Good Life Project - Groundbreaking Science on Bone Health (Your Genes Are Not Your Fate) | Belinda Beck

Episode Date: June 9, 2025

Defy gravity and rebuild your bones at any age with Dr. Belinda Beck's pioneering high-intensity resistance training protocols.In this groundbreaking conversation, the Professor of Exercise Science shatters myths around weightlifting for women and reveals how targeted loading can stimulate new bone growth - even for those with osteopenia or osteoporosis. Prepare to have your assumptions shattered and unlock a life without fear of fractures.You can find Belinda at: Website | LinkedIn | Episode TranscriptIf you LOVED this episode, you’ll also love the conversations we had with Dr. Adeel Khan about cutting-edge treatments like stem cells and gene therapy to heal the body.Check out our offerings & partners: Join My New Writing Project: Awake at the WheelVisit Our Sponsor Page For Great Resources & Discount Codes Hosted on Acast. See acast.com/privacy for more information.

So I am an age where for the first time I'm starting to think about the health of my bones. We tend to lose density and strength as we age. Although some people might argue I'm actually getting more dense as I age. And the effects on our bones can be pretty brutal from pain and fractures to serious limitations. You hear words like osteoporosis or osteopenia and wonder what exactly is that? And what does science say we can do to keep the bone we have and potentially even slow down or reverse any loss that we might be experiencing no matter how old you are? There is just so much misinformation

and mythology in this area. So I wanted to talk to somebody who's not only a leading voice, but also a primary researcher who is changing what we once believed was possible. My guest today is Dr. Belinda Beck, professor of exercise science at Griffith University and director of the Bone Clinic in Australia. With over two decades of research, her pioneering work has revealed some really powerful new insights to stimulating new bone growth through targeted high intensity resistance training,

even for people who had for years been written off as beyond being able to be helped. You're about to hear the remarkable stories of Dr. Beck's study participants who despite osteopenia and osteoporosis diagnoses and being later in life achieved astonishing increases in bone density and skeletal resistance. Though pretty much shatter every myth you've heard about women and weightlifting, in this mind blowing conversation,

you will discover a groundbreaking approach that defies conventional wisdom and unlocks your body's innate ability to fortify this foundational structure from within. So imagine unleashing a life without fear of fractures, moving with confidence, embracing activities you love. That is the transformation that Dr. Beck's evidence-based exercise protocols have delivered for countless individuals now worldwide. So excited to share this conversation with you.

I'm Jonathan Fields and this is Good Life Project. with you. I'm Jonathan Fields, and this is Good Life Project. Before we really dive into some of the details in Nitty Gritty, I'm also curious, just on a personal level, you chose this area as something to devote your professional life to, to really deepen into the research. What drew you to it? Was there something specific or was this sort of like just something you stumbled upon? I think most people who really get down in the weeds in a subject, there is a connection. For me, I was a runner and a hockey player and I used to suffer from medial tibial stress syndrome, what everybody used to call shin splints.

Shin splints, right. So my master's project was an anatomical study of the things that attach to the leg there because everybody thought it was a muscle problem. And it just became very obvious very quickly to me that this is a bone problem, not a muscle problem. And so my PhD, I wanted to know what it was that was signalling the bone to adapt because that was sort of the mystery at the time. And so I did an animal project to do that because you really can't do that in humans. Then I really discovered that I can't do animal research because it entails killing animals and I don't want to do that for my entire life. My postdoc was learning

clinical trials at Stanford and they were all about osteoporosis then rather than bone stress injuries. So I have continued studying bone stress injuries throughout my career, but you cannot get funding for it unless you go to the army. And it was very obvious that osteoporosis was a much, much bigger problem to the population, the world population at large. So I sort of went in that direction because it seemed like a more meaningful place to go, but it did allow me to keep my hand in because I'm an exercise physiologist at heart and I really do think that exercise is medicine. So it just seemed like the logical way to go. Bone stress injuries are from people doing too much too soon. Osteoporosis is probably not enough ever.

Dr. Justin Marchegiani Yeah, that's such an interesting contradiction or contrast. As you were describing what I grew up calling shin splints, I grew up when I was a kid, I was a competitive gymnast, I trained year round until I was about 20 years old. And I kind of lived with this pain in the front of my shins, perpetually, we were just sprinting down hardwood floors, like landing, and it was also a very different role, we trained differently back when I was doing this. And I was always told it was a soft tissue issue, you know,

like this has nothing to do with the bone. And it was just like, you just learned to live with it and you're walking around in pain. Yeah. The thing that I suppose the hook that really got me in was when I started, and this is as a PhD student, learning what an incredible tissue bone is. I mean, if we thought about all the structural materials that engineers use, if they could find a self-healing concrete, that would just transform engineering. But we've got one, and it doesn't heal with a scar. It heals with fabulous new tissue

and can be even stronger than it was. So it's wonderful stuff and we can't trick it either. We like to think that we can by giving people meds, bone medications that will lay down more bone and they work for that, but it will put that bone anywhere. Whereas exercise gives the bone a signal where the bone is bending the most because of that load and the bone adapts to avoid injury in that site. So it's this site-specific, really targeted, effective response. It's fabulous. I wanted to have a lot more into that, but before we get there, I want to understand bone a little bit better.

Because people we listen to, they're like, okay, I know that I have this thing inside of me called the skeleton. I have heard, and a lot of our listeners are in the middle years of their lives, a lot of them are women who are pre-menopause, pre-menopause, menopause, post-menopause, and a lot of them also probably have kids. So they're thinking about the full spectrum of that. When we think about bone, I think a lot of us, we kind of look at it as, okay, we have the skeleton side of us. It's this hard structural stuff that allows us to be upright and muscles and soft tissue can work against it. But kind of look at it as this thing where it's sort of like, it's this inert thing. It's not, I think a lot of folks don't look at bone as being alive.

So take me into like, what are we actually talking about when we're talking about bone? Well, nothing could be further from the truth. It is very much alive. It is full of cells, bone cells, which are called osteocytes. They're all throughout the bone. They live in tiny little caves of their own. The very cool thing is that they're not in isolation. There are channels

between those little caves where the bone cells reach out and actually hold hands if you like. So there's this massive system network of communication of all of these cells in bone. And not only that, there is a huge blood supply in bone. So that's why if you break a major bone, you are in danger of bleeding to death unless you stop that. So very much alive and very much able to adapt to stimuli because of that blood and that cellular network. So when we injure bone, probably everybody, if you get to a certain part of your life,

you've done something to a bone in your body, whether it's a bruise or a fracture or a break. I've certainly had my fair share. When bone heals itself, what is it actually doing? Well, it has not to get too much into the detail and send everyone to sleep, it has a cleanup crew that comes in first and sort of gets rid of all the mess. There are a bunch of chemicals that float around and pull other cells in to help do that. And then sometimes creates a little bit of a cartilaginous matrix and the cells can go into that then and convert that into bone and sometimes it just bone cells come along and actually lay new bone straight on to the fracture.

There are two kinds of cells osteoclasts which are the bone reservoirs and osteoblasts which are the bone builders. The osteoclasts, which are the bone resorbers, and osteoblasts, which are the bone builders. The osteoclasts will come along if there's a microcrack, so not a complete break, but a microcrack. They can detect there's a crack there because it probably has disrupted that network of cells I was telling you about. So the osteoclasts will munch along that crack and then the osteoblasts come along behind it and lay down perfectly

new bone. So just a little repress, and you wouldn't even know that the crack was there once it's done. So that's why I've had moments in my past where I've done something, I felt pain in a particular joint. A couple of months later, I've gone back and I'll get an x-ray and I would hear from the doctor, well, you had a fracture and it's basically healed itself. If you had a fracture in the middle of a long bone and broke it completely, so that's a fairly drastic kind of a thing, back in the day before orthopedic surgeons, people still

fused bones and if you get them roughly in alignment, the bone will fuse back together. If you get them perfectly in alignment you'll just get a little bit of a callus around the outside and over time that callus will resolve and then it'll look like nothing's happened. If you are unlucky enough to have a fracture you know right out in the bush and just stuck out there for months and maybe the bones don't align properly, maybe they'll elapse slightly, they can still fuse in that position. Unfortunately, that means you've probably lost a bit of length of that bone. They'll still fuse there and over time, they'll remodel a little bit, but you're almost certainly going to retain some of that defect because that's pretty full on.

But what was probably obvious about your previous fracture is that the callus was still evident, so the thickening around it was still evident. But over time, as I say, even the callus normally will resolve. So we have these osteoblasts that lay down, nubo and osteoclasts kind of go around as you described, munch it up. And as you're describing that, I'm also remembering years years ago I remember reading about this procedure that was I guess initially developed for kids who had a limb, generally a leg, that was substantially shorter than the other

where they would literally go in, take the large bones in the leg, cut them, effectively screw an exoskeleton on them, and then every day ratchet them apart a millimeter a day and then the bone would fill in. So I guess what you're describing is, I guess especially when you're a kid, this is probably much more efficient, that those osteoblasts would just create new bone effectively allowing you to lengthen it. How cool is that, hey? That's exactly right. I mean, it's, and you have to be pretty careful

with your lengthening timing and so on so that there's enough proximity for the signals to be getting through and because there are some cases where bone Doesn't heal because the ends are too far apart and they can't sense each other And you get a non-union fracture and that requires a bit of stimulation, but bone lengthening procedures are amazing in childhood because then you don't go through life with one leg longer than the other or which is going to mess with your back and all sorts of things. Yeah. Then I remember more recently reading an article

about how people were now doing this for cosmetic reasons. Fully grown adults, you know, 30s, 40s, 50s, and they just wanted to be taller. I remember the article describing this brutal experience of almost being bedridden for six months, and then when they finally stepped on it, it was a question about whether at that age, whether the regeneration of bone would be effective enough so that it could actually have the stability and the structure to carry their weight.

Yeah, there's so much problematic with what you were just describing. Where do we start, right? One that we're a society that values height so much that you would feel the need to put yourself through that major surgery, but there's all sorts of reasons why people might do that. I'm not judging. I tend to think your body is a bit of a temple and what you've got is pretty amazing and don't mess with it. I don't even have pierced ears.

I just think leave it alone. It's great. But for some people who do that, I think I would just bring to their attention the fact that if you are on bed rest and you would have to be non weight-bearing if this was a lower extremity procedure for a long time and then what's happening is you're essentially atrophying everything else that needs to be weight-bearing. So what

you're mentioning is can your body actually hold you up once that's happened? Well, yeah, it can. As I say, Bone's amazing, has this ability to adapt, but it will take a long time. And if you do the procedure quite late, you may never get back to what you originally had. And we'll be right back after a word from our sponsors. Good Light Project is sponsored

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DoorDash. Your door to big deals is on DoorDash right now. Sign up for DoorDash and enjoy a free Big Mac on your first McDonald's order of $20 or more. Only on DoorDash now until June 15th. Terms apply. Let's talk a little bit about bones and life cycle. I want to eventually get to what you brought up earlier, which is this notion of osteoporosis and the various different stages of that too. But let's start a little bit earlier in life because our bones

don't stay the same. We're not born with bones in a particular way and then they just kind of stay that way through life. So walk me through a bit, maybe starting out in childhood. Tell me, what are we looking at with the bone structure there? And then maybe we could sort of progress through the major life cycles and how that impacts bone. So starting right back, you know, in utero, we have our full skeleton in terms of the shape and all the little bits and pieces. This should blow your mind. It blows mine every time I think about it when we are eight weeks old in utero

The full skeleton is there in this tiny little bean, but it's cartilage It has to be because you need to be able to grow and develop a little human inside another human So it's a way to grow that skeleton quite quickly I shouldn't be calling it a skeleton because it's not until it's fully ossified. But that process of ossification begins in utero. All the major bones begin to have ossification centers in them because to be born as a little blob of cartilage would not be evolutionarily successful. So we have the bones of our skull are largely formed to protect the brain, the ribs are protecting the lungs and so on. But if you were to x-ray a baby's hand or a foot,

it would look like there was no bones in there because there's still all cartilage until that begins to ossify. By the time a baby is one years old and they're starting to walk, then there's a lot of bone in most of the weight-bearing parts of the body. So the reason why we don't ossify instantly is because if we did, we would be that size forever. Long bones have ossification in the middle of the bone and then an ossification at either end so that they're able to have a growth plate at either end and the bone can continue to grow. And when we're considered to have stopped growing, that's when your growth plates have also fused over and there's no cartilage there anymore. The bone is the length that it's going to be.

So that happens at very different times for people. It is an individual thing. The major growth spurts are when kids are very young, sort of between toddlerhood and the next stage of childhood and puberty. Now in puberty, there's a massive influx of growth hormones and so on and all of the sex hormones that change everything, those of us who've had teenagers. And women tend to have that growth spurt, and then they tend to have that growth spurt, and then they tend to stop growing round about 18, can be a little earlier or younger or later. Men tend to take a little longer to finish growing,

could be roughly about 25 when they actually stop growing. But again, the variation is enormous in that respect. But what we do know is that you almost certainly will have all the bone you're ever going to have by age 30. And in fact, you probably have 99% of all the bone you're ever going to have by age 20. So most of that, I guess the take home, if you're trying to build your bone bank, the window is childhood.

And from what I can tell from the work that has been published, the most important window is puberty. Keeping active and doing the right kinds of exercise. I'm actually gonna jump in, because I just wanna ask about that, sort of like 18 to 25 year window, or like the point where we quote peak.

Totally understand that in the context of the bones aren't going to get longer. Does that also apply to the bone mass, the density of the bone? Does that also basically peak in that same window? It does for, as a general rule, for most people. But whether it does depends on the person. So genes are largely determining what that peak bone mass is going to be when you stop growing and so

on. Certainly, the amount of exercise and you diet is going to be important in optimizing your peak bone mass, but genes are really the major determinant there. What happens next over the rest of your life is going to be very much determined by your lifestyle and that's when that sort of stuff kicks in. So yes is the answer to the question that's pretty much it for we measure bone by bone mineral density typically on a DEXA scan and typically that's the maximum BMD you'll ever have, it's the maximum length, width and so on. But there are caveats and I suspect you're going to ask me about those so I'll wait until you do. So if you know by the age of 30 or so at the latest, let's assume for the moment that we've got what we've got and granted we'll talk about I'm sure

some things where maybe we can actually alter that equation without doing anything substantial to intervene what is this sort of the the progression of your bone health your bone density as you move into the middle years of like 30s 40s 50s 60s and then beyond yeah so for most people if they don't have anything that stops them from being normally mobile, you know, normal amounts of activity and normal access to food and no major condition, life threatening condition or something, you will plateau for a while with your bone mineral density and then you'll begin to lose.

So for men, that is a very gradual process pretty much from any time between 30 and 40, roughly about 40 for men until the end of life. For women, because estrogen is such an important hormone for bone, because remember I talked about the bone munching cells, the osteoclasts, osteoclasts are inhibited by estrogen, so when estrogen is withdrawn at menopause, it's a bit like taking your hand away from underneath a running tap and suddenly the osteoclasts start resorbing bone like crazy and you lose much more rapidly for the next five to eight years through perimenopause as that's removed. Now, that does eventually level out again and the rate of loss tends to parallel men towards the end of life. But

there is a massive loss at menopause and this probably is one of the major reasons why women are more likely to have very low bone mass at the end of life compared to men. But of course you have to factor in that we don't gain as much bone at peak bone mass as men either. So we start lower and we lose more across life. And that does explain why more women than men are fracturing at end of life. If there's this process of quote natural, I don't want to say shedding, but reduction in density, reduction in mass that just happens year after year after year. And again, as you described, often different between men and women in no small part based

on the change in estrogen during menopause. As this process is unfolding, why does this matter to us? What are the changes that it makes in us and our abilities and our risks that would make us want to say, huh, I wonder if there's something I can do about this? For most people, that loss actually doesn't matter. You lose mass, but if you never do something that puts you in a position where you overload your skeleton and you never have a fracture, actually all you've done is lessen the load in your body and you use less energy to get around. However, most people do get to a point in their life where they have lost so much mass that they

are at increased risk of what we call a minimal trauma fracture. This is a fracture that would occur more likely in somebody with this reduced bone mass and it's why you would see the most commonly in the spine and you see that kyphotic deformity or the curvature of the spine when people have fractures in their spine. From little things like lifting up a grandchild or carrying a very big bag of groceries or jolting down a step when you thought you were on the ground but you forgot there was one step to go, that can actually cause a fracture. And these normally wouldn't cause a fracture in most people. But after the age of probably about 60, we're talking one in two or one in three women and about one in five men do have a fracture. This is something that is not insignificant, the risk is quite high. So I suppose the goal is

to prevent your skeleton getting to that point, preventing the loss across life, which, you know, many people think, used to think you couldn't do, but I tend to think that you can. So the risk really then is that will lead to fractures, which may lead to anything from pain to disability to all sorts of limitations, which is, I would imagine for the typical person to the extent we have control over this, something we'd rather not endure. One of the things that I think a lot of people hear about, well, if you reach an age where you're losing a certain amount of bone mass, that the risk of falls goes up. And then along with the risk of falls is fractures or entire breaks.

And often, you know, like the spine and the hip are things that people point to. I'm wondering, like, is there a chicken and egg thing going on here also? There is a very tiny percentage of times when that happens. If somebody has a very, very weak hip, that may happen. But 90% of hip fractures are a direct result of a fall. I would say 99% of all wrist fractures are a direct result of a fall. The three main osteoporotic fractures are wrist fracture, typically falling on an outstretched hand, and a wrist fracture isn't a really big deal for most people. It's an inconvenience. It heals over the course of six to eight weeks. You can survive with one other hand, you can move

around, it's okay. A spine fracture is probably the most prevalent. It causes considerable pain for most people, not everybody, not everyone even notices when they fracture a spine, but most people do. It causes pain in the actual fracture. But if you have such a bad fracture that you crush the spines to the extent that it squashes the nerves that come out of the spinal cord, then that's going to cause pain that will radiate to other parts of the body and become much more problematic. So severe spine fractures, it's not a place you want to go. And the hip fractures, of course, normally falling to the side and not being able to get your hand out to stop yourself falling directly onto your hip. Either you've been knocked over or you've moved suddenly or for whatever reason. So I guess I digress, but the

answer to your question is almost certainly the falls happen, not the other way around, fracture then fall. So then if you fall, whether you trip or not the other way around, fracture then fall. So then if you fall, whether you trip or whatever the cause may be, if your bones have already lost some mass, then when you fall, like if you had that exact same fall when you were 20 versus when you were 60, where you have a, you know, if you have a meaningful loss in bone mass, I guess in the likelihood of that fall leading to a fracture or a rake would go up dramatically. Dramatically, absolutely.

So talk to me about words like osteoporosis and osteopenia. What are these and how do we know if we quote have it? So osteopenia is a description of low bone mass and osteoporosis is very low bone mass. Now, to diagnose them, you would normally have a DEXA or a bone density scan. DEXA stands for dual energy x-ray absorptiometry. It is a very large x-ray machine that you lie on. It has very low dose radiation, so they're very safe, relatively inexpensive. And if your doctor had some idea that you may, even had a family history or whatever reason, they would send you for a scan and normally a hip and spine. Because as I mentioned, those are the two places that are most likely to fracture or if they do fracture cause the most trouble. When

determining whether you have osteopenia or osteoporosis your score your bimeneral density score is compared with the scores of a big database full of people who are like you. So in my case, a white woman. Your T score is your score compared to a young, or mine would be a young white woman. Not somebody the same age. Your Z score is compared to somebody the same age. But the T score is how osteoporosis is diagnosed.

If your value, your BMD value is more than two and a half standard deviations away from the score of somebody your sex and race at age roughly 20, you're considered to have osteoporosis. If your score is between minus one and minus 2.5, then it's osteopenia. So they're really just terms on the same scale and these cutoffs were created essentially so that doctors knew when you are most at risk for fracture and when they should be prescribing therapy? If I have it correctly, then this is a very low radiation test often, and it's generally comparing to two different standards.

One is sort of like you as a 20-year-old, and then also you probably like versus a population who's similar age to you. So it would be possible then to look at the comparison to the 20-year-old number and that come back and say, well, like you clearly have osteoporosis, but then compared to other people, your same gender, your same age, your same ethnicity, you might actually be a lot closer to what the typical person is. That's right. Because of the fact that everybody loses across life, your Z score, which is the comparison of your score to the average at your age, will be much closer. The

reason that it's compared to baseline is because at any stage during life, if your score is 2.5 standard deviations below that young normal score, you are at increased risk of fracture. That's what the big epidemiological studies say. How accurate is DEXA? I've always been curious about that. Oh, the million dollar question. On a population scale, it's great. It's a really great screening tool.

It gives us a very good snapshot of where we are. Can you get different scores on Dexa from one day to the next? Sure. Will they be in the ballpark of where you probably are? Yes. So there is error. There definitely is measurement error. Typically in a bone lab like mine, we do reliability studies where we test a new Dexa and scan people, we put them on the machine, we scan them, get them off, reposition them, scan them again, and that's considered to be our reliability number. And so when we do an intervention trial, we can see whether the effect of whatever we've tested is greater or lesser than that error that we measured in our reliability

study. Of course, not all the clinics are doing that, but the assumption is they're pretty close. There are all sorts of things to remember when you're having a DEXA in series. Oftentimes, it's recommended, particularly for women, to have a bone density scan at the time of menopause so that you can see where you started and so you can see how much you lose or hopefully don't and you need to make sure that your follow-up dexers are on the same dexer because you can't compare numbers that come from different machines. There are some machines that do have calibration standards the same model, the same type, the same brand of machine and they calibrate for all of them,

that's not quite so bad, but if you had a scan, for example, on a Hologic machine, and they went and had one on a Luna, you could not directly compare those two scans. That's so interesting. So then you could effectively, your doctor could order a DEXA scan, you could go get a scan,

you might choose one place or another place, they might have a different machine, and based on the fact that it was a different machine, you would potentially get a different score back. Correct. It's very frustrating for those of us who do research. But like I said, they're a good broad brush, pretty reliable and valid.

The thing about Dexter is that it is highly related to your risk of fracture. And it's easy to interpret the results on the plot, very easy to understand, and doctors are used to it. So it's a pretty good tool. It's definitely not perfect, but it's the best we have at the moment. There are various tools coming out, but for now, it's the best we have. I don't know if you...

I'm sure you're tracking this, if not involved in it, but it seems like AI is becoming really involved in a lot of imaging processes and I'm wondering if they're sort of like in a near future where AI actually becomes involved in the testing of bone mass and in some way makes it either like more accurate or more consistent. Yeah, that definitely is already happening. It's not my area, so I can't really speak too much to the specifics of it. There are other forms of detecting osteoporosis because most people don't even think about it. You don't think about your bones until you have a fracture. Some people are being screened for other conditions where perhaps you have a chest X-ray.

And in that case, there are some AI programs that are being used to also examine the density of the bone. It feels like we're on the cusp of just some really interesting stuff. Yeah. I feel like there are also some myths floating around. And maybe the biggest one that bridges the gap a little bit is that referencing what we talked about earlier, this idea that we have what

we have up until late 20s, around 30-ish, and then from that point forward, it's just going to get less and less dense. Your bone density is going to diminish over time, year after year after year. And there's nothing you can do about it. It's just the way it is. It's the natural process. Just accept it. You don't buy that. Oh, it's not true. So, I mean, it's absolutely not true. We've shown that over and over.

Bone is way ahead of us. You can absolutely do something about it. What about weight loss and bone density? Is there a relationship that you're aware of between losing weight and losing bone density? There absolutely is. And this is so frustrating for people who are doing something good for their body

by shedding excess weight that could be bad for all kinds of metabolic and joint reasons and so on. Because particularly if you lose a large amount of weight, you are also going to lose lean mass and muscle. And then some of us who are doing some work to see if our exercise program can prevent that loss. One study that we were doing was interrupted by COVID, so we don't have the answer yet. But there is certainly plenty of evidence that shows that some exercise can prevent some loss of bone and muscle during weight loss, so it's definitely better to do something. But in the past, those forms of exercise haven't been enough to stop

all of the loss. So I worry about drugs like Azempic, and that's the name that I always remember. I'm not singling it out. But these are highly effective weight loss drugs and they're almost miracle drugs for some people. They're really life-saving. But in the process of losing a lot of fat, in that case, also losing bone and muscle. Now, it's easy to put fat back on. It is not that easy to put bone and muscle back on. So people do need to be aware of that. Dr. Justin Marchegiani Yeah, I mean it's so interesting, right? Because it's like you're trying to do something that may really affect, you know, different health indicators in a very

positive way. And at the same time, what you're doing actually is very effective. It can have this potential other impact. And I know that the same as you described, the same as too, of muscle oftentimes when somebody loses a meaningful amount of weight, part of that is lean mass in the form of muscle and that is the metabolic engine of the body. So it has its own repercussions. So I guess the answer is that there is a relationship there, that it looks like maybe there is a way to stave off some of this, but the answer is not entirely in yet.

Can we actually completely maintain what we have while simultaneously losing weight? Because we haven't tested, as I'm sure we can talk about this, bone needs a very specific form of loading to actually grow. So if you're not doing that during weight loss, you're not going to be able to save your bone. So yeah, it's very targeted. So let's go there. Let's switch gears a little bit into, okay, so let's say we're at a certain point in life. Maybe we've just gotten a DEXA and we've gotten some numbers back, T-score, Z-score, and we're kind of like, oh, that's not what I wanted to see. I'm either heading in the direction of osteoporosis or maybe I'm already in it and really concerned.

I've been told by a lot of people traditionally that it is what it is or maybe there are pharmaceutical interventions and we'll talk a little bit about that. But you want to do something to reverse this if it's reversible or at least stop the progress of it. So much of your work focuses around exercise, but it's not just any form of movement that's really effective. So take me into how you approach this, what actually works and what doesn't work.

Maybe if we start with what doesn't work, because as an exerciseophile, as somebody who believes that exercise doesn't work because as an exercise what exercise is. Then finding in the literature just a dearth of evidence that a regular exercise program can improve bone mass and particularly in the people who need it most who already have low bone mass, I was a real head scratcher until we started drilling down and looking at the kinds of exercise that had been tested. So from that it became very clear walking is insufficient to grow bone. It's very good for your heart and lungs, great for your metabolism, probably really good for your mental health and socially, but it does not grow bone. A lifetime of walking is better for your bones than not ever

having done a lifetime of walking. But once your bones in older older age when you've got low bone mass choosing walking as your intervention is really I think wasting an opportunity to do something that might actually work. Same for swimming, same for cycling, same for activities like Pilates, Tai Chi, yoga, anything that is low intensity and anything that is not weight bearing. You need to be on your feet and you need to load the body at a higher intensity. Exercise is very site specific, only the loaded bones are going to adapt. It's not like go for a run and my skull bones will get thicker. That's not how exercise works. And we'll be right back after a word from our sponsors. Here's my question around this. I live in Boulder, Colorado. I live in the mountains and I hike on a regular basis. And I've wondered, is there a meaningful difference between walking and hiking? And in particular,

I will gain sometimes 1,500 feet in elevation on the way up. And I would imagine there isn't a meaningful difference there, but I'm wondering if I then have to come down 1,500 feet in elevation, which in my mind would mean that I'm loading the bone at some sort of, you know, like multiple of my body weight, or like it's more than just, you know, like one time the body weight as I descend. Do you know if that is anyway meaningfully different

than just really walking? It hasn't been measured empirically. But I would almost certainly say that that level of intensity of walking is gonna be better for your bones than just walking along flat pavement around a city street. I think that is going to be the case partly because walking uphill makes the muscles contract more, more loading on bones than just walking at a relaxed pace.

But also, I suspect when you're walking, sometimes you're on trails where you have to jump down a ledge. You're getting a little impacts here and there around the place, and slightly unusual kinds of movements. Bone loves that to be surprised. And also you're almost certainly carrying a pack on your back. So you've added to your load already. And if that's quite heavy, if you're camping at the time and you've got quite a bit of gear, then absolutely that is a different form of walking. The only time I've ever seen a research study show that there is an effect of walking on bone is when I believe a weighted vest was worn and the walking was very rapid.

So it's the same concept. Put an extra load on the body and the muscles with forces on the bones are probably greater as they're trying to move you more quickly. Okay, so tell me what does work then. Heavy loads and impact. We came to this conclusion because even looking at regular gym programs, which are beautifully designed to work all the muscle groups in the body. If you're doing high numbers at relatively low loads, that is not going to grow bone. It may help to maintain bone. So

remembering that across life, we've got this trajectory of downward movement. Doing a regular gym program is almost certainly slowing that loss. But if you want to gain bone, you have to load it more than you ordinarily would. There was a season where the trend was do three sets of like 30 reps of each of these things in a gym. It was just lighter weight over and over and over and over and over and often too fatigued. And maybe there are other, I'm sure there are other like health and fitness and well-being benefits of that, but what you're saying is that's not really going to get you there when we're talking about bone. Not for bone. However, as you mentioned before, falls are important and we're trying to stop

people from falling. There are some people who either can't or won't lift heavy. It's just not something that they are willing to do, in which case that loading to fatigue isn't such a bad idea because there are multiple ways to get to the same end when it comes to improving muscle strength. There's certainly a school of thought that thinks, yes, heavy loads done a small number of times, it's probably what we all assume is the most effective way to increase muscle strength. But actually, if you load at a lower weight to failure, so you cannot lift it one more time, there's evidence to show that that also increases muscle strength. Now, I am a very busy person

and there are many, many people like me who want to get in and do their exercise quickly and get out. I know which one of those protocols is going to suit me because exercising to fatigue takes much, much longer. When you talk about heavy loading then, I guess what my brain hears is heavier weight and oftentimes substantially heavier weight. When is this and when is it not safe for somebody, especially for somebody who maybe is further into their life,

maybe already has a DEXA or some sort of diagnosis that shows there is some level of osteopenia or even osteoporosis, it seems like there's this dance that you would have to do. On the one hand, you need to lift heavy to effectively either preserve or even rebuild bone. But is there a simultaneous risk of doing that when you already have some bone degradation? Absolutely. And that's the reason when I was scratching my head and started working

in this area thinking, why are people doing these low intensity exercise interventions for people with osteoporosis when we kind of know that that's not what bone adapts to? Well, it's because everyone's scared of hurting people, and I was too. So we never want to put somebody at risk. You don't want to cause the fracture you're trying to prevent because then that person's had a fracture and having one fracture increases the risk of having another by four times. So you have to be very careful. And I would say the very first rule of loading heavy for osteoporosis is supervision. Just because you might have done quite a bit of exercise in your life doesn't mean you don't need to be supervised on heavy lifting if you have very

weak bones. Your technique is everything and you can't see your technique properly even by looking in a mirror. In fact sometimes when you're lifting by looking in the mirror you're messing with your technique. Unfortunately the way to have an effective exercise program for osteoporosis is to have somebody who is qualified supervise you and take you through that program because they will know by looking at your lifting technique whether you are over and under loaded and at what amount they should be progressing you. You know, I often get asked, so how do I know what's heavy enough? Well, somebody who's expert will know that

and they can help you. And I guess, you know, part of this also is that you don't walk into a gym the first day and say, I wanna lift hefty, or I wanna lift heavy if you've been largely sedentary. You know, for- You're not. I think this brings us nicely also

to the study that you did, the Liftmore study. Walk me through this because, you know, the Lippemore study. Walk me through this because it sounds like it's a population, it's basically the population we're talking about now where there is a concern and the outcomes were stunning. Yeah. So there were two things that hadn't been done. I mean, there had been a couple of studies that had examined the osteoporotic population, but not very many because normally in these exercise trials, people were too scared, so

they were screening people with osteoporosis out. Now that's the other thing. If your bones are already quite strong and you load them, the bone goes, I'm strong enough. I don't need to adapt. So that's the other reason it looked like it wasn't working. What you need to do is recruit people who actually need the adapt. So that's the other reason it looked like it wasn't working. What you need to do is recruit people who actually need the exercise. So in Liftmore, we recruited people who had low to very low bone mass, and some of them had prevalent fractures already. So this would be somebody with a T score of minus one and as low as it went. I think the lowest we had was minus four, and we

were terrified, but we took her anyway. The other thing is nobody had tested these very high loads before. We didn't know how conservative we had to be, so we just started very conservative. We taught technique to begin with, very, very light loads, taught the movement patterns, and then just gradually added the loads. Now, curiously, it was the study participants who were frustrated with us that we were going way too slow. They could do way more than we thought they could. And we had originally planned for a one-month sort of lead-in period. And after a while, it was just, come on. So after two weeks of teaching them technique, we then started loading them up and away they

went getting them to be able to lift as heavy as they could in what we call the 85% one repetition max. So 85% of what they can lift maximally once. That process, we were very nervous about it. But at the end of it, we had a group of women who had gained considerable bone at the spine, bone mineral density from Dexa. At the hip, they had gained a little bit, it was statistically significant from the control group, mainly because the control group lost BMD at the hip. We were scratching our head a little bit because we couldn't understand why they weren't growing a lot of bone at the hip until we used some software I have in my lab that allows us to do a 3D analysis of the hip and it showed us that actually the bone of

your thigh, where it connects to your pelvis, that's what people call the hip, but actually the hip is the joint. It's the femur we're looking at. That bone doesn't adapt by becoming more dense. It adapts by changing its shape and getting thicker. That 3D hip software, thankfully, because I was just tearing my hair out thinking, how can this not be working, actually it turns out almost 30% greater increase in thickness at the femoral neck in our intervention group. And that's right where the fractures happen at the femoral neck. So this was a big a half moment for us. Number one, we were growing bone at the spine,

and number two, we were showing that we were actually changing the structure of the proximal femur in such a way that it was becoming stronger and more resistant to the kinds of loads that we put on the bone during everyday activities. So if I remember correctly, this study, it was women who were post-menopausal and sort of

like clearly passed any symptomology or past menopause. As you described, many of them already, I guess, to qualify for this study, they had to have some level of loss of bone mass or bone density. What was the duration of how long, how many months did you measure? Normally when you do bone research, interventions run for a year because bone is so slow to adapt. In our case, this was a PhD student study and we have to get them out the door. So we brought it down to eight months because I knew that if there was something to be seen, we would be able to detect it in eight months. So the intervention was eight months long. Turns out it was sufficient to be able to detect it in eight months. So the intervention was eight months long. Turns out it was sufficient to be able to detect a change. When we measure these days at the clinic,

we do allow a full year in between our testing. So yeah, twice a week for eight months. What they were doing also, it wasn't some sort of crazy complex or complicated. From what I remember, these were very fundamental movements. I mean, they were dynamic movements that involved the whole body, but these are like the basic things

that you see somebody do in a gym. There was nothing fancy or complicated about it. No, well, we wanted, I mean, feasibility for me, whenever I'm doing research, testing something just for the sake of testing it, it doesn't make a lot of sense. Research is expensive and you've only got a certain amount of time to do it.

So test something that is feasible, acceptable, people will actually do. I wanted it to be brief, so these are only 30 minute sessions, and I wanted it to hit everything that, you know, in the body that needed to be hit. I don't normally talk about the actual exercises publicly because people do silly things. When they hear me say that, they run out to a gym and do it. And what I'm trying to emphasize is that it really does need to be supervised. But what I can say is these were complex compound movements that are pretty straightforward, plus we added in some impact. The transfer of those compound movements to everyday activities like getting down and

up out of a chair and in and out of a car, onto the toilet, reaching above the head to pull something out of a cupboard, the movements that we did in this study translate directly to everyday activity, carrying a heavy basket of laundry, those things. The participants in the study reacted so positively because they just felt like they got their life back. To a point, we came for our bones, but we stayed because we just feel so much better and stronger. I don't have to ask my husband to undo this particular thing because I can

do it myself now. That's just music to my ears. There is this mythology that I've heard also that, quote, women shouldn't lift and women shouldn't lift heavy. You're basically saying that we have research that says, I mean, that was never true. It was probably dogma from a male-dominated gym scene. And in fact, it can be done in an intelligent, in a way that is guided with a professional who really knows what they're doing

so that they can monitor and make sure that your form is really good. It can be stunningly effective at not only building muscle and an effective lifestyle-oriented movement but also potentially rebuilding bone mass. I want to shift gears a little bit to talk about nutrition. And there are two things that tend to pop up. I've heard two different opinions on this lately.

For a long time, I feel like if you were diagnosed with osteoporosis and you went to somebody to get advice and you asked, well, what should I take? Without getting to pharmaceutical interventions, often calcium was the thing that was offered. And not as a kid, but as somebody in their 40s, 50s, 60s. And now I've heard conflicting research that shows that actually calcium is not the thing that you should be taking at all. What's your lens on this? Yeah, this is quite a polarized area in the research. I'm not a nutritionist, but I certainly spend a lot of time reading and listening to people talking about this. One school of thought is you should always get your calcium intake to a certain level. If you have osteoporosis,

that's 1300 milligrams a day. Another school of thought is you don't need to worry about it, just eat a healthy diet and you'll be fine and you should never ever supplement. I think I fall somewhere in the middle. I certainly am a food first person when it comes to nutrition. If you can avoid supplements you should. We didn't evolve taking great big boluses of one nutrient at a certain time every day. If you do that with calcium, you're most likely, if you take for example, a thousand milligram tablet of calcium, you'll get a big splurge of calcium in your system, most of which will be excreted. Some of it will actually lay down on the inside

of your arteries and if they're your coronary arteries, that's not a good thing. So that's where some of the pushback has come against calcium supplements because if you have too much in your system, there is a slight signal that you may be increasing your risk of heart attack. Now there are ways around that because if somebody is is really not getting enough calcium we use calcium in many systems of our body so we can't not have it in our blood. If you're not eating it where do you go? You go to the calcium bank. What's the calcium bank? That's your bones. So you do need to have enough that you're

either replacing what you've previously withdrawn from the bank for some of these processes, or that it's available circulating for you to use. I just use as a rough rule of thumb for adults about a thousand milligrams a day and try to get it through a very absorbable form. Now the most absorbable form is dairy. There is no getting away from that. There is a very anti-dairy culture online. My reading suggests that there are not negative health outcomes from eating dairy. Not any evidence that I can see convincing evidence. There does seem to be very positive things that come from having dairy in some form or other. Some people are lactose intolerant. Those people typically

can still have yogurt and hard cheese where the lactose is broken down. Some people have an actual allergy, a dairy allergy, and there are ways of getting around that, getting your calcium from other sources. Basically, if you can, try and get about 1,000 milligrams a day through your diet, something that's bioavailable. Your dietician will be able to tell you that. There are definite subtleties. You can't just go and look in a book and find out how much calcium is in a substance because for example in spinach

there's an element that prevents the absorption. You have to cook your spinach to be able to get calcium without the negative effects. So a dietician is probably the best person to see. So the answer is, long answer to a short question, You need a certain amount of calcium to keep your calcium bank full and not be depleting it. Best source is food. Make sure you speak to a dietitian to get the most bioavailable. If nothing's working, you cannot get it in your diet, take a calcium tablet that is also very absorbable like calcium citrate and have little bits throughout the day. Don't have a great big tablet, maybe 200 milligrams at a time and spread it throughout the day. Otherwise, you're putting your heart at

risk or you're peeing it out. And as you said, talk to a nutritionist who can work with you individually and really understand who you are and what your needs are. It's hard to have the calcium conversation with also and at least touching on vitamin D which again I feel like has become almost equally polarized in terms of like warring factions and you know like should you have it should you not should you supplement should you not should you just you know get 20 minutes of sun in the morning. What's your take on this in the context of bone health?

Yeah, well, you're quite right. You can't talk about calcium without vitamin D because if you're eating calcium, you won't be able to absorb it without vitamin D. So you do need to have that. Now, there are just massive differences of opinion as to how much vitamin D you need and how much you need in your bloodstream to be sufficient. But again, I try to take a very practical evolutionary approach in that how would we have got vitamin D in the past? Exposing our skin to a bit of sun is probably the most practical way to do it because food sources of vitamin D are things that we have probably been discouraged of eating that much of, red meat and butter.

There is some in salmon, mushrooms, high in vitamin D, but there's not a lot. There are some people who may need a vitamin D supplement, people who for whatever reason, perhaps culturally they cover up and they don't see any sun or they're in a nursing home and they don't get outside, those people probably do need a supplement. Whether or not you should be tested for vitamin D is also highly controversial because a vitamin D test from one day to the next can be vastly different. So a lot of doctors are moving away from testing. They're just advising on how to make sure you have enough. Now, I live in Queensland in Australia.

We have the highest rate of skin cancer in the world, I think, because we are white people living in a black person's country. And our skin, if we get too much sun, does develop skin cancer. This has made us very sun averse. We have a slip, slop, slap campaign here, slip on a shirt, slop on sunscreen and slap on a hat. So we keep the sun off us to the extent that many people in Australia are vitamin D deficient and that has repercussions not just for bone but for many things. So I've taken again an approach that I think is sensible getting some sun on my skin at a time where the sun is not at its most strong never ever getting even close to being sunburned so in

Australian summer you probably only need about 10 minutes or 10 o'clock in the morning. And that is not only good for vitamin D, but sunlight itself is good for us. There are all sorts of other things that benefit from sunlight, not just the vitamin D. So I think that's a healthy approach and should be enough. People with very dark skin need a little longer in the sun than people with very fair skin. If we move in the sun than people with very fair skin. If we move on to the last category here, and it's something that you referenced earlier, which is medication, pharmaceutical interventions, what's the state of that right now? Are there effective medications to help either prevent bone loss or even rebuild bone loss? And even if so, are they safe? Are there side effects that actually are without way the taking of them? What's your take on this?

The bone medications is also slightly fraught. I would say that there are certainly a slew of bone meds that will grow bone and many people need them, should be on them. If they have very low bone mass, that is one way of increasing your bone bank and reducing your risk of fracture. The caveat is that they don't work for everybody and the side effects can be quite negative for some people. Most people would be aware if they do even the smallest amount of online Google doctoring that the potential for osteonecrosis of the jaw and atypical femoral fracture is increased with bone drugs because many of the drugs, most of the drugs act to clamp the osteoclasts, the ones that chomp through bone. Now

one of the roles of that chomping through bone is replacing micro-damage as we've talked about. So if you clamp down on those osteoclasts too much, some of the roles that they perform are also inhibited. Now for someone who has jaw surgery, remember I was talking about what happens when you're healing a fracture. The first thing is the cleanup crew comes in, including osteoclasts. And if you stop them doing that cleanup, it actually stops the repair of the surgical

site. So, typically, I believe endocrinologists or GPs, whoever's in charge of the patient recommends that you stop your meds a little bit before you have your surgery and have the surgery allowed to recover and then go back on. There are some people who think that you don't need to do that. Some people who think that the incidence of ONJ or atypical femoral fracture is so low that it's worth staying on because the risk of fracture is so much higher and there is some evidence to show for every one person that has osteoanacrosis of a jaw. There are multiple people prevented for having fractures. So there are just many different ways of looking at it and I think really the answer is you have to have that conversation with

your doctor. How at risk are you of fracture? The higher risk you are, the more likely it is you do need to go on meds. Before you go on, maybe see a dentist. Check all of your teeth. Is it likely you're going to need to have oral surgery? Get that done before you go on the meds. Atypical femoral fracture is exactly as it says. It's a fracture that occurs lower on the femur, the thigh bone, than a typical hip fracture occurs. And nobody really knows why it occurs exactly where it occurs. But it seems to be because the osteoclasts are not chewing up the little microcracks in the bone and replacing and repairing it. And those little

microcracks sort of all eventually coalesce, form a complete fracture and the femur breaks. Because those little cracks are quite often painful, doctors will say you need to be aware if you have any upper thigh pain, aching pain, you need to be aware of that and tell me and we'll do an x-ray and we'll certainly stop the the drug and allow that to heal. Some drugs are more prone to that than others. It's a very fraught issue and I think there it's a very fraught issue and I think it's a conversation for your doctor. I would imagine on a similar vein,

not really, I guess you consider a pharmaceutical intervention or not, but hormone replacement therapy. As you were sharing earlier in our conversation, one of the main differences between the bone density outcomes between men and women later in life is that once estrogen goes dramatically lower, these osteoclasts basically get let loose.

That if you then start on hormone replacement therapy that increases at estrogen, it sounds like you would have similar issues to what we're talking about with certain pharma substances. The funny thing is with hormone therapy, they call it menopausal hormone therapy. These instead of HRT, they call it menopausal hormone therapy. Instead of HRT, they call it MHT these days. As far as I'm aware, it is not associated with the same problems, the same ONJ and AFF. I don't know that for certain, but that is my suspicion it's not. Now that hormone therapy, while you're going through menopause and in the years immediately after it can be safely started then and it is a very effective bone protecting agent and many

people are on it. What happened with that? Right back at the turn of the century, there was a study called the Women's Health Initiative. that was run in the US, a very big cohort study. And it was discovered that the people who were taking hormone therapy were at increased risk of certain things, thromboses and embolisms, a couple of other things. What it was good for was bone and I believe bowel cancer. I think it was protective there. So everybody dropped it like a hot rock and everyone went off hormone therapy and it is slowly coming back into the clinical milieu and is being used again because people realized they threw out the baby with the bath water. This is something that

probably the negative side effects happen if you start it in many years after menopause. You can't start somebody on hormone therapy when they're 70. It has to be in the years around menopause. Also, you don't want somebody who has a history, even a family history of breast cancer. They tend to avoid that. But for some people, it's very helpful. Whether or not I would go on it, that's a personal decision. People have different levels of acceptance of medication. It sounds like of everything that we've talked about, whether it's hormone replacement,

some sort of pharmaceutical substance, whether it's hormone replacement, some sort of pharmaceutical substance, whether it's different aspects of nutrition or calcium or vitamin D, you get people on different sides. The one thing that it sounds like has kind of become crystal clear now is that loading your frame by some form, whether it's classical weightlifting, but basically resistance training in some way, shape,

or form, would it be safe to say pretty much everyone who's even mildly informed now agrees this works and it's pretty accessible to almost anyone as long as it's done in a healthy, thoughtful, progressive, well-guided way? Okay, two things. Declaring my conflict of interest here, obviously, because we're from the Bone Clinic and we run our exercise program as Oniro and we are licensing

people all over the world with Oniro and they're running it very successfully. So this is because it does work and it is a targeted program that actually works. So not any resistance training is going to grow bone, but any resistance training is going to be better than nothing. So if you can't find an O'Neill provider, I would absolutely still be saying, a resistance training program is going to be good for you. If you are at risk of osteoporotic fracture, you still need to get some supervision. As to the other point, nobody would argue this. Oh man, I can tell you many, many very uninformed people will argue this. And it's because it's mainly in the primary care level, it's because GPs are so busy, they cannot keep across all the evidence that comes out for new therapies and they don't get any

training in exercise therapy and medical school. So it's not something that they have a really good understanding of. So I understand it. But what I would love is for rather than to be negative about it and say it won't work, it won't be helpful, is to maybe do a bit of just the briefest look. Look at some guidelines and you'll see that the evidence is there and you're doing your patients a real disservice if you don't mention it to them.

Particularly if you tell somebody with a T score of say minus three, oh Mrs. Smith, just go for a walk. That's actually worse than not telling them about an effective exercise intervention because not only will it not work but you're putting that person, if they haven't been active, at risk of falling. They will go for a walk and maybe trip over a tree root or the neighbor's dog will run out and they'll fall and they'll have a fracture. So it's not a no harm recommendation.

Walking is a fantastic exercise, but for some people it actually increases their risk of fracture. It also, whatever time they're allocating to the walking, that could have been time that is allocated to a type of exercise that actually potentially would help them, especially if they have a limited amount of time in their day. So it's actually stopping them because it's saying, I have a half an hour to do whatever it is I'm going to do.

I'll do the walking rather than saying, I'm going to do this other thing, which would potentially be much more effective. So as you described, you have your clinic where you do work with individuals. It's in Australia. You have been training and licensing professionals, I guess, pretty much around the world for a chunk of time now. We'll link to all this stuff in the show notes here so people can find out, do I actually have somebody qualified near me?

Even at that pace, I'm just curious, if we zoom the ones out with you and the work that you're so passionate about, it seems like the universe of people who need this type of help is so vastly larger than the world of people who are now sort of like equipped and skilled to help them. How do you dance with that? I'm an academic. I'm a scientist first and foremost, so you are quite right. This is a job that is too big for me. Because I did open the bone clinic so that the work that we do at the university in my

research lab could be tested in the real world, and it truly is a translational research facility. Every single person who comes is a research participant and we track them. We've been open for 10 years now, so we have some beautiful data. What I need is another one of me and I'm just in the process of employing another one of me so that I can get back into my lab, do what I love to do, and this person can help to disseminate the license a little more. It's very helpful when people like you take

an interest and really delve into the detail of this so people understand why it's so important to do it. I did another podcast recently that really raised the profile in the US. So that's what helped to get a lot of people licensed over there. And I'm getting probably 10 emails a day from people around the world, not everybody is eligible. You do need to have clinical training so that you can look after people but the demand is huge and we're just chipping away at it. One step at a time, one day at a time. Feels like a good place for us to come full circle in this conversation as well. So I always wrap with the same question in this container of Good Life Project. If I offer up the phrase, to live a good life, what comes up? To live a good life, you would want to be able to

do all the things that you wanted to do. And that means being physically and mentally able to do that. You need to have the time, space and capacity to do the things that you love. That's what I think is living a good life. Thank you. Hey, if you love this episode, say that you'll also love the conversation we had with Dr. Adeel Khan about cutting edge treatments like stem cells and gene therapy to heal the body. You can find a link to that episode in the show notes. This episode of Good Life Project was produced by executive producers Lindsay Fox and me, Jonathan Fields. Editing help by Alejandro Ramirez and Troy Young.

Christopher Carter crafted our theme music. And of course, if you haven't already done so, please go ahead and follow Good Life Project in your favorite listening app or on YouTube too. If you found this conversation interesting or valuable and inspiring, chances are you did because you're still listening here. Do me a personal favor, a second favor, share it with just one person. I mean if you want to share it with more that's awesome too, but just one person even, then invite them to talk with you about what you've both discovered, to reconnect and explore ideas that really matter, because that's how we all come alive together.

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