curiousnomad

@Ronnieman. Did you dry again with a non PG vehicle? K&B or stemoxydine perhaps?

I'm interested in this as well. I don't want to run lab work everytime i dial up the DHT suppression knob, but if there is a consensus that once weekly dutasteride is a healthy stair step on the way to full dutasteride, I'd like to hear it. 

Thanks for your response, Curious 25. I'm wondering if what those doctors are trying to communicate regarding the seemingly arbitrary 50% number is something along the lines of the following:

In androgen sensitive zones, some follicles will miniaturize faster that directly adjacent follicles. The faster a follicle miniaturizes, the faster the follicle approaches stem cell "death". What we're possibly seeing with slick bald people that recover decent coverage is the last man standing follicles that kept their stem cells "alive" had a chance to recover, whether that recovery be to 50% or 100% of its original diameter. I'm guessing at some point, a follicle's stem cell is in fact "dead" or so embedded in scar tissue that recovery is unachievable as these derms are opaquely communicating?

Lastly, I'd like to know what follicle "death" means, if anything. 

Does anyone have any technical understanding if a hair follicle, once miniaturized by androgens, can be un-miniaturized by the suppression of androgens? If not, does that mean then that the goal of any miniaturized follicle is to slow the miniaturization of that follicle via 5AR inhibitors as there's no restoring it to its former glory?

I think i heard the Hair Loss Show doctors claim once a follicle losses 50% of its diameter, it's toast. Maybe a miniaturized follicle will always produce a miniaturized hair, but minoxidil can keep that miniaturized hair in the anagen phase longer? Just wanting to better understand these mechanisms. Thanks for the feedback. Academic links welcome too