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Dianabol~Methandrostenolone

heavyiron

Chemistry Experiment
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Dianabol (Methandrostenolone)
Dianabol

Dbol - Methandrostenolone

By Anthony Roberts

This was more or less the second Anabolic Steroid ever produced. The first, as we all know was Testosterone, which was produced in the early 1900´s and experimented with by Nazi´s in WW2, in an attempt to produce a better soldier.

Russian Dianabol and Team Sports History

Russian athletes in the 1953 World Championships as well as the Olympic games then used testosterone with great success. After that, John Zeigler, who was a doctor working with the US Weightlifting Team, began a cooperative project with Ciba to develop an equalizer for US atheletes. Flash forward to 1956 and enter Dianabol ; the original trade name for Ciba´s Methandrostenolone... but called "Dbol" by athletes. The original package insert said that 10mgs/day was enough to provide full androgen replacement for a man and Dr.Zeigler recommended that athletes take 5-10mgs/day. Incidentally, this is also the dose that Bodybuilders were reputed to take from then until roughly the 1970´s. Yeah, this was allegedly Arnold´s dose, Zane´s dose, etc... simply stacked with some testosterone. (For any trivia buffs out there, Dan Duchaine´s mail order steroid business operated under the name "The John Zeigler Fan Club").

Dianabol Steroid Use

Enough with the history lesson, lets get into what this stuff is, and what it does. Well, first off, it´s usually found in pill form, though it can be found as an injectable also (Under the Trade name: Reforvit-B, which is 25mgs of methandrostenolone mixed with B-vitamins). It is a 17aa steroid, which means it has been altered at the 17th Carbon position, to survive its´ first pass through your liver, and make it into your blood stream. It´ll raise your blood pressure (4) and is also hepatoxic (Liver-Toxic), so be careful with it. Although I have known people to take up to 100mgs/day of this stuff and not suffer any ill-effects, and one study looked at that exact dose, and the people involved didn´t suffer any intolerable side effects ( 7). Lets examine this particular study a bit further, though:

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. I can only agree, having found this to be the case for me when I did my first cycle (which was 6 weeks of dbol alone at 25mgs/day), I gained roughly 25lbs and kept nearly ½ of it. Since then, Dbol has always had a special place in my heart.

Dianabol Side Effects

As with many other 17aa steroids, Dianabol is also a very weak binder to the Androgen Receptor, so most of it´s effects are thought to be non-receptor mediated, and are attributable to other mechanisms (i.e. protein synthesis as indicated by the production of muscle tissue with very high levels of nitrogen, etc... which was indicated in the 100mg/day study). This also means it only has a modest aromatase activity (2).

How strong is Dbol? Well...on a mg for mg basis, most people agree that it´s stronger than A50...but the reason most people don´t get the same gains off of Dbol is that almost nobody takes equivalent doses (I mean...I´ve heard of people taking 150mgs of A50, but not Dbol, even though the dbol would probably provide more solid gains and be less toxic, I suspect).

So how do we incorporate this stuff into our AAS regimen? Clearly, the inclusion of Dbol at any point in a cycle would contribute to gains, however, I´d speculate that Dbol is most regularly used for 2 reasons

1. At the start of a cycle to "Kick Start" gains.
2. As a "Bridge" between cycles, to maintain gains.

Lets examine these two uses.

Dianabol Cycle

In order to kick start a dianabol cycle, usually what you do is incorporate a fast acting oral like dianabol (or anadrol) and combine it with long acting injectables (such as Deca or Eq with some Testosterone). The reasoning here is that the oral (Dbol in this case) will give almost immediate results, while the injectable takes time to produce results. The end result is that you start seeing results within the first week of your cycle and continue up until the end with the injectables. This entails taking anywhere from 25-50mgs of dbol (although as little as 20mgs or as much as 100mgs have been reported) for 3-6 weeks at the start of a cycle (average time for a "Kick Start" is 4 weeks, though), and then ceasing their use as the injectables start to produce results.

In order to successfully bridge between cycles (and this means using a low dose of AAS, in this case dbol), you need to recover your natural hormonal levels to pre-cycle levels or to within acceptable parameters, and then you start your next cycle. The idea here is that you won´t lose any gains, but rather a low dose of an AAS will help you maintain them. Typically, you´d use around 10mgs/day of dbol and combine it with an aggressive Post-Cycle Therapy (PCT) course of Nolvadex (and/or Clomid) and HCG. This would give you full androgen replacement from the Dbol and a shot at recovering your natural hormonal levels via the other stuff you are taking. Remember, the 100mg/day dose of dbol in the study we looked at earlier did not suppress Test, LH, or FSH to a degree that would make recovery impossible and certainly not with 1/10th that dose in conjunction with an aggressive PCT.

All in all, this is a very good drug, and a potent tool for quick gains or retaining gains...when used properly and safely.

Dbol Facts

[17a-methyl-17b-hydroxy-1,4-androstadien-3-one]
Molecular Weight: 300.44
Formula: C20H28O2
Melting Point: N/A
Manufacturer: Ciba (originally)
Release Date: 1956
Effective dose: 25-50mgs (as low as 10 and as high as 100 have been reported)
Active Life: 6-8hours
Detection Time: up to 6 weeks
Anabolic/Androgenic Ratio (Range): 90-210:40-60


References:
  1. Serakovskii S, Mats´koviak I., Effect of methanedienone (methandrostenolone) on energy processes and carbohydrate metabolism in rat liver cells, Farmakol Toksikol 1981 Mar-Apr;44(2):213-7
  2. Brain Res. 1998 May 11;792(2):271-6.
  3. Chemfinder. Copyright 2004 CambridgeSoft Corporation. Cambridge, MA, USA.
  4. Br Med J. 1975 May 31;2(5969):471-3.
  5. www.steroid.com
  6. http://www.*****************.com
  7. Clin Sci (Lond). 1981 Apr;60(4):457-61
  8. Steroids. 1984 Dec;44(6):485-95.
  9. Vrach Delo. 1983 Nov;(11):34-6. Russian
  10. Acta Med Acad Sci Hung. 1975;32(1):27-34
  11. 4 Nesterin MF, Budik VM, Narodetskaia RV, Solov´eva GI, Stoianova VG., Effect of methandrostenolone on liver morphology and enzymatic activity, Farmakol Toksikol 1980 Sep-Oct;43(5):597-601
 
The effect of anabolic-androgenic steroids on aromatase activity and androgen receptor binding in the rat preoptic area.

Roselli CE.
Department of Physiology and Pharmacology, Oregon Health Sciences University, Portland, OR 97201-3098, USA. rosellic@ohsu.edu

The level of aromatase in the preoptic area of rats is transcriptionally regulated through a specific androgen-receptor mediated mechanism and can be used as a measure of central androgenic effect. Therefore, several commonly abused anabolic-androgenic steroids (AAS) were tested for their ability to induce aromatase activity in the preoptic area of castrated rats. In addition, we determined the relative binding affinities of these compounds for the androgen receptor, as well as their ability to bind androgen receptor in vivo following subcutaneous injections. All of the AAS compounds tested significantly stimulated POA aromatase activity above castrate levels. The compounds that produced the greatest stimulation of aromatase activity were those that bound most avidly to the androgen receptor in vitro (i.e., testosterone, dihydrotestosterone and nandrolone). In contrast, the 17alpha-alkylated compounds that were tested (stanozolol, danazol, methandrostenolone) modestly stimulated aromatase and were weak competitors for the androgen receptor. The subcutaneous injection of AAS compounds increased the concentrations of occupied nuclear androgen receptors in the brain, but the magnitude of effect was not related to their potency for inducing aromatase or their relative binding affinity for the androgen receptor suggesting that androgen receptor occupancy in POA is not correlated with the action of androgen on aromatase. The present results help explain the behavioral effects of AAS compounds in rats. Copyright 1998 Elsevier Science B.V.

PMID: 9593936 [PubMed - indexed for MEDLINE]
 
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Effect of methandrostenolone on postmenopausal bone wasting as assessed by changes in total bone mineral mass.

Chesnut CH 3rd, Nelp WB, Baylink DJ, Denney JD.
Abstract

To assess the efficacy of methandrostenolone in the treatment of osteoporosis a 26-mo double-blind study was performed with 13 treated and 13 control (placebo) postmenopausal osteoporotic females. Drug effect was assessed primarily by determinations of total body calcium (TBC) by neutron activation analysis, essentially a measurement of total bone mineral mass. Results in the 16 patients completing the study (10 treated and 6 placebo), as well as in all 26 patients participating in the study, showed significant (p less than 0.01) differences in the change in TBC between treated and control groups. In patients dropping out, TBC changes through the time of dropout were similar to those in patients completing the study. In those patients completing the study, TBC increased 2% in the treated group and decreased 3% in the placebo group. An approximate sixfold difference in extraskeletal calcium balance would be required to explain the magnitude of the observed intergroup TBC difference. The drug effect appeared to persist throughout the 26-mo observation period. Thus these data strongly suggest that long-term use of methandrostenolone in postmenopausal osteoporosis prevented bone loss; the possibility that it increased bone mass above initial values is less certain.
 
Effects of training and methandrostenolone (an anabolic steroid) on energy metabolism in the guinea pig: changes in enzyme activities in gastrocnemius muscle and myocardium.

Feraudi M, Weicker H.
Abstract

Modifications of enzyme activities (creatine kinase and its B subunit; adenylate kinase; hexokinase; phosphofructokinase; lactate dehydrogenase; malate dehydrogenase, isocitrate dehydrogenase; citrate synthase; acetylcarnitine transferase; beta-hydroxyacetyl-CoA dehydrogenase; cytochrome c oxidase) in gastrocnemius muscle and myocardium were reported after two forms of training with or without administration of anabolic steroid. Endurance training was on a horizontal motor-driven treadmill, 2 km X hr-1, 5 days a week for 0.5 hr per day for 5 weeks. In the case of power endurance training there was a slope of 45 degrees. Enzyme activities in controls and treated guinea pigs, as well as treatment-induced enzyme activity changes are time dependent. Some of these activities correlate linearly with one another; such correlations characterize the effect of adaptation. Endurance training and power endurance training in this study induce similar modifications and seem to differ essentially in the daily work load. The anabolic steroid methandrostenolone (dianabol) induces modifications which training does not bring about but which training at least partially eliminates.


PMID: 4076521 [PubMed - indexed for MEDLINE]
 
This may be the basis for why users report a sense of well being on Dianabol.

Br J Pharmacol. 1999 Mar;126(6):1301-6.

Increased dopaminergic and 5-hydroxytryptaminergic activities in male rat brain following long-term treatment with anabolic androgenic steroids.

Thiblin I, Finn A, Ross SB, Stenfors C.

Department of Forensic Medicine, Karolinska Institute, Stockholm, Sweden.

Abstract

1. The effects of treating groups of rats with four different anabolic androgenic steroids (AAS) (testosterone, nandrolone, methandrostenolone, and oxymetholone) on 5-hydroxytryptamine (5-HT) and dopamine (DA) neurones in different brain regions were examined. The AAS was injected six times with 1 week's interval and the rats were sacrificed 2 days after the final injection. 5-HT and its metabolite 5-hydroxyindoleacetic acid (5-HIAA), DA and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were measured. The effect on DA and 5-HT synthesis rate was analysed as the accumulation of 3,4-dihydroxyphenyl-alanine (DOPA) and 5-hydroxytryptophan (5-HTP), respectively, after inhibition of the amino acid decarboxylase with NSD-1015 (3-hydroxy-benzylhydrazine dihydrochloride). Additionally, the monoamine oxidase (MAO) activity was analysed in the hypothalamus. 2. The DOPAC + HVA/DA ratio was increased in the striatum in all treatment groups. However, the synthesis rate of DA was significantly increased only in the methandrostenolone treated group. 3. The 5-HIAA/5-HT ratio was increased in all treatment groups in the hippocampus, in the frontal cortex in the methandrostenolone-treated animals and in the hypothalamus in the testosterone- and oxymetholone-treated rats, while the 5-HT synthesis rate was not affected by the AAS-treatments. 4. The MAO-A activity was increased in the oxymetholone-treated rats while the other treatment groups were unaffected. The MAO-B activity was not changed. 5. The results indicate that relatively high doses of AAS increase dopaminergic and 5-hydroxytryptaminergic metabolism in male rat brain, probably due to enhanced turnover in these monaminergic systems.

full study

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1565900/
 
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