Discussion Why metribolone is the best ligand for maximum muscular hypertrophy (1 Viewer)

[R1881]

why it matters to run insane compounds rather than just test and EQ

so basically as we know physique is a crazy halo even for men especially if you are average height or above. I don't need to explain why I get some of you fat piece of shit will say "nah man its my height" yeah no shit I'm 5 foot 8 and if I were to stay here I might as well kms but physique is a crazy halo. in addition stronger androgens help with cD1 expression for chondrocytes. I will do a debunk on the maturative properties of androgens to the growth plate if anyone asks. tldr its the cell cycle. so basically the point with roids is because we are genetic failures we need to get a big physique as fast as possible

safety profile of metribolone
ok liver based on all anecdotes I have seen with inj. vs oral and I've read a half dozens peoeple blood works from metribolone injectably the liver damage from orals seems to be Cmax based rather than AUC based which aligns with the way the liver works. Also due to low substrate amount the toxicity from metribolone must be its androgenicity down regulating FXN which can be very easily fixed with TUDCA and its genomic interactions like honestly based on things I've seen inj. mtren is not that liver toxic the only reason oral was so bad in trials was because it was a crazy Cmax that drived so much androgenicity and took to long to clear than it downregulated BSEP and was just shit in general. so idk what to tell you I'm testing it on my unpaid client (I just test shit on him ik him irl) as we speak and he will get blood work soon. ik its n=1 but I'm not gonna run a fucking trial I've seen 10 peoples blood works chilling on inj mtren

why mtren mogs
basically for two reasons the first is the shape of the molecule. do you know why they make 19-nors? obv not because no one reads. the reason is because the A ring will shift out of the original plane that is in testoerone. so the molecule becomes more planar and the active site of the AR is planar so there u go. This is why dimethyltren and trimethyl tren is stupid and if you run it you should die. The Kd may be high (idk) but the transcriptional affinity is 0 because the methyl group sticks out. And then they put a triene core so it doesnt aromatize. And the 17aa makes it literally invincible to IC metabolism which is awesome so it yeah. And then the other reason is the fact that it doesn't go under metabolism IC so basically it stays in the cell really long unlike TREN which metabolizes.

theory behind using little mg of ligands
basically you have finite ARs and AMARU is also finite (3x estimate) feel free to fact check me if I am wrong. so basically you don't need that much ligand and using weaker ligands to saturate the AR will get mogged by stronger ligands. for the AR specifically 150 Tren mogs 10,000 EQ you know what I mean so basically all we need to do is run mtren for the perfect ar

the math

TREN/metribolone RECEPTOR OCCUPANCY
we are going to use Kd of 0.3 and 0.1 for TREN and mtren
gaddum childs equation to find the concentration needed ->
70kg man with Vd of 5 which is normal for AAS is 350L of volume
so we get for 90% saturation we need a trough of this many in the body:
we get 260mcg for tren
and 90mcg for metribolone
so wait? why is TREN so low? if I ran 260mcg of TREN daily I wouldn't feel it!
tren undergoes extenseive metabolism, It is by no means a metabolically stable molecule.
mtren ONLY gets metabolized in the liver, not IC, explaining its potency
anyway that was just to show u some cool stuff
250mcg of metribolone twice daily -> factor in tissue diffusion rate we can easily maintain a trough of 90mcg which is likely an overestimate
"but muh half life is 4 hours" thats serum, not tissue, refer to large Vd

so what else

no other androgens besides test and oxymetholone with the mtren or they will inhibit it as the Kd is not gapped with trenb for example but the transcriptional affinity is
uh use lantus hgh thyroid hormones humalog ghs try to keep e2 high if you worried about plates just take tamox and DNR

 

[R1881]

workout/diet
workout obviously should be FBEOD split avoiding technical compounds like squats and bench, SLDL is acceptable
train at MRV
eat at a surplus where body fat goes up very slightly week to week to ensure one is not in a systemic deficit (muscles will be in a surplus even on 1600 calories ofc haha don't starve your non AR expressive organs)

ancillaries
you know liver shit TUDCA and NACET are prolly the big ones

 

[Skull]

Hmm...

 

[R1881]

Hmm...

 

[ΜπιγκΜπλακΚοκ]

Damn you are actually smart
I thought you where using Jew-GBT for a second

 

[R1881]

Damn you are actually smart
I thought you where using Jew-GBT for a second

solid 80% chance you were raped as a child btw don't fucking complement me u down syndrome motherfucker

 

[goyboy.hero]

why it matters to run insane compounds rather than just test and EQ

so basically as we know physique is a crazy halo even for men especially if you are average height or above. I don't need to explain why I get some of you fat piece of shit will say "nah man its my height" yeah no shit I'm 5 foot 8 and if I were to stay here I might as well kms but physique is a crazy halo. in addition stronger androgens help with cD1 expression for chondrocytes. I will do a debunk on the maturative properties of androgens to the growth plate if anyone asks. tldr its the cell cycle. so basically the point with roids is because we are genetic failures we need to get a big physique as fast as possible

safety profile of metribolone
ok liver based on all anecdotes I have seen with inj. vs oral and I've read a half dozens peoeple blood works from metribolone injectably the liver damage from orals seems to be Cmax based rather than AUC based which aligns with the way the liver works. Also due to low substrate amount the toxicity from metribolone must be its androgenicity down regulating FXN which can be very easily fixed with TUDCA and its genomic interactions like honestly based on things I've seen inj. mtren is not that liver toxic the only reason oral was so bad in trials was because it was a crazy Cmax that drived so much androgenicity and took to long to clear than it downregulated BSEP and was just shit in general. so idk what to tell you I'm testing it on my unpaid client (I just test shit on him ik him irl) as we speak and he will get blood work soon. ik its n=1 but I'm not gonna run a fucking trial I've seen 10 peoples blood works chilling on inj mtren

why mtren mogs
basically for two reasons the first is the shape of the molecule. do you know why they make 19-nors? obv not because no one reads. the reason is because the A ring will shift out of the original plane that is in testoerone. so the molecule becomes more planar and the active site of the AR is planar so there u go. This is why dimethyltren and trimethyl tren is stupid and if you run it you should die. The Kd may be high (idk) but the transcriptional affinity is 0 because the methyl group sticks out. And then they put a triene core so it doesnt aromatize. And the 17aa makes it literally invincible to IC metabolism which is awesome so it yeah. And then the other reason is the fact that it doesn't go under metabolism IC so basically it stays in the cell really long unlike TREN which metabolizes.

theory behind using little mg of ligands
basically you have finite ARs and AMARU is also finite (3x estimate) feel free to fact check me if I am wrong. so basically you don't need that much ligand and using weaker ligands to saturate the AR will get mogged by stronger ligands. for the AR specifically 150 Tren mogs 10,000 EQ you know what I mean so basically all we need to do is run mtren for the perfect ar

the math

TREN/metribolone RECEPTOR OCCUPANCY
we are going to use Kd of 0.3 and 0.1 for TREN and mtren
gaddum childs equation to find the concentration needed ->
70kg man with Vd of 5 which is normal for AAS is 350L of volume
so we get for 90% saturation we need a trough of this many in the body:
we get 260mcg for tren
and 90mcg for metribolone
so wait? why is TREN so low? if I ran 260mcg of TREN daily I wouldn't feel it!
tren undergoes extenseive metabolism, It is by no means a metabolically stable molecule.
mtren ONLY gets metabolized in the liver, not IC, explaining its potency
anyway that was just to show u some cool stuff
250mcg of metribolone twice daily -> factor in tissue diffusion rate we can easily maintain a trough of 90mcg which is likely an overestimate
"but muh half life is 4 hours" thats serum, not tissue, refer to large Vd

so what else

no other androgens besides test and oxymetholone with the mtren or they will inhibit it as the Kd is not gapped with trenb for example but the transcriptional affinity is
uh use lantus hgh thyroid hormones humalog ghs try to keep e2 high if you worried about plates just take tamox and DNR

Mirin iq

 

[goyboy.hero]

why it matters to run insane compounds rather than just test and EQ

so basically as we know physique is a crazy halo even for men especially if you are average height or above. I don't need to explain why I get some of you fat piece of shit will say "nah man its my height" yeah no shit I'm 5 foot 8 and if I were to stay here I might as well kms but physique is a crazy halo. in addition stronger androgens help with cD1 expression for chondrocytes. I will do a debunk on the maturative properties of androgens to the growth plate if anyone asks. tldr its the cell cycle. so basically the point with roids is because we are genetic failures we need to get a big physique as fast as possible

safety profile of metribolone
ok liver based on all anecdotes I have seen with inj. vs oral and I've read a half dozens peoeple blood works from metribolone injectably the liver damage from orals seems to be Cmax based rather than AUC based which aligns with the way the liver works. Also due to low substrate amount the toxicity from metribolone must be its androgenicity down regulating FXN which can be very easily fixed with TUDCA and its genomic interactions like honestly based on things I've seen inj. mtren is not that liver toxic the only reason oral was so bad in trials was because it was a crazy Cmax that drived so much androgenicity and took to long to clear than it downregulated BSEP and was just shit in general. so idk what to tell you I'm testing it on my unpaid client (I just test shit on him ik him irl) as we speak and he will get blood work soon. ik its n=1 but I'm not gonna run a fucking trial I've seen 10 peoples blood works chilling on inj mtren

why mtren mogs
basically for two reasons the first is the shape of the molecule. do you know why they make 19-nors? obv not because no one reads. the reason is because the A ring will shift out of the original plane that is in testoerone. so the molecule becomes more planar and the active site of the AR is planar so there u go. This is why dimethyltren and trimethyl tren is stupid and if you run it you should die. The Kd may be high (idk) but the transcriptional affinity is 0 because the methyl group sticks out. And then they put a triene core so it doesnt aromatize. And the 17aa makes it literally invincible to IC metabolism which is awesome so it yeah. And then the other reason is the fact that it doesn't go under metabolism IC so basically it stays in the cell really long unlike TREN which metabolizes.

theory behind using little mg of ligands
basically you have finite ARs and AMARU is also finite (3x estimate) feel free to fact check me if I am wrong. so basically you don't need that much ligand and using weaker ligands to saturate the AR will get mogged by stronger ligands. for the AR specifically 150 Tren mogs 10,000 EQ you know what I mean so basically all we need to do is run mtren for the perfect ar

the math

TREN/metribolone RECEPTOR OCCUPANCY
we are going to use Kd of 0.3 and 0.1 for TREN and mtren
gaddum childs equation to find the concentration needed ->
70kg man with Vd of 5 which is normal for AAS is 350L of volume
so we get for 90% saturation we need a trough of this many in the body:
we get 260mcg for tren
and 90mcg for metribolone
so wait? why is TREN so low? if I ran 260mcg of TREN daily I wouldn't feel it!
tren undergoes extenseive metabolism, It is by no means a metabolically stable molecule.
mtren ONLY gets metabolized in the liver, not IC, explaining its potency
anyway that was just to show u some cool stuff
250mcg of metribolone twice daily -> factor in tissue diffusion rate we can easily maintain a trough of 90mcg which is likely an overestimate
"but muh half life is 4 hours" thats serum, not tissue, refer to large Vd

so what else

no other androgens besides test and oxymetholone with the mtren or they will inhibit it as the Kd is not gapped with trenb for example but the transcriptional affinity is
uh use lantus hgh thyroid hormones humalog ghs try to keep e2 high if you worried about plates just take tamox and DNR

Bookmarked and donated as well

 

[humanupgraded]

Omg no lol

 

[R1881]

Omg no lol

guy gets one water write up on bio.science and he thinks he's the shit

 

[humanupgraded]

guy gets one water write up on bio.science and he thinks he's the shit

Doesn't change what you said isn't wrong.

 

[R1881]

Doesn't change what you said isn't wrong.

did you mean is wrong

 

[humanupgraded]

did you mean is wrong

Yes lmao, the receptor occupancy is oversimplified but I can see where you are getting at about its potency.

 

[R1881]

Yes lmao, the receptor occupancy is oversimplified but I can see where you are getting at about its potency.

tell me what nuance could be added that would drastically shift the number involved for both ligands, especially metribolone
the more compartment extrapolations made reduces the theoretical accuracy of our ligand
the whole calculations were made to make a point: you don't need a lot of ligand if the Kd is low specifically for the AR

jfl

 

[humanupgraded]

I'm going to re write the receptor occupancy because it was kinda wrong but no one can tell I did it at 3am
do you know Dan he did the calculations but he drew from the blood levels. he got 50mg daily or less of tren. so did bio.science apparently and vig steve

the concept of the AUC vs Cmax is important though because it explains why people are not turning yellow in 2 weeks on 1mg

I was one of the first people to get this, you ask your Daddy Dan lol. Also the calculations aren't from blood levels what lmao. Its based off of testosterone which isn't reliable.

But who injects mtren at a weekly dose equating to trenbolone?
You'd probably Inject at most 14mg of mtren over 7 days. Compared to 200-400mg trenbolone. That means, by mere concentration difference, no, mtren doesn't have meaningful effects like that of tren. It's horrendous for hypertrophy

Just in case someone wants to pull up this study "https://www.ncbi.nlm.nih.gov/m/pubmed/3486322/"
This is a complete misrepresentation of the study linked. Mtren does, in-vitro, under an assay based on molecular weight concentration..

 

[humanupgraded]

tell me what nuance could be added that would drastically shift the number involved for both ligands, especially metribolone
the more compartment extrapolations made reduces the theoretical accuracy of our ligand
the whole calculations were made to make a point: you don't need a lot of ligand if the Kd is low specifically for the AR

jfl

Delete your last messages luckily i caught onto the second last one, I'm not going to bother continuing this. "Dan drew blood" LMAO

 

[ΜπιγκΜπλακΚοκ]

I was one of the first people to get this,

Nah you werent bu I respect the grind bucko

 

[humanupgraded]

Nah you werent bu I respect the grind bucko

What lol, you don't know me son lmao

 

[R1881]

haha jfl --->

you fail to understand the content of the table and its accuracy when applied to real world human beings. The method in the table for measuring the "activity" or "PAA" is idiotic. It is calculated by multiplying 1/Kd by the Bmax which is for the most part fixed in this study model design. So basically, this study that you claim people misinterpreted was horribly misinterpreted by YOU. This table literally scales Kd directly with transcriptonal efficacy which we know is not the case, You are unwittingly implying that mtren and tren have the exact same effect size per mole based on your idiotic statment

you rudimentarily try to find the efficacy of a ligands by multiplying its affinity (or efficacy? I don't think you know the difference as stated above) by the MG amount! stating that 400mg of Trenbolone will be vastly superior to 14mg of metribolone weekly. but do the kinetics agree with you? no lets look at 90% AR saturation. again, if you want to argue that AMARU is infinite be my guest but hopefully you are not that stupid, so finite receptor kinetics applies here. why are we looking at saturation? because we are looking at effect size itself solely AR mediated

if 1mg daily of mtren very significantly saturates the AR, it will mog any amount of Tren for AR mediated effects. using the standard Hill-Langmuir equation for receptor-ligand fractional occupancy we need a concentration of 1.25nM of metribolone to be present in the muscle. using a Kd of 0.15nm
and guess what using Vd is very accurate as only hepatocytes possess the ability to break down metribolone AND muscle tissue is preferred above average so we have non inferiority. so 1mg in a Vd of 350 would give us 10nm. the half life is likely much longer in tissues but we will use blood half life of 4 hours. in 12 hours we remain just at the 1.25mg in time for our next dose of 2mg

so we know both 14mg metribolone and 1000mg trenbolone give us significant AR occupancy which is basically our portion of our theoretical Emax and the mtren has much much higher transcriptional affinity due to its IC metabolism and WE KNOW THIS otherwise it wouldn't be more effective than Tren per mg anecdotally


but I will do the math even better because I was very lenient with everything here. the dose is likely far less than 2mg to achieve saturation

 

[humanupgraded]

haha jfl --->

you fail to understand the content of the table and its accuracy when applied to real world human beings. The method in the table for measuring the "activity" or "PAA" is idiotic. It is calculated by multiplying 1/Kd by the Bmax which is for the most part fixed in this study model design. So basically, this study that you claim people misinterpreted was horribly misinterpreted by YOU. This table literally scales Kd directly with transcriptonal efficacy which we know is not the case, You are unwittingly implying that mtren and tren have the exact same effect size per mole based on your idiotic statment

you rudimentarily try to find the efficacy of a ligands by multiplying its affinity (or efficacy? I don't think you know the difference as stated above) by the MG amount! stating that 400mg of Trenbolone will be vastly superior to 14mg of metribolone weekly. but do the kinetics agree with you? no lets look at 90% AR saturation. again, if you want to argue that AMARU is infinite be my guest but hopefully you are not that stupid, so finite receptor kinetics applies here. why are we looking at saturation? because we are looking at effect size itself solely AR mediated

if 1mg daily of mtren very significantly saturates the AR, it will mog any amount of Tren for AR mediated effects. using the standard Hill-Langmuir equation for receptor-ligand fractional occupancy we need a concentration of 1.25nM of metribolone to be present in the muscle. using a Kd of 0.15nm
and guess what using Vd is very accurate as only hepatocytes possess the ability to break down metribolone AND muscle tissue is preferred above average so we have non inferiority. so 1mg in a Vd of 350 would give us 10nm. the half life is likely much longer in tissues but we will use blood half life of 4 hours. in 12 hours we remain just at the 1.25mg in time for our next dose of 2mg

so we know both 14mg metribolone and 1000mg trenbolone give us significant AR occupancy which is basically our portion of our theoretical Emax and the mtren has much much higher transcriptional affinity due to its IC metabolism and WE KNOW THIS otherwise it wouldn't be more effective than Tren per mg anecdotally


but I will do the math even better because I was very lenient with everything here. the dose is likely far less than 2mg to achieve saturation

 

[R1881]

nah bro I'm sorry for being rude can we be friends I just want to learn more anyway

but I am correct

 

[humanupgraded]

nah bro I'm sorry for being rude can we be friends I just want to learn more anyway

but I am correct

You are incorrect, but doesn't matter because I am bound to make a video on this soon so I suppose you can wait for that. And I don't hate you lol it just a disagreement that we have not a big deal

 

[R1881]

You are incorrect, but doesn't matter because I am bound to make a video on this soon so I suppose you can wait for that. And I don't hate you lol it just a disagreement that we have not a big deal

ok can you tell me why because I plan to do this. which part is wrong because the table your provided basically said mtren and Tren are the exact same strength. the Bmax is largely irrelavent in tissues so idk why they added that

edit: by do this I mean either run Tren as my main AR ligand or mtren, I want to hear your argument as to which

 

[Skull]

You are incorrect, but doesn't matter because I am bound to make a video on this soon so I suppose you can wait for that. And I don't hate you lol it just a disagreement that we have not a big deal

nah bro I'm sorry for being rude can we be friends I just want to learn more anyway

but I am correct

 

[R1881]

You are incorrect, but doesn't matter because I am bound to make a video on this soon so I suppose you can wait for that. And I don't hate you lol it just a disagreement that we have not a big deal

what mistake I make

 

[R1881]

What lol, you don't know me son lmao

bro sad:w you don't know me son