Found a way to reopen growth plates (1 Viewer)

[DoorHandle5]

Abaloparatide for 3 weeks daily then hgh + AI

Explanation later in comments

 

[Biomaxx]

 

[Razi]

Nigga you ain’t in a TikTok video just explain

 

[bacland]

great job doorhandle5

 

[Dexter]

Explanation later in comments

 

[tyalak09128]

Abaloparatide for 3 weeks daily then hgh + AI

Explanation later in comments

Tales

 

[4psl]

So u gonna explain or not

 

[nineteen]

View attachment 40432

this made my day

 

[goyboy.hero]

Abaloparatide for 3 weeks daily then hgh + AI

Explanation later in comments

Ig bro

 

[DoorHandle5]

Nigga you ain’t in a TikTok video just explain

Alright big booty fakhr al din chill out

 

[DoorHandle5]

So u gonna explain or not

Yes one sec.

Dexter brother can you copy paste what we spoke about? The text I sent you first.

 

[Razi]

fakhr al din

 

[DoorHandle5]

View attachment 40432

Tales

So u gonna explain or not

proof that the stem cell niche remains. in all the images, stem cells are stained red, and in the bottom row of images, osteoblasts are stained green. you can see the line of scrimmage



once the osteoblast invasion of the proliferating zone (with the columnar chondrocytes) has come and passed, the stem cells are now subject to the whims of the osteoblasts forever after



fortunately, this new structure is heavily perfused, with plenty of vessels, meaning that systemic peptide administration will see peptide leaking into the stem cell niche



what's fascinating, and indeed, optimism inducing, is that the chondroprogenitors (stem cells that constitute the resting zone of a functional growth plate) develop the ability to self-replenish only postnatally. prior (fetal & neonatal), these cells constitute a reservoir that is otherwise depleted.



in a murine model, it only takes 14 days postnatally for these stem cells to reach peak concentrations in the growth plate



the theory is that you inject the abaloparstide for a few weeks to revive the growth plates, then you stop and start injecting hgh to grow + AI to keep the plates open



in the immature growth plate, angiogenesis only features towards the bottom of the apparatus in conjunction with osteogenic influences, like osteoblasts. obviously, maturation of the growth involves this region encroaching further and further up the plate with the aid of estrogen, crunching the proliferating & prehypertrophic zones until the resting zone becomes adjacent to the line of scrimmage



these blood vessels grapevining about the stem cell niche in our matured growth plates will ensure that systemically-injected abaloparatide will get its opportunity to impart impact



and do not doubt how plastic the growth plate can be; the concept of plasticity is useful, even if misapplied in heightmaxxing communities. a growth plate dissected and reimplanted in rabbit bones quickly re-establishes itself and functions normally. even when the growth plate is implanted in a perpendicular manner, it still operates as it would (albeit adding cells along the width as opposed length of the bone, but that's besides the point).



studies have even shown that "cartilaginous islands," otherwise known as "ectopic" cartilage, can be generated when stem cells are exposed to SOX9 or even hedgehog molecules



this tells me that the growth plate can be resuscitated with affairs are orchestrated correctly

 

[DoorHandle5]

good feedback, but it's not a matter of conflating dev bio with anything, rlly. the premise is that PTHrP (abaloparatide) will specifically inhibit osteogenic pressures while promoting chondrogenic pressures. this is what gives those stem cells the potential to develop into the columnar chondrocytes that can divide longitudinally to develop a new proliferating zone.

these stem cells operate based on the factors they're exposed to by their immediate environment most prominently. the reason why these stem cells do not behave like they once did postnatally is because they're now surrounded not by cartilage, but by bone. accordingly, they're exposed to osteogenic differentiation factors as opposed chondrogenic, and that's what ensures that any "activated" stem cells differentiate into osteoblasts rather than the chondrocytes that could then assemble into columns.

that written, there's a plethora of research done examining what transpires when SOX, PTHrP, and SMO agonists (or other Hedgehog pathway activators or enhancers) are applied to the growth plates of animal models, and from these studies, we can paint a picture of how plastic and flexible the system is, and how readily progenitors in the resting zone (mesenchymal stem cells) operate to generate chondrocytes if given the right circumstances. hell, in rabbits, they've even studied dissection of the growth plate and aberrant reinsertion (perpendicular to the original direction) and found that the growth plate would add length along the width of the bone. it demonstrates that the stem cells in the resting zone are polarized, and they will generate columns even if oriented in aberrant directions. they've studied constitutive Hedgehog activation (constantly active Hedgehog signaling) in murine models, done via PTCH1 knockout, and found that cartilaginous "islands" (ectopic cartilage) can be produced off the resting zone's chondroprogenitors. these studies elucidate that influencers like PTHrP, SOX, and even Hedgehog molecules can whip up a proliferative response dedicated to endochrondral ossification in theory. the trick is now seeing if we can harness that in vivo, which is admittedly extremely challenging to do! I will never take away from how difficult this is when local application of these agents is not possible. that is the crux of the problem to me. give me a way to ensure that the stem cell niche is constantly and specifically inundated with PTHrP & SOX proteins, and I will be much more optimistic. currently, no recourse therein. systemic circulation is the only hope

 

[PrettyBoyMaxxing]

View attachment 40583
proof that the stem cell niche remains. in all the images, stem cells are stained red, and in the bottom row of images, osteoblasts are stained green. you can see the line of scrimmage



once the osteoblast invasion of the proliferating zone (with the columnar chondrocytes) has come and passed, the stem cells are now subject to the whims of the osteoblasts forever after



fortunately, this new structure is heavily perfused, with plenty of vessels, meaning that systemic peptide administration will see peptide leaking into the stem cell niche



what's fascinating, and indeed, optimism inducing, is that the chondroprogenitors (stem cells that constitute the resting zone of a functional growth plate) develop the ability to self-replenish only postnatally. prior (fetal & neonatal), these cells constitute a reservoir that is otherwise depleted.



in a murine model, it only takes 14 days postnatally for these stem cells to reach peak concentrations in the growth plate



the theory is that you inject the abaloparstide for a few weeks to revive the growth plates, then you stop and start injecting hgh to grow + AI to keep the plates open



in the immature growth plate, angiogenesis only features towards the bottom of the apparatus in conjunction with osteogenic influences, like osteoblasts. obviously, maturation of the growth involves this region encroaching further and further up the plate with the aid of estrogen, crunching the proliferating & prehypertrophic zones until the resting zone becomes adjacent to the line of scrimmage



these blood vessels grapevining about the stem cell niche in our matured growth plates will ensure that systemically-injected abaloparatide will get its opportunity to impart impact



and do not doubt how plastic the growth plate can be; the concept of plasticity is useful, even if misapplied in heightmaxxing communities. a growth plate dissected and reimplanted in rabbit bones quickly re-establishes itself and functions normally. even when the growth plate is implanted in a perpendicular manner, it still operates as it would (albeit adding cells along the width as opposed length of the bone, but that's besides the point).



studies have even shown that "cartilaginous islands," otherwise known as "ectopic" cartilage, can be generated when stem cells are exposed to SOX9 or even hedgehog molecules



this tells me that the growth plate can be resuscitated with affairs are orchestrated correctly

Mouse growth plates do not fuse the way human growth plates do. They simply slow down drastically but retain a resting zone of cartilage well into adulthood.

the the niche no longer exists in adults.

as for abalo, PTHrP does keep chondrocytes in a proliferative state however, if you inject abalo systemically into someone with closed plates, it does not bring cartilage stem cells out of solid bone. it only binds on receptor bringing density. This is literally why abalo is prescribed to postmenopausal women to treat osteoporosis.

next, say you could forcefully induce ectopic cartilage (cartilage growing where it shouldn't), it wouldn't specifically be for the legs, you'd grow random lumps of cartilage in your joints and organ just for no gains (best case scenario) . Haha you could also trigger cancer, proliferation pathways are EXACTLY the same.

You will only gain palumboism and ir from gh

this is such a meme

 

[Hexum]

GOOD explanation gng i believe u

 

[PrettyBoyMaxxing]

the the niche no longer exists in adults.

*the niche no longer exists

 

[Hexum]

good feedback, but it's not a matter of conflating dev bio with anything, rlly. the premise is that PTHrP (abaloparatide) will specifically inhibit osteogenic pressures while promoting chondrogenic pressures. this is what gives those stem cells the potential to develop into the columnar chondrocytes that can divide longitudinally to develop a new proliferating zone.

these stem cells operate based on the factors they're exposed to by their immediate environment most prominently. the reason why these stem cells do not behave like they once did postnatally is because they're now surrounded not by cartilage, but by bone. accordingly, they're exposed to osteogenic differentiation factors as opposed chondrogenic, and that's what ensures that any "activated" stem cells differentiate into osteoblasts rather than the chondrocytes that could then assemble into columns.

that written, there's a plethora of research done examining what transpires when SOX, PTHrP, and SMO agonists (or other Hedgehog pathway activators or enhancers) are applied to the growth plates of animal models, and from these studies, we can paint a picture of how plastic and flexible the system is, and how readily progenitors in the resting zone (mesenchymal stem cells) operate to generate chondrocytes if given the right circumstances. hell, in rabbits, they've even studied dissection of the growth plate and aberrant reinsertion (perpendicular to the original direction) and found that the growth plate would add length along the width of the bone. it demonstrates that the stem cells in the resting zone are polarized, and they will generate columns even if oriented in aberrant directions. they've studied constitutive Hedgehog activation (constantly active Hedgehog signaling) in murine models, done via PTCH1 knockout, and found that cartilaginous "islands" (ectopic cartilage) can be produced off the resting zone's chondroprogenitors. these studies elucidate that influencers like PTHrP, SOX, and even Hedgehog molecules can whip up a proliferative response dedicated to endochrondral ossification in theory. the trick is now seeing if we can harness that in vivo, which is admittedly extremely challenging to do! I will never take away from how difficult this is when local application of these agents is not possible. that is the crux of the problem to me. give me a way to ensure that the stem cell niche is constantly and specifically inundated with PTHrP & SOX proteins, and I will be much more optimistic. currently, no recourse therein. systemic circulation is the only hope

make this a separate thread brah

 

[Hexum]

why would u post the explanation in the replys

 

[FatRetard]

Tales

 

[PrettyBoyMaxxing]

GOOD explanation gng i believe u

it's useless information

 

[Hexum]

it's useless information

IK just posting anything to get to the 700

 

[slogxER]

IK just posting anything to get to the 700

Like me?

 

[slogxER]

Say Wallahi bro that’s gonna make me 6’3

 

[Dexter]

proof that the stem cell niche remains. in all the images, stem cells are stained red, and in the bottom row of images, osteoblasts are stained green. you can see the line of scrimmage

you're assuming the stem cell niche remains viable post fusion. but once the growth plate fuses the resting zone is literally obliterated. the primary spongiosa anastomoses w epiphyseal vessels, replacing cartilage with bone marrow and trabecular bone. there are no residual chondroprogenitors left to revive in a fused GP.

in a murine model, it only takes 14 days postnatally for these stem cells to reach peak concentrations in the growth plate

growth plates in mice dont fuse the same way they do in humans. mice literally lack estrogen induced terminal fusion in long bones; their growth plates remain open throughout life but growth slows. the peak conc. at 14 days prolly refers to the establishment of the functional postnatal niche and not a reversible state. you cant use mice data for human related conclusions.

the theory is that you inject the abaloparstide for a few weeks to revive the growth plates, then you stop and start injecting hgh to grow + AI to keep the plates open

in the fused growth plate there is no proliferative zone to maintain. PTHrP works on prehypertrophic chondrocytes and resting zone progenitors that are still alive. once ur plates are fused, systemic administration of abaloparatide doesnt create a new proliferative zone ex nihilo in bone marrow

it increases bone turnover which in the case of fused plates would thicken the metaphyseal bone or maybe cause hyperostosis but not longitudinal growth

and do not doubt how plastic the growth plate can be; the concept of plasticity is useful, even if misapplied in heightmaxxing communities. a growth plate dissected and reimplanted in rabbit bones quickly re-establishes itself and functions normally. even when the growth plate is implanted in a perpendicular manner, it still operates as it would (albeit adding cells along the width as opposed length of the bone, but that's besides the point).



studies have even shown that "cartilaginous islands," otherwise known as "ectopic" cartilage, can be generated when stem cells are exposed to SOX9 or even hedgehog molecules

as far as i know, the rabbit reimplantation studies involve taking an intact living growth plate from a juvenile animal and surgically reimplanting it into the host. this basically shows the intrinsic polarity of the tissue and not the regeneration of a plate that has already undergone fusion

constitutive hedgehog activation (SMO agonists or PTCH1 knockout does induce cartilaginous islands, yes, but these are benign chondroid lesions or osteochondromas (Gorlin syndrome/PTCH1 mutations)) and not functional polarized growth plates capable of coordinated longitudinal growth. inducing these in a human leg would cause pathological bony deformities and not controlled height increase

that is the crux of the problem to me. give me a way to ensure that the stem cell niche is constantly and specifically inundated with PTHrP & SOX proteins, and I will be much more optimistic. currently, no recourse therein. systemic circulation is the only hope

even if the niche did still exist, systemic abaloparatide would affect every bone, every suture and every synovial joint simultaneously. in clinical trials PTH analogs cause systemic bone growth (acroosteolysis, widening of bones, hypercalcemia) when dosed continuously. theres no mechanism to confine the effect to the femoral/tibial growth plates while avoiding craniofacial abnormalities or pathological calcification of soft tissues

even if one could achieve perfect spatial specificity (like via locally implanted pumps or viral vectors) the fused growth plate lacks the requisite cellular substrate (a polarized resting zone with viable and uncommitted chondroprogenitors arranged in a stratified niche). local delivery of PTHrP and SOX9 to a fused epiphyseal line would, at best, induce disorganized fibrocartilage or osteophyte formation and not a functional growth plate. i think you can clearly see what the problem is bro.

what's fascinating, and indeed, optimism inducing, is that the chondroprogenitors (stem cells that constitute the resting zone of a functional growth plate) develop the ability to self-replenish only postnatally. prior (fetal & neonatal), these cells constitute a reservoir that is otherwise depleted.

the transition from a fetal "depleting" reservoir to a postnatal "muh self replenishing" pool kinda shows the establishment of a niche architecture (the formation of a structured resting zone w PTHrP gradient and hedgehog signaling feedback loops) but it doesnt imply that once depleted in adulthood the capacity for self renewal can be pharmacologically reinstated. the postnatal acquisition of self renewal is a one way developmental milestone and not a latent property that can be reactivated after the physical dissolution of the niche itself

 

[DoorHandle5]

Mouse growth plates do not fuse the way human growth plates do. They simply slow down drastically but retain a resting zone of cartilage well into adulthood.

the the niche no longer exists in adults.

as for abalo, PTHrP does keep chondrocytes in a proliferative state however, if you inject abalo systemically into someone with closed plates, it does not bring cartilage stem cells out of solid bone. it only binds on receptor bringing density. This is literally why abalo is prescribed to postmenopausal women to treat osteoporosis.

next, say you could forcefully induce ectopic cartilage (cartilage growing where it shouldn't), it wouldn't specifically be for the legs, you'd grow random lumps of cartilage in your joints and organ just for no gains (best case scenario) . Haha you could also trigger cancer, proliferation pathways are EXACTLY the same.

You will only gain palumboism and ir from gh

this is such a meme

you're assuming the stem cell niche remains viable post fusion. but once the growth plate fuses the resting zone is literally obliterated. the primary spongiosa anastomoses w epiphyseal vessels, replacing cartilage with bone marrow and trabecular bone. there are no residual chondroprogenitors left to revive in a fused GP.

growth plates in mice dont fuse the same way they do in humans. mice literally lack estrogen induced terminal fusion in long bones; their growth plates remain open throughout life but growth slows. the peak conc. at 14 days prolly refers to the establishment of the functional postnatal niche and not a reversible state. you cant use mice data for human related conclusions.

in the fused growth plate there is no proliferative zone to maintain. PTHrP works on prehypertrophic chondrocytes and resting zone progenitors that are still alive. once ur plates are fused, systemic administration of abaloparatide doesnt create a new proliferative zone ex nihilo in bone marrow

it increases bone turnover which in the case of fused plates would thicken the metaphyseal bone or maybe cause hyperostosis but not longitudinal growth

as far as i know, the rabbit reimplantation studies involve taking an intact living growth plate from a juvenile animal and surgically reimplanting it into the host. this basically shows the intrinsic polarity of the tissue and not the regeneration of a plate that has already undergone fusion

constitutive hedgehog activation (SMO agonists or PTCH1 knockout does induce cartilaginous islands, yes, but these are benign chondroid lesions or osteochondromas (Gorlin syndrome/PTCH1 mutations)) and not functional polarized growth plates capable of coordinated longitudinal growth. inducing these in a human leg would cause pathological bony deformities and not controlled height increase

even if the niche did still exist, systemic abaloparatide would affect every bone, every suture and every synovial joint simultaneously. in clinical trials PTH analogs cause systemic bone growth (acroosteolysis, widening of bones, hypercalcemia) when dosed continuously. theres no mechanism to confine the effect to the femoral/tibial growth plates while avoiding craniofacial abnormalities or pathological calcification of soft tissues

even if one could achieve perfect spatial specificity (like via locally implanted pumps or viral vectors) the fused growth plate lacks the requisite cellular substrate (a polarized resting zone with viable and uncommitted chondroprogenitors arranged in a stratified niche). local delivery of PTHrP and SOX9 to a fused epiphyseal line would, at best, induce disorganized fibrocartilage or osteophyte formation and not a functional growth plate. i think you can clearly see what the problem is bro.

the transition from a fetal "depleting" reservoir to a postnatal "muh self replenishing" pool kinda shows the establishment of a niche architecture (the formation of a structured resting zone w PTHrP gradient and hedgehog signaling feedback loops) but it doesnt imply that once depleted in adulthood the capacity for self renewal can be pharmacologically reinstated. the postnatal acquisition of self renewal is a one way developmental milestone and not a latent property that can be reactivated after the physical dissolution of the niche itself

I find that I have no retort.

 

[Dexter]

I find that I have no retort.

top 10 sentences of all time

 

[DoorHandle5]

View attachment 40432

 

[DoorHandle5]

Dexter PrettyBoyMaxxing

For the proliferating zone, I sent this to my boy cuz I have no retort honestly, he said this:







the proliferating zone, once resuscitated, will build a gap between the osteoblasts and the resting zone's stem cells. once the gap is created by these columnar chondrocytes stacking one atop the other, the PTHrP gradient will naturally become great enough that prehypertrophic and hypertrophic zones can develop. these zones develop organically without the need for us to act. the key is the proliferating zone. if that is resuscitated, all bets are off. the gradients that are vital develop naturally by virtue of spacing. hormones need to be managed (AI's), but the zones themselves will otherwise provide the signals they all need to maintain themselves.



that written, there's a plethora of research done examining what transpires when SOX, PTHrP, and SMO agonists (or other Hedgehog pathway activators or enhancers) are applied to the growth plates of animal models, and from these studies, we can paint a picture of how plastic and flexible the system is, and how readily progenitors in the resting zone (mesenchymal stem cells) operate to generate chondrocytes if given the right circumstances. hell, in rabbits, they've even studied dissection of the growth plate and aberrant reinsertion (perpendicular to the original direction) and found that the growth plate would add length along the width of the bone. it demonstrates that the stem cells in the resting zone are polarized, and they will generate columns even if oriented in aberrant directions. they've studied constitutive Hedgehog activation (constantly active Hedgehog signaling) in murine models, done via PTCH1 knockout, and found that cartilaginous "islands" (ectopic cartilage) can be produced off the resting zone's chondroprogenitors. these studies elucidate that influencers like PTHrP, SOX, and even Hedgehog molecules can whip up a proliferative response dedicated to endochrondral ossification in theory. the trick is now seeing if we can harness that in vivo, which is admittedly extremely challenging to do! I will never take away from how difficult this is when local application of these agents is not possible. that is the crux of the problem to me. give me a way to ensure that the stem cell niche is constantly and specifically inundated with PTHrP & SOX proteins, and I will be much more optimistic. currently, no recourse therein. systemic circulation is the only hope.



I’m trying to recreate resting & proliferating zones. That’s the fundamental mission, and if there are remnant stem cells present, enough stimulation with PTHrP & SOX could potentially inhibit osteogenic pressures and induce the chondrogenesis necessary to recreate a proliferating zone that can build space between the resting zone and the osteoblast-containing front.



if I'm not mistaken, I think there might actually be research currently ongoing in which the researchers are seeking to cause transdifferentiation (from osteoblast to chondrocyte) of the cells of the fused epiphysis. my fixation is on a parallel strategy that focuses instead on multipotent stem cells that may already be present. these cells obviously have the potential to differentiate chondrogenically if inundated with the right factors.



the premise is that a sliver of cartilage would need to be generated first. this will be the resting zone. if that resting zone can survive with continuous PTHrP & SOX pressure, the proliferating zone ensues. with continuing chondrogenic pressure, the proliferating zone expands enough to buy the resting zone enough of a buffer to no longer require the inundation of PTHrP & SOX proteins. at this point, exogenous PTHrP supply is abrogated, and a natural PTHrP gradient develops that allows for prehypertrophic and hypertrophic zones to develop distal to the resting zone.



and just to reiterate becuz we seem to continuously come circling back to the fact that a functional growth plate has prehypertrophic and hypertrophic zones, as well as the proliferating & resting zones that I've chosen to fixate on. the point is that these former zones will develop organically once PTHrP provision is ceased because of the AMPLE osteogenic pressure provided by the cells of the trabecular bone below the growth plate. PTHrP & SOX generated by chondroprogenitors of the resting zone will not diffuse far enough away from the resting zone, and the consequent gradient will allow for chondrocyte hypertrophy to begin. there's no need for us to manipulate anything to facilitate the development of prehypertrophic and hypertrophic zones; the bone will ensure that that happens, anyway.



the bone WILL NOT allow for a proliferating zone to develop sans heavy SOX pressure, though. that is the part we have to play God on. hence, inundation with abaloparatide that can induce SOX activity. this ensures MSC renewal (PTHrP) and chondrogenesis at the expense of osteogenesis (SOX)

 

[PrettyBoyMaxxing]

Dexter PrettyBoyMaxxing

For the proliferating zone, I sent this to my boy cuz I have no retort honestly, he said this:







the proliferating zone, once resuscitated, will build a gap between the osteoblasts and the resting zone's stem cells. once the gap is created by these columnar chondrocytes stacking one atop the other, the PTHrP gradient will naturally become great enough that prehypertrophic and hypertrophic zones can develop. these zones develop organically without the need for us to act. the key is the proliferating zone. if that is resuscitated, all bets are off. the gradients that are vital develop naturally by virtue of spacing. hormones need to be managed (AI's), but the zones themselves will otherwise provide the signals they all need to maintain themselves.



that written, there's a plethora of research done examining what transpires when SOX, PTHrP, and SMO agonists (or other Hedgehog pathway activators or enhancers) are applied to the growth plates of animal models, and from these studies, we can paint a picture of how plastic and flexible the system is, and how readily progenitors in the resting zone (mesenchymal stem cells) operate to generate chondrocytes if given the right circumstances. hell, in rabbits, they've even studied dissection of the growth plate and aberrant reinsertion (perpendicular to the original direction) and found that the growth plate would add length along the width of the bone. it demonstrates that the stem cells in the resting zone are polarized, and they will generate columns even if oriented in aberrant directions. they've studied constitutive Hedgehog activation (constantly active Hedgehog signaling) in murine models, done via PTCH1 knockout, and found that cartilaginous "islands" (ectopic cartilage) can be produced off the resting zone's chondroprogenitors. these studies elucidate that influencers like PTHrP, SOX, and even Hedgehog molecules can whip up a proliferative response dedicated to endochrondral ossification in theory. the trick is now seeing if we can harness that in vivo, which is admittedly extremely challenging to do! I will never take away from how difficult this is when local application of these agents is not possible. that is the crux of the problem to me. give me a way to ensure that the stem cell niche is constantly and specifically inundated with PTHrP & SOX proteins, and I will be much more optimistic. currently, no recourse therein. systemic circulation is the only hope.



I’m trying to recreate resting & proliferating zones. That’s the fundamental mission, and if there are remnant stem cells present, enough stimulation with PTHrP & SOX could potentially inhibit osteogenic pressures and induce the chondrogenesis necessary to recreate a proliferating zone that can build space between the resting zone and the osteoblast-containing front.



if I'm not mistaken, I think there might actually be research currently ongoing in which the researchers are seeking to cause transdifferentiation (from osteoblast to chondrocyte) of the cells of the fused epiphysis. my fixation is on a parallel strategy that focuses instead on multipotent stem cells that may already be present. these cells obviously have the potential to differentiate chondrogenically if inundated with the right factors.



the premise is that a sliver of cartilage would need to be generated first. this will be the resting zone. if that resting zone can survive with continuous PTHrP & SOX pressure, the proliferating zone ensues. with continuing chondrogenic pressure, the proliferating zone expands enough to buy the resting zone enough of a buffer to no longer require the inundation of PTHrP & SOX proteins. at this point, exogenous PTHrP supply is abrogated, and a natural PTHrP gradient develops that allows for prehypertrophic and hypertrophic zones to develop distal to the resting zone.



and just to reiterate becuz we seem to continuously come circling back to the fact that a functional growth plate has prehypertrophic and hypertrophic zones, as well as the proliferating & resting zones that I've chosen to fixate on. the point is that these former zones will develop organically once PTHrP provision is ceased because of the AMPLE osteogenic pressure provided by the cells of the trabecular bone below the growth plate. PTHrP & SOX generated by chondroprogenitors of the resting zone will not diffuse far enough away from the resting zone, and the consequent gradient will allow for chondrocyte hypertrophy to begin. there's no need for us to manipulate anything to facilitate the development of prehypertrophic and hypertrophic zones; the bone will ensure that that happens, anyway.



the bone WILL NOT allow for a proliferating zone to develop sans heavy SOX pressure, though. that is the part we have to play God on. hence, inundation with abaloparatide that can induce SOX activity. this ensures MSC renewal (PTHrP) and chondrogenesis at the expense of osteogenesis (SOX)

If the stem cell niche remains and can be 'resuscitated' so easily with existing drugs like abalo, why hasn't a single person with dwarfism or a growth hormone deficiency ever grown taller after fusion using this method in a clinical setting?

further more, why would you bring someone else into the claim you've made? you made the statement therefore you and you alone should be replying.

 

[DoorHandle5]

If the stem cell niche remains and can be 'resuscitated' so easily with existing drugs like abalo, why hasn't a single person with dwarfism or a growth hormone deficiency ever grown taller after fusion using this method in a clinical setting?

Because they haven’t used this method. Or they weren’t measuring for it. That’s a fallacy

further more, why would you bring someone else into the claim you've made? you made the statement therefore you and you alone should be replying.

because this is a JOINT theory, actually I’m not even the one who created it. The creator shared it with me first and we talked about it back and forth, and he gave me permission to share it with you guys. What’s wrong with that? Furthermore, who said that I’m the only one who should be replying? What makes that true? What objective moral framework said that this must be the case?

 

[Judenbänker]

If the stem cell niche remains and can be 'resuscitated' so easily with existing drugs like abalo, why hasn't a single person with dwarfism or a growth hormone deficiency ever grown taller after fusion using this method in a clinical setting?

Reasonable question

further more, why would you bring someone else into the claim you've made? you made the statement therefore you and you alone should be replying

Unreasonable bs because burden of proof does not need the person who proves to be the same as the one making the claim

 

[DoorHandle5]

Reasonable question

One that I just answered right now above

Unreasonable bs because burden of proof does not need the person who proves to be the same as the one making the claim

thank you. And I explained this further up.

 

[DoorHandle5]

Anyway it doesn’t matter who said what. Just focus on the theory. You don’t see all trying to improve here

 

[Judenbänker]

One that I just answered right now above

thank you. And I explained this further up.

Yeah while you sent that i was still typing and didnt see

My internet so bad rn it didnt even show me theres new replies jfl

 

[PrettyBoyMaxxing]

Because they haven’t used this method. Or they weren’t measuring for it. That’s a fallacy

This is objectively false. There are decades of clinical trials for PTH analogs, If these drugs "accidentally" reopened growth plates in adults, it would be a massive medical scandal but yeah lets just assume ooooo because nobody has used this specific cocktail of compounds, the entire medical community is missing it.

If the chondrocyte is dead, the method will never matter.

because this is a JOINT theory, actually I’m not even the one who created it. The creator shared it with me first and we talked about it back and forth, and he gave me permission to share it with you guys. What’s wrong with that? Furthermore, who said that I’m the only one who should be replying? What makes that true? What objective moral framework said that this must be the case?

We don't need a moral framework. Even if you have a 'joint theory,' the theory fails because it ignores terminal differentiation. In human adults, the DNA in those specific MSCs is methylated, you can't inundate a cell with SOX9 if its chromatin is closed to that signal.

Reasonable question

Unreasonable bs because burden of proof does not need the person who proves to be the same as the one making the claim

I don't recall asking for your opinion.

Synapse since when were forum users this retarded? never knew it was this bad.

 

[Judenbänker]

I don't recall asking for your opinion.

real sigma alpha male we got here

 

[Synapse]

This is objectively false. There are decades of clinical trials for PTH analogs, If these drugs "accidentally" reopened growth plates in adults, it would be a massive medical scandal but yeah lets just assume ooooo because nobody has used this specific cocktail of compounds, the entire medical community is missing it.

If the chondrocyte is dead, the method will never matter.

We don't need a moral framework. Even if you have a 'joint theory,' the theory fails because it ignores terminal differentiation. In human adults, the DNA in those specific MSCs is methylated, you can't inundate a cell with SOX9 if its chromatin is closed to that signal.


I don't recall asking for your opinion.

Synapse since when were forum users this retarded? never knew it was this bad.

That's the problem when people use extrapolated animal study data and try to apply it to humans ignoring the several biology differences between species, thats why extrapolating data is such a problem.

 

[Telmisartan]

Abaloparatide for 3 weeks daily then hgh + AI

Explanation later in comments

Yes g just open them again nice one

 

[PrettyBoyMaxxing]

That's the problem when people use extrapolated animal study data and try to apply it with humans ignoring the several biology differences between species, thats why extrapolating data is such a problem.

motherfuckers will look at you with a straight face telling you "yes bro I read studies on this trust me" without even being able to apply it, gets me laughing everytime, esp the so called heightmaxxers

 

[Synapse]

This is objectively false. There are decades of clinical trials for PTH analogs, If these drugs "accidentally" reopened growth plates in adults, it would be a massive medical scandal but yeah lets just assume ooooo because nobody has used this specific cocktail of compounds, the entire medical community is missing it.

If the chondrocyte is dead, the method will never matter.

We don't need a moral framework. Even if you have a 'joint theory,' the theory fails because it ignores terminal differentiation. In human adults, the DNA in those specific MSCs is methylated, you can't inundate a cell with SOX9 if its chromatin is closed to that signal.


I don't recall asking for your opinion.

Synapse since when were forum users this retarded? never knew it was this bad.

Read the replies of you and dexter, you guys are totally right, this is just wishful thinking at its finest.

 

[Synapse]

motherfuckers will look at you with a straight face telling you "yes bro I read studies on this trust me" without even being able to apply it, gets me laughing everytime, esp the so called heightmaxxers

yeah even my older thread fails at doing so, now i doubt really hard height is even remotely changeable even with all the pharma intervention possible, its all just tales and theory. I used to believe it was possible but i really hadn't done proper research.

 

[PrettyBoyMaxxing]

Read the replies of you and dexter, you guys are totally right, this is just wishful thinking at its finest.

that's what I Initially thought but it was pretty clear he was using some form of ai (dexter)

 

[Synapse]

that's what I Initially thought but it was pretty clear he was using some form of ai (dexter)
View attachment 40597

wow.

 

[PrettyBoyMaxxing]

yeah even my older thread fails at doing so, now i doubt really hard height is even remotely changeable even with all the pharma intervention possible, its all just tales and theory. I just to believe it was possible but i really hadn't done proper research.

took me a while to realize that as well, just at about 2022

 

[Telmisartan]

that's what I Initially thought but it was pretty clear he was using some form of ai (dexter)
View attachment 40597

Imagine dnring a nigga so hard u blindly copy their reply and ask chatgpt to respond

 

[Synapse]

took me a while to realize that as well, just at about 2022

yuh, im gonna revamp it but im just gonna label it as "theory", the LL guide will stay tho.

 

[Synapse]

Imagine dnring a nigga so hard u blindly copy their reply and ask chatgpt to respond

ngl i kinda get him, not even worth putting that much effort into debunking something that stupid.

 

[DoorHandle5]

This is objectively false. There are decades of clinical trials for PTH analogs, If these drugs "accidentally" reopened growth plates in adults, it would be a massive medical scandal but yeah lets just assume ooooo because nobody has used this specific cocktail of compounds, the entire medical community is missing it.

That’s just a fallacy. Simply put they aren’t measuring for GP opening so they won’t see it. Plus this specific theory was not put into place

We don't need a moral framework

you do if ur gonna say I should be the only one replying

 

[DoorHandle5]

Read the replies of you and dexter, you guys are totally right, this is just wishful thinking at its finest.

ngl i kinda get him, not even worth putting that much effort into debunking something that stupid.

You call it stupid yet you provided no logical counterpoint. Ur the only stupid one