Theory Heightmaxx Post Puberty (1 Viewer)

[virtuous1]

Credits to this: https://************/threads/height-growth-post-puberty-possible-shortcels-gtfih.1833342/

Height Growth as an Adult?

Once your growth plates are closed, most people think it's over unless you get LL Surgery. I may have found a way to elongate the bones, without endochondral ossification (growth plate growth).

Now we know banded sleeping works for spinal decompression and gives 1-2 inches over months, however this effect fades away over a few months when you decide to stop. I think this can possibly be turned to real permanent height. Most people don't know but bones have plasticity,they are able to bend and compress without breaking (ex. people with rickets). They can go through deformation.

Now there are two types of deformation,
- elastic deformation
- plastic deformation

Elastic is temporary (bone springs back into original shape). Plastic, however, is permanent, the bone stays in the state its deformed in. In theory, it is possible to permanently elongate bone through carefully applied, sustained axial tension. If a long bone is subjected to tension above its yield point but below the fracture threshold, it can plastically deform.

With induced microfractures in bone combined with banded sleeping, it could gradually lengthen by along that axis. Plastic deformation in this way is irreversible, and once the bone remodels under these new mechanical stresses, it could retain the longer shape as the material adapts to reinforce its structure along the new orientation. This principle is analogous to the surgical procedure of distraction osteogenesis, otherwise known as limb lengthening surgery, except that here it relies purely on mechanical stress instead of osteotomy to creating a physical gap.


Applying this concept to banded sleeping, the idea is that by stretching the bone during sleep WITH induced microfractures could induce sustained axial tension along the spine, femur, and tibia gradually stretching the vertebrae, intervertebral discs, and bone over months. In theory, if this tension were maintained consistently and precisely, the bones could undergo plastic deformation, while the discs adapt to the stress, potentially increasing end-to-end length. Over time, this process could create a permanent increase in stature, as the reinforced bones retain their new elongated geometry via osteogenesis.

I estimate this to cause 5-12mm per year of elongation (0.2-0.5in). It may not seem like much, but over a long period of time (ex. 10 years) it could give 37-92mm (1.5-3.6in) And that not accounting for the fast temporary spinal decompression gains of 1-2 inches in the first 3-6 months.

It may seem ridiculous and difficult but if you're a shortcel I wouldn't complain.

(just a bullshit theory, but I want to try to perform an experiment on myself to see if its really possible)

 

[Judenbänker]

dnr

 

[virtuous1]

read + repped

Thanks!

 

[SinisterTRADition]

 

[FS51]

Credits to this: https://************/threads/height-growth-post-puberty-possible-shortcels-gtfih.1833342/

Height Growth as an Adult?

Once your growth plates are closed, most people think it's over unless you get LL Surgery. I may have found a way to elongate the bones, without endochondral ossification (growth plate growth).

Now we know banded sleeping works for spinal decompression and gives 1-2 inches over months, however this effect fades away over a few months when you decide to stop. I think this can possibly be turned to real permanent height. Most people don't know but bones have plasticity,they are able to bend and compress without breaking (ex. people with rickets). They can go through deformation.

Now there are two types of deformation,
- elastic deformation
- plastic deformation

Elastic is temporary (bone springs back into original shape). Plastic, however, is permanent, the bone stays in the state its deformed in. In theory, it is possible to permanently elongate bone through carefully applied, sustained axial tension. If a long bone is subjected to tension above its yield point but below the fracture threshold, it can plastically deform.

With induced microfractures in bone combined with banded sleeping, it could gradually lengthen by along that axis. Plastic deformation in this way is irreversible, and once the bone remodels under these new mechanical stresses, it could retain the longer shape as the material adapts to reinforce its structure along the new orientation. This principle is analogous to the surgical procedure of distraction osteogenesis, otherwise known as limb lengthening surgery, except that here it relies purely on mechanical stress instead of osteotomy to creating a physical gap.


Applying this concept to banded sleeping, the idea is that by stretching the bone during sleep WITH induced microfractures could induce sustained axial tension along the spine, femur, and tibia gradually stretching the vertebrae, intervertebral discs, and bone over months. In theory, if this tension were maintained consistently and precisely, the bones could undergo plastic deformation, while the discs adapt to the stress, potentially increasing end-to-end length. Over time, this process could create a permanent increase in stature, as the reinforced bones retain their new elongated geometry via osteogenesis.

I estimate this to cause 5-12mm per year of elongation (0.2-0.5in). It may not seem like much, but over a long period of time (ex. 10 years) it could give 37-92mm (1.5-3.6in) And that not accounting for the fast temporary spinal decompression gains of 1-2 inches in the first 3-6 months.

It may seem ridiculous and difficult but if you're a shortcel I wouldn't complain.

(just a bullshit theory, but I want to try to perform an experiment on myself to see if its really possible)

Maybe

 

[Judenbänker]

Thanks!

Epic.

Just for that I will read and rep

 

[virtuous1]

Yay!

 

[Judenbänker]

How would you want to get those microfractures? As its unnatural growth you would need to manually select all the right bones no? Im not so educated on there

 

[virtuous1]

Nobody here wants to grow

 

[virtuous1]

Nobody :(

 

[virtuous1]

Credits to this: https://************/threads/height-growth-post-puberty-possible-shortcels-gtfih.1833342/

Height Growth as an Adult?

Once your growth plates are closed, most people think it's over unless you get LL Surgery. I may have found a way to elongate the bones, without endochondral ossification (growth plate growth).

Now we know banded sleeping works for spinal decompression and gives 1-2 inches over months, however this effect fades away over a few months when you decide to stop. I think this can possibly be turned to real permanent height. Most people don't know but bones have plasticity,they are able to bend and compress without breaking (ex. people with rickets). They can go through deformation.

Now there are two types of deformation,
- elastic deformation
- plastic deformation

Elastic is temporary (bone springs back into original shape). Plastic, however, is permanent, the bone stays in the state its deformed in. In theory, it is possible to permanently elongate bone through carefully applied, sustained axial tension. If a long bone is subjected to tension above its yield point but below the fracture threshold, it can plastically deform.

With induced microfractures in bone combined with banded sleeping, it could gradually lengthen by along that axis. Plastic deformation in this way is irreversible, and once the bone remodels under these new mechanical stresses, it could retain the longer shape as the material adapts to reinforce its structure along the new orientation. This principle is analogous to the surgical procedure of distraction osteogenesis, otherwise known as limb lengthening surgery, except that here it relies purely on mechanical stress instead of osteotomy to creating a physical gap.


Applying this concept to banded sleeping, the idea is that by stretching the bone during sleep WITH induced microfractures could induce sustained axial tension along the spine, femur, and tibia gradually stretching the vertebrae, intervertebral discs, and bone over months. In theory, if this tension were maintained consistently and precisely, the bones could undergo plastic deformation, while the discs adapt to the stress, potentially increasing end-to-end length. Over time, this process could create a permanent increase in stature, as the reinforced bones retain their new elongated geometry via osteogenesis.

I estimate this to cause 5-12mm per year of elongation (0.2-0.5in). It may not seem like much, but over a long period of time (ex. 10 years) it could give 37-92mm (1.5-3.6in) And that not accounting for the fast temporary spinal decompression gains of 1-2 inches in the first 3-6 months.

It may seem ridiculous and difficult but if you're a shortcel I wouldn't complain.

(just a bullshit theory, but I want to try to perform an experiment on myself to see if its really possible)

Bump

 

[birthdefect]

Credits to this: https://************/threads/height-growth-post-puberty-possible-shortcels-gtfih.1833342/

Height Growth as an Adult?

Once your growth plates are closed, most people think it's over unless you get LL Surgery. I may have found a way to elongate the bones, without endochondral ossification (growth plate growth).

Now we know banded sleeping works for spinal decompression and gives 1-2 inches over months, however this effect fades away over a few months when you decide to stop. I think this can possibly be turned to real permanent height. Most people don't know but bones have plasticity,they are able to bend and compress without breaking (ex. people with rickets). They can go through deformation.

Now there are two types of deformation,
- elastic deformation
- plastic deformation

Elastic is temporary (bone springs back into original shape). Plastic, however, is permanent, the bone stays in the state its deformed in. In theory, it is possible to permanently elongate bone through carefully applied, sustained axial tension. If a long bone is subjected to tension above its yield point but below the fracture threshold, it can plastically deform.

With induced microfractures in bone combined with banded sleeping, it could gradually lengthen by along that axis. Plastic deformation in this way is irreversible, and once the bone remodels under these new mechanical stresses, it could retain the longer shape as the material adapts to reinforce its structure along the new orientation. This principle is analogous to the surgical procedure of distraction osteogenesis, otherwise known as limb lengthening surgery, except that here it relies purely on mechanical stress instead of osteotomy to creating a physical gap.


Applying this concept to banded sleeping, the idea is that by stretching the bone during sleep WITH induced microfractures could induce sustained axial tension along the spine, femur, and tibia gradually stretching the vertebrae, intervertebral discs, and bone over months. In theory, if this tension were maintained consistently and precisely, the bones could undergo plastic deformation, while the discs adapt to the stress, potentially increasing end-to-end length. Over time, this process could create a permanent increase in stature, as the reinforced bones retain their new elongated geometry via osteogenesis.

I estimate this to cause 5-12mm per year of elongation (0.2-0.5in). It may not seem like much, but over a long period of time (ex. 10 years) it could give 37-92mm (1.5-3.6in) And that not accounting for the fast temporary spinal decompression gains of 1-2 inches in the first 3-6 months.

It may seem ridiculous and difficult but if you're a shortcel I wouldn't complain.

(just a bullshit theory, but I want to try to perform an experiment on myself to see if its really possible)

how much force would you need to actually cause plastic deformation
i feel like that level of force would surely cause damage to soft tissue
perhaps if this worked it would be help to upregulate bone remodelling, with intermittent periods of potent bone modelling

 

[Dexter]

In theory, it is possible to permanently elongate bone through carefully applied, sustained axial tension. If a long bone is subjected to tension above its yield point but below the fracture threshold, it can plastically deform.

barely accurate for the isolated biomechanical principle in a lab setting. not even close to being accurate for it's proposed application in vivo.

in controlled in vitro experiments a fresh bone can be plastically deformed. but, in in vivo this isn't controllable. applying tension over its yield point means you're micro damaging the bone. body's response would be a pain induced muscular spasm to stop the stress, then there'd be an inflammatory healing response to repair the fuck up not elongate the bone.

With induced microfractures in bone combined with banded sleeping, it could gradually lengthen

"induced microfractures" are literally injuries. body's response would be to strengthen the area by remodeling and not by elongating it for whatever reason. this concept fundamentally misunderstands osteogenesis. actual lengthening would require distraction osteogenesis + slow and controlled distraction in a stable frame which allows callus to form.

This principle is analogous to the surgical procedure of distraction osteogenesis, otherwise known as limb lengthening surgery, except that here it relies purely on mechanical stress instead of osteotomy

the osteotomy in LL is a literal surgical requirement to proceed. it creates a low strain gap in a stabilized bone segment. that in itself will make the body fill the gap with callus. you're applying tension to an intact and micro fractured bone which will only promote fibrous scar tissue formation instead of organized bone griwth (this is malunion)

Applying this concept to banded sleeping, the idea is that by stretching the bone during sleep WITH induced microfractures could induce sustained axial tension along the spine, femur, and tibia gradually stretching the vertebrae, intervertebral discs, and bone over months. In theory, if this tension were maintained consistently and precisely, the bones could undergo plastic deformation

for spine: nighttime banded sleeping can decompress the discs and you'll gain 1-3cm in the morning. but this is an elastic deformation of discs and not a plastic one of bone. it reverses within hours or even minutes of staying upright. never permanent.
for tibia/femur: simply impossible. there is no biomechanical rule that allows to apply meaningful axial tensile load to the long bones will cause growth. the. body's wight and the mattress provide compressive force and not tension. 0/100 for accuracy here.

Over time, this process could create a permanent increase in stature, as the reinforced bones retain their new elongated geometry via osteogenesis.

again, completely misunderstanding bone physiology. the "reinforced bones" you're referring to aren't longer but thicker and stronger

I estimate this to cause 5-12mm per year of elongation (0.2-0.5in). It may not seem like much, but over a long period of time (ex. 10 years) it could give 37-92mm (1.5-3.6in) And that not accounting for the fast temporary spinal decompression gains of 1-2 inches in the first 3-6 months.

not true. these are a speculative extrapolation from a flawed premise. even if it were true, 0.35in averaged per year is nothing, and no one is doing this for 10 years lmao.

 

[virtuous1]

induced microfractures" are literally injuries. body's response would be to strengthen the area by remodeling and not by elongating it for whatever reason. this concept fundamentally misunderstands osteogenesis. actual lengthening would require distraction osteogenesis + slow and controlled distraction in a stable frame which allows callus to form.

Another thing I’d like to add is microfractures are localized and asymmetrical. You can’t lengthen an entire structure with only microcracks, not only are they too small, but what about the surrounding healed/normal area? It’s like trying to expand or lengthen a tree long but making a few cracks on it. I fully agree that if we look at it from the perspective of microfractures then it’s a BS method.

Although I do want to dive more into plastic deformation and understand how this method is still not possible after the fact?

 

[NorthAfricanRopemaxxer]

Another thing I’d like to add is microfractures are localized and asymmetrical. You can’t lengthen an entire structure with only microcracks, not only are they too small, but what about the surrounding healed/normal area? It’s like trying to expand or lengthen a tree long but making a few cracks on it. I fully agree that if we look at it from the perspective of microfractures then it’s a BS method.

Although I do want to dive more into plastic deformation and understand how this method is still not possible after the fact?

Water

 

[virtuous1]

barely accurate for the isolated biomechanical principle in a lab setting. not even close to being accurate for it's proposed application in vivo.

in controlled in vitro experiments a fresh bone can be plastically deformed. but, in in vivo this isn't controllable. applying tension over its yield point means you're micro damaging the bone. body's response would be a pain induced muscular spasm to stop the stress, then there'd be an inflammatory healing response to repair the fuck up not elongate the bone.

"induced microfractures" are literally injuries. body's response would be to strengthen the area by remodeling and not by elongating it for whatever reason. this concept fundamentally misunderstands osteogenesis. actual lengthening would require distraction osteogenesis + slow and controlled distraction in a stable frame which allows callus to form.

the osteotomy in LL is a literal surgical requirement to proceed. it creates a low strain gap in a stabilized bone segment. that in itself will make the body fill the gap with callus. you're applying tension to an intact and micro fractured bone which will only promote fibrous scar tissue formation instead of organized bone griwth (this is malunion)

for spine: nighttime banded sleeping can decompress the discs and you'll gain 1-3cm in the morning. but this is an elastic deformation of discs and not a plastic one of bone. it reverses within hours or even minutes of staying upright. never permanent.
for tibia/femur: simply impossible. there is no biomechanical rule that allows to apply meaningful axial tensile load to the long bones will cause growth. the. body's wight and the mattress provide compressive force and not tension. 0/100 for accuracy here.

again, completely misunderstanding bone physiology. the "reinforced bones" you're referring to aren't longer but thicker and stronger


not true. these are a speculative extrapolation from a flawed premise. even if it were true, 0.35in averaged per year is nothing, and no one is doing this for 10 years lmao.

So ur saying that weakening the bone via exercise and then stretching over night won’t take advantage of the bone’s plasticity and stretch the bone?

 

[virtuous1]

So ur saying that weakening the bone via exercise and then stretching over night won’t take advantage of the bone’s plasticity and stretch the bone?

Dexter

 

[virtuous1]

in controlled in vitro experiments a fresh bone can be plastically deformed. but, in in vivo this isn't controllable. applying tension over its yield point means you're micro damaging the bone. body's response would be a pain induced muscular spasm to stop the stress, then there'd be an inflammatory healing response to repair the fuck up not elongate the bone.

To be fair, you’re merely positing this and didn’t actually prove why this is not a possibility.

 

[darkie+]

Credits to this: https://************/threads/height-growth-post-puberty-possible-shortcels-gtfih.1833342/

Height Growth as an Adult?

Once your growth plates are closed, most people think it's over unless you get LL Surgery. I may have found a way to elongate the bones, without endochondral ossification (growth plate growth).

Now we know banded sleeping works for spinal decompression and gives 1-2 inches over months, however this effect fades away over a few months when you decide to stop. I think this can possibly be turned to real permanent height. Most people don't know but bones have plasticity,they are able to bend and compress without breaking (ex. people with rickets). They can go through deformation.

Now there are two types of deformation,
- elastic deformation
- plastic deformation

Elastic is temporary (bone springs back into original shape). Plastic, however, is permanent, the bone stays in the state its deformed in. In theory, it is possible to permanently elongate bone through carefully applied, sustained axial tension. If a long bone is subjected to tension above its yield point but below the fracture threshold, it can plastically deform.

With induced microfractures in bone combined with banded sleeping, it could gradually lengthen by along that axis. Plastic deformation in this way is irreversible, and once the bone remodels under these new mechanical stresses, it could retain the longer shape as the material adapts to reinforce its structure along the new orientation. This principle is analogous to the surgical procedure of distraction osteogenesis, otherwise known as limb lengthening surgery, except that here it relies purely on mechanical stress instead of osteotomy to creating a physical gap.


Applying this concept to banded sleeping, the idea is that by stretching the bone during sleep WITH induced microfractures could induce sustained axial tension along the spine, femur, and tibia gradually stretching the vertebrae, intervertebral discs, and bone over months. In theory, if this tension were maintained consistently and precisely, the bones could undergo plastic deformation, while the discs adapt to the stress, potentially increasing end-to-end length. Over time, this process could create a permanent increase in stature, as the reinforced bones retain their new elongated geometry via osteogenesis.

I estimate this to cause 5-12mm per year of elongation (0.2-0.5in). It may not seem like much, but over a long period of time (ex. 10 years) it could give 37-92mm (1.5-3.6in) And that not accounting for the fast temporary spinal decompression gains of 1-2 inches in the first 3-6 months.

It may seem ridiculous and difficult but if you're a shortcel I wouldn't complain.

(just a bullshit theory, but I want to try to perform an experiment on myself to see if its really possible)

if u want a test subject just find someone suicidal on a forum and tell them their death doeant have to go to waste

 

[Dexter]

Although I do want to dive more into plastic deformation and understand how this method is still not possible after the fact?

plastic deformation is a constitutive material and not a biologically permissible adaptation in living bone. the moment cortical or trabecular bone approaches it's yield strain in vivo the body classifies it as structural damage instead of remodeling stimulus. osteocytes are mechanosensors and respond to supraphysiologic strain by starting targeted remodeling aimed at RESTORING PRE INJURY GEOMETRY, no preserving the deformation.
empirically, adult cortical bone yield strain is 0.75-0.89% (if i recall correctly) and fracture occurs at like 1.7% or something. there is no physiological window where sustained strain above yield strain can be applied again n again without triggering nociception, reflexive muscle contraction, inflammatory signaling and osteoclastic resorption followed by osteoblastic infill. this converges back to the original length, but, if i recall correctly, with higher cross sectional moment of inertia (thicker/stiffer bone)
and an important point is that plastic deformation observed in ex vivo bone samples is only possible because neural pain signaling is absent, muscular guarding is absent, cellular remodeling pathways are inactive.

once bone is living, plastic deformation can't accumulate longitudinally because remodeling enforces geometric homeostasis. this is why no longitudinal elongation of intact adult bones has ever been documented outside distraction osteogenesis (LL) or some pathological deformity

So ur saying that weakening the bone via exercise and then stretching over night won’t take advantage of the bone’s plasticity and stretch the bone?

correct. and the reason is that fatigue induced micro damage and axial elongation are governed by OPPOSITE physiological mechanisms.

exercise induced "weakening" of bone produces diffuse microcracks (45-100 micrometer, iirc.) that activate targeted remodeling units. these cracks are spatially random, non collinear and discontinuous. the biological response is osteoclastic resorption followed by osteoblastic deposition that restores original length and alignment while increasing mineral density and cortical thickness. this is a protective adaptation.

intact long bones don't experience any useful axial tensile load during sleep. using whatever retarded distraction frame you have in mind would result in termination by pain mediated muscle contraction before yield strain is reached

why distraction osteogenesis succeeds and your idea fails because an osteotomy creates a low strain interfragmentary gap, mechanical fixation prevents collapse, controlled distraction of 1mm/day maintains strain within osteogenic window (2-10% iirc), bone forms by intramembranous ossification within the gap not by deformation of intact cortex. sorry son, but stretching an intact and fatigued bone doesn't place it into an osteogenic stretch regime. there's only an injury-repair loop and its outcome is reinforcement and not axial elongation.


i hope you learned something from this free bio class

 

[virtuous1]

plastic deformation is a constitutive material and not a biologically permissible adaptation in living bone. the moment cortical or trabecular bone approaches it's yield strain in vivo the body classifies it as structural damage instead of remodeling stimulus.

Okay you state that the body sees this as damage instead of remodeling. Yet when the bone experiences damage, does it not remodel itself (heal) to become even stronger? Why doesn’t this count as remodeling then?

structural damage instead of remodeling stimulus. osteocytes are mechanosensors and respond to supraphysiologic strain by starting targeted remodeling aimed at RESTORING PRE INJURY GEOMETRY, no preserving the deformation.

okay, so you’re saying basically only saying that when remodeling does occur it only happens as a mechanism to restore it to its original size, not alter the actual geometry (size,length, etc). Again; this is an assertion without substantiation. You claim this yet studies effectively show that size does increase. I’ll admit no study shows an increase in length, this is why it’s a theory. But so far you haven’t actually refuted said theory.

and fracture occurs at like 1.7% or something. there is no physiological window where sustained strain above yield strain can be applied again n again without triggering nociception, reflexive muscle contraction, inflammatory signaling and osteoclastic resorption followed by osteoblastic infill. this converges back to the original length, but, if i recall correctly, with higher cross sectional moment of inertia (thicker/stiffer bone)
and an important point is that plastic deformation observed in ex vivo bone samples is only possible because neural pain signaling is absent, muscular guarding is absent, cellular remodeling pathways are inactive.

This is interesting and I’ll admit could be a flaw in the theory. But now what if we keep it below the yield point?

once bone is living, plastic deformation can't accumulate longitudinally because remodeling enforces geometric homeostasis. this is why no longitudinal elongation of intact adult bones has ever been documented outside distraction osteogenesis (LL) or some pathological deformity

I 100% agree that no empirical evidence exists.

exercise induced "weakening" of bone produces diffuse microcracks (45-100 micrometer, iirc.) that activate targeted remodeling units. these cracks are spatially random, non collinear and discontinuous. the biological response is osteoclastic resorption followed by osteoblastic deposition that restores original length and alignment while increasing mineral density and cortical thickness. this is a protective adaptation.

Im glad we agree on this at least. I do remember some dude trying to refute my claim on the localization of microfractures by stating that microfractures occur along the axis of tension, I don’t see how that’s a valid rebuttal in his case though.

intact long bones don't experience any useful axial tensile load during sleep. using whatever retarded distraction frame you have in mind would result in termination by pain mediated muscle contraction before yield strain is reached

id like to dig a little deeper in this point. You said the yield strain or whatever would be counteracted by the muscle contractions. I don’t really understand the correlation between the two however.

i hope you learned something from this free bio class

i did actually and im very glad we can have this conversation! Are you a doctor/medical student by any chance? I admit you are far more educated than me on this topic

 

[virtuous1]

plastic deformation is a constitutive material and not a biologically permissible adaptation in living bone. the moment cortical or trabecular bone approaches it's yield strain in vivo the body classifies it as structural damage instead of remodeling stimulus. osteocytes are mechanosensors and respond to supraphysiologic strain by starting targeted remodeling aimed at RESTORING PRE INJURY GEOMETRY, no preserving the deformation.
empirically, adult cortical bone yield strain is 0.75-0.89% (if i recall correctly) and fracture occurs at like 1.7% or something. there is no physiological window where sustained strain above yield strain can be applied again n again without triggering nociception, reflexive muscle contraction, inflammatory signaling and osteoclastic resorption followed by osteoblastic infill. this converges back to the original length, but, if i recall correctly, with higher cross sectional moment of inertia (thicker/stiffer bone)
and an important point is that plastic deformation observed in ex vivo bone samples is only possible because neural pain signaling is absent, muscular guarding is absent, cellular remodeling pathways are inactive.

once bone is living, plastic deformation can't accumulate longitudinally because remodeling enforces geometric homeostasis. this is why no longitudinal elongation of intact adult bones has ever been documented outside distraction osteogenesis (LL) or some pathological deformity


correct. and the reason is that fatigue induced micro damage and axial elongation are governed by OPPOSITE physiological mechanisms.

exercise induced "weakening" of bone produces diffuse microcracks (45-100 micrometer, iirc.) that activate targeted remodeling units. these cracks are spatially random, non collinear and discontinuous. the biological response is osteoclastic resorption followed by osteoblastic deposition that restores original length and alignment while increasing mineral density and cortical thickness. this is a protective adaptation.

intact long bones don't experience any useful axial tensile load during sleep. using whatever retarded distraction frame you have in mind would result in termination by pain mediated muscle contraction before yield strain is reached

why distraction osteogenesis succeeds and your idea fails because an osteotomy creates a low strain interfragmentary gap, mechanical fixation prevents collapse, controlled distraction of 1mm/day maintains strain within osteogenic window (2-10% iirc), bone forms by intramembranous ossification within the gap not by deformation of intact cortex. sorry son, but stretching an intact and fatigued bone doesn't place it into an osteogenic stretch regime. there's only an injury-repair loop and its outcome is reinforcement and not axial elongation.


i hope you learned something from this free bio class

I think overall I might concede on this point, you seem far more well versed on this. Although I do want to touch upon another subject that is similar albeit different to this method.

 

[Dexter]

Okay you state that the body sees this as damage instead of remodeling. Yet when the bone experiences damage, does it not remodel itself (heal) to become even stronger? Why doesn’t this count as remodeling then?
okay, so you’re saying basically only saying that when remodeling does occur it only happens as a mechanism to restore it to its original size, not alter the actual geometry (size,length, etc). Again; this is an assertion without substantiation. You claim this yet studies effectively show that size does increase. I’ll admit no study shows an increase in length, this is why it’s a theory. But so far you haven’t actually refuted said theory.

yes bone remodels after damage and often becomes stronger but the strengthening occurs via increase in mineral density, cortical thickening and altered trabecular orientation and not via axial elongation.
osteocyte mediated remodeling is constrained by geometric homeostasis, remodeling units operate locally and restore baseline length and alignment and any increase in "size" documented in studies refers to CSA, moment of inertia or volumetric BMD and not length
this is why wolff’s law and frost’s mechanostat predict radial hypertrophy under load and not longitudinal growth. longitudinal growth is biologically restricted to endochondral ossification at growth plates which are absent in adults

Are you a doctor/medical student by any chance? I admit you are far more educated than me on this topic

no. not yet, atleast. im only 16, still learning.

 

[virtuous1]

yes bone remodels after damage and often becomes stronger but the strengthening occurs via increase in mineral density, cortical thickening and altered trabecular orientation and not via axial elongation.
osteocyte mediated remodeling is constrained by geometric homeostasis, remodeling units operate locally and restore baseline length and alignment and any increase in "size" documented in studies refers to CSA, moment of inertia or volumetric BMD and not length
this is why wolff’s law and frost’s mechanostat predict radial hypertrophy under load and not longitudinal growth. longitudinal growth is biologically restricted to endochondral ossification at growth plates which are absent in adults

Makes sense. So in the end remodeling only adds what was already there and not any more additional volume. So but no amounts of stretching and bone weakening whatsoever will take advantage of the bone plasticity and stretch them? I know bone isn’t exactly silly putty but they do have plasticity, which I suppose that’s what the theory hinged on; just stretching the bone little by little and over time it being effected. But if this was the case then bone would get much shorter over the years due to compression from gravity + standing. So even if my theory was true, I suppose the gravity + body force would fuck all the banded sleeping up.

What do you think about this:

im only 16, s

Damn. Incel at 16 already tho tbf that’s when I started to

 

[Dexter]

Makes sense. So in the end remodeling only adds what was already there and not any more additional volume. So but no amounts of stretching and bone weakening whatsoever will take advantage of the bone plasticity and stretch them? I know bone isn’t exactly silly putty but they do have plasticity, which I suppose that’s what the theory hinged on; just stretching the bone little by little and over time it being effected. But if this was the case then bone would get much shorter over the years due to compression from gravity + standing. So even if my theory was true, I suppose the gravity + body force would fuck all the banded sleeping up.

What do you think about this:

View attachment 27685




Damn. Incel at 16 already tho tbf that’s when I started to

adult vertebrae are connected by intervertebral discs, facet joints, longitudinal ligaments (ALL, PLL) and paraspinal musculature. whenn you stretch the spine, what increases is disc height via hydration, vertebral bodies do not separate and there is no interosseous gap
a spinal traction on MRI/CT would show transient disc expansion and no change in vertebral body length
if vertebrae did separate enough, it'd be classified as spinal instability or ligamentous failure
A "gap" caused by traction has no fracture signaling, no angiogenic response, no periosteal activation, no callus template
so even if a microscopic gap existed (it doesn’t), bone would not form across it
LIPUS and vibration platforms increase healing rate, increase bone density and enhance callus maturation and do not initiate bone formation in intact bone
if hormones did anything, acromegalycels would be 8 feet tall.