Newly Discovered Factor in Androgenetic Alopecia. The Cure is Near?

[rubend]

Hello there. Long time without posting here but today I read this entire thread and worth a short post at least.

This is a very interesting breakthrough and it's nice to keep discussing this subject. My question is... does someone tried something with this and actually had any result? Is there any real application that we could try without being too much dangerous?

 

[Agahi]

Ive been trying the cetirizine thing for a bit over a month now. Seems to be helping a bit, but who knows considering ive been on minoxidil for like 6 years, and finasteride about a year now.

 

[baldnesssadness]

its now been 10 days since i started with cetirizine 30 mg daily, and when i showered this morning i shed much... my temples have even reeceeded further, and it depresses me so much yet my itching and scalp problems are gone, the hair loss... continues its maybe too early to panic now .I will atleast used it a month before i consider it but shedding early like this is it a good sign does it mean that this works? because i shed a lot more than before , i also used together with propecia which i have used for some weeks maybe it was the propecia that cause the shedding? i quit that and right now im only gonna use cetirizine for a month from today. So boldy have gotten what u ordered?

 

[burns_15]

i quit that and right now im only gonna use cetirizine for a month from today. So boldy have gotten what u ordered?

I wouldn't quit it because if your hair continues to fall out, you won't know if it's from Ceterezine or because you quit propecia.

 

[rbr]

im trying to understand from this study if TM30089 is better than Ramatroban. I get the feeling that it has a longer lasting effect at blocking PGD2 at the DP2 receptor but im no expert so cant be sure. if anyone has time to read it i would appreciate your feedback

http://molpharm.aspetjournals.org/content/69/4/1441.full.pdf

 

[frankierl77]

Washington: Researchers have discovered an abnormal amount of a protein called Prostaglandin D2 in the bald scalp of men with male pattern baldness.

The discovery by researchers at Perelman School of Medicine at the University of Pennsylvania may lead directly to new treatments for the most common cause of hair loss in men.

In both human and animal models, researchers found that a prostaglandin known as PGD2 and its derivative, 15-dPGJ2, inhibit hair growth.

The PGD2-related inhibition occurred through a receptor called GPR44, which is a promising therapeutic target for androgenetic alopecia in both men and women with hair loss and thinning.

Male pattern baldness strikes 8 of 10 men under 70 years old, and causes hair follicles to shrink and produce microscopic hairs, which grow for a shorter duration of time than normal follicles.

Researchers took an unbiased approach when scanning for potential biological causes of baldness, looking in scalp tissue from balding and non-bald spots from men with male pattern baldness and then corroborating findings in mouse models.

They found that levels of PGD2 were elevated in bald scalp tissue at levels 3 times greater than what was found in comparative haired scalp of men with androgenetic alopecia.

When PGD2 was added to cultured hair follicles, PGD2-treated hair was significantly shortly, while PGD2``s derivative, 15-dPGJ2, completely inhibited hair growth.

“Although a different prostaglandin was known to increase hair growth, our findings were unexpected, as prostaglandins haven`t been thought about in relation to hair loss, yet it made sense that there was an inhibitor of hair growth, based on our earlier work looking at hair follicle stem cells,â€￾ said George Cotsarelis, MD, chair and professor of Dermatology, and senior author on the studies.

In a Penn study published last year, underlying hair follicle stem cells were found intact, suggesting that the scalp was lacking an activator or something was inhibiting hair follicle growth.

Prostaglandins are well characterized for their role in many bodily functions – controlling cell growth, constricting and dilating smooth muscle tissue – and a different prostaglandin (F2alpha) is known to increase hair growth.

Researchers found that as PGD2 inhibits hair growth, other prostaglandins work in opposition, enhancing and regulating the speed of hair growth.

While these studies looked at Androgenetic Alopecia in men, the researchers noted that prostaglandins may represent a common pathway shared by both men and women with Androgenetic Alopecia.

Future studies, potentially testing topical treatments that may target GPR44, can determine whether targeting prostaglandins will benefit woman with Androgenetic Alopecia as well.

The study has been published in Science Translational Medicine.

http://stm.sciencemag.org/content/4/126/126ra34

Yes, And the heavens will Part the ocean, Send down an alien with Thick head of hair, And grant All bald people their hair back..... Or how about this, "...scientists have now determined that if you wear a blue shirt on a monday, your hair will thicken." or, Researchers at MSU have found a link between extremly skilled or talented individuals and early onset of MPbaldness during teens." Mostly trivial, Any hope your looking at Is hope you can waste your money on a Different potentially harmful product.

 

[HairOutTheWazoo]

Yes, And the heavens will Part the ocean, Send down an alien with Thick head of hair, And grant All bald people their hair back..... Or how about this, "...scientists have now determined that if you wear a blue shirt on a monday, your hair will thicken." or, Researchers at MSU have found a link between extremly skilled or talented individuals and early onset of MPbaldness during teens." Mostly trivial, Any hope your looking at Is hope you can waste your money on a Different potentially harmful product.

Wow get a grip. I guess science isn't your thing. Preposterous analogies by the way.

 

[WarLord]

male pattern baldness is a result of inflammation that just getting worst with time and minoxidil cannot keep up..

People, where do you take this bullsh*t? There are people, who have been on minoxidil for 2 decades! I guess you are another of the whining losers, who did nothing for several years, and after they see their balding vertex, they eventually start to do something and expect miracles.

 

[squeegee]

People, where do you take this bullsh*t? There are people, who have been on minoxidil for 2 decades! I guess you are another of the whining losers, who did nothing for several years, and after they see their balding vertex, they eventually start to do something and expect miracles.

Do you have something to back up your claims? **** no.. the usual hater, looser on here.....Another bitching member that just surfaced overhere.. Why don`t you start reading the mother****ing threads first? For you ****ing info..I have been on experimental treatments for over 10 years and I am not ****ing bald. Why don`t you stay as a lurker... don`t need miserable pos on here polluting this thread . Read the last ****ing sentence miserable POS.

[h=1]Effect of minoxidil on platelet function and the synthesis of prostaglandins in platelets.[/h]O'Barr TP, Swanson EW, Fitzpatrick JE, Corby DG.
[h=3]Source[/h]Department of Clinical Investigation, Fitzsimons Army Medical Center.

[h=3]Abstract[/h]At the 12.5 micrograms level, minoxidil prevents the irreversible aggregation of platelets by 2 x 10(-6) mol/L adenosine diphosphate (ADP). Levels of minoxidil greater than 12.5 micrograms cause a reversal of primary aggregation by 2 x 10(-6) mol/L ADP. Aggregation of platelets in response to 125 micrograms of arachidonic acid is measurably reduced by 12.5 micrograms of minoxidil and totally suppressed by 30 micrograms. Concurrent with the inhibition of platelet aggregation, increasing concentrations of minoxidil cause a gradual reduction in the synthesis of prostaglandin E2 (PGE2) and thromboxane B2 (TxB2). In the presence of 100 micrograms of minoxidil, PGE2 is reduced from a control value of 87.7 +/- 2.2 pg/ml to 23.9 +/- 3.2 pg/ml. At this level of minoxidil, TxB2 drops from 105 +/- 3.3 ng/ml to 10.5 +/- 2.6 ng/ml. The effect of minoxidil on platelet aggregation is not associated with increased cyclic adenosine monophosphate synthesis. All data support the conclusion that minoxidil functions (in platelet metabolism) primarily as a cyclooxygenase inhibitor.

 

[Quadzilla99]

crucify em squeegee! send his *** directly to the tree of woe!

 

[rjmogka]

hahaha squeeqe I love your style.

 

[Sparky4444]

So what the hell is up with that??? I had a post edited by the Admin that was no way nears as bad as Warlords -- but no slap on the wrists for him??? Don't tell this forum is one of those -- like Gearslutz...cripes

 

[zeroes]

Guys let's all play nice.

I'm on my phone right now so I can't mod properly right now.

 

[odalbak]

"increasing concentrations of minoxidil cause a gradual reduction in the synthesis of prostaglandin E2 (PGE2)"

But I thought PGE2 was supposed to be beneficial and that minoxidil promoted it? Why is minoxidil helpful then?

"Supplemental PGE2 could be therapeutic. By correcting its deficiency and increasing its level in bald scalp, the inhibitory effects of PGD2 may be overcome." (Cotzarelis, 2012)

 

[squeegee]

Ok.. for the people inquiring about anybody on here trying new treatments reference this thread and the latest discovery.. I've been proactive as usual.. so went back on Minoxidil 5% from kirkland..the best on the market.. taking it with Miconazole Nitrate 2%. Also taking it with Diclofenac diethylamine (Voltaren gel). At night I put Ibuprofen gel capsule with naxopren sodium (aleve liquid gels) mixed aloe vera gel.. I always try to add some copper peptide as well. All this reduce both isoform of Cox in the skin so lowering PGD2.. Ibuprofen stay in the the dermis for few days days after application..so really cheap and effective. The goal is to reduces inflammation , INOS and ROS to the maximum. The skin on your body cycle every month.. but everything stops when chronic inflammation happened. this is why you hair cycle goes to ****. Just went to a crazy shed with this..but recovering very fast! Don't be shy if you have any questions... All this are otc stuff.. reduces Cox levels to the maximum, boost the good isoform of nitric oxide (enos) so the stem cell can start to migrate and **** goes back as per normal... The overdose of PGD2 on our scalps says it all. The main problem in hair loss is inflammation.
- - - Updated - - -

Odalbak..All prostaglandins can be pro-inflammatory because they all have vasodilation properties..this is why it is so complicated..Minoxidil is good because it inhibits Cox levels and boost the Enos.. the good nitric oxide isoform that contributes to the migration of stem cell.. INOS is the bad kind...

 

[WarLord]

Do you have something to back up your claims? **** no.. the usual hater, looser on here.....Another bitching member that just surfaced overhere.. Why don`t you start reading the mother****ing threads first? For you ****ing info..I have been on experimental treatments for over 10 years and I am not ****ing bald. Why don`t you stay as a lurker... don`t need miserable pos on here polluting this thread . Read the last ****ing sentence miserable POS.

Effect of minoxidil on platelet function and the synthesis of prostaglandins in platelets.

O'Barr TP, Swanson EW, Fitzpatrick JE, Corby DG.
Source

Department of Clinical Investigation, Fitzsimons Army Medical Center.

Abstract

At the 12.5 micrograms level, minoxidil prevents the irreversible aggregation of platelets by 2 x 10(-6) mol/L adenosine diphosphate (ADP). Levels of minoxidil greater than 12.5 micrograms cause a reversal of primary aggregation by 2 x 10(-6) mol/L ADP. Aggregation of platelets in response to 125 micrograms of arachidonic acid is measurably reduced by 12.5 micrograms of minoxidil and totally suppressed by 30 micrograms. Concurrent with the inhibition of platelet aggregation, increasing concentrations of minoxidil cause a gradual reduction in the synthesis of prostaglandin E2 (PGE2) and thromboxane B2 (TxB2). In the presence of 100 micrograms of minoxidil, PGE2 is reduced from a control value of 87.7 +/- 2.2 pg/ml to 23.9 +/- 3.2 pg/ml. At this level of minoxidil, TxB2 drops from 105 +/- 3.3 ng/ml to 10.5 +/- 2.6 ng/ml. The effect of minoxidil on platelet aggregation is not associated with increased cyclic adenosine monophosphate synthesis. All data support the conclusion that minoxidil functions (in platelet metabolism) primarily as a cyclooxygenase inhibitor.

First of all, I am irritated by people, who pollute the internet with unfounded mystifications inspired by their own failure. "finasteride buys you 4-6 years", "Minoxidil works for 16 weeks and then you will start to lose your hair like before". LOL

I started with minoxidil in 1997 and I have kept all my Norwood2 hair. I have never thought that it should stop working - until I started to visit these internet latrines full of misinformation and negativism.

 

[Jacob]

Speaking of inflammation..and I know there are tons of things out there for that... http://www.phytosomes.info/public/18beta_glycyrrhetinic_acid_phytosome.asp

Anti-inflammatory activity

18ß-Glycyrrhetinic Acid Phytosome[SUP]®[/SUP] was tested for its ability to reduce inflammation cellular response[SUP]([/SUP][SUP]2[/SUP][SUP])[/SUP]. In fact, inflammation, in particular during the acute phase, causes the migration of granulocytes towards the inflammation site by chemotaxis. It is also known that the degree of peroxidase activity is directly proportional to the number of granulocytes present in the tissue. By measuring a reduced activity of myeloperoxidase, one can conlcude that the cellular response to inflammation is reduced accordingly. Still after 24 hours, the enzymatic activity of peroxidase was almost 75% lower than the activity measured with the control product.

Mechanism of action
18ß-Glycyrrhetinic Acid Phytosome[SUP]®[/SUP] is the complexed form of 18ß-Glycyrrhetinic Acid with soy phospholipids[SUP]([/SUP][SUP]3[/SUP][SUP])[/SUP]. The passage of the compound through the skin takes place through the interaction with cutaneous structures. In the reticular layer of the dermis, the complex is thought to undergo a slow and progressive decomplexation resulting in the in situ release of the free active constituent[SUP](1)[/SUP].
The active component 18ß-Glycyhrretinic Acid is structurally similar to cortisol, and potentiates the anti-inflammatory activity of cortisol by inhibiting its intracellular inactivation.

I think this product contains it: http://www.alignpharma.com/products-healthcare-professionals-xclair-cream.htm Showed up in a search at least..could just be "plain" g-acid.

 

[odalbak]

Ok.. for the people inquiring about anybody on here trying new treatments reference this thread and the latest discovery.. I've been proactive as usual.. so went back on Minoxidil 5% from kirkland..the best on the market.. taking it with Miconazole Nitrate 2%. Also taking it with Diclofenac diethylamine (Voltaren gel). At night I put Ibuprofen gel capsule with naxopren sodium (aleve liquid gels) mixed aloe vera gel.. I always try to add some copper peptide as well. All this reduce both isoform of Cox in the skin so lowering PGD2.. Ibuprofen stay in the the dermis for few days days after application..so really cheap and effective. The goal is to reduces inflammation , INOS and ROS to the maximum. The skin on your body cycle every month.. but everything stops when chronic inflammation happened. this is why you hair cycle goes to ****. Just went to a crazy shed with this..but recovering very fast! Don't be shy if you have any questions... All this are otc stuff.. reduces Cox levels to the maximum, boost the good isoform of nitric oxide (enos) so the stem cell can start to migrate and **** goes back as per normal... The overdose of PGD2 on our scalps says it all. The main problem in hair loss is inflammation.
- - - Updated - - -

Odalbak..All prostaglandins can be pro-inflammatory because they all have vasodilation properties..this is why it is so complicated..Minoxidil is good because it inhibits Cox levels and boost the Enos.. the good nitric oxide isoform that contributes to the migration of stem cell.. INOS is the bad kind...

Thanks Squeegee. Very interesting post.


Does anyone know of potential health dangers from regular Miconazole Nitrate use in the long term? Nitrates are meant to be neuro toxic substances if my memory is right.

 

[Quadzilla99]

Thanks Squeegee. Very interesting post.


Does anyone know of potential health dangers from regular Miconazole Nitrate use in the long term? Nitrates are meant to be neuro toxic substances if my memory is right.

i'm not sure if it get absorbs systemically I know ketoconazole doesn't get absorbed enough from topical application (http://www.ncbi.nlm.nih.gov/pubmed/3280211) to enter your system. I would guess miconazole is the same way. Maybe some with more knowledge can say for certain but I think you need a carrier like DMSO to get something like that through to your system

 

[Saint-Loup]

i'm not sure if it get absorbs systemically I know ketoconazole doesn't get absorbed enough from topical application (http://www.ncbi.nlm.nih.gov/pubmed/3280211) to enter your system. I would guess miconazole is the same way. Maybe some with more knowledge can say for certain but I think you need a carrier like DMSO to get something like that through to your system

bull**** nizoral is systemically absorbed and it can be dangerous for the liver