Decca, Winny and The Joints

Ive been getting slammed with questions about these compounds and there effect on the joints. I ran across this read and thought it would be usefull to some of the newbs. I don not take credit for this info as it was written by Anthony Roberts. Hope you fellas get some use out of this.


One of the most annoying and often repeated “well known fact” is that Nandrolone Decanoate (Deca) improves and soothes your joints by storing water in them. And, conversely, Winstrol has a “reverse osmotic” effect on your joints, which makes them ache when you use it, because it draws water out of your body, joints included. Reverse Osmotic? Wow?if we use really big words, maybe we?ll sound smart and people will stop asking questions. I believe this to be the dictum most anabolic steroid boards are founded on, and probably the way the staff on those boards begin their evening prayers?

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.

I’ve read this before on MesoRX I think. It’s quality info in my opinion. I like the way AR thinks.

I want to bump up this - read it right now, guys. Just wanted to create a thread about P4 & DHT derivatives and joint-related problems (have cut my E2 levels too much recently, so I’m interested again), but the author did a great job already. The only thing I want to correct is too low E2 leads to excess water retention in reality.

What did you do that cut your E2 levels so low?

A cycle of testosterone, boldenone, oxandrolone and mesterolone has lowered E2 below my “perfect range” for the cycle so I’ve experienced all low-E2 symptoms including knee joint pain with a slight inflammation (can’t do any knee extension exercises for now). What’s funny, when on TRT dose, this E2 result I’ve been recently struggling with is just good (20-23 pg/mL).To counteract this, my testosterone to boldenone ratio has to be close to 1:0.7, and E2 concentration more than 25 pg/mL… Those oral DHT derivatives have more anti-estrogenic (in direct and indirect mechanisms) properties then I’ve expected. Every cycle is a bit different - this is the first time I don’t have to take any AI (haven’t used such big doses of DHT orals before) and was forced to leave my E2 spot towards higher values to feel good.

I didn’t realize that about Anavar & Mast possibly lowering E2. That’s interesting thanks for sharing. I had heard Boldenone having that effect.

If you don’t mind me asking what TRT dose puts you at E2 of 22? I’m guessing it’s very low. When I first started TRT and was subscribed to the E2 = 22 rule and was always a hair away from crashing E2. I would be ok for months even with a very low AI dose and then all of a sudden crashed and I’m someone who’s E2 is usually higher than most at the same dosage. Luckily I feel much better letting it ride but that took and a year with several crashes to figure out.

Boldenone metabolites are moderate to strong aromatase inhibitors. Anavar and Proviron as DHT derived hormones have some like-AI properties and inhibit E2 products on transcriptional level.

When on testosterone solo, even at the dose of 100-150 mg/wk (enanthate, e2d to minimize any blood peaks) I still have to take low anastrozole doses (like 0.1 mg/e2d or so) to keep the range. I’m a high-aromatizer, unfortunately.

I haven’t been on such low doses of T for many months, mainly because of my bodybuilding involvment. If I’d move to TRT (most probably I would in the next year, for health and a new job reasons), I’ll add some Primobolan or Equipoise to my test for bigger anabolic:androgenic ratio and to give up any AI.

So… I have a question for you (or questions)

Does nandrolone induce dyspnea? Is this a known side effect. I’ve notice this a bit recently (and honestly last time I tried nandrolone). It’s nothing serious, nor is cardiorespiratory function particularly affected. I’m unsure whether this effect is directly nandrolone mediated or whether it’s due to the fact that I’m sick (influenza). I suppose we will see when I’m all better, back training full time. (I’m going back today given all my symptoms are “above the neck”)

I’m currently on 75mg test 140mg nandrolone. After my reckless vacation (got back Jan 2), Post injury → catching the flu I’ve lost a decent amount of muscle mass as I haven’t had enough time to train consistently. I have ten 10mg dbol tablets, this should theoretically be able to give me a small push for when I begin training again (get me back to where I used to be). I could use 20mg for 5 days or so. I appear to prefer nandrolone to testosterone, the question is, how long can one realistically use it? I’m going to check my lipids tomorrow, though literature indicates in terms of cardiac toxicity it outshines test, these studies predominantly pertain to those of a rodent/in-vitro nature. I’d switch to primo but I worry 1-150mg weekly will fuck up my lipids. DHT derived AAS tend to be harsh on lipids (given estrogens purported effect on glucose and lipid metabolism), if it were for a few weeks that’d be fine, but I don’t want to talk around year round with HDL in the 20s/low 30s. I’m genetically prone to not having the greatest lipids. Last I checked HDL was 43, LDL was 100, trigs were extremely low, about 40)… this was on 200mg test

What happens in rodents due to differences within metabolic pathways, elimination mechanisms, susceptibility to damage etc may not always correlate with human interaction. Rodent studies showcase a HED of 50-100mg test weekly to induce cardiac enlargement with associated fibrosis… Yet TREN doesn’t appear to elicit substantial cardiotoxicity within our rodent friends. In Vitro studies factor out environmental variables/antioxidants/drug elimination etc… So how much worse than test is nandrolone… realistically. Neurologically speaking I don’t appear to have garnered any particular effect. Perhaps my libido has dropped off slightly at this point comparative to baseline, otherwise it’s preferable to testosterone alone (less acne, less water retention… this is the biggest plus, relief of joint pain). You may not believe in nandrolone inhibiting aches and pains, think it’s a cortisol mediated response… but in this case why doesn’t fluoxymesterone, a very potent 11 HSD inhibitor mediate joint pain within those taking it?

Finally, opinions on Mestanolone… I have a source that sells this, it’s otherwise very hard to get so I don’t think I can pass up a potentially once in a lifetime opportunity. I assume regarding

Methylated dihydrotestosterone will be very potent, esp given I’ve seen studies wherein pure DHT has been used to treat gynocomoastia (I expect some semblance of ER antagonism to occur). This has been replicated (my theory) within rodent models

If it isn’t directly DHT mediated, 3b androstanediol (DHT metabolite) appears to have an (albeit very low) affinity for the ER

Though this study dictates DHT itself has very low affinity for the ER. Hinting the blunting of ER synthesis as you said is probably related to inhibiting E2 prior to receptor binding

Backs that statement

Finally… regrading AAS induced neurotoxicity. New study has come out linking AAS use to profound cognitive impairment/stunting… thoughts on this? How worried should I be if I’m using between 200-300mg weekly, sometimes between 300-350 if I’m briefly experimenting with an oral

I’m very tired and riddled with influenza (actually probably shouldn’t go to gym today, it’d be profoundly inconsiderate given that I’m presumably still contagious), so I apologise if this post appears somewhat incoherent