T
Tyl3r4
Iron
- Joined
- Mar 21, 2025
- Posts
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Just bought a course and the OP claims that he has achieved growth from 5’7 to 5’10 after closed plates. Wanna know if what he’s saying is legit.
METHOD 1
Periepiphyseal administration of igf-1 lr3 and/or des, irrespective of growth plate status (closed or open), utilizing sub-periosteal microdiffusion techniques under constrained hydrostatic gradients, aims to induce paracrine-mediated mesenchymal activation and ectopic chondrogenesis via localized igfr axis potentiation and downstream pi3k-akt-mtor signaling cascade reactivation.
Method leverages the inherent plasticity of periosteal and perichondral mesenchymal progenitors, which remain bioresponsive even post-epiphyseal fusion. By creating a hyperlocalized anabolic microenvironment saturated with igf analogs, the protocol re establishes conditions that mimic early endochondral ossification. The mechanical stress from sub-periosteal pressure, combined with ligand saturation at the igfr receptor sites, initiates a forced re-entry of quiescent cells into the chondroproliferative cycle. This bypasses the need for open growth plates by inducing a pseudo-epiphyseal niche, allowing longitudinal ossification to proceed in defiance of conventional skeletal senescence.
Risks : 8.5 / 10
Fibrosis or cancer (esp. osteosarcoma/chondrosarcoma) from unregulated proliferation = real concern
Aberrant calcification or malformed bone islands are likely
Immune response or necrosis if delivery isn’t perfectly localized
Highly experimental, no existing literature supports success in humans using this exact approach
If it works, it rewrites adult skeletal biology. If it fails, it risks fibrosis or tumors.
METHOD 2
Systemic microdosing of IGF-1 LR3 paired with spinal decompression and axial loading aimed for vertical growth via vertebral disc expansion, connective tissue hypertrophy, and periosteal remodeling. Though less invasive than direct periepiphyseal administration, this method still exploits the anabolic potential of the IGF axis to induce gradual height gains through spinal elongation and intervertebral disc matrix restoration
By injecting 20–30 mcg of IGF-1 LR3 subcutaneously near the lumbar region 30 minutes before mechanical stimulation, users prime the vertebral column’s microenvironment for heightened ECM synthesis, disc hydration, and ligamentous adaptation. The repeated cycle of decompressive stress (e.g., inversion therapy, dead hangs) followed by controlled axial loading (e.g., yoke walks, trap bar carries) creates a mechanical signaling loop that encourages spinal tissues to remodel under anabolic pressure. When synchronized with elevated IGF-1 presence, the spine becomes a viable target for measurable elongation.
Stacking collagen II, MSM, glycine, vitamin C, magnesium, and hyaluronic acid supports structural integrity and disc resilience, while deep sleep and GH optimization (via melatonin, zinc, and ashwagandha) maximize recovery and reinforce the endocrine component of the protocol. Over time, adaptive hypertrophy of intervertebral discs, postural muscles, and connective tissues may result in permanent height gains despite closed growth plates.
Risks: 5.5 / 10
IGF-1 LR3 remains a potent mitogen, mismanagement may cause systemic effects (e.g., insulin sensitivity disruption, organomegaly)
Axial overloading or improper decompression can lead to spinal injury
Disc degeneration or nerve compression if recovery is ignored
Moderate risk, high effort, potential reward, best suited for calculated long-term experimentation
METHOD 3
Targeted Synergistic Stack: Native igf1+Mechanical Stretch+Periosteal Receptor Priming
This enhanced protocol builds on Method 1 and 2 but pushes further with precision timed synergistic triggers targeting latent growth potential in periosteal and cartilaginous zones, especially clavicle, costal cartilage, tibia, mandible, and iliac crest.
Mechanism of Action (Stacked):
1. Native igf1 (20 mcg): Injected locally (intradermal/subq) at the periosteum with microneedle or insulin pin. Half-life = ~15 minutes. Binds tightly to igf1r.
2. Pre-Priming with mgf (10–20 mcg): Injected 1–2 hours before igf1 at same location. Pre-activates mechano-sensitive satellite and mesenchymal progenitor cells.
3. Mechanical Stretch/Isometric Load (3–7 min): Immediately post igf1 injection. Use high-tension static holds over injection site:
Overhead shrug (clavicle)
Static wall sit (tibia)
Deep split lunge (pelvis)
Hanging shrug (spine)
Jaw clamp or resistance chewing (mandible)
4. Receptor Uptake Optimization:
Supplement: 5g glycine, 10g collagen peptides, 2g MSM, 1g vitamin C (30–60 min pre)
Optional: microcurrent stimulation pad placed near site post-injection to increase receptor sensitivity
Why it works :
mgf primes progenitors, igf1 binds receptors, static load opens growth response pathway
Tightly localized effect prevents systemic drift
Repeated microtrauma and saturation lead to edge bone and cartilage remodelling
May increase periosteal width, clavicular length, pelvic flare, facial projection even post-fusion
Risk Level: 5.5 / 10
Higher complexity, but low systemic risk.
main risks: asymmetry
METHOD 15: ANABOLIC OSTEOGENESIS PULSE
Compounds: Teriparatide & Abaloparatide
Goal: Targeted bone elongation and cortical expansion via direct osteoblast activation.
Mechanism
Teriparatide (PTH 1-34) and Abaloparatide (selective PTHrP analog) are potent bone-forming agents. Unlike growth hormone or IGF-1, they directly stimulate osteoblast activity and bone modeling. When injected using sub-periosteal or periepiphyseal techniques, they can induce localized bone formation, not just density, but also controlled longitudinal expansion in areas with residual metaphyseal or periosteal plasticity.
Protocol :
Compound & Dose:
Teriparatide: 10–20 mcg
Abaloparatide: 40–80 mcg
!! USE ONE AT A TIME !!
Site: Distal femur, proximal tibia, or clavicular periosteum.
Technique: Shallow sub-periosteal injection using 31G insulin syringe. Slow infusion to minimize diffusion.
Frequency: Daily, 5 days on/2 days off.
Cycle Length: 4–8 weeks max, then 8+ weeks off to avoid overstimulation.
Loading & Stimulus:
10 minutes of light mechanical load (vibration platform or isometric tension) post-injection to direct bone formation along desired vector.
Supporting Stack:
High-dose Calcium + Vitamin D3/K2
Magnesium, Boron
Collagen Peptides (15g daily)
Avoid NSAIDs, they can blunt anabolic bone response.
Expected Outcomes
Periosteal widening and slight longitudinal gains (0.5–1.5 cm over 6 months) via cortical drift.
Increased bone density and mineral apposition rate in target sites.
Possible use for facial and clavicular remodeling when applied selectively.
Risks: 8/10
Hypercalcemia, elevated urine calcium.
Possible osteosarcoma risk with long-term use (known in rodent studies).
Overstimulation can cause aberrant bone formation or ectopic mineralization.
Must be monitored via serum calcium, P1NP, and periodic DEXA/X-ray.
METHOD 16: CRYSTALLINE MATRIX DRIFT
Compound: Synthetic Calcitonin (Salmon-based preferred)
Goal: Induce targeted longitudinal drift and cortical expansion by leveraging calcitonin's unique dual-action as an osteoclast inhibitor and chondrocyte activator in specific mechanical environments.
Mechanism Breakdown
Calcitonin is not just an anti-resorptive agent, it directly suppresses osteoclast activity while promoting proteoglycan synthesis in cartilage and stimulating chondrocyte proliferation in growth plate remnants. When combined with mechanically-induced interstitial fluid shear and local igf-1 enrichment, it can reopen fused metaphyseal lines for controlled linear expansion.
Protocol
1. Compound & Dose:
Calcitonin: 20–50 IU daily
+ Optional Synergist: Low-dose IGF-1 LR3 (10–15 mcg) at same site
2. Injection Site:
Shallow sub-periosteal or periosteal-perichondral border of:
Distal femur
Proximal tibia
Clavicular head
3. Delivery Technique:
Use 31G insulin syringe
Slow infusion parallel to bone surface
Combine with piezoelectric vibration (10–15 mins post-injection) to stimulate fluid dynamics within the lacuno-canalicular network
4. Loading & Timing:
Inject 30 mins before moderate axial or tensile loading (banded walks, static holds)
Follow with 10 mins of low-frequency vibration plate standing to amplify interstitial shear
5. Cycle:
5 weeks on, 5 weeks off (prevents receptor desensitization)
Max 3 cycles per year
Supporting Stack
Calcium Citrate: 1200 mg/day (split doses)
Hyaluronic Acid + Collagen Type II: For ECM and cartilage support
Vitamin D3 + K2: Direct mineral deposition
Magnesium Glycinate: Optimizes calcitonin receptor sensitivity
Risks: 6/10
Nausea or flushing (common with calcitonin)
Transient hypocalcemia (manage with calcium supplementation)
Risk of irregular ossification if mechanical loading is misapplied
Contraindicated in patients with hypocalcemia or allergy to calcitonin
METHOD 1
Periepiphyseal administration of igf-1 lr3 and/or des, irrespective of growth plate status (closed or open), utilizing sub-periosteal microdiffusion techniques under constrained hydrostatic gradients, aims to induce paracrine-mediated mesenchymal activation and ectopic chondrogenesis via localized igfr axis potentiation and downstream pi3k-akt-mtor signaling cascade reactivation.
Method leverages the inherent plasticity of periosteal and perichondral mesenchymal progenitors, which remain bioresponsive even post-epiphyseal fusion. By creating a hyperlocalized anabolic microenvironment saturated with igf analogs, the protocol re establishes conditions that mimic early endochondral ossification. The mechanical stress from sub-periosteal pressure, combined with ligand saturation at the igfr receptor sites, initiates a forced re-entry of quiescent cells into the chondroproliferative cycle. This bypasses the need for open growth plates by inducing a pseudo-epiphyseal niche, allowing longitudinal ossification to proceed in defiance of conventional skeletal senescence.
Risks : 8.5 / 10
Fibrosis or cancer (esp. osteosarcoma/chondrosarcoma) from unregulated proliferation = real concern
Aberrant calcification or malformed bone islands are likely
Immune response or necrosis if delivery isn’t perfectly localized
Highly experimental, no existing literature supports success in humans using this exact approach
If it works, it rewrites adult skeletal biology. If it fails, it risks fibrosis or tumors.
METHOD 2
Systemic microdosing of IGF-1 LR3 paired with spinal decompression and axial loading aimed for vertical growth via vertebral disc expansion, connective tissue hypertrophy, and periosteal remodeling. Though less invasive than direct periepiphyseal administration, this method still exploits the anabolic potential of the IGF axis to induce gradual height gains through spinal elongation and intervertebral disc matrix restoration
By injecting 20–30 mcg of IGF-1 LR3 subcutaneously near the lumbar region 30 minutes before mechanical stimulation, users prime the vertebral column’s microenvironment for heightened ECM synthesis, disc hydration, and ligamentous adaptation. The repeated cycle of decompressive stress (e.g., inversion therapy, dead hangs) followed by controlled axial loading (e.g., yoke walks, trap bar carries) creates a mechanical signaling loop that encourages spinal tissues to remodel under anabolic pressure. When synchronized with elevated IGF-1 presence, the spine becomes a viable target for measurable elongation.
Stacking collagen II, MSM, glycine, vitamin C, magnesium, and hyaluronic acid supports structural integrity and disc resilience, while deep sleep and GH optimization (via melatonin, zinc, and ashwagandha) maximize recovery and reinforce the endocrine component of the protocol. Over time, adaptive hypertrophy of intervertebral discs, postural muscles, and connective tissues may result in permanent height gains despite closed growth plates.
Risks: 5.5 / 10
IGF-1 LR3 remains a potent mitogen, mismanagement may cause systemic effects (e.g., insulin sensitivity disruption, organomegaly)
Axial overloading or improper decompression can lead to spinal injury
Disc degeneration or nerve compression if recovery is ignored
Moderate risk, high effort, potential reward, best suited for calculated long-term experimentation
METHOD 3
Targeted Synergistic Stack: Native igf1+Mechanical Stretch+Periosteal Receptor Priming
This enhanced protocol builds on Method 1 and 2 but pushes further with precision timed synergistic triggers targeting latent growth potential in periosteal and cartilaginous zones, especially clavicle, costal cartilage, tibia, mandible, and iliac crest.
Mechanism of Action (Stacked):
1. Native igf1 (20 mcg): Injected locally (intradermal/subq) at the periosteum with microneedle or insulin pin. Half-life = ~15 minutes. Binds tightly to igf1r.
2. Pre-Priming with mgf (10–20 mcg): Injected 1–2 hours before igf1 at same location. Pre-activates mechano-sensitive satellite and mesenchymal progenitor cells.
3. Mechanical Stretch/Isometric Load (3–7 min): Immediately post igf1 injection. Use high-tension static holds over injection site:
Overhead shrug (clavicle)
Static wall sit (tibia)
Deep split lunge (pelvis)
Hanging shrug (spine)
Jaw clamp or resistance chewing (mandible)
4. Receptor Uptake Optimization:
Supplement: 5g glycine, 10g collagen peptides, 2g MSM, 1g vitamin C (30–60 min pre)
Optional: microcurrent stimulation pad placed near site post-injection to increase receptor sensitivity
Why it works :
mgf primes progenitors, igf1 binds receptors, static load opens growth response pathway
Tightly localized effect prevents systemic drift
Repeated microtrauma and saturation lead to edge bone and cartilage remodelling
May increase periosteal width, clavicular length, pelvic flare, facial projection even post-fusion
Risk Level: 5.5 / 10
Higher complexity, but low systemic risk.
main risks: asymmetry
METHOD 15: ANABOLIC OSTEOGENESIS PULSE
Compounds: Teriparatide & Abaloparatide
Goal: Targeted bone elongation and cortical expansion via direct osteoblast activation.
Mechanism
Teriparatide (PTH 1-34) and Abaloparatide (selective PTHrP analog) are potent bone-forming agents. Unlike growth hormone or IGF-1, they directly stimulate osteoblast activity and bone modeling. When injected using sub-periosteal or periepiphyseal techniques, they can induce localized bone formation, not just density, but also controlled longitudinal expansion in areas with residual metaphyseal or periosteal plasticity.
Protocol :
Compound & Dose:
Teriparatide: 10–20 mcg
Abaloparatide: 40–80 mcg
!! USE ONE AT A TIME !!
Site: Distal femur, proximal tibia, or clavicular periosteum.
Technique: Shallow sub-periosteal injection using 31G insulin syringe. Slow infusion to minimize diffusion.
Frequency: Daily, 5 days on/2 days off.
Cycle Length: 4–8 weeks max, then 8+ weeks off to avoid overstimulation.
Loading & Stimulus:
10 minutes of light mechanical load (vibration platform or isometric tension) post-injection to direct bone formation along desired vector.
Supporting Stack:
High-dose Calcium + Vitamin D3/K2
Magnesium, Boron
Collagen Peptides (15g daily)
Avoid NSAIDs, they can blunt anabolic bone response.
Expected Outcomes
Periosteal widening and slight longitudinal gains (0.5–1.5 cm over 6 months) via cortical drift.
Increased bone density and mineral apposition rate in target sites.
Possible use for facial and clavicular remodeling when applied selectively.
Risks: 8/10
Hypercalcemia, elevated urine calcium.
Possible osteosarcoma risk with long-term use (known in rodent studies).
Overstimulation can cause aberrant bone formation or ectopic mineralization.
Must be monitored via serum calcium, P1NP, and periodic DEXA/X-ray.
METHOD 16: CRYSTALLINE MATRIX DRIFT
Compound: Synthetic Calcitonin (Salmon-based preferred)
Goal: Induce targeted longitudinal drift and cortical expansion by leveraging calcitonin's unique dual-action as an osteoclast inhibitor and chondrocyte activator in specific mechanical environments.
Mechanism Breakdown
Calcitonin is not just an anti-resorptive agent, it directly suppresses osteoclast activity while promoting proteoglycan synthesis in cartilage and stimulating chondrocyte proliferation in growth plate remnants. When combined with mechanically-induced interstitial fluid shear and local igf-1 enrichment, it can reopen fused metaphyseal lines for controlled linear expansion.
Protocol
1. Compound & Dose:
Calcitonin: 20–50 IU daily
+ Optional Synergist: Low-dose IGF-1 LR3 (10–15 mcg) at same site
2. Injection Site:
Shallow sub-periosteal or periosteal-perichondral border of:
Distal femur
Proximal tibia
Clavicular head
3. Delivery Technique:
Use 31G insulin syringe
Slow infusion parallel to bone surface
Combine with piezoelectric vibration (10–15 mins post-injection) to stimulate fluid dynamics within the lacuno-canalicular network
4. Loading & Timing:
Inject 30 mins before moderate axial or tensile loading (banded walks, static holds)
Follow with 10 mins of low-frequency vibration plate standing to amplify interstitial shear
5. Cycle:
5 weeks on, 5 weeks off (prevents receptor desensitization)
Max 3 cycles per year
Supporting Stack
Calcium Citrate: 1200 mg/day (split doses)
Hyaluronic Acid + Collagen Type II: For ECM and cartilage support
Vitamin D3 + K2: Direct mineral deposition
Magnesium Glycinate: Optimizes calcitonin receptor sensitivity
Risks: 6/10
Nausea or flushing (common with calcitonin)
Transient hypocalcemia (manage with calcium supplementation)
Risk of irregular ossification if mechanical loading is misapplied
Contraindicated in patients with hypocalcemia or allergy to calcitonin
