BrahminBoss
Boatsman from river of Styx triple 6
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In a six-month randomized clinical trial by Noecker et al comparing bimatoprost and latanoprost, eyelash growth was noted in 14 of 133 patients in the bimatoprost group versus no patients in the latanoprost group. Other studies by Eisenberg et al and Tosti et al have found similar results, also reporting that hypertrichosis usually appears earlier with bimatoprost than with latanoprost.
Hypertrichosis basically means excessive lash growth.
6 months for eyelash growth and yet the chances of actually noting observable eyelash growth is 1/10 th is completely disgusting. I dont know how they managed to formulate it as a cosmetic product when the results aren't even achievable consistently. Maybe its old hags who would do anything for huge eyelashes to cope with age pill.
But after reading a few studies, there's something interesting I observed.
Firstly, a word on PGF alpha 2 - the prostaglandin which is said to account for the increash in lash density observed. Remember latisse is a glaucoma medication first and foremost and works by reducing Intra Ocular pressure which is the pressure exerted by the amniotic fluid on the eyeball.
Here's what Wikipedia says about Prostaglandin F2 alpha:
Now this is interesting because the same signalling molecule both induces labor and is also used for abortions.
However, From PubMed:
TLDR: Wikipedia claims PGF 2 decreases progesterone, but Pub Med clarifies that this is dose dependent and that in young people the PGF -2 alpha actually induces a progesterone secretion markedly overweighing the e2 secretion (progesterone of course being antagonistic to estrogen in most of its phenotypic actions unlike what is commonly thought ie. they do not work in synergy no matter how much Bayer shills they do). Id imagine the cells making up the lower eyelid also resemble SLC more simply due to the fact that it does not need a strong barrier as much as the placenta.
We can thus infer that topical bimatoprost increases progesterone through the signal transduction of PGF 2 which led to higher progesterone concentrations in tissue.
Mechanism would go somewhat like this:
PGF 2 --> estrogen e2 stimulation --> progesterone stimulation --> eyelash growth.
This of course could all be circumvented by simply applying topical progesterone and indeed there are many reports of women who take bioidentical progesterone (not progestins which have estrogenic action) reporting major lash growth. But they take megadoses orally and I think a small topical dose would be enough for that effect.
Another interesting thing I found was that Bimatoprost wasnt alone in glaucoma medications causing lash growth. Acetozalamide which is a carbonic anhydrase inhibitor does the same by reducing intra ocular blood pressure (or through vasodilation effect consistently observed) also somehow induces lash growth? Latter mechanism would make more sense as it would mean improved blood flow prolonging the anagen phase and since lashes have the lowest anagen: telogen phase of hair follicles in the body it would benefit the most from progesterone and acetozalamide as prog has also shown to increase the duration of the anagen phase.
I dont recommend taking anything else on that list except Acetozalamide. Pencillamine seems to be safe but have not done much research. Acetozalamide with potassium to replenish the lost salts (through urine ) is the safest one.
I think topical progesterone and acetozalamide over a period of three months would be more than enough to replicate Bimatoprost's actions without any of the side effects such as periorbital fat loss, darkening of iris etc. caused by prostaglandin.
Hypertrichosis basically means excessive lash growth.
6 months for eyelash growth and yet the chances of actually noting observable eyelash growth is 1/10 th is completely disgusting. I dont know how they managed to formulate it as a cosmetic product when the results aren't even achievable consistently. Maybe its old hags who would do anything for huge eyelashes to cope with age pill.
But after reading a few studies, there's something interesting I observed.
Firstly, a word on PGF alpha 2 - the prostaglandin which is said to account for the increash in lash density observed. Remember latisse is a glaucoma medication first and foremost and works by reducing Intra Ocular pressure which is the pressure exerted by the amniotic fluid on the eyeball.
Here's what Wikipedia says about Prostaglandin F2 alpha:
Prostaglandin F2α (PGF2α in prostanoid nomenclature), pharmaceutically termed carboprost is a naturally occurring prostaglandin used in medicine to induce labor and as an abortifacient.
It is released in response to an increase in oxytocin levels in the uterus, and stimulates both luteolytic activity and the release of oxytocin. Because PGF2α is linked with an increase in uterine oxytocin levels, there is evidence that PGF2α and oxytocin form a positive feedback loop to facilitate the degradation of the corpus luteum. PGF2α and oxytocin also inhibit the production of progesterone, a hormone that facilitates corpus luteum development. Conversely, higher progesterone levels inhibit production of PGF2α and oxytocin, as the effects of the hormones are in opposition to each other. This is directly exhibited following ovulation when there is a spike of progesterone levels, and then as progesterone levels decrease, PGF2 levels will peak
It is released in response to an increase in oxytocin levels in the uterus, and stimulates both luteolytic activity and the release of oxytocin. Because PGF2α is linked with an increase in uterine oxytocin levels, there is evidence that PGF2α and oxytocin form a positive feedback loop to facilitate the degradation of the corpus luteum. PGF2α and oxytocin also inhibit the production of progesterone, a hormone that facilitates corpus luteum development. Conversely, higher progesterone levels inhibit production of PGF2α and oxytocin, as the effects of the hormones are in opposition to each other. This is directly exhibited following ovulation when there is a spike of progesterone levels, and then as progesterone levels decrease, PGF2 levels will peak
Now this is interesting because the same signalling molecule both induces labor and is also used for abortions.
However, From PubMed:
As corpora lutea (CL) contain at least two different steroidogenic cell populations, fractions of the so called small (SLC) and large (LLC) luteal cells were prepared and tested in separate experiments. In SLC as well as LLC from young CL OXT and PGF2 alpha inhibited progesterone (P) production but induced a strong increase of estradiol (E2) release. In old SLC and LLC OXT and PGF2 alpha were still inhibitory to P release but OXT was ineffective and PGF2 alpha had a moderate stimulatory effect on luteal E2 secretion. In SLC cultures from young but not from old CL E2 exerted a powerful stimulatory effect on progesterone (P) secretion, i.e. E2 has strong luteotrophic effects in the early luteal phase. Indeed, the pronounced inhibitory effect of OXT and PGF2 alpha on P release from SLC could be counteracted by the addition of exogenous E2 to the culture media. Therefore, we suggest that in the early luteal phase OXT as well as PGF2 alpha have an indirect, E2-mediated luteotrophic effect on P release which is stronger than the direct inhibitory action on P secretion
TLDR: Wikipedia claims PGF 2 decreases progesterone, but Pub Med clarifies that this is dose dependent and that in young people the PGF -2 alpha actually induces a progesterone secretion markedly overweighing the e2 secretion (progesterone of course being antagonistic to estrogen in most of its phenotypic actions unlike what is commonly thought ie. they do not work in synergy no matter how much Bayer shills they do). Id imagine the cells making up the lower eyelid also resemble SLC more simply due to the fact that it does not need a strong barrier as much as the placenta.
We can thus infer that topical bimatoprost increases progesterone through the signal transduction of PGF 2 which led to higher progesterone concentrations in tissue.
Mechanism would go somewhat like this:
PGF 2 --> estrogen e2 stimulation --> progesterone stimulation --> eyelash growth.
This of course could all be circumvented by simply applying topical progesterone and indeed there are many reports of women who take bioidentical progesterone (not progestins which have estrogenic action) reporting major lash growth. But they take megadoses orally and I think a small topical dose would be enough for that effect.
Another interesting thing I found was that Bimatoprost wasnt alone in glaucoma medications causing lash growth. Acetozalamide which is a carbonic anhydrase inhibitor does the same by reducing intra ocular blood pressure (or through vasodilation effect consistently observed) also somehow induces lash growth? Latter mechanism would make more sense as it would mean improved blood flow prolonging the anagen phase and since lashes have the lowest anagen: telogen phase of hair follicles in the body it would benefit the most from progesterone and acetozalamide as prog has also shown to increase the duration of the anagen phase.
I dont recommend taking anything else on that list except Acetozalamide. Pencillamine seems to be safe but have not done much research. Acetozalamide with potassium to replenish the lost salts (through urine ) is the safest one.
I think topical progesterone and acetozalamide over a period of three months would be more than enough to replicate Bimatoprost's actions without any of the side effects such as periorbital fat loss, darkening of iris etc. caused by prostaglandin.
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