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How Does Deca Heal Ailing Joints?
- Thread starter Jacob Creutzfeldt
- Start date
From it's anti-cortisol effects on the joints as well it's lubricating effects bringing fluid within the joints to allow more ease in the range of motion and for a cushioning type effect. Also allows the joints to heal faster due to this lubricating effect as the joints don't keep getting worn down repeatedly.
G
Golfer18--old
Guest
graffixx said:
I don't know wouldnt growth help that though?
Lift or Die
New member
No it doesn't heal anything. It eases and masks the pain but the damage to the connective tissue is still there.
rottweiler75
New member
I asked the same question awhile back, was looking for the physiological reason for this but no one seems to know it. Im sure you werent looking for "it lubes the joints" either. And from what I know low levels of cortisol, even by means of blocking its receptor, is the cause of most joint pain, not the contrary. Fonz or macro might know the reason. It maybe have something to do with progesterone levels causing some other hormone response, I know it is linked to relaxin in women, but im not sure of the whole biochemical process in which nandrolone exhibits its effects.
***
New member
i've never heard of deca's effect on cortisol. it doesn't seem to make sense that decreasing cortisol would be of any benefit to the joints as cortisol is a hormone to help reduce inflamation.
deca binds to progesterone receptors and activates them. one side effect of this is the water retention and possible gyno. another side effect when progesterone receptors are activated is increased fluid to the joints. the increased fluid in the joints will reduce bone on bone friction, but this would only help you if you have a problem with too much bone on bone friction as is the case with too much winny.
deca does not heal cartiledge or tendons. it only increases fluid in the joints to reduce friction.
deca binds to progesterone receptors and activates them. one side effect of this is the water retention and possible gyno. another side effect when progesterone receptors are activated is increased fluid to the joints. the increased fluid in the joints will reduce bone on bone friction, but this would only help you if you have a problem with too much bone on bone friction as is the case with too much winny.
deca does not heal cartiledge or tendons. it only increases fluid in the joints to reduce friction.
*** said:
Well from what I read yes I know that too little cortisol is bad for your joints and for the whole body. But I'm talking about decreasing it. Not eliminating it. Too much cortisol is not good either. I'm not sure exactly where I read that it decreases cortisol's negative effect on the joints but I can recall reading something along the lines of this. I will wait for Huck or Zyg to see what they have to say.
***
New member
the following article states the effects of decreased cortisol and how detrimental it may be for the joints:
Anti-inflammatory cooperativity of corticosteroids and norepinephrine in rheumatoid arthritis synovial tissue in vivo and in vitro.
Straub RH, Gunzler C, Miller LE, Cutolo M, Scholmerich J, Schill S.
Division of Rheumatology, Department of Internal Medicine I, University Hospital, Regensburg, Germany. [email protected]
Corticosteroids (CS) and norepinephrine (NE) support each other's biological effects. Thus, deficiency of cortisol and reduced synovial sympathetic innervation (SSI) may be proinflammatory in rheumatoid arthritis (RA). This study tested the anti-inflammatory cooperativity of CS and NE in human RA synovial tissue. In an in vivo study, 32 patients with RA (with prior CS therapy/without SSI: n=7; without prior CS therapy/with SSI: 6; with prior CS therapy/with SSI: 19) were investigated for synovial inflammation. In an in vitro study with synoviocytes from RA and OA patients, the separate and combined effects of cortisol and NE were studied. In the in vivo study, patients with prior CS therapy/with SSI showed lower secretion of synovial IL-8 than the other groups, lower synovial density of T cells and macrophages, and lower overall inflammation. In the in vitro study, a cooperative suppressive effect of NE (10(-6) M to 10(-8) M) and cortisol (10(-6) M and 10(-7) M) on secretion of IL-8 and TNF from primary early culture mixed RA synoviocytes was observed. This cooperative effect was not observed in OA synoviocytes. In the same RA and OA patients, the cooperative effect was lost in 3rd passage synovial fibroblasts. This study demonstrates the cooperativity of cortisol and NE for inhibition of proinflammatory mediators produced in the synovial tissue of RA patients. These results underscore that coupling of an efficient secretion of systemic cortisol together with local production of NE is important in order to lower synovial inflammation.
Anti-inflammatory cooperativity of corticosteroids and norepinephrine in rheumatoid arthritis synovial tissue in vivo and in vitro.
Straub RH, Gunzler C, Miller LE, Cutolo M, Scholmerich J, Schill S.
Division of Rheumatology, Department of Internal Medicine I, University Hospital, Regensburg, Germany. [email protected]
Corticosteroids (CS) and norepinephrine (NE) support each other's biological effects. Thus, deficiency of cortisol and reduced synovial sympathetic innervation (SSI) may be proinflammatory in rheumatoid arthritis (RA). This study tested the anti-inflammatory cooperativity of CS and NE in human RA synovial tissue. In an in vivo study, 32 patients with RA (with prior CS therapy/without SSI: n=7; without prior CS therapy/with SSI: 6; with prior CS therapy/with SSI: 19) were investigated for synovial inflammation. In an in vitro study with synoviocytes from RA and OA patients, the separate and combined effects of cortisol and NE were studied. In the in vivo study, patients with prior CS therapy/with SSI showed lower secretion of synovial IL-8 than the other groups, lower synovial density of T cells and macrophages, and lower overall inflammation. In the in vitro study, a cooperative suppressive effect of NE (10(-6) M to 10(-8) M) and cortisol (10(-6) M and 10(-7) M) on secretion of IL-8 and TNF from primary early culture mixed RA synoviocytes was observed. This cooperative effect was not observed in OA synoviocytes. In the same RA and OA patients, the cooperative effect was lost in 3rd passage synovial fibroblasts. This study demonstrates the cooperativity of cortisol and NE for inhibition of proinflammatory mediators produced in the synovial tissue of RA patients. These results underscore that coupling of an efficient secretion of systemic cortisol together with local production of NE is important in order to lower synovial inflammation.
Nandi12 has some interesting ideas about nandrolone's effects on the joints. Pretty much shoots down the watered joints theory. Something to consider at the very least.
http://www.cuttingedgemuscle.com/Forum/showthread.php?s=&threadid=119&highlight=deca+joints
"Some steroids seem to have stronger effects than others. So when people say deca improves joints because it makes you hold water, that is nonsense. It is an antiinflmmatory because it suppresses cell mediated immunity, which controls inflammation. it has nothing to do with water.
Why is deca's reputation as an antiinflammatory better than testosterone's for example? My guess is the minimal aromatization and its progestogenic activity. If you link to the article below and open the graphic, you will see a couple of interesting things.
First, progesterone, like testosterone, stimulates humoral immunity (the TH2 mediated response in the graphic) and suppresses cellular immunity (TH1 response). So progesterone has antiinflammatory action.
Second, estrogen exerts a biphasic effect. At low doses it is proinflammatory, stimulating the TH1 arm of the immune system (cellular immunity) and inflammation.
Deca then works both as an androgen and a progestin to quell inflammation. Testosterone, by virtue of its aromatization to estrogen is an inferior antiinflammatory.
If you want to learn more about sex hormones and immunity, this is a good article to start with
http://www.sciencemag.org/cgi/conte...y=JsdA5F3s0DHFo "
http://www.cuttingedgemuscle.com/Forum/showthread.php?s=&threadid=119&highlight=deca+joints
"Some steroids seem to have stronger effects than others. So when people say deca improves joints because it makes you hold water, that is nonsense. It is an antiinflmmatory because it suppresses cell mediated immunity, which controls inflammation. it has nothing to do with water.
Why is deca's reputation as an antiinflammatory better than testosterone's for example? My guess is the minimal aromatization and its progestogenic activity. If you link to the article below and open the graphic, you will see a couple of interesting things.
First, progesterone, like testosterone, stimulates humoral immunity (the TH2 mediated response in the graphic) and suppresses cellular immunity (TH1 response). So progesterone has antiinflammatory action.
Second, estrogen exerts a biphasic effect. At low doses it is proinflammatory, stimulating the TH1 arm of the immune system (cellular immunity) and inflammation.
Deca then works both as an androgen and a progestin to quell inflammation. Testosterone, by virtue of its aromatization to estrogen is an inferior antiinflammatory.
If you want to learn more about sex hormones and immunity, this is a good article to start with
http://www.sciencemag.org/cgi/conte...y=JsdA5F3s0DHFo "
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