Starting topical Asprin to supress prostaglandins

[casperz]

I'm sure everyone has heard the news on prostaglandin D2:

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

Since aspirin works by inhibiting an enzyme that produces prostaglandins would topical aspirin have a chance of working to regrow hair?

http://chronicle.uchicago.edu/950817/aspirin.shtml

Regardless I think I'm going to start topical aspirin tonight. I'm thinking
about a 5% solution mixed into minoxidil.

Tell me why it wont work.

 

[Jacob]

I'm guessing the pills contain fillers that may not disolve well...haven't looked at an aspirin label lately though.

Just some aspirin topical related links:

http://www.thecompounder.com/alternative-treatments/pain-management/383-aspirin-topical

http://aspirinandarnica.com/

http://www.pkwy.k12.mo.us/pierre/documents/topicalprod.pdf

http://www.livestrong.com/article/93361-add-aspirin-skin-cream/

 

[casperz]

The study below is not related but talks about inflammation and COX signaling in mice which was inhibited by topical aspirin treatment and had an effect on fur.

PDF: http://alturl.com/64o6v

 

[casperz]

Wow... did not realize how many products contain aspirin or salicylic acid.

I've got to believe someone has tried topical aspirin to combat hair loss but
Google sure does not turn up any results showing it either working or not.

It would be amazing if something like aspirin could work, maybe some of the long time posters here have heard of it being used before.

 

[Jacob]

I remember it being discussed before..just not anyone using it for any length of time. "Aspirin" that is. Salicylic acid is in plenty of products..even some I've used.

 

[TravisB]

My guess is it won't work. It would be too simple if Aspirin which is on market for many, many years was an accidential treatment for baldness. First, I guess you would need a good vehicle, if it even has to work.

But if you have time and desire, then experiment! Why not?

 

[abcdefg]

Well someone trying to make this themselves did not take long. Here is the thing its still a work in progress I doubt its as simple as just inhibiting this. They mentioned this - prostaglandin PGD2 but also they said a derivative of this seemed to completely stop hair growth so you would need to inhibit both of those and who knows what other things could be found while they do this.
I really doubt asprin is going to work the same way with the same effectiveness as an actual treatment formulated to target these.

 

[yassin]

today I spent most of the day searching about this to find a way to inhibit prostaglandin D2 synthase enzyme

1. aspirin >
aspirin is a prostaglandin inhibitor but I'm not sure if it inhibits prostaglandin D2, as it's a special prostaglandin , and not much info are known about it
people used aspirin for years and didn't note any effect on hair, maybe because people on aspirin don't experience any type of hair loss

But I don't think that aspirin has any effect on AA

2. Inorganic selenium compounds
SeCl4, NaSeCo3, selenium disulfide
I think that the first two have never tried for Androgenic Alopecia and they don't have any clinical usage in medicine , so I think that they will be tried in the next few years orally & topically. but they will have significant side effects if they are used orally because PG-D2 is an important factor on the brain

selenium disulfide is already used topically on the scalp as a powerful antidandruff shamoo (head & shoulders clinical strength)
selenium disulfide shampoos are used in two concentrations
1% over the counter (head & shoulders clinical strength and other shampoos)
2.5% available with prescribtion

3. organic sources of selenium
"egg" not the most sources but it's the best to be taken in a daily routin
1 egg is sufficient for your daily requirement of selenium
tuna fish is also very rich in selenium
you can also find other sources of organic selenium in this link
http://nutritiondata.self.com/foods-000 ... 00000.html

4. mast cell stabilizers (e.g. chromoglicic acid)
as PG-D2 is only synthesized away from the brain by mast cells "only"
mast cell stabilizers are used in bronchial asthma as a nasal spray or an inhaler.


I think if you want to try on yourself don't try aspirin but try chromoglicic acid solution/sprays + head & shoulders clinical strength + eat food rich in selenium

 

[Anarch]

I hope Merck isn't the only company researching PG-D2 blockers.

 

[zeroes]

I'm kind of confused, isn't aspirin suppose to 'thin' your blood? Isn't lack of blood to the head one of the reason's people loss their hair?

 

[Kirby]

I'm kind of confused, isn't aspirin suppose to 'thin' your blood? Isn't lack of blood to the head one of the reason's people loss their hair?

I thought 'thinner' blood = more easily circulated, but I may be wrong on that detail.

 

[slurms mackenzie]

W. They mentioned this - prostaglandin PGD2 but also they said a derivative of this seemed to completely stop hair growth so you would need to inhibit both of those and who knows what other things could be found while they do this.

This is a very important point, it's PGD2 synthase which they were cartwheeling over.

 

[dam]

Niacin produces pgd2, so would products like revivigen that contain niacin as a active ingredient cause hairloss? also would coffee and energy drinks wich are high in niacin cause hairloss? Been looking for this answer for some time now i just got revivogen and dont want to use it because of the niacin in it, i do get a slight burning sensation after application, i figure it is the niacin. any help would be appreciated.

 

[el longhorn]

I'm kind of confused, isn't aspirin suppose to 'thin' your blood? Isn't lack of blood to the head one of the reason's people loss their hair?

I thought 'thinner' blood = more easily circulated, but I may be wrong on that detail.

Blood thinners refers to the inhibition of clotting. THey don't actually make your blood less viscous

 

[squeegee]

Sodium salicylate inhibits cyclo-oxygenase-2 activity independently of transcription factor (nuclear factor kappaB) activation: role of arachidonic acid.
Mitchell JA, Saunders M, Barnes PJ, Newton R, Belvisi MG.
Source

Department of Anaesthesia and Critical Care Medicine, The Royal Brompton Hospital, London, England. j.mitchell@rbh.nthames.nhs.uk
Abstract

Acetylsalicylic acid (aspirin) is the drug most commonly self-administered to reduce inflammation, swelling, and pain. The established mechanism of action of aspirin is inhibition of the enzyme cyclo-oxygenase (COX). Once taken, aspirin is rapidly deacetylated to form salicylic acid, which may account, at least in part, for the therapeutic actions of aspirin. However, where tested, salicylic acid has been found to be a relatively inactive inhibitor of COX activity in vitro, despite being an effective inhibitor of prostanoids formed at the site of inflammation in vivo. Recently, the identification of a cytokine-inducible isoform of COX, COX-2, has led to the suggestion that salicylate produces its anti-inflammatory actions by inhibiting COX-2 induction through actions on nuclear factor kappaB (NF-kappaB). We have used interleukin 1beta-induced COX-2 in human A549 cells to investigate the mechanism of action of salicylate on COX-2 activity. Sodium salicylate inhibited prostaglandin E2 release when added together with interleukin 1beta for 24 hr with an IC50 value of 5 microg/ml, an effect that was independent of NF-kappaB activation or COX-2 transcription or translation. Sodium salicylate acutely (30 min) also caused a concentration-dependent inhibition of COX-2 activity measured in the presence of 0, 1, or 10 microM exogenous arachidonic acid. In contrast, when exogenous arachidonic acid was increased to 30 microM, sodium salicylate was a very weak inhibitor of COX-2 activity with an IC50 of >100 microg/ml. Thus, sodium salicylate is an effective inhibitor of COX-2 activity at concentrations far below those required to inhibit NF-kappaB (20 mg/ml) activation and is easily displaced by arachidonic acid.

 

[odalbak]

The thing is we don't have a precise understanding of…

how various prostaglandin forms (PGD2, PGE2, PGE1,…) interact with each other. Could there be a balance system of interdependence and/or antagonism between all of them?

Isn't the beneficial effect of the increase of PGE2 and PGF2 by minoxidil caused by a resulting decrease of PGD2, or is the increase of PGE2 and PGF2 alone beneficial?

Would inhibiting ALL prostaglandins on the scalp result in a decrease of inflammation and as a consequence a solution to hair loss? Or are prostaglandins essential to hair growth?

The map we're navigating with is not complete.

 

[boobyinspector]

I do Aspirin face masks. Whenever I do the facemask I also get the top of my hairline where I have the receded jude law style area. I've been doing that forever and while I do have hair starting to lessen the receded area I think it's as a result of being on finasteride long enough.

 

[Sparky4444]

What about Alka-Seltzer??? Doesn't that have aspirin in it??? Easy -- just dissolve and splash your head

 

[casperz]

Hey guys, I started this tread when the news of PGD2 first broke. I was talked out of using aspirin by some other posts on this site and others, the conclusion I came to at the time was aspirin was not going to do anything for PGD2 and might even hurt.

 

[Jaded]

.

The study below is not related but talks about inflammation and COX signaling in mice which was inhibited by topical aspirin treatment and had an effect on fur.

PDF: http://alturl.com/64o6v

The arachidonic acid/COX/prostaglandin pathway has been shown to be an important regulator of inflammatory responses. Interestingly, this pathway is also in- volved in the regulation of hair cycling. Two independent studies have demonstrated that overexpression of COX-2 in mouse skin leads to alopecia (Bol et al. 2002; Muller-Decker et al. 2003). Therefore, we examined the expression of several genes in this pathway. The expression of both COX-1 and COX-2 genes were markedly increased in the affected skin (Fig. 3A), as was that of the prostaglandin transporter (PGT), which mediates the re- lease of newly synthesized prostaglandins from cells. Western blot analyses further confirmed these gene ex- pression changes at the protein level (Fig. 3C). As shown in Figure 3, A and C, COX-2 expression in the control skin declined in catagen (P17–P20) and was barely de- tectable in early telogen (P21), but increased again during anagen (P28–P40) (Muller-Decker et al. 2003). In con- trast, COX-2 expression in the affected skin was signifi- cantly elevated during catagen/telogen


So basically we need cox-2 blockers and cox-1 enhancers. Aspirin blocks both.


Minoxidil is a cox-1 enhancer:
http://www.nature.com/jid/journal/v108/n2/abs/5610282a.html

"We demonstrate here that minoxidil is a potent activator of purified PGHS-1 (AC50 = 80 M), as assayed by oxygen consumption and PGE2 production."

PGHS1 = Cox1


So minoxidil+aspirin is the cure!


cox-2 should be banned from our body lol
"COX-2 appears to be related to cancers and abnormal growths in the intestinal tract. COX inhibitors have been shown to reduce the occurrence of cancers and pre-cancerous growths."

We need to find a soluble COX-2 selective inhibitor.