Latest / Gladden Longevity Podcast / From Steroids to Stem Cells: Redefining Recovery, Regeneration and Longevity - Episode 264

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From Steroids to Stem Cells: Redefining Recovery, Regeneration and Longevity - Episode 264 · Gladden Longevity Podcast

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Welcome to the Gladden Longevity Podcast with Dr.
0:04
Jeffrey Gladden, where our passion is helping you to become an age hacker.
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On this show, we want to help you optimize your life energy, longevity, health, and human performance with impactful and actionable information by answering four questions.
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How good can we be?
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How do we make 100 the new 30?
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How do we live well beyond 120?
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And how do we live young for a lifetime?
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Now here's today's episode of the Gladden Longevity Podcast.
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Welcome everybody to this edition of the Gladden Long Joedy Podcast.
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I'm your host, Dr.
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Jeffrey Gladden.
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And in this particular episode, we're going to be talking with David Carley, spelled K-A-R-L-I.
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David is an MD.
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He's also working in the regenerative medicine space, working with PRP for quite some time, ever since it became popular back in the early 2000s.
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He has a long standing history of working in the orthopedic space.
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He's done an orthopedist himself, but now he's involved with cell therapies.
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And I think you're going to find this conversation really fascinating about the state of regenerative medicine and what his take is on it and what my take is on it and how those
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two kind of.
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compliment and yet are a little different at the same time and I think you'll really enjoy this conversation.
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Welcome everybody.
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I'm your host, Dr.
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Jeffrey Gladden.
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And I have the pleasure of having David Carley on the show today.
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David and I have not met before, so we're going to learn a little bit about each other, I suppose, in the course of the next however many minutes.
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But David, welcome to the show.
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Thanks, Jeff.
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Appreciate you having me on.
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And as always, the opportunity informed to talk about all the work we're doing and an interesting, albeit controversial space.
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Yeah, definitely.
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Definitely has a little controversy swirling for sure.
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We're going to be talking a lot about regenerative medicine on this particular show, which is kind of near and dear, I think, to both our hearts and maybe many of the hearts of our
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listeners as well.
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David, tell us a little bit, how'd you get into this?
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What's a little bit of your background?
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Do you have a story that kind of led you down this path?
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Yeah, it's a long one.
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I'll give you a more abbreviated version.
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at this for a long time.
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So was traditionally trained at University of Maryland Medical School.
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Harvard residency, initially physical medicine rehabilitation, but it kind of went into the anesthesia interventional pain world, did some fellowship work there.
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Well, at Harvard, stayed on his teaching doc and then ended up at the Stedman Clinic in Vail, Colorado, where I was for 20 years before recently relocating to South Florida after
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our practice was acquired.
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On the region front, interventional pain, everybody's familiar with that route.
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I was really good at it, but recognized over the course of many years that I wasn't offering solutions.
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I was offering, everyone says band-aids.
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I don't know what band-aids, a good term, but I was offering transient symptomatic benefit at best.
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Temporary pain relief, essentially.
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Temporary pain relief.
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we were brought up, steroids was our primary vehicle, what it is.
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Catabolic pathways and we probably, well, we definitely overuse them over the course of many years and even to date in traditional interventional pain.
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And we now know that that overuse is horrendous and causes as many problems as it solves.
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Have they really figured that out because I find that people come to me and they see somebody, let's call it in the orthopedic world or even the spine world.
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which may or may not be neuro orthopedics, but, you know, they talk about, they always come back and the doctors offer me a steroid injection or this or that.
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Right.
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So it seems like nobody's really gotten away from that paradigm.
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And yet we know that steroids really kind of cause greater deterioration in the joint or the cartilage, then it helps, right?
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It's short-term pain for long-term loss is the way I characterize it.
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Well, I think the reason we got away with it, maybe continue to get away with it is there wasn't a better solution.
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for people who were hurting and people who were hurting are desperate for some relief and they do work.
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Yeah.
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Very effective.
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I'll be it for a very short period of time.
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So when you're the one in pain, you'll take that two months or three months because there's no other alternative and maybe opioids is your alternative and that has its own
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issues, obviously.
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you know, I, we look at someone who's on systemic steroids, what happens to their body?
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It basically deteriorates.
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So that's about as good of an example as I think I can give.
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At a tissue level, same thing happens.
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If you've trimicinolone or something, it's fairly high dose in concentration for those local tissues.
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Use cartilage as an example if we put it intraarticulary.
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And that same catabolic response ensues.
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And if it's repeated over and over and over again, chase and pain, yeah, it's catabolic.
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It degenerates and deteriorates tissues.
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Yeah.
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Then you end up with a total knee, a total hip or, whatever it is, if, it's correctable in that way.
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yeah, so it's a model.
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your steroids until you need the replacement part.
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Right.
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And that's an interesting concept.
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Also this idea of avoiding a joint replacement or avoiding other interventions.
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I'll weave my story into your story here in just a minute, but
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But that's an interesting concept.
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want the audience to hold this because I think we've all learned this from our physician.
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Well, you know, you're not quite ready for this or that.
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So we'll give you this in the interim.
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And when you get to that, then we'll do this, right?
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It's like, that's like, you know, from medical school on everybody's heard that, right?
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And, and it's like, well, your knee's not doing so good, but you're still getting around.
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So we'll see you back in five years because blah, blah, blah.
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So anyway, I'll weave that back in here in a minute, but go ahead.
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So.
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Well, perhaps we're a little short-sighted.
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There is some systemic uptake.
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If you put steroidals into a joint or a tendon or a rotator cuff or whatever it might be.
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And we probably were blind to the systemic repercussions and we're focused more on the local histology and local repercussions.
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But there's a greater systemic issue here.
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And if you've ever seen one who's had adrenal shutdown, it's not a pretty thing.
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And we didn't run into it often.
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you we were pretty responsible limiting it to, I used to tell patients, if you can manage a problem, this is pre regenerative medicine, but if you can manage a problem with two or
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less steroidal interventions in a 12 month period, that was a reasonable give and take, right?
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Yeah.
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Back in that paradigm.
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And just so the audience understands what he's talking about is if you get too many steroids, and we're not talking about
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Anabolic steroids like a Bellity Builder.
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We're talking about, you know, like things like prednisone and cortisol, know, the steroids your body makes to handle inflammation.
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And that's how those, those injections work is they decrease inflammation, but they also have a catabolic or break down the tissue kind of effect.
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But if you get too much of that either orally, because you're taking an immunosuppressant for your asthma and you're on a lot of prednisone or something, or you're getting that in
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an injection, but you're getting too much of it in the injection.
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You're basically telling your adrenal glands, which are the little glands that sit on top of the kidney that are responsible for making the cortisol when your body needs it, you're
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pretty much telling them to just shut down production.
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And now, you know, it's hard for you to have a normal cortisol response to daily activity, let alone if you should get sick, right?
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So you end up in this really kind of very depleted space.
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Well, and you know, Doc, someone comes in for their shoulder, chances are they have a knee and a back and an elbow as well.
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So what was happening is, know,
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as a practitioner, maybe I was working with their spine and two other practitioners were working elsewhere and they ended up getting 8, 10 steroidal exposures in a 12 month
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period.
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And that's clearly too much.
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But to get back to your original point, how did that lead me to regen?
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Well, I was doing this year in and year out and we were keeping patients as happy as we could.
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But I knew I wasn't offering a solution and that was progressively frustrating me.
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I practiced at the Sedman Clinic in Bale, Colorado and Dr.
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Sedman who has passed and rest in peace.
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But Dr.
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Sedman had a lot of contacts in Europe and in Europe they were treating some soccer athletes with a licensed product that was basically fetal bovine serum, purified baby
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cowl.
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I'm sorry, what was it again?
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Say that again.
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It was fetal bovine serum.
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Okay, fetal bovine serum.
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So what he's talking about is he's talking about...
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the serum or plasma from a calf, not from a human, but serum bovine, right?
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So anyway, okay.
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So now we're using calf blood minus the red blood cells and white blood cells, right?
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So that's pretty interesting.
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Yeah.
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Well, and it was a licensed product, right?
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It was purified commercial grade, I knew we couldn't bring that back to the U.S.
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There was no way.
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But I like the concept and I saw it applied.
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I was one of the first US physicians to visit a few docs in Europe that were applying this to football athletes, to soccer athletes with a lot of muscle and soft tissue injuries and
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so forth.
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And they were achieving some good results.
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So coming back, I like the concept of working with the body as opposed to working against it and managing symptoms.
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And around that time, not just myself, but a number of colleagues
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stumbled across some old dental literature where they were using a platelet concentration to stimulate gums and oral surgery, gingival disease.
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long story short, this kind of evolved into a boutique sports medicine application.
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At the time, this was quite a few years ago, was very, very innovative and cutting edge in the next greatest thing.
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And we started working with it.
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our market in Vale was very much a destination market.
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So we had to stay on the cutting edge to attract people for the latest and greatest.
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And we did our part to try to establish scientific validation, what we did, but we had to stay on the lead edge.
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So this was a good fit for that patient population that was looking for the latest and greatest.
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So what about here?
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What are you talking about?
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Just to tell you, it was talking about PRP, right?
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Yeah.
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Play Ligurge Plus was essentially what we're talking about, just so you're in the loop here.
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So this was not...
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When did this become popular?
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think it was back in the 90s maybe or something like that we first started to hear about or maybe something.
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So foundational research was in the late 90s but application in musculoskeletal and orthopedic medicine was really in the early 2000s I would say.
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That's when we first started working with it.
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Okay.
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And very primitive at the time.
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They were basically centrifuge blood to isolate platelets and stick it in there and let the magic happen.
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So it was a pretty primitive model but at the time was very innovative.
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We started working with it in part initially as a research opportunity, but then the demand skyrocketed and people started to seek it out and we started to apply it.
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But we ran into a problem very early on that led me into my career with this stuff.
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Okay.
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What was that?
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So most of the blood products like PRP are processed with a little tabletop medical device that fits on a counter.
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So you put a blood sample in and it centrifuges it and it produces your
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platelet-rich plasma and it comes out the other end, but it's not quantified and there's zero quality control.
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So you don't actually know what's in there.
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That's right.
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assume it's a platelet concentrate, but to the naked eye, we can't actually tell.
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And I was putting this into patients and we were seeing trends of good results, but it was driving me crazy that I didn't know what my dose was.
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Where in medicine do we apply something without knowing the dose?
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Right.
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And to date, that's still happening routinely.
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So that led me into my career, which was to solve that problem of creating this concept of a cellular dose.
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Right.
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And researching the fact that there's a cause and effect relationship.
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You apply a dose in medicine, we give a drug, we give a dose, and there's an effect.
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We applied that same pharma-like model to biologics, and that led me to ultimately found a biotechnology company to research and develop these things, which has continued since
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2010.
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Okay.
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And I've been battling a bit of a disruptor early on that was not well received to the communities that were producing these things without any quantification, without any
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measurement.
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Right.
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And we battled and fought that fight for many years on podiums and academic conferences.
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And I'm pleased to see over the last couple of years adoption that, yeah, we need to be measuring what we're putting into people and studying.
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Optimization, right?
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You don't treat every single person the exact same way we're different beings.
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100%.
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No, that's a basic tenet of what we do in our space as Yet it wasn't happening.
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And it still isn't happening to date.
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99 % of the biologic application, biologic treatments that are done, cell therapies, doctor has absolutely no idea how many cells are going into that patient.
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And in my opinion, that's unacceptable and is not sustainable.
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Let me ask you this.
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When you draw blood from an individual and you send it in for a complete blood count, you get a red blood cell number or a white blood cell number and you get a platelet count,
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right?
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You get a platelet number.
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Does the platelet count that you get from that CBC, does that translate into anything related to the dose that happens when you centrifuge that volume of blood down to get
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that?
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Is there any connection between those two or is that?
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There is, it continues to evolve.
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So it was kind of a crawl, walk, run approach.
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So we had to kind of first establish a threshold.
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So above that threshold is good, below that threshold is bad.
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That was kind of step one.
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Yeah.
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Not bad, but inadequate, right?
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Correct.
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But that was our first hurdle, and we did that.
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Now what we've done from there is to...
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So basically we measure every platelet, every type of self, different types of white blood cells that are our samples, and that's imported into a database.
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And we run that...
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dose, that cellular dose in parallel with patient reported outcomes at different points in time.
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And then retrospectively looking back, we can say, well, these patients did well.
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What dose did they receive?
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Here were some failures.
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What dose did they receive?
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That was step two.
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Identify trends and patterns of success and failure.
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Predictive value.
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What predicts failure?
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What predicts success?
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Then once we cleared that hurdle, there was a third step, which was customization.
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I treat you, different than myself.
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because we have totally different blood, totally different blood numbers.
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how to treat a patient based on their health and age and body mass index and medications that they're on, and then the problem that we're treating.
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So patient and indication.
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So we might treat a 75 year old smoker different from a 23 year old athlete.
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We might treat an acute problem different from a chronic problem.
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That was phase three, customization and optimization protocols, which is where we are today.
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Yeah that makes perfect sense.
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I can imagine that in the data you're collecting as to who had benefit and who didn't have benefit that there's probably some overlap between the doses that is probably not a clean
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line between above this point you get benefit and below this line you don't get benefit.
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I can imagine that there's people that got benefit with a bit lower dose and people that didn't get benefit with a bit higher dose.
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Do you want to?
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comment on that?
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Is that true, not true, or is it just binary?
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It's evolving, but it's not linear, right?
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So probably what happens is there's a dose increase, know, increased doses better, better, better, better, and it's going to level off.
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And that's the point of decreasing return at that point.
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Okay.
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there's your threshold.
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Okay.
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So it's linear in that sense, but there's not a cutoff if you took all the people that didn't respond and put them at the bottom and all the people that did respond at the top
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and you looked at their counts.
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you're saying that those two clouds wouldn't intersect with each other?
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There was a good correlation with some overlap and some ranges, right?
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It wasn't a finite number due to this number of platelets.
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It was a range, you know, as with everything in medicine.
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what was even more interesting than that is that we lined up 10 people that were fairly similar, similar backgrounds, similar problems, and treat them with a standardized dose.
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About seven or eight...
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will respond pretty positively and then there was a couple that would not and there wasn't much difference between them.
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So what was the why that would explain the non-responders?
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And that's, we're actually applying for an NIH grant at the moment, which is going to actually take this a step further and start to look at genomics and epigenomics to see if
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that, is there a genetic reason, i.e.
17:39
someone's cells are more therapeutic or less therapeutic than someone else's?
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Or is it the epigenome, which influences the gene expression, as you know, which may be influencing that responder or non-responder?
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To the same point, how can I put a stem cell, and we use the patient's own stem cells just to clarify.
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There's a lot of laws and FDA regulations we can talk about.
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Why can I put some cells into an arthritic knee and that patient feels good for five, six, seven years when those cells are long gone after a matter of weeks?
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What is the mechanism?
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And that's kind of where we're at in terms of research to try to understand.
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just to go back to your prior point, I would imagine that there are probably some genetic predisposition.
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And of course, epigenetics will tell a lot.
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Epigenetics, of course, being a combination of the environment that's impacting how the genes are expressed, right?
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So we have that element.
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But I would also suspect that there's a metabolic aging component.
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in this equation also.
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And what I mean by that is one of the things that we know is that if you take stem cells, for example, and you throw them into a Petri dish and you have old plasma in there, right,
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which is full of what's called an aging cytokines, maybe from senescent cells that have had that senescence associated secretory status.
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so now you've got
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These SAS cells that are basically secreting all these inflammatory cytokines We know that the stem cells don't work nearly as well as if you put them into a young healthy
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environment and I explain to people all the time that You know before you do any kind of regenerative procedure Which is basically putting your Olympic swimmers into an Olympic
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sized pool.
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You got to clean out the pool You got to get the lawn chairs out.
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You got to get the logs out You can't expect them to set a world record if they got a
19:37
Swim through all the trash.
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So one of the things we do is plasma for Esis for people first to kind of clear the clear the slate, if you will, with or without young plasma, but then, you know, trying to trying
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to get people back to baseline.
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So I don't know, there may be an aging component to this.
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I don't know if that's something you're entertaining as well, probably.
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There's a number of ways to look at that.
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It's a great discussion in and of itself because I get that a lot clinically and subjectively when a patient's thinking about doing this.
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Do I still have good cells?
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I'm in my 60s, I'm in my 70s.
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This guy named Philippe Ernigo, French orthopedic surgeon, University of Paris, who has been doing research on bone marrow derived.
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I want get away from the word stem cell, right?
20:21
It's a little bit taboo.
20:22
The FDA doesn't like us using it.
20:24
A better term is probably progenitor cell, which stem cell is indicative of one cell type, right?
20:31
Progenitor cells are many cell types in our bone marrow, for example, that have therapeutic.
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So, but anyway, if you look at progenitor cells from 60 and 70 and 80 year olds, and he looked at non-unions and diabetics and really difficult problems, and was able to show
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that the potency of autologous, meaning from the patients, their own cells, applied to those problems still had very strong effects.
20:56
I.e.
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even though you're in your 70s and 80s, if you're in reasonably good health, you still have therapeutic capacity.
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Now there is, as you know, a natural decline.
21:04
but we're able to overcome that through concentration, right, in the lab.
21:08
Yes.
21:09
By increasing the concentration.
21:10
That's right.
21:10
What I'm talking about is the stem cells are remarkably durable, although they do fade out at some point in time, right?
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But they are remarkably durable in that regard, and they have a way to actually be regenerated.
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Stem cells themselves can be regenerated, right, from very small embryonic-like stem cells that sort of sit behind them and actually will recreate them.
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In that case, you still end up with long telomeres and healthy stem cells and things like that.
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Even later in life.
21:38
Right.
21:38
I'm talking about the environment that they're working in that sort of smothers them from being able to do their work.
21:44
Right.
21:44
So, and equally as important, Jeff, the environment we're putting them into is a crappy one in that's it in, in orthopedic application, not just the blood that they're coming
21:52
from, the environment we're putting them in.
21:54
Now, exactly.
21:55
We expect them to react to that environment.
21:58
That's how they produce their effect.
21:59
Right.
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They sense what's going on and react.
22:02
Right.
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And that's a secretory function.
22:04
They release proteins and buy an mRNA and exosomal activity that works with the native tissue to try to stabilize a problem.
22:12
Yep.
22:13
We don't at this phase of the game, and I'm talking about taking patient cells, concentrating them, and immediately putting them back into arthritis, for example, we
22:24
don't regenerate much.
22:26
We call this regenerative medicine.
22:28
But if you look at histology, MRIs before and after and things like that,
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we're not seeing a lot of change.
22:33
Yet, that patient often subjectively, their symptoms are dramatically improved and their function is improved, even though on MRI, the knee still looks arthritic, for example.
22:43
That's right.
22:43
Now, everyone wants to get to the point where we can reverse a problem in vivo, inside the body, from the inside out.
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We're not there today, but obviously that's the goal of where we want to go.
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for now, what we can do is manage the problem effectively from a subjective standpoint.
23:00
I feel better.
23:01
I function better, even though it's arthritic.
23:04
And we think it's gonna take a long time to look at this data, but we think we can probably slow the progression of these problems as well with these types of treatments.
23:13
And you know what's interesting is that it's a nice transition that you made from basically treating symptoms, short-term gain for long-term negative consequences into
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something that has short-term gain, but has long-term positive.
23:32
Consequences, right?
23:33
And that's kind of a thing, and particularly if you sort of start to stack these things together, either, you know, repeated injections or stacking them with other other
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elements, other cofactors, things like that.
23:47
What's the audience should understand?
23:48
We're really taking this away from a kind of maintenance of pain until the joint deteriorates and you need a joint replacement into, you know, enhancing activity, not
23:59
just.
24:00
reducing pain.
24:01
And so you're getting somebody back to a more functional state.
24:04
Correct me if I'm wrong, but that's just what you're saying, And it took a long time to learn this just through doing.
24:12
that was, when does it, where's the point in overturn?
24:15
If you use a knee arthritis, for example, is there a point where this model starts to not be appealing anymore?
24:22
It's just progressed too much and we're better off thinking about a joint replacement at that point.
24:27
And we've kind of learned where that sweet spot is, but it's deeper into the degenerative process than we originally thought it was.
24:33
Right.
24:34
I.E.
24:34
people with moderate to severe arthritis, not always, but often will still respond very nicely.
24:41
So the question then clinically is can we push the replacement out or can we prevent it from being necessary completely?
24:50
Right.
24:50
And it varies obviously from person to person, but it performed...
24:54
And this back in the early days when we were experimenting this, we really know how far this could go.
24:59
And I think for your listeners, most medical technology, as you know, has this huge upsurge in interest in it's, you I found myself in Wall Street Journal in USA Today for
25:10
applying PRP back in 2005, right?
25:13
Because it was so innovative back then.
25:15
Fairly simple thing.
25:16
But what happens with most technology is it starts to undergo the rigors of scientific.
25:21
Process and then what happens we realize it's not as good as we thought and it dies and that happens over and over and over again But what happened with these or it its
25:30
equilibrium?
25:30
It may not die, but it finds its its actual equilibrium, right?
25:33
Right, which is what happened here, right?
25:36
So there was this massive interest and it leveled off came back to earth a little bit But then instead of dying it leveled off and now is showing kind of a slow sustainability And
25:47
when we saw that I I knew that work
25:49
probably was worth engaging in long-term, putting more resources into because it had a future as opposed to snake oil that had its time in the limelight and really didn't work
25:59
as well as everyone else.
26:00
That's Yeah.
26:02
I'll just, I want to hear more about the technology, but I want to interject my own story for a moment for the audience's benefit.
26:13
And to get your comment, I had a knee injury.
26:17
I tore an ACL.
26:18
When I was probably in my late 20s skiing, I did my cardiology fellowship at the University of Colorado.
26:26
And so I would go up and ski occasionally, not very much because I was super busy, but I got up there a few times.
26:31
Right.
26:32
So anyway, I tore an ACL.
26:34
I never knew it.
26:35
just, you know, last run of the day fell broke, you know, hurt my knees swelled up.
26:40
And that always a case last right.
26:42
That's right.
26:43
Went to work.
26:44
Went to work the next day, worked through it, you know, blah, blah.
26:47
Eventually, the swelling went down and got better.
26:48
And I ended up playing soccer and mountain biking and running and doing everything else on it, right?
26:53
So never a problem, so to speak.
26:56
And then snowboarding and everything else.
27:00
And then I had a crash on an elliptical.
27:03
I don't know if you know what that is, but it's like an elliptical on wheels.
27:06
And I was out riding one on a trail close to me and I ended up
27:11
of getting cut off, very unexpectedly got cut off and ended up falling.
27:15
So you're falling from a fairly high position, right?
27:18
You're upright.
27:19
And anyway, I landed on my right knee, which was the knee in question, and it really hurt.
27:24
And I limped back and the bike itself was kind of jacked up.
27:30
So I had to walk at home.
27:31
But the point was, it was so sore.
27:35
I mean, I could hardly go down the stairs.
27:37
I could hardly get up the stairs.
27:39
So I went in and I got an MRI scan.
27:41
And and I but I waited two or three weeks and I was using some signaling peptides like BPC 157 you know some of the things we have access to and And it just wasn't getting it was
27:55
better, but it wasn't that great still difficult getting down the stairs so I got the MRI scan and then You know I could see what the problems were there was you know the menisci
28:05
were they were there, but they weren't perfect and the ACL
28:09
had a couple of threads holding it together.
28:11
And so I scheduled an appointment with a sports orthopedic guy that works on the Cowboys here in Dallas.
28:16
then I thought, know chronologically I don't fit his mold, but I'm 27.
28:21
I wake up 27 every day, right in my world.
28:23
So I was like, no, I want to get this knee fixed.
28:26
So anyway, I made the appointment to go in to see him.
28:31
prior to that, I had...
28:34
done some regenerative work in our office because we do regenerative work in our office.
28:38
And I did a combination of things, right?
28:41
We did activated PRP with a very special activation of it with a particular laser.
28:46
We did some embryonic factors that went in there.
28:49
We did hyaluronic acid.
28:51
We did ozone.
28:52
We did some other things.
28:53
I put all that in there.
28:54
was quite a good thing.
28:55
And quite honestly, I could hardly walk going in there.
29:00
And the next morning,
29:03
It was better in the next day.
29:04
was like walking down the stairs again.
29:06
So it's like, okay, well, this is good.
29:08
but I went to see him anyway, because I knew it was a problem and I still couldn't run, still couldn't do some other things.
29:16
and so I went to see him and he said, well, you know, I wouldn't, wouldn't repair it, know, but, he said, you got, you know, some, some loss.
29:25
said, had some valgus.
29:26
He did the X-rays and stuff.
29:27
have some.
29:28
Your knee kind of separates a little bit.
29:29
It's a little bit loose when you move.
29:31
And I said, yeah, I can feel that.
29:32
I don't think I could snowboard on it.
29:34
He said, joint replacements are actually amazingly good now.
29:37
And he said, if you got it replaced, you could do anything you want.
29:39
Or you could run, could snowboard, you could do anything you want.
29:41
And I'm like, well, I hadn't really thought about that, but I'm not opposed to it.
29:45
So I started to think about that.
29:47
made an appointment.
29:48
I have an appointment with a guy to talk about it.
29:50
In the meantime, I thought I'm going to do another round.
29:53
and so I went back to my knee about three weeks after the first round and put in a bunch of other stuff.
29:58
Same stuff.
29:59
And I started running again.
30:01
And what I realized was that it was, I had to retrain myself to run because even though I've run my whole life, when your body has an injury, you start to splint.
30:14
Your body starts to protect that and it, it reprograms your nervous system.
30:18
Your nervous system is there to protect you.
30:20
Right?
30:20
So it's there protecting the way that leg moves.
30:23
And so it was difficult to actually start running again.
30:26
And it was pretty interesting.
30:28
And my point was when I started running, I realized that I'd even though I was exercising, doing lots of other things, I didn't stop exercising.
30:34
We were doing VASPER and we were doing bicycling and all this other stuff.
30:39
I had lost a fair amount of function and it's like, okay, I've got to get this back.
30:44
So now I'm running like every other day to every third day.
30:48
I'm doing VASPER doing some other things and it's starting to come around.
30:51
But my point to the audience is that when you have an injury.
30:57
Particularly as you're later in your chronological years, so to speak, you're not in your twenties anymore.
31:02
I think it's incredibly important to jump on it as quickly as possible.
31:07
This idea of give it time to sort of heal, I think is a little bit misinformed because what happens is while you're allowing your hip, your shoulder, whatever else, this three,
31:18
four, six, eight, 10 weeks to do whatever it's going to do, your body is actually deteriorating very quickly, very quickly.
31:26
And I think to really preserve function, it makes a lot of sense to say, I've got an injury, let's get an MRI, let's get the x-rays.
31:35
And if it's something that you don't need surgery for, it's like, well, let's jump in and see what we can do to heal it up.
31:40
Because otherwise you've got to really kind of recover from this whole decline that's happened, right?
31:45
So I don't know how you feel about that, but it really kind of changed my whole philosophy around injury and recovery.
31:51
So that's just it.
31:52
We have to change our thinking when we have a tool that
31:55
can augment what the body is trying to do.
31:59
So there's a lot to unpack there on that story.
32:02
So I'll try to hit on a couple of points.
32:05
First,
32:09
When we treat someone and have a positive response, we treat an arthritic knee that may be hurting for 10 years and all of a sudden it's not.
32:15
We have a rehab problem still to address.
32:18
We're not done.
32:20
And that gets back to your point.
32:21
If you use ACL injury as an example, after ACL injury and repair, the vastus medialis muscle, the inside muscle of the quad shuts off.
32:33
And we have a hell of a time getting it to turn back on even though the ACL has been repaired.
32:38
It's a negative feedback loop.
32:40
And those things are going on within our bodies all the time.
32:43
So that's point one.
32:44
With regards to getting to problems early, I wish we could get to problems sooner.
32:52
I get them at the end.
32:54
And that's partly a cultural issue of the medical community and patients.
32:58
I'm not that bad, so I'm not going to go to the doctor.
33:02
Exactly.
33:03
So there's two premises with regenerative medicine I think are applicable to your story.
33:07
The first is when we can work with an acute injury to enhance the healing process.
33:15
That's always better.
33:17
So the body's always going to try to heal, but what tissues do we work with in orthopedics?
33:21
Avascular tissues, tissues that have a crappy blood supply.
33:25
So they're lousy healers to begin with.
33:28
So just waiting, you may improve, but that doesn't mean the process has gone back to normal.
33:35
And that sets up a...
33:37
degenerative cascade that continues and that's why we all deteriorate.
33:40
So if we could intervene early in that process and take a problem that may not complete healing and get it to complete that process with help, that would be huge.
33:52
That would be incredible.
33:53
I rarely get that opportunity.
33:55
I'm always getting them at the end.
33:58
So that's healing augmentation versus chronic management, management of a chronic problem that we cannot reverse.
34:05
So your point is very spot on.
34:06
If we can get to problems sooner, it gives us a much greater opportunity to change the course of a disease process as opposed to just managing it.
34:17
Very big in my world.
34:18
Yeah.
34:19
And that's what I realized because I work out every day.
34:21
I do something, lots of things.
34:25
I'm on the road to recovery, but I realized just what a big hole I fell into.
34:29
And so if you're listening to this and you've got an injury or you
34:34
have one in the future, you know, God forbid if something happens, if you're going to be active, something's going to happen.
34:39
Jump on it would be the take home message and realize that utilizing some of these regenerative technologies can be, can be amazing, particularly if you get to it early.
34:49
Right.
34:50
So
34:53
This episode of the Gladden Ongevity podcast is brought to you by the new molecular hydrogen formulas of chill and energy.
35:00
Yeah, chill and energy were a couple of things that I learned about through NES Health.
35:06
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35:16
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35:21
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35:29
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35:38
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35:50
if they were kind of anxious or feeling upset about something, if they drop the hydrogen in the water and let it dissolve and drank it, not only did they get the benefits of
35:59
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36:07
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36:09
And when we started using H2 energy and combining those two together,
36:14
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36:21
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36:29
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36:33
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37:05
Anyway, think about that.
37:06
Well, you mentioned another really important topic, I think, that we're very excited about.
37:10
And was happy to talk with you today about this.
37:13
And that is the convergence of kind of longevity medicine and regenerative medicine.
37:18
There are so many synergies and parallels as you know, but you described my nightmare.
37:24
What's my nightmare?
37:25
You did five different things at the same time and you better, which is fantastic.
37:31
But in my role, I have to try to figure out how things work so I can make them better.
37:36
And when physicians do...
37:38
HA plus cells plus PRP plus something else plus peptides I've got to try to unwind that process to see what actually worked right and it's kind of kitchen sink versus if we're if
37:52
this field has a future we have to understand the processes that create the effect So I've got to approach it from a little bit different perspective and perhaps were simplistic to
38:03
a fault for example apply PRP and see if it works
38:08
That's one intervention.
38:09
That doesn't mean it's perfect nor best, but my job is to try to understand those mechanisms to predict an outcome.
38:19
Everyone asks me, when is insurance going to cover this?
38:21
What's never going to recover it until we can predict its behavior?
38:26
Because if you can't predict its behavior, you can't translate that into cost savings that a third party payer might be interested in.
38:33
And that's a lot of our work is trying to create predictive models.
38:37
So you come in and we say, all right, you're a 75 year old with this medical history and this problem.
38:42
And based on 10,000 patients data, we need to make that biologic to give you an 82.3 % chance of 50 % improvement lasting three years, right?
38:52
That's the thought process of where we need to go.
38:55
Yeah.
38:55
And I get the thought process and I applaud you for the work you're doing because I think too many times we don't actually fully understand what we're doing, right?
39:04
And yet in our world of longevity medicine where we want to get the best for our clients, we've tried a thing by itself.
39:17
We've tried another thing by itself.
39:19
So we know what peptides alone can do.
39:21
They can be amazing in certain situations.
39:23
We know what PRP can do.
39:24
It can be great in certain situations.
39:27
We know what some of these other things can do as well.
39:29
And it brought us to the point though where they're not
39:32
getting this all the way there.
39:33
And so when you're not getting all the way there, then you, then you start to think about, what would be an intelligent way to stack these together?
39:40
Right.
39:41
If you start to understand them.
39:42
And so the concept of creating kind of the informed or what we might call intelligent or somewhat intuitive, or maybe it's just pure luck.
39:49
don't know, but stack of putting these things together because the client wants to get better.
39:54
Right.
39:55
And, so they don't want an 82.3 % chance.
39:58
They want a hundred percent chance for 99.9.
40:01
So that's kind of where that's evolved from.
40:03
But I think to your point, being a little bit more reductionist in the thought process to actually get to what is the underlying mechanism, how this works, it doesn't preclude you
40:14
in the future of saying, okay, now we understand this.
40:17
What happens if we add this to that?
40:19
Of course.
40:19
Now where do we go?
40:20
That's crawl, walk, run.
40:22
That's the crawl, walk, run.
40:24
And also in terms of longevity pathways, it creates the potential for prehab.
40:30
That's right.
40:31
Optimization prior to treatment.
40:33
if someone...
40:34
Let's use the epigenome as an example.
40:36
Let's say we were able to run genomics and identify that someone has a really suboptimal epigenome or glycation profile or any number of things, telomere length, whatever it might
40:48
be.
40:49
Well, a lot of that, not all, but some is modifiable, especially epigenome, telomere length.
40:54
That's modifiable.
40:56
So maybe before we invest in an expensive cell therapy, we might want to do some work for weeks to months beforehand, try to improve that.
41:07
That should translate into an improved therapeutic capacity of ourselves.
41:10
Now we're studying that.
41:11
It's going to take a lot of data to prove that out.
41:13
But theoretically, it makes perfect sense.
41:17
And we should be pursuing that stuff aggressively.
41:20
I think so too.
41:21
I think the other thing that
41:22
My own situation really kind of drove home for me is that there's a ticking, there's a ticking clock.
41:28
So we're actually, we're actually, we're trying to get it right, but we're also racing against the clock because the clock, the longer we wait, the more collateral damage there
41:38
is to the actual injury, right?
41:40
Whether with nervous system and the muscle atrophy and the bone atrophy and the way that tendons work and all of that stuff is going downhill.
41:47
So from my perspective, there's kind of this ticking clock.
41:50
And what we're trying to do is intervene as quickly as possible.
41:53
So there's as little decline and as much restoration as possible.
41:57
And I think in what you're doing, being able to understand the mechanisms, you're going to be able to figure out how to do that is kind of what I'm thinking.
42:06
It becomes a problem of scale, right?
42:08
Those issues take large numbers to try to answer those questions.
42:14
So as a practitioner and as a company, you know, studying and
42:19
constantly collecting data and with sophisticated algorithmic analyses, we can now look at hundreds of variables at the same time.
42:29
Whereas before with traditional statistical models, it would have been near impossible to throw all of these things into a database and try to pick the ones or the combinations of
42:38
things that have that predictive value that we're after.
42:42
Well, with the advent of AI and machine learning and all these things,
42:46
it's a perfect application to apply that stuff to move faster.
42:50
Because our patients don't wait 10 years.
42:52
They want a solution today.
42:53
Exactly.
42:54
And people ask me, why are you working in autologous models?
42:57
Why not go with the magical cell in a bottle model?
43:01
And the answer is because my patients want a solution now.
43:04
They don't want to wait.
43:05
And that's great for their grandkids.
43:07
They want a solution today.
43:09
So we need to work within the parameters of what we can do from a regulatory standpoint.
43:14
But also,
43:15
what keeps people safe and what we're able to track, right?
43:19
As long as there's measurable events, cause, effect, there's an opportunity for us to gather that data and dig into it and try to come up with some answers to the things you
43:29
describe.
43:30
Yeah, I agree with that.
43:31
I think it is interesting in this world of statistical analysis and AI and machine learning and all this kind of thing.
43:37
It's amazing how you can have data sets that look kind of random on one hand and yet
43:44
the computer can go in and actually pull out the associations and the things that you would otherwise not see ostensibly, which I think may give us, and I don't know, this is
43:54
really as much of a question as anything, but may give us the latitude to create trials where we are inherent or initially even stacking some of these things in ways that we
44:04
think will work and then running that against other stuff and being able to pull it out faster.
44:10
Cause ultimately, you know, people want to be treated and fixed, right?
44:13
So.
44:14
I don't know what you think about that.
44:15
Well, it's a source of frustration because med tech moves very slowly compared to this.
44:23
Right.
44:24
Right.
44:25
And if you look at the impact that has had on our lives versus our ability to cure cancer, for example, you know, go to Mars, right?
44:36
These are enormous problems, but other sectors are moving way faster than we are now that our capabilities have improved.
44:43
For example, our ability to measure cells and actually be accurate in those measurements.
44:48
Our ability to analyze complex data sets.
44:51
We better start to move faster as a field because there's no reason with these capabilities that we shouldn't be able to come up with solutions.
45:01
Historically, medicine, it was sick care.
45:04
You know this, right?
45:05
It was a sick care model, but we've transitioned now into more of a...
45:09
stay healthy as long as possible and we still have the sick care model to fall back on, but we want to stay out of that sick care model.
45:15
But we need to move more quickly.
45:17
And one of the benefits to artificial intelligence is that capacity is there.
45:23
But one of the limitations to artificial intelligence, as you're probably aware, is it requires very large data sets.
45:28
You can't use little teeny data sets.
45:31
So we've got to accrue that data.
45:33
And that's the scaling problem that I'm talking about.
45:35
in order to come up with those answers.
45:37
So we're working on that and trying to grow as quickly as we can, but that's not so easy in an expensive cash-based market.
45:44
Yeah.
45:44
Right?
45:45
Yeah.
45:45
There's also one of the things that we've played with, and I agree with you, one of the things that we've also played with is in silico testing.
45:53
We did this when we were developing some of our hydrogen products, trying to understand how hydrogen worked and how it could be such a great way to modulate redox and...
46:02
decrease pain and do all kinds how did it, how could it possibly do that?
46:05
So we did some in silico modeling with it to figure out what the pathways were that it was affecting and how it was actually working.
46:11
And, that, that really became very powerful for our understanding, which then we could convey to people and say, no, this actually appears to work, right.
46:20
And then, you know, and then we would see it work.
46:22
So I wonder if there's a, going to be an element of in silico modeling for these kinds of things where, you know, we'll have a digital twin of the individual.
46:32
Right.
46:32
And then we can actually run, well, what happens if we give you this or that or this or that, or, for you, it's this.
46:39
Right.
46:39
And I think that kind of almost real time, digital twin, in silico modeling of what the best solution is going to be could be incredibly powerful.
46:50
So I don't know if you're involved with that, I think very important.
46:55
so this is code breaking, right?
46:58
At the end of the day is what we're doing.
47:00
That's right.
47:00
But to break a code, you need a template, right?
47:02
You need the cipher.
47:04
So what we're trying to do is to create the foundational models that we can then use artificial intelligence to model and simulate, right?
47:13
But you have to have the foundation in order to run the simulations.
47:16
So we're still getting to the point where statistically we have that simulation to the point where we trust the results.
47:24
And then once we're at that point, then we can run scenarios.
47:26
Let's test the model.
47:28
You know, the modeling in this situation, in that clinical situation, let's increase, let's decrease, let's add a second element.
47:35
We can do those things once we establish the template.
47:38
We're working as fast as we can.
47:40
Part of the NIH grant is really to try to establish that template.
47:44
If we can establish a template, now we can model without having to do animal research and without having to do human clinical research.
47:52
Run a phase one clinical trial.
47:56
How long does that take?
47:58
Sure.
47:58
My God, that's why we're so slow.
48:00
But if we can model and create interesting artificial simulations, now when we see positive trends, we can go back and run a smaller, more compact clinical trial and move
48:11
more quickly.
48:11
So it's the integration of modern technology into our traditional way of looking at these problems.
48:17
You know, there's another model out there too that you're probably aware of that we've come across, which is really like organ on a chip type modeling.
48:26
where you can actually have a liver or brain or a kidney or a heart.
48:30
And I don't know if they have, orthopedic models there for cartilage, or bone, but, being able to, you know, have a, basically a batch of these organs on a chip where you've got,
48:45
you know, 80 different livers and you're going to basically try out a bunch of different things simultaneously and you can get your results so much faster.
48:54
Tony Attala.
48:56
over Wake Forest is running the Wake Forest regenerative medicine department over there and has gone down this pathway.
49:05
And it was fascinating.
49:07
There was a, I forget the name of the chemo drug, but there was a chemo drug that went through the whole FDA process, took 10 years, was released.
49:16
It was approved for a particular kind of cancer.
49:19
It was like eight years into its use that.
49:22
They figured out that there was a lung toxicity to it that they didn't know about even after all the clinical trials and all the other stuff.
49:29
Apparently he took the drug and put it into the organ on a chip model.
49:33
He put it in the liver, the kidney, the lung, the heart, to see if there might be toxicity inside of a week.
49:40
knew that it caused liver toxicity.
49:42
Yeah.
49:42
Yeah.
49:42
It's out of a week.
49:43
Right.
49:44
And so the power, the power of these, of moving outside of this very old construct of we got to try this in humans.
49:52
for X number of years to try to get to the answer, right?
49:56
I think we're moving into an age when hopefully we can get it right for people, but also move at a much faster speed.
50:03
Yeah, the folks at WIC and Tony and Julie Alexen when she was there, now Julie's at Mayo, believe, with their organ regeneration program and the bladder work and all the stuff they
50:13
did, remember, we're talking about really expensive work.
50:19
Yeah.
50:20
people may not realize is that the resources and support needs to be there.
50:25
Where does that come from?
50:28
Pharma is driving this and a lot of the model you described is used to test drugs because it's less expensive and faster than doing it in human beings or animals.
50:37
But those are big, robust markets and the resources are there to drive the research.
50:42
If you look at application of PRP,
50:47
Now there's a lot of growth in that market has blossomed, but is it there to conduct a hundred million dollar, you know, bench top clinical trial?
50:56
Probably not yet.
50:58
But, so, you know, I think part of the limitation in our movement there is the resources from the investment front going into those particular areas, whereas they could be
51:09
transferred into,
51:12
more of the genetic engineering model in cancer and IPS in CAR-T or induced potent cells or things like that, which is another area of fascinating research, but that's in the drug
51:23
pathway, obviously.
51:24
So much slower.
51:25
No, that's right.
51:27
Yeah.
51:27
And I think these models will get cheaper over time.
51:29
think, you know, technologies gets cheaper in general.
51:32
think there are so much interest in this whole longevity, regenerative space that there's, I think there's funding out there for, you know, to run up, you know,
51:41
$100 million study.
51:42
don't think that's outside the range of what could be orchestrated.
51:47
Well, goes back to the concept of your reward is comparable to the magnitude of the problem you solve.
51:55
That's right.
51:56
So if you look at osteoarthritis as an example, as a multi-billion dollar market, you solve that problem and the resources will be there.
52:03
what we're tasked with is doing that early foundational work that leads to the interest.
52:10
Yes.
52:11
You've got to do that first.
52:12
And we're making progress and we're seeing a lot more interest in the space, but we definitely have a long way to go and I hope we can move more quickly.
52:23
I think, yeah, I hope so too.
52:25
think all of us working together is what I've found.
52:29
Nobody knows everything and kind of interdigitating these different...
52:33
technologies and different thought processes can sometimes accelerate things in a way that's just good for humanity, quite honestly.
52:39
Well, yeah, some days we don't think we know anything at all.
52:42
And then other days we think we're pretty smart.
52:44
The question is, can we outsmart nature?
52:46
And when we start to talk about genetic engineering, the question is, do we have the capacity to outsmart hundreds of millions of years of evolution?
52:55
I don't know.
52:56
Maybe, maybe not.
52:58
Which is one of the reasons we continue to play in the autologous space is the risk profile.
53:02
these things are very favorable and you're not going to hurt people.
53:07
that's comforting.
53:09
That's comforting to be.
53:12
If you look at the longevity space though, I wanted to get your take on this.
53:15
So you're a great person to ask this.
53:17
I have said on podcasts before, if you look at Sinclair's work and Liz Clotis' work and people like that,
53:27
where there's a real possibility in the future we're going to have average lifespans in the 120s and 50s and beyond.
53:34
But we've got a big problem there.
53:37
If we can get brains and hearts and livers and lungs and kidneys to live that long, the orthopedic system is lagging way behind.
53:45
So you have a 120-year-old person who's got good organs but a disastrous orthopedic system and they live in a terrible...
53:53
And we can only replace so many parts.
53:55
So I believe one of the biggest limiting factors in real foresight longevity is the orthopedic limitations and systems, which we don't have solutions to yet.
54:08
And we need to get those in order to make that 120 year old still have a reasonable quality of life.
54:15
I think we can make the other organs maybe move a little faster than we can those avascular orthopedic tissues.
54:20
And I see it as a big problem moving forward.
54:24
I think those solutions will come.
54:26
think it's, know, our vision for longevity is basically when we're a hundred, we want to have a 30 year old body and a 300 year old mind.
54:34
Right.
54:35
So it's really a continued expansion of consciousness, equanimity, peace, tranquility, all these things.
54:41
And, and, and living from that space, right.
54:44
It's not just about more years of the same.
54:47
And the 30 year old body is really from a standpoint of function.
54:52
And I think.
54:53
I think those solutions will come.
54:55
But I also think that in the interim, this idea of if you have a problem and it's nagging you, your knee, your shoulder, your, you know, your, your elbow, your ankle, whatever it
55:06
is, your hip, go get it, go get it taken care of now, because it's not getting better on its own.
55:12
Right.
55:12
And the longer we wait, the more associated decline there is.
55:17
So if you really want to have a 30 year old body, if you're listening to this from a longevity perspective, Hey, I want to have a 30 year old body.
55:22
So there's a problem.
55:23
I would say jump in and fix it as best you can right now.
55:26
Well, and don't know what your perspective is, but we're very interested and in tune with the hormonal axis and its decline as a key mediator of that process across the board.
55:38
That's right.
55:39
You got to have testosterone, estrogen, you got to have growth hormone release, you got to have all those things.
55:44
You got to be able to be anabolic to heal anything.
55:46
Exactly.
55:47
We go down that pathway a lot.
55:49
Well, it just astounds me that it's controversial to fix testosterone in symptomatic men with a low level.
55:55
It's astounding.
55:56
for us.
55:57
Well, it's not for us.
55:58
But I just can't believe the data, as you know, is crystal clear that risk profile is good.
56:05
Who doesn't get cancers?
56:06
Who doesn't get problems?
56:07
Young men with good testosterone levels, right?
56:10
Yeah, exactly.
56:11
So that's another important piece that, you know, do we need to fix or address the hormonal axis when appropriate?
56:18
when we're thinking about a cell therapy, we haven't proven that out yet, but it's only logical that it would supplement what we're trying to do.
56:26
Well, that's another thing.
56:27
I make sure my testosterone levels are good.
56:29
make sure that I've got the BPC.
56:31
I make sure I've got the CJC 1295 with a primoral endorelease growth hormone two days on, two days off.
56:37
I'm doing all, I'm taking other nutraceuticals that augment stem cell function.
56:42
You basically are kind of...
56:45
From your perspective, it's the kitchen sink, but from my perspective, it's like, how do we integrate everything we know to actually heal this thing as quickly as possible?
56:52
So, right.
56:53
Well, again, we work in tough tissues, right?
56:56
We're crappy healer tissues.
56:58
But so if you look at a cartilage model, cartilage regeneration is a holy grail in our space.
57:04
But there's another problem.
57:06
Let's say we could regenerate it.
57:09
Regenerating it and keeping it alive after regeneration are two separate problems.
57:14
That's right.
57:15
That's right.
57:15
So we've got two problems to address, not just one, because part of what leads to cartilage deterioration is the nutrient supply to the cartilage deteriorates over time.
57:25
So we could regenerate those cartilage cells in your knee, but the blood supply above in the subcontra bone is still not addressed.
57:32
Right.
57:32
Then we're not going to be able to keep that cartilage alive.
57:34
So there's a lot to it.
57:37
Certainly the body works in mysterious ways, but it is all integrated.
57:43
But if you look at hormonal axis, we fix a guy with a testosterone deficiency, but if he's got an orthopedic disaster, then it's going to be hard to move that body to get the
57:54
maximal benefit out of that testosterone optimization.
57:58
So that's how longevity medicine, hormone optimization, urology, et cetera, works together with what we're trying to do, which is I don't want orthopedics to become the limiting
58:08
factor between you like the match in that guy.
58:11
His symptoms are improved, his drive is improved.
58:13
He has the energy and the gas to go in the gym, but his knee or his back is preventing him from doing so, missing a massive opportunity to reduce his all-cause mortality.
58:23
That's right.
58:24
And that's why if you get those things fixed along with his metabolic disorders or whatever you might have, insulin resistance, whatever else, you get all that dialed in and
58:34
you still have the knee or the hip or whatever it is.
58:37
I would say jump in on that, right?
58:39
If you're listening to this, jump in on that because you don't want that holding you back.
58:44
You don't want to, you want to be...
58:45
the good news though, Jeff, is even the more advanced stuff is responding pretty well, better than we'd hoped.
58:51
So it's not all doomsday, right?
58:53
We definitely want to get to problems earlier, but let's say we don't.
58:57
It's not just an inevitable joint replacement anymore.
59:00
There are situations where that's still the best option.
59:03
You're right.
59:03
But we certainly like to try to keep your parts as long as we can.
59:07
Exactly.
59:09
yeah, fun conversation, David.
59:11
Really, really enjoyed it.
59:13
So, likewise.
59:14
I appreciate you having me on and great work yourself.
59:17
And we appreciate, we'll keep keeping an eye on the stuff you guys are doing as it certainly helps our efforts on this.
59:23
Yeah.
59:23
Happy to collaborate with you going forward on and whatever we can be.
59:28
Sounds good.
59:28
Fingers crossed on the NIH grant.
59:30
Always difficult to secure those things, but really important work ahead if we're able to.
59:34
The team's done a great job putting that together and we're hopeful.
59:37
that we're going to be able to pull the trigger on that.
59:40
Yeah, exactly.
59:42
We'll wish you the best in that.
59:43
So if people want to learn more about you or hear more about you, where should they go?
59:47
How do they do that?
59:47
Yeah, two places are the company that are recently development company is called Greyledge Biotechnologies or Greyledge technologies.
59:54
that's for people.
59:55
Spell Greyledge.
59:56
G-R-E-Y-L-E-D-G.
59:58
Greyledge Technologies, just greyledgetechnologies.com.
1:00:02
And my clinical practice is just Carly Center, K-A-R-L-I Center.
1:00:08
grayledge is integrated into our center, right?
1:00:11
So grayledge processes the cells and then we share data back and forth between the biotech company and the clinical.
1:00:18
And then we have grayledge affiliates across the nation and now in Europe as well, all of whom are collecting data into our central database.
1:00:24
That's scale problem that we talked about that we're trying to solve.
1:00:28
So if we can get more people focused on standardizing, counting, knowing what we're putting in there, we have a model that we can actually study to try to
1:00:36
prove out those cause and effect relationships and then start to customize, move more towards a precision medical model, which you're very familiar with, which is, believe, the
1:00:44
direction we have to go.
1:00:46
Beautiful.
1:00:46
Love it.
1:00:47
All right.
1:00:48
I appreciate it.
1:00:49
Yeah, my Good talking with you, Yeah.
1:00:51
All right.
1:00:55
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