My take on Superdrol

[DAdams91982]

So would the LV-SD @ 10 mg be like 30 MG pill form?

Nope... it is a 17aa methyl, therefore a ~99% bioavail rate. The LV only gives you the benefit of modulating the dosage precisely... albeit a huge factor when dealing with SD.

 

[dumbhick3]

Nope... it is a 17aa methyl, therefore a ~99% bioavail rate. The LV only gives you the benefit of modulating the dosage precisely... albeit a huge factor when dealing with SD.

You're probably right but I still wander...that LV technology is a bit hard to understand for me (SEEDS, oral, eso****eal, and stomach lining absorbtion, etc).

The only reason I think that the LV could in theory make the same dose slightly stronger than cap form is by rough analogy the fact that injectable winstrol is more potent than oral winstrol since it misses the first pass metabolism in the liver when injected. Both forms are near 100% bioavailable, but the first pass metabolism metabolizes some of that 100% dose so avoiding it means more active in your system at least with winstrol.

I doubt it is anything that dramatic with the LV (if anything at all), and really, I don't think it would be desirable or necessary to enhance the absorption of a dimethyl like superdrol since it is already so resilient to being broken down by the liver (much more than the single methyls). But it has been suggested that absorption of the LV starts in the mouth and the eso****us which to me seems like an avenue for some of the superdrol to avoid first pass hepatic biotransformation (I'm really speculating here).

What say you Trauma?...

 

[RAZORBACK09]

Nope... it is a 17aa methyl, therefore a ~99% bioavail rate. The LV only gives you the benefit of modulating the dosage precisely... albeit a huge factor when dealing with SD.

Oh okay, I thought I had read that the absorption was 3-4 times more then the pills so I figured 10mg of LV would be maybe like a 30mg of pill.

I'm going to be running tren/SD together (3 weeks SD, 6 week tren) should I just run liver care for the 3 weeks or the whole cycle?

 

[DAdams91982]

You're probably right but I still wander...that LV technology is a bit hard to understand for me (SEEDS, oral, eso****eal, and stomach lining absorbtion, etc).

The only reason I think that the LV could in theory make the same dose slightly stronger than cap form is by rough analogy the fact that injectable winstrol is more potent than oral winstrol since it misses the first pass metabolism in the liver when injected. Both forms are near 100% bioavailable, but the first pass metabolism metabolizes some of that 100% dose so avoiding it means more active in your system at least with winstrol.

I doubt it is anything that dramatic with the LV (if anything at all), and really, I don't think it would be desirable or necessary to enhance the absorption of a dimethyl like superdrol since it is already so resilient to being broken down by the liver (much more than the single methyls). But it has been suggested that absorption of the LV starts in the mouth and the eso****us which to me seems like an avenue for some of the superdrol to avoid first pass hepatic biotransformation (I'm really speculating here).

What say you Trauma?...

I think your knowledge about these are a bit skewed. the whole point of being methylated is the first liver pass, there is no skipping a first liver pass, the first time it goes through the liver is the first liver pass. Methylation prevents the breakdown on the first pass. No matter the point of absorbtion, the molecule enters the blood stream and goes through the liver.

As for winny, I have used both to test out that theory and seen the exact same effects, as have others who have used in the past. I speculate the winny theory is a placebo effect, IE: It's injects = stronger.

 

[Dragon13]

Nope... it is a 17aa methyl, therefore a ~99% bioavail rate. The LV only gives you the benefit of modulating the dosage precisely... albeit a huge factor when dealing with SD.

99%? Never heard that before. Reference?

 

[DAdams91982]

99%? Never heard that before. Reference?

I did my research almost 5 years ago... here is a pretty comprehensive list of research.. knock yourself out.

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[Dragon13]

I did my research almost 5 years ago... here is a pretty comprehensive list of research.. knock yourself out.

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Uh, I've seen this page at Rx. NONE of the information there quotes 99% bioavailabilty, and NONE of those studies are even pertinent to the bioavailabilty of AAS.

If you don't have the source, just say so. In any event, absent data to the contrary, I am not quite on board wth ANY 17a- oral steroid being 99% bioavailable.

 

[Trauma1]

Trauma, it is interesting that you mentioned h-drol in presumably the ER setting. It gets touted as a mild methyl, and I suppose for many it is (including those who don't get blood work...), but it certainly did a number on my AST/ALT. GGT and Bilirubin were fine, but I think that "mild methyls" taken at 100+ mg/day aren't so mild at the end of the day (cumulatively). And if h-drol can do that, it stands to reason that superdrol can do much worse in bad hands and at wrong dosing and durations.

BTW, I don't know if you guys have seen this from the CEL forum (idiots in action; suing CEL and TFS over M-drol b/c they nearly pickled their livers through ignorance):

http://anabolicminds.com/forum/competitive-edge-labs/145506-c-e-l.html

I can tell you Halodrol being labeled as "mild" is a misnomer. Again, this is where guys read anecdotal reports around the internet and take them as some kind of valid and substantiated reference; when in reality, you should take them for nothing more than an entertaining read.

I'm all about the science, not the hearsay.

- John

 

[Trauma1]

You're probably right but I still wander...that LV technology is a bit hard to understand for me (SEEDS, oral, eso****eal, and stomach lining absorbtion, etc).

The only reason I think that the LV could in theory make the same dose slightly stronger than cap form is by rough analogy the fact that injectable winstrol is more potent than oral winstrol since it misses the first pass metabolism in the liver when injected. Both forms are near 100% bioavailable, but the first pass metabolism metabolizes some of that 100% dose so avoiding it means more active in your system at least with winstrol.

I doubt it is anything that dramatic with the LV (if anything at all), and really, I don't think it would be desirable or necessary to enhance the absorption of a dimethyl like superdrol since it is already so resilient to being broken down by the liver (much more than the single methyls). But it has been suggested that absorption of the LV starts in the mouth and the eso****us which to me seems like an avenue for some of the superdrol to avoid first pass hepatic biotransformation (I'm really speculating here).

What say you Trauma?...

I'll answer this tomorrow; my bed is calling me right now.

- John

 

[fueledpassion]

I thought Unreal said in his guide to superdrol that shutdown occurred much faster than that-like less than a week.

Yeah I read on one of Eric Potratz's articles on PP's website that it only takes about 3 days for near complete shutdown..( I think )

 

[RAZORBACK09]

So if stacking with tren, should it be used first 3 weeks or last 3? I've gotten mixed reviews so I'm trying to figure it out before I go on cycle.

 

[DAdams91982]

Uh, I've seen this page at Rx. NONE of the information there quotes 99% bioavailabilty, and NONE of those studies are even pertinent to the bioavailabilty of AAS.

If you don't have the source, just say so. In any event, absent data to the contrary, I am not quite on board wth ANY 17a- oral steroid being 99% bioavailable.

Suit yourself. You can go ask Matt from DS though, he will definitely reconfirm my statement... since he is the master of methyls... he keeps all his research by his side, I on the otherhand could care less if someone believes me or not.

Although checking the A;A ratio of these methyls, and seeing that something as low as 2.5mg of SD can give results, that would have to tell you logically that every last mg will have to be absorbed... be that as it may, it is your right to disagree.

 

[the GUNSHOW]

the theory that the 2-on-2-off protocol is based on says that you don't get actually suppressed until after 2 weeks into a cycle. I am just hihgly skeptical of this and I think that suppression occurs much faster than 2 weeks, especially with the strong, high-shutdown orals like 19-nor, M1T, and Superdrol.

Just like you said with M1T you can cycle it for 2 weeks and gain 14 pounds, most people still get sides like lethargy even in just 2 weeks and some libido loss, these are definitely signs that significant suppression is occurring.

I don't understand the 2 week number, it's too arbitrary and magical, nothing in the human body is going to function on an exact 14 day time scale for everybody... It may have some merit but until I see lots of bloodwork results, I'm not buying too deeply into it.

hey man how long of a cycle do you think some one can do at just 10mg?

 

[younganabolic]

So if stacking with tren, should it be used first 3 weeks or last 3? I've gotten mixed reviews so I'm trying to figure it out before I go on cycle.

I think you should do it the last 3 weeks just because superdrol takes a while to kick in

 

[p5sky]

I noticed some nice strength gains on day 2 of 5mg. I have never run SD so that may have an effect of the compound. I mostly have noticed gains in shoulders and legs. Squats I have been able to push more wt at good reps at the end of my sets. I usually did 3 sets 225x8, then 245x6, 275x2/3. My 2nd day of SD was squat day and I EASILY did my 3x225x10, 245x8, 275x8, 305x2. Still more energy but did not want to push it and get hurt. Yesterday I did 2 sets of 315x3 PR!

 

[dumbhick3]

Suit yourself. You can go ask Matt from DS though, he will definitely reconfirm my statement... since he is the master of methyls... he keeps all his research by his side, I on the otherhand could care less if someone believes me or not.

Although checking the A;A ratio of these methyls, and seeing that something as low as 2.5mg of SD can give results, that would have to tell you logically that every last mg will have to be absorbed... be that as it may, it is your right to disagree.

Sledge is quite knowledgable in these things. I wouldn't waste his time.

But sometimes there is more to the picture than just near 100% bioavailability (just my opinion).

I think your knowledge about these are a bit skewed. the whole point of being methylated is the first liver pass, there is no skipping a first liver pass, the first time it goes through the liver is the first liver pass. Methylation prevents the breakdown on the first pass. No matter the point of absorbtion, the molecule enters the blood stream and goes through the liver.

As for winny, I have used both to test out that theory and seen the exact same effects, as have others who have used in the past. I speculate the winny theory is a placebo effect, IE: It's injects = stronger.

This is more what I was inferring with the winstrol analogy:

I think that most hepatic-metabolized injectables (IM/IV/SC) do miss the first pass hepatic biotransformation in the liver by being absorbed into the bloodstream first (thus exerting immediate effects at 100% of the injected dose before reaching the liver and being metabolized for the first time-the "second metabolism" according to the article below).

On the other hand, orals go straight from the stomach to the liver and then exert their effects (and undergo more extensive hepatic metabolism consequently). I am oversimplifying here and leaving out some details.

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The difference between taking oral vs. injectable Winstrol, even though it’s technically the same drug, is how and when your body metabolizes it. When you consume a drug orally, that drug is absorbed from the Gastrointestinal tract, where it then passes via the portal vein into the liver -where some drugs are metabolised. This “first pass” can mean that only a certain portion of the drug reaches your body’s bloodstream. As previously discussed, a 17aa has been attached to Winstrol to allow a sizeable portion to survive this metabolism.

First pass metabolism can occur in both the gut and the liver, and where this happens can vary with different drugs. First pass metabolism actually occurs in your gut for some drugs and in the liver for others. Once it has been metabolized, it enters the bloodstream. It’s important to note that when a blood is metabolized in the Gastrointestinal tract, the blood leaving the Gastrointestinal tract does not go right to the heart, but actually still passes through liver via the hepatic portal vein and then ultimately returns to circulation via the hepatic vein. The liver is your body’s filtration unit, and removes large quantities of nutrients, dangerous toxins (or fun toxins, depending on what they are) and other substances from the blood.

So as you can see, when you take an oral steroid such as Winstrol, undergoes a first-pass metabolism in the both the intestines as well as liver. Some drugs can be absorbed more or less totally intact, after only moderate metabolic activity, while some are absorbed only after very extensive metabolic activity. Once it is through this first pass, a given drug then circulates in the blood until it is acquired by another tissue, such as skeletal muscle. Now, if the drug reaches the liver again, it may undergo what is cleverly known as “second-pass” metabolism. Of course, in the case of Winstrol, an injectable version is available, and when we compare the oral and injectable versions of Winstrol and their effects in your body, I think there’s some surprising differences. The injectable is (naturally) put right into your bloodstream and only undergoes the far less extensive second pass metabolism, while the oral must endure the gut and liver on it’s first pass before ending up in circulation.

Now, here’s the interesting part: When you inject Winstrol, instead of taking it orally, you actually get more nitrogen retention (4) (and hence we can infer, more new muscle tissue is being built). SO if you are trying to use Winstrol to build new muscle tissue, the injectable version is going to be far superior to the Oral version. However, there are some advantages that the oral version has over the injectable, including a possible “synergy” with other drugs- but only (primarily) when taken orally.

While in the liver, on it’s first pass, Winstrol is exposed to a variety of enzymes and proteins. To understand how a possible synergy between Winstrol and other steroids may be possible, a little background on Sex Hormone Binding Globulin (SHBG) is first necessary. For our purposes here, all we need to know is that SHBG is a glycoprotein produced in the liver, which binds to testosterone and makes it biologically unavailable to do all the things we want it to do- like building muscle. It serves to transport testosterone throughout the body, but while it remains bound to testosterone, the testosterone can not exert it’s anabolic effects.

Most ppl know what SHBG is (I hope), but this article got me thinking. Winstrol is usually not run solo if you have much respect for your joints (ppl do it, but not too often).

So could it be that oral winstrol seems as potent as injectable winstrol b/c the oral binds SHBG to a much greater degree than the injectable, and consequently, the other steroids that you are stacking the oral with benefits from lowered SHBG (and your own endogenous test for that matter since estrogen isn't going to be much of an issue with solo winstrol due its DHT-derivate AI-like effects)? This SHBG discussion is just a theory to try and explain oral vs inject winstrol subjective effects, though the above link has some interesting graphs and more commentary on the subject.

It's interesting that Anthony Roberts suggests that winstrol may have less than 100% bioavailability. If I didn't quote it above, I think it is somewhere in that article I linked to. By the way, I am not insinuating that he is an expert; maybe he is; I don't know honestly.

I guess another quasi-example would be morphine (I know; nothing like a steroid). It has very poor oral bioavailability and increasingly high bioavailability as you go from SC to IM to IV (the latter being 100%). It's not methylated (that would be codeine/methylmorphine, lol, and it still sux) as with the steroids being discussed, but the reason that morphine has such horrible oral bioavailability is due to the first pass hepatic metabolization which wipes out most of an oral dose of it, leaving about 10-15% or so to enter the bloodstream (rough guess). 17a-methylated steroids are much more resilient orally of course, though other methylations like 1a- and 3a- aren't necessarily so resilient. Also, with the morphine illustration again, the time to onset of effects is directly related to the route of administration and how fast 100% of it or 10% of it can reach the bloodstream, then opioid receptors, etc. And finally, the duration of effect of morphine is inversely related to how quickly it gets into the bloodstream.

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Peak effects generally are reached in 10 minutes with the intravenous route, 10-15 minutes after nasal insufflation (eg, butorphanol, heroin), 30-45 minutes with the intramuscular route, 90 minutes with the oral route, and 2-4 hours after dermal application (ie, fentanyl). Following therapeutic doses, most absorption occurs in the small intestine. Toxic doses may have delayed absorption because of delayed gastric emptying and slowed gut motility.

Most opioids are metabolized by hepatic conjugation to inactive compounds that are excreted readily in the urine. Certain opioids (eg, propoxyphene, fentanyl, buprenorphine) are more lipid soluble and can be stored in the fatty tissues of the body. All opioids have a prolonged duration of action in patients with liver disease (eg, cirrhosis) because of impaired hepatic metabolism. This may lead to drug accumulation and opioid toxicity.

Much of this isn't directly applicable to methylated steroids, but it is interesting to speculate that IM winstrol could possibly be acting like a "mini-depot" injection for lack of a better word due to its avoidance of first pass metabolism and entering the bloodstream before reaching the liver, and still being very resilient when it gets there due to 17a-methylation, etc. The "mini-depot" idea could explain why EOD injections are often used interchangeably with ED tabs. Again, just more speculation.

You have used both of them and are obviously quite knowledgable, so I don't question your opinion (I respect it).

My opinion (and it is just an opinion) is that based on anecdotal feedback from friends, some of Seth Roberts' comments in Anabolic Pharmacology regarding oral vs inject winstrol, and the article above, I am still inclined to believe that the injectable winstrol is more potent than the oral version (and possibly even a bit less strenuous on the liver, though I haven't read anything to substantiate that).

So back to Superdrone LV (lol), it seems like Trauma's got some 'splaining to do to let us know if any of that superdrol LV dose could possibly go directly into the bloodstream and avoid the first pass "gut metabolism" that a cap of superdrol would undergo in full (of course, there is microdrol-sublingual right? anybody try that?).

I am going to go out on a limb to answer one recurring question and say (speculatively) that no, 10mg of superdrol lv does not equal 30mg of superdrol caps. If there is a difference in end effects, it would be smaller than that.

Good discussion; I am learning quite a bit along the way.

 

[BigBlackGuy]

I have talked to Bill Roberts in the past about his 2-on 4-off cycle method. Here is the case study for reference: (cant link without 50 posts) mesomorphosis. com/articles/pharmacology/steroid-case-study-01.htm

You can see they have blood tests done on the "lab rat". Suppression had not begun, nor had liver damage, when the two weeks were up. In some cases (I believe it is mentioned in the above link) that his HPTA was upregulated after the 2 weeks, some kind of rebound effect. The above link also does not mention Superdrol or any other Sdrol clone.

Can this method be applied to Superdrol? Sure. Will it work? Maybe. You have to know how your body responds.

In reference to Unreal's comments about 2 weeks not being magical, he is right. Maybe 1 week and 6 days. Maybe 2 weeks and a day. The point is that 2 weeks worked. It isn't magical, not exact, but in the case above, yes it did work. That is the point. Bill has certainly never said anything like that either. I don't know of anyone else who supports 2-on 4-off.

Also, what is this 2-on 2-off? Is that even a real thing? Or do people just want fast results so they warp Bill's work? Although he HAS mentioned it, I don't think he has ever done a study on it. His recommendation is a 1-3 ratio of on and off. So don't expect to be on for half the year and be suppression/sides free.

As a side note, why would Sdrol be more suppressive than something like dbol? If taken at the correct effectiveness to dosage ratio... I feel as though Sdrol wouldn't be extra suppressive.

Bottom line? People seem to be wanting results too quickly. There's always a factor missing when people say that training, diet, and recovery are the only parts of the equation when it comes to building muscle and getting stronger. That factor is time!

 

[dumbhick3]

Also, what is this 2-on 2-off? Is that even a real thing?

I don't know where the 2 on/2 off idea came from myself; it seems like a hormonal rollercoaster, but that's just my opinion.

So don't expect to be on for half the year and be suppression/sides free.

Me and my nuts are tight, but I'd be most concerned about liver failure which I hear causes impotence and potentially death.

As a side note, why would Sdrol be more suppressive than something like dbol? If taken at the correct effectiveness to dosage ratio... I feel as though Sdrol wouldn't be extra suppressive.

Interesting question. My guess is that since neither has appreciable effects on the PR, superdrol may be more suppressive due to its dimethylation, differences in A:A ratios of 400:20 versus 90-210:40-60 which seem to pan out in real life and not just on paper (not a scientific answer I know), and anecdotal feedback on sdrol. Also, d-bol provides more androgenic support than sdrol by itself and via its highly androgenic 5AR metabolite M1T (900-1600:200-300). Bridging with low doses of d-bol is also not unheard of, so between d-bol and sdrol, I'd say that d-bol has more androgenic support and similarity to test than sdrol (so kind of a quasi-HRT effect). I don't know if anyone has gotten intracycle bloodwork done on superdrol though. I'd like to see some hormone values at 2, 3, or 4 weeks on cycle.

Taking the high dose approach, it seems anecdotally at least that 30mg/day of superdrol would be more suppressive than 100mg/day of d-bol, but I'm just speculating and still not really answering your question very well.

In this study, done in the early 80´s, a very high dose of Dbol (100mgs/day for 6 weeks) decreased plasma testosterone to about 40% of it´s normal value, plasma GH went up about a third, LH dropped to about 80% of it´s original value, and FSH went down about a third also (these are all approximate numbers, for the sake of brevity, but you get the idea). Body fat did not go up significantly and Fat Free Mass went up anywhere between 2-7kgs (3.3kgs average gain). The researchers concluded that Dbol increases Fat Free Mass as well as increasing strength and performance.

Clin Sci (Lond). 1981 Apr;60(4):457-61
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[BigBlackGuy]

I don't know where the 2 on/2 off idea came from myself; it seems like a hormonal rollercoaster, but that's just my opinion.

Agreed. I've only heard proposals for 2-on 2-off, never any that were completed. That's probably not a good sign.

Me and my nuts are tight, but I'd be most concerned about liver failure which I hear causes impotence and potentially death.

I think the liver failure is over stated. If every bad thing I heard about a steroid were true, half of this forum would be dead, not to mention there are tons of horrible clones being produced, along with the general disdain from the roid "vets" for designers.

Interesting question. My guess is that since neither has appreciable effects on the PR, superdrol may be more suppressive due to its dimethylation, differences in A:A ratios of 400:20 versus 90-210:40-60 which seem to pan out in real life and not just on paper (not a scientific answer I know), and anecdotal feedback on sdrol. Also, d-bol provides more androgenic support than sdrol by itself and via its highly androgenic 5AR metabolite M1T (900-1600:200-300). Bridging with low doses of d-bol is also not unheard of, so between d-bol and sdrol, I'd say that d-bol has more androgenic support and similarity to test than sdrol (so kind of a quasi-HRT effect). I don't know if anyone has gotten intracycle bloodwork done on superdrol though. I'd like to see some hormone values at 2, 3, or 4 weeks on cycle.

I didn't think about the ratio between Anabolic/Androgenic when I made the post. The ratio shows that Sdrol is going to better (anecdotally, of course) for retaining gains than Dbol, so if we talk strictly a Dbol only cycle (foolish, yes) or an Sdrol only cycle, Sdrol is probably going to come through. Of course, as you said Dbol is used generally for bridging, and it's rarely used alone.

Taking the high dose approach, it seems anecdotally at least that 30mg/day of superdrol would be more suppressive than 100mg/day of d-bol, but I'm just speculating and still not really answering your question very well.

True, I suppose it would have to be an issue of how long does it take to recover hormone levels compared to how well the gains last. If you do a dbol only cycle and gain 20 lbs, and recover fast, you might hold a decent amount of the gains. If you take sdrol and gain 20 pounds and dont recover quickly, even assuming sdrol is better for retaining gains innately, then you might not keep too much.