NORI PROTOCOL

The NORI Protocol

NORI has researched and developed a unique approach to cancer therapy that is very simple, effective, low-cost, nontoxic and can be implemented at home by the cancer patient. It is based on targeting common metabolic abnormalities present in nearly all types of cancer cells. A methionine restricted diet combined with a nontoxic chemotherapeutic cocktail is a unique and powerful approach to treating and managing malignancies.

An important feature of the NORI protocol is the synergy created between the methionine restricted diet and high dose selenium. Methionine restriction sensitizes cancer cells to sodium selenite by lowering glutathione which increases oxidative stress.

The NORI approach is to leverage diet for maximum benefit while using a straightforward and highly targeted method for selectively killing cancer cells.

Methionine Restricted Diet

Nutrition is a powerful tool in controlling tumor growth as well as making cancer cells much more susceptible to treatment. The trick is in supporting normal healthy cells while depriving cancer cells of essential nutrients. Cancer cells are highly dependent on several different amino acids for growth and cell division. Cancer cells are universally dependent on methionine. It is both practical and effective to limit the dietary intake of methionine as a means to starve cancer cells of this essential nutrient. Normal cells are unharmed by short term limitation of methionine. Methionine restriction is very powerful and may be sufficient as a standalone therapy for many early stage cancers. Click here to read an article on dietary methionine restriction published in 2001 by Dr Epner.

NORI does not encourage or support the use of nutritional supplements, herbs and juicing during cancer treatment. It is believed that these elements only help cancer cells grow and survive. Anti-cancer compounds are only helpful if they are adequately absorbed, are present in the bloodstream at a sufficient concentration and time interval.

Methionine restriction is individualized for each patient according to weight, nutritional status, disease progression and past dietary preferences. A methionine restricted diet may be continuous or cycled on and off depending on individual circumstances. Methionine restriction involves the elimination of many foods and a focus on mostly fruits. The natural sugars in fruits will not feed cancer cells or cause tumors to grow. It is a common misconception that fruit equals sugar and that fruits raise blood sugar. Fruit can be a problem if there is a high fat intake (greater than 10% of total caloric intake) which will cause insulin resistance.

High Dose Selenium

Selenium is an essential trace element found in foods and nutritional supplements.  Studies have shown that selenium not only can prevent cancer but can also treat it.  Click here to read one of the best papers on treating cancer with selenium by Eric Olm, PhD.

Sodium selenite is the most effective form of selenium for therapeutic use.  Cancer cells are triggered to self destruct (apoptosis) when exposed to sodium selenite at low concentrations.  Normal healthy cells are unharmed unlike treatment with conventional chemotherapy.  Sodium selenite can be administered intravenously or by the use of a specially formulated sublingual tablet.

Sodium selenite is combined with two other natural compounds to boost the effect so that very safe and low doses can be used very effectively.   The mechanism of action is pro-oxidative through a simple chemical reaction that generates excess reactive oxygen species within the mitochondria which releases a cascade of signals triggering apoptosis.

Sodium Selenite, Na2SeO3

Sodium Selenite, Na2SeO3

Important Note:

NORI does not sell therapeutic level sodium selenite supplements and IV solutions to individuals.  Sodium selenite is available to patients who are receiving care from an affiliated physician or who are participating in the NORI nutritional support program. The types and dosages of selenium available in health food stores and online will not have therapeutic value.  Selenized yeast at 200 mcg per day is the best form for cancer prevention.

 

Genipin

Genipin is a compound present in gardenia fruit extract (Zhi Zi) that has been found to inhibit a mitochondrial protein called UCP2. Genipin has been shown to trigger apoptosis through the generation of excess reactive oxygen species (ROS) by increasing the level of ATP generated by mitochondria.  UCP2 maintains the cancer cell at a low level of oxidative stress  by keeping the level of mitochondrial oxidative phosphorylation minimized.  Gardenia fruit extract (Zhi Zi) has been used in traditional Chinese medicine for thousands of years. Current scientific studies are demonstrating potent and selective anti-tumor activity.

Vitamin E Succinate

The semi-synthetic form of vitamin E, vitamin E succinate (VES) has been extensively studied as a cancer preventative and chemotherapeutic agent. NORI incorporates VES within a powerful cocktail designed to induce apoptosis through the generation of excess oxidative stress. VES has no antioxidant activity and is synergistic with the pro-oxidant effects of sodium selenite. VES reacts directly with mitochondrial complex II generating ROS and has been shown to trigger apoptosis in over 90% of cancer cell types. VES is completely nontoxic to normal cells. NORI uses a transdermal VES formulation in addition to oral administration to ensure optimal therapeutic blood plasma concentration.

A Simple but Powerful Approach

The NORI protocol is very simple to implement but may be one of the most powerful alternative cancer treatments ever developed.  By optimally timing and synchronizing cycles the methionine restricted diet with the administration of the cocktail, cancer cells loose all defenses and nutrients necessary for growth and division.  The NORI protocol directly targets the cancer cell’s mitochondria which is exactly the root of the problem from the onset of the disease process.

For more information about NORI Protocol, call 1-800-634-3804 or email us info@NutritionalOncology.net.

Scientific References Supporting the NORI Protocol

 

This is only a partial sampling of the scientific studies that form the foundation of the NORI Protocol. The links below will take you to the original published articles.

 

Methionine Restriction

Methionine Deprivation Suppresses Triple-Negative Breast Cancer Metastasis In Vitro and In Vivo

Methionine Restriction Increases Macrophage Tumoricidal Activity and Significantly Inhibits Prostate Cancer Growth

Methionine Restriction Induces Apoptosis of Prostate Cancer Cells Via the C-Jun N-Terminal Kinase-Mediated Signaling Pathway

Phase II Trial of the Association of a Methionine-Free Diet with Cystemustine Therapy in Melanoma and Glioma

Dietary Methionine Restriction Inhibits Prostatic Intraepithelial Neoplasia in TRAMP Mice

The Role of Methionine in Cancer Growth and Control

 

Sodium Selenite

Application of Sodium Selenite in the Prevention and Treatment of Cancers

Pharmacokinetics and Toxicity of Sodium Selenite in the Treatment of Patients with Carcinoma in a Phase I Clinical Trial: The SECAR Study

Sodium Selenite Induces Superoxide-Mediated Mitochondrial Damage and Subsequent Autophagic Cell Death in Malignant Glioma Cells

High-Dose Sodium Selenite Can Induce Apoptosis of Lymphoma Cells in Adult Patients with Non-Hodgkin’s Lymphoma

Sodium Selenite Induces Apoptosis in Colon Cancer Cells Via Bax-dependent Mitochondrial Pathway

Treatment of Lung Cancer Cells with Cytotoxic Levels of Sodium Selenite: Effects on the Thioredoxin System

Sodium Selenite Inhibits Proliferation of Gastric Cancer Cells by Inducing SBP1 Expression

Sodium Selenite-Induced Oxidative Stress and Apoptosis in Human Hepatoma HepG2 Cells

Sodium Selenite Alters Microtubule Assembly and Induces Apoptosis In Vitro and In Vivo

 

Selenomethionine

Is Selenium a Potential Treatment for Cancer Metastasis?

Methioninase Gene Therapy with Selenomethionine Induces Apoptosis in BCL-2-Overproducing Lung Cancer Cells

Inhibitory Effect of Selenomethionine on the Growth of Three Selected Human Tumor Cell Lines

Redox-Active Selenium Compounds—From Toxicity and Cell Death to Cancer Treatment

 

Vitamin K3 (Menadione)

The Utility of Vitamin K3 (Menadione) against Pancreatic Cancer

Vitamin K and Its Analogs: Potential Avenues for Prostate Cancer Management

Menadione Triggers Cell Death Through ROS-Dependent Mechanisms Involving PARP Activation Without Requiring Apoptosis

Menadione Induces Apoptosis in a Gastric Cancer Cell Line Mediated by Down-Regulation of X-Linked Inhibitor of Apoptosis

Menadione (Vitamin K3) Induces Apoptosis of Human Oral Cancer Cells and Reduces their Metastatic Potential by Modulating the Expression of Epithelial to Mesenchymal Transition Markers and Inhibiting Migration

 

Shikonin

Shikonin, vitamin K3 and vitamin K5 inhibit multiple glycolytic enzymes in MCF-7 cells

Shikonin Induces Apoptosis in the Human Gastric Cancer Cells HGC-27 Through Mitochondria-Mediated Pathway

Shikonin Selectively Induces Apoptosis in Human Prostate Cancer Cells Through the Endoplasmic Reticulum Stress and Mitochondrial Apoptotic Pathway

Shikonin Induces Apoptotic Cell Death via Regulation of P53 and NRF2 in AGS Human Stomach Carcinoma Cells

Shikonin Induces Mitochondriamediated Apoptosis and Enhances Chemotherapeutic Sensitivity of Gastric Cancer Through Reactive Oxygen Species

Effect of Shikonin on Human Breast Cancer Cells Proliferation and Apoptosis In Vitro

Shikonin Induces Apoptosis and Necroptosis in Pancreatic Cancer via Regulating the Expression of RIP1/RIP3 and Synergizes the Activity of Gemcitabine

Shikonin Induces Apoptosis, Necrosis, and Premature Senescence of Human A549 Lung Cancer Cells through Upregulation of P53 Expression

Shikonin Circumvents Cancer Drug Resistance by Induction of a Necroptotic Death

Shikonin Induces ROS-Based Mitochondria-Mediated Apoptosis in Colon Cancer

Shikonin, a Naphthoquinone Compound, Rapidly Induces Cell Death of Human Myeloma Cells via Production of Reactive Oxygen Species

Anti-Leukemic Activity of Shikonin: Role of ERP57 in Shikonin Induced Apoptosis in Acute Myeloid Leukemia

Shikonin Inhibits Thyroid Cancer Cell Growth and Invasiveness Through Targeting Major Signaling Pathways

 

Vitamin E Succinate

Vitamin E Succinate Induces Apoptosis via the PI3K/AKT Signaling Pathways in EC109 Esophageal Cancer Cells

Vitamin E Succinate Inhibits Survivin and Induces Apoptosis in Pancreatic Cancer Cells

Vitamin E Analogues as Inducers of Apoptosis: Structure–Function Relation

Mitochondrially Targeted Vitamin E Succinate Efficiently Kills Breast Tumour-Initiating Cells in a Complex II-Dependent Manner

Anticancer Mechanisms of Vitamin E Succinate

Differential Response of Human Ovarian Cancer Cells to Induction of Apoptosis by Vitamin E Succinate and Vitamin E Analogue, Alpha-TEA

Vitamin E Inhibits Melanoma Growth in Mice

 

Genipin

Genipin Induced Apoptosis Associated with Activation of the C-Jun NH2-Terminal Kinase and P53 Protein in HeLa Cells

Genipin Inhibits the Growth of Human Bladder Cancer Cells via Inactivation of PI3K/AKT Signaling

Genipin, a Constituent of Gardenia Jasminoides Ellis, Induces Apoptosis and Inhibits Invasion in MDA-MB-231 Breast Cancer Cells

Genipin-Induced Inhibition of Uncoupling Protein-2 Sensitizes Drug-Resistant Cancer Cells to Cytotoxic Agents

The Hydroxyl at Position C1 of Genipin Is the Active Inhibitory Group that Affects Mitochondrial Uncoupling Protein 2 in Panc-1 Cells

UCP2 Induces Metabolic Reprogramming to Inhibit Proliferation of Cancer Cells

Plant-Derived Anticancer Agents: Lessons from the Pharmacology of Geniposide and Its Aglycone, Genipin

P38 MAP Kinase Mediates Apoptosis After Genipin Treatment in Non–Small-Cell Lung Cancer H1299 Cells via a Mitochondrial Apoptotic Cascade

 

Pine Bark (Pycnogenol) and Grape Seed Extract

Pro‑Apoptotic Effects of Pycnogenol on HT1080 Human Fibrosarcoma Cells

Anti-Tumor Effect of Pinus Massoniana Bark Proanthocyanidins on Ovarian Cancer Through Induction of Cell Apoptosis and Inhibition of Cell Migration

Effects of Pinus Massoniana Bark Extract on Cell Proliferation and Apoptosis of Human Hepatoma BEL-7402 Cells

Involvement of the BCL-2 Family Members in Pinus Massoniana Bark Extract-Induced Apoptosis in HeLa Cells

Anticancer and Cancer Chemopreventive Potential of Grape Seed Extract and Other Grape-Based Products

 

FASN Inhibitor

Fatty Acid Synthase as a Potential Therapeutic Target in Cancer

Fatty Acid Synthase Regulates Estrogen Receptor-α Signaling in Breast Cancer Cells 

Targeting FASN in Breast Cancer and the Discovery of Promising Inhibitors from Natural Products Derived from Traditional Chinese Medicine

Quercetin Induces Apoptosis in Triple-Negative Breast Cancer Cells via Inhibiting Fatty Acid Synthase and β-Catenin

 

Green Tea Extract

Induction of Apoptosis in Human Bladder Cancer Cells by Green Tea Catechins

Green Tea Extract Induces Apoptosis in the AGS Gastric Carcinoma Cell Line

Anti-Proliferative and Apoptosis Induction Activity of Green Tea Polyphenols on Human Promyelocytic Leukemia HL-60 Cells

EGCG Inhibits Growth and Induces Apoptosis in Renal Cell Carcinoma Through TFPI-2 Overexpression

Pro‑Apoptotic and Migration‑Suppressing Potential of EGCG, and the Involvement of AMPK in the P53‑Mediated Modulation of VEGF and MMP‑9 Expression

In Vitro and In Vivo study of Epigallocatechin-3-Gallate-Induced Apoptosis in Aerobic Glycolytic Hepatocellular Carcinoma Cells Involving Inhibition of Phosphofructokinase Activity

 

Taurine

Effect of Taurine on the Proliferation and Apoptosis of Human Hepatocellular Carcinoma HepG2 Cells

Mechanism of Taurine-Induced Apoptosis in Human Colon Cancer Cells

Effect of Taurine on Cell Proliferation and Apoptosis in Human Lung Cancer A549 Cells

Taurine Induces the Apoptosis of Breast Cancer Cells by Regulating Apoptosis-Related Proteins of Mitochondria

 

Zinc Sulfate

Zinc Induces Apoptosis of Human Melanoma Cells, Increasing Reactive Oxygen Species, P53 and FAS Ligand

Induction of Apoptosis and Necrosis by Zinc in Human Thyroid Cancer Cell Lines

 

Alpha-Bisabolol

Pro-Apoptotic Activity of A-Bisabolol in Preclinical Models of Primary Human Acute Leukemia Cells

A-Bisabolol Inhibits Invasiveness and Motility in Pancreatic Cancer Τhrough KISS1R Activation

Involvement of Mitochondrial Permeability Transition Poreopening in A-Bisabolol Induced Apoptosis

Antitumor Effects of A‐Bisabolol Against Pancreatic Cancer

A-Bisabolol, a Nontoxic Natural Compound, Strongly Induces Apoptosis in Glioma Cells