Green Tea Elevates DHT?!
Kev
Kofi posted this awhile ago, but.. This study says:
"Green tea...tended to elevate (P = 0.14) the serum dihydrotestosterone
(DHT) concentration."
Considering that Green tea has been shown to inhibit 5-ar, that is a pretty
strange statement.
J Nutr. 2003 Feb;133(2):516-21.
Soy phytochemicals and tea bioactive components synergistically inhibit
androgen-sensitive human prostate tumors in mice.
Zhou JR, Yu L, Zhong Y, Blackburn GL.
Nutrition/Metabolism Laboratory, Department of Surgery, Beth Israel
Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
jrz...@caregroup.harvard.edu
Although high doses of single bioactive agents may have potent anticancer
effects, the chemopreventive properties of the Asian diet may result from
interactions among several components that potentiate the activities of any
single constituent. In Asia, where intake of soy products and tea
consumption are very high, aggressive prostate cancer is significantly less
prevalent in Asian men. The objective of the present study was to identify
possible synergistic effects between soy and tea components on prostate
tumor progression in a mouse model of orthotopic androgen-sensitive human
prostate cancer. Soy phytochemical concentrate (SPC), black tea and green
tea were compared with respect to tumorigenicity rate, primary tumor growth,
tumor proliferation index and microvessel density, serum androgen level and
metastases to lymph nodes. SPC, black tea and green tea significantly
reduced tumorigenicity. SPC and black tea also significantly reduced final
tumor weights. Green tea did not reduce final tumor weight, although it
tended to elevate (P = 0.14) the serum dihydrotestosterone (DHT)
concentration. The combination of SPC and black tea synergistically
inhibited prostate tumorigenicity, final tumor weight and metastases to
lymph nodes in vivo. The combination of SPC and green tea synergistically
inhibited final tumor weight and metastasis and significantly reduced serum
concentrations of both testosterone and DHT in vivo. Inhibition of tumor
progression was associated with reduced tumor cell proliferation and tumor
angiogenesis. This study suggests that further research is warranted to
study the role of soy and tea combination as effective nutritional regimens
in prostate cancer prevention.
PMID: 12566493 [PubMed - indexed for MEDLINE]
Kev
This also shows an increase in T, apparently because its an aromatase
inhibitor.
Food Chem Toxicol. 2002 Jul;40(7):925-33.
Inhibition of aromatase activity by green tea extract catechins and their
endocrinological effects of oral administration in rats.
Satoh K, Sakamoto Y, Ogata A, Nagai F, Mikuriya H, Numazawa M, Yamada K,
Aoki N.
Department of Toxicology, The Tokyo Metropolitan Research Laboratory of
Public Health, 24-1 Hyakunincho 3 chome, Shinjuku-ku, Japan.
sa...@tokyo-eiken.go.jp
We orally administered polyphenone-60 (P-60), green tea extract catechins,
in the diet (0, 1.25 and 5%) to male rats for 2, 4 and 8 weeks initiated at
5 weeks old. It was found that a 5% dose to male rats for 2-8 weeks induced
goiters and decreased weights of the body, testis and prostate gland.
Endocrinologically, elevating plasma thyroid stimulating hormone (TSH),
luteinizing hormone (LH) and testosterone levels and decreasing
tri-iodothyronine (T(3)) and thyroxine (T(4)) levels were induced by this
treatment. We also found that P-60 as a whole and some of its constituents
exhibited inhibitory effects on human placental aromatase activity by in
vitro assay. The concentration of P-60 that required producing 50%
inhibition of the aromatase activity (IC(50) value) was 28 microg/ml. The
IC(50) values of (-)-catechin gallate (Cg), (-)-epigallocatechin (EGC),
(-)-epigallocatechin gallate (EGCg) and (-)-gallocatechin gallate (GCg) were
5.5 x 10(-6), 1.0 x 10(-4), 6.0 x 10(-5) and 1.5 x 10(-5) M, respectively.
(-)- Epicatechin gallate (ECg) at 1.0 x 10(-4) M produced 20% inhibition.
(-)-Epicatechin (EC) and (+)-catechin (CT) exhibited no effects on aromatase
activity. The endocrinological changes observed in vivo were in conformity
with antithyroid effects and aromatase inhibition effects of P-60 and its
constituents.
PMID: 12065214 [PubMed - indexed for MEDLINE]
anon
wrote:
> Kofi posted this awhile ago, but.. This study says:
>
> "Green tea...tended to elevate (P = 0.14) the serum dihydrotestosterone
> (DHT) concentration."
>
> Considering that Green tea has been shown to inhibit 5-ar, that is a
> pretty
> strange statement.
Green tea extract inhibits 5-ar in solution but not in a whole cell
culture. Something about the way it's metabolized.
Bryan Shelton
>Green tea extract inhibits 5-ar in solution but not in a whole cell
>culture. Something about the way it's metabolized.
Yes it does. In some 'in vivo' experiments, topical EGCG was able
to inhibit the 5a-reductase in sebaceous glands and reduce
sebum production, so I don't know where you got that about
"whole cell cultures".
Bryan
Ams4matt
this about raising DHT.....reducing VEGF.....I have no clue what the real deal
is.
Kev
If it is high in EGCG, then it's probably good. If it is whole green tea, or
whole extract, I wouldnt. I just eat it though, I don't see the point in
applying it topically.
anon
wrote:
It increases keratinocyte proliferation. It also weakly inhibits NFKB
and MMP-9. It does inhibit VEGF but then so do most antiinflammatories.
It also reduces the risk of skin cancer from UV light.
Bryan Shelton
>Ams4matt at ams4...@aol.com wrote:
>
>> Can someone just tell me whether or not topical Green Tea is a good idea? All
>> this about raising DHT.....reducing VEGF.....I have no clue what the real deal
>> is.
>
>If it is high in EGCG, then it's probably good. If it is whole green tea,
>or whole extract, I wouldnt.
Why not?
>I just eat it though, I don't see the point in applying it topically.
The point would be to inhibit 5a-reductase.
Bryan
Bryan Shelton
>It does inhibit VEGF but then so do most antiinflammatories.
It depends on HOW it inhibits VEGF. If it does it by reducing androgens
(by way of inhibiting 5a-reductase), then it could very well _increase_
VEGF in scalp hair follicles, not decrease it. The opposite would be
the case in body hair follicles.
So where did you get that thing about "whole cell cultures"?
Bryan
Bryan Shelton
I think it's probably at least neutral, if not actually beneficial.
Bryan
Kev
>> If it is high in EGCG, then it's probably good. If it is whole green tea,
>> or whole extract, I wouldnt.
>
> Why not?
Because studies suggest EGCG is a 5-ar inhibitor, and antioxidant - all
kinds of good stuff. Other catechins may be aromatase inhibitors, and
something in whole green tea raises DHT.
>> I just eat it though, I don't see the point in applying it topically.
>
> The point would be to inhibit 5a-reductase.
So just eat it. You don't think that eating it will block 5-ar?
Ams4matt
So how are we supposed to know if it is high in EGCG? I have just been using
green tea bags steeped in hot water.
Ernie Primeau
evidenced by the shedding from the use of anti-androgens.
bryan shelton cannot tell us what it takes to grow scalp hair if not
androgens,the same as body hair.Ernie
anon
>
> It depends on HOW it inhibits VEGF. If it does it by reducing androgens
> (by way of inhibiting 5a-reductase), then it could very well _increase_
> VEGF in scalp hair follicles, not decrease it. The opposite would be
> the case in body hair follicles.
I agree completely with this statement. The problem is, if anyone out
there has tested green tea extract in the skin, nobody's said much about
it.
There was a lot of worry that green tea promoted apoptosis but that
turned out to only be for cancer cells. In skin keratinocytes, it
actually lengthens lifespan. What it does on VEGF may very well depend
on cell type.
>
> So where did you get that thing about "whole cell cultures"?
>
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&lis
t_uids=11931850&dopt=Abstract>
I've also seen a reference to it in one patent. They added a little
molecular doodad to EGCG and it stopped getting metabolized by cells,
stayed free and had a lot of 5AR inhibition...
Which I continue to say is not necessarily a good thing for your long
term health since it will weakly inhibit your GABAergic function.
Declining GABAergic function is behind several age-related disorders
including cognitive decline.
Large levels of green tea catechins (like, 5% of your diet) inhibit
aromatase.
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&lis
t_uids=12065214&dopt=Abstract>
The extract should also increase SHBG levels.
Green tea catechins appear to inhibit androgen dependent tissue growth
but not necessarily through 5AR inhibition.
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&lis
t_uids=11380153&dopt=Abstract>
I would suggest it may have to do with insulin signaling pathways, since
EGCG also shrinks the uterus and ovary in high doses.
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&lis
t_uids=10698173&dopt=Abstract>
Jacob
> Kev:
>
> So how are we supposed to know if it is high in EGCG? I have just been using
> green tea bags steeped in hot water.
Take it in supplement form, such as
http://store.yahoo.com/iherb/egcg.html
There is also white tea and combo's of white and green tea:
http://store.yahoo.com/iherb/greenwhitetea.html
Article on green tea and hair loss..which mentions white tea:
http://www.newhope.com/ffn/ffn_backs/sep-oct_01/feverfew.cfm
anon
ams4...@aol.com (Ams4matt) wrote:
Order an extract in powder or liquid form. Dissolve in DMSO and apply.
Ams4matt
Good idea. Can you suggest how much to dissolve into how much DMSO? I think I
would also use a 50/50 DMSO/Distilled water mix.
Bryan Shelton
>Bryan Shelton at br...@airmail.net wrote:
>
>>> If it is high in EGCG, then it's probably good. If it is whole green tea,
>>> or whole extract, I wouldnt.
>>
>> Why not?
>
>Because studies suggest EGCG is a 5-ar inhibitor, and antioxidant - all
>kinds of good stuff. Other catechins may be aromatase inhibitors, and
>something in whole green tea raises DHT.
Do you have a reference for that claim about something in green tea
raising DHT?
So do I understand correctly that it's your view that while pure EGCG
would probably be a good thing to apply topically, the beneficial effect
_may_ be overridden by whole green tea, because something else in there
raises DHT, presumably counteracting the 5a-reductase inhibiting
effect of pure EGCG?
>>> I just eat it though, I don't see the point in applying it topically.
>>
>> The point would be to inhibit 5a-reductase.
>
>So just eat it. You don't think that eating it will block 5-ar?
No I don't. Don't you think that if eating or drinking green tea really
inhibited 5a-reductase to any significant degree, we would ALL know
about it by now? Don't you think it would have long since passed into
folklore and traditional medicine as a "natural" cure for a variety of things
like acne and prostate problems and hairloss? As far as I know, there is
no tradition of using it for things like that, and drug companies have
been investing large sums of $$$ to find synthetic drugs that really
DO do that job well. So I strongly doubt that eating or drinking green
tea in anywhere near reasonable amounts is going to have much of an
effect on 5a-reductase.
Bryan
Bryan Shelton
>> So where did you get that thing about "whole cell cultures"?
>
><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&lis
>t_uids=11931850&dopt=Abstract>
That's very odd...yes, I see that comment about the "whole cell cultures"
in the abstract, but topical EGCG has apparently been shown to inhibit
5a-reductase in an 'in vivo' model (hamster flank organs) in the other study
you cite below, written by some of the same authors as the one above!
I believe it's safe to say that the fact that it seems to work topically on
LIVE ANIMALS trumps that strange claim about "whole cell cultures"!
>Large levels of green tea catechins (like, 5% of your diet) inhibit
>aromatase.
>
><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&lis
>t_uids=12065214&dopt=Abstract>
Uhhh....that wasn't in the dietary part of the experiment, that was in the
'in vitro' part of it.
>Green tea catechins appear to inhibit androgen dependent tissue growth
>but not necessarily through 5AR inhibition.
>
><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&lis
>t_uids=11380153&dopt=Abstract>
Yes. I don't know if you've read that whole study, but one thing they found
was simply astonishing: topical EGCG was also able to reduce by 97%
the DHT-stimulated growth of the hamster flank organs! That does make
one wonder how much of the testosterone-stimulated growth that was also
suppressed by EGCG was actually due to the direct inhibition of 5a-R, and
how much was due to the apparent androgen receptor-blocking ability
of EGCG. In any event, I've been saying for the last year or so that
the above study makes topical EGCG look _awfully_ attractive!
Bryan
Bryan Shelton
>>Because studies suggest EGCG is a 5-ar inhibitor, and antioxidant - all
>>kinds of good stuff. Other catechins may be aromatase inhibitors, and
>>something in whole green tea raises DHT.
>
>Do you have a reference for that claim about something in green tea
>raising DHT?
OOPS (slaps forehead with palm of hand).
Ok, that was in the post at the top of this thread. Nevermind!
(That's what I get for not checking this thread for about a week or so...
I forgot what was said in the rest of it!)
Bryan
Kev
> On Sat, 13 Dec 2003 03:08:05 GMT, Kev <Kevi...@aol.com> wrote:
>
>> Bryan Shelton at br...@airmail.net wrote:
>>
>>>> If it is high in EGCG, then it's probably good. If it is whole green tea,
>>>> or whole extract, I wouldnt.
>>>
>>> Why not?
>>
>> Because studies suggest EGCG is a 5-ar inhibitor, and antioxidant - all
>> kinds of good stuff. Other catechins may be aromatase inhibitors, and
>> something in whole green tea raises DHT.
>
> Do you have a reference for that claim about something in green tea
> raising DHT?
That's what this thread was about...
J Nutr. 2003 Feb;133(2):516-21.
Soy phytochemicals and tea bioactive components synergistically inhibit
androgen-sensitive human prostate tumors in mice.
Although high doses of single bioactive agents may have potent anticancer
effects, the chemopreventive properties of the Asian diet may result from
interactions among several components that potentiate the activities of any
single constituent. In Asia, where intake of soy products and tea
consumption are very high, aggressive prostate cancer is significantly less
prevalent in Asian men. The objective of the present study was to identify
possible synergistic effects between soy and tea components on prostate
tumor progression in a mouse model of orthotopic androgen-sensitive human
prostate cancer. Soy phytochemical concentrate (SPC), black tea and green
tea were compared with respect to tumorigenicity rate, primary tumor growth,
tumor proliferation index and microvessel density, serum androgen level and
metastases to lymph nodes. SPC, black tea and green tea significantly
reduced tumorigenicity. SPC and black tea also significantly reduced final
tumor weights. Green tea did not reduce final tumor weight, although it
tended to elevate (P = 0.14) the serum dihydrotestosterone (DHT)
concentration. The combination of SPC and black tea synergistically
inhibited prostate tumorigenicity, final tumor weight and metastases to
lymph nodes in vivo. The combination of SPC and green tea synergistically
inhibited final tumor weight and metastasis and significantly reduced serum
concentrations of both testosterone and DHT in vivo. Inhibition of tumor
progression was associated with reduced tumor cell proliferation and tumor
angiogenesis. This study suggests that further research is warranted to
study the role of soy and tea combination as effective nutritional regimens
in prostate cancer prevention.
> So do I understand correctly that it's your view that while pure EGCG
> would probably be a good thing to apply topically, the beneficial effect
> _may_ be overridden by whole green tea, because something else in there
> raises DHT, presumably counteracting the 5a-reductase inhibiting
> effect of pure EGCG?
Yes.
>>>> I just eat it though, I don't see the point in applying it topically.
>>>
>>> The point would be to inhibit 5a-reductase.
>>
>> So just eat it. You don't think that eating it will block 5-ar?
>
> No I don't. Don't you think that if eating or drinking green tea really
> inhibited 5a-reductase to any significant degree, we would ALL know
> about it by now? Don't you think it would have long since passed into
> folklore and traditional medicine as a "natural" cure for a variety of things
> like acne and prostate problems and hairloss? As far as I know, there is
> no tradition of using it for things like that, and drug companies have
> been investing large sums of $$$ to find synthetic drugs that really
> DO do that job well. So I strongly doubt that eating or drinking green
> tea in anywhere near reasonable amounts is going to have much of an
> effect on 5a-reductase.
All I have are some studies that show EGCG inhibits 5ar. We know EGCG is
absorbed when taken orally. Other of its positive effects have been
demonstrated when ingested. And, I see no reason to think it would not also
demonstrate 5ar inhibition as well when taken orally in the diet. If whole
green tea counteracts some of the actions of isolated EGCG, maybe thats why
green tea has not been used to treat BPH. Of course, Im only guessing.
Isolated EGCG has not been around very long to have become a folklore
medicine.
You believe using topically is effective, right? If it can be ingested, then
taking it orally should also be effective. Like Minoxidil, it probably works
better and at lower doses when taken orally. For acne, B5 appears to work
better orally than topically. The only reason to use Minoxidil topically is
because of the adverse effects of using it orally. Same with anti-androgens.
We don't use finasteride topically since it would take far too much and
would be no more effective. Why would EGCG be any different? I want to know.
Are there examples of agents that can be safely ingested and absorbed
orally, are effective topically, but are not effective orally?
Hong Kong Med J. 2001 Dec;7(4):369-74.
The medicinal action of androgens and green tea epigallocatechin gallate.
Liao S.
Unorthodox (non-traditional or alternative) medicinal practices have been
expanding very rapidly in western countries. Modern physicians, scientists,
and non-traditional medicine practitioners now must join forces to promote
evidence-based medicine to benefit patients. Green tea extracts are among
the most widely used ancient medicinal agents, while androgens are probably
the oldest drugs used in a purified form in traditional Chinese medicine. It
is now clear that a specific green tea catechin,
(-)epigallocatechin-3-gallate, can modulate the production and biological
actions of androgens and other hormones. Modulation of androgenic activity
and administration of (-)epigallocatechin-3-gallate may be useful for the
treatment of various hormone-related abnormalities, such as benign prostatic
hyperplasia, baldness, and acne, as well as androgen-dependent and
-independent prostate cancers. (-)Epigallocatechin-3-gallate has also been
shown to modulate appetite and control obesity in animals.
Endocrinology. 2000 Mar;141(3):980-7.
Modulation of endocrine systems and food intake by green tea
epigallocatechin gallate.
Kao YH, Hiipakka RA, Liao S.
Green tea polyphenols, especially the catechin, (-)-epigallocatechin gallate
(EGCG), have been proposed as a cancer chemopreventative based on a variety
of laboratory studies. For clear assessment of the possible physiological
effects of green tea consumption, we injected pure green tea catechins ip
into rats and studied their acute effects on endocrine systems. We found
that EGCG, but not related catechins, significantly reduced food intake;
body weight; blood levels of testosterone, estradiol, leptin, insulin,
insulin-like growth factor I, LH, glucose, cholesterol, and triglyceride; as
well as growth of the prostate, uterus, and ovary. Similar effects were
observed in lean and obese male Zucker rats, suggesting that the effect of
EGCG was independent of an intact leptin receptor. EGCG may interact
specifically with a component of a leptin-independent appetite control
pathway. Endocrine changes induced by parenteral administration of EGCG may
relate to the observed growth inhibition and regression of human prostate
and breast tumors in athymic mice treated with EGCG as well as play a role
in the mechanism by which EGCG inhibits cancer initiation and promotion in
various animal models of cancer.
Int J Cancer. 2004 Jan 1;108(1):130-5.
Protective effect of green tea against prostate cancer: a case-control study
in southeast China.
To investigate whether green tea consumption has an etiological association
with prostate cancer, a case-control study was conducted in Hangzhou,
southeast China during 2001-2002. The cases were 130 incident patients with
histologically confirmed adenocarcinoma of the prostate. The controls were
274 hospital inpatients without prostate cancer or any other malignant
diseases, and matched to the age of cases. Information on duration, quantity
and frequency of usual tea consumption, as well as the number of new batches
brewed per day, were collected by face-to-face interview using a structured
questionnaire. The risk of prostate cancer for tea consumption was assessed
using multivariate logistic regression adjusting for age, locality,
education, income, body mass index, physical activity, alcohol consumption,
tobacco smoking, total fat intake, marital status, age at marriage, number
of children, history of vasectomy and family history of prostate cancer.
Among the cases, 55.4% were tea drinkers compared to 79.9% for the controls.
Almost all the tea consumed was green tea. The prostate cancer risk declined
with increasing frequency, duration and quantity of green tea consumption.
The adjusted odds ratio (OR), relative to non-tea drinkers, were 0.28 (95%
CI = 0.17-0.47) for tea drinking, 0.12 (95% CI = 0.06-0.26) for drinking tea
over 40 years, 0.09 (95% CI = 0.04-0.21) for those consuming more than 1.5
kg of tea leaves yearly, and 0.27 (95% CI = 0.15-0.48) for those drinking
more than 3 cups (1 litre) daily. The dose response relationships were also
significant, suggesting that green tea is protective against prostate
cancer.
Biochem Pharmacol. 2002 Mar 15;63(6):1165-76.
Structure-activity relationships for inhibition of human 5alpha-reductases
by polyphenols.
Hiipakka RA, Zhang HZ, Dai W, Dai Q, Liao S.
Department of Biochemistry and Molecular Biology, The Ben May Institute for
Cancer Research, and The Tang Center for Herbal Medicine Research MC6027,
University of Chicago, 5841 S. Maryland, Chicago, IL 60637, USA.
The enzyme steroid 5 alpha-reductase (EC 1.3.99.5) catalyzes the
NADPH-dependent reduction of the double bond of a variety of 3-oxo-Delta(4)
steroids including the conversion of testosterone to 5
alpha-dihydrotestosterone. In humans, 5 alpha-reductase activity is critical
for certain aspects of male sexual differentiation, and may be involved in
the development of benign prostatic hyperplasia, alopecia, hirsutism, and
prostate cancer. Certain natural products contain components that are
inhibitors of 5 alpha-reductase, such as the green tea catechin
(-)-epigallocatechin gallate (EGCG). EGCG shows potent inhibition in
cell-free but not in whole-cell assays of 5 alpha-reductase. Replacement of
the gallate ester in EGCG with long-chain fatty acids produced potent 5
alpha-reductase inhibitors that were active in both cell-free and whole-cell
assay systems. Other flavonoids that were potent inhibitors of the type 1
5alpha-reductase include myricetin, quercitin, baicalein, and fisetin.
Biochanin A, daidzein, genistein, and kaempferol were much better inhibitors
of the type 2 than the type 1 isozyme. Several other natural and synthetic
polyphenolic compounds were more effective inhibitors of the type 1 than the
type 2 isozyme, including alizarin, anthrarobin, gossypol,
nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and
dodecyl gallates. The presence of a catechol group was characteristic of
almost all inhibitors that showed selectivity for the type 1 isozyme of 5
alpha-reductase. Since some of these compounds are consumed as part of the
normal diet or in supplements, they have the potential to inhibit 5
alpha-reductase activity, which may be useful for the prevention or
treatment of androgen-dependent disorders. However, these compounds also may
adversely affect male sexual differentiation.
Bryan Shelton
>>>>> I just eat it though, I don't see the point in applying it topically.
>>>>
>>>> The point would be to inhibit 5a-reductase.
>>>
>>> So just eat it. You don't think that eating it will block 5-ar?
>>
>> No I don't. Don't you think that if eating or drinking green tea really
>> inhibited 5a-reductase to any significant degree, we would ALL know
>> about it by now? Don't you think it would have long since passed into
>> folklore and traditional medicine as a "natural" cure for a variety of things
>> like acne and prostate problems and hairloss? As far as I know, there is
>> no tradition of using it for things like that, and drug companies have
>> been investing large sums of $$$ to find synthetic drugs that really
>> DO do that job well. So I strongly doubt that eating or drinking green
>> tea in anywhere near reasonable amounts is going to have much of an
>> effect on 5a-reductase.
>
>All I have are some studies that show EGCG inhibits 5ar. We know EGCG
>is absorbed when taken orally.
No we don't. At least, not to any major extent. From what I've read,
EGCG is very poorly absorbed from the GI tract.
>Other of its positive effects have been demonstrated
>when ingested. And, I see no reason to think it would not also
>demonstrate 5ar inhibition as well when taken orally in the diet.
Don't assume that its positive effects (decrease in prostate cancer,
etc.) are necessarily due to the systemic absorption of EGCG. It may
not be. In fact, EGCG is poorly absorbed, from what I've read.
There may be a whole raft of other reasons for its various health effects.
>If whole
>green tea counteracts some of the actions of isolated EGCG, maybe thats
>why green tea has not been used to treat BPH. Of course, Im only guessing.
So you admit that drinking green tea almost certainly does NOT
lower serum DHT? Don't you think that would have been noticed
DECADES ago?
>You believe using topically is effective, right?
I don't really "believe" it, I just think it's a distinct possibility.
It was shown to be effective in that hamster study, and that's
a giant step in the right direction.
>If it can be ingested, then taking it orally should also be effective.
I don't see any justification for believing that.
>Like Minoxidil, it probably works better
>and at lower doses when taken orally.
There is evidence that when you use topical minoxidil, there is both
a LOCAL and a SYSTEMIC component to its effect (I've been meaning
to post about that for several months). What I mean by that is that
topical minoxidil works partly because of systemic absorption, and
partly because of a direct "local" effect where it's actually applied.
>For acne, B5 appears to work
>better orally than topically. The only reason to use Minoxidil topically is
>because of the adverse effects of using it orally. Same with anti-androgens.
>We don't use finasteride topically since it would take far too much and
>would be no more effective. Why would EGCG be any different? I want to know.
Because EGCG is apparently very poorly absorbed from the GI tract.
>Are there examples of agents that can be safely ingested and absorbed
>orally, are effective topically, but are not effective orally?
Yes. Topical fatty acids (GLA, ALA, LA, etc).
Bryan
Ernie Primeau
Ernie Primeau
Kev
> On Fri, 19 Dec 2003 11:53:38 GMT, Kev <Kevi...@aol.com> wrote:
>
>>>>>> I just eat it though, I don't see the point in applying it topically.
>>>>>
>>>>> The point would be to inhibit 5a-reductase.
>>>>
>>>> So just eat it. You don't think that eating it will block 5-ar?
>>>
>>> No I don't. Don't you think that if eating or drinking green tea really
>>> inhibited 5a-reductase to any significant degree, we would ALL know
>>> about it by now? Don't you think it would have long since passed into
>>> folklore and traditional medicine as a "natural" cure for a variety of
>>> things
>>> like acne and prostate problems and hairloss? As far as I know, there is
>>> no tradition of using it for things like that, and drug companies have
>>> been investing large sums of $$$ to find synthetic drugs that really
>>> DO do that job well. So I strongly doubt that eating or drinking green
>>> tea in anywhere near reasonable amounts is going to have much of an
>>> effect on 5a-reductase.
>>
>> All I have are some studies that show EGCG inhibits 5ar. We know EGCG
>> is absorbed when taken orally.
>
> No we don't. At least, not to any major extent. From what I've read,
> EGCG is very poorly absorbed from the GI tract.
References?
>> Other of its positive effects have been demonstrated
>> when ingested. And, I see no reason to think it would not also
>> demonstrate 5ar inhibition as well when taken orally in the diet.
>
> Don't assume that its positive effects (decrease in prostate cancer,
> etc.) are necessarily due to the systemic absorption of EGCG. It may
> not be. In fact, EGCG is poorly absorbed, from what I've read.
>
> There may be a whole raft of other reasons for its various health effects.
None of the studies on EGCG are by ingesting? (I should answer that
myself...)
>> If whole
>> green tea counteracts some of the actions of isolated EGCG, maybe thats
>> why green tea has not been used to treat BPH. Of course, Im only guessing.
>
> So you admit that drinking green tea almost certainly does NOT
> lower serum DHT? Don't you think that would have been noticed
> DECADES ago?
Yes, I agree, in fact it may raise DHT. But, again, we are talking about two
different things, whole green tea vs. EGCG.
>> You believe using topically is effective, right?
>
> I don't really "believe" it, I just think it's a distinct possibility.
> It was shown to be effective in that hamster study, and that's
> a giant step in the right direction.
>
>> If it can be ingested, then taking it orally should also be effective.
>
> I don't see any justification for believing that.
>
>> Like Minoxidil, it probably works better
>> and at lower doses when taken orally.
>
> There is evidence that when you use topical minoxidil, there is both
> a LOCAL and a SYSTEMIC component to its effect (I've been meaning
> to post about that for several months). What I mean by that is that
> topical minoxidil works partly because of systemic absorption, and
> partly because of a direct "local" effect where it's actually applied.
>
>> For acne, B5 appears to work
>> better orally than topically. The only reason to use Minoxidil topically is
>> because of the adverse effects of using it orally. Same with anti-androgens.
>> We don't use finasteride topically since it would take far too much and
>> would be no more effective. Why would EGCG be any different? I want to know.
>
> Because EGCG is apparently very poorly absorbed from the GI tract.
>
>> Are there examples of agents that can be safely ingested and absorbed
>> orally, are effective topically, but are not effective orally?
>
> Yes. Topical fatty acids (GLA, ALA, LA, etc).
*Topical* fatty acids, haha, sounds like a trick answer. But you can't
digest those, they change upon digestion -- or they are not edible ...
Right? I mean, you could digest borage oil, but thats not the free fatty
acid anyway. So, thats a bad example. I want an example where you can digest
it, and it's effective topically but not orally. If, as you suggest, EGCG is
very poorly absorbed, then you are right, I agree, it wont work.
Kev
> Because EGCG is apparently very poorly absorbed from the GI tract.
Looks like 0.2%-2.0% gets absorbed. So, lets say 1% gets absorbed, and so
taking 100mg gets you 1mg in plasma. Yeah, you can argue that is poor. Im
taking BAC's extract. They claim ">80% catechins (40% EGCG!)" I don't know
if thats 40% of the total, or 40% of the catechins. Lets say its 40% of the
total. I take 600mg per day. Thats 240mg EGCG. So, Im absorbing 2.4mg EGCG.
Would that be worse than applying a 10% solution of this green tea extract?
10% is 100mg/ml. 100mg of extract would contain 40mg EGCG. Would 40mg twice
a day topically be better than 2.4mg systemically? Sounds like it, but I
dont know. It depends on how well it is absorbed through skin. If it were
Minoxidil, I think topically would win. If I took the 2.4mg twice a day, I
bet it would be close to the effectiveness of the topical if we were talking
about Minoxidil. Looks like I should triple my green tea extract dose.
Biosci Biotechnol Biochem. 1997 Dec;61(12):1981-5.
Dose-dependent incorporation of tea catechins,
(-)-epigallocatechin-3-gallate and (-)-epigallocatechin, into human plasma.
Tea catechins, (-)-epigallocatechin-3-gallate (EGCg) and
(-)-epigallocatechin (EGC), have been reported to suppress oxidation of
plasma low density lipoprotein (LDL) in vitro. If dietary catechins can be
efficiently incorporated into human blood plasma, anti-atherosclerotic
effects in preventing oxidative modification of LDL would be expected. In
this study, a newly developed chemiluminescence detection-high pressure
liquid chromatography (CL-HPLC) method for measuring plasma catechins was
used and the incorporation of EGCg and EGC into human plasma was
investigated. Healthy subjects orally ingested 3, 5, or 7 capsules of green
tea extract (corresponding to 225, 375, and 525 mg EGCg and 7.5, 12.5, and
17.5 mg EGC, respectively). The plasma EGCg and EGC concentrations before
the administration were all below the detection limit (< 2 pmol/ml), but 90
min after, significantly and dose-dependently increased to 657, 4300, and
4410 pmol EGCg/ml, and 35, 144, and 255 pmol EGC/ml, in the subjects who
received 3, 5, and 7 capsules, respectively. Both EGCg and EGC levels
detected in plasma corresponded to 0.2-2.0% of the ingested amount. Catechin
intake had no effect on the basal level of endogenous antioxidants
(alpha-tocopherol, beta-carotene, and lycopene) or of lipids in plasma.
These results suggested that drinking green tea daily would contribute to
maintain plasma catechin levels sufficient to exert antioxidant activity
against oxidative modification of lipoproteins in blood circulation systems.
Publication Types:
PMID: 9438978
J Int Med Res. 2003 Mar-Apr;31(2):88-101.
A single ascending dose study of epigallocatechin gallate in healthy
volunteers.
This randomized, double-blind, placebo-controlled study assessed the safety,
tolerability and plasma kinetic behaviour of single oral doses of 94% pure
crystalline bulk epigallocatechin gallate (EGCG) under fasting conditions in
60 healthy male volunteers. In each group of 10 subjects, eight received
oral EGCG in single doses of 50 mg, 100 mg, 200 mg, 400 mg, 800 mg or 1600
mg, and two received placebo. Blood samples were taken at intervals until 26
h later. The area under the concentration-time curve from 0 h to infinity
(AUC(0-infinity)), the maximum plasma concentration (Cmax) of EGCG, the time
taken to reach the maximum concentration (Tmax), and the terminal
elimination half-life (t1/2z) of EGCG were determined. Safety and
tolerability were assessed. In each dosage group, the kinetic profile
revealed rapid absorption with a one-peak plasma concentration versus time
course, followed by a multiphasic decrease consisting of a distribution
phase and an elimination phase. The mean AUC(0-infinity) of total EGCG
varied between 442 and 10,368 ng.h/ml. The according mean Cmax values ranged
from 130 to 3392 ng/ml and were observed after 1.3-2.2 h. The mean t1/2z
values were seen between 1.9 and 4.6 h. Single oral doses of EGCG up to 1600
mg were safe and very well tolerated.
PMID: 12760312
Cancer Epidemiol Biomarkers Prev. 2002 Oct;11(10 Pt 1):1025-32.
Pharmacokinetics of tea catechins after ingestion of green tea and
(-)-epigallocatechin-3-gallate by humans: formation of different metabolites
and individual variability.
Green tea and tea polyphenols have been studied extensively as cancer
chemopreventive agents in recent years. The bioavailability and metabolic
fate of tea polyphenols in humans, however, are not clearly understood. In
this report, the pharmacokinetic parameters of
(-)-epigallocatechin-3-gallate (EGCG), (-)-epigallocatechin (EGC), and
(-)-epicatechin (EC) were analyzed after administration of a single oral
dose of green tea or decaffeinated green tea (20 mg tea solids/kg) or EGCG
(2 mg/kg) to eight subjects. The plasma and urine levels of total EGCG, EGC,
and EC (free plus conjugated forms) were quantified by HPLC coupled to an
electrochemical detector. The plasma concentration time curves of the
catechins were fitted in a one-compartment model. The maximum plasma
concentrations of EGCG, EGC, and EC in the three repeated experiments with
green tea were 77.9 +/- 22.2, 223.4 +/- 35.2, and 124.03 +/- 7.86 ng/ml,
respectively, and the corresponding AUC values were 508.2 +/- 227, 945.4 +/-
438.4, and 529.5 +/- 244.4 ng x h x ml(-1), respectively. The time needed to
reach the peak concentrations was in the range of 1.3-1.6 h. The elimination
half-lives were 3.4 +/- 0.3, 1.7 +/- 0.4, and 2.0 +/- 0.4 h, respectively.
Considerable interindividual differences and variations between repeated
experiments in the pharmacokinetic parameters were noted. Significant
differences in these pharmacokinetic parameters were not observed when EGCG
was given in decaffeinated green tea or in pure form. In the plasma, EGCG
was mostly present in the free form, whereas EGC and EC were mostly in the
conjugated form. Over 90% of the total urinary EGC and EC, almost all in the
conjugated forms, were excreted between 0 and 8 h. Substantial amounts of
4'-O-methyl EGC, at levels higher than EGC, were detected in the urine and
plasma. The plasma level of 4'-O-methyl EGC peaked at 1.7 +/- 0.5 h with a
half life of 4.4 +/- 1.1 h. Two ring-fission metabolites,
(-)-5-(3',4',5'-trihydroxyphenyl)-gamma-valerolactone (M4) and
(-)-5-(3',4'-dihydroxyphenyl)-valerolactone (M6), appeared in significant
amounts after 3 h and peaked at 8-15 h in the urine as well as in the
plasma. These results may be useful for designing the dose and dose
frequency in intervention studies with tea and for development of biomarkers
of tea consumption.
PMID: 12376503
Cancer Epidemiol Biomarkers Prev. 1998 Apr;7(4):351-4.
Blood and urine levels of tea catechins after ingestion of different amounts
of green tea by human volunteers.
The inhibitory activity of tea against tumorigenesis has been demonstrated
in many animal models and has been suggested by some epidemiological
studies. Such activity has generally been attributed to tea catechins. To
understand the bioavailability of tea catechins in humans, we gave 18
individuals different amounts of green tea and measured the time-dependent
plasma concentrations and urinary excretion of tea catechins. After taking
1.5, 3.0, and 4.5 g of decaffeinated green tea solids (dissolved in 500 ml
of water), the maximum plasma concentration (Cmax) of
(-)-epigallocatechin-3-gallate (EGCG) was 326 ng/ml, the Cmax of
(-)-epigallocatechin (EGC) was 550 ng/ml, and the Cmax of (-)-epicatechin
(EC) was 190 ng/ml. These Cmax values were observed at 1.4-2.4 h after
ingestion of the tea preparation. When the dosage was increased from 1.5 to
3.0 g, the Cmax values increased 2.7-3.4-fold, but increasing the dose to
4.5 g did not increase the Cmax values significantly, which suggested a
saturation phenomenon. The half-life of EGCG (5.0-5.5 h) seemed to be higher
than the half-life of EGC or EC (2.5-3.4 h). EGC and EC, but not EGCG, were
excreted in the urine. Over 90% of the total urinary EGC and EC was excreted
within 8 h. When the tea dosage was increased, the amount of EGC and EC
excretion seemed to increase, but a clear dose-response relationship was not
observed. The present study provides basic pharmacokinetic parameters of
green tea catechins in humans; these parameters may be used to estimate the
levels of these compounds after drinking tea.
PMID: 9568793
Int J Toxicol. 2003 May-Jun;22(3):187-93.
Absorption, tissue distribution and elimination of 4-[(3)h]-epigallocatechin
gallate in beagle dogs.
Polyphenols found in tea are potent antioxidants and have inhibitory
activity against tumorigenicity. The purpose of the described study was to
assess the absorption, tissue distribution, and elimination of
epigallocatechin gallate (EGCG), the principal catechin found in green tea,
in a nonrodent species. 4-[(3)H]-EGCG was administered to beagle dogs by
intravenous (IV) and oral routes. Following IV administration of 25 mg/kg,
radioactivity in the bloodstream resided predominantly in the plasma.
Distribution occurred during the first hour, and the plasma levels of total
radioactivity declined with a mean half-life of approximately 7 hours. The
apparent volume of distribution (0.65 l/kg) indicated wide distribution, and
the total body clearance (1.01 ml/min-kg) was low. A subsequent single oral
dose (250 mg/kg) was rapidly absorbed, with peak plasma levels at about 1
hour after administration, followed by elimination with a mean half-life of
8.61 hours. The mean area under the curve (AUC) for total radioactivity was
approximately 20% of the value following IV administration (corrected for
dose administered). Excretion of radioactivity in the feces predominated
over urinary excretion following both IV and oral administration of
[(3)H]-EGCG. Tissue distribution was determined 1 hour after an IV dose (25
mg/kg) administered after 27 days of oral treatment with EGCG (250
mg/kg/day) to mimic chronic consumption of tea. Radioactivity was
distributed to a variety of epithelial tissues; the highest concentrations
were observed in the liver and gastrointestinal tract tissues. Repeat dose
oral administration of EGCG resulted in significantly lower blood
radioactivity compared to the concentration following a single dose. These
results are generally in accord with previous studies in rodents and
indicate that, after oral administration, EGCG (as parent compound and
metabolites) is widely distributed to tissues where it can exert a
chemopreventive effect.
PMID: 12851151
J Nutr. 2003 Dec;133(12):4172-7.
Epigallocatechin-3-gallate is absorbed but extensively glucuronidated
following oral administration to mice(,2).
Epigallocatechin-3-gallate (EGCG), the most abundant catechin in green tea
(Camellia sinensis), has shown cancer preventive activity in animal models.
The bioavailability of EGCG in the most commonly used animal species, mice,
is poorly understood. Moreover, the pharmacokinetic parameters of EGCG have
not been reported previously in mice. Here we report that after
administration of EGCG intravenously at 21.8 micro mol/kg or
intragastrically at 163.8 micro mol/kg, the peak plasma levels of EGCG in
male CF-1 mice were 2.7 +/- 0.7 and 0.28 +/- 0.08 micro mol/L, respectively.
EGCG was present mainly (50-90%) as the glucuronide. The plasma
bioavailability of EGCG after intragastric administration was higher than
previously reported in rats (26.5 +/- 7.5% vs. 1.6 +/- 0.6%). The conjugated
EGCG displayed a shorter t(1/2) (82.8-211.5 vs 804.9-1102.3 min) than
unconjugated EGCG (P < 0.01, Student's t test). EGCG was present in the
unconjugated form in the lung, prostate and other tissues at levels of
0.31-3.56 nmol/g after intravenous administration. Although intragastric
administration resulted in lower levels in most tissues compared with
intravenous administration (e.g., 0.006 +/- 0.004 vs. 2.66 +/- 1.0 nmol/g in
the lung), the levels in the small intestine and colon were high at 45.2 +/-
13.5 and 7.86 +/- 2.4 nmol/g, respectively. This is the first report of the
pharmacokinetic parameters of EGCG in mice. Such information provides a
basis for understanding the bioavailability of EGCG in mice and should aid
in understanding the cancer preventive activity of EGCG.
PMID: 14652367
Biol Pharm Bull. 1996 Feb;19(2):326-9.
Absorption of tea catechins into rat portal vein.
Food Research Laboratories, Mitsui Norin Co., Ltd., Fujieda-shi, Japan.
Following the oral administration of tea catechins, (-)-epicatechin,
(-)-epigallocatechin, (-)-epicatechin gallate and (-)-epigallocatechin
gallate, respectively, to rats, the presence of these catechins in the
portal blood was examined. It was confirmed by HPLC and mass spectrometry
analysis that each of the administered catechins was present in the blood.
These results clearly indicate that four predominant catechins in fresh tea
leaves are absorbed, at least in part, into the rat portal vein.
PMID: 8850335
Bryan Shelton
>> No we don't. At least, not to any major extent. From what I've read,
>> EGCG is very poorly absorbed from the GI tract.
>
>References?
I don't have the reference any more (it was from a couple of years ago),
but it was pretty much in agreement with your conclusions from your next
post after this one...namely, around 1% to 2% absorption. Not very much.
>>> Other of its positive effects have been demonstrated
>>> when ingested. And, I see no reason to think it would not also
>>> demonstrate 5ar inhibition as well when taken orally in the diet.
>>
>> Don't assume that its positive effects (decrease in prostate cancer,
>> etc.) are necessarily due to the systemic absorption of EGCG. It may
>> not be. In fact, EGCG is poorly absorbed, from what I've read.
>>
>> There may be a whole raft of other reasons for its various health effects.
>
>None of the studies on EGCG are by ingesting? (I should answer that
>myself...)
Kevin, I'm telling you not to assume that the health benefits are from the
SYSTEMIC ABSORPTION of the EGCG into the bloodstream!
Here's a simple example of what I'm talking about: EGCG could possibly
not be absorbed into the bloodstream AT ALL, and yet still have its various
health benefits simply by acting on other substances as it's passing through
the GI tract. For example, its strong antioxidant properties could possibly
be keeping relatively harmless substances from being converted into
dangerous carcinogens WITHIN the GI tract. See what I mean?? Don't
assume that if it's not being absorbed into the bloodstream, then it just
can't possibly be having any important effect on the body. Important things
(both good and bad) happen right there within the gut.
>>> Are there examples of agents that can be safely ingested and absorbed
>>> orally, are effective topically, but are not effective orally?
>>
>> Yes. Topical fatty acids (GLA, ALA, LA, etc).
>
>*Topical* fatty acids, haha, sounds like a trick answer.
Immediately after I posted that, I realized I should have simply said
"fatty acids", instead of "topical fatty acids". That would be more precise.
>But you can't
>digest those, they change upon digestion -- or they are not edible ...
I'm not entirely sure what happens when you take large oral amounts
of free fatty acids. When you swallow natural oils, they are digested
down into free fatty acids and glycerol, but then they are put back
into triglycerides before they are released into the bloodstream.
However, there are small amounts (traces) of free fatty acids
even in natural oils, so the body must have _some_ way of dealing
with them properly...
>Right? I mean, you could digest borage oil, but thats not the free fatty
>acid anyway. So, thats a bad example. I want an example where you can digest
>it, and it's effective topically but not orally. If, as you suggest, EGCG is
>very poorly absorbed, then you are right, I agree, it wont work.
There was also a recent study in which GLA was given in supplement
form to test subjects along with DHEA and some herbal substances,
and the GLA wasn't able to stop the increase in DHT from the DHEA.
However, I couldn't find out for sure whether the GLS was in its "free"
form, or just a triglyceride.
In any event, I stand by the fatty acids as an example of something
which works topically, but not orally. That's probably because
IN THEORY it could work orally, but it's just too expensive (or maybe
dangerous) to try to take enough of it orally to have much of an effect
on one specific part of your body (like your scalp), whereas it's fairly
easy to flood your scalp locally with those active substances (fatty
acids, EGCG, etc.).
Bryan
Bryan Shelton
>Bryan Shelton at br...@airmail.net wrote:
>
>> Because EGCG is apparently very poorly absorbed from the GI tract.
>
>Looks like 0.2%-2.0% gets absorbed. So, lets say 1% gets absorbed, and so
>taking 100mg gets you 1mg in plasma. Yeah, you can argue that is poor. Im
>taking BAC's extract. They claim ">80% catechins (40% EGCG!)"
Yeah, that's what I use, too! :-)
>I don't know
>if thats 40% of the total, or 40% of the catechins. Lets say its 40% of the
>total. I take 600mg per day. Thats 240mg EGCG. So, Im absorbing 2.4mg EGCG.
>Would that be worse than applying a 10% solution of this green tea extract?
I think so. 2.4 mg spread out over your entire body, compared to flooding
your scalp topically with a strong alcoholic solution of the stuff?? Seems
like a no-brainer to me! :-)
>10% is 100mg/ml. 100mg of extract would contain 40mg EGCG.
>Would 40mg twice a day topically be better than 2.4mg systemically?
I certainly think so!
>Sounds like it, but I dont know.
>It depends on how well it is absorbed through skin.
Yes, and being water soluble _may_ make it more difficult for EGCG
to be absorbed properly (once again the big issue raises its head again
about which is more important for hair follicles, true transdermal
absorption in the sense of passing through the stratum corneum,
or passing down through the hair follicle itself??). Because of that
possible little problem, I'm always careful to apply my topical green
tea solution to a THOROUGHLY hydrated scalp. Hydration should
assist the passage of water soluble substances even more than fat-
soluble substances, so this is definitely the time to take advantage
of that technique.
I personally use BAC's high-potency extract in about a 5%-10% solution
in a 50/50 water/Everclear vehicle to a THOROUGHLY hydrated scalp.
Bryan
Kev
>> I don't know
>> if thats 40% of the total, or 40% of the catechins. Lets say its 40% of the
>> total. I take 600mg per day. Thats 240mg EGCG. So, Im absorbing 2.4mg EGCG.
>> Would that be worse than applying a 10% solution of this green tea extract?
>
> I think so. 2.4 mg spread out over your entire body, compared to flooding
> your scalp topically with a strong alcoholic solution of the stuff?? Seems
> like a no-brainer to me! :-)
You are right, it seems like a no-brainer. Lets look at some examples.
Is 10mg of oral Minoxidil spread throughout the body better than flooding
your scalp topical with 100mg (2ml of 5%) of Minoxidil? Is that a
no-brainer? No.
Is 50mg of topical finasteride better than 1mg of oral finasteride? Is that
a no-brainer? No.
Is the antiandrogenic action of 100mg topical spironolactone better than
50mg oral spironolactone? Is that a no-brainer? No.
I realize that your argument seems good -- 2.4mg spread throughout the body
*seems* better than a concentrated amount on the skin. You can see from
these examples that this argument is frequently not a good one to make. And,
if its difficult to absorb orally its probably also difficult to absorb
through the skin.
kofi
> your scalp topically with a strong alcoholic solution of the stuff?? Seems
> like a no-brainer to me! :-)
>
I recommend DMSO.
If you want a good idea of what it does to keratinocytes, put some green
tea and DMSO on your face too (and a towel on your pillow).
kofi
these high levels (and one should always use decaf, which is what the
extract is anyway) is inhibiting vitamin B1.
kofi
br...@airmail.net (Bryan Shelton) wrote:
> On Sat, 13 Dec 2003 11:02:28 GMT, anon <an...@anon.anon> wrote:
>
> >> So where did you get that thing about "whole cell cultures"?
> >
> ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&lis
> >t_uids=11931850&dopt=Abstract>
>
> That's very odd...yes, I see that comment about the "whole cell cultures"
> in the abstract, but topical EGCG has apparently been shown to inhibit
> 5a-reductase in an 'in vivo' model (hamster flank organs) in the other study
> you cite below, written by some of the same authors as the one above!
>
> I believe it's safe to say that the fact that it seems to work topically on
> LIVE ANIMALS trumps that strange claim about "whole cell cultures"!
You don't know that it's inhibiting 5AR. For all the authors knew, the
EGCG could have been inhibiting VEGF-driven prostate inflammation (which
it does) or some other growth factor.
> >Green tea catechins appear to inhibit androgen dependent tissue growth
> >but not necessarily through 5AR inhibition.
> >
> ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&lis
> >t_uids=11380153&dopt=Abstract>
>
> Yes. I don't know if you've read that whole study, but one thing they found
> was simply astonishing: topical EGCG was also able to reduce by 97%
> the DHT-stimulated growth of the hamster flank organs! That does make
> one wonder how much of the testosterone-stimulated growth that was also
> suppressed by EGCG was actually due to the direct inhibition of 5a-R, and
> how much was due to the apparent androgen receptor-blocking ability
> of EGCG. In any event, I've been saying for the last year or so that
> the above study makes topical EGCG look _awfully_ attractive!
EGCG definitely interferes with the inflammatory process, as does grean
tea extract. I've been applying DMSO and green tea extract to my upper
body for several muscle, joint and nerve problems for the last year or
two. It's really, really potent (and the powder only lasts about two
months before oxidizes too much). I wouldn't have believed it if there
hadn't been such a direct, dramatic change in my health the next day
after applying it. Given my sensitivity to GABAergic inhibition (even
mild ones like 5AR inhibitors) I think I'd know if GTE were inhibiting
DHT. (I know consuming high doses of oral curcumin with piperine will,
along with T).
However, I think to regrow hair you need to do more than block the
androgen receptor or control downstream inflammation. Those two things
are very important, but they're hardly all judging from some of the
mildly pro-inflammatory signals involved in growing hair (MMP-2, VEGF,
etc.).
As to the issue of digestion, I think tannins may play a role here
although I'm told either catechins or polyphenols intefere with
thiaminase (and I can't remember what that does). It's a shame tannic
acid hasn't been better studied. Antioxidants in general have a
beneficial effect on gut mucosa.
High levels of consumption might also interfere with mineral metabolism
(although there's no link between osteoporosis and tea consumption).
The thing you guys keep failing to mention is the connection between
insulin and sex hormone-binding globulin. By lowering insulin, EGCG may
increase SHBG and bind up sex hormones before they have a chance to get
to their receptors. Do any of these studies break down readings into
things like "Free T?"
Finally, don't forget EGCG is a phytoestrogen. Although it appears to
have little, if any, estrogenic effects, it might plug into some minor
but beneficial metabolic pathways through that similarity.
Bryan Shelton
Kevin, you're missing the point here, which is that I'm basing my argument
above on EMPIRICAL EXPERIMENTS which have indeed shown topical
EGCG to be effective in both animal trials and a human experiment.
It's a free country, so you can go ahead and continue to take your 2.4 mg/day
of systemic EGCG, for which there is not an iota of evidence for any effect
on the scalp. I will continue to use it topically, for which there is definitely
some evidence for a possible beneficial effect.
Bryan
Bryan Shelton
I've never used DMSO, and I'm not particularly inclined to start!
Can you just TELL me what happens? ;-)
Bryan
Bryan Shelton
> br...@airmail.net (Bryan Shelton) wrote:
>
>> On Sat, 13 Dec 2003 11:02:28 GMT, anon <an...@anon.anon> wrote:
>>
>> >> So where did you get that thing about "whole cell cultures"?
>> >
>> ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&lis
>> >t_uids=11931850&dopt=Abstract>
>>
>> That's very odd...yes, I see that comment about the "whole cell cultures"
>> in the abstract, but topical EGCG has apparently been shown to inhibit
>> 5a-reductase in an 'in vivo' model (hamster flank organs) in the other study
>> you cite below, written by some of the same authors as the one above!
>>
>> I believe it's safe to say that the fact that it seems to work topically on
>> LIVE ANIMALS trumps that strange claim about "whole cell cultures"!
>
>You don't know that it's inhibiting 5AR. For all the authors knew, the
>EGCG could have been inhibiting VEGF-driven prostate inflammation
>(which it does) or some other growth factor.
I don't understand what you're saying...are you claiming that there's
some kind of VEGF-driven inflammation in the skin that's similar to what
occurs in the prostate, and is responsible for sebaceous gland stimulation?
Or are you DIRECTLY blaming something in the prostate for what happens
in the skin?? I don't follow you at all...
>> >Green tea catechins appear to inhibit androgen dependent tissue growth
>> >but not necessarily through 5AR inhibition.
>> >
>> ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&lis
>> >t_uids=11380153&dopt=Abstract>
>>
>> Yes. I don't know if you've read that whole study, but one thing they found
>> was simply astonishing: topical EGCG was also able to reduce by 97%
>> the DHT-stimulated growth of the hamster flank organs! That does make
>> one wonder how much of the testosterone-stimulated growth that was also
>> suppressed by EGCG was actually due to the direct inhibition of 5a-R, and
>> how much was due to the apparent androgen receptor-blocking ability
>> of EGCG. In any event, I've been saying for the last year or so that
>> the above study makes topical EGCG look _awfully_ attractive!
>
>EGCG definitely interferes with the inflammatory process, as does grean
>tea extract. I've been applying DMSO and green tea extract to my upper
>body for several muscle, joint and nerve problems for the last year or
>two. It's really, really potent (and the powder only lasts about two
>months before oxidizes too much).
Are you saying that the DMSO/GTE solution only lasts for a couple
of months, or the dry powder itself that you have in storage?
>I wouldn't have believed it if there
>hadn't been such a direct, dramatic change in my health the next day
>after applying it.
How much of the solution (and at what concentration) do you apply
over how big an area of your body? What specific beneficial effects
do you observe the next day?
>Given my sensitivity to GABAergic inhibition (even mild ones
>like 5AR inhibitors) I think I'd know if GTE were inhibiting DHT.
But the point is that topical GTE has a LOCAL effect, at least
according to the studies. So I doubt that there would be
a systemic effect for you to notice.
>(I know consuming high doses of oral curcumin with piperine will,
>along with T).
You really think that piperine enhances absorption?
>However, I think to regrow hair you need to do more than block the
>androgen receptor or control downstream inflammation. Those two things
>are very important, but they're hardly all judging from some of the
>mildly pro-inflammatory signals involved in growing hair (MMP-2, VEGF,
>etc.).
Agreed.
>The thing you guys keep failing to mention is the connection between
>insulin and sex hormone-binding globulin. By lowering insulin, EGCG may
>increase SHBG and bind up sex hormones before they have a chance to get
>to their receptors.
Do you really think that green tea consumption could make much
of an impact on circulating androgens, which in turn could have much
of an effect on the course of MPB? Personally, I doubt it.
>Finally, don't forget EGCG is a phytoestrogen. Although it appears to
>have little, if any, estrogenic effects, it might plug into some minor
>but beneficial metabolic pathways through that similarity.
Interesting idea!
Bryan
Bryan Shelton
What about the evidence suggesting that caffeine is necessary
to ensure at least some of green tea's beneficial effects?
Bryan
anon
(Bryan Shelton) wrote:
If stress hormones play a role in pathogenesis, why would you want to
add caffeine to the mix?
Caffeine is an adenosine receptor antagonist which may worsen chronic
inflammatory conditions.
anon
> >> That's very odd...yes, I see that comment about the "whole cell
> >> cultures"
> >> in the abstract, but topical EGCG has apparently been shown to inhibit
> >> 5a-reductase in an 'in vivo' model (hamster flank organs) in the other
> >> study
> >> you cite below, written by some of the same authors as the one above!
> >>
> >> I believe it's safe to say that the fact that it seems to work
> >> topically on
> >> LIVE ANIMALS trumps that strange claim about "whole cell cultures"!
> >
> >You don't know that it's inhibiting 5AR. For all the authors knew, the
> >EGCG could have been inhibiting VEGF-driven prostate inflammation
> >(which it does) or some other growth factor.
>
> I don't understand what you're saying...are you claiming that there's
> some kind of VEGF-driven inflammation in the skin that's similar to what
> occurs in the prostate, and is responsible for sebaceous gland
> stimulation?
> Or are you DIRECTLY blaming something in the prostate for what happens
> in the skin?? I don't follow you at all...
I'm not making any statement about what's going on in the skin.
I'm saying the resulting shrinkage in the flank organs may have had to
do with the effects of green tea on something other than testosterone or
it may have interfered with androgen-driven growth in a way that doesn't
necessarily translate to the skin the way we want it to.
> >
> >EGCG definitely interferes with the inflammatory process, as does grean
> >tea extract. I've been applying DMSO and green tea extract to my upper
> >body for several muscle, joint and nerve problems for the last year or
> >two. It's really, really potent (and the powder only lasts about two
> >months before oxidizes too much).
>
> Are you saying that the DMSO/GTE solution only lasts for a couple
> of months, or the dry powder itself that you have in storage?
The dry powder doesn't store well if you keep opening it up. I don't
know how long it would refrigerate in DMSO solution. I assume to use
the solution you'd have to repeatedly expose it to air.
Right now I'm more worried about the fluoride content in tea...
>
> >I wouldn't have believed it if there
> >hadn't been such a direct, dramatic change in my health the next day
> >after applying it.
>
> How much of the solution (and at what concentration) do you apply
> over how big an area of your body? What specific beneficial effects
> do you observe the next day?
It's an antinflammatory. I put it over a wide area. I'm getting good
results with aloe vera pulp too. As to proper percentages, I measured
out about 2-5ml of DMSO and threw in a teaspoonful of green tea. That's
part of the reason I chose it. I didn't need to worry about poisoning
myself.
>
> >Given my sensitivity to GABAergic inhibition (even mild ones
> >like 5AR inhibitors) I think I'd know if GTE were inhibiting DHT.
>
> But the point is that topical GTE has a LOCAL effect, at least
> according to the studies. So I doubt that there would be
> a systemic effect for you to notice.
If it reduced the damage to a pinched nerve elevating my stress system,
you can bet the effect would be systematic.
>
> >(I know consuming high doses of oral curcumin with piperine will,
> >along with T).
>
> You really think that piperine enhances absorption?
Yeah. Experience tells me so.
>
> >The thing you guys keep failing to mention is the connection between
> >insulin and sex hormone-binding globulin. By lowering insulin, EGCG may
> >increase SHBG and bind up sex hormones before they have a chance to get
> >to their receptors.
>
> Do you really think that green tea consumption could make much
> of an impact on circulating androgens, which in turn could have much
> of an effect on the course of MPB? Personally, I doubt it.
What's your evidence?
Check out the studies of women taking metformin for polycystic ovarian
syndrome.
>
> >Finally, don't forget EGCG is a phytoestrogen. Although it appears to
> >have little, if any, estrogenic effects, it might plug into some minor
> >but beneficial metabolic pathways through that similarity.
>
> Interesting idea!
This is what I keep saying about SERMs like tamoxifen and genistein
(BMP-2 stimulators).
Jacob
http://www.lipoxidil.com/site/liposomal.php
br...@airmail.net (Bryan Shelton) wrote in message news:<3febfd30...@news.airmail.net>...
make sure you can see me
I will give you a quick run down of my experience.
I first started topical applications that where pretty standard to what
everyone is mixing together over at alt.d. DMSO/Minox and MSM. They are
using Arginine and I actually use a tri-amino Arginine/Ornithine/Lysine
as that's what I had around.
After the first week, I had what resembled an extremely bad case of
dandruff that covered my whole scalp. One enormous lifting of dead skin
all at once. It was so bad, I just buzzed my head (I do this
occasionally so it wasn't a big deal for me). The hair in the tub was
filled with dead skin.
Week two brought three strange spots on my head (two at the front
hairline and one on top of my head), which I would most liken to wounds
that seemed to erupt as though they "healed from the inside". Its really
had to explain. They weren't any bigger than pencil erasers and
resembled large cists or zits. They seemed to enlarge, break through the
skin and then heal. Once they healed, nothing like them ever came back.
I've actually started using DMSO on my face and had no problems only
progress.
There is a bunch of good research at
http://www.dmso.org/subLevels/literature.htm, check it out.
You should also jump in at alt.baldspot.d with questions and thoughts,
there are a lot of good people over there that know more than me. Your
presence would be more than welcome, I'm sure.
It's standard NNTP at 216.119.247.100.
p.s. Since I have your attention a second, thanks for the years of posts
that I've read through over the past year. Even though we've never
spoken, I've read old archives of this group for hours and your
contributions are appreciated.
"Bryan Shelton" <br...@airmail.net> wrote in message
news:3febfc63...@news.airmail.net...
Bryan Shelton
>In article <3fec0572...@news.airmail.net>, br...@airmail.net
>(Bryan Shelton) wrote:
>
>> On Mon, 22 Dec 2003 06:06:14 GMT, kofi <ko...@anon.un> wrote:
>>
>> >The only thing you might want to worry about when ingesting green tea
>> >at these high levels (and one should always use decaf, which is what
>> >the extract is anyway) is inhibiting vitamin B1.
>>
>> What about the evidence suggesting that caffeine is necessary
>> to ensure at least some of green tea's beneficial effects?
>>
>> Bryan
>
>If stress hormones play a role in pathogenesis, why would you want to
>add caffeine to the mix?
Because there is evidence suggesting that caffeine is necessary
to ensure at least some of green tea's beneficial effects! ;-)
Bryan
Bryan Shelton
>I'm not making any statement about what's going on in the skin.
>
>I'm saying the resulting shrinkage in the flank organs may have had to
>do with the effects of green tea on something other than testosterone or
>it may have interfered with androgen-driven growth in a way that doesn't
>necessarily translate to the skin the way we want it to.
Yes, it may have had to do with that astonishing 97% inhibition of DHT-
stimulated growth of the flank organs! I'm surprised that more people
don't talk about that! Sheesh!
It seems to me very likely that the effect on the flank organs was
due in large part to a combined antiandrogenic effect of EGCG:
an action against 5a-reductase, androgen receptors, or both.
BTW, are you the same person as "kofi"? You're just listed as "anon"
here in this post, but you appear to be answering the same as in an earlier
post by "kofi". If you're also "kofi", what's with the multiple handles? :-)
>> Are you saying that the DMSO/GTE solution only lasts for a couple
>> of months, or the dry powder itself that you have in storage?
>
>The dry powder doesn't store well if you keep opening it up.
I keep my GTE in the fridge, and only open it on rare occasions
(once a month or so) to make a solution. I also keep the solution
in the fridge, with a few grains of BHT added to it.
>It's an antinflammatory. I put it over a wide area. I'm getting good
>results with aloe vera pulp too. As to proper percentages, I measured
>out about 2-5ml of DMSO and threw in a teaspoonful of green tea. That's
>part of the reason I chose it. I didn't need to worry about poisoning
>myself.
A teaspoon of green tea will dissolve in 2-5 mL of DMSO?? Damn....
>> >Given my sensitivity to GABAergic inhibition (even mild ones
>> >like 5AR inhibitors) I think I'd know if GTE were inhibiting DHT.
>>
>> But the point is that topical GTE has a LOCAL effect, at least
>> according to the studies. So I doubt that there would be
>> a systemic effect for you to notice.
>
>If it reduced the damage to a pinched nerve elevating my stress system,
>you can bet the effect would be systematic.
Well, I'm talking about sysemic absorption of the GTE, of course! :-)
>> >The thing you guys keep failing to mention is the connection between
>> >insulin and sex hormone-binding globulin. By lowering insulin, EGCG may
>> >increase SHBG and bind up sex hormones before they have a chance to get
>> >to their receptors.
>>
>> Do you really think that green tea consumption could make much
>> of an impact on circulating androgens, which in turn could have much
>> of an effect on the course of MPB? Personally, I doubt it.
>
>What's your evidence?
Just circumstantial evidence: with all the interest in recent years in the
health benefits of green tea, don't you think scientists would have noticed
by now if green tea consumption really does cause a significant reduction
in circulating androgens? As far as I know, they haven't...if you know
otherwise (you seem to be reading a lot of green tea studies), please
let me know. Furthermore, MPB is only weakly associated with circulating
androgens, anyway. Should it ever be proven that drinking green tea
does in fact slightly reduce them, I don't see how that could have much
of an impact on hairloss.
>Check out the studies of women taking metformin for polycystic ovarian
>syndrome.
What does that have to do with green tea?
Bryan
Ernie Primeau
to take something.Ernie
kofi
> here in this post, but you appear to be answering the same as in an earlier
> post by "kofi". If you're also "kofi", what's with the multiple handles?
> :-)
Anon is my crime-fighting alter-ego.
Or is it this one?
I forget.
Are you saying you're upset someone who's anonymous posted anonymously
under an anonymous pseudonym instead of under an anonymous pseudonym?
>
> A teaspoon of green tea will dissolve in 2-5 mL of DMSO?? Damn....
It's scared of black helicopters.
> Well, I'm talking about sysemic absorption of the GTE, of course! :-)
You're forgetting how well hair follicles on the scalp absorb topical
agents (at least 20x better than abdominal hairs).
>
> >> >The thing you guys keep failing to mention is the connection between
> >> >insulin and sex hormone-binding globulin. By lowering insulin, EGCG may
> >> >increase SHBG and bind up sex hormones before they have a chance to get
> >> >to their receptors.
> >>
> >> Do you really think that green tea consumption could make much
> >> of an impact on circulating androgens, which in turn could have much
> >> of an effect on the course of MPB? Personally, I doubt it.
> >
> >What's your evidence?
>
> Just circumstantial evidence: with all the interest in recent years in the
> health benefits of green tea, don't you think scientists would have noticed
> by now if green tea consumption really does cause a significant reduction
> in circulating androgens? As far as I know, they haven't...if you know
> otherwise (you seem to be reading a lot of green tea studies), please
> let me know. Furthermore, MPB is only weakly associated with circulating
> androgens, anyway. Should it ever be proven that drinking green tea
> does in fact slightly reduce them, I don't see how that could have much
> of an impact on hairloss.
>
> >Check out the studies of women taking metformin for polycystic ovarian
> >syndrome.
>
> What does that have to do with green tea?
Normalizing insulin and increasing SHBG is important for PCOS. Tea
consumption is linked to lowered circulating hormones (abstracts below).
Note that none of this suggests local synthesis and binding is greatly
affected - although it may be. Tea consumption definitely results in
lower hormone driven cancers but there's no evidence that, for instance,
drinking green tea makes you impotent the way a dose of proscar can
(although the L-theanine will certainly stimulate GABAergic pathways
resulting in less general excitability). I, for one, would like to know
what accounts for the different forms of hormonal inhibition.
Nutr Cancer. 1998;30(1):21-4. Related Articles, Links
Association of coffee, green tea, and caffeine intakes with serum
concentrations of estradiol and sex hormone-binding globulin in
premenopausal Japanese women.
Nagata C, Kabuto M, Shimizu H.
Department of Public Health, Gifu University School of Medicine,
Japan.
Caffeine intake has been proposed to influence breast cancer risk.
Its effect may be mediated by hormonal changes. The relationships
between caffeine-containing beverages (coffee, green tea, black tea,
oolong tea, and cola) and serum concentrations of estradiol and sex
hormone-binding globulin were evaluated in 50 premenopausal Japanese
women. Intakes of caffeine and caffeine-containing beverages were
assessed by a semiquantitative food-frequency questionnaire. Blood
samples were obtained from each woman on Days 11 and 22 of her menstrual
cycle. High intakes of caffeinated coffee, green tea, and total caffeine
were commonly correlated with increasing sex hormone-binding globulin on
Days 11 and 22 of the cycle after controlling for potential confounders
[Spearman correlation coefficients (r) ranged from 0.23 to 0.31]. Green
tea but not caffeinated coffee intake was inversely correlated with
estradiol on Day 11 of the cycle (r = -0.32, p = 0.04). Although the
effect of caffeine cannot be distinguished from effects of coffee and
green tea, consumption of caffeine-containing beverages appeared to
favorably alter hormone levels associated with the risk of developing
breast cancer.
PMID: 9507508 [PubMed - indexed for MEDLINE]
This effect is likely due to the polyphenols or other constituents as
these are known to increase insulin uptake and improved insulin leads to
improved SHBG. (Caffeine is always bad to mix with chronic inflammatory
conditions due to its HPA effects.)
Fertil Steril. 2001 Oct;76(4):723-9. Related Articles, Links
Click here to read
Early follicular phase hormone levels in relation to patterns of
alcohol, tobacco, and coffee use.
Lucero J, Harlow BL, Barbieri RL, Sluss P, Cramer DW.
Department of Obstetrics and Gynecology, University of California at
San Francisco Medical Center, San Francisco, California, USA.
OBJECTIVE: To examine the effects of alcohol, caffeine, and tobacco
use on early follicular phase FSH, LH, E2, and sex hormone-binding
globulin (SHBG). DESIGN: Cross-sectional study. SETTING: Academic
medical center. PATIENT(S): Four hundred ninety-eight women selected
from the general population, ages 36-45, who were not currently
pregnant, breast feeding, or using exogenous hormones. INTERVENTION(S):
A general questionnaire assessing demography, anthropometry, and smoking
habits and a standardized dietary questionnaire assessing food and
beverage frequencies, including sources of alcohol and caffeine. MAIN
OUTCOME MEASURE(S): FSH, LH, E2, and SHBG levels measured during the
early follicular phase of the menstrual cycle. RESULT(S): Significant
associations observed in a univariate analysis included age > or =40 and
current smoking associated with higher FSH; higher body mass index (BMI)
associated with lower SHBG levels; and daily alcohol use, cholesterol
consumption greater than the median, and coffee use >1 cup/d associated
with higher E2 levels. In a multivariate model, total caffeine use was
significantly associated with E2 levels after adjustment for age, BMI,
total calories, current smoking, alcohol, cholesterol consumption, and
day of sampling. Early follicular phase E2 increased from 28.2 pg/mL for
women consuming < or =100 mg of caffeine to 45.2 pg/mL for women
consuming > or =500 mg of caffeine per day, about a 70% increase.
CONCLUSION(S): Coffee consumption and total caffeine use may increase
early follicular phase E2 levels independent of related habits of
alcohol or tobacco use.
PMID: 11591405 [PubMed - indexed for MEDLINE]
It also helps that green tea polyphenols appear to intervene directly in
the bone morphogenic complex.
Biochem J. 2002 Dec 15;368(Pt 3):695-704. Related Articles, Links
Click here to read
The antioxidant (-)-epigallocatechin-3-gallate inhibits activated
hepatic stellate cell growth and suppresses acetaldehyde-induced gene
expression.
Chen A, Zhang L, Xu J, Tang J.
Department of Pathology, Louisiana State University Health Sciences
Center in Shreveport, Shreveport, LA 71130, USA.
Activated hepatic stellate cells (HSC) are the primary source of
excessive production of extracellular matrix during liver fibrogenesis.
Although the underlying mechanisms remain incompletely understood, it is
widely accepted that oxidative stress plays a critical role in liver
fibrogenesis. Suppression of HSC growth and activation, as well as
induction of apoptosis, have been proposed as therapeutic strategies for
treatment and prevention of this disease. In the present report, we
elucidated, for the first time, effects of the antioxidant
(-)-epigallocatechin-3-gallate (EGCG), a major (and the most active)
component of green tea extracts, on cultured HSC growth and activation.
Our results revealed that EGCG significantly inhibited cultured HSC
growth by inducing cell cycle arrest and apoptosis in a dose- and
time-dependent manner. In addition, EGCG markedly suppressed the
activation of cultured HSC as demonstrated by blocking transforming
growth factor-beta signal transduction and by inhibiting the expression
of alpha1(I) collagen, fibronectin and alpha-smooth muscle actin genes
induced by acetaldehyde, the most active metabolite of ethanol.
Furthermore, EGCG reacted differently in the inhibition of nuclear
factor-kappaB activity between cultured HSC with or without acetaldehyde
stimulation. Taken together, our results indicated that EGCG was a novel
and effective inhibitor for activated HSC growth and activation in
vitro. Further studies are necessary to evaluate the effect of this
polyphenol in prevention of quiescent HSC activation in vivo, and to
further elucidate the underlying mechanisms.
PMID: 12223099 [PubMed - indexed for MEDLINE]
Braz J Med Biol Res. 1997 Sep;30(9):1061-6. Related Articles, Links
Risk factors for decreased bone density in premenopausal women.
Krahe C, Friedman R, Gross JL.
Departamento de Ginecologia e Obstetricia, Faculdade de Medicina,
Pontificia Universidade Catolica do Rio Grande do Sul, Porto Alegre, RS,
Brasil.
Osteoporosis is a major health problem. Little is known about the
risk factors in premenopause. Sixty 40-50-year old patients with regular
menses were studied cross-sectionally. None of the patients were on
drugs known to interfere with bone mass. Patients answered a dietary
inquiry and had their bone mineral density (BMD) measured. The Z scores
were used for the comparisons. A blood sample was taken for the
determination of FSH, SHBG, estradiol, testosterone, calcium and
alkaline phosphatase. Calcium and creatinine were measured in 24-h
urine. A Z score less than -1 was observed for the lumbar spine of 14
patients (23.3%), and for the femur of 24 patients (40%). Patients with
a Z score less than -1 for the lumbar spine were older than patients
with a Z score > or = -1 (45.7 vs 43.8 years) and presented higher
values of alkaline phosphatase (71.1 +/- 18.2 vs 57.1 +/- 14.3 IU/l).
Multiple regression analysis showed that a lower lumbar spine BMD was
associated with higher values of alkaline phosphatase, lower calcium
ingestion, a smaller body mass index (BMI), less frequent exercising,
and older age. The patients with a Z score less than -1 for the femur
were shorter than patients with a Z score > or = -1 (158.2 vs 161.3 cm).
Multiple regression analysis showed that a lower femoral BMD was
associated with lower BMI, higher alkaline phosphatase and caffeine
intake, and less frequent exercising. A lower than expected BMD was
observed in a significant proportion of premenopausal women and was
associated with lower calcium intake, relatively lower physical activity
and lower BMI. We conclude that the classical risk factors for
osteoporosis may be present before ovarian failure, and their effect may
be partly independent of estrogen levels.
PMID: 9458965 [PubMed - indexed for MEDLINE]
Note the effects of fiber on SHBG. Fiber increases digestion time,
reducing the amount of glucose entering the bloodstream at any given
moment. The association of caffeine with SHBG may be due to potent
flavonoids in coffee and tea. If the relationship holds for soda pop,
then I'd have to sa it might have to do with adrenal stimulation, which
is not good long-term.
Am J Clin Nutr. 1991 Jan;53(1):166-71. Related Articles, Links
Alcohol and other dietary factors in relation to serum hormone
concentrations in women at climacteric.
London S, Willett W, Longcope C, McKinlay S.
Department of Preventive Medicine, University of Southern California
School of Medicine.
The relationships between concentrations of endogenous hormones in
serum and dietary intakes of alcohol, fats, fiber, and caffeine were
examined in 325 healthy Massachusetts women aged 50-60 y who reported
having a normal menstrual period within the previous 12 mo. Diet was
assessed by a semiquantitative food frequency questionnaire. Hormones
assayed were estrone, estradiol, percent free estradiol,
sex-hormone-binding globulin (SHBG), cortisol, and gonadotropins.
Alcohol intake was not associated with concentrations of estrogens or
gonadotropins. Neither total fat intake nor the fat composition of the
diet influenced hormone concentrations. Fiber intake was positively
correlated with SHBG; no associations with estrogens were seen. Caffeine
intake was inversely correlated with free estradiol and positively
correlated with SHBG. These data suggest that fat, fiber, and alcohol
intakes of US women at climacteric are not determinants of variations in
estrone and either total or percent free estradiol.
PMID: 1845789 [PubMed - indexed for MEDLINE]
Well, this study shows inverse correlation with caffeine and caloric
intake. I would still caution about drawing too many conclusions about
caffeine per se. It also shows fat intake increases T whereas caloric
intake lowers DHT. These contradictory studies are all I can find,
though.
: Genet Epidemiol. 1988;5(1):43-59. Related Articles, Links
The effect of nutritional factors on sex hormone levels in male
twins.
Bishop DT, Meikle AW, Slattery ML, Stringham JD, Ford MH, West DW.
Department of Medical Informatics, University of Utah, Salt Lake
City.
Dietary intake has been hypothesized as being associated with
several hormonally related cancers including prostate, breast, ovarian,
and endometrial cancer. Because diet may affect hormones directly, it is
logical to examine the effects of dietary factors on hormone production
and levels. Therefore, a set of 72 male MZ and 83 male DZ twin pairs was
ascertained from the Utah birth certificates. A quantitative food
frequency questionnaire was administered and blood samples were drawn
for hormonal assays. Heritability estimates for hormonal levels were
calculated indicating a range from no heritability for sex hormone
binding globulin (SHBG), estrone, and testosterone glucuronide to 70%
for androstanediol glucuronide and luteinizing hormone. To examine
nutritional factors, the difference in hormone and SHBG levels between
each MZ twin and his co-twin were correlated with the difference in
nutrient intake. Weight and obesity were significantly correlated with
plasma testosterone and follicle stimulating hormone. Fat intake showed
a significant association with testosterone. Androstanediol glucuronide,
a steroid that reflects tissue formation of dihydrotestosterone, was
inversely correlated with caloric intake, theobromine and caffeine.
Testosterone glucuronide exhibited significant correlations with
calories and vitamin A. This study suggests that dietary intake affects
plasma sex-steroid levels in men.
PMID: 3360302 [PubMed - indexed for MEDLINE]
Bryan Shelton
>> BTW, are you the same person as "kofi"? You're just listed as "anon"
>> here in this post, but you appear to be answering the same as in an earlier
>> post by "kofi". If you're also "kofi", what's with the multiple handles?
>
>Are you saying you're upset someone who's anonymous posted anonymously
>under an anonymous pseudonym instead of under an anonymous pseudonym?
No, I'm upset when I don't know if I'm discussing something with
one person, or two different people. Don't you think it would be
better to pick just one handle and stick with it?
>> Well, I'm talking about sysemic absorption of the GTE, of course! :-)
>
>You're forgetting how well hair follicles on the scalp absorb topical
>agents (at least 20x better than abdominal hairs).
Actually I was thinking of the hamster flank organ tests, which showed
a purely "local" effect despite a high density of hair follicles.
>> >Check out the studies of women taking metformin for polycystic ovarian
>> >syndrome.
>>
>> What does that have to do with green tea?
>
>Normalizing insulin and increasing SHBG is important for PCOS. Tea
>consumption is linked to lowered circulating hormones (abstracts below).
<snip abstracts>
>Well, this study shows inverse correlation with caffeine and caloric
>intake. I would still caution about drawing too many conclusions about
>caffeine per se. It also shows fat intake increases T whereas caloric
>intake lowers DHT. These contradictory studies are all I can find,
>though.
Thanks for the abstracts, although I'm still uncertain how much
of the effect of green tea on circulating steroids is due to the
EGCG per se (or other polyphenols), and how much to the caffeine.
I'd have to see some studies on human males consuming de-caffeinated
green tea, before I could conclude that it was a significant factor. And
even if there _were_ a significant effect, I'd still question how much impact
it would have on balding.
Bryan
Ernie Primeau
Ernie Primeau
take something.Ernie