oral only gains (nark would you comment?)

[Manpretty]

why is it harder to keep gains from an oral only cycle?
is it something about the compound or the lenght of cycle?
any other reason?

ps im asking nark to comment becuase he usually uses scientific reasoning to back up what he is saying. id still love to hear from the rest of you (experience, studies you know of and so on)

manpretty

[Mista Massive]

you know you could do your own studies. the internet can search other things other than forums

[crash187ct]

you know you could do your own studies. the internet can search other things other than forums

that is a good point.

[Mista Massive]

that is a good point.

i thought so too

[Manpretty]

you know you could do your own studies. the internet can search other things other than forums

thanks for the very useful info massive you contributed to this thead immensly

[Mista Massive]

thanks for wasting ppl's time in posting threads which can easily be answered.

i wouldn't have said a thing if you hadn't kicked up such a stink in the other thread. you are doing the same thing here. expecting studies and proof on things you can very well obtain yourself.

[Liftnainez]

you know you could do your own studies. the internet can search other things other than forums

whats the point of the forum if all your answers are "look it up"
hes entitled to ask any question he wants? whats your problem?

[Liftnainez]

why is it harder to keep gains from an oral only cycle?
is it something about the compound or the lenght of cycle?
any other reason?

ps im asking nark to comment becuase he usually uses scientific reasoning to back up what he is saying. id still love to hear from the rest of you (experience, studies you know of and so on)

manpretty

its harder to keep and maitain gains from a test cycle then it is a var only IMO.. dont let these parrots fool or talk shit to you..

[Mista Massive]

I’m sure you know the difference between orals and injectables, but do yourself a favor and read this article, because I’m going to explain some things in here that you can use in your next cycle. Actually, I’m going to explain how you can use Winstrol (Stanozolol ) as either an oral or injectable, and get a very different set of effects from the same drug- depending on which route of administration you choose to utilize.

First, lets go over the basics of Winstrol, so we’re all on the same page here.

Winstrol is a steroid derived from the base structure of Dihydrotestosterone (DHT). DHT is just testosterone which has been 5alpha-reduced, meaning it has had the c4-5 double bond removed by two hydrogen atoms. This is very interesting from a chemical/biological standpoint. Once this bond is removed, testosterone has become DHT, and DHT is the body’s most potent androgen. DHT has a slew of beneficial effects which are more pronounced than the hormone it’s created out of. DHT is able to increase androgen receptor proliferation for almost 24 full hours (1) DHT also has profound effects on the Central Nervous System (CNS), and this is why we often see profoundly increased aggression with athletes who are using DHT derivatives such as Masteron (which has a deceivingly low anabolic and androgenic rating). As an added benefit, DHT can not aromatize (convert via the aromatase enzyme) into estrogen. It’s also noteworthy that the injectable version of Winstrol is actually the same exact thing as the oral- it’s just micronized Stanozolol powder suspended in water (or sometimes oil).

So what we have in Winstrol is DHT with two modifications- an added c17 methylation, and a very weird “pyrazol” group. The c17 methylation has been added in order to allow Winstrol to survive oral ingestion and the subsequent first pass through the liver. The pyrazol group is a bit weirder- what this means to you and I is that it has another whole “ring” attached to the four ring Steran Nucleus of DHT. Take a look over at the lower left portion of the two molecules below, and you’ll notice that Winstrol has an added cyclopentane (5 sided) group (the pyrazol group):


DHT Winstrol

When we really take a look at Winstrol, the anabolic rating of this product is very high (320% that of testosterone) as compared to its androgenic actions (30% of testosterone). Despite this, Winstrol is really a disappointing drug for size gains. What we typically see with this stuff is some pretty decent strength gains and some nice fat loss if the user isn’t too sloppy with their diet. Not many people report huge weight gains off of Stanozolol. Although many drugs which bind tightly to the androgen receptor are suspected to exhibit their at least some of their lipolytic (fat-burning) effects through receptor binding affinity. The effects of androgens on the regulation of lipolysis in adipose precursor cells.(2), Winstrol remains a potent cutting drug, despite the fact that it has a relatively weak AR binding ability (3). What this tells me is that there’s some stuff going on with regards to Winstrol’s mechanism of action, which doesn’t involve androgen receptor mediated effects. Still, Winstrol is a very potent compound for enhancing protein synthesis (4-5 ) .

As previously discussed, it’s derived from DHT, and DHT is known to have ant-estrogenic effects (6) and Winstrol itself also has anti-progestenic properties (in at least some cases, where it may "block" that receptor) (7). So I think it’s safe to say that some of the “hard” look you can get in your physique from Winstrol is because of it’s ability to inhibit estrogen and progesterone- known culprits in making a physique appear smooth. Unfortunately, since it is 17aa, it is also liver toxic, especially more so when you inject it and it is subject to what is known as the “first pass” through the liver. 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.





As you can surmise, a very large portion of the testosterone in your body is bound to SHBG. Wouldn’t it be great if we could lower SHBG? With Winstrol we can.

A fairly conservative oral dose of .2mg/kg of Winstrol has been shown to lower SHBG by close to 50%. (8)For me (200lbs) this would mean I would only need around 18mgs/day to free up half of my SHBG bound testosterone! For my omnipresent and hypothetical “100kg bodybuilder”- only 20mgs would be needed (he’s 220 lbs for the metrically impaired among us). Now, with less SHBG floating around in me, my anabolic steroid cycle will be more effective, right? Right.

But why can we only expect such a dramatic lowering of SHBG with the oral? Well, obviously, we’re taking advantage of the first pass through the liver, where we can have our Winstrol interact with SHBG where it’s produced- in the liver…without going through the bloodstream first.

When we take a look at a study done comparing injectable vs. oral contraceptives, we find that the oral version at 70mgs/week (10mgs/day given orally) is more effective at affecting SHBG levels than 400mgs/week given via an injection! (9)In this study, testosterone undecanoate was given at a constant dose along with norestisterone (which raises SHBG). What we see is that when norestisterone is given orally, it produces a far greater effect on SHBG, than when it is administered via an injection. And this is even when the doses of the injectable are 4x higher!

Here’s a chart, illustrating exactly what I’m talking about in this study, which I think suggests very strongly that injectable versions of drugs, when compared with the oral version, will have nowhere near as much of an effect on SHBG:



Group I (Black Circles): Injections of 200 mg NETE at study wk 0, 6, 12, and 18 plus injections of 1000 mg TU at study wk 2, 6, 12, and 18 (T free window). Group II (White Diamonds): Injections of 1000 mg TU together with 400 mg NETE at study wk 0, 6, 12, and 18. Group III (Grey Squares): Injections of 1000 mg TU at study wk 0, 6, 12, and 18 combined with daily oral 10 mg norethisterone acetate (NETE) from week 0 to 24 (9)

Of course, in this study, they’re looking at oral vs. injectable versions of a SHBG raising drug- but what we can take away from it is that SHBG interaction with oral compounds is far more pronounced than it is with injectables.

So lets take a small amount of Winstrol with our cycles, and free up some of those steroids we’re taking, right? Right!

Unless of course, we’re talking about women here…I was recently asked why I recommend that women use the injectable version of Winstrol over the oral. I was asked this question by someone, who I assumed had a female friend who was considering using Winstrol. I then realized I was totally incorrect- not about Winstrol, but about the reason behind the question. You see…I saw a picture of the man who had first asked me the question, and it’s readily apparent to me that he probably doesn’t actually know any women. But still, his question is valid and bears repeating and answering here.

I recommend that women avoid the oral version of this product for the same reason that men will find that it gives them an increased synergy and effectiveness in their cycles.

When SHBG is lowered in women, there is more free testosterone floating around. And as we’ve seen, the oral is going to affect SHBG exponentially more than the injectable will. When we lower SHBG too much in women, we see a strong positive correlation with hyperandrogenism (10 ), and hirsuitism (abnormal growth of body hair), as well In fact, non-SHBG-bound testosterone may actually be the defining characteristic for identifying hyperandrogenism in women. In addition, low SHBG contributes to menstrual irregularity.(11)

Finally, and (partially) anecdotally, we also see a greater incidence of clitoral enlargement and acne when the oral version of Winstrol is used by women instead of the injectable. The reasons for this are obvious- When we increase free testosterone by lowering SHBG, we increase the amount of testosterone which is able to be 5a-reduced to DHT. DHT is the primary culprit for steroid induced acne, and is also the hormone responsible for external genital enlargement. Clearly, this is why we see the increased level of clitoral hypertrophy as well as acne when oral Winstrol is used by women.

We can also see increased acne when men use Winstrol orally, but these effects are relatively minor when a 2mg/kg dose is being used to increase the effectiveness of other steroids in a cycle. This isn’t carte blanche to go using Winstrol for an extended period of time under the excuse that it’s increasing the overall effectiveness of the cycle. Stanozolol has some of the worst liver toxicity (hepatoxicity) of any oral steroid on a mg for mg basis. In addition, it’s deleterious effects on your lipid profile (Cholesterol) are also very pronounced, even at low doses- 6mgs/day of Stanozolol can lower HDL (good cholesterol)by 33% and raise LDL (bad cholesterol) by 29% (12 ).

So, hopefully, you’ve reached the end of this article and realized that Winstrol can be used in any cycle to increase the effectiveness of it, but that it must be used sparingly due to it’s possible hepatoxicity and lipid profile effecting properties. Still, when used in heavy testosterone-based profiles, at a dose that will cut your SHBG levels in half, it can increase you other steroids effectiveness quite a bit…but when maximal protein synthesis is wanted, you need to inject it.

[*Narkissos*]

thanks for wasting ppl's time in posting threads which can easily be answered.

I'm sure you have no idea what the answer is.. Or you would've probably attempted to answer it.

i wouldn't have said a thing if you hadn't kicked up such a stink in the other thread. you are doing the same thing here. expecting studies and proof on things you can very well obtain yourself.

If you have a personal problem with a poster...keep out of their threads.

It's that simple.

This isn't preschool.

[Mista Massive]

sorry the charts didn't work

[T3/T4 GSR]

Hell if your diet is good you can keep plenty of gains from a dbol only cycle ran with an AI. Dbol only is probably only the most popular cycle in the world so if it didn't work I doubt it would be so popular. As long as your diet and training are on point through PCT and beyond there is no reason to lose all your gains. Anyone who says otherwise has no idea wtf they are talking about.

[Mista Massive]

There you go…the differences between oral and injectable Winstrol , and how you can use either form to maximize your gains! And yes, Lyle, you can drink Winny.

References:

Neural Androgen Receptor Regulation: effects of androgen and antiandrogen. Lu S, Simon NG, Wang Y, Hu S, J Neurobiol 1999 Dec; 41(4):505-12
Endocrinology. 1990 Feb;126(2):1229-34. Xu X, De Pergola G, Bjorntorp P
Endocrinology. 1984 Jun;114(6):2100-6.
Can J Vet Res. 2000 Oct;64(4):246-8.
J Am Vet Med Assoc. 1997 Sep 15;211(6):719-22
MacDonald PC, Madden JD, Brenner PF, Wilson JD, Siiteri PK 1979 Origin of estrogen in normal men and in women with testicular feminization. J Clin Endocrinol Metab 49:905–916
Agents Actions. 1994 Mar;41(1-2):37-43.
Sex Hormone Binding Globulin response to the Anabolic steroid : Stanozolol : Evidence for its suitability as a Biological Androgen Sensitivity test. J Clin Metab Endocrinol 68: 1195, 1989)
The Journal of Clinical Endocrinology & Metabolism Vol. 87,No. 2 530-539. An Effective Hormonal Male Contraceptive Using Testosterone Undecanoate with Oral or Injectable Norethisterone Preparations Axel Kamischke, Tanja Heuermann, Kathrin Krüger, Sigrid von Eckardstein, Ilka Schellschmidt, Alexander Rübig and Eberhard Nieschlag Institute of Reproductive Medicine of the University (A.K., T.H., K.K., S.V.E., E.N.), D-48129 Münster, Germany; and Schering AG (I.S., A.R.), D-13342 Berlin, Germany
Non-sex hormone-binding globulin-bound testosterone as a marker for hyperandrogenism DC Cumming and SR Wall J. Clin. Endocrinol. Metab., Nov 1985; 61: 873 - 876.
Menstrual Irregularity in Women with Acr*****ly G. A. Kaltsas, J. J. Mukherjee, P. J. Jenkins, M. A. Satta, N. Islam, J. P. Monson, G. M. Besser, and A. B. GrossmanJ. Clin. Endocrinol. Metab., Aug 1999; 84: 2731 – 2735
JAMA. 1989 Feb 24;261(8):1165-8






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[*Narkissos*]

I’m sure you know the difference between orals and injectables, but do yourself a favor and read this article, because I’m going to explain some things in here that you can use in your next cycle. Actually, I’m going to explain how you can use Winstrol (Stanozolol ) as either an oral or injectable, and get a very different set of effects from the same drug- depending on which route of administration you choose to utilize.

First, lets go over the basics of Winstrol, so we’re all on the same page here.

Winstrol is a steroid derived from the base structure of Dihydrotestosterone (DHT). DHT is just testosterone which has been 5alpha-reduced, meaning it has had the c4-5 double bond removed by two hydrogen atoms. This is very interesting from a chemical/biological standpoint. Once this bond is removed, testosterone has become DHT, and DHT is the body’s most potent androgen. DHT has a slew of beneficial effects which are more pronounced than the hormone it’s created out of. DHT is able to increase androgen receptor proliferation for almost 24 full hours (1) DHT also has profound effects on the Central Nervous System (CNS), and this is why we often see profoundly increased aggression with athletes who are using DHT derivatives such as Masteron (which has a deceivingly low anabolic and androgenic rating). As an added benefit, DHT can not aromatize (convert via the aromatase enzyme) into estrogen. It’s also noteworthy that the injectable version of Winstrol is actually the same exact thing as the oral- it’s just micronized Stanozolol powder suspended in water (or sometimes oil).

So what we have in Winstrol is DHT with two modifications- an added c17 methylation, and a very weird “pyrazol” group. The c17 methylation has been added in order to allow Winstrol to survive oral ingestion and the subsequent first pass through the liver. The pyrazol group is a bit weirder- what this means to you and I is that it has another whole “ring” attached to the four ring Steran Nucleus of DHT. Take a look over at the lower left portion of the two molecules below, and you’ll notice that Winstrol has an added cyclopentane (5 sided) group (the pyrazol group):


DHT Winstrol

When we really take a look at Winstrol, the anabolic rating of this product is very high (320% that of testosterone) as compared to its androgenic actions (30% of testosterone). Despite this, Winstrol is really a disappointing drug for size gains. What we typically see with this stuff is some pretty decent strength gains and some nice fat loss if the user isn’t too sloppy with their diet. Not many people report huge weight gains off of Stanozolol. Although many drugs which bind tightly to the androgen receptor are suspected to exhibit their at least some of their lipolytic (fat-burning) effects through receptor binding affinity. The effects of androgens on the regulation of lipolysis in adipose precursor cells.(2), Winstrol remains a potent cutting drug, despite the fact that it has a relatively weak AR binding ability (3). What this tells me is that there’s some stuff going on with regards to Winstrol’s mechanism of action, which doesn’t involve androgen receptor mediated effects. Still, Winstrol is a very potent compound for enhancing protein synthesis (4-5 ) .

As previously discussed, it’s derived from DHT, and DHT is known to have ant-estrogenic effects (6) and Winstrol itself also has anti-progestenic properties (in at least some cases, where it may "block" that receptor) (7). So I think it’s safe to say that some of the “hard” look you can get in your physique from Winstrol is because of it’s ability to inhibit estrogen and progesterone- known culprits in making a physique appear smooth. Unfortunately, since it is 17aa, it is also liver toxic, especially more so when you inject it and it is subject to what is known as the “first pass” through the liver. 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.





As you can surmise, a very large portion of the testosterone in your body is bound to SHBG. Wouldn’t it be great if we could lower SHBG? With Winstrol we can.

A fairly conservative oral dose of .2mg/kg of Winstrol has been shown to lower SHBG by close to 50%. (8)For me (200lbs) this would mean I would only need around 18mgs/day to free up half of my SHBG bound testosterone! For my omnipresent and hypothetical “100kg bodybuilder”- only 20mgs would be needed (he’s 220 lbs for the metrically impaired among us). Now, with less SHBG floating around in me, my anabolic steroid cycle will be more effective, right? Right.

But why can we only expect such a dramatic lowering of SHBG with the oral? Well, obviously, we’re taking advantage of the first pass through the liver, where we can have our Winstrol interact with SHBG where it’s produced- in the liver…without going through the bloodstream first.

When we take a look at a study done comparing injectable vs. oral contraceptives, we find that the oral version at 70mgs/week (10mgs/day given orally) is more effective at affecting SHBG levels than 400mgs/week given via an injection! (9)In this study, testosterone undecanoate was given at a constant dose along with norestisterone (which raises SHBG). What we see is that when norestisterone is given orally, it produces a far greater effect on SHBG, than when it is administered via an injection. And this is even when the doses of the injectable are 4x higher!

Here’s a chart, illustrating exactly what I’m talking about in this study, which I think suggests very strongly that injectable versions of drugs, when compared with the oral version, will have nowhere near as much of an effect on SHBG:



Group I (Black Circles): Injections of 200 mg NETE at study wk 0, 6, 12, and 18 plus injections of 1000 mg TU at study wk 2, 6, 12, and 18 (T free window). Group II (White Diamonds): Injections of 1000 mg TU together with 400 mg NETE at study wk 0, 6, 12, and 18. Group III (Grey Squares): Injections of 1000 mg TU at study wk 0, 6, 12, and 18 combined with daily oral 10 mg norethisterone acetate (NETE) from week 0 to 24 (9)

Of course, in this study, they’re looking at oral vs. injectable versions of a SHBG raising drug- but what we can take away from it is that SHBG interaction with oral compounds is far more pronounced than it is with injectables.

So lets take a small amount of Winstrol with our cycles, and free up some of those steroids we’re taking, right? Right!

Unless of course, we’re talking about women here…I was recently asked why I recommend that women use the injectable version of Winstrol over the oral. I was asked this question by someone, who I assumed had a female friend who was considering using Winstrol. I then realized I was totally incorrect- not about Winstrol, but about the reason behind the question. You see…I saw a picture of the man who had first asked me the question, and it’s readily apparent to me that he probably doesn’t actually know any women. But still, his question is valid and bears repeating and answering here.

I recommend that women avoid the oral version of this product for the same reason that men will find that it gives them an increased synergy and effectiveness in their cycles.

When SHBG is lowered in women, there is more free testosterone floating around. And as we’ve seen, the oral is going to affect SHBG exponentially more than the injectable will. When we lower SHBG too much in women, we see a strong positive correlation with hyperandrogenism (10 ), and hirsuitism (abnormal growth of body hair), as well In fact, non-SHBG-bound testosterone may actually be the defining characteristic for identifying hyperandrogenism in women. In addition, low SHBG contributes to menstrual irregularity.(11)

Finally, and (partially) anecdotally, we also see a greater incidence of clitoral enlargement and acne when the oral version of Winstrol is used by women instead of the injectable. The reasons for this are obvious- When we increase free testosterone by lowering SHBG, we increase the amount of testosterone which is able to be 5a-reduced to DHT. DHT is the primary culprit for steroid induced acne, and is also the hormone responsible for external genital enlargement. Clearly, this is why we see the increased level of clitoral hypertrophy as well as acne when oral Winstrol is used by women.

We can also see increased acne when men use Winstrol orally, but these effects are relatively minor when a 2mg/kg dose is being used to increase the effectiveness of other steroids in a cycle. This isn’t carte blanche to go using Winstrol for an extended period of time under the excuse that it’s increasing the overall effectiveness of the cycle. Stanozolol has some of the worst liver toxicity (hepatoxicity) of any oral steroid on a mg for mg basis. In addition, it’s deleterious effects on your lipid profile (Cholesterol) are also very pronounced, even at low doses- 6mgs/day of Stanozolol can lower HDL (good cholesterol)by 33% and raise LDL (bad cholesterol) by 29% (12 ).

So, hopefully, you’ve reached the end of this article and realized that Winstrol can be used in any cycle to increase the effectiveness of it, but that it must be used sparingly due to it’s possible hepatoxicity and lipid profile effecting properties. Still, when used in heavy testosterone-based profiles, at a dose that will cut your SHBG levels in half, it can increase you other steroids effectiveness quite a bit…but when maximal protein synthesis is wanted, you need to inject it.

And this has no relevance here.

[*Narkissos*]

why is it harder to keep gains from an oral only cycle?
is it something about the compound or the lenght of cycle?
any other reason?

ps im asking nark to comment becuase he usually uses scientific reasoning to back up what he is saying. id still love to hear from the rest of you (experience, studies you know of and so on)

manpretty

Personally i don't think gains are harder to keep with orals vs injectables.

First off, in answering this question, one must realise that it isn't that straight foward of a question.

Because different orals have different mechanisms of action.. etc.

First off, one must define 'gains'.

As the message board community usually equates 'gains' with an amalgamation of LBM; fat; and water weight.. which is wrong.

LBM is our major concern ...not fat nor water weight.

Honestly i couldn't see why it'd be harder to maintain LBM gained from orals v.s. LBM gained from injectables.

e.g. How many guys do you know who post-cessation of a tbol; var; or wintrol-only cycle reported that they lost everything?

[T3/T4 GSR]

The only reason people who do oral only cycles report more lost gains are due to the fact that by nature people who wont inject are usually not as dedicated and knowledgable and tend to skip PCT and have crap diets that depend on drugs to get them a little bigger and cause a lot of fake gains through water retention.

[*Narkissos*]

Personally i don't think gains are harder to keep with orals vs injectables.

First off, in answering this question, one must realise that it isn't that straight foward of a question.

Because different orals have different mechanisms of action.. etc.

First off, one must define 'gains'.

As the message board community usually equates 'gains' with an amalgamation of LBM; fat; and water weight.. which is wrong.

LBM is our major concern ...not fat nor water weight.

Honestly i couldn't see why it'd be harder to maintain LBM gained from orals v.s. LBM gained from injectables.

e.g. How many guys do you know who post-cessation of a tbol; var; or wintrol-only cycle reported that they lost everything?

Further the above is an oversimplified explanation.

The nature of the cycle must be taken into account.

e.g. On another board Ross and Bajanbastard were were having an argument on cycling. Bajan actually proposed that dbol for example, a drug normally flamed as just minimally muscle-building, might be more productive on a longer run... 10 weeks or so (at a lower dose)... like how the older BBs used to run it.

The limiting factor for more oral only cycles are dosage; and duration... v.s. potential for side effects.

So honestly i think the opening question/hypothesis is flawed.. as in the pure sense keeping LBM is a matter of PCT (gonadal stimulation; cortisol modulation etc.)..and not a matter of keepability via compound used.

I think also injectable cycles are perceived as having a higher propensity for kept gains... namely because overall gross gains are higher with injectable cycles... thus net keepability may be higher because there is simply more net muscle gained.

e.g. 8-12 weeks on winstrol only = 10 lbs lbm
16 weeks on test + tren = 25 lbs lbm

for example.

Post-pct

winstrol only cycle = 8 lbs kept
test + tren cycle= 18 lbs kept.

Cycle B would be perceived as having higher keepability (even tho net loss and the percentage of gross gains loss is higher)... simply because 18 lbs is more perceviably physique changing than 8 lbs.

Nark

p.s. this too is an oversimplification

[Manpretty]

The only reason people who do oral only cycles report more lost gains are due to the fact that by nature people who wont inject are usually not as dedicated and knowledgable and tend to skip PCT and have crap diets that depend on drugs to get them a little bigger and cause a lot of fake gains through water retention.

yeah this it probably true for most people ......i like to think of an oral only cycle an intro to injects.....personally im just finishing an oral only cycle made good gains to boot....i plan on doing inject in the future just wanted to see how my body would react to AAS in general before i start jabbing

[Manpretty]

Further the above is an oversimplified explanation.

The nature of the cycle must be taken into account.

e.g. On another board Ross and Bajanbastard were were having an argument on cycling. Bajan actually proposed that dbol for example, a drug normally flamed as just minimally muscle-building, might be more productive on a longer run... 10 weeks or so (at a lower dose)... like how the older BBs used to run it.

The limiting factor for more oral only cycles are dosage; and duration... v.s. potential for side effects.

So honestly i think the opening question/hypothesis is flawed.. as in the pure sense keeping LBM is a matter of PCT (gonadal stimulation; cortisol modulation etc.)..and not a matter of keepability via compound used.

I think also injectable cycles are perceived as having a higher propensity for kept gains... namely because overall gross gains are higher with injectable cycles... thus net keepability may be higher because there is simply more net muscle gained.

e.g. 8-12 weeks on winstrol only = 10 lbs lbm
16 weeks on test + tren = 25 lbs lbm

for example.

Post-pct

winstrol only cycle = 8 lbs kept
test + tren cycle= 18 lbs kept.

Cycle B would be perceived as having higher keepability (even tho net loss and the percentage of gross gains loss is higher)... simply because 18 lbs is more perceviably physique changing than 8 lbs.

Nark

p.s. this too is an oversimplification

nice this is the sort of anwser i was looking for....and i know it is over simplified..and im sure there are still factors that can be argued.. but for me it lays to rest "injects in every cycle" thinking

[*Narkissos*]

^^ np.

I don't think it lays to rest anything per se.. just pokes a hole in a fallacy used as the main argument on message boards.

"Don't do an oral-only cycle bro.. you'll lose everything!!"



Honestly, everyone's goals may differ.

So each cycle regime has its place.

[G-1000]

None of this stuff is cut and dry. There has to be 1000o facters that take place.

[G-1000]

You have to see how your body responds to each compound. Every one is diffrent.

[Mista Massive]

You have to see how your body responds to each compound. Every one is diffrent.

agreed

[guest589745]

I’m sure you know the difference between orals and injectables, but do yourself a favor and read this article, because I’m going to explain some things in here that you can use in your next cycle. Actually, I’m going to explain how you can use Winstrol (Stanozolol ) as either an oral or injectable, and get a very different set of effects from the same drug- depending on which route of administration you choose to utilize.

First, lets go over the basics of Winstrol, so we’re all on the same page here.

Winstrol is a steroid derived from the base structure of Dihydrotestosterone (DHT). DHT is just testosterone which has been 5alpha-reduced, meaning it has had the c4-5 double bond removed by two hydrogen atoms. This is very interesting from a chemical/biological standpoint. Once this bond is removed, testosterone has become DHT, and DHT is the body’s most potent androgen. DHT has a slew of beneficial effects which are more pronounced than the hormone it’s created out of. DHT is able to increase androgen receptor proliferation for almost 24 full hours (1) DHT also has profound effects on the Central Nervous System (CNS), and this is why we often see profoundly increased aggression with athletes who are using DHT derivatives such as Masteron (which has a deceivingly low anabolic and androgenic rating). As an added benefit, DHT can not aromatize (convert via the aromatase enzyme) into estrogen. It’s also noteworthy that the injectable version of Winstrol is actually the same exact thing as the oral- it’s just micronized Stanozolol powder suspended in water (or sometimes oil).

So what we have in Winstrol is DHT with two modifications- an added c17 methylation, and a very weird “pyrazol” group. The c17 methylation has been added in order to allow Winstrol to survive oral ingestion and the subsequent first pass through the liver. The pyrazol group is a bit weirder- what this means to you and I is that it has another whole “ring” attached to the four ring Steran Nucleus of DHT. Take a look over at the lower left portion of the two molecules below, and you’ll notice that Winstrol has an added cyclopentane (5 sided) group (the pyrazol group):


DHT Winstrol

When we really take a look at Winstrol, the anabolic rating of this product is very high (320% that of testosterone) as compared to its androgenic actions (30% of testosterone). Despite this, Winstrol is really a disappointing drug for size gains. What we typically see with this stuff is some pretty decent strength gains and some nice fat loss if the user isn’t too sloppy with their diet. Not many people report huge weight gains off of Stanozolol. Although many drugs which bind tightly to the androgen receptor are suspected to exhibit their at least some of their lipolytic (fat-burning) effects through receptor binding affinity. The effects of androgens on the regulation of lipolysis in adipose precursor cells.(2), Winstrol remains a potent cutting drug, despite the fact that it has a relatively weak AR binding ability (3). What this tells me is that there’s some stuff going on with regards to Winstrol’s mechanism of action, which doesn’t involve androgen receptor mediated effects. Still, Winstrol is a very potent compound for enhancing protein synthesis (4-5 ) .

As previously discussed, it’s derived from DHT, and DHT is known to have ant-estrogenic effects (6) and Winstrol itself also has anti-progestenic properties (in at least some cases, where it may "block" that receptor) (7). So I think it’s safe to say that some of the “hard” look you can get in your physique from Winstrol is because of it’s ability to inhibit estrogen and progesterone- known culprits in making a physique appear smooth. Unfortunately, since it is 17aa, it is also liver toxic, especially more so when you inject it and it is subject to what is known as the “first pass” through the liver. 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.





As you can surmise, a very large portion of the testosterone in your body is bound to SHBG. Wouldn’t it be great if we could lower SHBG? With Winstrol we can.

A fairly conservative oral dose of .2mg/kg of Winstrol has been shown to lower SHBG by close to 50%. (8)For me (200lbs) this would mean I would only need around 18mgs/day to free up half of my SHBG bound testosterone! For my omnipresent and hypothetical “100kg bodybuilder”- only 20mgs would be needed (he’s 220 lbs for the metrically impaired among us). Now, with less SHBG floating around in me, my anabolic steroid cycle will be more effective, right? Right.

But why can we only expect such a dramatic lowering of SHBG with the oral? Well, obviously, we’re taking advantage of the first pass through the liver, where we can have our Winstrol interact with SHBG where it’s produced- in the liver…without going through the bloodstream first.

When we take a look at a study done comparing injectable vs. oral contraceptives, we find that the oral version at 70mgs/week (10mgs/day given orally) is more effective at affecting SHBG levels than 400mgs/week given via an injection! (9)In this study, testosterone undecanoate was given at a constant dose along with norestisterone (which raises SHBG). What we see is that when norestisterone is given orally, it produces a far greater effect on SHBG, than when it is administered via an injection. And this is even when the doses of the injectable are 4x higher!

Here’s a chart, illustrating exactly what I’m talking about in this study, which I think suggests very strongly that injectable versions of drugs, when compared with the oral version, will have nowhere near as much of an effect on SHBG:



Group I (Black Circles): Injections of 200 mg NETE at study wk 0, 6, 12, and 18 plus injections of 1000 mg TU at study wk 2, 6, 12, and 18 (T free window). Group II (White Diamonds): Injections of 1000 mg TU together with 400 mg NETE at study wk 0, 6, 12, and 18. Group III (Grey Squares): Injections of 1000 mg TU at study wk 0, 6, 12, and 18 combined with daily oral 10 mg norethisterone acetate (NETE) from week 0 to 24 (9)

Of course, in this study, they’re looking at oral vs. injectable versions of a SHBG raising drug- but what we can take away from it is that SHBG interaction with oral compounds is far more pronounced than it is with injectables.

So lets take a small amount of Winstrol with our cycles, and free up some of those steroids we’re taking, right? Right!

Unless of course, we’re talking about women here…I was recently asked why I recommend that women use the injectable version of Winstrol over the oral. I was asked this question by someone, who I assumed had a female friend who was considering using Winstrol. I then realized I was totally incorrect- not about Winstrol, but about the reason behind the question. You see…I saw a picture of the man who had first asked me the question, and it’s readily apparent to me that he probably doesn’t actually know any women. But still, his question is valid and bears repeating and answering here.

I recommend that women avoid the oral version of this product for the same reason that men will find that it gives them an increased synergy and effectiveness in their cycles.

When SHBG is lowered in women, there is more free testosterone floating around. And as we’ve seen, the oral is going to affect SHBG exponentially more than the injectable will. When we lower SHBG too much in women, we see a strong positive correlation with hyperandrogenism (10 ), and hirsuitism (abnormal growth of body hair), as well In fact, non-SHBG-bound testosterone may actually be the defining characteristic for identifying hyperandrogenism in women. In addition, low SHBG contributes to menstrual irregularity.(11)

Finally, and (partially) anecdotally, we also see a greater incidence of clitoral enlargement and acne when the oral version of Winstrol is used by women instead of the injectable. The reasons for this are obvious- When we increase free testosterone by lowering SHBG, we increase the amount of testosterone which is able to be 5a-reduced to DHT. DHT is the primary culprit for steroid induced acne, and is also the hormone responsible for external genital enlargement. Clearly, this is why we see the increased level of clitoral hypertrophy as well as acne when oral Winstrol is used by women.

We can also see increased acne when men use Winstrol orally, but these effects are relatively minor when a 2mg/kg dose is being used to increase the effectiveness of other steroids in a cycle. This isn’t carte blanche to go using Winstrol for an extended period of time under the excuse that it’s increasing the overall effectiveness of the cycle. Stanozolol has some of the worst liver toxicity (hepatoxicity) of any oral steroid on a mg for mg basis. In addition, it’s deleterious effects on your lipid profile (Cholesterol) are also very pronounced, even at low doses- 6mgs/day of Stanozolol can lower HDL (good cholesterol)by 33% and raise LDL (bad cholesterol) by 29% (12 ).

So, hopefully, you’ve reached the end of this article and realized that Winstrol can be used in any cycle to increase the effectiveness of it, but that it must be used sparingly due to it’s possible hepatoxicity and lipid profile effecting properties. Still, when used in heavy testosterone-based profiles, at a dose that will cut your SHBG levels in half, it can increase you other steroids effectiveness quite a bit…but when maximal protein synthesis is wanted, you need to inject it.

Nice copy and paste

[guest589745]

e.g. On another board Ross and Bajanbastard were were having an argument on cycling. Bajan actually proposed that dbol for example, a drug normally flamed as just minimally muscle-building, might be more productive on a longer run... 10 weeks or so (at a lower dose)... like how the older BBs used to run it.

Could you PM me where this thread is if you have a spare moment ?

[Liftnainez]

^^ np.

I don't think it lays to rest anything per se.. just pokes a hole in a fallacy used as the main argument on message boards.

"Don't do an oral-only cycle bro.. you'll lose everything!!"



Honestly, everyone's goals may differ.

So each cycle regime has its place.

this is my point that I always try to get across.. I couldnt agree more bro

[evil pepsi]

man, must you guys quote the entire article? thats a lot of stuff to continually scroll through to get to the next post...

[BajanBastard]

Could you PM me where this thread is if you have a spare moment ?

It's on IFL.

[guest589745]

It's on IFL.

Alright. Coo.