akn
Musclechemistry Member
My first clue to solving this mystery was that Winstrol was DHT derived, as is masteron, and I have a friend who gets bad joint problems when using both of them. A little bit of research revealed many people shared his affliction. And it was very obvious that many people who’ve used Deca have found it to alleviate chronic joint problems and pains. I know that Deca is a 19-nor derived steroid, and I also know that it’s a progestin, and hence can stimulate the progesterone receptor (15) about 20% as well as progesterone. I also know that it aromatizes (converts to estrogen) at a much lesser rate than testosterone (16). Could the answer somehow lie in estrogen? Well, Deca doesn’t really aromatize much at all, so maybe there is a synergy between Deca’s PgR stimulating ability and its low(ish) estrogenic effects?
We certainly know that Estrogen depletion by menopause can decrease bone mineral density and the replacement of estrogen quickly restores the bone loss (18). In addition, we know that estrogen is aided in this by progesterone but that estrogen is more important (19). Collagen is also subject to improvement by addition of estrogen and progesterone (20). But is that all? Why do your joints “feel” better on deca?
And where would this leave us, in terms of Winstrol and Masteron causing pain in joints? I have always thought there was something more to this. And I think the answer lies in DHT.
You see, DHT administration has been found to decrease estrogen levels through a variety of mechanisms on peripheral tissue (1). DHT directly inhibits estrogenic activity on tissues, either by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen receptor binding. Either way, it has two clear mechanisms of possible action in peripheral tissue.
DHT and its metabolites have further been shown to inhibit aromatization itself, and this is a possible mechanism whereby it can reduce circulating levels of estrogen in your body. Indeed, DHT, androsterone, and 5alpha-androstandione are all potent inhibitors of the formation of estrone from androstenedione. Finally, DHT acts on the HPTA to decrease the secretion of gonadotropins (it inhibits it). In fact, it’s so potent at reducing estrogen that transdermal DHT gel applied to the affected area has been used to treat gynocomastia (5)(6). Estrogen is the primary culprit in gyno (8), although we know that progesterone can be synergistic with estrogen in this (and other) respects(s).
DHT also has a negative effect on Progesterone biosynthesis in cells (7), and even has the ability to inhibit progesterone elevation caused by estrogen (10). Therefore DHT would be (and is) very effective in reducing gyno because it reduces both estrogen as well as progesterone. This property holds with DHT-derived steroids, for the most part as well, since Masteron has been found in some cases to have positive effects in reducing breast tissue tumors(9), which is essentially what gyno is (albeit benign).
You still with me? Good, because I want you to hold that first idea (DHT reduces estrogen and progesterone), and put it in the back of your mind while you read this next part, which is about your immune system.
T helper 1 (TH1) cells secrete pro-inflammatory cytokines as well as promoting cell-mediated immune responses, whereas TH2 cells trigger antibody production (2). Sex hormones (such as progesterone) that promote the development of a TH2 response also happen to antagonize the emergence of TH1 cells. Hence, when progesterone levels are (or the PgR, progesterone receptor) stimulated, you’ll have more anti-inflammatory cytokines floating around and less pro-inflammatory cytokines. Aspirin, Tylenol, and all of the over the counter anti-inflammatories are also useful as painkillers. Anti-inflammatory effects are often highly correlated with pain killing activity. What happens when women with arthritis get pregnant? They typically see a reduction in joint pain. This, I contend, is due to the progesterone and estrogen increases seen during pregnancy, and the anti-inflammatory effects they generate.
Progesterone, like testosterone, both stimulates humoral immunity (the TH2) and suppresses cellular immunity (TH1 response). Ergo, progesterone has anti-inflammatory action. Deca is a progestin, meaning it stimulates the progesterone receptor. And that’s why it alleviates joint pains. Remember that old idea that deca promotes “water-retention” in the joints, and that’s why it helps your joints feel better? Bullshit. You just read the real reason deca helps joints. Deca actually works on two fronts as an androgen—which have well-documented effects on corticosteroids—and as a progestin to reduce inflammation.
Let’s move on….
Estrogen exerts what is known as a biphasic (two phase) effect. At low amounts, it is pro-inflammatory, because it stimulates the TH1 arm of the immune system (cellular immunity) and inflammation. In high(er) amounts, it is actually an anti-inflammatory (2). So when one takes very strong anti-estrogens (or aromatase inhibitors), one both loses water (because estrogen causes water retention) as well as experiences sore joints due to the pro-inflammatory effects generated from low estrogen levels.
Letrozole, which reduces blood plasma levels of estrogen due to aromatase inhibition, is the best example of this. It is infamous for causing aching joints. Letrozole decreases both aromatase activity as well as (obviously) plasma levels of estrogen, and in addition reduces progesterone levels (3). This is why when people use Letrozole, they claim it takes “water out of their joints” and makes them ache. Again, this is total bullshit.
Lowering estrogen will reduce water retention, but of equal importance it will also limit your body’s ability to produce estrogen-mediated anti-inflammatory reactions to weight training. You lose water and your joints hurt, which is why the myth exists that lost water in the joints is the source of discomfort. It is true that you one loses subcutaneous water when estrogen levels are low, but it’s simply not true that losing this water will make your joints hurt. It is the loss of estrogen and progesterone’s anti-inflammatory effects that is behind the aching joints. We can also make the claim that Testosterone can have some anti-inflammatory effects both through it’s aromatization to estrogen is as well as its effects on corticosteroids. This too, is well documented.
Now, let’s see if we can recall that first bit I asked you to remember….the bit where I told you that DHT reduces estrogen and progesterone. By now we have established that reductions in both of those hormones (Estrogen and Progesterone) are caused by DHT and DHT-derivatives, which carry many of the same properties and produce similar metabolites.
And this reduction in Estrogen/Progesterone, caused by DHT, reduces your body’s production of anti-inflammatory and painkilling cytokines. And this is what causes Winstrol, Masteron, etc to cause joint pain. And as noted at the beginning of this article, when one undergoes reductions in estrogen and progesterone, bone mineral density and collagen will suffer deleterious effects.
So there we have it, finally: a plausible explanation for the contrasting effects Deca and Winstrol have on joints.
curtsey anthoney robberts
References
1. MacDonald PC, Madden JD, Brenner PF, Wilson JD, Siiteri PK 1979 Origin of estrogen in normal men and in women with testicular feminization. J Clin Endocrinol Metab 49:905–916
2. Science, Vol 283, Issue 5406, 1277-1278 , 26 February 1999
3. Eur J Obstet Gynecol Reprod Biol. 2002 Nov 15;105(2):161-5.
4. J Clin Endocrinol Metab. 1995 Sep;80(9):2658-60.
5. Successful percutaneous dihydrotestosterone treatment of gynecomastia occurring during highly active antiretroviral therapy: four cases and a review of the literature.
6. Clin Infect Dis. 2001 Sep 15;33(6):891-3. Epub 2001 Aug 10.
7. Androgens and the immunocompetence handicap hypothesis: unraveling direct and indirect pathways of immunosuppression in song sparrows.
8. Am Nat. 2004 Oct;164(4):490-505. Epub 2004 Sep 1.
9. Nippon Sanka Fujinka Gakkai Zasshi. 1988 Mar;40(3):331-7.
10. Progesterone is not essential to the differentiative potential of mammary epithelium in the male mouse. Freeman, Topper. Endocrinology. 1978 Jul;103(1):186-92
11. Eur J Cancer Clin Oncol. 1983 Sep;19(9):1231-7.
12. Biol Reprod. 1989 Jun;40(6):1201-7.
13. Metabolism. 1990 Nov;39(11):1167-9.
14. Effects of nandrolone decanoate on bone mineral content R, Righi GA, Turchetti V, Vattimo A.
15. Cancer Res 1978 Nov;38(11 Pt 2):4186-98
16. Biosynthesis of Estrogens, Gual C. et al. Endocrinology 71 (1962) 920-25
17. Comparative effects and mechanisms of castration, estrogen anti-androgen, and anti-estrogen-induced regression of accessory sex organ epithelium and muscle.Invest Urol. 1981 Jan;18(4):229-34.
18. [Clinical aspects of estrogen and bone metabolism]
Clin Calcium. 2002 Sep;12(9):1246-51. Japanese.
19. The effects of progestins on bone density and bone metabolism in postmenopausal women: a randomized controlled trial.
20. Bone response to treatment with lower doses of conjugated estrogens with and without medroxyprogesterone acetate in early postmenopausal women.
Osteoporos Int. 2005 Apr;16(4):372-9. Epub 2005 Jan 15.
21. Am J Obstet Gynecol. 2005 Apr;192(4):1316-23; discussion 1323-4.
We certainly know that Estrogen depletion by menopause can decrease bone mineral density and the replacement of estrogen quickly restores the bone loss (18). In addition, we know that estrogen is aided in this by progesterone but that estrogen is more important (19). Collagen is also subject to improvement by addition of estrogen and progesterone (20). But is that all? Why do your joints “feel” better on deca?
And where would this leave us, in terms of Winstrol and Masteron causing pain in joints? I have always thought there was something more to this. And I think the answer lies in DHT.
You see, DHT administration has been found to decrease estrogen levels through a variety of mechanisms on peripheral tissue (1). DHT directly inhibits estrogenic activity on tissues, either by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen receptor binding. Either way, it has two clear mechanisms of possible action in peripheral tissue.
DHT and its metabolites have further been shown to inhibit aromatization itself, and this is a possible mechanism whereby it can reduce circulating levels of estrogen in your body. Indeed, DHT, androsterone, and 5alpha-androstandione are all potent inhibitors of the formation of estrone from androstenedione. Finally, DHT acts on the HPTA to decrease the secretion of gonadotropins (it inhibits it). In fact, it’s so potent at reducing estrogen that transdermal DHT gel applied to the affected area has been used to treat gynocomastia (5)(6). Estrogen is the primary culprit in gyno (8), although we know that progesterone can be synergistic with estrogen in this (and other) respects(s).
DHT also has a negative effect on Progesterone biosynthesis in cells (7), and even has the ability to inhibit progesterone elevation caused by estrogen (10). Therefore DHT would be (and is) very effective in reducing gyno because it reduces both estrogen as well as progesterone. This property holds with DHT-derived steroids, for the most part as well, since Masteron has been found in some cases to have positive effects in reducing breast tissue tumors(9), which is essentially what gyno is (albeit benign).
You still with me? Good, because I want you to hold that first idea (DHT reduces estrogen and progesterone), and put it in the back of your mind while you read this next part, which is about your immune system.
T helper 1 (TH1) cells secrete pro-inflammatory cytokines as well as promoting cell-mediated immune responses, whereas TH2 cells trigger antibody production (2). Sex hormones (such as progesterone) that promote the development of a TH2 response also happen to antagonize the emergence of TH1 cells. Hence, when progesterone levels are (or the PgR, progesterone receptor) stimulated, you’ll have more anti-inflammatory cytokines floating around and less pro-inflammatory cytokines. Aspirin, Tylenol, and all of the over the counter anti-inflammatories are also useful as painkillers. Anti-inflammatory effects are often highly correlated with pain killing activity. What happens when women with arthritis get pregnant? They typically see a reduction in joint pain. This, I contend, is due to the progesterone and estrogen increases seen during pregnancy, and the anti-inflammatory effects they generate.
Progesterone, like testosterone, both stimulates humoral immunity (the TH2) and suppresses cellular immunity (TH1 response). Ergo, progesterone has anti-inflammatory action. Deca is a progestin, meaning it stimulates the progesterone receptor. And that’s why it alleviates joint pains. Remember that old idea that deca promotes “water-retention” in the joints, and that’s why it helps your joints feel better? Bullshit. You just read the real reason deca helps joints. Deca actually works on two fronts as an androgen—which have well-documented effects on corticosteroids—and as a progestin to reduce inflammation.
Let’s move on….
Estrogen exerts what is known as a biphasic (two phase) effect. At low amounts, it is pro-inflammatory, because it stimulates the TH1 arm of the immune system (cellular immunity) and inflammation. In high(er) amounts, it is actually an anti-inflammatory (2). So when one takes very strong anti-estrogens (or aromatase inhibitors), one both loses water (because estrogen causes water retention) as well as experiences sore joints due to the pro-inflammatory effects generated from low estrogen levels.
Letrozole, which reduces blood plasma levels of estrogen due to aromatase inhibition, is the best example of this. It is infamous for causing aching joints. Letrozole decreases both aromatase activity as well as (obviously) plasma levels of estrogen, and in addition reduces progesterone levels (3). This is why when people use Letrozole, they claim it takes “water out of their joints” and makes them ache. Again, this is total bullshit.
Lowering estrogen will reduce water retention, but of equal importance it will also limit your body’s ability to produce estrogen-mediated anti-inflammatory reactions to weight training. You lose water and your joints hurt, which is why the myth exists that lost water in the joints is the source of discomfort. It is true that you one loses subcutaneous water when estrogen levels are low, but it’s simply not true that losing this water will make your joints hurt. It is the loss of estrogen and progesterone’s anti-inflammatory effects that is behind the aching joints. We can also make the claim that Testosterone can have some anti-inflammatory effects both through it’s aromatization to estrogen is as well as its effects on corticosteroids. This too, is well documented.
Now, let’s see if we can recall that first bit I asked you to remember….the bit where I told you that DHT reduces estrogen and progesterone. By now we have established that reductions in both of those hormones (Estrogen and Progesterone) are caused by DHT and DHT-derivatives, which carry many of the same properties and produce similar metabolites.
And this reduction in Estrogen/Progesterone, caused by DHT, reduces your body’s production of anti-inflammatory and painkilling cytokines. And this is what causes Winstrol, Masteron, etc to cause joint pain. And as noted at the beginning of this article, when one undergoes reductions in estrogen and progesterone, bone mineral density and collagen will suffer deleterious effects.
So there we have it, finally: a plausible explanation for the contrasting effects Deca and Winstrol have on joints.
curtsey anthoney robberts
References
1. MacDonald PC, Madden JD, Brenner PF, Wilson JD, Siiteri PK 1979 Origin of estrogen in normal men and in women with testicular feminization. J Clin Endocrinol Metab 49:905–916
2. Science, Vol 283, Issue 5406, 1277-1278 , 26 February 1999
3. Eur J Obstet Gynecol Reprod Biol. 2002 Nov 15;105(2):161-5.
4. J Clin Endocrinol Metab. 1995 Sep;80(9):2658-60.
5. Successful percutaneous dihydrotestosterone treatment of gynecomastia occurring during highly active antiretroviral therapy: four cases and a review of the literature.
6. Clin Infect Dis. 2001 Sep 15;33(6):891-3. Epub 2001 Aug 10.
7. Androgens and the immunocompetence handicap hypothesis: unraveling direct and indirect pathways of immunosuppression in song sparrows.
8. Am Nat. 2004 Oct;164(4):490-505. Epub 2004 Sep 1.
9. Nippon Sanka Fujinka Gakkai Zasshi. 1988 Mar;40(3):331-7.
10. Progesterone is not essential to the differentiative potential of mammary epithelium in the male mouse. Freeman, Topper. Endocrinology. 1978 Jul;103(1):186-92
11. Eur J Cancer Clin Oncol. 1983 Sep;19(9):1231-7.
12. Biol Reprod. 1989 Jun;40(6):1201-7.
13. Metabolism. 1990 Nov;39(11):1167-9.
14. Effects of nandrolone decanoate on bone mineral content R, Righi GA, Turchetti V, Vattimo A.
15. Cancer Res 1978 Nov;38(11 Pt 2):4186-98
16. Biosynthesis of Estrogens, Gual C. et al. Endocrinology 71 (1962) 920-25
17. Comparative effects and mechanisms of castration, estrogen anti-androgen, and anti-estrogen-induced regression of accessory sex organ epithelium and muscle.Invest Urol. 1981 Jan;18(4):229-34.
18. [Clinical aspects of estrogen and bone metabolism]
Clin Calcium. 2002 Sep;12(9):1246-51. Japanese.
19. The effects of progestins on bone density and bone metabolism in postmenopausal women: a randomized controlled trial.
20. Bone response to treatment with lower doses of conjugated estrogens with and without medroxyprogesterone acetate in early postmenopausal women.
Osteoporos Int. 2005 Apr;16(4):372-9. Epub 2005 Jan 15.
21. Am J Obstet Gynecol. 2005 Apr;192(4):1316-23; discussion 1323-4.
