The NORI Protocol

There are two major goals of the NORI protocol. The first is to slow down tumor growth. The main component for slowing tumor growth is a methionine restricted diet. There are other factors that provide additional tumor growth inhibitory effects that are associated with the NORI dietary approach.

The second goal is to trigger apoptosis in cancer cells using commonly available natural and nontoxic compounds. There are numerous choices avaialble. NORI has selected among thousands of options and narrowed the selection to just a few that have very strong scientific support and fit within the overall approach. The NORI protocol exploits the primary vulnerability of cancer cells which is the regulation of oxidative stress. Cancer cells are barely surviving under a very high level of oxidative stress while normal cells are at a very low level. By depleting antioxidant capacity of cancer cells and elevating ROS (reactive oxygen species) within cancer cells, a critical condition is created that triggers the natural process of apoptosis. Normal cells easily survive the elevation of oxidative stress while cancer cells succumb.

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 protocol is intended to complement conventional cancer therapy and is not intended as a standalone therapy. NORI recommends that all cancer patients seek appropriate medical care and make informed choices based on science-based evidence.

Cancer is best treated through an integrative approach that incorporates many elements including targeted nutrition, stress reduction, lifestyle modifications and weighing the risks and benefits of all treatment options. Information overload is probably the biggest challenge for the cancer patient, especially when researching all of the alternative treatment options. NORI offers consultations to help one sort through the enormous maze and find the most effective path towards long term management.

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 certain nutritional supplements, herbs and juicing during cancer treatment. It is believed that these elements only help cancer cells grow and survive. NORI believes that certain B vitamins such as B12, B1 and B9 can encourage tumor growth. NORI also believes that antioxidants support cancer cell survival. Prime examples are NAC and glutathione.

The idea of building and boosting the immune system is not a central core of the NORI approach. Cancer cells very effectively evade the immune system so immune enhancement is not emphasized within the NORI protocol.

It is strongly recommended that one seeks professional assistance in implementing a methionine restricted diet. NORI offers such guidance through our home-based nutritional support program. Contact NORI for details.


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 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. Oral adminstration of VES is ineffective because the succinate portion of the molecule is hydrolyzed in the gut.

A Simple but Powerful Approach

The NORI protocol provides cancer patients with a set of tools to enhance their treatment plan and post treatment recovery. Successful cancer treatment and long term management requires many elements beyond the standard of care. NORI offers cancer patients an opportunity to enhance their care to a level well beyond the standard options of chemotherapy, radiation and surgery. Every treatment option has its risks, benefits, costs and quality of life issues. Choosing treatment options is very challenging and requires careful research and decision making. Always seek multiple opinions.

For more information about NORI Protocol, call 1-800-634-3804 or email us

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



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, 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 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


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


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

Essential Oils

Exploitation of Cytotoxicity of Some Essential Oils for Translation in Cancer Therapy

Damper Effect of Carvacrol on T47-D, A Human Breast Cancer Cell Line

Anti-Cancer Activity of Essential Oils and Their Chemical Components – A Review

In Vitro and In Vivo Anti-Tumor Potential of Carvacrol Nanoemulsion Against Human Lung Adenocarcinoma A549 Cells via Mitochondrial Mediated Apoptosis


Multi-Targeted Therapy of Cancer by Lycopene

Multiple Molecular and Cellular Mechanisms of Action of Lycopene in Cancer Inhibition

Anti-Proliferative and Apoptosis-Inducing Activity of Lycopene Against Three Subtypes of Human Breast Cancer Cell Lines


Carotenoid Lutein Selectively Inhibits Breast Cancer Cell Growth and Potentiates the Effect of Chemotherapeutic Agents through ROS-Mediated Mechanisms

Lutein, But Not Other Carotenoids, Selectively Inhibits Breast Cancer Cell Growth Through Several Molecular Mechanisms

Effect of Lutein and Doxorubicin Combinatorial Therapy on S180 Cell Proliferation and Tumor Growth

Cannabis Research

NORI believes that cannabis derivatives may offer enormous therapeutic benefits to those suffering from cancer.  We have incorporated the use of CBD into our program.


Cannabinoid Receptors: Where They Are and What They Do

Prospective Analysis of Safety and Efficacy of Medical Cannabis in Large Unselected Population of Patients with Cancer