- Mar 24, 2022
I agree with the crux of your post (all of these enumerated complications can be attributed to androgen abuse).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
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.
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?