Did you notice any aesthetic benefit? (I recall somewhere else wherein you adknowledged using 10mg stanozolol/day to lower shbg). Did 10mg/day induce any aesthetical impact? Did you suffer from joint pain (many anecdotally get joint pain on winny), recovery time in the gym (was it increased/decreased?)
Also (probably doesn’t relate to 2.5mg/day) but statins + c17AA AAS are generally not the greatest combination
Totally unrelated, but just had my ECG done. I emailed you the results, if you don’t mind taking a peek! Doctor said everything looked great. 
Just to be clear I no longer use low dose stanozolol (Winstrol) or oxandrolone (Anavar) to lower my SHBG. When i did, i found that 5mg stanozolol (2.5m 2X/day) per day was sufficient. With oxandrolone, I needed to do 5mg 2X per day (10mg/day) for the same effect.
I did not notice any joint pain. I don’t think recovery time was any better, it was minimally effective at that low dose, if at all. I did do a short trial of a larger dose of Anavar (30mg/day) and did notice some awesome pumps in the gym. however, that’s not my goal, so I don’t do that any more. I just wanted to try it.
I am considering adding 12.5 to 25 mg per day of stanozolol to my TRT regimen (currently 80 mg/week of Test Cyp dosed weekly). This would be compounded stanozolol in troche form.
I’ve logged my experiences with oxandrolone (effect on free T/TT ratio, SHBG, lipids) and have also done two 19-week bouts of nandrolone decanoate.
Current BF ~8% and looking at 4-6 weeks of stanozolol with a cut down to 5-6% BF. Any other experiences folks want to share with legitimate pharmaceutical stanozolol. Note, I have not chemically analyzed my troches but they come from compounding pharmacy.
Comparison between oxandrolone and stanozolol on vascularity, appearance? I appreciate the info @galgenstrick / @hankthetank89 / @unreal24278 have shared previously.
I had a previous one time bout of AFIB so I am a little sensitive about that and have considered potential impact of adding other AAS on QTC interval, autonomic dysfunction, etc. In this post-COVID world, still not clear what caused AFIB but my thyroid is now in check. Compared to pre AFIB, I notice my peak power output and HRR seems to have been affected but it may be a mental side from the event.
Thanks in advance.
In terms of AAS anecdotally. Testosterone/nandrolone appear to be significant aggravators regarding autonomic dysfunction. I’ve never used stanozolol and presumably never will thus I can’t comment or give an anecdotal comparison.
I was running higher test than you when running stanozolol. It took about 3-5 days to kick in. Vascularity was amazing on week 2-4, but I was about 12% body fat. You might see it sooner. I was also running masteron, so how much vascularity was due to the masteron and how much the stanozolol? I’m not sure.
Strength gains were surprisingly as good as anadrol for me, but I had to supplement taurine to reduce the cramps in my feet. I’m not sure how well that worked to be honest. They weren’t debilitating or anything, just once in a while they would randomly cramp up and I would have to pull my toes back.
As for oxandrolone, I’m not a big fan. You don’t really get a “I’m on steroids” feel from it. It’s more of a low risk low reward type deal. It’s also processed by the kidneys which turns me off to it. It a way I think it’s more dangerous than taking a lower dose of something like stanozolol and letting your liver regenerate afterwords.
I’m taking a little bit of oxymetholone right now as I don’t always make the best decisions. The quick uptick in strength, the crazy fullness and increase in vascularity etc is unparalleled; probably due to the higher dosages per tab as opposed to oxandrolone, stanozolol etc. Lot of water retention though
I don’t take harsh substances like this for more than 5-7 days at a time as the beneficial effects appear to peak for me quickly prior to chronic heartburn, drop in appetite kicking in.
Thought you might find this interesting. I’m unsure as to how strong stanozolol is in terms of mediating sympathetic drive. I tend to believe the AAS that are strong modulators of sympathetic drive are probably going to be quite damaging due to the long term effects of consistently being in a “fight” (fight/flight) esque. This includes testosterone; in higher dosages I don’t believe testosterone is one of the more “benign” substances.
It only takes around seven days for effects on serum lipoproteins to peak, following which it doesn’t take very long for lipids to normalise when use is ceased.
Document heart rate variability and RHR + post workout HR recovery if you have the time. I’d be interested to see how stanozolol impacts these parameters.
For the last variable I’ve found cardio is the best way of ascertaining impact. Get on a treadmill, run a few miles. Check HR before, during, immediately after (like 90 seconds after) and 1.5 hours or so after. Do this before and whilst on the winny.
If you can’t run a couple/few miles as but everyone can (apparently I have unreasonable expectations as to what should constitute a normal level of fitness), cycling will do the trick.
Tell me how the winny effects lipids at 25mg/day. I have a rough estimate as to what 12.5mg would do. Get SHBG checked too… This is exciting
I wish I had the balls to pull labs on day 5-7 of running something like oxymetholone… I don’t want to see my HDL reeeeeaaalllllly low again though.
Above 15mg/dl coupled with a HDL/LDL ratio of less than 1/4 and I’m not freaking out. My standards are quite low.
Will do if I go this route. I have a firm handle on my HRR/RHR for baseline and after nandrolone use. I was pushing very hard cardio + HIIT session prior to my AFIB episode. That’s probably a bad thing to do while also taking AAS (extra oxidative damage exacerbated by AAS). Thanks for sharing your thoughts and experiences.
I was typically running 6:30-7 min miles prior to AFIB and had worked up to pretty decent FTP (400 W) on the bike. Major hurdle for me right now is ramping HR back up to redline where I used to routinely do it. Since having 200+ bpm ventricular tachycardia (along with AFIB) it is hard for me to go back to same level of intensity. Probably mental defense mechanism but maybe I had COVID complication, no idea.
Interesting rate study with stanozolol:
The verification of resting bradycardia in the exercise group (T group) demonstrated the effectiveness of the training protocol proposed in this study. Resting bradycardia has been considered to be the hallmark of the cardiovascular effect of exercise-training adaptation in both animals and humans [20].
Meanwhile, the STA treatment alone reduced the HR. This result is in agreement with the previous report of Beutel, Bergamaschi & Campos [3], who showed resting bradycardia in rats treated with STA. El-Mas et al. [21] showed that testosterone can act on the brainstem and preganglionic vagal cardiomotor neurons, modulating the autonomic cardiac control. Here, we also showed that STA promoted the increase of relative heart weight when combined with exercise, without changing the body weight gain. Our result is in agreement with Du Toit et al. [7], who also observed increased relative heart weight in rats submitted to exercise and AAS treatment. Many studies have shown that AAS may act on cardiomyocytes, leading to cardiac hypertrophy [3, 8]. Moreover, AAS abuse has been related to sometimes irreversible cardiomyocyte changes, such as concentric left ventricular hypertrophy [3, 6]. AAS anabolic effect is mainly mediated through androgenic receptors present in large amounts in skeletal and cardiac muscles. These androgenic receptors regulate transcription of target-genes promoting the accumulation of DNA required for muscle growth [22]. In our experiment, relative heart weight was significantly increased only in rats treated with STA and submitted to the exercise protocol (ST group). Both resistance training and long-term AAS exposure can enhance androgenic receptor content [23, 24]. This phenomenon would be a possible mechanism by which high doses of AAS, combined with exercise, could lead to cardiac hypertrophy [8]. Another factor of great importance regarding cardiac hypertrophy is collagen fiber content. Both STA and exercise can stimulate collagen synthesis in cardiac muscle, and the combination of these two factors could significantly increase the heart’s collagen content. Chronic AAS abuse, alone or combined with exercise, might promote pathological cardiac hypertrophy with cardiac function loss [7]. STA seems to stimulate collagen synthesis, due in large part to TGF- β1 (transforming growth factor- β1) action. This protein is a potent collagen stimulator that is normally secreted in the acute phase of inflammation and acts on tissue repair [2, 25].
STA promoted left axis deviation in the ST group; however, this deviation was within the normal range expected for rats. This result might be due to the increase in relative heart weight and cardiomyocyte area (data not shown). The mean cardiac axis represents the net direction and magnitude of cardiac electrical force. In essence, the QRS electrical axis is useful because it helps to determine the position of the heart in the chest, patency of electrical pathways and integrity of muscle mass. Despite some criticisms, a number of studies suggest that morphological aspect analysis of the electrical axis (amplitude and duration changes by ECG) is one of the primary tools to detect ventricular hypertrophy and sudden cardiac death [26]. QRS duration is frequently increased in left ventricular hypertrophy. The increased QRS duration might be attributed to the increased thickness of the left ventricle wall and to intramural fibrosis, which distorts and prolongs the transmural impulse propagation. Prolongation of the QT interval is indicative of potential risk of lethal arrhythmia and cardiac sudden death [27]. In our results, there was no difference in QRS, QT and QTc duration among experimental groups; hence, ventricular activation has not been impaired by STA treatment. Thus, the fact that duration of QT and QTc intervals have been presented with no changes among the experimental groups corroborates the values found for QRS, discarding the risk of sudden death (as verified in our experimental conditions) as suggested in previous studies as a consequence of AAS abuse [9, 28].
One question I have is why winny? I know you don’t like var, but other options exist (tbol). Tbol would be milder on lipids (at least that is the general consensus). Probably a lot nicer for your joints too.
Sorry I’m advance for using the street names for these compounds.
It isn’t. Plenty of anecdotal bloods with people who have HDL in the low/mid single digits from tbol use as an independent variable.
Probably cuz winny is fcking EPIC!!! 
Injectable proviron would probably be very good for “drying out” albeit not conducive for mass gain (affinity for 3a-HSD enzyme). I have a means to procure this, but it’s a cocktail of injectable proviron, turinabol, stanozolol and oxandrolone.
Not a chance in hell I’d take that. Proviron has an oral bioavailability of around 3%, look at the results people get from 50-100mg orally. Imagine injecting 10-20mg/day with a far, far, far, far higher bioavailability.
It’d screw lipids up fiercely though
My dick doesnt work too good for 3-4 hours after taking proviron. I hate it.
No worries, use those outdated trade names all you want.
Why stanozolol? Legally available by Rx and therapeutically indicated for a number of conditions, some of which I experience. Ok, of course the long term “safe” dosage of 0.5 to 2 mg/day isn’t going to cut it for muscle gain most likely unless goal is to go from being bed ridden to sitting up :-).
Also, given my current body composition I am in a good position to gauge its effects in comparison to oxandrolone at same/similar dosage.
I want to be as methodical as possible because I realize you guys want nothing less than the purest data, which may be valuable for hypothesis testing.
Not aware of CDMT available by Rx so as I mentioned in other posts there’s only a handful of options for legal use of AAS in my country.
Since CDMT is 17-AA and derivative of Methandrostenolone, I am not aware of any theoretical or anecdotal data suggesting its easier on the liver or lipids than stanzolol. Do you have such info? Please share.
Good case study with pretty high doses of mix of 17-AA AAS + injectables. Talk about throwing various compounds against the wall:
You may enjoy this read @bkb333, has some good time course data that shows the impact of lipids over 10 weeks. Drawback is there are multiple compounds in play so perhaps more amusing that anything in the way the “cycles” were constructed.
6 mg/day of stanzolol quite potent on HDL-c (Apo A-I):
Notice 200 mg/week of TE was termed supraphysiologic back in 1989 :-). Too bad these guys didn’t understand the profound apparent metabolic clearance rates of testosterone esters for the gentlemen of T-NATION :-).
Fascinating:
I can’t get the link to work. Legal reasons make the decision more clear to me. If that was a non factor, I would use Tbol, even if the lipid impact is equal. The impact to joints is not equal, and as a powerlifter, I would only use something like winny for a very short period to increase strength temporarily. The powerlifting alone is enough on the joints for me.
I guess if I pursue I will find out regarding the joint effect. I don’t think they could hurt any worse than they do now, but you never know individual effect until you evaluate. Also great to have stanozolol on hand in case of potential cytokine storm brought on by COVID episode from what I’ve read briefly.
I think lots of folks would still use this description (though obviously people have taken dosages to EXTREMES these days). I tend to think of performance TRT – like my 238/week – as ‘supraphysiologic.’
Do you have behcets disease or HAE?
