On an empty stomach - with food - or doesn't matter?
thanks -
thanks -
What he said.2mg twice day. spaced in 8~12 hours.
Absortion will be better with some fat. go with fish oil + bolasterone.
I hear taking methyls with carbs and EFAs makes it a little easier on the liver.
this is perfects, also to keep in mind, boladrol is a diol compound, and does not need to convert in order to bind to the androgen receptor.Its a pro hormone (will need to be converted in the body to bolasterone)so you may get better absorbtion on an empty stomach. The grapefruit juice could possibly help also.
this is right, or if you bought two bottles (does it come in bottles or packages?) you can run a higher dose after the first 2 weeks, (like 6-8mg)2mg twice day. spaced in 8~12 hours.
no, fats dont do much to help absorbtion of methylated compounds, best to take it on an empty stomach.Absortion will be better with some fat. go with fish oil + bolasterone.
Wait a second, Boladrol doesn't become active unless the 3 Beta Hydroxy Steroid enzyme converts it upon ingestion..and it stays inactive if this converts into something different upon interference. I could've sworn this was the case. Enlighten me?boladrol is a diol compound, and does not need to convert in order to bind to the androgen receptor.
whats this mean? it is already an active compound, but does have the potential to convert into a stronger one
Dimethyls are a lot worse. Superdrol and Dimethyzine for instance. But then again, single methyls are usually run at higher doses (besides a few) so it could be equally harsh.I don't know if dimethyls are equally harsh on the liver at methyls.
Wait a second, Boladrol doesn't become active unless the 3 Beta Hydroxy Steroid enzyme converts it upon ingestion..and it stays inactive if this converts into something different upon interference. I could've sworn this was the case. Enlighten me?
Ok that was very clear and concise. This explains why diols have a higher potency than diones. Thankyouboladrol is a andro-diol pro hormone. diols are different than diones in that d/t their structure, they are already able to bind to the androgen receptor.
the binding to the a.r. will not be as strong as say bolasterone, but still binds to the androgen receptor.
another common one is cdma, commonly known as halodrol. this is an already active compound which converts into a more potent compound, but does not need to convert in order to bind to the ar.
all diol compounds will have this ability.
just because something can convert into another more potent compound, doesn't mean it isn't already able to have interaction.
this is a common misconception.
and because it is 7,17 dimethylated, it has oral availability, and does not need to convert.
Now this I don't agree with. If all diols are incapable of aromatization then why does Methyl 1, 4-Diol have considerable amounts of estrogen conversion? Because of the abscence of the 4-chloro. Diols/diones have little to do with aromatizing. 4-androstenediol is another perfect example, it's a diol with considerable aromatization.another thing people dont realize is that diol's are incapable of aromatization. meaning, some users of this compound (those who don't see alot of water retention) who have poor conversion, will see possibly leaner gains, and may also have to dose higher, d/t it not binding as strongly as bolasterone to the androgen receptor.
because like bolasterone (converted boladrol) m14add converts into dianabol, which is also a compound which like bolasterone, converts into a more potent estrogen.Ok that was very clear and concise. This explains why diols have a higher potency than diones. Thankyou
Now this I don't agree with. If all diols are incapable of aromatization then why does Methyl 1, 4-Diol have considerable amounts of estrogen conversion? Because of the abscence of the 4-chloro. Diols/diones have little to do with aromatizing. 4-androstenediol is another perfect example, it's a diol with considerable aromatization.
Sorry not trying to pick apart your post, my original question was answered. Thanks
A steroid needs a 3-ketone in order to aromatize, which this (diols) does not have. this compound is also a diol, and should have some binding ability to the androgen receptor itself, needing no conversion to begin working.
I have a paper sent to me from henryv that I need to read that will give me more of an idea on the aromatization of bolasterone, which he says, looks like it will aromatize less than methyl testosterone.
This would, theoretically, mean that boladrol doesn't convert to Bolasterone at a high rate because many users are experiencing, like myself, lean gains. So if bolasterone has a higher estrogen conversion than Dianabol and M14ADD has a higher estrogen conversion than Boladrol then something must be interfering with Boladrol's conversion because Boladrol should aromatize at a higher rate than M14ADD.. see what i'm saying?because like bolasterone (converted boladrol) m14add converts into dianabol, which is also a compound which like bolasterone, converts into a more potent estrogen.
bolasterone + aromatase enzyme= di methyl estradiol
dianabol + aromatase enzyme= methyl estradiol.
but again, like I said, all this information I posted can be found in the original boladrol release thread.
Well one would have to run Bolasterone to see if it does aromatize as high as Dianabol. So I guess the di-methyl estradiol has no merit in that sense. How could a methylation at the 7th position reduce a dimethyl estrogen to being less potent in aromatization than a methyl estrogen? Wish I could see that paper you readwell, two things, it has been suggested in a paper that bolasterone's conversion into methyl estradiol is significantly less than that of methyl testosterone, which is just one less methyl (the 7a).
7a methylation greatly changes the compound, in the same sense that adding a 17a methyl changes a compound.
for example, boldenone has less aromatization than testosterone, but add a 17a methyl, and (now dianabol) has a higher rate or aromatization, also into a more potent estrogen.
so it is most likely the 7a methylation that changes up the compound in this way, as well as many others.
I do have it, here is some of what it says:Well one would have to run Bolasterone to see if it does aromatize as high as Dianabol. So I guess the di-methyl estradiol has no merit in that sense. How could a methylation at the 7th position reduce a dimethyl estrogen to being less potent in aromatization than a methyl estrogen? Wish I could see that paper you read
Cool that'd be greatif I ever email mw, i'll send that paper to him for you to read.
oh okactually, i have to edit this, I just looked for the paper, looks like i deleted it, i'll have to get another copy from henry v.
loledit again, I think, im looking again.
:bling:I do have it, here is some of what it says:
Thus it was suggested that structural
modifications (7a methylation) of a compound can lead to changes in its biological
activity based on binding affinity, differences in absorption,
binding to plasma proteins and/or susceptibility to the action of
metabolizing enzymes.
[...]
7-Alkyltestosterone derivatives show a progressive
loss in activity, as competitive inhibitors of aromatase, as chain
length increases. The change in binding affinity of these compounds
seems too gradual to be the result of an absolute lack
of bulk tolerance by the receptor.
The similar affinities found for
the 7-hydroxypropyl and the isosteric 7-butyl derivatives of
testosterone indicate that the reduction in affinity cannot arise
solely as a consequence of a hydrophobic chain into a hydrophobic
pocket.
This is talking about estrogen receptor affinity right? Is this the conclusion as to why it reduces affinity or just one of the reasons?I do have it, here is some of what it says:
Thus it was suggested that structural
modifications (7a methylation) of a compound can lead to changes in its biological
activity based on binding affinity, differences in absorption,
binding to plasma proteins and/or susceptibility to the action of
metabolizing enzymes.
[...]
7-Alkyltestosterone derivatives show a progressive
loss in activity, as competitive inhibitors of aromatase, as chain
length increases. The change in binding affinity of these compounds
seems too gradual to be the result of an absolute lack
of bulk tolerance by the receptor.
The similar affinities found for
the 7-hydroxypropyl and the isosteric 7-butyl derivatives of
testosterone indicate that the reduction in affinity cannot arise
solely as a consequence of a hydrophobic chain into a hydrophobic
pocket.
I saw he posted that. M14ADD looks like it would have trouble making the conversion to Dianabol. It has to gain a hydroxylation somehow and then dehydrate before it can make that conversion right? Is that via the 3b-HSD pathway or another enzyme pa is talking about because I always thought 17a-methyl-1,4-androstadiene-3b,17b-diol + 3b-HSD = 17a-methyl-1,4-androstadiene-3-one-17b-olim looking into some info of methyl 1,4-androstenediol (m14add) possibly being able to convert into estrogen via a non enzymatic reaction. (according to pa, this may be possible)
not sure if this would also pertain to all diols, like boladrol. 1,4ad seems to be different in how it would need to be converted. I think.
It's so complex, and I can access the paper pa told me to read.
No-one's said that bolasterone has a higher estrogen conversion than dianabol.This would, theoretically, mean that boladrol doesn't convert to Bolasterone at a high rate because many users are experiencing, like myself, lean gains. So if bolasterone has a higher estrogen conversion than Dianabol and M14ADD has a higher estrogen conversion than Boladrol then something must be interfering with Boladrol's conversion because Boladrol should aromatize at a higher rate than M14ADD.. see what i'm saying?
I've heard this information before so I know you're right.
Do you have any evidence that dianabol aromatises more readily than boldenone?well, it has been suggested in a paper that bolasterone's conversion into methyl estradiol is significantly less than that of methyl testosterone, which is just one less methyl (the 7a).
7a methylation greatly changes the compound, in the same sense that adding a 17a methyl changes a compound.
for example, boldenone has less aromatization than testosterone, but add a 17a methyl, and (now dianabol) has a higher rate or aromatization, also into a more potent estrogen.
so it is most likely the 7a methylation that changes up the compound in this way, as well as many others.
bolasterone's estrogen conversion would be more potent than dianabols, because of the extra 7a methylation, but this is also what is suggested to cause it's estrogen conversion to be so much less than that of methyl testosterone.
remember "more potent" and "the rate of estrogen conversion" are two different things, which bolasterone seems to have lowered conversion into estrogen, but that the estrogen converted will just hang around longer.
It's not talking about ER affinity. It's talking about the affinity of the compound for binding to the aromatase enzyme.This is talking about estrogen receptor affinity right? Is this the conclusion as to why it reduces affinity or just one of the reasons?
The point of 7 alkylation is to reduce the 5a-reductase enzyme, but it seems this change has effected potency of the compound and aromatization.
That's always been the assumption.I always thought 17a-methyl-1,4-androstadiene-3b,17b-diol + 3b-HSD = 17a-methyl-1,4-androstadiene-3-one-17b-ol
Of course not, I am probably committing the same error I accuse people of doing, in mixing up the potency of methyl estrogen vs estrogen & rate of aromatization.Do you have any evidence that dianabol aromatises more readily than boldenone?
What does it mean by "as the size of group at C-7 position increased?" What causes this size increase? ; as this excerpt makes it sound like this "size increase" of the carbon molecule at the 7th position is what's responsible for Bolasterone's and Calusterone's A/A ratio (or any 7a for that matter)7-alkyltestosterone derivatives were tested and were found to lose androgenic and anabolic activity rapidly as the size of the group at the C-7 position increased.
^One can only imagine how suppressive ment-dione will be. Good lord. 7a methylation, according to this text, only increases androgenicity in a 19 nor derivative like ment-dione..:dead: ~ EDIT: NVM, it says only if it has a 17a methylation, so disregard this one :biggthumpup:7-methylation of 19-nor androgens with a 17-methyl group causes a many fold increase in androgenicity due to a sufficient protection of the 17-methyl group that permits delivery of the highly active 19-nor steroid to the end organ
They tested a number of 7a-alkylated testosterone derivatives with different 7a-substituents. They found that smaller functional groups (like a methyl group) caused a significant increase in anabolic and androgenic activity, but the larger the substituent, the less anabolic and androgenic activity was seen.Two excerpts from the text jbry posted that really stuck out at me..
What does it mean by "as the size of group at C-7 position increased?" What causes this size increase? ; as this excerpt makes it sound like this "size increase" of the carbon molecule at the 7th position is what's responsible for Bolasterone's and Calusterone's A/A ratio (or any 7a for that matter)
They tested a number of 7a-alkylated testosterone derivatives with different 7a-substituents. They found that smaller functional groups (like a methyl group) caused a significant increase in anabolic and androgenic activity, but the larger the substituent, the less anabolic and androgenic activity was seen.
Oh duh, somehow I missed this part of the paper. So basically that means methyl substitution was the most prudent in comparison to a cyano group and the others that were tested (does not surprise me, it's always a methyl lmao). But how would that relate to size? Is a cyano larger than a methyl group or something?The substitution at the 7-position with a cyano or
acetylthio moiety resulted in lower binding affinity and decreased
biological activity compared to the 7-methyl substitution
A methyl group is a small functional group. This is why it is used at 17a. Its existence prevents the 17b-ol from becoming a 17-one, but it is small enough not to impair receptor binding. The same is true of the 7a position - a methyl group here imparts a number of positive receptor binding effects that larger substituents do not.Oh duh, somehow I missed this part of the paper. So basically that means methyl substitution was the most prudent in comparison to a cyano group and the others that were tested (does not surprise me, it's always a methyl lmao). But how would that relate to size? Is a cyano larger than a methyl group or something?
Ok thanks henry, yeah I knew it wasn't talking about anything specific I just drew conclusions from its context.A methyl group is a small functional group. This is why it is used at 17a. Its existence prevents the 17b-ol from becoming a 17-one, but it is small enough not to impair receptor binding. The same is true of the 7a position - a methyl group here imparts a number of positive receptor binding effects that larger substituents do not.
The paper it is referring to does not study bolasterone specifically, or a testosterone derivative with a 7a cyano group.
It would seem that way. It would've been more consumer friendly to make the tablets 3-4mg, At 8 mg I could feel it in full swing and leaned out nicelyso far it is looking like boladrol dosage should be dosed between 8-10mg
Split into 2 equal AM and PM doses?so far it is looking like boladrol dosage should be dosed between 8-10mg
Interesting.the next run will be 3 or 4mg per tablet we still did not make out minds up yet..lol
CorrectBoladrol is in tablet form and not a capped pill correct?
Don't split them, they are incredibly smallThanks. How big are the tabs? Just wondering if I could easily split them
It's like the size of an Aspirin. And there is no reason to take 1 mg of Boladrol.Thanks. How big are the tabs? Just wondering if I could easily split them
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