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Best Stack with EQ................
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Mr.X
Guest
EQ only cycle? not a good idea. You need a test base there.
Themachine01
New member
test
DieselGunz
New member
I learned the hard way run test 
krishna
New member
If you run eq as your base, you will have the ability to build collagen for healthier connective tissue. If you stack that with supraphysiological doses of test, you can kiss your collagen production good-bye. Not everybody is on the test bandwagon. With what your goals are, I'd say
eq: 600/wk
tren e: 375/wk
test: 125/wk
eq: 600/wk
tren e: 375/wk
test: 125/wk
krishna
New member
k6jatu37 said:
Yes that's exactly what I'm saying. Keeping test levels within range (on the high end of course) will actually help increase collagen even more when stacked with deca or eq. Once you go above about 125, it seriously hinders collagen production. Since test is a mass builder, it seems dangerous to build so much mass while weakening your joints. I'll never run over 125/wk of test because of this and other sides it causes.
very interesting......bump for another expert opinion.
DieselGunz
New member
krishna said:
after my post on my cycle I am thinking this
EQ-450mgs for 1-13
test-250mgs for 1-15
tbol 1-4 at 40mgs
DieselGunz
New member
krishna said:
makes sense and then i wont have to get another bottle. Not that i am questioning you but where did u read this?
krishna
New member
How to increase collegen synthesis!! (i.e. - strengthen those tendons and ligaments)
originally posted by AnimalMass on competitivemuscle.com
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 he****g.
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.
I cut and pasted this. This should give you an idea of what I'm talking about. I'll try to round up some more sources that are more reputable, but for now, this was just a quick find on the net. Most of the stuff I've read isn't from the net.
originally posted by AnimalMass on competitivemuscle.com
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 he****g.
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.
I cut and pasted this. This should give you an idea of what I'm talking about. I'll try to round up some more sources that are more reputable, but for now, this was just a quick find on the net. Most of the stuff I've read isn't from the net.
DieselGunz
New member
excellent read Krishna
k to you
k to you
krishna
New member
UFC22 said:
I have been looking into this also, but there isn't much info on it. The only steroid I've found so far that drastically inhibits collagen formation is test at supraphysiological levels. I would be nervous about using any test derived gear that is highly aromatizable such as dbol. I don't do any orals besides proviron anyway, so I really don't have to worry about this. I still wish I could find more info on it though. AND I WISH SOMEONE WHO KNOWS MORE ABOUT THIS WOULD RESPOND TO MY DAMN POSTS! Apparently not many people know much about this topic.
Last edited:
Sanel27
New member
UFC22 said:
OK, this doesnt sound as a bad idea in itself as im thinking about doing something similar its just that it will look like this
1-16 Test E - 500mgs /EW
1-16 EQ - 600mgs/EW
1-6 Tren - 100mgs/EOD
8-16 Anavar - 40mgs/ED
After that a killer PCT cycle...................
krishna
New member
Sanel27 said:OK, this doesnt sound as a bad idea in itself as im thinking about doing something similar its just that it will look like this
1-16 Test E - 500mgs /EW
1-16 EQ - 600mgs/EW
1-6 Tren - 100mgs/EOD
8-16 Anavar - 40mgs/ED
After that a killer PCT cycle...................
The whole point of this stack was to build muscle and collagen at the same time. You're defeating the purpose of our discussion by adding test doses that high. Guess you haven't been following, or just don't care.
Extra_Strong
Well-known member
Well I would think if this is true many of the HRT patients would be in constant joint pain.
the normal amount for them is like 200mg a week isent it?
R they having problems in this area? also for people that have had surgerys many develop extra scar tissue? why not just give them some Test at doses above 125mg a week.
the normal amount for them is like 200mg a week isent it?
R they having problems in this area? also for people that have had surgerys many develop extra scar tissue? why not just give them some Test at doses above 125mg a week.
krishna
New member
Extra_Strong said:
If you read the article I posted, 200mg/wk is the max you should go to increase collagen synthesis. At this dose, the test is probably still helping build collagen, although it is on the verge of hindering it as anything above 200 is claimed to drastically reduce collagen formation. I'm not sure what you're trying to suggest with giving surgery patients test for excess scar tissue. Scar tissue hasn't been mentioned thus far.
Sanel27
New member
krishna said:
Yeah dude, i get you, i was following, its just that not many of us are as knowledgeable in these drugs effect on collagen and the rest of the body as much as you. Its just that 'till now we all have used test at high doses and it was effective, i mean you could use it in a bulker as well as cutter.......
I use it as a base in all cycles, i mean i see where you're going with it and i do care about your opinion as its very informative, but as i said, that up there is my upcoming cycle.......
I didnt suggest that this bro does it......
. I really don't care what stacks people do. Everyone has different goals. good luck with yours.
krishna
New member
k6jatu37 said:
No dooood! It makes no difference what the ester is. Any test >200mg/wk will slow collagen formation. I run my tren longer than 8 weeks by injecting weeks 9-15 also. I don't know how else to answer that question. Anyway, I'll try to get some sources soon, but I'm going to bed. PEACE!
Themachine01
New member
No matter what your reasons are for not including test in your cycles, you cannot be ignorant to the fact that your body needs test for many physical and psychological reasons besides just building muscle. When running a cycle with compounds that will shut down your body's natural ability to produce testosterone, you are depriving your body of a very important chemical that it needs on many levels for a healthy male. This is something that you need to keep in mind when you are shutting your test engine off and not replacing it, this can lead to many unwanted side affects, especially with something as powerful as tren.
Extra_Strong
Well-known member
krishna said:
yes i did read the article but for some reason had 125 stuck in my head.
but still leads to the question of they guys that do long high doses of test.
do they have joint problems?
and as far as the scar tissue thing i was talking about. collagen formes scar tissue so I was saying if you are correct in this and U could be I dont know.
then it would be a good aid when havig surgery like ACL or something because in many cases scar tissure deveoples and later has to be removed.
talk to a few guys that have been on long periods of high doses of test and see how ther joints are?
njmuscleguy
New member
I'd definitely be interested in more feedback - I respect what Krishna has to say though - any of the vets or mods have any comments? macro? you normally have tons of chemistry and physiology tidbits to share...
my other question then is... aside from the collagen synthesis issue, would there be a huge difference in outcome / results between say 400mg/wk EQ + 200mg/wk test as opposed to the "generally accepted" dosage of say 400mg/week EQ + 500mg (and higher) Test?
my other question then is... aside from the collagen synthesis issue, would there be a huge difference in outcome / results between say 400mg/wk EQ + 200mg/wk test as opposed to the "generally accepted" dosage of say 400mg/week EQ + 500mg (and higher) Test?
Themachine01
New member
My joints are absolutely fine, I have had no problems to date, no pain, no joint injuries. The male body needs testosterone, period. Whether you like it or not, it doesnt matter, running a cycle without test is hurting you whether you can see it or not.
My answer to the question on this thread would be test and it would be at doses higher then the eq.
BUT, krishna's post about collagen synthesis has now peaked my interest. The one compound I've always stayed away from is winny because of the seemingly instantaneous joint pain. The theory I'd always heard was that it dried out and made brittle the tendons and ligaments. OK, so far my impression is consistent with fact.
Now, here's where I get concerned as a long time test user. No matter what cycle I've run test has been the dominant or the only compound. Therefore, per the info in krishna's post I am always in a negative collagen synthesis condition and I'm damaging tendons and ligaments. Is that safe to assume?
Look at 2 more issues here. 1) One of my favorite simple cycles has been, test e @750mg/wk, deca @ 600mg/wk usually with a heavy prop frontload. Without doing the math, even though I'm running deca at a decent dosage my collagen synthesis is still negative. Is that safe to assume? 2) My longer, high dose (1g) cycles of test are so negative that damage is almost certain and significant. Make sense?
Then add the fact that I've been pushing heavy weight (especially in the 3 basic movements) in amounts disproportionate to my size for many years and I should basically have major joint problems. Well this is my condition exactly, degenerative joint disease which is actually arthritis.
I have had 2 sports related accidents specific to tendons and ligaments but never any training incidents. Thus my one and only question, my arthritis is caused by damaged and diminished cartilage creating a bone on bone condition, is this potentially caused by or accelerated by negative collagen synthesis as suggested in krishna's post? I ask this because tendons and ligaments are mentioned but cartilage is not.
I did answer the original question to this thread but if you guys think I hijacked this thread I'll start a new one.
BUT, krishna's post about collagen synthesis has now peaked my interest. The one compound I've always stayed away from is winny because of the seemingly instantaneous joint pain. The theory I'd always heard was that it dried out and made brittle the tendons and ligaments. OK, so far my impression is consistent with fact.
Now, here's where I get concerned as a long time test user. No matter what cycle I've run test has been the dominant or the only compound. Therefore, per the info in krishna's post I am always in a negative collagen synthesis condition and I'm damaging tendons and ligaments. Is that safe to assume?
Look at 2 more issues here. 1) One of my favorite simple cycles has been, test e @750mg/wk, deca @ 600mg/wk usually with a heavy prop frontload. Without doing the math, even though I'm running deca at a decent dosage my collagen synthesis is still negative. Is that safe to assume? 2) My longer, high dose (1g) cycles of test are so negative that damage is almost certain and significant. Make sense?
Then add the fact that I've been pushing heavy weight (especially in the 3 basic movements) in amounts disproportionate to my size for many years and I should basically have major joint problems. Well this is my condition exactly, degenerative joint disease which is actually arthritis.
I have had 2 sports related accidents specific to tendons and ligaments but never any training incidents. Thus my one and only question, my arthritis is caused by damaged and diminished cartilage creating a bone on bone condition, is this potentially caused by or accelerated by negative collagen synthesis as suggested in krishna's post? I ask this because tendons and ligaments are mentioned but cartilage is not.
I did answer the original question to this thread but if you guys think I hijacked this thread I'll start a new one.
Extra_Strong
Well-known member
(How to increase collegen synthesis!! (i.e. - strengthen those tendons and ligaments)
originally posted by AnimalMass on competitivemuscle.com )
I have found this artical posted over and over the oldest one i seem to find is Dec 2003 I guess there is no longer a competitivemuscle.com
http://www.intense-training.com/forums/showthread.php?t=20010
http://anabolicminds.com/forum/329430-post3.html
I would really like to see the origanal thread or the source.
the ideas sound really good and i would love to know more about it.
But at the same time there seem like there would be more info if this were true.
It kinda goes along the debate of wether winny hurts the joints or just has a blocking of (anti imflamitory effect)
originally posted by AnimalMass on competitivemuscle.com )
I have found this artical posted over and over the oldest one i seem to find is Dec 2003 I guess there is no longer a competitivemuscle.com
http://www.intense-training.com/forums/showthread.php?t=20010
http://anabolicminds.com/forum/329430-post3.html
I would really like to see the origanal thread or the source.
the ideas sound really good and i would love to know more about it.
But at the same time there seem like there would be more info if this were true.
It kinda goes along the debate of wether winny hurts the joints or just has a blocking of (anti imflamitory effect)
krishna
New member
Themachine01 said:
Nobody is saying not to take test. If you look at my post's you will find that I recommend 125mg/wk, which is within the higher end of normal range. I agree that test plays a large role in male health and functioning. All I'm saying is to build collagen, you shouldn't go above 125mg.
BBBBig Phenom
New member
test
Extra_Strong
Well-known member
krishna said:
are there other articals that pack the one u posted??
I just know you said you did a lot of research.
krishna
New member
g mac said:
Thanks for the post. This lends evidence to the research I've been doing on AAS and collagen systhesis. I am simply sharing a theme or trend that I've started to notice while researching the topic. I do not claim to have absolute knowledge on this, and I too would love to hear from some more vets as I've been begging them to post on this issue for quite some time now.
krishna
New member
Extra_Strong said:
Do you go to college? I have found some articles through the library's electronic resource section at my college. That is a good place to look, and I recommend you try it. I really haven't been able to find much about this on the internet either as I stated in an earlier post. Try to find some medical journals if you can. It's hard to find information specifically documenting what I've been saying, but a lot of the research I've seen seems to reveal this as a trend or theme in collagen synthesis. I have made my own assumptions based on the research I've done. Still, I would really like someone else to chime in if they know anything.
krishna said:
You seem quite knowledgeable on this topic, very interesting. What I might do is drop the EQ like you said to 6oomgs weeks 1-12, and maybe front load some Prop at 300mg weeks 1-4, then start cyp on week 3-12 at 300mgs. We'll see, still up in the air as to what I will stack with the EQ. I like the thought of Prop as a front loader because of It's fast acting qualities.
This collagen synthesis issue and the ramifications it would have on the use of AAS is huge if it were to be proven to be fact. All cycles would have to be correctly balanced for collagen synthesis to avoid soft tissue damage around the joints. And important parts of the idea of test in every cycle would have to change as test doses would be lowered so much they would render the compound useless for any mass building.
This would put serious test users, like myself, in a tough spot. Interesting theories.
This would put serious test users, like myself, in a tough spot. Interesting theories.
krishna
New member
Author(s): Falanga V ; Greenberg AS ; Zhou L ; Ochoa SM ; Roberts AB ; Falabella A ; Yamaguchi Y
Affiliation: University of Miami School of Medicine, Department of Dermatology, Miami Veterans Affairs Medical Center, Florida, USA.
Title: Stimulation of collagen synthesis by the anabolic steroid stanozolol.
Source: The Journal of investigative dermatology. (J Invest Dermatol) 1998 Dec; 111(6): 1193-7
Additional Info: UNITED STATES
Standard No: ISSN: 0022-202X (Print); 1523-1747 (Electronic); NLM Unique Journal Identifier: 0426720
Language: English
Abstract: There is evidence that anabolic steroids, which are derived from testosterone and have markedly less androgenic activity, promote tissue growth and enhance tissue repair; however, the mechanisms involved in their anabolic activities remain unclear. In this report, we measured the effect of the anabolic steroid stanozolol on cell replication and collagen synthesis in cultures of adult human dermal fibroblasts. Stanozolol (0.625-5 microg per ml) had no effect on fibroblast replication and cell viability (p = 0.764) but enhanced collagen synthesis (p < 0.01) in a dose-dependent manner (r = 0.907). Stanozolol also increased (by 2-fold) the mRNA levels of alpha1 (I) and alpha1 (III) procollagen and, to a similar extent, upregulated transforming growth factor-beta1 (TGF-beta1) mRNA and peptide levels (p < 0.001). There was no stimulation of collagen synthesis by testosterone. The stimulatory effects of stanozolol on collagen synthesis were blocked by a TGF-beta1 anti-sense oligonucleotide, by antibodies to TGF-beta, and in dermal fibroblast cultures derived from TGF-beta1 knockout mice. We conclude that collagen synthesis is increased by the anabolic steroid stanozolol and that, for the most part, this effect is due to TGF-beta1. These findings point to a novel mechanism of action of anabolic steroids.
This one shows winstrol's ability to increase collagen synthesis, but does not address address it's inhibition of cross-linking activity. Notice that it says there was no increase of collagen synthesis by testosterone, but it does not say what the doses were, or whether or not it slowed collagen synthesis (it may in the full report). This is how my research has been going. There are bits and pieces in different articles, like pieces to the puzzle. Once you get all the pieces and put them together, you get an article like the one I posted earlier with complete information. I've spent a lot of time rounding up information on this. I am not going to hand feed you every study I've read. If you want more info on this, I suggest you research it for yourself. I'll try to get another study or two for all the doubters just to be nice, but I really don't care what stacks people do. I'm just trying to point out something I've come across--something that I know a lot of AAS users would like to know. I did not have access to the complete study either.
Affiliation: University of Miami School of Medicine, Department of Dermatology, Miami Veterans Affairs Medical Center, Florida, USA.
Title: Stimulation of collagen synthesis by the anabolic steroid stanozolol.
Source: The Journal of investigative dermatology. (J Invest Dermatol) 1998 Dec; 111(6): 1193-7
Additional Info: UNITED STATES
Standard No: ISSN: 0022-202X (Print); 1523-1747 (Electronic); NLM Unique Journal Identifier: 0426720
Language: English
Abstract: There is evidence that anabolic steroids, which are derived from testosterone and have markedly less androgenic activity, promote tissue growth and enhance tissue repair; however, the mechanisms involved in their anabolic activities remain unclear. In this report, we measured the effect of the anabolic steroid stanozolol on cell replication and collagen synthesis in cultures of adult human dermal fibroblasts. Stanozolol (0.625-5 microg per ml) had no effect on fibroblast replication and cell viability (p = 0.764) but enhanced collagen synthesis (p < 0.01) in a dose-dependent manner (r = 0.907). Stanozolol also increased (by 2-fold) the mRNA levels of alpha1 (I) and alpha1 (III) procollagen and, to a similar extent, upregulated transforming growth factor-beta1 (TGF-beta1) mRNA and peptide levels (p < 0.001). There was no stimulation of collagen synthesis by testosterone. The stimulatory effects of stanozolol on collagen synthesis were blocked by a TGF-beta1 anti-sense oligonucleotide, by antibodies to TGF-beta, and in dermal fibroblast cultures derived from TGF-beta1 knockout mice. We conclude that collagen synthesis is increased by the anabolic steroid stanozolol and that, for the most part, this effect is due to TGF-beta1. These findings point to a novel mechanism of action of anabolic steroids.
This one shows winstrol's ability to increase collagen synthesis, but does not address address it's inhibition of cross-linking activity. Notice that it says there was no increase of collagen synthesis by testosterone, but it does not say what the doses were, or whether or not it slowed collagen synthesis (it may in the full report). This is how my research has been going. There are bits and pieces in different articles, like pieces to the puzzle. Once you get all the pieces and put them together, you get an article like the one I posted earlier with complete information. I've spent a lot of time rounding up information on this. I am not going to hand feed you every study I've read. If you want more info on this, I suggest you research it for yourself. I'll try to get another study or two for all the doubters just to be nice, but I really don't care what stacks people do. I'm just trying to point out something I've come across--something that I know a lot of AAS users would like to know. I did not have access to the complete study either.
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Like Krishna said "125mgs test EW" If you go over 200 you might as well do 500mgs/EW bro! So if you were going to follow any of krishnas outlook/advice on this cycle it would be more like this.
1-12 - eq600mgs/EW
1-12 - test125mgs/EW
If you go over 200mgs the benefit no longer exists!
krishna
New member
Cen Y ; Li K ; Liu N ; Liu XX
Affiliation: Department of Burn and Plastic Surgery, West China Hospital, Sichuan University, Chengdu 610041, China.
Title: [Effect of nandrolone phenylpropionate on hepatic albumin mRNA and granulational alpha 1(I) procollagen mRNA in burned rats]
Source: Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition. (Sichuan Da Xue Xue Bao Yi Xue Ban) 2004 Jan; 35(1): 77-9
Additional Info: China
Standard No: ISSN: 1672-173X (Print); NLM Unique Journal Identifier: 101162609
Language: Chinese
Abstract: OBJECTIVE: To assess the mechanism for the effect of nandrolone phenypropionate (NP) on hepatic albumin mRNA and granulational alpha 1(I) procollagen mRNA in burned rats with the aim to underpin the clinical application of anabolic steroids. METHODS: Thirty-two Wistar rats with a deep second-degree cutaneous burn of 20% total body surface area were randomly divided into two groups to receive either 5 mg/kg NP (NP group) or normal saline as placebo(control group) every other day. The expression copy quantities of albumin-mRNA in liver tissue and alpha 1 (I) procollagen mRNA in granulation wound were measured by quantitative fluorescent RT-PCR respectively on the post-burned days 4, 7, 14 and 21. RESULTS: The expression levels of albumin-mRNA and alpha 1 (I) procollagen mRNA in NP group were much higher than those in control group. The 7th and 14th days were the periods in which the albumin-mRNA and alpha 1 (I) procollagen mRNA expression had been increasing obviously (P < 0.01). CONCLUSION: Nandrolone phenylpropionate could effectively up-regulate the expression of albumin-mRNA in liver tissue and the alpha 1 (I) procollagen mRNA in granulation wound
Here's another one that shows NPP does indeed increase collagen formation. Just another piece of the puzzle fellas.
Affiliation: Department of Burn and Plastic Surgery, West China Hospital, Sichuan University, Chengdu 610041, China.
Title: [Effect of nandrolone phenylpropionate on hepatic albumin mRNA and granulational alpha 1(I) procollagen mRNA in burned rats]
Source: Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition. (Sichuan Da Xue Xue Bao Yi Xue Ban) 2004 Jan; 35(1): 77-9
Additional Info: China
Standard No: ISSN: 1672-173X (Print); NLM Unique Journal Identifier: 101162609
Language: Chinese
Abstract: OBJECTIVE: To assess the mechanism for the effect of nandrolone phenypropionate (NP) on hepatic albumin mRNA and granulational alpha 1(I) procollagen mRNA in burned rats with the aim to underpin the clinical application of anabolic steroids. METHODS: Thirty-two Wistar rats with a deep second-degree cutaneous burn of 20% total body surface area were randomly divided into two groups to receive either 5 mg/kg NP (NP group) or normal saline as placebo(control group) every other day. The expression copy quantities of albumin-mRNA in liver tissue and alpha 1 (I) procollagen mRNA in granulation wound were measured by quantitative fluorescent RT-PCR respectively on the post-burned days 4, 7, 14 and 21. RESULTS: The expression levels of albumin-mRNA and alpha 1 (I) procollagen mRNA in NP group were much higher than those in control group. The 7th and 14th days were the periods in which the albumin-mRNA and alpha 1 (I) procollagen mRNA expression had been increasing obviously (P < 0.01). CONCLUSION: Nandrolone phenylpropionate could effectively up-regulate the expression of albumin-mRNA in liver tissue and the alpha 1 (I) procollagen mRNA in granulation wound
Here's another one that shows NPP does indeed increase collagen formation. Just another piece of the puzzle fellas.
krishna
New member
Title: Effects of gonadal and adrenal androgens in a novel androgen-responsive human osteoblastic cell line.
Source: Journal of cellular biochemistry. (J Cell Biochem) 1998 Oct 1; 71(1): 96-108
Additional Info: UNITED STATES
Standard No: ISSN: 0730-2312 (Print); 1097-4644 (Electronic); NLM Unique Journal Identifier: 8205768
Language: English
Abstract: While androgens have important skeletal effects, the mechanism(s) of androgen action on bone remain unclear. Current osteoblast models to study androgen effects have several limitations, including the presence of heterogeneous cell populations. In this study, we examined the effects of androgens on the proliferation and differentiation of a novel human fetal osteoblastic cell line (hFOB/AR-6) that expresses a mature osteoblast phenotype and a physiological number (approximately 4,000/nucleus) of androgen receptors (AR). Treatment with 5alpha-dihydrotestosterone (5alpha-DHT) inhibited the proliferation of hFOB/AR-6 cells in a dose-dependent fashion, while it had no effect on the proliferation of hFOB cells, which express low levels of AR (<200/nucleus). In hFOB/AR-6 cells, co-treatment with the specific AR antagonist, hydroxyflutamide abolished 5alpha-DHT-induced growth inhibition. Steady-state levels of transforming growth factor-beta1 (TGF-beta1) and TGF-beta-induced early gene (TIEG) mRNA decreased after treatment of hFOB/AR-6 cells with 5alpha-DHT, suggesting a role for the TGF-beta1-TIEG pathway in mediating 5alpha-DHT-induced growth inhibition of hFOB/AR-6 cells. In support of this, co-treatment of hFOB/AR-6 cells with TGF-beta1 (40 pg/ml) reversed the 5alpha-DHT-induced growth inhibition, whereas TGF-beta1 alone at this dose had no effect on hFOB/AR-6 cell proliferation. Furthermore, treatment of hFOB/AR-6 cells with 5alpha-DHT and testosterone (10(-8) M) inhibited basal and 1,25-(OH)2D3-induced alkaline phosphatase (ALP) activity and type I collagen synthesis without affecting osteocalcin production. Thus, in this fetal osteoblast cell line expressing a physiological number of AR, androgens decrease proliferation and the expression of markers associated with osteoblast differentiation. These studies suggest that the potential anabolic effect of androgens on bone may not be mediated at the level of the mature osteoblast.
Here's one that shows that while studying the effects of androgens on bone cell proliferation, they also found that the administration of DHT and testosterone inhibited collagen formation. Yet another piece of the puzzle. I'm done! If you want to do high doses of test, go ahead, I honestly don't care. I have made my decision as to how I would cycle from now on, and I could care less if it's different than everyone else's. I think I've made a legitimate case for not being on the test bandwagon!
Source: Journal of cellular biochemistry. (J Cell Biochem) 1998 Oct 1; 71(1): 96-108
Additional Info: UNITED STATES
Standard No: ISSN: 0730-2312 (Print); 1097-4644 (Electronic); NLM Unique Journal Identifier: 8205768
Language: English
Abstract: While androgens have important skeletal effects, the mechanism(s) of androgen action on bone remain unclear. Current osteoblast models to study androgen effects have several limitations, including the presence of heterogeneous cell populations. In this study, we examined the effects of androgens on the proliferation and differentiation of a novel human fetal osteoblastic cell line (hFOB/AR-6) that expresses a mature osteoblast phenotype and a physiological number (approximately 4,000/nucleus) of androgen receptors (AR). Treatment with 5alpha-dihydrotestosterone (5alpha-DHT) inhibited the proliferation of hFOB/AR-6 cells in a dose-dependent fashion, while it had no effect on the proliferation of hFOB cells, which express low levels of AR (<200/nucleus). In hFOB/AR-6 cells, co-treatment with the specific AR antagonist, hydroxyflutamide abolished 5alpha-DHT-induced growth inhibition. Steady-state levels of transforming growth factor-beta1 (TGF-beta1) and TGF-beta-induced early gene (TIEG) mRNA decreased after treatment of hFOB/AR-6 cells with 5alpha-DHT, suggesting a role for the TGF-beta1-TIEG pathway in mediating 5alpha-DHT-induced growth inhibition of hFOB/AR-6 cells. In support of this, co-treatment of hFOB/AR-6 cells with TGF-beta1 (40 pg/ml) reversed the 5alpha-DHT-induced growth inhibition, whereas TGF-beta1 alone at this dose had no effect on hFOB/AR-6 cell proliferation. Furthermore, treatment of hFOB/AR-6 cells with 5alpha-DHT and testosterone (10(-8) M) inhibited basal and 1,25-(OH)2D3-induced alkaline phosphatase (ALP) activity and type I collagen synthesis without affecting osteocalcin production. Thus, in this fetal osteoblast cell line expressing a physiological number of AR, androgens decrease proliferation and the expression of markers associated with osteoblast differentiation. These studies suggest that the potential anabolic effect of androgens on bone may not be mediated at the level of the mature osteoblast.
Here's one that shows that while studying the effects of androgens on bone cell proliferation, they also found that the administration of DHT and testosterone inhibited collagen formation. Yet another piece of the puzzle. I'm done! If you want to do high doses of test, go ahead, I honestly don't care. I have made my decision as to how I would cycle from now on, and I could care less if it's different than everyone else's. I think I've made a legitimate case for not being on the test bandwagon!
DieselGunz
New member
lol i was just going to bump this
