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Dihydrotestosterone (DHT)
By: Hypertrophy
DHT is an endogenous androgen sex steroid and hormone primarily involved in the growth and repair of the prostate and the penis as well as the production of sebum and body hair composition.
Testosterone converts into DHT in tissues expressing the enzymes of the 5 alpha reductase (5AR) family. These enzymes add an α-orientated hydrogen atom at carbon 5. This reaction yields DHT. These enzymes are expressed among the liver, skin, prostate, epididymis, seminal vesicles, testis, kidney, pancreas and brain. DHT also has a 5x greater affinity for the AR
There are two main types of 5AR enzymes, type 1 (SRD5A1) Which is expressed in the sebaceous glands, nongenital skin, liver and brain. Type 2 (SRD5A2) Which is expressed in the prostate, seminal vesicles, epididymis, genital skin and hair follicles
DHT is not utilized in skeletal muscle or bone.
**DHT is a Looksmin**
DHT is one of the most useless hormones for LM after 18 years old. Some people think that DHT is a good looksmax but this is not the case.
DHT cant be turned into estradiol because it is not a substrate for the aromatase enzyme. This is important because estradiol is a central mediator of bone mineralization. So due to the fact that DHT can't produce estrogenic metabolites, its ability to influence bone via the estrogen receptor pathway is none.
DHT acts mainly locally (inside certain tissues). The face and scalp have high levels of SRD5A which converts test into DHT. DHT can promote growth or shrinkage of tissues depending on the cell type. Bone cells also have AR but they are mainly influenced by estrogen and testosterone and since DHT cannot be turned into estrogen, it doesn't promote bone growth.
Androgenic alopecia (hair loss) is a common DHT looksmin. DHT AR transcriptional activity upregulates paracrine mediators in genetically susceptible follicles. This leads to shorter growth phase (anagen) and miniaturization of follicles
DHT can also make your skin worse by increasing oil production in the sebaceous glands through androgen receptor signaling. This causes increased sebum production which can lead to acne, oily skin and pore enlargement.
I have been arguing with retarded DHTcels in comment sections recently and it's crazy hearing the shit they spew, I mean someone had an argument that said DHT blockers cause recession in the face.
So to start off, no DHT blockers do NOT cause recession in your face. This is because the bones there don't have enough 5AR for DHT to even play a significant role, so this means that testosterone is the main androgen driving this growth. Sooo when you take DHT blockers, the androgen signal in the bone tissue is fine because testosterone levels don't change.
I would also like to cite a study that experiments with this. In the study 99 men aged 18-55 were randomly assigned fin, dut or a placebo daily for 1 year. What they found was that significant suppression of circulating DHT levels did not significantly affect bone mineral density or markers of bone metabolism.
Further proving this point, There have been studies on people with a 5 ARD (5 alpha reductase deficiency) meaning they can't produce DHT like normal. Soo with that being said, guess what the result was? Normal bone growth still ensued and they had normal bone mineral density. Literally the only thing that happened was that the male subjects had micropenises.
So now that we debunked DHT being relevant for bone growth, let's go over other things. People will fearmonger 5ARIs because of “muhh sexual problems and muhh DHT is a neurosteroid so you need it”
First of all ED influenced by 5ARIs affects a low percentage of people who take them, approximately 4-9% for dutasteride and 1.3-1.4% for finasteride. It's funny because these effects they fear monger are generally reversible.
One interesting thing to note about this is that a study in 1998 and 1999 showed that sexual side effects were generally comparable to those observed with the treatment with placebo. Also a large study including 17,313 subjects was observed. They were given 5mg of finasteride (5x higher dose than the typical 1mg). It was found that finasteride increased sexual dysfunction slightly, even at the high dosage. Also the impact diminished over time
In conclusion 5AR are placed in specific locations to amplify androgen signalling where it is needed. DHT does not act everywhere, its reach is limited by where 5AR expression is present. DHT is pretty much useless after development and there's no real reason not to nuke it.
Thats it bhais, rep it up
By: Hypertrophy
DHT is an endogenous androgen sex steroid and hormone primarily involved in the growth and repair of the prostate and the penis as well as the production of sebum and body hair composition.
Testosterone converts into DHT in tissues expressing the enzymes of the 5 alpha reductase (5AR) family. These enzymes add an α-orientated hydrogen atom at carbon 5. This reaction yields DHT. These enzymes are expressed among the liver, skin, prostate, epididymis, seminal vesicles, testis, kidney, pancreas and brain. DHT also has a 5x greater affinity for the AR
There are two main types of 5AR enzymes, type 1 (SRD5A1) Which is expressed in the sebaceous glands, nongenital skin, liver and brain. Type 2 (SRD5A2) Which is expressed in the prostate, seminal vesicles, epididymis, genital skin and hair follicles
DHT is not utilized in skeletal muscle or bone.
**DHT is a Looksmin**
DHT is one of the most useless hormones for LM after 18 years old. Some people think that DHT is a good looksmax but this is not the case.
DHT cant be turned into estradiol because it is not a substrate for the aromatase enzyme. This is important because estradiol is a central mediator of bone mineralization. So due to the fact that DHT can't produce estrogenic metabolites, its ability to influence bone via the estrogen receptor pathway is none.
DHT acts mainly locally (inside certain tissues). The face and scalp have high levels of SRD5A which converts test into DHT. DHT can promote growth or shrinkage of tissues depending on the cell type. Bone cells also have AR but they are mainly influenced by estrogen and testosterone and since DHT cannot be turned into estrogen, it doesn't promote bone growth.
Androgenic alopecia (hair loss) is a common DHT looksmin. DHT AR transcriptional activity upregulates paracrine mediators in genetically susceptible follicles. This leads to shorter growth phase (anagen) and miniaturization of follicles
DHT can also make your skin worse by increasing oil production in the sebaceous glands through androgen receptor signaling. This causes increased sebum production which can lead to acne, oily skin and pore enlargement.
I have been arguing with retarded DHTcels in comment sections recently and it's crazy hearing the shit they spew, I mean someone had an argument that said DHT blockers cause recession in the face.
So to start off, no DHT blockers do NOT cause recession in your face. This is because the bones there don't have enough 5AR for DHT to even play a significant role, so this means that testosterone is the main androgen driving this growth. Sooo when you take DHT blockers, the androgen signal in the bone tissue is fine because testosterone levels don't change.
I would also like to cite a study that experiments with this. In the study 99 men aged 18-55 were randomly assigned fin, dut or a placebo daily for 1 year. What they found was that significant suppression of circulating DHT levels did not significantly affect bone mineral density or markers of bone metabolism.
Further proving this point, There have been studies on people with a 5 ARD (5 alpha reductase deficiency) meaning they can't produce DHT like normal. Soo with that being said, guess what the result was? Normal bone growth still ensued and they had normal bone mineral density. Literally the only thing that happened was that the male subjects had micropenises.
So now that we debunked DHT being relevant for bone growth, let's go over other things. People will fearmonger 5ARIs because of “muhh sexual problems and muhh DHT is a neurosteroid so you need it”
First of all ED influenced by 5ARIs affects a low percentage of people who take them, approximately 4-9% for dutasteride and 1.3-1.4% for finasteride. It's funny because these effects they fear monger are generally reversible.
One interesting thing to note about this is that a study in 1998 and 1999 showed that sexual side effects were generally comparable to those observed with the treatment with placebo. Also a large study including 17,313 subjects was observed. They were given 5mg of finasteride (5x higher dose than the typical 1mg). It was found that finasteride increased sexual dysfunction slightly, even at the high dosage. Also the impact diminished over time
In conclusion 5AR are placed in specific locations to amplify androgen signalling where it is needed. DHT does not act everywhere, its reach is limited by where 5AR expression is present. DHT is pretty much useless after development and there's no real reason not to nuke it.
Thats it bhais, rep it up
Explain to me how my points are wrong, you've failed to do so thus far
