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Anabolic Steroid effects on the immune system (part 2)

bigdelt69

New member
Although I could not find any specific studies regarding how AAS effects immune function, I was able to piece together several articles and come up with a general idea of how this works.

As I stated in the previous thread (part 1) the immune system has two basic types of defense cells. The B cells which make up the Humoral immunity, and T cells that make up the cell immunity.

First the T cells are formed in the thymus. These T cells work directly by attacking the invading virus. Explaining all the actions of T cells would take forever to do. If you want to do more, there are loads of info on this available at other sites. Most AAS are known to suppress Cellular immunity, although they stimulate humoral immunity.

What first brought this to my attention were the vast number of articles relating to using AAS to treat autoimmune diseases. Most autoimmune diseases are caused by various T cells attacking your own body.

Small doses of winstrol, and deca, have been shown to have no effect on the cellular immunity, but still improves humoral immunity. It is also know that many AAS including deca have been shown to be antiinflammatory. Although I believe that deca accomplishes this through a different function as compared to the rest. This is greatly because cellular immunity is what causes inflammation.

Although I can not explain why short ester testosterones seem to cause mild flu like symptoms, I greatly assume that it has something to do with the suppression on cellular immunity. I came across one study that concluded shorter acting esters of testosterone have a greater effect on the suppression of cellular immunity. I have ordered the full text and I will post it as soon as I can.
 
"Although I can not explain why short ester testosterones seem to cause mild flu like symptoms, I greatly assume that it has something to do with the suppression on cellular immunity. I came across one study that concluded shorter acting esters of testosterone have a greater effect on the suppression of cellular immunity. I have ordered the full text and I will post it as soon as I can."

It is the conversion of testosterone to etiocholanolone (sp?) that makes you feel sick, especially with short acting esters, because they peak strongly.

Furthermore the immune system is suppressed, because the body is longing so much for proteins during AAS use, that if you don't supply extra protein, the body will tear down immunoproteins from the blood. So bump up the proteins during AAS use, but we all know this.
 
bigdelt69 said:
It is also know that many AAS including deca have been shown to be antiinflammatory. Although I believe that deca accomplishes this through a different function as compared to the rest. This is greatly because cellular immunity is what causes inflammation.

Although I can not explain why short ester testosterones seem to cause mild flu like symptoms, I greatly assume that it has something to do with the suppression on cellular immunity. I came across one study that concluded shorter acting esters of testosterone have a greater effect on the suppression of cellular immunity. I have ordered the full text and I will post it as soon as I can.

If I remember, Flu-like symptoms (and inflamation) are a result of cytokine(s) (such as) tumor neucrosis factor induced production of aracadonic acid derivatives.. Please post the article when you get it.. It will be interesting to see if testosterone acts at this pathway.

I'm sure you are aware of the relationship between glucocorticoids and inflamation. What's your theory on deca and it's relation to this pathway?

There is a lot of corilation between TNF-alpha expression and reactive oxyen species.. Alpha lipoic acid has been shown to alleviate this in some instances..

Although the subject of immunology is not something I have great desires for, new findings on odd-ball cells (other than immune cells) expressing cytokine genes in autocrine, paracrine fashion.. Nobody ever dreamed that gut epethelial cells, for instance, expressed IL-family proteins.

Andy
 
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