Thanks for your answer Experimentality. I have another question, you mentioned before that you were on TRT, have you by any chance ever had a look on anything related to GDF8 inhibition? This is my next step after I am happy with my hair lol.
Regards, Descended Dog.
Yes, I know about it vaguely. However, you have to realize that molecules that bind the AR (not myostatin) are not only beneficial for muscle hypertrophy. Specifically, the brain contains a lot of AR, and molecules that bind the AR will masculinize the brain (whereas myostatin will not. It
will surpress the HPTA though, and by this cause
brain deprivation of androgens.). Equivalently, molecules that bind the ER will feminize the brain (to different degrees, of course). Hence, it will not suffice to replace androgens with myostatin. Furthermore, I'm not sure if myostatin is safe. However, it will probably be a major target in the coming years for muscle wasting syndromes in the elderly. I have contemplated Nandrolone monotherapy seriously in the past. To be honest, it seems the closest we're going to have to a cure in the coming decade (with hardly any side effects. Supplementing exogenous E2 may be necessary since Nandrolone doesn't aromatize). However, what made me divert to TRT instead is the fact that you can't use 5ARI's on it (since it would impart the N > DHN conversion in skin, thus yielding a more androgenic profile than without a 5ARI). The reason this is troublesome is because there will always be leftover T from the adrenals when the gonads are surpressed. The leftover T will be converted to DHT in the skin, which will yield a small androgenic contribution. I think that oral + topical Dutasteride with testosterone is superior to Nandrolone monotherapy without 5ARI's (both can be safely combined with an AR antagonist of choice, of course). The topical component is very important, because oral only inhibits ~60% of scalp DHT. I'm not very sure of this theory, so if some day I were to start losing hair again I may look into Nandrolone again. I will not be using myostatin since it doesn't align with my anti-aging beliefs.
Well, asking because with topical dutasteride 0.2 mg/day and topical estriol used at 20 mg/day for several months and now at 5 mg/day, got regrowth, mainly in the mid area, but front is better than 12 months on oral finasteride , mid is definitely a different world , so more than maintainance.
I'm wondering if few mcg of E2 can do more than estriol. Left on hold WAY-200070 and probably made the right choice so far.
Started ARV-110, 0.2 mg delivered by weekly pen microneedling 0.5 mm front, 0.75 mm mid and surrounding areas. ARV-110 mw is 812 Da, 120 h oral half-life, so I had to replace my standard microneedling follica-like , 0.8-1.0 mm every other week, with this milder and more frequent treatment.
That's great news! I am becoming more and more convinced that Dutasteride
mesotherapy (that is, combined with needling to increase absorption) is extremely potent and useful. And yes, a few micrograms of E2 will be more potent than
any amount of E3. I've talked about this before, it has to do with the efficiency of the ligand at the receptor. E3 only activates about 15% of the ER-beta at saturated concentration. That means it misses out on 85% of the transcribeable genes of ER-beta. E2 is a full agonist meaning it will induce transcription of all ER-beta associated genes. I also talked about WAY in a similar setting: basically it's unknown what the efficiency of this ligand is at the receptor. Full agonists are actually quite rare, so it's not very likely to be one. Erteberel is one, and could induce a similar response at ER-beta as E2 while leaving ER-alpha. However, only a micrograms of E2 is needed to saturate the receptors, which will not give any systemic sides effects on ER-alpha. ER-alpha activation in the scalp won't happen, since the scalp hardly has any. Basically, E2 and Erteberel should be equally effective, where Erteberel is outrageously expensive and E2 basically free at the amounts that are used.
My opinion on AR degraders is this. When enough of an AR
antagonist is provided, all receptors will be blocked. The body can only upregulate AR so much, so at a certain point the AR antagonist is powerful enough to block all receptors even when receptor density increased. So, I think AR
degraders are superfluous and one may as well use an AR antagonist (Bica, Apa, Enza or Daro). However, I am very curious to see your results. Did you by chance use any AR antagonists in the past to serve as comparison?
Edit: everywhere I wrote myostatin should of course be myostatin
inhibitor.
