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Pls_NW-1

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What are we talking sides wise. I can afford it-- thats not the issue. Health is tho
You need one dominant sex hormone, a balance and strong levels to avoid osteoporosis and other issues related to lack of sex hormones. The best you can do is blocking the androgen signaling in scalp tissue and let the ER be flooded by endogenous estrogens. Anti-Androgens, which elevate androgen levels itself, elevate estrogens as well by 150%. (3×).

Hope this clarifies.

Androgens: transcribe balding informations

Estrogens: reverse transcription of balding information

Sexual sides are 100% not avoidable with any kind of estrogens, be prepared.
 

Isneezedsohard

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You need one dominant sex hormone, a balance and strong levels to avoid osteoporosis and other issues related to lack of sex hormones. The best you can do is blocking the androgen signaling in scalp tissue and let the ER be flooded by endogenous estrogens. Anti-Androgens, which elevate androgen levels itself, elevate estrogens as well by 150%. (3×).

Hope this clarifies.

Androgens: transcribe balding informations

Estrogens: reverse transcription of balding information

Sexual sides are 100% not avoidable with any kind of estrogens, be prepared.
I think im kind of understanding? I'm gonna reread in the morning LOL
 

GRme11

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What about Methyl Vanillate as a cheap alternative for WNT-Beta Catenin Activation?
1)https://www.forhair.com/images/stor..._activator_JOCD_12225_Final_Revised_Proof.pdf
Background: Activation of the WNT/b-catenin pathway has emerged as a potential therapeutic target in androgenetic alopecia (Androgenetic Alopecia). Methyl vanillate (MV) a safe plant-derived ingredient – has been recently shown to activate the WNT/b-catenin signaling.
Objectives: Two distinct substudies were conducted. First, we designed a 6-month, uncontrolled, open-label clinical study to investigate whether topically applied MV may increase hair count and hair mass index (HMI) in female Androgenetic Alopecia. Second, we conducted a molecular study on the effect of MV on WNT10B mRNA expression in scalp biopsies of women with Androgenetic Alopecia.
Methods: A total of 20 Caucasian women (age range: 2557 years) with Androgenetic Alopecia (Sinclair grade 12) were included. The research product was an alcohol-free formulation supplied in the form of a spray containing 0.2% MV as the active ingredient. (Application was 2ml Every Other Day. So, 4mg/ml in total when the product applied)
Results: In the clinical study, hair count and HMI were found to increase at 6 months by 6% (P < 0.01) and 12% (P < 0.001), respectively, compared with baseline. No participant discontinued treatment due to adverse effects, and the overall patient satisfaction was good. At the molecular level, the topical application of the research product resulted in a 32% increase in WNT10B mRNA expression levels in the temporal scalp area (P < 0.001).
Conclusion: Our pilot data suggest that topical MV can increase hair count and HMI by inducing WNT10B expression in the scalp, potentially serving as a novel treatment strategy for female Androgenetic Alopecia.
2) https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2230.2011.04019.x
Background: Wnt10b (wingless-related mouse mammary tumour virus integration site 10b) plays various roles in a wide range of biological actions, including hair-follicle development.

Aim: To assess the roles that Wnt10b plays in postnatal hair-follicle growth.

Methods: Adenovirus vectors AdWnt10b, AdGFP, AdGFP plus AdRFP, AdWnt10b plus AdFrzB, and AdWnt10b plus AdSimBC were co-cultured separately with vibrissae. In situ protein expression of Wnt10b, β-catenin and Lef1 was determined by immunohistochemistry, and the proliferation status of the hair follicle was detected by 5-bromo-2-deoxyuridine (BrdU) labelling. The presence of Wnt signalling molecules in the three stages of hair-follicle growth was detected by PCR-based microarray.

Results: AdWnt10b-infected cells were able to secrete bioactive Wnt10b, and when this was added into the basal medium, the vibrissae grew faster than in control medium or in medium containing canonical Wnt signalling antagonists. The in situ protein expression of Wnt10b was consistent with that of β-catenin and Lef1. The expression locus of Wnt10b was almost the same as the proliferating cells labelled by BrdU in the anagen hair follicle.

Conclusions: Wnt10b may promote hair-follicle growth by inducing the switch from telogen to anagen via a canonical Wnt signalling pathway to promote the proliferation of matrix cells.
3) https://portlandpress.com/bioscirep...10b-promotes-hair-follicles-growth-and-dermal (recent study in Rabbits though)

Abstract​

Wnt signaling plays an important role in the growth and development of hair follicles (HFs). Among the signaling molecules, Wnt10b was shown to promote the differentiation of primary skin epithelial cells toward the hair shaft and inner root sheath of the HF cells in mice in vitro. Whisker HFs were isolated from Rex rabbits and cultured in vitro to measure hair shaft growth. Meanwhile, dermal papilla cells (DPCs) were isolated and cultured in vitro. Treatment with AdWnt10b or the Wnt/β-Catenin Pathway inhibitor, XAV939, assessed the DPCs proliferation by CCK-8 assay. And the cell cycle was also analyzed by flow cytometry. We found that Wnt10b could promote elongation of the hair shaft, whereas XAV-939 treatment could eliminated this phenomenon. AdWnt10b treatment promoted the proliferation and induced G1/S transition of DPCs. AdWnt10b stimulation up-regulated β-Catenin protein in DPCs. Inhibition of Wnt/β-Catenin signaling by XAV-939 could decreased the basal and Wnt10b-enhanced proliferation of DPCs. And could also suppress the cell cycle progression in DPCs. In summary, our study demonstrates that Wnt10b could promote HFs growth and proliferation of DPCs via the Wnt/β-Catenin signaling pathway in Rex rabbits.
4) (Recent good study for the WNT beta Catenin Pathway in General)
From the study above:

Wnt.jpg

My "concerns":

Vanillic Acid: Vanillic acid (4-hydroxy-3-methoxybenzoic acid) is a dihydroxybenzoic acid derivative used as a flavoring agent. It is an oxidized form of vanillin. It is also an intermediate in the production of vanillin from ferulic acid.
Methyl Vanillate: Methyl vanillate is a benzoate ester that is the methyl ester of vanillic acid. It has a role as an antioxidant and a plant metabolite. It is a benzoate ester, a member of phenols and an aromatic ether. It derives from a vanillic acid.
http://www.biomolther.org/journal/view.html?volume=28&number=4&spage=354 ( Vanillic Acid Stimulates Anagen Signaling via the PI3K/Akt/ β-Catenin Pathway in Dermal Papilla Cells->Decent effects)

(Vanillic acid restores DHT-downregulated β-catenin level in DPCs

Dihydrotestosterone, implicated in the development of Androgenetic Alopecia, suppresses the cell-cycle progression and Wnt/β-catenin pathway in DPCs (Kang et al., 2015). To determine whether vanillic acid could restore the downregulation of β-catenin by DHT, DPCs were treated with DHT (100 nM) in the absence or presence of vanillic acid (10 μg/mL) for 24 h. The decreased levels of β-catenin and Cox-2, a target gene of β-catenin, observed in the DHT treated cells were restored by vanillic acid (Fig. 4A). Confocal microscopy data showed that DHT decreased the level of β-catenin, but pretreatment with vanillic acid attenuated the DHT-induced decrease of β-catenin level (Fig. 4B). These results suggest that vanillic acid can restore the DHT-induced downregulation of the Wnt/β-catenin pathway.)




Although,

To examine whether vanillic acid activates the Wnt/β-catenin pathway, DPCs were stimulated with vanillic acid (10 μg/mL) for 0-120 min. As shown in Fig. 3A, vanillic acid increased the levels of phospho(ser9)-GSK3β, phospho(ser552)-β-catenin, and phospho(ser675)-β-catenin after 15-120 min. Confocal microscopy data showed that vanillic acid increased the levels of phospho(ser552)-β-catenin and phospho(ser675)-β-catenin in the cytoplasm and nucleus (Fig. 3B, 3C). The phosphorylation of β-catenin by minoxidil was increased similarly to that by the vanillic acid (Fig. 3B, 3C). These results indicate that vanillic acid could increase the levels of active β-catenins via the regulation of GSK3β. GSK3β is a downstream target of PI3K/Akt, which in turn regulates the expression of β-catenin (Monick et al., 2001). To evaluate the mechanism underlying the activation of the Wnt/β-catenin pathway by vanillic acid via PI3K/Akt, we examined the levels of phospho(ser675)-β-catenin, β-catenin, and Cox-2, a target gene of β-catenin, following a 24 h treatment with vanillic acid in the presence or absence of wortmannin. As shown in Fig. 3D, vanillic acid increased the levels of phospho(ser675)-β-catenin, β-catenin, Cox-2, and cyclin D1, and the increased levels of these proteins were attenuated by wortmannin (Fig. 3D). These results suggest that the activation of the Akt pathway by vanillic acid contributes to the activation of the Wnt/β-catenin pathway.

From Conclusions:

(As shown in Fig. 3D, vanillic acid also upregulated the levels of Cox-2 and cyclin D1, which are the target genes of β-catenin, and the level of β-catenin. These changes were attenuated by wortmannin, indicating that the vanillic acid-mediated proliferation in DPCs is regulated by the PI3K/Akt/Wnt/β-catenin pathway. Consistent with this notion, minoxidil prolongs the duration of the anagen phase, possibly, due to the activation of the Wnt/β-catenin pathway by altering the PKA and Akt pathways in human DPCs (Kwack et al., 2011). Therefore, based on the above mechanism, vanillic acid could activate the anagen phase and promote hair growth.

DHT, a potent androgen, plays a crucial role in the pathogenesis of Androgenetic Alopecia (Sinclair, 1998). Our previous study partially supports the DHT-mediated Androgenetic Alopecia development, demonstrating that DHT can attenuate the cell cycle progression by inhibiting translocation of β-catenin into the nucleus in DPCs (Kang et al., 2015). In this study, we demonstrated that vanillic acid exhibits a protective effect on the downregulation of β-catenin by DHT (Fig. 4). In addition, we investigated the effects of vanillic acid on the levels of growth factors, the opening of KATP channels, and the inhibition of the TGF-β pathway related to the regulation of the hair growth (Guo et al., 1996; Suzuki et al., 2000; Yano et al., 2001; Soma et al., 2002; Shorter et al., 2008). However, we observed that vanillic acid does not affect the levels of VEGF, FGF-7, and FGF-10 mRNA, the opening of KATP channels, or the phosphorylation of smad2/3, a mediator of the TGF-β pathway (data not shown).
In conclusion, we evaluated the effects of vanillic acid on the proliferation of DPCs and verified that vanillic acid selectively regulates the PI3K/Akt/Wnt/β-catenin pathway. These findings suggest that vanillic acid could stimulate the anagen phase by activating the PI3K/Akt/Wnt/β-catenin pathway and potentially alleviate hair loss.)



So, if I understand correctly they are to 2 negative factors here from the Vanillic Acid but the positive effects, they seem very very good as well. The "negatives" : Regulation of GSK3β and the increased levels of Cox-2.
If I am not wrong, we need to inhibit GSK3β and the increment to the Cox-2, it will lead to an increment to PGE2 but PGD2 as well??

BUT Pegasus mentioned this:


PGE2 regulates wnt activity by direct phosphorylation of β-catenin and GSK3β

Our work shows that PGE2 acts via cAMP/PKA signaling to directly modify β-catenin stability and emphasizes the functional importance and evolutionary conservation of these interactions in organ development and regeneration. PGE2-mediated regulation of Wnt signaling was previously demonstrated in cell lines. The proposed biochemical mechanisms mediating the interaction are remarkably diverse and may depend on the particular cell line studied (Clevers, 2006). Castellone et al. used colon cancer cell lines to demonstrate PGE2/PI3K-mediated activation of Akt, leading to dissociation of Axin1 from the destruction complex (Castellone et al., 2005). While we cannot exclude the existence of this biochemical interaction in vivo, our studies suggest that activation of PKA is the functionally significant effector downstream of PGE2 in HSCs. Likewise, both phosphorylation of GSK3β and β-catenin by PGE2-based activation of PKA have been implicated in Wnt signaling regulation in vitro. (vanillic acid increased the levels of phospho(ser9)-GSK3β, phospho(ser552)-β-catenin, and phospho(ser675)-β-catenin after 15-120 min) Fujino et al. used the transformed HEK293 cell line and showed that both PKA and PI3K could function downstream of PGE2 to phosphorylate GSK3β (Fujino et al., 2002). However, PGE1-induced activation of PKA and phosphorylation of β-catenin at S675 was cell-line dependent (Hino et al., 2005). While we found both phosphorylation events occur in the presence of PGE2 in vivo, it remains to be determined if phosphorylation of β-catenin and GSK3β each play a significant role in the regulation of wnt activity by PGE2 in HSCs, especially given a recently proposed functional redundancy of GSK3β with GSK3α (Doble et al., 2007).

PGE2 may have co-evolved with Wnt as a mechanism to rapidly upregulate cellular proliferation to foster organ repair. In this setting, PGE2 - which is produced locally in response to tissue damage - is required for and can enhance the proliferative effects initiated by wnt activitation.

Evolutionarily, what was greatly beneficial for wound healing – the coordinated pro-proliferative, anti-apoptotic effects of wnt and PGE2, may be detrimental in cases of chronic inflammation or constitutive pathway activation and lead to tumor initiation and growth.

All these are by the Vanillic Acid. Although, I couldn't find any other properties for Methyl Vanillate (MV) but I believe that since it is derived from Vanillic Acid, as en ester, probably it will act the same way. (Both Vanillic Acid and MV are pretty cheap)

So, If have understood correctly, these regulations of GSK3β and Cox-2, provided only positive effects rather than negative effects??

If you have some spare time, please elaborate and shed some light. Thank you very much all of you.
(Sorry if I have mistakes in my text).
 
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GRme11

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Anyone that could shed some light here and explain better or even correct me? Sorry for the bump. Thank you very much.
 

Ganked By DHT

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Anyone that could shed some light here and explain better or even correct me? Sorry for the bump. Thank you very much.
Lots of things can target Wnt/β‐catenin, secondly 6% increase is pretty bad, thirdly the study is on women.
 

GRme11

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Lots of things can target Wnt/β‐catenin, secondly 6% increase is pretty bad, thirdly the study is on women.
Thanks for responding back. Yes I know efficacy it's not very strong plus the study on women. However, could be one of the alternatives for the WNT-Beta Catenin pathway. My problem now is if I have understood correctly that this regulation of GSK3β is positive, along with regulation of Cox-2 (Probably the regulation of Cox-2 will lead to an increment of both PGD2 and PGE2, so I don't know if still this increment will bad or not, since PGE2 will go up as well- but this is reffering to Vanillic Acid. I can't find any other information for MV).
 
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RagnarLothbrok

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Hi pegasus2, very inspired by your thread thanks for everything!

I only have access to Latanaprost in my compounding pharmacy (price dropped a lot actually) and not Bimatoprost/similars like you using which require higher dosage.

Everyone quotes the same study ( https://pubmed.ncbi.nlm.nih.gov/21875758/ ) for 0.1% Latanaprost, but the study actually used ONE DROP (50 μL) in a microarea of the patients. They also concluded this is close to the maximum tolerated dosage.

The only one internet user I found who tried replicate the 0.1% study adding all over scalp and reported horrible throat inflammation sides and had to stop.

The lab says standard Latanaprost dose for eye/lashes regrowth is 0.005%. I apply 2ML all over scalp, so 2ML at 0.005% would be equivalent to 100μL at 0.1% (2 drops of study dosage).

TLDR: Is 2ML 0.005% Latanaprost going to work or it wont do sh*t? can anyone suggest a reasonable Latanaprost dosage to guarantee results but no crazy sides without blindly quoting the same study that only used 1 drop? Thanks!
 
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mj9

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Is oral minoxidil twice a day more effective than once a day?
I'm taking once a day atm
 

mj9

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Is the following Estriol cream effective or is it just a waste of time and money? It's difficult to get estriol in the UK.

Evalon Cream (Estriol) 15g/Tube 0.1%
 

Ganked By DHT

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Is the following Estriol cream effective or is it just a waste of time and money? It's difficult to get estriol in the UK.

Evalon Cream (Estriol) 15g/Tube 0.1%
Some people use that one, it would give you 150mg estriol which is alright but I dont know what youre paying for it
 

Ganked By DHT

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Thanks for responding back. Yes I know efficacy it's not very strong plus the study on women. However, could be one of the alternatives for the WNT-Beta Catenin pathway. My problem now is if I have understood correctly that this regulation of GSK3β is positive, along with regulation of Cox-2 (Probably the regulation of Cox-2 will lead to an increment of both PGD2 and PGE2, so I don't know if still this increment will bad or not, since PGE2 will go up as well- but this is reffering to Vanillic Acid. I can't find any other information for MV).
I dont know either, I will research it. Vanillic acid is found in highest amount of plants in Angelica Sinesis / Dong Quai which is kind of interesting.
 

mj9

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Some people use that one, it would give you 150mg estriol which is alright but I dont know what youre paying for it
It costs about £25. How are people applying it?
 

Ganked By DHT

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It costs about £25. How are people applying it?
Just putting on their scalp topically but the penetration is not that good. Some people would dermaroll straight after applying to increase. For it to be really effective prob. need higher dose that will cause gyno etc.

It would be a lot cheaper to buy estriol powder prob.
 

GRme11

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It costs about £25. How are people applying it?
I used custom made solution by crushing Estriol Pills into Ethanol/PPG/Water. I was using it for about 2-3 months. I started with 0.5mg/ml and then increase to 1mg/ml. I was applying it 4 times/week. Also, a friend of mine, tested my solution in a Chemistry Lab and we evaluated that the Estriol, indeed was in the mixture that I made (He couldn't check the concentration though). My before and after E3 level blood test was:
Before Starting: 0.1 ng/ml (Ref: 0.0-2.0).
After about 3 months since I started and before dropping it: 1.1 ng/ml.

So, as you can see with this carrier there is/was a systemic absorption (I believe that is a reasonable one). The problem is that I never knew exactly what concentration I was making, because I was crushing the pills. From a math perspective, I was making as I said, 1mg/ml but it could be easily a lower concentration because I didn't use the pure Estriol powder. You can give a try to the cream though and check by yourself. Thank you.
 
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Ganked By DHT

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I used custom made solution by crushing Estriol Pills into Ethanol/PPG/Water. I was using it for about 2-3 months. I started with 0.5mg/ml and then increase to 1mg/ml. I was applying it 4 times/week. Also, a friend of mine, tested my solution in a Chemistry Lab and we evaluated that the Estriol, indeed was in the mixture that I made (He couldn't check the concentration though). My before and after E3 level blood test was:
Before Starting: 0.1 ng/ml (Ref: 0.0-2.0).
After about 3 months since I started and before dropping it: 1.1 ng/ml.

So, as you can see with this carrier there is/was a systemic absorption (I believe that is a reasonable one). The problem is that I never knew exactly what concentration I was making, because I was crushing the pills. From a math perspective, I was making as I said, 1mg/ml but it could be easily a lower concentration because I didn't use the pure Estriol powder. You can give a try to the cream though and check by yourself. Thank you.
Your E3 level increased by more than 10 times? That is concerning. You didnt even use that high of a dose.
 

mj9

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I used custom made solution by crushing Estriol Pills into Ethanol/PPG/Water. I was using it for about 2-3 months. I started with 0.5mg/ml and then increase to 1mg/ml. I was applying it 4 times/week. Also, a friend of mine, tested my solution in a Chemistry Lab and we evaluated that the Estriol, indeed was in the mixture that I made (He couldn't check the concentration though). My before and after E3 level blood test was:
Before Starting: 0.1 ng/ml (Ref: 0.0-2.0).
After about 3 months since I started and before dropping it: 1.1 ng/ml.

So, as you can see with this carrier there is/was a systemic absorption (I believe that is a reasonable one). The problem is that I never knew exactly what concentration I was making, because I was crushing the pills. From a math perspective, I was making as I said, 1mg/ml but it could be easily a lower concentration because I didn't use the pure Estriol powder. You can give a try to the cream though and check by yourself. Thank you.
Can the estriol powder be added to a bottle of minoxidil solution? Also, is it worth cycling so you're not always walking around with high estrogen levels (so maybe 1 month on and 1 month off)? Will this be enough for hair growth and maintenance by finasteride/dutasteride?
Am I missing something?

I'm on oral min, topical min, finasteride, nizoral, castor oil. I really want to add estriol or something to boost growth on my crown area.

Oh and did you see any results with your 1mg/ml solution?
 

GRme11

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Your E3 level increased by more than 10 times? That is concerning. You didnt even use that high of a dose.
Well.. Blood tests can be vary sometimes. Also, hormones are having lot of fluctuations, but yeah, there was a systemic absorption, at least the blood test shows that. I forgot to mention that I was using 3ml/4 times a week. So, in total I was using 12mg of Estriol/week (from a math perspective as I said). I believe that this dosage it was reasonable for systemic absorption but yes, I agree with you, for such a dosage, x10 times greater it's something to take under consideration. I didn't notice something regarding side effects though. Thank you.
 
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GRme11

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Can the estriol powder be added to a bottle of minoxidil solution? Also, is it worth cycling so you're not always walking around with high estrogen levels (so maybe 1 month on and 1 month off)? Will this be enough for hair growth and maintenance by finasteride/dutasteride?
Am I missing something?

I'm on oral min, topical min, finasteride, nizoral, castor oil. I really want to add estriol or something to boost growth on my crown area.

Oh and did you see any results with your 1mg/ml solution?
I can't ensure you about the stability inside the Minoxidil. For example, it could degrade Minoxidil or vice versa. I believe is better to either invest into the cream or make a seperate solution, otherwise, you can try into Minoxidil and it will work, I just making some assumptions. Cycling is something that I always consider as well, specifically, that's why I was using it 4 times/week. Although, after some further research, since Estriol is a short-acting estrogen, I guess it will be better to use it daily.
("Previous research has suggested that shortacting estrogens would not be effectual or antagonistic if present in a continuous fashion which would result in constant or longterm occupancy of the estrogen receptor" --- When it is present in a continuous fashion, estriol acts as an estrogen--- 1) https://pubmed.ncbi.nlm.nih.gov/6356176/ --- 2) https://pubmed.ncbi.nlm.nih.gov/6202959). So, my 4 times/week could be easily not a proper way to use it for such dosage or at least for this potency (crushing the pills). About results, I noticed a small reduction in my shedding but I can't be one hundred percent sure, as I was using and completing my 1 year into Oral Finasteride and for this reason, I am unable to do a proper assessment. I was using 3ml/4 times a week, so in total:12mg/week. I stopped due to the lack of pure powder for preparation, and because suddenly, from early January (and so on), my hair started to feel weird but I don't believe Estriol is responsible for that, it could happen earlier for example, not so out of sudden, I could be wrong though. If I ever retry in the future, it will be with pure powder this time. Thank you.
 
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pegasus2

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Hi pegasus2, very inspired by your thread thanks for everything!

I only have access to Latanaprost in my compounding pharmacy (price dropped a lot actually) and not Bimatoprost/similars like you using which require higher dosage.

Everyone quotes the same study ( https://pubmed.ncbi.nlm.nih.gov/21875758/ ) for 0.1% Latanaprost, but the study actually used ONE DROP (50 μL) in a microarea of the patients. They also concluded this is close to the maximum tolerated dosage.

The only one internet user I found who tried replicate the 0.1% study adding all over scalp and reported horrible throat inflammation sides and had to stop.

The lab says standard Latanaprost dose for eye/lashes regrowth is 0.005%. I apply 2ML all over scalp, so 2ML at 0.005% would be equivalent to 100μL at 0.1% (2 drops of study dosage).

TLDR: Is 2ML 0.005% Latanaprost going to work or it wont do sh*t? can anyone suggest a reasonable Latanaprost dosage to guarantee results but no crazy sides without blindly quoting the same study that only used 1 drop? Thanks!
The concentration is what matters most not the volume. The volume just needs to be enough to saturate the follicle, whether it's one drop or a thousand drops, you're still getting a .1% concentration at the follicle. Bimatoprost sold as Latisse for eyelashes has a concentration of .03%, that's six times higher than latanoprost's eyelash solution. The minimum dosage Allergan used for bimatoprost in phase II for Androgenetic Alopecia is 1%. So that would be equivalent to .167% latanoprost if you go by their respective effective concentrations on eyelashes. So according to Allergan you should use at least .1% latanoprost for Androgenetic Alopecia, or are they also blindly quoting an irrelevant study?

The person you referred to is probably a hypochondriac experiencing nocebo, or he had something completely unrelated happen and blamed it on latanoprost out of fear.
 
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pegasus2

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Anyone that could shed some light here and explain better or even correct me? Sorry for the bump. Thank you very much.
Phosphorylation can either activate or inactivate a protein. In this case it inactivates GSK3b, so it promotes b-catenin, which is what activates the transcription factors that turn on proliferative genes in the HF.
Is the following Estriol cream effective or is it just a waste of time and money? It's difficult to get estriol in the UK.

Evalon Cream (Estriol) 15g/Tube 0.1%
The concentration is too low, but you can get some effect by using a lot of it twice a day. If using the raw powder it will easily mix with topical minoxidil at a concentration of 1%. Cycling it won't work because you have to be consistent, but you're unlikely to get any estrogenic side effects from that dose beyond better skin and mental concentration. Estradiol is the estrogen that causes feminization, estriol is very weak in that regard but good for hair.
 
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