In a nutshell, relatively recent investigations by Dr. Garza of Johns Hopkins University and Dr. Cotsarelis of the University Of Pennsylvania School of Medicine found that prostaglandin D2 levels are elevated in balding scalps, and inhibiting PGD2 could prevent baldness from progressing. This research was featured in laymen’s terminology in the following feature in Science news.
The search for a viable PGD2 inhibitor has been the focus of many research teams in both the pharmaceutical and biotech industries. In 2015, Kythera Biopharmaceuticals purchased the global rights to Setipiprant, a PGD2 inhibitor. It is likely that Setipiprant represents a breakthrough treatment for both men and women with Androgenetic Alopecia. Unfortunately clinical trials for Setipiprant will not be completed for several years.
This just published study however may represent a breakthrough role for Antioxidants, specifically N-Acetyl-Cysteine, as readily accessible, health promoting PGD2 Inhibitors. They appear to function by blocking PDG2 induced up-regulation of androgens in keratinocytes, which would essentially neutralize any negative effects PDG2 may have on hair growth.
J Investig Dermatol Symp Proc. 2017 Oct;18(2):S81-S84. Prostaglandin D2 Uses Components of ROS Signaling to Enhance Testosterone Production in Keratinocytes.
Elevated levels of prostaglandin D2 (PGD2) have been shown to be present in the bald scalp of androgenic alopecia (AGA) patients and to functionally inhibit hair growth. However, its precise mechanism in AGA has yet to be clearly defined. Although testosterone plays a critical role in the initiation and progression of AGA, the existence of a possible link between PGD2 and testosterone in skin has not been investigated. Here we show that human keratinocytes treated with PGD2 show enhanced capacity to convert the weak androgen, androstenedione, to testosterone. At the same time, treatment with PGD2 induced reactive oxygen species as indicated by generation of the lipid peroxidation product, 4-hydroxynonenal. To determine whether these two events are linked, we used the reactive oxygen species scavenger N-acetyl-cysteine, which blocked the enhanced testosterone production from PGD2-treated keratinocytes.Our study suggests the existence of a possible crosstalk between the PGD2-reactive oxygen species axis and testosterone metabolism in keratinocytes. Thus, we propose that AGA patients might benefit from the use of N-acetyl-cysteine or other antioxidants as a supplement to currently available or emerging AGA therapies such as finasteride, minoxidil, and PGD2 receptor blockers.
N-Acetyl-Cysteine , should be used at a dose of at least 1,000mg or more a day. As with L-Cysteine, It is important to concurrently use at least 3 times as much Vitamin C with N-Acetyl-Cysteine, to maintain lipid soluability. Both Cysteine and N-Acetyl Cysteine increase hair shaft diameter and increase hair growth rate by approximately 20%, requiring one to get hair cuts more often.
In addition to N-Acetyl Cysteine, Resveratrol and Quercetin function as PDG2 inhibitors:
Also of significance is the fact mainstream researchers in a conservative journal are finally recommending anti-oxidants as a hair loss treatment, something we at MPB Research have been recommending for almost 20 years.
Emu Oil also has the rare characteristic of being an oil that actually possesses anti-oxidant properties.