I’d be interested in hearing others experience using oxandrolone troches instead of oral delivery (capsules) to bypass first-pass metabolism and reduce liver toxicity and lower minimum effective dose . Since oxandrolone has excellent oral bioavailability (97-98%) and is actually metabolized partially by kidneys (haven’t looked at the original studies to support this assertion), I have a hard time believing that sublingual/buccal administration is going to do much to lower liver damage for same dosage (i,e, you end up swallowing most of the troche as it dissolves?). I’ve pulled 10-15 studies and most seem to show similar pharmacokinetics for oral and sublingual administration of drugs that are metabolized similarly (ie CYP 3A4). I guess one way to find out with some rigorous n=1 experiments.
Here’s an example with DHEA troche, similar result to oral administration (pill).
I cannot imagine it being worthwhile. Anavar is already pretty mild as far as hepatotoxicity. Now if this was a novel delivery system for one of the more harsh orals I’d be interested. But for Anavar? Kind of meh.
Why not just try crushing the anavar and placing it under your tongue? Or dissolving in alcohol. Hell, you could even try DMSO for transdermal delivery.
Thanks for the replies folks. I see this thread has some real entertainment potential and 20 mg/day of oxandrolone has been studied and associated with mild hepatic effects:
Seems like oxandrolone’s reputation for “mildness” is related to dosage and individual’s genetic response. Running 50-100 mg/day of oxandrolone probably ain’t gonna give the same result as 20 mg/day so just wanted to daylight the obvious. I don’t think anyone is doing histology on the kidneys while trial participants are running oxandrolone but perhaps that’s another place to look.
I was just genuinely curious why oxandrolone is dispensed from legitimate pharmacies via troche when its oral (delivery via digestive system) bioavailability is so high. Seems like a hammer in search of a nail. What was I missing? Hence I thought about avoiding liver damage. But, just because the drug doesn’t get delivered to liver/circulation via portal system doesn’t mean it can’t come back to the liver/kidney via serum for additional metabolism. Seems to me a troche’s strength is to get molecules (which have low oral bioavailability) into circulation by increasing bioavailability (avoid digestive system) and not to minimize end-organ metabolism damage. I can’t find an example of the latter in the literature.
Now, with regard to the delivery systems mentioned by you guys, would be an interesting experiment to test these different delivery modes on CMP/SHBG, lipids (hepatic lipase etc.). Appears to be a challenge for some to keep serum T levels reasonable (even with exogenous T usage) while also running oxandrolone since SHBG heads toward zero.
CONCLUSIONS: Patients had erectile dysfunction in association with low testosterone and SHBG, in spite of exogenous testosterone replacement. Discontinuation of oxandrolone led to the normalization or improvement of testosterone levels in all three patients with symptomatic improvement in one patient. First pass metabolism of orally administered oxandrolone may decrease hepatic synthesis of SHBG, allowing exogenously supplied testosterone to be excreted. Further work is necessary to elucidate the relationship.
I understand you guys may not be concerned with oxandrolone’s safety in particular, but think about this concept with respect to other hepatotoxic 17-AA AAS as @iron_yuppie mentions and ability to decouple anabolic effect from SHBG hit, significant hepatic lipase rise which ain’t good for some vulnerable populations. Wishful thinking, theory vs practice? I admire your ruthless efficiency @zeek1414.
Aha, I will correct myself. If you can get drug into systemic circulation (while avoiding first pass) where it presents at reduced systemic serum concentration (vs concentration upon introduction into portal vein) and metabolic clearance typically first order function of serum concentration, I can see where this concept has legs although effect may be quite minimal with highly bioavailable oxandrolone. Especially if most of the metabolic clearance is done in kidneys anyway. In short, dilution may be the solution.
Nice demonstration of the measurements and procedure you’d leverage clinically to study this with oral vs sublingual / rectal ( @zeek1414) approaches:
Just because it is an injectable version does not mean it’s not hepatotoxic (sp?). For instance winstrol. The common misconception is injectable winstrol is not toxic like oral. Simply not the case.
I think tren is a bit toxic as well not 100% sure on that one maybe @readalot can chim in and keep it laymen so you understand
Just the use of simple testosterone can come with some serious risk. Google “risk of trt” it doesnt mean it will it means it can this is the main reason why it’s so important to keep a close eye on more than just your hormones when you get bloods drawn
I think you should start here at testosterone and fully understand the risks with that molecule first…
@Chris_Colucci: are we allowed to share info from other forums? I think I’ve got some information that may help here. Just wanted to clarify what external content we are allowed to link to?
Ok, I realize everybody typically does what they want to do but in case this helps someone. I have historically only used prescription androgens at “therapeutic” dosages (under cumulative 250 mg/week). I’ve been challenged with some issues that allows me to trial nandrolone and oxandrolone.
Combining 100 mg/week of TRT with 100-150 mg/week of nandrolone was an overall positive experience wrt chronic joint pain. As others here and literature mentions, even at 150 mg/week I seemed to be affected mentally through the hypothesized serotonin/dopamine interaction with nandrolone over the 19 weeks I tried ND. Nothing alarming popped up on the extensive blood work I run every 6 weeks. My excellent lipid profile stayed really good and SHBG dropped slightly from upper 50s down to mid 40s.
I recently decided to give oxandrolone a try using the troche option I discussed above. RX was for 50 mg/day (350 mg/week). I continued TRT at 100 mg/week. I started first week at 25 mg/day and then next 3.5 weeks I did the 50 mg/day (total androgen usage of 450 mg/week). I decided to run NMR lipoprofile after 4.5 weeks of oxandrolone and compare with same profile after 10 weeks of ND.
As you can see I’ve got reasonable insulin sensitivity and maintain 8-10% bodyfat. Diet and exercise program are dialed in and I have the genetics to do well eating modified Keto (meat/vegetables/nuts).
Ok, here’s the NMR data after 4.5 weeks on TRT+ oxandrolone (1 week at 25 mg/day and 3.5 weeks at 50 mg/day):
Only difference is the oxandrolone vs the lower dosage ND. I can confirm my baseline lipids on TRT look very close to the TRT+ND results above.
I admit I’ve read every study I could and realized it was a possibility but can honestly say I wasn’t prepared when I saw these data (rationalizing is amazingly easy before the fact). LDL-P almost tripled, triglycerides actually went up (whoa), and HDL dropped like a rock. Oxandrolone potently upregulates hepatic lipase and I unfortunately didn’t measure my cRP which historically runs < 0.1. But in any case these results would suggest I am not doing myself any favors from a cardiovascular standpoint.
For those that may have a clinical need for AAS, stick to the injectables and please leave the 17-AA orals alone. Or at least confirm you have the genetics to use them. I unfortunately do not. I was thinking that perhaps my ketogenic diet may have exacerabated the oxandrolone effect on my lipids. A fun control experiment would be to cut my 50-70% of calories from fat way down and try again. Unfortunately, I do not have the heart.
PS, my SHBG dropped from 50 to 9 with the oxandrolone. Serum test went from 1000 to 494. On the bright side my provider was amazed at my bioavailable test. I’m not so psyched. Amazing swings in just 4.5 weeks. Take care of yourself and understand the implications long term from the data above. I immediately stopped the oxandrolone once I saw these data.
Very interesting. Thanks for the detailed dataset. I especially like that you mention the genetic aspect. That’s an undersold element. I took anavar @ 50mg/d for almost 12 weeks and my cholesterol, AST, and ALT barely moved. Yours did something very different. Further proof that there is rarely a blanket answer about how any one drug will affect an individual.
Thanks for taking a look and congratulations. If your cRP doesn’t spike and lipids hang in there, then that’s encouraging. My ALT/AST didn’t budge much but I was also taking all the usual stuff for protection (taurine, NAC, A-LA). I was hoping I wouldn’t see much on the lipids but I’ve found out I’m part of the 5%-tile, an elite club that no one wants membership in. It must be more like 50%-tile club since medical literature is filled with examples of lipid dysregulation with oxandrolone therapy.
I always thought when I was younger that if I smoked 1 cigarette I’d be dead of cancer within the year. Looks like my instincts served me well.
For those interested, this article captures the pros/cons of increased HL activity based on the underlying genetics of the patient. I’m not willing to bet any potential improvement in reverse cholesterol transport overcoming a tripling of LDL-P. RCT still very much an active area of research. Nice bedtime reading:
Increased or decreased hepatic lipase (HL) activity has been associated with coronary artery disease (CAD). This is consistent with the findings that gene variants that influence HL activity were associated with increased CAD risk in some population studies but not in others. In this review, we will explain the conditions that influence the effects of HL on CAD. Increased HL is associated with smaller and denser LDL (sdLDL) and HDL (HDL(3)) particles, while decreased HL is associated with larger and more buoyant LDL and HDL particles. The effect of HL activity on CAD risk is dependent on the underlying lipoprotein phenotype or disorder. Central obesity with hypertriglyceridemia (HTG) is associated with high HL activity that leads to the formation of sdLDL that is pro-atherogenic. In the absence of HTG, where large buoyant cholesteryl ester-enriched LDL is prominent, elevation of HL does not raise the risk for CAD. In HTG patients, drug therapy that decreases HL activity selectively decreases sdLDL particles, an anti-atherogenic effect. Drug therapy that raises HDL(2) cholesterol has not decreased the risk for CAD. In trials where inhibition of cholesterol ester transfer protein (CETP) or HL occurs, the increase in HDL(2) most likely is due to inhibition of catabolism of HDL(2) and impairment of reverse cholesterol transport (RCT). In patients with isolated hypercholesterolemia, but with normal triglyceride levels and big-buoyant LDL particles, an increase in HL activity is beneficial; possibly because it increases RCT. Drugs that lower HL activity might decrease the risk for CAD only in hypertriglyceridemic patients with sdLDL by selectively clearing sdLDL particles from plasma, which would override the potentially pro-atherogenic effect on RCT.
Unfortunately I didn’t measure it this time (forgot to pull that lab). As I mentioned above my systemic inflammation appears quite low, it’s joint-specific inflammation that’s very elevated. Look up 14.3.3 eta assay (most doctors aren’t even aware of it, even specialists).
In US, if you look hard enough and come prepared, you can find them. Of course state regulatory environment plays a big role, so FL always comes up.
My nandrolone experience was positive regarding joint pain but negative for mood/depression. My understanding is that ND may increase cortisol production. As I continue to learn more and research, seems like there’s little that can be done to rehab bone spurs and osteophytes. There’s nothing to “regenerate” there.
My own personal experience is that starting these androgens opens up a whole new set of problems that then gets you potentially into polypharmacy (Hct goes up, BP goes up, gain 20 lb of lean mass, now do you consider ARB or medication?). Who is realistically is going to train with the same intensity and poundage on 350 mg/week of AAS compared to 100 mg/week TRT? I didn’t. Well if you are trying to tackle degenerative disc disease and chronic joint pain then that’s what you’d need to do to perform rigorous anecdotal experiment.
Reminds me of adventurer who goes looking for some lost city of gold and finds it. But then he gets stuck in the gold vault room and slowly dies there (and the gold does him no good). At your age if you need HRT at therapeutic dosages continue to explore that option. Leave the other stuff alone and take care of your health.
I’ve studied this stuff up and down for a few years now and can’t honestly state that the reward is worth the risk in my particular case. Of course I may have very poor genes to mess with this stuff. If you do find a provider to trial these medications, either you or your provider better know what to look for to ensure you aren’t hurting yourself. Fortunately for you, you seem to be an exception for a younger person. Your theoretical knowledge is exceptional.
In my case with oxandrolone, the provider only wanted to see LFT panel after 8 weeks. If I hadn’t pulled my own lipid panel, I would not have known how upside down I was after 4.5 weeks. Complexity is in the eye of the beholder and unfortunately AAS are a black box whose effects seems strongly dependent on an individual’s genetic expression and makeup. That’s a recipe for disaster if you aren’t being cautious. All in all it was an educational experience for me and I hope this information provides some context on why the cumulative cavalier use of AAS may be very bad news for some. And that’s what we see with cigarettes, alcohol, anything. Some folks are more robust that others. You better know how robust you are before going on these crazy cycles I see people post on here. Hence, learn how your body reacts with testosterone first.
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