Finasteride Linked To Erectile Dysfunction That Lasts For Years

ahmed wolf

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Day 17 or so, still recovering.
I don't have morning wood yet, and erections are there with stimulation but not strong.

Around the two week mark, it seemed like things got a little better, but have slowly bounced back.

I am aware this is seen by others as well. I'm just gonna have to ride this out, I look at similar cases and recovery time varies.

Sure takes a long time tho
wow ur not freaking out?
 

abcdefg

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Finasteride doesnt really bring down allo that much thou, the only study ive read uses mice and at that point it was a huge decrease because finasteride affects ar1 in mice. The only allo that should be affected by finasteride is in the spine and a very small amount in the brain like .7 %.
I wish theyd do a study on nuerosteriod in the spine and brain while on finasteride and dutasteride.

I think this is the biggest worry id have using finasteride or dutasteride. These neurosteroids in the brain/spine I mean no one has any idea what those do. Why does finasteride inhibit these at all? If this caused sides it be almost impossible to ever figure out why
 

tommyt123

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Finasteride doesnt really bring down allo that much thou, the only study ive read uses mice and at that point it was a huge decrease because finasteride affects ar1 in mice. The only allo that should be affected by finasteride is in the spine and a very small amount in the brain like .7 %.
I wish theyd do a study on nuerosteriod in the spine and brain while on finasteride and dutasteride.

Hey alk why wouldn't allo come down in the human brain by much, could you tell me why or link me to a study that shows this?
 

Regulate

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Me personally, I never had the 'crash' when I went off finasteride. I experienced extreme brain fog, anxiety, decreased and watery ejaculate, no more morning wood, ED, weird pains in my penis and short term memory loss 2 weeks after starting. Lowered the dosage immediately and most of the things seemed to subside.

Sometimes I still think my short term memory is a bit less than what it used to be, I still have almost no morning wood and my erection have recovered a little bit (9 months after stopping) but are still not what they used to be. I think those pains in the shaft of my penis are the explanation why things downstairs are still not the same... I don't know what it is but something changed there...
What was the dosage you started with?
 

Alk

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Hey alk why wouldn't allo come down in the human brain by much, could you tell me why or link me to a study that shows this?
Because allo is metabolized by 5ar1 in tour brain, finasteride inhibits 5ar2.
 

donsf448

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A lot of us already knew this, but it's great to see it confirmed.

The PFS deniers now have less room to stand on.

Glad to see people aren't even reading the study and making uninformed statements.

https://peerj.com/articles/3020/

"Of 4,284 young men exposed to finasteride ≤1.25 mg/day, and without prior sexual dysfunction and who were evaluated for new PED, 34 (0.79%) developed PED (median 1,534 days after stopping 5α-RI, IQR 651–2,351 days)."

Out of over 4,000 subjects sampled, 0.79% of young men taking <= 1.25mg finasteride reported persistent sides. That number is literally statistically insignificant. By statistically insignificant, I mean that figure is so low that even a 1% sampling error means that literally ZERO occurrences of persistent ED is equally likely to 1.79% rate of persistent ED (which is still very low).

If anything, this serves as evidence that there's no proof to conclude whether finasteride can even cause persistent ED. This is also based off the narratives of subjects. It's not a new study. They're just sampling existing data. The 1.2% figure lumps together ALL finasteride and dutasteride users at ALL dosages so that number is even more useless.

Come on people. Do a little more due diligence before making blanket claims.
 

Afro_Vacancy

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Glad to see people aren't even reading the study and making uninformed statements.

https://peerj.com/articles/3020/

"Of 4,284 young men exposed to finasteride ≤1.25 mg/day, and without prior sexual dysfunction and who were evaluated for new PED, 34 (0.79%) developed PED (median 1,534 days after stopping 5α-RI, IQR 651–2,351 days)."

Out of over 4,000 subjects sampled, 0.79% of young men taking <= 1.25mg finasteride reported persistent sides. That number is literally statistically insignificant. By statistically insignificant, I mean that figure is so low that even a 1% sampling error means that literally ZERO occurrences of persistent ED is equally likely to 1.79% rate of persistent ED (which is still very low).

If anything, this serves as evidence that there's no proof to conclude whether finasteride can even cause persistent ED. This is also based off the narratives of subjects. It's not a new study. They're just sampling existing data. The 1.2% figure lumps together ALL finasteride and dutasteride users at ALL dosages so that number is even more useless.

Come on people. Do a little more due diligence before making blanket claims.

You should try actually reading the study.
 

donsf448

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You should try actually reading the study.

I just quoted the study and the EXACT line where they specifically cite real data on men who are taking the dosage of finasteride to treat baldness. Its objectively a flawed study. No one here is even mentioning the fact that the study lumped together all finasteride and dutasteride users together regardless of the dosage (even 5mg daily) and the number was STILL just 1.25%.

As someone who works in statistics, I read that as the data is at best inconclusive and at worst builds an argument against the possibility of persistent ED but sure take it whichever way you want.
 

Afro_Vacancy

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I just quoted the study and the EXACT line where they specifically cite real data on men who are taking the dosage of finasteride to treat baldness. Its objectively a flawed study. No one here is even mentioning the fact that the study lumped together all finasteride and dutasteride users together regardless of the dosage (even 5mg daily) and the number was STILL just 1.25%.

As someone who works in statistics, I read that as the data is at best inconclusive and at worst builds an argument against the possibility of persistent ED but sure take it whichever way you want.

You did quote it, but you didn't understand it.

For example, you're complaining about dosage, but what you don't know is that finasteride has a nearly flat response curve above ~0.10 mg/day. So the fact that some people are taking 1.00 mg/day, and others 1.25 mg/day, will have no measurable effect on outcomes.
 

donsf448

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You did quote it, but you didn't understand it.

For example, you're complaining about dosage, but what you don't know is that finasteride has a nearly flat response curve above ~0.10 mg/day. So the fact that some people are taking 1.00 mg/day, and others 1.25 mg/day, will have no measurable effect on outcomes.

And what about taking 5 mg a day to treat prostate dysplasia? Still the same effect? No. Yet the paper still lumped them into one statistic.
 

Afro_Vacancy

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And what about taking 5 mg a day to treat prostate dysplasia? Still the same effect? No. Yet the paper still lumped them into one statistic.

Finasteride has a flat response curve in the serum and the skin. Your serum DHT levels will be indistinguishable regardless of whether you take 0.25, 0.5, 1.0, 1.25, or 5.00 mg/day.

Here's a statistical lesson for you: you don't want to give weight to variables that don't matter. When you do that you add degrees of freedom to your fit, you may end up with a better fit but it's actually less meaningful. Sometimes, this is methodologically encoded via a Bayesian information criterion.

Undergraduates often make a related mistake, where they fit 9th degree polynomials to data, get a perfect fit, and think they've acquired understanding. They have not.

It's important to have a reasonable hypothesis, and to understand your variables. Blind fitting is sometimes beneficial but usually just leads to non-truths.
 

Stupidon

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Finasteride has a flat response curve in the serum and the skin. Your serum DHT levels will be indistinguishable regardless of whether you take 0.25, 0.5, 1.0, 1.25, or 5.00 mg/day.

Here's a statistical lesson for you: you don't want to give weight to variables that don't matter. When you do that you add degrees of freedom to your fit, you may end up with a better fit but it's actually less meaningful. Sometimes, this is methodologically encoded via a Bayesian information criterion.

Undergraduates often make a related mistake, where they fit 9th degree polynomials to data, get a perfect fit, and think they've acquired understanding. They have not.

It's important to have a reasonable hypothesis, and to understand your variables. Blind fitting is sometimes beneficial but usually just leads to non-truths.
That works for both parts... Not only to make your point since he made a fair one. Compiling 0.25mg/day data with 5mg/day does not make any sense.

How can you explain some people stop experiencing sides by decreasing their dosage? You like claiming everywhere the side effects percentage should be higher based on anecdotal evidences collected on a forum, so please do the same for the other party. Not to remain you we are speaking about a drug which makes $500M+/year and where there is obviously a bad experience bias on the forum reviews - basically people asking for help.
 

tommyt123

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Finasteride has a flat response curve in the serum and the skin. Your serum DHT levels will be indistinguishable regardless of whether you take 0.25, 0.5, 1.0, 1.25, or 5.00 mg/day.

Here's a statistical lesson for you: you don't want to give weight to variables that don't matter. When you do that you add degrees of freedom to your fit, you may end up with a better fit but it's actually less meaningful. Sometimes, this is methodologically encoded via a Bayesian information criterion.

Undergraduates often make a related mistake, where they fit 9th degree polynomials to data, get a perfect fit, and think they've acquired understanding. They have not.

It's important to have a reasonable hypothesis, and to understand your variables. Blind fitting is sometimes beneficial but usually just leads to non-truths.
That is true but i still don't think that rationalises putting all 5alpha inhibitors together seeing as dutasteride inhibits an additional enzyme and DHT is not the only product of 5alpha activity that is being effected.
 

Afro_Vacancy

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That works for both parts... Not only to make your point since he made a fair one. Compiling 0.25mg/day data with 5mg/day does not make any sense.

How can you explain some people stop experiencing sides by decreasing their dosage? You like claiming everywhere the side effects percentage should be higher based on anecdotal evidences collected on a forum, so please do the same for the other party. Not to remain you we are speaking about a drug which makes $500M+/year and where there is obviously a bad experience bias on the forum reviews - basically people asking for help.

Is English your second language? Your post is very hard to read.

****************

The flat response curve refers only to DHT levels in the skin and in the blood.

The sides may be due to the dozens of other reactions affected by finasteride, completely independent of DHT levels in the serum and in the skin. They don't necessarily have the same response curve.

However once you make it to 1 mg, it's plausible you've inhibited everything.
 

Afro_Vacancy

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That is true but i still don't think that rationalises putting all 5alpha inhibitors together seeing as dutasteride inhibits an additional enzyme and DHT is not the only product of 5alpha activity that is being effected.

In most studies so far, finasteride and dutasteride have indistinguishable side effect profiles. It is a surprise admittedly.
 

tommyt123

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In most studies so far, finasteride and dutasteride have indistinguishable side effect profiles. It is a surprise admittedly.
i'd say comparable but often not the same from what i've seen, and PED was never reported in the original trials just because they have similar transient side effects doesn't mean that they have the same persistent profile of adverse side effects i think further stratification is warranted in this instance. However in saying that i do think this study suggest there is a link between 5alpha inhibition and PED(likely for both finasteride and dutasteride given there similar mechanism of action/short term side effect profile similarity), i just think further research is needed to tease out how high the PED rate is between doses/medications and a strong conclusion can not be made yet. A more blanket criterion was probably just used in this study to establish the effect is there in the first place which is not necessarily a bad thing!

Also David_mpn roughly how much does it cost you a week/month at your current dose of RU im also thinking about going down that route in the light of some of these new studies starting to doubt if the risk is worth it.
 
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Afro_Vacancy

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i'd say comparable but often not the same from what i've seen, and PED was never reported in the original trials just because they have similar transient side effects doesn't mean that they have the same persistent profile of adverse side effects i think further stratification is warranted in this instance. However in saying that i do think this study suggest there is a link between 5alpha inhibition and PED(likely for both finasteride and dutasteride given there similar mechanism of action/short term side effect profile similarity), i just think further research is needed to tease out how high the PED rate is between doses/medications and a strong conclusion can not be made yet. A more blanket criterion was probably just used in this study to establish the effect is there in the first place which is not necessarily a bad thing!

Also David_mpn roughly how much does it cost you a week/month at your current dose of RU im also thinking about going down that route in the light of some of these new studies starting to doubt if the risk is worth it.

Not that much money I forget the exact prices that Kane charges.

15 mg a day is 450 mg a month or 3 grams every six months approximately. So less than $15 a month.
 
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