Showing posts with label resveratrol. Show all posts
Showing posts with label resveratrol. Show all posts

Monday, July 8, 2013

Resveratrol - A Potential Height Increase Supplement

 Surprisingly Resveratrol is available for sale: 1000 MG Resveratrol Extreme Juice Capsules Resveratrol Juice capsules TM 3 Months 180 pills HIGHLY POTENT Pure Resveratrol pills. 3 MONTH GUARANTEE. TWICE AS POTENT AS many RESVERATROL, Resveratrol Juice Extreme.
Resveratrol may boost SIRT1 which is implicated in catchup growth.  This is accroding to Resveratrol boosts cognitive function by targeting SIRT1.  Metformin may boost SIRT1 also according to  Metformin Is a Direct SIRT1-Activating Compound: Computational Modeling and Experimental Validation.
Resveratrol has a similar structure to estrogen and may prevent binding of estrogen to various cells that would decrease growth.  Therefore, resveratrol may increase height if taken during development at the right dose.

 Resveratrol Treatment Delays Growth Plate Fusion and Improves Bone Growth in Female Rabbits

"Trans-resveratrol (RES), naturally produced by many plants, has a structure similar to synthetic estrogen diethylstilbestrol. Pre-pubertal ovary-intact New Zealand white rabbits received daily oral administration of either vehicle (control) or RES (200 mg/kg) until growth plate fusion occurred{We don't know if this will have the same effect on men}. Bone growth and growth plate size were longitudinally monitored by X-ray imaging, while at the endpoint, bone length was assessed by a digital caliper. In addition, pubertal ovariectomized (OVX) rabbits were treated with vehicle, RES or estradiol cypionate (positive control) for 7 or 10 weeks and fetal rat metatarsal bones were cultured in vitro with RES (0.03 µM–50 µM) and followed for up to 19 days. In ovary-intact rabbits, sixteen-week treatment with RES increased tibiae and vertebrae bone growth and subsequently improved final length. In OVX rabbits, RES delayed fusion of the distal tibia, distal femur and proximal tibia epiphyses and femur length and vertebral bone growth increased when compared with controls. RES-treated OVX rabbits had a wider distal femur growth plate, enlarged resting zone, increased number/size of hypertrophic chondrocytes, increased height of the hypertrophic zone, and suppressed chondrocyte expression of VEGF and laminin. In cultured fetal rat metatarsal bones, RES stimulated growth at 0.3 µM while at higher concentrations (10 μM and 50 μM) growth was inhibited. RES has the potential to improve longitudinal bone growth. The effect was associated with a delay of growth plate fusion resulting in increased final length. These effects were accompanied by a profound suppression of VEGF and laminin expression suggesting that impairment of growth plate vascularization might be an underlying mechanism."

Note that only the smallest dosage of Resveratrol had an anabolic effect on growth which is consistent with the view that estrogen has an equilibrium level for growth.  These rabbits were pre-puberty so estrogen levels should've been lower than puberty.  Since estrogen levels increase during puberty doses should increase during puberty as estrogen would be higher than equilibrium level.  It's hard to ascertain what that is for humans though.

"Trans-resveratrol (3, 5, 4′-trihydroxystilbene), is a polyphenol naturally produced by a variety of plants such as peanuts, berries, skin of red grapes in response to stress, injuries and infections."<-Does anyone have anecdotal accounts of tall people or groups that ate lots of peanuts, berries, or red grapes?  Or drink red wine?

"in weanling rats demonstrating that 6 days of treatment with very low doses of RES (1–100 μg/day) had no significant effect on radial bone growth"

The Rabbits were twelve weeks old.

"tibia length 111.6±0.6 mm in the RES group vs. 109.5±0.6 mm in control" over 8 weeks.  That's approximately a 5% increase in growth rate.  Vertebral height was increased as well.

"RES-treatment delayed the time of growth plate fusion in all studied growth plates."<this could be due to Resveratrol's effects on sirt1 and catch up growth

"After 10 weeks, 33% of the animals in the RES group had unfused distal femur growth plates while only 10% of control animals had"

Surprisingly, RES decreased the number of proliferative chondrocytes per area in growth plates versus control but this is consistent with the view that Resveratrol delays growth plate senescence.

"chondrocyte expression of VEGF to be clearly suppressed in RES-treated rabbits as compared to controls (265±54 vs. 626±50 VEGF positive cells/mm2) while in the E2 group VEGF expression was similar as in controls (632±153 vs. 626±50 positive cells/mm2). Also the expression of laminin was decreased in the RES-treated group as compared to controls (17.7±0.6 vs. 27.4±1.04 positive cells/mm2;). In contrast, laminin expression was elevated in E2 treated animals (44.4±0.8 vs. 27.4±1.04 positive cells/mm2 in control)"

"RES significantly improves bone growth by delaying the process of epiphyseal fusion in female animals. Animals treated with RES had wider growth plates with enlarged resting zone, fewer proliferative chondrocytes, increased number and size of hypertrophic chondrocytes and markedly suppressed VEGF and laminin expression."

Friday, February 25, 2011

Protein Kinase-D

Inhibition of protein kinase-D promotes cartilage repair at injured growth plate in rats.

"Using a rat model, this study investigated potential roles of protein kinase-D (PKD) in regulating expression of osteogenic transcription factor osterix and the growth plate bony repair. 4 days post injury at the proximal tibial growth plate, rats received four once-daily injections of vehicle or 2.35mg/kg gö6976 (a PKD inhibitor), and growth plate tissues collected at day 10 were examined histologically and molecularly. In addition, effects of PKD inhibition on osteogenic and chondrogenic differentiation were examined in vitro using rat bone marrow mesenchymal stromal cells.
Compared to vehicle control, PKD inhibition caused a decrease in bone volume, an increase in % of mesenchymal tissue, and an increase in cartilaginous tissue[over twice as much] within the injury site{so maybe PKD inhibition can help form new growth plates?}. Consistently, gö6976 treatment tended to decrease expression of bone-related genes (osterix, osteocalcin) and increase levels of cartilage-related genes (Sox9, collagen-2a, collagen-10a1). In support, in vitro experiments showed that gö6976 presence in the primary rat marrow stromal cell culture resulted in a decrease of alkaline phosphatase(+) CFU-f colonies formed and an increase in collagen-2a expression in chondrogenic pellet culture.
 PKD is important for growth plate bony repair and its inhibition after growth plate injury may result in less bone formation and potentially more cartilage repair."

Full-size image (65 K)
Growth plate height looks higher in go6976 treated group and the bone seems wider.



Full-size image (136 K)"mesenchymal tissue (Me), bony trabeculae (BT), cartilaginous tissue (Ca) and bone marrow (BM)"

Notice that there is no cartilage in the selected region in the vehicle.

Sox9 was upregulated 2 fold by Go6979 treatment which was less than LSJL where one isoform of Sox9 was upregulated 3 fold.

According to The potential use of protein kinase D inhibitors for prevention/treatment of epidermal tumors., Resveratol is Protein Kinase D inhibitor.

Resveratrol is available for sale: NutriGold Resveratrol GOLD, 500mg, 120 Vegetarian Capsules - trans-Resveratrol with Grape Seed and Red Wine Polyphenols (Featuring Patented ResVinol and ORAC-15M)

Friday, December 4, 2009

reseveratrol


Biological effects of the plant-derived polyphenol resveratrol in human articular cartilage and chondrosarcoma cells.

"RSV is chondroprotective for articular cartilage in rabbit models for arthritis{Can this translate to height benefits?}. Effects of RSV on human articular cartilage homeostasis were studied by assessing production of matrix-degrading enzymes (MMP-13, ADAMTS4, and ADAMTS5), as well as proteoglycan production and synthesis. The counteractions of RSV against catabolic factors (e.g., FGF-2 or IL-1β) were examined by in vitro and ex vivo using monolayer, three-dimensional alginate beads and cartilage explants cultures, respectively. RSV improves cell viability of articular chondrocytes and effectively antagonizes cartilage-degrading protease production that was initiated by catabolic and/or anti-anabolic cytokines in human articular chondrocytes. RSV significantly enhances BMP7-promoted proteoglycan synthesis. RSV inhibits the activation of transcription factors involved in inflammation and cartilage catabolic signaling pathways, including direct downstream regulators of MAPK (e.g., AP-1, PEA3) and NFκB. RSV selectively compromises survival of human chondrosarcoma cells, but not primary articular chondrocytes, revealing cell-specific activity of RSV on non-tumorigenic versus tumor-derived cells. RSV exerts its chondroprotective functions, in part, by deactivating p53-induced apoptosis in human primary chondrocytes, but not human chondrosarcoma."

"signaling cascades generated by inflammatory cytokines (e.g., IL-1) or fibroblast growth factor-2 (FGF-2 or basic FGF) favor catabolism by stimulating protease production and inhibiting proteoglycan deposition in human adult articular cartilage or intervertebral disc tissue via ERK/MAPK activation"

"FGF-2 mediates striking antagonistic effects on cartilage anabolic activity in conjunction with IGF-1 and BMP7, and both FGF-2 and IL-1 modify chondrocyte gene expression when stimulated by mechanical injury "

"p53 DNA binding activity is significantly stimulated by IL-1β (10 ng/ml) along with AP-1, AP-2, Ets1/PEA3, NFκB, p53, Sp1, and multiple STATs that are critical for cytokine signals"