Thought of this as a potential mechanism for why some people get persistent (maybe permanent) erectile dysfunction after years of zero side effects on finasteride:
The cavernous nerves surround the prostate on the posterior aspect. As finasteride blocks 5-alpha reductase, decreasing DHT, the prostate begins to shrink. As the prostate shrinks, the cavernous nerves begin to stretch. Stretching a nerve beyond 15% of its length can cause irreversible damage if stretching is faster than the body's ability to adapt its nerves to stretch. Some people's bodies may have a slower adaptation to nerve stretch; therefore, these people can't keep up with the rate at which finasteride is shrinking the prostate. This would explain why persistent sides show up after years of zero sides. Since the cavernous nerves allow the penis to become erect to begin with, irreversibly damaging it would ultimately lead to permanent erectile dysfunction. A potential treatment could be stem cell injections to try to regenerate the nerves. The same concept has been implemented successfully in a few paraplegic cases. Regarding the people who get persistent ED after stopping finasteride, that is most likely more due to receptors being damaged because of the rapid surge in DHT after stopping. A receptor damage mechanism for the latter would explain why many of them have signs of hypogonadism with normal hormonal profiles and don't respond to TRT.
Good points brought up by IdealForehead:
- Young men on finasteride for hair already have small prostates, so it doesn't have that far to stretch
Although the prostate is smaller in younger men so it doesn't have have to stretch as far, the nerves directly around the prostate are so small that a stretch of 15% would still be possbile.
- The nerves that run to the penis must by design have a lot of slack to them, or if they didn't you'd tear the nerves every time you get an erection or pull on your dick to stretch it.
True, the nerves around the penis have a lot of slack in them. However, the small nerves directly around the prostate do not have as much slack in them so shrinking of the prostate is directly stretching a different group of nerves, all still considered part of cavernous nerves, than when you get an erection or pull on your dick to stretch it.
- Nerves can both shrink and lengthen over time depending on the stresses that are applied to them as long as it is gradual. This is how guys can get leg lengthening surgery done without paralysis to the ankle and foot - the nerves grow and stretch to adapt.
True as well, however, when the lengthening of a nerve is faster than the body's ability to adapt to the stretch then a stretch of more than 15% of its length will cause irreversible damage. Thus, some people's nerves might have a slower adaptation to stretch causing the irreversible damage over time leading to permanent ED via damage to cavernous nerves directly around the prostate.
I know this is all somewhat rare, but I'm just a slowing balding med student so I find this stuff interesting. Please let me know your thoughts. All the best!
The cavernous nerves surround the prostate on the posterior aspect. As finasteride blocks 5-alpha reductase, decreasing DHT, the prostate begins to shrink. As the prostate shrinks, the cavernous nerves begin to stretch. Stretching a nerve beyond 15% of its length can cause irreversible damage if stretching is faster than the body's ability to adapt its nerves to stretch. Some people's bodies may have a slower adaptation to nerve stretch; therefore, these people can't keep up with the rate at which finasteride is shrinking the prostate. This would explain why persistent sides show up after years of zero sides. Since the cavernous nerves allow the penis to become erect to begin with, irreversibly damaging it would ultimately lead to permanent erectile dysfunction. A potential treatment could be stem cell injections to try to regenerate the nerves. The same concept has been implemented successfully in a few paraplegic cases. Regarding the people who get persistent ED after stopping finasteride, that is most likely more due to receptors being damaged because of the rapid surge in DHT after stopping. A receptor damage mechanism for the latter would explain why many of them have signs of hypogonadism with normal hormonal profiles and don't respond to TRT.
Good points brought up by IdealForehead:
- Young men on finasteride for hair already have small prostates, so it doesn't have that far to stretch
Although the prostate is smaller in younger men so it doesn't have have to stretch as far, the nerves directly around the prostate are so small that a stretch of 15% would still be possbile.
- The nerves that run to the penis must by design have a lot of slack to them, or if they didn't you'd tear the nerves every time you get an erection or pull on your dick to stretch it.
True, the nerves around the penis have a lot of slack in them. However, the small nerves directly around the prostate do not have as much slack in them so shrinking of the prostate is directly stretching a different group of nerves, all still considered part of cavernous nerves, than when you get an erection or pull on your dick to stretch it.
- Nerves can both shrink and lengthen over time depending on the stresses that are applied to them as long as it is gradual. This is how guys can get leg lengthening surgery done without paralysis to the ankle and foot - the nerves grow and stretch to adapt.
True as well, however, when the lengthening of a nerve is faster than the body's ability to adapt to the stretch then a stretch of more than 15% of its length will cause irreversible damage. Thus, some people's nerves might have a slower adaptation to stretch causing the irreversible damage over time leading to permanent ED via damage to cavernous nerves directly around the prostate.
I know this is all somewhat rare, but I'm just a slowing balding med student so I find this stuff interesting. Please let me know your thoughts. All the best!
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