Revivogen! Question
Dying
Jake
>Anyone who tried this, please share your experience! Thanks
I second that. Also I'm wondering how it compares to other
"natural" products such as Crinagen in terms of effectiveness,
cost, ingredients (e.g. how much azelaic acid in Revivogen?)
etc. Revivogen shares ingredients with Crinagen and has a few
extra (fatty acids) but appears considerably more expensive.
Crinagen ingrediants
Polysorbate 20; Azelaic acid (5%); Zinc acetate hydrate; Niacin;
Vitamin B6 (as Pyridoxal-5-phosphate); Saw palmetto extract
(serenoa repens); Ginkgo biloba extract
Crinagen 4 oz (118ml) costs $19.95 free postage
Revivogen ingredients
Alpha Linolenic Acid, Gamma Linolenic Acid, Linoleic Acid, Oleic
Acid, Palmitic Acid, Myristic Acid, Saw Palmetto Extract,
Azelaic Acid, Pyridoxine Hydrochloride (Vitamin B6), Zinc
Sulfate, Niacin (Vitamin B3), Tocopherol Acetate (Vitamin E)
2 x 60 ml + shampoo costs $99 + postage
* Sent from RemarQ http://www.remarq.com The Internet's Discussion Network *
The fastest and easiest way to search and participate in Usenet - Free!
melvin
irritated my scalp a little. Is anyone else having this expierence?
"Jake" <cytokine1...@hotmail.com.invalid> wrote in message
news:0222858d...@usw-ex0108-063.remarq.com...
Jake
>I just this second applied Revivogen for the first time. It
burned and
>irritated my scalp a little. Is anyone else having this
expierence?
That would probably be due to the Niacin which is known
to increase blod circulation where applied. I had the same
experience, (and was expecting it) with Nioxin scalp treatment
which also contains Niacin. Not a bad thing I'd say if its
bearable.
Bryan Shelton
wrote:
>>Anyone who tried this, please share your experience! Thanks
>
>I second that. Also I'm wondering how it compares to other
>"natural" products such as Crinagen in terms of effectiveness,
>cost, ingredients (e.g. how much azelaic acid in Revivogen?)
>etc. Revivogen shares ingredients with Crinagen and has a few
>extra (fatty acids) but appears considerably more expensive.
>
>Crinagen ingrediants
>
>Polysorbate 20; Azelaic acid (5%); Zinc acetate hydrate; Niacin;
>Vitamin B6 (as Pyridoxal-5-phosphate); Saw palmetto extract
>(serenoa repens); Ginkgo biloba extract
>
>Crinagen 4 oz (118ml) costs $19.95 free postage
>
>Revivogen ingredients
>
>Alpha Linolenic Acid, Gamma Linolenic Acid, Linoleic Acid, Oleic
>Acid, Palmitic Acid, Myristic Acid, Saw Palmetto Extract,
>Azelaic Acid, Pyridoxine Hydrochloride (Vitamin B6), Zinc
>Sulfate, Niacin (Vitamin B3), Tocopherol Acetate (Vitamin E)
>
>2 x 60 ml + shampoo costs $99 + postage
After reading the above lists of ingredients and prices, I find myself
leaning toward Crinagen as being the better product.
Several things bother me about Revivogen:
1) It contains all those fatty acids; I wonder what they think is the
purpose of those? GLA is *supposed* to inhibit 5AR, but what about
the others? Worse, the unsaturated fatty acids (the two linolenic acids
and the linoleic acid, and possibly the SP extract) are very susceptible
to oxidation, yet they have no antioxidant in the product to protect them
(the tocopherol acetate doesn't serve this function).
2) The pyridoxine hydrochloride continues to be an issue for me. Most
of us in this newsgroup are aware of the study that found that the
pyridoxine form applied to tissues *increased* DHT, but the pyridoxal
form *decreased* DHT levels. I'm still amazed that Revivogen would use
the "wrong" form of the vitamin. When Farrel questioned them about this
a while back, their answer was a rather lame, "Well, we've found that the
product as a whole works". This is not good enough for me! I want to know
if they were aware of that study when they were designing the product, and
if so, why did they take a chance by using the "wrong" form? If they were
unaware of the study, why didn't they know something the rest of us knew,
and why do they *continue* to use the "wrong" form?
3) Probably the one thing that bothers me the most is the inclusion
of the tocopherol acetate in the formula. I can't see any possible
function for this ingredient. Moreover, if they are under the mistaken
belief that this is serving as an antioxidant for the fatty acids, then this
would cast doubt for me on the entire product. If they are this clueless
about tocopherol acetate, then I can't help but wonder what other
mistakes they've made in the formulation and production of the product.
The bottom line is that Revivogen costs almost five times as much as
Crinagen, has lots of fatty acids that are probably unstable, has the
"wrong" form of B6, and has a ridiculously ineffective form of vitamin E.
So far, I'll have to vote for Crinagen as probably being the better product.
Bryan
Farrel
You have obviously have never seen either product ;-)
Crinagen, the last time I used it, was a thick soupy green mixture. OTOH
Revivogen is clear, non greasy and looks far more stable in my opinion.
Based on the consistencies I would say Revivogen would be far better at
penetrating into the follicle than Crinagen
Farrel
--
HAIRTODAY.COM - Your One Stop Hair Loss Shop
http://www.hairtoday.com
Bryan Shelton <br...@pointecom.net> wrote in message
news:757488B4258B2639.44D10A7A...@lp.airnews.net...
Bryan Shelton
>Bryan
>
>You have obviously have never seen either product ;-)
You're right, I haven't actually seen either one!
>Crinagen, the last time I used it, was a thick soupy green mixture. OTOH
>Revivogen is clear, non greasy and looks far more stable in my opinion.
Well, you can't always go by appearances. You may have heard that
vegetable oils can become dangerously oxidized even before they
start to smell bad.
>Based on the consistencies I would say Revivogen would be far better
>at penetrating into the follicle than Crinagen
Farrel, why don't you forward my post to the fine folks at Revivogen?
I'd truly like to hear their response.
Bryan
AkOnAtAk1
vellus hairs.
I was also thinking revivogen but ended up going with the crinagen as a cheaper
substitute.
Ill keep you all informed on my results
Randall Parker
the sagacious br...@pointecom.net Bryan Shelton perspicated:
>
> 3) Probably the one thing that bothers me the most is the inclusion
> of the tocopherol acetate in the formula. I can't see any possible
> function for this ingredient.
Yeah, doesn't it need to have the acetate cleaved off in order for it to
be an antioxidant and doesn't that cleaving normally happen during
digestion?
It is my impression that only free form tocopherols provide preservative
protection of foods and medicines.
>Moreover, if they are under the mistaken
> belief that this is serving as an antioxidant for the fatty acids, then this
> would cast doubt for me on the entire product. If they are this clueless
> about tocopherol acetate, then I can't help but wonder what other
> mistakes they've made in the formulation and production of the product.
>
> The bottom line is that Revivogen costs almost five times as much as
> Crinagen, has lots of fatty acids that are probably unstable, has the
> "wrong" form of B6, and has a ridiculously ineffective form of vitamin E.
They both have Saw Palmetto. But, heck, that's easy to add to one's own
formulation. Crinagen has Azelaic acid as well.
Why the zinc as acetate hydrate in Crinagen? Revivogen has it as sufate
and so does Prox N.
Bryan Shelton
>In <757488B4258B2639.44D10A7A...@lp.airnews.net>,
>the sagacious br...@pointecom.net Bryan Shelton perspicated:
>>
>> 3) Probably the one thing that bothers me the most is the inclusion
>> of the tocopherol acetate in the formula. I can't see any possible
>> function for this ingredient.
>
>Yeah, doesn't it need to have the acetate cleaved off in order for it to
>be an antioxidant and doesn't that cleaving normally happen during
>digestion?
>
>It is my impression that only free form tocopherols provide preservative
>protection of foods and medicines.
Yes, absolutely! The fact that they don't seem to know anything
about this or the pyridoxal/pyridoxine issue makes me wonder what
other mistakes they may have made in this product. Sheesh!
>>Moreover, if they are under the mistaken
>> belief that this is serving as an antioxidant for the fatty acids, then this
>> would cast doubt for me on the entire product. If they are this clueless
>> about tocopherol acetate, then I can't help but wonder what other
>> mistakes they've made in the formulation and production of the product.
>>
>> The bottom line is that Revivogen costs almost five times as much as
>> Crinagen, has lots of fatty acids that are probably unstable, has the
>> "wrong" form of B6, and has a ridiculously ineffective form of vitamin E.
>
>They both have Saw Palmetto. But, heck, that's easy to add to one's own
>formulation. Crinagen has Azelaic acid as well.
>
>Why the zinc as acetate hydrate in Crinagen? Revivogen has it as sufate
>and so does Prox N.
I doubt that the specific zinc salt makes much of a difference,
as long as there aren't solubility problems.
Bryan
mike
output in rats,Dr Razack may have seen this study?
Farrel
Based on my initial discussions they say the majority of the DHT inhibition
occurs from the GLA and ALA and not from the B6. That is the fundamental
difference between their product and Crinagen
Farrel
--
HAIRTODAY.COM - Your One Stop Hair Loss Shop
http://www.hairtoday.com
Bryan Shelton <br...@pointecom.net> wrote in message
news:2613DC7A403E1D1D.E5518EDD...@lp.airnews.net...
Bryan Shelton
>I have forwarded the post onto them for comment and they will be replying.
>Based on my initial discussions they say the majority of the DHT inhibition
>occurs from the GLA and ALA and not from the B6. That is the fundamental
>difference between their product and Crinagen
I'll also mention that there can't be very much GLA and ALA
in the product, if it's not even greasy...
Bryan
HairTalk
<757488B4258B2639.44D10A7A...@lp.airnews.net>,
> of the tocopherol acetate in the formula. I can't see any possible
mistaken
> belief that this is serving as an antioxidant for the fatty acids,
then this
> would cast doubt for me on the entire product. If they are this
clueless
> about tocopherol acetate, then I can't help but wonder what other
> mistakes they've made in the formulation and production of the
product.
>
> The bottom line is that Revivogen costs almost five times as much as
> Crinagen, has lots of fatty acids that are probably unstable, has the
> "wrong" form of B6, and has a ridiculously ineffective form of
vitamin E.
>
product.
>
> Bryan
>
Bryan, crazy as it sounds, is it possible they're using the fatty acids
to create a "protected" environment on the scalp? I read today on
www.salusmaster.com in the section on Folligen that Dr Pickart does
something with the product to try to create a "safe" . and "incubated"
environment by actually *increasing* sebum or oily coating on the scalp
to prevent dehydration and help "protect" follicles.
This is diametrically opposed to the comments Ive heard that when a man
hits his "change of life" at age 25, gets fat, and starts to lose hair,
that DHT and sebum production increase, which both can lead to hairloss.
Is salusmasters information incorrect? Why would folligen want to
create a fatty oily scalp environment? Is it possible this is what
Revivogen is doing with their fatty asses? I mean acids?
HT
--
****************************************
http://www.hairlosstalk.com
Live 1 on 1 with hot nasty balding men.
****************************************
Sent via Deja.com http://www.deja.com/
Before you buy.
Bryan Shelton
>Is salusmasters information incorrect? Why would folligen want to
>create a fatty oily scalp environment? Is it possible this is what
>Revivogen is doing with their fatty asses? I mean acids?
I doubt it. After all, Farrel quoted them as saying specifically that
the GLA and ALA do most of the DHT suppression, so that's
probably the only reason they put them in there.
Bryan
han...@my-deja.com
> create a fatty oily scalp environment? Is it possible this is what
> Revivogen is doing with their fatty asses? I mean acids?
>
>
> --Hello HT
I don't know too much about hair loss or the products but I have heard that
excess sebum contributes to hair loss. If Folligen is creating a sebum rich
scalp environment, first, is this a good idea and second, if this is truly a
good idea, what about other hair loss products that cut down on sebum? In
what circumstances should these other products be used and should they be
used in conjunction with folligen? Any thoughts?
Farrel
Ok here is their response, strangely enough they were able to comment in
spite of the many "regulations" that prevented Spamcorp from answering any
questions. ;-)
Farrel
----------------------------------------------------------------------------
------------
Thank you for forwarding the comments posted on the baldspot news group for
our reply. We appreciate the opportunity to answer any concerns and
questions about Revivogen and always welcome criticism, suggestions, and
questions.
First I like to provide you with some details about the formulation of
Revivogen. Unlike what seems to be the popular belief, Revivogen is not a
Crinagen mimic formula based on Azelaic Acid, Zinc, and B6. It actually is a
GLA, ALA, and Linoleic based formula with Azelaic acid and other ingredients
added as complementary and supportive ingredients. We have chosen GLA, ALA,
and Linoleic Acid because they are in fact the most potent and best
researched 5AR inhibitors known today. These ingredients have the proven
ability to block both type 1 and 2 forms of 5AR equally from 90 to 98%.
Also they are the only ingredients that have been actually proven to inhibit
5AR when applied topically and are highly absorbable into the skin which
makes them a great delivery vehicle for other ingredients.
Yet another unique quality of GLA and ALA is their potent anti-inflammatory
properties. In fact the most common usage of these fatty acids as oral
supplements is as anti-inflammatories for the treatment of inflammatory
arthritic conditions (rheumatoid arthritis, etc.). It is a known fact that a
low grade inflammation also occurs in androgenetic Alopecia which eventually
leads to scarring alopecia after a long time. As such anti-inflammatories
are of essence to any successful therapy for hair loss. Based on these facts
it is apparent why we have mainly relied on GLA, ALA and Linoleic acid as
our main active ingredients. They have the best scientific studies and the
best properties in one place.
The most important thing about these fatty acids is that they must be in the
free fatty acid form or they don't work. This means all natural oils
including Borage oil, Emu Oil, Flax Seed Oil, etc. which have less than 1%
free fatty acid in the natural form, will not work and are worthless. This
again is proven by the scientific studies. We only use pure fatty acids in
Revivogen which is very expensive and hard to make. The other fatty acids in
the formula are in much lower concentrations and they are there because it
is very difficult to distract and separate them and unnecessary. All studies
discussed here are published at the research section of our site at
www.revivogen.com/research.html for public viewing.
In regards to the formula's potency and preventing oxidation we have taken
very stiff measures to prevent this from happening which includes:
1. Producing small quantities to have fresh formulas on a regular basis.
2. Using smaller bottles for the formula to prevent prolonged exposure to
the air (we would have saved significant amount of money if we used one
single 4 oz. bottle).
3. Inclusion of Alcohol, vitamin E (alpha, gamma, and delta Tocopherol),
Ascorbyl palmitate and BHT in the formula to provide additional and reliable
anti-oxidant protection.
We have added Azelaic Acid (5%), Zinc, B6, Saw Palmetto Extract (98% fatty
acids) and Niacin (for inducing capillary dilation and increasing blood flow
to the scalp) to increase the formula's potency and to provide additional
means of 5AR inhibition. All of these ingredients have good research but the
only ingredient that seems to be bothersome to many is Pyridoxine HCl. We
are aware of the study about the differences of Pyridoxine vs. Pyridoxal.
The reason we chose Pyridoxine HCl was that as first documented in British
Journal of Dermatology the invivo (not invitro) studies have shown that
"Pyridoxine HCl potentiates the effects of zinc and Azaleic Acid in
inhibiting 5-alpha Reductase. Additionally when the three substances were
added together at very low concentrations which had shown to be ineffective
alone, 90% inhibition of 5 alpha-reductase activity was obtained". It is a
clinically proven fact that these ingredients work synergistically in
blocking 5AR and therefore one has to look at their combined effect rather
than each individual ingredients properties when studied alone. Now if you
look at the studies about saw palmetto and many other compounds you would
see that for every study claiming their effectiveness there is another study
claiming that they don't work or have a negative effect. We place more value
on the study published in the British Journal of Dermatology which has a
very high degree of scientific credibility than other journals.
In regard to the before and after pictures first I like to assure every one
that they are real. Obviously they represent our best results which did not
happen over night. If the quality is not great it is because during the past
three years as we were experimenting with the formula we were not planing to
market it or to turn it into a commercial product. As such we were taking
the pictures sparingly without much attention to lighting, angles, etc.. Our
interest was first intellectual and then a hobby rather than preparation for
a business venture. It was only during the last year that we learned about
other products available for hair loss on the Internet and decided to market
and sell our formula. So if the lighting is incorrect or the angles are not
the same it is not because we are trying to mislead anyone or create amazing
before and after pictures.
But an even more important and over looked fact is that any before and after
picture is useless for trying to comparing products with each other or for e
valuating what kind of results one should expect with using any product.
Each individual is different and results vary from person to person. If
Revivogen has worked for X it does not mean that it will work for Y or that
they will have similar results. We highly recommend that any one who is
using Revivogen or any other product to take their own before and after
pictures for evaluating their results.
Finally we do not guarantee results or claim that Revivogen grows hair or
prevents hair loss. If we do make such claims then FDA and FTC would
consider Revivogen as a new treatment for hair loss and require FDA studies
and approval which can take 7-10 years and millions of dollars. We leave it
to our customers to make an educated and reasonable decision as to what to
expect from Revivogen based on the scientific evidence and the facts.
However, we do guarantee our customers satisfaction with a hassle free 90
day money back guarantee.
We know that it is impossible to please every one, and that there is always
room for improvement. We welcome all constructive criticism, comments and
recommendations. We can never live up to every one's expectations but we do
our best to provide the most effective and safest product to our customers
around the world. As such I like to announce here that we are considering to
change the B6 in our formula from Pyridoxine to Pyridoxal in our next
production to ease the many concerns raised about this issue. We like to
hear from the members of baldspot as to which form of B6 they prefer, given
our reasoning that was provided here. They can cast their votes by sending
an email directly to me at in...@revivogen.com . Thank you again for bringing
this matter to our attention and providing us with an opportunity to
response.
Sincerely,
Dr. Alan Shargani
Advanced Skin and Hair, LLC
Niall
Farrel <far...@my-deja.com> wrote in message
news:SZyy4.10077$u8.3...@newsread2.prod.itd.earthlink.net...
Randall Parker
sagacious far...@my-deja.com Farrel perspicated:
> The most important thing about these fatty acids is that they must be in the
> free fatty acid form or they don't work. This means all natural oils
> including Borage oil, Emu Oil, Flax Seed Oil, etc. which have less than 1%
> free fatty acid in the natural form, will not work and are worthless.
Is this true? If so, how can one convert fatty acids to free form?
Is the problem that they are esters?
Also, ask them why they are using the acetate form of Vitamin E. I don't
think that is providing any preservative effect.
Bryan Shelton
>Ok here is their response...
-----------------------------------------------------------------------------------------------
>In regards to the formula's potency and preventing oxidation we have taken
>very stiff measures to prevent this from happening which includes:
>
>1. Producing small quantities to have fresh formulas on a regular basis.
>2. Using smaller bottles for the formula to prevent prolonged exposure to
>the air (we would have saved significant amount of money if we used one
>single 4 oz. bottle).
>3. Inclusion of Alcohol, vitamin E (alpha, gamma, and delta Tocopherol),
>Ascorbyl palmitate and BHT in the formula to provide additional and reliable
>anti-oxidant protection.
But this doesn't jive with information we were given before
by another poster about Revivogen; were we misinformed?
Here's the other info:
>Revivogen ingredients
>
>Alpha Linolenic Acid, Gamma Linolenic Acid, Linoleic Acid, Oleic
>Acid, Palmitic Acid, Myristic Acid, Saw Palmetto Extract,
>Azelaic Acid, Pyridoxine Hydrochloride (Vitamin B6), Zinc
>Sulfate, Niacin (Vitamin B3), Tocopherol Acetate (Vitamin E)
Which is right, and which is wrong?
Bryan
Bryan Shelton
>The reason we chose Pyridoxine HCl was that as first documented in British
>Journal of Dermatology the invivo (not invitro) studies have shown that
>"Pyridoxine HCl potentiates the effects of zinc and Azaleic Acid in
>inhibiting 5-alpha Reductase."
Actually, you're mis-remembering what the article said. The abstract
for this study clearly indicates that B6 potentiates the effects of zinc,
but NOT azelaic acid.
>"Additionally when the three substances were added together
>at very low concentrations which had shown to be ineffective alone,
>90% inhibition of 5 alpha-reductase activity was obtained". It is a
>clinically proven fact that these ingredients work synergistically in
>blocking 5AR and therefore one has to look at their combined effect
>rather than each individual ingredients properties when studied alone.
> [...]
>As such I like to announce here that we are considering to change
>the B6 in our formula from Pyridoxine to Pyridoxal in our next production
>to ease the many concerns raised about this issue. We like to hear from
>the members of baldspot as to which form of B6 they prefer, given our
>reasoning that was provided here.
On further reflection, I've had a change of heart on this issue. Rather
than change from pyridoxine to pyridoxal, why not simply take OUT both
the pyridoxine and the zinc?
Why would I suggest this? Because the pyridoxine has no effect on
the azelaic acid, so it's not needed for that. It *does* potentiate
the zinc, but then zinc only inhibits 5AR type 1. See:
"Cations inhibit specifically type I 5 alpha-reductase found in human skin"
Author: Sugimoto Y; López-Solache I; Labrie F; Luu-The V
J Invest Dermatol, 104: 5, 1995 May, 775-8
This study found that zinc ions had no effect on 5AR type 2, but
they did strongly inhibit 5AR type 1. But increasingly it appears
that the important isozyme in the follicle and the dermal papillae,
and the one responsible for hair-loss, is type 2.
So it's with a great sense of irony that I suggest that you take
out the B6 and zinc entirely, and rely on the fatty acids and
azelaic acid to do the job.
Bryan
donald...@my-deja.com
responsible for hair loss. If they are getting that solely from hearing
that finasteride users halt hair loss, then that is not sufficient
argument. What about the people for whom finasteride doesn't work?
Maybe these people are just not responding to the drug (i.e., their
bodies are not inhibiting 5AR type 2) or type 1 is also causing the
problem for them.
>
> "Cations inhibit specifically type I 5 alpha-reductase found in human
skin"
> Author: Sugimoto Y; López-Solache I; Labrie F; Luu-The V
> J Invest Dermatol, 104: 5, 1995 May, 775-8
>
> This study found that zinc ions had no effect on 5AR type 2, but
> they did strongly inhibit 5AR type 1. But increasingly it appears
> that the important isozyme in the follicle and the dermal papillae,
> and the one responsible for hair-loss, is type 2.
>
>
Fuzz
Randall Parker <rgpa...@west.net> wrote in message
news:MPG.13348528e...@news.onlynews.com...
> In <SZyy4.10077$u8.3...@newsread2.prod.itd.earthlink.net>, the
> sagacious far...@my-deja.com Farrel perspicated:
the
> > free fatty acid form or they don't work. This means all natural oils
> > including Borage oil, Emu Oil, Flax Seed Oil, etc. which have less than
1%
> > free fatty acid in the natural form, will not work and are worthless.
>
>
> Is the problem that they are esters?
Yeah -- what does this actually mean? How does one determine if these oils
(GLA's/LA's) are at least 1% free fatty acids in natural form? Are we just
talking topically here as well?
--Fuzz
mike
>>Journal of Dermatology the invivo (not invitro) studies have shown that
>>"Pyridoxine HCl potentiates the effects of zinc and Azaleic Acid in
>>inhibiting 5-alpha Reductase."
>
>for this study clearly indicates that B6 potentiates the effects of zinc,
>but NOT azelaic acid.
>
>>at very low concentrations which had shown to be ineffective alone,
>>90% inhibition of 5 alpha-reductase activity was obtained". It is a
>>clinically proven fact that these ingredients work synergistically in
>>blocking 5AR and therefore one has to look at their combined effect
>>rather than each individual ingredients properties when studied alone.
>>As such I like to announce here that we are considering to change
>>the B6 in our formula from Pyridoxine to Pyridoxal in our next production
>>to ease the many concerns raised about this issue. We like to hear from
>>the members of baldspot as to which form of B6 they prefer, given our
>>reasoning that was provided here.
>
>than change from pyridoxine to pyridoxal, why not simply take OUT both
>the pyridoxine and the zinc?
>
>Why would I suggest this? Because the pyridoxine has no effect on
>the azelaic acid, so it's not needed for that. It *does* potentiate
>the zinc, but then zinc only inhibits 5AR type 1. See:
>
>Author: Sugimoto Y; López-Solache I; Labrie F; Luu-The V
>J Invest Dermatol, 104: 5, 1995 May, 775-8
>
>This study found that zinc ions had no effect on 5AR type 2, but
>they did strongly inhibit 5AR type 1. But increasingly it appears
>that the important isozyme in the follicle and the dermal papillae,
>and the one responsible for hair-loss, is type 2.
>
>out the B6 and zinc entirely, and rely on the fatty acids and
>azelaic acid to do the job.
>
>Bryan
That's completely the opposite to what I think is the key ingredients
in revivogen.Zinc & b6 have glucocorticoid antagonistic properties as
well as androgen blocking.This in my opinion makes them more valuable
than anything else in the formulation.This zinc/b6 solution is talked
about at:www.mindspring.com/~bupper1/index.htm.Remember we've talked
about the general ineffectiveness of topical anti-androgens in the past.
If topical antiandrogens were as a _group_effective then the argument
would soundly favor the antiandrogen property at work.What we know is
that only a few antiandrogens have shown any success in treating mpb and
this in my opinion votes for a different way of working other than
antiandrogenic.
Bryan Shelton
>Bryan, how do they come up with the statement that only type 2 is
>responsible for hair loss. If they are getting that solely from hearing
>that finasteride users halt hair loss, then that is not sufficient
>argument.
Oops! I should have made crystal clear that _I_ am the one
making that claim, not the folks at Revivogen. I don't have any
idea what their thoughts are on this issue, but lately I've really
been re-thinking my own position and this is now what I believe.
And off the top of my head, here are three good reasons:
1) Yes, finasteride halts hair-loss (at least in most people). Its
activity is almost entirely against 5AR type 2, and only minimally
against 5AR type 1.
2) The medical journal article that I quoted from extensively
recently demonstrated that 5AR type 2 is indeed the major
player in the follicle itself, including the all-important dermal papilla.
3) Last, and certainly not least, is the fact that 5AR-deficient
pseudohermaphrodites, who never go bald, are deficient ONLY in
5AR type 2. They have perfectly *normal* levels of 5AR type 1.
These three facts taken together (and I might be able to think
of others) seem to me to strongly support the idea that 5AR type 2
is the villain in hair-loss, and type 1 apparently plays little or no role.
>What about the people for whom finasteride doesn't work?
>Maybe these people are just not responding to the drug (i.e., their
>bodies are not inhibiting 5AR type 2) or type 1 is also causing the
>problem for them.
We've speculated about this before, recently. It doesn't seem to be
that the failures simply don't respond to the drug, because somebody
pointed out that Merck found that their DHT levels were lowered just
like the successes. And again, the pseudohermaphrodites have plenty
of 5AR type 1, and it doesn't bother *them*.
I suspect that it's a matter of timing AND degree: we know that even
severely balding men can have their hairloss switched-off like a light-
switch when their DHT levels are *severely* reduced, like in castration;
but if levels are reduced by only around 65%, as happens with Propecia
use, this isn't quite enough to pick up everyone, and there are a few
unlucky outliers left behind. The reason the pseudohermaphrodites
apparently have complete success with a bit less DHT reduction than
what you get with Propecia, I would guess, is that they are that way
from birth and do not begin after hairloss has already commenced.
Bryan
Farrel
some men the 65% reduction just isnt enough. That why I encourage using the
full 1mg dosage rather than a 0.25 mg dose. There definately is a threshold
in my own experience where the Finasteride no longer works. In my own
experimentation with going from a 1mg dose to a 0.5mg dose I noticed an
almost immediate return of scalp itch and increased hair loss.
Farrel
--
HAIRTODAY.COM - Your One Stop Hair Loss Shop
http://www.hairtoday.com
Bryan Shelton <br...@pointecom.net> wrote in message
news:92C94CBEB50DF082.CA011E9D...@lp.airnews.net...
Bryan Shelton
>br...@pointecom.net (Bryan Shelton) wrote:
>>So it's with a great sense of irony that I suggest that you take
>>out the B6 and zinc entirely, and rely on the fatty acids and
>>azelaic acid to do the job.
>>Bryan
>
>That's completely the opposite to what I think is the key ingredients
>in revivogen.Zinc & b6 have glucocorticoid antagonistic properties as
>well as androgen blocking.This in my opinion makes them more valuable
>than anything else in the formulation.
Well, Mike, we'll have to agree to disagree on this! :-)
It's funny, isn't it, how we've split into these two opposing points of view?
I think it's pure speculation as to whether or not these glucocorticoid
antagonistic properties would have any actual benefit for human MPB.
And the androgen blocking in the case of zinc and B6 is the *wrong*
androgen, in a manner of speaking, so I'm rather indifferent to these
two ingredients.
>This zinc/b6 solution is talked
>about at:www.mindspring.com/~bupper1/index.htm.
I couldn't get this link to work! Is there a typo in it?
>Remember we've talked
>about the general ineffectiveness of topical anti-androgens in the past.
>If topical antiandrogens were as a _group_effective then the argument
>would soundly favor the antiandrogen property at work.What we know is
>that only a few antiandrogens have shown any success in treating mpb
>and this in my opinion votes for a different way of working other than
>antiandrogenic.
No, Mike, I think topical antiandrogens *would* be effective (and you
know what I mean by "effective") for MPB, but they have extremely
rarely ever been *tried* in humans. That phantom spiro study Dr. P
tells us about is the only one that comes to mind, and that worked!
And they have definitely worked in animals. Are you aware of any
other human studies of any kind of topical antiandrogen for MPB,
whether it worked or not?
Bryan
MARK DORAN
Bryan Shelton wrote in message
<26943FB8BD7EF24C.1CDD708D...@lp.airnews.net>...
Sorry, but what is that 'phantom spiro study'?
*Fascinating* debate, guys, BTW.
Thanks,
Mark D.
Bryan Shelton
>Sorry, but what is that 'phantom spiro study'?
Dr. P always used to tell us (he hasn't mentioned it in a long time)
that once at a medical conference or convention or something he
had attended, another doc was passing out reports of a little study
he had done on the effect of topical spironolactone on hairloss, and
the results were sorta, kinda, about what you get with finasteride.
Unfortunately (grrrr...), Dr. P didn't get a copy of this paper, and I
don't think he knows the name of the doctor anymore or where
to find him. Damn. I would KILL to have a copy of that study!
Dr. P, put your thinking cap on: can't you remember the name
of that guy and where to find him??
Bryan
donald...@my-deja.com
what does that mean? Does it mean that finally the suppressive forces
of the drug have won the battle (and at that point the DHT has begun to
be inhibited 65%)? Or, that after being inhibited from the time the
person began taking the drug, finally an effect is being seen on the
hair (follicles)?
If everyone responds (it would seem from the get-go), as you say, it
perplexes me why there is such a lag in some people seeing noticeable
results.
Does anyone know what might inhibit the other 35% of type 2? I know
there are a lot of 5AR inhibitors (including my mom), but which
specifically work on type 2?
And Bryan, I know you have gone over this many times before. But, by
your argument, a non-finasteride taker would probably be inclined to
start, since you make it look so promising to many individuals. So why
don't you take it??
Farrel
variables so thats why everyone responds differently to treatment.
The best analogy with how Propecia works is to compare DHT to a brake and
your hair to a car. If your car has recently stopped, by removing the brake
it will easily start moving again.
However if your car has been stationary for 5 years, chances are when you
remove the brake, nothing will happen.
Thats the reason, and if you are taking long to respond to Propecia you
should look at using other drugs and SODS to help "repair the engine"
Farrel
--
HAIRTODAY.COM - Your One Stop Hair Loss Shop
http://www.hairtoday.com
<donald...@my-deja.com> wrote in message
news:8aj33h$ure$1...@nnrp1.deja.com...
SaberR...@fmer.com
Were you an auto mechanic in a previous life?
honkee00
> spironolactone being used for hair loss, we can make an educated guess that it
> should be pretty effective at halting its progression. For one, we've got
> anecdotal evidence from Dr. Lee that 5% minox + 2% spiro is at least as
> effective as 5% minox + finasteride. There are also numerous studies showing
> topical spiro is effective against androgen-related skin disorders such as
> acne, which means it should do the same for baldness. Finally, we've seen that
> topical RU58841 is perfectly capable of reversing hair loss in stumptail
> macaques (not humans, but as close as you can get....). Assuming RU is just an
> antiandrogen and possesses no additional growth stimulating properties, spiro
> should be able to do just as well, as it has a comparable affinity for androgen
> receptors. -Mitch
>
>
mike
>On 13 Mar 2000 01:43:56 GMT, mike <emka...@dodgenet.com> wrote:
>
>know what I mean by "effective") for MPB, but they have extremely
>rarely ever been *tried* in humans. That phantom spiro study Dr. P
>tells us about is the only one that comes to mind, and that worked!
>other human studies of any kind of topical antiandrogen for MPB,
>whether it worked or not?
>
>Bryan
No there is indeed a shortage of studies out there on this,as you have
said.Women with androgenic alopecia also dont regrow hair,but can stop
balding with oral antiandrogens.If women cant reverse balding much with
antiandrogens,how can men expect to?
But in my opinion there have prolly been alot of mini-trials thru out
the years in trying to reverse balding by doctors with topical
antiandrogen formulations.The reason not many studies get done,is small
scale it doesnt work,why invest in major dollar consuming studies when
you already know the idea has been proved incorrect many times before?
Step 1 is proving your theory at least works in someone.
Step 2 is verifying that it is reproducable in a valid sample size.
Step 3 is marketing
We know that drugs can progress very rapidly from step 1 to step 3..fact.
Minoxidil is one successful example of this and minoxidil _doesnt_ have
near the "theory age" as androgen blocking.
So my point is,antiandrogenic theories have been floating around much
longer than minoxidil,yet look at all the minoxidil studies around,and
lack of topical antiandrogen studies.Does this to you signal anything
wrong with a kink in the development process?
The reason people dont progress further in the development process is
the idea isnt working! Lets say I said to you pumpkin seed extract was
an excellent pain killer.The first thing would be to try and reproduce
what I said.The fact is small scale you cant do it,do you want to invest
in a large scale study failure?
mike
>Hairloss in people is always at different stages, there are so many
>variables so thats why everyone responds differently to treatment.
>
>The best analogy with how Propecia works is to compare DHT to a brake and
>your hair to a car. If your car has recently stopped, by removing the brake
>it will easily start moving again.
>
>However if your car has been stationary for 5 years, chances are when you
>remove the brake, nothing will happen.
>
>Thats the reason, and if you are taking long to respond to Propecia you
>should look at using other drugs and SODS to help "repair the engine"
>
>Farrel
>--
> HAIRTODAY.COM - Your One Stop Hair Loss Shop
> http://www.hairtoday.com
>
the whole "motor".
Hey maybe this crude oil stuff on www.regrowth.com,isnt too far off.:)
donald...@my-deja.com
>
> No there is indeed a shortage of studies out there on this,as you have
> said.Women with androgenic alopecia also dont regrow hair,but can stop
> balding with oral antiandrogens.If women cant reverse balding much
with
> antiandrogens,how can men expect to?
>
>
Do you mean women "can stop balding" or they "can't stop balding" with
antiandrogens?
doct...@my-deja.com
argument
> would soundly favor the antiandrogen property at work.What we know is
> that only a few antiandrogens have shown any success in treating mpb
and
> this in my opinion votes for a different way of working other than
> antiandrogenic."
I may agree with some points of mike, DHT is not the only factor for MPB
and FPB. I do not rule out DHT maybe one factor of multi-factors.
However, we have to open mind to look something else. For example, we
can not ignore the non-precise or blocked blood supply to hair
follicles, we can not ignore Stress (Stress can change blood supply
conditions, studied by Harvard University and University of Texas by
using proton imaging technique) factor, especially for young students,
young men and young women. Many other factors, as pointed out by mike
may exist too, if I remember right, mike has a long list of potential
factors other than DHT..
Rogaine has worked for some people, this is a crystal clear evidence
that
some other factors exist beside the possible DHT factor. DHT can not be
the unique factor for hair loss, for MPB, for FPB. DHT is the only
factor that is only an opinion. Even Upjohn can not agree with that.
Hair loss, socalled MPB, so called FPB are multifactor problems.
Another issue, I would like to raise again, some common ground must
exist among hair problems of men and women. Some connections must exist.
Ph.D.
@ http://www.springhair.com
In article <8ahh4s$216$1...@ins20.netins.net>,
mike <emka...@dodgenet.com> wrote:
> br...@pointecom.net (Bryan Shelton) wrote:
> >Dr. Alan Shargani of "Revivogen" wrote:
> >
> >>The reason we chose Pyridoxine HCl was that as first documented in
British
> >>Journal of Dermatology the invivo (not invitro) studies have shown
that
> >>"Pyridoxine HCl potentiates the effects of zinc and Azaleic Acid in
> >>inhibiting 5-alpha Reductase."
> >
> >Actually, you're mis-remembering what the article said. The abstract
> >for this study clearly indicates that B6 potentiates the effects of
zinc,
> >but NOT azelaic acid.
> >
> >>"Additionally when the three substances were added together
> >>at very low concentrations which had shown to be ineffective alone,
> >>90% inhibition of 5 alpha-reductase activity was obtained". It is a
> >>clinically proven fact that these ingredients work synergistically
in
> >>blocking 5AR and therefore one has to look at their combined effect
> >>rather than each individual ingredients properties when studied
alone.
> >> [...]
> >>As such I like to announce here that we are considering to change
> >>the B6 in our formula from Pyridoxine to Pyridoxal in our next
production
> >>to ease the many concerns raised about this issue. We like to hear
from
> >>the members of baldspot as to which form of B6 they prefer, given
our
> >>reasoning that was provided here.
> >
> >On further reflection, I've had a change of heart on this issue.
Rather
> >than change from pyridoxine to pyridoxal, why not simply take OUT
both
> >the pyridoxine and the zinc?
> >
> >Why would I suggest this? Because the pyridoxine has no effect on
> >the azelaic acid, so it's not needed for that. It *does* potentiate
> >the zinc, but then zinc only inhibits 5AR type 1. See:
> >
> >"Cations inhibit specifically type I 5 alpha-reductase found in human
skin"
> >Author: Sugimoto Y; López-Solache I; Labrie F; Luu-The V
> >J Invest Dermatol, 104: 5, 1995 May, 775-8
> >
> >This study found that zinc ions had no effect on 5AR type 2, but
> >they did strongly inhibit 5AR type 1. But increasingly it appears
> >that the important isozyme in the follicle and the dermal papillae,
> >and the one responsible for hair-loss, is type 2.
> >
> >So it's with a great sense of irony that I suggest that you take
> >out the B6 and zinc entirely, and rely on the fatty acids and
> >azelaic acid to do the job.
> >
> >Bryan
>
> That's completely the opposite to what I think is the key ingredients
> in revivogen.Zinc & b6 have glucocorticoid antagonistic properties as
> well as androgen blocking.This in my opinion makes them more valuable
> than anything else in the formulation.This zinc/b6 solution is talked
> about at:www.mindspring.com/~bupper1/index.htm.Remember we've talked
> about the general ineffectiveness of topical anti-androgens in the
past.
> If topical antiandrogens were as a _group_effective then the argument
> would soundly favor the antiandrogen property at work.What we know is
> that only a few antiandrogens have shown any success in treating mpb
and
> this in my opinion votes for a different way of working other than
> antiandrogenic.
>
>
jayja...@my-deja.com
doct...@my-deja.com wrote:
> (Stress can change blood supply
> conditions, studied by Harvard University ...
Is this where you received your Ph.D., doctorsp? Does your wonderful
scientific expertise come from this esteemed institution? ;-)
> Ph.D.
> @ http://www.springhair.com
So, doctorsp, you admit that you're spamcorp. Did you finally realize
that you fooled nobody? Or were you unable to resist posting your URL
one more time in the continuing hope of selling your snake oil?
I hope that the termination of your account at atlantic.net has
taught you a lesson, spamcorp. Your behavior was unacceptable, and if
you repeat it you will pay again with the loss of another account. This
newsgroup has been a very nice place during the past week, so don't even
think about flooding it again with repeated postings of your spam.
Are you a little more humble now? Do you still think that you are
qualified to tell others about obeying the law? You really are a
fucking loser, spamcorp. I just used the "F" word on purpose to tempt
you. If you're thinking right now about posting your ridiculous "clean
language" lecture, think again, because the users of this newsgroup will
kick you out a second time if necessary. Don't forget that you're now
on the Internet's list of troublemakers, and that it's going to become
more difficult each time for you to get a new account.
JC
Bryan Shelton
>br...@pointecom.net (Bryan Shelton) wrote:
>>No, Mike, I think topical antiandrogens *would* be effective (and you
>>know what I mean by "effective") for MPB, but they have extremely
>>rarely ever been *tried* in humans. That phantom spiro study Dr. P
>>tells us about is the only one that comes to mind, and that worked!
>>And they have definitely worked in animals. Are you aware of any
>>other human studies of any kind of topical antiandrogen for MPB,
>>whether it worked or not?
>>
>>Bryan
>
>No there is indeed a shortage of studies out there on this,as you have
>said.Women with androgenic alopecia also dont regrow hair,but can stop
>balding with oral antiandrogens.If women cant reverse balding much with
>antiandrogens,how can men expect to?
There you go confusing me again, Mike. I hope that last question
was a purely rhetorical one, since it's already been well established
that antiandrogen therapy doesn't regrow much hair; its value lies
mainly in halting further loss. But this is a valid goal of treatment,
as all the finasteride enthusiasts like to point out. So I'm not clear
why you tacked on those last two sentences. Was it just to make me
wonder if I'm missing an important point? :-)
>But in my opinion there have prolly been alot of mini-trials thru out
>the years in trying to reverse balding by doctors with topical
>antiandrogen formulations.The reason not many studies get done,is small
>scale it doesnt work,why invest in major dollar consuming studies when
>you already know the idea has been proved incorrect many times before?
>Step 1 is proving your theory at least works in someone.
>Step 2 is verifying that it is reproducable in a valid sample size.
>Step 3 is marketing
>
>We know that drugs can progress very rapidly from step 1 to step 3..fact.
>Minoxidil is one successful example of this and minoxidil _doesnt_ have
>near the "theory age" as androgen blocking.
>So my point is,antiandrogenic theories have been floating around much
>longer than minoxidil,yet look at all the minoxidil studies around,and
>lack of topical antiandrogen studies.Does this to you signal anything
>wrong with a kink in the development process?
No; I'm beginning to wonder if maybe you're correct about these
"mini-trials" having been done over the years! But the catch is,
what if they were looking for the wrong thing? What if they were
looking for obvious regrowth à la minoxidil? If so, these mini-trials
were doomed to fail. So they may have been expecting the wrong
result from the antiandrogens, without considering another important
alternative, much like you've been doing!
I'm really wondering if this has had something to do with the nearly
total lack of full-scale topical antiandrogen studies in humans.
Bryan
Bryan Shelton
>So, when it takes someone a year or longer to "respond" to finasteride,
>what does that mean? Does it mean that finally the suppressive forces
>of the drug have won the battle (and at that point the DHT has begun to
>be inhibited 65%)? Or, that after being inhibited from the time the
>person began taking the drug, finally an effect is being seen on the
>hair (follicles)?
Everybody (even non-responders) gets their DHT levels lowered
by that typical 65% within 24 hours of their first dose (well, it's
about 50% after the initial dose but then increases, typically,
to about 65% after successive doses). Your second sentence
is correct: eventually the effect is seen on the follicles after
a period of time.
>If everyone responds (it would seem from the get-go), as you say, it
>perplexes me why there is such a lag in some people seeing noticeable
>results.
It seems reasonable to me that after years of being ravaged by the
immune system, most follicles aren't immediately going to spring back
into action and start sprouting hair merely because you reduce the
amount of DHT to which they're exposed. In fact, from what we've
seen with the eunuchs, most such follicles *never* come back
without some external stimulation. That's why hair-count increases
from finasteride alone are quite modest compared to what you get
with topicals.
I think actual *loss* can continue for a while after starting finasteride
because the DHT reduction is not complete, but an intermediate value.
I think it takes a while for that active degenerative process that has
been going on for years to slowly burn itself out.
>Does anyone know what might inhibit the other 35% of type 2? I know
>there are a lot of 5AR inhibitors (including my mom), but which
>specifically work on type 2?
You mean the other 35% of DHT? You could almost certainly lower
blood levels a bit more by simply increasing the dose of finasteride,
but with a higher risk of side-effects. An early study of finasteride
found reductions of about 80% after single doses of 12.5 mg or
higher. A whole 5 mg tablet of Proscar every day would probably
get this done. An additional 15% reduction may not sound like
much, but it might be a critical extra boost for someone who is an
"outlier" and living on that "hairy edge". BTW, this same study claims
that finasteride will never achieve a reduction of more than 80% at
*any* dose because it cannot affect the amount supplied by the
testes, and this contribution is 20% of the total. I think that
dutasteride should be limited by this, too, since it is also a competitve
inhibitor of 5AR, but perhaps it will be able to pass the 80% barrier
by also inhibiting 5AR type 1.
All of this implies that blood levels of DHT are important in the
first place, which I doubt. If the pictures at the Revivogen site
are legitimate, then clearly blood levels of DHT are not an issue,
and it's the local suppression of DHT (by finasteride or Revivogen)
that does the trick. I tend to believe that the pictures are real.
If so, that might be the final piece of the puzzle: only locally
produced DHT from 5AR type 2 is responsible for hair-loss.
>And Bryan, I know you have gone over this many times before. But, by
>your argument, a non-finasteride taker would probably be inclined to
>start, since you make it look so promising to many individuals. So why
>don't you take it??
God, I've come full-circle now! I'm now seen as a promoter of finasteride!
There are two reasons I don't take it. The price is too high, in terms
of potential side-effects; the benefit/risk ratio is not high enough to get
me interested. Furthermore, I don't really *need* it. I'm maintaining
my hair just fine on Proxiphen, Prox-N, etc.
Bryan
doct...@my-deja.com
<E92EC016ABBD82F8.B3970320...@lp.airnews.net>,
The above is just one opinion and one assumption. If hair problem is a
multi-factor problem, for some people, DHT may not be the factor or DHT
may not be the major factor. Then, no mater how hard you try to reduce
the DHT level, it may not work for those people (For example, some
young men and young women under high stress). I do not rule out the
possibility, for some people, DHT level maybe a factor, even a major
factor. Be scientific, nothing is for 100% of people.
Albertwas
>.What we know is
>>>that only a few antiandrogens have shown any success in treating mpb
>>>and this in my opinion votes for a different way of working other than
>>>antiandrogenic.
Mike, it never ceases to amaze me
why you cannot make the distinction
between correcting the cause of
hairloss and correcting the *damage*
that has been done by that cause.
If you take it as given that eliminating
dht will eliminate hairloss, this does NOT
mean that eliminating dht will
correct the damage to folicles that
has already been done. Can
you not understand this? If not,
please explain.
albertw
Farrel
> Farrel,
>
> Were you an auto mechanic in a previous life?
>
>
though, most people seem to get the concept when I explain it to them in
these terms.
Farrel
>
> Farrel wrote:
>
> > Hairloss in people is always at different stages, there are so many
> > variables so thats why everyone responds differently to treatment.
> >
> > The best analogy with how Propecia works is to compare DHT to a brake
and
> > your hair to a car. If your car has recently stopped, by removing the
brake
> > it will easily start moving again.
> >
> > However if your car has been stationary for 5 years, chances are when
you
> > remove the brake, nothing will happen.
> >
> > Thats the reason, and if you are taking long to respond to Propecia you
> > should look at using other drugs and SODS to help "repair the engine"
> >
> > Farrel
> > --
> > HAIRTODAY.COM - Your One Stop Hair Loss Shop
> > http://www.hairtoday.com
> >
> > <donald...@my-deja.com> wrote in message
> > news:8aj33h$ure$1...@nnrp1.deja.com...
> > > So, when it takes someone a year or longer to "respond" to
finasteride,
> > > what does that mean? Does it mean that finally the suppressive forces
> > > of the drug have won the battle (and at that point the DHT has begun
to
> > > be inhibited 65%)? Or, that after being inhibited from the time the
> > > person began taking the drug, finally an effect is being seen on the
> > > hair (follicles)?
> > >
> > > If everyone responds (it would seem from the get-go), as you say, it
> > > perplexes me why there is such a lag in some people seeing noticeable
> > > results.
> > >
> > > Does anyone know what might inhibit the other 35% of type 2? I know
> > > there are a lot of 5AR inhibitors (including my mom), but which
> > > specifically work on type 2?
> > >
> > > And Bryan, I know you have gone over this many times before. But, by
> > > your argument, a non-finasteride taker would probably be inclined to
> > > start, since you make it look so promising to many individuals. So
why
> > > don't you take it??
> > >
> > >
mike
Its more complicated than that.How do you explain castration can perfectly
stop balding with no regrowth and almost 100% reduction in serum dht,
while propecia with 65% or so reduction can at least in some cause
regrowth? Yah,I know the standard answer is..the follicles with castrates
have more damage and therefore wont produce hair again...etc.Well what
makes castrates such a unique sample that excludes them from damage
blocking regrowth,or for that matter minoxidil?
What I'm saying is,certainly propecia patients have damaged follicles
too(going along with this theory..)what makes them regrow hair with
less dht reduction than castration?
Dont try telling me propecia is acting directly on the follicle too,the
studies show it topically not to work,so whatever propecia does is thru
systemic dht reduction or something else.Its the something else that looks
viable,because of this above mentioned analogy and say it...lack of
studies(gee wonder why?)
Plus I'm sure you know that if some drug works,studies follow.Minoxidil
didnt have any problem generating studies,why havent studies followed
with topical antiandrogens?
Can
>you not understand this? If not,
>please explain.
>
>albertw
I understand the concept,it just doesnt work.
Farrel
mike <emka...@dodgenet.com> wrote in message
news:8akctl$72s$3...@ins20.netins.net...
> "Farrel" <far...@my-deja.com> wrote:
> >Hairloss in people is always at different stages, there are so many
> >variables so thats why everyone responds differently to treatment.
> >
> >The best analogy with how Propecia works is to compare DHT to a brake and
> >your hair to a car. If your car has recently stopped, by removing the
brake
> >it will easily start moving again.
> >
> >However if your car has been stationary for 5 years, chances are when you
> >remove the brake, nothing will happen.
> >
> >Thats the reason, and if you are taking long to respond to Propecia you
> >should look at using other drugs and SODS to help "repair the engine"
> >
> >Farrel
> >--
> > HAIRTODAY.COM - Your One Stop Hair Loss Shop
> > http://www.hairtoday.com
> >
> Farrel that's a kind of cool analogy.Hope someday Dr.Gho will clone
> the whole "motor".
> Hey maybe this crude oil stuff on www.regrowth.com,isnt too far off.:)
>
Lets hope ;-) hey maybe this motor thing will give Spamcorp a new marketing
angle, since every motor needs oil to keep running maybe a snake oil is
needed to keep that motor running smoothly. <G>
Farrel
mike
>albe...@aol.com (Albertwas) wrote:
>>mike <emka...@dodgenet.com> wrote:
>>
>>>.What we know is
>>>>>that only a few antiandrogens have shown any success in treating mpb
>>>>>and this in my opinion votes for a different way of working other than
>>>>>antiandrogenic.
>>
>>Mike, it never ceases to amaze me
>>why you cannot make the distinction
>>between correcting the cause of
>>hairloss and correcting the *damage*
>>that has been done by that cause.
>>
>>If you take it as given that eliminating
>>dht will eliminate hairloss, this does NOT
>>mean that eliminating dht will
>>correct the damage to folicles that
>>has already been done.
>
>Its more complicated than that.How do you explain castration can perfectly
>stop balding with no regrowth and almost 100% reduction in serum dht,
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7679038&form=6&db=
m&Dopt=b
mike
>In article
><E92EC016ABBD82F8.B3970320...@lp.airnews.net>,
>br...@pointecom.net (Bryan Shelton) wrote:
>> On Mon, 13 Mar 2000 15:56:36 GMT, donald...@my-deja.com wrote:
>>
>finasteride,
>> >what does that mean? Does it mean that finally the suppressive forces
>> >of the drug have won the battle (and at that point the DHT has begun
>to
>> >be inhibited 65%)? Or, that after being inhibited from the time the
>> >person began taking the drug, finally an effect is being seen on the
>> >hair (follicles)?
>>
>> by that typical 65% within 24 hours of their first dose (well, it's
>> about 50% after the initial dose but then increases, typically,
>> to about 65% after successive doses). Your second sentence
>> is correct: eventually the effect is seen on the follicles after
>> a period of time.
>>
>> >perplexes me why there is such a lag in some people seeing noticeable
>> >results.
>>
>> immune system, most follicles aren't immediately going to spring back
>> into action and start sprouting hair merely because you reduce the
>> amount of DHT to which they're exposed. In fact, from what we've
>> seen with the eunuchs, most such follicles *never* come back
>> without some external stimulation. That's why hair-count increases
>> from finasteride alone are quite modest compared to what you get
>> with topicals.
>>
>> I think actual *loss* can continue for a while after starting
>finasteride
>> because the DHT reduction is not complete,
>Bryan,
>The above is just one opinion and one assumption. If hair problem is a
>multi-factor problem, for some people, DHT may not be the factor or DHT
>may not be the major factor. Then, no mater how hard you try to reduce
>the DHT level, it may not work for those people (For example, some
>young men and young women under high stress). I do not rule out the
>possibility, for some people, DHT level maybe a factor, even a major
>factor. Be scientific, nothing is for 100% of people.
>>but an intermediate value.
>> I think it takes a while for that active degenerative process that has
>> been going on for years to slowly burn itself out.
>>
>> >there are a lot of 5AR inhibitors (including my mom), but which
>> >specifically work on type 2?
>>
>> blood levels a bit more by simply increasing the dose of finasteride,
>> but with a higher risk of side-effects. An early study of finasteride
>> found reductions of about 80% after single doses of 12.5 mg or
>> higher. A whole 5 mg tablet of Proscar every day would probably
>> get this done. An additional 15% reduction may not sound like
>> much, but it might be a critical extra boost for someone who is an
>> "outlier" and living on that "hairy edge". BTW, this same study claims
>> that finasteride will never achieve a reduction of more than 80% at
>> *any* dose because it cannot affect the amount supplied by the
>> testes, and this contribution is 20% of the total. I think that
>> dutasteride should be limited by this, too, since it is also a
>competitve
>> inhibitor of 5AR, but perhaps it will be able to pass the 80% barrier
>> by also inhibiting 5AR type 1.
>>
reduces serum dht by greater than 90%.Remember propecia does grow hair
in some at 65%,while castration none at 90%.Might be other factors huh.;)
>> All of this implies that blood levels of DHT are important in the
>> first place, which I doubt. If the pictures at the Revivogen site
>> are legitimate, then clearly blood levels of DHT are not an issue,
>> and it's the local suppression of DHT (by finasteride or Revivogen)
>> that does the trick. I tend to believe that the pictures are real.
>> If so, that might be the final piece of the puzzle: only locally
>> produced DHT from 5AR type 2 is responsible for hair-loss.
>>
>> >And Bryan, I know you have gone over this many times before. But, by
>> >your argument, a non-finasteride taker would probably be inclined to
>> >start, since you make it look so promising to many individuals. So
>why
>> >don't you take it??
>>
>> God, I've come full-circle now! I'm now seen as a promoter of
>finasteride!
>>
>> There are two reasons I don't take it. The price is too high, in terms
>> of potential side-effects; the benefit/risk ratio is not high enough
>to get
>> me interested. Furthermore, I don't really *need* it. I'm maintaining
>> my hair just fine on Proxiphen, Prox-N, etc.
>>
>> Bryan
>>
>
>
Farrel
<doct...@my-deja.com> wrote in message news:8almol$sbp$1...@nnrp1.deja.com...
> In article
> <E92EC016ABBD82F8.B3970320...@lp.airnews.net>,
> br...@pointecom.net (Bryan Shelton) wrote:
> > On Mon, 13 Mar 2000 15:56:36 GMT, donald...@my-deja.com wrote:
> >
<SNIP>
>>Be scientific, nothing is for 100% of people
ROTFLMAO!! Be Scientific???, be scientific!!!!! hahahahahaha This is the
funniest thing I have heard Spamcorp say. Spamcorp, Bryan has made more
scientific statements in one single post than you have ever made in the
thousand or so posts you have made on this newsgroup.
Nice try Doctor LOL!!!!! When are you going to reveal your field of
expertise??? Never I'm sure, because you dont want everyone to know you are
not a medical doctor and have no medical training. Don't you know it is not
scientific to withhold this information LOL!!
You are however a doctor of something, so since you no longer call yourself
spnacorp I hereby rename you Dr Snake Oil.
Farrel
doct...@my-deja.com
Some other factors must exist. We need to find out. Hair problem is and
must be a multi-factor problem for both of men and women.
>
> >> All of this implies that blood levels of DHT are important in the
> >> first place, which I doubt.
DHT was not, is not and will be not single factor for this multi-factor
problem. Bryan, you should doubt it.
Farrel
news:8amk3k$hsi$1...@nnrp1.deja.com...
Dr Snake Oil
You seem to have made many comments on this thread, most often disputing the
role of DHT. You mention other factors which are common to both men and
women, what are these "factors" if they are not related to Androgens. Also
what are your qualifications, ie what field of study do you hold a PhD in?
And what does Ginseng have to do with this newsgroup since there is no
evidence that it helps hairloss in any way. Also, are you, or are you not
the same person who previously posted as spna...@atlantic.net
Looking forward to your answers that will not be forthcoming
Farrel
donald...@my-deja.com
> You mean the other 35% of DHT? You could almost certainly lower
> blood levels a bit more by simply increasing the dose of finasteride,
> but with a higher risk of side-effects. An early study of finasteride
> found reductions of about 80% after single doses of 12.5 mg or
> higher. A whole 5 mg tablet of Proscar every day would probably
> get this done. An additional 15% reduction may not sound like
> much, but it might be a critical extra boost for someone who is an
> "outlier" and living on that "hairy edge". BTW, this same study claims
> that finasteride will never achieve a reduction of more than 80% at
> *any* dose because it cannot affect the amount supplied by the
> testes, and this contribution is 20% of the total.
Why can't finasteride reduce the testes-produced DHT?
I think that
> dutasteride should be limited by this, too, since it is also a
competitve
> inhibitor of 5AR, but perhaps it will be able to pass the 80% barrier
> by also inhibiting 5AR type 1.
So type 1 is important in this hair loss process?? A post of yours from
a day or so ago I thought said type one is not important. You were
responding about why zinc and B6 are not important in Revivogen because
they inhibit the "wrong" enzyme. Are you now saying that perhaps type 1
does play at least a tiny part?
>
> All of this implies that blood levels of DHT are important in the
> first place, which I doubt. If the pictures at the Revivogen site
> are legitimate, then clearly blood levels of DHT are not an issue,
> and it's the local suppression of DHT (by finasteride or Revivogen)
> that does the trick. I tend to believe that the pictures are real.
> If so, that might be the final piece of the puzzle: only locally
> produced DHT from 5AR type 2 is responsible for hair-loss.
>
>
Doesn't finasteride inhibit 5AR in skin? Some?
Bryan Shelton
>This 80% barrier is pure fiction.Check the pubmed study showing
>castration reduces serum dht by greater than 90%.
Mike, the study I was referring to was not talking about extreme
things like castration. It was referring specifically to competitively
blocking 5AR type 2, and they simply pointed out that any such
blocker is very unlikely to have any significant effect on the DHT
produced in the testes because the concentration of testosterone
in the testes is 100X the level in the blood. So you can't get enough
of the blocker into the testes to have an effect, and there will always
be that upper 80% limit when using a type 2 *blocker*.
>Remember propecia does grow hair in some at 65%,
>while castration none at 90%.Might be other factors huh.;)
I have some comments about this, too, which I'll address a little
later. I'm a little pressed for time at the moment...
Bryan
donald...@my-deja.com
<00CA1D31B6BACB8B.CD6EDE7D...@lp.airnews.net>,
br...@pointecom.net (Bryan Shelton) wrote:
> On 14 Mar 2000 20:57:09 GMT, mike <emka...@dodgenet.com> wrote:
>
>
> Mike, the study I was referring to was not talking about extreme
> things like castration. It was referring specifically to competitively
> blocking 5AR type 2, and they simply pointed out that any such
> blocker is very unlikely to have any significant effect on the DHT
> produced in the testes because the concentration of testosterone
> in the testes is 100X the level in the blood. So you can't get enough
> of the blocker into the testes to have an effect, and there will
always
> be that upper 80% limit when using a type 2 *blocker*.
>
>
concerned. If that 20% stays in the testes, then it certainly won't be
affecting scalp hair loss. Plus, aren't we more concerned about the dHT
conversion in skin?
Bryan Shelton
>br...@pointecom.net (Bryan Shelton) wrote:
>> Mike, the study I was referring to was not talking about extreme
>> things like castration. It was referring specifically to competitively
>> blocking 5AR type 2, and they simply pointed out that any such
>> blocker is very unlikely to have any significant effect on the DHT
>> produced in the testes because the concentration of testosterone
>> in the testes is 100X the level in the blood. So you can't get enough
>> of the blocker into the testes to have an effect, and there will always
>> be that upper 80% limit when using a type 2 *blocker*.
>>
>If that's the case, then 80% is really 100% as far as hair loss is
>concerned. If that 20% stays in the testes, then it certainly won't be
>affecting scalp hair loss.
No, no! That 20% *doesn't* stay in the testes. Out of all of the
DHT found in the blood, about 20% of it comes from the prostate,
about 20% of it comes from the testes, and the rest comes from
various other sources. The article was saying that you can greatly
reduce DHT production from 5AR type 2 from all sources in the body
EXCEPT for the testes. Finasteride (and dutasteride, it seems to me)
will never be able to affect that one source to any significant degree.
>Plus, aren't we more concerned about the dHT conversion in skin?
Yes; _I_ am, anyway, although others may not agree. I was just
mentioning this stuff about blood levels of DHT for the sake
of completeness and for the people who still think blood levels
are important.
Bryan
Bryan Shelton
>> You mean the other 35% of DHT? You could almost certainly lower
>> blood levels a bit more by simply increasing the dose of finasteride,
>> but with a higher risk of side-effects. An early study of finasteride
>> found reductions of about 80% after single doses of 12.5 mg or
>> higher. A whole 5 mg tablet of Proscar every day would probably
>> get this done. An additional 15% reduction may not sound like
>> much, but it might be a critical extra boost for someone who is an
>> "outlier" and living on that "hairy edge". BTW, this same study claims
>> that finasteride will never achieve a reduction of more than 80% at
>> *any* dose because it cannot affect the amount supplied by the
>> testes, and this contribution is 20% of the total.
>
>Why can't finasteride reduce the testes-produced DHT?
Finasteride works by competing with testosterone at the 5AR molecule.
The finasteride molecules "crowd out" the testosterone molecules and
end up joining with 5AR type 2 instead of the testosterone, so no DHT
can be produced as a result. But there is an extremely high concentration
of testosterone in the testes (100 times the concentration found in the
blood!), and the *finasteride* is the one that gets "crowded out", with
continuing production of DHT.
>>I think that dutasteride should be limited by this, too, since it is
>>also a competitve inhibitor of 5AR, but perhaps it will be able
>>to pass the 80% barrier by also inhibiting 5AR type 1.
>
>So type 1 is important in this hair loss process?? A post of yours from
>a day or so ago I thought said type one is not important. You were
>responding about why zinc and B6 are not important in Revivogen because
>they inhibit the "wrong" enzyme. Are you now saying that perhaps type 1
>does play at least a tiny part?
No, no; I still think type 2 is the critical one! I just included the above
remarks for the sake of completeness, and for the people who continue
to think that blood levels are important. BTW, I reserve the right to change
my views (again) if more information comes out. We're all kinda groping
in the dark on a lot of these issues!
>> All of this implies that blood levels of DHT are important in the
>> first place, which I doubt. If the pictures at the Revivogen site
>> are legitimate, then clearly blood levels of DHT are not an issue,
>> and it's the local suppression of DHT (by finasteride or Revivogen)
>> that does the trick. I tend to believe that the pictures are real.
>> If so, that might be the final piece of the puzzle: only locally
>> produced DHT from 5AR type 2 is responsible for hair-loss.
>>
>Doesn't finasteride inhibit 5AR in skin? Some?
Sure, or else it wouldn't have any effect on MPB, IMHO! ;-)
Bryan
Randall Parker
> So, when it takes someone a year or longer to "respond" to finasteride,
> what does that mean? Does it mean that finally the suppressive forces
> of the drug have won the battle (and at that point the DHT has begun to
> be inhibited 65%)? Or, that after being inhibited from the time the
> person began taking the drug, finally an effect is being seen on the
> hair (follicles)?
Donald,
Here's a slightly different car brake analogy: If you are going 100 mph and you apply enough braking action that the braking action is doing more to slow the car than the engine is doing to move it you will eventually stop.
However, just how heavily you apply the brake will determine just how soon you come to a stop.
A given amount of 5AR inhibitor is a different amount of braking than it is for others.
Also, since the DHT is a signal for a series of events that cause hair loss when you cut out the signal there is still considerable lag before all the follow-on effects stop as well.
> If everyone responds (it would seem from the get-go), as you say, it
> perplexes me why there is such a lag in some people seeing noticeable
> results.
It shouldn't be too surprising if you think about it. The growth of a hair and its loss and then the starting of the growth of a new hair is measured in months. Intervention in hair loss is not intervention in a high frequency system. Also, I think that for different people the stages are probably of different length.
> Does anyone know what might inhibit the other 35% of type 2? I know
> there are a lot of 5AR inhibitors (including my mom), but which
> specifically work on type 2?
>
> And Bryan, I know you have gone over this many times before. But, by
> your argument, a non-finasteride taker would probably be inclined to
> start, since you make it look so promising to many individuals. So why
> don't you take it??
Topical treatments have fewer systemic effects. They are safer. Since there are many useful topical treatments someone who wants to avoid long term side effects may opt to use topicals only.
Randall Parker
> That's completely the opposite to what I think is the key ingredients
> in revivogen.Zinc & b6 have glucocorticoid antagonistic properties as
> well as androgen blocking.This in my opinion makes them more valuable
> than anything else in the formulation.This zinc/b6 solution is talked
> about at:www.mindspring.com/~bupper1/index.htm
So one could make one's own equivalent by putting zinc and B6 into a cream?
Isn't Desitin ointment made from zinc oxide? Couldn't one just add B6 powder to that ointment and apply it?
Randall Parker
> Well, Mike, we'll have to agree to disagree on this! :-)
> It's funny, isn't it, how we've split into these two opposing points of view?
> I think it's pure speculation as to whether or not these glucocorticoid
> antagonistic properties would have any actual benefit for human MPB.
> And the androgen blocking in the case of zinc and B6 is the *wrong*
> androgen, in a manner of speaking, so I'm rather indifferent to these
> two ingredients.
Well, if anyone here is even slightly adventurous you could make up your own cream that contains zinc and B6 and just apply it to one side of your head. Then report back what the results are in a few months.
Randall Parker
> The reason people dont progress further in the development process is
> the idea isnt working!
That's one reason.
>Lets say I said to you pumpkin seed extract was
> an excellent pain killer.The first thing would be to try and reproduce
> what I said.The fact is small scale you cant do it,do you want to invest
> in a large scale study failure?
Even if the pumpkin seed extract worked it wouldn't get the investment due to intellectual property issues. No one wants to spend the money to provide something works unless they can get exclusive rights to sell it.
Randall Parker
> >
> > Is this true? If so, how can one convert fatty acids to free form?
> >
> > Is the problem that they are esters?
>
> Yeah -- what does this actually mean? How does one determine if these oils
> (GLA's/LA's) are at least 1% free fatty acids in natural form? Are we just
> talking topically here as well?
My vague recollection from undergrad organic chem and biochem classes is that acid solutions should de-esterify these fatty acids.
So a little vinegar to make GLA be in the right form for topical application?
Randall Parker
> If that's the case, then 80% is really 100% as far as hair loss is
> concerned. If that 20% stays in the testes, then it certainly won't be
> conversion in skin?
You are confusing testosterone and DHT. The high concentration of testosterone in the testes makes it very hard for finasteride to compete with it to bind with 5AR.
But then once the testosterone has been converted to DHT in the testes part of the DHT enters the blood.
So the real problem is that finasteride can't achieve a high enough concentration in the testes where testosterone is in a much higher concentration.
Albertwas
>>Its more complicated than that.How do you explain castration can perfectly
>>stop balding with no regrowth and almost 100% reduction in serum dht,
> correction ^^^ insert >90%
>
>http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7679038&form=6&db=
>m&Dopt=b
>
>
I tried this url but got a "bad or missing
data base" message.
albertw
Albertwas
> (Albertwas) wrote:
>>mike <emka...@dodgenet.com> wrote:
>>
>>>.What we know is
>>>>>that only a few antiandrogens have shown any success in treating mpb
>>>>>and this in my opinion votes for a different way of working other than
>>>>>antiandrogenic.
>>
>>Mike, it never ceases to amaze me
>>why you cannot make the distinction
>>between correcting the cause of
>>hairloss and correcting the *damage*
>>that has been done by that cause.
>>
>>If you take it as given that eliminating
>>dht will eliminate hairloss, this does NOT
>>mean that eliminating dht will
>>correct the damage to folicles that
>>has already been done.
>
>Its more complicated than that.How do you explain castration can perfectly
>stop balding with no regrowth and almost 100% reduction in serum dht,
>while propecia with 65% or so reduction can at least in some cause
>regrowth? Yah,I know the standard answer is..the follicles with castrates
>have more damage and therefore wont produce hair again...etc.Well what
>makes castrates such a unique sample that excludes them from damage
>blocking regrowth,or for that matter minoxidil?
Well, what exactly *do* we know about the Norwood
stages of castrates that were studied?
(thanks for responding by the way. at least i
finally see where you are coming from).
>What I'm saying is,certainly propecia patients have damaged follicles
>too(going along with this theory..)what makes them regrow hair with
>less dht reduction than castration?
>Dont try telling me propecia is acting directly on the follicle too,the
>studies show it topically not to work,so whatever propecia does is thru
>systemic dht reduction
no dispute here, or by anyone who's been reading
about finasteride on this group for the past few years,
I would think. yes, propecia's impact on hairloss is
a result of systemic dht reduction. has this ever
been in question??
>or something else.Its the something else that looks
>viable,because of this above mentioned analogy and say it...lack of
>studies(gee wonder why?)
okay, you lost me here. you're writing is unclear.
what do you mean, lack of studies? how do
you think Merck got propecia approved?
Are you saying that dht's impact on mpb sensitive
folicles is only part of the attack, or is not part
of it whatsoever?
Stay with me here and respond to this, please, Mike.
I would like to know where you are coming from
on this. Bryan, have you figured it out? I think
it may be just a matter of getting the communication clear.
>Plus I'm sure you know that if some drug works,studies follow.Minoxidil
>didnt have any problem generating studies,why havent studies followed
>with topical antiandrogens?
Because you are talking *topical*. Didn't Merck (or
study) find that *topical* finasteride didn't have
the same impact as oral?
albertw
mike
Part of it,but my feeling is thru indirectly regulating other systems,
maybe the prostate.Everyone is aware that pseudohermaphrodites who are
type 2 deficient dont bald,they also have incompletely developed
prostates.Since we know that topically finasteride a
type 2 inhibitor wont regrow hair,but orally it will.This points to SERUM
dht as the culprit or culprit mediator in balding.
What could be happening?
My guess is that injecting dht or testosterone will cause hypertrophy
of the prostate,it does.The prostate may be intervening into what it
"thinks" is the start of a cancerous lesion.Dht may be initiating a higher
prostatic tgf beta1 level,since tgf beta1 causes apoptosis.Tgf beta1 also
causes apoptosis in dermal papilla.The serum tgf beta1 levels are elevated
in bph,strong associations exist between bph & mpb .Is tgf beta1 acting on
dermal papilla in the scalp?
This prostate initiated balding seems to explain the contradictory dht
evidence.This is, propecia only lowers serum dht by 65%,castration by 90%.
Yet castration doesnt regrow hair but propecia does,how could this be?
Castration doesnt cause the prostatic involution that finasteride does.
These differences may involve prostatic tgf beta 1 levels and serum tgf
beta 1.
So then what if prostatic and then subsequently serum tgf beta1 reaches
the dermal papilla,what would happen?
Tgf beta 1 is pro-apoptotic while dht actually is anti-apoptotic.Check
into Sjogrens sydrome studies,it will show dht to be
anti-apoptotic.Afterall dht_causes_ tissue overgrowth in the prostate,so
it is acting anti-apoptotically.Actually invitro studies on dermal
papilla show the same thing,dht is increasing dna synthesis and acting
anti-apoptotically.
Maybe we're just seeing an increase in scalp dht to offset the apoptotic
tgf beta1?If that's the case do we really want to block dht at the scalp?
As Dr.P points out tgf beta1 & NO are heavily interrelated.The only 2
drugs to my knowledge that prevent balding are topical 5% minoxidil and
anti-androgens.The cyproterone acetate study on mice prevented androgenic
alopecia for them but was thought to be thru systemic means as stated
by the researchers.In other words the topical antiandrogen didnt act
on the dermal papilla directly,could this be due to an antiandrogenic
effect on the prostate and tgf beta1 levels in the prostate? Cyproterone
acetate does have the effect of reducing cortisol as does 4MA as does
chronic cyclosporin,as does phenytoin.So maybe cortisol is involved too?
Something else:
I might add in that niddm which has been associated to mpb also has
been thought to be partly causal in bph.Niddm could be caused by
hypercortisolism,so its all related somehow.
Bryan Shelton
>Its more complicated than that.How do you explain castration can perfectly
>stop balding with no regrowth and almost 100% reduction in serum dht,
>while propecia with 65% or so reduction can at least in some cause
>regrowth? Yah,I know the standard answer is..the follicles with castrates
>have more damage and therefore wont produce hair again...etc.Well what
>makes castrates such a unique sample that excludes them from damage
>blocking regrowth,or for that matter minoxidil?
>What I'm saying is,certainly propecia patients have damaged follicles
>too(going along with this theory..)what makes them regrow hair with
>less dht reduction than castration?
Mike, what's causing this confusion is your basic premise that castrates
don't regrow hair, while Propecia users do. If necessary, go back and
re-read that post, "The effect of castration on hair-loss". Hamilton
never said in that article that the castrates had NO hair regrowth, just
that there wasn't a whole lot of it. Hamilton didn't have the benefit
of all that high-tech equipment that Merck had to precisely measure
hairs; he only did comparisons between the patients and their old
photographs. So we'll never be able to settle this issue for sure,
but it has always been my assumption that the castrates very likely
DID grow a bit more hair than Propecia users, in addition to having
a complete halting of further loss.
Bryan
Bryan Shelton
>albe...@aol.com (Albertwas) wrote:
>>Are you saying that dht's impact on mpb sensitive
>>folicles is only part of the attack, or is not part
>>of it whatsoever?
>
>Part of it,but my feeling is thru indirectly regulating other systems,
>maybe the prostate. Everyone is aware that pseudohermaphrodites
>who are type 2 deficient dont bald, they also have incompletely
>developed prostates. Since we know that topically finasteride a
>type 2 inhibitor wont regrow hair, but orally it will. This points to
>SERUM dht as the culprit or culprit mediator in balding.
Phooey! Mike, you keep pointing to this one single study about
topical finasteride! But it doesn't impress me because there are
at least a couple of reasons that could explain the negative results.
What if there's some problem with the "pharmacodynamics", as Dr. P
would say? What if the finasteride in a topical solution is absorbed
so rapidly and completely into the bloodstream that it's unable to have
a sufficient effect on the local follicles?
More importantly, I have very grave suspicions about the overall design
of this study. We've only seen the abstract, so we don't know the nitty-
gritty details, like how long the study ran and what kind of results they
were looking for. Suppose they were looking for obvious regrowth, and
the study only ran for six weeks? What is the likelihood of success
given those constraints? Not very high, I'd say.
We know from the Merck Propecia trial that oral finasteride requires
a year to see pretty much full results on average, with some outliers
requiring up to a couple of years. Moreover, the improvement is subtle
enough (less than 10% average improvement in hair-counts) that while
it was clear to the high-tech measuring equipment, it was rather less
clear to the patients themselves and even to the doctors doing the
investigator assessment, because there were still things like placebo
effects when humans were involved.
Do you think the authors of that topical finasteride study used as much
rigor and precision as the Merck doctors did? Did it go for even ONE
year, much less two? Did they use the same scanning equipment and
hair-counting software that allowed Merck to get a remarkable precision
of plus or minus 3.4 hairs out of a starting baseline of 876 hairs? I rather
doubt this. The topical finasteride study may have been too quick-and-dirty
to see a positive result.
Besides, we have an apparent refutation of the "serum DHT" theory
in the form of those pictures at the Revivogen site. Assuming they
are real, then it's hard to deny that local DHT from 5AR type 2 is
the culprit in hairloss, not serum DHT. Apparently GLA and ALA
were able to block DHT when applied topically, while finasteride wasn't.
>What could be happening?
>My guess is that injecting dht or testosterone will cause hypertrophy
>of the prostate,it does.The prostate may be intervening into what it
>"thinks" is the start of a cancerous lesion.Dht may be initiating a higher
>prostatic tgf beta1 level,since tgf beta1 causes apoptosis.Tgf beta1 also
>causes apoptosis in dermal papilla.The serum tgf beta1 levels are elevated
>in bph,strong associations exist between bph & mpb .Is tgf beta1 acting on
>dermal papilla in the scalp?
>
>This prostate initiated balding seems to explain the contradictory dht
>evidence.
"Prostate initiated balding"?? Mike, have you been smoking
funny cigarettes? :-) Remember that 20 year-olds don't have
enlarged prostates!
>This is, propecia only lowers serum dht by 65%,castration by 90%.
>Yet castration doesnt regrow hair but propecia does,how could this be?
I've responded to this in another post. No need to summon forth a
"prostate initiated balding" theory. (Shiver...)
>Castration doesnt cause the prostatic involution that finasteride does.
Are you sure about this? I would have strongly expected that it DOES.
>These differences may involve prostatic tgf beta 1 levels and serum tgf
>beta 1.
>
>So then what if prostatic and then subsequently serum tgf beta1 reaches
>the dermal papilla,what would happen?
>Tgf beta 1 is pro-apoptotic while dht actually is anti-apoptotic.Check
>into Sjogrens sydrome studies,it will show dht to be
>anti-apoptotic.Afterall dht_causes_ tissue overgrowth in the prostate,so
>it is acting anti-apoptotically.Actually invitro studies on dermal
>papilla show the same thing,dht is increasing dna synthesis and acting
>anti-apoptotically.
>Maybe we're just seeing an increase in scalp dht to offset the apoptotic
>tgf beta1?If that's the case do we really want to block dht at the scalp?
Again, explain the Revivogen results!
>As Dr.P points out tgf beta1 & NO are heavily interrelated.The only 2
>drugs to my knowledge that prevent balding are topical 5% minoxidil and
>anti-androgens.The cyproterone acetate study on mice prevented androgenic
>alopecia for them but was thought to be thru systemic means as stated
>by the researchers.In other words the topical antiandrogen didnt act
>on the dermal papilla directly,could this be due to an antiandrogenic
>effect on the prostate and tgf beta1 levels in the prostate?
What is this study? I'd like to read the whole thing...
Bryan
mike
>On 16 Mar 2000 07:08:37 GMT, mike <emka...@dodgenet.com> wrote:
>
>>albe...@aol.com (Albertwas) wrote:
>>>Are you saying that dht's impact on mpb sensitive
>>>folicles is only part of the attack, or is not part
>>>of it whatsoever?
>>
>>Part of it,but my feeling is thru indirectly regulating other systems,
>>maybe the prostate. Everyone is aware that pseudohermaphrodites
>>who are type 2 deficient dont bald, they also have incompletely
>>developed prostates. Since we know that topically finasteride a
>>type 2 inhibitor wont regrow hair, but orally it will. This points to
>>SERUM dht as the culprit or culprit mediator in balding.
>
>Phooey! Mike, you keep pointing to this one single study about
>topical finasteride! But it doesn't impress me because there are
>at least a couple of reasons that could explain the negative results.
>
>What if there's some problem with the "pharmacodynamics", as Dr. P
>would say? What if the finasteride in a topical solution is absorbed
>so rapidly and completely into the bloodstream that it's unable to have
>a sufficient effect on the local follicles?
Oh my!Do you really believe this absorption with no uptake into dermal
papilla,and I thought absorption was a good thing?
>
>More importantly, I have very grave suspicions about the overall design
>of this study. We've only seen the abstract, so we don't know the nitty-
>gritty details, like how long the study ran and what kind of results they
>were looking for. Suppose they were looking for obvious regrowth, and
>the study only ran for six weeks? What is the likelihood of success
>given those constraints? Not very high, I'd say.
>
Of course failure to believe a study because it doesnt "fit",it prolly
doesnt fit your theory.I dont think denying studies is the way to
go about things,but whatever.Which other ones should we toss out? ;)
Who says? Benign hypertrophy could be a post puberty thing as far as you
know,just not full blown.What makes teenagers immune from other things
such as arterial plaque buildup studies as I posted before.These are
not full blown problems but just the start of heart disease,may still take
60 years to get ya,but started initially in the teenage years.
Are 20 year olds immune from aging in general or does that just occur
late in life? ;)
>>This is, propecia only lowers serum dht by 65%,castration by 90%.
>>Yet castration doesnt regrow hair but propecia does,how could this be?
>
>I've responded to this in another post. No need to summon forth a
>"prostate initiated balding" theory. (Shiver...)
>
You again have failed to explain how a 65% reduction can cause hair
regrowth,check www.propecia.com,while a 90% reduction via castration
doesnt.(double shiver)
I know you think type2 reductase at the dermal papilla causes balding,
but the topical finasteride and serum dht study on mice argue otherwise.
Will this be the second abstract you toss out? ;) (posted at bottom)
>>Castration doesnt cause the prostatic involution that finasteride does.
>
>Are you sure about this? I would have strongly expected that it DOES.
>
Not as much,as intraprostatic dht levels in castration are still present,
in finasteride virtually nil.
>>These differences may involve prostatic tgf beta 1 levels and serum tgf
>>beta 1.
>>
>>So then what if prostatic and then subsequently serum tgf beta1 reaches
>>the dermal papilla,what would happen?
>>Tgf beta 1 is pro-apoptotic while dht actually is anti-apoptotic.Check
>>into Sjogrens sydrome studies,it will show dht to be
>>anti-apoptotic.Afterall dht_causes_ tissue overgrowth in the prostate,so
>>it is acting anti-apoptotically.Actually invitro studies on dermal
>>papilla show the same thing,dht is increasing dna synthesis and acting
>>anti-apoptotically.
>>Maybe we're just seeing an increase in scalp dht to offset the apoptotic
>>tgf beta1?If that's the case do we really want to block dht at the scalp?
>
>Again, explain the Revivogen results!
You believe the topical antiandrogen studies of revivogen as significant,
I dont attribute antiandrogens as the working factor in revivogen.
Zinc & b6 coincidentally block the glucocorticoid receptor,dont know
how the GR plays into balding but suspect its apoptosis related too.
I know you'll bring up spiro again,check it out,a mild glucocorticoid
antagonist.
>
>>As Dr.P points out tgf beta1 & NO are heavily interrelated.The only 2
>>drugs to my knowledge that prevent balding are topical 5% minoxidil and
>>anti-androgens.The cyproterone acetate study on mice prevented androgenic
>>alopecia for them but was thought to be thru systemic means as stated
>>by the researchers.In other words the topical antiandrogen didnt act
>>on the dermal papilla directly,could this be due to an antiandrogenic
>>effect on the prostate and tgf beta1 levels in the prostate?
>
>What is this study? I'd like to read the whole thing...
>
>Bryan
Heres the study:
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2774656&form=6&db=
m&Dopt=b
Let me guess...I'll bet there's some design flaw in the study.
mike
You dont need hair count studies on the propecia site to see that they
grew hair. www.propecia.com
Was Hamilton blind? Here's the segment you posted...1 out 21 regrew any
hair and that was on the crown.Propecia even regrows up front where
castration didnt,not alot but certainly observable,and thats with
a 25% disadvantage in serum dht.
A study of 21 adolescent and young adult males, before castration and for
eight to eighteen years afterwards, showed that after orchiectomy there
was no development of male pattern baldness (MPB) nor of any grossly
recognizable denudation of the scalp. There was no expansion of bald
areas in existence at the time of castration. At the end of the study the
eunuchs, compared with intact males of similar age, exhibited a
significantly lower incidence of MPB (P=.01) and had no further loss of
coarse hairs in the pattern that in most males results in recession of the
frontal hairline (P<.01). After castration, ______no increase in the
number of coarse hairs was detected in bald or sparsely-haired areas of
the frontal hairline. It is concluded that the remedial value of drastic
reduction in androgenic stimulation is ***probably nil**** _____with
regard to return of coarse hairs which have been lost along the frontal
hairline in young men. In 3 men with baldness of the crown of the head at
the time of orchiectomy, a limited increase in the number of coarse hairs
occurred after the operation in 1 but not in the others. Further study is
required to ascertain the potential for partial regrowth of coarse hairs
in subjects with late-appearing forms of MPB involving the dorsum of the
head."
Fuzz
honkee00 <honk...@earthlink.net> wrote in message
news:38CD92B1...@earthlink.net...
> > Although we can't seem to get our hands on any studies of topical
> > spironolactone being used for hair loss, we can make an educated guess
that it
> > should be pretty effective at halting its progression. For one, we've
got
> > anecdotal evidence from Dr. Lee that 5% minox + 2% spiro is at least as
> > effective as 5% minox + finasteride. There are also numerous studies
showing
> > topical spiro is effective against androgen-related skin disorders such
as
> > acne, which means it should do the same for baldness. Finally, we've
seen that
> > topical RU58841 is perfectly capable of reversing hair loss in stumptail
> > macaques (not humans, but as close as you can get....). Assuming RU is
just an
> > antiandrogen and possesses no additional growth stimulating properties,
spiro
> > should be able to do just as well, as it has a comparable affinity for
androgen
> > receptors. -Mitch
What is the consensus on copper acting as a topical DHT (5AR)
reducer --mentioned at www.skinbiology.com?
I was always curious as to this claim. I have read the study where copper
was the best metal at reducing 5AR type 1 and 2, then zinc I believe. I
like Folligen for its SOD activity, but can it actually inhibit DHT
topically?
--Fuzz
Bryan Shelton
>br...@pointecom.net (Bryan Shelton) wrote:
>>Mike, what's causing this confusion is your basic premise that castrates
>>don't regrow hair, while Propecia users do. If necessary, go back and
>>re-read that post, "The effect of castration on hair-loss". Hamilton
>>never said in that article that the castrates had NO hair regrowth, just
>>that there wasn't a whole lot of it. Hamilton didn't have the benefit
>>of all that high-tech equipment that Merck had to precisely measure
>>hairs; he only did comparisons between the patients and their old
>>photographs. So we'll never be able to settle this issue for sure,
>>but it has always been my assumption that the castrates very likely
>>DID grow a bit more hair than Propecia users, in addition to having
>>a complete halting of further loss.
>>
>>Bryan
>
>You dont need hair count studies on the propecia site to see
>that they grew hair. www.propecia.com
Mike, *everybody* shows their best subjects with the most impressive
results. Merck does it. Revivogen does it. Even Dr. P does it.
(Sung to the tune of: "Birds do it...bees do it...even educated fleas
do it!") :-)
>Was Hamilton blind? Here's the segment you posted...1 out of 21
>regrew any hair and that was on the crown. Propecia even regrows
>up front where castration didnt, not a lot but certainly observable,
>and that's with a 25% disadvantage in serum dht.
The "anterior" Propecia study was done not on the hairline itself,
the most difficult part of the scalp of all, but only on the top of the
scalp *toward* the frontal area. And how did it do? It regrew the
underwhelming average of only 9.6 hairs per square centimeter.
I suggest to you that Mr. Hamilton would be hard-pressed to notice
a modest change of this magnitude while comparing patients with
their decades-old photographs. Modern automated technology
can do it, but one poor fellow looking at old photos? No way.
Not to mention that Hamilton had only three patients with loss
on the crown, one of which showed a detectable hair increase.
Three patients? Hardly a statistically significant sample. Perhaps
a larger sample would have done considerably better than one out
of three. And the rest of them with no noticeable extra hair on the
very front hairline? Not surprising that nothing was observable
here, which would be expected to be even more sparsely re-populated
than in the front hairline.
Mike, there just isn't enough evidence here to believe that there
is some kind of DHT "paradox" here, that Propecia does any better
than castration did in Hamilton's limited study of eunuchs.
Bryan
Bryan Shelton
>And the rest of them with no noticeable extra hair on the
>very front hairline? Not surprising that nothing was observable
>here, which would be expected to be even more sparsely re-populated
>than in the front hairline.
OOPS! I meant, of course, "...which would be expected to be even more
sparsely re-populated that the frontal area of the crown."
Bryan
Bryan Shelton
>br...@pointecom.net (Bryan Shelton) wrote:
>>
>>>As Dr.P points out tgf beta1 & NO are heavily interrelated.The only 2
>>>drugs to my knowledge that prevent balding are topical 5% minoxidil and
>>>anti-androgens.The cyproterone acetate study on mice prevented androgenic
>>>alopecia for them but was thought to be thru systemic means as stated
>>>by the researchers.In other words the topical antiandrogen didnt act
>>>on the dermal papilla directly,could this be due to an antiandrogenic
>>>effect on the prostate and tgf beta1 levels in the prostate?
>>
>>What is this study? I'd like to read the whole thing...
>>
>>Bryan
>
>Heres the study:
>http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2774656&form=6&db=
>m&Dopt=b
>
>Let me guess...I'll bet there's some design flaw in the study.
Hmmm...they've clearly demonstrated that cyproterone acetate
IS absorbed systemically, but they don't state in the abstract
why they think that the hair-loss inhibition is by THAT route
rather than the topical route. Might be good to read the whole
study.
Bryan
mike
>On 16 Mar 2000 19:47:00 GMT, mike <emka...@dodgenet.com> wrote:
>
>>br...@pointecom.net (Bryan Shelton) wrote:
>>>
>>>>drugs to my knowledge that prevent balding are topical 5% minoxidil and
>>>>anti-androgens.The cyproterone acetate study on mice prevented androgenic
>>>>alopecia for them but was thought to be thru systemic means as stated
>>>>by the researchers.In other words the topical antiandrogen didnt act
>>>>on the dermal papilla directly,could this be due to an antiandrogenic
>>>>effect on the prostate and tgf beta1 levels in the prostate?
>>>
>>>What is this study? I'd like to read the whole thing...
>>>
>>>Bryan
>>
>>Heres the study:
>>http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2774656&form=6&db=
>>m&Dopt=b
>>
>>Let me guess...I'll bet there's some design flaw in the study.
>
>IS absorbed systemically, but they don't state in the abstract
>why they think that the hair-loss inhibition is by THAT route
>rather than the topical route. Might be good to read the whole
>study.
>
>Bryan
concentration topicals and they had no effect,the prevention only occurred
at a 5% or greater concentration which he noted systemic absorbtion.
mike
>On 16 Mar 2000 19:55:04 GMT, mike <emka...@dodgenet.com> wrote:
>
>>br...@pointecom.net (Bryan Shelton) wrote:
>very front hairline? Not surprising that nothing was observable
>here, which would be expected to be even more sparsely re-populated
>than in the front hairline.
>
>is some kind of DHT "paradox" here, that Propecia does any better
>than castration did in Hamilton's limited study of eunuchs.
>
>Bryan
Heres a quote from Dr.P about this:
Perhaps 100K males a year get castrated ( more
recently, with testicular suppression ), generally for prostate cancer.
There are no particular reports about much baldness reversal, but I'll
bet they generally don't get a lot balder either..,
Peter H. Proctor, PhD, MD
http://www.drproctor.com
So I still feel a discrepancy exists between castration and finasteride,
certainly we can see a difference in some on finasteride,NO HAIR COUNTS
ARE NEEDED,its obvious.But what isnt obvious is balding reversal in
castrates,else you would get someone occasionally reporting this.
MARK DORAN
can't put this sentence out of my mind:
>>
>>Mike, *everybody* shows their best subjects with the most impressive
>>results. Merck does it. Revivogen does it. Even Dr. P does it.
Not because I want to object that *Spnacorp* -doesn't- do it, but because
I'm not all that impressed by two of the three Revivogen pictures. If you
get a moment, please have another peep at them... Makes me wonder what
*average* results would be like...
Mark D.
HairTalk
<92C94CBEB50DF082.CA011E9D...@lp.airnews.net>,
br...@pointecom.net (Bryan Shelton) wrote:
> On Sun, 12 Mar 2000 16:54:09 GMT, donald...@my-deja.com wrote:
>
> >Bryan, how do they come up with the statement that only type 2 is
> >responsible for hair loss. If they are getting that solely from
hearing
> >that finasteride users halt hair loss, then that is not sufficient
> >argument.
>
> Oops! I should have made crystal clear that _I_ am the one
> making that claim, not the folks at Revivogen. I don't have any
> idea what their thoughts are on this issue, but lately I've really
> been re-thinking my own position and this is now what I believe.
>
> And off the top of my head, here are three good reasons:
>
> 1) Yes, finasteride halts hair-loss (at least in most people). Its
> activity is almost entirely against 5AR type 2, and only minimally
> against 5AR type 1.
>
> 2) The medical journal article that I quoted from extensively
> recently demonstrated that 5AR type 2 is indeed the major
> player in the follicle itself, including the all-important dermal
papilla.
>
> 3) Last, and certainly not least, is the fact that 5AR-deficient
> pseudohermaphrodites, who never go bald, are deficient ONLY in
> 5AR type 2. They have perfectly *normal* levels of 5AR type 1.
>
> These three facts taken together (and I might be able to think
> of others) seem to me to strongly support the idea that 5AR type 2
> is the villain in hair-loss, and type 1 apparently plays little or no
role.
This is why I personally believe things like Saw Palmetto and Green Tea
don't do anything to help hairloss. Saw Palmetto acts against type 1
of 5-alpha, not predominantly against type 2. This might also be why
Duasteride might not work. As I stated in another post, I was very
diligent in contacting the makers of the Saw palmetto most of us have
posted on here about taking, and they themselves said it was proven
innefective for Type 2. Type 2 is most responsible for hairloss. also
that Type 1 is most predominant in the Prostate, and this is why
Propecia was fairly innefective in affecting the prostate. This is why
the Saw Palmetto bottles say "FOR PROSTATE HEALTH" on them.
Makes sense eh?
HT
--
****************************************
http://www.hairlosstalk.com
****************************************
Bryan Shelton
>/Pardon me if I'm butting in, but I think the two top pictures on the
>Revivogen site are a tad /problematic. The first guy's first picture shows
>him with his head back, so you can't see
>/whether he started with a bald spot; and his second picture shows him with
>his head /forward, so you can't tell what kind of regrowth he had at the
>front.
His head *is* tilted forward more in the second picture, but the
amount of loss in the first is so massive that surely we would
still be able to detect it in the second. It's not so far forward,
as far as I can tell, that we can't see the front part *at all*
in the second pic.
Bryan
HairTalk
Randall Parker <rgpa...@west.net> wrote:
> In <8an3qi$t6t$1...@nnrp1.deja.com>, the sagacious donalddonald@my-
deja.com donald...@my-deja.com perspicated:
> > If that's the case, then 80% is really 100% as far as hair loss is
> > concerned. If that 20% stays in the testes, then it certainly won't
be
> > affecting scalp hair loss. Plus, aren't we more concerned about the
dHT
> > conversion in skin?
>
> You are confusing testosterone and DHT. The high concentration of
testosterone in the testes makes it very hard for finasteride to
compete with it to bind with 5AR.
>
> But then once the testosterone has been converted to DHT in the
testes part of the DHT enters the blood.
Could one apply a tourniquet to the testes to inhibit this from
happening? Im thinking Propecia, Duasteride, and a Testicle Tourniquet
applied daily would end hairloss forever!
Farrel
HairTalk <ad...@hairlosstalk.com> wrote in message
news:8b0pqv$b68$1...@nnrp1.deja.com...
Dutasteride is a dual inhibitor of both type 1 and type 2. According to
reports that I've heard the results have been much better than Propecia. So
for guys taking Propecia Saw may be beneficial as well. This has been told
to me by both Dr Washenik and Dr Moss.
As far as Saw on its own I can just say from speaking to a lot of our
customers who frequently reorder the Bald Truth formula, they report having
slowed or stopped their hairloss. Hair regrowth is not as frequently
reported, but stopping the existing loss seems to be the most frequent
comment. Although one long term 5mg Proscar user said that when he added
the formula he noticed a new hair growth spurt.
Farrel
As I stated in another post, I was very
> diligent in contacting the makers of the Saw palmetto most of us have
> posted on here about taking, and they themselves said it was proven
> innefective for Type 2. Type 2 is most responsible for hairloss. also
> that Type 1 is most predominant in the Prostate, and this is why
> Propecia was fairly innefective in affecting the prostate. This is why
> the Saw Palmetto bottles say "FOR PROSTATE HEALTH" on them.
>
> Makes sense eh?
>
Bryan Shelton
>br...@pointecom.net (Bryan Shelton) wrote:
>> These three facts taken together (and I might be able to think
>> of others) seem to me to strongly support the idea that 5AR type 2
>> is the villain in hair-loss, and type 1 apparently plays little or no role.
>
>This is why I personally believe things like Saw Palmetto and Green Tea
>don't do anything to help hairloss. Saw Palmetto acts against type 1
>of 5-alpha, not predominantly against type 2. This might also be why
>Duasteride might not work. As I stated in another post, I was very
>diligent in contacting the makers of the Saw palmetto most of us have
>posted on here about taking, and they themselves said it was proven
>innefective for Type 2.
Did they quote you any studies that make this claim? I just got through
searching PubMed and found studies saying that it's effective for BOTH
type 1 and type 2. Here are a couple:
---------------------------------------------
Prostate 1999 Sep 1;40(4):232-41
Serenoa repens (Permixon): a 5alpha-reductase types I
and II inhibitor-new evidence in a coculture model of BPH.
Bayne CW, Donnelly F, Ross M, Habib FK
Prostate Research Group, University Department of Oncology,
Western General Hospital, Edinburgh, Scotland.
BACKGROUND: The aim of this study was to determine the effect
of the phytotherapeutic agent, Permixon, on a novel coculture model
of benign prostatic hyperplasia (BPH) in an effort to better understand
the mode of action of the drug in vivo. METHODS: The effect of Permixon,
at the calculated therapeutic concentration, on the activity of 5alpha-
reductase isoenzymes was evaluated utilizing a pH-specific assay. Prostate-
specific antigen (PSA) secretions into the medium were measured in the
presence and absence of Permixon and quantified by an ELISA assay. The
morphological patterns before and following Permixon treatment were also
examined by electron microscopy. All results were compared to controls.
RESULTS: Permixon at a concentration of 10 micrograms/ml
(calculated plasma concentration in patient receiving recommended therapeutic
dosage) was shown to be an effective inhibitor of both 5alpha-reductase types I
and II isoenzymes without influencing the secretion of PSA by the
epithelial cells, even after stimulation with testosterone. The morphology of
Permixon-treated cells was found to be markedly different from that of
untreated controls. Cells which had been treated with the drug demonstrated
extensive accumulation of lipids in the cytoplasm and widespread damage
of intracellular membranes, including mitochondrial and nuclear membranes.
CONCLUSIONS: Permixon is an effective dual inhibitor of 5alpha-reductase
isoenzyme activities in the prostate. Unlike other 5alpha-reductase inhibitors,
Permixon induces this effect without interfering with the cells' capacity to secrete
PSA, thus permitting the continued use of PSA measurements for prostate
cancer screening.
------------------------------------------------------------------------------------------------
J Steroid Biochem Mol Biol 1995 Sep;54(5-6):273-9
Human prostatic steroid 5 alpha-reductase isoforms--a
comparative study of selective inhibitors.
Iehle C, Delos S, Guirou O, Tate R, Raynaud JP, Martin PM
Laboratoire de Cancerologie Experimentale, Faculte de Medecine, Marseille, France.
The present study describes the independent expression of the type 1 and 2
isoforms of human 5 alpha-reductase in the baculovirus-directed insect cell
expression system and the selectivity of their inhibition. The catalytic properties
and kinetic parameters of the recombinant isozymes were consistent with
published data. The type 1 isoform displayed a neutral (range 6-8) pH optimum
and the type 2 isoform an acidic (5-6) pH optimum. The type 2 isoform had
higher affinity for testosterone than did the type 1 isoform (Km = 0.5 and 2.9
microM, respectively). Finasteride and turosteride were selective inhibitors
of the type 2 isoform (Ki (type 2) = 7.3 and 21.7 nM compared to
Ki (type 1) = 108 and 330 nM, respectively). 4-MA and the lipido-sterol extract
of Serenoa repens (LSESr) markedly inhibited both isozymes
(Ki (type 1) = 8.4 nM and 7.2 micrograms/ml, respectively;
Ki (type 2) = 7.4 nM and 4.9 micrograms/ml, respectively). The three azasteroids
were competitive inhibitors vs substrate, whereas LSESr displayed
non-competitive inhibition of the type 1 isozyme and uncompetitive
inhibition of the type 2 isozyme. These observations suggest that the lipid
component of LSESr might be responsible for its inhibitory effect by modulating
the membrane environment of 5 alpha-reductase. Partially purified recombinant
5 alpha-reductase type 1 activity was preserved by the presence of lipids
indicating that lipids can exert either stimulatory or inhibitory effects on
human 5 alpha-reductase.
------------------------------------------------------------------------------------------------
>Type 2 is most responsible for hairloss. also
>that Type 1 is most predominant in the Prostate,
No, type 2 is more predominant in the prostate!
>and this is why Propecia was fairly innefective in affecting the prostate.
Huh?? Finasteride reduces intraprostatic DHT levels by 85% and
consistently reduces prostate volume. It definitely affects the prostate!
Bryan
donald...@my-deja.com
created by 5AR type 2? Do they attach to different receptor sites in
the skin, or is it that the skin isn't sensitive to type 1-created DHT?
I am wondering whether type 1-created DHT can have a minor effect in
hair loss AFTER type 2-created DHT initiates the process.
Bryan Shelton
>What is the difference in DHT that is created from 5AR type 1 and DHT
>created by 5AR type 2? Do they attach to different receptor sites in
>the skin, or is it that the skin isn't sensitive to type 1-created DHT?
There IS no difference in DHT created from type 1 and type 2 5AR.
Only the two 5AR enzymes are different.
Bryan
doct...@my-deja.com
<21480E4546D3742D.2A0A3C3A...@lp.airnews.net>,
br...@pointecom.net (Bryan Shelton) wrote:
> On Wed, 15 Mar 2000 03:24:13 GMT, donald...@my-deja.com wrote:
>
> >> You mean the other 35% of DHT? You could almost certainly lower
> >> blood levels a bit more by simply increasing the dose of
finasteride,
> >> but with a higher risk of side-effects. An early study of
finasteride
> >> found reductions of about 80% after single doses of 12.5 mg or
> >> higher. A whole 5 mg tablet of Proscar every day would probably
> >> get this done. An additional 15% reduction may not sound like
> >> much, but it might be a critical extra boost for someone who is an
> >> "outlier" and living on that "hairy edge". BTW, this same study
claims
> >> that finasteride will never achieve a reduction of more than 80% at
> >> *any* dose because it cannot affect the amount supplied by the
> >> testes, and this contribution is 20% of the total.
> >
> >Why can't finasteride reduce the testes-produced DHT?
>
> Finasteride works by competing with testosterone at the 5AR molecule.
> The finasteride molecules "crowd out" the testosterone molecules and
> end up joining with 5AR type 2 instead of the testosterone, so no DHT
> can be produced as a result. But there is an extremely high
concentration
> of testosterone in the testes (100 times the concentration found in
the
> blood!), and the *finasteride* is the one that gets "crowded out",
with
> continuing production of DHT.
>
> >>I think that dutasteride should be limited by this, too, since it is
> >>also a competitve inhibitor of 5AR, but perhaps it will be able
> >>to pass the 80% barrier by also inhibiting 5AR type 1.
> >
> >So type 1 is important in this hair loss process?? A post of yours
from
> >a day or so ago I thought said type one is not important. You were
> >responding about why zinc and B6 are not important in Revivogen
because
> >they inhibit the "wrong" enzyme. Are you now saying that perhaps type
1
> >does play at least a tiny part?
>
> No, no; I still think type 2 is the critical one! I just included the
above
> remarks for the sake of completeness, and for the people who continue
> to think that blood levels are important. BTW, I reserve the right to
change
> my views (again) if more information comes out. We're all kinda
groping
> in the dark on a lot of these issues!
>
> >> All of this implies that blood levels of DHT are important in the
> >> first place, which I doubt. If the pictures at the Revivogen site
> >> are legitimate, then clearly blood levels of DHT are not an issue,
> >> and it's the local suppression of DHT (by finasteride or Revivogen)
> >> that does the trick. I tend to believe that the pictures are real.
> >> If so, that might be the final piece of the puzzle: only locally
> >> produced DHT from 5AR type 2 is responsible for hair-loss.
Hello Bryan,
I admire your courage to try to establish a new theory about hair loss.
However, frankly speaking, I agree with the view of Dr. P, hair loss
problem is a multi-factor problem for men and women. It can not be just
a piece of puzzle.
Hair loss of men and women can be caused by many different reasons, it
is a very complicated issue, can not be as simple as you have proposed.
A good theory can not be only based on two unknown pictures. Worldwide,
millions and millions of men and women have hair-loss problem, two
unknown pictures are very small fluctuations in the statistics view. As
Dr. P mentioned before, it is difficult to find something that does not
help hair.
DHT or the localized DHT proposed by you, was not, is not and can not
be the unique cause of hair loss. I think, we have to open mind, as mike
pointed out, we should look something else as well.
Please excuse my frank point. As you said, you may change your view
later. I think you will.
Ph.D
@ http://www.springhair.com
> >>
> >Doesn't finasteride inhibit 5AR in skin? Some?
>
> Sure, or else it wouldn't have any effect on MPB, IMHO! ;-)
>
> Bryan
Farrel
<doct...@my-deja.com> wrote in message news:8b35cu$r2g$1...@nnrp1.deja.com...
Never trust the word of a lying ginseng snake oil salesman who refuses to
give his name or his field of study.
Springhair tonic is a snake oil hair tonic that does not prevent hair loss
or regrow hair.
Farrel
donald...@my-deja.com
<071171EA234D2EBE.912BB7C7...@lp.airnews.net>,
If that's the case, then type 1 must play a role in hair loss, but only
after type 2-created DHT initiates the process. Perhaps those
pseudohermaphrodites (is that right?) in those studies didn't lose their
hair, even though they had type 1 at normal levels, for this reason.
Randall Parker
HairTalk perspicated:
> Could one apply a tourniquet to the testes to inhibit this from
> happening? Im thinking Propecia, Duasteride, and a Testicle Tourniquet
> applied daily would end hairloss forever!
Ouch, Pain!
I am laughing at that gruesome thought.
Bryan Shelton
>> There IS no difference in DHT created from type 1 and type 2 5AR.
>> Only the two 5AR enzymes are different.
>
>If that's the case, then type 1 must play a role in hair loss,
>but only after type 2-created DHT initiates the process.
Why do you feel this way?
Bryan
donald...@my-deja.com
<494EFA2B764807E0.F6A0A74D...@lp.airnews.net>,
Well, I am not yet at the level where I can spit out studies as you do
so well. But I am just theorizing based on your own comments. But if
the DHT from the two 5AR types is the same, then why would one kind be
any different in the way it interacts with the receptor sites? If they
interact the same way, then they are both the problem. That is why I
say that type 2-created DHT is the one that initiates the process
because the 5AR type 2-deficient men in specific studies never lost
their hair.
But the other side might argue that the two 5AR types create different
kinds of DHT, which interact differently with the receptor site. Do you
know if all DHT can attach to any DHT receptor (with considering their
location in the body)?
doct...@my-deja.com
<D4F129C40DBDE4DB.2099102F...@lp.airnews.net>,
br...@pointecom.net (Bryan Shelton) wrote:
> On Sat, 18 Mar 2000 20:44:19 GMT, HairTalk <ad...@hairlosstalk.com>
wrote:
>
> >br...@pointecom.net (Bryan Shelton) wrote:
> >> These three facts taken together (and I might be able to think
> >> of others) seem to me to strongly support the idea that 5AR type 2
> >> is the villain in hair-loss, and type 1 apparently plays little or
no role.
> >
> >This is why I personally believe things like Saw Palmetto and Green
Tea
> >don't do anything to help hairloss. Saw Palmetto acts against type 1
> >of 5-alpha, not predominantly against type 2. This might also be why
> >Duasteride might not work. As I stated in another post, I was very
> >diligent in contacting the makers of the Saw palmetto most of us have
> >posted on here about taking, and they themselves said it was proven
> >innefective for Type 2.
Any comment about Rittmaster's statement quoted below:"
"According to Rittmaster, men born with the type I 5-alpha reductase
enzyme but
without the type II 5-alpha reductase enzyme (the kind DHT blocks)
experience
hair loss when given Testosterone injections. He believes this shows
that the
type I enzyme does play a role in hair loss."
End of quote.
Ph.D
@ http://www.springhair.com
doct...@my-deja.com
HairTalk <ad...@hairlosstalk.com> wrote:
> In article <MPG.1339a71c4...@news.onlynews.com>,
> Randall Parker <rgpa...@west.net> wrote:
> > In <8an3qi$t6t$1...@nnrp1.deja.com>, the sagacious donalddonald@my-
> deja.com donald...@my-deja.com perspicated:
> > > If that's the case, then 80% is really 100% as far as hair loss is
> > > concerned. If that 20% stays in the testes, then it certainly
won't
> be
> > > affecting scalp hair loss. Plus, aren't we more concerned about
the
> dHT
> > > conversion in skin?
> >
> > You are confusing testosterone and DHT. The high concentration of
> testosterone in the testes makes it very hard for finasteride to
> compete with it to bind with 5AR.
> >
> > But then once the testosterone has been converted to DHT in the
> testes part of the DHT enters the blood.
>
> happening? Im thinking Propecia, Duasteride, and a Testicle Tourniquet
> applied daily would end hairloss forever!
Have you considered how serious the side-effect will be for all of them?
Ph.D
>
> HT
>
> --
> ****************************************
> http://www.hairlosstalk.com
> ****************************************
>
Farrel
<doct...@my-deja.com> wrote in message news:8b72cm$kq2$1...@nnrp1.deja.com...
> In article <8b0qhq$bjn$1...@nnrp1.deja.com>,
> HairTalk <ad...@hairlosstalk.com> wrote:
> > In article <MPG.1339a71c4...@news.onlynews.com>,
> > Randall Parker <rgpa...@west.net> wrote:
> > > In <8an3qi$t6t$1...@nnrp1.deja.com>, the sagacious donalddonald@my-
> > deja.com donald...@my-deja.com perspicated:
> > > > If that's the case, then 80% is really 100% as far as hair loss is
> > > > concerned. If that 20% stays in the testes, then it certainly
> won't
> > be
> > > > affecting scalp hair loss. Plus, aren't we more concerned about
> the
> > dHT
> > > > conversion in skin?
> > >
> > > You are confusing testosterone and DHT. The high concentration of
> > testosterone in the testes makes it very hard for finasteride to
> > compete with it to bind with 5AR.
> > >
> > > But then once the testosterone has been converted to DHT in the
> > testes part of the DHT enters the blood.
> >
> > Could one apply a tourniquet to the testes to inhibit this from
> > happening? Im thinking Propecia, Duasteride, and a Testicle Tourniquet
> > applied daily would end hairloss forever!
>
> Have you considered how serious the side-effect will be for all of them?
>
> Ph.D
>
Probably a lot less then from springhair tonic. At least you will grow hair
using them, not like your snake oil tonic.