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Finasteride to testosterone dose ratio?

I didn't have an "agenda," but it may become riling up Macchu Pikachu with factual data about things he and fellow Redditors like (high estradiol, progesterone, MENT).
Fair enough, but you have to realize you don’t speak from any sort of credible basis right? You have very little experience with AAS, you have no background in anything related to what we’re discussing.

What you might not realize is the sheer amount of people that read these forums. So when you disparage an idea that you have no basis to do so you’re actually inflicting harm on the readership if you’re not checked by somebody else. You don’t have to respond to this post. Just think for a minute about all of the members that have PMed me and told me the discussion on progesterone and pregnenolone supplement have literally changed their lives by improving their day-to-day life. Now do you want to fuck with that, seriously? Again it’s kind of rhetorical bro. Just think about the effect of your actions. This isn’t a game where you’re “winning”.
 
Fair enough, but you have to realize you don’t speak from any sort of credible basis right? You have very little experience with AAS, you have no background in anything related to what we’re discussing.

What you might not realize is the sheer amount of people that read these forums. So when you disparage an idea that you have no basis to do so you’re actually inflicting harm on the readership if you’re not checked by somebody else. You don’t have to respond to this post. Just think for a minute about all of the members that have PMed me and told me the discussion on progesterone and pregnenolone supplement have literally changed their lives by improving their day-to-day life. Now do you want to fuck with that, seriously? Again it’s kind of rhetorical bro. Just think about the effect of your actions. This isn’t a game where you’re “winning”.
Hm, so you actually think a post about progesterone not being all that helpful for GABA-R modulation and myelination in healthy men is harmful to the community? And you think I am a corrosive influence on your oh-so-positive contributions? And you communicate this to me as a threat? You've got some things to work through, Macchu.
 
I use finasteride 1 mg ED

No sexual or mental side effects

But they are prevalent given the neurosteroidal disruptions associated and mentioned

Pretty sure there's even a post finasteride syndrome organization comprised of men affected by it lol
 
I use finasteride 1 mg ED

No sexual or mental side effects

But they are prevalent given the neurosteroidal disruptions associated and mentioned

Pretty sure there's even a post finasteride syndrome organization comprised of men affected by it lol
The Thinker, as you call yourself: I invite you to give my posts an honest reading once more and ask whether I deny the existence of a small post-finasteride syndrome population and their legitimate grievances, or whether I am challenging the carte blanche remedy of progesterone/allopregnanolone for healthy men on T.

I'll allow you to answer truthfully.
 
I use finasteride 1 mg ED

No sexual or mental side effects

But they are prevalent given the neurosteroidal disruptions associated and mentioned

Pretty sure there's even a post finasteride syndrome organization comprised of men affected by it lol
How long have you been on? I've been on 1 month taking 5mg/day and no troubles. My father has been on for 15 years or more ,5mg day, and no sides either except maybe erectile problems, but he's 85 now!
 
The Thinker, as you call yourself: I invite you to give my posts an honest reading once more and ask whether I deny the existence of a small post-finasteride syndrome population and their legitimate grievances, or whether I am challenging the carte blanche remedy of progesterone/allopregnanolone for healthy men on T.

I'll allow you to answer truthfully.
I don't think you deny it, but it's also one thing to look at those numbers from the study and take them at complete face value. There is more than a few guys who have reported the adverse effects of this drug, and I don't disagree with the opinion of not using this drug and taking the hair loss associated with supraphys-DHT levels over the potential effects long term of 5ar inhibs

Remember, we're talking brain chemistry, it's a lot more complicated than what you "feel", we have no idea about long term effects. And the same can be said about backloading any of the hormones mentioned above to try to fulfill the gap; there's no real way to measure what you're replacing and the downstream effects of it since there isn't a "standard" blood test for it

I wouldn't recommend anyone to outright take it without doing their homework, and understanding the risks associated with it. I personally choose to take it, and luckily am perfectly fine without side effects. There are others who take it topically, and some who won't even touch it. All a choice

Androgens themselves effect brain chemistry, and are associated with a larger amygdala. I wouldn't take them if I was being tested for the next Dalai Lama

How long have you been on? I've been on 1 month taking 5mg/day and no troubles. My father has been on for 15 years or more ,5mg day, and no sides either except maybe erectile problems, but he's 85 now!
About 3+ months now. I started on 0.25 mgs ED and slowly went up to 1 mg total. I'm a pretty high converter to DHT so I didn't really notice much in terms of sides. Hair just got thicker and holds better on testosterone. I also dermaroll, use minox, and some topical RU
 
I know that if an enlarged prostate is an issue, an urologist won't want to start you on finasteride right away because it lowers your PSA significantly if you're on it for awhile. Measure PSA prior and do a MRI of the prostate is what my doctor did. Taking finasteride can in some ways mask a cancer because it lowers the PSA and shrinks the prostate.

My doc wanted to do a biopsy but I said no on that. My PSA was up around 5.
Thank you for sharing.
 
I don't think you deny it, but it's also one thing to look at those numbers from the study and take them at complete face value. There is more than a few guys who have reported the adverse effects of this drug, and I don't disagree with the opinion of not using this drug and taking the hair loss associated with supraphys-DHT levels over the potential effects long term of 5ar inhibs

Remember, we're talking brain chemistry, it's a lot more complicated than what you "feel", we have no idea about long term effects. And the same can be said about backloading any of the hormones mentioned above to try to fulfill the gap; there's no real way to measure what you're replacing and the downstream effects of it since there isn't a "standard" blood test for it

I wouldn't recommend anyone to outright take it without doing their homework, and understanding the risks associated with it. I personally choose to take it, and luckily am perfectly fine without side effects. There are others who take it topically, and some who won't even touch it. All a choice

Androgens themselves effect brain chemistry, and are associated with a larger amygdala. I wouldn't take them if I was being tested for the next Dalai Lama


About 3+ months now. I started on 0.25 mgs ED and slowly went up to 1 mg total. I'm a pretty high converter to DHT so I didn't really notice much in terms of sides. Hair just got thicker and holds better on testosterone. I also dermaroll, use minox, and some topical RU
Yes, there is a small risk of very real side effects with finasteride. It's a relevant risk-balancing consideration. For a guy with real hair loss issues and an objective rationale for androgen use, it's probably overly risk averse to avoid it at 1mg daily, unless he seriously fears the ramifications of post-finasteride syndrome. It's an unusual metabolism of 5alpha-reductase inhibitors that seems to cause these rare issues. I greatly respect your thoughtful response, though, nickname holds up.
 
In men that have been on hormone replacement therapy or testosterone replacement therapy DHEA and all pregnenolone are shown to be significantly lower than men that are not on HRT or trt

Finasteride does seem to lower my sex drive some. There's been one case I can remember with my girlfriend that it totally I couldn't get it up at all that said I didn't use Cialis and I was using Cialis regularly when I saw her. Recently I've been on 10 mg a day testosterone and 1.25 mg finasteride didn't seem to affect my sex drive that much.

There's many different factors though if I'm training intense and I take a few days off my sex drive will go up.
 
In men that have been on hormone replacement therapy or testosterone replacement therapy DHEA and all pregnenolone are shown to be significantly lower than men that are not on HRT or trt
This bolsters the argument that supplemental neurosteroids are irrelevant for treatment of adverse sexual function, anxiety, and depression for those on T, since TRT is an effective treatment for those symptoms in its patients, no?
 
This bolsters the argument that supplemental neurosteroids are irrelevant for treatment of adverse sexual function, anxiety, and depression for those on T, since TRT is an effective treatment for those symptoms in its patients, no?

Do you mean dhea and allpregnelone are useless?


For males on hormones a long time, whether it be trt, hrt, or both allpregnelone and dht have shown close to zero . Since allpregnelone increases GABA a of course this would reduce anxiety. Mediation and good sleep do as well. It's only a small piece of the puzzle. I'll use them here or there when on true trt. Like recently I e been on 70 mgs scripted test c and used maybe a couple days or few or the week of each.

I do think it's a good idea to supplement dhea and allpregnelone a small amount transdermal, as oral doesn't seem to work well while on trt doses , let's say 70-140 mgs. Even 200 mgs . The higher one goes with hormones I don't see the point as nandrolone raise allpregnelone, progesterone. Other hormones like dht derivative s may raise dhea levels.
 
Its not worth the risk taking it imho. I better live with my baldness than experiencing pfs (post finasterid Syndrom).
 
Its not worth the risk taking it imho. I better live with my baldness than experiencing pfs (post finasterid Syndrom).
People that dont use finasteride experience more side effects than people claiming Finasteride syndrome experience side effects.

 
People that dont use finasteride experience more side effects than people claiming Finasteride syndrome experience side effects.

Noones saying it doesnt effect libido because in my experience it can. Its dose dependent. If youre taking a higher testosterone dose , same thing, a dose of 1.25 mgs finasteride seems to reduce a 10 mgs sub-q testosterone some , although ive had days where my sex drive worked well on 10 mgs testosterone, and 1.25 finasteride, than a 1.25 mgs finasteride , and 125 mgs shot of testosterone that day and coming days. Many factors involved .
 
Men, not rats. And most important, brain and cerebrospinal fluid, not merely Blood level.

5α-R reaction is the rate limiting step in the conversion of testosterone, progesterone, cortisol, corticosterone, and DOC into their respective 5α-dihydro-deratitves, which serve as precursors for 3α-hydroxysteroid dehydrogenase which transfroms such precursors into their respective neurosteroids (androstanediol, allopregnanolone [AP], tetrahydrocortisol, tetrahdyrocorticosterone, and tetrahydrodeoxycorticosterone) (Fig. 1) [1, 2]. All three isoforms of 5α-R are expressed in the various regions of brain and are thought to be critical for brain development since fetal brain express high concentrations of 5α-R [1, 2].

It has recently been shown that patients who had been treated with finasteride have reduced or undetectable levels of neuroactive steroids in their cerebro-spinal fluid and plasma, and exhibited higher levels of precursor steroids [75]. This observation strongly suggests that 5α-RIs have a deleterious effect on the biosynthesis and function of neurosteroids in the central nervous system. Finasteride treatment resulted in decreased levels of 5α-DHT and 3α, 5α-tetrahydroprogesterone (AP) and increased levels of testosterone supporting the hypothesis that deleterious effects of finasteride may be persistent or irreversible. This may explain some of the noted symptoms such as anxiety, depression and suicide in patients who have been treated with finasteride [76].

NEUROPROTECTIVE EFFECTS OF NEUROSTEROIDS
Neuroactive steroids elicit important neuroprotective effects during trauma and injury to the central nervous system [75]. AP is shown to be beneficial in the treatment of traumatic brain injury, attenuating edema, trauma, stress, inflammation, apoptosis, and reducing oxidative stress [76, 77, 78]. AP is not only a protective agent in ischemia, but also in maintaining blood brain barrier integrity, and in memory and learning [78, 79, 80, 81]. Studies on CNS injury in which asphyxiation was induced in fetal sheep to stimulate neurological stressors, in the presence or absence of finasteride, showed an increase in apoptotic cell death in the cerebellum and hippocampus in the animals treated with finasteride (Fig. 5) [82]. Furthermore, treatment with an AP analogue, alfaxalone, prevented cell death as assessed by the increase in activity of caspace-3 and expression of ki-67 protein. This observation suggests that AP exerts a neuroprotective role in the brain, which is inhibited by finasteride.



The neuroprotective effect of AP was further illustrated during injury to the rat hippocampus slices induced by tributyltin treatment, which resulted in significant cell death. Administration of progesterone (P) with finasteride showed similar cell death to that induced by tributyltin treatment, in the various regions of the hippocampus. In contrast, P treatment without finasteride provided a protective effect. This is attributed to the conversion of P to 5α-DHP by 5α-Rs and to AP by 3α-HSD. To confirm that this is due to the neuroprotective effect of AP, the latter was administered with or without finasteride. While the tributyltin induced cell death was significant, administration of AP with and without finasteride produced a markedly protective effect as assessed by the reduced cell death [83]. These findings suggest that 5α-Rs play a pivotal role in neuroprotection.

Neurosteroid synthesis in the hippocampus is suggested to be critical for neuroplasticity in the brain [84]. Inhibition of 5α-R by finasteride is thought to contribute to reduced neuroplasticity due to structural changes resulting from inhibition of neurogenesis in the hippocampus. Finasteride treatment in mice showed decreased cell proliferation in the hippocampus, suggesting that inhibitors of 5α-R blocks neurogenesis [84].

As reported by Mellon [85] in an adult animal model of Niemann-Pick disease type C the biosynthesis of AP is significantly reduced, and this was supported by significant reduction in the activity of 5α-R and 3α-HSD in the brain of these animals [85]. The activity of 5α-R was markedly reduced with the progression of the disease. This reduced 5α-R activity may contribute to the observed accumulation of cholesterol in neurons and gangliosides, cerebro, perkinje cell degeneration, dysmyelination and neurodegeneration [85]. Thus, loss of 5α-R and 3α-HSD activity is attributed to loss of neurons expressing these enzymes. Treatment with AP early at postanatal day 7 was found most effective in preventing neurodegeneration and correlates with reduced tremor, ataxia, and increased lifespan. In the animal model, these findings indicate that the loss of neurosteroid biosynthesis may be responsible for the disease state and its progression. Therefore inhibition of 5α-R by finasteride and dutasteride in the course of treatment of nonlife threatening conditions, such as male pattern baldness (alopecia) or BPH may have detrimental effects on the CNS.

It has been reported that AP levels were significantly decreased in postmortem human brains of Alzheimer disease (AD) patients [86]. An inverse correlation was noted between AP levels and the degree of neurological degeneration in pathological section of AD patient [86]. One of the interesting findings was that pregnenolone levels were greater in the temporal cortex of AD patients suggesting that this may be a compensating mechanism for reduced 5α-R activity. We speculate that 5α-RIs may contribute to reduced levels of neurosteroids in the CNS and this may enhance the progression of neurodegenerative disease, such as AD.

Conversion of polyprenol into dolichol is critical for N-glycosylation of membrane proteins [3]. 5α-R type 3 was shown to be critical for catalyzing this reaction [3]. A mutation in this enzyme lead to mental retardation and opthamologic and cerebral defects [3]. Intraoperative Floppy Iris Syndrome (IFIS) is also a complication experienced during cataract extraction. The syndrome is defined by floppy, or flaccid iris. Studies have indicated a correlation between finasteride and the occurrence of cataracts and IFIS indicating inhibition of glycosylation may contribute to this pathology
 
Men, not rats. And most important, brain and cerebrospinal fluid, not merely Blood level.

5α-R reaction is the rate limiting step in the conversion of testosterone, progesterone, cortisol, corticosterone, and DOC into their respective 5α-dihydro-deratitves, which serve as precursors for 3α-hydroxysteroid dehydrogenase which transfroms such precursors into their respective neurosteroids (androstanediol, allopregnanolone [AP], tetrahydrocortisol, tetrahdyrocorticosterone, and tetrahydrodeoxycorticosterone) (Fig. 1) [1, 2]. All three isoforms of 5α-R are expressed in the various regions of brain and are thought to be critical for brain development since fetal brain express high concentrations of 5α-R [1, 2].

It has recently been shown that patients who had been treated with finasteride have reduced or undetectable levels of neuroactive steroids in their cerebro-spinal fluid and plasma, and exhibited higher levels of precursor steroids [75]. This observation strongly suggests that 5α-RIs have a deleterious effect on the biosynthesis and function of neurosteroids in the central nervous system. Finasteride treatment resulted in decreased levels of 5α-DHT and 3α, 5α-tetrahydroprogesterone (AP) and increased levels of testosterone supporting the hypothesis that deleterious effects of finasteride may be persistent or irreversible. This may explain some of the noted symptoms such as anxiety, depression and suicide in patients who have been treated with finasteride [76].

NEUROPROTECTIVE EFFECTS OF NEUROSTEROIDS
Neuroactive steroids elicit important neuroprotective effects during trauma and injury to the central nervous system [75]. AP is shown to be beneficial in the treatment of traumatic brain injury, attenuating edema, trauma, stress, inflammation, apoptosis, and reducing oxidative stress [76, 77, 78]. AP is not only a protective agent in ischemia, but also in maintaining blood brain barrier integrity, and in memory and learning [78, 79, 80, 81]. Studies on CNS injury in which asphyxiation was induced in fetal sheep to stimulate neurological stressors, in the presence or absence of finasteride, showed an increase in apoptotic cell death in the cerebellum and hippocampus in the animals treated with finasteride (Fig. 5) [82]. Furthermore, treatment with an AP analogue, alfaxalone, prevented cell death as assessed by the increase in activity of caspace-3 and expression of ki-67 protein. This observation suggests that AP exerts a neuroprotective role in the brain, which is inhibited by finasteride.



The neuroprotective effect of AP was further illustrated during injury to the rat hippocampus slices induced by tributyltin treatment, which resulted in significant cell death. Administration of progesterone (P) with finasteride showed similar cell death to that induced by tributyltin treatment, in the various regions of the hippocampus. In contrast, P treatment without finasteride provided a protective effect. This is attributed to the conversion of P to 5α-DHP by 5α-Rs and to AP by 3α-HSD. To confirm that this is due to the neuroprotective effect of AP, the latter was administered with or without finasteride. While the tributyltin induced cell death was significant, administration of AP with and without finasteride produced a markedly protective effect as assessed by the reduced cell death [83]. These findings suggest that 5α-Rs play a pivotal role in neuroprotection.

Neurosteroid synthesis in the hippocampus is suggested to be critical for neuroplasticity in the brain [84]. Inhibition of 5α-R by finasteride is thought to contribute to reduced neuroplasticity due to structural changes resulting from inhibition of neurogenesis in the hippocampus. Finasteride treatment in mice showed decreased cell proliferation in the hippocampus, suggesting that inhibitors of 5α-R blocks neurogenesis [84].

As reported by Mellon [85] in an adult animal model of Niemann-Pick disease type C the biosynthesis of AP is significantly reduced, and this was supported by significant reduction in the activity of 5α-R and 3α-HSD in the brain of these animals [85]. The activity of 5α-R was markedly reduced with the progression of the disease. This reduced 5α-R activity may contribute to the observed accumulation of cholesterol in neurons and gangliosides, cerebro, perkinje cell degeneration, dysmyelination and neurodegeneration [85]. Thus, loss of 5α-R and 3α-HSD activity is attributed to loss of neurons expressing these enzymes. Treatment with AP early at postanatal day 7 was found most effective in preventing neurodegeneration and correlates with reduced tremor, ataxia, and increased lifespan. In the animal model, these findings indicate that the loss of neurosteroid biosynthesis may be responsible for the disease state and its progression. Therefore inhibition of 5α-R by finasteride and dutasteride in the course of treatment of nonlife threatening conditions, such as male pattern baldness (alopecia) or BPH may have detrimental effects on the CNS.

It has been reported that AP levels were significantly decreased in postmortem human brains of Alzheimer disease (AD) patients [86]. An inverse correlation was noted between AP levels and the degree of neurological degeneration in pathological section of AD patient [86]. One of the interesting findings was that pregnenolone levels were greater in the temporal cortex of AD patients suggesting that this may be a compensating mechanism for reduced 5α-R activity. We speculate that 5α-RIs may contribute to reduced levels of neurosteroids in the CNS and this may enhance the progression of neurodegenerative disease, such as AD.

Conversion of polyprenol into dolichol is critical for N-glycosylation of membrane proteins [3]. 5α-R type 3 was shown to be critical for catalyzing this reaction [3]. A mutation in this enzyme lead to mental retardation and opthamologic and cerebral defects [3]. Intraoperative Floppy Iris Syndrome (IFIS) is also a complication experienced during cataract extraction. The syndrome is defined by floppy, or flaccid iris. Studies have indicated a correlation between finasteride and the occurrence of cataracts and IFIS indicating inhibition of glycosylation may contribute to this pathology
You say men not rats, then copy and pasted a whole lot of rat and sheep data, though.

Here's the funny thing to me about avoiding 5α-reductase inhibitors because they crush neurosteroids and self-administering progesterone in this context:

"[Exogenous] progesterone (P4) is anti-androgenic because it also binds to the 5α-reductase enzyme and will therefore interact with the conversion of testosterone in dihydrotestosterone, its active metabolite (2)"
Schumacher, M., Mattern, C., Ghoumari, A., Oudin et, J. P., Liere, P., Labombarda, F., … Guennoun, R. (2014). Revisiting the roles of progesterone and allopregnanolone in the nervous system: Resurgence of the progesterone receptors. Progress in Neurobiology, 113, 6–39. doi:10.1016/j.pneurobio.2013.09.004

So it functions analogously to dutasteride/finasteride with similar downstream effects. You're just playing whack-a-mole with hormones that are nonspecific in their action.
 
Do you mean dhea and allpregnelone are useless?


For males on hormones a long time, whether it be trt, hrt, or both allpregnelone and dht have shown close to zero . Since allpregnelone increases GABA a of course this would reduce anxiety. Mediation and good sleep do as well. It's only a small piece of the puzzle. I'll use them here or there when on true trt. Like recently I e been on 70 mgs scripted test c and used maybe a couple days or few or the week of each.

I do think it's a good idea to supplement dhea and allpregnelone a small amount transdermal, as oral doesn't seem to work well while on trt doses , let's say 70-140 mgs. Even 200 mgs . The higher one goes with hormones I don't see the point as nandrolone raise allpregnelone, progesterone. Other hormones like dht derivative s may raise dhea levels.
I think they're potently anxiolytic and antidepressant. So they'll make you feel pretty good. I think they're antiandrogenic and negatively inhibit the HPG axis. As long as all those factors are considered and you decide to supplement, more power to you. Just recognize that they're hormones and as such rather blunt instruments for anxiety/antidepressant qualities since they effect so many systems. If you're supplementing within the physiological male range and feel good and all systems are go, hell, I want to hear all about it.

When you say 200mg is that of allop? Or a mix of DHEA/allop?
 
People that dont use finasteride experience more side effects than people claiming Finasteride syndrome experience side effects.

Exactly. My father has been on 5mg/day for going on 20 years now. Suffers none of the big side effects of Finasteride syndrome. Just the erection difficulties, but libido is normal. He is 84 years old too.

I'm about 6 weeks in on 5mg/day and zero sides.
 
People that dont use finasteride experience more side effects than people claiming Finasteride syndrome experience side effects.

Noones saying it doesnt effect libido because in my experience it can. Its dose dependent. If youre taking a higher testosterone dose , same thing, a dose of 1.25 mgs finasteride seems to reduce a 10 mgs sub-q testosterone some , although ive had days where my sex drive worked well on 10 mgs testosterone, and 1.25 finasteride, than a 1.25 mgs finasteride , and 125 mgs shot of testosterone that day and coming days. Many factors involved .
5mg/ day has zero side effect on my libido or sexual performance I'm doing great there.. Am I just lucky? Good video you found. I'm 52 years old too, and many guys my age not on Finasteride have sexual problems.
 

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