• All new members please introduce your self here and welcome to the board:
    http://www.professionalmuscle.com/forums/showthread.php?t=259
Buy Needles And Syringes With No Prescription
M4B Store Banner
intex
Riptropin Store banner
Generation X Bodybuilding Forum
Buy Needles And Syringes With No Prescription
Buy Needles And Syringes With No Prescription
Mysupps Store Banner
IP Gear Store Banner
PM-Ace-Labs
Ganabol Store Banner
Spend $100 and get bonus needles free at sterile syringes
Professional Muscle Store open now
sunrise2
PHARMAHGH1
kinglab
ganabol2
Professional Muscle Store open now
over 5000 supplements on sale at professional muscle store
azteca
granabolic1
napsgear-210x65
advertise1
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
ashp210
UGFREAK-banner-PM
esquel
YMSGIF210x65-Banner
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store

What is it that makes Deca give that famous joint lubrication that other steroids can't rival?

Yep. Carrying a little extra water always makes my joints feel more secure as well. I like eq also for it’s supposed ability to increase collagen production
I ran a recomp cycle of Test with EQ and Var which worked wonders for ailing knees. I am a firm believer in the ability of Boldenone and Anavar to increase cartilage production, as my anecdotal experience serves to support such.
 
There is no miracle compound nor do any come close to being a panacea.

Some are helpful but will never take the place of restructuring training method and movements, rest, ice and compression, physical rehabilitation and deep tissue work just to name some necessary implementations.
 
I ran a recomp cycle of Test with EQ and Var which worked wonders for ailing knees. I am a firm believer in the ability of Boldenone and Anavar to increase cartilage production, as my anecdotal experience serves to support such.
Boldenone works even better for me than deca for joints. I like running eq in the 1000-1200 Mg range
 
Prolly related 2 d collagen synthesis increase. Which is why it also makes it safer against ur bones etc breaking.
If that is the case then deca (At least in micro doses of 50-75mg or even 100mg per week) should be an absolute staple in all TRT/cycle regimes. I know that amount may seem so insignificant but it's really not. We need all of the collagen synthesis and joint lubrication we can get in this game.
 
13 joint reconstructions later. Deca is not what people think it is. It’s a wolf in Sheep’s clothing gentleman. And it’s also very hard on the heart as well.
Can you speak more to the heart affects? I have a personal vested interest in this now
 
Nandrolone has immunomodulatory anti-inflammatrory effects and can be used in treatment of many diseases. Here are a few abstracts.

PMC7108994
PMID- 32257859
IS - 2223-4683 (Print)
IS - 2223-4691 (Electronic)
VI - 9
IP - Suppl 2
DP - 2020 Mar
DP - 2020 Mar
TI - Nandrolone decanoate relieves joint pain in hypogonadal men: a novel prospective
pilot study and review of the literature.
PG - S186-94
AB - Testosterone is an archetypal androgenic-anabolic steroid (AAS), while its
exogenous administration is considered to be the gold standard for the treatment
of male hypogonadism. The benefits are not due to its intrinsic nature alone but
are due to the result of its interactions with the androgen receptor (AR). As the
management of hypogonadism continues to advance into the modern era, it would be
preferable for modern andrologists to have multiple tools at their disposal to
influence AR activity. Nandrolone, or 19-nortestosterone, is one such compound.
In the following review of the literature, we examine the history, pharmacology,
and clinical applications of this medication. We also present the results of our
novel pilot study examining the favorable effects of nandrolone on joint pain for
hypogonadal men.
FAU - Tatem, Alexander J.
AU - Tatem AJ
AD - Men’s Health Center, Urology of Indiana, Greenwood, IN, USA;
FAU - Holland, Levi C.
AU - Holland LC
AD - McGovern Medical School, University of Texas Health Science Center, Houston, TX,
USA;
FAU - Kovac, Jason
AU - Kovac J
AD - Men’s Health Center, Urology of Indiana, Greenwood, IN, USA;
FAU - Beilan, Jonathan A.
AU - Beilan JA
AD - Advanced Urology Institute, Clearwater, FL, USA;
FAU - Lipshultz, Larry I.
AU - Lipshultz LI
AD - Scott Department of Urology, Baylor College of Medicine, Houston, TX, USA
LA - eng
PT - Journal Article
PT - Review
PHST- 2019/10/11 [received]
PHST- 2019/10/31 [accepted]
TA - Transl Androl Urol
JT - Translational Andrology and Urology
AID - tau-09-S2-S186 [pii]
AID - 10.21037/tau.2019.11.03 [doi]
SO - Transl Androl Urol. 2020 Mar;9(Suppl 2):S186-94. doi:10.21037/tau.2019.11.03.

PMC - PMC1537214
PMID- 6973425
IS - 0009-9104 (Print)
IS - 1365-2249 (Electronic)
VI - 44
IP - 1
DP - 1981 Apr
TI - The effects of nandrolone, testosterone and their decanoate esters on murine
lupus.
PG - 11-7
AB - Treatment of NZB/NZW F1 (B/W) female and castrated male mice with testosterone or
19-nortestosterone (nandrolone), either by implantation in silastic tubing or by
subcutaneous injections of their decanoate esters, reduced in a dose-dependent
manner symptoms associated with murine lupus (proteinuria, IgG antibodies to DNA)
and prolonged survival. These phenomena were observed under both prophylactic
(start at 3-4 weeks) and therapeutic treatments (start 27-29 weeks). Nandrolone
and its decanoate ester were at least as potent as testosterone and testosterone
decanoate. As the unwanted androgenic properties of nandrolone and its ester are
significantly less pronounced than those of testosterone and its ester, also in
these NZB/NZW mice, the beneficial effect on murine lupus does not seem to be
associated with these properties.
FAU - Verheul, H A
AU - Verheul HA
FAU - Stimson, W H
AU - Stimson WH
FAU - den Hollander, F C
AU - den Hollander FC
FAU - Schuurs, A H
AU - Schuurs AH
LA - eng
PT - Journal Article
TA - Clin Exp Immunol
JT - Clinical and Experimental Immunology
SO - Clin Exp Immunol. 1981 Apr;44(1):11-7.

PMC - PMC1536283
PMID- 6467680
IS - 0009-9104 (Print)
IS - 1365-2249 (Electronic)
VI - 57
IP - 3
DP - 1984 Sep
TI - Effect of nandrolone decanoate on Sjögren's syndrome like disorders in NZB/NZW
mice.
PG - 571-4
AB - The effects of 2.5-40 mg/kg nandrolone decanoate (ND) on the development and
growth of mononuclear cell infiltrations in the submandibular glands of NZB/W
(B/W) mice have been studied using a quantitative histological method. Injections
with ND for 9 months, once every 3 weeks, starting at 4 weeks of age, reduced the
number and total area of infiltrations in submandibular glands of female and
castrated male B/W mice. Since ND has relatively weak virilizing properties, this
substance may be useful for the treatment of Sjögren's syndrome in humans.Images:
Fig. 1
FAU - Schot, L P
AU - Schot LP
FAU - Verheul, H A
AU - Verheul HA
FAU - Schuurs, A H
AU - Schuurs AH
LA - eng
PT - Journal Article
TA - Clin Exp Immunol
JT - Clinical and Experimental Immunology
SO - Clin Exp Immunol. 1984 Sep;57(3):571-4.

PMC - PMC1001090
PMID- 6342550
IS - 0003-4967 (Print)
IS - 1468-2060 (Electronic)
VI - 42
IP - 2
DP - 1983 Apr
TI - Hormonal manipulation of the immune response in systemic lupus erythematosus: a
drug trial of an anabolic steroid, 19-nortestosterone.
PG - 155-7
AB - Ten patients (8 female, 2 male) with systemic lupus erythematosus (SLE) were
entered into an open trial with the anabolic steroid 19-nortestosterone (19-nor).
Their clinical condition did not improve, nor were significant changes observed
in the majority of laboratory data. However, overall the platelet count rose, and
in patients with abnormal levels of T lymphocytes bearing receptors for IgG Fc
treatment returned the values to normal. Despite this latter result, suppressor
cell activity remained slightly below the normal range throughout the study
period.
FAU - Hazelton, R A
AU - Hazelton RA
FAU - McCruden, A B
AU - McCruden AB
FAU - Sturrock, R D
AU - Sturrock RD
FAU - Stimson, W H
AU - Stimson WH
LA - eng
PT - Journal Article
TA - Ann Rheum Dis
JT - Annals of the Rheumatic Diseases
SO - Ann Rheum Dis. 1983 Apr;42(2):155-7.
 
Can you speak more to the heart affects? I have a personal vested interest in this now
Start digging you’ll find info on it.
If you're referring to the studies on blood vessels, I believe those were done on rats. A few of the science minds here like @Stewie have gone through them and they don't translate 100% to humans. Not saying there isn't any risk with it, but it's not a 1:1 comparison.
 
There are studies out there done on it. But my main concern was when my endocrinologist at university of Washington who is a doctor for many pro athletes advised me that they are aware that nandrolone has negative effects on the heart specifically. This doctor is well versed in anabolics that’s why I went to her.
 
There are studies out there done on it. But my main concern was when my endocrinologist at university of Washington who is a doctor for many pro athletes advised me that they are aware that nandrolone has negative effects on the heart specifically. This doctor is well versed in anabolics that’s why I went to her.
The reason why im pressing you for some details is bcuz of a previous thread I started. Had a nuclear stress test done after having chest pains and it showed my ejection fraction reduced to 38% and my heart was globally hypokinetic. I was a big deca guy for many years.

I still cant find any good studies beyond rat/mice stuff.
 
I've collated quite a bit on the topic and may write more about, for example, what makes stanozolol so bad for healthy joints despite increased collagen synthesis markers. But just to address this question, I'll use one relevant study that implicates the RAS, because I think it's probably the most relevant system in what's occurring with apparent joint benefits while on a deca cycle.

The two major mechanisms that may explain deca's effects on joints are:
A) increased collagen deposition in the tendon, and
B) synovial joint fluid retention

Both mechanisms (increased collagen deposition in i.e. flexor tendon) and synovial joint fluid retention may be positively acted upon by the renin-angiotensin system (RAS). The RAS regulates water and electrolyte balance, connective tissue cell growth, and the metabolism of loose and dense connective tissue and sites of tissue repair [1]. Pathologically, RAS activation increases vascoconstriction, cardiac hypertrophy, and fibrosis (resulting in myocardial infarction, fibrosis of the liver) [1]. Therefore, it is important to consider the duality of the potential joint-tendon (i.e., knee extensor tendon) augmentation while on nandrolone: you may have a transient benefit in tendon remodeling (i.e., extensor tendon) and fluid balance, but via this same mechanism, may be accruing fibrotic or cardiac/left ventricular maladaptations.


So, to the potential transient benefits: Angiotensin-I converting enzyme (ACE) is a marker positively correlated with collagen type I mRNA activity, and may reflect ECM remodeling wherein collagen synthesis outstrips degradation.

Whereas AAS generally decrease matrix metalloproteases (MMP), collagen gene expression, nandrolone increases ACE activity and increases matrix type I collagen deposition. The results of [1] showed Nand + jump training >> Nand > jump training > sedentary in ACE activity in tendon (i.e., knee extensor). Consider, however, that this same pathway is implicated in cardiac tissue remodeling and pathological action.

[1] Marqueti, R. de C., Hashimoto, N. Y., Durigan, J. L. Q., Batista e Silva, L. L., Almeida, J. A. de, Silva, M. da G. da, … Araújo, H. S. S. de. (2015). Nandrolone increases angiotensin-I converting enzyme activity in rats tendons. Revista Brasileira de Medicina Do Esporte, 21(3), 173–177. doi:10.1590/1517-869220152103143667
 
I've collated quite a bit on the topic and may write more about, for example, what makes stanozolol so bad for healthy joints despite increased collagen synthesis markers. But just to address this question, I'll use one relevant study that implicates the RAS, because I think it's probably the most relevant system in what's occurring with apparent joint benefits while on a deca cycle.

The two major mechanisms that may explain deca's effects on joints are:
A) increased collagen deposition in the tendon, and
B) synovial joint fluid retention

Both mechanisms (increased collagen deposition in i.e. flexor tendon) and synovial joint fluid retention may be positively acted upon by the renin-angiotensin system (RAS). The RAS regulates water and electrolyte balance, connective tissue cell growth, and the metabolism of loose and dense connective tissue and sites of tissue repair [1]. Pathologically, RAS activation increases vascoconstriction, cardiac hypertrophy, and fibrosis (resulting in myocardial infarction, fibrosis of the liver) [1]. Therefore, it is important to consider the duality of the potential joint-tendon (i.e., knee extensor tendon) augmentation while on nandrolone: you may have a transient benefit in tendon remodeling (i.e., extensor tendon) and fluid balance, but via this same mechanism, may be accruing fibrotic or cardiac/left ventricular maladaptations.


So, to the potential transient benefits: Angiotensin-I converting enzyme (ACE) is a marker positively correlated with collagen type I mRNA activity, and may reflect ECM remodeling wherein collagen synthesis outstrips degradation.

Whereas AAS generally decrease matrix metalloproteases (MMP), collagen gene expression, nandrolone increases ACE activity and increases matrix type I collagen deposition. The results of [1] showed Nand + jump training >> Nand > jump training > sedentary in ACE activity in tendon (i.e., knee extensor). Consider, however, that this same pathway is implicated in cardiac tissue remodeling and pathological action.

[1] Marqueti, R. de C., Hashimoto, N. Y., Durigan, J. L. Q., Batista e Silva, L. L., Almeida, J. A. de, Silva, M. da G. da, … Araújo, H. S. S. de. (2015). Nandrolone increases angiotensin-I converting enzyme activity in rats tendons. Revista Brasileira de Medicina Do Esporte, 21(3), 173–177. doi:10.1590/1517-869220152103143667
I just read over that brazilian article you cite. It's interesting that they are able to show differences in ACE I signaling but they show no data on collagen ynthesis, tendon strength measurements or other experiments to really monitor downstream effects of nandrolone dependant ACE I signaling. Nandrolone is still a bit of a mystery when it comes to reduced joint pain. Sicne it is used in a number of inflammatroy diseases it seems to me that other mechanisms may be in place. I think probably the drug also has impact on joint tissue renewal and/or repair but it's probably more complex than increased synthesis of one or a subset of collagen types. It is probably so that dysregulated collagen synthesis, or for instance, improper temporal or coordinated collagens I, II and III synth would not be an advantage to arthritic or injury repair. I can state that I used ND long in the past when I had a knee injury that would not heal and it worked very well.
 
I've collated quite a bit on the topic and may write more about, for example, what makes stanozolol so bad for healthy joints despite increased collagen synthesis markers. But just to address this question, I'll use one relevant study that implicates the RAS, because I think it's probably the most relevant system in what's occurring with apparent joint benefits while on a deca cycle.

The two major mechanisms that may explain deca's effects on joints are:
A) increased collagen deposition in the tendon, and
B) synovial joint fluid retention

Both mechanisms (increased collagen deposition in i.e. flexor tendon) and synovial joint fluid retention may be positively acted upon by the renin-angiotensin system (RAS). The RAS regulates water and electrolyte balance, connective tissue cell growth, and the metabolism of loose and dense connective tissue and sites of tissue repair [1]. Pathologically, RAS activation increases vascoconstriction, cardiac hypertrophy, and fibrosis (resulting in myocardial infarction, fibrosis of the liver) [1]. Therefore, it is important to consider the duality of the potential joint-tendon (i.e., knee extensor tendon) augmentation while on nandrolone: you may have a transient benefit in tendon remodeling (i.e., extensor tendon) and fluid balance, but via this same mechanism, may be accruing fibrotic or cardiac/left ventricular maladaptations.


So, to the potential transient benefits: Angiotensin-I converting enzyme (ACE) is a marker positively correlated with collagen type I mRNA activity, and may reflect ECM remodeling wherein collagen synthesis outstrips degradation.

Whereas AAS generally decrease matrix metalloproteases (MMP), collagen gene expression, nandrolone increases ACE activity and increases matrix type I collagen deposition. The results of [1] showed Nand + jump training >> Nand > jump training > sedentary in ACE activity in tendon (i.e., knee extensor). Consider, however, that this same pathway is implicated in cardiac tissue remodeling and pathological action.

[1] Marqueti, R. de C., Hashimoto, N. Y., Durigan, J. L. Q., Batista e Silva, L. L., Almeida, J. A. de, Silva, M. da G. da, … Araújo, H. S. S. de. (2015). Nandrolone increases angiotensin-I converting enzyme activity in rats tendons. Revista Brasileira de Medicina Do Esporte, 21(3), 173–177. doi:10.1590/1517-869220152103143667
What makes stanozolol cause joint pain is fairly simple, new collagen is type III and healthy tendons are type I. Type III are stiff and lack elasticity, which makes it extremely prone to tendinopathy, especially from resistance training. What makes it even worse is that many if not most weightlifters have some level of tendinosis plus tendonitis already present in many tendons which are rapidly exacerbated by the increase in type III collagen.

Just as a note for everyone, I've explained this many times in the past, how tendinosis and tendonitis work: Tendonitis is caused when the tendon is broken down from repetitive activity, it becomes frayed which leads to further tendon injury as it irritates itself in the tendon sheath. This tendon then repairs itself with type III fibers, these fibers need time and use to mature to type I, and before this happens they are less elastic and more prone to getting tendonitis, this is tendinosis. More tendonitis leads to more tendinosis and more tendinosis leads to more tendonitis. To make it even WORSE: resistance training is needed to mature type III fibers and this can lead to further tendonitis.

Writing tendonitis and tendinosis over and over is super annoying.

It's also possible there is some kind of anti-cortisol effect playing a role here, I'm just guessing but it certainly makes sense, especially because most will already have tendinopathy on some level as I mentioned above which would need cortisol to heal. However, all AAS are anti-cortisol to some degree and winny does have an oddly higher effect on collagen synthesis so you be the judge.
 
I just read over that brazilian article you cite. It's interesting that they are able to show differences in ACE I signaling but they show no data on collagen ynthesis, tendon strength measurements or other experiments to really monitor downstream effects of nandrolone dependant ACE I signaling. Nandrolone is still a bit of a mystery when it comes to reduced joint pain. Sicne it is used in a number of inflammatroy diseases it seems to me that other mechanisms may be in place. I think probably the drug also has impact on joint tissue renewal and/or repair but it's probably more complex than increased synthesis of one or a subset of collagen types. It is probably so that dysregulated collagen synthesis, or for instance, improper temporal or coordinated collagens I, II and III synth would not be an advantage to arthritic or injury repair. I can state that I used ND long in the past when I had a knee injury that would not heal and it worked very well.
Given the tone of the paper, you likely picked up on their tendency to REALLY want a different finding, and to be able to say "DECA BAD!" right? Given the Declaration of Helsinki we'll never get a perfect study to look at what we want, and all studies have limitations. Given practical limitations, the Brazilian article stands out because it used a relevant exercise model and looks at the RAS as a system, which can account for the likely mechanisms behind transient joint benefits in deca. We'll never get a study that perfectly suits our interests on this, unfortunately. There's no legitimate interest in following the thread left by this study to show joint benefits, when by the same mechanism, cardiac maladaptations are more justified.

Absolutely, though, by dysregulating collagen deposition you're not helping arthritis (interestingly, stanozolol has some efficacy in RA, possibly OA, due to its suppressing DNA synthesis in synovial fibroblasts, despite increased procollagenous activity in skin but not joints.
 
What makes stanozolol cause joint pain is fairly simple, new collagen is type III and healthy tendons are type I. Type III are stiff and lack elasticity, which makes it extremely prone to tendinopathy, especially from resistance training. What makes it even worse is that many if not most weightlifters have some level of tendinosis plus tendonitis already present in many tendons which are rapidly exacerbated by the increase in type III collagen.

Just as a note for everyone, I've explained this many times in the past, how tendinosis and tendonitis work: Tendonitis is caused when the tendon is broken down from repetitive activity, it becomes frayed which leads to further tendon injury as it irritates itself in the tendon sheath. This tendon then repairs itself with type III fibers, these fibers need time and use to mature to type I, and before this happens they are less elastic and more prone to getting tendonitis, this is tendinosis. More tendonitis leads to more tendinosis and more tendinosis leads to more tendonitis. To make it even WORSE: resistance training is needed to mature type III fibers and this can lead to further tendonitis.

Writing tendonitis and tendinosis over and over is super annoying.

It's also possible there is some kind of anti-cortisol effect playing a role here, I'm just guessing but it certainly makes sense, especially because most will already have tendinopathy on some level as I mentioned above which would need cortisol to heal. However, all AAS are anti-cortisol to some degree and winny does have an oddly higher effect on collagen synthesis so you be the judge.
Is it that simple? My understanding is stanozolol doesn't even increase collagen deposition except for in skin fibroblasts. Evidence that it suppresses DNA synthesis in synovial fibroblasts. GH increases collagen I mRNA by 2.3-fold and collagen III by 2.5-fold, so it's good for tendons, right?
 
Is it that simple? My understanding is stanozolol doesn't even increase collagen deposition except for in skin fibroblasts. Evidence that it suppresses DNA synthesis in synovial fibroblasts. GH increases collagen I mRNA by 2.3-fold and collagen III by 2.5-fold, so it's good for tendons, right?
It's possible there are other factors but given winny's unique effect on collagen and its definite effect on "joints," this seems by far the biggest contributor. GH does all sorts of positive things for joints, but I'm not sure it has a positive effect on tendinopathy in particular.

I just started up GH and I have lots of joint issues, they all feel great from the GH except for my biceps tendons that I know have issues.
 
Is it that simple? My understanding is stanozolol doesn't even increase collagen deposition except for in skin fibroblasts. Evidence that it suppresses DNA synthesis in synovial fibroblasts. GH increases collagen I mRNA by 2.3-fold and collagen III by 2.5-fold, so it's good for tendons, right?
Collagen fibers in tendon repair start out as type III so if GH is increasing type I then it has to be increasing the rate of type III becoming type I.
 
Collagen fibers in tendon repair start out as type III so if GH is increasing type I then it has to be increasing the rate of type III becoming type I.
It's possible there are other factors but given winny's unique effect on collagen and its definite effect on "joints," this seems by far the biggest contributor. GH does all sorts of positive things for joints, but I'm not sure it has a positive effect on tendinopathy in particular.

I just started up GH and I have lots of joint issues, they all feel great from the GH except for my biceps tendons that I know have issues.
Agreed, GH does seem good for joints and at least healthy tendons. There's some evidence it can be used (i.e., directly into the tendon) to accelerate procollagenous activity... now whether that's good, e.g., if it's leading to fibrotic tissue in some cases, not sure. I need to look into the mechanisms of tendon remodeling more.
 

Staff online

  • Big A
    IFBB PRO/NPC JUDGE/Administrator

Forum statistics

Total page views
558,010,554
Threads
135,749
Messages
2,768,452
Members
160,339
Latest member
Dann828
NapsGear
HGH Power Store email banner
your-raws
Prowrist straps store banner
infinity
FLASHING-BOTTOM-BANNER-210x131
raws
Savage Labs Store email
Syntherol Site Enhancing Oil Synthol
aqpharma
yourmuscleshop210x131
hulabs
ezgif-com-resize-2-1
MA Research Chem store banner
MA Supps Store Banner
volartek
Keytech banner
musclechem
Godbullraw-bottom-banner
Injection Instructions for beginners
Knight Labs store email banner
3
ashp131
YMS-210x131-V02
Back
Top