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How to combat dry & sore joints from Winstrol???
- Thread starter rosco141
- Start date
utahdiesel
New member
You're gonna hear Deca... but I've never tried it, so I can't say. I use glucosamine/chondroitin and have always thought it helped. But I just heard on the radio a couple of months ago that the only reason it works is because of placebo effect... go figure.
utahdiesel
New member
jon79 said:
Yep, it took about a month for me to feel greased.
thefantom1
New member
MSM may help.. try drinking ton of water.... the MSM should be taken at 3000mg a day..if it will help you should notice a difference in about 3 days.. for those of us with regular joint pain.. the stuff is amazing.. very cheap too
macrophage69alpha
New member
nandrolone is an option
glucosamine/ chondroiten
pregnenolone or even low dose progesterone
glucosamine/ chondroiten
pregnenolone or even low dose progesterone
thefantom1
New member
pregnenolone helps with joints?? Or just the winny joint pain??
macrophage69alpha
New member
thefantom1 said:
both
it binds to the GCR
it was used at one time to treat rheumatoid arthritis (though obviously that patent expired...)
wootool
New member
somebody should try hyaluronic acid - HA.
I've read lots of great anecdotal examples of why it would be GREAT for this application, havent seen any science tho.
for example (paraphrasing) I took glucosamine for 2 months before I saw some slight effect on my aching joints, but within a few days of strting HA, I saw an amazing improvement blah blah blah.
another example was somebody had an arthritic dog who couldnt climb steps any more, and within a week, he was climbing steps again like a puppy.
hey, its worth a shot.
here's some doc from source naturals
Hyaluronic acid is a major component of joint tissue. It helps to hold lubricating moisture in joints and cartilage, which affects their resilience, elasticity, and strength. Source Naturals Hyaluronic Acid is made from patented BioCell Collagen II™, which has undergone an absorption enhancing hydrolyzation process that yields low molecular weight hyaluronic acid, chondroitin sulfate, and Collagen Type II peptides. These elements make it a multifaceted ingredient, which may help support joint joint function and the appearance of healthy skin.*
http://www.discount-vitamins-herbs.net/store/PPF/parameters/813_0/more_info.asp
I've read lots of great anecdotal examples of why it would be GREAT for this application, havent seen any science tho.
for example (paraphrasing) I took glucosamine for 2 months before I saw some slight effect on my aching joints, but within a few days of strting HA, I saw an amazing improvement blah blah blah.
another example was somebody had an arthritic dog who couldnt climb steps any more, and within a week, he was climbing steps again like a puppy.
hey, its worth a shot.
here's some doc from source naturals
Hyaluronic acid is a major component of joint tissue. It helps to hold lubricating moisture in joints and cartilage, which affects their resilience, elasticity, and strength. Source Naturals Hyaluronic Acid is made from patented BioCell Collagen II™, which has undergone an absorption enhancing hydrolyzation process that yields low molecular weight hyaluronic acid, chondroitin sulfate, and Collagen Type II peptides. These elements make it a multifaceted ingredient, which may help support joint joint function and the appearance of healthy skin.*
http://www.discount-vitamins-herbs.net/store/PPF/parameters/813_0/more_info.asp
macrophage69alpha
New member
HA is an interesting compound
macrophage69alpha
New member
Agents Actions. 1994 Mar;41(1-2):37-43. Related Articles, Links
The differential effects of stanozolol on human skin and synovial fibroblasts in vitro: DNA synthesis and receptor binding.
Ellis AJ, Cawston TE, Mackie EJ.
Rheumatology Research Unit, Addenbrooke's Hospital, Cambridge, UK.
The anabolic steroid stanozolol stimulates the production of prostaglandin E2 (PGE2) and the matrix metalloproteinases collagenase and stromelysin in human skin fibroblasts but not in rheumatoid synovial fibroblasts. The basis for these differential responses was investigated at the levels of DNA synthesis and steroid receptor binding. Stanozolol inhibited fibroblast growth factor (FGF)-stimulated DNA synthesis in both the skin and synovial fibroblasts, showing that both cell types were capable of responding to the compound. Competitive binding assays indicated that stanozolol bound specifically to both the skin and synovial fibroblasts. Binding of stanozolol to both cell types could be partially displaced by progesterone, indicating that stanozolol binds to the progesterone receptor. Immunocytochemical studies confirmed the presence of progesterone receptors on skin and synovial fibroblasts. However, progesterone failed to elicit any response with respect to collagenase production in either cell type. Nortestosterone, dexamethasone and 17 beta-oestradiol had no effect on binding of stanozolol to either cell type. These results indicate that the inhibition of DNA synthesis by stanozolol is elicited through the progesterone receptor. The effects of stanozolol on collagenase and PGE2 production are mediated by a different receptor, present on skin but not synovial fibroblasts, and as yet unidentified.
The differential effects of stanozolol on human skin and synovial fibroblasts in vitro: DNA synthesis and receptor binding.
Ellis AJ, Cawston TE, Mackie EJ.
Rheumatology Research Unit, Addenbrooke's Hospital, Cambridge, UK.
The anabolic steroid stanozolol stimulates the production of prostaglandin E2 (PGE2) and the matrix metalloproteinases collagenase and stromelysin in human skin fibroblasts but not in rheumatoid synovial fibroblasts. The basis for these differential responses was investigated at the levels of DNA synthesis and steroid receptor binding. Stanozolol inhibited fibroblast growth factor (FGF)-stimulated DNA synthesis in both the skin and synovial fibroblasts, showing that both cell types were capable of responding to the compound. Competitive binding assays indicated that stanozolol bound specifically to both the skin and synovial fibroblasts. Binding of stanozolol to both cell types could be partially displaced by progesterone, indicating that stanozolol binds to the progesterone receptor. Immunocytochemical studies confirmed the presence of progesterone receptors on skin and synovial fibroblasts. However, progesterone failed to elicit any response with respect to collagenase production in either cell type. Nortestosterone, dexamethasone and 17 beta-oestradiol had no effect on binding of stanozolol to either cell type. These results indicate that the inhibition of DNA synthesis by stanozolol is elicited through the progesterone receptor. The effects of stanozolol on collagenase and PGE2 production are mediated by a different receptor, present on skin but not synovial fibroblasts, and as yet unidentified.
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