hopelessromanticc
High IQ Looksmaxxing Theories
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So levobunolol has been shown to lighten eye color in very rare conditions but here are some problems I’ve found that are pretty much the main wall
1. Rarity
Levobunolol is rarely prescribed anymore. Even finding a source to order from was hard to do. It’s not over the counter so unless you get a prescription you can’t get it unless you order overseas and even overseas markets rarely have it. And people rarely get prescribed levobunolol
2. Eye pigment turnover
Levobunolol works by blocking b androgenic receptors which are responsible for activating camp signaling. When camp signaling is blocked all this means is one of the main pathways of tyrosinase (make melanin) production is reduced
However there are two problems
- residual pigment already produced will still be on your eye for months to years. And if you don’t keep doing it consistently your eyes will just produce melanin and no change will occur
- emergency pigmentation through other pathways can occur. When beta blockers activate they only target one mechanism. Even though it is the main mechanism there are other mechanisms your body can still use to produce melanin. Depending on how strong those other pathways produce melanin it may your eyes still might produce a lot (however it will still result in a net loss of melanin in the eye regardless so this isn’t a significant issue for eye lightening)
But mechanistically it is guaranteed that beta blockers reduce camp signaling and reducing camp signaling will lower melanin production
Only problem is that eye pigment remains on eye permanently. In fact, if you really wanted to alter eye color blocking melanin production is like the least of your worries (and maybe not even needed at all). Eye color doesn’t work like skin, with skin when you block tyrosinase the skin on the bottom layers will be lighter as they will have less melanin and then will replace the skin on the top layers. Thats how the skin cycle works. However think of the eye as that top layer of skin and there is no skin underneath to replace it. If you were to block cmp in a child with undeveloped pigment then the child will permanently have blue eyes
Simply blocking tyrosinase wont do anything because the problem isn’t making new pigment the problem is the pigment already on skin
That’s the same thing for eyes and it’s the reason why for example when you get a eye laser depigmentation procedure done even though it’s just destroying the pigment on the surface it leads to permanent results
It is also the reason why sometimes eye laser don’t work because in some individuals who have high cmp signaling their eyes are still actively producing melanin which means that eyes will still be dark after the laser as it gets quickly replaced by new melanin cells
and this is also why I think levobunolol eye lightening occurs mainly in old people.
Because old people have degraded eye pigment cells due to a lifetime of oxidative stress so when you block cmp which is what produces new pigment and combine it with degraded active pigment you then go from brown to blue eyes
So if we could find a way to combine levobunolol + some way to break down eyes active pigment (outside of lasers cause their expensive) then it’s pretty much a easily repeatable way of lightening eye color
For any high iqcels propose some theories on how we could break down active melanin pigment (not inhibiting new pigment production like levobunolol would do by blocking cmp)
1. Rarity
Levobunolol is rarely prescribed anymore. Even finding a source to order from was hard to do. It’s not over the counter so unless you get a prescription you can’t get it unless you order overseas and even overseas markets rarely have it. And people rarely get prescribed levobunolol
2. Eye pigment turnover
Levobunolol works by blocking b androgenic receptors which are responsible for activating camp signaling. When camp signaling is blocked all this means is one of the main pathways of tyrosinase (make melanin) production is reduced
However there are two problems
- residual pigment already produced will still be on your eye for months to years. And if you don’t keep doing it consistently your eyes will just produce melanin and no change will occur
- emergency pigmentation through other pathways can occur. When beta blockers activate they only target one mechanism. Even though it is the main mechanism there are other mechanisms your body can still use to produce melanin. Depending on how strong those other pathways produce melanin it may your eyes still might produce a lot (however it will still result in a net loss of melanin in the eye regardless so this isn’t a significant issue for eye lightening)
But mechanistically it is guaranteed that beta blockers reduce camp signaling and reducing camp signaling will lower melanin production
Only problem is that eye pigment remains on eye permanently. In fact, if you really wanted to alter eye color blocking melanin production is like the least of your worries (and maybe not even needed at all). Eye color doesn’t work like skin, with skin when you block tyrosinase the skin on the bottom layers will be lighter as they will have less melanin and then will replace the skin on the top layers. Thats how the skin cycle works. However think of the eye as that top layer of skin and there is no skin underneath to replace it. If you were to block cmp in a child with undeveloped pigment then the child will permanently have blue eyes
Simply blocking tyrosinase wont do anything because the problem isn’t making new pigment the problem is the pigment already on skin
That’s the same thing for eyes and it’s the reason why for example when you get a eye laser depigmentation procedure done even though it’s just destroying the pigment on the surface it leads to permanent results
It is also the reason why sometimes eye laser don’t work because in some individuals who have high cmp signaling their eyes are still actively producing melanin which means that eyes will still be dark after the laser as it gets quickly replaced by new melanin cells
and this is also why I think levobunolol eye lightening occurs mainly in old people.
Because old people have degraded eye pigment cells due to a lifetime of oxidative stress so when you block cmp which is what produces new pigment and combine it with degraded active pigment you then go from brown to blue eyes
So if we could find a way to combine levobunolol + some way to break down eyes active pigment (outside of lasers cause their expensive) then it’s pretty much a easily repeatable way of lightening eye color
For any high iqcels propose some theories on how we could break down active melanin pigment (not inhibiting new pigment production like levobunolol would do by blocking cmp)
Last edited:
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