TAKE ELLAGIC ACID SERIOUSLY!

[Guest guest]

I can't believe that people are fighting this information. This is the most

promising answer to cancer in medical history; the clinical trials are

posted below and they cannot be argued with by any person or any

doctor. I am a holistic healer and a holistic researcher of fibromyalgia,

and I get products thrown at me daily; I have never seen anything

even close to this. This product has been clinically proven to cause

G-arrest (stop mitosis-cell splitting and duplicating) in 48 hours in

numerous strains of human cancer cells! It has also been clinically

proven to cause apoptosis (a natural cell death) in 72 hours to human

cancer cells.

Here are some clinical studies, and right now, the largest clinical trial

is taking place at a prestigious cancer institute in South Carolina. They

are doing a double blind study on 500 cervical cancer patients. They are

using Ellagic-red21 from 21st Century Neutriceuticals. I take this product

personally and I can help anyone get it wholesale. I am not here to make

money off of sick people darnet! I am here to help people with this

insidious disease which is the number two cause of death in our country

to adults and children. The cancer clinic in question is the Hollings

Cancer Institute at the Medical University of South Carolina. They are

listing all of their current progress on a Washington D.C. site.

<A HREF= " http://www.red-raspberry.com/received.html " >Washington D.C. Red

Raspberry Commission</A>

see current cervical cancer study at Hollings

<A HREF= " http://www.cancerlinksusa.com/centers.htm " >Major cancer clinics in

the U.S.</A>

See the Hollings website under S. Carolina

They are accepting calls from Oncologists.

Here are some current clinical studies on ellagic acid going back over

ten years. Please, please, please show these studies to your

Oncologist.

Take care,

Steve Podhouser

Healerstouch1@...

24 Hr. Testimonials on Ellagic-red21 (512) 404-2331

ELLAGIC ACID CLINICAL TRIALS

Cancer Lett 1999 Mar 1 1;136(2):215-21

Expression and its posssible role in G1 arrest and apoptosisi in ellagic

acid treated cancer cells.

Narayanan BA, Geoffroy O, Wilmington MC, Re GG, Nixon DWCANCER P

Prevention program, Hollings Cancer Center, Medical University of South

Carolina, ton 29425, USA.

Protective Effect of Curcumin, Ellagic Acid and Bixin on Radiation Induced

Genotoxicity

K.C. Thresiamma, J. and R. Kuttan Amala Cancer Research Centre, Amala

Nagar, Trichur, India

Induction of micronuclei and chromosomal aberrations produced by whole body

exposure of r-radiation (1.5-3.0 Gy) in mice was found to be significantly

inhibited by oral administration of natural antioxidants, curcumin (400 µ

moles), ellagic acid (200 µ moles)

and bixin (200 µ moles) per kilogram body weight. These antioxidants induced

inhibition of micronucleated polychromatic and normochromatic erythrocytes,

was comparable with a-tocopherol (200 µ moles) administration. Curcumin and

ellagic acid were also found to significantly reduce the number of bone

marrow cells with chromosomal aberrations and chromosomal fragments as

effectively as a-tocopherol. Moreover, administration of antioxidants

inhibited the DNA strand breaks produced in rat lymphocytes upon radiation as

seen from the DNA unwinding studies. These results indicated that antioxidant

curcumin, ellagic acid and bixin provide protection against chromosome damage

produced by radiation.

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Inhibitory effects of ellagic acid on the direct-acting mutagenicity of

aflatoxin B1 in the Salmonella microsuspension assay.

Loarca-Pina G, Kuzmicky PA, de Mejia EG, Kado NY

Departamento de Investigacion y Posgrado, Facultad de Quimica, Universidad

Autonoma de Queretaro, Qro., Mexico. Ellagic acid (EA) is a phenolic compound

that exhibits both antimutagenic and anticarcinogenic activity in a wide

range of assays in vitro and in vivo. It occurs naturally in some foods such

as strawberries, raspberries, and grapes. In the previous work, we used the

Salmonella microsuspension assay to examine the antimutagenicity of EA

against the potent mutagen aflatoxin B1 (AFB1) using tester strains TA98 and

TA100. Briefly, the microsuspension assay was approximately 10 times more

sensitive than the standard Salmonella/microsome (Ames) test in detecting

AFB1 mutagenicity, and EA significantly inhibited mutagenicity of all AFB1

doses in both tester strains with the addition of S9. The greatest inhibitory

effect of EA on AFB1 mutagenicity occurred when EA and AFB1 were incubated

together (with metabolic enzymes). Lower inhibition was apparent when the

cells were first incubated with EA followed by a second incubation with AFB1,

or when the cells were first incubated with AFB1 followed by a second

incubation with EA alone, all with metabolic enzymes. The result of these

sequential incubation studies indicates that one mechanism of inhibition

could involve the formation of an AFB1-EA chemical complex. In the present

study, we further examine the effect of EA on AFB1 mutagenicity, but without

the addition of exogenous metabolic enzymes. We report the mutagenicity of

AFB1 in the microsuspension assay using TA98 and TA100 without the addition

of S9. Neither the concentrations of AFB1 (0.6, 1.2, and 2.4 microg/tube) nor

the concentrations of EA (0.3, 1.5, 3, 10, and 20 microg/tube) were toxic to

the bacteria. The results indicate that AFB1 is a direct-acting mutagen, and

that EA inhibits AFB1 direct-acting mutagenicity. PMID: 9626978

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Expression and its possible role in G1 arrest and apoptosis in ellagic acid

treated cancer cells.

Narayanan BA, Geoffroy O, Willingham MC, Re GG, Nixon DW

Cancer Prevention Program, Hollings Cancer Center, Medical University of 

South Carolina, ton 29425, USA. bhagavati@... Ellagic acid is a

phenolic compound present in fruits and nuts including raspberries,

strawberries and walnuts. It is known to inhibit certain carcinogen-induced

cancers and may have other chemopreventive properties. The effects of ellagic

acid on cell cycle events and apoptosis were studied in cervical carcinoma

(CaSki) cells. We found that ellagic acid at a concentration of 10(-5) M

induced G arrest within 48 h, inhibited overall cell growth and induced

apoptosis in CaSki cells after 72 h of treatment. Activation of the cdk

inhibitory protein p21 by ellagic acid suggests a role for ellagic acid in

cell cycle regulation of cancer cells. PMID: 10355751

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Regression of atherosclerosis: role of nitric oxide and apoptosis.

Wang BY, Ho HK, Lin PS, Schwarzacher SP, Pollman MJ, Gibbons GH, Tsao PS,

Cooke JP

Section of Vascular Medicine, Division of Cardiovascular Medicine, Stanford

University School of Medicine, Stanford, Calif, USA. <0.01). In subsequent

studies, aortas were harvested for ex vivo studies. Aortic segments were

incubated in cell culture medium for 4 to 24 hours with

modulators of the NO synthase pathway. The tissues were then collected for

histological studies and the conditioned medium collected for measurement of

nitrogen oxides by chemiluminescence. Addition of sodium nitroprusside

(10(-5) mol/L) to the medium caused a time-dependent increase in apoptosis of

vascular cells (largely macrophages) in the intimal lesion. L-Arginine

(10(-3) mol/L) had an identical effect on apoptosis, which was associated

with an increase in nitrogen oxides released into the medium. These effects

were not mimicked by D-arginine, and they were antagonized by the NO synthase

inhibitor L-nitro-arginine (10(-4) mol/L). The effect of L-arginine was not

influenced by an antagonist of cGMP-dependent protein kinase, nor was the

effect mimicked by the agonist of protein kinase G or 8-BR cGMP. CONCLUSIONS:

These results indicate that supplemental L-arginine induces apoptosis of

macrophages in intimal lesions by its metabolism to NO, which acts through a

GMP-independent pathway. These studies are consistent with our previous

observation that supplementation of dietary arginine induces regression of

atheroma in this animal model. These studies provide a rationale for further

investigation of the therapeutic potential of manipulating the NO synthase

pathway in atherosclerosis. PMID: 10069793

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Epidemic of gastroenteritis of viral origin associated with eating imported

raspberries.

Gaulin CD, Ramsay D, Cardinal P, D'Halevyn MA

Centre de sante publique de Quebec, Beauport. Several episodes of food

poisoning affected the region of Quebec City in July and August 1997. In the

first two episodes, the analysis of two cohorts (A and demonstrated that

the consumption of a raspberry mousse with raspberry sauce increased the risk

of contracting gastroenteritis (A, RR = 2.6 p = 0.001; B, RR = 4.7 p = 0.02).

More than 200 people were sick after eating a raspberry dessert. The common

ingredient of all those desserts was raspberries imported from Bosnia. Viral

studies on the raspberry sauce (2) and stool samples (5) using the genome

amplification method by PCR indicated the presence of genomic material

compatible with a virus of the Caliciviruses family. Southern hybridization

and sequence analysis showed that the nucleotide sequences found in the

raspberry sauce and in the stool samples were identical. It is important to

maintain active surveillance to detect and limit the spread of this kind of

outbreak. PMID: 10189738

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Protective effects of antioxidants on experimental liver injuries.

Suzuki M, Kumazawa N, Ohta S, Kamogawa A, Shinoda M

Faculty of Pharmaceutical Science, Hoshi University, Tokyo, Japan. Protective

effects of 14 kinds of antioxidant on liver injury induced by carbon

tetrachloride (CCl4) were investigated in terms of serum enzyme activities

and bilirubin concentration. Consequently, the significant protective effects

were found in sesamol, ellagic acid, cysteamine and cysteine. These

antioxidants clearly decreased the lipid peroxide in the liver tissue. The

protective effects on CCl4-induced liver injury in vivo were independent of

the inhibitory activities on lipid peroxidation in hepatic mitochondria

fraction in vitro. PMID: 2262882

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Polyphenols as cancer chemopreventive agents.

Stoner GD, Mukhtar H

Department of Preventive Medicine, Ohio State University, Columbus 43210,

USA. This article summarizes available data on the chemopreventive efficacies

of tea polyphenols, curcumin and ellagic acid in various model systems.

Emphasis is placed upon the anticarcinogenic activity of these polyphenols

and their proposed mechanism(s) of action. Tea is grown in about 30 countries

and, next to water, is the most widely consumed beverage in the world. Tea is

manufactured as either green, black, or oolong; black tea represents

approximately 80% of tea products. Epidemiological studies, though

inconclusive, suggest a protective effect of tea consumption on human cancer.

Experimental studies of the antimutagenic and anticarcinogenic effects of tea

have been conducted principally with green tea polyphenols (GTPs). GTPs

exhibit antimutagenic activity in vitro, and they inhibit carcinogen-induced

skin, lung, forestomach, esophagus, duodenum and colon tumors in rodents. In

addition, GTPs inhibit TPA-induced skin tumor promotion in mice. Although

several GTPs possess anticarcinogenic activity, the most active is

(-)-epigallocatechin-3-gallate (EGCG), the major constituent in the GTP

fraction. Several mechanisms appear to be responsible for the

tumor-inhibitory properties of GTPs, including enhancement of antioxidant

(glutathione peroxidase, catalase and quinone reductase) and phase II

(glutathione-S-transferase) enzyme activities; inhibition of chemically

induced lipid peroxidation; inhibition of irradiation- and TPA-induced

epidermal ornithine decarboxylase (ODC) and cyclooxygenase activities;

inhibition of protein kinase C and cellular proliferation;

antiinflammatory activity; and enhancement of gap junction intercellular

communication. Curcumin is the yellow coloring agent in the spice tumeric. It

exhibits antimutagenic activity in the Ames Salmonella test and has

anticarcinogenic activity, inhibiting chemically induced preneoplastic

lesions in the breast and colon and neoplastic lesions in the skin,

forestomach, duodenum and colon of rodents. In addition, curcumin inhibits

TPA-induced skin tumor promotion in mice. The mechanisms for the

anticarcinogenic effects of curcumin are similar to those of the GTPs.

Curcumin enhances glutathione content and glutathione-S-transferase activity

in liver; and it inhibits lipid peroxidation and arachidonic acid metabolism

in mouse skin, protein kinase C activity in TPA-treated NIH 3T3 cells,

chemically induced ODC and tyrosine protein kinase activities in rat colon,

and 8-hydroxyguanosine formation in mouse fibroblasts. Ellagic acid is a

polyphenol found abundantly in various fruits, nuts and vegetables. Ellagic

acid is active in antimutagenesis assays, and has been shown to inhibit

chemically induced cancer in the lung, liver, skin and esophagus of rodents,

and TPA-induced tumor promotion in mouse skin. PMID: 8538195

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Ellagic acid induces NAD(P)H:quinone reductase through activation of the

antioxidant responsive element of the rat NAD(P)H:quinone reductase gene.

Barch DH, Rundhaugen LM

Department of Medicine, Lakeside Veterans Affairs Medical Center, Chicago,

IL. Induction of cellular detoxification enzymes can increase detoxification

of carcinogens and reduce carcinogen-induced mutagenesis and tumorigenesis.

To determine if the dietary anticarcinogen ellagic acid induced enzymes which

detoxify xenobiotics and carcinogens, we examined the effect of ellagic acid

on the expression of the phase II detoxification enzyme NAD(P)H:quinone

reductase (QR). QR is induced by xenobiotics and antioxidants interacting

with the xenobiotic responsive and antioxidant responsive elements of the 5'

regulatory region of the QR gene. Ellagic acid is structurally related to the

antioxidants which induce QR and we proposed that ellagic acid would induce

QR expression through activation of the antioxidant responsive element of the

QR gene. Rats fed ellagic acid demonstrated a 9-fold increase in hepatic and

a 2-fold increase in pulmonary QR activity, associated with an 8-fold

increase in hepatic QR mRNA. To determine if this increase in QR mRNA was due

to activation of the antioxidant responsive element, transient transfection

studies were performed with plasmid constructs containing various portions of

the 5' regulatory region of the rat QR gene. These transfection studies

confirmed that ellagic acid induces transcription of the QR gene and

demonstrated that this induction is mediated through the antioxidant

responsive element of the QR gene. PMID: 7522986

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Pulmonary carcinogenesis and its prevention by dietary polyphenolic compounds.

Castonguay A

Laboratory of Cancer Etiology and Chemoprevention, School of Pharmacy, Laval

University, Quebec City, Canada. The aims of this study were to define the

cumulative exposure of Canadian smokers to NNK and to characterize the

efficacy of ellagic acid to inhibit lung tumorigenesis induced by NNK. The

sales-weighted average of NNK deliveries from Canadian cigarettes was 73.2

ng/cigarette. NNK deliveries were highly correlated to declared tar values

and were linear with puff volumes between 20 and 50 ml. Ellagic acid

inhibited lung tumorigenesis induced by NNK in A/J mice. This inhibition was

related to the logarithm of the dose of ellagic acid added to the diet. The

biodistribution of ellagic acid was studied in mice gavaged with ellagic

acid. Pulmonary levels of ellagic acid were directly proportional to the dose

of ellagic acid between 0.2 and 2.0 mmol/kg b.w. PMID: 8512246

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Lung tumors in strain A mice: application for studies in cancer

chemoprevention.

Stoner GD, Adam-Rodwell G, Morse MA

Ohio State University, Department of Preventive Medicine, Arthur G.

Cancer Hospital and Research Institute, Columbus 43210. Strain A mice develop

a high incidence of spontaneous lung tumors during their lifetime. These

tumors may be found in some animals as early as 3 to 4 weeks of age,

increasing to nearly 100% by 24 months of age. The strain A mouse is also

highly susceptible to the induction of lung tumors by several classes of

chemical carcinogens and has been used extensively as a mouse lung tumor

bioassay for assessing the carcinogenic activity of a variety of chemicals.

In addition to its use in carcinogen detection, the strain A mouse lung tumor

model has been employed extensively for the identification of inhibitors of

chemical carcinogenesis. A number of chemopreventive agents including

beta-naphthoflavone, butylated hydroxyanisole, ellagic acid, phenethyl

isothiocyanate, phenylpropyl isothiocyanate, phenylbutyl isothiocyanate,

phenylhexyl isothiocyanate, indole-3-carbinol, etc., have been shown to

inhibit chemically induced lung tumors in strain A mice. In most instances,

inhibition of lung tumorigenesis has been correlated with effects of the

chemopreventive agent on the metabolic activation and/or detoxification of

carcinogens. To date, no chemopreventive agent has been shown to inhibit lung

tumorigenesis in strain A mice when administered after the carcinogen, i.e.,

during the promotion/progression stages of tumor development. Efforts should

be made to develop a standardized protocol in strain A mice for evaluating

chemopreventive agents as inhibitors of both the initiation and progression

stages of lung tumor development. PMID: 8412213

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Medical research confirms eating red raspberries may be one of the most

potent ways to fight cancer.

Dr. Nixon, Medical University of South Carolina

(JANUARY-1999) -- One of the most popular and flavorful fruits on the market

now has an entirely new reason for becoming a part of a healthy diet. Recent

medical tests have shown that the red raspberry is one of the most effective

all-natural ways to fight certain forms of cancer.

Red raspberries have the highest content of ellagic acid, a phenolic compound

that is a proven anti-carcinogen, anti-mutagen and anti-cancer initiator.

Tests conducted at the Hollings Cancer Center at the Medical University of

South Carolina have revealed that the ellagic acid from red raspberries is

readily absorbed by the human body. This ellagic acid has been clinically

shown to cause apoptosis (cell death) in cancer cells.

Additional tests have revealed that the ellagic acid in red raspberries

retains its potency after heating, freezing and concentration processing. So

whether consumed fresh, in juices, fruit spreads, preserves or sorbets, the

red raspberry should become a part of any healthy diet.