WEBVTT
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So I'm just gonna on a call with this guy who is uh I think he was in his mid forties.
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Uh he has been lifting for a few years now, like since he was fucking 20.
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And uh he was he was not a competitive athlete like some of the other guys that I that I coach.
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He was just a a dude, man, who just he just loves training, right?
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And he he literally built his whole life around it.
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And he right now he was telling me about this uh knee thing.
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It wasn't like like anything popped or or tore or anything like that, it was just this fucking discomfort, right?
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That he's just building over the course of the past few years.
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And it it starts like it normally starts, right?
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You just get a little bit of stiffness after like a heavy squat day, then it becomes you know a stiffness that lasts into the following day, and then it's like this low-level ache that is just always there.
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And he'll try all the shit that you guys tried already, like glucosamine for over a year.
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He tried chondroitine, he tried uh collagen peptides, he tried fish oil with like stupid fucking doses, and uh basically just like threw money at all of the joint supplements on the shelf.
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He tried BPC 157 for a few rounds, so some of it helped a little a little bit, and uh most of the day absolutely fuck all that he could actually measure.
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And he was uh not happy, right?
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He was he was pissed off.
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Like what wasn't the the about like the the pain itself, right?
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Because it wasn't severe pain, right?
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What what bothered him is this feeling that something was just falling apart, and none of the shit that he was doing, none of the shit that he was taking was actually even touching that same problem.
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So he was like sort of uh that's what I told him actually.
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I was like, you're just like patching your fucking symptoms, right?
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But the underlying structure itself is just fading to shit.
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And that conversation is what uh pushed me deeper into the bioregulator space with him, uh, specifically on the bioregulators for cartilage tissue, because the way that these compounds work is fundamentally different from anything else that I've seen in the in the in our space, right?
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So most people they have the wrong mental model for what's happening in their joints, okay?
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Because cartilage is not actually wearing down like the brake pads on a car.
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That is the model that most people have in their mind.
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But the problem is that the model is actually mostly not true.
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You use your joints, right?
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The the cartilage gets thinner and then eventually it hits the bone.
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That's the story, right?
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Mechanical wear is part of that equation, right?
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But the much bigger problem is happening at the cellular level, right?
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Inside of the cells that are supposed to be maintaining and repairing that cartilage for you.
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So the the thing that makes the the cartilage weird is that it has no blood supply.
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So it is what it's called avascular tissue, right?
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There's no capillaries that are ringing through it uh to feed it oxygen and nutrients the way that there is to muscle.
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So everything that the tissue needs to has to basically diffuse from the joint fluid, right?
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The synovial fluid, and it has to squeeze its way through this very dense matrix to basically reach the cells that are buried in the middle of it.
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So it's a big deal because it means that cartilage repair would work slower compared to everything else, right?
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Like even when everything else is working, and it also means that the tissue is completely dependent on this small population of cells that are living inside of it because there is no backup crude that's rushing through the bloodstream, right?
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It's just the resident cells.
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And if they check out, you're screwed because there's nothing that's gonna be able to replace them.
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So these cells they are called the chondrocytes, okay?
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So they're like uh a construction crude that's just basically gonna keep um that's gonna build and maintain the uh cartilage tissue, the matrix itself, right?
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Now, what is the matrix?
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The matrix is basically two things type one, type two collagen, right?
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So type two collagen is going to form there this uh it's like a mesh, a woven mesh that just gives the cartilage the tensile strength, right?
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The thing that's actually gonna stop it from tearing apart when you load the tissue.
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And then two, you have these things called proteoglycans, right?
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Which is mainly a molecule called agricane, which are these super, super, super huge sugar protein complexes that basically grab water and then hold on to it.
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So that trapped water is what gives the cartilage that squishy, like uh a feeling, right?
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That ability to compress, load, and then spring back.
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So the chondrocytes, they're constantly laying down new collagen, constantly building aggregate, constantly renewing the matrix around themselves, right?
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And as you become older, these chondrocytes they start to enter a state that is called cellular senescence.
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So these cells they stop dividing, they stop doing their repair job.
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The fucked up part is that they don't clear away, they don't leave.
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Like if you're not gonna do your job, just get the fuck out of the way.
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But these guys just sit there and they fucking just start pumping out a bunch of these inflammatory signals that are gonna wreck the shit out of your surrounding tissue.
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This is called the senescence associated secretory phenotype or SASP for short.
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So think of it kind of like a construction worker who uh basically stopped building, but he just started throwing trash at the window instead, right?
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The cell is not helping anyone and it's also actively making the neighborhood worse.
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This is not something that we assume off of like a rat study, right?
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The SASP has specific ingredients, we know this for a fact.
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Uh, it's basically pumping out this metal metalloproteases, the MMPs.
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And these are the enzymes that are literally gonna chew through collagen and agricantine.
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We also have MMP 13 in particular, that's gonna go straight after collagen type 2.
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So the senescent cell is not failing to build just, right?
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That's it's also secreting the exact scissors that are going to cut apart the matrix that the cells basically busted their ass to lay down, right?
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So it's pumping out a bunch of cytokines like IL6, T and F alpha, right?
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They're gonna be pushing the neighborhood up, like healthy chondrocytes towards senescence as well.
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So it is a cascade, right?
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Once there are enough of your chondrocytes flipping into this state, cartilage breakdown accelerates because the cells that are responsible for repaired fit basically shut down and they started to be demolished instead.
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So the research on this maps the whole process out for us, shows that basically decreasing sertuin production in de-aging chondrocytes leads to what is called an impaired matrix remodel, right?
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And they also activated cytokine production.
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The sirtuins matter a lot here.
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So these are these are a family of enzymes, cert one through cert seven, right?
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These are basically acting as the cell's stress and quality control managers.
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So they de-acillate proteins, they help stabilize DNA, they basically keep the mitochondria running clean and they hold these inflammatory transcription programs in check, right?
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On a on a tight ship.
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So when the Certune production starts dropping in an aging chondrocyte, you lose the break, right?
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The inflammatory programs run unopposed, so to speak, and the cell loses its ability to maintain its own genome and its own repair machinery.
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That is the root cause.
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It's not the break bad idea, right?
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Cellular dysfunction is what makes the tissue incapable of maintaining itself.
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And this is where I think most people, including a lot of coaches, unfortunately, and practitioners, are thinking about this completely wrong, okay?
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And this is not because I know better.
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This is just because I've been exposed to certain uh research that I would like to expose you guys to as well.
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So glucosamine and chondratine, they are raw materials, right?
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You're basically handing the tissue more tissue to uh uh more building blocks, right?
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But if if those cells that are like supposed to use the building blocks, they have gone senescence and then they stop running their construction program, more raw materials is not gonna do anything, right?
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You're basically wasting your money, you're delivering lumber to a job site that the workers already fucked off home.
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It's pointless.
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Collagen supplementation will be the same deal.
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It is fantastic in theory, right?
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Your body needs the collagen precursors to maintain the collagen matrix.
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But if the chondrocytes that are incorporating those precursors into type two functional collagen architecture, they have downregulated their repair programs, then the precursors just don't get used properly.
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You're you dudes, you can flood the fuck out of your system with amino acids all you want.
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But if nobody's picking up the tools, jack shit's gonna get built.
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And even BPC 157, guys, which I think it has some legitimate applications for soft tissue repair, I think it's working at a completely different level, right?
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It's basically doing healing and inflammation stuff.
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It's helping blood flow and intendon to bone signaling, but it's not reaching into the chondrocytes and switching gene programs back on that aging hit silence.
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It's a different mechanism, different target, good tool, but wrong tool for this shit.
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And this is why I keep coming back to this approach of bioregulators in general, right?
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These compounds, they're all operating at this level of biology that nothing else in my toolkit is built to touch.
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They're not anti-inflammatory in the usual sense, they're not raw materials, they're not growth factors.
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They are reaching into the cell and trying to restore the gene expression patterns that were running back when the tissue was young and doing its job.
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So let me explain how these compounds are proposed to work.
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And I want to be upfront about where the evidence I think is pretty solid, but it's very much emerging.
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Okay.
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So the bioregulator first, uh the bioregulator approach is uh to cartilage runs on two compounds specifically, uh conleutin and cartilax.
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So conleutin is a synthetic tripeptide, uh, which is just three amino acids long as glutamic acid, ospertic acid, and leucine.
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And then we also have a natural polypeptide complex called sigomere, right?
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So this guy is extracted from the cartilage and bone tissue of young animals.
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The synthetic one is basically designed to interact with some specific gene promoter regions in the chondrocytes.
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And that's the whole mechanistic bet of this entire class of drugs, right?
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The peptides, they're they're small enough and they're charged in the right way that they can just slip into the nucleus, physically settle in the groove of the DNA, add a specific promoter sequence, and change whether the genes get red or not.
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So a tripeptide is not feeding the cell absolutely anything, okay?
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It's basically just flipping the switches on the genome.
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So the natural one, the sigamere, that carries the full spectrum of regulatory peptides that you find in a young cartilage tissue.
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So it's more like handing the cell all of the signals related to this at once.
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Okay.
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Now, there's a 2023 study.
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Basically, look at how these shark peptides regulate the differentiation of stem cells.
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And they got specific on the chondrocyte pathway and the pathway that's producing this brand new cartilage-forming cells.
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So I think that that in particular detail is very important.
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Why?
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Because it means that these ultra-short peptides can actually influence not just the existing chondrocyte, but also the stem cell population that gives rights to new ones, right?
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So if you can push mesenchymal stem cells towards the chondrocyte lineage, you are potentially rebuilding workforce, right?
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You're not just trying to motivate guys who are already retired.
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Now, there's also a piece of evidence from a 2022 study.
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This one I found really interesting because it was an international collaboration.
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It was not just a Russian-only publication pattern.
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And if you want more details on all the studies that I cite in any of my videos here, just go to the engine, go to the uh deep dive section of the YouTube videos, and there's a deep fucking dive in there with all the research and all of the ideas broken down and everything that you need to do to apply this video to your life.
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So, in this 2022 study, they basically tested conluten on a human monocyte cells, and they basically hit an inflammatory stimulus.
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And what they found is that specifically this shutdown TNF production also dialed back the inflammatory cascade.
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Now, this was not tested in cartilage cells directly, it was tested in immune cells.
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Why is that still relevant?
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Because remember, the cartilage sits inside of a joint capsule, right?
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In the lining of that capsule, the synovium is where a lot of the joint inflammation actually comes from.
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So in an aging or an arthritic joint, the immune cells, they're going to infiltrate the synovium.
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And in there, they're going to dump a bunch of TNF and IL-6 onto the joint fluid.
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And because the cartilage is avascular and bathe in that fluid, whatever's floating in there just diffuses straight into the tissue and hits the chondrocytes.
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So if you can calm TNF signaling at the source, you're going to be cleaning up this exact environment that the chondrocytes are trying to work in, right?
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Because everything is connecting.
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And then there's a clinical application data.
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There's a study in older folks with temporomandibular joint disease.
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They found that basically adding sigomere into a treatment basically got rid of the pain very fast.
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So an increased mouth opening amplitude, which I know you're trying to work on, buddy.
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No judgment.
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Improved chewing function and also stopped the releases over the observation period.
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Now, sigomere was one piece of a multimodal treatment there.
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Okay, so you can't just isolate that contribution to that one study.
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But the pattern of clinical benefit in aging joint stacked on top of the cellularism data, I think you're starting to paint a pretty interesting picture.
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Now, I keep coming back to this point here about bioregulator space in general.
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In cartilage, I think it's one of the main examples of why this matters, right?
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With conventional joint supplements, you're basically working with the current state of the tissue.
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You're accepting that the chondrocytes are aging, that the SAS was active, that the MMPs are eating the matrix and the repair capacity is dropping, and you're trying to prop whatever function is left.
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So that's the management strategy, right?
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Management strategy, they're gonna help with symptoms, but they can't change the trajectory.
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So the joint keeps heading the same shitty fucking direction, just maybe a little bit slower.
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And the bioregulator approach is basically trying to be way more ambitious with this stuff.
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It's trying to restore the gene expression patterns in dose chondrocytes back towards a younger phenotype to reverse the SASP, to get Sertoans back up in the repair programs that depend on them running again.
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And and where it stands, the clinical evidence, human clinical evidence for that particular clean, it's still building.
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Okay, they're still working on it.
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The settler evidence and the animal evidence, 100%.
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The clinical observation from practice using these compounds lines up with the mechanism, but large-scale control trials just have not been done yet.
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Now, what I can tell you from working with clients who folded cartilage bioregulators into their protocols is that the pattern that I see is just very, very different from what I see in standard joint stacks.
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Okay.
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The timeline is different, the quality of the improvement is different.
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Instead of like the pain is a little bit less when I take this, it's more of like, yo, something just kind of changed in the way that my joint feels and moves.
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So that experimental line, that report, it does line up with what the mechanism would predict, which is just not just managing symptoms, you're potentially restoring cellular function.
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So I mentioned the uh 2023 study on chondrogenic cell differentiation.
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I think it's important to come back to that study because I think that's the most important piece on this whole puzzle.
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So your cells, they have the the your body has these mesenchymal cells.
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These are stem cells, okay?
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They're basically like blank slate cells that can turn into different tissue types depending on what signals they get.
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So some of them become bone cells, some have become fat cells, some of them become chondrocytes, the cartilage-forming cells.
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And then the pathway that turns into a stem cell into a chondrocyte is called chondrogenic differentiation.
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It's run by this cascade of signals that have to fire the right order at the right time.
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And there's a master switch there, SOX9, that basically commits the cell to the cardid lineage and then drives it to start cranking out collagen type 2 and as well as aggregate.
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So this isn't just a single gene, it is a whole program that has to boot up in the right order.
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Now, what the Linkova and the Cavinson research showed us is that specific short peptides can regulate the differentiation pathway.
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So they can influence whether a stem cell commits to the contract lineage in the first place.
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And that's fundamentally a different approach from joint repaired and anything else that's out there, right?
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You're not feeding existing cartilage cells more building blocks.
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You're not just quieting information around damaged tissue.
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Guys, you're potentially directing the stem cell pools to produce more cartilage-forming cells, replenishing the workforce at the source in a tissue that basically has no other way of bringing it into the cells because remember, it is avascular, nothing is arriving through the blood.
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So it's uh it's a pretty big deal, in my opinion.
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Now, from what I can gather from the data stuff, this is very much early, right?
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The study that uh establishes the mechanism does exist.
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The peptide-driven regulation of chondrocyte, uh, chondrogenesis is a real thing operating at a real molecular level.
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But but what it does, like does it translate directly into the clinical cartilage of a 45-year-old with a cranky knee, right?
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That's the gap between a lab and the real world, right?
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You can't say with the evidence that we are there.
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So I don't.
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But when it comes to personal experience and coaching people, guys, we need a database of this shit because I'm we literally see the results.
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No.
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What I find compelling here is just how consistent the mechanism is across the whole bioregulator space.
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So in every tissue that was studied, where the compounds have been studied, right, the pattern is always the same.
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You get short peptides that are interacting with gene regulatory regions to restore expression patterns towards a younger phenotype.
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And in the brain, in the thymus, in the vascular system, in the pancreas, and now in the cartilage and the joint tissue, it's the same mechanism that keeps showing up.
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It's not a different claim for each organ, it's the same biological principle applied to tissue by tissue and map consistency is what makes me take seriously about regulators instead of writing it off as woo-woo bullshit just because uh someone online who's a pretty big deal said that uh they don't do anything.
00:17:23.519 --> 00:17:26.559
Now, the training context matters here too, right?
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I want to bring this into something practical because I know that a lot of you guys watching, you guys are dealing with this joint stuff, and you're like, oh, okay, cool, like cellular senescence, stem cell differentiation, right?
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But what does this actually fucking mean for my knee, my man?
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So here's how I think about it.
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Okay, let's say let's say you're in your 20s, right?
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Your joints feel fine, right?
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Your chondrocyte population is probably just humming along, and uh your stem cell pool is still strong.
00:17:50.240 --> 00:17:52.480
And the standard approach is just keeping the joints loaded.
00:17:52.799 --> 00:17:57.680
Eat enough protein, eat enough collagen, manage inflammation, uh, get your omega-3s in place, right?
00:17:57.759 --> 00:17:59.839
It's probably just enough to keep your joint healthy.
00:17:59.920 --> 00:18:02.160
You don't need to go settler bananas yet.
00:18:02.319 --> 00:18:08.480
But if you're in your 30s, okay, and then you start noticing like, hey, my recovery from my heavy sessions just takes a little bit longer.
00:18:08.640 --> 00:18:11.839
It's it's kind of like it hurts, your joints hurt a little bit more every time I train, right?
00:18:12.000 --> 00:18:18.559
And maybe certain positions you start to feel a little bit stiffer and uh your stuff just cracks and pops like crazy, like more than it did five years ago.
00:18:18.720 --> 00:18:20.000
Those are all early signs, right?
00:18:20.079 --> 00:18:22.160
Your chondrocyte population is starting to shift.
00:18:22.319 --> 00:18:25.519
Some cells, they're going to be flipping into senescence, right?
00:18:25.599 --> 00:18:27.359
The repair capacity is dropping.
00:18:27.519 --> 00:18:32.799
And at this stage, being proactive about the cellular environment starts to actually matter for you.
00:18:33.039 --> 00:18:36.160
Now, let's say that you're in your 40s, let's say you're beyond your 40s, right?
00:18:36.240 --> 00:18:36.960
You're old as shit.
00:18:37.039 --> 00:18:37.759
I'm just kidding, guys.
00:18:37.920 --> 00:18:40.079
Uh, right, let's say you've been training hard for decades.
00:18:40.319 --> 00:18:45.039
That chondrocyte senescence is very likely, and sadly so, very well established.
00:18:45.359 --> 00:18:48.400
The SASP active, the MMP is chewing the matrix.
00:18:48.480 --> 00:18:53.680
The standard supplements are just dropping raw materials in front of the cells, but these cells don't do shit anymore.
00:18:53.839 --> 00:18:55.200
Okay, that's why it doesn't work.
00:18:55.359 --> 00:19:02.480
This is where the bioregulated approach starts to make the most sense because you're not just managing the downstream mess, you're also going after the upstream causes.
00:19:03.039 --> 00:19:04.880
I'm not saying this replaces anything, right?
00:19:04.960 --> 00:19:19.759
You still need to load your joints intelligent, you still need the raw materials, you still need to address inflammation, but adding a layer that actually addresses the cellular machinery itself, the gene expression patterns like driving cartilage maintenance, completely conversation, right?
00:19:19.839 --> 00:19:22.240
It's a conversation that almost nobody in our space is having.
00:19:22.400 --> 00:19:29.039
So the thing that genuinely drives me nuts about the joint health in our community is that everybody treats it as like it's inevitable.
00:19:29.200 --> 00:19:31.440
Oh, you're in your 40s, your joints are gonna hurt, right?
00:19:31.519 --> 00:19:32.559
Like that's just how it is.
00:19:32.799 --> 00:19:35.680
And sure, mechanical stress does pile up.
00:19:35.759 --> 00:19:36.240
That's true.
00:19:36.400 --> 00:19:51.599
Yeah, decades of loading are gonna create wear patterns, but the cellular aging component, the part where like your chondrocytes are actively shutting down their repair programs and then switching on the MMPs to eat your matrix, that is not an inevitable consequence of training.
00:19:51.680 --> 00:20:00.240
Okay, that's a biological process, and biological processes can be stimulated, they can be slowed and potentially maybe even reversed, okay?
00:20:00.400 --> 00:20:07.039
And the reason you don't hear about this in the entire like joint supplement industry is that that is built around raw materials and anti-inflammatories.
00:20:07.519 --> 00:20:15.440
There's no money to be made and like to to say, like, hey, the problem is not glucosamine, the problem is your cell stopped using glucosamine properly, right?
00:20:15.519 --> 00:20:19.440
That doesn't move a single cup of glucosamine, which is cheap off the shelf.
00:20:20.319 --> 00:20:24.319
But that's also a lot closer to the truth than what is actually going on in an aging joint.
00:20:24.480 --> 00:20:26.079
And it goes way past supplements.
00:20:26.240 --> 00:20:29.359
The medical side of things is not easier when it comes to this, okay?
00:20:29.440 --> 00:20:40.799
I don't know why I'm moving like right about like our orange man on the standard clinical approach to osteoarthritis in pain management and eventually like joint replacement, just NSA, right?
00:20:40.880 --> 00:20:45.759
Cortisone, uh cortisone injections, physical therapy, and then when the joint gets bad enough, it's just surgery.
00:20:45.920 --> 00:20:56.160
There's no treatment art, there's basically zero conversation in conventional orthopedics about what's happening at the chondrocyte level and why these repair cells they stop repairing and whether the process can be touched at all.
00:20:56.400 --> 00:21:06.480
The research is out there, the mechanism is published, it's right there, but it hasn't filtered into clinical practice because the whole treatment paradigm is still stuck in this manage and replace bullshit.
00:21:06.640 --> 00:21:16.240
The idea that you could restore cellular function instead of just waiting for the joint to degrade enough to justify cutting it out and bolting a fucking metal one, that's not even on the radar for most orthopedic surgeries.
00:21:16.480 --> 00:21:18.400
And that should piss you off too.
00:21:18.640 --> 00:21:31.359
Now, if you're someone who's dealing with joint degradation, okay, whether that's diagnosed with osteoarthritis or just the slow slide in joint quality that comes from years of training, here's the framework that I need from you, okay?
00:21:31.599 --> 00:21:34.000
The foundation is still in the basics.
00:21:34.160 --> 00:21:44.480
So adequate collagen take via pro via protein, omega-3 for systemic inflammation, training modifications that cut that peak joint stress, but keep you loading the stimulus and the cartilage that needs it.
00:21:44.640 --> 00:21:48.480
Because the thing is the cartilage needs loading to be squeezed to be healthy, right?
00:21:48.559 --> 00:21:55.440
Since a vascular, that squeeze and release of the joint under the load is literally how the nutrients get pumped and then the waste gets pushed out of the tissue.
00:21:55.599 --> 00:21:58.000
Uh so loaded right and you are feeding it.
00:21:58.160 --> 00:22:04.400
Load it wrong or not at all, you're kind of just be gonna be standing the chance of just uh shitting on it, right?
00:22:04.559 --> 00:22:06.400
So the type of loading also matters.
00:22:06.880 --> 00:22:09.839
I'm not telling you to throw out your join stack either.
00:22:10.000 --> 00:22:15.039
Now, what I'm telling you is that if the basics are not moving the needle, for a lot of people over 35, they're really not.
00:22:15.200 --> 00:22:18.799
And then at a cellular level, I think that's where you should look next, okay?
00:22:18.960 --> 00:22:20.799
Are your chondrocytes still working?
00:22:21.039 --> 00:22:22.559
Is the SASP still active?
00:22:22.720 --> 00:22:25.920
Is the repair machinery just running or has it gone kind of quiet?
00:22:26.000 --> 00:22:29.599
And if it's gone quiet, what tools do exist to potentially like wake it back up?
00:22:29.759 --> 00:22:36.799
And the bioregulator course that we put together inside of the Art Lab engine goes deeper than this in every single kind of decision tree that you can imagine.
00:22:36.960 --> 00:22:46.319
Every single organ, every single system that these compounds target, including the cartilage and the joints, it gets broken down by what's in the tissue level mechanism of aging in that system.
00:22:46.480 --> 00:22:49.599
What does the evidence actually show for the bioregulator compounds there?
00:22:49.759 --> 00:22:51.119
What are the dosing frameworks?
00:22:51.200 --> 00:22:52.240
What are the cycling patterns?
00:22:52.319 --> 00:22:55.440
And how do you layer the whole thing with everybody, everything else that we're taking?
00:22:55.599 --> 00:23:04.319
So I built this whole thing around how I think through these problems with clients, not just like a compound list, just telling you a bunch of shit about random compounds.
00:23:04.400 --> 00:23:05.920
I that's uh that's not how we go.
00:23:06.000 --> 00:23:11.599
And the course is live, and it's the it's definitely the most comprehensive bioregulator resource in the English language.
00:23:11.680 --> 00:23:20.559
And if you don't want to figure this out yourself, guys, the optimization lab is where the acceleration happens because look, I can look at your specific training history, your specific joint issues.
00:23:20.720 --> 00:23:28.720
What if you tried and then map out a protocol directly into your situation instead of you just having to just generalize more shit from a course module?
00:23:28.880 --> 00:23:42.799
So, some of the biggest breakthroughs that I've seen, it came from clients who've been managing their issues for years, and the standard cool toolkit just stopped working, and they had no fucking clue that there were other levers that could still be working and that could be pulled.
00:23:42.880 --> 00:23:50.480
Now, if you watch the thyroid video that I put out a few days ago, you already know how these biological systems they talk to each other in ways that most people don't expect, right?
00:23:50.640 --> 00:23:59.359
Thyroid function is going to affect tissue repair and regeneration everywhere, including cartilage, because T3 is going to be driving the metabolic machinery cells that are going to need to maintain themselves.
00:23:59.519 --> 00:24:04.559
And a chondrocyte is basically trying to rebuild a matrix, and that is running on that machinery like any other cell.
00:24:04.720 --> 00:24:09.039
It's not coincidence that hypothyroid people so often have joint issues.
00:24:09.200 --> 00:24:10.799
It's because the systems are wired together.
00:24:10.880 --> 00:24:13.839
So the full bioregulator course has dropped already.
00:24:13.920 --> 00:24:16.880
The Optolab engine is filled to the brain.
00:24:16.960 --> 00:24:20.000
We also have a new thyroid course, and uh, you guys should go check it out.
00:24:20.079 --> 00:24:21.359
And then that's it for this one.
00:24:21.440 --> 00:24:24.240
Go take care of your damn fucking joints, and uh, I'll catch you in the next video.
00:24:24.319 --> 00:24:24.960
Peace out, boo.
00:00:00.320 --> 00:00:05.759
So I'm just gonna on a call with this guy who is uh I think he was in his mid forties.
00:00:06.000 --> 00:00:11.199
Uh he has been lifting for a few years now, like since he was fucking 20.
00:00:11.279 --> 00:00:15.279
And uh he was he was not a competitive athlete like some of the other guys that I that I coach.
00:00:15.599 --> 00:00:20.160
He was just a a dude, man, who just he just loves training, right?
00:00:20.239 --> 00:00:22.480
And he he literally built his whole life around it.
00:00:22.640 --> 00:00:26.000
And he right now he was telling me about this uh knee thing.
00:00:26.480 --> 00:00:32.479
It wasn't like like anything popped or or tore or anything like that, it was just this fucking discomfort, right?
00:00:32.560 --> 00:00:34.960
That he's just building over the course of the past few years.
00:00:35.119 --> 00:00:37.280
And it it starts like it normally starts, right?
00:00:37.359 --> 00:00:48.799
You just get a little bit of stiffness after like a heavy squat day, then it becomes you know a stiffness that lasts into the following day, and then it's like this low-level ache that is just always there.
00:00:49.039 --> 00:00:53.280
And he'll try all the shit that you guys tried already, like glucosamine for over a year.
00:00:53.439 --> 00:01:04.079
He tried chondroitine, he tried uh collagen peptides, he tried fish oil with like stupid fucking doses, and uh basically just like threw money at all of the joint supplements on the shelf.
00:01:04.159 --> 00:01:11.680
He tried BPC 157 for a few rounds, so some of it helped a little a little bit, and uh most of the day absolutely fuck all that he could actually measure.
00:01:11.920 --> 00:01:14.319
And he was uh not happy, right?
00:01:14.400 --> 00:01:15.680
He was he was pissed off.
00:01:15.760 --> 00:01:19.439
Like what wasn't the the about like the the pain itself, right?
00:01:19.680 --> 00:01:21.680
Because it wasn't severe pain, right?
00:01:21.840 --> 00:01:33.040
What what bothered him is this feeling that something was just falling apart, and none of the shit that he was doing, none of the shit that he was taking was actually even touching that same problem.
00:01:33.280 --> 00:01:36.959
So he was like sort of uh that's what I told him actually.
00:01:37.040 --> 00:01:40.079
I was like, you're just like patching your fucking symptoms, right?
00:01:40.239 --> 00:01:44.319
But the underlying structure itself is just fading to shit.
00:01:44.480 --> 00:01:59.120
And that conversation is what uh pushed me deeper into the bioregulator space with him, uh, specifically on the bioregulators for cartilage tissue, because the way that these compounds work is fundamentally different from anything else that I've seen in the in the in our space, right?
00:01:59.200 --> 00:02:04.799
So most people they have the wrong mental model for what's happening in their joints, okay?
00:02:05.040 --> 00:02:09.599
Because cartilage is not actually wearing down like the brake pads on a car.
00:02:09.759 --> 00:02:11.840
That is the model that most people have in their mind.
00:02:11.919 --> 00:02:14.960
But the problem is that the model is actually mostly not true.
00:02:15.280 --> 00:02:17.039
You use your joints, right?
00:02:17.199 --> 00:02:21.039
The the cartilage gets thinner and then eventually it hits the bone.
00:02:21.199 --> 00:02:22.479
That's the story, right?
00:02:22.719 --> 00:02:25.599
Mechanical wear is part of that equation, right?
00:02:25.680 --> 00:02:28.960
But the much bigger problem is happening at the cellular level, right?
00:02:29.120 --> 00:02:35.360
Inside of the cells that are supposed to be maintaining and repairing that cartilage for you.
00:02:35.680 --> 00:02:41.199
So the the thing that makes the the cartilage weird is that it has no blood supply.
00:02:41.360 --> 00:02:44.400
So it is what it's called avascular tissue, right?
00:02:44.479 --> 00:02:50.319
There's no capillaries that are ringing through it uh to feed it oxygen and nutrients the way that there is to muscle.
00:02:50.479 --> 00:02:56.560
So everything that the tissue needs to has to basically diffuse from the joint fluid, right?
00:02:56.639 --> 00:03:05.520
The synovial fluid, and it has to squeeze its way through this very dense matrix to basically reach the cells that are buried in the middle of it.
00:03:05.680 --> 00:03:11.840
So it's a big deal because it means that cartilage repair would work slower compared to everything else, right?
00:03:11.919 --> 00:03:22.000
Like even when everything else is working, and it also means that the tissue is completely dependent on this small population of cells that are living inside of it because there is no backup crude that's rushing through the bloodstream, right?
00:03:22.080 --> 00:03:23.520
It's just the resident cells.
00:03:23.599 --> 00:03:28.240
And if they check out, you're screwed because there's nothing that's gonna be able to replace them.
00:03:28.400 --> 00:03:32.479
So these cells they are called the chondrocytes, okay?
00:03:32.800 --> 00:03:41.680
So they're like uh a construction crude that's just basically gonna keep um that's gonna build and maintain the uh cartilage tissue, the matrix itself, right?
00:03:41.840 --> 00:03:42.960
Now, what is the matrix?
00:03:43.120 --> 00:03:47.599
The matrix is basically two things type one, type two collagen, right?
00:03:47.680 --> 00:03:57.199
So type two collagen is going to form there this uh it's like a mesh, a woven mesh that just gives the cartilage the tensile strength, right?
00:03:57.280 --> 00:04:00.960
The thing that's actually gonna stop it from tearing apart when you load the tissue.
00:04:01.120 --> 00:04:04.000
And then two, you have these things called proteoglycans, right?
00:04:04.080 --> 00:04:13.599
Which is mainly a molecule called agricane, which are these super, super, super huge sugar protein complexes that basically grab water and then hold on to it.
00:04:13.759 --> 00:04:19.040
So that trapped water is what gives the cartilage that squishy, like uh a feeling, right?
00:04:19.120 --> 00:04:21.600
That ability to compress, load, and then spring back.
00:04:21.759 --> 00:04:30.720
So the chondrocytes, they're constantly laying down new collagen, constantly building aggregate, constantly renewing the matrix around themselves, right?
00:04:30.959 --> 00:04:38.240
And as you become older, these chondrocytes they start to enter a state that is called cellular senescence.
00:04:38.399 --> 00:04:41.839
So these cells they stop dividing, they stop doing their repair job.
00:04:42.000 --> 00:04:44.959
The fucked up part is that they don't clear away, they don't leave.
00:04:45.040 --> 00:04:47.279
Like if you're not gonna do your job, just get the fuck out of the way.
00:04:47.360 --> 00:04:55.279
But these guys just sit there and they fucking just start pumping out a bunch of these inflammatory signals that are gonna wreck the shit out of your surrounding tissue.
00:04:55.439 --> 00:05:00.639
This is called the senescence associated secretory phenotype or SASP for short.
00:05:00.800 --> 00:05:08.560
So think of it kind of like a construction worker who uh basically stopped building, but he just started throwing trash at the window instead, right?
00:05:08.879 --> 00:05:13.360
The cell is not helping anyone and it's also actively making the neighborhood worse.
00:05:13.600 --> 00:05:16.879
This is not something that we assume off of like a rat study, right?
00:05:16.959 --> 00:05:19.600
The SASP has specific ingredients, we know this for a fact.
00:05:19.759 --> 00:05:24.319
Uh, it's basically pumping out this metal metalloproteases, the MMPs.
00:05:24.399 --> 00:05:28.000
And these are the enzymes that are literally gonna chew through collagen and agricantine.
00:05:28.079 --> 00:05:32.560
We also have MMP 13 in particular, that's gonna go straight after collagen type 2.
00:05:32.720 --> 00:05:35.759
So the senescent cell is not failing to build just, right?
00:05:35.839 --> 00:05:45.120
That's it's also secreting the exact scissors that are going to cut apart the matrix that the cells basically busted their ass to lay down, right?
00:05:45.439 --> 00:05:49.680
So it's pumping out a bunch of cytokines like IL6, T and F alpha, right?
00:05:49.759 --> 00:05:54.399
They're gonna be pushing the neighborhood up, like healthy chondrocytes towards senescence as well.
00:05:54.560 --> 00:05:56.240
So it is a cascade, right?
00:05:56.480 --> 00:06:08.639
Once there are enough of your chondrocytes flipping into this state, cartilage breakdown accelerates because the cells that are responsible for repaired fit basically shut down and they started to be demolished instead.
00:06:08.800 --> 00:06:21.680
So the research on this maps the whole process out for us, shows that basically decreasing sertuin production in de-aging chondrocytes leads to what is called an impaired matrix remodel, right?
00:06:21.759 --> 00:06:23.920
And they also activated cytokine production.
00:06:24.079 --> 00:06:25.759
The sirtuins matter a lot here.
00:06:25.839 --> 00:06:29.759
So these are these are a family of enzymes, cert one through cert seven, right?
00:06:29.920 --> 00:06:34.720
These are basically acting as the cell's stress and quality control managers.
00:06:34.879 --> 00:06:44.399
So they de-acillate proteins, they help stabilize DNA, they basically keep the mitochondria running clean and they hold these inflammatory transcription programs in check, right?
00:06:44.480 --> 00:06:45.680
On a on a tight ship.
00:06:45.839 --> 00:06:51.040
So when the Certune production starts dropping in an aging chondrocyte, you lose the break, right?
00:06:51.120 --> 00:06:59.120
The inflammatory programs run unopposed, so to speak, and the cell loses its ability to maintain its own genome and its own repair machinery.
00:06:59.199 --> 00:07:00.560
That is the root cause.
00:07:00.639 --> 00:07:02.319
It's not the break bad idea, right?
00:07:02.399 --> 00:07:08.000
Cellular dysfunction is what makes the tissue incapable of maintaining itself.
00:07:08.160 --> 00:07:15.120
And this is where I think most people, including a lot of coaches, unfortunately, and practitioners, are thinking about this completely wrong, okay?
00:07:15.199 --> 00:07:17.120
And this is not because I know better.
00:07:17.360 --> 00:07:22.240
This is just because I've been exposed to certain uh research that I would like to expose you guys to as well.
00:07:22.560 --> 00:07:27.519
So glucosamine and chondratine, they are raw materials, right?
00:07:27.600 --> 00:07:32.399
You're basically handing the tissue more tissue to uh uh more building blocks, right?
00:07:32.560 --> 00:07:44.000
But if if those cells that are like supposed to use the building blocks, they have gone senescence and then they stop running their construction program, more raw materials is not gonna do anything, right?
00:07:44.079 --> 00:07:49.120
You're basically wasting your money, you're delivering lumber to a job site that the workers already fucked off home.
00:07:49.279 --> 00:07:50.240
It's pointless.
00:07:50.560 --> 00:07:52.959
Collagen supplementation will be the same deal.
00:07:53.120 --> 00:07:54.720
It is fantastic in theory, right?
00:07:54.800 --> 00:07:58.319
Your body needs the collagen precursors to maintain the collagen matrix.
00:07:58.399 --> 00:08:09.279
But if the chondrocytes that are incorporating those precursors into type two functional collagen architecture, they have downregulated their repair programs, then the precursors just don't get used properly.
00:08:09.439 --> 00:08:16.319
You're you dudes, you can flood the fuck out of your system with amino acids all you want.
00:08:16.480 --> 00:08:19.680
But if nobody's picking up the tools, jack shit's gonna get built.
00:08:19.759 --> 00:08:27.600
And even BPC 157, guys, which I think it has some legitimate applications for soft tissue repair, I think it's working at a completely different level, right?
00:08:27.680 --> 00:08:30.720
It's basically doing healing and inflammation stuff.
00:08:30.800 --> 00:08:38.000
It's helping blood flow and intendon to bone signaling, but it's not reaching into the chondrocytes and switching gene programs back on that aging hit silence.
00:08:38.080 --> 00:08:42.720
It's a different mechanism, different target, good tool, but wrong tool for this shit.
00:08:42.879 --> 00:08:46.320
And this is why I keep coming back to this approach of bioregulators in general, right?
00:08:46.399 --> 00:08:51.120
These compounds, they're all operating at this level of biology that nothing else in my toolkit is built to touch.
00:08:51.279 --> 00:08:55.039
They're not anti-inflammatory in the usual sense, they're not raw materials, they're not growth factors.
00:08:55.200 --> 00:09:03.840
They are reaching into the cell and trying to restore the gene expression patterns that were running back when the tissue was young and doing its job.
00:09:04.159 --> 00:09:06.559
So let me explain how these compounds are proposed to work.
00:09:06.639 --> 00:09:11.759
And I want to be upfront about where the evidence I think is pretty solid, but it's very much emerging.
00:09:11.840 --> 00:09:12.080
Okay.
00:09:12.240 --> 00:09:19.919
So the bioregulator first, uh the bioregulator approach is uh to cartilage runs on two compounds specifically, uh conleutin and cartilax.
00:09:20.000 --> 00:09:26.480
So conleutin is a synthetic tripeptide, uh, which is just three amino acids long as glutamic acid, ospertic acid, and leucine.
00:09:26.559 --> 00:09:31.200
And then we also have a natural polypeptide complex called sigomere, right?
00:09:31.279 --> 00:09:35.360
So this guy is extracted from the cartilage and bone tissue of young animals.
00:09:35.600 --> 00:09:42.480
The synthetic one is basically designed to interact with some specific gene promoter regions in the chondrocytes.
00:09:42.639 --> 00:09:47.039
And that's the whole mechanistic bet of this entire class of drugs, right?
00:09:47.200 --> 00:09:58.559
The peptides, they're they're small enough and they're charged in the right way that they can just slip into the nucleus, physically settle in the groove of the DNA, add a specific promoter sequence, and change whether the genes get red or not.
00:09:58.720 --> 00:10:03.759
So a tripeptide is not feeding the cell absolutely anything, okay?
00:10:04.000 --> 00:10:07.919
It's basically just flipping the switches on the genome.
00:10:08.080 --> 00:10:14.799
So the natural one, the sigamere, that carries the full spectrum of regulatory peptides that you find in a young cartilage tissue.
00:10:14.879 --> 00:10:19.039
So it's more like handing the cell all of the signals related to this at once.
00:10:19.200 --> 00:10:19.519
Okay.
00:10:19.679 --> 00:10:22.159
Now, there's a 2023 study.
00:10:22.320 --> 00:10:26.720
Basically, look at how these shark peptides regulate the differentiation of stem cells.
00:10:26.879 --> 00:10:32.240
And they got specific on the chondrocyte pathway and the pathway that's producing this brand new cartilage-forming cells.
00:10:32.480 --> 00:10:35.840
So I think that that in particular detail is very important.
00:10:35.919 --> 00:10:36.240
Why?
00:10:36.399 --> 00:10:46.720
Because it means that these ultra-short peptides can actually influence not just the existing chondrocyte, but also the stem cell population that gives rights to new ones, right?
00:10:46.879 --> 00:10:54.799
So if you can push mesenchymal stem cells towards the chondrocyte lineage, you are potentially rebuilding workforce, right?
00:10:54.879 --> 00:10:58.559
You're not just trying to motivate guys who are already retired.
00:10:58.799 --> 00:11:02.399
Now, there's also a piece of evidence from a 2022 study.
00:11:02.639 --> 00:11:06.639
This one I found really interesting because it was an international collaboration.
00:11:06.799 --> 00:11:09.039
It was not just a Russian-only publication pattern.
00:11:09.200 --> 00:11:25.519
And if you want more details on all the studies that I cite in any of my videos here, just go to the engine, go to the uh deep dive section of the YouTube videos, and there's a deep fucking dive in there with all the research and all of the ideas broken down and everything that you need to do to apply this video to your life.
00:11:25.679 --> 00:11:33.440
So, in this 2022 study, they basically tested conluten on a human monocyte cells, and they basically hit an inflammatory stimulus.
00:11:33.600 --> 00:11:38.639
And what they found is that specifically this shutdown TNF production also dialed back the inflammatory cascade.
00:11:38.720 --> 00:11:43.279
Now, this was not tested in cartilage cells directly, it was tested in immune cells.
00:11:43.519 --> 00:11:44.960
Why is that still relevant?
00:11:45.120 --> 00:11:49.120
Because remember, the cartilage sits inside of a joint capsule, right?
00:11:49.200 --> 00:11:54.320
In the lining of that capsule, the synovium is where a lot of the joint inflammation actually comes from.
00:11:54.480 --> 00:12:01.120
So in an aging or an arthritic joint, the immune cells, they're going to infiltrate the synovium.
00:12:01.279 --> 00:12:05.919
And in there, they're going to dump a bunch of TNF and IL-6 onto the joint fluid.
00:12:06.000 --> 00:12:14.720
And because the cartilage is avascular and bathe in that fluid, whatever's floating in there just diffuses straight into the tissue and hits the chondrocytes.
00:12:14.879 --> 00:12:21.759
So if you can calm TNF signaling at the source, you're going to be cleaning up this exact environment that the chondrocytes are trying to work in, right?
00:12:21.840 --> 00:12:23.039
Because everything is connecting.
00:12:23.120 --> 00:12:25.679
And then there's a clinical application data.
00:12:25.919 --> 00:12:28.960
There's a study in older folks with temporomandibular joint disease.
00:12:29.039 --> 00:12:33.919
They found that basically adding sigomere into a treatment basically got rid of the pain very fast.
00:12:34.080 --> 00:12:38.559
So an increased mouth opening amplitude, which I know you're trying to work on, buddy.
00:12:38.720 --> 00:12:39.519
No judgment.
00:12:39.679 --> 00:12:44.000
Improved chewing function and also stopped the releases over the observation period.
00:12:44.159 --> 00:12:48.639
Now, sigomere was one piece of a multimodal treatment there.
00:12:48.720 --> 00:12:52.240
Okay, so you can't just isolate that contribution to that one study.
00:12:52.320 --> 00:13:00.399
But the pattern of clinical benefit in aging joint stacked on top of the cellularism data, I think you're starting to paint a pretty interesting picture.
00:13:00.559 --> 00:13:04.159
Now, I keep coming back to this point here about bioregulator space in general.
00:13:04.320 --> 00:13:07.759
In cartilage, I think it's one of the main examples of why this matters, right?
00:13:07.919 --> 00:13:12.399
With conventional joint supplements, you're basically working with the current state of the tissue.
00:13:12.559 --> 00:13:20.799
You're accepting that the chondrocytes are aging, that the SAS was active, that the MMPs are eating the matrix and the repair capacity is dropping, and you're trying to prop whatever function is left.
00:13:20.879 --> 00:13:22.720
So that's the management strategy, right?
00:13:22.960 --> 00:13:26.879
Management strategy, they're gonna help with symptoms, but they can't change the trajectory.
00:13:27.039 --> 00:13:31.679
So the joint keeps heading the same shitty fucking direction, just maybe a little bit slower.
00:13:31.840 --> 00:13:35.919
And the bioregulator approach is basically trying to be way more ambitious with this stuff.
00:13:36.080 --> 00:13:46.799
It's trying to restore the gene expression patterns in dose chondrocytes back towards a younger phenotype to reverse the SASP, to get Sertoans back up in the repair programs that depend on them running again.
00:13:46.960 --> 00:13:53.600
And and where it stands, the clinical evidence, human clinical evidence for that particular clean, it's still building.
00:13:53.679 --> 00:13:54.879
Okay, they're still working on it.
00:13:55.039 --> 00:13:57.679
The settler evidence and the animal evidence, 100%.
00:13:58.080 --> 00:14:05.600
The clinical observation from practice using these compounds lines up with the mechanism, but large-scale control trials just have not been done yet.
00:14:05.759 --> 00:14:15.440
Now, what I can tell you from working with clients who folded cartilage bioregulators into their protocols is that the pattern that I see is just very, very different from what I see in standard joint stacks.
00:14:15.519 --> 00:14:15.679
Okay.
00:14:15.840 --> 00:14:18.399
The timeline is different, the quality of the improvement is different.
00:14:18.480 --> 00:14:26.480
Instead of like the pain is a little bit less when I take this, it's more of like, yo, something just kind of changed in the way that my joint feels and moves.
00:14:26.720 --> 00:14:36.159
So that experimental line, that report, it does line up with what the mechanism would predict, which is just not just managing symptoms, you're potentially restoring cellular function.
00:14:36.320 --> 00:14:40.320
So I mentioned the uh 2023 study on chondrogenic cell differentiation.
00:14:40.480 --> 00:14:45.440
I think it's important to come back to that study because I think that's the most important piece on this whole puzzle.
00:14:45.600 --> 00:14:51.279
So your cells, they have the the your body has these mesenchymal cells.
00:14:51.519 --> 00:14:53.120
These are stem cells, okay?
00:14:53.360 --> 00:14:59.200
They're basically like blank slate cells that can turn into different tissue types depending on what signals they get.
00:14:59.360 --> 00:15:04.240
So some of them become bone cells, some have become fat cells, some of them become chondrocytes, the cartilage-forming cells.
00:15:04.320 --> 00:15:09.840
And then the pathway that turns into a stem cell into a chondrocyte is called chondrogenic differentiation.
00:15:09.919 --> 00:15:13.679
It's run by this cascade of signals that have to fire the right order at the right time.
00:15:13.759 --> 00:15:24.960
And there's a master switch there, SOX9, that basically commits the cell to the cardid lineage and then drives it to start cranking out collagen type 2 and as well as aggregate.
00:15:25.120 --> 00:15:30.320
So this isn't just a single gene, it is a whole program that has to boot up in the right order.
00:15:30.559 --> 00:15:38.240
Now, what the Linkova and the Cavinson research showed us is that specific short peptides can regulate the differentiation pathway.
00:15:38.399 --> 00:15:42.480
So they can influence whether a stem cell commits to the contract lineage in the first place.
00:15:42.639 --> 00:15:46.559
And that's fundamentally a different approach from joint repaired and anything else that's out there, right?
00:15:46.720 --> 00:15:50.000
You're not feeding existing cartilage cells more building blocks.
00:15:50.159 --> 00:15:53.919
You're not just quieting information around damaged tissue.
00:15:54.080 --> 00:16:08.159
Guys, you're potentially directing the stem cell pools to produce more cartilage-forming cells, replenishing the workforce at the source in a tissue that basically has no other way of bringing it into the cells because remember, it is avascular, nothing is arriving through the blood.
00:16:08.320 --> 00:16:10.320
So it's uh it's a pretty big deal, in my opinion.
00:16:10.480 --> 00:16:13.919
Now, from what I can gather from the data stuff, this is very much early, right?
00:16:14.000 --> 00:16:16.960
The study that uh establishes the mechanism does exist.
00:16:17.120 --> 00:16:22.559
The peptide-driven regulation of chondrocyte, uh, chondrogenesis is a real thing operating at a real molecular level.
00:16:22.639 --> 00:16:29.519
But but what it does, like does it translate directly into the clinical cartilage of a 45-year-old with a cranky knee, right?
00:16:29.759 --> 00:16:32.240
That's the gap between a lab and the real world, right?
00:16:32.320 --> 00:16:34.799
You can't say with the evidence that we are there.
00:16:35.039 --> 00:16:35.679
So I don't.
00:16:35.759 --> 00:16:42.320
But when it comes to personal experience and coaching people, guys, we need a database of this shit because I'm we literally see the results.
00:16:42.399 --> 00:16:42.559
No.
00:16:42.799 --> 00:16:49.679
What I find compelling here is just how consistent the mechanism is across the whole bioregulator space.
00:16:49.840 --> 00:16:55.039
So in every tissue that was studied, where the compounds have been studied, right, the pattern is always the same.
00:16:55.279 --> 00:17:01.120
You get short peptides that are interacting with gene regulatory regions to restore expression patterns towards a younger phenotype.
00:17:01.279 --> 00:17:08.400
And in the brain, in the thymus, in the vascular system, in the pancreas, and now in the cartilage and the joint tissue, it's the same mechanism that keeps showing up.
00:17:08.480 --> 00:17:23.359
It's not a different claim for each organ, it's the same biological principle applied to tissue by tissue and map consistency is what makes me take seriously about regulators instead of writing it off as woo-woo bullshit just because uh someone online who's a pretty big deal said that uh they don't do anything.
00:17:23.519 --> 00:17:26.559
Now, the training context matters here too, right?
00:17:26.640 --> 00:17:36.160
I want to bring this into something practical because I know that a lot of you guys watching, you guys are dealing with this joint stuff, and you're like, oh, okay, cool, like cellular senescence, stem cell differentiation, right?
00:17:36.240 --> 00:17:39.200
But what does this actually fucking mean for my knee, my man?
00:17:39.359 --> 00:17:40.720
So here's how I think about it.
00:17:41.119 --> 00:17:44.319
Okay, let's say let's say you're in your 20s, right?
00:17:44.400 --> 00:17:45.200
Your joints feel fine, right?
00:17:45.279 --> 00:17:50.160
Your chondrocyte population is probably just humming along, and uh your stem cell pool is still strong.
00:17:50.240 --> 00:17:52.480
And the standard approach is just keeping the joints loaded.
00:17:52.799 --> 00:17:57.680
Eat enough protein, eat enough collagen, manage inflammation, uh, get your omega-3s in place, right?
00:17:57.759 --> 00:17:59.839
It's probably just enough to keep your joint healthy.
00:17:59.920 --> 00:18:02.160
You don't need to go settler bananas yet.
00:18:02.319 --> 00:18:08.480
But if you're in your 30s, okay, and then you start noticing like, hey, my recovery from my heavy sessions just takes a little bit longer.
00:18:08.640 --> 00:18:11.839
It's it's kind of like it hurts, your joints hurt a little bit more every time I train, right?
00:18:12.000 --> 00:18:18.559
And maybe certain positions you start to feel a little bit stiffer and uh your stuff just cracks and pops like crazy, like more than it did five years ago.
00:18:18.720 --> 00:18:20.000
Those are all early signs, right?
00:18:20.079 --> 00:18:22.160
Your chondrocyte population is starting to shift.
00:18:22.319 --> 00:18:25.519
Some cells, they're going to be flipping into senescence, right?
00:18:25.599 --> 00:18:27.359
The repair capacity is dropping.
00:18:27.519 --> 00:18:32.799
And at this stage, being proactive about the cellular environment starts to actually matter for you.
00:18:33.039 --> 00:18:36.160
Now, let's say that you're in your 40s, let's say you're beyond your 40s, right?
00:18:36.240 --> 00:18:36.960
You're old as shit.
00:18:37.039 --> 00:18:37.759
I'm just kidding, guys.
00:18:37.920 --> 00:18:40.079
Uh, right, let's say you've been training hard for decades.
00:18:40.319 --> 00:18:45.039
That chondrocyte senescence is very likely, and sadly so, very well established.
00:18:45.359 --> 00:18:48.400
The SASP active, the MMP is chewing the matrix.
00:18:48.480 --> 00:18:53.680
The standard supplements are just dropping raw materials in front of the cells, but these cells don't do shit anymore.
00:18:53.839 --> 00:18:55.200
Okay, that's why it doesn't work.
00:18:55.359 --> 00:19:02.480
This is where the bioregulated approach starts to make the most sense because you're not just managing the downstream mess, you're also going after the upstream causes.
00:19:03.039 --> 00:19:04.880
I'm not saying this replaces anything, right?
00:19:04.960 --> 00:19:19.759
You still need to load your joints intelligent, you still need the raw materials, you still need to address inflammation, but adding a layer that actually addresses the cellular machinery itself, the gene expression patterns like driving cartilage maintenance, completely conversation, right?
00:19:19.839 --> 00:19:22.240
It's a conversation that almost nobody in our space is having.
00:19:22.400 --> 00:19:29.039
So the thing that genuinely drives me nuts about the joint health in our community is that everybody treats it as like it's inevitable.
00:19:29.200 --> 00:19:31.440
Oh, you're in your 40s, your joints are gonna hurt, right?
00:19:31.519 --> 00:19:32.559
Like that's just how it is.
00:19:32.799 --> 00:19:35.680
And sure, mechanical stress does pile up.
00:19:35.759 --> 00:19:36.240
That's true.
00:19:36.400 --> 00:19:51.599
Yeah, decades of loading are gonna create wear patterns, but the cellular aging component, the part where like your chondrocytes are actively shutting down their repair programs and then switching on the MMPs to eat your matrix, that is not an inevitable consequence of training.
00:19:51.680 --> 00:20:00.240
Okay, that's a biological process, and biological processes can be stimulated, they can be slowed and potentially maybe even reversed, okay?
00:20:00.400 --> 00:20:07.039
And the reason you don't hear about this in the entire like joint supplement industry is that that is built around raw materials and anti-inflammatories.
00:20:07.519 --> 00:20:15.440
There's no money to be made and like to to say, like, hey, the problem is not glucosamine, the problem is your cell stopped using glucosamine properly, right?
00:20:15.519 --> 00:20:19.440
That doesn't move a single cup of glucosamine, which is cheap off the shelf.
00:20:20.319 --> 00:20:24.319
But that's also a lot closer to the truth than what is actually going on in an aging joint.
00:20:24.480 --> 00:20:26.079
And it goes way past supplements.
00:20:26.240 --> 00:20:29.359
The medical side of things is not easier when it comes to this, okay?
00:20:29.440 --> 00:20:40.799
I don't know why I'm moving like right about like our orange man on the standard clinical approach to osteoarthritis in pain management and eventually like joint replacement, just NSA, right?
00:20:40.880 --> 00:20:45.759
Cortisone, uh cortisone injections, physical therapy, and then when the joint gets bad enough, it's just surgery.
00:20:45.920 --> 00:20:56.160
There's no treatment art, there's basically zero conversation in conventional orthopedics about what's happening at the chondrocyte level and why these repair cells they stop repairing and whether the process can be touched at all.
00:20:56.400 --> 00:21:06.480
The research is out there, the mechanism is published, it's right there, but it hasn't filtered into clinical practice because the whole treatment paradigm is still stuck in this manage and replace bullshit.
00:21:06.640 --> 00:21:16.240
The idea that you could restore cellular function instead of just waiting for the joint to degrade enough to justify cutting it out and bolting a fucking metal one, that's not even on the radar for most orthopedic surgeries.
00:21:16.480 --> 00:21:18.400
And that should piss you off too.
00:21:18.640 --> 00:21:31.359
Now, if you're someone who's dealing with joint degradation, okay, whether that's diagnosed with osteoarthritis or just the slow slide in joint quality that comes from years of training, here's the framework that I need from you, okay?
00:21:31.599 --> 00:21:34.000
The foundation is still in the basics.
00:21:34.160 --> 00:21:44.480
So adequate collagen take via pro via protein, omega-3 for systemic inflammation, training modifications that cut that peak joint stress, but keep you loading the stimulus and the cartilage that needs it.
00:21:44.640 --> 00:21:48.480
Because the thing is the cartilage needs loading to be squeezed to be healthy, right?
00:21:48.559 --> 00:21:55.440
Since a vascular, that squeeze and release of the joint under the load is literally how the nutrients get pumped and then the waste gets pushed out of the tissue.
00:21:55.599 --> 00:21:58.000
Uh so loaded right and you are feeding it.
00:21:58.160 --> 00:22:04.400
Load it wrong or not at all, you're kind of just be gonna be standing the chance of just uh shitting on it, right?
00:22:04.559 --> 00:22:06.400
So the type of loading also matters.
00:22:06.880 --> 00:22:09.839
I'm not telling you to throw out your join stack either.
00:22:10.000 --> 00:22:15.039
Now, what I'm telling you is that if the basics are not moving the needle, for a lot of people over 35, they're really not.
00:22:15.200 --> 00:22:18.799
And then at a cellular level, I think that's where you should look next, okay?
00:22:18.960 --> 00:22:20.799
Are your chondrocytes still working?
00:22:21.039 --> 00:22:22.559
Is the SASP still active?
00:22:22.720 --> 00:22:25.920
Is the repair machinery just running or has it gone kind of quiet?
00:22:26.000 --> 00:22:29.599
And if it's gone quiet, what tools do exist to potentially like wake it back up?
00:22:29.759 --> 00:22:36.799
And the bioregulator course that we put together inside of the Art Lab engine goes deeper than this in every single kind of decision tree that you can imagine.
00:22:36.960 --> 00:22:46.319
Every single organ, every single system that these compounds target, including the cartilage and the joints, it gets broken down by what's in the tissue level mechanism of aging in that system.
00:22:46.480 --> 00:22:49.599
What does the evidence actually show for the bioregulator compounds there?
00:22:49.759 --> 00:22:51.119
What are the dosing frameworks?
00:22:51.200 --> 00:22:52.240
What are the cycling patterns?
00:22:52.319 --> 00:22:55.440
And how do you layer the whole thing with everybody, everything else that we're taking?
00:22:55.599 --> 00:23:04.319
So I built this whole thing around how I think through these problems with clients, not just like a compound list, just telling you a bunch of shit about random compounds.
00:23:04.400 --> 00:23:05.920
I that's uh that's not how we go.
00:23:06.000 --> 00:23:11.599
And the course is live, and it's the it's definitely the most comprehensive bioregulator resource in the English language.
00:23:11.680 --> 00:23:20.559
And if you don't want to figure this out yourself, guys, the optimization lab is where the acceleration happens because look, I can look at your specific training history, your specific joint issues.
00:23:20.720 --> 00:23:28.720
What if you tried and then map out a protocol directly into your situation instead of you just having to just generalize more shit from a course module?
00:23:28.880 --> 00:23:42.799
So, some of the biggest breakthroughs that I've seen, it came from clients who've been managing their issues for years, and the standard cool toolkit just stopped working, and they had no fucking clue that there were other levers that could still be working and that could be pulled.
00:23:42.880 --> 00:23:50.480
Now, if you watch the thyroid video that I put out a few days ago, you already know how these biological systems they talk to each other in ways that most people don't expect, right?
00:23:50.640 --> 00:23:59.359
Thyroid function is going to affect tissue repair and regeneration everywhere, including cartilage, because T3 is going to be driving the metabolic machinery cells that are going to need to maintain themselves.
00:23:59.519 --> 00:24:04.559
And a chondrocyte is basically trying to rebuild a matrix, and that is running on that machinery like any other cell.
00:24:04.720 --> 00:24:09.039
It's not coincidence that hypothyroid people so often have joint issues.
00:24:09.200 --> 00:24:10.799
It's because the systems are wired together.
00:24:10.880 --> 00:24:13.839
So the full bioregulator course has dropped already.
00:24:13.920 --> 00:24:16.880
The Optolab engine is filled to the brain.
00:24:16.960 --> 00:24:20.000
We also have a new thyroid course, and uh, you guys should go check it out.
00:24:20.079 --> 00:24:21.359
And then that's it for this one.
00:24:21.440 --> 00:24:24.240
Go take care of your damn fucking joints, and uh, I'll catch you in the next video.
00:24:24.319 --> 00:24:24.960
Peace out, boo.
