Good afternoon, everyone. If we could go ahead and share the speaker's screen. Hi, John. Hey, Maggie. So welcome to Session 413, the Impact of Aging on Workplace Injury and Illness Risk. My name is Maggie Cook-Szymanek. And I am pleased to provide a brief introduction for our speaker, Dr. John Shumpert, who will be presenting virtually. So after four years of service in the U.S. Marine Corps, Dr. Shumpert earned a Bachelor of Science at the University of Montana, a Doctor of Medicine from the University of California San Diego, and a Master of Public Health from the University of Minnesota School of Public Health, where he also completed his residency training in occupational and environmental medicine. Dr. Shumpert has worked as a staff physician at the corporate headquarters of 3M Company and has provided direct patient care and medical surveillance at Idaho National Laboratories and Benefice Health Systems in Great Falls, Montana. Dr. Shumpert established his current practice, Resources for Environmental and Occupational Health, in 2001. He's a faculty affiliate of the University of Montana Center for Environmental Health Sciences, and he was the first medical director for the Montana Department of Labor and Industry. Dr. Shumpert is known as a colleague and also a friend of mine in beautiful Missoula, Montana. So please join me in welcoming Dr. John Shumpert. Thank you, Mary, and thank you for that great introduction. I think I should probably introduce this topic of why I found it interesting. This really grew out of work in my own practice when I first started this practice. I noticed that a lot of the people that I was seeing, patients and people that I was doing independent medical evaluations on, were in their 20s and 30s, and they would have injuries that were related to more industrial and construction types of jobs. But as time went on, I found that the people that I was evaluating were aging. Being in their 20s and 30s, by the late 2000s, they were in their 30s and 40s. It was rare that I would see someone young in their 20s. Now, in the early part of the 2020s, I'm finding that the most common age that I am seeing is in their 50s, and it's not at all uncommon to see someone in their 60s and 70s. And these are people that are still working, but they're not. The other thing that was interesting is that these folks aren't necessarily working in physically demanding positions. They're simply having injuries or developing occupational diseases from pretty light employment tasks, driving trucks, working in retail locations, doing things like being housekeepers, and also being nurses, which actually can be a very heavy job. And then I had a case of a gentleman who was a retired mechanical engineer. He was in his 70s. He'd done his duty and worked for decades as a professional and retired to Montana and thought he was just going to chill and go fish and hunt, and after a few years, really got bored and decided to take a job just somewhere, anywhere, just doing something just to have something to do and interact with people. And he got a job at a local hardware store and was doing something that should have been really a non-issue, helping a customer out with some packages to their car, and he injured himself while trying to load these packages, which weren't particularly heavy, into this customer's car. I saw this gentleman to do an impairment rating and was struck by how this is an otherwise healthy man. I believe he was 72, but he was really struggling to regain his life and was not only physically struggling, but psychologically and emotionally struggling. He thought he was going to have a great retirement, and now it wasn't so great because of this new injury. An injury that really didn't have to happen. And so it really made me think about aging and really made me wonder just what is it about aging that causes things that should have been trivial injuries to become things that are very challenging. And so I looked into this and put together this presentation. I hope you enjoy it. I hope you get something out of this. I love Samuel Clemens, Mark Twain. He's got a wry sense of humor, and I really do think this slide kind of encapsulates the whole issue of aging. So I am a solo practitioner in Missoula, Montana. I do independent medical evaluations, impairment ratings, occupational disease evaluations. I do on-site visits. I design medical surveillance programs for companies that are doing novel processes. I also teach at the University of Montana. I don't have any conflicts of interest to disclose. What I hope you'll gain from this is an understanding of aging from multiple levels, first being the molecular, then the organismal and cellular levels, and then finally the organ system level. And because we're Achmed and because it really is a focus of my practice, I'm going to focus on the musculoskeletal aging process, so we won't be talking about things like the nervous system or cardiovascular or renal or any other system, which also has been studied in terms of aging. So first, I'd like to talk about who cares about aging. Why is aging important? Why is this something that we as ergoambientologists need to be thinking about? So there have been positive and negative views about aging. Obviously, we like to think of this positive side of aging as something that gives us wisdom and gives us an understanding of what our life really meant to ourselves and to those around us. But there have been people that have espoused a negative view of aging, depriving us of all of our pleasures and leaving us with only the appetite for those pleasures and bringing us nothing but suffering. But in the end, we fear death. We actually do desire old age. But aging is something that we also have to do to understand in the developed world. In the developed world, aging is something that is becoming a real issue. In 2012, there are 810 million individuals over 60 years old worldwide. By 2050, this will be 2 billion. The current ratio of individuals worldwide over 60 is 1 to 9. By 2050, that will become 1 to 5. Obviously, this assumes a worldwide population of somewhere around 10 billion people by 2050. One of the things that I think is really interesting to look at in terms of aging and in terms of the large populations is population pyramids. Here's a population pyramid of the U.S. in 1960. And as you can see, in 1960, it's fairly pyramidal. We have most of the population being young. There's a little bit of a tightening in the age group from 20 to 30. But then it widens out again, childbearing age. And then it starts to become narrower as we get older, middle-aged, and then finally elderly. Obviously, people are dying throughout all this middle and older age groups. As a comparison, I'd like to show you now the population pyramid from just last year, a year before last, 2020. You can see from this population pyramid that we have far fewer as a percentage of the total population, far fewer young people than we do older people. And you can also see that the proportion of older people is getting larger. A good thing to do also is compare developed and developing world populations. Here we have two population pyramids. One is for the United States and the other is for Nigeria. And as you can see, there are far more young people in Nigeria as a percentage of the population than there are in the U.S. And you can also see life expectancy is lower in Nigeria than it is in the U.S. Obviously, there are things like infant mortality and protection of young people in the developing world that is far more difficult than in the developed world. So, you know, one of the theories is that we make more babies when more of our babies die. And as we are able to protect them in the developed world, we are able to protect them and nurture them. We need fewer of them to replace us. But we can compare two developed countries. On the left is the U.S. and on the right is Japan. Japan is really struggling right now because they have so few young people and so many elderly people. One of the problems with having a population density, rather population pyramid like this is that those older people require a certain number of young people to support them as they age and retire. They call this the age dependency ratio. And it varies from country to country. It depends on a lot of factors, the total population, the population density, the productivity of the country, cost of living. But in Japan, having a very high cost of living and having very few older, rather younger people, and having a shrinking, if you will, work population, they're having a difficult time supporting all of their elderly people. And their life expectancy is going up. These are the current population pyramid for the U.S. in 1960 and comparing it with what they believe will happen by 2060. And as you can see, baby boomers are really going to expand the upper limits of the population pyramid. We can think that by 2030, one in every five U.S. residents will be of retirement age, that is age over 65. We believe that by 2030, also older people will outnumber children for the first time in U.S. history. Now, there's a problem with this. And the problem is that when you change the age composition of a population, the population composition of a population, you tend to have a downward trend in labor force participation rate. So labor force participation rate is the number of people or the rate of people either entering the workforce or remaining in the workforce. And this has been declining over the last 20 years in the U.S. By their sheer numbers, baby boomers, people like me, have always been a generator for change in whatever stage of life they entered the workforce. And so we began entering the workforce in the 70s, and that's when the American workforce saw a huge expansion in the number of people out there working. And now as the baby boomers leave the workforce, we're seeing a decline in workforce participation rates. The U.S. labor market is now experiencing a negative democratic compositional effect as baby boomers leave the workforce. And we expect to see this increase over the next 10 years, at least for the next 10 years, and hopefully by then we'll have a new resurgence in workforce participation. But this is not a problem that's going to go away quickly. So with fewer younger people entering the workforce, we have fewer people to support the elderly that are on pensions. This old age dependency ratio really matters, particularly in countries where we have really high life expectancy and we have very few young people. So our biggest problem in the U.S. and in Japan and in many developed countries is something that goes back to that population pyramid, and that's fertility rates. Fertility rate is just how many new viable births are you experiencing per year, and that's been declining in the U.S. for decades. And it's something that actually has a significant impact on our own workforce. Labor force participation rates have been declining as a result of these demographic changes, but also because of structural changes. A lot of the jobs that were previously done in the U.S. have been exported to other countries where they can be done less expensively. And so a lot of those jobs are gone, and people who are really not qualified to do anything more, if you will, intellectually demanding are finding themselves out of the workforce. There have also been cyclical changes in our workforce, things that have changed in the 90s. There was a huge expansion of the stock markets, and suddenly all kinds of people found themselves able to retire early and did. And 97 to 2000 saw a resurgence as those people that thought they could retire in the early 90s found themselves having to go back to work. And there was actually a peak in those pre-retirement age employees, if you will, during that time. And after that time, we found that those folks, 25 to 54, and their participation rates in the workforce actually declined. But while that was going on, we found that those folks that could not retire, those age 55 and older, actually had to return to the workforce. And over time, they have continued to return to the workforce. So if you will, we are seeing a greater proportion of older workers re-entering the workforce, and we're seeing a smaller proportion of younger workers actually seeking employment or trying to maintain employment. Population is the single most important factor in determining the size and composition of a labor force. I think that's pretty easily seen in those population pyramids. As you see a declining growth in the labor force, you see that is probably due to a declining growth rate in the population. More older Americans are working and seeking employment in the workforce. More older Americans are working and seeking employment than ever before. This is something that has been pretty well identified by Bureau of Labor and Statistics, and they've been tracking it for years, for decades, really. And as you can see, whereas men and women age 55 to 64 are fairly flat in terms of their participation rates in the labor force, men and women older than 65 are actually increasing their labor force participation. And there's a problem with this, and that is because life expectancy doesn't necessarily come with less disease. And so as you have older people re-entering the workforce, you're having to deal with those chronic managed disabilities and diseases. And this is just some research that was put together by the Bureau of the Census. It's 2010 data, just kind of gives you an idea of the kinds of diseases that we see in individuals 65 years and older, and gives you gender ratios. You can see hypertension, no surprise. Arthritis, no surprise. Heart disease, no surprise. Diabetes, I suspect, is actually higher now as we gain weight in our population. Lung diseases, that actually is declining over time as people quit smoking. Cerebrovascular disease is still a problem, but has been managed through management of heart disease and hypertension and those types of risk factors. But there are other issues that occur with aging. Almost half of elderly men and a third of elderly women admit to having difficulty hearing. Some elderly people, myself included, have visual problems, and up to 25% have no natural teeth. I don't know how many of you get to see people that are 65 years and older. I do quite a bit in my practice, and I'm surprised actually at how many people are edentulous. But there are other challenges to work, and they aren't all physical. The new workplace, and this has to do with those cyclical changes and changes in what is driving the US economy, those new jobs require fluid intelligence. You need to be able to do math. You need to be able to learn computer skills. You need to be able to adjust to rapidly changing situations. This is what they term fluid intelligence, and this begins to decline in middle age. So we're already talking about problems with our ability to work that are occurring when we're in our 40s and 50s, not in our 60s and 70s. So why aging matters in the workplace? Part of that is because fewer younger people are entering the workforce. That may mean that we as employers have to rely on older workers. Older, potentially less cognitively capable people may take longer to train and be less efficient on the job. Also, they're less physically resilient than younger workers, so they may be more susceptible to occupational injury and disease. And because they are older, we aren't going to just be managing workers. We're going to be thinking about their chronic health conditions that may make it difficult for them to maintain their employment, and it may challenge our HR staff to keep a factory or a company operating if it's relying on older workers. So I believe as ergo-ambientologists, occupational and environmental medicine physicians, we need to understand aging and its impact on work and the workforce. So now I want to go into the next little issue of this talk, and that is aging itself. And I hope to help you understand current thinking on what aging actually is. The classic definition is that aging is the last stage in the life cycle during which the organism experiences gradual loss of organ function and systemic regulation, and this eventually leads to the organism's death. But that happens if you actually get to get old. Wild animals don't typically age. Wild animals, animals in the wild actually never get a chance to age because of selective pressure. They have predation. They have adverse weather conditions, infections, diseases, injuries, food shortages. All of those things contribute to a very low likelihood of dying of old age, as it were. But for us, and I consider us as domesticated animals, old age actually happens. And for us, aging begins at the molecular level. So I want to just make sure everybody is on the same page, and we'll talk about some things that you probably haven't seen since medical school, macromolecules and cells. Of course, the cell is the smallest enclosed unit in the body. And unlike prokaryotic cells, bacterial cells, where eukaryotics were made of eukaryotic cells, and they are able to specialize and diversify in their function. So there are all kinds of types and subtypes of cells, bone and cartilage, tendon, nerve cells, gastrointestinal cells. We actually have three types of just muscle cells in our bodies. Cells are made up of macromolecules. This depiction of a cell membrane gives you an idea of the numbers of different types of macromolecules in a simple cell membrane in a eukaryotic cell. The phospholipid bilayer, it's pierced by all kinds of proteins and signaling molecules that are needed for a proper cell functioning. And obviously, all of these macromolecules change with the purpose of that particular cell, be it a nerve cell or a gastrointestinal cell. Of course, the most famous cell, the one that everybody is researching now is the oxyribonucleic acid or DNA. And what we are finding now is that the loss of molecular fidelity at the molecular level is the essence of aging. This is the ability of molecules to function as they are designed to function. So let's talk about macromolecular function. Obviously, there are a number of different kinds of macromolecules, polysaccharides and lipids that provide energy. Lipids also are the chief components of cell membranes. They mediate inflammation. Lipids are where we get our prostaglandins from. They also act as signaling molecules. Polysaccharides are also a source of energy. They also are components in musculoskeletal structures like cartilage and in body fluids, such as synovial fluid. DNA has a couple of different major functions. One is storing genetic information for cell function so that it can be transcribed into RNA and translated into proteins for use within the cell and as extracellular messengers. And of course, DNA stored in the sperm and ova are the storehouses of our genetic information for species reproduction. Proteins form many body structures and tissues. They carry messages between cells and within cells, and they combine with other macromolecules for specific purposes. I'm focusing here on hyaluronic acid because it's kind of a fun compound. We use it a lot, or we see it used a lot in people that get viscose supplementation injections of the knees, things like SynVisc and EuFlexa. These are basically hyaluronic acid that's been synthesized and is used to help supplement folks that have joint degeneration and forestall the day when they have to have a knee replacement. So let's talk about what happens to the macromolecules that causes them to age, to lose their ability to function as designed. The current theory is that macromolecular aging occurs due to oxidative stress. And this oxidative stress is imposed by reactive oxygen and reactive nitrogen species. And those species are produced by daily normal metabolism and by bad habits like smoking. These reactive oxygen and nitrogen species are typically neutralized by our own body's antioxidants and also by things in our diet that help also to reduce their effects. There's an age-associated functional loss due to an accumulation of these reactive oxygen and nitrogen species and the damage that they induce. So this little depiction kind of gives you an example of different types of reactive oxygen and nitrogen species. All of us have had at least some training rather in toxicology. So I'm sure you're at least familiar with some of these like hydrogen peroxide, superoxide, nitrate oxide. These are all bad actors when put in living tissues. Free radicals like superoxide and reactive oxygen species like hydrogen peroxide can oxidize these macromolecules. They will oxidize the thiol groups and proteins, guanine and DNA, and carbon atoms and lipids. And with that, we get changes. We have number of multiple reactions of multiple body functions that thwart these types of impacts. We have enzyme systems like superoxide dismutase. We take things in our diet like vitamin C and vitamin E that have antioxidant effects. And of course, with DNA, there are multiple DNA repair mechanisms that also help to reduce the impact of this so-called macromolecular aging. This depiction kind of puts it all together how different impacts from metabolism, the environment and intracellular and intraorganismal oxidative activity can cause oxidation of proteins, lipids, genetic material, alter cell signaling, cause dysfunction in genes and enzymes and in structural components of the cell, which worsen homeostasis or decrease homeostasis, increase our susceptibility to disease, but also decrease our ability to heal once disease occurs. All of this causes us to age. So I think it's better now to move on from the macromolecular level to the organelle level. Organelles are made of macromolecules. And if the macromolecules are being oxidized, they're going to decrease the function of organelles. Everyone will remember that an eukaryotic cell has a number of different types of organelles, mitochondria, the nucleus, endoplasmic reticulum, the Golgi apparatus, so where things are either produced or packaged for export from the cell, lysosomes. The cells that, or rather the organelles that are important for aging include the nucleus, the mitochondria, lysosomes and peroxisomes. Then there are cell functions that are important in aging. These include stem cells and last but not least, cell mitosis or cell division. So the nucleus is really the master planner of the cell. It directs protein synthesis and controls cell division. The mitochondria produce adenosine triphosphate, which is the energy currency of the cell, the energy needed for all cell functions, peroxisomes, oxidized fats and alcohols. Lysosomes are important for importing cell components from the interstitial fluid into the cell and from there into the mitochondria. And they're also important for recycling micro, correction, macromolecules, a process that's called autophagy. Mitosis is really important. Obviously we have to be able to duplicate cells and those cells have to be perfect duplicates of the parent cell. There are also a number of different functions, or rather a number of different organ systems in the body that require rapidly dividing cells. The one that comes to mind that we are now performing a lot of medical surveillance for is the GI tract, rapidly dividing cells, line B GI tract. And of course, if you are like me and you have to go in and get your colonoscopy, this is what we're looking for, is inaccurate or dysfunctional reproduction of GI tract mucosal cells, causing adenomatous growths that can lead to carcinoma. Stem cells are important for replacement of dysfunctional cells. These are newly grown cells, if you will. They are baby cells and they've been found in virtually all organs in the body, blood vessels, skeletal muscle, teeth, hair, the heart, the GI tract, bone marrow, the brain, all of these contain stem cells. And theoretically, if all of these stem cells continue to work properly, we shouldn't die. But they don't work properly. So what happens when organelles age? Well, with the nucleus, we have a thing called epigenetic changes. These are changes to the DNA that cause gene expression to go awry. One example is methyl groups that are added as adducts to the DNA. They cause problems with translation that then, excuse me, transcription that then causes inaccuracies in RNA that cause inaccuracies in the production or translation of RNA to proteins. With mitochondria, again, we have a problem with not only ATP production, which decreases, but also with their ability to divide. Mitochondria have to go through mitosis just as the cell does so that there are an adequate number of mitochondria in the daughter cells as in the parent cell. Peroxisomes have a decrease in their isolation of oxidative reactants. They also, what you see with loss of peroxisome function is an increase in hydrogen peroxide production within the cell. So now you have increased ability to oxidize macromolecules and increased ability by that to decrease the function of organelles in the cell. And then lysosomes, you have, now you have too many oxidized macromolecules, but with lysosome function decreased, you are no longer digesting those macromolecules. So they're accumulating in the cell. And another problem with a loss of lysosomal function is that you have a decrease in importation of necessary cellular components. With mitosis, again, you have slow or no cell duplication. This can leave a cell to become more sensitive to necrosis and then going back again to lysosomes if your cells are dying and lysosomal function is decreased, then there's no autophagy and those dysfunctional cells start to accumulate in the body tissues. And then with stem cells, the problem is a lack of a supporting environment for them. So they are no longer able to progress from the pluripotent stem cell to the ultimate stem cell, product, be it a white blood cell or a GI tract cell. So the consequences of aging are manifold. With the nucleus, we're no longer producing a functional gene, excuse me, proteins or enzymes. We're also no longer making accurate duplicate copies of cells. This can cause metaplasia and can cause dysplasia. Mitochondria, no longer having adequate energy production in the cell. This is really important with the muscles. You're also not accurately duplicating the mitochondria at mitosis. With peroxisomes, we increase reactive oxygen species into the cell and we get more oxidation of organelles and macromolecules. And with the lysosomal aging, we have difficulty importing cellular components into the cell. And that's important with the mitochondria because one of those components the mitochondria require are starting materials for oxidative phosphorylation and that's glucose. So each tissue in the body ages at a different rate. And so we see this in a lot of different people. This is why the deaf person is able to run a marathon. It doesn't matter. They don't need their ears, even though their ears are old. Their heart and the muscles work just fine. The person with a severe heart disease may be able to do higher mathematics because their brain works just fine. Their body just doesn't work. Each organ in the body is made up of cells that interact in a coordinated fashion. When the cells age, the organ ages. And that's a take home here. And what I really want to focus on now is the musculoskeletal system and how it ages. And we'll start with the muscles themselves. Everybody knows we've got three types of muscles, smooth muscle, cardiac muscle, and skeletal muscle. The smooth muscle and cardiac muscle are involuntary, whereas the skeletal muscle is a voluntary muscle. Cardiac and skeletal muscle are striated and work by a different mechanism than smooth muscle. And we'll start with the muscles themselves. And we'll start with the muscles themselves. And we'll start with the muscles themselves. And we'll start with the muscles themselves. And we'll start with the muscles themselves. And we'll start with the muscles themselves. And we'll start with the muscles themselves. And we'll start with the muscles themselves. And we'll start with the muscles themselves. And we'll start with the muscles themselves. And we'll start with the muscles themselves. And we'll start with the muscles themselves. And we'll start with the muscles themselves. Cardioid muscles are a group of functions of the multi-medicated muscle system, called myofibers. Myofibers are a group of functions of the myofibers, called myofibers, and are a part of the central nervous system. And they're responsible for the functional and structural unit of muscle. Consists of thick myosin filaments and thin adenine filaments. Keeps thick filaments centered during contraction. In muscle contraction, actin filaments slide past myosin filaments. Neater filaments change in length, yet the sarcomere becomes shorter. The force required for this movement is generated by myosin heads, which may cross bridge attachments to actin. Myosin heads walk along an actin filament using ATP for energy. Tropomyosin is part of the complex that prevents myosin from sliding along the thin filaments. A myosin head binds ATP, and as a result, detaches from the actin filament. It rebinds in a new position. Prostate release triggers a power stroke that moves the actin filament. ADP disassociates, and the process is repeated. There are two types of striated muscles that we need to be concerned with. The first is the slow-twitch, or type I muscle fiber. And these use oxidative phosphorylation to make ATP, and this requires a lot of energy. The second is the slow-twitch, or type II muscle fiber. And these use oxidative phosphorylation to make ATP, and this requires a lot of energy. The third is the slow-twitch, and this requires a lot of mitochondria. These slow-twitch muscles contract slowly, and they resist fatigue. They facilitate prolonged low-intensity activities. Part of the reason that researchers theorize older people are better at marathons than younger people is because they have predominantly slow-twitch muscles, whereas younger people have a lot of fast-twitch muscles, and so they fatigue much more quickly. The type II, or fast-twitch muscles, utilize glycolic enzymes to make ATP, and so they have fewer mitochondria. They contract very quickly, but they fatigue easily. They're great for short, high-intensity activities, but they don't have lasting power. So as we age, we have a gradual age-related loss in lean or fat-free muscle mass, and this occurs in every animal model that's been studied, from worms to flies to rodents, monkeys, and humans. And this gradual age-dependent decrease in muscle cross-sectional area is called sarcopenia. I'm sure everybody's heard of that term. So sarcopenia does account for a certain amount of loss of muscle strength, but in terms of actual loss of strength, it only explains about 10% of age-related loss of strength. The remaining 90% of muscle strength loss is related to another related condition called dynapedia, and this is an age-related loss of strength, and it's independent on muscle mass. It is more dependent, actually, on not only the molecular structure of the muscle, but also on the fidelity of the mitochondria. Improvement of muscle mass does not cause a parallel improvement in muscle strength in the elderly. Association between physical disabilities and dynapedia are statistically stronger than the association between physical disabilities and sarcopenia. So dynapedia and not sarcopenia is statistically associated with increased mortality, as well as a decrease in strength. What we see with sarcopenia is muscle atrophy, fewer type 2 or fast twitch muscles, decreased protein synthesis, and degradation of those sarcomere components, and inadequate muscle cell replacement. Things that contribute to sarcopenia are inadequate physical activity and lack of a high-quality protein diet. Obviously, the lack of protein and lack of a high-quality protein diet. Obviously, with aging, we also have decreased hormonal levels. The ones that are important are growth hormone, estrogen, and testosterone. With dynapedia, we have other manifestations, and these include poor-quality contractile proteins. Now, remember, we're going all the way back to the cell nucleus, where we have dysfunctional transcription and translation of DNA. And so proteins that are coming out aren't as good as they were when you were in your 20s. And this leads to these low-poor-quality contractile proteins. We also have decreased mitochondrial numbers. This is partly because the mitochondria are being impacted by a loss of energy, being brought into the cell by the lysosomes, but also by oxidative events that are occurring inside of them and outside of them within the cells of the cytosol. There's altered mitochondrial DNA. I'm sure everybody remembers that mitochondria have their own DNA, and it's slightly different from the DNA that's found in every other species on the planet. But their DNA is important to them, and it helps them function properly, and it is also altered. These dihydropyridine receptor number decreases. These are the voltage-gated calcium channels within the muscle. These are decreased, so you have less stimulus of the muscle. And then also there's decreased input for motor neurons in dynapedia. The things that contribute to this, other than age itself, is a sedentary lifestyle and no resistance in aerobic exercise. So the consequences of aging in sarcopenia, you have increased body fat, increased inflammatory factors, decreased resting metabolic rate, you get weight gain, you have an increased risk of type 2 diabetes, and altered thermogenesis. As we get older, we often find ourselves getting colder. Young people, I just saw a guy yesterday swimming in the Clark Fork River. The Clark Fork River is the major river that goes through Missoula, Montana. Clark Fork River is sitting at around 35 to 38 degrees. And there were two young guys in their early 20s swimming in there, let's just say in their birthday suits. And they were swimming. They weren't just jumping in and jumping out. They were having a great time. But they have really great thermogenesis. I would not get in that water. I would die. Dynapedia is another problem. And that is something that causes muscle weakness. These are some factors that are probably really important. We'll go into later. Muscle weakness, a decreased gait or ability to walk is also a problem with dynapenia. Decreased exercise tolerance, increased risk of falls. And obviously we talked about this before, increased morbidity and mortality. So to summarize muscle aging, it's more important, well, rather dynopenia is more important than sarcopenia, loss of muscle strength, and not actually the loss of muscle girth or size mass that matters. And dynopenia can be combated by a continuous program of resistance exercise. This helps to maintain mitochondrial numbers, helps to maintain motor neuron input to the muscle. The current sports medicine prescription for exercise includes four types of exercise for the elderly. These include aerobic exercise, resistance exercise, balance exercise, and flexibility exercise. And then I just wanted to put in this little note. This is one of the things where I think companies that want to employ older workers will have to consider is developing and maintaining wellness programs for those older workers so that they can maintain their ability to physically be active. We're gonna transition to bone aging now. Obviously there are a lot of bones in the body, about 206 of them. 80% are compact cortical bones, and these include the skull, the jaw, the long bones, and the outer edges of the joints. And then the trabecular bones, things like the hips, the pelvis, and the vertebral bodies. There are a number of different types of bones, and I'm not gonna, you can read the slide as easy as I can read it to you. The important thing to notice here is that the long bones are the ones that tend to be impacted by aging, and we'll go into some of the conditions that occur in the skeletal system with aging. Bone architecture is something that is impacted by aging. I, again, won't go into the details of just how bones are built, if you will. I do want to recognize, though, that in order for bone to work, not only do we have to have the bone structure, but we have to have the cellular components of the bone being healthy. And this is really where the aging process is impacted. We have three types, well, four types, if you count stem cells, of bone cells, the osteoblasts, which help to form bone by creating the collagen matrix and incorporating calcium phosphate salts into the bone, the osteocytes, which are the mechanoreceptors for the bone and basically modulate the activity of the osteoblasts, which form bone with the osteoclasts, which resorb bone, and then the osteoclasts, which dissolve the bony matrix and break down, if you will, the calcium phosphate salts, refreeing them and placing them into the bloodstream. The osteogenic cells, the stem cells, obviously, are used to make new osteoblasts, osteocytes, and osteoclasts. Bone resorption, or the extraction of minerals out of the bone, and bone formation, or the deposition of minerals into the bone, are a coordinated process. And this process is coordinated by the osteocytes, and this process responds to mechanical strains, or what is called the customary strain stimulus. So if you have a strain above this customary strain stimulus, it will increase bone remodeling rate and strengthen the bone. This is why resistance exercise is so important. If your strain is below the customary strain stimulus, this also increases bone remodeling, but this leads to increased bone resorption. In the elderly, bone resorption typically exceeds bone formation, and this causes bony loss. This is why astronauts in the International Space Station exercise daily. They have to maintain that customary strain stimulus in order to not suffer from demineralization of their bones and develop osteoporosis. Studies show that bone mineral density decreases with age in both genders. It's more pronounced in women than in men, but it occurs across both genders. There are multiple hormones and chemicals that contribute to bone health. Estrogen is probably the most important one, parathyroid hormone, which helps to bring calcium out of the bone when you have a low calcium level. Vitamin D obviously is important for incorporation of calcium in the bone, and of course, calcium itself. Adrenocorticosteroids are important in that they can cause resorption of minerals from the bony matrix and cause osteopenia and osteoporosis. Estradiol is the most important regulator of bone health for men and women. It slows bone remodeling, and what it does really is it preferentially stimulates osteoblasts and osteocytes, and it eliminates osteoclasts. It diminishes at menopause in women and what is so-called andropause in men. In men, we use testosterone, and we have an enzyme called aromatase that's expressed in a number of different cell types in the male genitalia, to produce estrogen, and that's how men maintain bony mineralization. But again, we lose that ability to produce testosterone as we get older, which causes us to lose the ability to make estrogen in our tissues. So factors that influence age-related bone loss, of course, mechanical strain is less, so you have less bone formation, and you have less bone loss. You have less bone formation and more bone resorption. Menopause in females, andropause in males. Vitamin D and calcium deficiency is a real problem, especially because not only does this, if you have a calcium deficiency, what you will do is activate parathyroid hormone, and that will draw more calcium out of the bone and exacerbate any osteopenia that may already be present. Decreased growth hormone is also a problem. This causes a loss of osteogenic effects, and that means the stem cells are less active. Increased adrenal steroids, this is something that occurs with stress, and if you're being treated with glucocorticoids, this will also cause a loss of bone mineralization by multiple mechanisms. So smoking, and I've got to put my plug in. We're all preventive medicine specialists, and smoking is a real problem. We see this, I see this in my practice, and folks that are going in for various types of musculoskeletal surgeries and fusions, and one of the things that was not previously addressed in over the last 10 or so years has been more and more addressed as smoking status in orthopedic surgery patients. It's an independent risk factor for osteoporosis. It's associated with low bone mineral density. Obviously, you don't heal well if you're a smoker. You generate lots of free radicals and reactive oxygen species. It decreases absorption of calcium, accelerates menopause, increases adrenal steroid production, and there is a dose-dependent effect of smoking, and it's partially reversed if you quit smoking. Now, I'm going to transition from the bones to the joints. There are multiple joints in the body, types of joints in the body. They act as swivels, pivots, hinges, shock absorbers. They all have common components. They all have ligaments that connect bone to bone, bone to bone, synovial membrane, synovial fluid. There is an articular cartilage that line the joints, and it turns out that osteoarthritis or joint degeneration is probably the most common musculoskeletal condition we see in the elderly, and there are diagnostic criteria for osteoarthritis. There's extra bone growth or osteophytosis, joint space narrowing, and then extra bone growth along the joint line and formation of subchondral cysts. We find that prevalence of osteoarthritis increases with age, knee being the most prevalent, followed by hips, and then third is the hands. Osteoarthritis can involve all parts of the joints, including the cartilage, the synovial fluid, subchondral bone, the bone marrow, synovial membranes, and the ligaments. There are a number of other risk factors for osteoarthritis that combine with aging. Probably the most prominent with knee osteoarthritis is obesity. Post-trauma is also a problem with osteoarthritis. Genetics, they believe that 50% of the propensity for osteoarthritis is heritable. Diet, again, vitamin D is really important. Calcium is really important. Physical exercise is a good thing, but too much can be a bad thing. We see osteoarthritis as more prevalent in elite athletes in their older years, and congenital or injury-related misalignment can cause osteoarthritis. We can see this with femoral acetabular impingement and with abnormal hip, knee, ankle alignment. Dynapedia is another risk factor for osteoarthritis, but it's unclear just how that works. It's just been found to be associated with osteoarthritis, and obviously osteopenia is a major risk factor for osteoarthritis. We found from animal studies that the chondrocyte numbers in the articular cartilage declines with age. Some of these chondrocytes express a stress-induced senescence identical to the destructive senescence-associated secretory phenotype. So this is a phenotype that is expressed by old cells, and these senescent cells actually produce pro-inflammatory and degradative enzymes that go through the interstitium to non-senescent cells and actually cause those non-senescent cells to begin to become senescent cells. So if you will, old cells, if you will, aging can be contagious in these cells. It's believed to be due to a low level of chronic inflammation that we see in the elderly. We also see this in other populations, particularly in smokers and in the obese. There are many people that never develop osteoarthritis, but in point of fact, the majority of us will develop some amount of osteoarthritis in our lifecycle. It's interesting to note, though, that this senescent-associated secretory phenotype that is expressed by senescent cells is being addressed as a possible target for treatment of senescence in all types of tissues, not just in the joints. We'll talk about tendon aging. Everybody knows what tendons do. They connect muscles to bones. We have terms for them. Musculotendinous junction is the junction between the muscle and the tendon. The osteotendinous junction is the junction between the bone and the tendon. Tendons are made up of a number of different structures. We have collagen fibers, and we have tenocytes that are the resident cells in the tendon, and they sense the load in the extracellular matrix of the tendon, and they are what help to adapt the tendon to varying amounts of stress placed upon it through the bones. Tendons consist mainly of type 1 collagen fibers, and these tendons consist of proteoglycans that are responsible for the elasticity of the tendon. So the problem with, or rather, the function of a tendon is not only to stretch, but also to contract and return to its original length. And when those tendons aren't able to do so, well, one of the issues that can occur is that they can rupture. And we see this in older folks with things like ruptures of the bicep tendons. Tendons have a significantly reduced blood supply around bony pulleys, and we see this manifest in things like stenosing tendosynovitis or trigger fingers. Just wanted to remind you that tendons aren't just in the musculoskeletal system. We have tendons in our eyes and tendons in our ears. And these tendons can become stiff, just like the tendons in your ankles and in your fingers and everywhere else in your body. Aged tendons exhibit structural, compositional, and biomechanical changes. Structural changes include disorganized collagen fibers. They lose blood flow and vascularity. And they develop tissues that are not native to them. The big one that we see is bone tissue or calcium. And so we see, if you will, the calcific tendonitis that you see in the shoulders. This can happen in other parts of the body. And the patellar tendon, heterotopic bone formation, can occur. This often can also occur in older patients who undergo orthopedic surgery. There are compositional changes in the tendons with decreased cellularity, which means fewer numbers of tenocytes, and de-differentiation of those tendons and de-differentiation of those tenocytes as they become senescent. And then biochemical changes with changes in collagen and proteoglycan content. Again, accumulation of advanced glycation in products and reduced proliferation of metabolic activity in the tenocytes themselves. So tendon aging is really a problem for smokers and for the obese. And if you will, because smoking at least is a modifiable risk factor, it is something that we can address as we take care of these folks. Obesity is a little bit harder to take care of. It's really hard once a person is obese to get them to lose weight. It requires a number of lifestyle changes that are often insurmountable for many patients. Females are at greater risk of tendon aging than men. And tendon aging can be at least partially mitigated by an exercise regimen. So now I want to switch to some common conditions of musculoskeletal aging. So this pathologic triad has been discussed by Minetto. And it's highly prevalent in elderly patients. And its components include sarcopenia or loss of muscle, bulk, tendinopathies, and arthritis. So with the bones, we have the highest risk of fracture in hips, the spine, the femur, and the wrists and arms. And then the secondary risk of aged bones is fracture non-healing. I've been noticing this occurring in my patient population with older folks that end up needing a fusion, a cervical fusion or a lumbar fusion, that go on to develop a non-fusion or pseudoarthrosis. I personally have never understood the recommendation by many surgeons that the person for stalls, major orthopedic surgery until they're older, when you consider all the risk factors for proper healing that occur in the elderly that aren't there in the younger patient. And so to tell a person that is in their 40s to wait until they're in their 60s or 70s to have that lumbar fusion makes no sense to me. There are numerous comorbidities that combine with the aging process to increase fracture risk and fracture non-healing. Obviously, diabetes is one. Smoking is one. Obesity is one. Osteoporosis or osteopenia. Chronic kidney disease is one. With the muscles, we find that we lose muscle mass over time. From the second to the eighth decade of life, the whole body and appendicular lean muscle mass declines by about 20% in men and 30% in women. A 2015 systematic review, and this was of Chinese population, or excuse me, British population in this study, found that sarcopenia actually increased over the life cycle in the community and between the community and between community, a comparison between community acute hospital and long-term care facilities. Obviously, this demonstrate that sarcopenia is more prevalent in those that are less active. Unlike tendon and joint research in the aging population, there isn't much research done on muscle aging. What has been done is a look at the, if you will, the effect of muscle aging. And this is where the concept of frailty comes in. A frail person is considered to be susceptible to stressors that result from a decreased physiologic reserve, or rather, excuse me, I misspoke. Frailty causes a decrease in physiologic reserve. And stressors can include anything from infection to disease. We've seen this. I see this in my population of COVID sufferers that are in their 50s and 60s. A change in medications can be a stressor. And obviously, mental stress, the 50 or rather the 65-year-old I just saw who had a 27-year marriage end abruptly with her husband becoming ill and dying over the course of a couple of weeks. And she was injured prior to his death. And after his death, she's just not rehabbing well at all. And her injury should have been trivial. Now it's become life, well, life-changing. An older fit person exposed to a sudden change in health status is more likely to return to stability and the same level of health as before, whereas a frail person will experience a minor stressor. They'll have an exaggerated response and will have very difficult time recovering and going back to where they were before that minor stressor. And this is what I see most often. People have no ability or very limited ability to rebound after what should have been a trivial injury. This is the gentleman that I mentioned earlier on, the gentleman who was a mechanical engineer, had a trivial shoulder injury, and just wasn't able to rehab and return to his previous state of health. Frailty was described by Freed and is based on the cardiovascular health study. The components of frailty include shrinking, weakness, lack of endurance, slowness, and low physical activity. They operationalized this to provide a diagnostic criteria for frailty. This includes unintentional weight loss of more than 5% over the course of a year. Unintentional weight loss of more than 5% over the previous year. Weakness is defined as a loss of grip strength that's measured using a dynamometer. Slowness is defined as a loss of gait speed. And then they use self-report questionnaires to document physical activity level and levels of exhaustion or lack of endurance. The prevalence of frailty has been measured in multiple populations over 65 and estimated between 4% and 59%. The overall weighted average prevalence of frailty is about 10% or 11%. That means that about 1 in 10 people over the age of 65 is frail. In 1990, the American Medical Association, the AMA estimated that about 40% of adults over the age of 80 are frail. And then frailty also has impacts on other conditions or rather other conditions have impact on frailty. About 44% of folks in heart failure are frail by definition. About 37% of people within state renal disease are frail. Depression has a fairly high prevalence of frailty at about 40%. And no surprise, malnutrition causes frailty or is associated with frailty in about two thirds of adults. Frailty matters because frail people work. Now, all of this data really is based upon people that are 65 years or older. In my population here in Montana, where people work very hard and often work two or three jobs, I find frailty and obesity to be the major risk factors in their musculoskeletal injuries and occupational diseases. If the person has a condition that has not improved over the course of a year to two years, and I'm seeing them for the independent medical evaluation, and the injury is stated to be something like a shoulder injury or a low back injury or a neck strain, the first thing I ask is, what is their BMI? Is it really high or is it really low? Problems of the tendons are really interesting in the elderly. This is something that we're all likely to see as we get older. Rotator cuff tendinopathy is really prevalent in the older population. The supraspinatus and subscapularis tendons are the most commonly involved. We see this a lot, and there's quite a bit of literature documenting a high proportion of people with tendons a high proportion of elderly men and women who have rotator cuff tears and have no idea that they are there. And it's because the rotator, the tendons have degenerated to the point and finally given up and torn. Those folks have lack of shoulder strength and range of motion, but really don't have any pain and don't even know that they have torn the rotator cuff some point in the past. We also see a lot of calcific tendinopathies. This is seen in the shoulder, most supraspinatus, infraspinatus and subscapularis. But I also see this in my practice in the patellar tendons and the Achilles tendons as well. Gluteal tendinopathy is another problem and is more prevalent in the elderly. Clinical characteristics are old age, female gender, obesity, altered gait parameters. And this feeds back to a problem we have with age-related muscle weakness. And we also see it in female gender. Psychological distress can cause this as well. I'm not so sure how that is measured in this study beyond it being self-report. Achilles tendinopathy is a most common sports-related injury, but it's also fairly prevalent in the elderly. The injury rate has changed from two in 100,000 to 12 in 100,000 over the last 10 years. You see it far more likely to occur in men and then in women. And it actually occurs more in younger, middle-aged instead of in the elderly. And it also turns out the Achilles tendon strain tolerance is far more impaired in the older than in the younger worker. This will have an impact for individuals. I see this in folks that return to work after retiring. They decide to take a job at Walmart or at Costco and they want to stock or they want to be a greeter and they have to push shopping carts or they have to climb ladders. And their Achilles tendons don't take the strain and they fall. Common problems of the joints. So the Johnston arthritis study found the lifetime risk of symptomatic knee osteoarthritis to be basically 50 to 67%. 50% of people overall will develop some amount of knee osteoarthritis. Two thirds of people that are obese will develop knee osteoarthritis. The global burden of disease study that WHO put on, that WHO sponsored found that 10% of men and 20% of women over the age of 60 have symptomatic osteoarthritis. This study is really interesting. It was a large meta-analysis and you can argue as to the validity of meta-analyses but this was conducted in China. And it was after looking at thousands of studies, they found 21 studies that met their inclusion criteria. 14 of these investigated people that were older than 40. Four of the studies investigated people older than 50 and three of these studies investigated people older than 60. So if you will, most of these studies were actually in only the middle-aged and not in the elderly. That being stated, they found that the prevalence of lumbar osteoarthritis was around 25% and that's starting at middle age. Prevalence of knee osteoarthritis was around 20%. The cervical osteoarthritis was around 20%. Hand osteoarthritis around 9%. And they found that there was a higher prevalence of hand, knee, lumbar, and cervical osteoarthritis in women and in Southern China. No idea why that is. Knee and hand osteoarthritis was found to increase in age and predictably so were lumbar and cervical osteoarthritis. But the interesting thing they found in their study and China had for a number of years had low life expectancy but life expectancy in China has been increasing. Since really the 2000s. And they found that osteoarthritis increases with age up to around 70 years old. And then the prevalence slightly decreases in older ages. Now this could be a survivor effect and not really have anything to do with the development of osteoarthritis at all. So I wanna summarize what I've talked about. We're almost out of time here. American workforce has fewer younger workers. And that's because we have a decreased population fertility rate. Older workers are challenged by both physically and cognitively demanding workplaces. A modest challenge to a younger worker can be an overwhelming challenge to an older worker. And I want you to remember that in the same way that organ systems age at different rates, people do too. And so the 60 year old may be a young 60, the 50 year old may be an old 50. Aging workforce is only becoming more prevalent as our population becomes older overall. I think we demonstrated that with the population pyramids I showed at the beginning of this talk. The effects of aging vary within individuals and vary between individuals within different organ systems within the same individual. Aging begins at the macromolecular level and then is manifested in the organelles, the cells, the tissues, the organisms, and then in the organism itself. Inflammation appears to be a very important factor for aging and this is why we see all the huge emphasis in the nutraceutical industry on antioxidants. Musculoskeletal aging affects all components of the musculoskeletal system. I did not address the nervous system, that's another talk, but it does affect the bones, the muscles, the tendons, and the joints, all in different ways. So in summary, the older worker may require a longer course of injury care or rehabilitation. In Montana, we have treatment guidelines for workers' compensation. They're called the Montana Utilization and Treatment Guidelines. And one of the general principles of the Montana Utilization and Treatment Guidelines is that a proportion of the people that are treated for a routine injury may require a longer time to rehab from that injury. And those people have a greater susceptibility or a greater vulnerability. One of the populations that is a part of that, if you will, population is the elderly. I see that a lot, older workers that just don't have the resiliency. I think that the sports medicine model of rehabilitation in the occupational setting is great if you're young. I don't know that it works well if you're old. Temporary total disability is probably more prevalent in the older worker than in the younger worker. When treating older workers, you also have to consider treating their comorbidities, their hypertension, their hypercholesterolemia. You have to get their diabetes under control. If it isn't, you have to get them to quit smoking. You have to get their weight down. All of those things cause an increased time of rehabilitation and the older worker often struggles to resume pre-injury functioning and often is unable to do so. So with that, I'll open it up for questions. Thank you for your attention. Appreciate you coming and taking a listen. And if you do have questions, please feel free to approach the microphone. In the meantime, Dr. Schumpert, there was a question from one of the online viewers, whether you could share your slide set on the SwapCard app through AECOM. Oh, yeah, I actually already did, but if it's not up, I'll do it again, no problem. Great, thank you. Any questions? Go ahead, go ahead. Yeah, good morning, Bill Barkman, Kansas. As the post-placement exams for older people over 65, do you change the criteria? And a second part of that, on people that are volunteering, whether at a hospital or whatever industry, do you routinely do exams on those or do you clear those simply by a questionnaire? The reason I ask is our volunteers are covered under Work Comp. And the issue is if they get injured and you'd have no idea, if you've never physically seen them, it gets to be a little tricky about causation. So thank you. So great question. And this is an interesting difference between Kansas and Montana. In Montana, pre-placement examinations or post-offer examinations are basically not done. The employers and the insurers in Montana as a matter of policy, prefer to deal with injuries and illnesses after the fact. So they hire folks as they are and deal with them as they are. You're right about volunteers. And I often find that my elderly evaluees are volunteers in hospitals and different non-governmental organizations. They just wanted to do something to keep busy or they wanted to contribute to their church or to an organization that they feel is important and then they get injured there. Those folks were never screened to see if they were physically capable to do the work that they were asked to do. That's just something that's not done. As to go back to the first part of your question though, I really do think it is important to consider the age of the person when evaluating them for a particular position. And I also think it's important to consider that that person, although they may be able to perform all the essential functions of that position now, may still have an increased risk of injury if performing that position in, let's say, a stressful environment. So maybe they're being asked to do it twice as fast as they usually do it, or maybe there is a change in the way workflow is done and they have to adapt to that new change. All of those things can have an impact on the older worker that may not be seen by the younger worker and that has to be taken into account. And I don't see that happening anywhere. We really are, in the same way that we are gender blind, we are age blind in our society. And I think that that's something that needs to change, particularly as we see more and more older workers entering the workforce. Thanks, John. Thank you, Dr. Shumpert. Tom McClure, Montana. In your research, did you find that anything other than smoking cessation and exercise had a significant impact, like all the nutraceuticals you referred to? Is there a product that really does make a big difference? You know, there are products out there that do. I found out just recently that one product that's actually the, oh, I'm gonna blank on the name of the actual compound, but it is the major component in chocolate, in dark chocolate, actually has been shown in a number of placebo-controlled trials to improve cognitive function, memory, and middle clarity, and agility. So chocolate is good for you. Eat dark chocolate. And obviously there are a lot of different products that are antioxidants. And then the other one that really has turned out to be an important factor, it's becoming more and more important because of sarcopenia and dynopenia, is a good protein diet. Protein is probably eaten in excess as we are young. We probably eat too much protein when we're younger, and then we don't eat enough protein when we're older. High-quality protein is really important. Obviously, you get to choose whether you want red meat or white meat or plant-based protein. I prefer white meat and plant-based protein because I've got some risk factors that I have to deal with that red meat precludes my use of. But as far as anything beyond that, no, I really didn't see a lot. There's a lot of stuff being looked at. But on all of these things, some of these things have marginal effects, but very few of them have really compelling, like there's no golden bee, there's no fountain of youth out there yet. There are a number of different lines of research looking at things like how do we control these factors put out by senescent cells that cause surrounding cells to become senescent? How do we take care of other processes like the deposition of calcium into soft tissues such as tendons? Those things are still up in the air. In general, though, four types of exercise are felt to be really important. Balance exercise, flexibility exercise, strength exercise, resistance, and aerobic exercise. Those are felt to be really important for mitigating the musculoskeletal effects and some of the psychological and mental effects of aging. Obviously, there's a lot of research that's been done that's found that cognitive aging can be slown by exercise and resistance exercise in particular. Thank you. Dr. Schemper, we have one question from an online participant. What is the approximate age where the total temporary and or permanent disability increases? You referenced this on your last slide. Could you repeat that question, please? Sure, I can. So when you're talking about age and its relationship to total temporary and or permanent disability, about what age do you think that risk increases? This is really asking just your opinion on that. Yeah, you know, I don't know. And this is the problem that I have with answering that question is that I don't think that's a one size fits all, probably something that would be a great research topic. And the reason I can't answer that is because people age differently. And that's partly because of lifestyle, partly because of genetics. I see people that I think, when I see them, I walk in the exam room and I'd swear this person is 10 or 15 years older than I am. And they end up being five years or 10 years younger than I am. And it isn't just how they look, but it's their demeanor. It's how they express themselves. It's, you know, how they move as they get out of the chair and move to the exam table, all of those things. And I see that playing out in, not only across different age groups of individuals, but also across genders. You see the young 70 year old and the old 45 year old. So I don't know if there is a specific, and I really reticent to say, oh yeah, at 60 years old, that's when you can expect the uptick. I really don't know where that number lies. Sorry, I can't give you any more clarity than that. Thanks. We have another Montana medical provider approaching the mic. Mike Fitch from Billings. I just had a question for you with the IMEs, if you find yourself resulting the cause saying it's more probably not due to your aging weight and smoke status and the injury that you suffered. Well, you know, that's okay. But you know, one of the, good point, but one of the, well, one of the assumptions in work comp is that we take the person as they are, right? And so it doesn't, we're not hiring Olympic gold medalists. We're hiring people off the street. And so that means we're hiring people with their hypertension and their smoking and their diabetes and their hypothyroidism and all of their other baggage and their depression and their anxiety and their college education and their work ethic, all of that. And so when I see someone and I see those kinds of risk factors, you know, I still have to say, well, okay, we've got a well-documented injury or not, or we have a well-documented occupational disease. We have someone who has a ergonomic or musculoskeletal exposures that would explain their current condition if it is an occupational disease. Yeah, this thing could have been better if this person, you know, had a BMI of, you know, 28 instead of 48, or this person might not have had such a great impact if they were, and I see this, this is actually where I see it most, is the person, you know, all they were doing was lifting a hose and they tore their rotator cuff. And if they were 20, they would have had no problem with it, but they were 60. And then the employer is going, well, gee, all they did was lift a, you know, a water hose. Yeah, but they were a 60-year-old lifting that water hose. And then that water hose, okay, well, they weighed it and turns out it weighed like 35 pounds. But this is a 60-year-old lifting 35 pounds with one arm. And this is a deconditioned 60-year-old. So do we say it's the fault of the person's age and deconditioning? Well, they still have the occupational exposure. And so I have to say, yeah, they have risk factors, but they still have that occupational exposure. They still got hurt. And it's still legitimately an occupational injury. With that, we're right at time. And so I'm gonna thank Dr. Shumpert for presenting virtually. This is a fascinating talk and also discussion. And I wanna thank everybody else for attending this session. Have a great day. Thank you.

aging

workplace injury

illness risk

older workers

physically demanding jobs

musculoskeletal system

sarcopenia

dynapenia

body fat

inflammation

fractures

osteoarthritis