Adding Height with Vitamin E‏?

Dl-alpha tocopheryl acetate is one of the key ingredients for peak height.  Dl-alpha tocopheryl acetate is also known as Vitamin E.  Peak Height may have some benefits for increasing height but it is really an overpriced vitamin supplement.  It may be possible to increase height with different forms of certain Vitamins.  For example, Cyp27b1 which converts Vitamin D to the active metabolite increases height when it is deactivated.  So ingesting a form of Vitamin D that can't be converted into the active metabolite may increase height.  It could either be that the active metabolite of Vitamin D reduces growth or it could be that the inactive metabolite of Vitamin D increases growth and conversion of Vitamin D into the active metabolite reduces the numbers of the inactive metabolite.  Both of these possible reasons would explain a benefit for a form of Vitamin D that can't be converted into the active metabolite form.

Vitamin E is available as a nutritional supplement: Kirkland Signature Vitamin E 400 IU, 500 Softgels

What effects does Vitamin E have on adding height? 

Vitamin E stimulates trabecular bone formation and alters epiphyseal cartilage morphometry. 

"The effects of dietary vitamin E (VIT E) and lipids on tissue peroxidation and fatty acid composition, epiphyseal growth plate cartilage development, and trabecular bone formation were evaluated in chicks. A 2 x 2 factorial design was followed using two levels (30 and 90 IU/kg of diet) of dl-alpha-tocopheryl acetate and two different dietary lipids. The basal semipurified diet contained one of the following lipid treatments: anhydrous butter oil (40 g/kg) + soybean oil (60 g/kg), [BSO], or soybean oil (100 g/kg), [SBO]. After 14 days of feeding, the level of alpha tocopheryl in plasma was higher and thiobarbituric acid reactive substances (TBARS) were less in plasma and liver of chicks supplemented with 90 IU of VIT E compared with those given 30 IU of VIT E. Body weights and tibiotarsal bone lengths were not affected by the dietary treatments. Saturated fatty acids (14:0, 15:0, 16:0, 17:0, and 18:0) were increased in the tibiotarsal bone of chicks fed the BSO diet. In contrast, total polyunsaturated fatty acids and the ratio unsaturated fatty acids/saturated fatty acids were higher is plasma of chicks fed SBO compared with the values from chicks fed BSO. The thickness of the entire growth plate cartilage and the lower hypertrophic chondrocyte zone was significantly greater in chicks fed 90 IU/kg of VIT E. Kinetic parameters on bone histomorphometry indicated that mineral apposition rate was higher in chicks fed 90 IU of VIT E. The interaction effect between the VIT E and BSO treatments led to the highest trabecular bone formation rate among the groups. VIT E protects against cellular lipid peroxidation in cartilage to sustain normal bone growth and modeling." 

Vitamin E is an anti-oxidant(it scavenges free radicals that can cause damage).  That would indicate that it's only necessary to have sufficient levels of Vitamin E in the diet to grow taller not that excess levels of Vitamin could help you grow taller. 

Synergistic chondroprotective effect of alpha-tocopherol, ascorbic acid, and selenium as well as glucosamine and chondroitin on oxidant induced cell death and inhibition of matrix metalloproteinase-3--studies in cultured chondrocytes. 

"Overproduction of reactive oxygen species and impaired antioxidant defence accompanied by chronic inflammatory processes may impair joint health. Pro-inflammatory cytokines such as interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) stimulate the expression of metalloproteinases which degrade the extracellular matrix. Little is known regarding the potential synergistic effects of natural compounds such as alpha-tocopherol (alpha-toc)[Vitamin E], ascorbic acid (AA)[Vitamin C] and selenium (Se) on oxidant induced cell death. Furthermore studies regarding the metalloproteinase-3 inhibitory activity of glucosamine sulfate (GS) and chondroitin sulfate (CS) are scarce. Therefore we have studied the effect of alpha-toc (0.1-2.5 micromol/L), AA (10-50 micromol/L) and Se (1-50 nmol/L) on t-butyl hydroperoxide (t-BHP, 100-500 micromol/L)-induced cell death in SW1353 chondrocytes. Furthermore we have determined the effect of GS and CS alone (100-500 micromol/L each) and in combination on MMP3 mRNA levels and MMP3 secretion in IL-1beta stimulated chondrocytes. A combination of alpha-toc, AA, and Se was more potent in counteracting t-BHP-induced cytotoxicity as compared to the single compounds. Similarly a combination of CS and GS was more effective in inhibiting MMP3 gene expression and secretion than the single components. The inhibition of MMP3 secretion due to GS plus CS was accompanied by a decrease in TNF-alpha production. Combining natural compounds such as alpha-toc, AA, and Se as well as GS and CS seems to be a promising strategy to combat oxidative stress and cytokine induced matrix degradation in chondrocytes." 

Selenium is available as a supplement as well, for cheap: Selenium 200mcg 100 caps. Note that the reason they consider MMP-3 as a bad thing is that they are trying to culture chondrocytes and they don't want a degradation of extracellular matrix then.  MMP-3 is one of the crucial MMPs involved in the formation of cartilage canals.  What's important to note in this article is that Vitamin E, Vitamin C, and Selenium all reduce TNF-Alpha and IL-1.  How much you need is based on the oxidative stress you undergo especially if you smoke. 

Ascorbic acid-induced chondrocyte terminal differentiation: the role of the extracellular matrix and 1,25-dihydroxyvitamin D. 

"Chondrocyte terminal differentiation is associated with cellular hypertrophy increased activity of plasma membrane alkaline phosphatase and the synthesis of collagen type X. The hypertrophic phenotype of cultured chondrocytes can be stimulated by ascorbic acid[Vitamin C] but the underlying mechanisms for this phenotypic change are unclear. As ascorbic acid is central to many hydroxylation reactions, the possibility was examined that its pro-differentiating effects are mediated by its effects on collagen and vitamin D metabolite formation. In vitro studies indicated that ascorbic acid-induced chondrocyte alkaline phosphatase activity was inhibited by the addition of both collagen and proteoglycan synthesis inhibitors. The addition of arginine-glycine-aspartic acid (RGD)-containing peptides also resulted in lower alkaline phosphatase activity. Chicks supplemented with dietary ascorbic acid had higher concentrations of both collagen and proteoglycans within their growth plates but the chondrocyte maturation rate was unaltered. No evidence was obtained to suggest that ascorbic acid-induced collagen production was mediated by lipid peroxidation[like Vitamin E]. In addition, supplementation with dietary ascorbic acid resulted in higher serum 1,25-dihydroxyvitamin D3 concentrations and increased chondrocyte vitamin D receptor number. Ascorbic acid-treated chondrocytes maintained in vitro also had increased vitamin D receptor numbers but chondrocyte receptor affinity for 1,25-dihydroxyvitamin D3 was unaltered. These results indicate that ascorbic acid promotes both chondrocyte matrix production and 1,25-dihydroxyvitamin D3 synthesis, accompanied by upregulation of the vitamin D receptor. Thus, ascorbic acid may be causing amplification of the vitamin D receptor-dependent genomic response to 1,25-dihydroxyvitamin D, resulting in promotion of terminal differentiation. Strong evidence is provided to support the hypothesis that ascorbic acid-induced chondrocyte terminal differentiation is mediated by interactions between integrins and RGD-containing cartilage matrix proteins." 

So Vitamin E doesn't seem to interact with Vitamin C.  These scientists think that the key to elongating the growth phase is by inhibiting Alkaline Phosphatase and Collagen X. LIPUS(and by extensions LSJL) blocked expression of Type X Collagen. This study also indicates that 1,25-dihydroxyvitamin D may result in the terminal differentiation of chondrocytes so now it seems that to increase height we must inhibit the active metabolite of Vitamin D.  We also increase height by increasing the number of peptides containing the RGD group. 

So proper amounts of Vitamin E can increase height by scavenging free radicals.  Cholecalciferol(one of the main ingredients of Peak Height), the inactive form of Vitamin D could increase height if it doesn't convert to the active form.  We'll have to go over those studies to see if it does or doesn't.