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haidut

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The neurosteroid androsterone has some very interesting properties, among which is potent GABA agonist activity. Most GABA agonists inhibit the synthesis and/or release of epinephrine (adrenaline) and norepinephrine (noradrenaline) in various animal models and in human trials. The studies below show that androsterone is no exception and is in fact quite potent at reducing the catecholamine release trigerred by nicotine through acetylcholine receptor activation. In addition, and in agreement with its anti-adrenaline effect, androsterone exhibited vasorelaxant properties.

Short term effect of steroids on catecholamine secretion from bovine adrenal medulla chromaffin cells. - PubMed - NCBI
"...As shown in Table 1, many steroid compounds produced marked inhibitory effects on the secretory response induced by ACh (100 PM) in adrenal chromaffin cells. Progesterone, androsterone, androstandione, 4A-androstene-3,17-dione, testosterone and dehyroisoandrosterone caused the most significant inhibition p<O.OOOl) of -60 to 90%, and inhibition by 17~ethinylestradiol, 5cr-androstane-17P-ol-3-one, 17a-hydroxyprogesterone, P-estradiol and 17a_hydroxypregnenolone was less pronounced and ranged between 20- 50%. Curiously, estradiol3-benzoate and estradiol-17/?- acetate caused a slight but significant (p < 0.05) elevation in catecholamine secretion induced by ACh. Pregnenolone, estrone and cholesterol did not significantly change the secretory effect of ACh."


[Activity induced by androsterone and hemisuccinate of androsterone on perfusion pressure and vascular resistance]. - PubMed - NCBI
"...RESULTS: The results showed that: (1) the hemisuccinate of androsterone [10(-9) M] increases the perfusion pressure and vascular resistance in comparison with the androsterone [10(-9) M]; (2) the effect of androsterone-derivative [10(-9) M-10(-5) M] on perfusion pressure not was inhibited by indometacin [10(-6) M]; (3) nifedipine [10(-6) M] blocks the effects exerted by hemisuccinate of androsterone [10(-9) M-10(-5) M] on perfusion pressure; and (4) the effect of androsterone-derivative [10(-9) M-10(-5) M] on perfusion pressure in presence of flutamide [10(-6) M] was inhibited.


Testosterone-induced relaxation of rat aorta is androgen structure specific and involves K+ channel activation. - PubMed - NCBI
"...Based on the sensitivity (EC(50)) of Endo- aortas, Tes, the active metabolite 5alpha-dihydrotestosterone, the major excretory metabolites androsterone and etiocholanolone, the nonpolar esters Tes-enanthate and Tes-hemisuccinate (THS), and THS conjugates to BSA (THS-BSA) exhibited relative potencies for vasorelaxation dramatically different from androgen receptor-mediated effects observed in reproductive tissues, with a rank order of THS-BSA > Tes > androsterone = THS = etiocholanolone > dihydrotestosterone >> Tes-enanthate. Pretreatment of aortas with 5 mM 4-aminopyridine attenuated Tes-induced vasorelaxation by an average of 44 +/- 2% (25-300 microM Tes). In contrast, pretreatment of aortas with other K+ channel inhibitors had no effect. These data reveal that Tes-induced vasorelaxation is a structurally specific effect of the androgen molecule, which is enhanced in more polar analogs that have a lower permeability to the VSM cell membrane, and that the effect of Tes involves activation of K+ efflux through K+ channels in VSM, perhaps via the voltage-dependent (delayed-rectifier) K+ channel."
 

Drareg

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The neurosteroid androsterone has some very interesting properties, among which is potent GABA agonist activity. Most GABA agonists inhibit the synthesis and/or release of epinephrine (adrenaline) and norepinephrine (noradrenaline) in various animal models and in human trials. The studies below show that androsterone is no exception and is in fact quite potent at reducing the catecholamine release trigerred by nicotine through acetylcholine receptor activation. In addition, and in agreement with its anti-adrenaline effect, androsterone exhibited vasorelaxant properties.

Short term effect of steroids on catecholamine secretion from bovine adrenal medulla chromaffin cells. - PubMed - NCBI
"...As shown in Table 1, many steroid compounds produced marked inhibitory effects on the secretory response induced by ACh (100 PM) in adrenal chromaffin cells. Progesterone, androsterone, androstandione, 4A-androstene-3,17-dione, testosterone and dehyroisoandrosterone caused the most significant inhibition p<O.OOOl) of -60 to 90%, and inhibition by 17~ethinylestradiol, 5cr-androstane-17P-ol-3-one, 17a-hydroxyprogesterone, P-estradiol and 17a_hydroxypregnenolone was less pronounced and ranged between 20- 50%. Curiously, estradiol3-benzoate and estradiol-17/?- acetate caused a slight but significant (p < 0.05) elevation in catecholamine secretion induced by ACh. Pregnenolone, estrone and cholesterol did not significantly change the secretory effect of ACh."


[Activity induced by androsterone and hemisuccinate of androsterone on perfusion pressure and vascular resistance]. - PubMed - NCBI
"...RESULTS: The results showed that: (1) the hemisuccinate of androsterone [10(-9) M] increases the perfusion pressure and vascular resistance in comparison with the androsterone [10(-9) M]; (2) the effect of androsterone-derivative [10(-9) M-10(-5) M] on perfusion pressure not was inhibited by indometacin [10(-6) M]; (3) nifedipine [10(-6) M] blocks the effects exerted by hemisuccinate of androsterone [10(-9) M-10(-5) M] on perfusion pressure; and (4) the effect of androsterone-derivative [10(-9) M-10(-5) M] on perfusion pressure in presence of flutamide [10(-6) M] was inhibited.


Testosterone-induced relaxation of rat aorta is androgen structure specific and involves K+ channel activation. - PubMed - NCBI
"...Based on the sensitivity (EC(50)) of Endo- aortas, Tes, the active metabolite 5alpha-dihydrotestosterone, the major excretory metabolites androsterone and etiocholanolone, the nonpolar esters Tes-enanthate and Tes-hemisuccinate (THS), and THS conjugates to BSA (THS-BSA) exhibited relative potencies for vasorelaxation dramatically different from androgen receptor-mediated effects observed in reproductive tissues, with a rank order of THS-BSA > Tes > androsterone = THS = etiocholanolone > dihydrotestosterone >> Tes-enanthate. Pretreatment of aortas with 5 mM 4-aminopyridine attenuated Tes-induced vasorelaxation by an average of 44 +/- 2% (25-300 microM Tes). In contrast, pretreatment of aortas with other K+ channel inhibitors had no effect. These data reveal that Tes-induced vasorelaxation is a structurally specific effect of the androgen molecule, which is enhanced in more polar analogs that have a lower permeability to the VSM cell membrane, and that the effect of Tes involves activation of K+ efflux through K+ channels in VSM, perhaps via the voltage-dependent (delayed-rectifier) K+ channel."

Will probably increase erection frequency by the sounds of it.
 

haidut

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haidut

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Haidut: do you know what kind of effects it has on blood pressure?

It seems to lower blood pressure in higher doses. GABA agonists lower cortisol and given the anti-adrenaline effects in the above studies, androsterone seems a lot like clonidine in that respect. So, a certain blood pressure lowering effect is expected.
 

OkayByTheSea

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Thanks, Haidut.

I have ordered a bottle already.

Would you have a range recommendation on timing (when to apply) and dosage pattern (beginning dose and as one progresses) for the indication of chronic stress?

Regards,
OBTS
 

haidut

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Thanks, Haidut.

I have ordered a bottle already.

Would you have a range recommendation on timing (when to apply) and dosage pattern (beginning dose and as one progresses) for the indication of chronic stress?

Regards,
OBTS

I think it is similar to DHEA - up to 15mg - 20mg daily is probably best. In combination with Pansterone, this thing turns into a monster. In a good way :):
 

haidut

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Thanks, Haidut.

I have ordered a bottle already.

Would you have a range recommendation on timing (when to apply) and dosage pattern (beginning dose and as one progresses) for the indication of chronic stress?

Regards,
OBTS

I think combined with progesterone it works very well as anti-stress tool. I would take a dose of say 2mg - 3mg of each steroid at a time. If taken at night it is usually good enough even as a single dose but you can take more during the day as needed. The only downside I see is that in higher doses that combo is very sedating, so not very useful if you have to drive or focus mentally.
 

haidut

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@haidut

Doesn't Peat view noradrenaline as being beneficial in some situations? I remember him talking about noradrenaline being something like the brain's locally produced anti-seizure chemical.

Also it seems to have other benefits: Norepinephrine: Good or Bad? (And Natural Ways to Increase It) - Selfhacked

Do you have a source of where Peat talks about noradrenaline in positive light? My research on it is that it is not something desirable to have elevated long term.
 

OkayByTheSea

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I think combined with progesterone it works very well as anti-stress tool. I would take a dose of say 2mg - 3mg of each steroid at a time. If taken at night it is usually good enough even as a single dose but you can take more during the day as needed. The only downside I see is that in higher doses that combo is very sedating, so not very useful if you have to drive or focus mentally.

As a male, I am advised to stay away from progesterone. I, however, do take pregnenolone. I feel a lot of anti-stress benefits from pregnenolone. I hope I could continue to take pregnenolone with androsterone. Please advice.

Regards,
 

haidut

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As a male, I am advised to stay away from progesterone. I, however, do take pregnenolone. I feel a lot of anti-stress benefits from pregnenolone. I hope I could continue to take pregnenolone with androsterone. Please advice.

Regards,

Don't see a reason why not, unless a doctor advises against it. In my opinion progesterone + androsterone or pregnenolone + androsterone would be a good way to get the benefits of the pregnanes without the anti-male effects.
 

thyrulian

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@haidut

Doesn't Peat view noradrenaline as being beneficial in some situations? I remember him talking about noradrenaline being something like the brain's locally produced anti-seizure chemical.

Also it seems to have other benefits: Norepinephrine: Good or Bad? (And Natural Ways to Increase It) - Selfhacked
My guess is that downregulated noradrenergic activity is partially why Ritanserin taken in the morning can improve slow wave sleep at night.

I took 2 drops of it the other day, noticed greater anxiety, but felt more relaxed than usual at bed time.
 

TubZy

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Might have to try this, I have been using nicotine in the form of gum and vape over the past two weeks for neurosteroid boost, which has been very helpful. Cigarettes don't really provide the same effect honestly. I have been using higher doses (close to 12mg nicotine a day).

The vasoconstriction has been kind of on and off, gelatin has helped and taurine, but didn't androsterone had a vasorelaxtion effect.
 

Regina

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I think it is similar to DHEA - up to 15mg - 20mg daily is probably best. In combination with Pansterone, this thing turns into a monster. In a good way :)
Do you have a source of where Peat talks about noradrenaline in positive light? My research on it is that it is not something desirable to have elevated long term.
I can't find any pathogenic bacteria that does not flourish in norepinephrine. I hate this stuff.
I just have to figure out some chicken and egg mystery with myself. Wiped-out iron : high NE. Which tail is wagging the dog?
 

Regina

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The neurosteroid androsterone has some very interesting properties, among which is potent GABA agonist activity. Most GABA agonists inhibit the synthesis and/or release of epinephrine (adrenaline) and norepinephrine (noradrenaline) in various animal models and in human trials. The studies below show that androsterone is no exception and is in fact quite potent at reducing the catecholamine release trigerred by nicotine through acetylcholine receptor activation. In addition, and in agreement with its anti-adrenaline effect, androsterone exhibited vasorelaxant properties.

Short term effect of steroids on catecholamine secretion from bovine adrenal medulla chromaffin cells. - PubMed - NCBI
"...As shown in Table 1, many steroid compounds produced marked inhibitory effects on the secretory response induced by ACh (100 PM) in adrenal chromaffin cells. Progesterone, androsterone, androstandione, 4A-androstene-3,17-dione, testosterone and dehyroisoandrosterone caused the most significant inhibition p<O.OOOl) of -60 to 90%, and inhibition by 17~ethinylestradiol, 5cr-androstane-17P-ol-3-one, 17a-hydroxyprogesterone, P-estradiol and 17a_hydroxypregnenolone was less pronounced and ranged between 20- 50%. Curiously, estradiol3-benzoate and estradiol-17/?- acetate caused a slight but significant (p < 0.05) elevation in catecholamine secretion induced by ACh. Pregnenolone, estrone and cholesterol did not significantly change the secretory effect of ACh."


[Activity induced by androsterone and hemisuccinate of androsterone on perfusion pressure and vascular resistance]. - PubMed - NCBI
"...RESULTS: The results showed that: (1) the hemisuccinate of androsterone [10(-9) M] increases the perfusion pressure and vascular resistance in comparison with the androsterone [10(-9) M]; (2) the effect of androsterone-derivative [10(-9) M-10(-5) M] on perfusion pressure not was inhibited by indometacin [10(-6) M]; (3) nifedipine [10(-6) M] blocks the effects exerted by hemisuccinate of androsterone [10(-9) M-10(-5) M] on perfusion pressure; and (4) the effect of androsterone-derivative [10(-9) M-10(-5) M] on perfusion pressure in presence of flutamide [10(-6) M] was inhibited.


Testosterone-induced relaxation of rat aorta is androgen structure specific and involves K+ channel activation. - PubMed - NCBI
"...Based on the sensitivity (EC(50)) of Endo- aortas, Tes, the active metabolite 5alpha-dihydrotestosterone, the major excretory metabolites androsterone and etiocholanolone, the nonpolar esters Tes-enanthate and Tes-hemisuccinate (THS), and THS conjugates to BSA (THS-BSA) exhibited relative potencies for vasorelaxation dramatically different from androgen receptor-mediated effects observed in reproductive tissues, with a rank order of THS-BSA > Tes > androsterone = THS = etiocholanolone > dihydrotestosterone >> Tes-enanthate. Pretreatment of aortas with 5 mM 4-aminopyridine attenuated Tes-induced vasorelaxation by an average of 44 +/- 2% (25-300 microM Tes). In contrast, pretreatment of aortas with other K+ channel inhibitors had no effect. These data reveal that Tes-induced vasorelaxation is a structurally specific effect of the androgen molecule, which is enhanced in more polar analogs that have a lower permeability to the VSM cell membrane, and that the effect of Tes involves activation of K+ efflux through K+ channels in VSM, perhaps via the voltage-dependent (delayed-rectifier) K+ channel."
Yip yip. And androgens improve anemia:
Google
 

Antonello

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@haidut If Andro show up some underlying issue with my metabolism and I ended up with adrenaline and anxiety, exactly the opposite of what I wanna to achieve and with a calories intake under control and a daily thyroid combo of t3/t4, does it mean I need more thyroid for support the extra boost in metabolism? Because Im not the first one that report the same crash issue and this happens just in various occasion what is the missing link to give the body the ability to convert andro in a proper way?
I’m thinking about thyroid but I don’t know if it’s need more T3 or T4. Please can you clarify this?:)
 
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