supernature
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FINASTERIDE SIGNIFICANTLY UPREGULATES ANDROGEN RECEPTOR in this study ( PROTOCOLS and discussions for PFS)
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@Slayo @supernature
I had the same, when I was very sick, my eyes color from blue became grey and kind of not sharp.
When you fast, the color becomes blue again and very sharp color and the whites get very white.
I think part of it since ammonia load goes down. Ammonia usually makes your eyes tired
I had the same, when I was very sick, my eyes color from blue became grey and kind of not sharp.
When you fast, the color becomes blue again and very sharp color and the whites get very white.
I think part of it since ammonia load goes down. Ammonia usually makes your eyes tired
supernature
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Goose12
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That's exactly how I was as a kid. I would literally have dreams of the future. It was always just random things nothing important. It's slowed down a lot now that I am older but every now and then I will still have one. Wish I could have one about the stock market lol.
Also when I was younger I could do things like read a book and solve math problems at the same time. It was like I had 2 brains. It would be awsome to do that again.
This was all before I was hit with mild cfs that I have had most off my life. Currently, on tei, its greatly improved.
This statement that you mentioned just caught my eye:
"In cases of downregulated receptors, dutasteride will work. or any 5 AR antagonist. with no progestin line action, Just blocks 5 AR"
Are you saying that Dustasteride does not act as progestin up regulating receptors but instead just inhibits 5AR enzymes?
I ask because I actually took Avodart (Dustastride) when I was twenty two years old for a whole month and did not develop PFS or have any problems for that matter. It was not until I was twenty six when I took Saw P that I developed PFS...
I have always wondered why I was able to take Dustastride a powerful duel action 5ar inhibitor and not develop PFS but I was able to get PFS from Saw P. Do you think Saw P acts as a progestin like fin? while Dustasterdie does not?
I mean if this is the case this is hugh because it could be a big clue as to if I am dealing with down regulated or up regulated receptors correct?
Hey @5 alpha whats up?
Couple points:
The last sentence of this study
Dutasteride affects progesterone metabolizing enzyme activity/expression in human breast cell lines resulting in suppression of cell proliferation and detachment | J P Wiebe | Request PDF
“This study provides the first evidence that dutasteride is a potent progesterone 5alpha-reductase inhibitor and that such inhibition may be beneficial in breast cancer”
So I’m not sure if they’re saying duta is a potent progesterone *based* 5alpha-reductase...
My 2nd point tho is we’ve seen a common pattern where ppl use a 5ARi and stop, recover without issue and then try again only to suffer the post 5ARi sides.
However, jack has proven something that I recently started trying too. Going back on may relieve the symptoms and bring about another chance to come off.
Jack has used fin but settled on duta which may be not only due to its longer half life but, if it’s not synthetic prog like fin, it could be why it’s safer and working.
I’m on other stuff so it’s not a clean trial but I’m using a single drop of fin with 3 drops dmso on my forearm. The science is all about receptors. Fingers crossed bro
Couple points:
The last sentence of this study
Dutasteride affects progesterone metabolizing enzyme activity/expression in human breast cell lines resulting in suppression of cell proliferation and detachment | J P Wiebe | Request PDF
“This study provides the first evidence that dutasteride is a potent progesterone 5alpha-reductase inhibitor and that such inhibition may be beneficial in breast cancer”
So I’m not sure if they’re saying duta is a potent progesterone *based* 5alpha-reductase...
My 2nd point tho is we’ve seen a common pattern where ppl use a 5ARi and stop, recover without issue and then try again only to suffer the post 5ARi sides.
However, jack has proven something that I recently started trying too. Going back on may relieve the symptoms and bring about another chance to come off.
Jack has used fin but settled on duta which may be not only due to its longer half life but, if it’s not synthetic prog like fin, it could be why it’s safer and working.
I’m on other stuff so it’s not a clean trial but I’m using a single drop of fin with 3 drops dmso on my forearm. The science is all about receptors. Fingers crossed bro
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Joe, PFStinks has been doing this for far longer than Jack17 and trying to come off. But it does not work for him. He was using fin though and not dutasteride.
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@joekool I think to try to come off dutasteride is better, since the rise in DHT happens slower, and if we assume that AR is overexpressed, then it will be better to slowly downregulate the expression. by switching off silencing mechanism and slowly downregulating expression.
This is true only if the brain shut down AR trancription since ARs density was overexpressed
This is true only if the brain shut down AR trancription since ARs density was overexpressed
Yea I’m seriously leaning to order duta and go that route. I think it’s smarter to drop all 5AR (both type 1 & 2) for the SnapBack / up regulation. In fact, I’m thinking the fin plus dht/randro I’m using isn’t smart. It should be one or the other , alternating.
Still testing things... but Monday night when I did the drop and dht drops, I got a very healthy random erection showing me I was immediately responding to dht
Still testing things... but Monday night when I did the drop and dht drops, I got a very healthy random erection showing me I was immediately responding to dht
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I think you are confused about androgens and DHT. DHT if high kills erections, and libido by putting calcium inside of the cell. and in prostate by using PTX G protein
PTX G protein is gaba. so DHT by gaba mechanism increases calcium in the cell.
so for people with high DHT , by lowering 5AR and killing DHT and its metabolites, that increases their metabolism similar to thyroid.
Calcium activation decreases, by kiling 5ar. and this allows more potassium to enter the cell. which turns progesterone which is high into cortisol, and increases estrogen.
Since potassium enters the cell, body is allowed to convert histidine into histamine, and thus you get libido. since histamine itself lowers potassium in the cell.
So this manipulation kills 3 adiol, 3 allopregnenolone, kills gaba. GABA suppresses dopamine release. and thus increases prolactin. Prolactin is the thing that activates calcium vitamin D to active form conversion.
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@5 alpha people crash from dutasteride same as they crash from finasteride. Many were taking finasteride, then came off got PFS, then started dutasteride came off and got even more sides which they did not have with finasteride, like totally inability to experience pleasure. So it is hard to see the differences.
Also people crashed on RU -45888 which does not even touch 5AR. and crashed the same as on finasteride.
No one came off dutasteride and got fixed. so we don't know if it works. PFSstinks has been doing this for a year now. trying to go back on fin low dosage feeling normal and trying to come of , but it does not work.
We know that Jack17 had high DHT levels and felt great while he was taking dutasteride, before. Then when he came off dutasteride he crashed. He came off dutasteride just for the sake of it. not because he felt bad on it.
Now he went back on dutasteride again, and feeling normal again
So there is 2 possibilities,
1) If indeed body used some silencing mechanism to lower transcription of the AR since density was highly overexpressed. then may be just may be. doing micro doses of duta can switch off silencing mechanism for the whole numbers of ARS. and downregulate density overtime. since DHT will be rising constantly and more slowly , and body will have time to downregulate density. instead of just turning off all ARs. by silencing mechanism
2) it has zero to do with androgen receptors and going back on duta in Jack17s case means what I described to Joe in the previous post.
LIBIDO has nothing to do with DHT and androgens, LIBIDO is histamine, and estrogen. and penis growth is nitric oxide.
Nitric oxide is made by nitric oxide synthase.
It needs iron to start the reaction. then it needs FAD NADPH, BH4 then SODs, and glutathione peroxidase and all of this trigggered by calcium.
Testosterone starts IRON and puts it into blood. DHT puts calcium into the cell. Estrogen provides methylation and SODS, so keeps nitric oxide instead of superoxide.
and then selenium and cysteine, and glutathione get rid of hydrogen peroxide.
So if DHT is too high . then it just puts too much calcium in the cell. which slow metabolism. Estrogen lowers thyroid. so it is only allowed in the body when metabolism is high .
So when DHT puts too much calcium in the cell. estrogen is turned off. that is how DHT is antiestrogen.
Without estrogen you get no SODS. and thus no nitric oxide.
Highest nitric oxide production,= highest tissue growth and expansion. PUMP. as you can see from all of this stuff. If people think that androgens provide growth of tissue, they are wrong. you need like 5 balanced systems, to have this growth.
this is why that guy who was trying to cycle finasteride and DHT to grow penis. cycling finasteride is not done to increase some AR receptors. it is done to lower intracellular calcium, by killing DHT which increases metabolism speed.. and thus increases estrogen, so then later on, when you add DHT, you have both estro and DHT for maximum nitric oxide production.
This is why many people feel totally cured from all PFS side from taking test plus thyroid. or thyroid estro dht.
Which JN and justquitdut described in their protocols.
This is why when Jack17 went back on fin. his metabolism sped up, he lost weight. Fin was created to get rid of calcium from the cell and speed up metabolism. and thus getting rid of hairloss for some people.
this is why people with high DHT levels, like in prostate cancer. take DUTA inhibit DHT 90% and feel insane libido. with zero problems. since their metabolism is low and DHT is not even needed for their metabolism for a while.
Good example would be Stud. the young guy who has no PFS and never took finasteride but likes to experiment with DHT. When he went on high dose DHT, he lost libido, erections, and got anxiety. And it is a normal reaction for a healthy person.
Also people crashed on RU -45888 which does not even touch 5AR. and crashed the same as on finasteride.
No one came off dutasteride and got fixed. so we don't know if it works. PFSstinks has been doing this for a year now. trying to go back on fin low dosage feeling normal and trying to come of , but it does not work.
We know that Jack17 had high DHT levels and felt great while he was taking dutasteride, before. Then when he came off dutasteride he crashed. He came off dutasteride just for the sake of it. not because he felt bad on it.
Now he went back on dutasteride again, and feeling normal again
So there is 2 possibilities,
1) If indeed body used some silencing mechanism to lower transcription of the AR since density was highly overexpressed. then may be just may be. doing micro doses of duta can switch off silencing mechanism for the whole numbers of ARS. and downregulate density overtime. since DHT will be rising constantly and more slowly , and body will have time to downregulate density. instead of just turning off all ARs. by silencing mechanism
2) it has zero to do with androgen receptors and going back on duta in Jack17s case means what I described to Joe in the previous post.
LIBIDO has nothing to do with DHT and androgens, LIBIDO is histamine, and estrogen. and penis growth is nitric oxide.
Nitric oxide is made by nitric oxide synthase.
It needs iron to start the reaction. then it needs FAD NADPH, BH4 then SODs, and glutathione peroxidase and all of this trigggered by calcium.
Testosterone starts IRON and puts it into blood. DHT puts calcium into the cell. Estrogen provides methylation and SODS, so keeps nitric oxide instead of superoxide.
and then selenium and cysteine, and glutathione get rid of hydrogen peroxide.
So if DHT is too high . then it just puts too much calcium in the cell. which slow metabolism. Estrogen lowers thyroid. so it is only allowed in the body when metabolism is high .
So when DHT puts too much calcium in the cell. estrogen is turned off. that is how DHT is antiestrogen.
Without estrogen you get no SODS. and thus no nitric oxide.
Highest nitric oxide production,= highest tissue growth and expansion. PUMP. as you can see from all of this stuff. If people think that androgens provide growth of tissue, they are wrong. you need like 5 balanced systems, to have this growth.
this is why that guy who was trying to cycle finasteride and DHT to grow penis. cycling finasteride is not done to increase some AR receptors. it is done to lower intracellular calcium, by killing DHT which increases metabolism speed.. and thus increases estrogen, so then later on, when you add DHT, you have both estro and DHT for maximum nitric oxide production.
This is why many people feel totally cured from all PFS side from taking test plus thyroid. or thyroid estro dht.
Which JN and justquitdut described in their protocols.
This is why when Jack17 went back on fin. his metabolism sped up, he lost weight. Fin was created to get rid of calcium from the cell and speed up metabolism. and thus getting rid of hairloss for some people.
this is why people with high DHT levels, like in prostate cancer. take DUTA inhibit DHT 90% and feel insane libido. with zero problems. since their metabolism is low and DHT is not even needed for their metabolism for a while.
Good example would be Stud. the young guy who has no PFS and never took finasteride but likes to experiment with DHT. When he went on high dose DHT, he lost libido, erections, and got anxiety. And it is a normal reaction for a healthy person.
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@joekool Joe, may be it is a good idea to inhibit 5AR and take r andro at the same time. it is like taking fin with 5a-dhp. since r andro is gaba agonist. May be this way gaba does not get upregulated and then when you come off. DHT converts more into 3 adiol. and causes less problems.
I actually wondered what would happen if people took fin and 5a-dhp at the same time. Would it interfere with hairloss saving properties of fin.
and would it eliminate the crash after coming off fin.
I remember recently some guy on the forum, who was taking finasteride and gettting ready to come off. added 5 dhp and that lifted his sides while on finasteride.
I actually wondered what would happen if people took fin and 5a-dhp at the same time. Would it interfere with hairloss saving properties of fin.
and would it eliminate the crash after coming off fin.
I remember recently some guy on the forum, who was taking finasteride and gettting ready to come off. added 5 dhp and that lifted his sides while on finasteride.
RebelWithACause
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Yes so does GHB while on finasteride - I tried that myself when I was on finasteride. incl libido, erections was back everything. I think that will work. Don't know about the hairloss since I only used it for a night every time.
Nina
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I always thought finasteride dropped potassium in the cell? Do i have the wrong info?
5a-DHP would not address THDOC though, the final metabolite of cortisol.
GHB would address 5a-DHP, Allo and THDOC but I recall I also read a study where GHB's benefits on neurosteroids were not existent if one was also taking finasteride.
well i guess this explains why I got worse when I took arimidex. About three months after I got PFS at 26 my total Testosterone. Free Testosterone, LH and FSH were all low. An endo who was open minded and trying to learn about PFS tried a "2 year clomid restart protocol" on me. Essentially it was taking 50 mg of clomid every other day while lowering the dose until I was off completely over course of two years. When I first went on the Clomid it raised my Total T and Free T from almost being flagged low to being flagged high over the 1000 range. This did very little for my symptoms. The endo noticed that with the significant increase in T my estrogen raised high enough to be flagged as high so he put me on Armide to inhibit estrogen. About two weeks after taking the armidex all the sexual sides got worse despite follow up labs showing my estrogen being right in the middle on the labs reference range. I stopped taking the armidex had more labs which showed my estrogen went right back up to being flagged high and I improved...
So yea what you are saying about the estrogen is consistent with my experience.
I need to figure out what the difference between dusesteride and saw P is as far as what its doing and how they effect the prog receptors. I still think that the difference between how both are working is a clue for what has happened in my case at least. I was fine on Dutesteride to the extent that I was in healthy relationship with my girlfriend before during and after the one month I took it for. Sex 1-2 every day... no problems at all.
It's so odd that only 4 years later I would take Saw P and develop PFS while on the Saw P. So I did not get hit with the PFS crash people speak of after coming off the Saw P. I was on it and it was just like something is obvious wrong and came off of it and never recovered. I always figured it's like an accumulative effect type of thing that at 22 my body overcame and failed to over come only 4 years later while still in my prime. But I no longer think this is the case. I think they work by different mechanisms
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@5 alpha I think finasteride and dutasteride use NADPH's hydrogen to form complex with NADP and this way they inhibit 5AR. so for inhibition of 5AR NADPH is required. thus both drugs raise insulin while you are on the drug, since insulin is trying to make more NADPH. by putting more sugar in the cell.
Saw palmetto, just kills cholesterol binding. so to me it kills all enzymes where there is iron cysteine cluster. Like cortisol forming enzyme., 5 ar, pregnenolone forming enzyme. estrogen forming enzyme. the enzymes which RU blocks.
and since you are not using NADPH. then you get high iron high manganese on the hairtest of saw palmetto victims. and b1 is probably flushed out also. since body is trying to inhibit NADPH production, since probably those receptors for those hormones got overexpressed.
SO when you block those receptors of overexpressed hormones., my guess is that you start using that iron and manganese and b1 again, and not just flush it out. since the body wants to make NADPH again, and it needs iron cysteine cluster, and manganese and b1 to do that , to make those enzymes.
and this raises your nitric oxide.
same tests we saw from @Goose12 and @Walker Identical hairtests for saw palmetto people. I think someone else had the exactly same balance.
Saw palmetto, just kills cholesterol binding. so to me it kills all enzymes where there is iron cysteine cluster. Like cortisol forming enzyme., 5 ar, pregnenolone forming enzyme. estrogen forming enzyme. the enzymes which RU blocks.
and since you are not using NADPH. then you get high iron high manganese on the hairtest of saw palmetto victims. and b1 is probably flushed out also. since body is trying to inhibit NADPH production, since probably those receptors for those hormones got overexpressed.
SO when you block those receptors of overexpressed hormones., my guess is that you start using that iron and manganese and b1 again, and not just flush it out. since the body wants to make NADPH again, and it needs iron cysteine cluster, and manganese and b1 to do that , to make those enzymes.
and this raises your nitric oxide.
same tests we saw from @Goose12 and @Walker Identical hairtests for saw palmetto people. I think someone else had the exactly same balance.
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Goose12
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Olski69 had high iron also https://hackstasis.com/threads/saw-palmetto-sufferer-log-hair-test-included.923/
Goose,
I posted these same questions in olaski69's thread after reading through it. I am posting it here as well just in case it is missed there seeing that it's an old thread.
If I am I following correctly myself, Goose, Walker and Olaski69 are all Saw P victims?
Goose is it correct that both you and Olaski69 both get worse from inhibiting Estrogen? (I ask because I get worse from inhibiting estrogen)
Olaski69 said he is 6 foot 4 ? I am pretty sure Walker is also 6 foot 4 if I am remembering correctly from Swole Source when he posted as Maxout? (I ask because I am 6 foot 4 so it's just an interesting pattern if I am correct on Olaski69's and Walker's hight)
Goose what is your hight if you don't mind me asking?
Goose, walkers and Olaski69 all have high iron from hair test. I will need to get a hair test done sooner than late. . I am curious about this
Does anyone know if Walker gets worse from inhibiting estrogen ?