Taller Height by inhibiting PGE2 and Cox-2?

LSJL downregulates COX2. Listed on the study as prostaglandin-endoperoxin synthase 2. According to Molecular pathways mediating mechanical signaling in bone, connexin hemi channels can be knocked down during fluid shear thus inhibiting PGE2 release.  Although it mentions also that in other cases PGE2 can be stimulated.

Alkoclar made an interesting statement via email "Enhanced cnp expression coupled with partial activin antagonism enables the fused tissue to gain elasticity and degrades pge2 and cox-2 expression,re-enabling vertical bone growth over time. Pge1 release is also enhanced through this stimuli,literally softening hardened periosteum.this process requires cnp signal accumulation in order to undo the long period it had been fused"


Activin inhibits cellular differentiation. Which would inhibit cells from differentiation into chondrocytes. CNP is a guanyl cyclase activator which is involved in the nitric oxide pathway. The end result is an increase in chondrocyte hypertrophy which makes you taller. Now I don't see how this would help the fused tissue gain elasticity but it is certainly worth investigating.


LIPUS enhances Prostaglandin E2 which is regulated by Cox-2. Shear Stress also increased PGE2 levels.

Here's a study that shows that contraindicates LSJL but like anything that's anabolic helping cancer to spread faster I don't think it's anything to worry about as LSJL itself won't cause the necessary changes to induce osteoarthritis or you want to take anti-oxidants to go against the inflammatory effects(although inflammation may be good for height growth).

Shear-induced interleukin-6 synthesis in chondrocytes: roles of E prostanoid (EP) 2 and EP3 in cAMP/protein kinase A- and PI3-K/Akt-dependent NF-kappaB activation.

"Mechanical overloading of cartilage producing hydrostatic stress, tensile strain, and fluid flow can adversely affect chondrocyte function and precipitate osteoarthritis (OA)[A couple of things, you are loading the epiphysis and not the cartilage; osteoarthritis has some anabolic properties and this shows that hydrostatic pressure and tensile strain have anabolic properties; Osteoarthritis also involves CD44 and an alteration in the OPG/RANKL gradient which isn't caused by hydrostatic pressure or tensile strain]. Application of high fluid shear stress to chondrocytes [stimulates the] release of pro-inflammatory mediators, matrix degradation, and chondrocyte apoptosis. Elevated levels of cyclooxygenase-2 (COX-2), prostaglandin (PG) E(2), and interleukin (IL)-6 have been reported in shear-activated chondrocytes in vitro[this is circumstantial evidence, correlation not equal causation]. PGE(2) positively regulates IL-6 synthesis in chondrocytes. Using the human T/C-28a2 chondrocyte cell line as a model system, we demonstrate that COX-2-derived PGE(2) signals via up-regulation of E prostanoid (EP) 2 and down-regulation of EP3 receptors to raise intracellular cAMP[cAMP is involved in the Nitric Oxide pathway], and activate protein kinase A (PKA)[PKA enhances Sox9 transcriptional activity and thus may help with height growth] and phosphatidylinositol 3-kinase (PI3-K)/Akt pathways. PKA and PI3-K/Akt transactivate the NF-kappaB p65 subunit via phosphorylation at Ser-276 and Ser-536, respectively. Binding of p65 to the IL-6 promoter elicits IL-6 synthesis in sheared chondrocytes. Selective knockdown of EP2 or ectopic expression of EP3 blocks PKA- and PI3-K/Akt-dependent p65 activation and markedly diminishes shear-induced IL-6 expression. Similar inhibitory effects on IL-6 synthesis were observed by inhibiting PKA, PI3-K, or NF-kappaB using pharmacological and/or genetic interventions."

IL-6 is involved in Osteoclast formation  Since PGE2 increases IL-6 synthesis it may increase osteoclast production giving chondrocytes more room to grow.  It seems like then if anything you'd want to enhance PGE2 and COX2 to soften tissue(Alkoclar recommends LIPUS which upregulates PGE2 and COX-2).

"PGE2 exerts its biological functions via binding to four distinct transmembrane G-protein-coupled receptors (GPCRs) termed E prostanoid (EP) 1, EP2, EP3, and EP4. Following PGE2 binding, the EP receptors activate distinct intracellular signaling pathways, which may account for the pleiotropic effects of this prostaglandin. EP1 couples to Gq protein and raises intracellular calcium. EP2 and EP4 elevate intracellular cAMP levels by activating adenylate cyclase via stimulatory G (Gs) proteins. The major signaling pathway of the EP3 receptor is the inhibition of adenylate cyclase, and thus reduction of intracellular cAMP, via inhibitory G (Gi) proteins. Human chondrocytes primed with exogenous PGE2 synthesize IL-6."<-may it's the raising of intracellular calcium that stimulates chondrogenesis.

"Application of fluid shear to T/C-28a2 chondrocytes induces p65 phosphorylation at both Ser-536 and Ser-276 without affecting total p65 protein levels"

If you do decide to inhibit PGE2 and COX2...

Inhibition of cyclooxygenase-2 expression and prostaglandin E2 production in chondrocytes by avocado soybean unsaponifiables and epigallocatechin gallate.'

"Production of type II collagen and aggrecan was verified by immunohistochemistry and Western blot. Chondrocytes were incubated with: (1) control media alone, (2) ASU (4 microg/ml; 8.3 microg/ml), (3) EGCG (4, 40, 400 ng/ml), or (4) the combination of ASU[Avocado Soybean unsaponifiables] and EGCG[epigallocatechini gallate, it's found in green tea] for 24h. Cells were next incubated with control medium alone or with IL-1beta (10 ng/ml) and TNF-alpha (1 ng/ml). COX-2 gene expression by real-time PCR analysis and NF-kappaB nuclear translocation by immunohistochemistry were performed after 1h of incubation. PGE(2) production was determined by immunoassay after 24h of incubation.
Equine chondrocytes responded to cytokine activation by up-regulated gene expression of COX-2 and increased PGE(2) production. Activation was associated with NF-kappaB translocation. Individually, ASU and EGCG marginally inhibited COX-2 expression and PGE(2) production in activated chondrocytes. In contrast, the combination of ASU and EGCG reduced COX-2 expression close to non-activated control levels and significantly inhibited PGE(2) production. These reductions were statistically greater than those of ASU or EGCG alone. The inhibition of COX-2 expression and PGE(2) production was associated with inhibition of NF-kappaB translocation."


PGE2 and COX2 have an affect on vertical body growth.  Whether it augments or hinders growth is unclear.  But Green Tea and Avocados affect PGE2 and COX2.


Prostaglandin E2 inhibits BMP signaling and delays chondrocyte maturation.


"While cyclooxygenases are important in endochondral bone formation during fracture healing, mechanisms involved in prostaglandin E2 (PGE2) regulation of chondrocyte maturation are incompletely understood. The present study was undertaken to determine if PGE2 effects on chondrocyte differentiation are related to modulation of the bone morphogenetic protein (BMP) signaling pathway. In primary murine sternal chondrocytes, PGE2 differentially regulated genes involved in differentiation. PGE2 induced type II collagen and MMP-13[Remember F-spondin which reduces height growth increased MMP-13 levels by as much as 30%], had minimal effects on alkaline phosphatase, and inhibited the expression of the maturational marker, type X collagen. In BMP-2-treated cultures, PGE2 blocked the induction of type X collagen. All four EP receptors were expressed in chondrocytes and tended to be inhibited by BMP-2 treatment. RCJ3.1C5.18 chondrocytes transfected with the protein kinase A (PKA) responsive reporter, CRE-luciferase, showed luciferase induction following exposure to PGE2, consistent with activation of PKA signaling and the presence of the EP2 and EP4 receptors. Both PGE2 and the PKA agonist, dibutyryl cAMP, blocked the induction of the BMP-responsive reporter, 12XSBE, by BMP-2 in RCJ3.1C5.18 chondrocytes. In contrast, PGE2 increased the ability of TGF-beta to activate the TGF-beta-responsive reporter, 4XSBE. Finally, PGE2 down-regulated BMP-mediated phosphorylation of Smads 1, 5, and 8 in RCJ3[Phosphorylating Smad 1/5/8 means to inhibit them and Smad 1/5/8 phosphorylation is  a way to grow taller!  PGE2 downregulates this.]1C5.18 cells and in primary murine sternal chondrocytes. Altogether, the findings show that PGE2 regulates chondrocyte maturation in part by targeting BMP/Smad signaling and suggest an important role for PGE2 in endochondral bone formation."


PGE2 downregulates Phosphorylation 1/5/8 and raises levels of MMP-13.  Therefore, PGE2 is bad for height growth.  Therefore, you can grow taller with avocados(100% Avocado Oil 8 Oz (Refined, light color)) and green tea(NOW Foods Green Tea Extract, 250 Capsules / 400mg) as they inhibit PGE2.  Does anyone know any other ways to inhibit PGE2?  So inhibiting PGE2 does help vertical body growth but I don't see how inhibiting PGE2 will enable elasticity.

However there's evidence that PGE2 enhances chondrogenesis.

NSAIDS inhibit in vitro MSC chondrogenesis but not osteogenesis: implications for mechanism of bone formation inhibition in man.

"Non-steroidal anti-inflammatory drugs (NSAIDs) may inhibit bone formation. We investigated whether the reported NSAID effect on bone is related to inhibition of bone marrow mesenchymal stem cell (MSC) proliferation and osteogenic and chondrogenic differentiation and evaluated both cyclooxygenase (COX)-1 and COX-2 specific drugs. The effects of seven COX-1 and COX-2 inhibitors on MSC proliferation and osteogenic and chondrogenic differentiation were tested using Vybrant, sodium 3'-[1-(phenylaminocarbonyl)- 3,4-tetrazolium]-bis (4-methoxy-6-nitro) benzene sulfonic acid hydrate (XTT), functional and quantitative assays of MSC differentiation. The MSC expression of COX-1 and COX-2 and prostaglandin E2 (PGE-2) levels were evaluated serially during lineage differentiation by quantitative PCR and ELISA. None of the NSAIDs at broad range of concentration (range 10(-3) to 100 μg/ml) significantly affected MSC proliferation. Surprisingly, MSC osteogenic differentiation inhibition was not evident. However, NSAIDs affected chondrogenic potential with a reduction in sulphated glycosaminoglycans (sGAG) content by 45% and 55% with diclofenac and ketorolac, respectively (P < 0.05 compared to controls). Parecoxib and meloxicam, more COX-2 specific reagents inhibited sGAG to a lesser degree, 22% and 27% respectively (P < 0.05 compared to controls). Cartilage pellet immunohistochemistry confirmed the above results. Pellet chondrogenesis was associated with increased COX-1 expression levels but not COX-2, and COX-1 specific drugs suppressed MSC PGE-2 more than COX-2 specific inhibitors. These findings suggest that NSAIDs may inhibit bone formation via blockage of MSC chondrogenic differentiation."

So non-steroidal anti-inflammatory drugs may decrease chondrogenesis thus decreasing height.

"[PGE2] can stimulate new bone formation, increase bone mass and also regulate both bone morphogenetic protein 2 (BMP-2) and BMP-7 expression"