The Effect of 5 {alpha}-Reductase Inhibitors on Erectile Function
J Androl. 2008 Apr 17
Five alpha-reductase inhibitors, which inhibit conversion of testosterone to dihydrotestosterone, are used for miscellaneous clinical applications, including the treatment of benign prostatic hyperplasia, male pattern hair loss, and possibly to reduce the risk of prostate cancer. Erectile dysfunction has been associated with 5 alpha-reductase inhibitors.
Overall reports in the literature suggest rates of erectile dysfunction to be between 0.8%-33% in men using these medications. However, randomized controlled studies report the rates of erectile dysfunction to be between 0.8%-15.8%.
The possible risk association is that these medications impact on androgen function which is understood to contribute to normal erectile physiology.
5 alpha-reductase inhibitors result in a drop in median serum dihydrotestosterone levels by 60%-93% within 2 years, but there is no major change in testosterone levels.
In this review, we surveyed studies on erectile dysfunction in patients treated with 5 alpha-reductase inhibitors and critically examined the evidence which associates 5 alpha-reductase inhibitors and erectile dysfunction.
We conclude that 5 alpha-reductase inhibitors do not lead to erectile dysfunction to a significant degree and we support the position that dihydrotestosterone is less relevant than testosterone in erectile function.
» Is ED really a problem with 5 AR inhibitors?
»
» The Effect of 5 {alpha}-Reductase Inhibitors on Erectile Function
»
» J Androl. 2008 Apr 17
»
» Five alpha-reductase inhibitors, which inhibit conversion of testosterone
» to dihydrotestosterone, are used for miscellaneous clinical applications,
» including the treatment of benign prostatic hyperplasia, male pattern hair
» loss, and possibly to reduce the risk of prostate cancer. Erectile
» dysfunction has been associated with 5 alpha-reductase inhibitors.
»
» Overall reports in the literature suggest rates of erectile dysfunction
» to be between 0.8%-33% in men using these medications. However, randomized
» controlled studies report the rates of erectile dysfunction to be between
» 0.8%-15.8%.
»
» The possible risk association is that these medications impact on androgen
» function which is understood to contribute to normal erectile physiology.
»
» 5 alpha-reductase inhibitors result in a drop in median serum
» dihydrotestosterone levels by 60%-93% within 2 years, but there is no major
» change in testosterone levels.
»
» In this review, we surveyed studies on erectile dysfunction in patients
» treated with 5 alpha-reductase inhibitors and critically examined the
» evidence which associates 5 alpha-reductase inhibitors and erectile
» dysfunction.
»
» We conclude that 5 alpha-reductase inhibitors do not lead to erectile
» dysfunction to a significant degree and we support the position that
» dihydrotestosterone is less relevant than testosterone in erectile
» function.
I think the impact of antiadros on ED could be overstated. It would be difficult to construct a control group that was free from ED prior to the beginning of the study. As it is a sensisitive subject for most men, I doubt many would be honest about it if asked. If people lie about whether or not they experience it prior to the beginning of studies, then how can one be certain that the subject didn’t suffer from it prior to the use of antiandros? I for one have never had that side effect; if anything, its been the opposite. From the anecdotal evidence drawn from this board, it seems that many have experienced the same thing.
We mustn’t be attending the same board. I consider myself a perfect and honest control group. I was horny as much as one may desire to be when I didn’t take propecia. When I started to take it, I didn’t realize the nasty side effect since sex was correct and decent when needed. 5 years later I switched from the nominal daily 1mg to 2.5mg with no idea that I could have a problem. Within 3 months, my libido nosedived (in all senses) and has remained low eversince.
And I am in good and plentiful company: propeciahelp.com
» We mustn’t be attending the same board. I consider myself a perfect and
» honest control group. I was horny as much as one may desire to be when I
» didn’t take propecia. When I started to take it, I didn’t realize the nasty
» side effect since sex was correct and decent when needed. 5 years later I
» switched from the nominal daily 1mg to 2.5mg with no idea that I could have
» a problem. Within 3 months, my libido nosedived (in all senses) and has
» remained low eversince.
» And I am in good and plentiful company: propeciahelp.com
Its funny you should mention that - I took fin at 1.25 mg for a couple of years with seemingly no problem. Then I switched to dut after it came out at a low dose for about 6 months and it thickened up my hair while I dont think I had a single errection on it the entire time. Going back to fin things got better but…it was never quite the same. And eventually things got almost as bad as they were on dut. Now while off fin things are more or less fine (though they didnt get better straight away) but if I ever go back - problems again.
I had attributed this to getting older and a fall in natural test production but now I havealso wondered if going to the more aggressive level of 5-AR inhibition didnt change something. I wonder if others have the same experience? I know some have said they didnt notice any problems on fin/dut but then stopped taking it for awhile and suddenly realised that their sensation/interest in sex had gradually left while on the drug but they had never actually noticed it happen until it left their system. I cant say if this had actually happened to me before I tried dut and ran into a sexual brick wall.
hh
Oh and I’m not entirely sure but I think the above study might have been supported by GSK or Merck from memory which made me a little suspicious of its conclusions.
How do you know whether the ED is caused by the medication or due to other reasons?
How did you rule out psychological causes and age related ED ?
Why cant ED that is reported by a few be a coincidental symptom?
Why is ED NOT reported by everyone taking DHT blockers, if ED is such a significant side effect of those medications?
» » We mustn’t be attending the same board. I consider myself a perfect
» and
» » honest control group. I was horny as much as one may desire to be when
» I
» » didn’t take propecia. When I started to take it, I didn’t realize the
» nasty
» » side effect since sex was correct and decent when needed. 5 years later
» I
» » switched from the nominal daily 1mg to 2.5mg with no idea that I could
» have
» » a problem. Within 3 months, my libido nosedived (in all senses) and has
» » remained low eversince.
» » And I am in good and plentiful company:
» propeciahelp.com
»
» Its funny you should mention that - I took fin at 1.25 mg for a couple of
» years with seemingly no problem. Then I switched to dut after it came out
» at a low dose for about 6 months and it thickened up my hair while I dont
» think I had a single errection on it the entire time. Going back to fin
» things got better but…it was never quite the same. And eventually things
» got almost as bad as they were on dut. Now while off fin things are more or
» less fine (though they didnt get better straight away) but if I ever go
» back - problems again.
» I had attributed this to getting older and a fall in natural test
» production but now I havealso wondered if going to the more aggressive
» level of 5-AR inhibition didnt change something. I wonder if others have
» the same experience? I know some have said they didnt notice any problems
» on fin/dut but then stopped taking it for awhile and suddenly realised that
» their sensation/interest in sex had gradually left while on the drug but
» they had never actually noticed it happen until it left their system. I
» cant say if this had actually happened to me before I tried dut and ran
» into a sexual brick wall.
» hh
» Oh and I’m not entirely sure but I think the above study might have been
» supported by GSK or Merck from memory which made me a little suspicious of
» its conclusions.
» How do you know whether the ED is caused by the medication or due to other
» reasons?
»
» How did you rule out psychological causes and age related ED ?
»
» Why cant ED that is reported by a few be a coincidental symptom?
»
» Why is ED NOT reported by everyone taking DHT blockers, if ED is such a
» significant side effect of those medications?
»
Haroldo: you’ve dropped fin altogether as I understand. When did you? Did you have a huge shed? What did you replace fin with?
Hairsite:
» How do you know whether the ED is caused by the medication or due to other
» reasons?
When ED is brutal and accompanied by an obvious decrease of semen, your memory makes a quick round up of the possible brutal possible causes. In my case, fin was the only possible one.
» How did you rule out psychological causes and age related ED ?
Same answer.
» Why cant ED that is reported by a few be a coincidental symptom?
Same answer. (Would you please stop asking the same question)
» Why is ED NOT reported by everyone taking DHT blockers, if ED is such a
» significant side effect of those medications?
1°) The effects of fin on hormone serum levels is variable. The total T bloodtest may remain good though the sexual behaviour deteriorates. Specialists think that the relevant data to be considered is free T or even the ratio freeT/total T.
2°) Age is an important factor in terms of adaptability to brutal hormonal changes as DHT’s.
3°) Intricacy of conversion mechanisms. Who knows from a given amount of dht inhibitor and a given patient what the resulting distribution will be in DHT, free T, total T, androstenedione, estradiol, to name just… a few. And what are the ideal proportions to be given to these hormones for an optimum sexual health? No answer.
» How do you know whether the ED is caused by the medication or due to other
» reasons?
Well when you lose all sexual function within days if not hours of starting a medication it kind of clues you in. When you go from whacking off multiple times to day to being able to watch hardcore porn after months without sex and feeling no arousal its another clue.
» How did you rule out psychological causes and age related ED ?
I had only aged a few days anbd I was otherwise feeling fine.
» Why cant ED that is reported by a few be a coincidental symptom?
In large numbers of people some of it almost certainly is.
» Why is ED NOT reported by everyone taking DHT blockers, if ED is such a
» significant side effect of those medications?
An interesting question. Probably for the similar reasons as why some people will continue to bald while on several mg of dutasteride per day. Speculation is that the sexual response of some is more dependent on DHT than others is. In a recent study on semen/sperm production/quality and 5AR inhibitors most people saw a slight if significant fall in sperm quantity, motility etc roughly proportional to the degree of 5-ar inhibition - ie less for fin, more for increasing doses of dut. The reseearchers noted that there was a subgroup of men whose sperm count dropped massively while on a 5-ar inhibitor.
“Some individuals (approximately 5% of the subjects on
active treatment) demonstrated greater sensitivity to the effects
of 5-reductase inhibition, with decreases in total sperm
count to less than 10% of their baseline values during
treatment.”
There was no baseline hormonal characteristics to distinguish this group from others.
»
»
»
» » » We mustn’t be attending the same board. I consider myself a perfect
» » and
» » » honest control group. I was horny as much as one may desire to be
» when
» » I
» » » didn’t take propecia. When I started to take it, I didn’t realize the
» » nasty
» » » side effect since sex was correct and decent when needed. 5 years
» later
» » I
» » » switched from the nominal daily 1mg to 2.5mg with no idea that I
» could
» » have
» » » a problem. Within 3 months, my libido nosedived (in all senses) and
» has
» » » remained low eversince.
» » » And I am in good and plentiful company:
» » propeciahelp.com
» »
» » Its funny you should mention that - I took fin at 1.25 mg for a couple
» of
» » years with seemingly no problem. Then I switched to dut after it came
» out
» » at a low dose for about 6 months and it thickened up my hair while I
» dont
» » think I had a single errection on it the entire time. Going back to fin
» » things got better but…it was never quite the same. And eventually
» things
» » got almost as bad as they were on dut. Now while off fin things are more
» or
» » less fine (though they didnt get better straight away) but if I ever go
» » back - problems again.
» » I had attributed this to getting older and a fall in natural test
» » production but now I havealso wondered if going to the more aggressive
» » level of 5-AR inhibition didnt change something. I wonder if others
» have
» » the same experience? I know some have said they didnt notice any
» problems
» » on fin/dut but then stopped taking it for awhile and suddenly realised
» that
» » their sensation/interest in sex had gradually left while on the drug
» but
» » they had never actually noticed it happen until it left their system. I
» » cant say if this had actually happened to me before I tried dut and ran
» » into a sexual brick wall.
» » hh
» » Oh and I’m not entirely sure but I think the above study might have
» been
» » supported by GSK or Merck from memory which made me a little suspicious
» of
» » its conclusions.
» » How do you know whether the ED is caused by the medication or due to
» other
» » reasons?
» »
» » How did you rule out psychological causes and age related ED ?
» »
» » Why cant ED that is reported by a few be a coincidental symptom?
» »
» » Why is ED NOT reported by everyone taking DHT blockers, if ED is such a
» » significant side effect of those medications?
» »
»
»
» Haroldo: you’ve dropped fin altogether as I understand. When did you?
Consistently dropped it about October last year.
» Did you have a huge shed? What did you replace fin with?
Well there hasnt been an “End of Days” shed yet but yeah I have lost a lot of overall hair quality and thickness since then. I think the fall has been softened by the fact that I have experimented with so much topical fin, dut and other even more extreme antiandrogens since then that it hasnt been quite that long that my hair has had zero protection from DHT. I have even wimped out a few times and gone back to the old oral fin as nothing has been truly satisfactory.
hh
» Hairsite:
» » How do you know whether the ED is caused by the medication or due to
» other
» » reasons?
» When ED is brutal and accompanied by an obvious decrease of semen, your
» memory makes a quick round up of the possible brutal possible causes. In my
» case, fin was the only possible one.
» » How did you rule out psychological causes and age related ED ?
» Same answer.
» » Why cant ED that is reported by a few be a coincidental symptom?
» Same answer. (Would you please stop asking the same question)
» » Why is ED NOT reported by everyone taking DHT blockers, if ED is such a
» » significant side effect of those medications?
» 1°) The effects of fin on hormone serum levels is variable. The total T
» bloodtest may remain good though the sexual behaviour deteriorates.
» Specialists think that the relevant data to be considered is free T or even
» the ratio freeT/total T.
» 2°) Age is an important factor in terms of adaptability to brutal hormonal
» changes as DHT’s.
» 3°) Intricacy of conversion mechanisms. Who knows from a given amount of
» dht inhibitor and a given patient what the resulting distribution will be
» in DHT, free T, total T, androstenedione, estradiol, to name just… a
» few. And what are the ideal proportions to be given to these hormones for
» an optimum sexual health? No answer.
Overall reports in the literature suggest rates of erectile dysfunction to be between 0.8%-33% in men using these medications. However, randomized controlled studies report the rates of erectile dysfunction to be between 0.8%-15.8%.
We conclude that 5 alpha-reductase inhibitors do not lead to erectile dysfunction to a significant degree and we support the position that dihydrotestosterone is less relevant than testosterone in erectile function.
They got two figures: 1-16%, or 1-33%.
They concluded from that data that ED is not a significant problem with this stuff.
What does that say about their intentions here?
It looks to me like they literally just threw out the data they didn’t like and went with the low figures as the only “correct” ones.
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