AAS and joint pain

[Glycomann]

Looking at the near-term (vs the long-term use of AAS that I gather the OP was referring to) impact of different compounds, I think the stack of winny + deca is traditional and a great illustration of use of a cutter (wintrol) that causes hella joint pain if you run it alone as a cycle (which I doubt anyone here is going to recommend anyway), but coupling it w/ deca as aromatizing compound to keep some estrogen / water in the mix to support your joints. Also winstrol appears to not only not aromatise, but actually acts as an aromatase inhibitor itself.

Including AIs is recommended to manage your estrogen levels (for guys) resulting from aromatizing compounds, but needs to be balanced to allow some estrogen to enable muscle growth for the stress you're putting on your body already as a result of choosing to run a cycle. I.e. no estrogen at all is bad. You need some estrogen to build muscle mass, and you need some estrogen --> water to keep your joints from feeling brittle.

If you couple dry joints w/ an increase in lifting capability (while not promoting connective tissue) you are also promoting an environment for further joint / tendon / ligament damage.

I think there are a few different components involved in such cycling that can effect bone and joint tissue. Stanozolol, at least in part, i effective in treatment of hereditary angioedema by increasing production of C1 inhibitor, which in turn leads to more fibrin formation through pro clotting function. Essentially, in normal persons this results in less subcutaneous fluid leading to a "drier look". This probably leads to some joint tissue "drying". The second major fator in such cycling is effects on proper estrogen signaling in joint and bone tissues. There is a wealth of literature exploring estrogen signaling in osteoblasts and chondrocytes among other cells such as tissue macrophages. These cells are involved in bone and joint tissue metabolism and health. A group of proteins affected are the bone matrix proteins (BMPs). In post menopausal women the BMPs are diminished as estrogens are diminished. Estrogens, and other steroids, are involved in a delicate interplay of joint health. Performance enhancing manipulation can be expected to impact joint and bone tissue health among other tissues.

 

[Ravager]

Test alone will reduce your natural collagen synthesis levels by 66%, meaning your cartilage and tendons will be weaker than when your natty by 2/3...

DECA will increase your collagen synthesis by like 250% OVER natty levels, meaning your cart and tendons will be able to grow/repair/strengthen at a rate 2 1/2 times your natty levels.

EQ actually boosts your collagen synthesis MORE than deca in the 300% range.

SO, I think a cycle is 'safer' with a collagen boosting AAS in the mix.

Else, your muscles will grow fast, as your joints/cart/tendons degrade, resulting in the muscle possibly tearing off the tendon. This is how most people get injured using AAS.

 

[Glycomann]

Test alone will reduce your natural collagen synthesis levels by 66%, meaning your cartilage and tendons will be weaker than when your natty by 2/3...

DECA will increase your collagen synthesis by like 250% OVER natty levels, meaning your cart and tendons will be able to grow/repair/strengthen at a rate 2 1/2 times your natty levels.

EQ actually boosts your collagen synthesis MORE than deca in the 300% range.

SO, I think a cycle is 'safer' with a collagen boosting AAS in the mix.

Else, your muscles will grow fast, as your joints/cart/tendons degrade, resulting in the muscle possibly tearing off the tendon. This is how most people get injured using AAS.

These percentages, from what I can gather, can't be verified. At least that is my recollection. I think that's correct though in general. At some serum concentration of androgen some collagen synthesis is compromised. Some of them are among the BMPs. There are others in skin, yet others in joint tissue and so on. There are over 20 subtypes so we have to be careful about making general statements about the group. But in general, yes, I believe dysmorphic collagen production profiles are part of the AAS induced joint problems.

 

[TGB1987]

I think there are a few different components involved in such cycling that can effect bone and joint tissue. Stanozolol, at least in part, i effective in treatment of hereditary angioedema by increasing production of C1 inhibitor, which in turn leads to more fibrin formation through pro clotting function. Essentially, in normal persons this results in less subcutaneous fluid leading to a "drier look". This probably leads to some joint tissue "drying". The second major fator in such cycling is effects on proper estrogen signaling in joint and bone tissues. There is a wealth of literature exploring estrogen signaling in osteoblasts and chondrocytes among other cells such as tissue macrophages. These cells are involved in bone and joint tissue metabolism and health. A group of proteins affected are the bone matrix proteins (BMPs). In post menopausal women the BMPs are diminished as estrogens are diminished. Estrogens, and other steroids, are involved in a delicate interplay of joint health. Performance enhancing manipulation can be expected to impact joint and bone tissue health among other tissues.

Very informative! I am learning some new stuff in this thread. Thanks for posting about this Glycomann.

 

[GrappleStrong]

you should run somthing along that strengthens the bones like eq/deca/ and not lift super heavy all the time go light do it right is the motto. and you can still make great gains off of lighter weight and higher volume