Quantum Cat
Senior Member
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- 137
you mean nobody wants to market it as a male pattern baldness treatment, or the FDA doesn't think it's safe?
Free radical scavengers: the bane of PGE2 (read to get your hopes crushed)
- Thread starter beholder
- Start date
you mean nobody wants to market it as a male pattern baldness treatment, or the FDA doesn't think it's safe?
What I wanted to say above is that we need to literally rape our fcking skulls [to hyperproduce PGE2 and thus get lower PGD2, lower androgens, induce growth factors, etc etc]. Think about the worst fcking rape you ever saw on TV. The Irréversible (2002) class rape, allright? THAT is what we need to do to our damn skulls. Another poster (AnteUp) in another thread called it inducing cancer-like changes or something like that. I agree. There is no golden ratio for hair growth, no PG love waiting for you, hon. Just bloody a*** rape with a violent knock-out at the end waiting for the skull and its cells.
I am almost writing nonsense, I must stop already.
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both. It's really expensive and it's not a hairloss panacea. Hell, people got insomnia from this OCxxxxx stuff they used.
I am only interested in pretty much over-the-counter remedies which are readily available. I don't care for unreachable enzymes. I have my own success (albeit very short, crossing my fingers it works in long-term).
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Oh forgot to write people took it with luteolin [COXes blocker] and stuff like that.. they could have taken aspirin in the very same way with similar results IMO. And much much cheaper.
I am almost writing nonsense, I must stop already.
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both. It's really expensive and it's not a hairloss panacea. Hell, people got insomnia from this OCxxxxx stuff they used.
I am only interested in pretty much over-the-counter remedies which are readily available. I don't care for unreachable enzymes. I have my own success (albeit very short, crossing my fingers it works in long-term).
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Oh forgot to write people took it with luteolin [COXes blocker] and stuff like that.. they could have taken aspirin in the very same way with similar results IMO. And much much cheaper.
K
karankaran
Guest
Just to add, if this has already not been discussed:
MAP (Magnesium abscorbyl phosphate) has been used with MSM in one study and i guess i saw it mentioned in this thread or some other.
http://img.kisti.re.kr/soc_img/society/ksp/OOOMB4/2009/v17n3/OOOMB4_2009_v17n3_241.pdf
A lot of people use it for wrinkles or sun damage and so it can be easily (alright, relatively!) prepared because various reliable online retailers sell it. MAP is more stable than L-ascorbic acid but i am not sure if it will have the same effect on decreasing DKK-1 and increasing IGF-1 as L-ascorbic acid.
Second, Aspirin might not be good for those who have already problems such as hiatus hernia like I do. Among alternatives, as it is mentioned, luteolin is a cox-2 blocker and as it is also noted in this thread, some of these compounds also inhibit PGE2 and this is done by luteolin. But as this is already considered, i want to share my knowledge of luteolin. Luteolin bio-availability is on the low side. However, peanut hull extract can improve its bio-availability.
http://www.ncbi.nlm.nih.gov/pubmed/18052241
Peanut hull extract might be difficult to find and might only be available from vendors on Alibaba or something. It is 20$-100$ for a kg. One more benefit of luteolin is that it inhibits CD38 at "sufficient doses" and this has been shown to increase NAD+ -> something that is strongly anti-aging and it also reduces inflammation.
Just sharing my knowledge on supplements as i have researched on them a lot in peer reviewed scientific studies.
MAP (Magnesium abscorbyl phosphate) has been used with MSM in one study and i guess i saw it mentioned in this thread or some other.
http://img.kisti.re.kr/soc_img/society/ksp/OOOMB4/2009/v17n3/OOOMB4_2009_v17n3_241.pdf
A lot of people use it for wrinkles or sun damage and so it can be easily (alright, relatively!) prepared because various reliable online retailers sell it. MAP is more stable than L-ascorbic acid but i am not sure if it will have the same effect on decreasing DKK-1 and increasing IGF-1 as L-ascorbic acid.
Second, Aspirin might not be good for those who have already problems such as hiatus hernia like I do. Among alternatives, as it is mentioned, luteolin is a cox-2 blocker and as it is also noted in this thread, some of these compounds also inhibit PGE2 and this is done by luteolin. But as this is already considered, i want to share my knowledge of luteolin. Luteolin bio-availability is on the low side. However, peanut hull extract can improve its bio-availability.
http://www.ncbi.nlm.nih.gov/pubmed/18052241
Peanut hull extract might be difficult to find and might only be available from vendors on Alibaba or something. It is 20$-100$ for a kg. One more benefit of luteolin is that it inhibits CD38 at "sufficient doses" and this has been shown to increase NAD+ -> something that is strongly anti-aging and it also reduces inflammation.
Just sharing my knowledge on supplements as i have researched on them a lot in peer reviewed scientific studies.
Can you create a separate thread will all the directions and ingredients you would need to "rape your skull"? So what some of us try and maybe we can get something from it. I know there was a guy here long ago named Rambo and he had a huge stack of vitamins and topicals and had the most impressive growth I have ever seen.
- Reaction score
- 1,332
Neogenic is a prolyl-4-hydroxylase inhibitor. Hypoxia signalling is mediated by HIF-1A and this in turn is degraded by prolyl-4-hydroxylase-mediated hydroxylation. In short it induces hypoxia, so I wouldn't exactly call it a "oxidant". That said using it won't hurt you.
minoxiDjunkie
Established Member
- Reaction score
- 5
you know
if you have ever been to a real sedative state of mind (usually from drugs or deep deep sleep)
you would feel blood in your boody in places you never felt before.
your head will start to warm up and feet as well (for me i have cold feet and palm most of the time if im not doing something)
recently i started taking valium,
yesterday i went to sleep after a 5mg pill and a few weed bong hits, and thats exactly what happened -
hypoxia is a lack of oxigen in the blood right ?
well i almost stopped breathing completely, which made me really calm (and not afraid to die because of lack of oxi) and warm, and my head too,
i felt as if it was kind of a much better way to live,
at least during restings....
its something i think about for a while now -
we breath too much (hyperventilating) without even know that because of modern way of life and stress.
this may be a big cause for hair loss and inflammation and more - all in a single package.
i also have asthma if that means anything to you.
it always remind me one of the final scenes in the film - "I Legend"
good film about zombies with will smith (and i hate zombie movies more than everything, but thats a good one)
and in that scene you see him (will) try to sedate a zombie which all looks bald, pale and basically really ugly, but most of all - he breathes like a car engine in 5000RPM
if you have ever been to a real sedative state of mind (usually from drugs or deep deep sleep)
you would feel blood in your boody in places you never felt before.
your head will start to warm up and feet as well (for me i have cold feet and palm most of the time if im not doing something)
recently i started taking valium,
yesterday i went to sleep after a 5mg pill and a few weed bong hits, and thats exactly what happened -
hypoxia is a lack of oxigen in the blood right ?
well i almost stopped breathing completely, which made me really calm (and not afraid to die because of lack of oxi) and warm, and my head too,
i felt as if it was kind of a much better way to live,
at least during restings....
its something i think about for a while now -
we breath too much (hyperventilating) without even know that because of modern way of life and stress.
this may be a big cause for hair loss and inflammation and more - all in a single package.
i also have asthma if that means anything to you.
it always remind me one of the final scenes in the film - "I Legend"
good film about zombies with will smith (and i hate zombie movies more than everything, but thats a good one)
and in that scene you see him (will) try to sedate a zombie which all looks bald, pale and basically really ugly, but most of all - he breathes like a car engine in 5000RPM
Thanks for the reply, Swoop.
And thank you for this amazing amazing compilation, Beholder. Please keep the info coming. I'm updating my regimen based on your sharings.
I will incorporate Vitamin C and Vitamin E topically and orally as those are the ingredients you mentioned to both inhibit PGD2 and promote PGE2.
Any information about:
-JAK, WNT?
-Brevilin A (Litsea Glutinosa)
-Beta Glucan (It is supposed to promote macrophages)
Thank you again
And thank you for this amazing amazing compilation, Beholder. Please keep the info coming. I'm updating my regimen based on your sharings.
I will incorporate Vitamin C and Vitamin E topically and orally as those are the ingredients you mentioned to both inhibit PGD2 and promote PGE2.
Any information about:
-JAK, WNT?
-Brevilin A (Litsea Glutinosa)
-Beta Glucan (It is supposed to promote macrophages)
Thank you again
Sure, thanks man.
As for information on those other things, I have only this: this thread is not about them. I will research them a bit soon, may post findings later.
Hairismylife
Established Member
- Reaction score
- 77
I agree, please create a new thread and I will follow that for trial. Thanks Beholder!
HairShocka
Member
- Reaction score
- 1
Regarding inhibited both COX-1 and COX-2 I found this:
Therefore, we obtained blood samples before and after 5 days administration of 200 mg Pycnogenol to five healthy humans. The plasma moderately inhibited both COX-1 and COX-2 activities ex vivo. In a second approach, 10 volunteers received a single dose of 300 mg Pycnogenol. Only 30 min after ingestion of the pine bark extract the serum samples induced a statistically significant increase in the inhibition of both COX-1 (P < 0.02) and COX-2 (P < 0.002). This suggests a strikingly rapid bioavailability of bioeffective compounds after oral intake of the extract.
http://www.ncbi.nlm.nih.gov/pubmed/16330178
Would this fit somewhere in your research beholder?
Therefore, we obtained blood samples before and after 5 days administration of 200 mg Pycnogenol to five healthy humans. The plasma moderately inhibited both COX-1 and COX-2 activities ex vivo. In a second approach, 10 volunteers received a single dose of 300 mg Pycnogenol. Only 30 min after ingestion of the pine bark extract the serum samples induced a statistically significant increase in the inhibition of both COX-1 (P < 0.02) and COX-2 (P < 0.002). This suggests a strikingly rapid bioavailability of bioeffective compounds after oral intake of the extract.
http://www.ncbi.nlm.nih.gov/pubmed/16330178
Would this fit somewhere in your research beholder?
Not really. COX inhibitors are common drugs (NSAIDs) and work quite well. However they all may work in one specific way, so any other compound - like the ones I listed in the 1st post - is welcome. Or not, depending on the angle you approach hairloss-hairgrowth problem.
I am now more interested in what could get PGE2 up and/or PGD2 down (without taking out PGE2). Once we figure this out -- and I do feel I am on the right way -- then we're pretty much half-way there, I believe.
I am now more interested in what could get PGE2 up and/or PGD2 down (without taking out PGE2). Once we figure this out -- and I do feel I am on the right way -- then we're pretty much half-way there, I believe.
jimmyhairte
New Member
- Reaction score
- 8
Well OC blocks PGD2 receptors:
http://www.atopixtherapeutics.co.uk/04_03_oc459.html
http://www.thekaneshop.com/index.php/oc000459-ethanol-1g.html
There are some reports over on HLH saying it at least stopped their shedding quite abruptly. No / very little regrowth though.
And one possible explanation for why minoxidil works might be an increase in PGE2 production:
http://www.ncbi.nlm.nih.gov/pubmed/9008235
Add some DHT inhibition or receptor blocking to the mix, some dermarolling for WIHN. Theoretically that should be it but I'm pretty sure it isn't.
HairShocka
Member
- Reaction score
- 1
Posting a link from a different forum. I felt they may be relevant to your research but what they're talking about is way over my head.
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http://www.hairlosshelp.com/forums/messageview.cfm?catid=7&threadid=103917
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http://www.hairlosshelp.com/forums/messageview.cfm?catid=7&threadid=103917
Attachments
Yep, that pic is what I was talking about.
Thanks for the HLH thread, already started reading it.
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As I have written before, an awesome thread! What I got from it is this, now get this guys:
http://www.ncbi.nlm.nih.gov/pubmed/21034532
Those Koreans should get an applause. So now I have some more proof that ascorbic acid (one of its metabolites is the L-threonate) MAY actually be one of the keys opening the door. One guy from that thread even tried the threonate on himself however he probably didn't get high enough concentration for it to penetrate dermis. Ascorbic acid may need pH below 3.5 to be useful topically (which is very acidic/sour, I tried, think vinegar), according to http://www.nordicselfcare.com/pdf/1.09_percutaneousabsorption.pdf
Thanks for the HLH thread, already started reading it.
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As I have written before, an awesome thread! What I got from it is this, now get this guys:
http://www.ncbi.nlm.nih.gov/pubmed/21034532
Those Koreans should get an applause. So now I have some more proof that ascorbic acid (one of its metabolites is the L-threonate) MAY actually be one of the keys opening the door. One guy from that thread even tried the threonate on himself however he probably didn't get high enough concentration for it to penetrate dermis. Ascorbic acid may need pH below 3.5 to be useful topically (which is very acidic/sour, I tried, think vinegar), according to http://www.nordicselfcare.com/pdf/1.09_percutaneousabsorption.pdf
HairShocka
Member
- Reaction score
- 1
Why exactly is L-threonate special compared to L-ascorbic? From what I could learn, it sounds like a fancy type of Magnesium that crosses the bbb and the effect is the same effect of repressing DHT-induced DKK-1 expression in dermal papilla cells.
It's pretty expensive stuff, but is this something you would personally add to the ascobic acid, MSM solution you use?
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Wait a sec, the stuff talked about in the study is L-ascorbic acid 2-phosphate is not plain L-ascorbic acid. http://www.ncbi.nlm.nih.gov/pubmed/2910890
According to this page: http://examine.com/supplements/L-Threonate/
L-Threonate is a deriviative of L-ascorbic acid 2-phosphate (which in and of itself is a derivative of Ascorbic Acid, otherwise known as Vitamin C).
L-threonate is able to repress the expression of a gene known as dickkopf-1 (DKK-1) which is upregualted by Dihydrotestosterone (DHT) in male pattern baldness when co-cultured.[1] It seems to work similarily to L-ascorbic acid 2-phosphate via alkaline phosphatase activity and releasing ascorbic acid into the cell.[2][3]
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So do you think we're covered by using high concentration of ascorbic crystals, or do you think L-Threonate/L-ascorbic acid 2-phosphate has its own unique strengths and is better?
It's pretty expensive stuff, but is this something you would personally add to the ascobic acid, MSM solution you use?
-----
Wait a sec, the stuff talked about in the study is L-ascorbic acid 2-phosphate is not plain L-ascorbic acid. http://www.ncbi.nlm.nih.gov/pubmed/2910890
According to this page: http://examine.com/supplements/L-Threonate/
L-Threonate is a deriviative of L-ascorbic acid 2-phosphate (which in and of itself is a derivative of Ascorbic Acid, otherwise known as Vitamin C).
L-threonate is able to repress the expression of a gene known as dickkopf-1 (DKK-1) which is upregualted by Dihydrotestosterone (DHT) in male pattern baldness when co-cultured.[1] It seems to work similarily to L-ascorbic acid 2-phosphate via alkaline phosphatase activity and releasing ascorbic acid into the cell.[2][3]
-------
So do you think we're covered by using high concentration of ascorbic crystals, or do you think L-Threonate/L-ascorbic acid 2-phosphate has its own unique strengths and is better?
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HairShocka
Member
- Reaction score
- 1
Some things on melatonin I found, which I think backs up your recommendation to put in with Ascorbic/MSM solution for topical use. Sounds like it's good for halting hairloss which is my goal. What do you think?
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In the search for alternative agents to oral finasteride and topical minoxidil for the treatment of androgenetic alopecia (Androgenetic Alopecia), melatonin, a potent antioxidant and growth modulator, was identified as a promising candidate based on in vitro and in vivo studies.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3681103/
Using a digital software-supported epiluminescence technique (TrichoScan) in 35 men with Androgenetic Alopecia, after 3 and 6 months in 54.8% to 58.1% of the patients a significant increase of hair density of 29% and 41%, respectively was measured (M0: 123/cm2; M3: 159/cm2; M6: 173/cm2
(P < 0,001). (4) In 60 men and women with hair loss, a significant reduction in hair loss was observed in women, while hair loss in men remained constant (P < 0.001). (5) In a large, 3-month, multi-center study with more than 1800 volunteers at 200 centers, the percentage of patients with a 2- to 3-fold positive hair-pull test decreased from 61.6% to 7.8%, while the percentage of patients with a negative hair-pull test increased from 12.2.% to 61.5% (P < 0.001). In addition, a decrease in seborrhea and seborrheic dermatitis of the scalp was observed.
Based on the positive effects of melatonin on hair growth, ASATONA AG (Zug, Switzerland) developed a topically applied cosmetic hair solution with a melatonin content of 0.0033%, which was intended to slow the hair's aging process and be used as an adjuvant treatment for Androgenetic Alopecia.
In order to provide a reliable, technically and methodologically objective assessment of the therapeutic benefits of the cosmetic melatonin solution a further open-label, clinically controlled study was carried out based on the TrichoScan method to determine the efficacy and tolerability of the melatonin hair solution, which was applied to the scalp each night by 35 men (aged 18-41 years) with Stage I or II Androgenetic Alopecia (Hamilton/Norwood scale) for a period of 6 months.[39] The study was carried out from April 2004 to April 2005 at the Instituto Dermatologico Europeo (European Dermatological Institute) (IDE) in Milan, Italy following review and approval by the corresponding Ethics Committee in accordance with GCP. Prior to participating in the study the patients signed a written informed consent form. TrichoScan is a digital software-supported epiluminescence technique for measuring hair count (number of hairs/0.7cm2), hair density (number of hairs/cm2), hair diameter, anagen/telogen ratio, and vellus hair/terminal hair ratio.[40,41] The results of this study showed an increase in the hair count (number of hairs/0.7cm2) in 54.8% of participants after 3 and 6 months, respectively, and improved hair density (number of hairs/cm2) in 54.8% and 58.1% of participants after 3 and 6 months, respectively.
The increase in the hair count was 29.2% (3 months vs. 0 month) and 42.7% (6 months vs. 0 month); both values were statistically significant (P < 0.001) (Month 0: 85.76 ± 27.0; Month 3: 110.82 ± 31.7; Month 6: 122.35 + 40.5). In the case of hair density an increase of 29.1% and 40.9% was determined after 3 and 6 months, respectively (Month 0: 123.15 ± 39.0; Month 3: 159.03 ± 46.8; Month 6: 173.56 ± 58). The differences among the hair density values were also significant (P < 0.001).
Objective assessment of treatment with the cosmetic melatonin solution by the medical investigator at each visit found improved hair loss in 26.6% (Day 30), 48.2% (Day 90) and 32.1% (Day 180) of patients, whereby the proportion of patients showing improvement was greatest after 90 days and even included a small group of patients with new hair growth. In addition, the proportion of patients exhibiting no change in hair loss during the period from Day 30 to Day 90 decreased from about 73.3% to 48.2% and this value was maintained through Day 180. Hair loss continued in 3.4% of patients (at 90 days) and in 19.3% (at 180 days)
Receptor-mediated melatonin effects are theoretically possible because the MT1 membrane receptor has been detected in both human hair follicle keratinocytes and fibroblasts of the dermal hair papillae by means of Real Time Polymerase Chain Reaction (RT-PCR)[30] as well as in situ in the human scalp at the center of the outer and inner root sheath of the hair follicle.[28] An aberrant form of the MT2 membrane receptor has also been detected in human fibroblasts of the dermal hair papillae.[30] A specific, hair cycle-dependent expression of MT2 in the skin has been demonstrated in the C57BL/6 mouse model.[34] Thus, this receptor could have a functional influence on the hair cycle if the knowledge gained from the mouse model can be applied to humans. To date only weak expression of MT2 in the human hair follicle has been detected in the inner root sheath using immunohistochemical techniques.[28] While individual human skin cells (keratinocytes, melanocytes, fibroblasts) contain the MT3 receptor or NQO2, it has not been detected to date in individual hair follicle cells or in situ in the hair follicle.[27] MT3/NQO2 could play a role in the prevention of oxidative stress in HF catagen regression or in oxidative stress-induced hair aging.[12] The nuclear melatonin receptor RORα performs a biological function in hair growth because RORα-knock-out mice had significantly thinner coats.[33] Hair cycle-dependent regulation of the nuclear receptor in the inner and outer root sheath was also able to be identified in C57BL/6 mice.[34] The melatonin receptors identified to date are all in the root sheath of the hair, which assists in the regulation of hair growth in addition to mechanically stabilizing the hair shaft. Thus, it can be inferred that the growth-promoting properties of melatonin are at least partially regulated by its receptors in the root sheath of the hair.
The effect of melatonin on hair growth may also be mediated by interaction with androgens and estrogens as well as their receptors, as evidenced by the antiandrogenic effect of melatonin on benign prostate cells.[50] While the antiandrogenic effect on prostate cells is accompanied by an inhibition of proliferation, antiandrogenic effects on hair follicles include prolongation of the hair cycle and decreased miniaturization.[2] Human benign prostate cells and human skin express functionally active melatonin receptors (MT1),[30,51] making it possible to also assume a melatonin receptor-mediated, antiandrogenic effect in the skin and hair follicles.
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Hey. I've been reading a lot. Learned a lot but also confused a lot.
Should we be focusing on decreasing PGD2, leaving PGE2 alone, and increasing PGE1??
DGLA (Dihomo-γ-linolenic acid) is the immediate precursor of PGE1. (Prostaglandin E1). PGE1 counteracts PGE2 as well. Also, Cox-1 is needed for the production of PGE1.
This is all stuff I'm getting from Squegee's posts.
You should read this as well: http://www.hindawi.com/journals/jar/2012/121390/#B145
In healthy endothelium, these vasodilators and vasoconstrictors, coexisting with other vasoactive factors, are held in balance to maintain normal vascular functions. The aging process shifts this balanced profile toward a proconstrictive mediator profile [76, 77].
------
In the search for alternative agents to oral finasteride and topical minoxidil for the treatment of androgenetic alopecia (Androgenetic Alopecia), melatonin, a potent antioxidant and growth modulator, was identified as a promising candidate based on in vitro and in vivo studies.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3681103/
Using a digital software-supported epiluminescence technique (TrichoScan) in 35 men with Androgenetic Alopecia, after 3 and 6 months in 54.8% to 58.1% of the patients a significant increase of hair density of 29% and 41%, respectively was measured (M0: 123/cm2; M3: 159/cm2; M6: 173/cm2
(P < 0,001). (4) In 60 men and women with hair loss, a significant reduction in hair loss was observed in women, while hair loss in men remained constant (P < 0.001). (5) In a large, 3-month, multi-center study with more than 1800 volunteers at 200 centers, the percentage of patients with a 2- to 3-fold positive hair-pull test decreased from 61.6% to 7.8%, while the percentage of patients with a negative hair-pull test increased from 12.2.% to 61.5% (P < 0.001). In addition, a decrease in seborrhea and seborrheic dermatitis of the scalp was observed.Based on the positive effects of melatonin on hair growth, ASATONA AG (Zug, Switzerland) developed a topically applied cosmetic hair solution with a melatonin content of 0.0033%, which was intended to slow the hair's aging process and be used as an adjuvant treatment for Androgenetic Alopecia.
In order to provide a reliable, technically and methodologically objective assessment of the therapeutic benefits of the cosmetic melatonin solution a further open-label, clinically controlled study was carried out based on the TrichoScan method to determine the efficacy and tolerability of the melatonin hair solution, which was applied to the scalp each night by 35 men (aged 18-41 years) with Stage I or II Androgenetic Alopecia (Hamilton/Norwood scale) for a period of 6 months.[39] The study was carried out from April 2004 to April 2005 at the Instituto Dermatologico Europeo (European Dermatological Institute) (IDE) in Milan, Italy following review and approval by the corresponding Ethics Committee in accordance with GCP. Prior to participating in the study the patients signed a written informed consent form. TrichoScan is a digital software-supported epiluminescence technique for measuring hair count (number of hairs/0.7cm2), hair density (number of hairs/cm2), hair diameter, anagen/telogen ratio, and vellus hair/terminal hair ratio.[40,41] The results of this study showed an increase in the hair count (number of hairs/0.7cm2) in 54.8% of participants after 3 and 6 months, respectively, and improved hair density (number of hairs/cm2) in 54.8% and 58.1% of participants after 3 and 6 months, respectively.
The increase in the hair count was 29.2% (3 months vs. 0 month) and 42.7% (6 months vs. 0 month); both values were statistically significant (P < 0.001) (Month 0: 85.76 ± 27.0; Month 3: 110.82 ± 31.7; Month 6: 122.35 + 40.5). In the case of hair density an increase of 29.1% and 40.9% was determined after 3 and 6 months, respectively (Month 0: 123.15 ± 39.0; Month 3: 159.03 ± 46.8; Month 6: 173.56 ± 58). The differences among the hair density values were also significant (P < 0.001).
Objective assessment of treatment with the cosmetic melatonin solution by the medical investigator at each visit found improved hair loss in 26.6% (Day 30), 48.2% (Day 90) and 32.1% (Day 180) of patients, whereby the proportion of patients showing improvement was greatest after 90 days and even included a small group of patients with new hair growth. In addition, the proportion of patients exhibiting no change in hair loss during the period from Day 30 to Day 90 decreased from about 73.3% to 48.2% and this value was maintained through Day 180. Hair loss continued in 3.4% of patients (at 90 days) and in 19.3% (at 180 days)
Receptor-mediated melatonin effects are theoretically possible because the MT1 membrane receptor has been detected in both human hair follicle keratinocytes and fibroblasts of the dermal hair papillae by means of Real Time Polymerase Chain Reaction (RT-PCR)[30] as well as in situ in the human scalp at the center of the outer and inner root sheath of the hair follicle.[28] An aberrant form of the MT2 membrane receptor has also been detected in human fibroblasts of the dermal hair papillae.[30] A specific, hair cycle-dependent expression of MT2 in the skin has been demonstrated in the C57BL/6 mouse model.[34] Thus, this receptor could have a functional influence on the hair cycle if the knowledge gained from the mouse model can be applied to humans. To date only weak expression of MT2 in the human hair follicle has been detected in the inner root sheath using immunohistochemical techniques.[28] While individual human skin cells (keratinocytes, melanocytes, fibroblasts) contain the MT3 receptor or NQO2, it has not been detected to date in individual hair follicle cells or in situ in the hair follicle.[27] MT3/NQO2 could play a role in the prevention of oxidative stress in HF catagen regression or in oxidative stress-induced hair aging.[12] The nuclear melatonin receptor RORα performs a biological function in hair growth because RORα-knock-out mice had significantly thinner coats.[33] Hair cycle-dependent regulation of the nuclear receptor in the inner and outer root sheath was also able to be identified in C57BL/6 mice.[34] The melatonin receptors identified to date are all in the root sheath of the hair, which assists in the regulation of hair growth in addition to mechanically stabilizing the hair shaft. Thus, it can be inferred that the growth-promoting properties of melatonin are at least partially regulated by its receptors in the root sheath of the hair.
The effect of melatonin on hair growth may also be mediated by interaction with androgens and estrogens as well as their receptors, as evidenced by the antiandrogenic effect of melatonin on benign prostate cells.[50] While the antiandrogenic effect on prostate cells is accompanied by an inhibition of proliferation, antiandrogenic effects on hair follicles include prolongation of the hair cycle and decreased miniaturization.[2] Human benign prostate cells and human skin express functionally active melatonin receptors (MT1),[30,51] making it possible to also assume a melatonin receptor-mediated, antiandrogenic effect in the skin and hair follicles.
- - - Updated - - -
Hey. I've been reading a lot. Learned a lot but also confused a lot.
Should we be focusing on decreasing PGD2, leaving PGE2 alone, and increasing PGE1??
DGLA (Dihomo-γ-linolenic acid) is the immediate precursor of PGE1. (Prostaglandin E1). PGE1 counteracts PGE2 as well. Also, Cox-1 is needed for the production of PGE1.
This is all stuff I'm getting from Squegee's posts.
You should read this as well: http://www.hindawi.com/journals/jar/2012/121390/#B145
In healthy endothelium, these vasodilators and vasoconstrictors, coexisting with other vasoactive factors, are held in balance to maintain normal vascular functions. The aging process shifts this balanced profile toward a proconstrictive mediator profile [76, 77].
Hey beholder, I'm doing some of the same research that you have done and coming to the same conclusions unfortunately. It's been awhile since you wrote this and now we have the Proastgladin protocol by swiss with sulfasalazine or setipripant and topical PGE2, but I'm looking for a way to accomplish the same protocol without the expensive/prescription drugs that are hard to obtain.
I'm contemplating doing the same thing you suggested - taking COX inhibitors with growth stimulants. For the last six months I took curcumin, resveratrol, and minoxidil and had epic regrowth. I'm about to start this protocol again and see what happens but add oral castor oil for PGE2.
I'm contemplating doing the same thing you suggested - taking COX inhibitors with growth stimulants. For the last six months I took curcumin, resveratrol, and minoxidil and had epic regrowth. I'm about to start this protocol again and see what happens but add oral castor oil for PGE2.
I.D WALKER
Senior Member
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Good luck with your resolve plans Yum.
If you could add pics with periodic updates that would be extra-appreciated.
Thanks.
If you could add pics with periodic updates that would be extra-appreciated.
Thanks.
There's a very high chance that you would have had similar hair growth by just using minoxidil. Curcumin actually increases TRPV1 pathway, making the scalp more prone to inflammation. Also, curcumin inhibits phase 1 detoxification pathway in the liver. I have no doubt in my mind that high dose of curcumin is harmful for the body.
I am totally baffled by the dumb comments on this thread. When someone takes time to research and post a thread in a concise format, read the damn content.
I really appreciated the thread Beholder. Thanks.