Deca, Winstrol and your joints.

[Deacon]

Ok I have been flooded with emails from MESO to check out this article and I have; well so have some other board VET's and we have soem concerns. You see it would appear that some of Mr. Roberts information; in fact complete sentences in some cases have been taken from Nandi - a very well known and respected bro who also a scientist. He also passed away tragically a while back.
Anyway it is doubly tragic that MR Roberts appears to be borrowing heavily from his articles published 3 years ago without listing any reference to Nandi. I have to wonder how many other bro's work I might find in his new book?


This article was originally published September 9, 2005 at http://www.mindandmuscle.net)

Separating Fiction from Fact

I’ve been somewhat plagued by certain questions ever since I started reading about steroids a decade ago. Certain ideas just never sat well with me…and unfortunately, when I asked more questions, I only received similar answers. When I was introduced to the world of internet steroid boards about half a decade ago, I posed these same questions to the "powers that be" on the boards I was a member of. I received many of the same answers, but my private messages and e-mails to moderators and staff members on various boards asking for references or some kind of logic were all left unanswered. On occasion I was offered the profound advice that it’s "well known that…etc…" and told to stop asking. Well known to whom? It’s certainly not well known to me.

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…

Well, this mode of thinking isn’t good enough for me, and if you’re reading MESO-Rx or Avant’s website or Mind and Muscle magazine, it’s not good enough for you either. Hold on, because we’re about to engineer a paradigm shift!

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.

[Deacon]

this was Nandi's work;

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

[Deacon]

more of Nandi;

Yes, that is my theory. 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 disorders.

[Deacon]

another Nandi post;

Hormonal 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.

[unt0ld]

thx for taking the time deacon, you have the most informative posts on these boards. Your the man bro.

[kethnaab]

no doubt, deacon is the man.

on a side note, deacon, what are your thoughts on anthony roberts' pct article?

[Deacon]

well if you were to research the work already done by Pheedno and on the boards for the last 4-5 years you would find much the same information except for the actual protocol; once again many old board bro's are stating that Mr Roberts has done nothing more than rehash what Pheedno has already done. I would strongly caution Mr Roberts in his use of others work especially printed articles. The entire reason I am bringing any of this up is simply because I wonder if Mr Roberts is writing this stuff or simply taking from others and adding his own little slant to it.

As far as the PCT protocol he advises; I see no reason for the vitamin e or other vitamins he adds - every bb should be using a multi anyway.
I also disagree that 20 mgs of nolva is enough - I prefer the 40/20 recipe and if the cycle was extreme - tren or deca for a long period - I believe that you must mix clomid and nolva at 100/40 - 50/20 for 28 days - I simply dont see his PCT giving you a proper recovery. On a test only cycle yes it would.

Also as far as Aromasin being added there are many arguments for or against this and I have yet to be convinced it should be a part of PCT.

I do agree with his use of HCG - however I shake my head when he says he is one of the few who advise this - HCG useage is the norm these days not the abstract.
Overall I think Mr Roberts is taking a lot of credit for things he has nothing to do with and did nothing to bring about.

[Deacon]

for those who wonder here is Pheedno's PCT;

Pheedno's PCT

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My post cycle therapy is a three compound administration which is designed so that there is a primary and secondary LH stimulator which both are maximizing potential early in the duration; with the primary being phased out in extended protocol. With the addition of an AI, which makes the above possible, the individual will also endure less of an increase in SHBG, which allows free testosterone levels to reach base line
at a much quicker pace. The individual will also see less of a problem in most cases with sexual libido as the bounding SHBG is controlled(to an extent). Below you will find my suggested bare minimum, as well as a sample of an extended protocol. Extended PCT protcol is cycle length dependant so the below is not the standard for all cycles


PCT for cycles 8-16wks:
Day 1-30- .25mg L-dex + 100mg Clomid + 20mg Nolva

Extended protocol sample for a 12+ month cycle:
Day 1-15_ .25mg L-dex + 100mg Clomid + 20mg Nolva
Day 16-45_.25mg L-dex + 75mg Clomid + 20mg Nolva
Day 46-65_.25mg L-dex + 20mg Nolva
Day 66-80_.25mg L-dex

Now, IMO clomid is selective to the suprapituitary, while Nolva is selective to breast, bone, and liver ERs. I've come to this conclusion based on the comparison of studies on both SERMs. In every study showing benefit to HPTA from tamoxifin, the duration of the administration is 3-12months(This includes studies cited by William Llewellyn in his Nolva vs Clomid article). In studies showing levels of LH, FSH, and Testosterone checked after short durations of tamox, they were either insignificant, or their was an actual drop. I believe this is because tamox selectively works at the mammery(as well as bone and liver), thus taking longer for LH stimulation to occur.
With clomid, benefit to gonadotphin concentrations, LH, FSH, and serum testosterone can be seen in short periods of 2-6wks. Because of the apparent selective nature of the two, and given our usual PCT duration, clomid is by far superior at LH stimulation than Nolva. Now both is the wise choice for a couple of reasons:

1. Nolva acts as the preventive measure to the estrogen flux
occured PC while clomid is the primary LH stimulator(Even more so in the case an AI is not used).
2. If your running a longer PCT, clomid needs to be discontinued after a while as it has been shown to desensitize GnRH, this due, IMO, to it's selective nature to the suprapituitary. In the longer forms of PCT, the clomid will be phased out, leaving Nolva and L-dex

Arimidex(or L-dex)
Estrogen is the main inhibitence of restoring HPTA, and AI administration has been shown to increase gonadotrophin concentrations and serum Testosterone by up to 50%. In addition, by adding L-dex, the inhibitence of excess estrogen allows Tamox to work greater at LH stimulation in the begining stages of PCT, since the need to prevent binding in the mammery is lessened by the reduction in estrogen biosynthesis.

[solo47]

Aromasin or Arimidex, that's the question. Clom & Nolva, sure.

[novicebb]

Great posts deacon especially the last one- really found it helpful. I would like if some would sticky this.