According to Orthopedics at about.com "Glucosamine and chondroitin are two molecules that make up the type of cartilage found within joints. Inside your joints, cartilage undergoes a constant process of breakdown and repair. However, to be properly repaired, the building blocks of cartilage must be present and available. The theory behind using the glucosamine and chondroitin joint supplements is that more of the cartilage building blocks will be available for cartilage repair.
- Glucosamine is a precursor to a molecule called a glycosaminoglycan-this molecule is used in the formation and repair of cartilage.
- Chondroitin is the most abundant glycosaminoglycan in cartilage and is responsible for the resiliency of cartilage.
Glucosamine seems to be the more important of these two molecules as it has the ability to aid in formation of new cartilage although chondroitin can reduce degeneration of discs and cartilage by strengthening cartilage thereby reducing wear and tear damage.
"Oral consumption of glucosamine and chondroitin has not been shown to alter the availability of these cartilage building blocks inside an arthritic joint. It has not been shown that consumption of joint supplements increases the quantity of these cartilage building blocks within any joint."
The current methods of getting glucosamine and chondroiton may just be ineffective and there may be natural ways of increasing the levels of glucosamine and chondroiton in the joint and discs areas. The studies so far have shown glucosamine and chondroiton to aid in pain reduction. And how could glucosamine and chondroiton aid in pain reduction? By increasing the space between discs and joints thereby decreasing the amount that nerves are impinged.
Effects of chondroitin sulfate and glucosamine in adult patients with Kaschin-Beck disease.
"The purpose is to investigate the effects of chondroitin sulfate and glucosamine on adult patients with Kaschin-Beck disease (KBD). A total of 80 patients, aged over 40 years, were randomized into two groups receiving either 1,600 mg oral mixture of chondroitin sulfate and glucosamine or placebo twice daily for 8 months. Posteroanterior radiographs of bilateral knee in full extension were taken at enrollment and after 8 months. Mean joint-space width of the assigned six points on the tibiofemoral joint compartment was measured by a graduated magnifying lens. The mean joint space decreased significantly in the placebo group (4.3 +/- 1.09 versus 4.1 +/- 1.07 mm, P < 0.0001) after 8 months and was unchanged in the experimental group (P = 0.51). There was no statistical significance in the mean joint space between two groups at baseline and follow-up (P = 0.65 and P = 0.84, respectively). But the overall mean change in joint space was significant between the two groups (P < 0.0001). Knee joint space of the experimental group narrowed slowly compared to the control group. Therefore, chondroitin sulfate and glucosamine might play a protective role in preserving articular cartilage and provide evidence for therapeutic drugs in adult patients with KBD."
Effect of glucosamine or chondroitin sulfate on the osteoarthritis progression: a meta-analysis.
"The aim of this study was to assess the structural efficacies of daily glucosamine sulfate and chondroitin sulfate in patients with knee osteoarthritis (OA). The authors surveyed randomized controlled studies that examined the effects of long-term daily glucosamine sulfate and chondroitin sulfate on joint space narrowing (JSN) in knee OA patients using the Medline and the Cochrane Controlled Trials Register, and by performing manual searches. Meta-analysis was performed using a fixed effect model because no between-study heterogeneity was evident. Six studies involving 1,502 cases were included in this meta-analysis, which consisted of two studies on glucosamine sulfate and four studies on chondroitin sulfate. Glucosamine sulfate did not show a significant effect versus controls on minimum JSN over the first year of treatment (SMD 0.078, 95% CI -0.116 to -0.273, P = 0.429). However, after 3 years of treatment, glucosamine sulfate revealed a small to moderate protective effect on minimum JSN (SMD 0.432, 95% CI 0.235-0.628, P < 0.001). The same was observed for chondroitin sulfate, which had a small but significant protective effect on minimum JSN after 2 years (SMD 0.261, 95% CI 0.131-0.392, P < 0.001). This meta-analysis of available data shows that glucosamine and chondroitin sulfate may delay radiological progression of OA of the knee after daily administration for over 2 or 3 years."
Conclusion: Chondroitin and glucosamine do have an effect on joint space. Joint space does increase height. Chondroitin and glucosamine could be used to increase height(barring homeostatic negative feedback loops).
Of course, the big height increasing effect would be if chondroitin and glucosamine had an affect on intervertebral discs.
Glucosamine and chondroitin sulfate supplementation to treat symptomatic disc degeneration: biochemical rationale and case report.
"Glucosamine and chondroitin sulfate preparations are widely used as food supplements against osteoarthritis, but critics are skeptical about their efficacy, because of the lack of convincing clinical trials and a reasonable scientific rationale for the use of these nutraceuticals. Most trials were on osteoarthritis of the knee, while virtually no documentation exists on spinal disc degeneration. The purpose of this article is to highlight the potential of these food additives against cartilage degeneration in general, and against symptomatic spinal disc degeneration in particular, as is illustrated by a case report. The water content of the intervertebral disc is a reliable measure of its degeneration/ regeneration status, and can be objectively determined by Magnetic Resonance Imaging (MRI) signals. Oral intake of glucosamine and chondroitin sulfate for two years associated with disk recovery (brightening of MRI signal) in a case of symptomatic spinal disc degeneration. We provide a biochemical explanation for the possible efficacy of these nutraceuticals. They are bioavailable to cartilage chondrocytes, may stimulate the biosynthesis and inhibit the breakdown of their extracellular matrix proteoglycans. The case suggests that long-term glucosamine and chondroitin sulfate intake may counteract symptomatic spinal disc degeneration, particularly at an early stage. However, definite proof requires well-conducted clinical trials with these food supplements, in which disc de-/regeneration can be objectively determined by MRI. A number of biochemical reasons (that mechanistically need to be further resolved) explain why these agents may have cartilage structure- and symptom-modifying effects, suggesting their therapeutic efficacy against osteoarthritis in general."
The full text was available for this study and the conclusion was essentially that it worked. So that means yeah Glucosamine and Chondroitin can increase height and I hate supplements because most biological materials are readily available in foods. Glucosamine and Chondroitin aren't available in food are they? Glucosaberries, chondroicolates?
The effect of beta-xylosides on the chondrogenic differentiation of mesenchymal stem cells.
"Chondroitin/dermatan sulphate (CS/DS) sulphation motifs on cell and extracellular matrix proteoglycans (PGs) within stem/progenitor cell niches are involved in modulating cell phenotype during the development of many musculoskeletal connective tissues. Here, we investigate the importance of CS/DS chains and their motifs in the chondrogenic differentiation of bone marrow mesenchymal stem cells (bMSCs), using p-nitrophenyl xyloside (PNPX) as a competitive acceptor of CS/DS substitution on PGs. Comparison of cultures grown in control chondrogenic medium, with those grown in the presence of PNPX showed that PNPX delayed the onset of chondrogenesis, characterised by cell rounding and aggregation into spheroidal beads. PNPX reduced gene expression of SOX-9, aggrecan and collagen type II, and caused reduced levels of collagen type II protein. PNPX-treated cultures also showed delayed expression of a native CS/DS sulphation motif epitope recognised by antibody 6C3. This epitope appeared associated with a range of PGs, particularly biglycan, and its close association was lost after PNPX treatment. Overall our data show that perturbation of PG glycosylation with CS/DS GAGs using PNPX significantly delays the onset of chondrogenic differentiation of bMSCs, highlighting the importance of CS/DS during the initial stages of chondrogenesis. The delayed expression of the CS/DS sulphation motif recognised by 6C3 suggests that this motif, in particular, may have early involvement in chondrogenesis."
"Elevated gene expression levels of SOX-9, aggrecan and collagen type II within the 3D aggregates of control cultures between 3 and 4 weeks indicate the establishment of a differentiated chondrogenic phenotype after 4 weeks. The gene expression data for aggrecan were more variable than those of SOX-9 and collagen type II"
"interference with chondroitin-0-4-sulphotransferase expression on CS/DS chains releases the selective binding of the Wnt-3a protein"
"the sulphated CS/DS chains in glypican-5 have been shown to contribute to the binding and stabilisation of Hedgehog"
"The CS/DS chains on biglycan are believed to have involvement in growth factor binding and collagen fibrillogenesis"
Chondroprotective effects of glucosamine involving the p38 MAPK and Akt signaling pathways.
"The purpose of the present study was to elucidate the possible signal transduction pathway involved in the underlying mechanism of glucosamine (GLN)'s influence on the gene expression of matrix metalloproteinases (MMPs) in chondrocytes stimulated with IL-1beta. Using chondrosarcoma cells stimulated with IL-1beta, the effects of GLN on the mRNA and protein levels of MMP-3, the activation of JNK, ERK, p38, NF-kappaB, and AP-1, the nuclear translocation of NF-kappaB/Rel family members, and PI3-kinase/Akt activation were studied. GLN inhibited the expression and the synthesis of MMP-3 induced by IL-1beta, and that inhibition was mediated at the level of transcription involving both the NF-kappaB and AP-1 transcription factors. Translocation of NF-kappaB was reduced by GLN as a result of the inhibition of IkappaB degradation. A slightly synergistic effect on the activation of AP-1 induced by IL-1beta was shown in the presence of GLN[If activation of AP-1 plays a role in chondrogenic differentiation than maybe glucosamine can play a role in chondrogenic differentiation]. Among MAPK pathways involved in the transcriptional regulation of AP-1, phosphorylation of JNK and ERK was found to increase with the presence of GLN under IL-1beta treatment, while that for p38 decreased. It was also found that GLN alone, but also synergistically with IL-1beta, was able to activate the Akt pathway[Akt is pretty much always anabolic]. The requirements of NF-kappaB translocation and p38 activity are indispensably involved in the induction of MMP-3 expression in chondrosarcoma cells stimulated by IL-1beta. Inhibition of the p38 pathway in the presence of GLN substantially explains the chondroprotective effect of GLN on chondrocytes that regulate COX-2 expression, PGE(2) synthesis, and NO expression and synthesis. The chondroprotective effect of GLN through the decrease in MMP-3 production and stimulation of proteoglycan synthesis may follow another potential signaling pathway of Akt."
"IL-1β binds to the IL-1 receptor type I (IL-1RI) that activates tumor necrosis factor receptor molecule-associated factor-6 (TRAF-6), leading to activation of the NF-κB-inducing kinase (NIK) and thereby freeing up NF-κB to interact with the nuclear importation machinery and be translocated to the nucleus, where it binds its target gene to upregulate the expression of many proinflammatory genes, such as COX-2 and iNOS in rheumatic disease. Alternatively, TRAF-6 can also activate MAPK. The MAPK pathways (ERKs, JNKs, and p38) promote phosphorylation of other substrates, such as c-Jun N-terminal kinase and the Jun and Fos family, all of which are associated with the transcriptional activity of AP-1, which regulates T cell activation, cytokine production, and production of matrix metalloproteinases (MMPs)"
"GLN is able to fully prevent the upregulation of stromelysin (MMP-3)[upregulated by LSJL] mRNA expression induced by IL-1β, but the addition of GLN with IL-1β only decreased the activation of the NF-κB, not AP-1"
"IGF-1 stimulation of proteoglycan synthesis by articular chondrocytes requires activation of the PI 3-kinase/Akt/mTOR/p70S6 kinase signaling pathways but not the Ras/Raf/MEK/ERK pathways. Thus, the phosphorylating activation of Akt in the presence of GLN downregulates ASK1 activity, which in turn decreases activation of JNK and p38 which may be induced followed by binding of IL-1β to its membrane receptor."
"Akt activation by GLN is not mediated by PI 3-kinase"<-Thus glucosamine may be a useful adjunct to LSJL by activating Akt by a different method as LSJL likely works by the PI3K pathway.
Haven't tested any of those yet. You might want to snoop around on amazon or your store to find the best deal. I've seen some with MSM but I'm not sure if it does anything. If you're not happy with the product give it a bad review and the product owner will probably contact you to see if he can change your mind :)