TheLastHairbender said:
I wanted to take the time to give you the full story in my experience so far before someone else starts telling you to slather home-compounded RU Myristate all over your head without even giving finasteride+minoxidil a shot first.
tedlin01 said:
Put the money on some more potent experimental treatments as RU58841, ASCJ-9. ... Save some "space" for Minoxidil and/or OSH101 and/or Bitamoprost.
Ahh tedlin beat me to it while I was typing that whole dissertatio
n! It's not that this is bad advice; RU, 17ap, ASC, OSH, OC, and especially bimatoprost all show tremendous promise. Just give yourself time on the big 3 first, then come back and re-evaluate the state of the art with these treatments after a year. Hopefully at that time we'll know more about the optimal dosages, best delivery vehicles, necessary application frequencies, and have established some safety guidelines for their use. You might not even have to buy them out of someone's basement and compound them on your kitchen counter at that point! It's also possible that after a year on the big 3 you, like me, will have regrown so much damn hair that there isn't even a need for more inconvenient, costly, and potentially hazardous treatments. Instead you can save the add-ons for five years down the road when finasteride and minoxidil start to lose their punch. ...It's like feeding a starving person at a five-start gourmet - the luxury would be wasted when plain rice would seem like a Michelin-star dinner. Enjoy your rice for a while, then when you're sick of that we'll take you out to a nice fancy dinner, and you'll enjoy it all over again.
As a final precautionary tale, look at that list of experimental stuff: RU58841, CB-03-01, ASCJ-9, OSH101, OC000459, bimatoprost
(aka 7-[3,5-dihydroxy-2-(3-hydroxy-5-phenyl-pent-1-enyl)-cyclopentyl]-N-ethyl-hept-5-enamide). That's just six of the more prominent ones right now. It seems almost assured that ten years from now, out of all those experimental treatments, there's going to be one that we're like "dang, I can't believe people were putting that lymphoma bait directly on their skin for hair loss". ...So which one are you going to pick? Hope it doesn't turn out to be that one.
There are many more too: P45, KF19418, LGD1331, Thymosin B4, Naminidil, Diazoxide, Panacidil, Bicalutamide, steroid sulfatase inhibitors, Cromkalin, etc. Just because something inhibits 5a-reductase or activates potassium channel ions doesn't mean it's ok to start rubbing it on your head. Most of this isn't new either. Use Google Trends and see how long people have been talking about this stuff. OSH101? Yeah that was called PS1 back in 2003 and nothing has come of it since. RU? Not new. It has been the 'next big thing' since at least 2004. If safety and effectiveness were so assured with these novel treatments one surely would have been brought to this $10 billion market with how many commercial drugs under unique patent? zero?
There's a lot of lunacy in the hair loss community. UCLA released a study last year in which a new peptide regrew hair on five baldness-induced mice. There are already people lining up on the forums to have it synthesized and begin topical application. Nevermind that man's only experience with the stuff is on five mice, receiving it via injection, for a whopping
five days and studied for all of four months. Topical Astressin-B is as likely to cause melanoma as it is to regrow hair. (The study itself shows a more immediate impact on melanocytes than on hair follicles, but you don't hear anybody talking about that). But inevitably someone is going to come along and tell you to try rubbing
D-Phe-His-Leu-Leu-Arg-Glu-Val-Leu-Glu-Nle-Ala-Arg-Ala-Glu-Gln-Leu-Ala-Gln-cyclo(-Glu-Ala-His-Lys)-Asn-Arg-Lys-Leu-Nle-Glu-Ile-Ile-NH[SUB]2 [/SUB]into your scalp twice a day.
RU is praised for a reported lack of systemic absorption, yet some people are reporting E.D., clear semen, and shrunken testes. Some ASC experimenters are reporting joint pain throughout their bodies. OSH's class of peptides has been linked to Parkinson's disease. Bimatoprost can turn your iris permanently brown if it gets in your eyes (oh and you have to buy it in raw bulk powder and mix the preparation yourself - hope you have a steady hand). Not trying to scare you, I curse propeciahelp.com for that, but the fact is that we don't have safety profiles for much of this stuff, let alone an understanding of proper methods of administration, dosages, etc.
To recommend you start using anything but finasteride, minoxidil, and keto is downright reckless. (Ok spironolactone, Retin-A, and the AHK volume in Tricomin get a pass because their safety has at least been established). You'll find a lot of desperate people willing to try anything in the hair loss community. You don't need to be one of them yet.
- - - Updated - - -
OK I wanted this to be a separate post but since there is no intermediate reply the new system is adjoining it to the former.
Please post references showing spironolactone topically having systemic effects and pm these to me to
I think you will have a hard time finding research support for that view. Early studies, as far back as 1988, suggested a lack of systemic absorption from topically applied spironolactone:
Rey FO, Valterio C, Locatelli L, Ramelet AA, Felber JP. "Lack of endocrine systemic side effects after topical application of spironolactone in man." J Endocrinol Invest. 1988 Apr;11(4):273-8.
Berardesca E, Gabba P, Ucci G, Borroni G, Rabbiosi G. "Topical spironolactone inhibits dihydrotestosterone receptors in human sebaceous glands: an autoradiographic study in subjects with acne vulgaris." Int J Tissue React. 1988;10(2):115-9.
Messina M, Manieri C, Musso MC, Pastorino R. "Oral and topical spironolactone therapies in skin androgenization." Panminerva Med. 1990 Apr-Jun;32(2):49-55.
These early results remain unchallenged in the literature as far as I'm aware.
Still, there has been a non-negligible number of reports of gynecomastia from topical spironolactone use, which seem to follow the discontinuation of oral anti-androgens for the same reason. It's possible that individuals exist in the hair loss community with sensitivities to estrogen that were not well-represented in the small
N studies referenced. Let me attempt to reconcile these observations:
Noting that the first study used
N=6 "healthy" males, a single application of spironolactone, and 72 hours of post-treatment observation, the hypothesis that certain estrogen-sensitive individuals may demonstrate non-severe systemic side effects after medium- or long-term use can not be immediately refuted. Put more convincingly: I conjecture that topically applied spironolactone may be systemically absorbed after long-term use in sufficient quantity so as to generate systemic side effects in particularly sensitive individuals while remaining at undetectable levels after 72 hours of a single application among healthy individuals. The experiment from the first referenced study is of insufficient duration and contains insufficient variation in its sample group to refute this conjecture. In fact both can be true: a single application of topical spironolactone may be systemically undetectable for 72 hours among healthy individuals and also exhibit long-term systemic absorption among sensitive individuals, even if only in small amounts (the question about amount is more a question of how much it takes to generate gynecomastia among individuals already demonstrated to be gynecomastia-prone when on 5a-reductase suppression, which could be argued to be very little).
The second study, which I believe provides the strongest basis for our beliefs in spironolactone's safety and effectiveness, is more convincing. Study participants apply 100mg of spironolactone to 25 square centimeters of their back, approximately the same area I typically cover when applying to my vertex and temples. A 5% strength cream yields 47.5mg/mL, so the experimental application volume was 2.1mL, roughly double what I attempt to apply at one time (although my metering out of spironolactone is anything but scientific, one of my main complaints about its application), and was maintained under occlusion, further amplifying typical absorption rates. This heavy application, combined with their long-term results from one month of twice daily application without occlusion, presents a stronger confirmation of spironolactone's strictly local influence (and its effectiveness for selective AR competition). Still, the tiny sample size of six can surely not be expected to span the population space.
The third paper is a survey and I have other things to do with my life right now.
If you're of the belief that spironolactone is not systemically absorbed. . . then I'm in agreement with you, at least up to the 98 or 99th percentile in terms of sensitivity. In that sense, the small-sample findings can still be logically reconciled with the observation that several among many, many individuals, particularly those that have previously demonstrated sensitivity to DHT inhibition, may exhibit side effects consistent with systemic absorption. I am personally comfortable with the general belief in topical spironolactone's safety (and efficacy for that matter).