Ingesting collagen has been stated to improve nutrition when combined with vegetables and one spokeswoman even claims that "Collagen is a kind of protein that forms bones, skin and many other tissues. It especially forms large parts of inner skin. Studies imply that eating or drinking collagen improves bone metabolism and is good for people suffering joint inflammation and osteoporosis." In addition, it has been reported in a preliminary experiment that eating or drinking collagen helps the skin stay moist.
The woman did not go so far as to say ingesting collagen is more effective than other types of protein. (Collagen is digested into amino acids just like fish, chicken, eggs, etc...).
Collagen accounts for a third of protein forming animal bodies, so it is correct to say it is a very necessary protein. Also, it accounts for 70 percent of the weight of inner skin when it is completely dehydrated, apparently.
However, I haven't actually read any of the studies done and this is all just apparent from some articles published in Japan Times.
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There is however one supplements that I take, which I believe is key to helping the body repair for Penis Enlargement. It's a combination of Glucosamine, Chondroitin, and MSM.
Glucosamine is a compound found naturally in the body, made from glucose and the amino acid glutamine. Glucosamine is needed to produce glycosaminoglycan, a molecule used in the formation and repair of cartilage and other body tissues. Production of glucosamine slows with age, so therefore nutritional supplementation can benefit individuals who suffer from osteoarthritis and other conditions such as rheumatoid arthritis, inflammatory bowel disease (Crohn's disease and ulcerative colitis), chronic venous insufficiency, and skin conditions.
Glucosamine is often combined with chondroitin sulfate, a molecule naturally present in cartilage. Chondroitin gives cartilage elasticity and is believed to prevent the destruction of cartilage by enzymes. Glucosamine is sometimes combined with MSM (methylsulfonylmethane), in nutritional supplements.
Here are a couple studies.
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Int J Mol Med. 2011 Apr 29. doi: 10.3892/ijmm.2011.686. [Epub ahead of print]
Effect of glucosamine, a therapeutic agent for osteoarthritis, on osteoblastic cell differentiation.
Igarashi M, Sakamoto K, Nagaoka I.
Department of Host Defense and Biochemical Research, Graduate School of Medicine, Juntendo University, Bunkyo-ku, Tokyo 113-8421, Japan.
Abstract
Osteoarthritis (OA) is characterized by qualitative and quantitative changes in the architecture and composition of all the joint structures. Glucosamine (GlcN) has been used to treat OA in humans, because GlcN is present in the cartilage tissues as a component of glycosaminoglycans, and exhibits the symptom-modifying effect on OA by normalizing cartilage metabolism. On the other hand, the pathological change of subchondral bone is associated with the initiation and progression of cartilage damage in OA. However, the effect of GlcN on bone metabolism remains unsolved. In the present study, we determined the effect of GlcN on bone metabolism (osteoblastic cell differentiation) using mouse osteoblastic MC3T3-E1 cells by evaluating the expression of early (type I collagen and alkaline phosphatase), middle (osteopontin) and late (osteocalcin and mineralization) stage differentiation markers, and further compared its effects to those of N-acetyl-D-glucosamine (GlcNAc), a derivative of GlcN. The results indicated that the mineralization of mature osteoblasts was increased by treatment with GlcN and GlcNAc. Furthermore, reverse transcription-polymerase chain reaction (RT-PCR) analyses revealed that GlcN and GlcNAc substantially increased the expression of a middle stage marker and a late stage marker, although they did not essentially affect the expression of early stage markers. In addition, GlcN and GlcNAc suppressed the expression of receptor activator of NF-κB ligand (RANKL), a key factor involved in the osteoclastic cell differentiation and activation. Together these observations suggest that both GlcN and GlcNAc may have a potential not only to induce osteoblastic cell differentiation especially at middle-late stages, but also to suppress the osteoclastic cell differentiation, thereby possibly increasing bone matrix deposition and decreasing bone resorption, and eventually modulating bone metabolism in OA.
PMID: 21537831 [PubMed - as supplied by publisher]
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Eur Cell Mater. 2011 Mar 15;21:259-71; discussion 270-1.
A preliminary study of the effects of glucosamine sulphate and chondroitin sulphate on surgically treated and untreated focal cartilage damage.
Kamarul T, Ab-Rahim S, Tumin M, Selvaratnam L, AHydromaxad TS.
Department of Orthopaedic Surgery (NOCERAL), University of Malaya, Kuala Lumpur, Malaysia.
Abstract
The effects of Glucosamine Sulphate (GS) and Chondroitin Sulphate (CS) on the healing of damaged and repaired articular cartilage were investigated. This study was conducted using 18 New Zealand white rabbits as experimental models. Focal cartilage defects, surgically created in the medial femoral condyle, were either treated by means of autologous chondrocyte implantation (ACI) or left untreated as controls. Rabbits were then divided into groups which received either GS+/-CS or no pharmacotherapy. Three rabbits from each group were sacrificed at 12 and 24 weeks post-surgery. Knees dissected from rabbits were then evaluated using gross quantification of repair tissue, glycosaminoglycan (GAG) assays, immunoassays and histological assessments. It was observed that, in contrast to untreated sites, surfaces of the ACI-repaired sites appeared smooth and continuous with the surrounding native cartilage. Histological examination demonstrated a typical hyaline cartilage structure; with proteoglycans, type II collagen and GAGs being highly expressed in repair areas. The improved regeneration of these repair sites was also noted to be significant over time (6 months vs. 3 months) and in GS and GS+CS groups compared to the untreated (without pharmacotherapy) group. Combination of ACI and pharmacotherapy (with glucosamine sulphate alone/ or with chondroitin sulphate) may prove beneficial for healing of damaged cartilage, particularly in relation to focal cartilage defects.
PMID: 21409755 [PubMed - in process]
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I take a supplement 2 times/day, once in the AM and once before bed, by NOW foods called Glucosamine & Chondroitin with MSM. I think it has helped me recover from heavy stretching. Every morning when I wake up, I feel fresh and ready to stretch. I almost never take days off, and I believe it really helps.
To completely change topics, I have heard that IGF-1 may exhibited better cartilaginous features than chondroitin. Here's another study.
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J Cell Physiol. 2011 Aug;226(8):1981-8. doi: 10.1002/jcp.22530.
Differential effect of ECM molecules on re-expression of cartilaginous markers in near quiescent human chondrocytes.
Chiu LH, Chen SC, Wu KC, Yang CB, Fang CL, Lai WF, Tsai YH.
Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan; Graduate Institute of Cell and Molecular Biology, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Abstract
The limited source of healthy primary chondrocytes restricts the clinical application of tissue engineering for cartilage repair. Therefore, method to maintain or restore the chondrocyte phenotype during in vitro expansion is essential. The objective of this study is to establish the beneficial effect of ECM molecules on restoring the re-expression of cartilaginous markers in primary human chondrocytes after extensive monolayer expansion. During the course of chondrocyte serial expansion, COL2A1, SOX9, and AGN mRNA expression levels, and GAG accumulation level were reduced significantly in serially passaged cells. Exogenous type II collagen dose-dependently elevated GAG level and induced the re-expression of cartilaginous marker mRNAs in P7 chondrocytes. Chondroitin sulfate did not show significant effect on P7 chondrocytes, while hyaluronic acid inhibited the expression of SOX9 and AGN mRNAs. Upon treatment with type II collagen, FAK, ERK1/2, and JNK were activated via phosphorylation in P7 chondrocytes within 15 min. Furthermore, GFOGER integrin blocking peptide, MEK inhibitor and JNK inhibitor, not p38 inhibitor, significantly reduced the type II collagen-induced GAG deposition level. Finally, in the presence of TGF-β1 and IGF-I, P7 chondrocytes cultured in 3D type II collagen matrix exhibited better cartilaginous features than those cells cultured in the type I collagen matrix. In conclusion, type II collagen alone can effectively restore cartilaginous features of expanded P7 human chondrocytes. It is probably mediated via the activation of FAK-ERK1/2 and FAK-JNK signaling pathways. The potential application of type II collagen in expanding a scarcity of healthy chondrocytes in vitro for further tissue engineering is implicated. J. Cell. Physiol. 226: 1981-1988, 2011. © 2010 Wiley-Liss, Inc.
Copyright © 2010 Wiley-Liss, Inc.
PMID: 21520049 [PubMed - in process]
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I haven't tried IGF-1 yet, and I believe Supra has a log or has done some experimentation with that. I'd be a willing lab-rat in the near future though! For now, I'll stick with my current nutritional supplementation of aminos and the a fore mentioned NOW foods product.
