False.
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
what about testosterone esters?
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?
In a nutshell: Info is fine, links are not.
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.
Here’s the lipoprofile after 10 weeks of ND+TRT:
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.
Did you’re cRP spike on oxandrolone?
And where are these awesome doctors prescribing nandrolone and oxandrolone?
I have terrible joint pain year round dammit … However the evidence for use of nandrolone to help with joint pain is, as of current, purely anecdotal
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.
Nandrolone interacts with dopamine on a receptor level, reducing dopamine receptor density (D1 and D2 subtypes I believe), alters mRNA expression of dopamine. 19-nors in general also tend to deplete serotonin. Hence the negative impact on mood (nandrolone and n metabolites also act on numerous other neurotransmitters, however those two are the most glaringly obvious causes of N induced behavioral/mood changes.
Using concurrent androgens in general is a type of polypharmacy. Generally it’s best to either A: reduce dose or B: find natural remedies to combat side effects rather than use medication for a solution, however sometimes (for instance I use a low dose of a beta blocker for social anxiety/mild autonomic instability) medication can work wonders, and the absence of side effects one may experience with a medication (such as me and Atenolol) allows one’s body to reach a level of equilibrium where everything’s great
Post TRT I have experimented with additional androgens. I’ve used
Oxandrolone, in total about 5 weeks use, between 12.5-25mg/day (believe it was spiked with something else). Used for 1st 4 wks at 12.5, 5th wk at 25
Nandrolone (phenylpropionate ester), bout 3-4 wks at something like 75-100mg/wk, can’t remember exactly dose. Helped with joint pain tremendously towards end of 2nd week.
1-androsterone: 2 weeks
Have also used high doses of testosterone, up to 250mg/wk, not all of this was done at the same time. I tend to introduce each individual variable independently so I know how I react.
Over the past 1-1/2 years I’ve probably gone up 25-30lbs in LBM (although my weight itself hasn’t fluctuated much. Prior to TRT (with my chronic pain and all) I’d dropped down to 59kg, at about 18-20%+ bodyfat… Was terrible, now I’m 73KG bout 15-16%. Haven’t grown since age 15 (ephysial plates are/have been fused, my medical history is actually quite interesting, what happened to me was just baaaaaadddd luck). Never had any issues from the increased mass.
Reason for my high BF at the moment is due to a recent flare up of my chronic pain, making it very difficult for me to exercise intensely, unfortunately I put on fat very easily.
I’d be happy to take an ace inhibitor for cardioprotective effect. Other drugs I’d be happy to trial are
Lifestyle isn’t terrible, but not great either. I never consume alcohol. Used to on occasion, but I see absolutely no point in drinking. I love the taste of beer, with beer and soda water being my two fav beverages, but they have non alcoholic beer so I can drink that without the toxic effect on my body. (legal age is 18 here, 16 at parties which are private venues, used to be 16 if with an adult eating a meal but law changed on March). I use cannabis socially but don’t touch anything else, the fact that it helps with pain is a huge bonus, esp if I’m at a party where one has to dance and move around a lot. drug use (hard drugs too)/drinking is very rampant among youth in my area (much more so than when I lived in America). Eat fairly healthy, exercise as much as possible (including cardio, both LISS and moderate to high intensity aerobic exercise).
Sleep 9-12 hours a day (I have problems with fatigue, I sleep a loooooooooooooooooooooooooooottttt.
Make sure to get adequate water, vegetable and mineral intake. I have OCD style tendencies with many things, and thus I do tend to meticulously track my intake of vital essentials otherwise I don’t feel right (it’s placebo/in my head, but it irritates me and if it doesn’t harm me then why fix it)
Also have a merck manual and a bunch of other medical books that I sometimes read because i’m a rather strange individual
Furthermore I should add I’m very aware of the risks associated with the use of anabolic steroids. I’m not oblivious to the potential long term effects on my cardiovascular system, potential neurotoxicity, nephro/hepatotoxicity, haematological alterations etc. The doses I use are low, which may somewhat mitigate the risk (or not, who knows).
Feel free to give me backlash regarding my decisions. I don’t mind criticism/ judgement, I’m fully aware my decisions regarding experimentation with androgens aren’t responsible. It’s not that I don’t care or can’t comprehend my own mortality (as appears to be a common trait of many teenagers), it’s that when I weigh out the pros and cons, I don’t see particularly significant risk/ an imbalance between benefit/risk assessment. I view my benefit/risk ratio/assessment based on how much something impacts my quality of life, health and wellbeing, and the potential impact on my longevity. While androgen experimentation certainly doesn’t do any good for my long term health, the impact of low doses (as specified above) on my overall quality of life and general wellbeing is significant, and with the absence of creeping HCT/ other parameters, a clean echocardiogram (both recently and at birth), multiple EKG’s checking out etc I think “ehhhhhhhhh, not too worried”. The neurotoxicity/ cardiovascular toxicity is my biggest worry by far.
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 . . . .
Really bro…
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.
DRUG ABSORPTION BY SUBLINGUAL AND RECTAL ROUTE
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.
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
