Review of Growth Flex V Pro Scam

Growth Flex V Pro contains Arginine and Ornithine.  It's $100 for a one month supply!  You can get Arginine and Ornithine for about 16$ Vitamin Shoppe - L-Arginine-Ornithine 2000 Mg, 2000 mg, 100 capsules.  Arginine may help increase height via HGH, CARM-1(An arginine associated methyltransferase), and the Nitric Oxide Pathway.  How can Ornithine affect height growth? 

Polyamine depletion inhibits apoptosis following blocking of survival pathways in human chondrocytes stimulated by tumor necrosis factor-alpha. 

"Chondrocyte apoptosis can be an important contributor to cartilage degeneration[and can cause a reduction in height growth], thereby making it a potential therapeutic target in articular diseases. To search for new approaches to limit chondrocytic cell death, we investigated the requirement of polyamines for apoptosis favored by tumor necrosis factor-alpha (TNF), using specific polyamine biosynthesis inhibitors in human chondrocytes. The combined treatment of C-28/I2 chondrocytes with TNF and cycloheximide (CHX) resulted in a prompt effector caspase activation and internucleosomal DNA fragmentation. Pre-treatment of chondrocytes with alpha-difluoromethylornithine (DFMO), an ornithine decarboxylase (ODC) inhibitor, markedly reduced putrescine and spermidine content as well as the caspase-3 activation and DNA fragmentation induced by TNF and CHX. DFMO treatment also inhibited the increase in effector caspase activity provoked by TNF plus MG132, a proteasome inhibitor. DFMO decreased caspase-8 activity and procaspase-8 content, an apical caspase essential for TNF-induced apoptosis. Although DFMO increased the amount of active, phosphorylated Akt, inhibitors of the Akt pathway failed to restore the TNF-induced increase in caspase activity blunted by DFMO. DFMO also reduced the increase in caspase activity induced by staurosporine, but in this case Akt inhibition prevented the DFMO effect. Pre-treatment with CGP 48664, an S-adenosylmethionine decarboxylase (SAMDC) inhibitor markedly reduced spermidine and spermine levels, and provoked effects similar to those caused by DFMO. Finally DFMO was effective even in primary osteoarthritis (OA) chondrocyte cultures. These results suggest that the intracellular depletion of polyamines in chondrocytes can inhibit both the death receptor pathway by reducing the level of procaspase-8, and the apoptotic mitochondrial pathway by activating Akt." 

Phosphorylation of Akt is good and height increasing substances like IGF-II increase phosphorylation of Akt. But anything that enhances TNF-alpha like Ornithine decarboxylase is bad.  You can increase phosphorylation of Akt with methods other than Ornithine and avoid feed TNF-alpha with Ornithine decarboxylase. 

Induction of ornithine decarboxylase in T/C-28a2 chondrocytes by lysophosphatidic acid: signaling pathway and inhibition of cell proliferation. 

"Among several extracellular messengers tested, lysophosphatidic acid (LPA) was able to cause the most marked induction of ornithine decarboxylase (ODC) in serum-starved human T/C-28a2 chondrocytes. LPA also induced the activation/phosphorylation of Src, Akt and p44/42 MAPK, and the translocation of PKC-delta from cytosol to membrane coupled to its tyrosine phosphorylation. Experiments with selective signaling inhibitors indicate that LPA leads to Src activation through Gi protein-coupled receptors. In turn Src can activate PI3K and PKC-delta, and all these signaling proteins are required for ODC induction. In conclusion these results show that chondrocytes may be a novel target for LPA action. However, although LPA is considered a mitogen for several cell types and ODC induction is generally correlated to cell growth, LPA was not able to stimulate chondrocyte growth, but rather exerted an anti-proliferative effect." 

So the positive effects on ornithine decarboxylase on cell growth(Akt phosphorylation among other effects) are less than the negative effects of ornithine decarboxylase on TNF-alpha.  Ornithine decarboxylase may reduce height growth!  Although the negative effects of Ornithine Decarboxylase on TNF-Alpha and other inflammatories may be mitigated by anti-inflammatories. 

Does Ornithine increase HGH? 

Arginine and ornithine supplementation increases growth hormone and insulin-like growth factor-1 serum levels after heavy-resistance exercise in strength-trained athletes. 

"This placebo-controlled double-blind study was designed to investigate the effect of arginine and ornithine (arg and orn) supplementation during 3-week heavy-resistance training on serum growth hormone/insulin-like growth factor-1/insulin-like growth factor-binding protein 3 (GH/IGF-1/IGFBP-3), testosterone, cortisol, and insulin levels in experienced strength-trained athletes. The subjects were randomly divided between a placebo group (n = 8) and the l-Arg/l-Orn-supplemented group (n = 9), and performed pre and posttraining standard exercise tests with the same absolute load, which consisted of the same exercise schedule as that applied in the training process. Fasting blood samples were obtained at rest, 2 minutes after the cessation of the strength exercise protocol, and after 1 hour of recovery. The resting concentrations of the investigated hormones and IGFBP-3 did not differ significantly between the study groups. In response to exercise test, all the hormones were elevated (p < 0.05) at both time points. Significant increases (p < 0.05) were observed in both GH and IGF-1 serum levels after arg and orn supplementation at both time points, whereas a significant decrease was seen in IGFBP-3 protein during the recovery period. Because there was no between-group difference in the remaining hormone levels, it appears that the GH/IGF-1/IGFBP-3 complex may be the major player in muscle tissue response to short-term resistance training after arg and orn supplementation." 

Here's another study that supports arginine and ornithine's affects on HGH: 

Arginine increases growth hormone gene expression in rat pituitary and GH3 cells. 

"The effect of arginine (Arg) and Ornitargin (OT) [a compound containing the aminoacids Arg, citrulline (Cit) and ornithine (Orn)] administration upon growth hormone (GH) gene expression was studied both in vivo and in vitro (hemipituitaries and GH3 cells) by Northern blot analysis. For in vivo studies, adult male Wistar rats were anesthetized, subjected to i.v. infusion of 200 microl of 150 mM NaCl (control group), Arg (15 or 150 mg) or OT (15 mg of Arg, 1 mg of Cit and 4 mg of Orn) at a rate of 20 microl/min, and killed 50 min thereafter. For the in vitro studies, hemipituitaries or GH3 cells were incubated in 1 ml of appropriate medium containing Arg (15 or 150 mg) or OT (15 mg of Arg, 1 mg of Cit and 4 mg of Orn) for 60 min. The pituitaries of the in vivo and in vitro studies and GH3 cells were subsequently processed for RNA extraction. Total RNA was subjected to electrophoresis in agarose (1%)/formaldehyde gel, transferred to a nylon membrane and subjected to hybridization with a rat GH (32)P-cDNA, and (32)P-18S rRNA probe to correct for the variability in RNA loading. After autoradiography of the membrane, the abundance of GH mRNA and 18S rRNA bands was quantified by densitometry. The in vivo study demonstrated that Arg and OT infusion induced a 2.3-fold increase in GH mRNA expression, which could result from the Arg-mediated inhibition of somatostatin release. In addition, in vitro Arg, but not OT, induced GH gene expression in hemipituitaries and GH3 cells, indicating that the aminoacid can act per se at the pituitary somatotrope level. In conclusion, our data show for the first time that arginine stimulates GH gene expression in parallel to its recognized GH-releasing activity." 

Note this is infusion of Ornithine and Arginine. Arginine may be better than Ornithine because of how Ornithine Decarboxylase "feeds" TNF-alpha.  Arginine could also increase inflammation via Nitric Oxide.  It's possible that Ornithine plus anti-inflammatories could increase height.  There are tons of anti-inflammatories such as Phlomis Umbrosa and Eleutherococcus senticosus.  You could also supplement with Folinic and Folic Acid to help prevent DNA damage.  In puberty, I would worry about the anti-inflammatories first and then start taking growth boosters that cause inflammation like Arginine and Ornithine.  You should never take Growth Flex V Pro, it is an overpriced vitamin supplement.

Grow Taller with Arginine

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.