Question for Sweetjade!

[Karl2]

Hi Sweetjade/everyone,

Sweetjade I have a question regarding the DHT inhibitors Finasteride and Dutasteride; I've read that the '...primary metabolite of testosterone in the prostate and the skin' is DHT. So, following this theory, I guess the average acne sufferer has to preclude testosterone from developing into DHT. My question: If we inhibit DHT with one of these effective drugs aren't we still left with androgens to contend with, or, is it adequate to inhibit DHT alone. And, if DHT is the primary metabolite of testosterone in the skin, how on earth is it affecting our faces. I was led to believe that we have no DHT receptors on our face; this is why men lose the hair on their head, but not their facial hair as a consequence of DHT (DHT receptors are in scalp but not facial tissue). Does this mean that DHT sets our faces off even though we don't have DHT receptors there, by binding to plain old androgen receptors. I would love to have this clarified. Thank-you. Please forgive any ignorance on my part.

[SweetJade1]

Karl,
So glad you asked that question because it's a big one and I'm currently in debate with another male about the usefulness of such drugs. Duatasteride is supposed to inhibit Type I (skin, sebum) and Type II (hair follicle) DHT enzymes. Now, Finasteride is a Type II, and this is why it is promoted for helping men with androgenic alopecia. DHT had the ability to:

Produce Acne & Inflammation

Produce sebum

Enlarge sebacous glands and/or prostate glands (thanks to the aid of IGF-1),

Activate secondary terminal hair follicles in men and women (produce hirsuitsim),

Deactivate hair follicles on the scalp (androgenic alopecia, male pattern baldness).

Isn't it amazing??? Uggh. I suppose if you are a body builder it's good thing because it will help make you nice and muscular, if you don't mind the above side effects of either producing too much or being oversensitive to normal amounts.

My question: If we inhibit DHT with one of these effective drugs aren't we still left with androgens to contend with, or, is it adequate to inhibit DHT alone. And, if DHT is the primary metabolite of testosterone in the skin, how on earth is it affecting our faces.

YES, you will be left with more of either the inactive testosterones or Free Testosterone (testostorone). However, this isn't as potent as DHT or Testosterone and may not be a problem. If you want to reduce this amount, you must raise your estrogen levels or your SHBG levels, but that relies or estrogen anyway. The safest way for a male to do that would be to follow a lower carbohydrate type diet. Insulin and SHBG are inversely related, so you lower one and you will raise the other.

Does this mean that DHT sets our faces off even though we don't have DHT receptors there, by binding to plain old androgen receptors. I would love to have this clarified.

Ha ha, I'm still trying to figure this out myself, however, it appears that what happens is that the inactive forms of testosterone, including DHEA, will bind to androgen receptors in the Skin, Muscle, Hair follicle, and/or Prostate gland and from there will be "reduced" (ha) to become their more active forms, usually DHT. It is repeatedly said that most (90%) acne sufferers, do not produce too much testosterone in their blood, but that they do have a higher sensitivity and likeliness of producing more DHT in the sebecous glands.


So you are correct. Depending on your gender here, there are several ways to attack DHT and possibly excess tesoterone production:

Prevent excess testosterone (anti-androgens, dietary changes)

Bind Testosterone (anti-androgens, dietary changes)

Prevent the conversion of T or DHEA into DHT (DHT Inhibitor)

Block DHT from binding at the receptors (Anti-androgen)

Bind DHT (DHT Inhibitors - Equol)

Encourage the breakdown of Testosterone & DHT - (Inhibit liver enzymes such as Type I 17-beta hydroxysteriod dehyrdogenase [Type I 17b-HSD] or 3 alpha-androstanediol glucuronide enzyme [3 alpha-diol G].

Encourage the elimination of excess hormones - (liver functions such as Glucuronidation - eliminates estrogens, but what eliminates Testosterones?)


To answer your other question, Finasteride (Propecia, Proscar) help males with Male Patterned Baldness, but not females, yet help females with hirsutism. Duatasteride (Avodart) and Finasteride are not reccomended for the treatment of acne. Some say it has helped their skin, others say that these drugs, caused them to breakout with acne & white heads, even when they never had acne before! This is probably why Spironolactone is the preferred choice at treating acne and hirsutism.

Spiro, acts as an Anti-androgen by binding to the Androgen receptors so that DHT or T can't and it is also a Type II 17-beta HSD inhibitor so it encourages the active forms of Estrogen and Androgen, but Testosterone won't be as active because it's still being blocked. As such, Spironolactone actually has the ability to indirectly lower your Free Testosterone levels by 20% - 30% (probably because estrogen is still active, hence boosting SHBG). It's dose-dependent and weaker compared to the above DHT inhibitors (inhibit DHT by up to 60% - 90%) and I believe Saw Palmetto inhibits by up to 50%. Saw Palmetto is also an anti-androgen, so this may explain why it may be more effective than Spiro and has been found to be just as effective as Finasteride.

Anyway, did that help some? Are you planning on taking any of these in natural or prescription drug form? If so, your natural anti-androgens are Curcumin, NAC, Beta-Sitosterol, and possibly Indole 3-Carbinole (DIM, but it can also act as an anti-estrogen).

Quercitin and Green Tea (EGCG is an anti-androgen) are your Type I 5alpha reductase DHT inhibitors. Chromium, NAC, B5, Pantathine, Guggul, Niacin (not niacinamide), work to metabolize excess lipids, so they won't be synthesized into Testosterone. Folic Acid, PABA, Acidolphilus, Bee Propolis, and Boron (may also boost androgens), boost Estrogen, thus SHBG. OF course, dietary changes preferrably involving maintaining healthy Cholesterol & Insulin Levels, will also help. =)

Bye for now

P.S. There's PLENTY of confusion for all of us ;-)

[Karl2]

Hi Sweetjade,

I want to thank-you for getting back to me as promptly as you did. I agree with you, it is definitely confusing.

Quote:
"YES, you will be left with more of either the inactive testosterones or Free Testosterone (testosterone). However, this isn't as potent as DHT or Testosterone and may not be a problem."

This is very interesting; so what you're saying is that once someone has taken Dutasteride (for example) they will be left with considerably more inactive testosterones or free testosterone, and this is significantly less potent than Testosterone. So, I guess, you have taken care of DHT, but your left with inactive forms of testosterone which ultimately/theoretically could potentiate DHT, but is precluded from doing so, thanks to Dutasteride.

Quote:
"Ha ha, I'm still trying to figure this out myself, however, it appears that what happens is that the inactive forms of testosterone, including DHEA, will bind to androgen receptors in the Skin, Muscle, Hair follicle, and/or Prostate gland and from there will be "reduced" (ha) to become their more active forms, usually DHT. It is repeatedly said that most (90%) acne sufferers, do not produce too much testosterone in their blood, but that they do have a higher sensitivity and likeliness of producing more DHT in the sebaceous glands."

This sounds as though a DHT inhibitor is the answer to our problem. But I'm wondering about those people who have been on Dutasteride, and break out when they report never having a problem with acne in the past. Now, even though their inactive forms of testosterone have risen, thanks to drug, it shouldn't really be a problem, because DHT is being inhibited. Or, maybe it is the inactive testosterones, which are still to blame. I guess, as a working hypothesis, this is what is happening to those people who are breaking out as a result of these drugs without acne histories.

It seems like the problem with Dutasteride and Finasteride is that although they inhibit DHT, this in itself, may not be sufficient. From what you have said, it seems that Spironolactone is the best choice, even though it doesn’t specifically inhibit DHT (or does it?), but, rather, functions by binding to Androgen receptors, and decreases the level of Testosterone produced from the Adrenal gland (I've read). I'm guessing that although it doesn’t specifically preclude DHT from forming, it does still block DHT from registering at receptor sites, be they DHT, or, plain old androgen receptor sites.

Quote:
"Anyway, did that help some? Are you planning on taking any of these in natural or prescription drug form?"

Yes, that did help, and I an incredibly indebted to you, as are many others. Umh, well, I have taken Spironolactone, in the recent past (20mgs daily), and it rocked. Oil production was down to nil, and pores were on the verge of extinction, seriously. Problem was I lost a significant amount of water weight, and Potassium levels were quite low. My blood pressure dropped to about 80, and I was feeling terrible, but happily looking good. I had to get off. I was thinking of trying one of the others, hence the question. I've tried Saw Palmetto, and at best, I've found it to be O.K.; I think you've reported similar experiences with S.P.

Sweetjade thanks again, and I owe you big time.