How to make good, cheap, spironolactone cream

CCS

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Byan posted a study showing that the following alcohol based spironolactone did nothing for hirutism, whereas the cream worked reduced hair counts by 50% I think, both with 1% spironolactone. The alcohol one did not have PPG.

1% spironolactone in a cream base alone:
(59.4% water,

13% propylene glycol,
3.2% cetyl alcohol,

7.5% mineral oil, 6% stearyl alcohol, 5.5% white petrolatum,

2.7% sodium lauryl sulfate, 2.6% spermaceti, and 0.1% potassium sorbate).

That is water, alcohol like stuff, thicker stuff, emulsifiers.
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1% spironolactone in an alcohol-based vehicle made by Neutrogena:

53% water

41.5% ethyl alcohol,
6.0% isopropyl alcohol,

Laureth-4).
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Here is what I want to make:

2% spironolactone
49% water
10% 70% isopropyl
16% PPG
22% oils
1% emulsifier

That is, for 100 grams of cream, I using
2g of spironolactone,
49 mL water,
10 mL 70% isopropyl rubbing alcohol,
16 mL PPG (I must buy that, but it is cheap),
22 mL of flax, borageseed, and essentials oils, saw palmeto and maybe oleic acid
1mL baby shampoo (emulsifier that does not lather).

The spironolactone is cheap; 10g total (100 of 100mg) for $25.
PPG is $30 for 1L and I think $5 for
rubbing alcohol is $1 per pint.
i have all the oils already. you can use corn oil if you want.
baby shampoo is 99 cents for 15 ounces.

i just need a swimmers cap for when i apply it at night.

the spironolactone probably is incased in lactose or dextrose (glucose). grind it up and dissolve it in water. spironolactone is insoluble in water, but sugar is soluble in water, especially warm water. get rid of the water and use the remainder in your cream. i'm going to weight it to see if it is 100mg.


and when I analyze finasteride, I'll use water first to get ride of the sugars, and alcohol second to get the finasteride out of the starch that is left.
 

CCS

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that is around 30% the cost of Dr Lee's 2%, if the tablets are real, and you get to pick the oils.

Product 205
5% Spironolactone Lotion

Quantity and Ingredients:
2 oz / 60 grams. 5% spironolactone (50mg spironolactone / gm) in a lotion base
of water, aloe vera gel, stearic acid, cetyl alcohol, alkyl octanoate, mineral oil,
dimethicone, tocopherol acetate, magnesium aluminum silicate, sorbitol, disodium
EDTA, methylparaben, dimethlydimethyl hydantoin.

Most of those ingredients are in my baby shampoo. the tocopherol is vitamin E. I guess i might buy a little aloe very just in case, if it is cheap.

Make it 5% if you want. I probably should if I just use it at night.
 

Old Baldy

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Oleic acid is NOT a replacement for oils, it acts as an emuslifying agent usually.
 

CCS

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an oil as an emulsifying agent?

My biology fatty acid knowledge is a bit behind right now. I know that there are saturated fatty acids, and that saturated FATS are three fatty acids combined to a glycerol. I don't know how the classification goes if one or two of those fatty acids is not saturated.

I know oils are fats that are liquid at room temperature and usually, but not always, are non-saturated. What I don't know is if all oils are bonded to a glycerol like satureated fats, and if companies that make 80% oleic safflower oil from 20% oleic safflower oil just distill out the oleic acid or if they have to chemically remove the glycerol and separate the individual fatty acids and then re-add the glycerol.

I hope that new guy with the biology degree who has been talking in other threads with brian about prostate cancer will explain so I don't have to get off my butt and do a google search. I''ll go to that thread and tell him to look here.

Anyway, you say you have oleic acid, but you don't say what it is from. (here. I think you told me where you buy it once. I'll have to go look that up again).

I just find it hard to believe that an oil could be an emulsifying agent.
Could you post the link to where you buy it once more? Thanks.

....
Actually, a true free fatty acid would have a carboxylic group that is soluble in water, and a tail that is soluble in fat. So that would make it an emulsifier. So you are not buying high-oleic acid oil. You are buying actually free oleic acid. Interesting.

Bubbka, does the skin have free oleic acid or oil with oleic acid in it or both?
 

CCS

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I think I answered my own question. Yours just does not have glycerol.

I looked up spironolactone prices. Some pet places sell the 25mg tablets without a prescription, and are in the US and clearly state their address. So I guess it is not tightly regulated. But the 100mg tablets are all Rx only. It looks like I was wrong about the price. One hundred 100mg tablets is $40. So my solution is not as cheap as I thought compared to Dr. Lee's. I wonder how Felk plants to make his for under $10 per month. Maybe he can get it cheaper in the land down under.
 

Bryan

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Re: an oil as an emulsifying agent?

collegechemistrystudent said:
My biology fatty acid knowledge is a bit behind right now. I know that there are saturated fatty acids, and that saturated FATS are three fatty acids combined to a glycerol. I don't know how the classification goes if one or two of those fatty acids is not saturated.

I may be wrong, but I don't think there's any particular "classification" describing that situation. It's just a triglyceride containing a mixture of saturated and unsaturated fatty acids.

collegechemistrystudent said:
Actually, a true free fatty acid would have a carboxylic group that is soluble in water, and a tail that is soluble in fat. So that would make it an emulsifier. So you are not buying high-oleic acid oil. You are buying actually free oleic acid. Interesting.

Hmmm....I don't think these typical fatty acids (the C:18 ones, anyway) have any significant solubility in water. Metallic salts of fatty acids turn them into soap, of course, which will be more water-soluble.

Bryan
 

CCS

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Yeah, the acid hydrogen is more likely to come off at a lower pH. A metal in a salt will come off at just about any pH, though it would be replace by a hydrogen quickly at a low pH. I am working with formic acid in my summer research (fenton reaction) right now, and know half of it is dissociated at a pH 2.8, wheras acedic acid is half dissociated at a pH of about 4.5.

So I believe you that the really long ones probably don't dissociate much, if i can draw a pattern from those first two based on the fact that formic has only one carbon and acedic two. Our measuring technique depends on this fact. because we change the pH to selectively evaporate stuff out of solution.

my professor was telling me that ionic molecules will stay in a polar solvent much more strongly than polar molecules. while fromic acid is prefectly solube, the fatty acids have long tails that pull them into the fat, and the polar non-dissociated end won't stop that, whereas an ionic dissociated end will stay in the water and drag fats in with it.

The most common metal salt in soap is the sodium salt, from sodium hydroxide, which lowers the pH. in order to make a soap, you need a non-polar molecule with one end that will dissociate even at a pH of 4 (shampoos), though most soaps have a pH of 9 or 10 and just change your skin pH.
 

CCS

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$15 per gallon is as cheap as corn oil.
 

CCS

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good anti-androgens, and reasons.

I read that chart Bryan gave us, with the relative strengths of adrogens, and it explains a lot. I just want to explain some concepts to people.

1. 0.5 mg/day dutasteride inhibits almost all type 2 5ar, so that the 7% of serum DHT remaining is coming from the half of of 5ar1 that is not inhibited.
2. Since the scalp has more 5ar1 compared to the rest of the body, blood DHT levels there are inhibited only 55%.
3. Only the DHT activity in the follicle matters, so if 5ar2 produces DHT in the follicle, that DHT causes the vast majority of the damage.
4. 2.5 mg/day dutasteride inibits about 85% of 5ar1, so that scalp blood DHT levels are inhibbited 84%. Since 2.5mg/day dutasteride grows about 20% more hair than 0.5 mg/day, and 0.5 mg/day inhibits almost all 5ar2, this shows that when 5ar2 DHT contribution is small, the effect of DHT diffusing in from the blood from 5ar1 matters.

So 5ar1 does play a small role in hair loss.

5. A new drug Merk experimented with inhibits almost all 5ar1, but does not seem to affect hair loss. This shows that reducing the DHT in the follicle by a small amount has little effect on hair loss.

6. 5ar1 is in the brain, so inhibiting it could affect the brain. 0.1mg/day dutasteride does not inhibit much 5ar1, and inhibits 84% of type 2. It is therefore a safe dose.
7. 0.5mg twice a week inhibits (guessing from the graph) 93% of type2 and 15% of type1. I think this is still safe, much more effective, and easier to stay on schedule with than a pill every 5 days.
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to avoid side effects in the brain and body, topical anti-androgens are needed.

1. oral flutamide is much stronger than oral spironolactone because both quickly react in the body to form metabolites, and hydroxyflutamide is far stronger than the spironolactone metabolite.
2. flutamide is not as strong as hydroxy flutamide, and is absorbed systemically when applied topically. it affects the whole body equally at all dose.
3. spironolactone is powerful, but needs a good vehicle, such as the right cream.
4. if the same concentration of spironolactone as DHT is in a celll, the spironolactone will occupy 67% as many androgen receptors as the DHT will, assuming i am interpretting the table brain posted. logically, if it has equal strength, and is assigned a value of 100% like DHT, it would occupy 50% of the receptors.
5. Assuming you had a vehicle that could deliver this much spironolactone to the cells, it would have the effect of inhibiting 40% of DHT. This is weaker than propecia, which inhibits 70% produced by 5ar2. This is why topical spironolactone has little effect.
6. spironolactone's metabolite is so weak that it can't have systemic effects. I think spironolactone is used for water retension, which should interest people who believe minoxidil cause water retention.
7. If finasteride inhibits 70% of 5ar2 DHT, and spironolactone blocks 40% of the remaining 30, that combo blocks 82% of the DHT activity, and all the testosterone and other androgens, and some of the DHT that enters from the blood.
8. Again, the concentratin of spironolactone matters, and so does the vehicle.
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9. I don't know how strong fluridil is, but it looks similar to hydroxy flutamide, but has a tail on it that should make it stronger. 2, 4, and 6% twice a day all have the same effect as 2% once a day, which does indicate it might be strong.

10. I did not see a table of RU compared head to head with other anti-androgens, but Bryan said it is 85% as strong as castration, which means that it would occupy 85% of androgen receptors and leave only 15% for DHT, which means it is 85/15 = 5.7 times as strong as DHT. If this is true, then by itself it is about as strong as proscar. This, as everyone knows, is not enough to regrow your hair like majic. But if you combine it with proscar, and eliminate 85% of the remaining 15%, that gives you the effect of 98% DHT inhibition. Combine RU with dutasteride twice per week, and you get safe results that are stronger than the once a day. Note: DHT from 5ar1 can enter from the blood and affect the weakest hairs, specifically the ones that are almost peach fuzz or below the surface. RU can block 85% of that DHT. Even 2.5 mg/day dutasteride only inhibits 75% of 5ar1, though only a fraction of what is left will enter the follicle.

So I predict that combining RU with dutasteride 0.5mg/ twice a week would be slighly more effective than 2.5mg/day, partially because of the protection from testosterone.

fluridil and RU do not go systemic
 

CCS

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and taking 0.5mg/dutasteride twice a week combined with spironolactone should be a little stronger than take 0.5mg dutasteride/day, partially because of the testosterone protection.

if the concentration of spironolactone in the cell is different from the concentration of DHT, or if number of molecules is not greater than the number of receptors, this will change these predictions. I'm sure the number of receptors is small compared to grams of spironolactone, though only a small percent of the spironolactone enters the scalp and a smaller percent enters the follicle.
 

CCS

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CCS

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my eucapil arrived

i got my eucapil today. they had to send it twice because it got returned. they said that only happens in 5% of cases.

I'll make my first application in 5 hours, after my prox-n dries. i just took a shower. i'm just going to apply it to the front of my head. i'll use the full 2mL this time until i get silly puddy to use 1mL per day. then i'll use it every other day alternating with spironolactone once my spironolactone arrives, though I can probably only use the spironolactone on my hairline. but I think the eucapil will stay in the scalp longer than they say, and I don't think a quick shower will hurt it. i think the only time it is volunerable to mosture is when it is on your scalp and getting absorbed.



my spironolactone cream will have free fatty acids in it as the cream base. wow, that will be good. bryan and i suspect the only reason saw palmetto has any hair loss benifits is it has a higher percentage of free fatty acids than most oils do. oils are fatty acids bonded to glycerol. i did not read the studies bryan has, but the fatty acids are very good DHT inhibitors, and maybe a solution for people with propecia side effects. I think the slow evaporation rate might entice me to add 4 dutasteride capsules to my cream, especially if it will last over a month.
 

CCS

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my folligen just arrived from follica, 10 days after I ordered it. i live in the western USA.
 

Felk

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My folligen just arrived a few days ago too. Its a massive bottle, i have to say. Im just wondering what it is in ml, college? 8oz, is it 240ml?

Anyway, i think i might actually use the spray instead of the dropper, because with long hair spreading drops around is hell. And with folligen's cheapness, i coudl use a bit more.

Also, i don't really mind the scalp staining. If you use it straight, it goes away after a while.
 

CCS

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Bryan just posted that 80% of the pill is filler, and I'm not sure if any of it is water soluble, except for the lactose, which is a small part. The spironolactone is ethanol soluble, but you need a lot of ethanol, and evaporating it is no fun. I'm trying to find away to make pure spironolactone. Until then, I am very convinced the extra powder detracts from its effectitivenss.
 

Felk

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collegechemistrystudent said:
I wonder how Felk plants to make his for under $10 per month. Maybe he can get it cheaper in the land down under.

I was basing that figure on Iamnakes recipe, which is a 2.5% mixture using nothing but the spironolactone. tabs and rosewater glycerin. I can't vouch for it's effectiveness.
 
G

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college,

what about eventually combining RU daily with Dutas 0.5 mg per day? Would that achieve close to 100% DHT inhibition and take care of the testosterone and other androgens?

what other androgens does RU block besides test and DHT? are there exact numbers on how much RU blocks?

thanks
 

CCS

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I've never seen any numbers and I know it is dose dependent and the dose that gets into the skin is based in large part on the vehicle used.

it affects all androgens. Any thing that binds to the AR will have an RU in the way.

I'm much more interested in finding a company that will buy a gallon of borage seed oil and make it into fatty acids and sell it to me, if I can't do it myself. Though maybe once male pattern baldness starts, it is necessary to hit it with RU as well since maybe it is more sensitive then. I suspect though that GLA reverses sensitivity.

Bryan has studies which show that GLA reduces flank organ size, and appears to block 5ar. Oleic acid blocks both 5ar and AR, and is the only 18 carbon fatty acid tested on both. But here is the kicker. They don't know these do either. They don't know the mechanism. It is entirely possible GLA reduces the production rate of 5ar, instead of actually blocking it. The experiments would get the same results either way and we would not know the difference. I have a strong suspicion this is what happens. When you get off propecia, all the 5ar's are still there and kill the follicle. They are worse than every, but were just clogged this whole time. When you get off GLA, the cell may need time to make more 5ar, and I suspect it will take more than a week. I think GLA and other fatty acids may prevent skin aging. I'd like to use RU temporarily while GLA goes to work. Once GLA makes its repairs, I would then want to stop the RU, and not use spironolactone or eucapil.

I'm really tempted to go buy revivogen right now, but I don't have the money, and could make my GLA for my face and scalp for $5 a month if I just get the chemistry down.
 

Felk

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JayMan said:
college,

what about eventually combining RU daily with Dutas 0.5 mg per day? Would that achieve close to 100% DHT inhibition and take care of the testosterone and other androgens?

what other androgens does RU block besides test and DHT? are there exact numbers on how much RU blocks?

thanks

JayMan, I think once you're on dutasteride and some sort of AA i don't think you need to worry about DHT/androgens anymore!

Remember, taking out androgens is only one part of fighting baldness. The most successful approach will always be addressing it from different angles.
 
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