Interesting Thought on D-bol

Drveejay11

I am banned!
(By Andy13....and 2 other people that responded with intelligent remarks)

Dbol during first few weeks of a cycle.
1. A lot of guys will take dbol for (only) the first 2,3,4 weeks in a cycle. This is very popular, but what is the reasoning behind this type of plan?

This could be an effort to minimize toxicity associated with the compound, although I see doses >50mg/day being used. If this is the case, I don't think there would be much difference (as far as toxicity) in taking 50mg/day for 4 weeks or 25mg/day for 8 weeks. In fact, the longer, lesser dose may be less toxic.

The second reason for this type of dosing would be to "kick start" a cycle..

I don't think taking dbol in the beginning of a cycle is nearly as effective as font end loading injectables..

Here's why. Dbol is a poor AR agonist. It's primary mode of action is unknown... Everyone agrees that a "dbol only" cycle is near worthless, right? That's because the 'unknown' muscle building effects of dbol allegedly occur outside the AR and are supposedly "synergystic" with strong AR binders. So using dbol early in the cycle until injectables are built up to maximal theraputic blood concentration is a lot like doing a dbol only cycle for the first few weeks. So, in all actuality, the dbol is not really "kick starting" your cycle. To really kick start your cycle, you need to load your injectables.

If dbol is alleged to be synergystic with AR binding androgens, why not take dbol for the full 8 weeks?

-Andy13


RESPONSE #1:
A lot of "experts" feel that b-bol is actually pretty damn benign from a hepatotoxicity standpoint.From what I've gathered,if there happens to be any liver strain,damage or whatever it is almost always totally reversible upon discontinuation.
A russian friend translated the package insert that follows with the russian dbol and therapeutic dosage was up to 50mg for 8 weeks.It also said "large overdoses over long periods of time may cause jaundice but is totally reversible upon discontinuation".

The whole hepatotoxicity issue is debated alot.The potential is real but probably overstated,IMO.I have several friends who have ingested gross overdosages of dbol,like 40-50 tabs per day or 2000 pinks over a 12 weeks stack and none of them seem to have gotten liver damage.Enzymes have been normal several weeks after the cycle.
1. http://magazine.mindandmuscle.net/p...ID=84&issueID=8

RESPONSE #2:

I think oral toxicity is overrated. I read a study about anadrol, the supposed most toxic of them all. It was done on elderly men, ages 65-80. They were divided into 3 groups. One placebo, one 50mg ed, and one 100mg ed. In 6 weeks, there were no siginifigant changes in PSA, total or LDL chloresterol levels, or fasting triglycerides. However in the 50 and 100mg groups, HDL chloresterol was reduced by 19 and 23 points respectively. Liver values increased only in the 100mg group(transaminases AST and ALT), but they were not dramatic, and not accompanied by hepatic enlargement or the development of a serious liver condition.

refs cited:
Effects of oral androgens on muscle and metabolism in older, community-dwelling men. Schroeder et al. A, J Physiol Endocrinal Metab 284: E120-28
 
Good post Bro, I've heard a 17aa is good to have in your cycle when using hgh. Any thoughts on that. I'm tring to get all the info I can.

Thanks Bro
JohnnyB
 
17aa's useful during HGH cycling... i think the reason may have something to do with oral meds causing increased IGF output from the liver.

I remember reading this about Winstrol (winny). Not sure if this is the relation though?????
 
rj420 said:
17aa's useful during HGH cycling... i think the reason may have something to do with oral meds causing increased IGF output from the liver.

I remember reading this about Winstrol (winny). Not sure if this is the relation though?????
I thought I remembered reading somewhere, that d-bol helped. But maybe it was Winstrol (winny), I know it was a 17aa, I can remember that:p

JohnnyB
 
JohnnyB said:
Good post Bro, I've heard a 17aa is good to have in your cycle when using hgh. Any thoughts on that. I'm tring to get all the info I can.

Thanks Bro
JohnnyB

Hmmmmmm....I wish I could help here bro..........rj420 brings up an interesting "theory"?!?!

Maybe HHajdo will chime in soon...............
 
yes, becuase as they make two passes thru the liver, it increase igf-1 release, and this is what you are after when using GH, igf-1 release
 
iced said:
yes, becuase as they make two passes thru the liver, it increase igf-1 release, and this is what you are after when using GH, igf-1 release
Would 10-20mg do the trick?

JohnnyB
 
DRveejay11 said:
Hmmmmmm....I wish I could help here bro..........rj420 brings up an interesting "theory"?!?!

Maybe HHajdo will chime in soon...............
I you you would if you could Bro;)

JohnnyB
 
of dbol? i would imagine, also the higher the GH dose, the lower i would think you would have to go on mgs. I would use something like Halo or dbol.
 
iced said:
of dbol? i would imagine, also the higher the GH dose, the lower i would think you would have to go on mgs. I would use something like Halo or dbol.
I'm going with 2 or 3 iu. I don't like d-bol because of it's effect on BP. How's the halo on BP?

JohnnyB
 
i dont believe halo aromatizes, so your water retention shouldnt be bad, so im guessing BP wouldnt be too bad.
 
Most AS cause an increase in GH which than acts on the liver to produce IGF-1.

An example:

Testosterone administration increases insulin-like growth factor-I levels in normal men.

Hobbs CJ, Plymate SR, Rosen CJ, Adler RA.

Department of Clinical Investigation, Madigan Army Medical Center, Tacoma, Washington 98493.

Although testosterone (T) administration can increase insulin-like growth factor-I (IGF-I) when administered to hypogonadal men, no studies have examined whether this occurs in normal men. The present study was undertaken to determine if an increase in IGF-I may be part of the anabolic effect of androgens. We enrolled 11 normal men in a randomized, double-blinded cross-over study. Subjects were assigned to receive either T enanthate (TE) (300 mg im, each week) or nandrolone (ND) decanoate (300 mg im, each week) for 6 weeks. After a washout period subjects were administered the alternate treatment. Pre- and posttreatment serum was analyzed for IGF-I by RIA after acid-ethanol extraction. Results expressed as mean +/- SEM (Table 1). IGF-binding protein-3 was measured by RIA and was unchanged in the TE treatment and decreased significantly after ND treatment. Although GH levels were not significantly different after either TE or ND treatment, they tended to increase after TE treatment (1.23 +/- 0.28 ng/mL vs. 3.3 +/- 1.03 ng/mL) but remained unchanged after ND treatment (1.68 +/- 0.68 ng/mL vs. 1.89 +/- 0.64 ng/mL). Serum total T levels increased 32 +/- 0.05 nmol/L in the TE-treated men, but fell by 7 +/- 0.02 nmol/L in the ND-treated men (P < 0.0001). Serum estradiol levels rose by 193.04 +/- 19.82 pmol/L in the TE-treated men although falling by 50.65 +/- 34.50 pmol/L in the ND-treated men (P < 0.0002). These data indicate that when normal men are given TE, serum IGF-I levels increase after 6 weeks of treatment. Treatment with ND did not change serum levels of IGF-I but did decrease the level of the major serum IGF-BP and therefore the level of bioavailable IGF-I may be increased in the ND group.



Stanozolol at 0.1 mg/kg didn't have any impact on GH/IGF in this study:

http://jcem.endojournals.org/cgi/content/full/82/11/3710

eg1174379005.jpeg
 
DRveejay11 said:
(By Andy13....and 2 other people that responded with intelligent remarks)

Dbol is a poor AR agonist

I'm not sure about that...

from December 29, 2000 Issue #27 "Q&A WITH PAT ARNOLD" on anabolicextreme.com

Q: I hear that there are two classes of steroids. Class I bind to the androgen receptor to impart their activity and they include nandrolone and testosterone. Class II do not bind to the androgen receptor but impart their actions by as yet undetermined means. Class II steroids include d-bol and 4-AD and these are supposed to stack awesomely with Class I. Do I have this right?

A: There are not two classes of anabolic steroids. This theory has no acceptance, let alone mention, in the scientific literature, but is instead the belief of the exceptionally outspoken dudes over at Testosterone.net.

This theory can be blown out of the water by one simple fact. D-bol, 4-AD, anadrol and the other so called“Class II” steroids have very high androgenic activity. Androgenic activity is manifested through the classic androgen receptor and there is no argument about that. Therefore these “Class II” compounds, like the “Class I”, are exerting at least some part of their effects through the androgen receptor.

You want proof? Consider the following article:



Effect of steroids with antiandrogenic properties on androgenic and myotrophic activity of testosterone and some of its derivatives. Neurosci Behav Physiol.,1980

May-Jun;10(3):227-31.

In this article they use an anti-androgen (receptor antagonist) to test
effects on various tissues when taken along with a variety of
anabolic steroids. The effect with dianabol is described as follows:
"The results obtained upon joint administration of dianabol and the
antagonist were somewhat unexpected. The latter in doses of 2.5 and
7.5mg/rat/day caused a decrease in the response to dianabol only on the
part of the muscle and inhibited the stimulatory effect of dianabol on
the mass of the accessory (androgen sensitive) organs only in the
maximum dose."



Dianabol is described by the T-Mag theorists as being a classic "Class
2" (acts anabolically not by the androgen receptor). This study
completely contradicts their theory because when administered with an
androgen receptor antagonist, dianabol's anabolic activity was vastly
reduced
. Reduced even more so than it was with testosterone (a
purported "Class 1" steroid). I mean, these results are the total opposite of what
would be expected from the “Class Theory” of steroids!!

There is a very simple explanation why some steroids do not bind much to the androgen receptor in-vitro, yet exert strong anabolic / androgenic effects in-vivo. Hey, I did not make up this explanation, it is the one accepted by the scientists themselves. You see, many drugs do not exert their effects in their original form but are instead metabolized into the active compounds. Such drugs are termed “prodrugs”. So even though these Class II compounds have negligible binding to the androgen receptor in their parent form, they have metabolites that do bind very well. For instance, oxymetholone (anadrol) metabolizes into 17alpha methyl-DHT (mestanolone) which binds very strongly to the AR. Furthermore, 4-AD metabolizes into testosterone doesn’t it? Well duh!!

No, there are not two classes of anabolic steroids. The evidence does not suggest this at all. So why did such a theory get proclaimed with such confidence? Why did it get accepted by the lame ass public just because “they said so”? I dunno!
 
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I tend to beleive hhajdo side of things. Test causes a rise in IGF-1 also, as long as most if not all gear i beleive. I have never seen anything backing the fact that orals create this large spike in IGF-1 as opposed to injectables. I may be wrong, but i was under the impression that that was one of the dispelled myths.
 
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