Functional medicine providers have the best tools and scientific understanding of topics like immunology, the microbiome and mitochondria. This constellation of knowledge and tools makes functional and integrative doctors optimally equipped to address osteoarthritis. Dr. Thomas Guilliams is an expert in nutrition research and immunology, and he has written several books on the therapeutic uses of nutritional supplements.

During this conversation, we hear about the gut-joint relationship and an expanded understanding of osteoarthritis. We also explore best practices for nutrition and supplementation alongside lifestyle modifications to resolve chronic conditions.

Listen in to learn more about:

  • The evolution of the scientific understanding of osteoarthritis
  • Issues with nutrition and supplementation research
  • Addressing autoinflammatory conditions (as differentiated from autoimmunity)
  • Dr. Guilliams’ take on the paleo dietary pattern
  • And much more!



Nutrition, Lifestyle and Supplementation Support for Osteoarthritis | Ep 279


James Maskell:
Welcome to the Evolution of Medicine podcast, the place health professionals come to hear from innovators and agitators leading the charge. We cover the latest clinical breakthroughs in health technology, as well as practical tools to help you transform your practice and the health of your community. This podcast is brought to you by the Lifestyle Matrix Resource Center, who provide a range of options to help you deliver successful, effective, functional, and integrative medicine. To find out more and to get started, go to goevomed.com/lmrc. That’s goevomed.com/lmrc.

Hello, and welcome to the podcast. This week, we are talking to Dr. Tom Guilliams about osteoarthritis. At a recent conference, we had a chance to just sort of touch on this topic and just realized that this was something where, not only do integrative and functional medicine doctors possibly have the best tools and understanding, but also the science on things like immunology, the microbiome, mitochondria is actually helping us understand this condition that was once thought to be very simple in its understanding.

So, Tom is great in that he really understands the history of the research and where it’s gone. We’re going to be talking about the gut-joint axis. We’ll be talking about the best practices from nutrition and supplementation alongside lifestyle medicine to get to the root cause of some of these conditions. It was a really interesting half an hour. Enjoy.

So a warm welcome to the podcast. Dr. Tom Guilliams. Welcome back, Doc.

Dr. Thomas G. Guilliams:
Yeah, thank you, James. Great to be back with you.

James Maskell:
Yeah. So look, this is going to be a part of our series here on different clinical topics and just bringing the most cutting-edge research, and really grateful for you to be here. When we met up recently, we were talking about, I guess, the topic broadly of osteoarthritis because that’s something where there’s a lot of interesting things happening. I guess, since we spoke, it sounds like you’ve been, I guess, reexamining the evolution of our understanding of osteoarthritis. And so, why don’t we start there? For clinicians that maybe haven’t been in the functional, integrative space for more than a decade, I know that this conversation has been going on for five decades. So, where should we start?

Dr. Thomas G. Guilliams:
Yeah, well, thanks James. This is something, as I do in a lot of my projects, I do deep dives into certain areas, and of course, I don’t do deep dives into everything all the time. So, I was in a deep dive recently on where are things with osteoarthritis, especially in the lifestyle, integrative medicine, nutrition, nutraceuticals, and this kind of thing, especially since osteoarthritis still does not have an approved drug. There’s really no approved drug for osteoarthritis, at least nothing that really changes the dynamic of it.

So, as I was doing that, and I’ve come out with kind of a new updated review on this topic, it kind of caused me to really think about just this whole history because osteoarthritis is one of the first things that I started thinking about back in the mid-nineties, when I really got into the industry. And it was kind of like going a little bit of nostalgia. So, for those who have been in the industry a couple decades, this might also function as a little nostalgia for you. And if you haven’t, I think some of these little anecdotes along the way, I think will be informative to help explain how the industry sort of got where it was.

So 1996, for those of you who remember, that was the publication of the book, The Arthritis Cure by Jason Theodosakis. And that really opened up, especially in the United States, the whole world of glucosamine and chondroitin sulfate as a potential therapy. Now I think maybe The Arthritis Cure was maybe a little too strong of a title, but what it did is it took this… I mean, glucosamine was being used quite a bit in Europe a lot, and most of the research was being done in Europe by the manufacturers of glucosamine, glucosamine sulfate primarily. And a few people were starting to use it and bring it over to the United States.

But that book really began not only the popular use of these supplements—where they were available, they weren’t always quite readily available—but also changed the dynamic of the research. So obviously, people want to know: Does it work? Does it work? And so there was all these publications in the ‘80s, ‘70s and 1980s, and it wasn’t until really a book like this came out that people started buzzing about, “Well, is the data good enough? Do we need to do more research?”

And that eventually set up what—we can talk about here in a minute—was called the Gate Trial. The NIH funded really probably even to date the largest clinical trial on glucosamine and chondroitin sulfate and the combination for knee osteoarthritis because of a book like that. So, that kind of brought me back because I remember even writing about that book and it was kind of, like I said, it was a big book right when I was brought into this industry.

A few years after that, a book called The Miracle of MSM was also published. And at that time, MSM and DMSO and some of these other compounds were being used and explored. And of course, The Miracle of MSM—again, the title of some of these books may be a little bit over-promising, under-delivering—but in some ways, that started, I would say, a scrutiny on MSM which I don’t think MSM really proved itself, at least on the osteoarthritis side, to be as good as glucosamine and chondroitin sulfate. So, that’s kind of something, and I’ll come back to the Gate Trial here in a minute.

But one of the things that I think struck me the most about sort of the evolution of thinking in osteoarthritis—really since 1996, so it’s quite a few years—is looking at the disease. In the ‘80s and ‘90s, it was very much thought as just a wear and tear, just the articular cartilage on the end of the bone just wears away. It was really thought not to be an inflammatory process like rheumatoid arthritis and all the inflammatory conditions, and it’s just the wear and tear. And of course, it’s called degenerative joint disease or wear and tear arthritis, and that still does define it in some capacity as opposed to the hyper-inflammatory conditions like rheumatoid arthritis.

But as you know, in the last 20 years, the exploration of the inflammatory response in aging or what we call the senescent phenotype of aging tissue, which we see in osteoarthritic chondrocytes and things like that, and the role of the gut microbiome, the role of the mitochondria, the role of circadian biology, and all of these things… All of a sudden, you start looking in, and you realize… Over the last 15 years, we realized there is a gut-joint axis.

We talk about the gut-brain axis, but there’s a gut-joint axis where changes in gut microbiome influence, let’s say lipopolysaccharides, are allowing things, because of gut permeability issues, allowing more of these toxins to get around the body. And they seem to accumulate or can accumulate in the joint and create this inflammatory process.

So, it’s pretty amazing when, if you’ve studied other aging diseases as you have with other clinicians, you know that all of these factors that I just mentioned are involved in almost all the aging diseases that we talk about. Then it shouldn’t surprise us then that osteoarthritis, which seemed like this very simplistic, almost like a mechanical disease, turns out to be this highly complex aging disease that is influenced by all of these factors. So, that was kind of one of the aha moments that I had, and thankfully I was able to write and include a lot of this information in the new review that I put together.

James Maskell:
Yeah, it’s really interesting. I’m glad you said that. And I think just in general, even the last 25 years, we’ve certainly seen how books have triggered new interest in the public, new interest in science and so forth. And it’s even interesting to think, “What books in 2022 will have that same influence, and what will it look like?” I mean, early in the year, I did a whole forum on uric acid and Perlmutter’s new take on that. So in five years, what will be the impact of this sort of new scrutiny on this one marker that used to be about gout, now potentially about metabolic flexibility? What will it be? And I guess, I mean, the answer to all of these things in a certain way is it’s more complicated than we thought and there are more pathways that affect it than we thought, I guess, with all chronic illness maybe.

Dr. Thomas G. Guilliams:
And that’s true. I mean, I was thinking back, as I was thinking, “What are the seminal books that came out in those years?” I think Barry Sears and The Zone Diet book that came out and then later on, he talked about the omega, and so that plus other things that really started the omega-3 revolution. Books may be positive, negative. I’ve talked about the adrenal fatigue phenomena that was started somewhat on my book. I mean, I think it started a new conversation around stress, some of which needed to be corrected, but nonetheless, it really influenced a lot of people. And it influenced a lot of people in the way that they did research.

So, when we start thinking about all of these phenomena, I think you’re right. I think the gluten phenomenon with some of the books that came out, all of these are dynamics, which not only change the way clinicians practice, of course. A lot of it’s driven also by the patient because the patient comes in asking a whole bunch of new questions, and then the research community then begins to respond on the both positive and negative. Sometimes, they go in, “We’re going to try to debunk this person.” But then other times, they go in and actually do some research to find out. Obviously, like you said, it’s nuanced. There’s all these nuances.

So going back to our discussion, I’ll just kind of bring this full circle on the Gate Trial, the glucosamine and chondroitin sulfate trial that was done by NIH. And essentially what they did is… It was 16 different clinics, I think over 1500 patients, and essentially what they did is they gave some placebo, some glucosamine, some chondroitin. They gave a combination of glucosamine and chondroitin, and then they gave them Celebrex® as a fifth arm. And essentially, it’s kind of funny because I actually talk about this as a way to understand research. They went into this idea thinking that the placebo would be about 30% responders, meaning 20% improvement in their pain scores. So, if they saw 20% improvement in their pain scores, they were a responder. They responded to the drug or whatever, and they thought it was going to be about 30%.

Well, it turns out they had 60% of the placebo arm have a response, which again, that completely blew out of the water their expectations. But it probably had something to do with the fact that they were recruiting people who knew they were going to be in a glucosamine chondroitin trial and probably were hoping for a response. So that’s probably a recruitment problem. But when they looked at all these patients, they pooled them all together. And they basically showed that, even though they all had a slight improvement over that 60%, which is very hard to do, only the drug in this case, the NSAID Celebrex®, had a statistical benefit. And so, for those people—and that was the primary outcome of the trial—and they said, “Okay, well, glucosamine chondroitin didn’t work.”

But if you actually read the paper, and actually if you saw what was actually the conferences given by the authors before the publication, they were all positive. Why were they all positive? Well, it’s because within the data, they showed that the patients with moderate to severe pain all were benefited statistically only with the glucosamine chondroitin combination. The placebo in that group was only 50%, which is still pretty high, but they had a 79% improvement in the glucosamine chondroitin group. And the Celebrex® group there did not reach statistical significance. So, interpreting that group of data, the moderate to severe patients, everybody in the industry championed, “Well, glucosamine chondroitin sulfate was vindicated,” whereas the actual article in the abstract basically said it didn’t work.

So, it’s not uncommon in our industry when you have big publications like this, especially when there’s bias on both sides, that a big trial will come out, and you’ll hear both sides of things. Very similar to—for those in the community that are familiar with—the NIH funded trial to assess a chelation therapy. When that came out, there was an 18% drop in secondary events in people getting chelation, and it was statistically significant. Of course, the chelation people said, “This vindicates everything we’ve been saying.” But the other answer came out that there’s no justification for use and kind of it wasn’t as big of a deal within the community. So, that’s kind of a frustrating thing that we see. And if you’re in our industry, hopefully you’re getting thick-skinned realizing that’s a little bit of how the publication world is.

James Maskell:
Well, I think COVID taught us that if nothing else, many other things, but for sure that. I was actually at the ACAM conference in 2012, I think, when that was announced. And I remember just sort of like a weird feeling in the room in that it was obviously given a positive spin because ACAM was teaching everyone how to do chelation, but at the same time, it wasn’t like chelation took off in the years after that. If anything, it kind of went the other direction.

Dr. Thomas G. Guilliams:
Which is kind of odd, which is kind of odd, but yeah. After it was vindicated, it kind of like maybe people just moved on to something else. I don’t know. And of course, over those years, more and more drugs have come out. So, we’ve got obviously more and more sophisticated statins and other drugs that have come out. So I think people have moved on for various reasons. So coming back… Well, go ahead.

James Maskell:
One question I just had to ask is, obviously in the functional medicine world, and we were at a conference last month where there was a lot of this: Our understanding of autoimmune disease is getting better. And maybe our understanding of autoimmune disease in functional medicine is like way ahead of conventional care, and certainly, I think you’ve been on the cutting edge of that. Have there been things that you or we as a community have learned about rheumatoid arthritis in the autoimmune and the inflammatory side that teaches us anything about osteoarthritis that we were maybe missing before?

Dr. Thomas G. Guilliams:
Yeah. I mean, when you think about, well, obviously there are two different sort of etiologies, or we think of them. But I would say the other kind of thing that’s occurred in the autoimmune community over the last 20 years is sort of a recognition of what’s called auto-inflammatory conditions, and there’s been a lot of overlap in these ideas. So, when we think of autoimmune diseases, traditionally, we think of there’s an antibody or there’s a T-cell that cross reacts or starts attacking our own tissue. But an auto-inflammatory condition is where you have the innate immune system that is constantly being triggered.

And as it turns out, something I mentioned earlier on this idea of a senescent cell or a senescent associated secretory phenotype (SASP). It turns out that certain tissues when they age—and we find that this happens in osteoarthritic chondrocytes—that they age, they’re still very metabolically active, but they really should be killed or taken out. They should go through apoptosis or autophagy or something where they’re destroyed, and they somehow don’t. And they start producing mostly pro-inflammatory destructive sort of secretions, and those then begin damaging the tissue, in this case, the cartilage and whatnot.

And that damaged cartilage floats around, and guess what, it combined to pattern recognition receptors, toll-like receptors—a lot of people are familiar with these in immune systems and auto-inflammatory diseases. But as it turns out, chondrocytes also have toll-like receptors. And when this debris hits them, what do they do? They turn on the inflammatory cycle, NF-kappaB, all the things that people are pretty familiar with. So, in thinking of the auto-inflammatory condition, which is very similar to an autoimmune condition, that is probably present in osteoarthritis.
And when you start expanding the definition or the changes, you start asking questions like,

“Well, obviously we know that obesity, for instance, increases the risk for knee osteoarthritis.” And logically we would say, “Okay, well, that’s just more pressure on the knee.” But we also know that obese individuals have more inflammation, so they have this sort of backdrop of inflammation. And interestingly, they also have a different microbiome.

For instance, there was a paper I ran into where there was actually a meta-analysis of studies looking at curcumin, a standard anti-inflammatory phytochemical, and it works in some cases, it doesn’t work in others. And they found that the heterogeneity in some of these trials, the thing that came up the most was a patient’s BMI. So the higher their BMI the less the curcumin worked. Well, why would that be? Well, it turns out curcumin needs probably a proper microbiome to be converted into all of its active constituents. So, is it possible that many of the therapies that we’re using, phytochemical therapies, because of somebody’s microbiome—in this case, an obese microbiome—actually limits their ability to use curcumin as an anti-inflammatory for OA, for osteoarthritis?

So, just in thinking through all of these layers, there’s a lot more going on. Actually, it turns out that the microbiome might also influence the absorption of glucosamine. There’s actually several papers that have come out recently to suggest that not everyone absorbs glucosamine as well as the other, which may also influence all the heterogeneity of our clinical trials. And now we’re discovering that the microbiome may actually be influencing glucosamine absorption. So, these are all things that weren’t even contemplated back when The Arthritis Cure was written 25 years ago. And now, because of all of that intriguing dialogue, we’ve been doing research on things we probably would never have thought to do, and we’re discovering all these interesting things.

James Maskell:
Yeah, that reminds me, so I had Brett Weinstein on the podcast a few months ago, and he’s an evolutionary biologist, and I kind of asked him about the paleo diet. His thought was it’s not ideal because obviously there wasn’t just one type of paleolithic human. There were all types of people living all around the world eating different stuff. But to give it its fair shot, he was like, “It’s not a bad first approximation. It’s not where we need to get to eventually, but it’s a good first approximation.” Then obviously, science continues to build from that. And we understand that probably it goes a little bit further, and there’s more individualization. So, I think it’s that same thing that you are seeing there where it’s like you just have to make a first approximation, which is like The Arthritis Cure. There’s something else going on we don’t understand, and then over time it gets looked at and understand more.

One of the things that I experienced with gout was that it’s worse in the morning, and I know that’s also something with OA. So what’s going on? Why is stiffness in OA worse in the morning? Is it something to do with cortisol, inflammation, lubrication, inactivity? What’s going on there?

Dr. Thomas G. Guilliams:
Well, I mean morning stiffness is sort of like the initial early sign, and obviously, maybe I’m getting a little of that as well as I’m getting over 50. But yeah, I think a lot of it has to do with hydration. So if you’re not moving a joint, especially knee and spine particularly, if you’re not moving them, you’re not creating fluidity. You’re not bringing in because I basically explain… And most people realize this that hyaluronic acid and other glycosaminoglycans, they’re sulfated, and they can bring in all this water. So I think hyaluronic acid can expand by like 10,000 times its weight in water. So, if you’re sleeping for eight hours or whatever, however many hours, and that joint has not been moving and hydration—you don’t have water in that joint. When you wake up and you put a little pressure on it, you’re probably going to have that sense of feeling. Then as soon as you move around, then all of a sudden, you regain that hydration.
The effects of cortisol, interestingly, are highest in the morning, but cortisol sensitivity is lowest in the morning. So whether or not that anti-inflammatory component kicks in, that’s kind of interesting. You see that more in rheumatoid arthritis than you see with osteoarthritis. So that cyclical pain cycle you see quite a bit in autoimmune conditions, it’s less prominent in osteoarthritis, I think, from an immune standpoint. From a cortisol standpoint, probably has more to do with that morning stiffness and the lack of hydration in the joint itself.

But no, I think these are all things that, like you mentioned, going even back to the paleo ideas, what are we taking away versus what are we giving? So, if somebody starts doing a quote unquote paleo diet, which obviously they can’t do. Paleolithic humans didn’t go to Kroger’s to get their beets for juicing or whatever. But nonetheless, if you start thinking about not eating foods that are prepackaged with all the different chemicals in them, just removing a lot of those from your diet can have a dramatic effect.

And it’s hard to know exactly which things you’re adding to the diet. Of course, the whole paleo versus vegan debate, whether meat is appropriate versus avoiding meat. And so, I don’t want to get into that debate because I don’t know that… I think my take on this usually is humans are very adaptable. And I think we can adapt to different dietary patterns if we avoid some of the major problems which is basically the Western diet. If we avoid the industrialized Western diet, I think our body responds to most other patterns pretty well.

James Maskell:
So, what role does the immune system play in osteoarthritis?

Dr. Thomas G. Guilliams:
So, that’s interesting because we typically think of rheumatoid arthritis being sort of the immune component of the arthritic world. It turns out osteoarthritis, when you start looking at and looking at what kind of cells are in there, it’s not so much the T and B cells, but of course they’re there. It’s really the monocytes and the macrophages, and that’s probably recruited because of this whole auto-inflammatory condition. So, remember, I talked about this SASP, this senescent associated secretory phenotype. And that’s again, if you can imagine a cell going through this, it’s just spraying out inflammatory biomarkers, IL-1, IL-6, these kind of things, TNF-alpha. Also, it’s spewing out proteases. A lot of these are what we call matrix metalloproteinases, which are going to degrade the collagen and whatnot.

And of course, when that is happening, the immune system is going to sense that. There’s going to be a sense of, wait a minute, there’s something going on because a lot of these are immune signaling compounds. And so, the innate immune system is typically the one that’s going to come in there and hopefully try to get rid of those senescent cells. But these senescent cells are very resistant to being destroyed right away, and so that’s why you have this constant degradation and osteoarthritis continues. So yeah, I would say the innate immune system… We know monocytes and macrophages in particular are drawn to the tissue. And so, while it’s not maybe the traditional immune response that we see in rheumatoid arthritis, it clearly does involve the immune system, and we’ve kind of learned that really over the last couple decades.

James Maskell:
Great. Alright. So look, there’s a lot there. I think anyone who was interested in sort of a deep dive into sort of the evolving science, we’ve definitely… You’ve given people a lot to think about, I’ll put it that way. So, let’s just talk about practical application now, I guess. So, now that we understand everything that you’ve said, what would you sort of have most doctors in the functional integrative lifestyle medicine world… What would you have them thinking about with regard to treatment in light of this information?

Dr. Thomas G. Guilliams:
So, I think one of the things that I’ve learned about this is sometimes what we know… We’re always looking for new things. Everybody wants to know what’s the newest thing on the shelf. As it turns out, the things that have been on the shelf for a long time work very well, and I think shouldn’t be dismissed. So, if we’re thinking—what I call glycosaminoglycan precursors, chondroitin sulfate and glucosamine—I think they are still the first line therapy in the non-pharmacological approach to OA. And, you know, they’re on board. Also in that family is hyaluronic acid, so that’s also available. But I would say that should be probably the primary thing that clinicians should be recommending. Probably, if you go back to the original doses, 1,500 milligrams of glucosamine, and that could be glucosamine sulfate or hydrochloride. And then at least 800 milligrams of a really good chondroitin sulfate.

And I would usually say a pharmaceutical grade, although that may be somewhat misleading. But chondroitin sulfate is actually a pharmaceutical in Europe, and those same ingredients are available as dietary supplements in the US. So, I would say there is a difference in the quality of chondroitin sulfates, so make sure you’re getting a high-quality chondroitin sulfate, 800 milligrams, with a glucosamine. And then hyaluronic acid is one you could add to that. But then beyond that, I would say relying upon polyphenolics that are anti-inflammatory. I think curcumin is the one we think of the most. Curcumin, ginger, boswellic acid… I think those should be the primary ones that you’re using. And then, other polyphenols that we know have been helpful are things like resveratrol and baicalin, which might be not known as well from Chinese skullcap and things like that.

So, I think the clinician should be using those. There’s plenty of data to suggest that—especially if you try different ones, different doses—typically, you can dose a little higher at the beginning. When patients start feeling the pain benefits of some of those, the pain relieving benefits of some of those, you can often reduce the dose. Some of these are a little more costly than some other supplements, so instead of doing it every day, you can maybe move to every other day once they get down to like three to six months later when they’ve had some of the pain relief. And there’s good data to suggest that intermittent dosing of things like chondroitin sulfate can be very helpful in the long run. You don’t have to have the high dose forever.

I think because we have a condition for which there is no drug treatment except for palliative care, a lot of people are taking NSAIDs on their own. And we know that these are very harmful not only for their biology, their GI tract, but also likely preventing chondrocytes from forming cartilage. There’s some data to suggest in animal models that NSAIDs actually decrease cartilage production. So, since patients are already self-medicating, this is sort of low-hanging fruit for the functional medicine/integrative medicine clinician to be using these studied ingredients.
And like I said, they’re not going to work in every patient. You might have to be working with obesity. You might have to be looking at their microbiome and some other things. But this is a comprehensive aging condition for which a functional medicine/integrative medicine approach really does work, and there’s sufficient evidence to direct us in how to do this. So, after 20 years of coming back full circle, it still is one of the conditions for which integrative medicine clinicians may have still the best tools available.

James Maskell:
Yeah, absolutely. Well, I’m glad you shared that, and I think there’s some great starting points there. Obviously, there’s a lifestyle medicine piece to dealing with sort of just optimal function on sort of bottom of the matrix. But yeah, those are great supplements, and I think there’s a lot of great tools there. Next week, I’m actually going to a conference that’s sort of on the edge, I guess, of conventional medicine and functional medicine, more like ortho-biological kind of stuff. And I’m just wondering, there they’re talking about stem cells and prolotherapy and that kind of stuff. And I guess, do you have an opinion on that and their effectiveness in this issue, or do you not have an opinion about that?

Dr. Thomas G. Guilliams:
Well, I don’t have a strong opinion. I kind of try to stay out of that area a little bit because there’s other experts, but I think, as we’re learning, these are all newer technologies using stem cells, using enriched plasma and these sorts of therapies. I think clinicians should… I think there’s going to be some patients that are going to be more receptive or more able to tolerate. And I’ve had personal people that I’ve known that have tried some of these, and sometimes they’ve worked and sometimes they haven’t. And that’s true of the other things that I’ve mentioned as well. So, I think due diligence… Do your diligence in understanding which patients may respond well to those.

James Maskell:
Great. Awesome, Tom. Well, look, I really appreciate this deep dive. I think it’s super critical for all of our community to understand this. We are committed here at the Evolution of Medicine to taking these clinical topics and bringing in leaders who are treating this either successfully or understand the science very rigorously on it. So, I really appreciate you coming to share. If you have more questions about osteoarthritis, feel free to get in touch with us, and we’ll try and get you the answers that you need. But I think there’s probably some learnings in this, Tom, I would say, for other conditions. I mean, I guess some of the ideas that you’ve shared in here, are there other conditions that you think the conversation is relevant for?

Dr. Thomas G. Guilliams:
Well, probably all of them, meaning, I think we need to go back into the literature. We need to really ask where things have come. I mean, I think a lot of clinicians, and this happens both on the functional medicine and the conventional side, once they get into a groove of the things they know and the things that they use to treat whatever it is and the biomarkers they use to measure, they sometimes stay there for a decade. And a lot of research is moving on, and they’re not always willing to change.

So, I think as we’re learning about the complexity of chronic disease, this is going to be true of not just joint tissue, in the brain, in the liver, in the cardiovascular system, in the gut. All of these things that we’re learning about auto-inflammatory condition, the senescent patterns, we’ll be able to leverage this information really for probably most chronic diseases. And as we learned from the pandemic, these chronic disease conditions put us at risk for acute viral infections as well. So, you really can’t separate chronic disease from acute diseases as we once thought were so clearly delineated.

James Maskell:
Beautiful. Well, Doc, thanks so much for being part of the Evolution of Medicine podcast. Always great to get you on, so much value for our community. I’m really grateful to have you as part of, I guess, leadership in terms of the kind of experts that we go to, and it’s been great to just continue that relationship together. Thanks for being part of the Evolution of Medicine podcast. My name’s James Maskell; I’m the host. I’ve been here with Dr. Tom Guilliams. We’ve been talking all things osteoarthritis. I think this has been super valuable content no matter what kinds of conditions you’re treating. Thanks so much for tuning in, and we’ll see you next time.

Thanks for listening to the evolution of medicine podcast. Please share this with colleagues who need to hear it. Thanks so much to our sponsors, the Lifestyle Matrix Resource Center. This podcast is really possible because of them. Please visit goevomed.com/lmrc to find out more about their clinical tools like the group visit toolkit. That’s goevomed.com/lmrc. Thanks so much for listening and we’ll see you next time.

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