Friday, June 29, 2012

Height increase with Chitosan?

Chitosan is a soluble dietary fiber but it is insoluble in water.  The trouble is getting it from the stomach to the bone.  PCL beads are used for the controlled release of drugs.  Chitosan scaffolds have been used to induce chondrogenesis before. Chitosan is available for sale but can it increase serum levels in the epiphyseal bone marrow is the question: NOW Foods Chitosan 500mg, 240 Caps.

Chondrogenesis of human bone marrow mesenchymal cells by transforming growth factors β1 through cell shape changes on controlled biomaterials.

"The phenotypic responses of human bone marrow mesenchymal cells (hBMSCs) on different ratio of chitosan/polycaprolactone (PCL) blends were investigated in this study. The results showed that hBMSCs existed different morphology on chitosan/PCL blends due to the different adhesion characteristic of cell on neat PCL and neat chitosan. Interestingly, comparing to hBMSCs on neat PCL, hBMSCs aggregated to form spheroid and to express ascendant trend of transforming growth factor β1, collagen type II, collagen type X, and Sox9 mRNA on the chitosan/PCL blended substrates with the decrease of PCL content. To confirm chondrogenesis of hBMSCs with spheroid on test substrates, Alcian Blue and Safranin O staining were used to detect the cartilaginous extracellular matrix (ECM). It revealed hBMSCs with spheroid on neat chitosan and 10 wt % PCL did turn to chondrogenic differentiation and synthesize cartilaginous ECM. Therefore, these findings provided new insights into the role of chitosan/PCL blended material could mediate the endogenous gene expression of hBMSCs to alter the phenotypic behavior through mediating the cell shape."

"The cell–materials interaction is generally considered to be a multistep process involving the adsorption of extracellular matrix (ECM) proteins onto the substrate surface and the recognition between the transmembrane receptors on the cell surface (i.e., integrin) and the cell-binding domain of ECM proteins."

"Focal adhesion kinase is a cytoplasmic tyrosine kinase that is activated on integrin ligating to the ECM at sites of focal adhesion, which results in changes of actin cytoskeleton organization and in the cell spreading, growth, and phenotype"<-Maybe LSJL by inducing Lateral compression and thus alter integrin linking.  Note that lateral compression is much easier to achieve than axial compression.

"[The] gene of transforming growth factor-β1 (TGF-β1) could be upregulated by breaking the cytoskeleton with chemical reagent to make dermal fibroblasts presenting round shape."<-We find out what this chemical reagent is to help us grow taller.

" the TGF-β1 gene expression of cell could be regulated by modulating the cell shape. TGF-β1 was needed for the in vitro chondrogenic differentiation of hBMSCs. We hypothesized that using the chitosan and PCL blended material could alter the gene expression and the phenotypic response of hBMSCs through mediating hBMSCs to present different cell shape on the chitosan and PCL blends."

"On chitosan, hBMSCs exhibited round shape and formed short radial-growth of filopodia. With the increase of PCL content in the blends, hBMSCs presented more flattened shape and spindle-like morphology."<-So this is what we want to happen more rounded shape and more radial growth of filopodia in the stem cells of the epiphyseal bone marrow.

There has to be some way to increase the chitosan content of the bone marrow.

Here's the study that talks about chemical regeants to break up the actin cytoskeleton:

Cytoskeleton Regulates Expression of Genes for Transforming Growth Factor-b1 and Extracellular Matrix Proteins in Dermal Fibroblasts

"Cytoskeleton not only controls cell morphology but also regulates cell growth, migration, differentiation, and gene expression. We have recently reported that reorganization of cytoskeleton induces expression of mRNA for transforming growth factor-beta 1 (TGF-beta 1), collagenase, and tissue inhibitor of metalloproteinase-I (TIMP-I){up in LSJL} in dermal fibroblasts[it's possible that the same chemicals will work on stem cells as well]. In this report we have examined the role of gene transcription in this induction. As judged by nuclear run-on assay, trypsin, EGTA (ethylene glycol-bis (beta-aminoethyl ether) N, N, N', N', tetra-acetic acid), or cytochalasin C (Chs) increased the rate of transcription of the TGF-beta 1 gene by 2.0, 2.7, and 1.6 fold, respectively[So EGTA was most effective], and of the collagenase gene by 5.3, 6.2, and 3.3 fold. The rate of transcription of the TIMP-I gene was increased by trypsin (4.3 fold) or EGTA (3.8 fold) but unaffected by Chs. Cytochalasin induced an increase in the rate of transcription of procollagen I (alpha 1), procollagen I (alpha 2), and fibronectin genes by 1.4, 1.5, and 1.9 fold respectively, while trypsinization or EGTA treatment had no or little effects on these gene. Since transcription of the TGF-beta 1 gene is believed to be largely governed by the activating protein 1 (AP1) complex, we also examined the expression of mRNA for c-fos[LSJL upregulates c-fos] and c-jun protoon-coproteins. Trypsinization induced rapid (within 30 min) and transient expression of c-fos mRNA. A 2.4 fold increase in c-jun mRNA was apparent after 4 hr and persisted for at least 24 hr. Actinomycin D (Act D) suppressed the induction of TGF-beta 1 mRNA by Chs but had less effect on the TGF-beta 1 mRNA in trypsinized cells which had been replated for 4 hr, suggesting that the half life of TGF-beta 1 mRNA is reduced in cells with a disassembled cytoskeleton. Simultaneous treatment with Chs and cycloheximide (Cxm) resulted in a superinduction of TGF-beta 1 mRNA by 88 +/- 23% (n = 4, P < 0.05), which was abrogated by preexposure to Act D. In contrast, the induction of collagenase mRNA by Chs was totally blocked by Cxm, indicating that the Cxm-mediated superinduction is selective and that protein synthesis is required for induction of this mRNA. Our results suggest that the activities of genes for proteins involved in the structure (Type I collagen and fibronectin), turnover (collagenase and TIMP-1) and regulation (TGF-beta 1) of extracellular matrix (ECM), are all governed at least in part by the status of the cytoskeleton."

This study mentioned that chitosan(and GMS) increased serum levels of GH and IGF-1 but didn't directly mention Chitosan serum levels: Effect of dietary supplementation of chitosan and galacto-mannan-oligosaccharide on serum parameters and the insulin-like growth factor-I mRNA expression in early-weaned piglets.

Chitosan is insoluble in water so if it does get past the digestive system and into the blood stream it should stay intact and increase the serum content of chitosan in the epiphyseal bone marrow.

According to Effects of habitual chitosan intake on bone mass, bone-related metabolic markers and duodenum CaBP D9K mRNA in ovariectomized SHRSP rats.,  chitosan can cause bone loss which may favor neo-growth plate formation by making room for it.

So maybe supplementing with chitosan and a glass of water could help you grow taller by encouraging epiphyseal bone marrow stem cells to become a more rounded pro chondrogenic shape.  


  1. could you do some research on what makes the growth plates grow in width? and how the chondrocytes line up, (i remember you saying that the people were growing in width with lsjl and that may be because the chodnrocytes are not lined up properly)

    1. Collagen Type 9 may play a role in growth plate width. I'll look into it further.

  2. Tyler,

    In your thread previous to this one, you mentioned sleep which made me remember another topic.

    I heard that eating at late hours affects the amount of hormones your body produces due to spikes in insulin (other something like that).

    My son goes to bed early and eats rather well, but I am wondering if his late night snacking affects his growth potential if at all. My wife and I are rather short and I want him to be able to reach his optimum height.

    Could you possibly do an article on how diet affects your sleep hormones which affects height?