I'm travelling now for another few weeks. My plan is once I get back I'll go to a doctor and ask for a finasteride prescription. I tried that with a doctor before travelling but he pissed me off with his ignorance and I decided to wait another month or two and go with a better doctor.
I'm hoping the better doctor (I know who I'm going to) will also be willing to prescribe an aromatase inhibitor. I'm worried about finasteride because I already have moderate ED.
I can add minoxidil in a year, that's a good idea. Thank you.
Yeah some doctors are a joke. Find someone who is willing to think and work with you. I switched from doctor too. The one I have now currently is way better.
I think it's a smart move to go with finasteride asap. Minoxidil can wait.
Perhaps you can get a baseline of E2, if you are worried a potential increase? Then measure it again while being on finasteride. I doubt that you want to use a aromatase inhibitor on a continual basis. Then again I haven't looked that deep into that so you probably know more about that.
Nothing wrong with starting with a low dosage with finasteride too and working your way up. If it exacerbates your ED then just drop it immediately.
Good luck man
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There are some people who get more growth on just finasteride or Min.
I haven't really researched Seti but it will be interesting to see if stopping something down the chain can halt Androgenetic Alopecia as effectively as dealing with DHT. My guess is no. But until there are large scale trials, double blinded, placebo, for Androgenetic Alopecia patients we won't know.
Jup definitely Wolf_Pack, no contest.
About your second point, we already know that to some degree and I am curious if you agree with me. You work somewhere research related right?
In terms of anti-androgens (AR antagonists) and 5ar2 inhibitors we see that something happens, at least in a subset group of people. Cosmetic improvement right? One just has to look at the success section here and see how people can get literally good improvement of the hair that is notable not only by the person itself but by the observer too. Cosmetic improvement just often doesn't go unnoticed, or actually any hair related changes.
In fact we see the same happen too with minoxidil. After all that is how the compound got discovered for hair growth and to no surprise other compounds with similar biological activity induce hair growth too some extent too (diazoxide, pinacidil etc.) Case reports of all those have been shown.
Exactly the same thing with PGF2a. Also discovered by accident. Both bimatoprost and latanoprost (both analogues of pgf2a similar biological activity) have shown to induce hair growth too.
If we look further we see several case reports that have been released either because hair growth was noticed or hair alterations, some examples;
http://erj.ersjournals.com/content/46/suppl_59/PA4293 (Unexpected hair growth induced by gefitinib treatment in two patients with EGFR gene mutation-positive adenocarcinoma of the lung)
http://www.ncbi.nlm.nih.gov/pubmed/24153140 (Partial reversal of androgenetic alopecia with methotrexate therapy for psoriasis.)
http://www.ncbi.nlm.nih.gov/pubmed/3090984 (Valproic acid, curly hair and weight gain)
I could dump more but you see where I'm heading at. Case reports are often shown or simply described when such hair changes are seen.
Now Androgenetic Alopecia in men is quite prevalent. Let's be honest. If you look at older men quite many people suffer from Androgenetic Alopecia to some extent.
So in terms of setipiprant, ultimately it's a selective DP2 antagonist. However there are several other compounds with the same biological activity! Even stronger ones. Even setipiprant has failed 7 clinical trials not related to Androgenetic Alopecia.
So ultimately that means we have hundreds of people that have been implicated in clinical trials that focuses on DP2 antagonism right? Well is anybody going to tell me that nobody of these participants actually suffers from Androgenetic Alopecia? That would be foolish to assume wouldn't it.
That begs the question; Why haven't hair related changes been reported in all of these clinical trials or at least case reports shown? Compounds that hit the androgen/AR angle do give cosmetic improvement in some people so why wouldn't DP2 antagonist if they actually work upstream?
Remember Kythera argues that it works like this Androgens > AR > PGD2 synthase > PGD2 production > PGD2 receptor > hair loss
It would be logical to assume that if the pathway works like this antagonizing the PGD2 receptor would yield some cosmetic improvement in some people too. Actually it should probably work even better, at least some compounds. When we look at the AR angle for example we don't have viable treatment that antagonize the AR sufficiently. RU58841 for example is only able to block 70% of DHT, being already a very potent anti-androgen. In terms of PGD2 receptor antagonizing compounds have run clinical trials that pretty much show full antagonistic activity towards the receptor.
This already to me displays that it's extremely unlikely that it can stop hair loss as efficiently as dealing with DHT.
Sure there is always a possibility that these hair growth effects went unnoticed. But in hundreds of people dude? How big are those odds? Come on.
Then people always argue; But but dude, it's Cotsarelis and Kythera has picked up the compound. There must be something to it!
Well yeah dude, some fun facts;
1. Cotsarelis has been wrong on multiple occasions in the past. Promising a cure 2 times. Not only that if you give Cotsarelis 2 million he will have a better hair growth agent than minoxidil and if you give him 20 millions he will give you a full head of hair. Although that might take some time. LOL, can you actually believe he said that? But it's true. This is not unique to researchers though. After all they need to hype things up, attract publicity, funding to survive etc.. I think the most cited study on PLOS goes well with this "Why Most Published Research Findings Are False"";
http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0020124. I bet you know what I mean with this
.
2. Setipiprant is bought for pocket change. Literally for pocket change.
3. If we look at drugs overall we see from the statistics that the overwhelming majority actually fails.
Ok, sure it's excellent that they are running double blinded placebo controlled trials for Androgenetic Alopecia ultimately that will give the
final answer. But in terms of odds? Dude I would know where to bet my money on immediately! The odds for it to deal as effectively as dealing with DHT are low to non-existent in my opinion. If I would place my money I would say that it's going nowhere after the 2nd phase. Obviously this is not only based on the above but also on the literature provided by other researchers and discussions I have had with researchers.
Research is research though and when it doesn't actually work out we will actually learn some more.
Curious to your opinion about this all.
One thing is for sure dude. I'm happy that some of us can deal with Androgenetic Alopecia by hitting the androgen angle. I mean imagine yourself if Androgenetic Alopecia was something like cicatrial alopecia for where no single treatment has been found? Holy sh*t that would be something...
Excited for the future though. In terms of gene therapy for example;
It would be damn nice to silence that androgen receptor for a very long period of time
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