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SERIOUS Question about AS and Immune System

TheStromba

New member
Hope some of the experts can help

Can AS lower your White Blood Cell Count ?

If it does, how long post cycle do levels return to normal ?

My count has always been a bit below normal. Very healthy otherwise, matter of fact I really don't often catch a cold.

My latest blood work showed a drop in my white cell count from before I did AS. (3.2 1 year ago to 2.7)

I have just started my second cycle and I dont want to drive my levels so low that I get sick.

Thanks
 
Androgens are generally antiinflammatory (in the literature) and are immunosuppressive, you are correct! Estrogens exert negating effects on this. I hope this helps!
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Androgens and estrogens modulate the immune and inflammatory responses in rheumatoid arthritis.

Cutolo M, Seriolo B, Villaggio B, Pizzorni C, Craviotto C, Sulli A.

Laboratory and Division of Rheumatology, Department of Internal Medicine and Medical Specialities, University of Genova, Genova, Italy. [email protected]

Generally, androgens exert suppressive effects on both humoral and cellular immune responses and seem to represent natural anti-inflammatory hormones; in contrast, estrogens exert immunoenhancing activities, at least on humoral immune response. Low levels of gonadal androgens (testosterone/dihydrotestosterone) and adrenal androgens (dehydroepiandrosterone and its sulfate), as well as lower androgen/estrogen ratios, have been detected in body fluids (that is, blood, synovial fluid, smears, salivary) of both male and female rheumatoid arthritis patients, supporting the possibility of a pathogenic role for the decreased levels of the immune-suppressive androgens. Several physiological, pathological, and therapeutic conditions may change the sex hormone milieu and/or peripheral conversion, including the menstrual cycle, pregnancy, the postpartum period, menopause, chronic stress, and inflammatory cytokines, as well as use of corticosteroids, oral contraceptives, and steroid hormonal replacements, inducing altered androgen/estrogen ratios and related effects. Therefore, sex hormone balance is still a crucial factor in the regulation of immune and inflammatory responses, and the therapeutical modulation of this balance should represent part of advanced biological treatments for rheumatoid arthritis and other autoimmune rheumatic diseases.

PMID: 12114267 [PubMed - in process]
 
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More evidence
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Effect of gonadal steroids on proliferative responses and subset alterations in cultured chicken lymphocytes.

Landsman T, Leitner G, Robinzon TB, Helle ED.

Department of Animal Sciences, Faculty of Agriculture, The Hebrew University of Jerusalem, Rehovot, Israel.

The effect of gonadal steroids (GS) on proliferation of lymphocytes and distribution of lymphocyte subpopulations in cell culture was examined. The involvement of protein kinase C (PKC) and calcium ionophore in the proliferative response was tested. Estradiol benzoate (EB) or testosterone propionate (TP) had no significant influence on proliferation of peripheral blood lymphocytes (PBL) when cells were not stimulated by mitogen. At high concentration (10-6 M), EB and dihydrotestosterone (DHT) decreased lymphocyte proliferative response to concanavalin A (ConA) and lipopolysaccharide (LPS) at 24 and 72 h of incubation. However, at physiological doses (10(-12) to 10(-16) M), EB significantly enhanced the proliferative response at 24 h of incubation, whereas DHT had no effect. The inhibitory effect of the high dose of EB or DHT on proliferation of T and B lymphocytes was independent of time of hormone presentation to the cells or age and gender of cell donor. In all cultures, pre-incubation of lymphocytes with 10(-6) M of EB or DHT significantly reduced their proliferative responses to ConA, phytohemagglutinin (PHA), and LPS. The percentage of CD3+ cells was significantly reduced by EB, whereas DHT had no such effect. In contrast to inhibition of proliferation in response to mitogens, 10(-6) M EB dramatically enhanced the proliferation of lymphocytes in response to the PKC activator, phorbol 12-myristate 13-acetate, and calcium ionophore, A23187. Results suggest that high doses of EB do not damage the viability or proliferation capability of lymphocytes and, therefore, suppress the proliferative response to mitogens in a different manner, perhaps by reducing gene transcription for receptors that recognize the mitogens, or suppressing some postreceptor events. The enhancement of proliferation in response to mitogens by low doses of EB may support this assumption, because the biphasic effects of steroids on gene transcription are well documented.

PMID: 11558919 [PubMed - indexed for MEDLINE]
 
GH and IGF-1 have a general immune stimulating effect but are not essential for immune system development or normal function. GH acts to oppose the immune depressing effects of cortisol. Some of the specific effects of GH and IGF-1 that I have seen described are:

- an increase thymus size and thymocyte numbers

- IGF-I can potentiate B lymphopoiesis ( B cell formation)

- they stimulate the growth of antigen-responsive clones of B and
T cells

- they stimulate T cells to secrete cytokines ( immune modulating
chemicals ) that can stimulate bone marrow production of
immune cells.
 
I have read many times that deca actually improves the immune system but i ahve never done scientific research to support that!:D
 
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.


Here is a link to an excellent summary of all this, called "Gender Gap in AutoImmunity"

http://www.sciencemag.org/cgi/content/full/283/5406/1277?ijkey=JsdA5F3s0DHFo
 
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