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

[TMNK]

Good to hear Agahi. Where do you get this stuff, and is it topical only? Sorry to be one of those guys now, but I can't read the whole thread.

 

[Agahi]

I get mine at walmart (store in the USA) for 10 dollars for a 45 day supply. I eat the pills, I dont make a topical from it. I think topical is likely better, but eating them is working well enough for me.

 

[TMNK]

I'm on the big 3, and I consider to add this to my regime. Do you have a link for it? What is the full name for CIT?

 

[Agahi]

cetirizine, brand name is usually zyrtec. What I use is a generic called Equate indoor and outdoor allergy. Walmart has it on their website, I don't wanna direct link it because I dont know if that is allowed sorry.

 

[Aks20]

Ok in all seriousness, why on earth do people comment so specifically about hair shedding? Some people actually claim they know the exact numbers of hair that shed that day. Can anyone explain this to me? The guy above me claims he reduced shedding by 60%, that is an absolutely absurd estimate based on absolutely nothing. in a 24 hour period, between sleeping, showering, performing activities, touching your head, etc. You honestly think you know exactly how much hair you lose a day? a Normal male head sheds 50-100 on average and women generally shed 75-150, so that already gives you a inaccurate baseline, then throw in male pattern baldness/shedding or topical medicine and that can change the number of hairs you shed. So by claiming you know the percentage of reduced shedding is saying that you know exactly how many hairs you would shed that day naturally, how much hair you would shed on top of the natural shedding, how much of that hair you actually did shed, and exactly how many hairs less you shed do to the reduction of shedding. And to add to all of that, you would have to know exactly how many shed hairs are still anchored on the scalp and haven't been removed.

Anyone who claims to know how much hair they shed a day is a lunatic.

Some of us who are already into advanced hair loss, NW3 and above, can reasonably estimate how many hairs we shed every day. Each time I comb, I lose around ten hairs, and on the bed etc, I can pick out a few. When you have few to begin with its easier to notice the loss.

 

[Sparky4444]

Some of us who are already into advanced hair loss, NW3 and above, can reasonably estimate how many hairs we shed every day. Each time I comb, I lose around ten hairs, and on the bed etc, I can pick out a few. When you have few to begin with its easier to notice the loss.

yep....it gets to a point where shedding has a bigger impact on appearance and you can't hide it AT ALL...critical tipping point...I am at that point now...

 

[Aks20]

yep....it gets to a point where shedding has a bigger impact on appearance and you can't hide it AT ALL...critical tipping point...I am at that point now...

very irritating thing this male pattern baldness is...
I tried the Cet thing, worked for me, worth a try..


Squeegee....can you suggest a safe (non sides) alternative approach to the hair loss issue..

Thanks

 

[Aks20]

Interesting...today I had eye twitching...same as with Latisse eyedrops...but at much reduced intensity....this Cet stuff seems to be doing some thing with Prostaglandins...

 

[Kirby]

Anyone here using OC000459 at the moment?

 

[Quadzilla99]

 

[squeegee]

Best bump ever!!!

 

[squeegee]

Still don't know why you guys all think that PGD2 is the bad guy? PGD2 Major biological activities: inhibits platelet and leukocyte aggregation, decreases T-cell proliferation and lymphocyte migration and secretion of IL-1? and IL-2; induces vasodilation and production of cAMP.

PGD2 is just a response to inflammation. Kill inflammation, no more expression of PGD2. No more Hairloss.

 

[Iloveindie]

Anarch-How can you say it made a lot difference? Regrowth? Itching stopped? Anyway aspirin helps indirectly with the pgd2 inhibiting COX-2.

Squeege-If you read the study of Cotsarelis you find out that when pgd2 get inhibited the hair regrow directly, so it's clear the pgd2 is the cause of balding.

 

[Iloveindie]

Good to hear Anarch! Do you apply all over the scalp or front only? Do you notice less inflammation or similar? How many mg is one pill of Aspirin?

 

[boobyinspector]

More Quackery. Remember back when Beta-sitosterol was the big thing and there was science behind it and guys were posting pics of their hair growing. Well it was all a quackery as usual.

Terfenadine also reduced vascular permeability as reflected in decreased albumin levels. In this model, cetirizine reduced sneezing, TAME-esterase activity, and albumin levels, whereas histamine release and PGD2 levels remained unaffected.

http://www.ncbi.nlm.nih.gov/pubmed/7690526

 

[squeegee]

Anarch-How can you say it made a lot difference? Regrowth? Itching stopped? Anyway aspirin helps indirectly with the pgd2 inhibiting COX-2.

Squeege-If you read the study of Cotsarelis you find out that when pgd2 get inhibited the hair regrow directly, so it's clear the pgd2 is the cause of balding.

First thing I did after reading the study is asking myself why PGD2 inhibits hair growth which most of you guys never did. Why should I block PGD2 which the main role is to inhibit platelet aggregation and inflammatory leukocyte?

 

[zeroes]

Squeeze should we be blocking pgd2 or is pgd2 required to keep diseases etc away?

 

[squeegee]

Zeroes.. I don't see why people in the first place are obsess with blocking PGD2. PGD2 presence during the balding phase shows that the environment is in an inflammation state. Don't kill the messenger, kill the problem ( Inflammation). Yep, nobody really knows the side effects of blocking PGD2 as well. PGD2 is just trying to fix the inflammation, but it is chronic, Cell apoptosis goes to **** which included your hair cycle. All chronic diseases have the same problems and results. TNF-A and NF-KB are the problem, not PGD2. We should boost it instead. PGD2 or others prostagladins are just metabolite of COX.

Contrary prostaglandins: the opposing roles of PGD2 and its metabolites in leukocyte function.

Sandig H, Pease JE, Sabroe I.

Source

Department of Asthma, Allergy and Respiratory Science, King's College London, 5th Floor Thomas Guy House, Guy's Hospital, London, UK. Hilary.sandig@kcl.ac.uk

Abstract

Traditionally, PGD(2) has been considered to be a pro-inflammatory mediator, acting via classical PG receptors, such as the PGD(2) receptor (DP). PGD(2) is degraded rapidly in vitro and in vivo to a variety of metabolites, the majority of which were thought, until recently, to be physiologically inactive. Several "inactive" metabolites, particularly 15d-PGJ(2), have been shown to have wide-ranging effects on leukocytes and other cell types, however, and a potentially important anti-inflammatory role for PGD(2) has now been recognized, and the complexity of PGD(2) signaling is beginning to be elucidated. PGD(2) and its metabolites are biologically active over a broad concentration range, and, intriquingly, it appears that there are marked concentration-dependent variations in the consequences of signaling by these eicosanoids, which have the potential to exert pro- and anti-inflammatory effects. For example, the actions of PGD(2) can influence multiple stages in the life of the mature eosinophil, from causing its release from the bone marrow to inducing its recruitment and activation and, ultimately, regulating its apoptosis. This review is concerned with the diverse responses induced in leukocytes by PGD(2) and its metabolites and the signaling mechanisms which are thought to be responsible for them.

 

[Vox]

Don't kill the messenger, kill the problem ( Inflammation).

Aspirin is one of the best known general anti-inflammatory medications. I am not saying that this has something to do with the results reported by Anarch, but who knows?

 

[squeegee]

DHT Activates Inflammatory NFkB (and Block Nerve Apoptosis?)

Prolonged exposure of cerebral blood vessels to DHT has been shown to activate the inflammatory transcription factor NFkB. Conversion of testosterone to DHT by 5-alpha reductase may amplify the inflammatory impact of testosterone by virtue of the stronger activation of the androgen receptor by DHT. Activation of NFkB also suppresses apoptosis and may be necessary to maintain some neural cells. Reducing DHT production by 5-alpha reductase inhibitors, may reduce NFkB activation in the brain and expose androgen-sensitive parts of the brain to apoptosis. This loss of brain cells may result in loss of sexual behavior.