My new plan...

[CCS]

My new plan is to buy RU, mail half to my brother, use 5g in 5 months, store most in the freezer with descicator sand, and store a 1 or 2 month supply in pure borage and flax seed free fatty acids. That is 1.5% RU at 1.5 mL per day for $40 per month. If it esterifies at all with any of the the fatty acids, that will increase its solubility. I'd like to store it all in the fatty acid, but I'm not sure if it will break down. When I'm ready to apply some of it, I will dissolve 0.25mL of fatty acid/ RU mixture in 1.25 mL of ethanol/ 1% spironolactone mixture, stored separatedly. I will use two separate minoxidil droppers to get the liquids and mix them on a hard surface, and suck them back up and apply to my thinning and smooth areas. After a year, I will reduce the RU dose to 0.5% to save money.

For the spironolactone, I'll do a water extraction of the lactose first, to get as pure of spironolactone in ethanol as possible. And only if the spironolactone does not stink. That is about $60 for 1000mL of solution, would last me just over a year. So $5 per month, only 2/3 of which is the spironolactone. RU is needed only to compete with DHT. spironolactone can handle testosterone just fine.

It might not make sense getting both, but the investment is small. I can split the $60 with my brother and do 5-6 month increments.

Yeah, I'm definitely doing 20% PPG in the ethanol.

I'll use my eucapil daily until my RU arrives, and after a year or less of using it, I will alternate with eucapil and then evenually use up the eucapil and then just use the RU spironolactone at a lower dose. It is cheaper than Eucapil.

 

[CCS]

Now I know why Bryan did not respond. GLA blocks 5ar. It does not block androgen receptors. That is why it does not make sense to compare it to spironolactone. It would make more sense to compare it to finasteride, except the vehicle would be an issue. It has not been tested orally, nor would some people want to do so, since the goal is a local effect, unless the stuff returns hormones to normal, non balding levels, instead of lowering them all.



My previous post to bryan:



You posted an abstract that gave the strength order of fatty acids, but was there ever a study that measured the adrogen receptor affinity compared to testosterone or spironolactone or DHT, and the concentrations used?

Also, do you think GLA would have structural changes at 100 degrees C?

 

[Bryan]

Now I know why Bryan did not respond. GLA blocks 5ar. It does not block androgen receptors.

Hey, not so fast! As I mentioned a while back, there is evidence that unsaturated fatty acids seem to have SOME kind of activity against androgen receptors. In the hamster test, GLA did have some activity against even the DHT-stimulated growth of the pigmented macules, although it didn't reach statistical significance. It caused a 26% inhibition in one of the experiments.

There's other evidence supporting that idea, too, like the following study: "Inhibitory Effect of Fatty Acids on the Binding of Androgen Receptor and R1881", Mitsuhashi et al, Endocrinol Japon 1998, 35 (1), 93-96. They found in an in vitro study of rat prostate cytosol that oleic acid caused a greater than 60% inhibition of binding of androgen receptors with the potent androgen R1881. Arachidonic acid and DHA caused inhibitions slightly over 80%. And there's at least one other study with similar findings, too.

So topical unsaturated fatty acids may have a bit of a double-whammy against androgens: they mostly inhibit 5a-reductase, but they also probably interfere directly with the binding of androgens to androgen receptors, by some as yet unknown mechanism.

Bryan