Increase your Height with S-Adenosyl methionine

Earlier, we discussed how DNA Methylation was involved in growth plate cessation.  Yes, Estrogen handles growth plate fusion but growth plate fusion will not occur until after growth plate cessation.  Then we discussed how folic and folinic acid were involved in producted DNA from damage(And in turn damage to DNA Methyltransferase).  S-Adenosyl Methionine is available for purchase:Nature Made SAM-e Complete 200 mg - 90 Enteric Coated Tablets

Now, S-Adenosyl Methionine has a methyl group that can be donated to different proteins.  If methyl groups were continuously donated to growth plate chondrocytes the body would keep growing!

Exploring the mechanisms behind S-adenosylmethionine (SAMe) in the treatment of osteoarthritis

"Clinical trials have shown reduced pain and stiffness [in osteoarthritis] while in vitro and animal studies have shown SAMe can stimulate the production of cartilage which is critical in reversing the disease process. The author examines many potential mechanisms of action including: reduction of inflammatory mediators; increasing levels of glutathione; direct or indirect signaling of cartilage synthesis or survival; maintenance of DNA methylation. Research into the mechanisms of supplemental SAMe in osteoarthritis is necessary to evaluate the clinical effectiveness and safety of this dietary supplement."

"Osteoarthritic chondrocytes are particularly sensitive to the inflammatory cytokines because they have increased levels of their activating enzymes and receptors. Part of the catabolic role of IL-1 could be due to its ability to up regulate the inducible form of nitric oxide synthase and cyclooxygenases (COX)-2, leading to the increased production of nitric oxide and prostaglandin E2. Nitric oxide can induce apoptosis and decrease proteoglycan synthesis in chondrocytes by interfering with β 1-integrin mediated cell to matrix signal transduction mechanism. Over time, the cartilage would disintegrate, resulting in narrowing of the joint space and damage to the surrounding bone"

"joint space narrowing occurs at < 0.1 mm per year"

"intramuscular injection with 30 mg/kg and 60 mg/kg of SAMe for 12 weeks resulted in an increased number of cells and depth of cartilage in a partial meniscectomy model of osteoarthritis in rabbits compared to placebo"

"positive effects after treatment with both 1 μ g/ml and 10 μ g/ml SAMe, with 10 μ g/ml being the most effective at increasing proteoglycan synthesis and secretion, while 100 μ g/ml had an inhibitory effect"

"SAMe plays a vital role in three biochemical pathways; methylation, transsulfuration and aminopropylation. The loss of a methyl group from SAMe triggers the transsulfuration pathway creating all endogenous sulfur compounds. With the loss of its methyl group to different acceptors (i.e. DNA, proteins, phospholipids, and neurotransmitters) SAMe is converted into s-adenosylhomocysteine, which is hydrolyzed to adenosine and homocysteine. When methionine is needed, homocysteine is remethylated by methyltetrahydrofolate homocysteine methyltransferase with B12 as a cofactor. When methionine is in excess, homocysteine is converted to cystathionine by β cystathionine-synthase with vitamin B6 as a cofactor. Cystathionine is then converted to cysteine, which can act as a reducing agent either alone or as an active part of glutathione. Polyamines are synthesized via the aminopropylation pathway which begins when SAMe is converted to decarboxylated SAMe via SAMe decarboxylase. As an aminopropyl group is transferred to putrescine, methylthioadenosine is formed, which is followed by the production of spermidine and spermine. Methylthioadenosine is then converted back to methionine"

Well, in osteoarthiritis the cartilage is already turning into bone so we don't know if SAMe consumption will result in endochondral ossification of the articular cartilage.  But, SAMe can stimulate the production of cartilage when ordinarily cartilage production is very limited so taking SAMe during development could lead to extra height growth(If you take SAMe you also need to take Folic acid as well to cope with the additional cellular proliferation).  SAMe is produced by the body.

Moderate or supranormal folic acid supplementation does not exert a protective effect for homocysteinemia and methylation markers in growing rats

"Folic acid (FA) deficiency/supplementation effects seem to be dependent on age group and/or physiological status. The aim was to evaluate changes associated with rapid growth in relation to methionine metabolism in rats.
Four groups (n = 10 each) of male Sprague Dawley rats (5 weeks old) were on diets that varied in their FA content: 0 mg FA/kg diet (deficient), 2 mg FA/kg diet (control), 8 mg FA/kg diet (moderate supplementation), 40 mg FA/kg diet (supranormal supplementation). Animals were fed ad libitum for 30 days. Biomarkers of methionine metabolism and antioxidant status were evaluated.
Serum total homocysteine concentration increased (p < 0.01) in FA deficient animals, with no differences between the supplemented groups. The hepatic 'methylation ratio' (S-adenosylmethionine/S-adenosylhomocysteine) of the FA content groups reached similar values, which were significantly higher compared to the deficient group. The brain 'methylation ratio', however, remained unmodified independently of FA content in the diet. FA deficiency induced hepatic DNA hypomethylation, and supranormal FA supplementation exerted the most protective effect (p < 0.01). Serum folate levels increased according to FA dietary level, whereas no differences were seen for vitamin B(12) and vitamin B(6).
FA deficiency compromises methionine metabolism whereas supplementation does not show an additional positive effect compared to the control diet in growing animals"

"The main dietary components that act as methyl groups donors are folates, methionine, vitamin B 12 and choline"

"The methionine cycle is nutritionally regulated by FA, and vitamins B 6 and B 12"

"The so-called methylation ratio (AdoMet/AdoHcy) of the 3 groups whose diet included FA reached similar values, significantly higher compared to the deficient group"

"Serum folate levels are increased, as expected, in accordance with the vitamin supplementation level of the diet. However, serum vitamin B 6 and B 12 in the different groups remained unmodified regardless of dietary FA content"

"neither FA deficiency nor supplementation altered the average weight gain of the animals
throughout the study. These results are comparable to other studies that show neither deficiency nor supplementation of FA in the diet inhibits or improves animal response in relation to growth"

After 200 micrograms/a day of FA, Folic acid is no longer metabolized and floats in the serum.

"high-dose FA supplementation does not seem to induce higher transmethylation activity"

The conclusions seem to differ from the results as they say that supranormal FA supplementation exerts a protective effect and serum folate levels increased with Folic acid supplementation.  But this shows that SAMe supplementation will have an effect independent of Folic acid supplementation as in all the groups the SAMe level in the blood normalized on a particular level.

SAMe hasn't really been tested on healthy adults and it's effects on cell growth but in theory SAMe supplementation should result in some extra height growth as a result of more chondrocytes getting methylating and thus proliferating and differentiating for a longer period.