DHT-blocking Topicals (Please submit information)

[MPBWarrior]

I want to start this thread to see what people have to say on DHT-blocking topicals like Revivogen, spironolactone, etc., as i am thinking of starting to use one and i´m sure a lot of people would love to hear information on them. Thanks.

 

[CCS]

I speak from rehashed posts and some intuition, not my experiece:

spironolactone cream is good but not nearly as effective by itself as propecia. it is good for applying to hairlines and bald spots you want to grow in more than propecia would. While it can get you there faster, once you have more than propecia would have given you, that extra should fall out within a year or two of quiting the spironolactone.

Revivogen in theory should be work, but they don't report their GLA and ALA concentrations. They have oleic acid, which is weaker and cheaper than these other fatty acids. I suspect the reason they include it is just so they can say on some hard to find part of their site that their product is 40% fatty acid, most of which I guess is the oleic acid, though they hope you will assume they have more of the potent ones.

RU is 10x as powerful as spironolactone, and 5.7 times as powerful as DHT. But the vehicle is everything. You must get some in the follicle a somewhere near the concentration of DHT for it to do its job. If you could get it in the follicle at the same concentration as DHT, it would be a bit stronger than proscar, but maybe not quite as strong as dutasteride 0.5mg/day.

Flutamide only has systemic effects, which help hair since hair is part of the whole system.

Eucapil dries in seconds but is pricey, and may be weaker than spironolactone, but perhaps has a better delivery.

Topical finasteride has only worked in creams. I believe it is very important for absorption to last 2 hours or even 3, since that is how long it takes the complexing of 5ar2 and finasteride. That means slow evaporation, and minoxidil is not slow enough. The PPG free minoxidil should be slow enough. I would consider adding oils, or having a separate topical of oil and isopropyl alcohol mixed to a slow evaporation. Even then, there are no experiments to say if it reaches the follicle, or goes into the blood and to the heart and back again.

azelaic acid does not work, despite what lee says. 98% is way better than propecia, yet i don't see his minoxidil customers getting by as good as avodart users.

I don't know about zink.

 

[MPBWarrior]

Thanks college! which oils do u suggest? and also, how do i go about making a solution or cream or whatever with these oils to apply to my scalp? thanks!

 

[ShedMaster]

collge, in your opinion what method/order should folligen be applied to the scalp when combined with 5% generic minoxidil?


minoxidil 1st? if so, how long to let it dry before applying folligen?

 

[CCS]

shed master,
i don't know the answer to that. I would assume the order would not matter much. I just advice to apply any oily stuff like PPG minoxidil last, since the oil can keep watery stuff like CPs from getting into the pours. I would apply the one you want the most of first. In my case, I apply prox-n first to make sure it is fully absorbed, and i wait a few hours before applying anything else, but this might not be necessary.

As a result of my long wait, I usually only get one each of 4 topicals each day, instead of 2 each.

 

[CCS]

MPBwarrior,

i think the main purpose of oils in a cream is to slow and prolong the absorption of the topical by making it more viscous and slowing the evaportation. 90% alcohol will get a lot more into your scalp, but the wave will likely rush into your blood faster than you vessels (for minoxidil) or follicles (for other topicals) can absorb them, and is gone in 30 minutes. Because spironolactone is broken down into an extremely weak anti-androgen quickly, it is good to use a cream that gives a 4+ hour delivery. If it can bind to the androgen receptor strongly enough and fast enough, and completely enough, i guess a 5 minute dose would be OK. but it looks like this does not happen, I think, because cream works and alcohol does not in a study bryan posted. However, the PPG could have done something. until i see more studies, i can't say for sure.

as for oils, it does not matter a lot. flax or borage might be a little better than corn oil, but for dramatically better results, you must break the flax and borage oil apart into their fatty acids and glycerol, and maybe remove the glycerol, mainly so they don't reform together. The fatty acids are not only good penetration enhancers, but they inhibit 5ar in vivo at very low doses. I don't know if revivogen has enough. that is why i am making my own. they can be good by themself, or you can use them to make spironolactone cream. most likely you will need water and a pressure cooker to make fatty acids, but it will take loner and be much less pure than i can make it with acid and base.

i don't know now to separate all the filler from spironolactone cream. water will take care of the lactose, but there is a lot of other stuff that is not water soluble, and a lot of ethanol is required to dissolve spironolactone, more than i would want in the cream for that dose of spironolactone. i could dissolve spironolactone in fatty acids, but I'm affraid the viscosity would make a suspension and the filler would not settle out. i will experimiment with oleic acid first, since corn oil is cheap.

 

[momo]

Many people, Including myself, could not bear finasteride side effects, that's why they seek for a topical dht inhibitor. I had a tremendous success with finasteride within only 3 months, so I know dht is a big factor in my hairloss.

Three months on liquid spironolactone 2% did nothing to my hair (matching byran's research).

College, ppg free (lee's version) dries faster than regular minoxidil (based on personal experience). Few months ago I put some finasteride in lee's minoxidil (which dries and/or absorbs very fast). I had some minor results but also experienced side effects.

I'm no expert but I do believe that you need a vehicle that releases the the chemical (finasteride/minoxidil/whatever) slowly, so it won't flush with the blood, making it effective and not causing sides.

I made a chocolate cake the other day and had it covered with tons of thick film of chocolate syrup. Every time I had a slice I could see the chocolate slowly absorbed few milimeters down. The cake did not regrew hairs, in case you wonder, but it did make think for a few seconds about absorption. Going to have another one.

 

[CCS]

I wonder if GLA is as strong as spironolactone. At least it is easily absorbed and avaiable in mass quantity and may have other benifits, and does not stink.

 

[MPBWarrior]

so to summarise for people like me (which i´m sure there are many of)searching a dht-inhibitting topical, is spironolactone the most obvious choice? and on that note, is dr lee´s the best one? 2% or 5%? and from what i gather, the cream is better right?

 

[JWM]

A guy named Waseda mentioned this years ago on Hairsite. He claimed that he got good results on topical finasteride by grinding it up with Dermovan AND Horse Oil.

 

[Bryan]

Revivogen in theory should be work, but they don't report their GLA and ALA concentrations. They have oleic acid, which is weaker and cheaper than these other fatty acids. I suspect the reason they include it is just so they can say on some hard to find part of their site that their product is 40% fatty acid, most of which I guess is the oleic acid, though they hope you will assume they have more of the potent ones.

Hmmm....when you say "they include [oleic acid]...", you seem to be implying that they pick-and-choose specific fatty acids to include in Revivogen. But that's not the case! Again, my understanding is that they take certain natural oils (flax and borage were mentioned in this regard at one time), and then de-esterify them en masse for inclusion into the product. So Revivogen has the same fatty acid profile as whatever specific oil(s) they happen to be using.

RU is 10x as powerful as spironolactone, and 5.7 times as powerful as DHT. But the vehicle is everything. You must get some in the follicle a somewhere near the concentration of DHT for it to do its job. If you could get it in the follicle at the same concentration as DHT, it would be a bit stronger than proscar, but maybe not quite as strong as dutasteride 0.5mg/day.

College, all this theorizing and number-crunching you do makes me dizzy!

I'm not sure what you mean when you say RU is "5.7 times as powerful as DHT".

When you say that RU is "10x as powerful as spironolactone", I rather prefer a simpler, more intuitive bottom-line biological way of comparing the two. Since topical RU58841 reduces hamster sebaceous glands by a maximum of about 60% (near-castration levels) and the greatest reduction I've ever seen with topical spironolactone was about 39% (30% is more typical), I feel that it's more intuitive to say that RU is approximately twice as effective as spironolactone, at least in that specific animal model.

Bryan

 

[CCS]

To say RU is twice as strong as spironolactone would be to say a drug that grows twice as much hair as propecia is twice as strong as propecia. This seems fair, but when I said RU is 10x (actually 8.5x) as strong as spironolactone, I meant it in terms of the androgen supression, not the therapudic effect. Avodart only grows about 50% more hair than propecia 1mg, yet it reduces DHT to a small fraction the level that propecia brings DHt down to. That is the way I meant with the RU and spironolactone, kind of like the 100% scale with DHT being 100%.

I assume if an anti-androgen on this scale is ranked 50%, that means at the same concentration as DHT, it will occupy half as many androgen recptors. Or it takes twice the concentration to occupy an equal number of receptors. I could be wrong on what that scale means.

I don't remember how I came up with the numbers. You said in another post that castration reduces flank organ size by 75%. Maybe I divided by 60% (which would be a lapse in logic), or maybe there was another post I used, but somehow I thought that RU would occupy 85% of androgen receptors when at the same concentration as DHT. From that, I did 85%/15% = 5.7 times as strong as DHT = 570% = 8.5 times as strong as spironolactone.

I guess I did not have a good reason to come up with the 85% figure, and either way, calculating how much DHT is blocked is not as important as the actually effect. However, when choosing which anti-androgen to use, and knowing you can use higher concentration, and that there are different prices, this information does become useful.

 

[CCS]

"1) The most suppression of flank-organs I've ever seen by the topical application of spironolactone was 39.3%, for a dose of 0.3 mg/day. A larger dose of 3 mg/day actually produced LESS suppression (29.5%), suggesting that 0.3 mg/day is close to an optimum dose for that drug, at least in hamsters. There was no suppression of the other flank-organ in either case, indicating that the effect was apparently a local one only.

2) The same study as the previous one (for spironolactone) also tested topical cyproterone acetate. At a dose of 0.3 mg/day, it achieved a suppression of 39.7% on the treated side, and a suppression of 30.3% on the untreated side, suggesting that maybe it worked partly by a direct local effect, but mostly by systemic absorption.

3) As I mentioned earlier, the Chen et al study found an even greater 52% reduction in the flank-organ size from the same dose of 0.3 mg of flutamide, but BOTH flank-organs were affected to the same degree, suggesting a completely systemic route of absorption.

4) A study of topical RU58841 by Matias et al found a maximum reduction of about 60% in hamster sebaceous glands, with no apparent systemic effects!! So I think it's crystal clear that of all these antiandrogens that have been tested topically, RU58841 is the clear winner. Now you know why I'm so interested in RU!"

The doses and vehicles are not given, particularly with the RU.

Back to the flutamide. The small dose had that much effect on the whole animal, suggesting that either spironolactone has a short half life, or hydroxyflutamide is very strong. I noticed hydroxyflutamide was not on the list of androges you posted.
http://www.gourmetstylewellness.com/discussions ... n&start=40
I mention this only because I'm trying to guess the strength of fluridil, which looks kind of like hydroxyflutamide but with a longer tail.

 

[CCS]

What is the approximate surface area that topicals are applied to on hampsters?

 

[Bryan]

To say RU is twice as strong as spironolactone would be to say a drug that grows twice as much hair as propecia is twice as strong as propecia. This seems fair...

Even in a case like that, you still need to compare hairgrowth with the drugs to what happens with the placebo. Think about this hypothetical example: you've developed two new 5a-reductase inhibitors, but they aren't as effective as finasteride. In fact, they are just barely able to lower DHT levels enough to cause any regrowth at all. The placebo haircounts drop by an average of 30 hairs after a year, but one of the drugs causes an average increase of ONE hair after a year, and the other drug grows TWO hairs. Would anybody be crazy enough to say that one of the drugs was "twice as effective" as the other because it grew "twice as much hair" (2 versus 1)? Of course not. The difference between the two drugs isn't 2 versus 1, it's 32 versus 31. They're both nearly the same effectiveness.

...but when I said RU is 10x (actually 8.5x) as strong as spironolactone, I meant it in terms of the androgen supression, not the therapudic effect.

Yeah, but how on earth would you go about computing the true "androgen suppression" of the two drugs? It's too difficult and unreliable to try to figure that out. Just go by the therapeutic effect, which is the bottom-line, anyway. Screw what it OUGHT to be on paper, go by what happens in the Real World.

Avodart only grows about 50% more hair than propecia 1mg...

I doubt that it's even that much. And it's even less significant still when you take into consideration the changes versus placebo, like I mentioned above.

I don't remember how I came up with the numbers. You said in another post that castration reduces flank organ size by 75%. Maybe I divided by 60% (which would be a lapse in logic), or maybe there was another post I used, but somehow I thought that RU would occupy 85% of androgen receptors when at the same concentration as DHT. From that, I did 85%/15% = 5.7 times as strong as DHT = 570% = 8.5 times as strong as spironolactone.

I believe that RU58841 is generally considered to have about the same Relative Binding Affinity to androgen receptors as testosterone (not DHT). I could probably dig-up the RU study again that said that, if you're curious to see it.

Bryan

 

[CCS]

I would like to see it, mainly because I'm curious what the binding affinity of testosterone is compared to DHT, when ever both 5ar's are blocked.

http://www.gourmetstylewellness.com/discussions ... n&start=40

In that list, testosterone is equal to DHT because it is converted to DHT.

What is meant by DHT being 30 times as potent as testosterone?

And do you know the surface area of the spironolactone applications on the flank organs? That would give me a ball park idea of what concentration to use.

 

[CCS]

It just seems odd that if spironolactone is 67, and DHT is 100, and RU is between the two, that spironolactone would shrink the gland 30%, and RU a whole 60%, unless the 52% experiment for spironolactone was more accurate.

 

[Bryan]

I wonder if GLA is as strong as spironolactone.

It would appear to be AT LEAST as effective as spironolactone.

It's always somewhat risky to try to compare different studies that used different kinds of testing, but there's not much else available. The hamster study of GLA and the other fatty acids measured the changes in the area of the pigmented macule on the flank organs, rather than the size or mass of the flank organs themselves. That shouldn't be that much of an issue, because my understanding is that there's a reasonably good correlation between the size of the pigmented macule and the flank organ itself.

Here are the results of one of the experiments. They used castrated hamsters, and applied ethanol only to the left flank organ. They applied ethanol containing testosterone with or without the test fatty acid to the right flank organ every day for 21 days. After that period of time, the pigmented macule on the right flank organs (the ones that didn't get any fatty acids at the same time) grew to 10 times the size of the one on the left flank organ. The flank organs that also got fatty acids had pigmented macules whose growth was inhibited to various extents, depending on the specific fatty acid that was used. Here are the degrees of inhibition from each fatty acid that was tested (1 mg was applied each time):

undecylenic acid: 16% p>0.05
palmitic acid: 25% p>0.05
oleic acid: 43% p<0.01
elaidic acid: 5% p>0.05
linoleic acid: 52% p<0.01
linolelaidic acid: 6% p>0.05
alpha-linolenic acid: 44% p<0.01
GAMMA-LINOLENIC ACID: 66% p<0.01
arachidonic acid: 28% p>0.05
erucic acid: 29% p>0.05
nervonic acid: 10% p>0.05

Another experiment they did was with intact (non-castrated) newborn hamsters. They applied 2 mg of gamma-linolenic acid to the right flank organ every day and measured the growth of the pigmented macules over the next 24 days. The final two measurements made near the end of the trial showed reductions of 58% and 52%, compared to the hamsters that were treated with ethanol alone. The left flank organs were unaffected, showing no systemic effects.

Bryan

 

[CCS]

That is informative. It is nice to know linoleic acid and ALA are close behind. I must point out that here linoleic acid out performed ALA, whereas in the PubMed abstracts you posted, ALA outperformed linoleic acid. It is also interesting that even oleic acid did decently, perhaps similarly to how spironolactone would have done.

Since RU costs 10x as much as spironolactone for the same dose, I'm tempted to go with the spironolactone.

I read that borage seed oil is supposed to be 57% GLA, but the bulk stuff is 22% GLA. I wonder if that means they remove GLA before selling the bulk stuff. That makes me tempted to go with flax oil, which is 57% ALA, 20% oleic, and 20% linoleic, and cheaper. I'd really like that GLA if I can get it in the 57%.

 

[Felk]

So the question is, do we go with college's idea and try to get the stuff in bulk, or just go for revivogen? Especially because on ebay i seem to be able to get 9 bottles for $99 (unless its just worded badly, saying 3 boxes of 3, and its really just 3 bottles) I wouldn't mind saving myself the hassle and just sloshing that on my head.