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

[2020]

Re: A recently discovered new factor in AA, the cure is near

http://www.sciencedaily.com/releases/2012/03/120321143013.htm

cool link.Like the pic. unk:

you haven't read that article yet?

underlying hair follicle stem cells were found intact, suggesting that the scalp was lacking an activator or something was inhibiting hair follicle growth.

could it be all that excess PGD2?

 

[TravisB]

Re: A recently discovered new factor in AA, the cure is near

Someone needs to get rid of this PGD2 and see what happens. And fast.

Very cool pic. It literally shows how the hair shaft is filled with PGD2 (green), making it impossible for hair to grow through.

If getting rid of PGD2 in scalp turned out to be the true cure for baldness, all the baldies in the world would go apeshit.

This was probably talked here, but what role does DHT play in it then? Does lowering DHT also causes lowering of PGD2?

 

[franciscosalta]

Re: A recently discovered new factor in AA, the cure is near

I was thinking.. DHT cant cause the increase in PGD2 production... let me explain..
finasteride inhibits DHT production...
if someone uses finasteride for a year for example... and stops hair loss
then use finasteride and minoxidil for another year, he recovers hair because minoxidil increases PGE2
but if after a year, he stops using minoxidil (but continue to use finasteride), he will lose the hair he recovered using minoxidil because the pge2 levels are again low... but the DHT levels are low too because of the finasteride..
so, dht isn't causing the high pgd2 levels :/

 

[franciscosalta]

Re: A recently discovered new factor in AA, the cure is near

I was thinking.. DHT cant cause the increase in PGD2 production... let me explain..
finasteride inhibits DHT production...
if someone uses finasteride for a year for example... and stops hair loss
then use finasteride and minoxidil for another year, he recovers hair because minoxidil increases PGE2
but if after a year, he stops using minoxidil (but continue to use finasteride), he will lose the hair he recovered using minoxidil because the pge2 levels are again low... but the DHT levels are low too because of the finasteride..
so, dht isn't causing the high pgd2 levels :/

year 0 : scalp = pgd2 + dht + low pge2 => hair loss
year 1: scalp + finasteride = pgd2 + low pge2 => stops hair loss
year 2: scalp + finasteride + minoxidil = pgd2 + normal pge2 => previous hair +new hair
year 3: scalp + finasteride = pgd2 + low pge2 again => previous hair

:dunno: :dunno: :dunno:
am i wrong?
also i've read that castrated adults doesn't recover lost hair, only stop loosing hair

 

[franciscosalta]

Re: A recently discovered new factor in AA, the cure is near

I was thinking.. DHT cant cause the increase in PGD2 production... let me explain..
finasteride inhibits DHT production...
if someone uses finasteride for a year for example... and stops hair loss
then use finasteride and minoxidil for another year, he recovers hair because minoxidil increases PGE2
but if after a year, he stops using minoxidil (but continue to use finasteride), he will lose the hair he recovered using minoxidil because the pge2 levels are again low... but the DHT levels are low too because of the finasteride..
so, dht isn't causing the high pgd2 levels :/

year 0 : scalp = pgd2 + dht + low pge2 => hair loss
year 1: scalp + finasteride = pgd2 + low pge2 => stops hair loss
year 2: scalp + finasteride + minoxidil = pgd2 + normal pge2 => previous hair +new hair
year 3: scalp + finasteride = pgd2 + low pge2 again => previous hair

:dunno: :dunno: :dunno:
am i wrong?
also i've read that castrated adults doesn't recover lost hair, only stop loosing hair

I think we must investigate this with scientific method... think in a hypothesis, and try to refute it or prove it.. and then go on...

I'll start with:

1. PGD2 needs DHT to cause hair loss.
2. PGD2 without DHT doesn't cause hair loss.
3. DHT without PGD2 doesn't cause hair loss.
4. PGE2 makes the hair grow.
5. PGE2 counteract PGD2 effects.

 

[franciscosalta]

Re: A recently discovered new factor in AA, the cure is near

I was thinking.. DHT cant cause the increase in PGD2 production... let me explain..
finasteride inhibits DHT production...
if someone uses finasteride for a year for example... and stops hair loss
then use finasteride and minoxidil for another year, he recovers hair because minoxidil increases PGE2
but if after a year, he stops using minoxidil (but continue to use finasteride), he will lose the hair he recovered using minoxidil because the pge2 levels are again low... but the DHT levels are low too because of the finasteride..
so, dht isn't causing the high pgd2 levels :/

year 0 : scalp = pgd2 + dht + low pge2 => hair loss
year 1: scalp + finasteride = pgd2 + low pge2 => stops hair loss
year 2: scalp + finasteride + minoxidil = pgd2 + normal pge2 => previous hair +new hair
year 3: scalp + finasteride = pgd2 + low pge2 again => previous hair

:dunno: :dunno: :dunno:
am i wrong?
also i've read that castrated adults doesn't recover lost hair, only stop loosing hair

I think we must investigate this with scientific method... think in a hypothesis, and try to refute it or prove it.. and then go on...

I'll start with:

1. PGD2 needs DHT to cause hair loss.
2. PGD2 without DHT doesn't cause hair loss.
3. DHT without PGD2 doesn't cause hair loss.
4. PGE2 makes the hair grow.
5. PGE2 counteract PGD2 effects.

First, "PTGDS and its product PGD2 are elevated in the bald-scalp areas of men with male pattern baldness" .. so I think something is causing an excess of PTGDS (PTGDS is PGD2 Synthase, so, the stuff that converts PGH2 to PGD2). But! PGH2 also can be converted to PGE2!! So, perhaps an excess of PGD2 Synthase (PTGDS) makes a lot of PGD2, leaving less PGH2 for making PGE2! That could explain the high PGD2 levels and the low PGE2 levels.

PTGDS catalyzes the conversion of prostaglandin H2 (PGH2) to prostaglandin D2 (PGD2).

PGE Synthase generates prostaglandin E2 (PGE2) from prostaglandin H2

Perhaps DHT causes high Prostaglandin D2 Synthase for any reason! :dunno: :dunno: :dunno: Sorry for too much spam! :whistle: :whistle: :whistle:

 

[odalbak]

Re: A recently discovered new factor in AA, the cure is near

"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 PGD2 study)

minoxidil + some anti PGD2 product could be enough at least to stop hair loss.

 

[TA45]

Re: A recently discovered new factor in AA, the cure is near

What about the people who can't tolerate minoxidil?

 

[franciscosalta]

Re: A recently discovered new factor in AA, the cure is near

"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 PGD2 study)

minoxidil + some anti PGD2 product could be enough at least to stop hair loss.

What about the people who can't tolerate minoxidil?

yes :thumbdown2: i don't use minoxidil because I used for 5 months some years ago and I got some wrinkles in my forehead and worst dark eye circles... Now I use finasteride 1mg once a day and kotoconazole shampoo 2% 3 times a week since 11 months ago... stopped totally the hair loss and recover some hair but I need more a lot more to be like before I discovered that I suffer male pattern baldness :sobbing: :sobbing: :sobbing: So , I was thinking to use minoxidil, but I dont wan't a youger hair with older face :shakehead: :shakehead: :shakehead:

 

[2020]

Re: A recently discovered new factor in AA, the cure is near

then don't mind the minoxidil... you can always just buy a direct PGE2 analog but that will cost you a lot more than minoxidil

 

[squeegee]

This is why you are suffering from male pattern baldness:

Biol Reprod. 2000 Sep;63(3):775-80.
Androgen control of cyclooxygenase expression in the rat epididymis.
Cheuk BL, Leung PS, Lo AC, Wong PY.
Source

Department of Physiology, The Chinese University of Hong Kong, Shatin, N.T, Hong Kong.
Abstract

Bradykinin and a number of peptide hormones such as angiotensin, endothelin, and vasopressin stimulate anion secretion in rat epididymis via local formation of PGE(2). These effects are mediated by cyclooxygenase (COX)-1 isozyme. The present study was undertaken to assess the androgen control of COX expression in the epididymis. Adult male Sprague-Dawley rats were bilaterally castrated through a scrotal route. Reverse transcription-polymerase chain reaction was used to measure COX-1 and COX-2 mRNAs in the epididymis in normal and castrated rats. Anion secretion in epithelia grown from the epididymides of these rats was studied by the short-circuit current technique. In normal rats, COX-1 and COX-2 mRNAs were detected in the intact epididymis. Elimination of spermatozoa by the technique of efferent duct ligation or flushing out spermatozoa did not affect the expression of either enzyme in the epididymis, indicating that the epithelium, but not spermatozoa, expressed the enzymes. Castration caused a time-dependent decrease in expression of COX-1 and COX-2 mRNAs, which were partially restored upon testosterone replacement. In epithelia cultured from castrated rats, there was a complete loss of bradykinin-induced anion secretion. This effect was reversible upon testosterone replacement. Although epithelia from castrated rats did not respond to bradykinin, they could respond to cAMP, forskolin, and PGE(2) with only 20% loss of response magnitude when compared with epithelia from normal rats. These results suggest that the expression of COX-1 and COX-2 are dependent on androgen. The loss of COX-1 expression after castration correlates with the specific loss of anion secretion induced by bradykinin and possibly other hormones.

 

[Selo]

Dihydrotestosterone alters cyclooxygenase-2 levels in human coronary artery smooth mu

And DHT influences COX-2 expression in HUMAN coronary artery smooth muscle cells aswell. So regulating DHT (say by using finasteride/dutasteride) can possibly helps to regulate COX-2 which then may have a flow on effect on prostaglandin levels which regulate hair cycling.


http://ajpendo.physiology.org/content/298/4/E838.full

Dihydrotestosterone alters cyclooxygenase-2 levels in human coronary artery smooth muscle cells
Kristen L. Osterlund1,2,
Robert J. Handa1, and
Rayna J. Gonzales1

Abstract
Both protective and nonprotective effects of androgens on the cardiovascular system have been reported. Our previous studies show that the potent androgen receptor (AR) agonist dihydrotestosterone (DHT) increases levels of the vascular inflammatory mediator cyclooxygenase (COX)-2 in rodent cerebral arteries independent of an inflammatory stimulus.

Little is known about the effects of androgens on inflammation in human vascular tissues. Therefore, we tested the hypothesis that DHT alters COX-2 levels in the absence and presence of induced inflammation in primary human coronary artery smooth muscle cells (HCASMC). Furthermore, we tested the ancillary hypothesis that DHT's effects on COX-2 levels are AR-dependent. Cells were treated with DHT (10 nM) or vehicle for 6 h in the presence or absence of LPS or IL-1β. Similar to previous observations in rodent arteries, in HCASMC, DHT alone increased COX-2 levels compared with vehicle.

This effect of DHT was attenuated in the presence of the AR antagonist bicalutamide. Conversely, in the presence of LPS or IL-1β, increases in COX-2 were attenuated by cotreatment with DHT. Bicalutamide did not affect this response, suggesting that DHT-induced decreases in COX-2 levels occur independent of AR stimulation.

Thus we conclude that DHT differentially influences COX-2 levels under physiological and pathophysiological conditions in HCASMC. This effect of DHT on COX-2 involves AR-dependent and- independent mechanisms, depending on the physiological state of the cell.

 

[Saint-Loup]

And DHT influences COX-2 expression in HUMAN coronary artery smooth muscle cells aswell. So regulating DHT (say by using finasteride/dutasteride) can possibly helps to regulate COX-2 which then may have a flow on effect on prostaglandin levels which regulate hair cycling.


http://ajpendo.physiology.org/content/298/4/E838.full

Dihydrotestosterone alters cyclooxygenase-2 levels in human coronary artery smooth muscle cells

Very interesting...
production of PGE2 seems to be independant of DHT level.

Surprisingly, DHT did not affect PGE2 levels in the absence or presence of IL-1β-induced inflammation. This result could have been due to increases in COX-1 activity that arise to compensate for the decreased COX-2 protein levels; however, our data show that COX-1 protein levels were decreased by DHT in the presence of IL-1β, making compensatory COX-1 activity seem unlikely. Since PGE2 is not the only COX-2-derived end product, further studies are needed to determine which end product (prostacyclin, PGF2α, or PGD2) may be altered by DHT treatment.

 

[Selo]

Very interesting...
production of PGE2 seems to be independant of DHT level.

Which might explain why using finasteride/dutasteride doesn't give you much regrowth.

Reducing DHT might only reduce PGD2 levels preventing further loss but doesn't upregulate PGE2 to get growth because PGE2 is independent of DHT. :dunno:

 

[Saint-Loup]

Jacob! I bought Ibuprofen gel capsules today for cheap at the drugstore.. I mixed it with aloe vera (Cox 2 inhibitor as well).. works really good. I also tried it with Diclofenac sold under Voltaren.. which is another Cox 2 inhibitor..works good as well.

Have you seen some results?

The exposure to paracetamol after 24 h and for aspirin at all time-points led to modest decreases in PGD2 production. Surprisingly, the highest concentration (100 μm) of paracetamol actually increased the secretion of this PG at 72 h. A similar increase was also seen with the paracetamol metabolite, AM404, at a concentration of 10 μm (data not shown).
[..]
Similar to paracetamol and aspirin, indomethacin had a marked anti-androgenic effect when used at 10 μm. However, the indomethacin-induced inhibition of testosterone, unlike that induced by other mild analgesics, was associated with a concomitant inhibition of PGD2. As indomethacin inhibits both cyclooxygenases (COX1 and 2) (PGHS1 and PGHS2) whereas paracetamol mainly inhibits COX2 (Mitchell et al., 1994), but nevertheless induce anti-androgenic effects in rats (Kristensen et al., 2011a), this may suggest that both COX enzymes are involved.

http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2605.2012.01282.x/full

 

[zombiehair]

hi as you can see by my join date ive been checking in on these forums for a while.havent posted much at all.
this pgd2 stuff is the first thing to really get my attention.
the more i look into it reading the study looking for ways to lower pgd2 and raise pge2 as i can see many of you have been as well.
a few things have caught my attention.
first is minoxidol raising pge2 ive seen this mentioned a few times.
cetirizine lowering pgd2 (posts from years ago people reporting regrowth while taking it )
caffine supposedly raising pge2 (alpecin ?)
old remedys and more recent reports of them regrowing hair.
onions = queritine supposedly lowers pgd2
scar creams growing hair some of these are onion based.
various oils
castor oil supposedly raises or mimics pge2
miconzole contains castor oil
alpecin liquid contains castor oil
im sure their are more i cant remember now been a bit of a google frenzie
whats interesting is this pgd2 study give many of the above a viable mode of action where as before they were either hear say wives tales or unknowing.
lets hope this all leads some where maybe even barbers.
if anyones been trying out any pg related stuff please post results.

 

[squeegee]

The problem is not at the prostagladins level.. It is at the Cyclooxygenase level where it is upregulated by DHT.

Minoxidil inhibit Cyclooxygenase
Miconazole Nitrate inhibit Cyclooxygenase
Inhibition of DHT by finasteride reduce COX.

Look up the studies in this thread.

The problem is mother****ing COX level.period. This is why the prostaglandins level are imbalanced and in a pro-inflammatory state.

 

[Selo]

The problem is not at the prostagladins level.. It is at the Cyclooxygenase level where it is upregulated by DHT.

Minoxidil inhibit Cyclooxygenase
Miconazole Nitrate inhibit Cyclooxygenase
Inhibition of DHT by finasteride reduce COX.

Look up the studies in this thread.

The problem is mother****ing COX level.period. This is why the prostaglandins level are imbalanced and in a pro-inflammatory state.

So the question is will reregulating at the COX level cause hair to grow? And how do you regulate COX? You would need a topical COX-2 inhibitor to do that.

 

[zombiehair]

I hear you squeegee ,so pg s are a down stream event.
Nice find with the studys,i can see you put a lot into finding and reading these studys.
so in your opinion walking a pg tight rope isnt the way to go.we want to target Cyclooxygenase.
I remember while id been looking for pg related info seeing Cyclooxygenase mentioned.
Onions inhibit Cyclooxygenase.
Ill have another google see what i can find.

 

[squeegee]

non selective cox inhibition is the way to go... Cox-1 and Cox-2 inhibition.

- - - Updated - - -

Somebody is finally getting it!!! People were using onions juice on here as an hairloss remedy!!! The problem is COX which is controlled by androgen in the skin. This is why female don't have this problem but only when they have PCOS..when their body go androgenic...and this is why castrated people at young age don't go bald as well. the level of COx in the skin stay low. PGs are products of COX. No elevated COX no elevated PGD2.