Neogenic by L’Oréal
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pretty simple
On a different note.. in another thread about OC000459, one of the users who started applying it to his scalp said that his acne started going away. That could mean that the PGD-2 was truly being blocked, sebaceous glands were dissipating, and acne was ceasing due to lack of oil on the skin. That could be good news.Comment
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It's not pretty simple. I have read the whole study and it is not clear in specifying that PGD-2 is the absolute cause of MPB. It does nothing to disprove my previous comment. PGD-2 is always present before the Telogen stage for the hair to stop growing (read the study). It may continue to be present because the follicle is damaged or never signaled to go into the Anagen stage. And with its continued presence it could cause the formation of the sebaceous glands. Yes, blocking the PGD-2 receptor may very well stop the inhibition, just like limiting DHT will (for the same reason). And it may be a more elegant way to do so than previous methods, but it doesn't seem to be the cause to me, its just an effect. And it does not necessarily mean that it will move the follicle into the Anagen stage for hair regrowth.
On a different note.. in another thread about OC000459, one of the users who started applying it to his scalp said that his acne started going away. That could mean that the PGD-2 was truly being blocked, sebaceous glands were dissipating, and acne was ceasing due to lack of oil on the skin. That could be good news.
Given the correlation of increased levels of PGD2 with balding scalp in humans and the presumptive inhibitory role of PGD2 on the mouse follicle, we hypothesized that mice with high levels of PGD2 in the skin might develop features of AGA. Because Ptgs2 (cyclooxygenase 2, prostaglandin G/H synthase) is the enzyme upstream to Ptgds, we further hypothesized that mice overexpressing Ptgs2 would have elevated PGD2 levels. Transgenic mice that overexpress Ptgs2 in the epidermis had been developed previously for carcinogenesis studies. The hair follicles in these K14-Ptgs2 transgenic mice were noted to enter catagen prematurely, and these mice reportedly developed alopecia and sebaceous gland enlargement "
the only reason pgd2 is being hyped by dr C is because its the only pathway he can exploit to profit from its not the root
we already know different prostgaldnisn are elevated and lowerd as hairs cycle through some are more prominent eg pge2 in the anagen stage...its possible pgd2 is elevated because the hairs in those sampled balding men had hairs that were in the telogen stage of the cycle hence its only logical to find an abundance of pgd2...but its still possible lowering this pgd2 results in more pge2 being produced...this is what dr c is gambling on with his new product thats been announced to successfully have an impact on the ballance of prostglandins to regrow hair
im pretty confident one of the root cause is cox2 overexpression (initiated because of excess dht(another roots cause) in hair and skin cells...i think the same stem cells are used to renew skin as well as hair.Comment
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The root cause is in the follicle. Not hormones, not in our blood. Its so stupid to look at things from that direction, because if that was the case.. the follicles on the back and sides of our head would be effected. Hypothesize all you want, but thats a fact. Tell me hair transplants dont work cause they are in the Anagen stage when they are transplanted lol. The study proved that PGD-2 inhibits healthy follicles as well, so that rules out blood and hormonal issues as the root cause.Comment
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The root cause is in the follicle. Not hormones, not in our blood. Its so stupid to look at things from that direction, because if that was the case.. the follicles on the back and sides of our head would be effected. Hypothesize all you want, but thats a fact. Tell me hair transplants dont work cause they are in the Anagen stage when they are transplanted lol. The study proved that PGD-2 inhibits healthy follicles as well, so that rules out blood and hormonal issues as the root cause.
you to can hypothesize all you want...but i am 1000% confident there is no differneces between hair on the top and than hair on the sides and back but of course im no scientist so i cant prove this...but its still easily provable with an easy experiment.
anyway, the only mystery remaining is why isnt the back and sides affected, which isnt going to be figured out anytime soon.Comment
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Heres my total hypothesis... over the years UV rays from the sun damage the follicles on the top of our head. This results in abnormal follicular cells which get "confused" and dont respond to signaling from our body, or dont provide appropriate signaling to our body. This may be accelerated by genetic structure. They are then stuck in the Talogen stage for whatever reason. In a situation like that, limiting DHT or PGD-2 would not FIX the follicle, and would not promote regrowth. Great for those people who still have their hair. Not great for us NW6's.Comment
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I keep seeing you say that the problem is an over-expression of COX2-> PGD2, so many times.. like its a definite thing. The study only shows that its elevated, not WHY ITS ELEVATED in the scalp. It also says its naturally elevated with hair in the Talogen stage. It's more realistic to assume our hair is stuck in the Talogen stage.. and thats the problem, and the clinical findings are consistant with that. Now how do we signal it to change to the Anagen stage. My bet is thats exactly what Histogen figured out.
Heres my total hypothesis... over the years UV rays from the sun damage the follicles on the top of our head. This results in abnormal follicular cells which get "confused" and dont respond to signaling from our body, or dont provide appropriate signaling to our body. This may be accelerated by genetic structure. They are then stuck in the Talogen stage for whatever reason. In a situation like that, limiting DHT or PGD-2 would not FIX the follicle, and would not promote regrowth. Great for those people who still have their hair. Not great for us NW6's.Comment
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No expert, just wanted to add that the hairs that usually fall out are the ones that point directly upwards in most people, where the sun has the most exposure to direct scalp. With the sides and back of your hair, its all angled downward. Again that could have nothing to do with it all. It certainly doesn't explain temple loss, but it is interestingComment
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I keep seeing you say that the problem is an over-expression of COX2-> PGD2, so many times.. like its a definite thing. The study only shows that its elevated, not WHY ITS ELEVATED in the scalp. It also says its naturally elevated with hair in the Talogen stage. It's more realistic to assume our hair is stuck in the Talogen stage.. and thats the problem, and the clinical findings are consistant with that. Now how do we signal it to change to the Anagen stage. My bet is thats exactly what Histogen figured out.
you need to look back on dht, this is why cox 2 is eleveated - this is still a problem too. Science knows that hermphrodites never go bald and castrates can stop any further loss by getting castrated - > dht is still involved, but not as modern day science describes it as...my hypothesis - is that it is excess dht...its the levels of dht(or levels of 5 alpha reductase enzymes) in the body over one persons early life, or trapped levels of dht in that region of the scalp.
theres science that states dht does indeed interact with cox2 and its possible it has a wider role in skin too.
Heres my total hypothesis... over the years UV rays from the sun damage the follicles on the top of our head. This results in abnormal follicular cells which get "confused" and dont respond to signaling from our body, or dont provide appropriate signaling to our body. This may be accelerated by genetic structure. They are then stuck in the Talogen stage for whatever reason. In a situation like that, limiting DHT or PGD-2 would not FIX the follicle, and would not promote regrowth. Great for those people who still have their hair. Not great for us NW6's.
funny thing that you should mention uv rays
-> http://www.ncbi.nlm.nih.gov/pubmed/9635856
your hypothesis was created out of thin air. It can easily be debunked by saying "why do some men not go bald, despite being in the sun or why do castrates/hermaphrodites never fo bald despite being in the sun" i guess your response would be "because of genetics"...whereas science has already implicated cox2 and shown hair can be regrown using a cox2 inhibitor.
The only genetical aspect that may be an aspect in mpb is the differnces in expression of cox2 between people.
it truley is dht->cox2 that is the true culprit with mpb...anyway hopefully it will be proven by academic researchers sometime in the future.Comment
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Also, using castrated men as an example just contradicts your theory. They probably have almost no DHT in their blood stream, which means their PGD-2 levels are extremely low. Yet they proved that castrated men DO NOT REGROW hair. So LOW PGD2 does not equal REGROWTH. We will find out soon enough though.Comment
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Also, using castrated men as an example just contradicts your theory. They probably have almost no DHT in their blood stream, which means their PGD-2 levels are extremely low. Yet they proved that castrated men DO NOT REGROW hair. So LOW PGD2 does not equal REGROWTH. We will find out soon enough though.
blocking cox2 or pgd2 may or may not regrow hair but we will find out soon...
dormancy is part of baldness...as described earlier overexpression of cox2 is associated with cancers and its probably a cancer protection mechanism thats used by the body.
increasing pge2 may help in regrowing hair and if dr c holds the patent to it may bring this out to regrow hair in bald scalps.
i suspect the the pgd2 blockers would not regrow hair just prevent any further baldness.Comment
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http://www.quithairloss.com/hair-solar-radiation.html Hmmm. Guess someone already thought of and documented the sun theory.Comment
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