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Here's an old post by Bryan discussing topical green tea extract, etc.
It's a good read. Something that should be brought up now and then IMHO:
It's a good read. Something that should be brought up now and then IMHO:
From: Bryan Shelton - view profile
Date: Mon, Aug 13 2001 8:58 pm
Email: b...@airmail.net (Bryan Shelton)
Groups: alt.baldspot
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Guys, I'm all excited about a new study which just came out. I have to give
Waseda a tip of the hat for mentioning it on the newsgroup a couple of weeks
ago. Since then, I've gotten the full study and carefully read it. I think it has
some very interesting implications: "Growth suppression of hamster flank
organs by topical application of catechins, alizarin, curcumin, and myristoleic
acid", Shutsung Liao et al., Arch Dermatol Res (2001) 293:200-205.
Most of you know that I've been experimenting with a topical green tea extract
(from http://www.beyond-a-century.com) that is supposed to be 45% EGCG (epigallo-
catechin-3-gallate), which is one of the main antioxidant polyphenols found
in green tea. The rationale for doing this is that EGCG and certain others
of this chemical group have been found to be potent inhibitors of the 5alpha-
reductase enzyme. This was first verified in an earlier study: "Selective
inhibition of steroid 5alpha-reductase isozymes by tea epicatechin-3-gallate
and epigallocatechin -3-gallate", Shutsung Liao and Richard Hiipakka,
Biophys Biochem Res Commun 214:833-838. This was just an "in vitro"
study, but it did find that EGCG and certain others of these compounds
inhibited BOTH forms of 5a-R, although they were more potent against
the type 1 version. However, as with all things like this, you can make up
with quantity what you lack in quality! ;-) And near the end of this study,
they added a little afterthought: they mentioned an "unpublished observation"
of theirs, which was that the topical application of either GLA (gamma-linolenic
acid) or EGCG to the foreheads of human male subjects decreased their
sebum excretion rate. Since the activity of sebaceous glands is under
androgenic control, this was a clear indication that these compounds are
able to work topically in humans, at the very least in sebaceous glands.
Now we have a newer study by these same researchers, and this time they
test these substances (and a few others) in an "in vivo" experiment, using
hamster flank organs. And they made a *very* unexpected and fascinating
finding which I will get to in just a moment, but first let me mention the more
conventional results: in one part of the experiment they duplicated yet another
earlier study, and tested a combination of testosterone and 1 mg of GLA on one
flank organ of a group of hamsters, and found that the GLA reduced the growth
of the pigmented macules (a direct function of the growth of the flank organ
itself) by 82%, which agrees with the previous study. In other parts of the
experiment they tested EGCG along with testosterone, and as you can guess,
they got significant inhibitions that ranged up to 64% from 1 mg of EGCG, in one
of the trials! Now think about that: 1 mg of the very inexpensive and easily
obtainable EGCG (from green tea) was in the same general neighborhood
of effectiveness as 1 mg of the extremely expensive, exotic, and exemplary
GLA (yes, I just love alliteration)! Results from 1 mg of the tea catechins
alizarin and curcumin were even *more* impressive, with inhibitions of 87%
for both of those compounds.
Ok, now we're getting closer to the real punchline of this study! Consider
this: GLA, ALA, LA, oleic acid, and the other fatty acids have no effect
whatsoever on DHT itself. In this new study and the older one, they were
very effective at inhibiting hamster flank organs and hair follicles because
they are good at stopping the conversion of testosterone to DHT, via the
5a-R enzyme. But they have no effect on the androgen receptor, so they
cannot affect pre-existing DHT. When GLA and the other fatty acids are
applied to hamster flank organs along with pure DHT, there is no effect
at all; the growth of the flank organs is not inhibited at all.
Question: what would you expect to happen if you applied some cheap
EGCG from green tea to hamster flank organs, along with pure DHT??
Would it also turn out to be ONLY a 5alpha-reductase inhibitor??
That's what Liao et al. wanted to know, and that's what they tried.
(BTW, they found that pure DHT was almost exactly 50% more potent
than the same dose of testosterone at stimulating flank organs: the
extra testosterone-stimulated growth of the macules in control animals
was 13.83 mm^2, and the DHT-stimulated growth was 20.80 mm^2)
Ok, here's the kicker: 1 mg of EGCG applied with pure DHT inhibited
the flank organ growth by an absolutely *astonishing* 97%!! EGCG was
even MORE effective against DHT than it was against testosterone!!
Suddenly, things are put in a whole new light. Previously it was assumed
that cheap green tea might possibly function as an inexpensive additional
5alpha-reductase inhibitor; perhaps something to use as an adjunct
to Propecia, to inhibit the type 1 form of the enzyme. But now it appears
to be a distinct possibility that this substance performs not just as a *dual*
inhibitor of 5a-R, but as some kind of an agent that interferes directly with DHT!
Could it be possible that the most effective antiandrogenic agent to date
(at the very least, the most cost-effective) has been literally right under
our noses all this time??I think this is something to consider....
I now present the entire "Discussion" section of this new study. I've added
a couple of comments of my own in brackets. Any comments afterwards
are certainly welcome:
"DISCUSSION"
"In this study we showed that all four green tea catechins inhibited hamster
flank organ growth to various degrees. Like gamma-LA (Liang and Liao 1992;
Liao and Hiipakka 1995), in an in vitro enzyme assay ECG and EGCG have
been shown to be potent inhibitors (IC50 10-20 uM) of 5alpha-reductase,
while EC and EGC are not active inhibitors of 5alpha-reductase at 200 uM
(Liao and Hiipakka 1995). Consistent with these in vitro tests, EGCG and
ECG inhibited the testosterone-dependent growth of flank organs. However,
EC and EGC, though inactive against 5alpha-reductase in vitro, had an
inhibitory effect on flank organ growth. The suppression of flank organ
growth by catechins, therefore, does not appear to be due simply to inhibition
of the formation of DHT from testosterone in flank organs. In line with this
observation, EGCG was inhibitory even when DHT instead of testosterone
was used as the androgen (Table 1). [That refers to the 97% figure --- Bryan]
This is in contrast with GLA, which inhibited testosterone-stimulated flank
organ growth but not DHT-stimulated flank organ growth (Liang and Liao
1997). Therefore, even though EGCG and EGC can inhibit 5alpha-reductase,
inhibition of flank organ growth by catechins may occur through other mechanisms.
Whether these catechins affect androgen receptor activity in hamster flank
organs is not known.
"The possibility that polyphenolic catechins and other inhibitory compounds
act simply by interacting with topically applied androgens and reduce androgenic
activity is unlikely since these compounds when topically applied inhibited
endogenous androgen-dependent growth of flank organs of normal (not castrated)
male hamsters (results not shown). We have previously shown that topically
applied GLA inhibits flank organ growth in normal hamsters (Liang and Liao
1997).
"Previous studies of the effect of fatty acids on flank organ growth suggest that
compounds with fewer than 18 carbons are ineffective (Liang and Liao 1997).
We showed here that MA [this is myristoleic acid --- Bryan], containing 14 carbons
is as effective as GLA in inhibiting flank organ growth. In addition, the effects
of MA and GLA in preventing testosterone-induced growth of flank organs were
similar to the effect of EGC-gamma-linoleneate and EGC-myristoleate esters.
No differences were noted in the effects of EGCG and that of the synthetic
esters which contained GLA and MA in place of the gallate group of EGCG.
"Alizarin and curcumin may inhibit flank organ growth primarily by inhibiting
5alpha-reductase. This conclusion is supported by data showing that alizarin
and curcumin inhibited testosterone-induced flank organ growth, but did not
curb growth stimulated by DHT. Furthermore, in an in vitro enzyme assay,
both compounds have been shown to be potent inhibitors of 5alpha-reductase
(IC50 5-10 uM) (Hiipakka and Liao, unpublished results). These observations
support our previous conclusion (Liang and Liao 1997) that flank organ growth
is dependent on local conversion of testosterone to DHT as is prostate growth
in rodents and humans. Histological observations show that pigments of flank
organs were localized in the hair shaft and near the orifice of hair follicles. This
finding suggests that catechins, alizarin, and curcumin inhibit androgenic effects
not only in dermal melanocytes, but also in hair follicles of the flank organ.
"An inhibitor of a 5alpha-reductase with systemic activities would be teratogenic
to embryos (Imperato-McGinley and Guatier 1986; Russell and Wilson 1994).
For this reason a topical preparation of 5alpha-reductase inhibitor that does not
produce systemic activity is desirable for treating androgen-dependent skin
diseases. Since local application of GLA and other active compounds described
in this report did not exhibit a systemic effect on the contralateral flank organs
or on prostate organ weights in hamsters, they may be useful for treatment
of androgen-dependent skin disorders. Additional studies are needed
to determine whether the findings described in this report for the hamster
model are applicable to human skin."
Bryan
