i was wondering how fast it usually takes deca to take effect on the joints and help lube them?
i was wondering how fast it usually takes deca to take effect on the joints and help lube them?
lube them ??
"Deca stores water in connective tissue, thus alleviating joint pain"
When I used deca before I didn't notice it much until I stopped and my joints got alittle sore.
wouldnt anything that caused you to retain water have the same effect then..
think its more than likely caused by decas action as an antiinflammatory..
I normally feel joint relief from deca in the first 3-4 weeks.
I also find that the relief occurs within the first several weeks. For me it was like a miracle. Went from chronic shoulder tendonitis to zero pain. It was great.
Do you think frontloading will help with the joint relief sooner?
My joint pain was due to a high TSH. My endo increased my synthroid to 175mcg and all pain went away!!
I tried every narcotic/otc pain relivers and Prednisone was the only thing that worked until we found the problem.
Yeah I know but i was thinking maybe it was something that will take some time to build.
just to explain how it works..written by nandi in 2002.. way before hooker stole it and wrote his article on the same topic claiming it to be his own.. after nandi passed i might add.. nandi was on the cutting edge..one of the brightest minds in the game..way ahead of the times
Androgens, Estrogens, and The Immune Response
I posted this reply recently on another board to the question "Do androgens suppress or stimulate the immune system"
It's really not quite correct to say androgens suppress or stimulate the immune system. It is a bit more complicated than that, not surprisingly.
Here is Immunology 101 in a nutshell. The immune system has two "arms of attack": the cell mediated arm and the humoral arm. The cell mediated arm, or cellular immunity, responds to general assaults on the body by sending out immune cells to do things like attack invading organisms, or degrade necrotic tissue, in a non specific manner. By non specific it is meant that the immune cells do not recognize the invader as a specific target with which they are familiar. Inflammation is an example of a cell mediated response. When you get a sliver or strain a muscle the body sends immune cells there to wall off the site, increase blood flow, remove damaged tissue, etc.
Humoral immunity involves B lymphocytes that secrete antibodies that bind to the target and allow immune cells to recognize the target immediately as an invader and launch an attack. When you are vaccinated for something, like smallpox, you are injected with a small inactive piece of the virus. This primes your body to make large numbers of B cell clones that, if ever challenged with smallpox for real, pump out antibodies that mark the virus for destruction by other cells. The big advantage of this system is that it is fast and efficient. The disadvantage is that it is very specific. The cellular response is not as efficient but it works against any invader, not just one for which there already exist primed clonal B cells.
There is an emerging model of how the sex steroids regulate the two arms of the immune system. It is thought that testosterone stimulates the humoral arm and suppresses the cellular arm. This paradigm arose from the study of autoimmune diseases which overwhelmingly plague women more than men. The majority of autoimmune diseases involve a cellular immune system gone wild. Since in men testosterone suppresses cellular immunity, men are much less likely to suffer from these diseases, like rheumatoid arthritis.
So when NFG123 mentioned that androgens are antiinflammatory, this is kind of what it means technically. 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
Deca has been used in several trials to treat the inflammatory symptoms of different autoimmune diseases like Sjogren's Syndrome and rheumatoid arthritis, with varying degrees of success. It is hardly a magic bullet but eases the symtoms and improves well being somewhat.
If that "lubing the joints" stuff were true, then other steroids that cause more bloating than deca would work better, and they don't seem to. There is just no evidence to support it, as you point out. The TH1 suppression caused by androgens/progestins makes perfect sense, agrees with the research, and is consistent with the clinical trials of deca in inflammatory disordersHormonal influences. T helper 1 (TH1) cells secrete proinflammatory cytokines and promote cell-mediated immune responses, whereas TH2 cells trigger antibody production. In multiple sclerosis (MS) and rheumatoid arthritis (RA), there are features characteristic of a TH1 immune response directed against autoantigens in the central nervous system and joints, respectively. Pregnancy and systemic lupus erythematosus (SLE) favor a TH2 environment. Sex hormones (such as progesterone) that promote the development of a TH2 response antagonize the emergence of TH1 cells. This may explain why in multiple sclerosis and rheumatoid arthritis disease symptoms improve during pregnancy, whereas in lupus, they do not.
From
http://www.sciencemag.org/cgi/conte...83/5406/1277/F1
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