Possible to grow taller with huperzine a?

There doesn't seem to be strong directions between huperzine a and height growth but it is available for sale: Source Naturals Huperzine A, 200mcg, 120 Tablets.

Effects of huperzine A on memory deficits and neurotrophic factors production after transient cerebral ischemia and reperfusion in mice.


"Oral administration of huperzine A (0.2 mg/kg, once per day, started 2 days before surgery and lasted for 7 days after surgery)... significantly increased the mRNA and protein levels of  TGF-beta(1), and potentiated phosphorylation of MAPK/ERK 1/2[so increased phosphorylation of MAPK]"<-MAPK plays some sort of mediary role in cell proliferation.  This was in the brain not the bone though.

Huperzine A is an acetylcholinesterase inhibitor and it was linked to bone in this study "Acetylcholinesterase inhibitors and the risk of hip fracture in Alzheimer's disease patients: a case-control study."

Human osteogenesis involves differentiation-dependent increases in the morphogenically active 3' alternative splicing variant of acetylcholinesterase.

"The extended human acetylcholinesterase (AChE) promoter contains many binding sites for osteogenic factors, including 1,25-(OH)2 vitamin D3 and 17beta-estradiol[Vitamin D and estrogen are chondrogenic factors too]. In differentiating osteosarcoma Saos-2 cells, both of these factors enhanced transcription of the AChE mRNA variant 3' terminated with exon 6 (E6-AChE mRNA), which encodes the catalytically and morphogenically active E6-AChE isoform[both estrogen and Vitamin D have some height decreasing effects and benefits maybe inhibiting AChE with something like huperzine A will eliminate the negatives and allow you to keep the benefits]. In contrast, antisense oligodeoxynucleotide suppression of E6-AChE mRNA expression increased Saos-2 proliferation in a dose- and sequence-dependent manner. The antisense mechanism of action was most likely mediated by mRNA destruction or translational arrest, as cytochemical staining revealed reduction in AChE gene expression. In vivo, we found that E6-AChE mRNA levels rose following midgestation in normally differentiating, postproliferative fetal chondrocytes but not in the osteogenically impaired chondrocytes of dwarf fetuses with thanatophoric dysplasia[so AChE is likely involved in ossification so you need some AChE or you'll just have cartilage and poorly developed bone]."

"AChE is expressed in [mesenchymal] cells"

"direct correlation between E6-AChE mRNA expression and chondrocyte differentiation, itself inversely correlated with chondrogenic proliferation"

Getting Estrogen to equilibrium levels may be a way to grow taller.  Using Huperzine A may be a way to get AChE to equilibrium levels.  However, we don't know what those equilibrium levels are.  Still, Huperzine A is more readily available than Estrogen inhibitors so it's a step forward.

Huperzine A is an NMDA receptor antagonist and that has effects on chondrogenesis as well.

Interference with cellular differentiation by D-serine through antagonism at N-methyl-D-aspartate receptors composed of NR1 and NR3A subunits in chondrocytes.

"Serine racemase (SR) is responsible for the biosynthesis of D-serine (D-Ser), an endogenous co-agonist for the glycine (Gly)-binding site on N-methyl-D-aspartate (NMDA) receptors, from L-Ser in the brain. We have previously demonstrated high expression of SR by chondrocytes in cartilage. In this study, we attempted to elucidate the possible functional role of D-Ser in chondrogenesis. Expression of mRNA and corresponding protein was seen for SR in cultured rat costal chondrocytes, while the addition of L-Ser significantly increased intracellular and extracellular levels of D-Ser. In organotypic cultured mouse embryonic metatarsals isolated before vascularization, SR mRNA was highly localized in hypertrophic and calcified chondrocytes. Exposure to D-Ser not only suppressed several chondrocytic maturation markers, including alkaline phosphatase (ALP) activity, Ca2+ accumulation, nodule formation, and osteopontin expression, in rat chondrocytes, but also delayed chondral mineralization in mouse metatarsals[this may or may not have an impact on height as chondrocytes have a finitie proliferative capacity and altering the terminal stage won't effect that unless the terminal stage occurs before finite chondrocyte proliferation]. Either NMDA or Gly alone significantly increased Ca2+ accumulation in cultured chondrocytes[there's an optimal level of Ca2+ accumulation and we won't know whether we're above or below that level], whereas D-Ser significantly prevented Ca2+ accumulation by Gly, but not by NMDA. Gly alone also significantly increased gene transactivation by the introduction of runt-related transcription factor-2 (Runx2) in COS7 cells transfected with NR1 and NR3A subunits, while D-Ser significantly prevented the increase by Gly without affecting the promoter activity of Runx2. In both cultured chondrocytes and metatarsals from NR1-null mice, significant decreases were seen in ALP activity and chondral mineralization, respectively. These results suggest that D-Ser may negatively regulate cellular differentiation through inhibiting NMDA receptors composed of NR1 and NR3A subunits in a manner related to Runx2 transcriptional activity in chondrocytes."

So Huperzine A is an over the counter supplement that could have an impact on height growth.  However, AChE needs to be at a specific equilibrium and there's an optimal amount of Ca2+ accumulation in chondrocytes and stem cells.  We don't know what that serum level is and there's no over the counter way to test these levels.