Arginine is an amino acid that is often taken by height seekers in an attempt to grow taller. Arginine is taken to try to increase growth hormone levels and growth hormone may increase height(GH has been to shown to increase height in GH transgenic mice and in tumors in the pituitary gland plus other homeostatic altering places but those contain several confounding variables that may increase the height other than the GH itself such as altered homeostatic mechanisms in GH transgenic mice). Arginine also increases height via the Nitric Oxide/Guanyl Cyclase/cGMP pathways. CARM1(co-activator associated arginine methyltranferase 1) is a critical regulator of chondrocyte proliferation by regulating the arginine methylation of Sox9. CARM1 disrupts the interaction of Sox9 with Beta-Catenin (which could induce hypertrophic chondrocytes to differentiate into bone) so someone with more CARM1 may grow taller.
L-Arginine is also a key ingredient of Peak Height, Height Maximizer.
Ibuprofen-arginine generates nitric oxide and has enhanced anti-inflammatory effects.
"Ibuprofen, a chiral non-steroidal anti-inflammatory drug chemically related to fenoprofen and naproxen, has moderate but definite anti-inflammatory, analgesic and antipyretic properties. Bioavailability of ibuprofen is increased by salification with various salts. Ibuprofen-arginine [is] of biological interest because l-arginine acts as substrate of the nitric oxide (NO) synthesising enzymes. Using epithelial HeLa cells expressing the endothelial NO synthase we show that ibuprofen-arginine releases NO and that this NO protects against the cytotoxic apoptogenic effects of staurosporine. Ibuprofen-arginine is endowed with enhanced anti-inflammatory effects with respect to ibuprofen, as shown by reduced hind paw oedema, neutrophil infiltration and chondrocyte apoptosis in collagen-induced mouse arthritis, a model of chronic inflammation. NO has pleiotropic beneficial effects that may contribute to limit inflammation and anti-inflammatory compounds able to release NO display higher efficacy than the parent drugs in defined clinical settings. NO generation contributes to the enhanced anti-inflammatory effects of ibuprofen-arginine vs. ibuprofen."
Ibuprofen-arginine may be a potential way to grow taller by increasing NO expression which increases cGK II expression. Nitric Oxide may have negative effects on growth too but this can be alleviated by TP508.
Thrombin peptide TP508 prevents nitric oxide mediated apoptosis in chondrocytes in the endochondral developmental pathway.
"TP508 is a 23-amino acid peptide derived from human prothrombin that increases cartilage matrix production and reduces alkaline phosphatase activity without changing chondrocyte proliferation. TP508 acts by blocking the onset of apoptosis associated with hypertrophy. Rat costochondral resting zone chondrocytes and human auricular chondrocytes were cultured in DMEM containing 50microM ascorbic acid and 10% FBS. Apoptosis was induced by treatment of confluent cultures with chelerythrine, tamoxifen, or inorganic phosphate (Pi) for 24h[chelerythrine, tamoxifen, and inorganic phosphate are bad for growth]. One half of the cultures received TP508 (0, 0.7, or 7microg/ml). Apoptosis was assessed as a function of DNA fragmentation ([3H]-thymidine labeled DNA fragments), TUNEL staining, and cell viability using the MTT assay, as well as by assessing the Bcl-2/Bax mRNA and protein ratios and caspase-3 activity. The universal NO synthase inhibitor l-NMMA was used to assess the effect of NO production on chondrocyte apoptosis and specific NO synthase subspecies were identified using iNOS inhibitor 1400W and nNOS inhibitor vinyl-l-NIO, as well as l-NAME, which inhibits both iNOS and eNOS. Finally, we assessed if TP508 would block NO production induced by the apoptogens. Chelerythrine, tamoxifen and Pi-induced apoptosis and this was reversed by TP508. All apoptogens increased NO production and this was reduced by TP508. TP508 reduced NO levels to the same extent as 1400W but not to the same extent as l-NAME, suggesting that its effects are mediated primarily by iNOS. In addition, TP508 reduced the effect of chelerythrine to the same extent as 1400W and l-NAME, again indicating that it acts via inhibition of an iNOS pathway. TP508 also regulated Bcl-2/Bax[mostly via upregulation of Bax] mRNA in a time and dose-dependent manner. The Bcl-2/Bax mRNA ratio was 0.11 in the absence of TP508 at 1h and 4.95 at 7microg/ml TP508; by 3h the ratio was approximately 1 in both groups. The Bcl-2/Bax protein ratio also increased by 63% at 1h. TP508 did not affect caspase-3 activity. TP508 also caused a dose-dependent increase in protein kinase C (PKC) activity within 9min that was maximal at 270min. TP508 prevents apoptosis in growth plate chondrocytes via inhibition of iNOS-dependent NO [with] PKC [involvement]."
NO activity may result in chondrocyte apoptosis but NO also has positive activities as well. TP508 inhibits the specific pathway that causes growth plate chondrocyte apoptosis. TP508 inhibits apoptosis in human chondrocytes as well.
L-Arginine should increase Nitric Oxide levels by providing more raw materials to increase Nitric Oxide(Nitric Oxide should be increased first by a mechanism like Viagra or Tribulus Terristris). Viagra might be best because it doesn't increase NO but rather it's a PDE5 inhibitor so it doesn't cause Chondrocyte Apoptosis.
Growing taller with a supplement that increases NO(or inhibits PDE5), L-arginine, or TP508 should be possible. If you take something like Viagra which doesn't specifically increases NO but rather targets a by-product on the pathway then you may not need TP508.