IHateFin
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Do a nice taper when you come off. Increases your chances of a fruitful snap back
cnb30
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Ok, I'll do 1/2 a pill for the next few days and eventually 1/4th a pill before stopping.
I should also mention that I've also been on Abilify for the past 8 months. While I realize that there are some pretty nasty side effects (and I notice them, especially when I skip a day), I also achieve a state of mental stability that I haven experienced in about 6 years (if I recall what mental stability feel like). Still the most frustrating thing about it is that I can't feel romantic on it (I think it does something to block dopamine which is VERY concerning), but doing that allows me to think straighter. Anyway the point I'm trying to get at is do you think being on Abilify could keep the Finasteride from restoring my sex drive?
IHateFin
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well i dont know a lot about this drug but it seems to be a selective serotonin agonist, antagonist, inverse agonist, NMDA antagonist, SERT blocker and a partial agonist of most of the dopamine receptors (thanks to good ol wiki). thats a whole lot of fuckery, man. @Ghost may be able to get you better answers on this one, but i mean its possible that it could interfere with fin snap back benefits.
also keep in mind that if you are feeling mentally off due to fin it could be possibly due to reversing whatever the current drug your taking is doing. what would maybe be a positive effect on your brain is now one that feels off or unstable due to this other drug. very unpredictable. honestly dont take it from me on this one, but if brain chemistry is changing from a drug (fin) while another drug has already changed your brain chemistry and is still active its hard to say what is causing what you are feeling or if libido can come back. im sure it can.
also when you get to 1/4 pil every day. start taking that same dose every 3rd day for a bit then every 4 th day to complete the taper.
IHateFin
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look at this:
Regulation of androgen receptor gene expression by steroids and retinoic acid in human breast-cancer cells. - PubMed - NCBI
Abstract
Although the androgen receptor (AR) has been detected by ligand-binding assays, there is little known about the expression and regulation of the AR gene in human breast-cancer cells. AR mRNA, measured by Northern analysis in 18 cell lines, was found to be expressed predominantly in oestrogen- and progesterone-receptor-positive (ER+, PR+) lines as a single species of approximately 10.5 kb but was also comparatively abundant in I ER- and PR-negative cell line, MDA-MB-453. Dexamethasone (Dex), Organon 2058 (Org 2058), dihydrotestosterone (DHT), and all-trans-retinoic acid (RA) down-regulated AR mRNA levels in T-47D (ER+, PR+) cells 6 hr after treatment, whereas oestradiol (E2) had no effect. In MDA-MB-453 (ER-, PR-) cells, regulation of AR mRNA by RA differed from the other cell lines: RA increased the level of AR mRNA. DHT-binding assays indicated a corresponding increase in AR protein. Transfection of the androgen-responsive mouse mammary tumour virus long-terminal repeat (MMTV LTR) linked to a chloramphenicol acetyltransferase (CAT) reporter gene was used to examine the effect of altered AR levels on androgen action. The increased level of AR following RA pre-treatment in MDA-MB-453 cells resulted in enhanced induction of CAT activity by DHT and, conversely, a decrease in the level of AR following RA pretreatment in T-47D cells resulted in reduced induction of CAT activity by DHT. These data demonstrate that AR is expressed predominantly in ER+ and PR+ cell lines and its expression is regulated by ligands also known to regulate ER or PR, including progestins and retinoids. Androgen responsiveness measured by a transfected reporter gene was altered according to the extent of up- or down-regulation of AR expression, demonstrating that responsiveness is dependent on receptor concentration.
this study just blew my mind
Retonic acid (like fin which accutaine is a derrivative of) seemed to increase androgen receptors at first, but then after treatment the increase in CAT activity from dht actually caused a down regulation of gene expression. this must be the reason dht makes us feel like shit. chloramphenicol acetyltransferase (CAT) seems to be the reason dht doesnt work for us anymore and makes us feel like shit. PFS could be a matter of purely androgen insensitivity along with PAS, but maybe PAS is a much worse condition. this is definitely some epi-genetics shit going on here.
Regulation of androgen receptor gene expression by steroids and retinoic acid in human breast-cancer cells. - PubMed - NCBI
Abstract
Although the androgen receptor (AR) has been detected by ligand-binding assays, there is little known about the expression and regulation of the AR gene in human breast-cancer cells. AR mRNA, measured by Northern analysis in 18 cell lines, was found to be expressed predominantly in oestrogen- and progesterone-receptor-positive (ER+, PR+) lines as a single species of approximately 10.5 kb but was also comparatively abundant in I ER- and PR-negative cell line, MDA-MB-453. Dexamethasone (Dex), Organon 2058 (Org 2058), dihydrotestosterone (DHT), and all-trans-retinoic acid (RA) down-regulated AR mRNA levels in T-47D (ER+, PR+) cells 6 hr after treatment, whereas oestradiol (E2) had no effect. In MDA-MB-453 (ER-, PR-) cells, regulation of AR mRNA by RA differed from the other cell lines: RA increased the level of AR mRNA. DHT-binding assays indicated a corresponding increase in AR protein. Transfection of the androgen-responsive mouse mammary tumour virus long-terminal repeat (MMTV LTR) linked to a chloramphenicol acetyltransferase (CAT) reporter gene was used to examine the effect of altered AR levels on androgen action. The increased level of AR following RA pre-treatment in MDA-MB-453 cells resulted in enhanced induction of CAT activity by DHT and, conversely, a decrease in the level of AR following RA pretreatment in T-47D cells resulted in reduced induction of CAT activity by DHT. These data demonstrate that AR is expressed predominantly in ER+ and PR+ cell lines and its expression is regulated by ligands also known to regulate ER or PR, including progestins and retinoids. Androgen responsiveness measured by a transfected reporter gene was altered according to the extent of up- or down-regulation of AR expression, demonstrating that responsiveness is dependent on receptor concentration.
this study just blew my mind
Retonic acid (like fin which accutaine is a derrivative of) seemed to increase androgen receptors at first, but then after treatment the increase in CAT activity from dht actually caused a down regulation of gene expression. this must be the reason dht makes us feel like shit. chloramphenicol acetyltransferase (CAT) seems to be the reason dht doesnt work for us anymore and makes us feel like shit. PFS could be a matter of purely androgen insensitivity along with PAS, but maybe PAS is a much worse condition. this is definitely some epi-genetics shit going on here.
cnb30
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Depression. It seems to help too.
cnb30
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Hey guys, my in some weird way my libido appears to be returning slightly. It’s more pronounced some ways than others and it’s definitely more of a psychological thing (not like easier erections or whatnot at the moment). Hopefully it is more than just spring. I’m thinking that taking finasteride might have harmed me somewhat psychologically but let’s see.
IHateFin
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cnb30
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Do you mean to say that the benefits don’t start until after you finish the fin?
IHateFin
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From what I've read the benefits are there, but moderate while on fin; however, after you quit everything surges back with a SnapBack. Probably CNS 5ar1 coming back which will raise 5AR and androgen sensativity everywhere else
cnb30
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I’ve tapered down to 1/4th a pill but I haven’t noticed too many positive effects. Who knows, it might take more than 1 cycle for me.
IHateFin
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