Does dbol reduce?

Taken from Big Cat:
It has a rather weak androgenic component and an obviously quite strong and visible anabolic component. Its effects are largely non-AR mediated, which is documented by its rather low influence on the natural endocrine system2 and the fact that it decreases rather than increases red blood cell content in the blood. Which means that one worry users of Dianabol, especially short term, needn't fear is the dramatic shutdown of natural Testosterone production as is often the case with very androgenic compounds. Of course this effect is dose-dependent. It still has a mild androgenic component, meaning in high doses (30+ mg daily) androgen-mediated side-effects can be noted (acne, male pattern hair loss).

-Just read this (for the 100th time) regarding D-bol: "a simple application of only 10 mg results in a 5-fold increase in the average testosterone concentration in the male." Is this the most important part of how d-bol works? Especially if this is so, it would seem that the 5AR pathway to explain the d-bol to DHT process may hold true.

-If the test levels are increased 5x ....technically it would directly affect DHT levels since 4% of testosterone is converted to DHT. But then I don't know off hand if that convertion rate would stay proportional with such highly elevated test levels.

I don't see how it could convert directly to DHT without first converting to test since it's a direct metabolite of test....here's some info on test DHT conversion.

The plasma content of DHT is one tenth that of testosterone, approximately 400 ug produced daily compared to 5 grams of test. The reaction is catabolized by the NADPH-dependent 5 alpha reductase enzymes. There are two types of the 5AR enzyme.... type I found in the liver.... type II found in reproductive tissue and other specific tissues.

If I'm reading this correctly then it is reduced by the 5-alpha reductase enzyme and causes a dramatic rise in test levels. This in turn would yield a higher DHT level but not necessarily at a proportional rate. I do know that dbol is known to be rather harsh on the hairline though I've never lost hair due to any compound. I hope this answers your questions, I was a little confused.

Posted by: GettinSwole

Taken from Big Cat:
it decreases rather than increases red blood cell content in the blood.

-Just read this (for the 100th time) regarding d-bol: "a simple application of only 10 mg results in a 5-fold increase in the average testosterone concentration in the male."

The reaction is catabolized [ooops] by the NADPH-dependent 5 alpha reductase enzymes. There are two types of the 5AR enzyme.... type I found in the liver.... type II found in reproductive tissue and other specific tissues.

I hope this answers your questions, I was a little confused.

oh yeah?!

Its not reduced. Except it might be.

The problem, and the reason I go nuts reading stuff like BC's [sans cites], is without knowing the primary source you just can't trust it. For eg, Dianabol INCREASES hematocrit, it does not decrease it like BC claims. Dianabol is actually a little known treatment for anemia for this reason. So what are we to think of the remainder?

Increases test? Hmmm.....makes me wonder how those guys in the Lancet article which found no suppression from am dosing. Forget the dbol, where the otherwise suppressive test go at night? In fact, the test would HAVE TO aromatize so there would be a bunch of FSH (and maybe LH) suppressing estrogen floating around.

I think the pragmatic answer for a dbol only cycle is take your Proscar and pray, but I wish I could get a firmer handle on all this.

I decided to figure this out myself (god I hate biochem).....and came up with interesting results: dbol, contrary to everything you read on the web, IS in fact *itself* reduced by 5ar to a more androgenic species (PMID: 860289).

I was always under the impression that dbol was a very poor substrate for 5 alpha reductase. Instead its 5 reduced metabolites were all of the 5 beta configuration (1).

As you can see from the abstract below regarding M (dbol),

"the weak activity of M may be attributable to a lack of reduction to 5alphaM"

Dbol actually causes the prostrate to shrink because it both reduces testosterone production, and binds to the prostate AR and displaces DHT.

Steroids 1977 Mar;29(3):331-48

Relative importance of 5alpha reduction for the androgenic and LH-inhibiting activities of delta-4-3-ketosteroids.

Steele RE, Didato F, Steinetz BG.

The significance of 5alpha reduction of c19, delta1,4-3-ketosteroids in regulating growth of the rat ventral prostate (VP) was examined. The androgenic and LH-inhibiting activities of a C19 delta1,4-3-detosteroid which does not undergo appreciable 5alpha reduction were compared with those of its 5alpha reduced analogue and those of testosterone (T). In intact rats M (17beta-hydroxy-17alpha-methyl-androsta-1:4-dien-3-one) caused a suppression of VP weights and plasma testosterone concentrations, and in castrated rats suppressed plasma LH concentrations. M was considerably less androgenic and moderately less potent as an inhibitor of LH secretion than either T or the 5alpha reduced analogue of M [17beta-hydroxy-17alpha-methyl-5alpha-androst-1-ene-3-one; (5alphaM)]. 5alphaM was found to be at least as androgenic and as active as an inhibitor of LH as T, suggesting that the weak activity of M may be attributable to a lack of reduction to 5alphaM. Following incubation of 3H-M with VP minces, over 96% of the radioactivity recovered corresponded with M by TLC. Under identical conditions 32-48% of the radioactivity recovered from incubations with 14C-T corresponded with 5alpha reduced metabolites of T. This study demonstrates the importance of 5alpha reduction for both the androgenic and LH-inhibiting activities of delta4-3-ketosteroids.

(1) Clin Chem 1996 Jul;42(7):1001-20 Related Articles, Links

Clin Chem. 1996 Jul;42(7):999-1000.

Metabolism of anabolic androgenic steroids.

Schanzer W.

Institute of Biochemistry, German Sports University Cologne, Germany.

It is also disappointing to hear so many people say things like dbol's effects

"are largely non-AR mediated, which is documented by its rather low influence on the natural endocrine system2 and the fact that it decreases rather than increases red blood cell content in the blood'

There is no evidence for any non androgen receptor mediated actions of dbol. Testosterone (and probably other AAS) have non genomic actions, but they are poorly characterized. Just because one anabolic steroid has different actions than another (like the supposed effects on red blood cells) does not mean that the actions of the drug are nongenomic.

The study below (which I think I've posted before) shows that testosterone and various AAS bind to and activate androgen responsive genes differently because the have different affinities to different gene promoters.

A gene which is androgen sensitive (like the gene for IGF-1 in muscle) consists in part of an exon, which actually codes for IGF-1, and one or more promoters, which are stretches of DNA upstream and downstream from the exon.

The steroid/receptor complex binds the so called "androgen response element" which is a part of the promoter region. This activates other transcription factors which detemine whether the gene will be transcribed (or repressed) and the rate of transcription.

There is no need to invoke non AR mediated actions for AAS. They may exist, but the varying effects of the different AAS are much more likely determined by which promoters they bind to and activate.

For instance, if a certain androgen suppressed hematopoiesis instead of stimulating it, all it means is most likely the androgen/receptor complex has bound to a promoter that represses transcription of the gene(s) responsible for red blood cell production.

J Steroid Biochem Mol Biol 2002 Nov;82(4-5):269-275

Anabolic steroids, testosterone-precursors and virilizing androgens induce distinct activation profiles of androgen responsive promoter constructs.

Holterhus PM, Piefke S, Hiort O.

Department of Pediatrics, Medical University of Lubeck, Lubeck, Germany

Different androgens, e.g. virilizing androgens such as testosterone and its precursors as well as synthetic anabolic steroids, respectively, induce diverse biological effects. The molecular basis for this variety in biological actions, however, is not well understood. We hypothesized that this variability of actions may be due to steroid-specific target gene expression profiles following androgen receptor (AR)-activation. Therefore, we investigated androgen receptor dependent transactivation of three structurally different androgen responsive promoter constructs ((ARE)(2)TATA-luc, MMTV-luc, GRE-OCT-luc) in co-transfected Chinese hamster ovary (CHO)-cells as an artificial model simulating different natural target genes. Three virilizing androgens (dihydrotestosterone, testosterone, methyltrienolone), three anabolic steroids (oxandrolone,Stanozolol, nandrolone) and two testosterone-precursors of gonadal and adrenal origin (dehydroepiandrosterone, androstenedione) were used as ligands (0.001-100nM). All steroids proved to be potent activators of the AR. Remarkably, anabolic steroids and testosterone-precursors showed characteristic promoter activation profiles distinct from virilizing androgens with significantly lower (ARE)(2)TATA-luc activation. Hierarchical clustering based on similarity of activation profiles lead to a dendrogram with two major branches: first virilizing androgens, and second anabolics/testosterone-precursors. We conclude that steroid-specific differences in gene transcription profiles due to androgen receptor activation could contribute to differences in biological actions of androgens.

quote:

---

the fact that it decreases rather than increases red blood cell content in the blood

---

quote:

---

For instance, if a certain androgen suppressed hematopoiesis instead of stimulating it, all it means is most likely the androgen/receptor complex has bound to a promoter that represses transcription of the gene(s) responsible for red blood cell production.

---

This is the first time I've heard about this.Do you know where Big Cat got this info from?And is red blood cell increase the same as increased blood volume(can you get more blood yet less red blood cells)?

Anadrol is often thought to be one steroid that binds poorly to the AR but I read somewhere that one of its main metabolites actually binds very strongly to the AR.

I'd never heard it. I was just using it as a hypothetical. In fact everything I have seen suggests the opposite. For example:

Eksp Klin Farmakol 1997 May-Jun;60(3):41-4

[The results of experimental study of phytoecdysteroids as erythropoiesis stimulators in laboratory animals]

Syrov VN, Nasyrova SS, Khushbaktova ZA.

Phytoecdysteroids alpha-ecdysone, 2-desoxyecdysterone, ecdysterone, sileneoside A, and turkesterone isolated from Rhaponticum carthamoides (Willd.) IIjin, Silene brahuica Boiss and Ajuga turkestanica (Rgl.) Repeated administration of brig increased the content of erythrocytes and hemoglobin in the blood of intact rats. The most active of them--ecdysterone, sileneoside A, and, particularly turkesterone, cause also a marked effect on red blood regeneration in hemotoxic phenylhydrazine anemia. In its capacity for simulating erythropoiesis turkesterone resembles the well-known steroidal anabolic drug nerobol [dianabol].

re RBC, as I pointed out above BigCat is wrong.

lol......great minds think alike.

Posted by: Nandi12

Dbol actually causes the prostrate to shrink because it both reduces testosterone production, and binds to the prostate AR and displaces DHT.

M was considerably less androgenic and moderately less potent as an inhibitor of LH secretion than either T or the 5alpha reduced analogue of M [17beta-hydroxy-17alpha-methyl-5alpha-androst-1-ene-3-one; (5alphaM)]. 5alphaM was found to be at least as androgenic and as active as an inhibitor of LH as T, suggesting that the weak activity of M may be attributable to a lack of reduction to 5alphaM.

1. Dbol *lowering* test levels makes much, much more sense to me.

2. Dbol DOES reduce via 5alpha. Which means folks should take proscar (assuing that the reduced version has more affinity for the androgen receptors in the scalp, which seems reasonable given the above.

3. How significant the alpha pathway is I don't know (I don't know the pathways and ain't gonna try to figure them out.....this probably would show help figure out the pathways and you could then back out from the 1:3:8 ratio thereafter if anyone cares: ). But I find it hard to reconcile dbol displacing DHT from the androgen receptor when dbol is less androgenic than 5alphaDBOL OR test (and we know DHT has more affinity to the AR than test). Perhaps it really is 5alpha that is displacing the DHT.....just because it binds doesn't mean it has the same impact?

4. I understand (sort of) what you are thinking with respect to this sentence "weak activity of M may be attributable to a lack of reduction to 5alphaM" ... but it is really, really unclear what the author's are saying in this portion of the abstract. Presumably the weak action refers to inhibiting LH. I don't know what that has to do with ARs. I don't know how they could measure the impact on LH (in fact, I don't think anybody to this day has really effectively shown the impact of just test on LH...as opposed to say estrogen). Frankly I don't buy this portion of the abstract, or at least I don't put much stock in it. In other words, I have no idea how much dbol goes the alpha pathway, just that #2 above probably makes sense.

Posted by: Nandi12

So it looks like according to the study in humans, the 5beta reduced metabolite, 17 alpha-methyl-5 beta-androstane-3 alpha,17 beta-diol, is about 4 (3.8) times more abundant than the 5 alpha reduced version, 17 alpha-methyl-5 alpha-androstane-3 alpha,17 beta-diol.

Maintaining prostate weight vs muscle mass is a standard way of measuring androgenicity v the anabolic potency of a drug.

1. Looks like there is an alpha=>beta pathway so the second set of numbers don't mean anything....some may go through 5ar. As I said, I'm too lazy to figure out the pathways.

2. As opposed to, say, hair loss count vs. muscle mass? The unanswered questions are how does Dbol/5alphaD displace DHT from prostate? Or for young uns, why do folks think it is so hard on the hair? My vote goes to finasteride now.

So it looks like according to the study in humans, the 5beta reduced metabolite, 17 alpha-methyl-5 beta-androstane-3 alpha,17 beta-diol, is about 4 (3.8) times more abundant than the 5 alpha reduced version, 17 alpha-methyl-5 alpha-androstane-3 alpha,17 beta-diol.

So rats aren't people when it comes to dbol. Or when the first paper was published instrumentation was not sophisticated enough to detect the different metabolites.

Maintaining prostate weight vs muscle mass is a standard way of measuring androgenicity v the anabolic potency of a drug. If it maintains skeletal muscle but the prostate shrinks, it is considered to have a high anabolic/androgenic ratio, or at least one higher than test. This is the case with dbol.

In the 1970's it was quite difficult to measure LH. In castrated animals LH is very high; it is easier to detect a drop due to AAS. In intact animals I suspect the drop in LH due to the dbol was outside the detection limits of their equipment.