Grow Taller with Vitamin D?

Vitamins are a lot more complicated than you would think.  Vitamins can influence height growth but it's not a simple matter of supplementing with vitamins.  Their are several forms of each vitamin and each has different effects.

The big vitamin that people point to when height growth is involved is Vitamin D.  Vitamin D is needed for bone growth but as Vitamin D is not a regulator of bone growth supra-maximal levels of Vitamin D will not result in supra-maximal bone growth.  The big factor in height growth that Vitamin D can affect is that it is involved in regulating cellular proliferation, differentiation, and apoptosis(all three of which occur in the growth plate).  But you'd need a Vitamin D mutation to get altered growth.

Vitamin D is the most promising Vitamin aside from Vitamin B12(which helps to regulate DNA synthesis which can affect everything) that could affect height growth.  Although obviously, you can't increase your height when you're dead and all Vitamins help you live.

Vitamin D is way more powerful than calcium although calcium is needed in repair. 

Chondrocyte-specific modulation of Cyp27b1 expression supports a role for local synthesis of 1,25-dihydroxyvitamin D3[One of the forms of Vitamin D] in growth plate development. 

"The Cyp27b1 enzyme (25-hydroxyvitamin D-1alpha-hydroxylase) that converts 25-hydroxyvitamin D into the active metabolite, 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)], is expressed in kidney but also in other cell types such as chondrocytes[Vitamin D conversion enzyme is expressed in chondrocytes]. This suggests that local production of 1,25(OH)(2)D(3)[Vitamin D] could play an important role in the differentiation of these cells. To test this hypothesis, we engineered mutant mice that do not express the Cyp27b1 gene in chondrocytes. Inactivation of both alleles of the Cyp27b1 gene led to decreased RANKL expression and reduced osteoclastogenesis, increased width of the hypertrophic zone of the growth plate at embryonic d 15.5, increased bone volume in neonatal long bones, and increased expression of the chondrocytic differentiation markers Indian Hedgehog and PTH/PTHrP receptor. The expression of the angiogenic marker VEGF was decreased, accompanied by decreased platelet/endothelial cell adhesion molecule-1 staining in the neonatal growth plate, suggesting a delay in vascularization. In parallel, we engineered strains of mice overexpressing a Cyp27b1 transgene in chondrocytes by coupling the Cyp27b1 cDNA to the collagen alpha(1)(II) promoter[transgenic refers to a heightened expression of the gene, so a heightened expression of the gene that converts Vitamin D into a metabolite]. The transgenic mice showed a mirror image phenotype when compared with the tissue-specific inactivation, i.e. a reduction in the width of the hypertrophic zone of the embryonic growth plate, decreased bone volume in neonatal long bones, and inverse expression patterns of chondrocytic differentiation markers. These results support an intracrine role of 1,25(OH)(2)D(3) in endochondral ossification and chondrocyte development in vivo."  

This study makes it seem like 25-hydroxyvitamin D could be used to enhance height growth and that the other form of Vitamin D is bad for height growth.  Genetic engineered deactivation of the Cyp27b1 gene could also enhance height growth or a Cyp27b1 enzyme inhibitor could also enhance height growth. 

"Ihh and Hif1α mRNA expression was decreased in transgenic mice"

"A role for 1,25(OH)2D3 in growth plate function is further supported by the observation that rescuing mineral homeostasis of Cyp27b1-deficient mice with a high-calcium, high-lactose diet corrected all aspects of the phenotype except long bone growth "

"Despite a stimulation in the expression of Ihh mRNA, we measured an increase in the size of the hypertrophic zone without changes in chondrocyte proliferation in Cyp27b1−/CHΔ mutant mice "

"locally synthesized 1,25(OH)2D3 regulates VEGF expression and signaling in the developing growth plate. In the absence of Cyp27b1, decreased VEGF expression would lead to a decrease in blood vessel formation. In turn, the vasculature delay reduces osteoclast invasion at the chondroosseous junction. Because osteoclasts resorb the calcified cartilaginous matrix that serves as the scaffold for woven bone formation, a reduction in osteoclast invasion would result in an increased scaffold size and thus a larger bone volume at the primary spongiosa. The model predicts that this phenotype is transient as blood vessels eventually invade the chondroosseous junction and normalize osteoclast recruitment and bone turnover."

"The expression of Fgf23 was reduced in the metaphysis of chondrocyte-specific VDR mutant mice"<-Vitamin D may affect FGF23 production from osteoblasts.

Vitamin D could also be involved with Estrogen which some say is the big height increase killer... 

Vitamin D modulation of the activity of estrogenic compounds in bone cells in vitro and in vivo. 

"Vitamin D [induce] creatine kinase (CK) activity. Skeletal organs from vitamin D-depleted rats showed lower constituent CK than those from vitamin D-replete rats. Moreover, estradiol-17beta (E2) or dihydrotestosterone (DHT), which increased CK in organs from intact female or male rats, respectively, stimulated much less CK in vitamin D-depleted rats. Treatment of intact female rats with noncalcemic vitamin D analogs significantly upregulated E2- and DHT-induced CKresponse. These analogs upregulated the CK response to selective estrogen receptor modulators (SERMs) in organs from intact or ovariectomized (Ovx) female rats but abolished SERMs' inhibitory effect on E2-induced CK. These analogs significantly increased estradiol receptor alpha (ERalpha) protein in skeletal organs as well as histomorphological and biochemical changes due to this treatment followed by E2 or DHT. The analogs alone markedly altered the growth plate and the trabeculae and increased trabecular bone volume (%TB V) and trabecular width. The addition of E2 or DHT to this treatment restored all parameters as well as increased %TBV and cell proliferation. Treatment of Ovx female rats with JK 1624 F2-2 (JKF) decreased growth-plate width and increased %TB V, whereas QW1624 F2-2 (QW) restored growth-plate width and %TB V. Treatment of E2 with JKF restored %TBV and growth-plate width, whereas E2 with QW restored all parameters, including cortical width. There was also upregulation of the response of CK to E2 in both combined treatments. Our human-derived osteoblast (hObs)-like cell cultures respond to estrogenic compounds, and pretreating them with JKF upregulated the CK response to E2, raloxifene (Ral), and some phytoestrogens. ERalpha and ERbeta proteins, as well as mRNA, were modulated by CB 1093 (CB) and JKF. JKF increased specific nuclear E2 binding in female hObs but inhibited specific membranal E2 binding. hObs express 25 hydroxyvitamin D3-1alpha hydroxylase (1-OHase)-mRNA and its biological activity[Remember we established this compound as bad in the previous study], which are both modulated by parathyroid hormone (PTH) and estrogenic compounds[another way to tackle this bad form of vitamin D would be a change in parathyroid or estrogenic compounds]. Our results demonstrate mutual interaction between vitamin D and estrogenic compounds."  

Supplementing with Vitamin D won't work above your needs to increase height growth unless it's a Cyp27b1 inhibitor.

Here's a study that states that Vitamin D deficiency actually increases growth rate:

Vitamin D deficiency and whole-body and femur bone mass relative to weight in healthy newborns.

"We measured plasma 25-hydroxyvitamin D [25(OH)D] as an indicator of vitamin D status in 50 healthy mothers and their newborn term infants. In the infants, anthropometry and lumbar, femur and whole-body BMC were measured within 15 days of delivery. Mothers completed a 24-hour recall and 3-day food and supplement record. We categorized the vitamin D status of mothers and infants as deficient or adequate and then compared infant bone mass in these groups using nonpaired t tests. Maternal and infant variables known to be related to bone mass were tested for their relation to BMC using backward stepwise regression analysis.

Twenty-three (46%) of the mothers and 18 (36%) of the infants had a plasma 25(OH)D concentration consistent with deficiency. Infants who were vitamin D deficient were larger at birth and follow-up[Note though that larger individuals are more likely to need more Vitamin D and thus more likely to be deficient]. Absolute lumbar spine, femur and whole-body BMC were not different between infants with adequate vitamin D and those who were deficient, despite larger body size in the latter group. In the regression analysis, higher whole-body BMC was associated with greater gestational age and weight at birth as well as higher infant plasma 25(OH)D.
A high rate of vitamin D deficiency was observed among women and their newborn infants. Among infants, vitamin D deficiency was associated with greater weight and length but lower bone mass relative to body weight. Whether a return to normal vitamin D status, achieved through supplements or fortified infant formula, can reset the trajectory for acquisition of BMC requires investigation."

No information is provided in the study about how low Vitamin D could make bones longer.

Here's a study that states that Vitamin D receptors have minimal effects on human height:

Vitamin D receptor gene polymorphisms have negligible effect on human height.

"Human height is a highly heritable trait, with genetic factors explaining up to 90% of phenotypic variation. The vitamin D receptor (VDR) gene has been reported as contributing to variation in height. A meta-analysis of 13607 adult individuals found a small but significant association with the rs1544410 (BsmI) polymorphism. In contrast, the meta-analysis found no effect in a sample of 550 children. Two recent studies reported variants with large effect on height elsewhere in VDR (rs10735810 [FokI] and rs7139166 [-1,521] polymorphisms). We genotyped large Caucasian samples from Australia (N = 3,906) and the Netherlands (N = 1,689) for polymorphisms in VDR. The Australian samples were twin families with height measures from 3 time points throughout adolescence. The Dutch samples were adult twins. We use the available family data to perform both within and between family tests of association. We found no significant associations for any of the genotyped variants after multiple testing correction. The (non-significant) effect of rs1544410 in the Australian adolescent cohort was in the same direction and of similar magnitude (additive effect 0.3 cm) to the effect observed in the published adult meta-analysis. An effect of this size explains approximately 0.1% of the phenotypic variance in height - this implies that many, probably hundreds, of such variants are responsible for the observed genetic variation. Our results did not support any role for two other regions (rs10735810, rs7139166) of VDR in explaining variation in height."

So it could be the amount of Vitamin D having an effect on human height rather than mutations in the receptor.

High-dose vitamin D supplements are not associated with linear growth in a large Finnish cohort.

"High vitamin D intake in childhood has been suggested to have an adverse influence on linear growth. In Finland, in the mid-1960s the official recommendation for infant vitamin D supplementation was 2000 IU/d (50 μg/d). We investigated whether high-dose vitamin D supplementation in infancy was associated with subsequent growth in height. We used data from a prospective population-based birth cohort study including all children due to be born in the 2 northernmost provinces in Finland in 1966 (12,058 live-births, coverage 96%). Information on each participant's height was collected at birth and ages 1, 14, and 31 y, as were possible confounding factors (data for analyses available from 10,060 singletons). Information on the frequency and dose of vitamin D supplementation was collected in 1967 when participants were 1 y of age. A weak association was found between frequency of vitamin D supplementation with greater height at age 1 y (P = 0.005), which was explained by birth characteristics and maternal and social factors (adjusted P = 0.34). Neither frequency nor dose of vitamin D supplementation was associated with height at 14 or 31 y (P > 0.13). To conclude, contrary to proposed evidence suggesting that vitamin D has a negative influence on growth rate at a dosage of ~2000 IU/d, supplementation at this level in the Northern Finland Birth Cohort was not associated with reduced height at any age studied."

"after adjustment for increased dose and their own adult height at 31 y, participants with rickets were 0.48 cm shorter compared with others"


Arachidonic acid directly mediates the rapid effects of 24,25-dihydroxyvitamin D3 via protein kinase C and indirectly through prostaglandin production in resting zone chondrocytes.

"24,25-dihydroxyvitamin D3 [24,25-(OH)2D3] plays a major role in resting zone chondrocyte differentiation and that this vitamin D metabolite regulates both phospholipase A2 and protein kinase C (PKC) specific activities. Arachidonic acid is the product of phospholipase A2 action and has been shown in other systems to affect a variety of cellular functions, including PKC activity. The aim of the present study was to examine the interrelationship between arachidonic acid and 24,25-(OH)2D3 on markers of proliferation, differentiation, and matrix production in resting zone chondrocytes and to characterize the mechanisms by which arachidonic acid regulates PKC, which was shown previously to mediate the rapid effects of 24,25-(OH)2D3 and arachidonic acid on these cells. Confluent, fourth passage resting zone cells from rat costochondral cartilage were used to evaluate these mechanisms.

[ 3H]Thymidine incorporation[measure of cell proliferation] was increased (10–100μ M), and alkaline phosphatase activity was decreased (10–100 μM), but [35S]sulfate incorporation was unaffected [by arachidonic acid]. 24,25-(OH)2D3 inhibited [3H]thymidine incorporation[decreased proliferation] and stimulated alkaline phosphatase, proteoglycan sulfation, and PKC activity. In cultures treated with both agents, the effects of 24,25-(OH)2D3 were reversed by arachidonic acid. The PKC isoform affected by arachidonic acid was PKCalpha; cytosolic levels were decreased, but membrane levels were unaffected, indicating that translocation did not occur. Arachidonic acid had a direct effect on PKC in isolated plasma membranes and matrix vesicles, indicating a nongenomic mechanism. Plasma membrane PKCalpha was inhibited, and matrix vesicle PKCzeta was stimulated; these effects were blocked by 24,25-(OH)2D3. Studies using cyclooxygenase and lipoxygenase inhibitors indicate that the effects of arachidonic acid are due in part to PG production, but not to leukotriene production. This is supported by the fact that H8-dependent inhibition of protein kinase A, which mediates the effects of PGE2, had no effect on the direct action of arachidonic acid but did mediate the role of arachidonic acid in the cell response to 24,25-(OH)2D3. Diacylglycerol does not appear to be involved, indicating that phospholipase C and/or D do not play a role. Gamma-linolenic acid, an unsaturated precursor of arachidonic acid, elicited a similar response in matrix vesicles but not plasma membranes, whereas palmitic acid, a saturated fatty acid, had no effect. These data suggest that arachidonic acid may act as a negative regulator of 24,25-(OH)2D3 action in resting zone chondrocytes."

"Within minutes of exposure of resting zone cells to 24,25-(OH)2D3, release of arachidonic acid is decreased, calcium ion flux is altered, plasma membrane fluidity is decreased, and production of diacylglycerol via phospholipase D is increased"

So Vitamin D decreases chondrocyte proliferate and increases chondrocyte differentiation.

"After 24 h of treatment with 24,25-(OH)2D3, there is a decrease in PGE2, and matrix vesicle phospholipase A2 (PLA2) is also decreased" 

"the PKA inhibitor H8 had no effect on proliferation, but it preserved the stimulatory effect of 24,25-(OH)2D3 on alkaline phosphatase and proteoglycan sulfation at lower concentrations of arachidonic acid, but not at higher concentrations of the fatty acid. These observations suggest that some of the effects of arachidonic acid are via PG[proteoglycan]"

"arachidonic acid induces expression of early growth response genes c-fos and Egr-1"<-both upregulated by LSJL.

"diacylglycerol, which is involved in the 24,25-(OH)2D3-dependent stimulation of PKC in resting zone cells, caused an increase in cytosolic PKC together with a marked increase in membrane PKC"

"exogenous PGE2 causes a decrease in PKC activity"


1,25(OH)2D3 alters growth plate maturation and bone architecture in young rats with normal renal function.

"1,25(OH)(2)D(3) is used in pediatric patients with chronic kidney disease and mineral and bone disorder (CKD-MBD) and is strongly associated with growth retardation. Here, we investigate the effect of 1,25(OH)(2)D(3) treatment on bone development in normal young rats, unrelated to renal insufficiency. Young rats received daily i.p. injections of 1 µg/kg 1,25(OH)(2)D(3) for one week, or intermittent 3 µg/kg 1,25(OH)(2)D(3) for one month. Histological analysis revealed narrower tibial growth plates, predominantly in the hypertrophic zone of 1,25(OH)(2)D(3)-treated animals in both experimental protocols. This phenotype was supported by narrower distribution of aggrecan, collagens II and X mRNA, shown by in situ hybridization. Concomitant with altered chondrocyte maturation, 1,25(OH)(2)D(3) increased chondrocyte proliferation and apoptosis in terminal hypertrophic cells. In vitro treatment of the chondrocytic cell line ATDC5 with 1,25(OH)(2)D(3) lowered differentiation and increased proliferation dose and time-dependently. Micro-CT analysis of femurs from 1-week 1,25(OH)(2)D(3)-treated group revealed reduced cortical thickness, elevated cortical porosity, and higher trabecular number and thickness. 1-month administration resulted in a similar cortical phenotype but without effect on trabecular bone. Evaluation of fluorochrome binding with confocal microscopy revealed inhibiting effects of 1,25(OH)(2)D(3) on intracortical bone formation. This study shows negative effects of 1,25(OH)(2)D(3) on growth plate and bone which may contribute to the exacerbation of MBD in the CKD pediatric patients."

"Analysis of transgenic VDR or 1α-hydroxylase null mice revealed phenotypic abnormalities characteristic of vitamin D-dependent rickets, with decreased bone mineralization, growth retardation and aberrant growth plate development after weaning. Impaired apoptosis of hypertrophic chondrocytes, with ordinary proliferation, was demonstrated to cause the significant widening and disorganization of the epiphyseal growth plates"

"[There's] a direct inhibitory role of 1,25(OH)2D3 in osteogenesis"

"Two additional transgenic mice models with chondrocytes-specific 1α-hydroxylase ablation or overexpression, revealed a “mirror image” growth plate phenotype with increased hypertrophic zone width, reduced osteoclastogenesis and delayed angiogenesis in the former, while decreased hypertrophic zone width, enhanced osteoclastogenesis and induced angiogenesis in the later"

"Short-term treatment of uremic rats with 1,25(OH)2D3 resulted in a reduced number of chondro-osseous junction chondroclasts compared to uremic control"

"1-month intermittent administration of 1,25(OH)2D3 induces chondrocyte proliferation and compresses chondrocytes maturation zone in young rats."

"1,25(OH)2D3 treatment increased the metabolic cleavage of XTT, indicative of higher cell proliferation, over a range of cell densities. mRNA levels of key transcription factors Sox 9, Runx 2, mRNA of Collagen type II, as well as mRNA and enzymatic activity of the matrix metalloproteinases MMP2 and MMP9, measured by gelatin-zymography, were all downregulated by 1,25(OH)2D3 in a dose and time dependent manner throughout differentiation"


Vitamin D signaling in osteocytes: Effects on bone and mineral homeostasis.

"1,25(OH)(2)D is crucial to maintain normal calcium and bone homeostasis and accomplishes this through this primarily through stimulation of intestinal calcium transport. When insufficient calcium is acquired from the diet (severe dietary calcium restriction, lack of intestinal VDR activity), 1,25(OH)(2)D levels will increase and will directly act on osteoblasts and osteocytes to enhance bone resorption and to suppress bone matrix mineralization. Preservation of serum calcium levels has priority over skeletal integrity."

"VDR action in osteoblasts influences the maintenance of the hematopoietic stem cell (HSC) niche"<- since HSCs may be inhibitory towards chondrogenic differentiation of progenitor cells this is important.

VDR deletion from intestines and chondrocytes has no specific effects on the growth plate.

"chondrocytes and osteoblasts are important for RANKL production during the growth of the long bones, but tosteocytes are the predominant source of RANKL during remodeling of bone. Consistent herewith, Rankl mRNA levels and bone resorption are not altered in young adult (8 weeks old) osteoblast/osteocyte-specific Vdr null (Dmp1-promoter) mice during a positive calcium balance. Bone resorption is stimulated to a similar extent in wild-type and osteoblast/osteocyte-specific Vdr null mice following 1,25(OH)2D treatment, indicating that the response of immature osteoblasts and chondrocytes to 1,25(OH)2D is sufficient to increase bone resorption in young adult mice"

"1,25(OH)2D suppresses mineralization by increasing the pyrophosphate (PPi) levels, which are highly potent mineralization inhibitors."

"extracellular PPi levels depend on PPi generation by ectonucleotide pyrophosphatase phosphodiesterase (ENNP) 1 and 3, the transport of PPi to the extracellular environment by progressive ankylosis (ANK), and degradation by tissue-nonspecific alkaline phosphatase (TNAP). 1,25(OH)2D treatment increases the expression of Enpp1, Enpp3 and Ank in in vitro cultured osteoblasts"

"A decrease in serum Ca2 + levels triggers the release of PTH, which enhances Cyp27b1 expression in the kidney, the enzyme responsible for the final hydroxylation of vitamin D precursors to 1,25(OH)2D, the active ligand. 1,25(OH)2D stimulates several processes to restore normocalcemia, i.e. intestinal and renal calcium (re)absorption, and when these processes are insufficient, a release of calcium from bone. 1,25(OH)2D overproduction is prevented by the normalization of the trigger (serum Ca2 +) and by several feedback loops, one of them being the osteocytic production of FGF23 via VDR-mediated signaling. FGF23 restrains further 1,25(OH)2D production by suppressing Pth and Cyp27b1 transcription "

"1,25(OH)2D administration increases femoral Fgf23 expression and serum FGF23 levels"

"FGF23 suppresses renal Cyp27b1 transcription and subsequently further 1,25(OH)2D activation"

"VDR signaling is required for the mobilization of HSC from the bone marrow into the blood stream induced by granulocyte colony-stimulating factor (G-CSF)"

"hypocalcemic Vdr null mice (standard diet) have less HSC in their bone marrow but an increased number in the spleen"<-If HSCs do have an inhibitory effect on chondrocyte differentiation of progenitor cells maybe less Vitamin D could be permissive to chondrocyte differentiation.