BIG NEWS FOR SHORTCELS First Official Heightmaxxing Research Just Came Out

[monecel]

Dogshit, obviously AI generated then put through a processor to make it detection resistant absolute water dnr

 

[Corpuscula]

this is not water wtf, its like opposite,not in a good way

there is just so many things wrong and the only things that could theoritically work there would barely yield any result if not none

 

[shredded4summer]

there is just so many things wrong and the only things that could theoritically work there would barely yield any result if not none

):

 

[shredded4summer]

BUMP

 

[Corpuscula]

put into AI checker.. smart doesnt equal chatgpt

View attachment 3532105

 

[Corpuscula]

JFL the idiots that fell for this. sorry

end it all

 

[LoveAllRaces]

BUMP, BOTB WORTHY

 

[shredded4summer]

REP farming has never been easier

 

[shredded4summer]

BUMP, BOTB WORTHY

 

[shredded4summer]

end it all

let a man have fun

 

[sluttysuzy420]

Somatic Elongation & Epiphyseal Reactivation: A Multi-Pathway Approach to Skeletal Maximization​

Height augmentation is not merely a function of growth plate availability—it is an intricate process dictated by endocrine synchronization, mechanotransductive osteogenic stimulation, and epiphyseal chondrocyte hyperproliferation. By leveraging exogenous peptide therapy, neuroendocrine recalibration, and biomechanical axial decompression, one can transcend the genetic limitations imposed by physeal senescence and reinitiate longitudinal osteogenesis post-adolescence.

View attachment 3532047

Phase 1: Growth Plate Reanimation via Senolytic Chondrocyte Induction​

Traditional height-maxxing protocols falter due to the epiphyseal plate's ossification post-puberty. To counteract this, we employ a targeted senolytic approach to selectively purge senescent chondrocytes, thereby reactivating dormant proliferative zones. This involves:
View attachment 3532048

Dasatinib (5 mg EOD) + Quercetin (500 mg ED): Eliminates senescent mesenchymal progenitor cells, restoring the extracellular matrix's pro-chondrogenic microenvironment.
Fisetin (500 mg biweekly): Induces autophagic recycling of calcified chondrocytes, allowing the deposition of newly proliferative chondrogenic clusters.
Rapamycin (1 mg every 3rd day): Inhibits mTORC1, shifting cellular energy allocation from hypertrophic calcification to chondrocyte self-renewal.

Phase 2: Peptidergic Growth Axis Amplification​

To initiate longitudinal osteogenesis, the body's endogenous IGF-1 & GH axis must be maximized while simultaneously inhibiting premature fibrocartilaginous ossification. This is achieved through rhythmic peptide cycling to manipulate somatic growth cascades.

View attachment 3532050
GHRH Analog + Ghrelin Mimetic: Administered pre-sleep in alternating pulses to induce ultradian growth hormone surges, simulating the endocrine profile of a prepubescent adolescent.
PEG-MGF (Mechano-Growth Factor): Injected directly into tibial periosteum, promoting localized osteoblastic hyperplasia and inhibiting epiphyseal fibrosis.
Thymosin Beta-4: Facilitates angiogenesis within the growth plate, optimizing nutrient diffusion rates to sustain chondrocyte proliferation longevity.
Liraglutide (GLP-1 Agonist): Enhances insulin-mediated IGF-1 secretion, biasing the body's anabolic state toward skeletal elongation rather than muscular hypertrophy.

Phase 3: Biomechanical Axial Tension & Epiphyseal Decompression​

To maximize osteogenic elongation, targeted tensile loading of the axial skeleton is required to mechanotransduce osteoblastic signaling pathways. The goal is to induce a continuous low-grade microfracture cycle, allowing for incremental periosteal apposition.

View attachment 3532051
Inverted Decompression Therapy (30 min daily at -45°): Encourages vertebral hydration expansion while reducing axial compression, enhancing the fluid permeability of the intervertebral discs.
Tibial Mechanical Stretching Device (1 mm daily elongation): Uses a modified Ilizarov external fixator, creating a controlled distraction osteogenesis effect without requiring surgical corticotomy.
Pulse Electromagnetic Field (PEMF) Therapy: Directs osteogenic differentiation through targeted electrical stimulation of osteoprogenitor cells, increasing collagen matrix deposition at the physeal junctions.
Low-Intensity Vibration Plate (35 Hz, 0.4 g acceleration): Enhances mesenchymal stem cell chondrogenesis, facilitating the deposition of epiphyseal cartilage layers essential for sustained bone elongation.

Phase 4: Circadian Hormonal Synchronization for Nocturnal Elongation​

Peak skeletal growth occurs during deep sleep, where GH surges coincide with bone remodeling cycles.


Melatonin + GABA Microdosing (3 mg + 500 mg, 30 min pre-sleep): Prolongs deep-wave sleep stages, increasing GH release duration.
Nandrolone Phenylpropionate (50 mg biweekly): Unlike testosterone, NPP exhibits preferential binding to osteoblast androgen receptors, promoting skeletal matrix deposition without premature physeal closure.
GH Secretagogue: Maintains a steady-state GH elevation, preventing overnight catabolic cortisol spikes that would otherwise inhibit longitudinal growth factor activity.
Sodium Butyrate: Epigenetically enhances RUNX2 transcription, biasing stem cell differentiation toward osteogenic lineages rather than adipogenesis.
View attachment 3532052

Phase 5: Extracellular Matrix Expansion & Soft Tissue Adaptation​

As skeletal elongation progresses, soft tissue structures must adapt proportionally to prevent postural imbalances.


Hyaluronic Acid Loading (1,500 mg ED): Expands interfibrillar hydration, increasing ligament extensibility to accommodate increased skeletal length.
GHK-Cu Peptide Application: Enhances collagen fibril cross-linking, preventing ligamentous laxity post-elongation.
Pentosan Polysulfate Sodium (PPS): Stimulates glycosaminoglycan synthesis, reinforcing joint integrity as new growth occurs.
View attachment 3532054

Conclusion: The Path to Transcendental Statural Augmentation​

By orchestrating a multidimensional interplay of peptide signaling, biomechanical elongation, and senolytic epiphyseal reactivation, one can bypass the conventional limitations of post-pubertal growth cessation. The result is a meticulously engineered statural transformation, allowing for unprecedented longitudinal skeletal hypertrophy beyond the constraints of genetic predetermination.

View attachment 3532056

read through briefly this can all work in thory but wont thigns like PEG MGF cant actually stimuate the same fucntins as ur own as MGF is an autocryn hormien produced by the bodyss own cells. Thsi wont do shit best best is to get some money and buy some NGENLA and run it at 10 IU a day for as long as u can

 

[ascension124]

Tagging some short cels @Edgarpill @Clavicular @Celestial Empire @Loruki @monecel @brownmutt42

I can never view them the same now

 

[goober55]

Somatic Elongation & Epiphyseal Reactivation: A Multi-Pathway Approach to Skeletal Maximization​

Height augmentation is not merely a function of growth plate availability—it is an intricate process dictated by endocrine synchronization, mechanotransductive osteogenic stimulation, and epiphyseal chondrocyte hyperproliferation. By leveraging exogenous peptide therapy, neuroendocrine recalibration, and biomechanical axial decompression, one can transcend the genetic limitations imposed by physeal senescence and reinitiate longitudinal osteogenesis post-adolescence.

View attachment 3532047

Phase 1: Growth Plate Reanimation via Senolytic Chondrocyte Induction​

Traditional height-maxxing protocols falter due to the epiphyseal plate's ossification post-puberty. To counteract this, we employ a targeted senolytic approach to selectively purge senescent chondrocytes, thereby reactivating dormant proliferative zones. This involves:
View attachment 3532048

Dasatinib (5 mg EOD) + Quercetin (500 mg ED): Eliminates senescent mesenchymal progenitor cells, restoring the extracellular matrix's pro-chondrogenic microenvironment.
Fisetin (500 mg biweekly): Induces autophagic recycling of calcified chondrocytes, allowing the deposition of newly proliferative chondrogenic clusters.
Rapamycin (1 mg every 3rd day): Inhibits mTORC1, shifting cellular energy allocation from hypertrophic calcification to chondrocyte self-renewal.

Phase 2: Peptidergic Growth Axis Amplification​

To initiate longitudinal osteogenesis, the body's endogenous IGF-1 & GH axis must be maximized while simultaneously inhibiting premature fibrocartilaginous ossification. This is achieved through rhythmic peptide cycling to manipulate somatic growth cascades.

View attachment 3532050
GHRH Analog + Ghrelin Mimetic: Administered pre-sleep in alternating pulses to induce ultradian growth hormone surges, simulating the endocrine profile of a prepubescent adolescent.
PEG-MGF (Mechano-Growth Factor): Injected directly into tibial periosteum, promoting localized osteoblastic hyperplasia and inhibiting epiphyseal fibrosis.
Thymosin Beta-4: Facilitates angiogenesis within the growth plate, optimizing nutrient diffusion rates to sustain chondrocyte proliferation longevity.
Liraglutide (GLP-1 Agonist): Enhances insulin-mediated IGF-1 secretion, biasing the body's anabolic state toward skeletal elongation rather than muscular hypertrophy.

Phase 3: Biomechanical Axial Tension & Epiphyseal Decompression​

To maximize osteogenic elongation, targeted tensile loading of the axial skeleton is required to mechanotransduce osteoblastic signaling pathways. The goal is to induce a continuous low-grade microfracture cycle, allowing for incremental periosteal apposition.

View attachment 3532051
Inverted Decompression Therapy (30 min daily at -45°): Encourages vertebral hydration expansion while reducing axial compression, enhancing the fluid permeability of the intervertebral discs.
Tibial Mechanical Stretching Device (1 mm daily elongation): Uses a modified Ilizarov external fixator, creating a controlled distraction osteogenesis effect without requiring surgical corticotomy.
Pulse Electromagnetic Field (PEMF) Therapy: Directs osteogenic differentiation through targeted electrical stimulation of osteoprogenitor cells, increasing collagen matrix deposition at the physeal junctions.
Low-Intensity Vibration Plate (35 Hz, 0.4 g acceleration): Enhances mesenchymal stem cell chondrogenesis, facilitating the deposition of epiphyseal cartilage layers essential for sustained bone elongation.

Phase 4: Circadian Hormonal Synchronization for Nocturnal Elongation​

Peak skeletal growth occurs during deep sleep, where GH surges coincide with bone remodeling cycles.


Melatonin + GABA Microdosing (3 mg + 500 mg, 30 min pre-sleep): Prolongs deep-wave sleep stages, increasing GH release duration.
Nandrolone Phenylpropionate (50 mg biweekly): Unlike testosterone, NPP exhibits preferential binding to osteoblast androgen receptors, promoting skeletal matrix deposition without premature physeal closure.
GH Secretagogue: Maintains a steady-state GH elevation, preventing overnight catabolic cortisol spikes that would otherwise inhibit longitudinal growth factor activity.
Sodium Butyrate: Epigenetically enhances RUNX2 transcription, biasing stem cell differentiation toward osteogenic lineages rather than adipogenesis.
View attachment 3532052

Phase 5: Extracellular Matrix Expansion & Soft Tissue Adaptation​

As skeletal elongation progresses, soft tissue structures must adapt proportionally to prevent postural imbalances.


Hyaluronic Acid Loading (1,500 mg ED): Expands interfibrillar hydration, increasing ligament extensibility to accommodate increased skeletal length.
GHK-Cu Peptide Application: Enhances collagen fibril cross-linking, preventing ligamentous laxity post-elongation.
Pentosan Polysulfate Sodium (PPS): Stimulates glycosaminoglycan synthesis, reinforcing joint integrity as new growth occurs.
View attachment 3532054

Conclusion: The Path to Transcendental Statural Augmentation​

By orchestrating a multidimensional interplay of peptide signaling, biomechanical elongation, and senolytic epiphyseal reactivation, one can bypass the conventional limitations of post-pubertal growth cessation. The result is a meticulously engineered statural transformation, allowing for unprecedented longitudinal skeletal hypertrophy beyond the constraints of genetic predetermination.

View attachment 3532056

I believe.

 

[shredded4summer]

read through briefly this can all work in thory but wont thigns like PEG MGF cant actually stimuate the same fucntins as ur own as MGF is an autocryn hormien produced by the bodyss own cells. Thsi wont do shit best best is to get some money and buy some NGENLA and run it at 10 IU a day for as long as u can

just sleep good theory

 

[tonsack]

JFL cope? the three people i tried it on grew +2 inches in under 2 months

Tldr pls I'm a retarded and a manlet

 

[shredded4summer]

Tldr pls I'm a retarded and a manlet

Just sleep good

 

[Seong Gi-Hun]

This is massive news for science man.. nothing like this has been discovered before. the early adopters can literally grow 3-5+ inches depending on consistency assuming they are under 20

Fr? So I just spam melatonin

 

[AuggyDauggy]

Tldr pls I'm a retarded and a manlet

this shit doesn't work nigga. none of this makes sense

 

[tonsack]

How can I use this info in my everyday life

 

[tonsack]

How can I use this info in my everyday life

Also is there not a limit to how much u grow from just sleep ??

 

[tweaqo]

Skimmed through, is there any way you could make a summary of what u need to do on a daily basis ie what to take and at what dosages etc etc

 

[ioneiwon]

Somatic Elongation & Epiphyseal Reactivation: A Multi-Pathway Approach to Skeletal Maximization​

Height augmentation is not merely a function of growth plate availability—it is an intricate process dictated by endocrine synchronization, mechanotransductive osteogenic stimulation, and epiphyseal chondrocyte hyperproliferation. By leveraging exogenous peptide therapy, neuroendocrine recalibration, and biomechanical axial decompression, one can transcend the genetic limitations imposed by physeal senescence and reinitiate longitudinal osteogenesis post-adolescence.

View attachment 3532047

Phase 1: Growth Plate Reanimation via Senolytic Chondrocyte Induction​

Traditional height-maxxing protocols falter due to the epiphyseal plate's ossification post-puberty. To counteract this, we employ a targeted senolytic approach to selectively purge senescent chondrocytes, thereby reactivating dormant proliferative zones. This involves:
View attachment 3532048

Dasatinib (5 mg EOD) + Quercetin (500 mg ED): Eliminates senescent mesenchymal progenitor cells, restoring the extracellular matrix's pro-chondrogenic microenvironment.
Fisetin (500 mg biweekly): Induces autophagic recycling of calcified chondrocytes, allowing the deposition of newly proliferative chondrogenic clusters.
Rapamycin (1 mg every 3rd day): Inhibits mTORC1, shifting cellular energy allocation from hypertrophic calcification to chondrocyte self-renewal.

Phase 2: Peptidergic Growth Axis Amplification​

To initiate longitudinal osteogenesis, the body's endogenous IGF-1 & GH axis must be maximized while simultaneously inhibiting premature fibrocartilaginous ossification. This is achieved through rhythmic peptide cycling to manipulate somatic growth cascades.

View attachment 3532050
GHRH Analog + Ghrelin Mimetic: Administered pre-sleep in alternating pulses to induce ultradian growth hormone surges, simulating the endocrine profile of a prepubescent adolescent.
PEG-MGF (Mechano-Growth Factor): Injected directly into tibial periosteum, promoting localized osteoblastic hyperplasia and inhibiting epiphyseal fibrosis.
Thymosin Beta-4: Facilitates angiogenesis within the growth plate, optimizing nutrient diffusion rates to sustain chondrocyte proliferation longevity.
Liraglutide (GLP-1 Agonist): Enhances insulin-mediated IGF-1 secretion, biasing the body's anabolic state toward skeletal elongation rather than muscular hypertrophy.

Phase 3: Biomechanical Axial Tension & Epiphyseal Decompression​

To maximize osteogenic elongation, targeted tensile loading of the axial skeleton is required to mechanotransduce osteoblastic signaling pathways. The goal is to induce a continuous low-grade microfracture cycle, allowing for incremental periosteal apposition.

View attachment 3532051
Inverted Decompression Therapy (30 min daily at -45°): Encourages vertebral hydration expansion while reducing axial compression, enhancing the fluid permeability of the intervertebral discs.
Tibial Mechanical Stretching Device (1 mm daily elongation): Uses a modified Ilizarov external fixator, creating a controlled distraction osteogenesis effect without requiring surgical corticotomy.
Pulse Electromagnetic Field (PEMF) Therapy: Directs osteogenic differentiation through targeted electrical stimulation of osteoprogenitor cells, increasing collagen matrix deposition at the physeal junctions.
Low-Intensity Vibration Plate (35 Hz, 0.4 g acceleration): Enhances mesenchymal stem cell chondrogenesis, facilitating the deposition of epiphyseal cartilage layers essential for sustained bone elongation.

Phase 4: Circadian Hormonal Synchronization for Nocturnal Elongation​

Peak skeletal growth occurs during deep sleep, where GH surges coincide with bone remodeling cycles.


Melatonin + GABA Microdosing (3 mg + 500 mg, 30 min pre-sleep): Prolongs deep-wave sleep stages, increasing GH release duration.
Nandrolone Phenylpropionate (50 mg biweekly): Unlike testosterone, NPP exhibits preferential binding to osteoblast androgen receptors, promoting skeletal matrix deposition without premature physeal closure.
GH Secretagogue: Maintains a steady-state GH elevation, preventing overnight catabolic cortisol spikes that would otherwise inhibit longitudinal growth factor activity.
Sodium Butyrate: Epigenetically enhances RUNX2 transcription, biasing stem cell differentiation toward osteogenic lineages rather than adipogenesis.
View attachment 3532052

Phase 5: Extracellular Matrix Expansion & Soft Tissue Adaptation​

As skeletal elongation progresses, soft tissue structures must adapt proportionally to prevent postural imbalances.


Hyaluronic Acid Loading (1,500 mg ED): Expands interfibrillar hydration, increasing ligament extensibility to accommodate increased skeletal length.
GHK-Cu Peptide Application: Enhances collagen fibril cross-linking, preventing ligamentous laxity post-elongation.
Pentosan Polysulfate Sodium (PPS): Stimulates glycosaminoglycan synthesis, reinforcing joint integrity as new growth occurs.
View attachment 3532054

Conclusion: The Path to Transcendental Statural Augmentation​

By orchestrating a multidimensional interplay of peptide signaling, biomechanical elongation, and senolytic epiphyseal reactivation, one can bypass the conventional limitations of post-pubertal growth cessation. The result is a meticulously engineered statural transformation, allowing for unprecedented longitudinal skeletal hypertrophy beyond the constraints of genetic predetermination.

View attachment 3532056

Where do I get ts

 

[AscendableReal]

Somatic Elongation & Epiphyseal Reactivation: A Multi-Pathway Approach to Skeletal Maximization​

Height augmentation is not merely a function of growth plate availability—it is an intricate process dictated by endocrine synchronization, mechanotransductive osteogenic stimulation, and epiphyseal chondrocyte hyperproliferation. By leveraging exogenous peptide therapy, neuroendocrine recalibration, and biomechanical axial decompression, one can transcend the genetic limitations imposed by physeal senescence and reinitiate longitudinal osteogenesis post-adolescence.

View attachment 3532047

Phase 1: Growth Plate Reanimation via Senolytic Chondrocyte Induction​

Traditional height-maxxing protocols falter due to the epiphyseal plate's ossification post-puberty. To counteract this, we employ a targeted senolytic approach to selectively purge senescent chondrocytes, thereby reactivating dormant proliferative zones. This involves:
View attachment 3532048

Dasatinib (5 mg EOD) + Quercetin (500 mg ED): Eliminates senescent mesenchymal progenitor cells, restoring the extracellular matrix's pro-chondrogenic microenvironment.
Fisetin (500 mg biweekly): Induces autophagic recycling of calcified chondrocytes, allowing the deposition of newly proliferative chondrogenic clusters.
Rapamycin (1 mg every 3rd day): Inhibits mTORC1, shifting cellular energy allocation from hypertrophic calcification to chondrocyte self-renewal.

Phase 2: Peptidergic Growth Axis Amplification​

To initiate longitudinal osteogenesis, the body's endogenous IGF-1 & GH axis must be maximized while simultaneously inhibiting premature fibrocartilaginous ossification. This is achieved through rhythmic peptide cycling to manipulate somatic growth cascades.

View attachment 3532050
GHRH Analog + Ghrelin Mimetic: Administered pre-sleep in alternating pulses to induce ultradian growth hormone surges, simulating the endocrine profile of a prepubescent adolescent.
PEG-MGF (Mechano-Growth Factor): Injected directly into tibial periosteum, promoting localized osteoblastic hyperplasia and inhibiting epiphyseal fibrosis.
Thymosin Beta-4: Facilitates angiogenesis within the growth plate, optimizing nutrient diffusion rates to sustain chondrocyte proliferation longevity.
Liraglutide (GLP-1 Agonist): Enhances insulin-mediated IGF-1 secretion, biasing the body's anabolic state toward skeletal elongation rather than muscular hypertrophy.

Phase 3: Biomechanical Axial Tension & Epiphyseal Decompression​

To maximize osteogenic elongation, targeted tensile loading of the axial skeleton is required to mechanotransduce osteoblastic signaling pathways. The goal is to induce a continuous low-grade microfracture cycle, allowing for incremental periosteal apposition.

View attachment 3532051
Inverted Decompression Therapy (30 min daily at -45°): Encourages vertebral hydration expansion while reducing axial compression, enhancing the fluid permeability of the intervertebral discs.
Tibial Mechanical Stretching Device (1 mm daily elongation): Uses a modified Ilizarov external fixator, creating a controlled distraction osteogenesis effect without requiring surgical corticotomy.
Pulse Electromagnetic Field (PEMF) Therapy: Directs osteogenic differentiation through targeted electrical stimulation of osteoprogenitor cells, increasing collagen matrix deposition at the physeal junctions.
Low-Intensity Vibration Plate (35 Hz, 0.4 g acceleration): Enhances mesenchymal stem cell chondrogenesis, facilitating the deposition of epiphyseal cartilage layers essential for sustained bone elongation.

Phase 4: Circadian Hormonal Synchronization for Nocturnal Elongation​

Peak skeletal growth occurs during deep sleep, where GH surges coincide with bone remodeling cycles.


Melatonin + GABA Microdosing (3 mg + 500 mg, 30 min pre-sleep): Prolongs deep-wave sleep stages, increasing GH release duration.
Nandrolone Phenylpropionate (50 mg biweekly): Unlike testosterone, NPP exhibits preferential binding to osteoblast androgen receptors, promoting skeletal matrix deposition without premature physeal closure.
GH Secretagogue: Maintains a steady-state GH elevation, preventing overnight catabolic cortisol spikes that would otherwise inhibit longitudinal growth factor activity.
Sodium Butyrate: Epigenetically enhances RUNX2 transcription, biasing stem cell differentiation toward osteogenic lineages rather than adipogenesis.
View attachment 3532052

Phase 5: Extracellular Matrix Expansion & Soft Tissue Adaptation​

As skeletal elongation progresses, soft tissue structures must adapt proportionally to prevent postural imbalances.


Hyaluronic Acid Loading (1,500 mg ED): Expands interfibrillar hydration, increasing ligament extensibility to accommodate increased skeletal length.
GHK-Cu Peptide Application: Enhances collagen fibril cross-linking, preventing ligamentous laxity post-elongation.
Pentosan Polysulfate Sodium (PPS): Stimulates glycosaminoglycan synthesis, reinforcing joint integrity as new growth occurs.
View attachment 3532054

Conclusion: The Path to Transcendental Statural Augmentation​

By orchestrating a multidimensional interplay of peptide signaling, biomechanical elongation, and senolytic epiphyseal reactivation, one can bypass the conventional limitations of post-pubertal growth cessation. The result is a meticulously engineered statural transformation, allowing for unprecedented longitudinal skeletal hypertrophy beyond the constraints of genetic predetermination.

View attachment 3532056

rapamycin is straight poison bro

 

[HostSamurai]

I believe.

 

[fzris]

extremely high effort post bhai

 

[ScramFranklin]

This is retarded. Sounds like one of those patents someone comes up with that isn’t any actual research or studies, someone just plugging in hypotheticals.

This wasn’t actually done.

 

[HostSamurai]

It's still LL or death.

 

[Setif]

Too broke to buy these shits

 

[SubhumanCurrycel]

I thought this was going to be a post on relevant research not a scientific schizo ramble but I appreciate the quality