Why testosterone is useless without dht

20/04/2008

20/04/2008

Zephir
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Why testosterone is useless without dht



Who here thinks that DHT is just a stronger version of testosterone?

Well, I’m here to tell you that the DHT has unique benefits that testosterone doesn’t have, and this is why it’s important to maximize your DHT.

You can have high levels of testosterone and still feel like you have low androgens because your DHT is not on point and/or your 5 alpha to 5 beta reductase ratio is not being optimized.



DHT basics

So we do know that DHT is about 10 times stronger than testosterone. This is because DHT has 4 times higher binding affinity to the androgen receptor than testosterone. And DHT binds 3 to 5 times longer to the androgen receptor than testosterone


DHT is much more capable of exerting what it’s supposed to do than testosterone.

Even though DHT is found in 10 times lower amounts than testosterone, it’s 10 times stronger. If you maximize 5 alpha-reductase (5AR) and testosterone, you’ll have a much greater total androgen pool than someone with low 5AR. This means you will have more androgens to bind to the androgen receptor, making you more anabolic and androgenic.


Androgens binding to the androgen receptor​

Here’s what happens when androgens bind to the androgen receptor.

image.png

Heat shock protein 70 and 90 are bound to the androgen receptor. Once the androgen binds to the receptor, the heat shock proteins detach and the androgen receptor can enter the nucleus. Once inside, it binds to the androgen response element (ARE). Various cofactors can then also bind to the AR/ARE complex. There are also multiple androgen response elements as well as co-regulators



Selective ARE is a mechanism for ligand-specific regulation of AR function (R).

So as you can see, it’s more complicatedthan just binding to the androgen receptor and exerting 1 action.


Different androgens on the androgen receptor​

Because the structure of each androgen is different, they will bind differently to the androgen receptor and exert different effects.

Different-androgen-structure.png

As you can see from the structures above, these androgens are about 95% similar, but they vary a lot in how potently they bind to the androgen receptor.

And they induce slightly different configurations despite binding to the same receptor.

It’s the same thing with SARMs. SARMs act on the androgen receptor.

The hypothesis for how SARMs work, and how they are anabolic but not androgenic, are those two hypotheses.

1)Hypothesis 1 (coactivator hypothesis): This hypothesis presumes that testosterone-bound AR and SARM-bound AR have different coregulator proteins, which leads to transcriptional activation of a differentially regulated collection of genes
  • Meaning, SARMs, and androgens regulate genes differently despite acting on the same receptor.
2) Hypothesis 2: This hypothesis assumes that distinctive ligand classes have unique thermodynamic partitioning and are expressed into conformationally different states. The conformational modifications in the ligand-binding domain are induced by the ligand binding and might change surface topology, thus modifying protein-protein interactions between AR and other coregulators


  1. don’t know about you, but that makes little sense to me
Additionally, testosterone is less effective at stabilizing AR than DHT. These observations suggest that DHT, by enhancing the stabilization of AR and its action, amplifies the T signal in those tissues which contain 5a-reductase


Without DHT you have weaker AR signalling.

So as I mentioned, the androgen receptor binds differently to these different compounds, and this creates the conformational modifications in the ligand binding domain induced by ligand binding and might change surface topology, thus modifying protein-to-protein interaction between the androgen receptor and other co-regulators.

Summary​

It’s complex stuff, but because the structures of these molecules are different, they induce different changes when binding to the same receptor. And also testosterone and DHT induce different androgen response elements.

It’s different co-regulators and different androgen response elements. And this is actually why studies have shown that there are unique benefits to DHT that testosterone does not have. So when you give, for example, DHEA or testosterone to a human or an animal, and you inhibit 5 alpha-reductase with, for example, finasteride, you don’t get the same benefit as not blocking it, right?

So there are unique benefits to DHT. A lot of people would say that DHT plays no role in the adult. You only need testosterone. That’s not true. DHT is not just a stronger version of distortion. It’s different and induces different changes to the androgen receptor and gives unique benefits that testosterone will not give you.

So you might be thinking: “Well, I’m just going to use DHT.” Now that’s also a wrong conclusion because there are unique benefits of testosterone and DHT. If you were to use just DHT, you would miss out on the benefits of testosterone. But if you use just testosterone and you don’t optimize your 5 alpha reductase enzyme or block it, you might miss out on the benefits of DHT.

Make sure that your 5 alpha reductase is working properly so you can convert your testosterone and DHEA and androstenedione into the 5 alpha reduced steroids so you can benefit from that.

Also, 5AR doesn’t just create DHT, it also deactivates cortisol and aldosterone and activates progesterone to create allopregnanolone. 5 alpha reductase is very important, not just for creating DHT.

Tags:@Hexmask
 
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Reactions: nuclearlooksmaxxer, halloweed, JohnDoe and 4 others
Why testosterone is useless without dht



Who here thinks that DHT is just a stronger version of testosterone?

Well, I’m here to tell you that the DHT has unique benefits that testosterone doesn’t have, and this is why it’s important to maximize your DHT.

You can have high levels of testosterone and still feel like you have low androgens because your DHT is not on point and/or your 5 alpha to 5 beta reductase ratio is not being optimized.



DHT basics

So we do know that DHT is about 10 times stronger than testosterone. This is because DHT has 4 times higher binding affinity to the androgen receptor than testosterone. And DHT binds 3 to 5 times longer to the androgen receptor than testosterone


DHT is much more capable of exerting what it’s supposed to do than testosterone.

Even though DHT is found in 10 times lower amounts than testosterone, it’s 10 times stronger. If you maximize 5 alpha-reductase (5AR) and testosterone, you’ll have a much greater total androgen pool than someone with low 5AR. This means you will have more androgens to bind to the androgen receptor, making you more anabolic and androgenic.


Androgens binding to the androgen receptor​

Here’s what happens when androgens bind to the androgen receptor.

image.png

Heat shock protein 70 and 90 are bound to the androgen receptor. Once the androgen binds to the receptor, the heat shock proteins detach and the androgen receptor can enter the nucleus. Once inside, it binds to the androgen response element (ARE). Various cofactors can then also bind to the AR/ARE complex. There are also multiple androgen response elements as well as co-regulators



Selective ARE is a mechanism for ligand-specific regulation of AR function (R).

So as you can see, it’s more complicatedthan just binding to the androgen receptor and exerting 1 action.


Different androgens on the androgen receptor​

Because the structure of each androgen is different, they will bind differently to the androgen receptor and exert different effects.

Different-androgen-structure.png

As you can see from the structures above, these androgens are about 95% similar, but they vary a lot in how potently they bind to the androgen receptor.

And they induce slightly different configurations despite binding to the same receptor.

It’s the same thing with SARMs. SARMs act on the androgen receptor.

The hypothesis for how SARMs work, and how they are anabolic but not androgenic, are those two hypotheses.

1)Hypothesis 1 (coactivator hypothesis): This hypothesis presumes that testosterone-bound AR and SARM-bound AR have different coregulator proteins, which leads to transcriptional activation of a differentially regulated collection of genes
  • Meaning, SARMs, and androgens regulate genes differently despite acting on the same receptor.
2) Hypothesis 2: This hypothesis assumes that distinctive ligand classes have unique thermodynamic partitioning and are expressed into conformationally different states. The conformational modifications in the ligand-binding domain are induced by the ligand binding and might change surface topology, thus modifying protein-protein interactions between AR and other coregulators


  1. don’t know about you, but that makes little sense to me
Additionally, testosterone is less effective at stabilizing AR than DHT. These observations suggest that DHT, by enhancing the stabilization of AR and its action, amplifies the T signal in those tissues which contain 5a-reductase


Without DHT you have weaker AR signalling.

So as I mentioned, the androgen receptor binds differently to these different compounds, and this creates the conformational modifications in the ligand binding domain induced by ligand binding and might change surface topology, thus modifying protein-to-protein interaction between the androgen receptor and other co-regulators.

Summary​

It’s complex stuff, but because the structures of these molecules are different, they induce different changes when binding to the same receptor. And also testosterone and DHT induce different androgen response elements.

It’s different co-regulators and different androgen response elements. And this is actually why studies have shown that there are unique benefits to DHT that testosterone does not have. So when you give, for example, DHEA or testosterone to a human or an animal, and you inhibit 5 alpha-reductase with, for example, finasteride, you don’t get the same benefit as not blocking it, right?

So there are unique benefits to DHT. A lot of people would say that DHT plays no role in the adult. You only need testosterone. That’s not true. DHT is not just a stronger version of distortion. It’s different and induces different changes to the androgen receptor and gives unique benefits that testosterone will not give you.

So you might be thinking: “Well, I’m just going to use DHT.” Now that’s also a wrong conclusion because there are unique benefits of testosterone and DHT. If you were to use just DHT, you would miss out on the benefits of testosterone. But if you use just testosterone and you don’t optimize your 5 alpha reductase enzyme or block it, you might miss out on the benefits of DHT.

Make sure that your 5 alpha reductase is working properly so you can convert your testosterone and DHEA and androstenedione into the 5 alpha reduced steroids so you can benefit from that.

Also, 5AR doesn’t just create DHT, it also deactivates cortisol and aldosterone and activates progesterone to create allopregnanolone. 5 alpha reductase is very important, not just for creating DHT.

Tags:@Hexmask
Very good thread bump.
 
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Reactions: GenesBeans, Jonas2k7 and 20/04/2008
Last edited:
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Why testosterone is useless without dht



Who here thinks that DHT is just a stronger version of testosterone?

Well, I’m here to tell you that the DHT has unique benefits that testosterone doesn’t have, and this is why it’s important to maximize your DHT.

You can have high levels of testosterone and still feel like you have low androgens because your DHT is not on point and/or your 5 alpha to 5 beta reductase ratio is not being optimized.



DHT basics

So we do know that DHT is about 10 times stronger than testosterone. This is because DHT has 4 times higher binding affinity to the androgen receptor than testosterone. And DHT binds 3 to 5 times longer to the androgen receptor than testosterone


DHT is much more capable of exerting what it’s supposed to do than testosterone.

Even though DHT is found in 10 times lower amounts than testosterone, it’s 10 times stronger. If you maximize 5 alpha-reductase (5AR) and testosterone, you’ll have a much greater total androgen pool than someone with low 5AR. This means you will have more androgens to bind to the androgen receptor, making you more anabolic and androgenic.


Androgens binding to the androgen receptor​

Here’s what happens when androgens bind to the androgen receptor.

image.png

Heat shock protein 70 and 90 are bound to the androgen receptor. Once the androgen binds to the receptor, the heat shock proteins detach and the androgen receptor can enter the nucleus. Once inside, it binds to the androgen response element (ARE). Various cofactors can then also bind to the AR/ARE complex. There are also multiple androgen response elements as well as co-regulators



Selective ARE is a mechanism for ligand-specific regulation of AR function (R).

So as you can see, it’s more complicatedthan just binding to the androgen receptor and exerting 1 action.


Different androgens on the androgen receptor​

Because the structure of each androgen is different, they will bind differently to the androgen receptor and exert different effects.

Different-androgen-structure.png

As you can see from the structures above, these androgens are about 95% similar, but they vary a lot in how potently they bind to the androgen receptor.

And they induce slightly different configurations despite binding to the same receptor.

It’s the same thing with SARMs. SARMs act on the androgen receptor.

The hypothesis for how SARMs work, and how they are anabolic but not androgenic, are those two hypotheses.

1)Hypothesis 1 (coactivator hypothesis): This hypothesis presumes that testosterone-bound AR and SARM-bound AR have different coregulator proteins, which leads to transcriptional activation of a differentially regulated collection of genes
  • Meaning, SARMs, and androgens regulate genes differently despite acting on the same receptor.
2) Hypothesis 2: This hypothesis assumes that distinctive ligand classes have unique thermodynamic partitioning and are expressed into conformationally different states. The conformational modifications in the ligand-binding domain are induced by the ligand binding and might change surface topology, thus modifying protein-protein interactions between AR and other coregulators


  1. don’t know about you, but that makes little sense to me
Additionally, testosterone is less effective at stabilizing AR than DHT. These observations suggest that DHT, by enhancing the stabilization of AR and its action, amplifies the T signal in those tissues which contain 5a-reductase


Without DHT you have weaker AR signalling.

So as I mentioned, the androgen receptor binds differently to these different compounds, and this creates the conformational modifications in the ligand binding domain induced by ligand binding and might change surface topology, thus modifying protein-to-protein interaction between the androgen receptor and other co-regulators.

Summary​

It’s complex stuff, but because the structures of these molecules are different, they induce different changes when binding to the same receptor. And also testosterone and DHT induce different androgen response elements.

It’s different co-regulators and different androgen response elements. And this is actually why studies have shown that there are unique benefits to DHT that testosterone does not have. So when you give, for example, DHEA or testosterone to a human or an animal, and you inhibit 5 alpha-reductase with, for example, finasteride, you don’t get the same benefit as not blocking it, right?

So there are unique benefits to DHT. A lot of people would say that DHT plays no role in the adult. You only need testosterone. That’s not true. DHT is not just a stronger version of distortion. It’s different and induces different changes to the androgen receptor and gives unique benefits that testosterone will not give you.

So you might be thinking: “Well, I’m just going to use DHT.” Now that’s also a wrong conclusion because there are unique benefits of testosterone and DHT. If you were to use just DHT, you would miss out on the benefits of testosterone. But if you use just testosterone and you don’t optimize your 5 alpha reductase enzyme or block it, you might miss out on the benefits of DHT.

Make sure that your 5 alpha reductase is working properly so you can convert your testosterone and DHEA and androstenedione into the 5 alpha reduced steroids so you can benefit from that.

Also, 5AR doesn’t just create DHT, it also deactivates cortisol and aldosterone and activates progesterone to create allopregnanolone. 5 alpha reductase is very important, not just for creating DHT.

Tags:@Hexmask
Unbenannt 4
 
Dht is for gods!:blackpill:
 
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Reactions: 20/04/2008
DHT is rapidly metabolised 3-alpha-hydroxysteroid dehydrogenase in muscle tissue

/thread
 
DHT is rapidly metabolised 3-alpha-hydroxysteroid dehydrogenase in muscle tissue

/thread
You read the thread in 1 min
Are you fucking crazy do you want me to believe you actually read it 😂😂😂
 
You read the thread in 1 min
Are you fucking crazy do you want me to believe you actually read it 😂😂😂
Not going to read garbage produced by a dht worshipping tranny faggot.

You will 100% come to same conclusion as I did down the line when your hair is dropping in swathes and your skin quality goes to shit.

My skin has never been better, my hairline has never been better, my body has never been better, my LOOKS have never been better. All after adding dutasteride in.
 
Not going to read garbage produced by a dht worshipping tranny faggot.

You will 100% come to same conclusion as I did down the line when your hair is dropping in swathes and your skin quality goes to shit.

My skin has never been better, my hairline has never been better, my body has never been better, my LOOKS have never been better. All after adding dutasteride in.
You know im on fucking gear for 2 years now
No hair sheeding like wtf do you talk about
 
No hair sheeding like wtf do you talk about
That's awesome. Good for you. You have great genetics

That isn't my problem, my problem is you faggots who dissuade other potential steroid users from using 5ar inhibitors simply because YOU don't experience hairloss.
 

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