Do you have the link for the study showing caffeine is bad for hair?
There is none for that specifically but there's solid theory behind it. Let me explain the situation. There are conflicting reports about COX1 and COX2 inhibitors. In general they both inhibit the conversion of Arachidonic Acid to PGH2 which will lower both your PGD2 and your PGE2/PGF2a. The second is something we don't want. Cetirizine for example was trialed by the german forum alopezie.de, it's a relatively "clean" cox inhibitor and ended up hurting their hair more than helping them (no doubt because they killed their beneficial prostaglandins as well). On the other hand, there is caffeine. Now caffeine is absolutely dirty. It's not just a cox inhibitor but it has dozens of other biological actions. One of them for example is its direct antagonism of adenosine, in fact that's how caffeine "wakes you up". Sounds good? Well, not really! Because adenosine itself is beneficial to hair, there are several products such as Adenogen which contain it and their efficacy is well known and presented in several studies. Some even saying that it has a similar effect to 2% Minox. Now, caffeine also does have some beneficial actions. In some way it does actually manage to raise pge2/pgf2a, at least if we're going to believe some animal intestine studies and then also believe those to be true in humans as well.
So, long story short. COX inhibitors at large are wildly different and affect too many pathways to be predictable. There are very few "pure" inhibitors, but the pure ones that people tested ended up hurting them. This makes sense theoretically as well as I already pointed out since killing COX will kill your beneficial prostaglandins. Is it worth lowering an extremely important angle (benefiicial prostaglandins) for some other vaguely positive effect? I believe not. With cox inhibitors you are shooting in the dark and most likely you're going to shoot yourself in the foot.
The correct way to approach this is by sticking to direct manipulation of what we know and can change efficiently. Such as blocking the PGD2 receptor which is well researched and for which we have several different candidates. COX inhibition should be avoided at all cost unless *maybe* when you're already using exogenous PGE2 and PGF2a (but even in that case I would not recommend it).
Hope that helps to clear up the confusion a bit.
So, long story short. COX inhibitors at large are wildly different and affect too many pathways to be predictable. There are very few "pure" inhibitors, but the pure ones that people tested ended up hurting them. This makes sense theoretically as well as I already pointed out since killing COX will kill your beneficial prostaglandins. Is it worth lowering an extremely important angle (benefiicial prostaglandins) for some other vaguely positive effect? I believe not. With cox inhibitors you are shooting in the dark and most likely you're going to shoot yourself in the foot.
The correct way to approach this is by sticking to direct manipulation of what we know and can change efficiently. Such as blocking the PGD2 receptor which is well researched and for which we have several different candidates. COX inhibition should be avoided at all cost unless *maybe* when you're already using exogenous PGE2 and PGF2a (but even in that case I would not recommend it).
Hope that helps to clear up the confusion a bit.
