:02:33.060 estrogen matters. And this might be a reason for me to consider HRT as part of my decision matrix.

01:02:40.140 They might think, well, let me go through these two miserable years of perimenopause,

01:02:44.600 wait till I'm completely amenorrheic. My estradiol levels are unmeasurable and my FSH is through the

01:02:51.340 roof and now we should start doing it. No, it turns out that there are data that suggests that

01:02:56.440 they've actually lost quite a bit of bone up until that point, which again, to me is, it's so

01:03:02.660 preventable. I hope that women listening to this are sitting with doctors who can help them through

01:03:08.080 that transition. I'm sure many people listening to us have had a DEXA scan. So when you get a DEXA scan,

01:03:15.260 let's put aside the body composition part of it, where you see body fat and lean mass.

01:03:20.400 Sometimes when you get a DEXA scan, it shows you total bone density and it says your total bone

01:03:27.840 density Z score is this and your T score is that, but it doesn't give any segmental information. It

01:03:34.980 doesn't tell you about the lumbar spine or the hips or the femurs or anything like that. And if you look

01:03:40.680 closely, it might even give you a number in grams per centimeter squared as an actual number. Do you

01:03:46.860 want to just help people make sense of what all those numbers mean? Why, for example, is it grams

01:03:52.240 per centimeter squared, not grams per centimeter cubed as a density? And maybe explain to people the

01:03:58.480 difference between their Z scores and their T scores. And if anything can be understood from the

01:04:04.620 total body Z score and T score, or if we must be looking at segmental. I know there's a lot in there,

01:04:10.140 but have at it. Okay. So dual energy X-ray absorptiometry is a low dose radiation tool,

01:04:19.700 much lower dose than a X-ray of your chest, where the name describes what it's doing. It's sending two

01:04:26.300 energies through the body in a way to determine the density of the tissue it's going through. Now it is

01:04:32.340 a misnomer. It is an aerial density, which is a contradiction because it is a planar view. The X-ray

01:04:42.680 source is underneath and you lie on the bed and the detector is in the arm above. And it is a projected

01:04:48.380 image of this two-dimensional density. They call it aerial bone mineral density because without going into

01:04:57.060 too much detail and I may screw it up, not being a medical physicist, the method of measuring is looking

01:05:02.960 at what is detected according to the density of the material. So it's not volumetric at all. If you want a

01:05:09.940 volumetric density, you have to look at a three-dimensional method of measuring. So you can also get

01:05:16.860 bone mineral content and area from the same scan and they're derived from this density measure.

01:05:22.420 So they talk about it in grams per centimeter squared because it's an aerial measure. So

01:05:28.880 the answer to the question about total BMD, bone mineral density, that is the amount of bone that

01:05:37.380 you're observing from a whole body scan. And normally if your doctor wants to know if you

01:05:43.020 have osteopenia or osteoporosis, they will send you to their radiology clinic and they will do a

01:05:49.700 standard spine and hip scan. They're the normal ones from which you would diagnose those conditions,

01:05:56.800 not a whole body scan. The only reason you would do a whole body scan is if like us,

01:06:02.360 we want to look at body composition because we're interested in lean mass. I wouldn't use the value,

01:06:07.640 the BMD value that I get from the total scan as a marker or as any index for osteopenia or osteoporosis

01:06:16.860 because the who definition was actually based at the hip. In fact, it was based on femoral neck.

01:06:23.580 We've moved away from looking at femoral neck as the standard and we look at total hip now because

01:06:28.840 it can be quite a bit of variation of femoral neck because of the way that you analyze it.

01:06:34.340 So osteoporosis should be really diagnosed from hip BMD according to the definition of the World

01:06:42.560 Health Organization was that a T score of minus 2.5 is definitive of osteoporosis, but a T score

01:06:50.120 between minus one and minus 2.5 is osteopenia or low bone mass. Now that's essentially a T score is

01:06:57.340 a standard deviation. So what is that compared to? Your value is compared to a reference database

01:07:04.900 and the T score is actually comparing your score to what they call a young normal. It depends on the

01:07:13.760 site and that does vary, but let's just say it is roughly a 20 year old between 20 and 30 of the same

01:07:23.580 race and sex. So a 52 year old woman is going, let's say a 50 year old white woman, her value,

01:07:32.440 her BMD value is going to be compared to the average BMD value of a white woman age 20.

01:07:41.320 That's the T score. The Z score is comparing your value to someone the same age and sex. So

01:07:48.500 compared to the average BMD of a 52 year old white woman. So that is, if you're looking at the plot

01:07:57.100 and you have the average score goes up, like David was talking about, and if he doesn't go up because

01:08:03.140 we started at age 20, it's pretty much plateauing and then it begins to go down. So your score will

01:08:09.020 be plotted on there, age 52. If you went straight up to the average value, that is what your BMD Z score

01:08:17.720 is being compared to. So it's a standard deviation from there. The T score is being compared to right at

01:08:24.540 the start of that plot. The reason why they give us these two values is because it's thought that at

01:08:32.100 any stage of your life, if you are two and a half standard deviations away from the amount of bone

01:08:38.600 that you probably started with, then you are at increased risk of fracture. And obviously the

01:08:45.720 problem with that is the fact that you could have started higher or lower than that average. And most of

01:08:50.820 us did, few of us are actually average, but the Z score gives us information about where you lie in

01:08:57.960 relation to your peers, how normal that is. The Z score is normally not as scary as the T score because

01:09:07.180 you will have lost some bone. Yeah. The way I try to help my patients understand it is that, as you said,

01:09:14.000 like I always give them an example, right? Like if your Z score is zero, you're at the 50th percentile

01:09:19.620 of the population. If your Z score is one, you're a full standard deviation above the mean. So what's that?

01:09:27.040 You're in the 85th percentile, if I'm doing the math correctly. And obviously, as you said, the T score

01:09:33.000 is always going to be lower because we're comparing you to a perfect standard. We're comparing you to that

01:09:38.600 super healthy 20 to 30 year old. So what we say to patients is, look, we want your T score. If you show up

01:09:46.000 with a decent T score, your T score is zero and your Z score is plus 0.8, we say the win is keeping

01:09:55.440 that T score where it is and watching the Z score go up. Because over time, we want you being better

01:10:03.900 and better and better than your age matched peers because they're going down and we're going to hold

01:10:08.500 you plateau. And that means we can't improve you relative to the T score. Although I'd love to hear in

01:10:14.460 your experience what you're finding there, but we can improve you relative to your peers.

01:10:19.820 Yeah, it's a good example. And yes, you're right. We can improve the T score.

01:10:24.460 Let's get right to it because this is going back to the outside of this discussion. I learned about you.

01:10:30.240 I don't even know how. I think I was like literally just watching stuff on YouTube and

01:10:33.760 somehow saw a clip. It's probably many years old from local news in Australia highlighting you

01:10:41.640 talking about the Lift More study. And there's just something like if you look at the things that

01:10:47.880 I can get sucked into on YouTube, it's car videos, F1 videos. There's this world that just sucks me in.

01:10:57.120 But I'll tell you another one of the things that sucks me in. Videos of elderly people lifting weights.

01:11:03.560 I can go down that rabbit hole. I mean, it's ridiculous. You show me a 90-year-old woman

01:11:11.160 deadlifting and I could watch that for days. It must be that the algorithm knows that.

01:11:16.820 It served you up to me. So let's talk about the Lift More study.

01:11:21.380 I suppose around about 2013, I got to a point in my research career where I looked around and thought

01:11:31.360 the exercise guidelines for osteoporosis are get your kids jumping and running and playing as much

01:11:37.440 sport as possible. Keep doing that for as long as you can. But then when you get osteoporosis,

01:11:43.320 stop doing all that and just prevent falls so you don't break. So are we done? Is this the best we can

01:11:50.180 do? This is lame. All my animal research experience had told me that even with very low bone mass animals,

01:11:57.820 if you load them, they can grow bone. The only reason we hadn't been doing that in research is

01:12:04.100 because we were terrified of hurting someone. And so it seemed to me we hadn't really tried.

01:12:11.780 And at the risk of hurting somebody, we decided to do it. So we had three physiotherapists on that

01:12:19.600 trial, including the PhD student who ran it, Steve Watson. We decided to do a brief because bone

01:12:27.600 doesn't need a lot of loading. You don't need to run a marathon. You just need to do one sprint to get

01:12:31.820 those bone cells stimulated. So we had twice a week, 30 minutes, four exercises, and we wanted them

01:12:40.660 lifting heavy. So it was 85% 1RM. We used compound movements. This needed to be an efficient project.

01:12:48.340 We wanted to involve as much muscle as possible. It needed to be weight bearing. And we wanted something

01:12:53.260 that would transfer to really useful daily activities. So clearly a squat and a deadlift was going to be

01:13:01.080 fundamental. These are fabulous compound movements that they tick all those boxes. And these are not

01:13:06.520 on machines. This is with free weights because you want to engage as much of those other systems and

01:13:13.140 capacities as possible. We're trying to improve balance because we're trying to stop people falling.

01:13:17.500 So away we went. Ideally, we wanted it to be 12 months because you do need a fair amount of time

01:13:23.580 to be able to detect change on DEXA because DEXA, ionizing radiation, picks up mineral. So you can't

01:13:30.560 just measure new bone, which would be the osteoid, unmineralized. You need a full period of time to

01:13:36.020 allow for a full remodeling cycle and mineralized bone. Because it was a PhD project, we couldn't afford

01:13:42.260 a full year for each person. So we just made it an eight-month intervention, which I was confident would be

01:13:47.380 enough to detect a change. We did really comprehensive bone and functional measures at baseline. We

01:13:56.480 recruited about 100 people, randomly allocated them to this high-intensity resistance and impact

01:14:01.680 training. Exercise research is really hard to blind to your participants, and blinding is so important

01:14:07.960 in clinical trials. So we had to not tell our participants which was the intervention that we

01:14:14.320 thought was going to be effective. We just said, if you got randomized to this low-intensity home

01:14:19.200 program, we were trying to see whether that worked too. Of course, we knew that that was not going to

01:14:23.820 work because we've got years of experience to know that that is not going to improve bone.

01:14:27.760 But we gave them things like walking, stretching, some body weight lunges and toe raises, and things that

01:14:35.080 would potentially improve their balance. So we weren't completely ripping them off. So then we had

01:14:42.400 eight months of this intervention. It was supervised. Sorry, once again, Belinda, you said the treatment

01:14:47.120 group was 20 minutes, three times a week? No, 30 minutes, two times a week.

01:14:52.580 Got it. Yeah. Maximum group size was eight, and we recruited post-menopausal women. So we were looking

01:15:00.400 for people, we advertised for over 60, but I think we did recruit one person who was 58 because she had

01:15:06.820 been through menopause when she was young and they just needed to be well clear of menopause. We didn't

01:15:12.600 want to be fighting that withdrawal of estrogen phase and they needed to have low bone mass. So

01:15:18.440 they needed to be at least a T-score of minus one at either the spine or the hip. So away we went.

01:15:26.680 And I have to say, we were looking through our fingers for a little bit and we were so incredibly

01:15:32.300 conservative to begin with and just being very careful that we weren't hurting anybody. It became

01:15:38.200 abundantly clear very quickly that we weren't hurting anybody. In fact, we were making people

01:15:43.100 feel a lot better. Let me just ask you about that because the video, which we'll link to in the show

01:15:48.700 notes, even though it was just a local news segment, was just really inspiring. I think there were women

01:15:54.520 there that were at some point basically able to pick up their body weight. Am I remembering that

01:15:59.020 correctly? Like literally these women were deadlifting their body weight. How did you even

01:16:05.020 train them to do this? These women show up to this study and they're probably told it's an exercise

01:16:11.420 study. So they think, great, I'll be doing pool jogging or something. And then you drag them into

01:16:17.440 a weight room with Olympic bars. How did you even go about getting them to do this safely? How much

01:16:23.420 resistance was there on their part to the fear of weightlifting? I assume prior weightlifting

01:16:29.380 experience was not an inclusion criteria? No, they could have had it, but they couldn't have been

01:16:34.220 doing anything in the past 12 months because you know bone is a use it or lose it tissue. So

01:16:38.800 they needed to not be already doing this. We told them what the basic exercises were. So these had to be

01:16:45.500 people who were willing to do this. We never throw somebody straight into lifting something extremely

01:16:52.740 heavy. And certainly nobody would have expected that we would end up with people lifting their

01:16:57.560 body weight. Certainly, at least of all us. We just did it very systematically. You start with a broomstick

01:17:05.700 and you make sure that people's technique is good. And I have to tell you, we had people with fractures,

01:17:12.240 so they had existing kyphosis. And you know what a kyphotic curvature looks like in a deadlift position.

01:17:17.980 This is not a pretty thing. But as long as they had an extensor moment, it was okay. We don't want

01:17:25.300 people flexing and lifting weight because then we're putting them at risk of fracture. But it's

01:17:30.100 all in the coaching. And this is the reason why it's so important that the person who is coaching

01:17:34.580 somebody with osteoporosis knows what they're doing. They can't just be a strength and conditioning

01:17:40.080 coach, although that really helps. They have to have some clinical training. So because people come

01:17:45.940 to you in a clinic with not just osteoporosis, but pelvic floor dysfunction, frozen shoulder,

01:17:53.360 spondylolisis, vertigo, knee OA, you've got to be able to manage that. Many of those conditions were

01:18:01.420 actually screened out of the Liftmore study because it was the first time we were doing it. We didn't

01:18:05.700 want to have to manage all of that. But I just put it out there because it's something I want to

01:18:10.640 remember to talk about. So it was all about just systematically training them in the technique

01:18:16.700 and then gradually increasing the load. And a lot of people think of older people and particularly

01:18:24.100 older women and particularly post-menopausal women who the assumption is they go completely loopy

01:18:29.300 through menopause, which is not true. They think about old people as completely incapable,

01:18:34.800 incapable of doing stuff and incapable of learning. But old people are you and me who just kept living

01:18:41.300 longer. We have the capacity to learn and older people are perfectly capable of learning how to

01:18:47.640 do a deadlift and a squat. It might be pretty ugly to start with, but they get better. And as they get

01:18:53.660 stronger, they get even better. I just love it so much. I cannot, for people listening and not

01:19:00.320 watching right now, just the grin on my face listening to you talk about this, it just warms

01:19:05.280 my heart. I just agree with all of that. I think that one of the saddest, I think, misconceptions people

01:19:11.460 have is that once they get to a certain age, it's too late and they sort of accept their fate. And,

01:19:17.380 oh, I have this kyphotic spine and, oh, my bones are too brittle and I guess I'm just going to spend the

01:19:24.180 next decade of my life doing nothing. And studies like this demonstrate that that's not the case.

01:19:28.980 I'm looking for some of the other kind of soft stuff as you think about the evolution of this

01:19:32.740 study. I mean, what else did you notice in the subjects? What did they tell you? How did this

01:19:36.820 translate into the rest of their lives? Because obviously you as an investigator are looking for

01:19:42.680 something very specific. You want to probably understand how much muscle mass they put on,

01:19:47.220 what their bone density did, how much their T-score has changed. But were there other things that you

01:19:51.900 learned about these women as the study went on that spoke to their quality of life?

01:19:56.120 Yeah. Undoubtedly. And for them, that was the most important thing. And that is what made me

01:20:01.240 want to open the clinic. This is a quality of life issue. It turns out this is not a bone issue.

01:20:08.540 I'm a bonehead. I care about what their BMD scores did. But the reality is comments like,

01:20:15.640 oh, my God, Belinda, I can see my shoulders in the mirror again because their posture changed.

01:20:20.360 When you do a clinical trial, you measure height and weight as the standard baseline,

01:20:24.300 how to describe your population. Who knew that we would actually be citing height as an outcome

01:20:31.660 because the control group shrank, whereas the intervention group grew a little. Of course,

01:20:37.940 they didn't grow, but their posture improved to the extent that they were taller at the end of the

01:20:42.820 study. And the difference between groups was significant. It was only half a centimeter, but hey.

01:20:48.620 That's in eight months.

01:20:50.600 Yeah. If you like soft outcomes, people saying, my husband is hiking the Kokoda Trail and I just

01:20:57.320 thought I was going to be cheerleading. I can go with him now. I've got this incredible strength.

01:21:02.180 I've basically got my life back. I can get into the garden and I can push the wheelbarrow full of

01:21:08.220 potting mix around now and I don't feel like I'm going to break. I can lift my grandchild again.

01:21:13.720 I can get my own shopping out of the car. It's all about independence. Yeah. Quality of life,

01:21:22.000 major quality of life as well. And at the clinic, it's pretty obvious that that is something that

01:21:27.060 is improving.

01:21:28.560 So what did you find after eight months with respect to muscle mass, bone density,

01:21:32.200 and the other sort of clinical metrics?

01:21:34.040 We ended up with a net benefit of a bit over 4% at the spine. That equated to about 3% improvement

01:21:42.620 at the spine in BMD and about one and a half or one and a bit loss in controls. I would say that

01:21:49.920 this program definitely has the biggest effect of the spine. That is a good thing because it's one

01:21:55.300 of the places that fractures most frequently. At the hip, it was a real head scratcher. When I first

01:22:02.600 looked at the results, we had something like a 0.6% improvement at the femoral neck. And I'm

01:22:08.340 thinking, these women deadlifting and squatting 70 kilos, how can that be? We ended up with a

01:22:14.540 significant difference because the controls lost two and a half percent. There was a net benefit,

01:22:19.120 but I couldn't figure it out. Luckily, I have some 3D hip software, which allows me to reanalyze my

01:22:27.080 2D BMD data from DEXA and look at the changes in geometry. From that, you could see things like

01:22:37.860 cross-sectional area of the femoral neck, cortical thickness, and so on. When you look at cortical

01:22:43.340 thickness of the total femoral neck, there was a 13% net benefit in the intervention group. And if you

01:22:51.860 looked specifically at the lateral femoral neck cortex, there was a 27% improvement. So it turns

01:23:00.580 out that if you were just looking at BMD from DEXA, it would look like this kind of lifting only has a

01:23:06.980 maintenance effect at the hip. But actually what's happening is it's changing the geometry. It's

01:23:12.260 making it stronger by making the cortex, that cortical bone, thicker and more resistant to bending.

01:23:19.720 So that was another of those fantastic moments where I had only just got this software and was just

01:23:27.520 in time to show this really novel outcome. I think that's such an important point, by the way.

01:23:33.880 And given that most of us clinicians don't have access to that, can we, in your opinion, rely on

01:23:41.080 the stabilization of the Z-score or the improvement of the Z-score, the stabilization of the T-score as a

01:23:46.620 win if we're in that situation? So we have that patient who comes in at a minus two, you get them

01:23:52.420 on a strength training program, they're putting on muscle mass, the Z-score gets better, but the T-score

01:23:57.660 does not. You still say, look, you're probably winning, even though you don't have the radiographic

01:24:03.340 tool to document the cortical bone thickening? Yeah. If you can maintain bone mass at the hip,

01:24:08.960 bone mineral density, yes, that is absolutely a win. Don't get me wrong, there were some people who,

01:24:14.160 probably the largest gain we had at the hip in the lift more study was about 6%. So there were some

01:24:19.180 people who improved BMD, but yeah, on average, it's something that you don't always see.

01:24:24.920 The important thing I think for people to understand here is even if going on this type of a training

01:24:31.560 program at best maintained you, let's assume even the cortical thickening was maintained.

01:24:37.860 There's two important points to consider. The controls are having the floor dropped from

01:24:44.520 underneath them. So that gap between what you would be doing and what you're doing is widening,

01:24:51.640 even if you're not getting better. So the fact that you're even getting better slightly is mind

01:24:56.060 boggling. But even if you don't, the gap between where you are and where you would be is enormous.

01:25:01.840 The second point is your fall risk is going down dramatically because you're putting on muscle

01:25:10.860 mass. And to the very important point you made, you're using these free weights and you're improving

01:25:17.420 your balance. So you have more muscle, more balance, more motor control. The likelihood of falling to get

01:25:24.280 in the position that you're going to break a bone is going down so much. So when you add to the fact

01:25:29.060 that, oh, and by the way, cortical bone is increasing by 13 percent, this is just a win,

01:25:33.220 win, win, win, win across the board. And show me a bone drug that does that.

01:25:38.620 If you look at our functional outcomes, we had back extensor strength, leg extensor strength,

01:25:43.980 and then we had tandem walk, timed up and go, sit to stand, vertical jump. And we also measured

01:25:51.540 kyphosis. All of those things improved, but especially lower extremity strength and back extensor

01:25:58.100 strength. Now, people think, oh, well, back extensor strength, yes, it's just making them

01:26:02.140 stand up straighter. There's no just about it. If somebody has kyphosis and their posture is such

01:26:08.060 that their vision is angled downwards, they've lost that peripheral vision for, say, when they're

01:26:15.380 walking to their car at the shopping center, which is not their comfortable environment. Perhaps a

01:26:22.020 little kid runs out in front of them and they haven't seen them coming. And that's when a fall can

01:26:27.460 happen on a hard supermarket floor, walking outside their own home and the neighbor's dog runs out.

01:26:33.780 They don't see it coming, they get a fright and they'll fall. So posture is actually really,

01:26:38.700 really important to full risk and risk of fracture because we know pretty much half the time you fall,

01:26:43.760 you're going to fracture. I would add something even more to that, which is we have a couple of

01:26:48.700 folks in our practice who are really forward thinking in their understanding of the role of

01:26:54.280 vision in brain health. And we know this is true with auditory stimuli as well. So we know that

01:26:59.840 hearing loss is a risk for dementia because it's reducing sensory input to the brain.

01:27:06.240 And we would argue that you see the same thing with a reduction of visual input. So a reduction of

01:27:12.000 visual input is a reduction of cortical stimulation, cortical meaning brain cortical, and that's also

01:27:18.680 increasing problem. So in addition to everything you said, which is this increased risk of falling

01:27:23.300 as vision is getting narrower, you're also reducing brain input. And I think you run the risk of also

01:27:30.460 exacerbated or accelerated degeneration of the brain. So yeah, I agree with you completely. It's not that

01:27:36.760 you just reversed kyphosis. That's a really big deal to get somebody looking up and forward.

01:27:43.640 The other things that I'm sure you saw were improvement in grip strength. So there's another

01:27:48.360 benefit because you can't deadlift without grip strength. If a woman's picking 70 kilos off the

01:27:53.800 ground, think of how strong her hands are and think of the implication of that on mitigating fall risk.

01:28:01.080 You think about that person walking down a flight of stairs. Now imagine the grip they have on the

01:28:06.220 handrail as they confidently walk down the steps. You think of the devastating injuries that people can

01:28:12.900 have of any age, but certainly older people when they can't hold onto a handrail, and then they

01:28:18.040 don't have the leg strength to stop themselves. Just to reiterate this point that we can't make

01:28:22.480 enough, which is, yes, there are some really interesting and exciting drugs on the horizon

01:28:26.300 for the management of this. Yes, pharmacology and endocrinology play a very important role in

01:28:32.540 managing these things. I would argue estrogen more than any other drug out there, but none of these

01:28:37.880 things compare or should ever be thought of as a substitute for what you're describing.

01:28:43.440 No, that's right. I briefly mentioned the tandem walk and sit to stand and timed up and go and

01:28:49.180 vertical jump, and all of those things are risk factors or predictive of your risk of falling. So yeah,

01:28:55.520 we do know that improving those things reduce your risk of falling. You're quite right about grip

01:29:00.460 strength. I do as much of this lifting as I can, but I'm frequently, I've just been to Europe for a

01:29:05.860 month. I've been to the US for a month and my lifting falls away. So I come back to the gym and

01:29:11.500 go to lift again. And whereas my muscles, my major lifting muscles may be okay, but I end up on my

01:29:18.760 last set. I am just holding onto that bar with my fingertips because my grip strength goes.

01:29:23.800 So it is absolutely part and parcel. This is why these Olympic lifts are so incredibly helpful

01:29:30.080 because they are compound movements using virtually every muscle in your body, including if you're

01:29:36.500 frowning while you're doing it. So Belinda, there's no chance that anybody listening to us

01:29:42.440 at this point would call into question the value of this type of intervention. So now the question is

01:29:48.940 for virtually everybody listening to us, they don't have access to you and they don't have access to

01:29:53.700 your clinic. What would be the advice for the men and women who are coming to this discussion or people

01:30:02.000 listening to this who want to send it to their parents or loved ones who really are showing up

01:30:06.760 and are in the same state that the women were in at the beginning of your study? How can we take that

01:30:14.160 person, provide them with the safest environment to go forth and conquer? Because again, if you're saying

01:30:21.040 all you got to do is 30 minutes twice a week of this very, very specific type of lifting protocol,

01:30:28.000 which is again, very straightforward in concept, obviously in technique, it requires execution.

01:30:34.500 How can they go about doing that? Who would you recommend they see? What type of individual to coach

01:30:39.620 them? So there's levels to that answer. And without turning this into an advertisement for Onira, which is

01:30:46.780 what the program is called, that we deliver through the bone clinic, we get that question all the time.

01:30:52.040 The minute I opened the bone clinic, everybody wanted the program. And the problem is I didn't want to

01:30:57.380 initiate an avalanche of fractures for people doing the program and hurting themselves. So we decided to

01:31:04.620 license it and provide that program to physiotherapists, what you guys call physical therapists,

01:31:11.960 and accredited exercise physiologists, all their equivalent. And we have licensed, there's probably

01:31:18.240 about 60 in Australia at the moment and a growing number overseas now. It's just starting to take on

01:31:24.160 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

01:31:29.800 they get it. The training for that is a very comprehensive six hours online. You must have these

01:31:36.220 qualifications to do it. And then you're ready to deliver it to your patients in your clinic,

01:31:41.780 as long as you have the gear. And they've always got access to me and a lot of supportive information

01:31:46.860 to do that safely. The reason I want physios and EPs to deliver it is because they have that

01:31:53.040 background information that I was telling you about, that clinical training that allows them

01:31:57.260 to look after the millions of different comorbidities that are going to come into their clinic.

01:32:03.520 So tell us again, Belinda, just to make sure everyone's hearing this, and we'll link to it

01:32:07.500 in the show notes. But what's the name of the program? Where can somebody go as an exercise

01:32:12.740 physiologist or a physio to become accredited in this program?

01:32:17.920 O-Nero is the name of the program, and they just need to Google O-Nero Academy.

01:32:23.860 O-N-E-R-O?

01:32:26.040 That's right. Yeah.

01:32:27.540 Okay. We'll link to it. Yep.

01:32:29.220 And they can read about it.

01:32:30.360 This is not something that the patients go to. This is something

01:32:34.040 that the trainers go to to become accredited. So if a person is listening to this and they want

01:32:40.480 to be trained, can they go to that site and find out where the accredited people are?

01:32:47.180 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,

01:32:53.200 you'll see a little red tag. If you click on the tag, the contact details of that O-Nero provider

01:32:59.620 will pop up. Now, as I say, at least in the US, not a huge number of them at the moment, but

01:33:05.060 the demand is so incredibly high in the US. Really, the best thing that you could do if you were in

01:33:12.460 that situation and you wanted to go to an O-Nero provider is go to your local PT or kinesiologist,

01:33:19.140 exercise physiologist, some equivalent, and say, okay, you need this program. Here's the website.

01:33:26.140 Contact Belinda. And I can get them licensed and away they go. For me, it's research. There is a

01:33:32.360 way for them to contribute to our research program. I give them access to our database. I'm really

01:33:37.420 interested in making sure that this works, not just in our hands. And so that's part of my research.

01:33:44.700 But for them, of course, it's a revenue stream. So it is a win-win for them.

01:33:48.480 For the patients who cannot convince anybody to do O-Nero, then the next best thing would still be

01:33:56.380 to contact the bone clinic. We can do a telehealth appointment with them and give them our very best

01:34:01.260 advice for a program that they can do either at home or at a gym. If they don't want to do that,

01:34:07.220 then the next best thing they can do is just go to the gym and get some gym program. Just anything

01:34:15.200 is better than nothing and start lifting weights and try to get some supervision because if you've

01:34:21.100 got a T-score of minus four, I'm not comfortable with you training by yourself. So even if you're not

01:34:26.320 doing O-Nero, get somebody to look after you. So those are the sort of three levels. If you can find

01:34:32.120 an O-Nero provider, do supervise O-Nero. If you can't, call, email the bone clinic and we'll do a telehealth

01:34:39.120 appointment and get you a program that you can do, which would be the very best that we can come up

01:34:44.260 with that you could do unsupervised. And then the next level down, just get yourself to the gym with

01:34:50.940 someone supervising you and do some weights of some kind. I guess I'm going to add a fourth one,

01:34:56.580 which is I've been to the Gold Coast many times. It's absolutely spectacular. I think a trip to

01:35:02.580 Australia is never a bad thing. Maybe scrap the telemedicine visit and just take a two-week

01:35:07.940 vacation to the Gold Coast and get some time at the clinic maybe. We'd love to see you. Actually,

01:35:13.100 the clinic's in Brisbane. I live on the Gold Coast because that's where the university is,

01:35:16.940 but the clinic's just up there. Well, Brisbane's gorgeous as well. Belinda,

01:35:21.040 this has been excellent. I'm just so excited to make sure that everybody out there who's listening to

01:35:26.620 us has access to this type of information. I think this is a remarkable demonstration of the

01:35:32.540 power of exercise. People hear me say this all the time, and I'm sure they're sick of hearing me say

01:35:36.760 it. It is the most potent drug available. I am a very pro-pharma guy, but there's just no denying

01:35:45.500 the evidence. There is nothing that a pill can do to touch the benefits of exercise. This is about as

01:35:53.140 pointed as an example as you will see. I love hearing about how in such a relatively short period

01:35:59.880 of time, these women had such a dramatic improvement in their quality of life. It's

01:36:05.140 such an exciting story. It's really had a greater impact on their quality of life than I can think

01:36:09.580 of any other intervention that any healthcare provider could demonstrate. Anyway, thank you

01:36:14.600 for your work, and thank you for, like I said, getting up early this morning to share it with us.

01:36:18.680 It's my pleasure. It's lovely to meet a kindred spirit.

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The Peter Attia Drive - October 21, 2024

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

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