Equol.

TheOliviaTremorControl

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Hey, there's this new stuff called equol. Check it out!!!!111!!:) :) :) L0L!!!!!!!!!










Haha, just kidding, I'm sure you've all heard of Equol, that enzyme (?) produced in 35-40% of male digestion systems.

When do you guys think an Equol supplement will be available on the market? A couple of months? A year?

Last I heard some american scientists were trying to put a patent on it...
Given what can be ascertained from their results, I'm surprised there isn't a lot more talk about equol in the hairloss groups.
I did a search for Equol on the forum and found but a few posts.


I read one post on this forum that mentioned a hairloss treatment called multiflora, and it read "Soy equol isoflavones" as one of the ingredients.

For starters, I thought equol wasn't available on the market yet, even if its only an ingredient?

Secondly, something that makes me think this is a "snake oil" is that it mentions "soy equol", which would indicate that either equol comes exclusively from soy, or that equol produced from soy acts different than other foods that are high in isoflavines that produce equol (broccoli?)
I was under the influence that all equol was the same. I mean, its equol. Equol produced from broccoli would be the same as equol produced from soy, right?

Thirdly, since I'm fairly sure Equol itself isn't an ingredient in this product, merely only the isoflavines that produce equol (in 30-40% of people), would a topical treatment be remotely useful? The isoflavines would need to be digested to produce equol, and the equol would need to be in the bloodstream for it to bind with the DHT.

What are you guys thoughts on all this?
I mean, come on guys, with the very promising information on equol, you guys think you all would have gotten the ball rolling on this already.

Mainly, I want to hear what you guys have to say about when equol will start being produced in supplement form.
 

Bryan

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There's nothing particularly "promising" about equol that I can see. Its effects should be very similar to finasteride or dutasteride, and those drugs are MUCH easier to obtain and very likely much cheaper than equol.

Bryan
 

Bryan

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Somebody posted a reply that started with the following words, then it got deleted somehow:

"if one assumes testosterone has the potential to negatively affect hair, equol could potentially be more useful than finasteride. also, increased sebum..."

I want to emphasize again that equol should have essentially the same effects as finasteride and dutasteride; namely, a similar increase in testosterone levels, along with a deactivation of DHT.

Bryan
 

pleasegodno

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explain why equol should increase T levels to the extent typical of finasteride users. are you suggesting that the inhibition of the conversion of T to DHT doesn't contribute to higher T levels in finasteride users? and do you contend that equol wouldn't decrease sebum production via local inactivation of DHT produced by type I 5ar?
 

Bryan

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pleasegodno said:
explain why equol should increase T levels to the extent typical of finasteride users. are you suggesting that the inhibition of the conversion of T to DHT doesn't contribute to higher T levels in finasteride users?

Sure it does, but probably not for the reason you think. It raises testosterone production because the potent androgen DHT is a player in the hypothalamic/pituitary/gonadal axis which provides feedback control of T synthesis. You lower DHT, and the brain senses that and releases more LH (luteinizing hormone) to increase T production. Equol would have the same effect.

pleasegodno said:
and do you contend that equol wouldn't decrease sebum production via local inactivation of DHT produced by type I 5ar?

I suppose we might EXPECT it to do that, but then again MK386 had no effect on acne in that recent clinical trial. It'll be interesting to see what effect equol (or dutasteride, for that mattter) really does have on sebum production.

Bryan
 

TheOliviaTremorControl

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Bryan, I don't know how much into Equol you've read, but it works completely different than DHT Inhibitors.

Equol itself binds with the DHT, so that the DHT cannot bind with your androgen receptor. Thus, you are not messing around with hormones, unbalencing them and whatnot.

Finasteride, however, inhibits the creation of DHT, which in some (rare) cases causes permanent damage to your DHT production, which would mean any side effects would be indefinate.

Basically, Equol is estimated to be even more powerful at *stopping* dht from binding with your androgen receptors than Dutasteride is, but there is none of the side effects (theoretically).

So, for all those people that want something as powerful as Dutasteride, but are too afraid of the side effects, this ones for you.
 

Bryan

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TheOliviaTremorControl said:
Bryan, I don't know how much into Equol you've read, but it works completely different than DHT Inhibitors.

First of all, let's use the precise term "5a-reductase inhibitor", rather than the vague, ambiguous expression "DHT inhibitor". Second of all...yes, equol works by a different mechanism than 5a-reductase inhibitors, but they should still end-up having similar effects on androgen-sensitive tissues.

TheOliviaTremorControl said:
Equol itself binds with the DHT, so that the DHT cannot bind with your androgen receptor. Thus, you are not messing around with hormones, unbalencing them and whatnot.

What PRECISELY does "messing around with hormones" mean, in this context? What PRECISELY does "unbalancing them" mean? I repeat what I said before: equol and 5a-reductase inhibitors should have essentially the same effect on DHT-sensitive tissues, even though they arrive at that point by a different route. Both the desired effects and the side-effects should be about the same. They should both cause a mild reflexive increase in testosterone production.

TheOliviaTremorControl said:
Finasteride, however, inhibits the creation of DHT, which in some (rare) cases causes permanent damage to your DHT production, which would mean any side effects would be indefinate.

Show me some evidence that finaseride causes "permanent damage" to DHT production.

TheOliviaTremorControl said:
Basically, Equol is estimated to be even more powerful at *stopping* dht from binding with your androgen receptors than Dutasteride is, but there is none of the side effects (theoretically).

What evidence do you have that it's more powerful than dutasteride? And what on earth makes you think that equol would (theoretically) have none of the side-effects?? (I'm particularly interested in that second claim, so please explain that one to me in detail! :wink: )

TheOliviaTremorControl said:
So, for all those people that want something as powerful as Dutasteride, but are too afraid of the side effects, this ones for you.

I ask you again, just for added emphasis: what on earth makes you think that equol wouldn't have the same side-effects that dutasteride does?? PLEASE EXPLAIN.

As I said before, the side-effects should be similar, whether you use finasteride, dutasteride, or equol.

Bryan
 

michael barry

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Equol is made by roughly 35% of people who eat soy isoflavens.

It is made explicitly in the digestion process. Soy supposedly is now linked in delay of genital devlopment in pre-pubescent males and females. Japanese dermatologist not that rural Japanese almost always have headfulls of hair, but are of smaller stature than city Japanese. They also eat alot more soy.

Ive not heard of anything that suggests that their sex drives are lower however.

There was a similar buzz about a phytonutient in broccholi a while back. An indole therein apparently binds with androgen receptors and keeps DHT from doing so in test tubes. The Doctor that made the find was looking for research grant money to study male pattern baldness with this discovery.
Perhaps soy/equol might work in a similar way..................binding with the same androgen receptors or who knows, maybe it chemically knocks of the two extra hydrogen from the DHT AFTER IT IS FORMED.

At any rate, synthesizing Equol chemically would be MUCHO expensive.
 

Bryan

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michael barry said:
There was a similar buzz about a phytonutient in broccholi a while back. An indole therein apparently binds with androgen receptors and keeps DHT from doing so in test tubes. The Doctor that made the find was looking for research grant money to study male pattern baldness with this discovery.
Perhaps soy/equol might work in a similar way..................binding with the same androgen receptors or who knows, maybe it chemically knocks of the two extra hydrogen from the DHT AFTER IT IS FORMED.

We don't have to wonder about how equol works, we already KNOW how it works: yes, it binds directly with the DHT molecule and deactivates it. It's not supposed to have any effect on androgen receptors.

michael barry said:
At any rate, synthesizing Equol chemically would be MUCHO expensive.

Yes. MUCH cheaper just to stick with finasteride.

Bryan
 

Bryan

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SE-freak said:
Sometimes, I think that Bryan must feel very lonely.

I was feeling very lonely until YOU came along. Come here and give me a hug, big guy! :fun:

Bryan
 

SE-freak

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Mine was a comment on differences in scientific depth and language.
I did not imply any other kind of solitude. :)
 

Dave001

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TheOliviaTremorControl said:
Bryan, I don't know how much into Equol you've read, but it works completely different than DHT Inhibitors.

Equol itself binds with the DHT, so that the DHT cannot bind with your androgen receptor. Thus, you are not messing around with hormones, unbalencing them and whatnot.

Wow!!!!!one!!!one!!! No way!!!one!!!two!!!!three!!

Naturally, I'm fascinated by the possibility that one could prevent the hormone, DHT, from binding to the androgen receptor, without "messing around with" or potentially "unbalencing [sic]" his hormones.

TheOliviaTremorControl said:
Basically, Equol is estimated to be even more powerful at *stopping* dht from binding with your androgen receptors than Dutasteride is, but there is none of the side effects (theoretically).

Estimated by whom?
 

TheOliviaTremorControl

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*hugs bryan*


Bryan said:
First of all, let's use the precise term "5a-reductase inhibitor", rather than the vague, ambiguous expression "DHT inhibitor".
Yes sir!



Bryan said:
What PRECISELY does "messing around with hormones" mean, in this context? What PRECISELY does "unbalancing them" mean? I repeat what I said before: equol and 5a-reductase inhibitors should have essentially the same effect on DHT-sensitive tissues, even though they arrive at that point by a different route. Both the desired effects and the side-effects should be about the same. They should both cause a mild reflexive increase in testosterone production.

Because Equol does not alter hormone levels in the body, it simply blocks the effects. The body should not have an increase in testosterone, because testosterone is still being converted to DHT at the same rate that a particular subject would convert it without equol.

Bryan said:
Show me some evidence that finaseride causes "permanent damage" to DHT production.
If anything people say on the internet can be taken for face value, I've come across a lot of angry consumers that claim they remain impotent years after stopping finasteride consumption. Sorry, I don't have any scientific evidence for you.

Bryan said:
And what on earth makes you think that equol would (theoretically) have none of the side-effects?? (I'm particularly interested in that second claim, so please explain that one to me in detail! :wink: )
Explained earlier. Equol doesn't affect the hormone level in your body, it simple stops the negative effects of DHT binding with certain things. (excessive body hair, acne, miniturization of the hair follicle)


Dave001 said:
"unbalencing [sic]"
Oh christ, you're correcting a typo? Congratulations, you possess mastery of one of the easier languages on this planet to learn! Go spread your superior knowledge of grammar in a video game message board.
Thanks for wasting our time!
 

Dave001

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Bryan said:
michael barry said:
There was a similar buzz about a phytonutient in broccholi a while back. An indole therein apparently binds with androgen receptors and keeps DHT from doing so in test tubes. The Doctor that made the find was looking for research grant money to study male pattern baldness with this discovery.
Perhaps soy/equol might work in a similar way..................binding with the same androgen receptors or who knows, maybe it chemically knocks of the two extra hydrogen from the DHT AFTER IT IS FORMED.

We don't have to wonder about how equol works, we already KNOW how it works: yes, it binds directly with the DHT molecule and deactivates it. It's not supposed to have any effect on androgen receptors.

We do? I knew hardly anything about equol prior to five minutes ago, apart from its role as one of ten billion or so estrogenic soy isoflavones. A quick search of PubMed revealed the following study, which supports the mechanism you propose:

Lund, T. D., D. J. Munson, et al. (2004). "Equol is a novel anti-androgen that inhibits prostate growth and hormone feedback." Biology of Reproduction 70(4): 1188-1195.

I didn't bother to search any further. Is that mechanism agreed upon by other studies? What is the origin of the recent interest in equol that I've seen in the hair loss forums?
 

Dave001

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Bryan said:
michael barry said:
There was a similar buzz about a phytonutient in broccholi a while back. An indole therein apparently binds with androgen receptors and keeps DHT from doing so in test tubes. The Doctor that made the find was looking for research grant money to study male pattern baldness with this discovery.
Perhaps soy/equol might work in a similar way..................binding with the same androgen receptors or who knows, maybe it chemically knocks of the two extra hydrogen from the DHT AFTER IT IS FORMED.

We don't have to wonder about how equol works, we already KNOW how it works: yes, it binds directly with the DHT molecule and deactivates it. It's not supposed to have any effect on androgen receptors.

[quote="michael barry":45aa5]At any rate, synthesizing Equol chemically would be MUCHO expensive.

Yes. MUCH cheaper just to stick with finasteride.[/quote:45aa5]

Unless of course it were topically effective and without significant systemic absorption, but that has not been demonstrated (or tested, AFAIK). How expensive is it, anyway?

BTW, I remember reading that it's fairly lipophilic for a plant isoflavone:

Rothwell, J. A., A. J. Day, et al. (2005). "Experimental Determination of Octanol-Water Partition Coefficients of Quercetin and Related Flavonoids." Journal of Agricultural and Food Chemistry 53(11): 4355-4360.

I don't recall the exact LogP reported, but it is listed as 3.032 in PubChem.

Topical equol?

Reeve, V. E., S. Widyarini, et al. (2005). "Protection Against Photoaging in the Hairless Mouse by the Isoflavone Equol." Photochemistry and Photobiology.

Abstract: "Topical application of the isoflavone equol immediately following solar simulated UV (SSUV) radiation exposure has previously been demonstrated to have significant photoprotective effects. Equol reduced both the inflammatory edema and the systemic suppression of the contact hypersensitivity reaction in hairless mice. Furthermore, daily topical equol application immediately following irradiation during a 10-week chronic SSUV exposure regime, also reduced the photocarcinogenesis severity in the mouse. This study examines the potential for topical equol to prevent photoaging in response to chronic SSUV irradiation for up to 30 weeks. We did not find consistent expression of the characteristic markers of photoaging until 30 weeks, although moderate epidermal hyperplasia and a transient increase in dermal mast cell numbers were evident after 1 week. Daily application of 10 uM equol lotion significantly reduced these early changes. However after 30 weeks of SSUV exposures, photoaging was well developed, shown histologically by markedly increased epidermal hyperplasia, increased dermal mast cell number, pronounced focal elastotic deposits, degraded dermal collagen and deposition of GAGs in the lower dermis. Topical equol treatment protected significantly from each of these impairments, demonstrated histologically and quantitatively. Additionally, equol was found to have strong antioxidant action against acute UVA-induced lipid peroxidation of the mouse skin, this property accounting for its anti-photoaging mechanism. The evidence for equol's anti-photoaging activity, taken together with its anti-inflammatory, immunoprotective and anti- carcinogenic efficacy against SSUV irradiation in the mouse, suggests that equol could be developed as a helpful topical photoprotective agent for daily use by humans."
 

Bryan

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TheOliviaTremorControl said:
Because Equol does not alter hormone levels in the body, it simply blocks the effects. The body should not have an increase in testosterone, because testosterone is still being converted to DHT at the same rate that a particular subject would convert it without equol.

But the body WILL have an increase in testotsterone, just like with finasteride and dutasteride, and the rat studies appear to demonstrate that (LH levels rose with equol administration).

I've already explained to you why testosterone rises with finasteride/dutasteride, and it's not the superficial reason that people always seem to think. It's because DHT is a player in the feedback loop which the brain uses to regulate testosterone production. You deactivate DHT, and the brain will release more LH (luteinizing hormone) as a signal to the testes to start making more T as a countermeasure. The same thing happened with the rats, when they were given equol.

TheOliviaTremorControl said:
Bryan said:
Show me some evidence that finasteride causes "permanent damage" to DHT production.
If anything people say on the internet can be taken for face value, I've come across a lot of angry consumers that claim they remain impotent years after stopping finasteride consumption. Sorry, I don't have any scientific evidence for you.

Yes, but that's not what I asked you! :) There are indeed anecdotal reports of continuing long-term side-effects after stopping finasteride usage; however, the point I tried to make to you above is that there is no evidence that there is permanent damage to DHT production. In other words, once you stop using finasteride, DHT levels will definitely rise back up to "normal", pre-finasteride levels. I've never heard of any evidence to the contrary.

If people are really still experiencing problems years after discontinuing finasteride, then it must have something to do OTHER than with levels of DHT. Furthermore, there's no reason to blame that on finasteride; the very same problem would be likely to occur with equol use, too.

TheOliviaTremorControl said:
Bryan said:
And what on earth makes you think that equol would (theoretically) have none of the side-effects?? (I'm particularly interested in that second claim, so please explain that one to me in detail! :wink: )
Explained earlier. Equol doesn't affect the hormone level in your body, it simple stops the negative effects of DHT binding with certain things. (excessive body hair, acne, miniturization of the hair follicle)

And _I_ explained earlier. Equol will affect hormone levels in your body, just like finasteride. There's no question about that.

Bryan
 

Bryan

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Dave001 said:
I didn't bother to search any further. Is that mechanism agreed upon by other studies?

Yep. Everything I've seen about equol says that.

Dave001 said:
What is the origin of the recent interest in equol that I've seen in the hair loss forums?

It's the latest antiandrogen du jour. People think that it's going to have advantages (lack of side-effects) that the other similar drugs don't, despite my continuing efforts to squash that idea.

Bryan
 

Dave001

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Bryan said:
Dave001 said:
What is the origin of the recent interest in equol that I've seen in the hair loss forums?

It's the latest antiandrogen du jour. People think that it's going to have advantages (lack of side-effects) that the other similar drugs don't, despite my continuing efforts to squash that idea.

Yeah, but is there a specific study or article that has caused this recent excitement?
 
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