what exactly is 6 bromo

[martel04]

ive searched and nothing comes up. just wondering if anyone has any studies on this compound. what exactly it is and what it does. thanks

[Regular_Ryan]

http://anabolicx.com/store/hyperdrol.html

[Regular_Ryan]

6-Bromodione: There are two types of estrogen aromatase inhibitors and application of only one leaves the other pathway open for feminizing potential.

1.

6 alpha-Bromodione is a competitive inhibitor of aromatase enzymes. Basically this means it works by way of binding to the active binding site of the aromatase enzyme resulting in prevention of interaction with other steroids that aromatize like testosterone and the rest of our favorite male androgens. This is great for rapid binding and short term aromatase control, but unfortunately a competitive inhibitor will eventually let go of the enzyme and allow it to do feminizing things to manly hormones. So, only half of the job is done, but it has its important role as well.

2.

6 beta-Bromodione is a mechanism-based irreversible inhibitor of the aromatase enzyme. An irreversible aromatase inhibitor is also referred to as a suicide inhibitor. It’s pretty cool in that it acts similar to a competitive inhibitor in the way it binds, but like a pissed-off ex-girlfriend, it is both highly selective and it will not let go until death do they part.

Together the two analogs in 6-Bromodione make sure that estrogen is under control, and many would assume that less estrogen means the prolactin would be under control as well. Often, once prolactin increases are stimulated, shutting it back down takes some extra effort and a protracted period of time.

[Viado]

ive searched and nothing comes up. just wondering if anyone has any studies on this compound. what exactly it is and what it does. thanks

A new revenue generating compound that is clinically unproven to do anything at this time.

[Regular_Ryan]

6) Stereochemistry of the functional group determines the mechanism of aromatase inhibition by 6-bromoandrostenedione.
Endocrinology. 1987 Sep;121(3):1010-6.

[Viado]

Has a randomized controlled study been done testing it's effects on humans? safety? efficay?

[OMMID]

6-bromo-testosterone

[ironLifeBG]

okay i'll translate that for those of you who don't speak endocrine.

compound #1 basically binds with estrogen to keep free testosterone and other male androgens from binding, but the binds aren't permanent and they will break ...this is a similar mechanism to DS ActivaTe, i believe except i believe activate targets SHGB (sex hormone binding globulin) directly.

compound #2 suicide inhibitor...similar mechanism to any ATD, AT product...ie it binds with the estrogen and the bond is permanent, however the compound is highly selective in its choice of mates and will probably float around for a couple days before binding (this is why it takes a couple days to notice body composition changes)


very interesting indeed


has anyone ever tried stacking activate and hyperdrol?

[martel04]

yea ever hear of NHA stack from ds. RR and activate. RR is almost the same as HD

[ironLifeBG]

yea ever hear of NHA stack from ds. RR and activate. RR is almost the same as HD

yes i ran and logged an NHA stack consisting of rebound XT and ActivaTe Beta about 10 months ago

i didn't realize that rebound reloaded was "almost the same" as hyperdrol and jungle warfare. i will however let you know how well it works.

[uhockey]

Reloaded is not "almost the same" at all, as it is standardized for specific 6-bromo isomers and specific lignans from the white button mushroom.

And, although I can't be sure due to the proprietary blend of Hyperdrol, I believe ActivaTe's dosing of Divanil is significantly higher.

[Viado]

It is interesting to get negative reps for simply saying the truth, ie where in the literature has this compound been tested for safety and efficacy in humans? Any randomized controlled trials? Any data?

Simply because an article shows up on pub med, (of which I have access to 75% of the article in simple text or pdf form, and also where publications I have authored can be found) does not make it gospel nor should it render credibility.

[bigsexysd7]

Ohhhh viado, pubmed is all that matters on this board. If it ain't on pubmed, it ain't true. It is the only check too many on here use. I wouldn't be surprised if people on here had a link to pubmed on their myspace.

On a side note, I have yet to be disappointed with a DS product. I am using the RR now in PCT, and I must sa i like it more than the RXt.

[uhockey]

Ohhhh viado, pubmed is all that matters on this board. If it ain't on pubmed, it ain't true. It is the only check too many on here use. I wouldn't be surprised if people on here had a link to pubmed on their myspace.

On a side note, I have yet to be disappointed with a DS product. I am using the RR now in PCT, and I must sa i like it more than the RXt.

It's funny because it's true. I prefer my literature from JAMA, but they don't talk much about supplements......then again they don't talk much about Rats either.

Suffice it to say, much of this industry is a cost/benefit analysis of relatively new compounds with unknown long term safety.

No one is forcing you to take anything.

[Androgenic]

JAMA is on PUBMED.

http://www.ncbi.nlm.nih.gov/entrez/q...arch&DB=PubMed

"Suffice it to say, much of this industry is a cost/benefit analysis of relatively new compounds with unknown long term safety. "

Uhockey do you find this being at least partially in conflict with what the healthcare system is supposed to represent. The rolling the dice with one's health especially with hormones whether benign or not without more knowledge of the compound seems questionable. I expect that a bit more from the mavericks that throw health to the wind for the potential of one more pound of muscle, but I would expect at least a bit more caution from you, given your life's direction. My research has turned up some red flags on this compound that at least would make me less than quick to be a Guinea Pig. You are aware with most hormones, that there is a hormonal cascade and numerous effects throughout the body. This compound was discovered many, many years ago and it's interesting that there is so little real data available. Wouldn't you in your position as a Med Student recommend something with a bit more documented safety or data (that still has potential risk) such as AT/6-oxo or Formestane/4-hydroxyandrostenedione. Even if it is truly effective with little side effects, shutting down estrogen is not a desirable thing. Read Bill Llewellyn's thoughts in his Encyclopedia on AI's (that are not SERMs). It can have numerous health implications and strength implications...and this is from a steroid guru, not even a medical community member.

[xGhostinGx]

Ohhhh viado, pubmed is all that matters on this board. If it ain't on pubmed, it ain't true. It is the only check too many on here use.

Good comment. Lets start using various articles that anyone writes. Screw the truth! Pubmed is a joke of a standard.

[xGhostinGx]

It is interesting to get negative reps for simply saying the truth, ie where in the literature has this compound been tested for safety and efficacy in humans? Any randomized controlled trials? Any data?

You got a neg rep for asking that question? LOL. Who? Exposure can be a good thing, so we can see whos being a little sensetive.

[xGhostinGx]

It is interesting to get negative reps for simply saying the truth, ie where in the literature has this compound been tested for safety and efficacy in humans? Any randomized controlled trials? Any data?

Simply because an article shows up on pub med, (of which I have access to 75% of the article in simple text or pdf form, and also where publications I have authored can be found) does not make it gospel nor should it render credibility.

Ill pos rep you when im charged up tonight.

[Bloute]

Reloaded is not "almost the same" at all, as it is standardized for specific 6-bromo isomers and specific lignans from the white button mushroom.

And, although I can't be sure due to the proprietary blend of Hyperdrol, I believe ActivaTe's dosing of Divanil is significantly higher.

Bump for the comment about Divanil. I haven'T finish my Hyperdrol log but I don't feel the pumps and the muscle hardness I had from Activate with Hyperdrol.

[Viado]

JAMA is on PUBMED.

http://www.ncbi.nlm.nih.gov/entrez/q...arch&DB=PubMed

"Suffice it to say, much of this industry is a cost/benefit analysis of relatively new compounds with unknown long term safety. "

Uhockey do you find this being at least partially in conflict with what the healthcare system is supposed to represent. The rolling the dice with one's health especially with hormones whether benign or not without more knowledge of the compound seems questionable. I expect that a bit more from the mavericks that throw health to the wind for the potential of one more pound of muscle, but I would expect at least a bit more caution from you, given your life's direction. My research has turned up some red flags on this compound that at least would make me less than quick to be a Guinea Pig. You are aware with most hormones, that there is a hormonal cascade and numerous effects throughout the body. This compound was discovered many, many years ago and it's interesting that there is so little real data available. Wouldn't you in your position as a Med Student recommend something with a bit more documented safety or data (that still has potential risk) such as AT/6-oxo or Formestane/4-hydroxyandrostenedione. Even if it is truly effective with little side effects, shutting down estrogen is not a desirable thing. Read Bill Llewellyn's thoughts in his Encyclopedia on AI's (that are not SERMs). It can have numerous health implications and strength implications...and this is from a steroid guru, not even a medical community member.

I think that the saddest part is that when someone posts a log, for the most part is is treated as something along the lines of an individual study - where one person's gains could directly translate into one's personal gains on said product. Little do we know that there are many individuals on this board that are in fact posting these logs that may have a direct or indirect affiliation with the manufacturer. It owuld almost be appreciated if those testing the products disclose or deny their affiliation with manufacturer X. Clinicla trials for safety adn efficacy go through an expensive process that takes years until an agent makes it onto the market - even then, post approval some products are dicontinued (ie Vioxx as a recent example). The bottom line is that one should be weary about testing a new product witha new or novel compound. Compromising your health is truly not worth it. Do your research, have a doc sift through the literature or even prin out some of these COMPLETE articles on line. There are way too many abstact readers here that really don't see the details, ie if a compound doubled the incidence of something from 1% to 2% - it is still low, but can be spun via clever marketing as DOUBLING! I could go on and on. Just be on the lookout.

It's what I tell my patients.

[weightsanyway]

I think that the saddest part is that when someone posts a log, for the most part is is treated as something along the lines of an individual study - where one person's gains could directly translate into one's personal gains on said product. Little do we know that there are many individuals on this board that are in fact posting these logs that may have a direct or indirect affiliation with the manufacturer. It owuld almost be appreciated if those testing the products disclose or deny their affiliation with manufacturer X. Clinicla trials for safety adn efficacy go through an expensive process that takes years until an agent makes it onto the market - even then, post approval some products are dicontinued (ie Vioxx as a recent example). The bottom line is that one should be weary about testing a new product witha new or novel compound. Compromising your health is truly not worth it. Do your research, have a doc sift through the literature or even prin out some of these COMPLETE articles on line. There are way too many abstact readers here that really don't see the details, ie if a compound doubled the incidence of something from 1% to 2% - it is still low, but can be spun via clever marketing as DOUBLING! I could go on and on. Just be on the lookout.

It's what I tell my patients.

Excellent post.

You'll get the standard answer here about testing costing too much, etc. etc. But the ironic thing here is that as supplements evolve and become even more drug-like/effective, there's an even greater need for something like that. For the love of God, many of these steroidal AIs that the companies are digging up these days have been around for decades and, same as the new prohormones, have been passed over for development because of the risk of use, sides, etc.

There's dozens of AI's out there, reading a few studies from the 1950's and determining that their safe for use is a far cry from setting up a controlled study today and applying the medical knowledge and testing that we have available 50 years later...

[Androgenic]

Excellent post.

You'll get the standard answer here about testing costing too much, etc. etc. But the ironic thing here is that as supplements evolve and become even more drug-like/effective, there's an even greater need for something like that. For the love of God, many of these steroidal AIs that the companies are digging up these days have been around for decades and, same as the new prohormones, have been passed over for development because of the risk of use, sides, etc.

There's dozens of AI's out there, reading a few studies from the 1950's and determining that their safe for use is a far cry from setting up a controlled study today and applying the medical knowledge and testing that we have available 50 years later...

Precisely. This is exactly the train of thought one should have. Why was it discovered so long ago and not used by pharmaceutical companies, why didn't the hardcore bodybuilding community cry out for it's development and have a black market for it, why is there NO real data and the few studies that sort of allude to it are from dates prior to electronic data recording (no abstract or online study). Then to top it off the name gets altered...bromodione (or could've done bromo-etiochol, but in this case it's more beneficial to play up the andro, being it's an AI with less legal loopholes necessary)...and how much in the product...unknown...proprietary (which means it could be altered for dosages whenever without scrutiny). I have not even got to why I think this compound may not be a good selection in terms of organic/biochemistry, much of it theoretical given what data is available on the compositional groups and molecules of comparable nature.

[Androgenic]

I'd like to know where this information is legitimately referenced. I have found nothing regarding 6-bromoandrostenedione having an alpha and beta with these characteristics. Actually, I found some data pointing to them being anti-androgens. I did find one 1978 abstract on bromoandrostenedione with alpha and beta...but it is not 6-bromo (rather 16) and well, read on...
__________________________________________________ ______________
Steroids, 1978 Nov, 32(4), 519 - 27
Improved synthesis of 16alpha-hydroxylated androgens: intermediates of estriol formation in pregnancy; Numazawa M et al.; 16alpha-Hydroxyandrostenedione (16alpha-hydroxyandrost-4-ene-3,17-dione), 16alpha-hydroxytestosterone (16alpha,17beta-dihydroxyandrost-4-en-3-one) and 16alpha-hydroxydehydroepiandrosterone 3-sulfate (3beta, 16alpha-dihydroxyandrost-5-en-17-one 3-monosulfate) were synthesized by a new chemical approach with much improved yield . 16alpha-Bromoandrostendione was converted to the hydrazone of 16alpha-hydroxyandrostenedione which gave 16alpha-hydroxyandrostenedione on acid hydrolysis in total 63% yield . Oxidation of 16alpha-hydroxydehydroepiandrosterone with Jones' reagent also selectively afforded 16alpha-hydroxyandrostenedione . 16alpha-Hydroxytestosterone was observed by selective reduction of 16alpha-hydroxyandrostenedione with sodium borohydride . Reaction of 16alpha-hydroxydehydroepiandrosterone with chlorosulfonic acid in pyridine selectively gave the 3-monosulfate . The structure of the sulfate was deduced from its solvolysis to the starting material, and its acetylation and subsequent solvolysis to 16alpha-hydroxydehydroepiandrosterone 16-acetate . All procedures are suitable for large scale synthesis without the use of microorganisms.
__________________________________________________ _______________

6-Bromodione: There are two types of estrogen aromatase inhibitors and application of only one leaves the other pathway open for feminizing potential.

1.

6 alpha-Bromodione is a competitive inhibitor of aromatase enzymes. Basically this means it works by way of binding to the active binding site of the aromatase enzyme resulting in prevention of interaction with other steroids that aromatize like testosterone and the rest of our favorite male androgens. This is great for rapid binding and short term aromatase control, but unfortunately a competitive inhibitor will eventually let go of the enzyme and allow it to do feminizing things to manly hormones. So, only half of the job is done, but it has its important role as well.

2.

6 beta-Bromodione is a mechanism-based irreversible inhibitor of the aromatase enzyme. An irreversible aromatase inhibitor is also referred to as a suicide inhibitor. It’s pretty cool in that it acts similar to a competitive inhibitor in the way it binds, but like a pissed-off ex-girlfriend, it is both highly selective and it will not let go until death do they part.

Together the two analogs in 6-Bromodione make sure that estrogen is under control, and many would assume that less estrogen means the prolactin would be under control as well. Often, once prolactin increases are stimulated, shutting it back down takes some extra effort and a protracted period of time.

[Viado]

In all honestly, does it make one really want to try this compound if this is all that is available on it? *sigh*

Great work!

[jrkarp]

okay i'll translate that for those of you who don't speak endocrine.

compound #1 basically binds with estrogen to keep free testosterone and other male androgens from binding, but the binds aren't permanent and they will break ...this is a similar mechanism to DS ActivaTe, i believe except i believe activate targets SHGB (sex hormone binding globulin) directly.

compound #2 suicide inhibitor...similar mechanism to any ATD, AT product...ie it binds with the estrogen and the bond is permanent, however the compound is highly selective in its choice of mates and will probably float around for a couple days before binding (this is why it takes a couple days to notice body composition changes)

Actually completely inaccurate. They bind to the aromatase enzyme, which
converts androgens (like testosterone) to estrogens. They do not bind to estrogen.

ActivaTe binds to SHBG.

[Androgenic]

Well, I found where this data is being drawn from. It does exert anti-aromatase activity, but in this case at the expense of, as a competitive inhibitor of, androstenedione...which as we all know by know is a few steps away in testosterone's production. This gets back to why one would do this unless its for a short period in a hyperestrogenic state, further, as stated previously it will be at the expense of testosterone, as anti-androgen as well if used for any notable period of time. This is from 1. 1987 2. Hardly, a strong credentialed, peer-referenced, stringently reviewed journal 3. Is with rabbits regarding placental aromatase. But taking it for a noteworthy place to start, it is that. There is another Japanese journal publication that uses the 1987 data and elaborates further on the rabbit data with the discussion on the activity of various groups in the molecule...which is a bit more conflicting then stated above in the typical muscle magazine marketing sort of way. But for anyone interested here's the elusive data that's being somewhat distorted and extrapolated.

Endocrinology, Vol 121, 1010-1016, Copyright © 1987 by Endocrine Society
--------------------------------------------------------------------------
Stereochemistry of the functional group determines the mechanism of aromatase inhibition by 6-bromoandrostenedione
Y Osawa, Y Osawa and MJ Coon


A selective inhibitor of aromatase (estrogen synthetase) would be a useful pharmacological tool with potential therapeutic application. We have found that 6 alpha-bromoandrostenedione (6 alpha-BrA) is a competitive inhibitor of human placental aromatase with respect to androstenedione, with an apparent Ki of 3.4 nM, while 6 beta-BrA is a mechanism-based irreversible inhibitor with an apparent Ki of 0.8 microM and a kinact of 0.025 min-1. Aromatase activity was measured by tritium release into water from the 1 beta position of [1(-3)H,4(- 14)C]androstenedione in reaction mixtures containing NADPH and the aromatase. Time-dependent inhibition was assessed by preincubation of inhibitors with either the 900 X g placental pellet or placental microsomes in the presence of NADPH. Aliquots were taken at intervals, diluted, and assayed for aromatase activity with androstenedione and additional NADPH. The time-dependent inhibition by 6 beta-BrA was dependent on the concentration of this compound and the presence of NADPH, while the addition of excess substrate in the preincubation mixture hindered the inactivation. Both epimers were ineffective in inhibiting rabbit liver microsomal drug-metabolizing activities in a competitive or time-dependent manner. This indicates a high selectivity of 6-BrA inhibition among P-450 cytochromes. These and other 6- substituted androgens may be useful probes into the nature of the active site and mechanism of action of aromatase.
__________________________________________________ ______________

Biol Pharm Bull. 2004 Nov;27(11):1878-82. Related Articles, Links


Synthesis and biochemical properties of 6-bromoandrostenedione derivatives with a 2,2-dimethyl or 2-methyl group as aromatase inhibitors.

Numazawa M, Handa W, Yamada K.

Tohoku Pharmaceutical University, Sendai, Japan. numazawa@tohoku-pharm.ac.jp

To gain insight into the mechanism for irreversible inactivation of aromatase by 6beta-bromoandrostenedione (1), one of the earliest discovered suicide substrates, in relation to the catalytic function of the enzyme, the 2,2-dimethyl derivative of compound 1, steroid 4, and its 6alpha-isomer 5, as well as 2-methyl-1,4-diene steroid 8 and its 6alpha-bromide 10, were synthesized. All of the steroids inhibited aromatase activity in human placental microsomes with apparent K(i)'s ranging between 10 and 81 nM. The 2,2-dimethyl-6beta- and 6alpha-bromo steroids 4 and 5 were extremely powerful inhibitors (K(i): 14 and 10 nM, respectively), but these two did not cause a time-dependent inactivation of aromatase in the presence of NADPH; in contrast, the 2-methyl-1,4-diene steroids 8 and 10 caused time-dependent inactivation with apparent k(inact) of 0.035 and 0.071 min(-1), respectively, in a suicide manner. These results indicate that the 2,2-dimethyl function of the 6beta-bromide 4 would prevent the inactivation of aromatase caused by inhibitor 1 in a suicide manner, probably through steric activity, whereas the 2-methyl group of steroid 8 did not significantly affect the suicidal inactivation by the parent 1,4-diene steroid, a typical suicide substrate.

[jrkarp]

Well, I found where this data is being drawn from. It does exert anti-aromatase activity, but in this case at the expense of, as a competitive inhibitor of, androstenedione...which as we all know by know is a few steps away in testosterone's production. This gets back to why one would do this unless its for a short period in a hyperestrogenic state, further, as stated previously it will be at the expense of testosterone, as anti-androgen as well if used for any notable period of time. This is from 1. 1987 2. Hardly, a strong credentialed, peer-referenced, stringently reviewed journal 3. Is with rabbits regarding placental aromatase. But taking it for a noteworthy place to start, it is that. There is another Japanese journal publication that uses the 1987 data and elaborates further on the rabbit data with the discussion on the activity of various groups in the molecule...which is a bit more conflicting then stated above in the typical muscle magazine marketing sort of way. But for anyone interested here's the elusive data that's being somewhat distorted and extrapolated.

Endocrinology, Vol 121, 1010-1016, Copyright © 1987 by Endocrine Society
--------------------------------------------------------------------------
Stereochemistry of the functional group determines the mechanism of aromatase inhibition by 6-bromoandrostenedione
Y Osawa, Y Osawa and MJ Coon


A selective inhibitor of aromatase (estrogen synthetase) would be a useful pharmacological tool with potential therapeutic application. We have found that 6 alpha-bromoandrostenedione (6 alpha-BrA) is a competitive inhibitor of human placental aromatase with respect to androstenedione, with an apparent Ki of 3.4 nM, while 6 beta-BrA is a mechanism-based irreversible inhibitor with an apparent Ki of 0.8 microM and a kinact of 0.025 min-1. Aromatase activity was measured by tritium release into water from the 1 beta position of [1(-3)H,4(- 14)C]androstenedione in reaction mixtures containing NADPH and the aromatase. Time-dependent inhibition was assessed by preincubation of inhibitors with either the 900 X g placental pellet or placental microsomes in the presence of NADPH. Aliquots were taken at intervals, diluted, and assayed for aromatase activity with androstenedione and additional NADPH. The time-dependent inhibition by 6 beta-BrA was dependent on the concentration of this compound and the presence of NADPH, while the addition of excess substrate in the preincubation mixture hindered the inactivation. Both epimers were ineffective in inhibiting rabbit liver microsomal drug-metabolizing activities in a competitive or time-dependent manner. This indicates a high selectivity of 6-BrA inhibition among P-450 cytochromes. These and other 6- substituted androgens may be useful probes into the nature of the active site and mechanism of action of aromatase.

Um, the way I read that, it says that 6-A-BrA competes with andro... at the aromatase enzyme. It doesn't say that it competes with andro at the 17B-hydroxysteroid dehydrogenase, which is what converts andro to test.

This seems to say that this compound keeps androstenedione away from aromatase, which is a good thing. Androstenedione + Aromatase = Estrone

[Androgenic]

Aromatase is an enzyme and its simply an additive chemical reaction like was stated. It is above the arrow (catalyzing in one direction, but there reversible portion of the reaction too, unlike with "suicide inhibition", metioned above, which apparently is what the beta is). Competitive inhibition, with the alpha form, can lead to feedback and ultimately raised levels of estrone with cessation and lower testosterone prior (in a cascade...not one direction, not even really two directions, but multiple loops in multiple direction with numerous impact on enzymatic production, tissues, etc.) to that...hence the chronic use I was discussing. It does work in the short term according to this data. But as discussed previously, this scenario is only desirable in a basic bodybuilding magazine sort of way and not fully understanding the hormonal cascade and enzymatic relationships. And if I was to go this route I would use a product that has been studied more such as 4-hydroxyandrostenedione that is just as obtainable. AI overuse of any kind could lead to osteoporosis, lower strength, lower libido and testosterone and ultimately less muscle. Estrogen is tied into strength and muscle and the most muscle and strength gained are often with the most aromatizable steroids. Not that hyperestrogenemia is a positive situation and these drugs can be used to normalize PCT...but the potent the brief this situation should be. I believe for this very reason people have better long term results with 6-oxo over ATD, related to potencty. Potency is not ultimately the best thing with regards to estrogen/aromatase. Again read Bill Llewelyn's thoughts on AI's being overused or misappropriately used, that aren't SERMs.

If you read my article on DGL, you might get a feel for may grasp on biochem./organic.

[wild1poet2]

Reading this thread is blocking estrogen conversion...LOL but my head is going to explode.

It's a great thread. What my simple mind is taking away is that 6 bromo is of questionable efficacy. Even more disconcerting could cause adverse hormonal response. Are these fair conclusions?

[jrkarp]

Aromatase is an enzyme and its simply an additive chemical reaction like was stated. It is above the arrow (catalyzing in one direction, but there reversible portion of the reaction too, unlike with "suicide inhibition", metioned above, which apparently is what the beta is). Competitive inhibition, with the alpha form, can lead to feedback and ultimately raised levels of estrone with cessation and lower testosterone prior (in a cascade...not one direction, not even really two directions, but multiple loops in multiple direction with numerous impact on enzymatic production, tissues, etc.) to that...hence the chronic use I was discussing. It does work in the short term according to this data. But as discussed previously, this scenario is only desirable in a basic bodybuilding magazine sort of way and not fully understanding the hormonal cascade and enzymatic relationships. And if I was to go this route I would use a product that has been studied more such as 4-hydroxyandrostenedione that is just as obtainable. AI overuse of any kind could lead to osteoporosis, lower strength, lower libido and testosterone and ultimately less muscle. Estrogen is tied into strength and muscle and the most muscle and strength gained are often with the most aromatizable steroids. Not that hyperestrogenemia is a positive situation and these drugs can be used to normalize PCT...but the potent the brief this situation should be. I believe for this very reason people have better long term results with 6-oxo over ATD, related to potencty. Potency is not ultimately the best thing with regards to estrogen/aromatase. Again read Bill Llewelyn's thoughts on AI's being overused or misappropriately used, that aren't SERMs.

If you read my article on DGL, you might get a feel for may grasp on biochem./organic.

I was not questioning your grasp of biochem/organic.

I was questioning an implication you were making.

It does exert anti-aromatase activity, but in this case at the expense of, as a competitive inhibitor of, androstenedione...which as we all know by know is a few steps away in testosterone's production.

Where in those studies does it say that 6-bromo inhibits androstenedione? It does not.

You were implying that 6-bromo will compete to reduce androstenedione levels, and in turn reduce testosterone. If there is an ultimate reduction in test levels, it is not a result of a direct influence of 6-bromo on androstenedione.

I agree with what you are saying about AI overuse.