A Potential Mechanism Behind Male Pattern Balding

jbrog1987

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Doing research on male pattern baldness, DHT and now PGD2 I theorized what the real mechanism behind male pattern baldness might be. My theory is that DHT's presence isn't what causes hair follicles to shrink. My thought is men with the male pattern baldness genes do indeed have a sensitivity to DHT, but DHT's presence is only the initial trigger. What I believe is men with male pattern baldness have a physiological immune system reaction when DHT levels reach a certain level and the DHT trigger creates a chain reaction that results (among other things) in high PGD2 production. PGD2 is already known as an inflammatory compound and has an active roll in asthma and constriction within the lungs. It only makes sense that PGD2 may have more of a causative and direct role in follicular miniaturization then previously established.


The inflammation one feels in thinning and balding areas is easily explained by PGD2 and it's potentially a major player in the progression of hair loss and not simply a side effect. It makes sense that PGD2 in excess directly causes the blood vessels within the follicle to begin to shrink and become constricted. Slowly but surely shrinking the blood supply and eventually the health of the follicle. So just as an asthma inhaler relieves inflammation and constriction, I imagine a PGD2 inhibitor for the scalp may have equally beneficial effects on hair growth and follicle health. Particularly if caught early.


I just wish science would stop dragging it's feet when it comes to clinical trails of PGD2 inhibition and it's effect on hair but the three pronged approach of DHT inhibition, PGD2 inhibition and minoxidil for regrowth (once the constriction is relieved, making minoxidil more effective if needed at all) could become a much more effective and potent "BIG 3" or "BIG 2" if minoxidil can be jettisoned if this theory rings true. The likes of esernecipp and others are putting these scientist to shame. Thoughts?
 

jasonbourne

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"Particularly if caught early"

Define early.

A diffuse thinner with no bald spot but thin hair is early? Or earlier than that?
 

Wolf Pack

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Nothing new here. It's been know for like ages that DHT is only the initial trigger. Although it's a very deadly and important step that must be stopped. Theoretically you can inhibit the chain of male pattern baldness anywhere. That's actually another reason I don't want to use minoxidil. If a better treatment comes out you can maybe quit finasteride as you can stop the chain at any point potentially. Allows you to hold your "real hairs" with another drug instead of finasteride. With minoxidil, hairs are absolutely dependent on it as it grows hair via a complex/unknown mechanism so it truly is a life treatment. Unless a viable cure comes out. I suppose you could quit it and lose the benefits in the area you applied but still.
 

jbrog1987

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"Particularly if caught early"

Define early.

A diffuse thinner with no bald spot but thin hair is early? Or earlier than that?
Good question. I think it's simply a matter of progression of male pattern baldness. If you're slick bald in large areas of your scalp, you're in the later stages. Thinning but decent coverage is early in my book. But who knows how much hair can be recovered if this theory rings true. There isn't really any precedent there.

- - - Updated - - -

Nothing new here. It's been know for like ages that DHT is only the initial trigger. Although it's a very deadly and important step that must be stopped. Theoretically you can inhibit the chain of male pattern baldness anywhere. That's actually another reason I don't want to use minoxidil. If a better treatment comes out you can maybe quit finasteride as you can stop the chain at any point potentially. Allows you to hold your "real hairs" with another drug instead of finasteride. With minoxidil, hairs are absolutely dependent on it as it grows hair via a complex/unknown mechanism so it truly is a life treatment. Unless a viable cure comes out. I suppose you could quit it and lose the benefits in the area you applied but still.
No doubt it's known that it's known that male pattern baldness is more complex then DHT = dead follicles but my general point is if PGD2 might have a much more significant role in male pattern baldness then any other known mechanism besides DHT, and its inhibition COULD be a huge addition to our arsenal. Maybe not. Could be just another fangless saw pallmetto esque "treatment". Who knows. This post is made moreso out of anxiousness directed at science and to explore PGD2's potential role in balding.
 
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