Boladrol - A Brand New PH from IBE!

Damn, I just remembered this: my only side affect from adrol was severe agrression culminating with me tring to attack a Rottweiler who growled at me on the beach while my girlfriend held me back (she was clueless about my AAS use but I wonder what was going through her mind at the time) Anyway, see the crazy animal metaphor? Sorry guys for derailing this thread!

No, that was the PCP.
 
Man, I can feel a boladrol/epi stack coming on with some 6-bromo thrown in and a kick-ass aggressive PCT!! I say again "THANK YOU IBE!!!" I will adjust when I read some logs as I think that people are jumping to conclusions on the wet sides just by looking at the compound without any empirical evidence to back up their fears.

Wow
 
I've always though that this was the mechanism i.e DHEA metabolites that Trauma1 theorizes and hence a suicide inhibitor (6-OXO etc) would work to stop that DHEA from converting to estrogen

Conversion of DHEA to estrogen is low. It has to convert to 4-androstenedione or testosterone to then be aromatized to estrone and estradiol respectively. The estrogenic actions of DHEA primarily occur through the conversion to 5-androstenediol which has estrogen receptor agonist ability on it's own. An anti aromatase would thus not stop the majority of estrogenic effects from DHEA. You would need a SERM.
 
I don't know that m1t and sd work through the same moa either, sd is super dry usually and m1t is def wet, would be hard pressed to be convinced their estrogenic activity is similar.

I don't think estrogenic potential is the issue with m1t. Water retention can be due to mineralcorticoid agonism, altering mineralcorticoid production, or altering mineralcorticoid metabolism as well. I don't think structurally m1t has any ability to act on the ER. Could be wrong though.
 
First off who are you and why don't you post more? Lol

Awesome info man

Also I was speaking about the possibility that superdrol could effect the er, not m1t. So your take on anadrols estrogenic effects as well?

I don't think estrogenic potential is the issue with m1t. Water retention can be due to mineralcorticoid agonism, altering mineralcorticoid production, or altering mineralcorticoid metabolism as well. I don't think structurally m1t has any ability to act on the ER. Could be wrong though.
 
Beta testers just received their product this week. I'm sure logs will start on monday. I find it strange that it's only a 15 day supply though.

Yeah, I know about these people but I wanted to see the original beta testers. As in, the people who worked for the company that tested the product when it was first finished. I thought that IBE stated there were a few?
 
Yeah, I know about these people but I wanted to see the original beta testers. As in, the people who worked for the company that tested the product when it was first finished. I thought that IBE stated there were a few?

wait, is the recommendation 15 days, or are the pills only good for 15 days ???
 
Conversion of DHEA to estrogen is low. It has to convert to 4-androstenedione or testosterone to then be aromatized to estrone and estradiol respectively. The estrogenic actions of DHEA primarily occur through the conversion to 5-androstenediol which has estrogen receptor agonist ability on it's own. An anti aromatase would thus not stop the majority of estrogenic effects from DHEA. You would need a SERM.

Yeah, I think you're right about this. Forgot about 5-androstenediol having er agonist properties. I need to dust off my steroid pharmacology hat! Anyway, boladrol has got my interest up in this field. Haven't really thought about this stuff in a while.
 
Yeah, I know about these people but I wanted to see the original beta testers. As in, the people who worked for the company that tested the product when it was first finished. I thought that IBE stated there were a few?

Even though I havent gotten my test bottle. I think that IBE is proffesional enough that they wouldnt bring something to market that gave marginal results. This should be as good as anything hitting the market in this time span. There is competition, particularly when this niche has been teetering on the edge for so long.
 
Tester

Yes, you heard it right! IBE is releasing a new PH to the market.
We have already sent out about 15 bottles to beta-testers and we are still looking for some tester/loggers to try this amazing compound before the projected 2-3 week release date of Bolodrol to the public. We are giving away 30+ bottles total to our beta-test groups to get the best data logged as possible while the caps, labels and bottles are finishing up for our big release. If any of you guys are interested in beta-testing contact me via PM because we still have a few bottles left to send out.

Fairly new to these forums which makes me unable to PM people yet. But I am interested if you are still looking for testers.:saroll:
 
I don't think estrogenic potential is the issue with m1t. Water retention can be due to mineralcorticoid agonism, altering mineralcorticoid production, or altering mineralcorticoid metabolism as well. I don't think structurally m1t has any ability to act on the ER. Could be wrong though.

your username looks very familiar but I can't remember where I have seen it before.
 
Even though I havent gotten my test bottle. I think that IBE is proffesional enough that they wouldnt bring something to market that gave marginal results. This should be as good as anything hitting the market in this time span. There is competition, particularly when this niche has been teetering on the edge for so long.

Not to sure why you stated that but I have specific reasons for asking about the A testers, not this current group.
 
I don't think estrogenic potential is the issue with m1t. Water retention can be due to mineralcorticoid agonism, altering mineralcorticoid production, or altering mineralcorticoid metabolism as well. I don't think structurally m1t has any ability to act on the ER. Could be wrong though.

You are speaking about m1t that was released by legal gear several years ago?

Are you saying that it is impossible to have any actions that contribute to estrogenic activity?

Not sure the edge here but are you stating this from actual test ran on people that used the original m1t or white paper research?
 
I saw where someone said dhea converts minimally into estrogen. just want to point out this statement is incorect.

dhea can actually convert directly into estrogen. and it is also a parent hormone for other hormones, not just estrogen, and test.
 
I saw where someone said dhea converts minimally into estrogen. just want to point out this statement is incorect.

dhea can actually convert directly into estrogen. and it is also a parent hormone for other hormones, not just estrogen, and test.

Thats what I thought too. Thanks for clarifying :)

//CC
 
I saw where someone said dhea converts minimally into estrogen. just want to point out this statement is incorrect.
dhea can actually convert directly into estrogen.

As far as I am aware, it is indeed correct. Please point out a metabolic pathway for the DIRECT coversion of DHEA to estrogen, without going through one or more intermediates. I pointed out two off the top of my head, there is also another I can think of with one intermediate. DHEA -> 16 alpha oh DHEA -> 16-alpha OH estrone. One with a couple intermediates is dhea to 4-androstenedione to test to 16 alpha hydroxy test to 16 alpha hydroxy estradiol. All conversions that I am aware of from DHEA to estrogen involve intermediates and are not primary metabolites. If you know of a direct path from dhea to estrogen with a source, please inform me. All studies I have come across have primary metabolites of various dhea hydroxylates, dhea sulfate, and 5-alpha androstanediol. Also, conversion is different from male to female, with male DHEA supplementation yielding fairly small increases in free estrogen, with females having free estrogen double. This is likely from it's greater conversion to testtosterone in women, hence higher aromatization to estrogen. Keep in mind, I am not arguing that DHEA can convert to estrogen downstream through multiple conversions. Rather, I am saying the primary estrogenic effect of DHEA in men comes from its high conversion to 5-androstenediol and it's inherent estrogenic effects.
 
You are speaking about m1t that was released by legal gear several years ago?

Are you saying that it is impossible to have any actions that contribute to estrogenic activity?

Not sure the edge here but are you stating this from actual test ran on people that used the original m1t or white paper research?

It doesn't matter who made the M1T or what anyone thinks it does in real life. 17aa dihydroboldenone (1-test) cannot aromatise, since it is already 5a-reduced. If you used something called M1T and it actually increased estrogen, it was just mislabeled.
 
You are speaking about m1t that was released by legal gear several years ago?

I am speaking about the compound m1t, not any specific manufacturer.

Are you saying that it is impossible to have any actions that contribute to estrogenic activity?

No, otherwise I would have put that in the post. I believe to m1t water gains to be due to either cross reactivity at the PR causing progestenic effects, mineralcorticoid receptor cross reactivity causing Na+ retention, or alterations in mineralcorticoid production and/or metabolism. Which one is it from? I don't know. It is not as well researched a compound as many others.

Not sure the edge here but are you stating this from actual test ran on people that used the original m1t or white paper research?

Going off the structure. M1t is 5-alpha reduced. 5-alpha reduced steroids are generally not agonists at the ER. Anadrol was brought up because it's weird in that it is 5-alpha reduced yet has possible estrogenic activity. I would have to bust out with some research to be sure. It should be somewhere, as it is a well researched steroid. I know some people have speculated the hydroxymethylene to change in vivo resulting in a metabolite that could bind to the er. PA would be a good guy to ask.
 
Ya, in all the profiles I've read on anadrol they've mentioned its intrinsic estrogenic effects but none can pinpoint its moa....

Most the studies done on it too I've found are regarding its use in preventing muscle wasting and its toxicity but nothing significant regarding its estrogenic effects.... Just speculation that it direct binds or possibly a metabolite does...

Wonder if it releases bound by shbg estrogen and that's part of it...
 
Also I was speaking about the possibility that superdrol could effect the er, not m1t. So your take on anadrols estrogenic effects as well?

Anadrol is a mystery to me that I should look into when I have time. Might convert to an estrogenic metabolite. Or, it could be this:

neither convert to DHT. anadrol is a DHT derivative however. halo OTOH is not a DHT derivative, it is a testosterone derivative

Also, neither should aromatize to estrogens. However, anadrol may have intrinsic estrogenic activity (binds directly to the estrogen receptor). I say this because like estrogens, anadrol has an acidic proton on the outer side of the A-ring (and this property may be very important to estrogen's binding to estrogen receptor)
Source: forum.bodybuilding.com/showpost.php?p=7414027&postcount=20

That is an old quote (2005) from Patrick Arnold. He may have come across research indicating something else since then. Someone should ask.

As far as superdrol, some say it is more androgenic than Vida tests etc. would indicate. If so, it shouldn't cause estrogenic sides, as it wouldn't seem to be able to bind to the ER being 5-alpha reduced, and its androgenic activity would oppose estrogenic effects. If it is indeed as low on the androgenic potency as Vida says, that could be the cause, but I would still think the lengthy action (long half life from 17a-methylation) of it and decent androgenic potency, along with being taken in supraphysiological levels for an androgen would combat estrogenic sides. In that case, it could be from contamination with another steroid from the manufacturer.
Another question is this; when are the estrogenic sides experienced? Many 17a methyls lower SHBG. If the steroid is administered and SHBG is reduced in the first few days, the initial circulating T and E, much of it bound to SHBG and serum albumin produced before HPTA shutdown starts could be freed up to act at the ER. The freed estrogen could act directly, and the freed testosterone would be likely to convert via aromatase to estrogen and do the same. Circulating aromatase can't act on superdrol so it would be available to act on the freed T. So estrogenic sides at the cycle onset might be possibly reasonable. Also, estrogenic sides post cycle while T/E ratio is low and superdrol is no longer circulating to oppose estrogen makes sense as well. Estrogenic effects during the cycle would be the toughest to explain. I am just throwing out ideas here.
 
Wonder if it releases bound by shbg estrogen and that's part of it...

Ha. Exactly what I was just thinking. One of these days when I get a chunk of free time I should do some research on it. Post any studies you find on it. The chemical is well researched enough and around long enough for the answer to be somewhere.
 
And you posted what I was thinking about anadrol DIRECTLY binding to the ER....

hell why not? Its binding affinity for the AR is nill not withstanding it Is derived from dht, yet its def exerting a typical steroidal/hormonal effect SO its def possible its still binding to the ER as well as exerting direct effects on muscle protein mitochondria...

This is all just me thinking out loud though and likely is completely wrong, but I'm a technician and trouble shooting its what i do .... Eliminate other factors and what your left with is most likely the answer .... Prob is I don't know the machine that the body is as much as I know electronic/mechanic systems.... Could be plenty other moa's I don't even know exist.
 
It doesn't matter who made the M1T or what anyone thinks it does in real life. 17aa dihydroboldenone (1-test) cannot aromatise, since it is already 5a-reduced. If you used something called M1T and it actually increased estrogen, it was just mislabeled.


If was looking at structure then, yes, I would have not added the name brand because I know what the chemical makeup says. I am not ignorant to the structure by any means.

You are questioning what I am posting as if you are saying that i am lying...I don't get YOUR POINT.

That is MY point. There is or was no "THINKING in real life" or whatever you are talking about.

There were blood works done on subjects using M1t by legal gear, IN REAL LIFE, in which their estrogen increased, me being one of them. So, it DOES matter about the manufacturer if said manufacturer was mislabeling their products. This is why I placed the comment in there about original/legal gear.
 
I am speaking about the compound m1t, not any specific manufacturer.



No, otherwise I would have put that in the post. I believe to m1t water gains to be due to either cross reactivity at the PR causing progestenic effects, mineralcorticoid receptor cross reactivity causing Na+ retention, or alterations in mineralcorticoid production and/or metabolism. Which one is it from? I don't know. It is not as well researched a compound as many others.



Going off the structure. M1t is 5-alpha reduced. 5-alpha reduced steroids are generally not agonists at the ER. Anadrol was brought up because it's weird in that it is 5-alpha reduced yet has possible estrogenic activity. I would have to bust out with some research to be sure. It should be somewhere, as it is a well researched steroid. I know some people have speculated the hydroxymethylene to change in vivo resulting in a metabolite that could bind to the er. PA would be a good guy to ask.

Thanks, just clearing it up. This conversation has been done on this board and bb, elite fitness, etc several years ago. I was only stating that during my time with that PARTICULAR manufacturer, I experienced issues with estrogen increasing. Also, i have read the blood work of a few others with the same issues.

I am very aware of what you stated here.
 
I stand corrected, after viewing all the pathways & metabolism of cholesterol, pregenolone, & dhea, I was mis informed (how, im not sure) but it looks like it must first convert into androstenedione first.

but, how much converts into estrogen or testosterone will vary person to person, and will have a number of factors that come into play.
 
As far as I am aware, it is indeed correct. Please point out a metabolic pathway for the DIRECT coversion of DHEA to estrogen, without going through one or more intermediates. I pointed out two off the top of my head, there is also another I can think of with one intermediate. DHEA -> 16 alpha oh DHEA -> 16-alpha OH estrone. One with a couple intermediates is dhea to 4-androstenedione to test to 16 alpha hydroxy test to 16 alpha hydroxy estradiol. All conversions that I am aware of from DHEA to estrogen involve intermediates and are not primary metabolites. If you know of a direct path from dhea to estrogen with a source, please inform me. All studies I have come across have primary metabolites of various dhea hydroxylates, dhea sulfate, and 5-alpha androstanediol. Also, conversion is different from male to female, with male DHEA supplementation yielding fairly small increases in free estrogen, with females having free estrogen double. This is likely from it's greater conversion to testtosterone in women, hence higher aromatization to estrogen. Keep in mind, I am not arguing that DHEA can convert to estrogen downstream through multiple conversions. Rather, I am saying the primary estrogenic effect of DHEA in men comes from its high conversion to 5-androstenediol and it's inherent estrogenic effects.

Great post. All of the research I've done on this subject concurs with what you've stated here.



-John
 
Nice little tidbit on gynodrol manifestion there brah.

How would you counteract this "theory".. Specifically, what type of product?

I must have missed this before, sorry bro.

I'll get a response back tonight when i have a bit more time.



-John
 
Is there any recommendations on stacking anything with this??? not referring to another ph really, just supplements in general
 
Cycle assist
Multi vitamin
Taurine (in case of back pumps like I had with sd and m1t)
Pottasium (in case of back pumps)
Have an ai in hand and serm, if not used on cycle then of course use for pxt
Bcaa's can be helpful
P5P or 1- carboxy/mucuna pruriens/l-dopa for possible prolactin (who knows its new)


I also like to dose extra leucine in my shakes and bcaas but that's not necessary....

I'm sure I'll think of more but that's basically what I'm sitting on ready to use with my run...
 
Oh ya, also the l-dopa is great for sleep, given some compounds give some guys trouble with on cycle and sleep is crucial since its when you grow.
 
Oh ya, also the l-dopa is great for sleep, given some compounds give some guys trouble with on cycle and sleep is crucial since its when you grow.

Not to mention it's good insurance against prolactin induced gyno and just an all around great supp!
 
forgive me if this has been mentioned (10 pages is too much to go through) but when is this product going to be available? Just curious... :)
 
I think what HeretoStudy was trying to say was that those that have run some of the harsher ph's would know what to do if a bad side effect occurs and have experience handling the sides. I don't think he meant it would necessarily be safer..
 
i guess that guy uses nothing when he goes to get a toof pulled... i mean, what's the difference? you have a ton of pain you take a pill... you want a little more nutrition, you take a shake... you want an advantage in the gym, you take a pill... it's all the same to me... :cheers:

So take a pill to eat.
Take a pill to s hit.
Take a pill to stop the side effects of another pill.
Take a pill to sleep.
Take a pill to wake up.
Take a pill to go to the gym.

Where does it stop?. Supplementation is fine with me. However some people go overboard. They do cycle after cycle after cycle. If these people really gained the muscle they say they do from taking PH/PS products than within only a few years they would all be entering Mr.O!.
 
all in all, i dont think it matters enough to make a statistical difference. but, if one wanted maximum absorbtion of active methylated steroids, they would take them on an empty stomach.

steroids are fat soluble, and some of the steroid could get passed through along with the undigested fat.


That makes no sense.
 
Wait....so for those with experience it would be safer?:think:

T-Bone, did I do something to upset you? I feel like you are trying to call me out often. As mentioned, it is obvious that I meant someone who knows what to expect out of a harsh cycle would be better off running something that at this point most are predicting to be very harsh. I in no way attempted to argue that someone who has done harsher steroids is immune side effects.
 
So take a pill to eat.
Take a pill to s hit.
Take a pill to stop the side effects of another pill.
Take a pill to sleep.
Take a pill to wake up.
Take a pill to go to the gym.

Where does it stop?. Supplementation is fine with me. However some people go overboard. They do cycle after cycle after cycle. If these people really gained the muscle they say they do from taking PH/PS products than within only a few years they would all be entering Mr.O!.

some of the BEST physiques i have ever seen have been in NATURAL bodybuilding competition where size isnt everything but quality is
 
some of the BEST physiques i have ever seen have been in NATURAL bodybuilding competition where size isnt everything but quality is

I think he meant that there are a large number of sites with members and many of those members piss away money but get little to no results.

Most of those lack of results coming from a lack of knowledge.
 
T-Bone, did I do something to upset you? I feel like you are trying to call me out often. As mentioned, it is obvious that I meant someone who knows what to expect out of a harsh cycle would be better off running something that at this point most are predicting to be very harsh. I in no way attempted to argue that someone who has done harsher steroids is immune side effects.

No I wasn't trying to call you out. Just trying to get a feel for what you were trying to say. In general on this board and many others people have the mentality that if its a harsher PH/PS product than it should only be used by those with experience. Now, besides the knowledge that this "experienced person" may or may not have about steroids what is the point?.

The inexperienced person can do the research on the product on his or her own. However,if it is a new untested product with extremely limited research and findings, than I would think whether the experienced person took it or the newbie it wouldn't make much difference. They both have the same knowledge about this new product and only got that knowledge from reading things on the internet that may or may not be truth.

I'm not trying to argue, just trying to start up an interesting conversation and get some answers and opinions on this subject.
 
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