Anabolic/Androgenic Ratios

[KBD]

Lets get this out here, so alot of idiots realize what they are dealing with.

Anadrol 50:
Androgenic: Anabolic Ratio: 45:320

Anavar:
Anabolic/Androgenic Ratio (Range): 322-630:24

Androil:
Anabolic/Androgenic Ratio (Range): 100:100

Andropen 275:
Anabolic/Androgenic Ratio (Range):100:100

Deca-Durabolin:
Anabolic/Androgenic ratio: 125:37

Dianabol:
Anabolic/Androgenic Ratio (Range): 90-210:40-60

Equipoise:
Anabolic/ Androgenic ratio: 100:50

Halotestin:
Anabolic/Androgenic ratio:1,900/850

Masteron:
Anabolic/Androgenic Ratio:62:25

NPP:
Androgenic/Anabolic ratio: 37:125

Omnadren:
Anabolic/Androgenic Ratio: 100:100

Oral Turnibol:
Anabolic/ Androgenic ratio: >100:>0

Parabolan (Tren):
Anabolic/Androgenic ratio: 500/500

Primobolan:
Anabolic/Androgenic Ratio (Range): 88:44-57

Proviron:
Androgenic: Anabolic Ratio:30-40/100-150

Sustanon 250:
Anabolic/Androgenic ratio:100/100

Testosterone Cyp, Enanthate, Prop, Suspension
Anabolic/Androgenic ratio:100/100

Winstrol:
Androgenic/Anabolic Ratio:30:320

 

[Bill Roberts]

What these numbers specify is the measured ratio of growth in rats of the levator ani muscle versus the prostate.

The levator ani is not a skeletal muscle, but is analogous to the human PCG muscle. It really is not a good assay for effect on skeletal muscle.

And prostate growth is of course a measurement only of that particular possible side effect. In rats.

So perhaps the reason that "anabolic/androgenic ratios" are useless in bb'ing is because they are derived from measurements which aren't useful: that is to say, they aren't good predictors.

There was a Russian protocol that actually may have been useful -- would have had a better chance, anyway, I think -- where anabolic effect was assayed by means of evaluating growth of the exercise-stimulated soleus muscle in rats. The soleus was stimulated by means of cutting the gastrocnemius while still in some way requiring the rats to walk or run, forcing the soleus to carry the entire load.

But I've never seen data from these measurements.

 

[Lizard King]

I believe you were just owned by Bill Roberts.

 

[KBD]

I believe you were just owned by Bill Roberts.

Thats ok i just gathered useful information. Sorry we cant all be right all the time like "the Great Lizard King"...

But the point of this thread was to show that most AAS are androgenic. Which can lead to hairloss

In which IronCore does not believe, hence his dbol comment on my last thread.

Dbol can cause hairloss because of it being androgenic, but i didnt expect him to know that.

Anyways Thanks Bill roberts

We all make mistakes. Glad you corrected me

 

[Bill Roberts]

Really I didn't view it as "correction" -- there is nothing wrong with having the numbers. Rather it was bringing out what the numbers are.

Your point that every anabolic steroid is androgenic is absolutely correct. This is why there is no anabolic steroid that doesn't at some dose have virilization risk for women, for example.

 

[KBD]

Really I didn't view it as "correction" -- there is nothing wrong with having the numbers. Rather it was bringing out what the numbers are.

Your point that every anabolic steroid is androgenic is absolutely correct. This is why there is no anabolic steroid that doesn't at some dose have virilization risk for women, for example.

So then you agree that any Androgenic steroid CAN cause hair loss. correct?

 

[Bill Roberts]

My understanding is that any anabolic steroid at anabolically quite-effective dosages can promote hair loss in individuals susceptible to male pattern baldness.

Testosterone is a worse offender than the synthetics in general, but I think any anabolic steroid can do it. But some will allow a higher mg/week amount, for any given risk to the hair, than testosterone allows. It isn't an exact science though. In principle it could be, with suitable studies, but I don't think that's ever been done and it would be unlikely to be done today. It would be hard to obtain Independent Review Board approval -- probably impossible -- for administering "health risking" doses of trenbolone, Dianabol, and various other anabolic steroids to see how they compared with each other for hair loss effect.

And it seems too hard to pick out subtle differences from informal observation. Even the same individual following the same protocol can have different results in different cycles. One of them can have a hair-shedding phase (not actual permanent hair loss) and the other can happen not to have it. If the person had done only one of those cycles, he'd come to quite different conclusions purely from chance. So it is hard to say, except broadly that testosterone is a worse offender or at least somewhat worse offender than others, for anabolically-comparable dosages.

 

[KBD]

My understanding is that any anabolic steroid at anabolically quite-effective dosages can promote hair loss in individuals susceptible to male pattern baldness.

Testosterone is a worse offender than the synthetics in general, but I think any anabolic steroid can do it. But some will allow a higher mg/week amount, for any given risk to the hair, than testosterone allows. It isn't an exact science though. In principle it could be, with suitable studies, but I don't think that's ever been done and it would be unlikely to be done today.

So lets say, we compare deca to test in hairloss..

Test is going to have a much more dramatic effect correct?

 

[Bill Roberts]

For anabolically equivalent dosages and for individuals susceptible to male pattern baldness, generally yes, except sometimes such an individual will get away with effective high dose testosterone use with no apparent post-cycle difference, and so in those cases, there's no way to be dramatically better than that.

(In this example we know the individual is susceptible to MPB because of already having started losing hair simply from natural testosterone.)

 

[KBD]

For anabolically equivalent dosages and for individuals susceptible to male pattern baldness, generally yes, except sometimes such an individual will get away with effective high dose testosterone use with no apparent post-cycle difference, and so in those cases, there's no way to be dramatically better than that.

(In this example we know the individual is susceptible to MPB because of already having started losing hair simply from natural testosterone.)

So if one were to use a topical anti-androgen such as Spiro with testosterone at a low dose, than hair loss effects should be somewhat inhibited?

 

[Bill Roberts]

So if one were to use a topical anti-androgen such as Spiro with testosterone at a low dose, than hair loss effects should be somewhat inhibited?

Yes.

Spironolactone smells bad, though.

 

[KBD]

Yes.

Spironolactone smells bad, though.

So i hear.. Lol

 

[ergomaniac]

nandrolone should be good as ists less androgenic than test or dht and so should their derivatives. thats because it is metabolized into a less potent structure, dihydronandrolone. test into dht and dht, just dht. and alterations to structue seem to be geared towards less androgenic or estrogenic effects. pun intended. more muscle building is what we want. hence sarms. they have selectivitey. seems like everything theres a ying and a yang. dihydronandrolone i think is why you get deca dick, and why everyone runs test with everything.

 

[Bill Roberts]

Hirshberg, the developer of the above-described assay measuring "anabolic/androgenic ratio," certainly hoped it would be useful and it was certainly reasonable science to try such things.

And indeed the developers of anabolic steroids did use these ratios as (supposed) indicators of success in separating therapeutic effect from undesired side effects, but as it happened NO MATTER WHAT THEY DID the result was virtually always much "better" than testosterone.

Actually what was happening is that most compounds don't metabolize via 5-AR to a more potent substance.

So it wasn't really that side effects in general were being minimized by increase in anabolic/androgenic ratio, but rather that in almost all cases such metabolism was abolished. Really it wasn't ratios involved so much as it was an either/or matter with regard to metabolism.

 

[KBD]

nandrolone should be good as ists less androgenic than test or dht and so should their derivatives. thats because it is metabolized into a less potent structure, dihydronandrolone. test into dht and dht, just dht. and alterations to structue seem to be geared towards less androgenic or estrogenic effects. pun intended. more muscle building is what we want. hence sarms. they have selectivitey. seems like everything theres a ying and a yang. dihydronandrolone i think is why you get deca dick, and why everyone runs test with everything.

Deca dick is caused by a rise in prolactin levels.

 

[Reinheart]

Deca dick is caused by a rise in prolactin levels.

Yes and one can avoid this side effect by inducing Dostinex to his cycle.

 

[IronCore]

or prami...

 

[Bill Roberts]

Deca dick is caused by a rise in prolactin levels.

The problem with this is that it is from no evidence. It's the kind of statement that if true would be quite provable: prolactin is measurable.

The one study I've read that reported prolactin levels with anabolic steroid usage showed approximately the same results for testosterone and nandrolone both for average increase in prolactin levels and percent of individuals showing any increase. (I don't, unfortunately, still have the study and I've found it hard to find again, but it quite definitely exists.)

The dopamine agonists are prosexual for many individuals even where there is no prolactin problem, so an improvement in libido with these drugs does not prove that prolactin was the cause of the poor libido.

It is true that high prolactin can yield low libido.

But it's not proven that this is the cause of Deca's unusual unfavorableness in this regard: if it were, testosterone should be about as bad a culprit because it too often increases prolactin and by about as much.

(Most likely via increase in estrogen.)

 

[Jeton]

The problem with this is that it is from no evidence. It's the kind of statement that if true would be quite provable: prolactin is measurable.

The one study I've read that reported prolactin levels with anabolic steroid usage showed approximately the same results for testosterone and nandrolone both for average increase in prolactin levels and percent of individuals showing any increase. (I don't, unfortunately, still have the study and I've found it hard to find again, but it quite definitely exists.)

The dopamine agonists are prosexual for many individuals even where there is no prolactin problem, so an improvement in libido with these drugs does not prove that prolactin was the cause of the poor libido.

It is true that high prolactin can yield low libido.

But it's not proven that this is the cause of Deca's unusual unfavorableness in this regard: if it were, testosterone should be about as bad a culprit because it too often increases prolactin and by about as much.

(Most likely via increase in estrogen.)

well that's certainly very interesting, bcuz i'd come to believe prolactin as the deca-dick culprit based on my own experiences compared with those of others...specifically, being on 200-400mg of deca continuously from 4/07 to summer 09 put me in a state where it took a fairly long time to orgasm during intercourse...my body "felt" like i was in a refractive state, as if i'd just ejaculated, so "no need" to orgasm. however, keeping at it every produced exhausted and sore partners, and a generally cataclysmic orgasm on my part.

thing is, i've always been multi-orgasmic...as a young teen i basically trained myself to be that way, so the sense of "i've cum already" wasn't a total roadblock for me. in contrast, "one shot and i'm going to sleep" guys i know who go on deca awhile get get it up at all, as if they shot their wad n were done for the nite.

i came to this conclusion BEFORE i knew about the deca-prolactin popular wisdom (which i read of here on meso), so coming across this common belief made perfect sense to me.

incidentally, now i cycle deca off-longer-than-on, n i can shoot in 5 minutes or less if i need to.

still, i guess the Mystery Of Deca-Dick continues...opcorn:

 

[Bill Roberts]

Yes, it's a mystery because the claims for this mechanism don't have any evidence to support the theory.

What would be good evidence would be if an author or researcher found that everyone or nearly everyone studied who has the complaint with Deca indeed had high prolactin, whereas among the Deca users -- which is about half or two-thirds -- that don't have high prolactin, none or nearly none had the complaint.

Then we could say that among the Deca users the problem is correlated with prolactin.

But generally the claims of "high prolactin" are made without even a measurement of prolactin.

We don't know that the many Deca users claiming "high prolactin" is causing their problem actually have high prolactin, or that if they do, that the prolactin alone is the full or even primary cause for their low libido, as testosterone users often have raised prolactin but still good libido.

And it would remain a mystery how it is that similarly high prolactin from testosterone use doesn't cause the same problem.

Just as, for example, an anabolic steroid can as a side effect interact with glucocorticoid receptors, an anabolic steroid can also interact with receptors in the brain such as the GABA receptor. An apparent example in my experience was that 17b-hydroxyandrost-1-ene-3-one (popularly known as "1-testosterone" though it's a misnomer) proved in a product I developed back in 2002 or so, which delivered a very large amount of it, to be able to cause fairly black depression. Pretty awful.

On the theory that the cause might be allopregnanolone-like activity in the brain, I included pregnenolone in the product, which is an antagonist to that effect.

Problem solved. There wasn't a single reported customer complaint about effect on mood.

Now that doesn't prove that the steroid actually had allopregnanolone-like activity but it is at least consistent with it.

It might be that nandrolone has a neurosteroid-like activity, or antagonist activity, that is anti-sexual. It's as good a theory as any -- no evidence behind it, but neither is there for the prolactin theory. But at least it doesn't have the inconsistency problem that the prolactin theory has, the inconsistency being that testosterone has similar prolactin-raising properties but doesn't have the same tendency to reduce libido.

So it's a mystery, to date.