Vit C and Cancer: hard evidence

CMAJ. 2006 Mar 28; 174(7): 937–942.

doi: 10.1503/cmaj.050346

PMCID: PMC1405876

PMID: 16567755

Intravenously administered vitamin C as cancer therapy: three cases

Sebastian J. Padayatty, Hugh D. Riordan, Stephen M. Hewitt, Arie Katz, L. John Hoffer, and Mark Levine

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Early clinical studies showed that high-dose vitamin C, given by intravenous and oral routes, may improve symptoms and prolong life in patients with terminal cancer. Double-blind placebo-controlled studies of oral vitamin C therapy showed no benefit. Recent evidence shows that oral administration of the maximum tolerated dose of vitamin C (18 g/d) produces peak plasma concentrations of only 220 μmol/L, whereas intravenous administration of the same dose produces plasma concentrations about 25-fold higher. Larger doses (50–100 g) given intravenously may result in plasma concentrations of about 14 000 μmol/L. At concentrations above 1000 μmol/L, vitamin C is toxic to some cancer cells but not to normal cells in vitro. We found 3 well-documented cases of advanced cancers, confirmed by histopathologic review, where patients had unexpectedly long survival times after receiving high-dose intravenous vitamin C therapy. We examined clinical details of each case in accordance with National Cancer Institute (NCI) Best Case Series guidelines. Tumour pathology was verified by pathologists at the NCI who were unaware of diagnosis or treatment. In light of recent clinical pharmacokinetic findings and in vitro evidence of anti-tumour mechanisms, these case reports indicate that the role of high-dose intravenous vitamin C therapy in cancer treatment should be reassessed.

Thirty years ago Cameron, Campbell and Pauling reported beneficial effects of high-dose vitamin C (ascorbic acid) therapy for patients with terminal cancer.1–4 Subsequent double-blind, randomized clinical trials at the Mayo Clinic failed to show any benefit,5,6 and the role of vitamin C in cancer treatment was discarded by mainstream oncologists.7,8 Vitamin C continues, however, to be used as an alternative cancer therapy.9,10

A key distinction between conventional, science-based medicine and alternative therapy is the presence or absence of scientific plausibility.11 In conventional medicine, the efficacy of treatment is proven by properly conducted clinical trials. Many treatments are still used if there is moderately good, albeit inconclusive evidence of efficacy (“clinical plausibility”), especially when treatment rationale agrees with biologic facts (conferring “biological plausibility”).11 Vitamin C is an alternative cancer therapy because the results obtained in original studies that suggested clinical benefit were not confirmed by controlled clinical trials, and the notion that high-dose vitamin C was selectively toxic to cancer cells was biologically implausible.

New information is available pertaining to biological plausibility. Although similar doses of vitamin C were used in the Cameron–Pauling and Mayo Clinic studies, the Cameron–Pauling studies combined intravenous and oral administration whereas the Mayo Clinic studies used only oral administration.1,2,12–14 Recent pharmacokinetics modeling15 indicates that with oral administration, even very large and frequent doses of vitamin C will increase plasma concentrations only modestly, from 70 μmol/L to a maximum of 220 μmol/L, whereas intravenous administration raises plasma concentrations as high as 14 000 μmol/L. Concentrations of 1000–5000 μmol/L are selectively cytotoxic to tumour cells in vitro,16–20 and emerging evidence indicates that ascorbic acid at concentrations achieved only by the intravenous route may function as a pro-drug for hydrogen peroxide delivery to tissues.20 The in vitro biologic evidence and clinical pharmacokinetics data confer biological plausibility to the notion that vitamin C could affect cancer biology and may explain in part the negative results of the Mayo Clinic trials.13,15,21,22 Thus, sufficient evidence has accumulated, not to use vitamin C as cancer treatment, but to further explore the therapeutic concept. One way to increase the clinical plausibility of alternative cancer therapies is rigorous, well-documented case reporting, as laid out in the US National Cancer Institute (NCI) Best Case Series guidelines (,24 Such case series might identify alternative therapies that merit further investigation.23,24

Case reports of apparent responses by malignant disease to intravenous vitamin C therapy have appeared,25–30 including those of 2 of the 3 patients presented below.25,26 However, they were reported without sufficient detail or with incomplete follow-up for evaluation and without conforming to NCI Best Case Series guidelines. They also lacked objective pathologic confirmation, which is a pillar of NCI guidelines. In this article, we use NCI Best Case Series guidelines to report 3 cases of patients with usually progressive malignant disease who received intravenous vitamin C therapy as their only significant cancer therapy and whose clinical courses were unusually favourable. Original diagnostic material obtained before treatment with vitamin C was reviewed by pathologists at the National Institutes of Health (NIH) who were unaware of the diagnoses and treatments.

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Patient 1

This case was previously reported but without long-term follow-up, without detail, and with no independent pathologic confirmation.25,26 A 51-year-old woman was found in August 1995 to have a tumour involving her left kidney. At nephrectomy in September 1995 this was shown to be a renal cell carcinoma 9 cm in diameter with thrombus extending into the renal vein. Chest radiography results were normal, and there was no evidence of metastatic disease on CT scan of the chest and abdomen. In March 1996 a CT scan of the chest indicated several new, small, rounded and well-defined soft tissue masses no larger than 5 mm in diameter; they were judged consistent with metastatic cancer. By November 1996 chest radiography revealed multiple cannonball lesions (Fig. 1).


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Fig. 1:Chest radiography, November 1996, about 1 month after intravenous vitamin C therapy was started. Cannonball lesions are evident in both lung fields, as indicated by the arrows and lines.

The patient declined conventional cancer treatment and instead chose to receive high-dose vitamin C administered intravenously at a dosage of 65 g twice per week starting in October 1996 and continuing for 10 months. She also used other alternative therapies: thymus protein extract, N-acetylcysteine, niacinamide and whole thyroid extract (Table 1). In June 1997 chest radiography results were normal except for one remaining abnormality in the left lung field, possibly a pulmonary scar (Fig. 2).

Table 1


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Fig. 2:Chest radiography, June 1997, showing regression of the lesions; the arrow indicates one residual abnormality.

In October 2001 a new mass 3.5 cm in diameter in the anterior right lung was detected on radiography. A transthoracic biopsy revealed small-cell carcinoma of the lung. The patient opted for intravenous vitamin C injections. The lung mass remained constant in size in radiograpy taken in May and August 2002 but had increased to 4 cm in views taken in October 2002. In early November hyponatremia developed. Two weeks later the patient was admitted to hospital with abdominal distension and constipation. Barium studies revealed slow transit but no intestinal obstruction. Results of a CT scan of the abdomen were normal. She died shortly afterward, and no autopsy was performed. Histopathologic review of the primary renal tumour at the NIH confirmed the diagnosis of clear-cell renal carcinoma, type, nuclear grade III/IV, with the largest diameter measuring 6.5 cm. The tumour involved the renal vein and hilar perinephric fat. Pathologic review of the lung tumour biopsy specimen of October 2001 was not conducted at the NIH. Local pathologists diagnosed this specimen as indicating small-cell lung cancer and not recurrent metastatic renal cell carcinoma.

This case describes the regression of pulmonary metastatic renal cancer in a patient receiving high-dose intravenous vitamin C therapy. According to the NCI Best Case Series guidelines, the credibility of this case would be increased by biopsy proof that the multiple slowly growing bilateral cannonball lung nodules in this patient with known renal cell carcinoma were actually malignant. However, in this case, the clinical characteristics and evolution of the pulmonary lesions, in the absence of bacterial infection or other systemic disease, make any other diagnosis unlikely. The clinician attending the patient deemed a confirmatory biopsy to be unnecessary and inappropriate in this setting. A plausible alternative explanation to the conclusion that this patient’s metastatic renal cell cancer responded to intravenous vitamin C therapy is that the tumours spontaneously regressed. Spontaneous regression has been reported in renal cell cancer, but it is rare, occurring in fewer than 1% of cases and typically after nephrectomy, radiation to the primary tumour or primary tumour embolization.31,32 Here, metastatic disease appeared several months afternephrectomy, rather than regressing in response to it. As well, the primary cancer was nuclear grade III/IV and involved the renal vein, factors associated with a highly unfavourable prognosis.31

Of note, more than 4 years after stopping intravenous vitamin C therapy and with the renal cell cancer in complete remission, primary small-cell lung cancer was diagnosed in this patient, who was a long-standing cigarette smoker. The second cancer did not respond to high-dose vitamin C therapy. From the clinical history it appears the tumour remained a constant size for many months and likely slowly progressed until her death about a year after diagnosis despite the resumption of intravenous vitamin C therapy.

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Patient 2

A 49-year-old man presented to his physician in 1996 with hematuria and was found at cystoscopy to have a primary bladder tumour with multiple satellite tumours extending 2–3 cm around it. Transurethral resection of the primary tumour and its surrounding tumour satellites was carried out until apparently normal muscle was reached and the tumour base was fulgurated. The patient declined systemic or intravesical chemotherapy or radiotherapy and instead chose intravenous vitamin C treatment. He received 30 g of vitamin C twice per week for 3 months, followed by 30 g once every 1–2 months for 4 years, interspersed with periods of 1–2 months during which he had more frequent infusions. Histopathologic review at the NIH revealed a grade 3/3 papillary transitional cell carcinoma invading the muscularis propria. Now, 9 years after diagnosis, the patient is in good health with no symptoms of recurrence or metastasis. The patient used the following supplements: botanical extract, chondroitin sulfate, chromium picolinate, flax oil, glucosamine sulfate, α-lipoic acid, Lactobacillus acidophilusand L. rhamnosusand selenium (Table 2).

Table 2


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Complete or partial bladder removal is the standard treatment for stage T2 (muscle invasive) bladder cancer, since the presence of muscle invasion appears to be the best predictor of aggressive behaviour. When treated only locally, as in this case, invasive transitional cell bladder cancer almost invariably develops into clinically apparent local or metastatic disease within a short period.33–35 There are reports of transurethral tumour resection being offered as the sole initial therapy in carefully selected patients with T2 disease. In one report 20% of patients with muscle invasive bladder cancer treated only with transurethral resection remained free of recurrent disease after 3–7 years of follow-up.36 However, such minimal therapy is considered an option only when the cancer is solitary, well defined and completely excised as documented by pathologic evaluation,37 whereas this patient presented with multiple tumours and associated muscle invasion.

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Patient 3

This case was previously reported but without detail and without independent pathologic confirmation.26,30 A 66-year-old woman was found in January 1995 to have a large left paraspinal mass medial to the iliopsoas muscle at the L4–5 level. On imaging the mass measured 3.5–7 cm transversely and 11 cm in the craniocaudal direction, with evidence of extension into the posterior paraspinal muscle and bone invasion. Chest radiography results were normal. An open biopsy specimen was diagnostic of a diffuse large B-cell lymphoma. The patient’s oncologist recommended local radiation therapy and chemotherapy. Although she agreed to a 5-week course of local radiation therapy, the patient refused chemotherapy, electing instead to receive vitamin C intravenously. She received 15 g of vitamin C twice per week for about 2 months, 15 g once to twice per week for about 7 months, and then 15 g once every 2–3 months for about 1 year. This began in mid-January 1995 concurrently with the radiation therapy, which was given as AP/PA parallel opposed 18 MEV x-rays and between 1–18 and 2–28–95, 5040 Centi Gray in 28 fractions delivered to the mid-plane of the body with 3:2 loading from the back. At this time a left axillary lymph node 1 cm in diameter and a right axillary lymph node 1.5 cm in diameter were palpable.

Two weeks later, in early February 1995, the right and left axillary lymph nodes remained palpable and a new left cervical lymph node 1 cm in diameter and a new left supraclavicular lymph node larger than 1 cm were apparent on physical examination. Intravenous vitamin C therapy continued. Three weeks later the supraclavicular and cervical lymph nodes were no longer palpable, the left axillary node had disappeared, and the right axillary node had decreased in size to less than 1 cm. After a further 3 weeks, in mid-March 1995, there was no lymphadenopathy in the neck and no palpable axillary lymphadenopathy. In late April 1995 a new left cervical lymph node was detected, and histopathologic review identified a biopsy specimen as identical to the original tumour. The patient once again refused chemotherapy and continued her program of intravenous vitamin C injections. Two months later, in June 1995, there was marked left supraclavicular lymphadenopthy 3 cm in size, with shotty right axillary nodes but no adenopathy in the left axilla. Four months later, in October 1995, a single right submandibular node was palpable, but the supraclavicular and all other areas, including the axillas, had no palpable lymph nodes. In May 1996 a left anterior cervical node 1.5 cm in size was present, but there was no other adenopathy. Intravenous vitamin C therapy continued through late December 1996, at which time the patient was in normal health and had no clinical sign of lymphoma. The patient remains in normal health 10 years after the diagnosis of diffuse large B-cell lymphoma, never having received chemotherapy. The patient used additional products: β-carotene, bioflavonoids, chondroitin sulfate, coenzyme Q10, dehydroepiandrosterone, a multiple vitamin supplement, N-acetylcysteine, a botanical supplement and bismuth tablets (Table 3). Histopathologic examination of the original paraspinal mass at the NIH confirmed a diffuse large B-cell lymphoma at stage III, with a brisk mitotic rate.

Table 3


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Patients with untreated stage III diffuse B-cell lymphoma have a dismal prognosis. This case, like the preceding one, is unusual in that the patient refused chemotherapy, which might have produced a long-term remission. It appears, nonetheless, that a cure occurred in connection with intravenous vitamin C infusions.

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These cases were analyzed in accordance with the NCI’s Best Case Series process, which reports and interprets apparent responses to alternative therapies.23,24 Apart from its implications regarding vitamin C, this article illustrates the use of the Best Case Series approach in assessing the clinical plausibility of novel therapies. None of these case histories provides definitive proof that intravenous vitamin C therapy was responsible for the patient’s unusually favourable clinical course. It is often difficult to prove definitively that a given treatment is responsible for a specific clinical outcome. When the treatment is unorthodox, alternative explanations, even if highly unlikely, tend to be preferred.38,39 However, although they do not provide grounds for advocating intravenous vitamin C therapy as a cancer treatment, these cases increase the clinical plausibilityof the notion that vitamin C administered intravenously might have effects on cancer under certain circumstances.

The overall plausibility of ascorbic acid administered intravenously as a cancer therapy is enhanced by recent insights into clinical pharmacokinetics and in vitro cancer-specific cytotoxicity of vitamin C.15–20 Pharmacokinetics data show that orally administered vitamin C results in tightly controlled plasma and cell concentrations. Subjects consuming 200–300 mg per day of vitamin C in 5 or more daily servings of fruits and vegetables have fasting steady state plasma concentrations of about 70–80 μmol/L.40,41 Even with maximally tolerated oral doses of 3 g every 4 hours, peak plasma concentrations are estimated to not exceed 220 μmol/L.15 Intravenous administration of vitamin C bypasses tight control for several hours, until homeostasis is restored by renal excretion. Depending on the dose and infusion rate, peak plasma concentrations obtained intravenously are estimated to reach 14 000 μmol/L, and concentrations above 2000 μmol/L may persist for several hours. Emerging in vitro data show that extracellular ascorbic acid selectively kills some cancer but no normal cells by generating hydrogen peroxide.20 Death is mediated exclusively by extracellular ascorbate, at pharmacologic concentrations that can be achieved only by intravenous administration. Vitamin C may serve as a pro-drug for hydrogen peroxide delivery to extravascular tissues, but without the presence of hydrogen peroxide in blood. These data are consistent with clinical pharmacokinetics of vitamin C administered intravenously.15 Of note, only a minority of cancer patients reported by Cameron and colleagues responded to intravenous and oral vitamin C therapy,1–4 and not all cancer cells were killed by ascorbic acid in vitro.20 Further basic investigation of pharmacologic vitamin C concentrations in mediating cell death will facilitate discovery of the mechanisms responsible for sensitivity and resistance in vitro and in vivo. On the basis of emerging clinical and in vitro data, early-phase clinical trials of intravenous vitamin C therapy alone and in combination with conventional chemotherapy are currently in the planning and execution phase, including a formal phase I trial in progress at McGill University.42–44

The cases reported here do not prove that vitamin C induced the favourable outcomes observed. These patients received other alternative medicine therapies. Spontaneous remission of some tumours may occur rarely, although the 3 cancers reported here are dissimilar. Accretion of more cases meeting NCI Best Case Series guidelines may indicate whether vitamin C or other factors contribute to such remissions.

It is likely that high vitamin C intakes have low toxicity, except under certain conditions.45,46 Intravascular hemolysis was reported after massive vitamin C administration in people with glucose-6-phosphate dehydrogenase deficiency.46 Administration of high-dose vitamin C to patients with systemic iron overload may increase iron absorption and represents a contraindication.46,47 Ascorbic acid is metabolized to oxalate, and 2 cases of acute oxalate nephropathy were reported in patients with pre-existing renal insufficiency given massive intravenous doses of vitamin C.48,49 Therefore, patients with renal insufficiency or renal failure, or who are undergoing dialysis, should not receive high doses of vitamin C.46 It is controversial whether high-dose vitamin C use is associated with oxalate kidney stones, and patients with hyperoxaluria or a prior history of oxalate kidney stones have a relative contraindication to high-dose vitamin C.46 Rare cases of acute tumour hemorrhage and necrosis were reported in patients with advanced cancer within a few days of starting high-dose intravenous vitamin C therapy, although this was not independently verified by pathologic review.1,50 Although tumour hemorrhage suggests an anticancer potential for ascorbate, there is the potential for risk to some patients.

The cases reported here are of tumours confirmed by histopathologic examination to have poor prognosis but that instead had long clinical remissions. Most previous case reports lacked independent pathologic confirmation of the tumour and did not follow the NCI Best Case Series guidelines, which makes their interpretation difficult. Recent findings show that only high-dose intravenous, but not oral, vitamin C therapy results in very high plasma vitamin C concentrations (e.g., 14 000 μmol/L). At these concentrations, the vitamin is toxic to some cancer cells, possibly because at these concentrations the vitamin is a pro-drug for hydrogen peroxide formation in extracellular fluid. Accumulated data confer some degree of biological and clinical plausibility to the notion that high-dose intravenous vitamin C therapy may have anti-tumour effects in certain cancers. When all available data are considered, further clinical study as to safety and efficacy of intravenous vitamin C is warranted.

@ See related article page 956

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The writing of this paper was supported in part by the Intramural Research Program of the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health (Z01 DK 54506).

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Editor’s take

• Intravenous administration of the maximum tolerated dose of vitamin C produces plasma levels 25 times that achieved when the same dose is administered orally. At high plasma concentrations vitamin C is toxic to some cancer cells but not to normal cells in vitro.

• Using the National Cancer Institute Best Case Series guidelines, the authors reviewed 3 cases of advanced cancer where patients had unexpectedly long survival times after receiving high-dose intravenous vitamin C therapy.

Implications for practice:In a setting of biological plausibility and clinical plausibility, further research into vitamin C as a treatment for cancer is warranted.

This article has been peer reviewed.

Contributors:Sebastian Padayatty, Arie Katz and Mark Levine wrote the first draft, Hugh Riordan contributed to data acquisition, Stephen Hewitt conducted pathology reviews and John Hoffer revised this article. All of the authors contributed to the conception, design and critical review of the paper. All of the authors approved the final version of the paper, excepting Hugh Riordan. Hugh Riordan died before the final version was accepted but had reviewed and approved an earlier version of the paper.

Hugh D. Riordan died suddenly during the final preparation of this article. We dedicate it to his memory.

Competing interests:None declared.

Correspondence to:Dr. Mark Levine, Molecular and Clinical Nutrition Section, Bldg. 10, Rm 4D52–MSC 1372, National Institutes of Health, Bethesda MD 20892–1372;vog.hin.liam@LkraM

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Vitamin C and Cancer

In 1976, Pauling and Dr. Ewan Cameron, a Scottish physician, reported that a majority of one hundred “terminal” cancer patients treated with 10,000 mg of vitamin C daily survived three to four times longer than similar patients who did not receive vitamin C supplements [11,12]. However, Dr. William DeWys, chief of clinical investigations at the National Cancer Institute, found that the study was poorly designed because the patient groups were not comparable [13]. The vitamin C patients were Cameron’s, while the other patients were under the care of other physicians. Cameron’s patients were started on vitamin C when he labeled them “untreatable” by other methods, and their subsequent survival was compared to the survival of the “control” patients after they were labeled untreatable by their doctors. DeWys reasoned that if the two groups were comparable, the lengths of time from entry into the hospital to being labeled untreatable should be equivalent in both groups. However, he found that Cameron’s patients were labeled untreatable much earlier in the course of their disease—which means that they entered the hospital before they were as sick as the other doctors’ patients and would naturally be expected to live longer.

Nevertheless, to test whether Pauling might be correct, the Mayo Clinic conducted three double-blind studies involving a total of 367 patients with advanced cancer. The studies, reported in 1979, 1983, and 1985, found that patients given 10,000 mg of vitamin C daily did no better than those given a placebo[14-16]. Pauling criticized the first study, claiming that chemotherapeutic agents might have suppressed the patients’ immune systems so that vitamin C couldn’t work [17]. But his 1976 report on Cameron’s work stated clearly that: “All patients are treated initially in a perfectly conventional way, by operation, use of radiotherapy, and the administration of hormones and cytotoxic substances.” And during a subsequent talk at the University of Arizona, he stated that vitamin C therapy could be used along with all conventional modalities [18]. The participants in the 1983 study had not undergone conventional treatment, but Pauling dismissed its results anyway.

Science aside, it is clear that Pauling was politically aligned with the promoters of unscientific nutrition practices. He said his initial interest in vitamin C was aroused by a letter from biochemist Irwin Stone, with whom he subsequently maintained a close working relationship. Although Stone was often referred to as “Dr. Stone,” his only credentials were a certificate showing completion of a two-year chemistry program, an honorary chiropractic degree from the Los Angeles College of Chiropractic, and a “Ph.D.” from Donsbach University, a nonaccredited correspondence school.

In a little-publicized chapter in Vitamin C and the Common Cold, Pauling attacked the health-food industry for misleading its customers. Pointing out that “synthetic” vitamin C is identical with “natural” vitamin C, he warned that higher-priced “natural” products are a “waste of money.” And he added that “the words ‘organically grown’ are essentially meaningless—just part of the jargon used by health-food promoters in making their excess profits, often from elderly people with low incomes.” But Vitamin C, the Common Cold and the Flu, issued six years later, contained none of these criticisms. This omission was not accidental. In response to a letter, Pauling informed me that, after his first book came out, he was “strongly attacked by people who were also attacking the health-food people.” His critics were so “biased,” he decided, that he would no longer help them attack the health-food industry while another part of their attack was directed at him [19].

The Linus Pauling Institute of Science and Medicine was founded in 1973 and operated under that name until 1995 [20]. The institute was dedicated to “orthomolecular medicine.” For many years, its largest corporate donor was Hoffmann-La Roche, the pharmaceutical giant that produces most of the world’s vitamin C. Many of the institute’s fundraising brochures contained questionable information. During the 1980s, for example, they falsely stated that no significant progress had been made in cancer treatment during the previous twenty years.

A dispute between Pauling and Arthur Robinson, Ph.D., gives additional evidence of Pauling’s defense of vitamin C megadosage was less than honest. Robinson, a former student and long-time associate of Pauling, helped found the institute and became its first president. According to an investigative report by James Lowell, Ph.D., in Nutrition Forum newsletter, Robinson’s own research led him to conclude in 1978 that the high doses (5-10 grams per day) of vitamin C being recommended by Pauling might actually promote some types of cancer in mice [18]. Robinson told Lowell, for example, that animals fed quantities equivalent to Pauling’s recommendations contracted skin cancer almost twice as frequently as the control group and that only doses of vitamin C that were nearly lethal had any protective effect. Shortly after reporting this to Pauling, Robinson was asked to resign from the institute, his experimental animals were killed, his scientific data were impounded, and some of the previous research results were destroyed. Pauling also declared publicly that Robinson’s research was “amateurish” and inadequate. Robinson responded by suing the Institute and its trustees. In 1983, the suit was settled out of court for $575,000. In an interview quoted in Nature, Pauling said that the settlement “represented no more than compensation for loss of office and the cost of Robinson’s legal fees.” However, the court-approved agreement stated that $425,000 of the settlement was for slander and libel. The Institute’s own legal fees were close to a million dollars [21].

In 1994, Robinson and two colleagues summarized the results of four mouse studies he had carried out while working at the Pauling Institute [22]. Nearly all of the mice developed skin cancers (squamous cell carcinomas) following exposure to ultraviolet radiation. Altogether, 1,846 hairless mice received a total of 38 different diets. The researchers found that (a) the rate of onset and severity of tumors could be varied as much as 20-fold by just modifying dietary balance; (b) diets with the worst balance of nutrients had the greatest inhibitory effect on cancer growth; and (c) no cures or remissions were observed (although the researchers were not looking for this). In 1999, Robinson commented:

The results of these experiments caused an argument between Linus and me, which ended our 16-year period of work together. He was not willing to accept the experimentally proved fact that vitamin C in ordinary doses accelerated the growth rate of squamous cell carcinoma in these mice.

At the time, Linus was promoting his claim that “75% of all cancer can be prevented and cured by vitamin C alone.” This claim proved to be without experimental foundation and not true. . . . Vitamin C increased the rate of growth of cancer at human equivalents of 1 to 5 grams per day, but suppressed the cancer growth rate at doses on the order of 100 grams per day (near the lethal dose), as do other measures of malnutrition [23].

Recent laboratory studies have found that vitamin C may interfere with the effectiveness of five anti-cancer drugs. First, the researchers gave a vitamin C product to cancer cells that were treated with chemotherapy and found that the 30% to 70% fewer cancer cells were killed. Then they injected mice with cancer cells, administered chemotherapy, and found that cells grew into tumors much faster in the mice that received pre-treatment vitamin C. The researchers warned that although results in animals are not necessarily applicable to humans, vitamin C supplementation during cancer treatment may interfere with the effect of chemotherapy in humans [24].

Other Questionable Activities

During the mid-1970s, Pauling helped lead the health-food industry’s campaign for a federal law that weakened FDA protection of consumers against misleading nutrition claims. In 1977 and 1979, Pauling received awards and presented his views on vitamin C at the annual conventions



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