HairShocka
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I've been reading a lot on PGD2, PGE2, PGE1, and how fixing their levels on the scalp might help halt hairloss. And of course as a result, I'm utterly confused. lol
Below, I will list what I've gotten out of my research so far while asking questions along the way. Please point out if any points I'm making are true/false, useful/irrelevant.
According to many studies including the Costarelis study, PGD2 is high in balding scalp.
1. Blocking PGD2 could be part of the solution to halt hair loss from progressing because PGD2 has inhibitory effects on hair growth.
2. Others say, PGD2 is high as the body's natural reaction to the chronic inflammatory activity going on in the scalp. What is the function of PGD2 in the body? Could lowering PGD2 on the scalp cause more trouble than good?
PGE2 which according to the Costarelis study, was found to be lowered in balding scalp.
1. PGE2 on scalp, lowers Testosterone/ androgens in the scalp, which lowers pgd2 and pgf2alpha, which also means lower testosterone topically in the scalp.
2. However, PGE2 is also known to cause inflammation. wtf!
PGE1 is the major hair growth booster from the prostaglandins family. DGLA is the immediate precursor of PGE1. (Prostaglandin E1). PGE1 counteracts PGE2. Minoxidil, Miconazole Nitrate or Nitroglycerin cream all upregulates PGE1.
What is the safest way to increase PGE1?
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Do you guys feel that manipulating pge2/pgd2/pge1 on the surface is a viable way to halt loss? Ideally, I feel it's best if we can somehow figure out why PGD2 is higher and PGE2 lower on us baldies and find a way to get the balance right. I'm guessing that this is what lab researchers are trying to figure out. If anyone has any information or theories on what's going on, I'd like to hear them. From my findings, DHT-induced DKK-1 expression in dermal papilla cells seems like a good place to look into.
With that said, what do you guys think about a highly concentrated ascorbic acid topical to halt hairloss? Beholder and I (i'm sure others as well) are experimenting with a topical with ascorbic acid, msm, and melatonin. You can see the original post by Beholder here: http://www.hairlosstalk.com/interac...f-PGE2-(read-to-get-your-hopes-crushed)/page4
I'm copying some stuff he had to say about this:
Ascorbic acid (vitamin C) dose-dependently inhibited interleukin-1beta (IL-1beta)-mediated PGE2 synthesis in the human neuronal cell line. Furthermore it dose-dependentlyproduced a significant reduction in IL-1beta-mediated production of 8-iso-prostaglandin F2alpha (PGF2a), a reliable indicator of free radical formation, suggesting that the effects of ascorbic acid on COX-2-mediated PGE2 biosynthesis may be the result of the maintenance of the neuronal redox status since COX activity is known to be enhanced by oxidative stress. http://arxiv.org/abs/0708.0548
In a previous study, we recently claimed that dihydrotestosterone (DHT)-inducible dickkopf-1 (DKK-1) expression is one of the key factors involved in androgen-potentiated balding. We also demonstrated that L-ascorbic acid 2-phosphate (Asc 2-P) represses DHT-induced DKK-1 expression in cultured dermal papilla cells. Here, we investigated whether or not L-threonate could attenuate DHT-induced DKK-1 expression. We found that DHT-induced activation of DKK-1 promoter activity was significantly repressed by L-threonate. Moreover, a co-culture system featuring outer root sheath (ORS) keratinocytes and DPCs showed that DHT inhibited the growth of ORS cells, which was then significantly reversed by L-threonate. Collectively, these results indicate that L-threonate inhibited DKK-1 expression in DPCs and therefore is a good treatment for the prevention of androgen-driven balding. http://www.ncbi.nlm.nih.gov/pubmed/21034532
Ascorbic acid (one of its metabolites is the L-threonate) MAY actually be one of the keys opening the door. One guy from that thread even tried the threonate on himself however he probably didn't get high enough concentration for it to penetrate dermis. Ascorbic acid may need pH below 3.5 to be useful topically (which is very acidic/sour, I tried, think vinegar), according to http://www.nordicselfcare.com/pdf/1.09_percutaneousabsorption.pdf
Below, I will list what I've gotten out of my research so far while asking questions along the way. Please point out if any points I'm making are true/false, useful/irrelevant.
According to many studies including the Costarelis study, PGD2 is high in balding scalp.
1. Blocking PGD2 could be part of the solution to halt hair loss from progressing because PGD2 has inhibitory effects on hair growth.
2. Others say, PGD2 is high as the body's natural reaction to the chronic inflammatory activity going on in the scalp. What is the function of PGD2 in the body? Could lowering PGD2 on the scalp cause more trouble than good?
PGE2 which according to the Costarelis study, was found to be lowered in balding scalp.
1. PGE2 on scalp, lowers Testosterone/ androgens in the scalp, which lowers pgd2 and pgf2alpha, which also means lower testosterone topically in the scalp.
2. However, PGE2 is also known to cause inflammation. wtf!
PGE1 is the major hair growth booster from the prostaglandins family. DGLA is the immediate precursor of PGE1. (Prostaglandin E1). PGE1 counteracts PGE2. Minoxidil, Miconazole Nitrate or Nitroglycerin cream all upregulates PGE1.
What is the safest way to increase PGE1?
------
Do you guys feel that manipulating pge2/pgd2/pge1 on the surface is a viable way to halt loss? Ideally, I feel it's best if we can somehow figure out why PGD2 is higher and PGE2 lower on us baldies and find a way to get the balance right. I'm guessing that this is what lab researchers are trying to figure out. If anyone has any information or theories on what's going on, I'd like to hear them. From my findings, DHT-induced DKK-1 expression in dermal papilla cells seems like a good place to look into.
With that said, what do you guys think about a highly concentrated ascorbic acid topical to halt hairloss? Beholder and I (i'm sure others as well) are experimenting with a topical with ascorbic acid, msm, and melatonin. You can see the original post by Beholder here: http://www.hairlosstalk.com/interac...f-PGE2-(read-to-get-your-hopes-crushed)/page4
I'm copying some stuff he had to say about this:
Ascorbic acid (vitamin C) dose-dependently inhibited interleukin-1beta (IL-1beta)-mediated PGE2 synthesis in the human neuronal cell line. Furthermore it dose-dependentlyproduced a significant reduction in IL-1beta-mediated production of 8-iso-prostaglandin F2alpha (PGF2a), a reliable indicator of free radical formation, suggesting that the effects of ascorbic acid on COX-2-mediated PGE2 biosynthesis may be the result of the maintenance of the neuronal redox status since COX activity is known to be enhanced by oxidative stress. http://arxiv.org/abs/0708.0548
In a previous study, we recently claimed that dihydrotestosterone (DHT)-inducible dickkopf-1 (DKK-1) expression is one of the key factors involved in androgen-potentiated balding. We also demonstrated that L-ascorbic acid 2-phosphate (Asc 2-P) represses DHT-induced DKK-1 expression in cultured dermal papilla cells. Here, we investigated whether or not L-threonate could attenuate DHT-induced DKK-1 expression. We found that DHT-induced activation of DKK-1 promoter activity was significantly repressed by L-threonate. Moreover, a co-culture system featuring outer root sheath (ORS) keratinocytes and DPCs showed that DHT inhibited the growth of ORS cells, which was then significantly reversed by L-threonate. Collectively, these results indicate that L-threonate inhibited DKK-1 expression in DPCs and therefore is a good treatment for the prevention of androgen-driven balding. http://www.ncbi.nlm.nih.gov/pubmed/21034532
Ascorbic acid (one of its metabolites is the L-threonate) MAY actually be one of the keys opening the door. One guy from that thread even tried the threonate on himself however he probably didn't get high enough concentration for it to penetrate dermis. Ascorbic acid may need pH below 3.5 to be useful topically (which is very acidic/sour, I tried, think vinegar), according to http://www.nordicselfcare.com/pdf/1.09_percutaneousabsorption.pdf