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roger_that

MARYLAND,
08.12.2012, 18:48
(edited by roger_that, 08.12.2012, 19:10)
 

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2 (Hair Multiplication & Stem Cells Treatment)

First of all I want to say that I just went out and bought my first bottle of NasalCrom (Cromolyn Sodium) for use on my hair. I have been using NC for years, on and off, for my allergies. It completely eliminates my allergies, so I'm confident the stuff has some real potency at what it does -- which is stabilizing the Mast cells and preventing their degranulation. The spray bottle cost me, as usual, $16.99.

Now I want to call everyone's attention to a concern that occurred to me, which nobody seems to be addressing on this forum or -- especially -- on some of the other forums where lots of people are using and discussing Cromolyn Sodium.

I think this is a big point people have overlooked.

People are just assuming that Mast cells are the only major source of PGD2 in the scalps of people with MPB.

To me, there is no reason to make that assumption.

In fact, it is entirely possible that Mast cells are a relatively minor source of PGD2 in the scalps of people with MPB.

In that case, Cromolyn Sodium might not help that much at all.

I am still going to use it, to determine that, however.

People are assuming that everything is essentially the same with respect to "sources of PGD2" in the scalps of normal people as compared with balding people, and I think that's a hasty and uninformed assumption.

Remember that all PGD2 is created by the enzyme called PGD2 Sythase.

To my mind, PGD2 Synthase can theoretically be present and active in almost any cell, not just in Mast cells. (Parenthetically we know that another form of PGD2 Synthase exists in the brain and nervous system -- but that form is not relevant to this discussion.)

All it would take is for the PGD2 Synthase gene to become activated, for a cell to express PGD2 Synthase and start making a lot of PGD2.

We know that Mast cells exist in the skin of people with MPB and people without MPB.

Normally, the function of Mast cells is to produce and excrete chemicals called "cytokines", which include things like histamine, heparin, and PGD2, in response to allergens.

Therefore by inductive reasoning we can conclude that Mast cells have a lot of activated PGD2 Synthase genes and PGD2 Synthase enzyme, cranking out a relatively large amount of PGD2, in comparison with most other skin cells, which don't.

But where does that PGD2 Synthase enzyme come from? Probably in the Mast cells, their DNA expresses the PGD2 Synthase gene a lot -- significantly more than in the neighboring normal skin cells.

In people with MPB, we know that DHT interacts with the androgen receptors and that DHT/Receptor complex then affects the DNA inside the nucleus of skin cells, causing something to happen.

We now suspect that what happens is the creation of a lot of PGD2 Synthase in those cells. The PGD2 Synthase then goes on to create a lot of PGD2.

But there is absolutely no reason I can think of to assume that in people with MPB, that process is restricted to the Mast cells alone. That process could theoretically happen in ANY tissue cell. All you need is DHT exposure and the process would be kicked into effect.

So that means that if PGD2 Synthase is being expressed in non-Mast cells, and PGD2 is being created in those non-Mast cells, then a drug which "stabilizes the Mast cells" won't be able to take care of PGD2 being created in non-Mast cells.

If that is the case (and I don't know that it is, I just know that it is theoretically possible unless someone can explain to me why it actually doesn't happen in fact), then Cromolyn Sodium wouldn't really help us much, because it wouldn't have any effect on PGD2 being created outside of the Mast cells, in MPB affected people.

Does anyone get what I'm trying to say here?

I really hope I am wrong about this. This is just a suspicion, I very well may be wrong, and so I am going to try this experiment anyway.




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

jarjarbinx

08.12.2012, 20:14

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

I fully understand your point and I'm also concerned about whether or not PGD2 originates entirely, or even mostly, in the mast cells. In addition, I'm not so convinced that NasalCrom will be able to absorb into the skin to the level of the complete follicle, and I'm also concerned that even if PGD2 only originates in the mast cells NasalCrom still won't be potent enough to ameliorate hair growth. I understand that NasalCrom completely eliminates your allergies but that's a different biological task than reversing hair loss. It may be an easier biological task to eliminate allergies than it is to reverse hair loss. Eliminating allergies may require only the elimination of a small amount of PGD2 whereas reversing hair loss may require the elimination of a lot of PGD2. We just don't know.

All that having been said I'm still hopeful that your experiment works because it would be a lot easier on all of us if we could use NasalCrom to reverse our hair los.

While I have some questions about whether or not NasalCrom has what it takes to reverse hair loss I have no evidence that it doesn't. If you use NasalCrom + minox and you grow hair then that means that the answers to all 3 of my questions regarding NasalCrom are favorable for hair growth with NasalCrom.

Good luck.




» First of all I want to say that I just went out and bought my first bottle
» of NasalCrom (Cromolyn Sodium) for use on my hair. I have been using NC
» for years, on and off, for my allergies. It completely eliminates my
» allergies, so I'm confident the stuff has some real potency at what it does
» -- which is stabilizing the Mast cells and preventing their degranulation.
» The spray bottle cost me, as usual, $16.99.
»
» Now I want to call everyone's attention to a concern that occurred to me,
» which nobody seems to be addressing on this forum or -- especially -- on
» some of the other forums where lots of people are using and discussing
» Cromolyn Sodium.
»
» I think this is a big point people have overlooked.
»
» People are just assuming that Mast cells are the only major source of PGD2
» in the scalps of people with MPB.
»
» To me, there is no reason to make that assumption.
»
» In fact, it is entirely possible that Mast cells are a relatively minor
» source of PGD2 in the scalps of people with MPB.
»
» In that case, Cromolyn Sodium might not help that much at all.
»
» I am still going to use it, to determine that, however.
»
» People are assuming that everything is essentially the same with respect to
» "sources of PGD2" in the scalps of normal people as compared with balding
» people, and I think that's a hasty and uninformed assumption.
»
» Remember that all PGD2 is created by the enzyme called PGD2 Sythase.
»
» To my mind, PGD2 Synthase can theoretically be present and active in
» almost any cell, not just in Mast cells. (Parenthetically we know that
» another form of PGD2 Synthase exists in the brain and nervous system -- but
» that form is not relevant to this discussion.)
»
» All it would take is for the PGD2 Synthase gene to become activated,
» for a cell to express PGD2 Synthase and start making a lot of PGD2.
»
» We know that Mast cells exist in the skin of people with MPB and people
» without MPB.
»
» Normally, the function of Mast cells is to produce and excrete chemicals
» called "cytokines", which include things like histamine, heparin, and PGD2,
» in response to allergens.
»
» Therefore by inductive reasoning we can conclude that Mast cells have a lot
» of activated PGD2 Synthase genes and PGD2 Synthase enzyme, cranking out a
» relatively large amount of PGD2, in comparison with most other skin cells,
» which don't.
»
» But where does that PGD2 Synthase enzyme come from? Probably in the Mast
» cells, their DNA expresses the PGD2 Synthase gene a lot -- significantly
» more than in the neighboring normal skin cells.
»
» In people with MPB, we know that DHT interacts with the androgen receptors
» and that DHT/Receptor complex then affects the DNA inside the nucleus of
» skin cells, causing something to happen.
»
» We now suspect that what happens is the creation of a lot of PGD2 Synthase
» in those cells. The PGD2 Synthase then goes on to create a lot of PGD2.
»
» But there is absolutely no reason I can think of to assume that in
» people with MPB, that process is restricted to the Mast cells alone. That
» process could theoretically happen in ANY tissue cell. All you need is DHT
» exposure and the process would be kicked into effect.

»
» So that means that if PGD2 Synthase is being expressed in non-Mast cells,
» and PGD2 is being created in those non-Mast cells, then a drug which
» "stabilizes the Mast cells" won't be able to take care of PGD2 being
» created in non-Mast cells.
»
» If that is the case (and I don't know that it is, I just know that it is
» theoretically possible unless someone can explain to me why it actually
» doesn't happen in fact), then Cromolyn Sodium wouldn't really help us much,
» because it wouldn't have any effect on PGD2 being created outside of the
» Mast cells, in MPB affected people.
»
» Does anyone get what I'm trying to say here?
»
» I really hope I am wrong about this. This is just a suspicion, I very well
» may be wrong, and so I am going to try this experiment anyway.




jarjarbinx is located in [NA] and he is available to meet: NO

hairman2

08.12.2012, 20:18

@ jarjarbinx

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

You sound a lot more skeptical about nasalcrom than you do about Iron Dragons Cromolyn solution. Why is that, especially considering that its basically the same thing.

» I fully understand your point and I'm also concerned about whether or not
» PGD2 originates entirely, or even mostly, in the mast cells. In addition,
» I'm not so convinced that NasalCrom will be able to absorb into the skin to
» the level of the complete follicle, and I'm also concerned that even if
» PGD2 only originates in the mast cells NasalCrom still won't be potent
» enough to ameliorate hair growth. I understand that NasalCrom completely
» eliminates your allergies but that's a different biological task than
» reversing hair loss. It may be an easier biological task to eliminate
» allergies than it is to reverse hair loss. Eliminating allergies may
» require only the elimination of a small amount of PGD2 whereas reversing
» hair loss may require the elimination of a lot of PGD2. We just don't
» know.
»
» All that having been said I'm still hopeful that your experiment works
» because it would be a lot easier on all of us if we could use NasalCrom to
» reverse our hair los.
»
» While I have some questions about whether or not NasalCrom has what it
» takes to reverse hair loss I have no evidence that it doesn't. If you use
» NasalCrom + minox and you grow hair then that means that the answers to all
» 3 of my questions regarding NasalCrom are favorable for hair growth with
» NasalCrom.
»
» Good luck.




hairman2 is located in [NA] and he is available to meet: NO

roger_that

MARYLAND,
08.12.2012, 20:41

@ hairman2

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» You sound a lot more skeptical about nasalcrom than you do about Iron
» Dragons Cromolyn solution. Why is that, especially considering that its
» basically the same thing.

Can't speak for jarjar, but I am of the exact same mind about both of them, they are both essentially the same product.

ID's cromolyn solution has all of the same potential as well as the same potential drawbacks of NasalCrom.

I'm just focusing on NC here because I'm very familiar with the drug, having used it for a long time, and I know it's safe, causes no side effects, and I have easy access to it. Why buy it from some chemical company online and pay a lot more? The stuff is available in pharmacies all over North America for about $17.




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

neversaynever

08.12.2012, 20:50

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» » You sound a lot more skeptical about nasalcrom than you do about Iron
» » Dragons Cromolyn solution. Why is that, especially considering that its
» » basically the same thing.
»
» Can't speak for jarjar, but I am of the exact same mind about both of them,
» they are both essentially the same product.
»
» ID's cromolyn solution has all of the same potential as well as the same
» potential drawbacks of NasalCrom.
»
» I'm just focusing on NC here because I'm very familiar with the drug,
» having used it for a long time, and I know it's safe, causes no side
» effects, and I have easy access to it. Why buy it from some chemical
» company online and pay a lot more? The stuff is available in pharmacies
» all over North America for about $17.

I think it will have the same effect. Mast cells are essential to hair cycling, so supressing them will just 'pause' the whole process. Or at least slow it down.

Dr cots referenced to this study in his 2012 study publication:

"while inhibitors of mast cell degranulation (cromoglycate, tiacrilast) and antagonists of selected MC products (clemastin, ranitidine, ketanserin) significantly retarded the induced development of anagen follicles in these mice"

Somewhere between pge2, f2a, mast cell supressing...there might be something that helps.

But at least nasalcrom is relatively cheap.




neversaynever is located in [NA] and he is available to meet: NO

neversaynever

08.12.2012, 20:54

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» First of all I want to say that I just went out and bought my first bottle
» of NasalCrom (Cromolyn Sodium) for use on my hair. I have been using NC
» for years, on and off, for my allergies. It completely eliminates my
» allergies, so I'm confident the stuff has some real potency at what it does
» -- which is stabilizing the Mast cells and preventing their degranulation.
» The spray bottle cost me, as usual, $16.99.
»
» Now I want to call everyone's attention to a concern that occurred to me,
» which nobody seems to be addressing on this forum or -- especially -- on
» some of the other forums where lots of people are using and discussing
» Cromolyn Sodium.
»
» I think this is a big point people have overlooked.
»
» People are just assuming that Mast cells are the only major source of PGD2
» in the scalps of people with MPB.
»
» To me, there is no reason to make that assumption.
»
» In fact, it is entirely possible that Mast cells are a relatively minor
» source of PGD2 in the scalps of people with MPB.
»
» In that case, Cromolyn Sodium might not help that much at all.
»
» I am still going to use it, to determine that, however.
»
» People are assuming that everything is essentially the same with respect to
» "sources of PGD2" in the scalps of normal people as compared with balding
» people, and I think that's a hasty and uninformed assumption.
»
» Remember that all PGD2 is created by the enzyme called PGD2 Sythase.
»
» To my mind, PGD2 Synthase can theoretically be present and active in
» almost any cell, not just in Mast cells. (Parenthetically we know that
» another form of PGD2 Synthase exists in the brain and nervous system -- but
» that form is not relevant to this discussion.)
»
» All it would take is for the PGD2 Synthase gene to become activated,
» for a cell to express PGD2 Synthase and start making a lot of PGD2.
»
» We know that Mast cells exist in the skin of people with MPB and people
» without MPB.
»
» Normally, the function of Mast cells is to produce and excrete chemicals
» called "cytokines", which include things like histamine, heparin, and PGD2,
» in response to allergens.
»
» Therefore by inductive reasoning we can conclude that Mast cells have a lot
» of activated PGD2 Synthase genes and PGD2 Synthase enzyme, cranking out a
» relatively large amount of PGD2, in comparison with most other skin cells,
» which don't.
»
» But where does that PGD2 Synthase enzyme come from? Probably in the Mast
» cells, their DNA expresses the PGD2 Synthase gene a lot -- significantly
» more than in the neighboring normal skin cells.
»
» In people with MPB, we know that DHT interacts with the androgen receptors
» and that DHT/Receptor complex then affects the DNA inside the nucleus of
» skin cells, causing something to happen.
»
» We now suspect that what happens is the creation of a lot of PGD2 Synthase
» in those cells. The PGD2 Synthase then goes on to create a lot of PGD2.
»
» But there is absolutely no reason I can think of to assume that in
» people with MPB, that process is restricted to the Mast cells alone. That
» process could theoretically happen in ANY tissue cell. All you need is DHT
» exposure and the process would be kicked into effect.

»
» So that means that if PGD2 Synthase is being expressed in non-Mast cells,
» and PGD2 is being created in those non-Mast cells, then a drug which
» "stabilizes the Mast cells" won't be able to take care of PGD2 being
» created in non-Mast cells.
»
» If that is the case (and I don't know that it is, I just know that it is
» theoretically possible unless someone can explain to me why it actually
» doesn't happen in fact), then Cromolyn Sodium wouldn't really help us much,
» because it wouldn't have any effect on PGD2 being created outside of the
» Mast cells, in MPB affected people.
»
» Does anyone get what I'm trying to say here?
»
» I really hope I am wrong about this. This is just a suspicion, I very well
» may be wrong, and so I am going to try this experiment anyway.

I think youre right. When you factor in DHT, mast cells seem less the culprit and its the keratinocyte and other 'hair cells' that are creating a sort of feedback loop. Mast cells being vital to the hair cycle get caught up in it maybe.

But if keratinocytes are made to stop producing pgd2, we have no idea what will happen.




neversaynever is located in [NA] and he is available to meet: NO

roger_that

MARYLAND,
08.12.2012, 20:57

@ neversaynever

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» I think it will have the same effect. Mast cells are essential to hair
» cycling, so supressing them will just 'pause' the whole process. Or at
» least slow it down.
»
» Dr cots referenced to this study in his 2012 study publication:
»
» "while inhibitors of mast cell degranulation (cromoglycate,
» tiacrilast) and antagonists of selected MC products (clemastin, ranitidine,
» ketanserin) significantly retarded the induced development of anagen
» follicles in these mice"

Not sure, but I think you're taking some things out of context here.

If he says cromoglycolate (Cromolyn) "significantly retarded the induced development of anagen follicles", then that would mean that cromoglycolate HURTS your hair growth, not helps it... wouldn't it?

Thanks for calling our attention to it, but we have to calm down here and see what all this stuff means, and be sure we're not taking things out of context.

When you say "suppressing them will just 'pause' the whole process", if you're talking about pausing the process, what process do you mean?

It is my understanding that PGD2 has already paused the process of follicle cycling, and by removing PGD2 we are trying to re-start the process, not pause it.




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

jarjarbinx

08.12.2012, 20:58

@ hairman2

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

For starters, alecbaldone is not indicating he's experiencing hair growth but some of the people using OC are indicating that they are having hair growth.



» You sound a lot more skeptical about nasalcrom than you do about Iron
» Dragons Cromolyn solution. Why is that, especially considering that its
» basically the same thing.
»
» » I fully understand your point and I'm also concerned about whether or
» not
» » PGD2 originates entirely, or even mostly, in the mast cells. In
» addition,
» » I'm not so convinced that NasalCrom will be able to absorb into the skin
» to
» » the level of the complete follicle, and I'm also concerned that even if
» » PGD2 only originates in the mast cells NasalCrom still won't be potent
» » enough to ameliorate hair growth. I understand that NasalCrom completely
» » eliminates your allergies but that's a different biological task than
» » reversing hair loss. It may be an easier biological task to eliminate
» » allergies than it is to reverse hair loss. Eliminating allergies may
» » require only the elimination of a small amount of PGD2 whereas reversing
» » hair loss may require the elimination of a lot of PGD2. We just don't
» » know.
» »
» » All that having been said I'm still hopeful that your experiment works
» » because it would be a lot easier on all of us if we could use NasalCrom
» to
» » reverse our hair los.
» »
» » While I have some questions about whether or not NasalCrom has what it
» » takes to reverse hair loss I have no evidence that it doesn't. If you
» use
» » NasalCrom + minox and you grow hair then that means that the answers to
» all
» » 3 of my questions regarding NasalCrom are favorable for hair growth with
» » NasalCrom.
» »
» » Good luck.




jarjarbinx is located in [NA] and he is available to meet: NO

neversaynever

08.12.2012, 20:58

@ neversaynever

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

Im getting nasalcrom tomorow, and im interested in Ricinoleic acid aswell.




neversaynever is located in [NA] and he is available to meet: NO

neversaynever

08.12.2012, 21:00

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

Thats why im posting it here. Hoping together we can find the right context :)

By pause I mean stop further hairloss but also stop further re-growth. ie. Stop shedding, and not get regrowth.

Something that is very encouraging is that if nasalcrom stops the shedding, we have easy access to something cheap that halts or slows down hairloss without a limp dick or ordering expensive chemicals from overseas.

It has been proven effective in penetrating the skin for various skin issues (with positive results)




neversaynever is located in [NA] and he is available to meet: NO

neversaynever

08.12.2012, 21:10

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» » I think it will have the same effect. Mast cells are essential to hair
» » cycling, so supressing them will just 'pause' the whole process. Or at
» » least slow it down.
» »
» » Dr cots referenced to this study in his 2012 study publication:
» »
» » "while inhibitors of mast cell degranulation (cromoglycate,
» » tiacrilast) and antagonists of selected MC products (clemastin,
» ranitidine,
» » ketanserin) significantly retarded the induced development of anagen
» » follicles in these mice"
»
» Not sure, but I think you're taking some things out of context here.
»
» If he says cromoglycolate (Cromolyn) "significantly retarded the induced
» development of anagen follicles", then that would mean that cromoglycolate
» HURTS your hair growth, not helps it... wouldn't it?
»
» Thanks for calling our attention to it, but we have to calm down here and
» see what all this stuff means, and be sure we're not taking things out of
» context.
»
» When you say "suppressing them will just 'pause' the whole process", if
» you're talking about pausing the process, what process do you mean?
»
» It is my understanding that PGD2 has already paused the process of follicle
» cycling, and by removing PGD2 we are trying to re-start the process,
» not pause it.

Has PGd2 paused hair cycling or put it into hyperdrive? ie, shorter and shorter anagen phases.

Not being sarcastic, just curious...

My assumption was that elevated levels of pgd2 induces early telogen or catagen, and the anagen time becomes shorter and shorter.

I believe thats where mast cells are involved. They induce catagen (according to cots and others)




neversaynever is located in [NA] and he is available to meet: NO

roger_that

MARYLAND,
08.12.2012, 21:50

@ neversaynever

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» Thats why im posting it here. Hoping together we can find the right context
» :)
»
» By pause I mean stop further hairloss but also stop further re-growth. ie.
» Stop shedding, and not get regrowth.

I'm not following you. I like to avoid terms like "shedding" because they're scientifically misleading.

»
» Something that is very encouraging is that if nasalcrom stops the shedding,
» we have easy access to something cheap that halts or slows down hairloss
» without a limp dick or ordering expensive chemicals from overseas.

I don't think you can have a drug that "stops shedding" and yet doesn't promote hair growth. The only reason people with MPB experience more "shedding" in the first place is because their follicles are being miniaturized. Shedding is just one outward sign of miniaturization -- the two are connected, not independent of each other. If you stop one of these processes, you stop both.

»
» It has been proven effective in penetrating the skin for various skin
» issues (with positive results)




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

neversaynever

08.12.2012, 21:56
(edited by neversaynever, 08.12.2012, 22:14)

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

By shedding I mean the miniturization procress.

During mpb the miniturization causes hairs to shed more often, because the anagen phases are become shorter and shorter. For me, RU seems to have slowed that miniturization procress big time, and thus, im seeing far far less shedding (almost nothing compared to what it was) ie...less or halted shedding.

Regrowth would be growing hairs where there was no hair, or turning vellus hairs into terminal ones.




neversaynever is located in [NA] and he is available to meet: NO

jarjarbinx

08.12.2012, 23:35
(edited by jarjarbinx, 09.12.2012, 00:05)

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» » Thats why im posting it here. Hoping together we can find the right
» context
» » :)
» »
» » By pause I mean stop further hairloss but also stop further re-growth.
» ie.
» » Stop shedding, and not get regrowth.
»
» I'm not following you. I like to avoid terms like "shedding" because
» they're scientifically misleading.
»
» »
» » Something that is very encouraging is that if nasalcrom stops the
» shedding,
» » we have easy access to something cheap that halts or slows down hairloss
» » without a limp dick or ordering expensive chemicals from overseas.
»
» I don't think you can have a drug that "stops shedding" and yet doesn't
» promote hair growth. The only reason people with MPB experience more
» "shedding" in the first place is because their follicles are being
» miniaturized. Shedding is just one outward sign of miniaturization -- the
» two are connected, not independent of each other. If you stop one of these
» processes, you stop both.
»


I disagree with you here. I think that stopping hair loss and reversing hair loss are two different biological tasks, and I think reversing hair loss is the harder of the two biological tasks.



» »
» » It has been proven effective in penetrating the skin for various skin
» » issues (with positive results)




jarjarbinx is located in [NA] and he is available to meet: NO

neversaynever

08.12.2012, 23:55

@ jarjarbinx

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» » » Thats why im posting it here. Hoping together we can find the right
» » context
» » » :)
» » »
» » » By pause I mean stop further hairloss but also stop further re-growth.
» » ie.
» » » Stop shedding, and not get regrowth.
» »
» » I'm not following you. I like to avoid terms like "shedding" because
» » they're scientifically misleading.
» »
» » »
» » » Something that is very encouraging is that if nasalcrom stops the
» » shedding,
» » » we have easy access to something cheap that halts or slows down
» hairloss
» » » without a limp dick or ordering expensive chemicals from overseas.
» »
» » I don't think you can have a drug that "stops shedding" and yet doesn't
» » promote hair growth. The only reason people with MPB experience more
» » "shedding" in the first place is because their follicles are being
» » miniaturized. Shedding is just one outward sign of miniaturization --
» the
» » two are connected, not independent of each other. If you stop one of
» these
» » processes, you stop both.
» »
»
»
» I disagree with you here. I think that stopping hair loss and reversing
» hair loss are two different biological tasks, and I think reversing hair
» loss is the harder of the two biological tasks.
»
» I used to be intensely focused on anti-androgens and 5-alpha reductase
» inhibitors. I used to know where to find evidence showing that it takes
» more anti-androgenic activity to reverse hair loss than to arrest hair loss
» but that was years ago so I don't remember where I found that evidence.
» But I don't know where it is. I have given up on anti-androgens and 5-alpha
» reductase inhibitors. RU was definitely the most effective thing I ever
» used. It grew me some new hair. Neither proscar or dutasteride could grow
» me new hair. They both slowed down or arrested my hair loss.
»
»
»
»
» » »
» » » It has been proven effective in penetrating the skin for various skin
» » » issues (with positive results)

Why did you stop RU? Supply problems? Did you use it with minox? If so how?

Im interested in something that will be far more effective than minox, theres always hope :)




neversaynever is located in [NA] and he is available to meet: NO

jarjarbinx

09.12.2012, 00:19

@ neversaynever

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» » » » Thats why im posting it here. Hoping together we can find the right
» » » context
» » » » :)
» » » »
» » » » By pause I mean stop further hairloss but also stop further
» re-growth.
» » » ie.
» » » » Stop shedding, and not get regrowth.
» » »
» » » I'm not following you. I like to avoid terms like "shedding" because
» » » they're scientifically misleading.
» » »
» » » »
» » » » Something that is very encouraging is that if nasalcrom stops the
» » » shedding,
» » » » we have easy access to something cheap that halts or slows down
» » hairloss
» » » » without a limp dick or ordering expensive chemicals from overseas.
» » »
» » » I don't think you can have a drug that "stops shedding" and yet
» doesn't
» » » promote hair growth. The only reason people with MPB experience more
» » » "shedding" in the first place is because their follicles are being
» » » miniaturized. Shedding is just one outward sign of miniaturization
» --
» » the
» » » two are connected, not independent of each other. If you stop one of
» » these
» » » processes, you stop both.
» » »
» »
» »
» » I disagree with you here. I think that stopping hair loss and reversing
» » hair loss are two different biological tasks, and I think reversing hair
» » loss is the harder of the two biological tasks.
» »
» » I used to be intensely focused on anti-androgens and 5-alpha reductase
» » inhibitors. I used to know where to find evidence showing that it takes
» » more anti-androgenic activity to reverse hair loss than to arrest hair
» loss
» » but that was years ago so I don't remember where I found that evidence.
» » But I don't know where it is. I have given up on anti-androgens and
» 5-alpha
» » reductase inhibitors. RU was definitely the most effective thing I ever
» » used. It grew me some new hair. Neither proscar or dutasteride could
» grow
» » me new hair. They both slowed down or arrested my hair loss.
» »
» »
» »
» »
» » » »
» » » » It has been proven effective in penetrating the skin for various
» skin
» » » » issues (with positive results)
»
» Why did you stop RU? Supply problems? Did you use it with minox? If so
» how?
»
» Im interested in something that will be far more effective than minox,
» theres always hope :)

1. Sometimes it worked and sometimes it didn't. I did it for about 2 years.
One time I got complete regrowth after the 4th month. Total regrowth. But then the next batch wouldn't work. It would work when I would get it fresh but I couldn't get it fresh every time. I felt that he would say it was fresh but sometimes it would be fresh and sometimes it wouldn't be.

2. I had a problem with customs once. They were upset at first. They withheld my delivery at their office for two weeks at room tempurature.

3. I got gyno, which I reversed with arimidex, but it was quite disturbing at fist.


I don't want to use an anti-androgen again. I want to try to ameliorate my hair loss downstream of the angrogens if I can. I'm hoping that by targeting the problem downstream of the androgens then that won't trigger the gyno again. I still have a VERY TINY case of gyno that is not visible, and I think that if I use anti-androgens again it will agravate the tiny case of gyno that I have and turn it into a big case of gyno.




jarjarbinx is located in [NA] and he is available to meet: NO

neversaynever

09.12.2012, 00:40

@ jarjarbinx

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

Of course pgd2 inhibition wont induce gyno.

How long were you using RU before you got gyno? And what dose? Any other sides? Ive had no sides at all upto 80mg.

I agree that it would be much better if we can do the same as RU downstream, and im confident we can. Though youre the only person ive read about who had regrowth with RU alone.

Im quite happy to halt the miniturizing procress (or at least slow it down greatly), but in terms of regrowth we have even more limited options.

Curious about all this PG stuff because i dont want to mess with DHT. After alot of reading ive got a feeling one of the big issues is at the catagen phase (where mast cells are responsible). Thats not to say mast cells are the reason for balding, i think the cause comes from the follicles primary cells, which are creating a sort of feedback loop with the mast cells creating ultra short anagen phases by inducing catagen phase too early. Round and round it goes. Mast cells produce pgd2 to induce catagen, but if the DP cells and K cells in the follicle are also producing pgd2 as some kind of response to over expressed DHT, then it equals too much pgd2.

Im quite confident that blocking the gpr44 receptor will at least slow down / stop the follicle shrinking process.

Ordered nasalcrom. Very curious to try it.




neversaynever is located in [NA] and he is available to meet: NO

Mr. Z

09.12.2012, 01:23

@ neversaynever

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

You guys may be interested in this publication.

http://www.ncbi.nlm.nih.gov/pubmed/9354767

Activated skin mast cells are involved in murine hair follicle regression (catagen).
Maurer M, Fischer E, Handjiski B, von Stebut E, Algermissen B, Bavandi A, Paus R.
Source
Department of Dermatology, Charité, Humboldt-Universität zu Berlin, Germany.
Abstract

Increasing evidence supports a role for mast cells (MC) in the control of tissue remodeling. Using the cyclic growth and regression activity of the murine hair follicle (HF) as a model, we have previously demonstrated that MC are involved in regulating the HF transformation from resting (telogen) to active hair growth (anagen). In the present study, we investigated the potential role of skin MC in spontaneous HF regression (catagen), a rapid and highly controlled process of organ involution characterized by massive epithelial cell apoptosis. By histochemistry, immunohistochemistry, and electron microscopy, we first assessed the number, location, and granulation status of perifollicular MC during the anagen-catagen-telogen transformation of back skin HF. Spontaneous catagen induction was associated with a dramatic reduction of dermal MC numbers, preceded by an increase in the percentage of degranulated MC. In vivo, the MC-secretagogues substance P and adrenocorticotropic hormone induced premature and dystrophic catagen development in anagen HF, whereas inhibitors of MC degranulation retarded normal catagen development. Comparing HF cycling in MC-deficient WBB6F1-KitW/KitWv and congenic normal (+/+) mice, catagen development was retarded in the virtual absence of MC. These data support the notion that MC function as hair cycle regulators and are involved in the control of HF regression. The mouse model employed here offers an excellent tool for dissecting the physiologic role of MC as "central switchboards of tissue remodeling" in developmentally regulated systems, specifically in organ involution processes.

I've got some sodium cromolyn and will begin testing tonight.




Mr. Z is located in [NA] and he is available to meet: NO

Mr. Z

09.12.2012, 01:27

@ Mr. Z

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

More:

Dermal fibrosis in male pattern hair loss: a suggestive implication of mast cells.
Arch Dermatol Res. 2008 Mar;300(3):147-52. Epub 2008 Feb 20.
Won CH, Kwon OS, Kim YK, Kang YJ, Kim BJ, Choi CW, Eun HC, Cho KH.
Department of Dermatology, Seoul National University College of Medicine, Yongon-Dong 28, Chongno-Gu, Seoul, 110-744, Republic of Korea.

A relationship has been suggested between mast cells (MCs) and male pattern hair loss (MPHL), because of histological evidence of perifollicular fibrosis and increased mast cell numbers. Two paired punch biopsies were taken from balding vertexes and non-balding occipital promontory areas of ten patients with MPHL (Ludwig-Hamilton IIIv to IV) and from five normal subjects aged from 20 to 35 years. Masson trichrome and Victoria blue staining were performed to observe collagen frameworks and elastic fiber structures. Numbers of immunoreactive MCs stained with anti-tryptase or anti-chymase antibody were counted. It was found that collagen bundles were significantly increased in balding vertexes than in non-balding occiput scalp skin. A near 4-fold increase in elastic fibers was observed in both vertex and occiput scalp skins with MPHL versus controls. Total numbers of MCs (tryptase-positive) in site-matched scalp samples were about 2-fold higher in MPHL subjects than in normal controls. Percentage elastic fiber (%) was found to be relatively well-correlated with tryptase and chymase-positive MCs. These findings suggest that accumulated MCs might be responsible for increased elastic fiber synthesis in MPHL, and indicate that future investigations are warranted.




Mr. Z is located in [NA] and he is available to meet: NO

hairman2

09.12.2012, 01:27

@ Mr. Z

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

hmmm that is very interesting... I think I need to order some cromo as well :)

» You guys may be interested in this publication.
»
» http://www.ncbi.nlm.nih.gov/pubmed/9354767
»
» Activated skin mast cells are involved in murine hair follicle regression
» (catagen).
» Maurer M, Fischer E, Handjiski B, von Stebut E, Algermissen B, Bavandi A,
» Paus R.
» Source
» Department of Dermatology, Charité, Humboldt-Universität zu Berlin,
» Germany.
» Abstract
»
» Increasing evidence supports a role for mast cells (MC) in the control of
» tissue remodeling. Using the cyclic growth and regression activity of the
» murine hair follicle (HF) as a model, we have previously demonstrated that
» MC are involved in regulating the HF transformation from resting (telogen)
» to active hair growth (anagen). In the present study, we investigated the
» potential role of skin MC in spontaneous HF regression (catagen), a rapid
» and highly controlled process of organ involution characterized by massive
» epithelial cell apoptosis. By histochemistry, immunohistochemistry, and
» electron microscopy, we first assessed the number, location, and
» granulation status of perifollicular MC during the anagen-catagen-telogen
» transformation of back skin HF. Spontaneous catagen induction was
» associated with a dramatic reduction of dermal MC numbers, preceded by an
» increase in the percentage of degranulated MC. In vivo, the
» MC-secretagogues substance P and adrenocorticotropic hormone induced
» premature and dystrophic catagen development in anagen HF, whereas
» inhibitors of MC degranulation retarded normal catagen development.
» Comparing HF cycling in MC-deficient WBB6F1-KitW/KitWv and congenic normal
» (+/+) mice, catagen development was retarded in the virtual absence of MC.
» These data support the notion that MC function as hair cycle regulators
» and are involved in the control of HF regression. The mouse model
» employed here offers an excellent tool for dissecting the physiologic role
» of MC as "central switchboards of tissue remodeling" in developmentally
» regulated systems, specifically in organ involution processes.
»
» I've got some sodium cromolyn and will begin testing tonight.




hairman2 is located in [NA] and he is available to meet: NO

neversaynever

09.12.2012, 02:31

@ Mr. Z

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» More:
»
» Dermal fibrosis in male pattern hair loss: a suggestive implication of mast
» cells.
» Arch Dermatol Res. 2008 Mar;300(3):147-52. Epub 2008 Feb 20.
» Won CH, Kwon OS, Kim YK, Kang YJ, Kim BJ, Choi CW, Eun HC, Cho KH.
» Department of Dermatology, Seoul National University College of Medicine,
» Yongon-Dong 28, Chongno-Gu, Seoul, 110-744, Republic of Korea.
»
» A relationship has been suggested between mast cells (MCs) and male pattern
» hair loss (MPHL), because of histological evidence of perifollicular
» fibrosis and increased mast cell numbers. Two paired punch biopsies were
» taken from balding vertexes and non-balding occipital promontory areas of
» ten patients with MPHL (Ludwig-Hamilton IIIv to IV) and from five normal
» subjects aged from 20 to 35 years. Masson trichrome and Victoria blue
» staining were performed to observe collagen frameworks and elastic fiber
» structures. Numbers of immunoreactive MCs stained with anti-tryptase or
» anti-chymase antibody were counted. It was found that collagen bundles were
» significantly increased in balding vertexes than in non-balding occiput
» scalp skin. A near 4-fold increase in elastic fibers was observed in both
» vertex and occiput scalp skins with MPHL versus controls. Total numbers of
» MCs (tryptase-positive) in site-matched scalp samples were about 2-fold
» higher in MPHL subjects than in normal controls. Percentage elastic fiber
» (%) was found to be relatively well-correlated with tryptase and
» chymase-positive MCs. These findings suggest that accumulated MCs might be
» responsible for increased elastic fiber synthesis in MPHL, and indicate
» that future investigations are warranted.

I read these studies earlier too. Its of great interest that mast cell numbers are increased (confirmed by Dr Cots and others too) and the mast cell is involved heavily with catagen. There was also some kind of link to nerve fibres aswell.

What I missed before was collagen. Im so sure I read somewhere yesterday that minoxidil helps to prevent collagen formation.

Interesting stuff.

Will start Crom Sodium next week.




neversaynever is located in [NA] and he is available to meet: NO

neversaynever

09.12.2012, 03:48

@ neversaynever

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

"In miniaturized hair follicles in balding human scalp, sebaceous gland and hair follicle keratinocytes outside of the bulge (Fig. 4, C and E), and in some cases within the suprabasal bulge (Fig. 4D), expressed PTGDS. We also detected PTGDS outside of the hair follicle epithelium, indicating potential sources of PGD2 in the dermis (Fig. 4, E and F). In hair follicles undergoing catagen, PTGDS was present in mast cells within the fibrous streamer, which is the former site of the regressed follicle (Fig. 4E)"

"Corrob- orating our results from the spontaneous hair cycle, Ptgds mRNA also fluctuated with the hair cycle in depilated animals. Ptgds mRNA peaked in late anagen, followed by the peak of PGD2 in catagen (Fig. 3C). PGD2 production peaked on day 19.5 (catagen), with 199.9 ng/g tissue compared to a nadir of 27.6 ng/g tissue on day 37. We also noted a unique peak of PGD2 production within hours of depila- tion, which was not seen in the spontane- ous hair cycle in Fig. 3B. This coincides with degranulation of mast cells observed previously after depilation"

Seems catagen is the peak of pgd2 production (mast cells) and possibly from keratinocytes and the sebaceous gland during growth stages (which is where DHT might be involved in messing up the sync of everything).




neversaynever is located in [NA] and he is available to meet: NO

rogfar71

09.12.2012, 06:41

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» » You sound a lot more skeptical about nasalcrom than you do about Iron
» » Dragons Cromolyn solution. Why is that, especially considering that its
» » basically the same thing.
»
» Can't speak for jarjar, but I am of the exact same mind about both of them,
» they are both essentially the same product.
»
» ID's cromolyn solution has all of the same potential as well as the same
» potential drawbacks of NasalCrom.
»


I had ordered some from the Iron Dragon website to try but it was on backorder. Are you saying that their formula is the same thing? I don't know anything about chemicals. They list theirs as Chromoglycate / Indomethacin. If that's the case, I'd rather save my money and just buy the cheaper version.




rogfar71 is located in [NA] and he is available to meet: NO

TheThing

09.12.2012, 10:01

@ neversaynever

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

Roger and never, how with you both be applying this to your scalp? Will you simply be spraying it directly or will you be making a topical?

Thanks.




TheThing is located in [NA] and he is available to meet: NO

roger_that

MARYLAND,
09.12.2012, 15:45
(edited by roger_that, 09.12.2012, 16:12)

@ neversaynever

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» Has PGd2 paused hair cycling or put it into hyperdrive? ie, shorter and
» shorter anagen phases.
»
» Not being sarcastic, just curious...
»
» My assumption was that elevated levels of pgd2 induces early telogen or
» catagen, and the anagen time becomes shorter and shorter.
»
» I believe thats where mast cells are involved. They induce catagen
» (according to cots and others)

Neversaynever, you've posted a lot of information and it's really good info, and I appreciate all your research, you've taken the time to really understand all this stuff.

My take on this is a bit different from yours. I don't know whether it's because I have a background in biochemistry plus other graduate background in biochem, pharma and human physiology... Not saying I'm the only one with such background on the board discussing these things, but here's my take at least.

You're talking about the role of the Mast cells, but I think you're getting how Mast cells play into this slightly confused between the normal state in a person without MPB (or areas of the skin not affected by MPB in any person), and a person in the MPB disease state.

Let's take the non-MPB example first. In skin unaffected by DHT (the "normal" case), Mast cells act as a triggering mechanism and put out synchronized signals to the hair follicles.

Remember at any given time, 2/3 of your scalp hair follicles are in anagen (growing terminal hairs) and roughly 1/3 are in telogen (sleeping, growing no hair or only tiny vellus).

The Mast cells of your scalp send local signals to the hair follicles through prostaglandins, most importantly PGD2.

Statistically 1/3 (completely randomly spaced) are putting out enough PGD2 to shut down 1/3 of the follicles.

The PGD2 spike happens just before the follicle goes into catagen stage, which is really just the prelude to telogen phase.

So we can deduce that a spike in PGD2 above a certain baseline level is a signal to the follicle to shut down, i.e. go into its dormant phase.

Let's leave PGE2 and the other prostaglandins out of it for now, as not enough is known about their role.

What happens in the person with MPB is quite a bit different.

In the MPB disease state, you have DHT inducing more PGD2 Synthase enzyme which leads to an absolutely massive increase in the amount of PGD2 throughout the balding areas of the scalp. (This is of course very localized to specific follicles, because prostaglandins act only very locally; nonetheless, it manifests itself in visible "zones" of the scalp being affected.)

Whether this excess PGD2 is mainly being made in the Mast cells, or also in other cells such as the keratinocytes and others, I don't know. I am going to assume it's in both Mast cells and other cells like keratinocytes, possibly also in dermal papilla cells, sheath cells, epithelial cells of the sebaceous glands, and even in roaming platelets and other cells around the area.

But what happens here is that you have that same PGD2 signaling, but now it's happening 24/7 and everywhere. In other words, you have a massive PGD2 "white noise" signal, which is constantly telling all the follicles to go into catagen phase, and then telogen.

The key here is that in people without MPB, the signaling is mainly happening through the Mast cells in an ordered and synchronized way, to turn the follicles on and off like clock-work.

In people with MPB, there is so much massive induction of the PGD2 Synthase enzyme everywhere, probably not just in the Mast cells but including in a lot of other cells, like hair follicle epithelial cells, that the normal signaling regime gets completely overridden and you have a permanent background noise signal telling the follicles to cease growing and remain in resting stage.

Since this abnormal signaling is huge and constant, it basically tricks all the follicles in the area to go to sleep and stay asleep, i.e. putting them into a permanent coma.

I think your theory about excess PGD2 accelerating the cycling is unnecessary. It's not accelerating the cycles, it is elongating telogen and shortening anagen, progressively, until telogen is the permanent "new normal" state of the follicle, and basically anagen doesn't exist for all practical purposes.

You're focusing on the signal that Mast cells give with PGD2 for follicles to go into catagen phase, in a normal person without MPB, and assuming the same thing is happening in MPB, but just much more of it, resulting in a lot of "tiny" cycles.

What I'm saying is that the incessant PGD2 signaling coming from everywhere is simply tricking the follicles to stay asleep indefinitely, so it's basically elongating one part of the cycle (telogen), not shortening it.

So in MPB you have a PGD2 signal and then a millsecond after that you have another PGD2 signal, and a millisecond after that you have another PGD2 signal, continuing indefinitely. (That's just an exaggeration to serve as an example; I don't know how the signals are really spaced.) This is a completely abnormal state. It short-circuits the normal cycling of the follicle.

Picture the PGD2 Synthase enzyme like little microscopic factories cranking out PGD2 non-stop. The longer the MPB affected area is exposed to DHT, the more of these little factories there will be, and the more PGD2 there will be.

The more PGD2 Synthase enzyme is activated in a specific area of the scalp, the more background noise of PGD2 signaling you'll have, and the higher the telogen:anagen ratio will be in that area.

When the PGD2 background noise goes beyond a certain point, you basically have all the follicles in that area permanently sleeping, i.e. in a coma.

They are getting a non-stop signal to stay in telogen phase. This is a very abnormal state and basically takes the normal state, where the signaling is timed, and turns it on its head and makes it permanent.




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

neversaynever

09.12.2012, 16:17

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

Nice post, I was hoping for a reply (Im no scientist!).

I totally agree that we dont know where the excess PGd2 is coming from. From the cells of the hair, or the mast cells, or all of them!

There is however, indication of a rise in amount of mast cells in balding scalp. Maybe thats because of the longer telogen phase and early catagen induction. Mast cells can also have androgen receptors.

It would be fair to say the DP cells and others are causing the issue, because we have hair that dont suffer from MPB (those with fewer androgen receptors).

What I find interesting is the cavity that forms after a follicle has regressed, it is primarily (as pointed out by Dr Cots and co) filled with PTGDS and a certain type of mast cell.

My basic point is, while we have no idea exactly where the PGD2 is coming from, its just worth a shot with these mast cell stabilizers (such as nasalcrom). We know at least that mast cells are part of a bigger problem, and through stablizers we might not reverse the balding process, but might be able to halt the miniturization procress (like RU has done for me).

You said in a previous post that pgd2 essentially pauses the hair growth cycle. I agree once a follicle is dormant it is paused. But while hair is still being produced, i would say the excess pgd2 is sending the cycles into a sort of hyperdrive, but inducing earlier catagen, longer telogen, and shorter anagen.

Im not saying mast cells are the cause of the balding process, simply that they play a downstream role. We can only attack with whats available, and mast cell stablizers are available cheaply, which you know obviously.

My hope is that we can stablize our loss with over the counter stuff, rather than importing expensive chemicals from abroad. The source of excess pgd2 remains a mystery, for now.

As for other PG's, a few studies have indicated the positive roles of F2a and E2, but we dont have enough knowledge yet about their direct relationship to pgd2, especially when there is excess pgd2. In some situations (such as asthma) pge2 actually prevents pgd2 production, but I have a feeling it wont be the same for hair because the causes of both conditions are quite different.

You started nasalcrom yet?




neversaynever is located in [NA] and he is available to meet: NO

roger_that

MARYLAND,
09.12.2012, 16:31

@ neversaynever

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

First, regarding your "hyperdrive" theory, I just don't think it explains things because I don't think there's any evidence of it. I don't think there's evidence that hair follicles in any stage of MPB, are going through and completing the entire cycle any faster than in people without MPB. I also don't see why your theory is necessary; it's an over-complication of what is actually a pretty simple and "elegant" (as they say in science) idea.

» As for other PG's, a few studies have indicated the positive roles of F2a
» and E2, but we dont have enough knowledge yet about their direct
» relationship to pgd2, especially when there is excess pgd2. In some
» situations (such as asthma) pge2 actually prevents pgd2 production, but I
» have a feeling it wont be the same for hair because the causes of both
» conditions are quite different.

They shouldn't be any different because MPB and allergies are two outward manifestations of things happening with the same prostaglandins, but the underlying physiology of how the PGs are made, how they interact biochemically with other molecules, etc., has to be the same all around.

»
» You started nasalcrom yet?

Just started it this morning!




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

roger_that

MARYLAND,
09.12.2012, 16:34

@ TheThing

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» Roger and never, how with you both be applying this to your scalp? Will you
» simply be spraying it directly or will you be making a topical?
»
» Thanks.

I sprayed it on this morning. So far I haven't put it in a topical applicator, but I may eventually get some Rogaine and mix them together, using the Rogaine applicator.




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

roger_that

MARYLAND,
09.12.2012, 16:42

@ neversaynever

Your information on different cells secreting PGD2

» My basic point is, while we have no idea exactly where the PGD2 is coming
» from, its just worth a shot with these mast cell stabilizers (such as
» nasalcrom). We know at least that mast cells are part of a bigger problem,
» and through stablizers we might not reverse the balding process, but might
» be able to halt the miniturization procress (like RU has done for me).

Yes, and you posted some good information that indicates that both Mast cells and other cells (e.g., keratinocytes) express the androgen receptor AND PGD2S and produce PGD2, right? Look at that information again.

If it's true, then even if other cells are making PGD2 too (not just Mast cells), using NasalCrom should be good enough to deal with those other cells as well!




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

neversaynever

09.12.2012, 16:43

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» First, regarding your "hyperdrive" theory, I just don't think it explains
» things because I don't think there's any evidence of it. I don't think
» there's evidence that hair follicles in any stage of MPB, are going through
» and completing the entire cycle any faster than in people without MPB. I
» also don't see why your theory is necessary; it's an over-complication of
» what is actually a pretty simple and "elegant" (as they say in science)
» idea.
»
» » As for other PG's, a few studies have indicated the positive roles of
» F2a
» » and E2, but we dont have enough knowledge yet about their direct
» » relationship to pgd2, especially when there is excess pgd2. In some
» » situations (such as asthma) pge2 actually prevents pgd2 production, but
» I
» » have a feeling it wont be the same for hair because the causes of both
» » conditions are quite different.
»
» They shouldn't be any different because MPB and allergies are two outward
» manifestations of things happening with the same prostaglandins, but the
» underlying physiology of how the PGs are made, how they interact
» biochemically with other molecules, etc., has to be the same all around.
»
» »
» » You started nasalcrom yet?
»
» Just started it this morning!

Im causing confusing with my laymans terminology. Hyperdrive is the wrong word. Essetially the complete cycle stays the same, but because the 'sync' is altered in mpb, the early catagen and longer telegen create a far shorter anagen phase. So it would seem anagen is in a sort of hyperdrive, but let me re-phrase and just say anagen becomes shorter and shorter until there is a 'coma'.




neversaynever is located in [NA] and he is available to meet: NO

roger_that

MARYLAND,
09.12.2012, 16:46

@ neversaynever

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» Im causing confusing with my laymans terminology. Hyperdrive is the wrong
» word. Essetially the complete cycle stays the same, but because the 'sync'
» is altered in mpb, the early catagen and longer telegen create a far
» shorter anagen phase. So it would seem anagen is in a sort of hyperdrive,
» but let me re-phrase and just say anagen becomes shorter and shorter until
» there is a 'coma'.

OK, then -- I agree with that!




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

neversaynever

09.12.2012, 16:47

@ roger_that

Your information on different cells secreting PGD2

» » My basic point is, while we have no idea exactly where the PGD2 is
» coming
» » from, its just worth a shot with these mast cell stabilizers (such as
» » nasalcrom). We know at least that mast cells are part of a bigger
» problem,
» » and through stablizers we might not reverse the balding process, but
» might
» » be able to halt the miniturization procress (like RU has done for me).
»
» Yes, and you posted some good information that indicates that both Mast
» cells and other cells (e.g., keratinocytes) express the androgen receptor
» AND PGD2S and produce PGD2, right? Look at that information again.
»
» If it's true, then even if other cells are making PGD2 too (not just
» Mast cells), using NasalCrom should be good enough to deal with those other
» cells as well!


I think nasal crom goes for the Fc epsilon receptor, which quite a few cells have including the keratinocytes, platelets, mast cells and morphages (spelling).

What is not clear is if the fc epsilon receptor (cd23) on keratinocytes can halt halt pgd2 production in keratinocytes because there seems to be multiple pathways to produce pgd2.

Thats where i lose my mind and hit my limit with understanding things.

I think ill lose more hair reading this stuff!

How would you mix minox with nasal crom?




neversaynever is located in [NA] and he is available to meet: NO

hairman2

09.12.2012, 16:48

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» Neversaynever, you've posted a lot of information and it's really good
» info, and I appreciate all your research, you've taken the time to really
» understand all this stuff.

we would really need an M.D. here so that he could prescribe us all sorts of crap... off label :)

» But what happens here is that you have that same PGD2 signaling, but now
» it's happening 24/7 and everywhere. In other words, you have a massive
» PGD2 "white noise" signal, which is constantly telling all the follicles to
» go into catagen phase, and then telogen.


» In people with MPB, there is so much massive induction of the PGD2
» Synthase enzyme everywhere, probably not just in the Mast cells but
» including in a lot of other cells, like hair follicle epithelial cells,
» that the normal signaling regime gets completely overridden and you have a
» permanent background noise signal telling the follicles to cease growing
» and remain in resting stage.


» Since this abnormal signaling is huge and constant, it basically tricks all
» the follicles in the area to go to sleep and stay asleep, i.e. putting them
» into a permanent coma.

» I think your theory about excess PGD2 accelerating the cycling is
» unnecessary. It's not accelerating the cycles, it is elongating telogen
» and shortening anagen, progressively, until telogen is the permanent "new
» normal" state of the follicle, and basically anagen doesn't exist for all
» practical purposes.

» What I'm saying is that the incessant PGD2 signaling coming from everywhere
» is simply tricking the follicles to stay asleep indefinitely, so it's
» basically elongating one part of the cycle (telogen), not shortening it.

» So in MPB you have a PGD2 signal and then a millsecond after that you have
» another PGD2 signal, and a millisecond after that you have another PGD2
» signal, continuing indefinitely. (That's just an exaggeration to serve as
» an example; I don't know how the signals are really spaced.) This is a
» completely abnormal state. It short-circuits the normal cycling of
» the follicle.


I was under the impression that it has been well established that during AGA, the hair follicles undergo a miniaturization process in which the telogen phases become increasingly longer and anagen phases shorter? If however, there was an ubiquitous presence of hightend levels of PGD2 at all times then how could the miniaturization process of follicular cycling be explained? Wouldn't in the abundance of PGD2 the follicle could go straight into their telegon state and remain throughout he MPB lifetime. How do you explain the miniaturization and vellus hair phase before the follicles completely stop growing?

» Picture the PGD2 Synthase enzyme like little microscopic factories cranking
» out PGD2 non-stop. The longer the MPB affected area is exposed to DHT, the
» more of these little factories there will be, and the more PGD2 there will
» be.

» The more PGD2 Synthase enzyme is activated in a specific area of the scalp,
» the more background noise of PGD2 signaling you'll have, and the higher the
» telogen:anagen ratio will be in that area.

I guess this is the answer to my question above right? If i understand correctly you are suggesting that with increased exposure to DHT, the background level PGD2 slowly increases, making the anagen phase less profound (not sure if this is the right word) and allowing the follicles to get pushed back into their telegon phase more easily/earlier due to the already heightened background level of PGD2?

» When the PGD2 background noise goes beyond a certain point, you basically
» have all the follicles in that area permanently sleeping, i.e. in a coma.

i guess this theory sounds reasonable




hairman2 is located in [NA] and he is available to meet: NO

roger_that

MARYLAND,
09.12.2012, 16:49

@ neversaynever

Your information on different cells secreting PGD2

» I think nasal crom goes for the Fc epsilon receptor, which quite a few
» cells have including the keratinocytes, platelets, mast cells and morphages
» (spelling).
»
» What is not clear is if the fc epsilon receptor is halt pgd2 production in
» keratinocytes because there seems to be multiple pathways to produce pgd2.

As far as the effect of NC, I was always taught that it blocks degranulation of the Mast cells -- in other words, it prevents the heparin, histamine, PGD2, etc. from getting out of the MCs. I never knew it also stops production of PDG2. If that's so, then it's an added bonus!

»
»
» How would you mix minox with nasal crom?

Just pour the NC liquid into Minox solution!




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

hairman2

09.12.2012, 16:55

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

any regrowth yet? :)

» I sprayed it on this morning. So far I haven't put it in a topical
» applicator, but I may eventually get some Rogaine and mix them together,
» using the Rogaine applicator.




hairman2 is located in [NA] and he is available to meet: NO

neversaynever

09.12.2012, 16:55

@ roger_that

Your information on different cells secreting PGD2

» » I think nasal crom goes for the Fc epsilon receptor, which quite a few
» » cells have including the keratinocytes, platelets, mast cells and
» morphages
» » (spelling).
» »
» » What is not clear is if the fc epsilon receptor is halt pgd2 production
» in
» » keratinocytes because there seems to be multiple pathways to produce
» pgd2.
»
» As far as the effect of NC, I was always taught that it blocks
» degranulation of the Mast cells -- in other words, it prevents the heparin,
» histamine, PGD2, etc. from getting out of the MCs. I never knew it also
» stops production of PDG2. If that's so, then it's an added bonus!
»
» »
» »
» » How would you mix minox with nasal crom?
»
» Just pour the NC liquid into Minox solution!

Oh god, me and my words again.

Yea NC blocks degranulation of mast cells, preventing inflammatory elements from being released. Thats what I mean with 'stop pgd2 production' hahaha. How it will effect things like keratinocytes producing pgd2 is beyond me.




neversaynever is located in [NA] and he is available to meet: NO

roger_that

MARYLAND,
09.12.2012, 17:06

@ hairman2

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» I was under the impression that it has been well established that during
» AGA, the hair follicles undergo a miniaturization process in which
» the telogen phases become increasingly longer and anagen
» phases shorter? If however, there was an ubiquitous presence of
» hightend levels of PGD2 at all times then how could the miniaturization
» process of follicular cycling be explained? Wouldn't in the abundance of
» PGD2 the follicle could go straight into their telegon state and remain
» throughout he MPB lifetime. How do you explain the miniaturization and
» vellus hair phase before the follicles completely stop growing?

Complex question but I think it has to do with levels of PGD2. It's not a binary switch where if you have "+" PGD2 then the thing swings completely into telogen. We're talking about levels of PDG2 and their influence on hair -- in other words, the more PGD2 there is, the higher is the ratio of telogen:anagen.

Everything in molecular biology is based on statistics and mass numbers of millions of reactions per unit time and billions of molecules. When you take a snapshot of that statistical profile, there is a corresponding phenotypic picture.




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

roger_that

MARYLAND,
09.12.2012, 17:10

@ hairman2

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» I guess this is the answer to my question above right? If i understand
» correctly you are suggesting that with increased exposure to DHT, the
» background level PGD2 slowly increases, making the anagen phase less
» profound (not sure if this is the right word) and allowing the follicles to
» get pushed back into their telegon phase more easily/earlier due to the
» already heightened background level of PGD2?

Exactly.




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

neversaynever

09.12.2012, 17:28

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

A combination of mast cell stablizer, gpr44 blocker, Ricinoleic acid and minox would be interesting.




neversaynever is located in [NA] and he is available to meet: NO

jarjarbinx

09.12.2012, 18:26

@ rogfar71

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

»
» I had ordered some from the Iron Dragon website to try but it was on
» backorder. Are you saying that their formula is the same thing? I don't
» know anything about chemicals. They list theirs as Chromoglycate /
» Indomethacin. If that's the case, I'd rather save my money and just buy the
» cheaper version.


I don't think the irondragon formulation is the same thing. I think the irondragon formulation works by two different modes of action, one being at the mast cell level, but I think it also works by another mode of action.




jarjarbinx is located in [NA] and he is available to meet: NO

roger_that

MARYLAND,
09.12.2012, 18:30

@ jarjarbinx

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» I don't think the irondragon formulation is the same thing. I think the
» irondragon formulation works by two different modes of action, one being at
» the mast cell level, but I think it also works by another mode of action.

Yes, because the ID formulation actually has 2 completely different drugs in it, indomethacin and cromoglycolate (cromolyn). The indo works in a completely different way, it works on the COX-2 pathway.




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

rogfar71

09.12.2012, 19:50

@ jarjarbinx

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» »
» » I had ordered some from the Iron Dragon website to try but it was on
» » backorder. Are you saying that their formula is the same thing? I
» don't
» » know anything about chemicals. They list theirs as Chromoglycate /
» » Indomethacin. If that's the case, I'd rather save my money and just buy
» the
» » cheaper version.
»
»
» I don't think the irondragon formulation is the same thing. I think the
» irondragon formulation works by two different modes of action, one being at
» the mast cell level, but I think it also works by another mode of action.


JarJar and Roger,

Thanks for the additional info, but is it worth it to go with the Iron Dragon version? There's a huge price difference.




rogfar71 is located in [NA] and he is available to meet: NO

roger_that

MARYLAND,
09.12.2012, 19:54

@ rogfar71

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» JarJar and Roger,
»
» Thanks for the additional info, but is it worth it to go with the Iron
» Dragon version? There's a huge price difference.

I think the price difference, plus the fact that the Indomethacin in the Iron Dragon mix might be suppressing PGE2 (which plays a role in triggering hair growth -- to what extent we really don't know yet), indicates for me at least that NasalCrom is the better option.

I can't see how ID justifies that price for what is essentially NasalCrom (available at $16.99/bottle in the US) and Indomethacin, which is a well-known prescription medication which you might be able to get a doctor to prescribe for you off label, and have formulated into a topical at the pharmacy.




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

neversaynever

09.12.2012, 20:05

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» » JarJar and Roger,
» »
» » Thanks for the additional info, but is it worth it to go with the Iron
» » Dragon version? There's a huge price difference.
»
» I think the price difference, plus the fact that the Indomethacin in the
» Iron Dragon mix might be suppressing PGE2 (which plays a role in triggering
» hair growth -- to what extent we really don't know yet), indicates for me
» at least that NasalCrom is the better option.
»
» I can't see how ID justifies that price for what is essentially NasalCrom
» (available at $16.99/bottle in the US) and Indomethacin, which is a
» well-known prescription medication which you might be able to get a doctor
» to prescribe for you off label, and have formulated into a topical at the
» pharmacy.

Roger, Dr cots highlighted that Lpgds is elevated, is it true that mast cells produce only Hpgds? Will then render nasalcrom useless?




neversaynever is located in [NA] and he is available to meet: NO

Mr. Z

09.12.2012, 20:25

@ neversaynever

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» A combination of mast cell stablizer, gpr44 blocker, Ricinoleic acid and
» minox would be interesting.

Never, do you notice any sides from RU?




Mr. Z is located in [NA] and he is available to meet: NO

roger_that

MARYLAND,
09.12.2012, 20:37

@ neversaynever

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» Roger, Dr cots highlighted that Lpgds is elevated, is it true that mast
» cells produce only Hpgds? Will then render nasalcrom useless?

Neversaynever -- it doesn't matter.

LPGDS and HPGDS are just two alternative types of the same enzyme, with very similar chemical structures (almost exactly the same) which both make the exact same molecule, PGD2.

While the enzymes have slightly different chemical structures (because they are big enzyme molecules, a small number of changes in the right places won't affect what the molecule does), the chemical that they make is a much, much smaller molecule, a short-chain prostaglandin. There is no difference in the structure of the PGD2 that these enzymes make.

Because NasalCrom is just blocking the release of the PGD2 from the Mast cells, it doesn't matter what the exact structure of the PGDS enzyme that is creating the PGD2 happens to be. NasalCrom isn't affecting the PGDS, it's affecting a receptor on the Mast cell membrane that stabilizes the Mast cell so it won't "explode" and release its contents of histamine, cytokines, PGD2, etc.




roger_that is located in MARYLAND and he is available to meet: YES
email hairsite@aol.com to arrange a meeting.

rogfar71

09.12.2012, 21:17

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» » JarJar and Roger,
» »
» » Thanks for the additional info, but is it worth it to go with the Iron
» » Dragon version? There's a huge price difference.
»
» I think the price difference, plus the fact that the Indomethacin in the
» Iron Dragon mix might be suppressing PGE2 (which plays a role in triggering
» hair growth -- to what extent we really don't know yet), indicates for me
» at least that NasalCrom is the better option.
»
» I can't see how ID justifies that price for what is essentially NasalCrom
» (available at $16.99/bottle in the US) and Indomethacin, which is a
» well-known prescription medication which you might be able to get a doctor
» to prescribe for you off label, and have formulated into a topical at the
» pharmacy.

Thanks. I'm in the U.S., so obtaining the NC is a lot easier. Do I need to do anything other than just spray on the scalp?




rogfar71 is located in [NA] and he is available to meet: NO

neversaynever

09.12.2012, 21:24

@ Mr. Z

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» » A combination of mast cell stablizer, gpr44 blocker, Ricinoleic acid and
» » minox would be interesting.
»
» Never, do you notice any sides from RU?

No sides noticed. 75mg doses mostly, kb solution vehicle.




neversaynever is located in [NA] and he is available to meet: NO

Mr. Z

09.12.2012, 21:27

@ neversaynever

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» » » A combination of mast cell stablizer, gpr44 blocker, Ricinoleic acid
» and
» » » minox would be interesting.
» »
» » Never, do you notice any sides from RU?
»
» No sides noticed. 75mg doses mostly, kb solution vehicle.


Thanks!




Mr. Z is located in [NA] and he is available to meet: NO

Mr. Z

09.12.2012, 21:32

@ Mr. Z

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

Quercetin is more effective than cromolyn in blocking human mast cell cytokine release and inhibits contact dermatitis and photosensitivity in humans
Full Text
By Weng, Zuyi; Zhang, Bodi; Asadi, Shahrzad; Sismanopoulos, Nikolaos; Butcher, Alan; Fu, Xueyan; Katsarou-Katsari, Alexandra; Antoniou, Christina; Theoharides, Theoharis C.
From PLoS One (2012), 7(3), e33805. | Language: English, Database: CAPLUS


Mast cells are immune cells crit. in the pathogenesis of allergic, but also inflammatory and autoimmune diseases through release of many pro-inflammatory cytokines such as IL-8 and TNF. Contact dermatitis and photosensitivity are skin conditions that involve non-immune triggers such as substance P (SP), and do not respond to conventional treatment. Inhibition of mast cell cytokine release could be effective therapy for such diseases. Unfortunately, disodium cromoglycate (cromolyn), the only compd. marketed as a mast cell "stabilizer", is not particularly effective in blocking human mast cells. Instead, flavonoids are potent anti-oxidant and anti-inflammatory compds. with mast cell inhibitory actions. Here, we first compared the flavonoid quercetin (Que) and cromolyn on cultured human mast cells. Que and cromolyn (100 μM) can effectively inhibit secretion of histamine and PGD2. Que and cromolyn also inhibit histamine, leukotrienes and PGD2 from primary human cord blood-derived cultured mast cells (hCBMCs) stimulated by IgE/Anti-IgE. However, Que is more effective than cromolyn in inhibiting IL-8 and TNF release from LAD2 mast cells stimulated by SP. Moreover, Que reduces IL-6 release from hCBMCs in a dose-dependent manner. Que inhibits cytosolic calcium level increase and NF-kappa B activation. Interestingly, Que is effective prophylactically, while cromolyn must be added together with the trigger or it rapidly loses its effect. In two pilot, open-label, clin. trials, Que significantly decreased contact dermatitis and photosensitivity, skin conditions that do not respond to conventional treatment. In summary, Que is a promising candidate as an effective mast cell inhibitor for allergic and inflammatory diseases, esp. in formulations that permit more sufficient oral absorption.

Maybe we need to add quercetin into the mix?




Mr. Z is located in [NA] and he is available to meet: NO

jarjarbinx

09.12.2012, 21:38

@ roger_that

BIG Question on Cromolyn Sodium not being addressed: Non-Mast Sources of PGD2

» » Roger, Dr cots highlighted that Lpgds is elevated, is it true that mast
» » cells produce only Hpgds? Will then render nasalcrom useless?
»
» Neversaynever -- it doesn't matter.
»
» LPGDS and HPGDS are just two alternative types of the same enzyme, with
» very similar chemical structures (almost exactly the same) which both make
» the exact same molecule, PGD2.
»
» While the enzymes have slightly different chemical structures (because they
» are big enzyme molecules, a small number of changes in the right places
» won't affect what the molecule does), the chemical that they make is a
» much, much smaller molecule, a short-chain prostaglandin. There is no
» difference in the structure of the PGD2 that these enzymes make.
»
» Because NasalCrom is just blocking the release of the PGD2 from the Mast
» cells, it doesn't matter what the exact structure of the PGDS enzyme that
» is creating the PGD2 happens to be. NasalCrom isn't affecting the PGDS,
» it's affecting a receptor on the Mast cell membrane that stabilizes the
» Mast cell so it won't "explode" and release its contents of histamine,
» cytokines, PGD2, etc.



Roger-that,

I remember you told me that the IronDragon formula suppressed PGD2 at the mast cell level but I think you also said it worked by a second mode of action - preventing the body from forming any prostaglandins. That is why I think that minox might be useless in combo with the IronDragon formulation since minox works by stimulating the body to produce more PGE2 but one mode of action of IronDragon's formulation should prevent minoxidil from getting the body to produce more PGE2.

Please remind what are the two modes of action of the IronDragon formula.

I can't think of any reason why the drug you've chosen (a mast cell level PGD2 supression) wouldn't combine well with minox. So it really just gets down to whether or not the drug you've chosen negates enough of the prostaglandins that cause hair loss.

I am so hoping that your experiment works because if it works it has so many advantages over everything else.

1. Cheaper

2. Legally available

3. Easy to access.

4. No possibility of an interruption to the supply line. We would be able to get it easy, indefinitely, without interuption.




jarjarbinx is located in [NA] and he is available to meet: NO

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