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Inflamation/ PGD-2 and Mast Cell Degranulation?

I’ve been on this site for like 15 years. Dont post hardly ever anymore and just check in once in a while to see if anything new is happening. I posted this in the HM section and got 0 response. Perhaps I will get something here.

It seems there is a lot of stuff about inflammation and its inhibition being talked about.

I’ve always been interested in Mast Cell Inhibitors like Sodium Chromolyn.

Im hoping some of the brighter folks here can talk about cox-2 inhibition and PGD-2 as it relates to Mast Cell Degranulation. How much is thought to be related to the pro inflammatory cytokine cascade produced by mast cell degranulation.

The reason I ask is I am wondering about a Sodium Chromolyn topical as a treatment or adjunct treatment. I had actually experimented for a while putting Nasalcrom on my scalp many years ago but did not follow through long term.

Reason: Expensive ( you can go through the small bottles of nasalcrom pretty quickly applying constantly) and Mast cell inhibitors need to be used 4 times a day to exert their influence. Work best for allergies and other things related to mast cell degranulation after 4-6 weeks. Also it may need to be much higher concentration when used on scalp over larger area as apposed to inhaling it.

Some questions and comments for those that might know. SC is easily absorbed through mucus mebranes and lungs. Does its molecular weight make it a candidate for a topical?

Its been around for ever and has a super safe profile. Again the main issue is its short action.

However Im thinking it should be easy and cheap to get made. Could be added to shampoo/conditioner ( for one application). Then perhaps added to a spritz type topical for another app. Then perhaps to something like an oil or something else that would take longer to dry and have more of a long term effect. Perhaps using an occlusive while sleeping getting 8 or so hours of effect.

I was also thinking if pro inflamatory cytokines were the issue or part of the issue you could add a anti histamine in the topical to mop any of the stuff that escapes if some of the mast cells do pop. Perhaps put the nite time stuff in a base of emu oil with some other known natural anti inflammatory’s.

I consume relatively large amounts of tumeric and use a coco butter hand and face product from palmers as a pomade that I work through my hair and onto my scalp. I also take aspirin everyday. I eat alot of wild blueberries ( where i live you can pick pounds for free in a day). They are supposed to be the best anti inflammatory food you can eat and the absolute highest amount of resveratol (SP?) possible from foods. 2-3 times the amount in commercially grown berries and of course no pesticides ( commercial blueberries have some of the highest pesticide counts of any fruit… organic pesticides can be worse the man made).

My life long itchy scalp, dandruff,scaly scabs, dermatitis is gone. My hairloss is pretty progressed and been in action for over 25 years. The tumeric coco butter blueberry regimen is pretty new so I cant say I am growing my hair back. But it is definately a bit thicker and healthier and my scalp condition is pretty much 100% better. I also have much less body pain in general. Considering I have had a lot of musco skeletal injuries including a torn pec/ shoulder opperation 8 months ago this sais quite a bit I think.

I take no anti andros or minox either.

So I do think alot can be done through diet, spices, aspirin and the coco butter product for scalp. But wondering if adding the SC and perhaps a topical anti histamine to this would be a big/medium/small help or adjunct to re growing/maintaining ones hair. Especially for people in earlier stages.

I think it (SC) would be a worthy thing to experiment with as it should be easy to get (SUPER SAFE AND EFFECTIVE) and many people have tried much scarrier and expensive things. If inflamation is a crucial part of HL and you can stop mast cell degranulation to any degree I cant see how this would not be of use.

Sorry for the long winded post that may a bit allover the place. Would love to hear what people say and ideas for getting SC compounded and such.


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Have you seen this? GangsterBoy posted it over at HLH

PGD2 in hair folicles is not caused by HPGDS - hematopoietic prostaglandin D synthase BUT, by LPGDS lipocalin pgds.

Source? read the 22 march study of DR. cots. LPGds levels are highly elevated…


Increased PGD2 pathway activity in balding scalp of men with AGA. (A) Expression of lipocalin-type PTGDS mRNA in bald versus haired scalp, as tested by qPCR. Data are means ± SEM (n = 4). (B and C) The amount of PTGDS protein in paired bald (B) and haired (H) scalps (n = 4), as shown by Western blotting with Ponceau stain used for verification of equal loading (B) and its quantitation as normalized to haired scalp ©. Data are means ± SEM. (D) PGD2 production in bald scalp, as tested by ELISA. Data are means ± SEM (n = 3). (E and F) Fold change in PGD2 (n = 17), 15-dPGJ2) (n = 7), and PGE2 (n = 17) expression in bald scalp compared to haired scalp (E). Total prostaglandin content is quantified in (F). Data are means ± SEM. *P < 0.05; **P < 0.01. In (F), P value compares haired versus bald samples for each prostaglandin.

knowing this, explain why cetrizine and other mastcell stabelizers, will NOT help against the elevated PGD2 in hairflocles… so your basically missing the boat with hpgds stabilizers.

The distinction between H-PGD2 and L-PGD2 could be significant. AT-56 looks like the right formula to inhibit L-PGD2, with no antagonism toward PGE2 or H-PGD2:


Since H-PGD2 is involved in sleep regulation, etc. and is very present in the brain, should a topical inhibitor be absorbed into the blood and cross the blood-brain barrier it might cause problems (unknown at this point I think, but worrisome). Also, taking oral preparations that significantly inhibit any PGD activity systemically, if taken in sufficient dosage to induce hair growth, the inflammation necessary for wound healing, etc. could be adversely affected. At this point, hoping for a topical solution that doesn’t circulate too much in the rest of the body seems the best thing to hope for. Maybe At-56…?

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