For my part, my issues are more than just the joint itself, but using adequan has reduced the pain and increased my tolerance to work and stress of the joint to such an extent I will forever swear by it/use it.
Could you elaborate on that?
What’s the joint in question?
One issue I have observed (aside from miss-diagnosing the cause of the pain) is that many do not follow the veterinary use of Adequan. Looking into vet recommended usage, what many consider the treatment is refereed to as a “loading phase” of a number of administrations close together for a number of days. The vet then moves the animal down to a maintenance dose, which is equivalent in dosing to a preventative dose. This is continued generally until the end of the horses “working days”.
I follow this procedure. Having done a full loading phase, I administer an as-needed maintenance dose, seemingly needing fewer and fewer as the months progress. I now go 2-4 weeks between injections with about 50-80% less pain in the joint than before any adequan administration, despite greatly increased workload and stress of the joint.
Thanks for the details.
So, how do you differentiate between actual cartilage regrowth and simply more ‘cushioning’ due to an increase in synovial fluids?
Many also love Nandrolone Decanoate for joint support.
I’m worried about Nandrolone Decanoate (and other anabolic steroids purported to be able to actually repair joints) to only provide temporary relief due to the cushioning effect by pulling water into the joints. I’m not going to cross the threshold to ASS (and thus have to deal with stuff like PCT etc.) until I know for sure they can repair joints
I omitted the specific joint in question so as to maintain anonymity. I would be happy to discuss such details via PM if you are interested, but would rather leave it out of the public forum. I can say, however, the joint in question was rarely trained before, and when it was, only with excruciating pain. Now I am able to train it regularly (2+ times per week) with nearly none of the pain during training, and 50-80% less pain in every day life.
While I have little subjective measurements of if the cause of the pain relief is actual reconstruction of the collagen, or simply an increase in synovial fluid, I can say that as an FDA approved drug (but not for human use), research indicates that the action of adequan is that of increasing synovial fluid, increasing and triggering collagen synthesis in joints, and stopping enzymatic processes of joint catabloism (I believe it MMP family enzymes). So, while my subjective experience is reduced joint pain, and increased ROM/tolerance, I might point to the available literature to address the WHY.
If looking JUST for joint relief, I too would not take Nandrolone for such purposes, and (as always), I can never recommend use of AAS. However, since it’s a good read, I will post an article by Anthony Roberts addressing the issue and the cause. It is less of an IF article, then a WHY article, being that Nandrolone has been fairly well established as a joint aid.
Deca, Winstrol, and your Joints
By Anthony Roberts
Separating Fiction from Fact
IÃ¢??ve been somewhat plagued by certain questions ever since I started reading about steroids a decade ago. Certain ideas just never sat well with meÃ¢?Â¦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 itÃ¢??s “well known thatÃ¢?Â¦etcÃ¢?Â¦” and told to stop asking. Well known to whom? ItÃ¢??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? WowÃ¢?Â¦if we use really big words, maybe weÃ¢??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 prayersÃ¢?Â¦
Well, this mode of thinking isnÃ¢??t good enough for me, and if youÃ¢??re reading MESO-Rx or AvantÃ¢??s website or Mind and Muscle magazine, itÃ¢??s not good enough for you either. Hold on, because weÃ¢??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 whoÃ¢??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 itÃ¢??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 doesnÃ¢??t really aromatize much at all, so maybe there is a synergy between DecaÃ¢??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 thatÃ¢??s why it alleviates joint pains.
Remember that old idea that deca promotes “water-retention” in the joints, and thatÃ¢??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 androgenÃ¢??which have well-documented effects on corticosteroidsÃ¢??and as a progestin to reduce inflammation.
LetÃ¢??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 progesteroneÃ¢??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, letÃ¢??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.