Revolutionizing Healing: Dr. David Karli On Regenerative Medicine, Stem Cell Therapy, & Longevity
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Forget frequently asked questions. Common sense, common knowledge, or Google. How about advice from a real genius? 95% of people in any profession are good enough to be qualified and licensed. 5% go above and beyond. They become very good at what they do, but only 0.1%.

are real geniuses. Richard Jacobs has made it his life's mission to find them for you. He hunts down and interviews geniuses in every field, sleep science, cancer, stem cells, ketogenic diets, and more. Here come the geniuses. This is the Finding Genius Podcast with Richard Jacobs. Hello, this is Richard Jacobs with the Finding Genius Podcast. My guest today is Dr. David Carley. He's an orthopedic

stem cell therapist. We're going to talk about what's called micronized fat and platelet-rich plasma, PRP. So welcome, David. Thanks for coming. Hey, Richard. Thank you. Thank you so much for having me on. Good to be here. Yeah. Tell me a bit about your background, how you got into this area of research, and then we'll talk about the Coralie Center and your current work. Yeah. So I'm a traditionally trained doc, medical school, University of Maryland, residency in the Harvard system.

And I stayed on at Harvard. My background's in physical medicine rehabilitation as well as interventional pain management. So our job is to ultrasound and x-ray guide needles into tiny little places to deliver therapies. And that was a great segue for an eventual landing spot in regenerative medicine. So I practiced kind of traditional interventional pain for a number of years and got

got progressively frustrated with an inability to alter disease courses. All we really could do was manage symptoms with the tools we had at our disposal. And that led me, you know, over 15 to 20 years into researching alternative ways to try to achieve non-surgical management of orthopedic problems. And that started in Europe with a number of stints in

in research and eventually led us into kind of the PRP and autologous cell therapy world. So our space utilizes the patient's own cells. In the U.S., as you know, there are some regulatory limitations to what we can and can't do. So we are an FDA-registered and audited company.

I started a biotech company to do this that is a vendor to our clinic. But we like to think we're innovating within the rules. And I know this stem cell space can be kind of a wacky Wild Wild West type of run. And one of the things we've tried to do is to create academic and scientific pockets of legitimacy around those FDA requirements.

guidelines, what we can and can't do in the United States. And so long story short, that led me into progressively more and more researching, developing these types of therapies, integrating them into my practice first 20 years at the Steben Clinic in Vail, Colorado, which is a very well-known sports medicine orthopedic practice. And then more recently relocated here, relocating here to South Florida, where we've created a fully integrated regenerative medicine practice that also kind of

is slowly working in elements of functional medicine and longevity medicine to try to improve the capacities and therapeutic capabilities of our stem cells isolated from the patient's own body. Okay. So what kind of conditions are people coming to you for where you can use this procedure?

Yeah. So it's routine orthopedic stuff. A lot of it is arthritis, osteoarthritis driven knees, shoulders, hips, spine, back pain, neck pain, and then a lot of soft tissue injuries, partial thickness, rotator cuff tears, Achilles tendon injuries, tendon and ligament tears, things of that nature. Your bread and butter ortho stuff.

And our job is to try to find ways wherever possible to manage those things with a needle as opposed to arthroscopic surgery. All right. So what would happen in a typical surgery? Let's say you're...

I don't know, you tore your ACL in your knee. What would happen and what's a new procedure that does better? Well, historically, and it depends on the level of the tear. So a tear can mean a lot of different things. A complete tear is where there's two fully torn pieces, right? We can't

two ends of pieces and reattach them with a cell therapy. That still requires a surgical fixation. Surgeon goes in, takes one end, reconnects it to the other end. Now what we'll do in that scenario is we'll actually work with our surgeons to apply cell therapies. Patients own stem cells from bone marrow derived

blood or from adipose tissue, that's the micronized adipose or MFAT type of model, right there at the surgical correction. For partial thickness tears, where it's not completely torn, so 25% or 50% or 70% of the tendon or ligament is torn, there's still two pieces of it that are still attached. And we're progressively working more and more to try to manage those problems without having to go in and repair it surgically.

Because there's healthy tissue still attached to work from to try to stimulate healing and repair in a non-surgical model. Yeah, but how? Like, what would you do? What would be a stem cell-based intervention to fix a partially torn meniscus? Maybe it was jagged, you know, in the knee. Yeah.

Well, I mean, this is an interesting one, but so we can't, we're not throwing hand grenades here. We have to be extremely precise to implant cells into the injured tissue. So it's typically ultrasound guided or fluoroscopically guided injection, not a blind injection. We don't want to get close. We have to go into the pathology and that's critical. We can make a great biologic product if we miss the mark.

obviously that's not going to get the job done. So this field involves not only producing a good biologic, and we can talk about what that means, but also highly, highly accurate

extremely precise implantations into the injured tissue, not around it, but into it. And then those cells trigger a healing response coordinating with the local tissues to try to drive repair in orthopedic tissues, which historically don't fix themselves very well. What would be the intercellular glue or bandaid over the area, metaphorically, after you input the cells so that they don't get sloughed off or damaged or taken away?

It's interesting. So stem cell theory has changed over the years. We used to think years ago that you implant stem cells or a better term, by the way, Richard, for stem cells is progenitor cells because there's not one type of stem cells. There's actually many different types of stem cells or progenitor cells. Anyway, we used to think that those cells would be implanted into an injured tendon. Let's use that as an example, our meniscus, and just become new tissue, new meniscus, new ligament. Scientifically, over a

the past 10, 12 years, that original theory and hypothesis kind of been defunct. And what we now know is these cells secrete signals which work and coordinate with the native tissue to drive and stimulate healing. So they're telling the tissues through signaling pathways, hey, repair, heal, recruit other cells into the

the area. Some of them do because it's like it's the exosomes or something that are being produced. Exactly. So exosomes are the vehicles that cells use to communicate with each other. And there's a model where we can isolate those exosomes or the cell signal and basically just little vesicles or little balls of fat that contain genetic and protein materials, which coordinate the healing process. But what's interesting about exosomes is there are good exosomes, bad exosomes. There's exosomes that

induce cancer. There's exosomes that induce healing. So one of the challenges is the message in the bottle, so to speak, a reactive message. For example, if we put stem cells into an arthritic joint, are the exosomes that are released reactive to the environment that those cells find themselves? So this is a toxic, inflamed arthritic environment. They're going to release a signal in those exosomes to try to control that environment, reduce pain and inflammation, and stimulate healing. If we induce that process in a lab, in

in a test tube, for example, is the message in the bottle because those conditions aren't the same. So in exosome products, those are artificially collected and created in a laboratory. So the limitation of an exosome model where you're just injecting exosomes that are isolated from the lab, the critical way to look at that is, is the message in the bottle the same? We believe in the cell therapy world that they're not. And I don't know that we have enough control

in the laboratory to consistently think about a batch and a lot number from bottle to bottle to bottle to bottle to make that signal consistent.

and predictable in terms of the response. So that's why we like to use fresh whole cells and tissue because we believe it's a reactive message to the environment that these stem cells find themselves. Well, I mean, what about analyzing the typical signaling that you get from the remaining healthy tissue around a knee or a shoulder or wherever it may be? Sure, of course. But in an exosome, let's just, they're tiny, tiny, tiny, tiny little things, obviously. In a mepsisome...

Pre-feeding them, though. Could you harvest the exosomes that are in and around the joint and then precondition the stem cells in a bath of that fluid and then put them in place? You could, and there's work being done at this point to try to precondition exosomes from platelets or cells or even from birthing tissue. There's a lot of different models out there. But again, it's very, very expensive to measure. So one of the things that we do is, for example, if we make a cell therapy,

We want to know exactly how many cells, all the different types of cells, the phenotypes, the number of platelets, et cetera, as consideration for a cellular dose, quote unquote. What is the cellular dose? You could apply that to exosomes. What's the number of exosomes? In any given exosome, there might be 150 different things.

So they're very complicated little tiny vesicles. And again, the question on exosomes is, is it a reactive thing that we should just let nature drive? Or do we have the capacity to control that message effectively? More like a drug where we can precondition or basically manufacture the message in the bottle to make it the one that we want every single time. And that's something that's evolving in the space.

getting better. Right now, to my knowledge, in an orthopedic application, there's no licensed exosome product that we can routinely stick into a knee arthritis, for example, outside of a clinical trial. But there's a lot of pipeline work being done, and it's definitely an exciting area to kind of keep track of from our perspective.

But how do you know you've got what you need? Will the cells attach faster or will they fail to attach? Will healing, you know, like, I don't know, will the stem cells kick in and the healing will be much faster? Like, how can you tell if you've created the right environment or not? Well, we track every single patient and there's a number of things to track. There's really three levels of determining was a stem cell treatment successful or unsuccessful. The first is subjective. Do they feel better? Okay. So that's easy, right? We track.

we track patients, you know, one month, three months, six months, and 12 months with patient reported outcomes. So subjective is the first, do I feel better? Objective is the second, am I functioning better? So if you take a knee, for example, you do pre-treatment questionnaires and you follow up with indexes that are validated for knee functionally. So you have the subjective, a functional or objective outcome. And the third is radiographic. Can you find a histological difference? A

a difference in a pre and post MRI, for example, which shows that tissue is changed or regenerated or healed or improved. We call this field regenerative medicine, but in truth, we're not regenerating a whole lot yet. The microscopic level, there's regenerative activity. But if you look at a lot of pre and post MRIs, no matter what the stem cell model is, there's not major difference in chronic generative pathologies.

Now, if we catch problems early, like an acute meniscus tear or acute ACL tear, for example, we can stimulate and drive healing in those situations and pick that up on an MRI. But in the more chronic degenerative models, we cannot. So the goal of all this is eventually to kind of rebuild the body from the inside out. Are we there today? No. Are we making progress? Yes, most certainly we are.

Before we continue, I've been personally funding the Finding Genius podcast for four and a half years now, which has led to 2,700 plus interviews of clinicians, researchers, scientists, CEOs, and other amazing people who are working to advance science and improve our lives and our world. Even though this podcast gets 100,000 plus downloads a month, we need your help to reach hundreds of thousands more worldwide. Please visit findinggeniuspodcast.com and click on support us.

We have three levels of membership from $10 to $49 a month, including perks such as the ability to see ahead in our interview calendar and ask questions of upcoming guests, transcripts of podcasts you're interested in, the ability to request specific topics or guests, and more. Visit FindingGeniusPodcast.com and click support us today. Now back to the show. Okay. So what kind of conditions are stem cells used for successfully? What kind of orthopedic conditions?

Well, OA, osteoarthritis, is probably the most common one that kind of fills up our halls. Knee arthritis, hip arthritis, shoulder arthritis. Spine is a little bit different, much more complex than peripheral joints, but low back pain, and we're starting to venture up higher into the spine, into the cervical spine and neck area. Of course, all the soft tissue itises, right? Tendonitis, tennis elbow. These are areas where PRP has been studied pretty exhaustively with level one trials and has shown success.

excellent outcomes. My background and what I have brought to the field really is more in the quality control end. So one of the limitations in autologous cell therapies or cell therapies isolated from the patient's own body is that physicians process blood or fat in a little class two medical device, and there's no quality control to measure the cellular output.

So to the naked eye, you can't tell if it's good, bad, or indifferent final product. So what we did back in 2010 was to say that's an unacceptable long-term solution. We need to know ahead of time exactly how many cells, platelets, different types of cells, stem cells, et cetera, are in these products to track them from a cellular dose perspective, dose and response, just like a pharma type of model. So we've brought a pharma approach

to cell therapies. And it took a long time to figure that out. Obviously, again, as I mentioned, it's an FDA registered process, but that's the work that we've done in the hopes of not only identifying, you know, what's kind of the threshold dose, if you will, to optimize a patient's best potential for a successful outcome, but also to create predictive models. If we can predict the behavior of a stem cell therapy isolated from your bone marrow, for example, that can ultimately drive

third-party payer models, building encoding channels. Because every patient that comes in my door asks me, when's this going to be covered by insurance? Because these are cash pay expensive procedures. The only way I see to drive that model forward is to create predictions so that we could go to a third-party payer and say, if we apply our predictive model to these eight diagnoses, we can save you $400 million.

And until you can translate it in a language that they understand, dose, predictable response, I don't think you're going to see a lot of activity and a lot of action moving this towards a standard of care where it would be covered by

by a third-party payer. So a lot of this work isn't just because it's a responsible way to think about developing these paths, these biological paths. It's also to try to make it more available to the general public. It's expensive. Not everyone can afford to do it. So how do you scale this to the point where everyone would have access to it? Well, one way is to create third-party billing and coding channels, and that's part of the work that we do. Okay.

So these stem cells can be induced from blood or fat in the person? And is there any difference, you know, where you get it from in the person? Yeah, there is. What's the sex to do here?

Not a lot of adverse effects. So again, there's a regulator. I won't dive into the details and bore everyone with the regulations, the code of federal regulations of the FDA, but there are things, rules that we have to follow in order to apply this clinically without an FDA approval. So autologous biologics, as long as they're harvested, concentrated, and immediately put back into the patient, don't require an FDA approval. Now,

Even though they don't require approval, that doesn't mean they don't require FDA compliance, i.e. you can do whatever you want with them. There are rules governing how we need to process these samples and then how we need to apply them. So everyone asks, are these FDA approved therapies? They are not because they don't need to be based on the code of federal regulation. So that was a loophole that allowed this field to evolve and develop.

relatively quickly. Whereas, for example, a placental-derived cell that's cultured in a laboratory and then re-implanted, that's considered a biological drug that has to go through a typical FDA approval process, preclinical animal testing, phase 1, 2, 3, etc. That 10, 12, 15 years costs hundreds of millions of dollars. So it was fortunate because we had

Safety. Your cells can't really harm you as long as there's no sterility issues or potential that we induce an infection, which as long as you process them correctly is incredibly small. They can't really- Or if you somehow picked up cancer cells, I guess, and cultured them and re-injected them, but that seems rare.

It would be really rare. And of course, that's one of the contraindications is an active cancer, especially an active blood cancer like a leukemia or a lymphoma that wouldn't be appropriate for bone marrow derived stem cell therapy. So there are some simple screening questions that have to go into the workup prior to offering this to the patient. But by and large, if someone's in good health, the risk is extremely low.

So now it was an issue of, okay, how do we get control over the standardization? How do we create predictive modeling? And then how do we create a customization pathway? For example, I don't treat you, Richard, the same as a 78-year-old diabetic smoker, which would be different from a 23-year-old professional athlete. You're totally different people. And to think that a one-size-fits-all cellular dosing solution would apply equally to all of you is unrealistic.

So by measuring, we're able to look at or consider customization and precision medicine protocols. You have a partial thickness rotator cuff tear, 50%. You're 56 years old. You're a non-smoker. You're on these medications. You have this past medical history. We're developing in a data cloud overriding

a way in which to input all of that information, consider it along with a baseline blood count, right? An analysis of your blood and then an assessment of your pathology, which would prospectively tell us what biologic to make in order to give you the best chance for a successful return on your health investment.

So a lot of this data collection also drives these customization pathways, thinking that, you know, throw it in there and let the magic happen, got us to a certain point. But the future of this requires a much more detailed, much more scientific, much more evidence-driven approach than has guided the field, you know, up to this point. And that's a disruptive concept. And that wasn't always well received on podiums over the years, I can tell you, but over

But over time, the physician culture has kind of adopted that, yes, indeed, we need to think of this much more in terms of quality control, much more in terms of standardization, and much more in terms of predictability models. What are you seeing from overseas clinics that are, you know, kind of skirting the law? Any good or bad learnings from them? Well, there's not much, you know, we're not seeing it on podiums. We're not seeing it in publication. My

My biggest, you know, critical comment to that is I don't know what you got. So I get a lot of second and third opinions from patients who've gone offshore and maybe didn't have a positive outcome. They're out $20,000, $30,000 and they're showing up at my door saying, well, it didn't work. You know, what do you have to offer me? And my first question to them is, well, okay, what did you get? Did your doctor know how many cells were in it?

Did they know how many cells were viable or actually alive? We've tested, you know, cryopreserved, colleagues of mine have tested cryopreserved samples, you know, the cells in a bottle model, and they were all dead in multiple batches and lot. When we rethought them, took them out of cryopreservation with protocol and then tried to culture them and nothing grew. So if- Does that mean that the cryopreservation

Preservation method was faulty or that certain cells just can't be cryopreserved? Could be either, or it could have been the free stall process and protocol where they fall too quickly, where they fall too slow. When you culture cells, we can't assume that the cell doesn't change in some way.

right? Cells and culture to grow from, you know, millions to billions have to go through what we call passages or you grow cells, wash them to remove the cells you don't want, and then grow more and wash and grow and wash. Those are called passages. And

in culture. And you end up with a single cell line, a mesenchymal stem cell, for example, which is what people want to isolate from birthing tissue, umbilical cord or placenta, which are felt to be rich in these types of cells. And that's interesting, but it ends up producing what's called a monotherapy. So it's a single cell therapy. But if you think about healing in the body and you understand healing, that is many, many, many different types of cells and exosomes and signaling and biological proteins. It's a very complex process. So the question becomes,

Can a single cell implanted into that healing pathway induce the same response as all of the cells in a fresh preparation? We take all of the cells out of blood in the same ratio as they would normally be found.

We concentrate them to amplify their potential and then reapply them, which is better. The answer is we don't know yet because there's no head-to-head comparative data where you match patient cohorts. 500 people with knee arthritis get umbilical cord cells, culture expanded, and 500 get fresh autologous bone marrow concentrator, bone marrow stem cells isolated from their own body. And we go head-to-head and track these people. Not a single study, to my knowledge, exists in the orthopedic space which can

definitively prove that these younger, more vibrant, more vital cells are better than your own. So the knock on aging people is that my stem cells don't work anymore. I don't have any stem cells. We don't treat people in their 20s. All of our patients that we've collected data on, we have 5,300 patients in our database alone, 5,300 treatments. All of our patients are in their 50s, 60s, and 70s. Some of my colleagues have done autologous stem cell research in people in their 80s.

And shown positive results. So this notion that... Yeah, I thought it was... The older you get, you get encouraged to bank your cells. And if you do it when you're older, you're not as efficacious. Is that not true? There is a drop-off in the density of stem cells with time, but they're not gone. You'd be dead if you didn't have any stem cells, right? So yes, there is a reduction. And this concept of, as we age, our stem cells lose therapeutic capacity due to genetic anomalies or

you know, epigenomic changes or glycation or all these different things. That's true. That does happen. But what we don't know is if that translates into a loss of clinical capacity when you apply those cells to a knee arthritis. And what we're seeing in the data is

and we have a lot of data now on autologous cell therapies, is that the patients do just fine and their outcomes are very strong. So it really kind of, you know, it throws kind of a monkey wrench into this concept that I see over and over again and celebrity endorsements and hundreds of millions of dollars going into developing cells from someone else when in fact the data suggests that yours work quite well

as long as they're produced in doses that show a strong correlation with positive outcome. And that's the data that we're collecting. So, you know, again, I'm a bit disruptive and prickly in the space because, you know, the one advantage to the cells in the bottle model is it's just easy to commercialize. You know, you do one donor and you can generate, you know, 500 bottles of, quote, stem cells. Well, that's an easy way to make lots of money if you can prove that that model works. And I'm not saying it doesn't.

What I am saying is I know your cells won't hurt you. I know it's compliant with the Food and Drug Administration. And I know that we have a whole lot of data suggesting that your cells, if you're in reasonably good health, even in your 50s, 60s, 70s, work quite well. Why wouldn't we use that? We're in this age of biohacking. Biohacking is everywhere you look, right?

At the end of the day, biohacking really is just a push towards improving your cellular health. So we have patients that spend thousands and thousands and thousands of dollars on all these health-oriented biohacking, nutrition, supplementation, hormone optimization, peptides, you name it.

They do all of this and then they choose to take someone else's cells. Why would you do all that work and then abandon your own cells, which you're working so hard to improve for your longevity, for your general health? So we say, well, if you're going to work so hard to improve your cells, why don't you use them? But what are the trade-offs between autologous versus donor? Who's the donor, right? I don't know. But what are the trade-offs? Like if you, I don't know, let's say I'm 65, my knee is really messed up, I need to have

and had some surgeries on that for the ACL or whatever. Yeah. And I have a chance to either do my own cells where I'm 65 or like some young 25 year old that has, you know, that's compatible. Here's how I would approach it. I would say, okay, Richard, we've seen, I don't know the number off my top of my head, but we've seen 637 patients with your type of problem at your age and with your general health. And from those patients, we know that at

Two years, we have a 72% restoration in function holding at two years and a reduction in pain from six out of 10 to one out of 10 or something like that. I can counsel you based on our data and our outcomes. I can't do that with someone else's cells. Number one, I don't know who they are. The donor isn't identified partly due to HIPAA reasons. We can't.

I don't know what was screened. I don't know the genetics. I like to, we can always make light of it. So I always say, think of the most annoying person on the planet that you can possibly think of, Richard. How do you know that wasn't your donor? You want to use their cells, right? How do we know this person, even though the cells are quote younger, has

has good genetics. How do we know they have good epigenetics? We just applied for an NIH grant, unfortunately delayed with all of the turmoil of the administration change, but nonetheless an important study where we're going to take 200 knee arthritis patients and treat them with bone marrow concentrates, so stem cells isolated from their bone marrow. And we're going to use complicated flow cytometry to identify all the subpopulations of progenitor cells, but we're also going to measure their entire genome sequence

and their epigenome at the time of treatment. And for your listeners who may not know, your genome obviously is your DNA. Three billion base pairs. We're going to measure all three billion. And there's a lot of incredible technology that can do that cost-effectively now. And the epigenome, which is the environment in your body which influences gene expression, which is modifiable. So if you have terrible diabetes and you're a smoker and high blood pressure and sickly, your epigenome's not going to be so good. If you're in very good health, your epigenome might be better. Anyway,

epigenome influences what genes are expressed and when and how robustly and so forth. So we're measuring not only the genes that you have and the differences from person to person, but also the epigenomic influence on how those genes are expressed in stem cells. And can we use that as a predictor to determine if your stem cells and your genetics and your epigenome will

cause success or failure, or we need to alter your protocol based on what we find. So we're diving from the first layer of what we talked about earlier of understanding cell dose to now going deeper into the precision medical pathway where we're actually looking at genomics and epigenomics to help us predict, number one, whether you should do this, and two, what's the likelihood if you do of a positive effect, and three, on our end,

Do we have to make a different biologic product to account for what we find in your genome and epigenome? So you can really run this. These are living cells, just whether they're yours or someone else's. And we've taken it kind of to the moon and really done it. What criteria do you look for to see if the cells are suitable and healthy?

Well, for a long time, we tracked viability. Are they even alive? I mentioned earlier that one of the questions when you get a frozen sample in a bottle and thaw it out, are they still alive? And unless you do an assay prior to...

putting those cells back into the patient, which no one does at the bedside. Oh, you don't know. So you have to assume. So we track that for a long time. And when you use a fresh frozen sample, meaning it's taken out of the body, processed, and 30, 40 minutes later, re-implanted back into the patient, the viability is 97, 96, 98%, very, very high. We lose very, very little in that process. So are they still alive is one question. What are the doses or the levels of those cells? That will vary from patient to patient.

and vary from day to day in patient in terms of their cell counts, especially if you think about peripheral blood for PRP. So we're dynamic organisms. We're different from day to day. So what we do when we get a blood sample, for example, is we measure the baseline

And then we use that to estimate how much blood we need to draw, knowing that this is just a math equation because we want to get to a final dose. And you can use math if you know your baseline to know how much you need to draw to concentrate to a dose that you know will give you the best chance for success. So we want to know the viability.

We want to know the concentration and baseline concentrations of all the different cell types that we apply. And then we want to study those. So we talked about monotherapies. Well, fresh autologous therapies are the complete opposite of that. It's many different types of cells, isolated, concentrated, and reapplied.

So we have to think about each one as individual variables. We have to think about combinations of them. And we have to think about ratios. This one compared to the dose of another one, plus a different one, plus a third one. And historically, statistically, that was a nightmare. But modern algorithmic analyses, machine learning,

AI, et cetera, common buzz term. It really has been a game changer for us to analyze immensely complex datasets, large datasets, and literally scour continuously looking for those positive and negative predictors and the things that will prove success and the things that will prove failure.

failure. So it's A plus B, A plus B plus C, A plus D plus F minus G plus R in that sequence. Endless connotations of possibilities of things that could influence success and failure. Once you unlock that code and you know your secret sauce, so if we know if we make this biologic product for a grade two knee arthritis, then we know for certain that will lead to an 89% chance of a 70% improvement at three years. Well, we're going to make that every time.

But it's about taking, collecting, first measuring, collecting, analyzing what are the positive predictors. And then once you know that, you make that product every time. Well, if you don't measure, you can't make that product.

that product. So it gets, it gets really difficult. And I always say it's easy to practice regenerative medicine poorly. Oh, take some cells out of the bottle, squirt them in the knee and let the magic happen. How much better results are you able to get before you started doing all these analysis, you know, compared to now? Like what's, how are you measuring improved efficacy? What does it look like? Well, the general trends in the field and for

you know, 10, 15 years, there weren't these analyses. It was make PRP with these medical devices, put it into whatever it is you were putting it in and measure whether there was success or failure. The general trend suggested that there was success, but if it succeeded, I didn't know why it succeeded. And if it failed, I didn't know why it failed. So the reasons we mentioned earlier. So as we've started tracking, we know now there is an actual dose response effect, i.e. weaker biologic products, lower dose biologic products don't work as well as higher dose biologic products.

And we've teased out over time, not just myself, but many colleagues as well. We've just been kind of in the lead in that regard on the dose issue, that if you're not paying attention, if you do 10 different patients and make 10 PRPs, you'll get 10 totally wildly different final products. So it's like giving a blood pressure medication with five doses and you want to see if it works to control blood pressure, but you don't know what dose you gave. So we were seeing general trends without measuring that these things had generally positive outcomes, but

That wasn't a long-term sustainable thing. And because we couldn't predict it accurately nor improve it, we didn't feel there was really a long-term future if we didn't make it more farm-like. So long-winded answer to your question, the general trends were good, but we want to do better than good. We want to be able to predict and optimize to maximize a return on the patient-consumer's investment. And that's really all the work that we do.

Okay. Well, very good. What's the best place for people to find out more about stem cell therapies and where can you help people? Yeah. So Grayledge Technologies is our bio company, www.grayledgebiotech.com, G-R-E-Y, Grayledge.

And that outlines a lot of the work we do on the biological manufacturing side, how we make these products, how we measure them, how we analyze them and collect the data, et cetera. My clinic is carlycenter.com. Carly is K-A-R-L-I, carlycenter.com. And that's here in South Florida, just south of downtown Miami. And Grayledge is kind of integrated fully into that clinic, whereby we're treating patients with product made from our biologic and

tracking very carefully in a registry type format, every single patient data from every single patient that we treat. So grayledgebiotech.com and carlycenter.com really gives you a good feel for the work that we're doing. And there's lots of educational material on there. If you're a consumer interested in this, I highly recommend that you check those out because it helps you to understand what questions you should ask to give you the best chance to find a practitioner who is going to be at a higher level and give you a better chance for a successful return.

Well, very good. Well, thank you, David, so much for coming on the podcast. I appreciate it. Thank you, Richard. Appreciate being here. Thanks for having me. If you like this podcast, please click the link in the description to subscribe and review us on iTunes. You've been listening to the Finding Genius Podcast with Richard Jacobs.

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