Combined usage of testosterone and nandrolone may cause heart damage?

[Type-IIx]

AAS are known to cause:
1. Negative cardiac effects
2. Focal segmental glomerulosclerosis (why tons of BBers end up on dialysis)
3. Heart hyperplasia/hypertrophy
4. Proteinuria
5. Malignant hypertension
6. Collagen remodeling
7. Fibrosis in different tissues (e.g. kidneys, tendons, etc)

More variables than that, and usually it's the uncontrolled hypertension that will cause the kidney diseases.

Collagen synthesis is increased with AAS (e.g. higher cross-sectional area of tendons) but the extracellular matrix/framework is dysfunctional, and the cause for the huge amount of AAS users who get tendon tears/ruptures.

Plenty of data on negative heart/cardiac effects from AAS use.

You can't have your cake and eat it too, but many AAS users refuse to believe that and won't take necessary actions to mitigate the deleterious effects of AAS use. I was once that stubborn, too.

I agree with the crux of your post (all of these enumerated complications can be attributed to androgen abuse).

My question pertains to the statement that "Collagen synthesis is increased with AAS (e.g. higher cross-sectional area of tendons) but the extracellular matrix/framework is dysfunctional, and the cause for the huge amount of AAS users who get tendon tears/ruptures."

Is this categorically true?

While I am aware of rodent data that T increases tendon stiffness, thereby affecting the tensile strength of rat tendon that may then cause failure with less elongation - is this definitely true for humans? I believe it likely is, but can you speak to your thought process extrapolating from the studies in rodents to man on this question?

My thinking is something like this: there are benefits to performance with increased tendon stiffness, though this could logically lead to traumatic injury in combination with dramatically increased muscular strength.

But has it been borne out that androgens as a class - (what about nandrolone, oxandrolone, what about in combination with rhGH) - cause dysfunction in the ECM?

Also, I am aware of the fact that markers of soft tissue collagen metabolism seem enhanced by AAS, but are you able to speak to the evidence on AAS-induced i) collagen deposition (as opposed to serum and urinary markers) and ii) dysfunctional vs. functional ECM remodeling?

 

[bybon]

I agree with the crux of your post (all of these enumerated complications can be attributed to androgen abuse).

My question pertains to the statement that "Collagen synthesis is increased with AAS (e.g. higher cross-sectional area of tendons) but the extracellular matrix/framework is dysfunctional, and the cause for the huge amount of AAS users who get tendon tears/ruptures."

Is this categorically true?

While I am aware of rodent data that T increases tendon stiffness, thereby affecting the tensile strength of rat tendon that may then cause failure with less elongation - is this definitely true for humans? I believe it likely is, but can you speak to your thought process extrapolating from the studies in rodents to man on this question?

My thinking is something like this: there are benefits to performance with increased tendon stiffness, though this could logically lead to traumatic injury in combination with dramatically increased muscular strength.

But has it been borne out that androgens as a class - (what about nandrolone, oxandrolone, what about in combination with rhGH) - cause dysfunction in the ECM?

Also, I am aware of the fact that markers of soft tissue collagen metabolism seem enhanced by AAS, but are you able to speak to the evidence on AAS-induced i) collagen deposition (as opposed to serum and urinary markers) and ii) dysfunctional vs. functional ECM remodeling?

Sure. I don't feel like staying on Google Scholar (tendon morphology is a good start)

I agree with the crux of your post (all of these enumerated complications can be attributed to androgen abuse).

My question pertains to the statement that "Collagen synthesis is increased with AAS (e.g. higher cross-sectional area of tendons) but the extracellular matrix/framework is dysfunctional, and the cause for the huge amount of AAS users who get tendon tears/ruptures."

Is this categorically true?

While I am aware of rodent data that T increases tendon stiffness, thereby affecting the tensile strength of rat tendon that may then cause failure with less elongation - is this definitely true for humans? I believe it likely is, but can you speak to your thought process extrapolating from the studies in rodents to man on this question?

My thinking is something like this: there are benefits to performance with increased tendon stiffness, though this could logically lead to traumatic injury in combination with dramatically increased muscular strength.

But has it been borne out that androgens as a class - (what about nandrolone, oxandrolone, what about in combination with rhGH) - cause dysfunction in the ECM?

Also, I am aware of the fact that markers of soft tissue collagen metabolism seem enhanced by AAS, but are you able to speak to the evidence on AAS-induced i) collagen deposition (as opposed to serum and urinary markers) and ii) dysfunctional vs. functional ECM remodeling?

It's not the stiffness I focus on, it's the change in the morphology of tendons/tendon repair/matrix metallopeptidases/ECM remodeling that I want awareness on.

A great start in Google Scholar can be had by searching "anabolic steroid tendon morphology". I'm being lazy.

Studies with mice shouldn't be dismissed either. Sure, some data can be ignored, but not every research conclusions

Oh, type "anabolic steroid glomerulosclerosis" into Google Scholar. You'll enjoy that data.

Plenty of AAS users get tendon tears/ruptures (including me). A couple of surgeons I know even joked about having a lot of PTs with tendon injuries.

I don't feel people truly think about the adverse effects of AAS or they just ignore the possibilities of detrimental side effects from AAS use.

 

[Glycomann]

AAS are known to cause:
1. Negative cardiac effects
2. Focal segmental glomerulosclerosis (why tons of BBers end up on dialysis)
3. Heart hyperplasia/hypertrophy
4. Proteinuria
5. Malignant hypertension
6. Collagen remodeling
7. Fibrosis in different tissues (e.g. kidneys, tendons, etc)

More variables than that, and usually it's the uncontrolled hypertension that will cause the kidney diseases.

Collagen synthesis is increased with AAS (e.g. higher cross-sectional area of tendons) but the extracellular matrix/framework is dysfunctional, and the cause for the huge amount of AAS users who get tendon tears/ruptures.

Plenty of data on negative heart/cardiac effects from AAS use.

You can't have your cake and eat it too, but many AAS users refuse to believe that and won't take necessary actions to mitigate the deleterious effects of AAS use. I was once that stubborn, too.

There was what use to be called an off portion of the cycle. People don't cycle anymore. They're just on. Off portion of the cycling approach probably negates a lot of this damage.

 

[rawdeal]

There was what use to be called an off portion of the cycle. People don't cycle anymore. They're just on. Off portion of the cycling approach probably negates a lot of this damage.

I'm splitting hairs on words here, but goodgod I hope you're right ... and that this applies to those of us who are past cycling and substitute moderate blast + cruise ... I hope

 

[Type-IIx]

Sure. I don't feel like staying on Google Scholar (tendon morphology is a good start)

It's not the stiffness I focus on, it's the change in the morphology of tendons/tendon repair/matrix metallopeptidases/ECM remodeling that I want awareness on.

A great start in Google Scholar can be had by searching "anabolic steroid tendon morphology". I'm being lazy.

Studies with mice shouldn't be dismissed either. Sure, some data can be ignored, but not every research conclusions

Oh, type "anabolic steroid glomerulosclerosis" into Google Scholar. You'll enjoy that data.

Plenty of AAS users get tendon tears/ruptures (including me). A couple of surgeons I know even joked about having a lot of PTs with tendon injuries.

I don't feel people truly think about the adverse effects of AAS or they just ignore the possibilities of detrimental side effects from AAS use.

I've begun delving in. Have you read Jones, I. A., Togashi, R., Rick Hatch, G. F., Weber, A. E., & Vangsness JR, C. T. (2018). Anabolic Steroids and Tendons: A Review of their Mechanical, Structural and Biologic Effects. Journal of Orthopaedic Research®. doi:10.1002/jor.24116? It's a good recent meta-analysis of the topic and Table 2 summarizes the highly heterogenous (and rather conflicting/contradictory) evidence well.

There is very likely a drug- and dose- dependency to the likely deleterious impacts on mechanical & structural tendon properties (for our purposes, we are particular concerned with the effects of exercise + AAS). As well, there is likely a time- dependency, i.e., a suggested compensatory mechanism that seems to counter the initial/short-term likely deleterious impacts (including effects on MMPs, tendinocyte proliferation and differentiation, mechanical property changes, etc.)

The ongoing investigation into the clinical efficacy of oxandrolone in rotator cuff repair (e.g., the Hatch Oxandrolone Rotator Cuff Trial [ORCT]) that is in Phase 2 indicates some potential beneficial effects (i.e., halting fatty infiltration, attenuating muscle atrophy, enhancing healing/repair) on tendon at least peri- & post- operatively.

 

[Wilson6]

I've begun delving in. Have you read Jones, I. A., Togashi, R., Rick Hatch, G. F., Weber, A. E., & Vangsness JR, C. T. (2018). Anabolic Steroids and Tendons: A Review of their Mechanical, Structural and Biologic Effects. Journal of Orthopaedic Research®. doi:10.1002/jor.24116? It's a good recent meta-analysis of the topic and Table 2 summarizes the highly heterogenous (and rather conflicting/contradictory) evidence well.

There is very likely a drug- and dose- dependency to the likely deleterious impacts on mechanical & structural tendon properties (for our purposes, we are particular concerned with the effects of exercise + AAS). As well, there is likely a time- dependency, i.e., a suggested compensatory mechanism that seems to counter the initial/short-term likely deleterious impacts (including effects on MMPs, tendinocyte proliferation and differentiation, mechanical property changes, etc.)

The ongoing investigation into the clinical efficacy of oxandrolone in rotator cuff repair (e.g., the Hatch Oxandrolone Rotator Cuff Trial [ORCT]) that is in Phase 2 indicates some potential beneficial effects (i.e., halting fatty infiltration, attenuating muscle atrophy, enhancing healing/repair) on tendon at least peri- & post- operatively.

 

[Wilson6]

The dose and drug is the poison. The problem is, you have one extreme (the genetic altered farm animal wannabees) that throw caution to the wind and are destined to have problems, and the other (clinicians and law makers) that say any dose of any AAS including testosterone is the great evil and will not prescribe, monitor and want any use beyond very strict limitations criminalized. Thus you have the problems we have. There are so many potential benefits that can come from reasonable dosing of AAS for various clinical conditions and anti-aging but given the current legal and political climate, they are not being explored or studied. As well, there are probably a large percentage of cosmetic users that would be just fine using lower doses, from a compounding pharmacy under medical supervision to accomplish perhaps not their dream goals but close enough to reduce most risk and live a normal life span, and contribute to a large data base so we know what drugs do what (good and bad), not just bro science. I doubt we'll ever find middle ground and there will be a day either will become the norm but who knows.

 

[Type-IIx]

The dose and drug is the poison. The problem is, you have one extreme (the genetic altered farm animal wannabees) that throw caution to the wind and are destined to have problems, and the other (clinicians and law makers) that say any dose of any AAS including testosterone is the great evil and will not prescribe, monitor and want any use beyond very strict limitations criminalized. Thus you have the problems we have. There are so many potential benefits that can come from reasonable dosing of AAS for various clinical conditions and anti-aging but given the current legal and political climate, they are not being explored or studied. As well, there are probably a large percentage of cosmetic users that would be just fine using lower doses, from a compounding pharmacy under medical supervision to accomplish perhaps not their dream goals but close enough to reduce most risk and live a normal life span, and contribute to a large data base so we know what drugs do what (good and bad), not just bro science. I doubt we'll ever find middle ground and there will be a day either will become the norm but who knows.

I agree completely. Thank you for the excellent and highly relevant paper. Hopefully, there'll be an explosion in research and trials into these applications. These drugs (AAS; synthetic androgens) have clear benefits for medicine but are still largely relegated to use in third world nations for conditions like hereditary angioedema, inoperable malignant breast cancer (as an absolute last resort), anemia, etc.

 

[LITTLEMAGS]

AAS are known to cause:
1. Negative cardiac effects
2. Focal segmental glomerulosclerosis (why tons of BBers end up on dialysis)
3. Heart hyperplasia/hypertrophy
4. Proteinuria
5. Malignant hypertension
6. Collagen remodeling
7. Fibrosis in different tissues (e.g. kidneys, tendons, etc)

More variables than that, and usually it's the uncontrolled hypertension that will cause the kidney diseases.

Collagen synthesis is increased with AAS (e.g. higher cross-sectional area of tendons) but the extracellular matrix/framework is dysfunctional, and the cause for the huge amount of AAS users who get tendon tears/ruptures.

Plenty of data on negative heart/cardiac effects from AAS use.

You can't have your cake and eat it too, but many AAS users refuse to believe that and won't take necessary actions to mitigate the deleterious effects of AAS use. I was once that stubborn, too.

same here stubborn as fuck until shit started happening. Now it is just a low low dose sub dermal test.

 

[gunslinger]

There was what use to be called an off portion of the cycle. People don't cycle anymore. They're just on. Off portion of the cycling approach probably negates a lot of this damage.

That's exactly how I did it for years and most ppl with common sense did as well. Somewhere around 5-10 years ago it seemed to shift to most people just staying on all year long. Their "off cycle" was 500mg of test per week and 6iu of GH per day. There is a huge difference in someone doing a cycle or two per year and staying on extremely high doses of multiple compounds year round.

Thats real close to what a buddy of mine use to do up until his sudden death a couple years ago. He told me on more than one occasion "nah bro, I'm off right now. Just 500 test and 200 Deca and my normal GH." His idea of off was that and eating ice creme.

 

[rosoo]

That's exactly how I did it for years and most ppl with common sense did as well. Somewhere around 5-10 years ago it seemed to shift to most people just staying on all year long. Their "off cycle" was 500mg of test per week and 6iu of GH per day. There is a huge difference in someone doing a cycle or two per year and staying on extremely high doses of multiple compounds year round.

Thats real close to what a buddy of mine use to do up until his sudden death a couple years ago. He told me on more than one occasion "nah bro, I'm off right now. Just 500 test and 200 Deca and my normal GH." His idea of off was that and eating ice creme.

off cycle still need 500 test and 200 deca and growth hormone - is that considered overdose?

why would one need such high test and deco off cycle?

 

[gunslinger]

off cycle still need 500 test and 200 deca and growth hormone - is that considered overdose?

why would one need such high test and deco off cycle?

This was his idea of "off cycle"

"On cycle" was 3-4 grams of test, 600mg to a gram of tren, 10iu of GH per day and 2-3 orals for 6-8 months at a time. I guess he figured thats what he needed to maintain his size and condition.