It’s dependent on the individual… but no, the progressive docs giving HIV+ patients deca prescribed considerably higher dosages
Within the book “built to survive” if I recall (read it a while ago), the dosages prescribed/reccomended was 2-400mg weekly, not to say 100mg isn’t effective, it’s dependent on the severity of the disease (progression). Trials using 100-150mg e2w were quite conservative, if I recall correctly the amount of LBM accrued over 16 wks was about 1.5 kg… not much
There are trials that exist regarding hiv/nandrolone decanoate with dosages approaching 600mg weekly
Other drugs trialed/used for hiv/aids are
- Oxandrolone: 20-80mg daily
- Oxymetholone: 50-150mg daily
- Nandrolone: 50-600mg weekly
In terms of cardiac damage I’d garner just about all c17aa orals induce far more cardiac damage when used comparative to deca. The problem with deca vs other AAS is we simply have more data (pertaining solely to rodent studies) comparative to other AAS.
Do I think it’s harsher on cardiac parameters/functioning comparative to test? Probably… but it’s not tren, winny, dbol etc
No data exists regarding long term effects, however there are individuals who have been using low dosages of the stuff for 30+ years (there’s one MD in particuar I know… not personally though… of who still uses the stuff in low dosages after decades of using supraphysiologic dosages of the compound)
The one study indicating the compound is 11x more harmful compared to test regarding vasculature/inducing apoptosis in endothelial cell culture (in vitro)… the thing is though, differences between what occurs in a microbiological vs macrobiological context is fairly significant. In vitro antioxidants, elimination pathways etc don’t exist, not to mention the concentration of nandrolone required to induce said cellular damage was enormous (11 micromolar, equiv to 11,000 nmol, granted blood concentration can differ from concentrations achieved in differing tissues, still I’d garner the amount that’d need to be taken would be astronomical.
However all AAS (like deca for instance) impair antioxidant enzyme balances, induce a net vasoconstrictive effect etc. There are numerous mechanisms behind AAS induced cardiac toxicity
- Hypertension stemming from RAAS modification + systemic vascular resistance
- increased sensitivity to release of catecholamines + beta adrenergic receptor upregulation (this seems to effect some far more than others)
- dyslipidemia + pro oxidive effect
- direct myocardial injury (once again due to the notion of macro vs microbiology this is hotly debated), and aside from a few small scale studies regarding the cardiac dimensions of prior/current AAS users we don’t have an accurate conclusion… Some studies state the impact on cardiac dimensinos/function is minimal/doesn’t exist
- oxidative stress
- diabetic induced cardiac alterations
https://www.sciencedirect.com/science/article/pii/0735109792904786
Whereas others state the dysfunction induced is serious, potentially life threatening
https://www.ahajournals.org/doi/full/10.1161/circulationaha.116.026945
https://www.researchgate.net/publication/335501604_Long-term_anabolic_steroids_in_male_bodybuilders_induce_cardiovascular_structural_and_autonomic_abnormalities
Interestingly, in this case the left ventricular hypertrophy observed is very significant… but the mean BP of all subjects is within hypertensive ranges… thus the question begs is the cardiac alterations induced by sympathetic nervous system upregulation, direct myocardial injury or prolonged hypertension
Or subclinical
And even in the studies in which cardiac dysfunction appears to be subclinical, certain subjects appear to have cardiac dimensions/functinoal measurements that meet the criteria for the diagnosis of CHF, in a cohort of 100 men, if 2-3 have CHF from AAS, those odds aren’t fantastic…
However these studies don’t typically account for lifestyle factors, other drugs that may or may not have been taken, whether individuals are lying about their doses etc… This is why I get so frustrated when yolotards come on here casually blasting two grams of tren per week etc… they’re killing themselves, and have no idea and/or are in denial. I’m dropping my total weekly dose to 250mg weekly next week (from 270).
Problem is, in once study (can’t post it on here as it’s a payed study to access) individuals were monitored while they underwent cycles, some were pretty fat cycles… no echocardiographic changes could be detected in up to 20 weeks of prolonged usage… you’d think something would occur during that timeframe no?
Furthermore, there was recently a rodent study in which nandrolone failed to replicate the cardiac alterations induced within other studies, many of these rodent studies aren’t particularly large enough to come to a definite consensus… BUT, given the amount we have, it’s fair to assume a strong correlation exists (but this can be observed with test, eq, deca, dbol, winny…) the only compounds not shown to induce cardiac enlargement in rodents are
DON’T take that as tren being safe, we have profoundly differing elimination/antioxidation enzymes, and doses of test equiv to LESS than that of physiology (5mg/kg) appears to induce cardiomyopathy/significant fibrosis. Tren is ABSOLUTELY the most harmful thing one can take in terms of injectable preparations of AAS (and probably beats most orals too in terms of cardiac toxicity)
Deca isn’t safe, there are potentially profound neurological, cardiovascular etc consequences involved… As is the case with most other AAS… like all the effect is likely dose dependent
@blshaw @36_grit
No, the studies using 2-400mg didn’t experience any SAE’s because of the incredibly short durations of the trials… don’t think that means it’s safe… there are trials using 600mg test for 20 wks with no observable sides… doesn’t account for potential changes in cardiac morphology (on a cellular level or measurable as these variables weren’t accounted for in any studies)
One study compares the effect of 200mg test wkly for 4 wks vs same dose of deca… interestingly the TESTOSTERONE appeared to induce a non significant alteration in cardiac structure, while the deca didn’t have any measurable effect
Yes, I’d say it’s probably more dangerous to use AAS in high dosages than to regularly smoke tobacco tbh, tobacco statistically takes 10 years off one’s lifespan… anabolic steroids CAN take 30-40 off according to anecdotal reports and perhaps the preliminary findings from some of these studies