Equol inhibits Hormone Feedback

[goata007]

This study is quite old (2003) but I don't remember seeing it here, so posting it:

Equol Is a Novel Anti-Androgen that Inhibits Prostate Growth and Hormone Feedback

"The possibility exists that equol can have anti-androgenic actions on a number of tissues throughout the body. In particular, blockade of androgen action could be beneficial not only for preventing growth of reproductive tissues with DHT dependency such as prostate and epididymis, other androgen-responsive tissues may also benefit from equol therapy. Such conditions include female- and male-pattern baldness [42–44]; facial and body hair growth [42–44]; skin health (acne, anti-aging, and anti-photo aging) [42, 45]; skin integrity (collagen and elastin robustness) [42, 45]; and emotional and mental health issues, such as, mood, depression, anxiety, learning, and memory "

It says that equol could help depression, learning etc, then why do people on finas get brain fog? isn't the brain fog primarily due to androgen inhibition?

I'm really surprised about the inhibition of negative feedback. Equol looks like a promising anti-androgen?

 

[el_duterino]

Interesting..thanks for the info.
I still have my 500mg of pure R/S-Equol in the freezer waiting to be applied on my scalp.
I have one question though, if we apply a topical Equol once a day, say 2 mg a day on the scalp, how long would that work to inhibit DHT ?
we know that 5ar take a few days to be resplenished..that's why finasteride/dutasteride ar so effective.
Lets suppose that all the molecules in the Equol topical would inhibit all the DHT molecules at that time of application or shortly after...., what would happens to the "new" DHT that will be converted from then on and during the next 24 hours ?
That would perhaps limit the effectiveness of a topical Equol since DHT is produced "round-the-clock". But it would be a perhaps good addition to an exisiting 5ar inhibitor to "clean-up" the left over of DHT in the follicules.

In any case, pure Equol is currently extremely expensive and not available on the market to individuals, so that's another limitation to be considered for a "life-long" regimen. Japanese researchers at Otsuka Pharma. have discovered in 2006 a mehod to create Equol using bacteria so that they don't have to collect it form human or horse urine..but again i did some searches (I am in Japan) and cannot find any of that Equol sold in Japan on the market at present.

 

[Bryan]

I'm really surprised about the inhibition of negative feedback. Equol looks like a promising anti-androgen?

They're just talking about the inhibition of negative feedback from DHT itself, since equol inactivates DHT. But there will still be an increase in LH, and more testosterone production as a result, just like when you take finasteride or dutasteride.

I've never been very interested in equol, for the simple reason that its bottom-line effects ARE so similar to what happens when you take finasteride or dutasteride. And those drugs are a LOT cheaper than equol! Why spend money on a highly experimental drug like equol, when you can get essentially the same effect with thoroughly tested and approved finasteride/dutasteride?

 

[goata007]

They're just talking about the inhibition of negative feedback from DHT itself, since equol inactivates DHT. But there will still be an increase in LH, and more testosterone production as a result, just like when you take finasteride or dutasteride.

I don't think Testosterone is the problem, well not as much as DHT.

I've never been very interested in equol, for the simple reason that its bottom-line effects ARE so similar to what happens when you take finasteride or dutasteride. And those drugs are a LOT cheaper than equol! Why spend money on a highly experimental drug like equol, when you can get essentially the same effect with thoroughly tested and approved finasteride/dutasteride?

They are very different in their method of action. Finasteride Blocks/Decreases conversion of Testosterone -> DHT by acting on 5alpha-reductase. The sideeffect of which is higher estrogen levels and thus gyno etc. Equol on the otherhand, competes with DHT for binding with AR. Thus it results in higher levels of serum DHT, so even if there is higher testosterone it won't have same side effects as finas, because it's not affecting the T -> DHT conversion.

As of the availability, the study said that its common in soy etc, so I don't think it's that expensive to include in ones daily life.

 

[Bryan]

They're just talking about the inhibition of negative feedback from DHT itself, since equol inactivates DHT. But there will still be an increase in LH, and more testosterone production as a result, just like when you take finasteride or dutasteride.

I don't think Testosterone is the problem, well not as much as DHT.

I didn't say that testosterone is the problem. The point I was making is that there will be an upregulation of testosterone production with equol, just like there is with finasteride/dutasteride. I'm trying to point out the similarity of effects between equol and finasteride/dutasteride.

They are very different in their method of action.

True, but the bottom-line effects are very similar.

Finasteride Blocks/Decreases conversion of Testosterone -> DHT by acting on 5alpha-reductase. The sideeffect of which is higher estrogen levels and thus gyno etc. Equol on the otherhand, competes with DHT for binding with AR. Thus it results in higher levels of serum DHT, so even if there is higher testosterone it won't have same side effects as finas, because it's not affecting the T -> DHT conversion.

You didn't understand that study! Equol doesn't compete with DHT for binding to AR. In fact, equol doesn't bind with AR at all. Equol binds with DHT, causing it to be inactivated. Go back and re-read the study!

Equol should have virtually the same side effects as finasteride/dutasteride.

As of the availability, the study said that its common in soy etc, so I don't think it's that expensive to include in ones daily life.

Having trace levels of equol in your diet is one thing, having large enough levels of it in your system to have a finasteride/dutasteride-like effect is quite another. I suggest you stick with finasteride/dutasteride. Those are reliable, and proven to work.

 

[DuCharme]

They're just talking about the inhibition of negative feedback from DHT itself, since equol inactivates DHT. But there will still be an increase in LH, and more testosterone production as a result, just like when you take finasteride or dutasteride.

I don't think Testosterone is the problem, well not as much as DHT.

I didn't say that testosterone is the problem. The point I was making is that there will be an upregulation of testosterone production with equol, just like there is with finasteride/dutasteride. I'm trying to point out the similarity of effects between equol and finasteride/dutasteride.

They are very different in their method of action.

True, but the bottom-line effects are very similar.

Finasteride Blocks/Decreases conversion of Testosterone -> DHT by acting on 5alpha-reductase. The sideeffect of which is higher estrogen levels and thus gyno etc. Equol on the otherhand, competes with DHT for binding with AR. Thus it results in higher levels of serum DHT, so even if there is higher testosterone it won't have same side effects as finas, because it's not affecting the T -> DHT conversion.

You didn't understand that study! Equol doesn't compete with DHT for binding to AR. In fact, equol doesn't bind with AR at all. Equol binds with DHT, causing it to be inactivated. Go back and re-read the study!

Equol should have virtually the same side effects as finasteride/dutasteride.

As of the availability, the study said that its common in soy etc, so I don't think it's that expensive to include in ones daily life.

Having trace levels of equol in your diet is one thing, having large enough levels of it in your system to have a finasteride/dutasteride-like effect is quite another. I suggest you stick with finasteride/dutasteride. Those are reliable, and proven to work.

Not to nitpick, but I have several issues with this thread. For one, equol is not a 'drug' as Bryan indicates, but a metabolite of daidzein, a soy isoflavone; it is produced naturally in the body by bacterial flora in the intestines. Supplementing with it, if it is even possible and so far I have never read anywhere that it has been done successfully anyway, is similar to taking finasteride in that it is taking a pill, but...that's all.

Finasteride is a drug because it is a synthetic substance ingested to obtain a specific end--halting the production of Type II 5-AR. Equol cannot be considered a drug; something that forced the body to produce equol would be a drug. The difference is semantic, but I think a relevant one. Apples and oranges.

My second problem is the insinuation that the binding of DHT is the same as halting its production by inhibiting 5-AR and in this, I am sorry to say, you are very wrong Bryan. The ends do not always justify the means ; similar result, very, very different process. Caveat: I'm not out to bash finasteride or rabble rouse; the drug works and is relatively safe. But it is not perfect and should not be assumed so. The problem lies in 5-AR's cross-compatibility--it creates DHT, the enemy, but it also plays a major role in the production of allopregnanolone, as we all know. That is why Dutasteride is very dangerous in my humble opinion, as it suppresses Type I and Type II. At any rate, the role of 5-AR in other parts of the body is not very well understood and its inhibition, frankly put, should be avoided if there is another way. And that's the difference I think is important with equol. In theory it could bind with DHT without hampering 5-AR; the end result without the risk.

Is that to say a "Natural Supplement" is the great solution, flush your finasteride, hoorah? Of course not; there aren't even any descent double blinds that show you can supplement equol. So far you can either produce it through some lovely quirk in genetics out of daidzein, or you can't.

I highly respect your contributions Bryan, but the point being: finasteride works similar to equol, but not through the same method; it should not be lightly dismissed because another substance can supply the same effect. Twenty years ago if everyone stuck with what is "reliable, and proven to work" wigs would still be the only solution! Discussion, exploration, DEMAND drive discovery! Twenty hopefuls on a message board mixing supplements into their Rogaine isn't going to change anything, but this IS the most read and respected one of the bunch. If the diehards here aren't asking for something more from the pharmaceutical industry...why would they ever create anything new (...and unpatented...)?

 

[CCS]

Even if you could inject yourself with Eqoul, it might not get some of the side effects of finasteride, but it would get rid of DHT from 5ar1 and 5ar2 about equally. You might need to get rid of 70% to have the effect you want. But who knows if DHT is needed in places like the brain and other tissues.

I'd still rather find a topical that inhibits 5ar2 locally.

 

[Bryan]

Not to nitpick, but I have several issues with this thread. For one, equol is not a 'drug' as Bryan indicates, but a metabolite of daidzein, a soy isoflavone; it is produced naturally in the body by bacterial flora in the intestines.

I'm curious as to how you would answer this question: do you consider Accutane to be a "drug"?

My second problem is the insinuation that the binding of DHT is the same as halting its production by inhibiting 5-AR and in this, I am sorry to say, you are very wrong Bryan.

I didn't say or "insinuate" that the binding of DHT is the same as halting its production by inhibiting 5a-reductase. I was careful to state in plain English that the BOTTOM-LINE EFFECTS are similar.

The ends do not always justify the means ; similar result, very, very different process.

Of course.

Caveat: I'm not out to bash finasteride or rabble rouse; the drug works and is relatively safe. But it is not perfect and should not be assumed so. The problem lies in 5-AR's cross-compatibility--it creates DHT, the enemy, but it also plays a major role in the production of allopregnanolone, as we all know. That is why Dutasteride is very dangerous in my humble opinion, as it suppresses Type I and Type II. At any rate, the role of 5-AR in other parts of the body is not very well understood and its inhibition, frankly put, should be avoided if there is another way. And that's the difference I think is important with equol. In theory it could bind with DHT without hampering 5-AR; the end result without the risk.

I'd be curious to hear what you think is the specific cause of the finasteride and dutasteride side effects that we hear about so much on these hairloss forums (loss of libido, failure to maintain erection, watery semen, "brain fog", etc.). Do you think it's the sharp reduction in DHT, or do you think it's the inability of the 5a-reductase enzyme to perform those other chemical conversions (BTW, the formation of allopregnanolone isn't the only such conversion performed by that enzyme)?

I highly respect your contributions Bryan, but the point being: finasteride works similar to equol, but not through the same method;

Yeah, I know.

 

[chore boy]

Has it been discussed that Equol and Daidzein may be steroid sulfatase inhibitors?

Recent studies have associated high dietary isoflavone intake with low incidence of breast cancer. Since estrogenic steroids are important factors in the evolution of breast cancer, and in breast tumors they are derived mainly from the sterol sulfatase pathway, we have therefore investigated effects of the isoflavone daidzein and its sulfoconjugates, daidzein-4?-O-sulfate and daidzein-7,4?-di-O-sulfate, on sterol sulfatase acitivity using dehydroepiandrosterone sulfate as substrate. While daidzein does not affect sterol sulfatase, its sulfoconjugates are potent inhibitors of this enzyme. Kinetic analyses reveal that daidzein-4?-O-sulfate and daidzein-7,4?-di-O-sulfate inhibit sterol sulfatase competitively with respect to the steroid substrate and with Kivalues of 5.9 and 1 ?M, respectively. Daidzein sulfo-conjugates also inhibit hydroxysteroid and phenol sulfotransferases but at much higher concentrations. These results provide a biochemical basis for the putative chemopreventive role of dietary isoflavones against breast cancer.

http://www.sciencedirect.com/science?_o ... a39772a75b


5-dihydrotestosterone is known to play a crucial part in the regulation of hair growth and in the development of androgenetic alopecia. 5-dihydrotestosterone is formed locally within the hair follicle from the systemic precursor testosterone by cutaneous steroid 5-reductase. Moreover, adrenal steroids such as dehydroepiandrosterone are converted to 5-dihydrotestosterone by isolated hair follicles, which may provide an additional source of intrafollicular 5-dihydrotestosterone levels. Elevated urinary dehydroepiandrosterone and serum dehydroepiandrosterone sulfate have been reported to be present in balding young men. These reports suggest that dehydroepiandrosterone sulfate may act as an important endocrine factor in the development of androgenetic alopecia. Hence the question arises whether the dehydroepiandrosterone sulfate can be metabolized within the hair follicles to yield dehydroepiandrosterone by the microsomal enzyme steroid sulfatase, and where steroid sulfatase might be localized. We therefore performed immunostaining for steroid sulfatase on human scalp biopsies as well as analysis of steroid sulfatase enzyme activity in defined compartments of human beard and occipital hair follicles ex vivo. Using both methods steroid sulfatase was primarily detected in the dermal papilla. Steroid sulfatase activity was inhibited by estrone-3-O-sulfamate, a specific inhibitor of steroid sulfatase, in a concentration-dependent way. Furthermore, we show that dermal papillae are able to utilize dehydroepiandrosterone sulfate to produce 5-dihydrotestosterone, which lends further support to the hypothesis that dehydroepiandrosterone sulfate contributes to androgenetic alopecia and that steroid sulfatase inhibitors could be novel drugs to treat androgen-dependent disorders of the hair follicle such as androgenetic alopecia or hirsutism.

http://www.nature.com/jid/journal/v117/ ... 1298a.html

 

[chore boy]

http://www.molekula.co.uk/index.php?mai ... _id=167027

 

[DuCharme]

I'm curious as to how you would answer this question: do you consider Accutane to be a "drug"?

Accutane: drug or…gooey stuff? True, Accutane is a retinoid, or a biological compound related to Vitamin A. Does that make it a ‘natural’ compound, demonized as charlatan lore though the term may be? Yes and no. It is similar to vitamin A, but is is not vitamin A, it is a synthetic duplicate, and one so incredibly concentrated it is considered a teratogenic, or birth defect causing compound. That really should have been a no-brainer, as high concentrations of actual vitamin A are toxic—as low as 15,000 IU per day to 1.4 million IU per day.

And don’t tell me “well, Retin-A is also useful in hair loss!â€

Efficacy of 5% Minoxidil versus Combined 5% Minoxidil and 0.01% Tretinoin for Male Pattern Hair Loss: A Randomized, Double-Blind, Comparative Clinical Trial.
Original Research Article
American Journal of Clinical Dermatology. 8(5):285-290, 2007.
Shin, Hyo Seung 1; Won, Chong Hyun 2; Lee, Seung Ho 1; Kwon, Oh Sang 1; Kim, Kyu Han 1; Eun, Hee Chul 1
Abstract:
Background: 5% topical minoxidil solution has been widely used to stimulate new hair growth and help stop hair loss in men with androgenetic alopecia (Androgenetic Alopecia). However, it is not convenient for patients to continue applying the solution twice daily on a regular basis. Tretinoin is known to increase the percutaneous absorption of minoxidil and, therefore, to enhance the response of Androgenetic Alopecia to minoxidil. For this reason, it was assumed that tretinoin would be helpful in alleviating the inconvenience associated with the recommended twice-daily application of minoxidil.
Objective: To compare the efficacy and safety of therapy using a combined solution of 5% minoxidil and 0.01% tretinoin once daily with those of the conventional 5% topical minoxidil therapy applied twice daily in the treatment of Androgenetic Alopecia.
Methods: A total of 31 male patients (aged 28-45 years, mean 39.7 +/- 4.5) with Androgenetic Alopecia (Hamilton-Norwood classification type III-V) were randomly assigned into two groups, one in which 5% minoxidil was applied to the scalp twice daily and the other in which the combined agent was applied once daily at night together with a vehicle placebo in the morning. The efficacy parameters were: (i) changes in total hair count, non-vellus hair count, anagen hair ratio, linear hair growth rate, and mean hair diameter assessed by macrophotographic image analysis; and (ii) the patient's and investigator's subjective assessments.
Results: After therapy, increases in the macrophotographic variables of total hair count and non-vellus hair count were shown in both treatment groups. There were no statistically significant differences between the two treatment groups with respect to changes in macrophotographic variables or scores on subjective global assessments by patients and the investigator. The incidence of adverse effects such as pruritus or local irritation was similar in the 5% minoxidil group (4 of 14 subjects) and the combined agent group (5 of 15 subjects).
Conclusion: The efficacy and safety of combined 5% minoxidil and 0.01% tretinoin once-daily therapy appear to be equivalent to those of conventional 5% minoxidil twice-daily therapy for the treatment of Androgenetic Alopecia.
Copyright 2007 Adis Data Information BV

I'd be curious to hear what you think is the specific cause of the finasteride and dutasteride side effects that we hear about so much on these hairloss forums (loss of libido, failure to maintain erection, watery semen, "brain fog", etc.). Do you think it's the sharp reduction in DHT, or do you think it's the inability of the 5a-reductase enzyme to perform those other chemical conversions (BTW, the formation of allopregnanolone isn't the only such conversion performed by that enzyme)?

…and what’s your answer to that question, Bryan? Doesn’t that answer the question? There is no consensus; in fact, the only solid answer among dedicated finasteride users seems to be “they’re just hypochondriacs.†Clearly the question of “brain fog†is related to allopregnanolone. Allopregnanolone is a neurosteroid in the brain synthesized from progesterone via two compounds: 3-alpha HSD and 5-Alpha Reductase. Interestingly enough, 3-alpha HSD acts in the body as a sort of natural counterweight to 5-Alpha Reductase. Moot point, as there isn’t a whole lot to be done to boost 3-alpha levels. But allopregnanolone is a key modulator in the production of the neurotransmitter Gamma-aminobutyric acid (GABA)—a mood and anxiety stabilizer.

As for sexual side effects? Those very well could be a product of the systemic lose of DHT. Shouldn’t that make the case even stronger for the development of better topicals? opsblush:

 

[Bryan]

Accutane: drug or…gooey stuff? True, Accutane is a retinoid, or a biological compound related to Vitamin A. Does that make it a ‘natural’ compound, demonized as charlatan lore though the term may be? Yes and no. It is similar to vitamin A, but is is not vitamin A, it is a synthetic duplicate, and one so incredibly concentrated it is considered a teratogenic, or birth defect causing compound. That really should have been a no-brainer, as high concentrations of actual vitamin A are toxic—as low as 15,000 IU per day to 1.4 million IU per day.

Accutane is a derivative of the vitamin A molecule and is normally present in the human body, although obviously in smaller amounts (at least, that's my understanding). So for you to be consistent with what you said before about equol, won't you also have to maintain that even ACCUTANE, of all things, isn't a "drug"?

 

[chore boy]

Bump for Bryan.

 

[DuCharme]

:bravo: Since Accutane is sort of made from a vitamin in titanic quantities it is therefore somewhat similar to equol, the latter being derived from a soy isoflavone, so equol is a drug and it is therefore perfectly analogous with Finasteride. Thank you for clearing that up.

 

[goata007]

Here is a press release (march 2004) regarding the study that I posted, it also includes comments from the lead researchers Trent Lund:

http://www.newsinfo.colostate.edu/index.asp?page=news_item_display&news_item_id=927584798

Important bits:

"To date, no other compound has been shown to directly bind DHT; rather, all other drugs target the receptor for DHT or the enzymes that are involved in the synthesis of DHT," added Trent Lund, lead author of the study and assistant professor in the biomedical sciences department at Colorado State.

In recent years, the pharmaceutical industry has developed drugs that inhibit a certain enzyme that converts testosterone to DHT. Unfortunately, these drugs have side effects. Equol, on the other hand, does not prevent DHT from being made but prevents it from functioning. It puts "handcuffs" on DHT, preventing it from binding to the androgen receptor and thereby preventing the prostate from growing. This may be particularly important for men who have been diagnosed with either an enlarged prostate (benign prostatic hyperplasia), or cancer of the prostate

In other words, equol did not change hormone levels but completely blocked the effects of DHT in rats.

The researchers have initiated further studies of equol to assess its potential as a treatment for a variety of other androgen-mediated conditions. The team has filed patent applications on equol and hopes to commercialize the technology.

 

[Bryan]

In recent years, the pharmaceutical industry has developed drugs that inhibit a certain enzyme that converts testosterone to DHT. Unfortunately, these drugs have side effects. Equol, on the other hand, does not prevent DHT from being made but prevents it from functioning. It puts "handcuffs" on DHT, preventing it from binding to the androgen receptor and thereby preventing the prostate from growing.

I'm ashamed of them for making such a misleading statement. I expect side effects with equol to be similar to those with finasteride.

 

[el_duterino]

in Asian countries 50% of the people can produce Equol and some of them eat a lot of soy and produce Equol. but we don't have reports of side effects such as being on Finasteride.

In addition, women who produce equol, eat soy and are pregnant do not produce babies with deformed sex organs such as what would happen if they were taking finasteride or androgen-receptors blockers.
DHT plays a crucial role in the formation of the external male genitalia and prostate during fetal life.

So we draw 3 assumptions:
1) Equol is not very effective at inhibiting DHT in vivo
2) Not enough Equol is produced in the body on soy foods to have an impact in the body DHT
3) Equol serum life is short so its gets eliminated quickly in blood.
> this would make it a very good candidate for a topical hairloss

 

[DuCharme]

In recent years, the pharmaceutical industry has developed drugs that inhibit a certain enzyme that converts testosterone to DHT. Unfortunately, these drugs have side effects. Equol, on the other hand, does not prevent DHT from being made but prevents it from functioning. It puts "handcuffs" on DHT, preventing it from binding to the androgen receptor and thereby preventing the prostate from growing.

I'm ashamed of them for making such a misleading statement. I expect side effects with equol to be similar to those with finasteride.

I still don't agree that the effects would be the same as finasteride exactly but--how can you prevent a hormone from functioning and not expect some problems, especially if done systemically? They might be different problems, strength, duration, or type, but...come on now...

My real question for a topical of equol vs. a topical of finasteride: does it matter where DHT is made--in the blood or on the scalp?

Immunohistochemical localization of types 1 and 2 5?-reductase in human scalp
Auteur(s) / Author(s)
BAYNE E. K. (1) ; FLANAGAN J. (1) ; EINSTEIN M. (1) ; AYALA J. (1) ; CHANG B. (1) ; AZZOLINA B. (1) ; WHITING D. A. (2) ; MUMFORD R. A. (1) ; THIBOUTOT D. (3) ; SINGER I. I. (1) ; HARRIS G. (1) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Merck Research Laboratories, PO Box 2000, Rahway, NJ 07065, ETATS-UNIS
(2) Department of Dermatology and Pediatrics, Southwestern Medical Center, Baylor Hair Research and Treatment Center, Dallas, TX 75246, ETATS-UNIS
(3) Division of Dermatology, Pennsylvania State University, Hershey, PA 17033, ETATS-UNIS
Résumé / Abstract
The predominant form of 5?-reductase (5aR) in human scalp is 5aR1. None the less, clinical studies have shown that finasteride, a selective inhibitor of 5aR2, decreases scalp dihydrotestosterone and promotes hair growth in men with androgenetic alopecia. Immunolocalization studies were thus carried out to examine 5aR isozyme distribution within scalp and, in particular, to determine whether 5aR2 might be associated with hair follicles. 5aR2 was localized using both a rabbit polyclonal and a mouse monoclonal antibody. 5aR1 was detected with a mouse monoclonal antibody. The specificity of these reagents was demonstrated both by immunofluorescence and Western blot analyses of COS cells overexpressing human 5aR1 or 5aR2. When cryosections of scalp from men with androgenetic alopecia were stained with antibody against 5aR2, using immunoperoxidase avidin-biotin complex methodology, immunostaining was observed in the inner layer of the outer root sheath and, in more proximal regions of the follicle, in the inner root sheath. Staining was also prominent in the infundibular region of the follicle, with less intense staining extending throughout the granular layer of the epidermis. Some staining was also seen in sebaceous ducts. Similar results were obtained with both the polyclonal and monoclonal 5aR2 antibodies. In contrast, in scalp cryosections stained with antibody to 5aR1, no immunostaining was observed within hair follicles. Intense staining for the type 1 isozyme was, however, detected within sebaceous glands. Our immunolocalization data suggest that the results seen in clinical trials of men with male pattern hair loss treated with finasteride may be due, at least in part, to local inhibition of 5aR2 within the hair follicle.

So...mostly Type I is in the scalp, but some Type II is as well. If we're talking topicals then would it not make more sense to talk anti-androgens like spironolactone and, perhaps, equol? Maybe spironolactone would be a better approximate to equol than finasteride, provided this team has actually solved the synthesizing problems.

...and doesn't SHBG also "put handcuffs on" DHT?

 

[Bryan]

I still don't agree that the effects would be the same as finasteride exactly but--how can you prevent a hormone from functioning and not expect some problems, especially if done systemically? They might be different problems, strength, duration, or type, but...come on now...

My hunch is that the side effects from finasteride are due mainly to the sharp reduction in DHT, not from blocking those other chemical conversions made by the 5a-reductase enzyme. That's why I expect the side effects from equol and finasteride to be similar: I don't expect there to be much difference between stopping the actual manufacture of DHT, and merely stopping DHT's effects by binding to it and inactivating it.

My real question for a topical of equol vs. a topical of finasteride: does it matter where DHT is made--in the blood or on the scalp?

DHT isn't made in the blood. It "leaks" into the blood from the various body tissues where it's actually synthesized, like hair follicles, the prostate, the liver, the kidneys, etc.

BTW, it's always been my opinion that DHT made right there in the hair follicle is much more important than serum DHT.

So...mostly Type I is in the scalp, but some Type II is as well.

Happle and Hoffmann did an important study showing that the 5a-reductase in human dermal papillae seems to be almost exclusively type II.

 

[hairrific]

I am allot confused as to why there is so little talk about EQUOL. Just because finasteride and dutasteride. is the same difference and is cheaper?

Sort of like saying Tang is better than fresh squeezed orange juice. I still resent drinking this commercial Tang crap as a child, and in Florida of all places, we had huge orange trees in our yard, oh never mind, the big corporate commercial line won in those days over mother nature.

So far I can't find info on if there is a practical way to find out if I am one of the lucky 30-50% of people that have intestinal bacteria that makes equol. Is there a way to tell?

If I am not a producer then does that mean the soy isoflavonoids, daidzein, genistein, ect. supplement I am taking would be not doing much for me or at least converting to equol that is? Does that mean there is no practical why to increase EQUOL in my body?

Also, does EQUOL act on inhibiting type I and II 5-alpha reductase or does it just do something to DHT only?

At least someone comment on my new avatar I made in photoshop! Hey I am an blond artist, expect much insanities!