Question about Tren when adding it to a cycle.

[ironmaster73]

I read that Tren competes hard for the AR. Hence when adding Tren to a cycle it was said that because it binds hard to the AR that it will kick testosterone off. So most of your test will be redirected causing more side effects. The recommended cause of action is to use a trt dose or nothing over 300mg/wk of test when using Tren. I guess this comes back to the low test higher Tren protocol. I must say I have noticed more side effects when I had my test at 750mg and Tren 300mg. Also I have found when I add equal amounts of Mast to Tren side effect seem to be less. But back to my original question. Does Tren compete for the AR and make it harder for test to bind to the AR.

 

[juggy38]

the answer depends on binding affinity, onff rates, and % receptor occupancy/plasma drug levels.

Easy answer….yes in a competitive antagonism match, tren wins 1 on 1. But this matters about fuck all in vivo

Luckily, this doesn’t really matter. Allegedly, estimated receptor saturation doesn’t happen until around 4g of drugs (this might be a bullshit fourm folklore repeated over and over). Nonetheless, it’s not 1g like your example.


“Sides” being less with low test……this has MUCH more to do with it have high progestogenic activity. Its progestogenic effects along with estrogen levels will dictate “feels”

this ^^^ is why women are fucjing nuts. These two hormones can drastically affect neurotransmitter pathways that regulates mood

 

[Mufasa123]

the answer depends on binding affinity, onff rates, and % receptor occupancy/plasma drug levels.

Easy answer….yes in a competitive antagonism match, tren wins 1 on 1. But this matters about fuck all in vivo

Luckily, this doesn’t really matter. Allegedly, estimated receptor saturation doesn’t happen until around 4g of drugs (this might be a bullshit fourm folklore repeated over and over). Nonetheless, it’s not 1g like your example.


“Sides” being less with low test……this has MUCH more to do with it have high progestogenic activity. Its progestogenic effects along with estrogen levels will dictate “feels”

this ^^^ is why women are fucjing nuts. These two hormones can drastically affect neurotransmitter pathways that regulates mood

Fucking all around epic answer.

 

[danieltx]

Fucking all around epic answer.

@juggy38 is one of the underappreciated scientific minds on here.

 

[Stewie]

There's billions upon billions of several different cell types in the human body. In the vast majority of these billions of cells, there are different organelles (subcellular machinery)-mitochondria and endoplasmic reticulum that the androgen receptors (including splice variants and orphan receptors) take up residence in.

So most of your test will be redirected causing more side effects

This premise doesn't make sense. Wouldn't there need to be binding->activation-> expression to create a "side effect"? What's it being redirected to?

Nuclear receptors, such as the androgen receptor has multiple binding sites. Low(er) affinity ligands (less potent androgens) possess the ability to active full-lenght gene expression through androgen response elements. Once testosterone localizes and binds to the AR, Tren isn't going to kick (dissociate) testosterone to the curb. Its going to carry out it's genomic, and potentially non-genomic actions if it doesn't translocate to DNA domain- androgen response element.

 

[juggy38]

There's billions upon billions of several different cell types in the human body. In the vast majority of these billions of cells, there are different organelles (subcellular machinery)-mitochondria and endoplasmic reticulum that the androgen receptors (including splice variants and orphan receptors) take up residence in.



This premise doesn't make sense. Wouldn't there need to be binding->activation-> expression to create a "side effect"? What's it being redirected to?

Nuclear receptors, such as the androgen receptor has multiple binding sites. Low(er) affinity ligands (less potent androgens) possess the ability to active full-lenght gene expression through androgen response elements. Once testosterone localizes and binds to the AR, Tren isn't going to kick (dissociate) testosterone to the curb. Its going to carry out it's genomic, and potentially non-genomic actions if it doesn't translocate to DNA domain- androgen response element.

I think from the old forums, the groupthink which gets repeated often, was the misunderstanding that if trenbolone is bound to the receptor, test will do nothing but float around and be aromatized at higher rates or something to that nature, causing more sides.

I think if everyone that plays this game would just go find an old molecular biology textbook, a pharmacology textbook and read them….they would be 1000 leagues ahead of 99% of gym rats understanding of how these drugs actually work. Even if they only retained the general principles.

Also good reading to pass out at night while on said tren lol

 

[Mufasa123]

I think from the old forums, the groupthink which gets repeated often, was the misunderstanding that if trenbolone is bound to the receptor, test will do nothing but float around and be aromatized at higher rates or something to that nature, causing more sides.

I think if everyone that plays this game would just go find an old molecular biology textbook, a pharmacology textbook and read them….they would be 1000 leagues ahead of 99% of gym rats understanding of how these drugs actually work. Even if they only retained the general principles.

Also good reading to pass out at night while on said tren lol

For what it's worth you were one of the old AFBoard/Ulter's that I saw posting here that made me decide to join. Always a good guy sharing quality knowledge and thinking.

 

[Stewie]

I think from the old forums, the groupthink which gets repeated often, was the misunderstanding that if trenbolone is bound to the receptor, test will do nothing but float around and be aromatized at higher rates or something to that nature, causing more sides.

I think if everyone that plays this game would just go find an old molecular biology textbook, a pharmacology textbook and read them….they would be 1000 leagues ahead of 99% of gym rats understanding of how these drugs actually work. Even if they only retained the general principles.

Also good reading to pass out at night while on said tren lol

There's a tremendous amount yet to understand. More than I'll ever know.

Like most of my posts, I tend to leave bits and pieces out.

As for the previously aforementioned given the multitude on the diversity of cells that occupy different receptor types. There's plenty of binding sites for a-many ligands (molecules) to go around. The androgen receptor is an allosteric receptor, essentially meaning they can bind several different ligands at one time. The queries remains... do they create a complex towards a heterodimerization with two distinctively different androgenic molecules? It's recognized as a homodimer. Although...?

Correct me if I'm mistaken, you're in psych?

 

[mexbeast]

Great info, it would be great if you guys gave this kind of responses more often!

 

[bbxtreme]

Great info, it would be great if you guys gave this kind of responses more often!

Most of these discussions are had in DM’s here as of late sadly. If we could all keep this place clear of the drama and feeding the trolls and troubled members I would venture to say you’d see a lot more of this back on the open forums.

 

[juggy38]

There's a tremendous amount yet to understand. More than I'll ever know.

Like most of my posts, I tend to leave bits and pieces out.

As for the previously aforementioned given the multitude on the diversity of cells that occupy different receptor types. There's plenty of binding sites for a-many ligands (molecules) to go around. The androgen receptor is an allosteric receptor, essentially meaning they can bind several different ligands at one time. The queries remains... do they create a complex towards a heterodimerization with two distinctively different androgenic molecules? It's recognized as a homodimer. Although...?

Correct me if I'm mistaken, you're in psych?

I wish we had the ability (technology and previous literature) to confirm that conformational changes upon ligand binding could result in an AR receptor creating herterodimers. I would weakly bet that there isn’t literature confirming this happening in NORMAL physiological processes.

But lord knows 1g test with 700mg tren is a fucking far and away place from “normal circumstances”.

Possible? Yea i believe so. The body is a magical machine.

Yes, my background is in psych/medical. We are the pack that think every problem can be solved with a pill

But in seriousness, we literally throw shit at the wall, relying on theoretical knowledge of a disease process, theoretical knowledge of neurotransmitters and their impact, and zero diagnostics.

Example…catatonia….what causes it? Well, we are not sure. How do we fix it? Umm….welp….these 3-4 things have fixed kt
In the past…..ok….risk/reward cost/benefit….and is safe? Umm…ok that leaves 2……ok….whos got a quarter to flip?

 

[juggy38]

Most of these discussions are had in DM’s here as of late sadly. If we could all keep this place clear of the drama and feeding the trolls and troubled members I would venture to say you’d see a lot more of this back on the open forums.

Agreed. It’s the “oh well, that doesn’t matter man, take Benadryl for sleep and run at least 350mg Ace a week and hit your calories. This is overthinking”

Some people like to squat and are fascinated by drug-receptor dynamics and the physiological implications of such lol.

If me and @Stewie nerd out, and if there’s anything applicable, we usually say that also. Most of this is literally just talking about HOW the cellular dominos fall. It doesn’t change what needs to be done to change a physique.

 

[juggy38]

For what it's worth you were one of the old AFBoard/Ulter's that I saw posting here that made me decide to join. Always a good guy sharing quality knowledge and thinking.

AFBoard was a great place!

 

[danieltx]

Yes, my background is in psych/medical. We are the pack that think every problem can be solved with a pill

But in seriousness, we literally throw shit at the wall, relying on theoretical knowledge of a disease process, theoretical knowledge of neurotransmitters and their impact, and zero diagnostics.

Example…catatonia….what causes it? Well, we are not sure. How do we fix it? Umm….welp….these 3-4 things have fixed kt
In the past…..ok….risk/reward cost/benefit….and is safe? Umm…ok that leaves 2……ok….whos got a quarter to flip?

And that's why they call it 'practicing medicine'!

 

[Stewie]

I wish we had the ability (technology and previous literature) to confirm that conformational changes upon ligand binding could result in an AR receptor creating herterodimers. I would weakly bet that there isn’t literature confirming this happening in NORMAL physiological processes.

But lord knows 1g test with 700mg tren is a fucking far and away place from “normal circumstances”.

Possible? Yea i believe so. The body is a magical machine.

Yes, my background is in psych/medical. We are the pack that think every problem can be solved with a pill

But in seriousness, we literally throw shit at the wall, relying on theoretical knowledge of a disease process, theoretical knowledge of neurotransmitters and their impact, and zero diagnostics.

Example…catatonia….what causes it? Well, we are not sure. How do we fix it? Umm….welp….these 3-4 things have fixed kt
In the past…..ok….risk/reward cost/benefit….and is safe? Umm…ok that leaves 2……ok….whos got a quarter to flip?

I thought that was the area of med you're in. My youngest son is finishing up his PMHNP at Saint Francis College of Nursing.

 

[Flex500]

just wanted to say @juggy38 and @Stewie great posts! Love when you two get going with these types of posts.

And juggy you are 100% right. it is from thinking the test "just floats around and does bad stuff" because it "beats out the test it's competing with and has nowhere to go".

I vividly remember this because I used to post in the bbing.com forums when they had a steroid section and this premise was posted all the time literally 20 years ago lol.

 

[Stewie]

just wanted to say @juggy38 and @Stewie great posts! Love when you two get going with these types of posts.

And juggy you are 100% right. it is from thinking the test "just floats around and does bad stuff" because it "beats out the test it's competing with and has nowhere to go".

I vividly remember this because I used to post in the bbing.com forums when they had a steroid section and this premise was posted all the time literally 20 years ago lol.

I've seen the same fallacious discussion several times, too. If you don't know, understandable. If presented as pseudoauthoritarian facts, without seemingly plausible facts. I'm hard pressed to buy into that type of selling point. Yet, the naive or not well read will buy into such less than stellar nonsense. Wash, rinse and repeat for the next person to regurgitate.

Some individuals fail to conceive the thought, if a biochemical pathway (charted) directively creates a reaction. This doesn't necessarily mean it will happen. Nor does it tell us how quantitatively un/important it is. This aligns with the original topic at hand- binding affinity.

Singling out estradiol floating around haphazardly makes zero sense. The peripheral conversion of androgens isn’t specific to just aromatization to fractionated estrogens. There's a lot of moving parts that may potentially lead to "side effects" so to speak.

This all falls within the same grasp of know-it all's on social media platforms. Namely -Facebook Hormone Replacement sites spitting out, and pimping aromatase inhibitors to obese individuals due to slightly elevated E2. Look at the big picture. Not by suppressing an action created by a more concerning underlying condition(s). The more concerning part. These so-called Optimizing Hormone Clinics, Rx'n AI's unnecessarily.

I'll step off my soapbox.

 

[Neuro1234]

I've seen the same fallacious discussion several times, too. If you don't know, understandable. If presented as pseudoauthoritarian facts, without seemingly plausible facts. I'm hard pressed to buy into that type of selling point. Yet, the naive or not well read will buy into such less than stellar nonsense. Wash, rinse and repeat for the next person to regurgitate.

Some individuals fail to conceive the thought, if a biochemical pathway (charted) directively creates a reaction. This doesn't necessarily mean it will happen. Nor does it tell us how quantitatively un/important it is. This aligns with the original topic at hand- binding affinity.

Singling out estradiol floating around haphazardly makes zero sense. The peripheral conversion of androgens isn’t specific to just aromatization to fractionated estrogens. There's a lot of moving parts that may potentially lead to "side effects" so to speak.

This all falls within the same grasp of know-it all's on social media platforms. Namely -Facebook Hormone Replacement sites spitting out, and pimping aromatase inhibitors to obese individuals due to slightly elevated E2. Look at the big picture. Not by suppressing an action created by a more concerning underlying condition(s). The more concerning part. These so-called Optimizing Hormone Clinics, Rx'n AI's unnecessarily.

I'll step off my soapbox.

You and @juggy38 are welcome on any soapbox at any time as far as I’m concerned.

 

[specter]

There's billions upon billions of several different cell types in the human body. In the vast majority of these billions of cells, there are different organelles (subcellular machinery)-mitochondria and endoplasmic reticulum that the androgen receptors (including splice variants and orphan receptors) take up residence in.



This premise doesn't make sense. Wouldn't there need to be binding->activation-> expression to create a "side effect"? What's it being redirected to?

Nuclear receptors, such as the androgen receptor has multiple binding sites. Low(er) affinity ligands (less potent androgens) possess the ability to active full-lenght gene expression through androgen response elements. Once testosterone localizes and binds to the AR, Tren isn't going to kick (dissociate) testosterone to the curb. Its going to carry out it's genomic, and potentially non-genomic actions if it doesn't translocate to DNA domain- androgen response element.

Also as far as i can remember long term usage of androgens makes the body produce more receptors.. but as a whole people overthink things they hardly have any control over..

 

[specter]

Most of these discussions are had in DM’s here as of late sadly. If we could all keep this place clear of the drama and feeding the trolls and troubled members I would venture to say you’d see a lot more of this back on the open forums.

man when i started 20+ years ago nothing was more effin nice then see the then big minds discussing/deabting shit and just sitting there soaking it all up.. those where the days..