The Revici Method

Lipid Replacement Therapy (LRT) can restore and help maintain mitochondrial membrane function by replacing damaged mitochondrial membranes so the perfect form of selenium would have selenium bonded to a lipid. This form was developed by a surgeon in New York who used to inject it to treat cancer.

Lipid Replacement Therapy, the use of functional oral supplements containing cell membrane phospholipids and antioxidants, has been used to replace damaged, usually oxidized, membrane glycerophospholipids in mitochondria that accumulate during aging and in various clinical conditions in order to restore cellular function.

The Revici Method is an unconventional therapy for the treatment of cancer developed by Emanuel Revici, MD. Dr. Revici believed that pathologic conditions were due to a chemical imbalance within the body that could be modified using natural substance. Revici’s cancer therapy was a nontoxic chemotherapy that used lipids, lipid-based substances, and essential elements to correct an underlying imbalance in the patient’s chemistry.

Revici’s research has demonstrated that lipids have an affinity for tumors and other abnormal tissues. Because of this, the lipids or lipid-like synthetic compounds administered to the patient, either by mouth or injection, travel directly to the tumor or lesion. Cancerous tissue is abnormally rich in free lipids, and the lipidic agents introduced into the bloodstream are readily taken up by the tumor.

His method was a blend of clinical observations, laboratory analyses, and chemotherapy. Basically, Revici would analyze the urine, blood, and body temperature and place patients in specific categories based on the “imbalance” that was discovered from these tests. He knew that low body temperature tracks perfectly with immune system strength.

The Romanian-born physician, who practiced in New York City, applied his wide-ranging discoveries for over sixty years to the treatment of cancer as well as many other disorders, including AIDS, arthritis, Alzheimer’s disease, chronic pain, drug addiction, schizophrenia, allergies, shock, and burns. The great majority of his cancer patients were in advanced stages of the illness.

Dr. Revici was the first physician to develop selenium compounds low enough in toxicity to give cancer patients doses far in excess of safety limits for ordinary forms of selenium. He did this by chemically bonding the mineral selenium to a lipid. Independent validations of Revici’s findings accumulated over the years concerning the development of a safe, effective means of lipid transport and the use of selenium in a virtually non-toxic form to treat cancer.

Revici, who died at a ripe old age of 101, was hounded by the authorities of his time. Dr. Seymour Brenner, a respected radiation oncologist in private practice in New York, testified on Revici’s behalf. He had investigated a number of patients in very advanced stages of cancer, incurable by orthodox means, whom Revici had put into long remissions. Dr. Brenner had an independent panel of pathologists confirm the diagnosis and stage of illness prior to each patient’s initial visit to Revici. He testified that his personal findings strongly suggest Revici has a cancer treatment deserving further study, and he proposed that such an evaluation be conducted by the FDA.

Revici, who holds patents for his numerous chemical compounds, claims to have devised a novel technique to open double bonds in molecules of unsaturated fatty acids in order to incorporate different metallic elements at precise points in the molecules. The result is an entirely new series of therapeutic compounds, exceedingly low in toxicity and incorporating selenium, copper, sulfur, zinc, calcium and other elements. In general, these compounds reportedly have a toxicity less than one-thousandth of that of the elements in the forms normally available. His revolutionary techniques converted toxic substances into safe anticancer agents.”

In this form, he can administer up to 1 gram of selenium per day, which corresponds to 1 million micrograms per day, reportedly with no toxic side effects. In contrast, too much selenite (hexavalent-positive selenium) has toxic effects on animals, so human intake of commercial selenite is limited to a dosage of only 100 to 150 micrograms by mouth. Dr. Revici often administers his nontoxic form of selenium by injection, usually considered to be four times more powerful than the form given orally.

Revici’s use of selenium in the treatment of cancer predates mainstream interest in this mineral by more than twenty years. Selenium is one of the major trace elements always found deficient in cancer-prone populations. Research has shown that it is of value not only in preventing cancer but also in treating it. Revici used a special molecular form of selenium (bivalent-negative selenium) incorporated in a molecule of fatty acid.

In this form, he could administer up to 1 gram of selenium per day, which corresponds to 1 million micrograms, reportedly with no toxic side effects. In contrast, too much selenite (hexavalent-positive selenium) has toxic effects on animals, so human intake of commercial selenite is limited to a dosage of only 100 to 150 micrograms by mouth. Dr. Revici often administers his nontoxic form of selenium by injection, usually considered to be four times more powerful than when given orally.

By 1948, Revici had begun exploring the use of selenium in treating cancer and as a means for rendering radiation less harmful. His promising findings on radiation came to the attention of United States Navy scientists testing A-bombs in the Pacific. Twice, the scientists invited him to join them in studying radiation’s harmful effects.

Working at Roswell Park Memorial Institute in the early 1960s (not long after selenium’s nutritional essential nature was established), Dr. Raymond Shamberger and colleagues envisioned an anti-carcinogenic role for selenium. Knowing that free radical-generating drugs increase the yield of cancers in carcinogen-treated mouse skin, they hypothesized that topical application of certain antioxidants including selenium might lessen the incidence of skin cancers. Their study documented a profound reduction of skin cancer incidence in the carcinogen-treated mice given topical sodium selenide indeed, the selenium was far more effective than any other antioxidant they tested.8 Their report, published in 1966, encouraged a great number of subsequent animal studies which over the next two decades demonstrated that selenium was the most versatile and potent anticarcinogenic agent known, at least with respect to animal models of cancer induction.

Dr. Emanuel Revici’s greatest discovery was that if we want to deliver a nutrient to a sick cell – attach it to a fat. Unsaturated fats are the ultimate and perfect vehicle to deliver nutrients to stressed cells. Revici used a special molecular form of selenium (bivalent-negative selenium) incorporated in a molecule of fatty acid. In this form, he can administer up to 1 gram of selenium per day, which corresponds to 1 million micrograms per day, reportedly with no toxic side effects. In contrast, too much selenite (hexavalent-positive selenium) has toxic effects on animals, so human intake of commercial selenite is limited to a dosage of only 100 to 150 micrograms by mouth. Dr. Revici often administered his nontoxic form of selenium by injection, usually considered to be four times more powerful than the form given orally.

In 1954, Revici’s fund-raising organization financed the purchase of Beth David Hospital in Manhattan. Renamed Trafalgar Hospital, this general-care facility employing over 200 resident and visiting physicians enabled Revici, as the chief of oncology, to provide round-the-clock care for critically ill patients.

Selenium improves mitochondrial function even in the absence of oxidative stress. Selenium has beneficial effects of endogenous antioxidant activity via GPx, restoration of mitochondrial function and stimulation of biogenesis, and may also reduce oxidative stress driven inflammation. Selenium protects neurons against hypoxic/ischemic damage by reducing oxidative stress, restoring mitochondrial functional activities and stimulating mitochondrial biogenesis. Selenium restores the activity of important antioxidant enzymes and decreases lipid peroxidation. Selenium supplementation reduced glutamate-induced ROS production, prevented mitochondrial hyperpolarization, preserved oxygen utilization, maintained mitochondrial dynamic balance and ameliorated autophagy activation, hence showed neuroprotection from glutamate toxicity.[1]

Tissue damage in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis is accompanied by the arrest of mitochondrial respiration, loss of mitochondrial DNA, and the expression of nuclear-encoded mitochondrial proteins. Selenium effectively protects colon mitochondria prevented inflammatory and necrotic changes. Selenium in a high dose is therefore a potential therapeutic agent in inflammatory bowel disease.[2]

Extra selenium in the diet drastically reduces the spontaneous occurrence of cancer in mice. In human populations, high selenium intake correlates with low cancer rates. In a 140 patient study of cancer victims treated with selenium, Dr. R. Donaldson of the St. Louis Veterans’ Administration Hospital reported in 1983 that some patients deemed terminal with only weeks to live were completely free of all signs of cancer after four years; all the patients showed a reduction in tumor size and in pain.

Adequate selenium nutritional status may help protect against some of the neurological effects of iodine deficiency. Researchers involved in the Supplementation en Vitamines et Mineraux AntioXydants (SU.VI.MAX) study in France, which was designed to assess the effect of vitamin and mineral supplements on chronic disease risk, evaluated the relationship between goiter and selenium in a subset of this research population. Their findings suggest that selenium supplements may be protective against goiter.[3] 

Selenium (Se) in the form of selenocysteine is an essential component of the family of the detoxifying enzymes glutathione peroxidase (Gpx) and of the iodothyronine selenodeiodinases that catalyze the extrathyroidal production of tri-iodothyronine (T(3)). Thus, Se deficiency may seriously influence the generation of free radicals, the conversion of thyroxine (T(4)) to T(3) and a thyroidal autoimmune process.

[1] Glutamate Induces Mitochondrial Dynamic Imbalance and Autophagy Activation: Preventive Effects of Selenium

2012https://doi.org/10.1371/journal.pone.0039382

[2] High selenium diet protects against tnbs-induced acute inflammation, mitochondrial dysfunction, and secondary necrosis in rat colon. TIROSH Oren ; LEVY Eran; REIFEN Ram; Hebrew University of Jerusalem. ISSN 0899-9007  2007, vol. 23, no11-12, pp. 878-886

[3] https://ods.od.nih.gov/factsheets/selenium-HealthProfessional/#h5