Male Pattern Baldness 99% cured if you can get on meds???

Experimentality

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Thanks for such an elaborarate answer. I have further questions, so if you have time please share your thoughts:

- Why do you use both oral Dutasteride and oral Finasteride? Do you believe that one of them will make any fuction the other will not?

- Has it been documented the level of scalp DHT reduction with Dutasteride mesotherapy? I tried to find but I didn't see numbers. It trully sounds like a really good choice given that you don't even get systemic effect of the drug... I believe this is the route I'm gonna take rather than oral.

- Are you following the research on prolactin receptor antibody? If so, what is the difference between the PRLR antibody developed by Bayer compared to any other monoclonal PRLR antibody that may already be accesible?

Thank you,

Descended Dog
I use both since the mechanisms through which they inhibit 5AR are very likely different. I do not know any genetic polymorphisms I might possess, but theoretically one could respond to finasteride while being unresponsive to dutasteride. There is no research on combined therapy, so I am my own guinea pig. Actually, I am not really comfortable with systemic 5AR inhibitors, mainly due to the fact that they promote neurodegradation due to decreased neurosteroidogenesis. Most people will probably be fine, but my job involves a lot of thinking and I am very cautious of anything that imparts brain functioning. That is why I am taking ultra-low dose Fluoxetine to increase cerebral 5a-DHP conversion to allopregnenolone (see here) which seems to be working very well. Again, I do not recommend doing this, but realise 5AR inhibitors are really nuclear options (just as anything else I am using). Unfortunately, fighting male pattern baldness is an (impossible) uphill battle without the use of 5ARI's.

Regarding your second question: there is a lot of research available (for example here) that dutasteride mesotherapy is very effective. The problem is that dosage-response curves of finasteride and dutasteride are very flat: this means any tiny amount entering the bloodstream will inhibit a good chunk of systemic DHT. I would not recommend topical/mesotherapy of 5ARI's for individuals that are not comfortable with possible systemic inhibition.

I think the prolactin research is really promising. Hair loss (yes, also male pattern baldness) is definitely not restricted to androgens and estrogens. In fact, I believe that prolactin may even be a bigger contributor to male pattern baldness than androgens. Systemic inflammation is also underestimated: I think diet does matter (a lot) when fighting male pattern baldness. Gut inflammation releases cytokines, endotoxins and histamines which are all systemically pro-inflammitory. There is a reason some people are using things like oral cetirizine or montelukast to decrease the release or actions of these pro-inflammitory compounds. I am not aware of any currently existing PRL antibodies. I think the Bayer antibody is still a long way off, and the ones interested in this pathway would be better off looking into ways to decrease systemic PRL (lisuride, metergoline or other dopamine agonists, which may very well be a more effective approach as well).
 
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Experimentality

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Upon location. It can be DIYed, which I might be able to replicate if I have it done once.

The frequency depends. They recommend "one intensive treatment every 3 months" for "regrowth" and "just 2 or 3 injections per year for maintenance".

What I am interested about this is how much of scalp DHT you can inhibit given that there is a limitation with oral Dutasteride. So if you go high enough it could actually be really effective at least stopping progression, something I could be happy with.
There are no studies on this, but there will be a limitation to topical applications as well. The reason for this is the androgen backdoor pathway. 5AR is not the only way to synthesize DHT:

ABP.png


As you can see in the lower right of the picture, the backdoor pathway starts at Allo to 17OH-Allo (P450), to Andro (P450), to 5a-andro (17bHSD) to DHT (mainly 17bHSD). Note that nowhere this involves 5AR. Ironically, by increasing my Allo (as per my previous post) I am actually feeding my backdoor pathway. That is how twisted this whole thing is. I believe that this is where the remaining ~30% of scalp DHT comes from. However, I also think that the vast, vast majority of men do not have to consider this pathway even if it is somehow upregulated (and anyway, there is not much to be done about it. Messing with dehydrogenases is not safe and not worth the damage you may cause to your body and brain). I would get a quality AR antagonist if you are worried about the remnant DHT.
 
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