THEORY DISCUSSION: inositol trisphosphate maximizing.

[KLEORB]

Inconclusion theories that are less primary compared to mainstream like, GHRH,GHRN, PTH1R ETC.
IP₃ solos both in many ways, rather much of the positives and negatives.
summary table:

Drug / Hormone	Receptor	Second Messenger	Effect
Teriparatide / Abaloparatide / PTH	PTH1R (Gs-coupled)	↑ cAMP → PKA	Stimulates osteoblasts, ↑ bone formation
		Can also weakly ↑ IP₃ via PLC in some cells	Minor, mostly anabolic bone effect via cAMP

Hormone	Receptor	Second Messenger	Effect
Calcitonin	Calcitonin receptor (Gs-coupled)	↑ cAMP → PKA	Inhibits osteoclasts → ↓ bone resorption
		IP₃?	Minimal; mostly cAMP

THIS STIMULATES THE CALCITONIN RECEPTOR THAT GIVES U UNGODLY OSTEOBLAST COMPOUNDS IN UR ANALOGS. MEANING ↓ Bone breakdown, Stabilizes bone density in conditions like osteoporosis or Paget’s disease, Useful for acute reduction of bone turnover.

NO THIS IS NOT A PROMOTION TO USING THIS. THIS IS A DISCUSSION FOR RESEARCH PURPOSES ON THE EFFECTS AND TURNOVERS.
IF YOUR A FUCKING RETARD READING THIS DECIDING "SARR I MIGHT HAVE TO TAKE THIS" WELL FUCKING GUESS WHAT.

Risk	Mechanism
Excess bone turnover	Continuous PTH analog can stimulate both osteoblasts AND osteoclasts → net bone loss instead of gain
Hypercalcemia	Too much PTH → ↑ calcium release from bone → ↑ blood calcium → nausea, kidney stones, arrhythmias
Receptor desensitization	Chronic activation → PTH1R becomes less responsive → body stops responding to hormone

System	Possible effect of excess
Heart / blood vessels	β-agonists or vasopressin analogs → arrhythmias, hypertension
Kidneys	Calcium or phosphate imbalance
Hormone feedback	Natural hormone production may shut down (endogenous suppression)

YOU'LL BE DESCENDING LIKE CRAZY.

"SARR SARR but i have hypoparathyroidism"
Mirin. this will save your life.
how>? ---------------------------------------|

• Teriparatide or full-length PTH can restore cAMP signaling giving <>
• Effects like Stimulating osteoblasts → normal bone formation, Maintains proper calcium levels in blood, Restores normal bone remodeling

but since 99% of you guys don't have hypoparathyroidism u wont need this.

SUMMARY CHART:

Age Group	Growth Plate Status	Bone Mass / Density Effect	Facial Bone Effect	Approximate % Change*	Notes
Early teens (13–14)	Growth plates mostly open	↑ Trabecular & cortical bone formation	Slight increase in jaw/facial bone density; minor structural growth possible	Bone mass: 5–10%; Facial density: 2–5%	Peak growth velocity; bone very responsive to anabolic signals
Mid teens (15–16)	Growth plates partially closing	↑ Bone density; cortical thickness increases	Slight density increase; structural growth slowing	Bone mass: 3–6%; Facial density: 1–3%	Most facial growth mostly complete
Late teens (17–18)	Growth plates mostly closed	↑ Bone microarchitecture; prevents bone loss	Very slight density improvements; no new growth	Bone mass: 2–4%; Facial density: <1–2%	Effects mainly protective; facial shape adult

therefore, this is unironic cope. minimal reward

 

[monecel]

dnr

 

[KLEORB]

dnr

dont blame u

 

[BonesGrowth]

Inconclusion theories that are less primary compared to mainstream like, GHRH,GHRN, PTH1R ETC.
IP₃ solos both in many ways, rather much of the positives and negatives.
summary table:

Drug / Hormone	Receptor	Second Messenger	Effect
Teriparatide / Abaloparatide / PTH	PTH1R (Gs-coupled)	↑ cAMP → PKA	Stimulates osteoblasts, ↑ bone formation
		Can also weakly ↑ IP₃ via PLC in some cells	Minor, mostly anabolic bone effect via cAMP

Hormone	Receptor	Second Messenger	Effect
Calcitonin	Calcitonin receptor (Gs-coupled)	↑ cAMP → PKA	Inhibits osteoclasts → ↓ bone resorption
		IP₃?	Minimal; mostly cAMP

THIS STIMULATES THE CALCITONIN RECEPTOR THAT GIVES U UNGODLY OSTEOBLAST COMPOUNDS IN UR ANALOGS. MEANING ↓ Bone breakdown, Stabilizes bone density in conditions like osteoporosis or Paget’s disease, Useful for acute reduction of bone turnover.

NO THIS IS NOT A PROMOTION TO USING THIS. THIS IS A DISCUSSION FOR RESEARCH PURPOSES ON THE EFFECTS AND TURNOVERS.
IF YOUR A FUCKING RETARD READING THIS DECIDING "SARR I MIGHT HAVE TO TAKE THIS" WELL FUCKING GUESS WHAT.

Risk	Mechanism
Excess bone turnover	Continuous PTH analog can stimulate both osteoblasts AND osteoclasts → net bone loss instead of gain
Hypercalcemia	Too much PTH → ↑ calcium release from bone → ↑ blood calcium → nausea, kidney stones, arrhythmias
Receptor desensitization	Chronic activation → PTH1R becomes less responsive → body stops responding to hormone

System	Possible effect of excess
Heart / blood vessels	β-agonists or vasopressin analogs → arrhythmias, hypertension
Kidneys	Calcium or phosphate imbalance
Hormone feedback	Natural hormone production may shut down (endogenous suppression)

YOU'LL BE DESCENDING LIKE CRAZY.

"SARR SARR but i have hypoparathyroidism"
Mirin. this will save your life.
how>? ---------------------------------------|

• Teriparatide or full-length PTH can restore cAMP signaling giving <>
• Effects like Stimulating osteoblasts → normal bone formation, Maintains proper calcium levels in blood, Restores normal bone remodeling

but since 99% of you guys don't have hypoparathyroidism u wont need this.

SUMMARY CHART:

Age Group	Growth Plate Status	Bone Mass / Density Effect	Facial Bone Effect	Approximate % Change*	Notes
Early teens (13–14)	Growth plates mostly open	↑ Trabecular & cortical bone formation	Slight increase in jaw/facial bone density; minor structural growth possible	Bone mass: 5–10%; Facial density: 2–5%	Peak growth velocity; bone very responsive to anabolic signals
Mid teens (15–16)	Growth plates partially closing	↑ Bone density; cortical thickness increases	Slight density increase; structural growth slowing	Bone mass: 3–6%; Facial density: 1–3%	Most facial growth mostly complete
Late teens (17–18)	Growth plates mostly closed	↑ Bone microarchitecture; prevents bone loss	Very slight density improvements; no new growth	Bone mass: 2–4%; Facial density: <1–2%	Effects mainly protective; facial shape adult

therefore, this is unironic cope. minimal reward

nice thread