reduce pgd2

block pgd2 :

aspirin,
niacinamide,
caffeine, all as a topical or internal

coconut oil
Vitamin E
astaxanthin - a maybe
butter

Quercetin
luteolin
resveratrol


won't block pgd2 (mistakenly believed to do so) :

fish oil
walnut oil
chia oil
common unsaturated cooking oils
blackcurrant oil
topical oils. (exception = coconut oil)
certainly not topical fish oil.

That's interesting about coconut oil being a pgd2 inhibitor. Maybe that's why sage's topical works for him.

Almost pieced together all the ingredients to make a topical, peat style. But some bits aren't adding up:

1. Working the hypothesis PGD2, supresses hair growth, so we want to nix that / And PGE2 encourages hair growth, or at least hair maintenance, so we want to raise that

These results define PGD2 as an inhibitor of hair growth in AGA and suggest the PGD2-GPR44 pathway as a potential target for treatment.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319975/

PGE2 did not induce distinct telogen-to-anagen conversion, but showed moderate growth stimulatory effects on early anagen hair follicles.

http://www.ncbi.nlm.nih.gov/pubmed/15854125

2. Aspirin does decrease PGD2, but it also decrease PGE2, so what's the net value to us?

This model also explains why agents such as aspirin, which inhibit upstream prostaglandin synthesis enzymes (PTGS1 and PTGS2), have minimal effects on hair growth because of likely equally decreased production of PGE2 and PGD2.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319975/

It appears that 325 mg of aspirin is sufficient to affect PGE2 production and that increasing the dosage to 650 mg daily provides an additional decrease in PGE2 synthesis.

http://www.ncbi.nlm.nih.gov/pubmed/18831918

3. And Niacin does increase PGE2 but  also seems to increase PDG2, again, what's the net end result here?

On the other hand, niacin administration sometimes induces adverse effects, including niacin flushing, as a result of excessive production of PGD2

http://www.nature.com/srep/2013/131017/srep02973/full/srep02973.html

http://www.ncbi.nlm.nih.gov/m/pubmed/1373750/

Specifically, levels of PGD2, PGE2, PGI2 and their metabolites have been shown to be increased as quickly as 12?45 min after niacin treatment (15,26,32,43)

http://onlinelibrary.wiley.com/doi/10.1111/j.1742-1241.2009.02099.x/abstract;jsessionid=1A77F33A12AFB804CF28C9BEDF187500.f03t01

4. Caffeine increase PGE2, good, but can't find anything on its effect on PGD2

Furthermore, the increases in the synthesis and release of PGE2 and 6-keto-PGFI alpha.

http://www.ncbi.nlm.nih.gov/pubmed/7529107

Confused  

This stuff .... 15-dPGJ2 ... sounds like the stuff we may want to target perhaps, focusing further upstream in the PG pathway to PGD2?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319975/

Quercertin, suppresses PGE2.

In accordance with inhibition of COX-2 expression, quercetin reduced PGE2 production

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319975/

LET THERE BE LIGHT!? Maybe us baldies are natural light deficient? I'd sure like some "hypertrichosis" on my noggin; UVB increases PGE2 and decreases PGD2...

Twenty-four hours after treatment with UVB (25 mJ/cm(2)), production of PGE(2) and PGJ(2) increased, while PGD(2) production decreased.

http://www.ncbi.nlm.nih.gov/pubmed/18597804

Interestingly, Minox reduces PGE2:

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).

http://www.ncbi.nlm.nih.gov/pubmed/2553835

After all this forum rambling my current train of thought, either...

1. It's about the relative ratios of PGE2:PGD2 more so than quantities;
2. Understanding how the various options of aspirin, niacin etc. effects that ratio and to what extent seems crucial (e.g. a small decrease may in PGE2 may be worth it so long as you get a bigger decrease in PGD2);
3. And/or there's probably a lot more to all this than meets the eye
4. The blindingly obvious starting place should be to reduce inflammation, generally

Alternate hypothesis, that directly contradicts the PGE2 hypothesis above but seems to possibly explain why I'm not able to make sense of the studies: WE DON'T WANT TO INCREASE PGE2 -- WE DON'T EVEN MIND IF IT GOES DOWN A BIT // PGE1, MAY BE A KEY PLAYER IN THE EQUATION INSTEAD

"Minoxidil, Miconazole Nitrate or Nitroglycerin cream all upregulates PGE1. PGE1 is the major hair growth booster from the prostaglandins family. DGLA is the immediate precursor of PGE1. (Prostaglandin E1). PGE1 counteracts PGE2 as well."

1. Why is counteracting PGE2 good? Isn't there a lot of evidence pointing to block PGD2 and increase PGE2 to combat hairloss? I'm confused about this since Minox increases PGE1 but also PGE2, but PGE2 also causes inflammation. My guess is it's not the up regulation of PGE2 from minox that is beneficial for hair at all, in fact it's what makes minox sort of a double edged sword: allows dead hairs to grow back, but in the meantime it's also causing inflammation and causing more hairloss underneath.

2. DGLA or Dihomo-γ-linolenic acid, I think is a pretty rare form of omega 6 fatty acid. "They" say that the omega 3 to omega 6 balance is important and the western diet is too rich in omega 6, but if we are able to get just DGLA, would taking it do you think would cause inflammation? since it is omega-6. I'm trying to figure out how I can increase PGE1 without increasing PGE2.

WHERE the activity takes place seems key and may also explain some of the inconsistencies....

"...It is interesting to note that α-tocopherol inhibits (pro-inflammatory) PGE2 production in macrophages, but enhances (anti-inflammatory) PGE2 production in endothelial cells..."

lots of good stuff here

http://www.hairlosshelp.com/forums/messageview.cfm?catid=10&threadid=99832

the best way is to avoid rancid oils and omega 6 oils

but the supplements I mentioned, vitamin e, astaxanthin, etc,
will hinder their damage

that's the dietary link with hair loss - rancid oils like margarine, sunflower oil, etc etc

I'm not completely up to date on PGE2, d2 etc, but I looked into castor oil, it is 95% Ricinoleic acid
According to wikipedia, it activates EP3 receptor for PGE2.

Sage 1 is using castor oil in his mixture, I'm gonna give it a try too.

iuyyigh, still feeling confident with the solban-like combo?

still not sure how PGEs figure into this equation. Intuitively...

That Alpecin seems to be helping quite a few people suggests caffeine/niacin worth a crack

Still not sure about aspirin. But the fact it's obviously linked to healthy anti-inflammatory effects and helps blood flow function but does topical application provide the same benefits as internal?!

Also dose seems important... "Low-dose aspirin selectively inhibits COX-1, and high-dose aspirin inhibits both COX-1 and COX-2."

In the midst of all this confusion, I've learned capers are mega high in quercertin. I bloody love capers, woohoo

And if you want to get really bamboozled by possible nuances of this all, have a read of this page

http://www.hairlosshelp.com/forums/messageview.cfm?catid=7&threadid=103917

Columbo wrote:iuyyigh, still feeling confident with the solban-like combo?

why wouldn't I ?

I have tried everything and own most topicals and supplements. I think I know when something is working.

Yes, based on that, I am pretty confident.

I think right now trying to get your head around all of the disparate research on prostaglandin signalling is going to be like chasing the breeze. You're talking about inflammatory signalling and cross-talk happening at the cellular level in every tissue of the body, and its far from understood much less understood in the context of hairloss. When you get to trying to flick the machinery around at that level of detail, you are talking about prescription drugs. And the kind of research materials and expertise required mean this stuff is going on in labs where clinical and research dermatologists are able to circle jerk about these pathways whereby just listening would make your head explode.

My point is you must ask yourself what the point of trying to get to the minutia of this is? Is it worth your time and energy? What would be the result if you did? Because I'm assuming you believe that even if you did find the penultimate step in the causal molecular chain, that there would be a plant chemical available OTC that would just knock it out. Or some plant oil. Yet millions upon millions have tried every commercially available supplement, every plant chemical, every known human vitamin and mineral, and any effect such as that would probably have been realized by sheer accident (and by now) rather than starting with a hypothesis and experimenting.

Given what this forum is dedicated to and where people's hearts are here...the natural, non-drug approach.....you already have all of the information you need. And here they are in order of importance:

(1) Lower ratio of omega-6 to omega-3 fats in the diet to as close to a 4:1 or 3:1 level as possible. This is absolutely the most CRUCIAL and EFFECTIVE natural, lifestyle means for controlling inflammation. This is how you naturally balance the inflammatory vs. anti-inflammatory pathways. Forget downstream prostaglandin synthesis, this is where it all starts. If the cell membrane is made up of an ideal constituency of fatty acids, everything downstream falls into a better place.

(2) Fat soluble and insoluble antioxidant therapies. Substantial dose vitamin E and C. Also some plant pigments within reason.

(3) Avoiding highly unsaturated or processed seed oils.

(4) Favoring fats with a fatty acid makeup more similar to that of human beings with a balance of saturated to monounsaturated FAs. ANIMAL FATS.

(5) Adequate energy flux, i.e. intake and output. You're a physical engine, either of these parameters is off-balance, you are in a stress state. Adequate carbohydrate intake to curb cellular stress response. Adequate exercise to ensure hormonal sensitivity to make cells use that energy properly. Along with antioxidant intake.

(6) Controlling inflammation through other important routes discussed everywhere here: blood sugar control, the stress response, etc. etc. etc.

If you're discussing the more minute aspects of the pathways for purely academic (hobby) purposes, that's fine. But if you are trying to find something workable and non-drug from going over the research, do NOT waste your time. The interventions that will give you the biggest bang for your buck (speaking in terms of non-drug interventions!), are known and available. Problem is, if you read the list, its not flashy, its not fun, requires discipline and splitting hairs about diet, and doesn't totally come in a little capsule you take with a glass of water or from some exotic sounding plant.

it has been figured out. all of it has.

but

the man who discovered it,Dr George Cotsarelis,  and goes around america lecturing on hair loss and pgd2,
said "take fish oil to reduce pgd2"

Yes, absolutely. The point of taking fish oil being to correct the balance of n-6:n-3 fats, by adding in a greater amount of omega 3 FA's to the diet. All of the molecules that eventually become the inflammatory mediators start as chunks of FAs cleved from the inner cell membrane. So if you want to attack it from as upstream a point as possible, you start with what your cells are building their membranes with. And that is largely determined by the ongoing, long-term fat content of your food. Eat a hugely imbalanced ratio of omega-6:omega-3 like a 20:1 or 30:1 ratio like many westerners, your cell membranes will display that ratio and you'll have a lot more of the starting materials for inflammatory pathways. You set yourself up for it. Eat a better ratio like 4:1, and you give your physiology more materials to balance the inflammatory pathways with the anti-inflammatory ones.

Besides just taking fish oil, there are foods that are higher in omega-3 FAs that should also be included in the diet to offset the omega 6 content. Also trying to lower the amount of seed oils is HUGE. If you look at the vast majority of processed foods, you'll find that seed oils are always high on the list (corn, cottonseed, soybean, sunflower, safflower). Look at the data for the FA content of these oils in particular. Omega 6 dominates substantially. Also, the PUFA content just in general of these is far too high.

Favor fats that are higher in saturated FAs naturally, or where the mono- are at least balanced well with the fully saturated FAs (such as palm oil). Besides this, where it concerns PUFA, look for the lowest omega 6:omega 3 ratio.

Gates, I agree with the sentiment of your last but one post. Can drive oneself loopy trying to figure out what's what with barely a partial picture at best. On the hand always worth doing a bit of due diligence first

Regarding the fat balancing act, seems this is now agreed wisdom, mainly. My guess it will help many maintain what hair they have more easily. The more PUFA I ditched / more SFA I've consumed the more my hair has been stable (plus skin has improved)

The question is how can we kick hair loss into reverse and actually regrow some? Think I've read enough to give the Solban combo a go, hopefully it will help

The point of my previous post was to say that poring over the studies on the finer molecular details in the process of inflammation (unless only for personal interest) is essentially pointless for practical purposes, especially where it concerns hollistic/lifestyle types of therapy/medicine.

As it applies to curbing inflammation with whole food or crude plant substances (non drug fractions), there is nothing new under the sun.

Yes, ah yes. The regrowth dilemma. Columbo, will look forward to your experience and feedback with what you're trying.

fish oil won't reduce pgd2

not eating any overt omega 3, or overt omega 6, will reduce pgd2

and the supplements i mentioned help too

and that guy is the world leader in pgd2 research, and still got it wrong

The data indicated that omega-3 PUFAs can effectively inhibit niacin-induced synthesis of PGD2 and PGE2, the key mediators of flushing caused by niacin intake. The possible inhibitory mechanisms appear to be diminished niacin receptor expression and reduced availability of AA, a substrate for PGD2 and PGE2 synthesis. These effects are mediated within cellular membranes and are based on the enhanced incorporation of omega-3 PUFAs into membrane phospholipids.

"Attenuation of niacin-induced prostaglandin D2 generation by omega-3 fatty acids in THP-1 macrophages and Langerhans dendritic cells"
(cannot post a link yet)

Reducing the availability of n-6 fats in the membrane reduces PGD2. You do this by railroading them in the diet with a higher intake of n-3 relatively. The AA being referred to being an n-6 FA.

My very first natural regimen I'm now noticing contained nearly everything in this thread said to reduce pgd2. I did both topical, and interncal caffeine, took 1,000mg+ of niacinamide daily, vit e daily, astax daily...and here is the craziest thing, I ingested 3-6 tbsp of extra virgin coconut oil daily. My digestive system eventually adjusted to all the added fat.

Anyway sorry to say but the regimen didn't hold up. I lost my hair, but maybe it will work for others.

SonofOdin wrote:My very first natural regimen I'm now noticing contained nearly everything in this thread said to reduce pgd2. I did both topical, and interncal caffeine, took 1,000mg+ of niacinamide daily, vit e daily, astax daily...and here is the craziest thing, I ingested 3-6 tbsp of extra virgin coconut oil daily. My digestive system eventually adjusted to all the added fat.

Anyway sorry to say but the regimen didn't hold up. I lost my hair, but maybe it will work for others.

and topically ?

as someone who has tried every internal supplement, I believe all of the resources of the supplement are used on the body, and then hair last. the only supplement where I thought, yes, this is directly affecting hair, was gelatine and lysine

so that's why i go topical, and as people know, I have tried a lot of supplements

I must also mention, that minoxidil works BY intefering with pgd2

If Solban = Minox (sort of) then are you considering rolling too?

"82% of the patients (Dermaroller + Minoxidil) reported more than 50% improvement (hair growth) vs 4.5% with Minoxidil only"

Columbo wrote:If Solban = Minox (sort of) then are you considering rolling too?

"82% of the patients (Dermaroller + Minoxidil) reported more than 50% improvement (hair growth) vs 4.5% with Minoxidil only"

topical treatments like dermarolling can help, yes