what hormone makes a male horny besides dht and test

kambally

kambally

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im horny most of the time but i look like low t what hormones makes a male horny besides dht and t ??
 
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kambally said:
how
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Estrogen's role in libido starts with the aromatization of testosterone into estradiol. In males, a significant portion of estrogen is derived from the aromatization of testosterone in the brain, catalyzed by the enzyme aromatase, which is highly expressed in regions critical to sexual behavior regulation, such as the medial preoptic area (mPOA) and the bed nucleus of the stria terminalis.
1728331747030

Once converted, estradiol binds to estrogen receptors (ERs), specifically ERα and ERβ, which are widely expressed in the central nervous system, particularly in areas that govern sexual motivation, like the hypothalamus. Estrogen receptor signaling through ERα in the mPOA is crucial for male sexual motivation. The activation of these receptors leads to both genomic and non-genomic signaling cascades.

Upon estrogen binding, ERα/ERβ translocate into the nucleus, where they act as transcription factors that regulate the expression of genes associated with sexual behavior, such as those influencing dopamine synthesis, receptor density, and nitric oxide (NO) pathways. The increased expression of these genes enhances the dopaminergic transmission in areas like the nucleus accumbens and the ventral tegmental area (VTA), which are involved in reward processing and sexual arousal.

1728331727815


Estrogen can also act via rapid, membrane-initiated signaling cascades, engaging membrane-bound ERs or G-protein-coupled estrogen receptors (GPER), which can activate second messenger systems such as MAPK/ERK or PI3K/Akt pathways. This results in rapid modulation of neurotransmitter release, particularly dopamine and nitric oxide. These non-genomic actions are crucial for the rapid modulation of sexual drive, as they affect neurotransmitter systems that govern immediate sexual motivation.

Dopamine, the primary neurotransmitter associated with reward and motivation, is heavily modulated by estrogen. In males, estrogen's effect on the dopaminergic system is critical for libido. Estrogen promotes the release and synthesis of dopamine in the hypothalamus and the mPOA, which then influences the mesolimbic reward system. Increased dopamine in these circuits enhances the reward feedback mechanisms associated with sexual activity, boosting sexual desire.

1728331714948

Furthermore, estrogen modulates the expression of dopamine receptors, particularly D1 receptors, which are involved in promoting sexual arousal and behaviors. By enhancing D1 receptor expression and increasing dopamine release, estrogen sets the stage for heightened libido and sexual motivation.

Estrogen also plays a pivotal role in the regulation of nitric oxide (NO) synthase, particularly neuronal nitric oxide synthase (nNOS) in the brain. NO acts as a vasodilator, increasing blood flow to erectile tissues and enhancing sexual function. Estrogen stimulates NO release both centrally, facilitating dopaminergic transmission, and peripherally, promoting vasodilation in the penile arteries. This two-pronged influence of NO leads to both the psychological arousal (through enhanced neurotransmission) and the physiological readiness for sexual activity (through increased blood flow).
Estrogen's involvement in the HPG axis adds another layer of complexity to its role in libido regulation. High levels of estradiol provide negative feedback on the hypothalamus, particularly on the secretion of gonadotropin-releasing hormone (GnRH). While excessive estrogen can suppress libido by downregulating GnRH and thereby reducing testosterone levels, moderate estradiol levels maintain the delicate balance necessary for proper HPG axis function.

However, estradiol also exerts positive feedback on certain neurons in the hypothalamus that regulate sexual behavior directly, independent of the testosterone-driven pathways. For instance, estrogen-sensitive neurons within the mPOA, particularly those rich in aromatase and estrogen receptors, integrate signals from both circulating testosterone and local estradiol production, fine-tuning sexual motivation.
1728331700482


Estrogen doesn't act in isolation; it has a complex interaction with androgens, particularly testosterone. The simultaneous action of estradiol and testosterone on different receptor pathways synergistically enhances libido. Testosterone, acting on androgen receptors (ARs), directly promotes sexual desire. When testosterone is aromatized to estradiol, the resulting estrogenic signaling augments this effect, creating a more potent, finely-tuned response. Moreover, testosterone's direct effects on erectile function complement estrogen's influence on sexual motivation, creating an integrated hormonal environment conducive to both physical arousal and sexual drive.
 
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NZb6Air said:
Estrogen's role in libido starts with the aromatization of testosterone into estradiol. In males, a significant portion of estrogen is derived from the aromatization of testosterone in the brain, catalyzed by the enzyme aromatase, which is highly expressed in regions critical to sexual behavior regulation, such as the medial preoptic area (mPOA) and the bed nucleus of the stria terminalis.
View attachment 3224548
Once converted, estradiol binds to estrogen receptors (ERs), specifically ERα and ERβ, which are widely expressed in the central nervous system, particularly in areas that govern sexual motivation, like the hypothalamus. Estrogen receptor signaling through ERα in the mPOA is crucial for male sexual motivation. The activation of these receptors leads to both genomic and non-genomic signaling cascades.

Upon estrogen binding, ERα/ERβ translocate into the nucleus, where they act as transcription factors that regulate the expression of genes associated with sexual behavior, such as those influencing dopamine synthesis, receptor density, and nitric oxide (NO) pathways. The increased expression of these genes enhances the dopaminergic transmission in areas like the nucleus accumbens and the ventral tegmental area (VTA), which are involved in reward processing and sexual arousal.

View attachment 3224544

Estrogen can also act via rapid, membrane-initiated signaling cascades, engaging membrane-bound ERs or G-protein-coupled estrogen receptors (GPER), which can activate second messenger systems such as MAPK/ERK or PI3K/Akt pathways. This results in rapid modulation of neurotransmitter release, particularly dopamine and nitric oxide. These non-genomic actions are crucial for the rapid modulation of sexual drive, as they affect neurotransmitter systems that govern immediate sexual motivation.

Dopamine, the primary neurotransmitter associated with reward and motivation, is heavily modulated by estrogen. In males, estrogen's effect on the dopaminergic system is critical for libido. Estrogen promotes the release and synthesis of dopamine in the hypothalamus and the mPOA, which then influences the mesolimbic reward system. Increased dopamine in these circuits enhances the reward feedback mechanisms associated with sexual activity, boosting sexual desire.

View attachment 3224539
Furthermore, estrogen modulates the expression of dopamine receptors, particularly D1 receptors, which are involved in promoting sexual arousal and behaviors. By enhancing D1 receptor expression and increasing dopamine release, estrogen sets the stage for heightened libido and sexual motivation.

Estrogen also plays a pivotal role in the regulation of nitric oxide (NO) synthase, particularly neuronal nitric oxide synthase (nNOS) in the brain. NO acts as a vasodilator, increasing blood flow to erectile tissues and enhancing sexual function. Estrogen stimulates NO release both centrally, facilitating dopaminergic transmission, and peripherally, promoting vasodilation in the penile arteries. This two-pronged influence of NO leads to both the psychological arousal (through enhanced neurotransmission) and the physiological readiness for sexual activity (through increased blood flow).
Estrogen's involvement in the HPG axis adds another layer of complexity to its role in libido regulation. High levels of estradiol provide negative feedback on the hypothalamus, particularly on the secretion of gonadotropin-releasing hormone (GnRH). While excessive estrogen can suppress libido by downregulating GnRH and thereby reducing testosterone levels, moderate estradiol levels maintain the delicate balance necessary for proper HPG axis function.

However, estradiol also exerts positive feedback on certain neurons in the hypothalamus that regulate sexual behavior directly, independent of the testosterone-driven pathways. For instance, estrogen-sensitive neurons within the mPOA, particularly those rich in aromatase and estrogen receptors, integrate signals from both circulating testosterone and local estradiol production, fine-tuning sexual motivation.
View attachment 3224531

Estrogen doesn't act in isolation; it has a complex interaction with androgens, particularly testosterone. The simultaneous action of estradiol and testosterone on different receptor pathways synergistically enhances libido. Testosterone, acting on androgen receptors (ARs), directly promotes sexual desire. When testosterone is aromatized to estradiol, the resulting estrogenic signaling augments this effect, creating a more potent, finely-tuned response. Moreover, testosterone's direct effects on erectile function complement estrogen's influence on sexual motivation, creating an integrated hormonal environment conducive to both physical arousal and sexual drive.
Click to expand...
so high estrogen femboys are horny??
 
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NZb6Air said:
Estrogen's role in libido starts with the aromatization of testosterone into estradiol. In males, a significant portion of estrogen is derived from the aromatization of testosterone in the brain, catalyzed by the enzyme aromatase, which is highly expressed in regions critical to sexual behavior regulation, such as the medial preoptic area (mPOA) and the bed nucleus of the stria terminalis.
View attachment 3224548
Once converted, estradiol binds to estrogen receptors (ERs), specifically ERα and ERβ, which are widely expressed in the central nervous system, particularly in areas that govern sexual motivation, like the hypothalamus. Estrogen receptor signaling through ERα in the mPOA is crucial for male sexual motivation. The activation of these receptors leads to both genomic and non-genomic signaling cascades.

Upon estrogen binding, ERα/ERβ translocate into the nucleus, where they act as transcription factors that regulate the expression of genes associated with sexual behavior, such as those influencing dopamine synthesis, receptor density, and nitric oxide (NO) pathways. The increased expression of these genes enhances the dopaminergic transmission in areas like the nucleus accumbens and the ventral tegmental area (VTA), which are involved in reward processing and sexual arousal.

View attachment 3224544

Estrogen can also act via rapid, membrane-initiated signaling cascades, engaging membrane-bound ERs or G-protein-coupled estrogen receptors (GPER), which can activate second messenger systems such as MAPK/ERK or PI3K/Akt pathways. This results in rapid modulation of neurotransmitter release, particularly dopamine and nitric oxide. These non-genomic actions are crucial for the rapid modulation of sexual drive, as they affect neurotransmitter systems that govern immediate sexual motivation.

Dopamine, the primary neurotransmitter associated with reward and motivation, is heavily modulated by estrogen. In males, estrogen's effect on the dopaminergic system is critical for libido. Estrogen promotes the release and synthesis of dopamine in the hypothalamus and the mPOA, which then influences the mesolimbic reward system. Increased dopamine in these circuits enhances the reward feedback mechanisms associated with sexual activity, boosting sexual desire.

View attachment 3224539
Furthermore, estrogen modulates the expression of dopamine receptors, particularly D1 receptors, which are involved in promoting sexual arousal and behaviors. By enhancing D1 receptor expression and increasing dopamine release, estrogen sets the stage for heightened libido and sexual motivation.

Estrogen also plays a pivotal role in the regulation of nitric oxide (NO) synthase, particularly neuronal nitric oxide synthase (nNOS) in the brain. NO acts as a vasodilator, increasing blood flow to erectile tissues and enhancing sexual function. Estrogen stimulates NO release both centrally, facilitating dopaminergic transmission, and peripherally, promoting vasodilation in the penile arteries. This two-pronged influence of NO leads to both the psychological arousal (through enhanced neurotransmission) and the physiological readiness for sexual activity (through increased blood flow).
Estrogen's involvement in the HPG axis adds another layer of complexity to its role in libido regulation. High levels of estradiol provide negative feedback on the hypothalamus, particularly on the secretion of gonadotropin-releasing hormone (GnRH). While excessive estrogen can suppress libido by downregulating GnRH and thereby reducing testosterone levels, moderate estradiol levels maintain the delicate balance necessary for proper HPG axis function.

However, estradiol also exerts positive feedback on certain neurons in the hypothalamus that regulate sexual behavior directly, independent of the testosterone-driven pathways. For instance, estrogen-sensitive neurons within the mPOA, particularly those rich in aromatase and estrogen receptors, integrate signals from both circulating testosterone and local estradiol production, fine-tuning sexual motivation.
View attachment 3224531

Estrogen doesn't act in isolation; it has a complex interaction with androgens, particularly testosterone. The simultaneous action of estradiol and testosterone on different receptor pathways synergistically enhances libido. Testosterone, acting on androgen receptors (ARs), directly promotes sexual desire. When testosterone is aromatized to estradiol, the resulting estrogenic signaling augments this effect, creating a more potent, finely-tuned response. Moreover, testosterone's direct effects on erectile function complement estrogen's influence on sexual motivation, creating an integrated hormonal environment conducive to both physical arousal and sexual drive.
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Legit. there are countless reports of guys on aromatase inhibitors tanking their sexual desire
 
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97baHater said:
PMs nigga
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i saw a femboy on tt like a month ago she was literally a high htb or low stacylite i was wondering why didnt that "girl" had no boobs until i read the caption said "im a male"(maybe it was fake but his body was a body of a male so idk)
 
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kambally said:
i saw a femboy on tt like a month ago she was literally a high htb or low stacylite i was wondering why didnt that "girl" had no boobs until i read the caption said "im a male"(maybe it was fake but his body was a body of a male so idk)
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Yeah yeah ask @NZb6Air to send you some femboy this fag has female looking niggas on his hard drive
kambally said:
send that shi to me too
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@NZb6Air
 
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NZb6Air said:
i can send you're gonna coom in ur pants lol but mods will delete/ban
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RealSurgerymax said:
“Just get OBO and Tripods and make sure it’s custom and modified so you don’t need craniotomy and get Infraorbital and malar implants at the same time and add in skull implants and make sure all the plates and guides are used perfectly and each and every one of the 20 individual implants fit together perfectly without any misplacement and don’t have any complications theory.”
 
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97baHater said:
?
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you immediately wanted to see that shit lol, you wanted to see a chick with a cock, to prove your claim? :forcedsmile::forcedsmile:

if you knew your claim was right you would've stood your ground and not asked for evidence, im only gonna say that for this because its more of a biased arguement
 
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dookielooksmaxxer said:
you immediately wanted to see that shit lol, you wanted to see a chick with a cock, to prove your claim? :forcedsmile::forcedsmile:

if you knew your claim was right you would've stood your ground and not asked for evidence, im only gonna say that for this because its more of a biased arguement
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nigger said absolutely nothing, the only thing i know is that i'd crush your torso in mere seconds
 
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dookielooksmaxxer said:
you immediately wanted to see that shit lol, you wanted to see a chick with a cock, to prove your claim? :forcedsmile::forcedsmile:

if you knew your claim was right you would've stood your ground and not asked for evidence, im only gonna say that for this because its more of a biased arguement
Click to expand...
Shut the fuck up faggot I piss in your throat
NZb6Air said:
nigger said absolutely nothing, the only thing i know is that i'd crush your torso in mere seconds
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Tell him king
 
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NZb6Air said:
wtf unignore him

just apologize for accusing him of evil without proof
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alr bhai, I apologize for my accusations, I do not wish to start on the wrong foot, I truly believe my fellow incel bhais are truly a great gift to me, as I have a community to share my dark experiences of being an incel @97baHater

- written by an actual human
 
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NZb6Air said:
wtf unignore him
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Never actually ignored him
dookielooksmaxxer said:
alr bhai, I apologize for my accusations, I do not wish to start on the wrong foot, I truly believe my fellow incel bhais are truly a great gift to me, as I have a community to share my dark experiences of being an incel @97baHater

- written by an actual human
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Okay ✅
 
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