In your extensive reading have you came across studies of rectal administration for AAS ? I’m thinking here, maybe a slow release suppository to even out the admin of oral steroids, and maybe even avoid liver damage for the harsher compounds . . . .
I prefer to inject my sphincter…
None particular to AAS but some of these examples would partition similarly to 17-AA oral AAS. This is a nice review with examples. You have to give credit to @zeek1414 who already raised this possibility earlier in the thread. This was all tongue in cheek though.
My point above was that troche with auxiliary supplements for liver seemed to be working just fine (ALT and AST were barely out of range). You have to be disciplined with the troches and do them buccal route. Sublingual route and you are just effectively swallowing all the medication. The problem was my lipids which took an incredible hit as well as my SHBG. As SHBG drops, the metabolic clearance rate of testosterone shoots way up and you need more exogenous Testosterone to maintain the same free Test.
For you genetically gifted, I have absolutely no comments on non-prescription AAS, but a stevia sweetened, raspberry oxymetholone troche would be an interesting alternative to regular tablet. You definitely don’t want all that extra sugar pushing you out of ketosis
Whether you are getting USP grade oxymetholone is another important consideration.
I never even considered this.
Help me understand.
So if I’m using drugs that greatly reduce shbg will my then current dose of testosterone essentially be less effective?
Or is it that it’s even more effective just displaying a lower serum level?
My experience was consistent with paper I posted earlier in this thread above:
Here’s my approximate T-values on 100 mg/week of Tcyp (50 mg twice weekly):
Now add on top of the TRT add the 50 mg/day of oxandrolone. After 4.5 weeks (1 week at 25 mg/day + 3.5 weeks at 50 mg/day):
There’s competing effects here.
- SHBG drops significantly which speeds up testosterone MCR and reduces total serum testosterone by about 50% (the testosterone is getting secreted more rapidly and the lower SHBG is effectively reducing half-life/binding efficiency).
- The lower SHBG results in less of the remaining total serum testosterone being bound vs free. So you can see I ended up with close to the same free T (18.7 ng/dL before vs 17 ng/dL after). Bioavailable went from 438 to 399.
As SHBG gets closer to zero you’ll lose even more ground. So don’t crash your SHBG (just like estradiol) otherwise you risk having no testosterone (and hence lower estradiol) to balance synthetic AAS that you may also be administering. Depending on whether synthetic AAS is aromatizing/5-alpha reduced, this may or may not be a huge deal. For the guys in article above, they had ED effects that may be attributed to significant reduction in SHBG while on exogenous T.
Here’s a hypothetical example on same 100 mg/week of Tcyp but now you’ve taken your SHBG down to 1 (your liver is extremely sensitive to oxandrolone here, let’s say your total T is now 200 ng/dL (I’m just giving example):
Almost all of your serum T is bioavailable (96.8%) but there’s not much around because you’re hyperexcreting it compared to an SHBG of 30 or 50. So another consideration to keep in mind.
Zeeks method does show some promise . . . . so would his technique, or buccal admin for that matter , be effective with non 17α-alkylated versions? thereby sidestepping hepatoxicity.
In your specific case, do you think your low bodyfat (8-10 %) had any bearing on your adverse lipid reaction to AAS ? . . . . thinking along the lines of reduced conversion to estrogen.
Adverse lipids from c17AA is due to further activation of hepatic lipase, hepatic strain etc
For the interested reader:
Update after trialing oxandrolone a second time at 7.5 mg/day mean (15 mg capsule EOD)…
LDL particle count up signficantly and HDL-c / SHBG crushed at either 7.5 mg /d avg or 50 mg /d.
So for me oxandrolone risk profile exceeds anabolic profile at low dose (7.5 or 50 mg/day, to clarify).
Have you looked into pahrmacogenomic testing? I just had it done by GeneSight Psychtropic. I’d be interested in your take.
Commented over on your post. No I haven’t yet since I’ve tried to avoid the medications this testing is used to screen for. Sounds like you’ve learned quite a bit and I am glad it was helpful. I’ll study up on this some more. Thanks!
Additional details and Rx pricing current as of Nov 2019:
Ok, let’s pretend Oxo didn’t hurt lipids, how did you feel with a SHBG of 9 and TT 50% lower? Better, worse or the same?
Honestly, workouts were a little better with the oxandrolone and no real difference in well being with modified TT/SHBG. Joint pain may have been better with oxandrolone, placebo?
Right now I take 70 mg/week of TC (once per week) injection and feel no different on day 2 vs day 7. Peak is 900 ng/dL and trough about 300 ng/dL. Current SHBG is about 50 nmol/L.
My “debate” last week has me revisiting the impact of oxandrolone on the CNS and cardiac beta-adrenergic receptors.
I’ve read this paper which suggests oxandrolone does not appreciably modulate β-adrenergic receptor signaling:
While the cardiac effects of PROP are well known, there is little information regarding the effect of oxandrolone on the myocardium. Clinical data regarding the effect of testosterone on the heart are controversial, with some studies reporting that androgen administration is detrimental and others reporting that it is cardioprotective. Exogenous androgen administration has been implicated in prothrombotic, prohypertrophic signaling (reviewed in  In addition, there is a solid body of basic science research indicating that testosterone modulates β-adrenergic receptor signaling. For example, studies in isolated cardiomyocytes demonstrate that testosterone administration significantly increases β-adrenergic receptor expression after testosterone treatment. Alterations in the β-adrenergic receptor signaling system were also seen after testosterone treatment in an animal model of heart failure.
Any other data out there that folks are aware of? Thanks in advance.
Oxandrolone or stanozolol for least impact on cardiac electrical system and complications for arrhythmia? Oxandrolone seems to be best of the worst in this respect. Others thoughts/analysis?
Interesting I had no issues with 350 mg/week of oxandrolone combined with 100 mg/week of TC (when my TSH was in range) but 325 mg/week of TC by itself sent me to a bad place (but my TSH at the time was in the range of 8-10). Make sure you’ve got your thyroid under control before doing any supra-levels of Test or AAS add-on.
I’ve got access to both oxandrolone and stanozolol from my Accelerated Aging (AA) clinic so curious how the stanozolol would work at very low dose (say 12.5 - 25 mg/day). As I’ve detailed, oxandrolone at up to 50 mg/week tore up my lipids/HDL/particle counts but so does 7.5 mg/day.
In conclusion, the chronic use of supraphysiological doses of STA induced bradycardia and increased cardiac SOD and CAT activities. STA combined with swimming led to an increase in systolic and diastolic blood pressure, relative heart weight and left cardiac axis deviation. Although MEL did not prevent cardiac hypertrophy in exercised animals treated with STA, it prevented blood pressure elevation and the increase of cardiac catalase activity. MEL also prevented the STA-induced electric cardiac axis deviation. Hence, under our experimental conditions, the adverse effects of STA on the cardiovascular system were partly attenuated by MEL treatment. New experiments are now underway in our laboratory to investigate how MEL treatment could improve and minimize the side effects produced in the cardiovascular system. by STA administration.
Anecdotally I’ve noted primo was the mildest regarding exacerbation of autonomic dysfunction
I tried “Anavar” once, though I don’t think it was anavar (legitimate reason for suspecting it wasn’t Anavar, not just the “but it’s often faked” schtick). For me, if this WAS actually Anavar it was the second worst for aggravating cardiac autonomic dysfunction with nandrolone being at the top.
As to stanozolol. I’ve never tried it, I’ve heard it causes joint pain and good GOD I don’t want to be in even more pain on a daily basis.
What’s more, have you seen what stanozolol does to lipids? It’s arguably the harshest AAS for lipids barring perhaps methyldrostanolone.
5mg/day = 40% + reduction in HDL and 30% ish increase in LDL.
For longevity you’re best off not using c17-aa drugs. See if you can contact the guy on the T-replacement/Pharma forum whose clinic compounded him primo. Not recommending you use AAS or anything, but it’s (probably) safer than winny.
I do find it interesting LV global longitudinal strain and LV mass in controls is on average borderline/abnormal in comparison to AAS users of which have marketedly abnormal results indicative of cardiovascular abnormalities.
Wonder how much they’re using… Wonder whether some of the controls are LYING…
Regardless, be aware any AAS use probably takes years off your life. I’m not one to make decisions for others, but you should probably come to terms with this prior to experimenting again.
And if you’re going to do it again, I’d highly advise against concomitant high dose T3, using beta 2 agonists or stimulants. It’s a 1+1=6 scenario
All of the study participant were claiming to pump the iron. Lifting weights works that LV.
I agree AAS take off the years. At least I can’t claim ignorance any more or really ever :-). Thanks for your feedback. I believe the T3 use induced hypothyroidism / pseudo-hypothyroidism (TSH went above normal and fT4 dropped below normal range). Clearly for people who don’t need it (probably very small minority), using high dosage of T3 with out without T4 to titrate TSH is really dumb. Will be interesting but risky to see if I have same experience with well managed TSH on T4 monotherapy now that I am back to physiologically relevant treatment for thyroid. I’ll lay off the pre-workout formula as well.