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Any actual science supporting Deca & Joint health?

weltweite

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Sep 29, 2008
Messages
713
Is there any actual study showing Deca's ability to increase collagen synthesis?

I see a lot of people copy & pasting that little article saying Deca increases collagen synthesis by 370% and Test lowers collagen synthesis by 50% and Winstrol increases collagen synthesis but weakens the tendons.. and anavar and eq.. etc.

I can say from my own experience that EQ did NOTHING for my joints. Anavar did NOTHING for my joints. Winstrol is a risk as stated..

Deca made my joints feel wonderful, and test makes my joints feel awful..

which leads me into why I am asking..

Someone is currently on a cycle of Test and Anavar.. and their joints and tendons never felt worse. This person wants to avoid Deca use due to it lowering interferon levels in the body and a few other negative side effects with red blood cell lining, and its long duration in the system after use.

My question is... is there any studies showing Deca actually raises collagen synthesis? Is the results seen with deca because of anti-inflammatory effects? If so, couldn't turmeric pills, fish oils, bromelain, cissus.. mimic those benefits?

And is Deca really a benefit in that case if its only MASKING the problem.. and not actually improving joints. Do you all notice bad joints after it's long gone from your system?

This "someone" really doesn't want to do Deca again, but may have too if their joint are preventing them from working out properly. It's getting sort of ridiculous, and pathetic for this person.


I have read many threads over the years regarding Deca, but never seen the studies. Any help, opinions, feedback, would be MUCH appreciated.
 

weltweite

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Sep 29, 2008
Messages
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This was the best I could do so far. (Deca and tendons)

Anabolic steroids may improve surgical repair of torn shoulder tendons

New research from the University of North Carolina at Chapel Hill indicates that treatment with anabolic steroids may improve surgical repair of massive or recurrent tears of the shoulder's rotator cuff tendons.

Such injuries extend well beyond the world of high-performance athletes, professional and collegiate - often occurring among older weekend athletes, including tennis and golf players. The study, which appears in the June issue of the American Journal of Sports Medicine, was led by Dr. Spero Karas, assistant professor of orthopedic surgery in UNC's School of Medicine.

Dr. Albert J. Banes, professor of orthopedics and biomedical engineering at UNC, developed a bioengineered tendon that figured prominently in the study's experiments. Through a company he founded 18 years ago, Banes developed a special tissue plate in which cells in a liquid collagen gel could remodel on their own to form a tissue-like matrix or structure. The structure then could be placed under mechanical load by a computer-driven pressure-controlled system.

In 2002, his laboratory announced it had successfully bioengineered a rhythmically beating experimental model of heart muscle.

Anabolic steroids benefit millions of people a year, said Karas, including those with deficiencies in sex hormones and burn victims who need to build up their metabolism to repair musculoskeletal tissue. They also are FDA-approved for treating anemia for their ability to help the body rebuild blood.

As it's widely known that anabolic steroids can build muscle mass and strength, Karas said he thought these properties might apply to shoulder tissue and that Banes' bioartificial tendon might provide the appropriate model for testing.

"In this new study, supraspinatus tendon cells were harvested from my patients during rotator cuff surgery, isolated and then sent to Albert's lab," Karas said. "The cells were then grown in his culture media to coalesce and form this experimental tendon model, the bioartificial tendon."

Prior to applying mechanical strain, the researchers treated some of the developing tissue with the anabolic steroid nandrolone decoanate. The steroid was administered directly into the lab dish via pipette, or dropper.

"We clearly found that when you looked at the bioartificial tendon matrices that were treated with anabolic steroid and then mechanical load or strain, we saw significant increases in their biomechanical properties," Karas said.

"The tendons were smaller, more dense, stronger, more elastic and had better remodeling properties than tissue cells not treated with steroid or placed under strain," he said. "They responded better to the load and formed a more normal appearing tendon, versus a more disorganized matrix we see in the untreated bioartificial tendon."

Thus, said Karas, it appeared that load and anabolic steroid "act synergistically" to improve the characteristics of tendon.

Karas said the research had clinical applications, including the possibility of a day when bioartificial tendon matrices might literally help bridge the gap between deficient human tissue and the normal state - that is, to bridge the holes that remain following surgery for large rotator cuff tears.

In the less distant future, the new study's crucial implications may apply to the post-surgery healing of tendons that have been torn or retracted for a long time, he said.

"Orthopedic surgeons, especially those who specialize in the shoulder, tend to have one vexing dilemma in front of them: There are certain states that make rotator cuff repair extremely difficult, and that would be a tendon that has experienced atrophy and degeneration, that has been torn for a long time. In other words, not a fresh tear.

"With FDA-approved drugs taken at the appropriate dosages for the appropriate occasions, we might be able to modulate tendon-to-bone healing in this postoperative period," he said, adding that the next step is to explore the use of anabolic steroids in the animal model.

Most of these patients are between 50 and 70 years of age and have their athletic years behind them. But many are very active and comprise a much larger demographic in society than the athlete, Karas said.

"And these weekend warriors who play tennis and golf are represented far more in most orthopedic practices than professional or collegiate athletes." Support for the study came from the National Institutes of Health.
 

dece870717

Banned
Joined
May 18, 2009
Messages
627
http://www.ironmagazine.com/article545.html

"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."
 

weltweite

New member
Registered
Joined
Sep 29, 2008
Messages
713
Deca, Winstrol and Your Joints - 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."
I really appreciate you taking the time to post that. Learned something new today. Thank you

The only thing I was a little "iffy" on was the part that says "Testosterone can have anti-inflammatory effects" because my joints kill me when taking Test. So perhaps the conversion to DHT has more effect on the joints than the estrogen increase that comes with it.. and visually I don't really bloat on Test, I actually get leaner and harder looking so that probably explains that.

Well, I think I will try out higher dosings of other anti-inflammatory supplements, and see if that helps. (High dose turmeric pills, injectable resveratrol I have lying around, bromelain, cissus)

I'm doing research on Alflutops right now too.
 

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