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alisalamaz
Iron
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Have you read this study https://www.oncotarget.com/article/1886/pdf/?They even have patent where they claim that minoxidil is effective in the treatment of acne https://patentimages.storage.googleapis.com/01/9e/e8/15c102fa38a5ed/EP2991653B1.pdf.
Their study begins with the fact that the mechanism of minoxidil in the treatment of AR-related disease,AGA,is unknown and they hypothesized that minoxidil affects AR receptors.And their hypothesis was allegedly confirmed.But they did not explain why minoxidil causes hair growth even on the beard where hair grows through the activation of androgens,they also did not explain why Bicalutamide or other AR receptor blocker cannot preserve hair that has been grown by minoxidil after the withdrawal of minoxidil.
Last paragraph of Introduction from study: Previous studies have consistently concluded that minoxidil does not act directly through an androgen effect [19, 20]. However, it nevertheless influences the androgen-AR pathway-dominant disease, AGA, prompting us to hypothesize that minoxidil does indeed affect AR-related functions. To test this speculative relationship between minoxidil and AR, we performed a series of experimental and modeling studies.
If previous studies have stated that minoxidil is not an anti-androgen, then what is the point of hypothesizing something?It's really weird.
Let's take a look at their discussion
“Minoxidil actions as an anti-hypertension agent have been mainly attributed to its potassium channel-opening effect, which has been linked to the hypertrichosis phenomenon associated with minoxidil [37]. However, this mechanism is not compatible with certain findings, including the observations that potassium channel antagonists are unable to block minoxidil effects and potassium channels are not expressed in hair follicle cells [38, 39]» According to them, it turns out that minoxidil lowers blood pressure through the blocking of androgen receptors but not through the opening of potassium channels.
“AGA is closely associated with androgen-AR pathway activity. Previous studies using a golden Syrian hamster model found no anti-androgenic potential of minoxidil on androgen-dependent cutaneous structures [19]. However, female animals were used in these studies, and testosterone, which can be converted to estradiol in hair follicles [40], rather than DHT was chosen”
They claim that
Previous studies using a golden Syrian hamster model found no anti-androgenic potential of minoxidil on androgen-dependent cutaneous structures and this is wrong because female animals were used and testosterone can be converted to estradiol in the hair,rather dht. This is complete nonsense!Female flank organ is as responsive as that of male to hormonal stimulation,and that females can easily be used in place of castrated males to study the effects of topically anti-androgens. Take a look at Trans man.After stimulation with testosterone, the beard begins to grow and the voice also becomes rough.
Their study begins with the fact that the mechanism of minoxidil in the treatment of AR-related disease,AGA,is unknown and they hypothesized that minoxidil affects AR receptors.And their hypothesis was allegedly confirmed.But they did not explain why minoxidil causes hair growth even on the beard where hair grows through the activation of androgens,they also did not explain why Bicalutamide or other AR receptor blocker cannot preserve hair that has been grown by minoxidil after the withdrawal of minoxidil.
Last paragraph of Introduction from study: Previous studies have consistently concluded that minoxidil does not act directly through an androgen effect [19, 20]. However, it nevertheless influences the androgen-AR pathway-dominant disease, AGA, prompting us to hypothesize that minoxidil does indeed affect AR-related functions. To test this speculative relationship between minoxidil and AR, we performed a series of experimental and modeling studies.
If previous studies have stated that minoxidil is not an anti-androgen, then what is the point of hypothesizing something?It's really weird.
Let's take a look at their discussion
“Minoxidil actions as an anti-hypertension agent have been mainly attributed to its potassium channel-opening effect, which has been linked to the hypertrichosis phenomenon associated with minoxidil [37]. However, this mechanism is not compatible with certain findings, including the observations that potassium channel antagonists are unable to block minoxidil effects and potassium channels are not expressed in hair follicle cells [38, 39]» According to them, it turns out that minoxidil lowers blood pressure through the blocking of androgen receptors but not through the opening of potassium channels.
“AGA is closely associated with androgen-AR pathway activity. Previous studies using a golden Syrian hamster model found no anti-androgenic potential of minoxidil on androgen-dependent cutaneous structures [19]. However, female animals were used in these studies, and testosterone, which can be converted to estradiol in hair follicles [40], rather than DHT was chosen”
They claim that
Previous studies using a golden Syrian hamster model found no anti-androgenic potential of minoxidil on androgen-dependent cutaneous structures and this is wrong because female animals were used and testosterone can be converted to estradiol in the hair,rather dht. This is complete nonsense!Female flank organ is as responsive as that of male to hormonal stimulation,and that females can easily be used in place of castrated males to study the effects of topically anti-androgens. Take a look at Trans man.After stimulation with testosterone, the beard begins to grow and the voice also becomes rough.
