There are actually quite a few studies implementing testosterone at high dosages for long periods of time. Ranging from 200-600mg/wk. We also have studies regarding oxymetholone at up to 150mg/day, oxandrolone at up to 80mg/day, methenolone at up to 1200mg/wk and nandrolone at up to 600mg/wk.
The prospect of testosterone being safer then synthetic AAS is IMO a fallacy. Testosterone is neuroprotective, has anti-oxidant capacity when administered within the realms of therapeutic dosing. When dosages climb, testosterone is likely neurotoxic and acts as a promotor of oxidative stress.
Testosterone (probably) isn’t particularly safer regarding the cardiac pathology observed following prolonged AAS abuse. Testosterone may not alter lipids quite as much as say, nandrolone, drostanolone or methenolone, but other mechanisms come into play. Elevated homocysteine, CRP, RAAS dysfunction (and thus altered BP), autonomic dysfunction/catecholamine up-regulation, direct AR binding within cardiac myocytes etc all exist with testosterone. If anything, something like methenolone might have a lesser effect on cardiac parameters as it generally has less of an effect on BP (11b HSD2 inhibition is also stronger with testosterone) and mg/mg primo is less potent.
There are genetic discrepancies regarding how prone one is to the more serious side effects induced via AAS. There is ample data (in vitro, rodent models and case reports) indicative that testosterone alone can induce deleterious long term outcomes. If cardiac pathology is partly mediated via direct AR binding, all AAS would be culpable. Testosterone doesn’t get a magic free pass just because it’s naturally produced (well… it does in therapeutic concentrations, but the body wasn’t designed to run with a TT of like 2500ng/dl for decades on end)
Old school bodybuilders in Europe/parts of the USA (60s, 70s) purportedly didn’t use a whole lot of testosterone. Cyclic templates from those eras were mostly compromised of 19-nortestosterone, methenolone, dehydromethyltestosterone, oxandrolone and stanozolol. Testosterone became more commonplace within the late 70s/early 80s.
I’m not sure of the mortality rates regarding golden era bodybuilders. But it does seem as if a large proportion of them (who used more conservatively within the 60’s/70’s) are still around today. That being said, many suffered from coronary artery disease/had myocardial infarctions in their 60s and 70s.
Back then it was common knowledge that stanozolol was a mild drug, we know better today (lipiiiiiddddddsss)
Do you know a lot of people who have died from AAS? Legitimately curious, and if so… what dosages are we talking about? I’ve always pondered as to whether risk is heavily dependant on dose/genetics and lifestyle (there’s obviously a compound dependant risk)… or if it’s like cigarettes wherein any amount (referring to supra dosages, not TRT) practically triples heart disease risk