The Dr. Ewan Cameron Vitamin C Treatment Protocol for Cancer

Cameron Protocol


"It has been known for many years that cancer patients have depressed circulating, cellular, and tissue ascorbate reserves, and ascorbate (vitamin C) is involved in many aspects of host resistance to cancer." 


by Ewan Cameron, MD, FRCS, Medical Director, Linus Pauling Institute of Science and Medicine. Formerly Chief of Surgery, Vale of Leven Hospital, Lochlomondside, G83 OUA, Scotland

Reprinted with permission of the Linus Pauling Institute, Oregon State University

(Note: Within this paper, Dr. Cameron cited 38 references, and recommended 11 additional sources. The complete bibliography is posted at )

Important Note: This paper is designed specifically for, and addressed specifically to, licensed medical physicians.


More than one thousand (as of 1986) cancer patients have been treated by supplemental ascorbate (vitamin C) in a few canters in Scotland and Japan. In addition, it has been reliably estimated that at least 100,000 cancer patients in the United States are currently ingesting ascorbates with or without the tacit consent and knowledge of their physicians. Nevertheless this form of treatment must still be considered experimental and unproven. Before initiating treatment, the physician must obtain signed informed consent stressing this point. The administration of ascorbate either orally or intravenously is not illegal anywhere in the United States or Canada.


The reasons for the expectation that supplemental ascorbate should be of some benefit to all cancer patients have been given in detail elsewhere. To summarize, it has been known for many years that cancer patients have depressed circulating, cellular, and tissue ascorbate reserves, and ascorbate (vitamin C) is involved in many aspects of host resistance to cancer. Moreover, ascorbate administered in pharmacological doses enhances many parameters of the immune response to levels far above the somewhat arbitrary "normal" range, including cell-mediated immunity and the endogenous production of interferon. There is also some laboratory evidence behind the strong clinical impression that in certain situations attainable concentrations of ascorbate may have a selective cytotoxic effect on malignant cells while being harmless to normal cells, resulting in cancer regression in rare instances.


Despite the above, it is understandably difficult to believe that a simple cheap and safe substance such as vitamin C could have any possible value against such a bafflingly complex disease as cancer. Such reasonable skepticism was seemingly confirmed by the publication of two negative trials carried out by respected investigators at the Mayo Clinic. However, careful reading of these two papers shows that these much publicized results were far from conclusive. Both trials relied upon oral medication only, and in the form of 20 ascorbate capsules to be swallowed per day, compared to controls swallowing 20 capsules of an easily recognized placebo. In the first trial 127 far-advanced patients suffering from miscellaneous cancers were studied, almost all of whom had already been unsuccessfully treated by chemotherapy or radiation therapy and often both. Such immune-compromised patients would be the least likely to derive any benefit from vitamin C. Furthermore no checks were carried out to ensure that controls were not self-medicating with this freely available substance. 

The second trial was even more inconclusive. Ascorbate or placebo was administered to 100 patients with inoperable colon cancer, abruptly discontinued when tumor progression was detected at a median time of 10 weeks, then replaced in the majority by chemotherapy. From the published data in the second paper it is clear that the few controls tested were also self-medicating with vitamin C. Thus the ascorbate treatment of cancers remains unproven and experimental, but by no means disproved.


Cancer treatment must never be regarded as an alternative to proven conventional methods of cancer treatment, but instead as a supportive measure employed alongside whatever standard method is indicated. There is some evidence of synergism. Thus ascorbate has long been known to promote healing, and should accelerate convalescence from major cancer surgery. Ascorbic acid and its metabolite dehydroascorbic acid radiosensitize hypoxic tumor cells with the potential to enhance the therapeutic effects of radiation. Ascorbate enhances the chemotherapeutic activity of some chemotherapeutic drugs, including adriamycin, while there is considerable anecdotal evidence that ascorbate diminishes to a certain extent the unpleasant side-effects of cytotoxic chemotherapy without apparently interfering with the effectiveness of such drugs, although the latter point has not been completely investigated.


As with any cancer treatment, it is important to establish certain baseline data before commencing treatment, in order to monitor future therapeutic response. Such baseline data will naturally vary depending on the type and extent of the particular cancer being treated but will include patient's weight, performance on the Karnovsky scale, full hematological profile, SMAC-16 biochemical profile, measurement of serum tumor marking proteins if present, and clinical and radiological (including CAT-scan and NMR imaging if appropriate) measurement of the extent of tumor load.


Clinical experience indicates that the best responses are obtained if one can maintain a continuous high plasma ascorbate level. Ascorbate, however administered, is rapidly excreted in the urine, so that administration should be continuous or at very frequent intervals. Furthermore, exposure to high circulating levels of ascorbate induces over-activity of certain hepatic enzymes concerned with its degradation and metabolism. These enzymes persist for some time after sudden cessation of high intakes, resulting in depletion of circulating levels of ascorbate to well below normal unsupplemented values. This is known as the rebound effect. It causes a sharp decrease in immunocompetence and must be avoided in the cancer patient. Clinical experience has shown that the best responses are observed when vitamin C is administered intravenously, so insuring a high plasma level. However, because long-term continuous intravenous administration is impractical, we recommend an initial intravenous course of ten days duration, followed by continuous maintenance oral regimen. If the patient's condition deteriorates, further intravenous "booster" courses are recommended.


Vitamin C intravenously can be given by intermittent injection, but this is not recommended, particularly if the intervals between injections extend to several days. Because of the rebound effect, such administration would produce a sawtooth plasma ascorbate profile with abnormally low levels in the troughs just prior to the next injection. We recommend continuous administration via slow drip infusion.

It is recommended that the patient be hospitalized for initial evaluation and commencing the intravenous regimen. Intravenous vitamin C can cause troublesome chemical phlebitis if injected directly into a superficial vein. Fo0r this reason it is recommended that infusion be given via a C.V.P. (Central Venous Pressure, or similar) line, with routine A-P portable chest X-ray taken after placement to ensure that the catheter tip is correctly positioned in the Superior Vena Cava. Alternately a "Hep-Lock" (or similar) cannula may be used in a forearm vein with appropriate precautions against clotting.

(Additional information on intravenous vitamin C administration is found in the Riordan Intravenous Vitmain C Protocol); in Dr. Robert F. Cathcart's paper Preparation of Sodium Ascorbate for IV and IM Use posted at ; and in Clinical Guide to the Use of Vitamin C, by Lendon Smith, MD. The full text of Dr. Smith’s book is posted at . These sources discuss details including needle gauges and buffers, among other topics.)

The recommended "carrier solution" is Ringer's Lactate Solution, readily available in liter packs or flasks, and infused at the steady rate of 2 liters (two packs) every 24 hours. Isotonic Dextrose should never be used as the carrier solution. Vitamin C for parenteral use comes in sterile ampules of sodium ascorbate preferably without preservative. Standard ampules contain 0.5g (500 milligrams), or as "multiuse" 50 ml ampules containing 25 grams. The ampules should be added to the infusion packs under full sterile conditions in the Hospital Pharmacy or Infusion Fluids Department.

In patients not previously exposed to high levels of ascorbate, a gradual "wind-up" dose regimen is recommended, along the following lines:

Day One to the first flask add 0.5g sodium ascorbate

to the second 1.0g sodium ascorbate

to the third 1.5g sodium ascorbate

to the fourth 2.0g sodium ascorbate

Day Two to the fifth flask add 2.5g sodium ascorbate

(continuing at that level infuses 10g sodium ascorbate per day)

Much higher doses can be and have been infused with perfect safety, the limiting factor being sodium overload with water retention, and not the ascorbate ion itself. The wind-up dosage schedule is not necessary in patients receiving "booster" repeat courses.

PRECAUTIONS: Standard continuous infusion procedure must be followed. It is not necessary to monitor serum electrolyte levels except in patients with gross cardiac or renal impairment.

SIDE-EFFECTS There are two recognized side-effects, one very common and relatively harmless, the other very rare and highly dangerous. The common side-effect is transient fluid retention due to sodium overload resulting in some ankle edema in the ambulant and sacral pad edema in those confined to bed. Inpatients with cardiac impairment dangerous pulmonary edema may develop and require intravenous frusemide for its control.

The rare side-effect, seen only in patients with highly anaplastic very rapidly growing tumors and a heavy tumor load, is the sudden precipitation of widespread tumor necrosis. Clinically this is heralded by sudden pain in all tumor deposits, rapid swelling of known tumors, tumor hemorrhage, both internal and external, hyperpyrexia, severe hypotension,

tachycardia and azotemia. This very rare complication can be fatal and must be vigorously treated. If suspected, the ascorbate infusion should be immediately stopped, and the patient treated as for septicemic shock. The patient may require transfer to the Intensive Care Unit for close monitoring and support by oxygen, plasma or blood, and intravenous steroids. If resuscitation is successful, it will be found that any residual tumor has shrunk considerably or even disappeared. Although highly dangerous, this reaction might also be termed the best possible response to ascorbate treatment of wide-spread cancer.


On the day planned to terminate intravenous ascorbate, the patient should be commenced on oral ascorbate at the same daily intake. The medication should be taken every six hours (four times a day), and once commenced should never be abruptly discontinued because of the rebound effect. The dose varies between individuals in the 10 to 30g a day range. The aim should be to maintain plasma ascorbate levels of at least 3mg/dl for effective therapy. Leukocyte ascorbate concentration, a technically more difficult estimation to perform, is of much less value in predicting response to treatment.


As with any other form of cancer treatment, therapeutic response will vary between individual patients, with paradoxically the best responses seen with individuals with far advanced disease. Therapeutic responses may be listed as follows:

1. No response detectable (a very few)

2. Some retardation of progressive tumor growth (very many)

3. Stasis or standstill effect (considerable number)

4. Tumor regression (a few)

5. Tumor necrosis (very rare)

A typical response to ascorbate can be described as follows:

An improvement in well-being, vigor and Karnovsky performance status will be apparent in 5 to 7 days. Originally thought to be a purely subjective response, it is now realized to be objective and due to restoration of endogenous carnitine biosynthesis, carnitine being responsible for transporting triglycerides across the mitochondrial membrane where they are burned for muscle energy.

If painful skeletal metastases are present, relief of bone pain will occur in about 5 to 7 days, enabling opiates to be withdrawn without withdrawal symptoms. Skeletal or widespread visceral metastases are associated with increased urinary hydroxyproline (UHP) excretion reflecting collagen breakdown. Within 5 days of commencing ascorbate therapy, a sharp and sustained fall in UHP excretion will be noted.

Response to treatment will also be reflected in a drop in the sedimentation rate and fall in the titer of any serum tumor protein markers (CEA etc.) if present.

Radiological signs of good response include the slow conversion of osteolytic skeletal metastases to dense osteosclerotic lesions over a period of months. In favorable cases, resorption of malignant pleural effusions and reduction in size of pulmonary metastases have been observed.


Oral ascorbate should be continued indefinitely and the patient carefully monitored at least every month. The usual course of events is that the patient instead of slowly declining will enter a plateau of comparative well-being that may continue for many months or even years, and then enter an abrupt downhill phase with explosive metastases. At the first suspicion of this change, a "booster" course of intravenous ascorbate is recommended, even though individual responses can never be predicted. Over a period of three years, one patient with widespread leiomyosarcoma had six such booster courses with clear benefit from each one except the last. Many other patients have shown no benefit from even the first booster course, but it is always worth trying.


Isotonic solutions of sodium ascorbate (2.97g sodium ascorbate in 100 ml sterile distilled water for injection) have been instilled in the peritoneal and pleural cavities after paracentesis or thoraocentesis for malignant effusions. Benefit appeared to ensue in the sense of reduction in the rate of effusion accumulation, although without controls this impression is difficult to prove. At least clinical experience has shown that the procedure is quite painless and perfectly safe.


There is a widespread belief in the medical profession that large intakes of vitamin C might somehow cause kidney damage. This apparently stems from a (1954) study that showed that in some individuals (5 percent of those tested) intakes of vitamin C above 4 grams per day resulted in a measurable increase in urinary oxalate levels with a theoretical risk of oxalate stone formation. Doubts have been expressed about the specificity of the assay method used, and studies on healthy individuals ingesting large amounts of vitamin C for years have shown plasma and urinary oxalate levels well within normal range. No instance of this complication has been encountered in over 100 cancer patients under the author's care, or in many other patients ingesting multigram amounts of ascorbate for many years. The risk of stone formation, if it exists at all, must be extremely remote, and more than offset by the potential benefit to the cancer patient. (Additional information refuting alleged vitamin-caused kidney stones is found in The Vitamin C Connection, by Emanuel Cheraskin, MD, et al, and How to Live Longer and Feel Better, by Linus Pauling, PhD.)

(Note: Within this paper, Dr. Cameron cited 38 references, and recommended 11 additional sources. The complete bibliography is posted at

Andrew Saul is the author of the books FIRE YOUR DOCTOR! How to be Independently Healthy (reader reviews at ) and DOCTOR YOURSELF: Natural Healing that Works. (reviewed at )



Andrew W. Saul


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