Please Scroll Down to See Forums Below It's been a good while since I've been on these boards, but I've found my way back. Let's say One were to plan on running a cycle after a tendon injury. Cut through a flexor carpi ulnaris (sp?). Are there any precautions to take or substances to avoid? I'm thinking about running maybe 500-750mg of test a week, with a little something else, maybe. any input is greatly appreciated.
cut tendon, need some advice
- Thread starter JKerry
- Start date
needtogetarmy
CEO of Project Mayhem
tendons take a banging when running a cycle because of the increase in strength. Additionally, some substances, namely winstro.l can wreck havoc on joints and tendons. My recommendation would be to lay off the gear until the tendon is properly healed. Bombarding it with heavy weights is not prudent.
Pat_McCrotch
New member
agreed.
A
ALIN
Guest
The Old Vet said:
I have to agree. wait until your healed and give it 100%
holy ghost
New member
I have heard theories about anavar being used as tendon repair at moderate dosages
6FULLMETALTRUCKIE9
New member
really anavar humm, I hope that's a true one! was it a full cut or partial tear? another thing how long ago was it? What I'm going to try is Hexalin and IGF-R3 after i have my knee tendons reconstructed . i'll keep ya posted when it happens bro!
holy ghost
New member
IGF and some GH.
Tatyana
Elite Mentor
Cissus quadralangaris is a herbal supp that is specific to muscle and tendon repair.
Get it capped, it tastes MANK.
I ruptured my achilles last year. Tendons take AGES to heal because of reduced blood flow, so continue to stay active.
The body is wired such that if you train your healthy side lightly, it will also stimulate the muscles on your damaged side.
Keep training your legs as this will also stimulate the muscles in the upper half of your body.
With regards to steroids, muscles grow faster than tendons, even with normal training, the tendons and ligaments need to 'get tougher', and they do so slower than muscle.
I found I had to train lighter on my legs as the tendons in my damaged leg REALLY hurt for awhile.
I would avoid steroids and heal naturally.
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Get it capped, it tastes MANK.
I ruptured my achilles last year. Tendons take AGES to heal because of reduced blood flow, so continue to stay active.
The body is wired such that if you train your healthy side lightly, it will also stimulate the muscles on your damaged side.
Keep training your legs as this will also stimulate the muscles in the upper half of your body.
With regards to steroids, muscles grow faster than tendons, even with normal training, the tendons and ligaments need to 'get tougher', and they do so slower than muscle.
I found I had to train lighter on my legs as the tendons in my damaged leg REALLY hurt for awhile.
I would avoid steroids and heal naturally.
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tatyana_zadorozny said:
Good post. Agreed.
6FULLMETALTRUCKIE9
New member
funny my ortho told me that stuff is a step above snake oil for tendons and ligaments . stuff like that's in the "ben gay" rub on stuff is more or less better for aching joints ands muscle strains!!!
Tatyana
Elite Mentor
evilb said:
I think you mean Tiger Balm or Double Dragon (the knock off version).
Great for muscle ache, but if he had it surgically repaired, he will not be able to put anything on the suture for awhile.
Tiger Balm is also fantastic when you will be around a lot of stinky people (hard core dance clubs, underground, gym sometimes) put a wee bit of it just below your nose, and no stink, also clears your sinuses.
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slat1
New member
I will cut through all the rumors.
Anavar does nothing for tendon repair.
Deca does nothing for tendon repair.
HGH does nothing for tendon repair.
I have partially torn BOTH my bicep tendons. The tears were identical.
With one I used growth, deca and var on the recomendation of people on this board.
The other I used nothing.
The first one took twice as long to heal and I actually cause micro tears from using gear/hgh.
The second one I was clean and it healed up nicely.
My dr looked at me the second time and said "are you going to fuck this one up like the first one by taking shit?"
The first arm is fucked for life. The second is fine.
I have had multiple MRI's on both to show how they healed.
AAS will only cause more injury. Same with growth.
Use nothing and let it heal. Trust me!
Anavar does nothing for tendon repair.
Deca does nothing for tendon repair.
HGH does nothing for tendon repair.
I have partially torn BOTH my bicep tendons. The tears were identical.
With one I used growth, deca and var on the recomendation of people on this board.
The other I used nothing.
The first one took twice as long to heal and I actually cause micro tears from using gear/hgh.
The second one I was clean and it healed up nicely.
My dr looked at me the second time and said "are you going to fuck this one up like the first one by taking shit?"
The first arm is fucked for life. The second is fine.
I have had multiple MRI's on both to show how they healed.
AAS will only cause more injury. Same with growth.
Use nothing and let it heal. Trust me!
Tatyana
Elite Mentor
Tren and collagen synthesis
originally posted by hooker on qualitymuscle
Actually, it stands to reason that Tren does, in fact, stimulate collagen synthesis.
You see, tren increases IGF-1 to a great degree, which ought to stimulate the growth of tendons, as we all know.
Endocrinology. 1989 May;124(5):2110-7.
Trenbolone alters the responsiveness of skeletal muscle satellite cells to fibroblast growth factor and insulin-like growth factor I.
Thompson SH, Boxhorn LK, Kong WY, Allen RE.
Department of Animal Sciences, University of Arizona, Tucson 85721.
The potential role of satellite cells in mediating the effect of trenbolone [17 beta-hydroxyestra-4,9-11-trien-3-one (TBOH)] on skeletal muscle hypertrophy was examined. Young female Sprague-Dawley rats received TBOH injections daily for 2 weeks; growth, body composition, and the composition of selected muscles were assessed. Treated rats grew more rapidly and deposited less body lipid and more protein. The semimembranosus muscle from treated rats was larger and had approximately 60% more DNA per muscle than muscles from control rats. The addition of trenbolone directly to the medium of cultured satellite cells did not stimulate cell proliferation, nor did it augment the stimulatory response of these cells to fibroblast growth factor (FGF) or insulin-like growth factor I (IGF-I). In contrast, satellite cells cultured from TBOH-treated rats exhibited greater proliferative responses to FGF and IGF-I than satellite cells from control rats. In addition, serum from TBOH-treated rats stimulated greater cell proliferation in satellite cell cultures than serum from control rats. These experiments suggest that one possible mechanism responsible for the ability of TBOH to stimulate skeletal muscle hypertrophy may be through enhanced proliferation and differentiation of satellite cells as a result of the increased sensitivity of these cells to IGF-I and FGF.
PMID: 2707149 [PubMed - indexed for MEDLINE]
You will also note that Tren treated satellite cells showed an increased response to FGF (fibroblast growth factor). Again, as we know, (basic)FGF stimulates collagen synthesis:
Sports Med. 2003;33(5):381-94.The roles of growth factors in tendon and ligament healing.
Molloy T, Wang Y, Murrell G.
Orthopaedic Research Institute, St George Hospital Campus, University of New South Wales, Sydney, Australia.
Tendon healing is a complex and highly-regulated process that is initiated, sustained and eventually terminated by a large number and variety of molecules. Growth factors represent one of the most important of the molecular families involved in healing, and a considerable number of studies have been undertaken in an effort to elucidate their many functions. This review covers some of the recent investigations into the roles of five growth factors whose activities have been best characterised during tendon healing: insulin-like growth factor-I (IGF-I), transforming growth factor beta (TGFbeta), vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), and basic fibroblast growth factor (bFGF). All five are markedly up-regulated following tendon injury and are active at multiple stages of the healing process. IGF-I has been shown to be highly expressed during the early inflammatory phase in a number of animal tendon healing models, and appears to aid in the proliferation and migration of fibroblasts and to subsequently increase collagen production. TGFbeta is also active during inflammation, and has a variety of effects including the regulation of cellular migration and proliferation, and fibronectin binding interactions. VEGF is produced at its highest levels only after the inflammatory phase, at which time it is a powerful stimulator of angiogenesis. PDGF is produced shortly after tendon damage and helps to stimulate the production of other growth factors, including IGF-I, and has roles in tissue remodelling.In vitro and in vivo studies have shown that bFGF is both a powerful stimulator of angiogenesis and a regulator of cellular migration and proliferation. This review also covers some of the most recent studies into the use of these molecules as therapeutic agents to increase the efficacy and efficiency of tendon and ligament healing. Studies into the effects of the exogenous application of TGFbeta, IGF-I, PDGF and bFGF into the wound site singly and in combination have shown promise, significantly decreasing a number of parameters used to define the functional deficit of a healing tendon. Application of IGF-I has been shown to increase in the Achilles Functional Index and the breaking energy of injured rat tendon. TGFbeta and PDGF have been shown separately to increase the breaking energy of healing tendon. Finally, application of bFGF has been shown to promote cellular proliferation and collagen synthesis in vivo.
Therefore, Trenbolone, by stimulating (b)FGF as well as IGF-1 - certainly would stimulate collagen synthesis. I don't know of anyone who claims tren healed any injuries...but the evidence is here to suggest it.
originally posted by hooker on qualitymuscle
Actually, it stands to reason that Tren does, in fact, stimulate collagen synthesis.
You see, tren increases IGF-1 to a great degree, which ought to stimulate the growth of tendons, as we all know.
Endocrinology. 1989 May;124(5):2110-7.
Trenbolone alters the responsiveness of skeletal muscle satellite cells to fibroblast growth factor and insulin-like growth factor I.
Thompson SH, Boxhorn LK, Kong WY, Allen RE.
Department of Animal Sciences, University of Arizona, Tucson 85721.
The potential role of satellite cells in mediating the effect of trenbolone [17 beta-hydroxyestra-4,9-11-trien-3-one (TBOH)] on skeletal muscle hypertrophy was examined. Young female Sprague-Dawley rats received TBOH injections daily for 2 weeks; growth, body composition, and the composition of selected muscles were assessed. Treated rats grew more rapidly and deposited less body lipid and more protein. The semimembranosus muscle from treated rats was larger and had approximately 60% more DNA per muscle than muscles from control rats. The addition of trenbolone directly to the medium of cultured satellite cells did not stimulate cell proliferation, nor did it augment the stimulatory response of these cells to fibroblast growth factor (FGF) or insulin-like growth factor I (IGF-I). In contrast, satellite cells cultured from TBOH-treated rats exhibited greater proliferative responses to FGF and IGF-I than satellite cells from control rats. In addition, serum from TBOH-treated rats stimulated greater cell proliferation in satellite cell cultures than serum from control rats. These experiments suggest that one possible mechanism responsible for the ability of TBOH to stimulate skeletal muscle hypertrophy may be through enhanced proliferation and differentiation of satellite cells as a result of the increased sensitivity of these cells to IGF-I and FGF.
PMID: 2707149 [PubMed - indexed for MEDLINE]
You will also note that Tren treated satellite cells showed an increased response to FGF (fibroblast growth factor). Again, as we know, (basic)FGF stimulates collagen synthesis:
Sports Med. 2003;33(5):381-94.The roles of growth factors in tendon and ligament healing.
Molloy T, Wang Y, Murrell G.
Orthopaedic Research Institute, St George Hospital Campus, University of New South Wales, Sydney, Australia.
Tendon healing is a complex and highly-regulated process that is initiated, sustained and eventually terminated by a large number and variety of molecules. Growth factors represent one of the most important of the molecular families involved in healing, and a considerable number of studies have been undertaken in an effort to elucidate their many functions. This review covers some of the recent investigations into the roles of five growth factors whose activities have been best characterised during tendon healing: insulin-like growth factor-I (IGF-I), transforming growth factor beta (TGFbeta), vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), and basic fibroblast growth factor (bFGF). All five are markedly up-regulated following tendon injury and are active at multiple stages of the healing process. IGF-I has been shown to be highly expressed during the early inflammatory phase in a number of animal tendon healing models, and appears to aid in the proliferation and migration of fibroblasts and to subsequently increase collagen production. TGFbeta is also active during inflammation, and has a variety of effects including the regulation of cellular migration and proliferation, and fibronectin binding interactions. VEGF is produced at its highest levels only after the inflammatory phase, at which time it is a powerful stimulator of angiogenesis. PDGF is produced shortly after tendon damage and helps to stimulate the production of other growth factors, including IGF-I, and has roles in tissue remodelling.In vitro and in vivo studies have shown that bFGF is both a powerful stimulator of angiogenesis and a regulator of cellular migration and proliferation. This review also covers some of the most recent studies into the use of these molecules as therapeutic agents to increase the efficacy and efficiency of tendon and ligament healing. Studies into the effects of the exogenous application of TGFbeta, IGF-I, PDGF and bFGF into the wound site singly and in combination have shown promise, significantly decreasing a number of parameters used to define the functional deficit of a healing tendon. Application of IGF-I has been shown to increase in the Achilles Functional Index and the breaking energy of injured rat tendon. TGFbeta and PDGF have been shown separately to increase the breaking energy of healing tendon. Finally, application of bFGF has been shown to promote cellular proliferation and collagen synthesis in vivo.
Therefore, Trenbolone, by stimulating (b)FGF as well as IGF-1 - certainly would stimulate collagen synthesis. I don't know of anyone who claims tren healed any injuries...but the evidence is here to suggest it.
Tatyana
Elite Mentor
AAS and Collagen Synthesis
--------------------------------------------------------------------------------
by AnimalMass on competitivemuscle
While injecting test increases protein syntesis by roughly 50 times, depending on dose and time, most bodybuilders forget that it will reduce collagen synthesis by more than 50% -- more like 80%, giving you the collagen synthesis rate of a senior citizen. Since collagen makes up tendons, bros are very prone to injury if they continue to lift very heavy, unless they cycle off T and let their collagen synthesis get back to normal. It's like having the skeletal muscle of a gorilla with the tendons of a very old man.
Winstrol increases collagen synthesis. It will give you bigger tendons. However, your body compensates for this by making them more brittle, weaker, and more prone to injury. I can't tell you how many bros work out anaerobically and become injured while on winstrol. Guys who lift in the 1-5 rep range while on winstrol, to baseball players who sprint all out from a stationary position -- winstrol should be the LAST drug they choose. Most of them like winstrol because they don't get the weight gain from it but it is very detrimental to bros who train for any sport anaerobically. Tendons tear easily on it.
Also, the drugs I mention increase collagen syn while also increasing collagen cross-linking integrity, making for a much stronger tendon.
Winstrol, on the other hand, will dramatically increase collagen syn, but ironically it decreases collagen cross-linking integrity, thus making a much weaker tendon.
You can plan a cycle of AAS which will increase collagen synthesis and skeletal muscle growth at the same time. The key is the drug(s) you choose.
Deca, Equipoise, Anavar, and Primobolan will ALL increase skeletal muscle while at the same time dramatically increase collagen syn and bone mass and density, leaving you with a substantially reduced chance of becoming injured than if you choose to use AAS like sus, cyp, or enth.
While testosterone will increase bone mass and density, even at supra-physiological levels, the result is weaker tendons due to inhibition of collagen syn.
To plan a cycle where the goal is to increase skeletal muscle mass/strength while at the same time increase joint/tendon/ligament strength, enough to keep up with the dramatic increase in skeletal muscle, you must choose drugs like Eq, Deca, Anavar, or Primo as the base of your cycle. Testosterone and its esters can be added to your cycle to keep levels within a 'normal' physiological range (ie, 100-200 mg/wk) but must not go above this. Since drugs like eq, deca, anavar and primo will reduce endogenous, natural levels of test, these levels may be maintained with exogenous test in the 100-200 mg/wk range. Test at this dose will not inhibit collagen syn, but paradoxically, will help increase it. It is when exogenous testosterone is used > 200 mg/wk that collagen syn is inhibited.
Deca @ 3 mg/kg a week(about 270 mg/wk for a 200 lb male) will increase procollagen III levels by 270% by week 2. Procollagen III is a primary indicator used to determine the rate of collagen syn. As you can see, deca is a very good drug at giving you everything you want -- an increase in collagen syn, an increase in skeletal muscle, and increases in bone mass and density. The one thing it does not give you is wood
Primobolan, @ 5 mg/kg, will increase collagen synthesis by roughly 180% -- less than deca and equipoise but still substantial.
Equipoise @ 3 mg/kg will increase procollagen III by approximately 340% -- slightly better than deca.
Oxandrolone has over a hundred studies documenting its effectiveness at treating patients needing rapid increases in collagen syn to enhance healing.
These drugs have longer half-lives than most other AAS, so this should be considered when timing your post cycle clomid use. Here they are:
Deca: 15 days Equipoise: 14 days Primobolan: 10.5 days
Anavar has a half-life of only 8 hours so it should not pose a problem.
GH is probably the most remarkable drug at increasing collagen synthesis. It increases collagen syn in a dose dependant manner -- the more you use, the more you will increase collagen syn. It has also demonstrated this ability in short and long term studies. From what I've read, hGH at 6 iu/day increased the collagen deposition rate by around 250% in damaged collagen structures. This result indicates that the increased biomechanical strength of wounds to collagen structures treated with biosynthetic human growth hormone was produced by an increased deposition of collagen in the collagen structures.
Eq, primo, anavar, and deca are all good -- they increase several biomakers of collagen syn -- ie, type III, II, I, procollagen markers. GH just seems to do so most dramatically.
Use of any of these drugs @ supra-physiological levels with a maintenance dose of test will increase collagen syn while at the same time increase skeletal muscle mass. Skeletal muscle mass gains will not be as dramatic as with large testosterone doses but you have to weigh the risk/reward basis for yourself. Also, these drugs do not satisfy the libido like testosterone, but that is not the point of this thread. It is only to demonstrate that you can increase skeletal muscle and collagen syn at the same time with certain AAS -- the decision is up to you.
__________________
--------------------------------------------------------------------------------
by AnimalMass on competitivemuscle
While injecting test increases protein syntesis by roughly 50 times, depending on dose and time, most bodybuilders forget that it will reduce collagen synthesis by more than 50% -- more like 80%, giving you the collagen synthesis rate of a senior citizen. Since collagen makes up tendons, bros are very prone to injury if they continue to lift very heavy, unless they cycle off T and let their collagen synthesis get back to normal. It's like having the skeletal muscle of a gorilla with the tendons of a very old man.
Winstrol increases collagen synthesis. It will give you bigger tendons. However, your body compensates for this by making them more brittle, weaker, and more prone to injury. I can't tell you how many bros work out anaerobically and become injured while on winstrol. Guys who lift in the 1-5 rep range while on winstrol, to baseball players who sprint all out from a stationary position -- winstrol should be the LAST drug they choose. Most of them like winstrol because they don't get the weight gain from it but it is very detrimental to bros who train for any sport anaerobically. Tendons tear easily on it.
Also, the drugs I mention increase collagen syn while also increasing collagen cross-linking integrity, making for a much stronger tendon.
Winstrol, on the other hand, will dramatically increase collagen syn, but ironically it decreases collagen cross-linking integrity, thus making a much weaker tendon.
You can plan a cycle of AAS which will increase collagen synthesis and skeletal muscle growth at the same time. The key is the drug(s) you choose.
Deca, Equipoise, Anavar, and Primobolan will ALL increase skeletal muscle while at the same time dramatically increase collagen syn and bone mass and density, leaving you with a substantially reduced chance of becoming injured than if you choose to use AAS like sus, cyp, or enth.
While testosterone will increase bone mass and density, even at supra-physiological levels, the result is weaker tendons due to inhibition of collagen syn.
To plan a cycle where the goal is to increase skeletal muscle mass/strength while at the same time increase joint/tendon/ligament strength, enough to keep up with the dramatic increase in skeletal muscle, you must choose drugs like Eq, Deca, Anavar, or Primo as the base of your cycle. Testosterone and its esters can be added to your cycle to keep levels within a 'normal' physiological range (ie, 100-200 mg/wk) but must not go above this. Since drugs like eq, deca, anavar and primo will reduce endogenous, natural levels of test, these levels may be maintained with exogenous test in the 100-200 mg/wk range. Test at this dose will not inhibit collagen syn, but paradoxically, will help increase it. It is when exogenous testosterone is used > 200 mg/wk that collagen syn is inhibited.
Deca @ 3 mg/kg a week(about 270 mg/wk for a 200 lb male) will increase procollagen III levels by 270% by week 2. Procollagen III is a primary indicator used to determine the rate of collagen syn. As you can see, deca is a very good drug at giving you everything you want -- an increase in collagen syn, an increase in skeletal muscle, and increases in bone mass and density. The one thing it does not give you is wood
Primobolan, @ 5 mg/kg, will increase collagen synthesis by roughly 180% -- less than deca and equipoise but still substantial.
Equipoise @ 3 mg/kg will increase procollagen III by approximately 340% -- slightly better than deca.
Oxandrolone has over a hundred studies documenting its effectiveness at treating patients needing rapid increases in collagen syn to enhance healing.
These drugs have longer half-lives than most other AAS, so this should be considered when timing your post cycle clomid use. Here they are:
Deca: 15 days Equipoise: 14 days Primobolan: 10.5 days
Anavar has a half-life of only 8 hours so it should not pose a problem.
GH is probably the most remarkable drug at increasing collagen synthesis. It increases collagen syn in a dose dependant manner -- the more you use, the more you will increase collagen syn. It has also demonstrated this ability in short and long term studies. From what I've read, hGH at 6 iu/day increased the collagen deposition rate by around 250% in damaged collagen structures. This result indicates that the increased biomechanical strength of wounds to collagen structures treated with biosynthetic human growth hormone was produced by an increased deposition of collagen in the collagen structures.
Eq, primo, anavar, and deca are all good -- they increase several biomakers of collagen syn -- ie, type III, II, I, procollagen markers. GH just seems to do so most dramatically.
Use of any of these drugs @ supra-physiological levels with a maintenance dose of test will increase collagen syn while at the same time increase skeletal muscle mass. Skeletal muscle mass gains will not be as dramatic as with large testosterone doses but you have to weigh the risk/reward basis for yourself. Also, these drugs do not satisfy the libido like testosterone, but that is not the point of this thread. It is only to demonstrate that you can increase skeletal muscle and collagen syn at the same time with certain AAS -- the decision is up to you.
__________________
Tatyana
Elite Mentor
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.
__________________
For info about personal training consultations email me at [email protected]
__________________
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.
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thanks for all the responses guys. it's been around 7 months since the cut. i've been doing weights for a month and a bit already, though they've been lighter than i used to do primarily due to atrophy. i've been given the go ahead to weight train, but i'd rather take it slow than risk doing damage to the progress i've already made. thanks again
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