Why you stop minoxidil? Won't you hair fall without it?
Aggressive Regemin - Recovery From Norwood-6.5
- Thread starter cocona
- Start date
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Congrats! Wow that's really amazing! We should all be so lucky!
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Really great progress, Cocona. Your posts in other threads are informative and very helpful, and now just for the first time I saw your progress thread here. Really, really amazing. The last 12 months must have been such a wonderful change for you... in your hair and in your life! 
You wrote briefly about drug timings. I'm curious about the interaction of different treatments and which treatments can NOT be used simultaneously. It's a big issue when building out a regimen with lots of parts. In hair research, I haven't seen much published about the topic (what I've found is mostly about interactions with sleep cycles, e.g. with melatonin, PGD2). Of forum guys, there's a little about interactions and timings, but not much. I've seen that Swiss emphasizes to separate by several hours what he considers PGE1 treatments from PGE2 treatments, while Antydhtor has a schedule where he keeps oral minoxidil at least 1 hour away from 5ar inhibitors, cyproterone acetate 3 hours away from 5ar inhibitors, and estrofem 1 hour away from cyproterone acetate.
You wrote a bit about it in your regimen:
You've done tons of research for quite a while, so I'm genuinely curious what you think now about the interactions and timings of the different hair treatments we all look at. In your opinion, which can NOT be used simultaneously?
Taking your regimen as an example, how did you decide on separating stemoxydine and castor oil 12 hours away from minoidil and nizoral? I'm not saying you're wrong or criticizing, it's that I'm honestly very interested in your thinking on these interaction/timing issues because it's not clear to me how to evaluate/classify treatments, consider possible interactions, and decide on timing.
My question is about all treatments in general, but using your regimen as an example, the first questions I had were:
- How exactly do PGE1 and PGE2 antagonize each other? If applied topically, is it local only? How about systemic effects, how would their antagonizing work from systemic use?
- You classified minoxidil as a PGE1 agonist, and therefore made sure that it's used 12 hours apart from the PGE2-expressing castor oil. What makes you classify minoxidil as a PGE1 agonist? From research I've seen, I thought it was still a pretty open question how minoxidil works. Two fairly recent studies:
- Stemoxydine: I'd thought its benefit, if any, is its hypoxic effect. What interaction does that have with other treatments, minoxidil for example? There's not much research on stemoxydine in the last years, but when L'Oreal developed it in the mid-2000s, the idea was that:
You wrote briefly about drug timings. I'm curious about the interaction of different treatments and which treatments can NOT be used simultaneously. It's a big issue when building out a regimen with lots of parts. In hair research, I haven't seen much published about the topic (what I've found is mostly about interactions with sleep cycles, e.g. with melatonin, PGD2). Of forum guys, there's a little about interactions and timings, but not much. I've seen that Swiss emphasizes to separate by several hours what he considers PGE1 treatments from PGE2 treatments, while Antydhtor has a schedule where he keeps oral minoxidil at least 1 hour away from 5ar inhibitors, cyproterone acetate 3 hours away from 5ar inhibitors, and estrofem 1 hour away from cyproterone acetate.
You wrote a bit about it in your regimen:
You've done tons of research for quite a while, so I'm genuinely curious what you think now about the interactions and timings of the different hair treatments we all look at. In your opinion, which can NOT be used simultaneously?
Taking your regimen as an example, how did you decide on separating stemoxydine and castor oil 12 hours away from minoidil and nizoral? I'm not saying you're wrong or criticizing, it's that I'm honestly very interested in your thinking on these interaction/timing issues because it's not clear to me how to evaluate/classify treatments, consider possible interactions, and decide on timing.
My question is about all treatments in general, but using your regimen as an example, the first questions I had were:
- How exactly do PGE1 and PGE2 antagonize each other? If applied topically, is it local only? How about systemic effects, how would their antagonizing work from systemic use?
- You classified minoxidil as a PGE1 agonist, and therefore made sure that it's used 12 hours apart from the PGE2-expressing castor oil. What makes you classify minoxidil as a PGE1 agonist? From research I've seen, I thought it was still a pretty open question how minoxidil works. Two fairly recent studies:
- The 2012 Garcia paper:
"Although minoxidil alters potassium channel kinetics, it is also known to increase production of PGE2. Given the decreased amount of PGE2 present in bald scalp versus haired scalp, minoxidil may normalize PGE2 levels. Future studies should address whether minoxidil can concomitantly decrease PGD2 levels and thus normalize multiple prostaglandin species as a mechanism to improve Androgenetic Alopecia."
- This 2011 Korean study on mice claims that minoxidil's effect is on the Wnt signalling pathway:
"Our results strongly suggest that minoxidil extends the anagen phase by activating β-catenin activity in the [dermal papilla cells]."
- Stemoxydine: I'd thought its benefit, if any, is its hypoxic effect. What interaction does that have with other treatments, minoxidil for example? There's not much research on stemoxydine in the last years, but when L'Oreal developed it in the mid-2000s, the idea was that:
"[H]ypoxia signaling is mediated by HIF1, a subunit of which is degraded in an oxygen-dependent manner through prolyl-4-hydroxylase (P4H)-mediated hydroxylation... stemoxydine is a P4H competitive inhibitor... [hypoxia is] favourable to stem cells functioning (especially CD34+ stem cells in the lower reservoir of follicle) that are responsible for triggering to neogen phase and then conduct to new hair growth (new follicle cycle)... the longer the kenogen phase is, the more empty bulbs there are and thus the density decreases. Stemoxydine acts as a hair kenogen phase shortener, leading to an increase in visible scalp hair density. More dormant bulbs wake up...”. [quotes from several L'Oreal articles]
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- 1,155
Obviously not true
- Reaction score
- 338
Really great progress, Cocona. Your posts in other threads are informative and very helpful, and now just for the first time I saw your progress thread here. Really, really amazing. The last 12 months must have been such a wonderful change for you... in your hair and in your life!
You wrote briefly about drug timings. I'm curious about the interaction of different treatments and which treatments can NOT be used simultaneously. It's a big issue when building out a regimen with lots of parts. In hair research, I haven't seen much published about the topic (what I've found is mostly about interactions with sleep cycles, e.g. with melatonin, PGD2). Of forum guys, there's a little about interactions and timings, but not much. I've seen that Swiss emphasizes to separate by several hours what he considers PGE1 treatments from PGE2 treatments, while Antydhtor has a schedule where he keeps oral minoxidil at least 1 hour away from 5ar inhibitors, cyproterone acetate 3 hours away from 5ar inhibitors, and estrofem 1 hour away from cyproterone acetate.
You wrote a bit about it in your regimen:
You've done tons of research for quite a while, so I'm genuinely curious what you think now about the interactions and timings of the different hair treatments we all look at. In your opinion, which can NOT be used simultaneously?
Taking your regimen as an example, how did you decide on separating stemoxydine and castor oil 12 hours away from minoidil and nizoral? I'm not saying you're wrong or criticizing, it's that I'm honestly very interested in your thinking on these interaction/timing issues because it's not clear to me how to evaluate/classify treatments, consider possible interactions, and decide on timing.
My question is about all treatments in general, but using your regimen as an example, the first questions I had were:
- How exactly do PGE1 and PGE2 antagonize each other? If applied topically, is it local only? How about systemic effects, how would their antagonizing work from systemic use?
- You classified minoxidil as a PGE1 agonist, and therefore made sure that it's used 12 hours apart from the PGE2-expressing castor oil. What makes you classify minoxidil as a PGE1 agonist? From research I've seen, I thought it was still a pretty open question how minoxidil works. Two fairly recent studies:
- The 2012 Garcia paper:
"Although minoxidil alters potassium channel kinetics, it is also known to increase production of PGE2. Given the decreased amount of PGE2 present in bald scalp versus haired scalp, minoxidil may normalize PGE2 levels. Future studies should address whether minoxidil can concomitantly decrease PGD2 levels and thus normalize multiple prostaglandin species as a mechanism to improve Androgenetic Alopecia."
- This 2011 Korean study on mice claims that minoxidil's effect is on the Wnt signalling pathway:
"Our results strongly suggest that minoxidil extends the anagen phase by activating β-catenin activity in the [dermal papilla cells]."
- Stemoxydine: I'd thought its benefit, if any, is its hypoxic effect. What interaction does that have with other treatments, minoxidil for example? There's not much research on stemoxydine in the last years, but when L'Oreal developed it in the mid-2000s, the idea was that:
"[H]ypoxia signaling is mediated by HIF1, a subunit of which is degraded in an oxygen-dependent manner through prolyl-4-hydroxylase (P4H)-mediated hydroxylation... stemoxydine is a P4H competitive inhibitor... [hypoxia is] favourable to stem cells functioning (especially CD34+ stem cells in the lower reservoir of follicle) that are responsible for triggering to neogen phase and then conduct to new hair growth (new follicle cycle)... the longer the kenogen phase is, the more empty bulbs there are and thus the density decreases. Stemoxydine acts as a hair kenogen phase shortener, leading to an increase in visible scalp hair density. More dormant bulbs wake up...”. [quotes from several L'Oreal articles]
You are more educated than me on this subject. I'm sorry I cant help you.
- Reaction score
- 2,720
Hey girl, awesome regrowth. Looking like you’re well on your way to some solid locks! I have some questions.
Sadly since you on a trans regimen coming from male hormones, I realise things are different for us, but I will ask anyway since technically I started with male pattern baldness from having no estrogen.
I just started dutas 0.5mg per week (low because I’m scared of starting high and really screwing my hormones). I started shedding hugely THREE DAYS after and still and a week later. My question is: did you notice a shed or sheds after taking it? Any sides? Do you shed now?
Sadly since you on a trans regimen coming from male hormones, I realise things are different for us, but I will ask anyway since technically I started with male pattern baldness from having no estrogen.
I just started dutas 0.5mg per week (low because I’m scared of starting high and really screwing my hormones). I started shedding hugely THREE DAYS after and still and a week later. My question is: did you notice a shed or sheds after taking it? Any sides? Do you shed now?
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- 3,456
probably just a shed but maybe using once a week is the reason? I dont think having ups and downs in hormones is good for hair so consider using dutasteride everyday to keep Dht consistently and maximumly suppressed. Dht is terrible, you dont need it for anything as a woman. f*** Dht.
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Haha I love that last part of what you said. Amen to that. After doing a lot of reading however, I have seen many great accounts of hair regrowth for women with PCOS (similar to my own hormone profile and also I the pill) using 250mg Flutamide a day. I am a little worried about annihilating my liver for The sake of hair regrowth however, and dutas 0.5mg is a VERY high dose. 0.1mg is the equivalent of 5mg finas. So perhaps if I choose to stay on it, it’s better up up the dose to twice weekly thereby equaling 5mg finas a day but with greater 5-alpha reductase inhibition.
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Bicalutamide is similiar to flutamide but with less side effects, Ive heard its like a newer better version of flut. I'm afraid to try Bic or flut because they actually increase T in men while blocking the receptors because it increases LH and LH is what activates testicles or ovaries to produce sex hormones, so probably it would increase estrogen for a woman? Lol yeah you could try that, maybe dutasteride everyday is overkill but less dht is always better for hair and blocking it should increase estrogen some too since some of extra T will aromatize. There's a transwoman on this site who actually stopped taking finasteride completely and continued to regrow with cypro and estrogen. Maybe you could consider Flut, Bic, or Cypro? However, all receptor blockers seem to be not so healthy in some way.
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You read my mind. I’ve been lurking on PCOS and trans hairloss sites and Flutamide + estrogen (the pill) + minoxidil seems to yield the best results. You are right about Flutamide raising estrogen, but in fact lowers test levels in women which i beleive is key in treating female hairloss. I am also going to start RU as per @IdealForehead suggestion.Bicalutamide is similiar to flutamide but with less side effects, Ive heard its like a newer better version of flut. I'm afraid to try Bic or flut because they actually increase T in men while blocking the receptors because it increases LH and LH is what activates testicles or ovaries to produce sex hormones, so probably it would increase estrogen for a woman? Lol yeah you could try that, maybe dutasteride everyday is overkill but less dht is always better for hair and blocking it should increase estrogen some too since some of extra T will aromatize. There's a transwoman on this site who actually stopped taking finasteride completely and continued to regrow with cypro and estrogen. Maybe you could consider Flut, Bic, or Cypro? However, all receptor blockers seem to be not so healthy in some way.
That Diane 35 is nasty stuff be careful. You could try cypro ,12.5 mg every two to three days should not be to harsh on liver. dutasteride has very long half life so maybe twice a week ? I use the oral minoxidil too. 10mg. seems to have helped alot
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I have to take Diane for the estrogen since I don’t produce any of my own sadly. It’s just the best choice because it also has anti androgenic properties. I’ve found through research that drugs which ultimately raise testosterone levels like Dutasteride and Finasteride are not the best option for female hairloss, as our hairloss can be linked to raised levels of test moreso than raised levels of dht. In lieu of this I plan to start using topical 5% ru58841 as it acts as a powerful 5 alpha inhibitor without systemic hormonal effects. Also, since casodex seems to be safer than Flutamide with almost the same mechanisms, I shall look into that.
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- 338
Answer to your question:
Nope within even a week I had tons of new hair I didn't have before. Compare early May to June photos to see the kind of regrowth I got in the first 2 months. Sides are standard antiandrogen sides. Impotence, lower muscle mass etc. Around oct. I stopped it because I was also getting short term memory loss issues. Those stopped when I stopped it. I used Dr. Reddys Dutas from inhousepharmacy.vu If you are interested in it I have just over 4 months of it left I could mail you if you like.
More information:
I just got my hormone profile done 2 weeks ago and my my testosterone was at 4 ng/dl and am only on 50 mg spironolactone/day since Oct. My previous measurement was at 4 ng/dl in Aug. so it appears my testosterone production has shut down completely now which is great.
What sorts of sites? (I'm interested.)
Apology:
Also sorry for the lateness I have just been completely distracted from tackling hair loss. There are no positive updates for me to give its still more of the same mostly.
About future updates to this thread:
I am getting ffs March 29th and it is devouring all my funds so I wont do much on here for a few months. One of the parts of my ffs is a scalp advancement included as part of my brow reduction so that's a thing that's relevant to hair loss. Other than that the plans to try are topical cetirizine if I can get it, pge2 and seti from kane and a hair transplant. The hair transplant may be the first to happen since It is covered under my insurance at 90% of the cost as part of my transition. (I have amazing insurance through boeing that is great for transpeople.) The plan is Dr Arocha in Texas if I can get him but this is still in its preliminary stages. side note my hair is still too thin on the top to grow out. when I do it becomes very obvious there are density issues so the plan is to solve those then maybe in a year and a half I can have hair that is 6 inches long or so.
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you could try the cetrizine,pge2, and seti first before getting a transplant to see if you happen to regrow any more hairs? maybe it will save you some grafts in the long run.
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- 118
Can you share the blood report? For science/curiosity
Also have you wondered switching to estrogen shots instead of pills? If twohen's info and timeline is accurate, it seems he used estrogen shots to regrow his hair.
- Reaction score
- 338
Been on the fence about this for a while. Maybe idk. Honestly I'm exhausted and I just want some f*****g hair. A 3500 fue would be a huge step in the right direction, maybe even make me passable without a wig. That'd be great.
Too much editing... sorry.
https://www.hairlosstalk.com/intera...mizing-growth-and-minimizing-scarring.109363/
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