peterandrew
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Searching for the proper site for discussion hope this site would help me...
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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.
Pay attention, people. This is how scientists think.
Science is the process of hypothesis formation and testing with the purpose of trying to falsify the hypothesis.
Too many people come up with a story (not really a falsifiable hypothesis) and seek only to confirm it. That's how myths are made and propagated.
Hence, alot of bullshit made up in the steroid world.
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.
Thank you for the kind words!
The dopamine agonists such as Dostinex or pramipexole commonly increase libido for many people with or without anabolic steroid use.
They definitely merit consideration and where this works well, excellent! By no means am I knocking their use or their usefulness.
It's worth pointing out though they are drugs to be cautious with and overdoing definitely is not wise.
Thank you for the kind words!
The dopamine agonists such as Dostinex or pramipexole commonly increase libido for many people with or without anabolic steroid use.
They definitely merit consideration and where this works well, excellent! By no means am I knocking their use or their usefulness.
It's worth pointing out though they are drugs to be cautious with and overdoing definitely is not wise.
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
With pramipexole 0.5 mg/day seems a reasonable maximum, with some having room for a somewhat higher dose than this but if trying that I would do so only quite carefully.
I don't know if there are permanent issues from overdoing this drug but withdrawal can be difficult with sustained use particularly at higher dosages.
I haven't worked with these drugs long enough to have any worked-out protocols that I have confidence will cover the bases for everybody.
But basically for a reasonable-length steroid cycle such as 12 weeks or less -- but with no implication that somewhat more may be okay -- a dosage of 0.5 mg/day pramipexole seems to be easy to discontinue and generally to be a dosage without problems.
A dose can be recognized as being too high from symptoms of excessive somnolence (however, improved sleep can be a favorable side effect), dizziness, nausea, dry mouth, muscle spasms, bloating, fatigue, constipation, or addictive behaviors.
It is not a proven method but personally I like the idea and have used the principle of sometimes deliberately skipping a dosing to see if the system has become dependent on the drug. If no adverse symptom exists and it is also easy to skip a dose, then probably the dose is not too high.
All that said, still I have doubts, for most individuals anyway, about taking the dose past 0.75 mg/day. And just as a personal guess it would seem safest to me to cycle these drugs rather than to use them 365 days a year.
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.
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.)
Back to the conversation about hairloss.
Its my understanding that aas test is pretty much the same test that runs through all our bodies so if unless you're already having problems with hairloss, I dont think losing hair is somthing to worry about.
Bump for someone to correct me if im wrong
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.
ironmagazineforums.com/threads/108597-Is-Deca_Durabolin-Less-Likely-Than-Testosterone-to-Cause-Hair-Loss
wow. old post. heres another post. thank you google. first link. I think ive heard of this guy, and the source.
whatever. Ive got a full head of hair. barber always make a comment like, "wow, you got a full head of hair." no shit. you said that last time. I think he thinks, more hair, bigger tip .
I think there was a misprint in that article. said Deca was less Anabolic than Test. which is backwards.
there is no article, it a post, by Bill Roberts.
which has little to do on the subject of hair loss .