Cancer and Vitamin C: Crossroads of New Research

[Part 9 of 9]

In 2018, a third edition of Ewan Cameron and Linus Pauling’s book, Cancer and Vitamin C, was published. Released nearly a quarter century after Pauling’s death, this edition marked the first time that someone other than Pauling or Cameron contributed to the volume. The second edition, which was published in 1993, included an updated preface and a few new indices, but the text itself remained entirely Cameron and Pauling’s. The 2018 edition also includes a new preface and a new index, but both were written by Stephen Lawson of the Linus Pauling Institute at Oregon State University. Lawson used the new additions to ably present recent scholarship connecting the efficacy of vitamin C to the treatment of cancer.


One bit of background that Lawson sought to clarify at the outset was the story of why vitamin C treatments for cancer had not been initially supported by outside research. As noted in our previous posts, Pauling and Cameron believed that external research corroborating their results would provide an effective avenue for convincing skeptics of the curative powers of vitamin C. The Mayo Clinic eventually agreed to conduct a study of this sort, but found that vitamin C did not improve cancer patients’ prognoses, and in some instances their outcomes were actually worse.

Even though Pauling and Cameron did not agree with the Mayo Clinic’s findings, they had a hard time making their case to the public about why the study was in error. But as described by Lawson in the 2018 preface, Pauling and Cameron recognized that the Mayo Clinic’s treatment protocols were different than their own in important ways. Specifically, Cameron and Pauling had always delivered vitamin C intravenously, whereas the Mayo Clinic researchers dosed their patients orally. At the time, Pauling and Cameron could not prove why this should make a difference, but they believed that it was a key reason why the Mayo Clinic did not get positive results. While science could not confidently address this scenario in 1979 – or even in 1993 at the time of the second edition – by 2018 researchers had developed a much clearer idea of the importance of intravenous application.

Beginning in 1999, a team of researchers began actively exploring the absorption of vitamin C and, in particular, whether or not there was a difference between oral and intravenous applications. As they conducted their work, the group discovered a previously unknown vitamin C transport molecule in the stomach, which helped to deliver ascorbic acid into the bloodstream. The team subsequently learned that there was an upper limit to how much vitamin C the transport molecules could carry. This effectively meant that no matter how much vitamin C a person ingested orally – vitamin C that would end up in the stomach – only a finite amount could actually be absorbed and utilized, due to the limited carrying capacity of the transport molecule. The exact amount of vitamin C that a transport molecule can carry is still being researched, with data to this point indicating that quantities may vary based on factors such as age.

In tandem with this discovery, researchers were also interested in understanding what happens when vitamin C enters the bloodstream, be it intravenously or through transport molecules in the stomach. As Lawson notes, studies found that one byproduct of high levels of vitamin C in the bloodstream (regardless of how it got there) is hydrogen peroxide. Hydrogen peroxide has the ability to fight cancer by altering its DNA, robbing its cells of ATP (the “muscle” of the cell), and fatally damaging its energy-producing mitochondria. When deployed at scale, this three-pronged attack might be presumed to fight cancer very effectively.

That said, hydrogen peroxide therapy has not been used with cancer patients, because there is no safe and effective way to deliver the substance into the bloodstream without damaging other healthy cells. While the connection between vitamin C dosing and internal hydrogen peroxide production is not well-understood, these preliminary findings suggest that high blood concentrations of vitamin C could create hydrogen peroxide in sufficient quantity as to be effective at neutralizing cancer cells.


Several other new areas of research were highlighted in the 2018 edition, including the connection between vitamin C and hypoxia inducing factor (HIF). Some cancer tumors grow so fast that blood vessels cannot be created quickly enough to deliver oxygen to the expanding mass. To compensate for this lack of blood vessels in these hypoxic (or low oxygen) environments, tumor cells induce HIF, which stimulate the growth of blood vessels within the tumor. This inducement of HIF allows fast-growing tumors to continue to propagate and wreak havoc, rather than succumbing to oxygen starvation. For reasons that remain unclear, when vitamin C is introduced into a fast-growing tumor it represses the activation of HIF, compelling the tumor to remain in its hypoxic state and eventually die.

Emerging research on the relationship between vitamin C and dehydroascorbic acid (DHA) is also included in the 2018 edition. DHA is an oxidation product of vitamin C, and when present has been shown to reduce the amount of colorectal cancer in the body.

A collection of sixteen relatively recent clinical trials are likewise surveyed in the book, all of which examined the outcomes of different kinds of cancer patients when given vitamin C in conjunction with other chemotherapeutics. All sixteen found that patients’ outcomes improved once they were given the vitamin C in concurrence with their chemotherapy treatment. Five other studies were conducted on cancer patients given vitamin C but not chemotherapy. Results of these trials were mixed but, as Lawson points out, the non-chemotherapy researchers were primarily interested in determining optimal doses of vitamin C and measuring how quickly patients depleted their vitamin C infusions. Many of the trials also found that patient outcomes improved.

As with the original text of the book, a collection of case studies were also discussed by Lawson. And though they serve mostly as anecdotal evidence, Lawson shows that significant improvements in patients’ health have been documented once they have been administered vitamin C treatment.


One of the biggest takeaways that a reader might glean from the 2018 edition is that, even though a significant amount of research has been conducted on the vitamin C and cancer connection, medical practitioners have been hesitant to deploy the treatment because the studies have seemed less than rigorous, or because other practitioners have found that it does not work with their patients. Lawson counters these sentiments by noting that most cancer research is novel and that only the most promising ideas go on to clinical trials. Further, because an optimum vitamin C dose has not yet been codified, doctors commonly administer vitamin C on an ad hoc basis. Worse still, doctors also sometimes administer the treatment as a “last ditch” effort after chemotherapy and all other treatments have failed. Pauling and Cameron demonstrated in their first edition that vitamin C needs to be administered continuously and before chemotherapy to be maximally effective. Clearly much remains to be done before the work that Pauling and Cameron started with their first edition can be called complete.

Why Vitamin C? Cancer Fighting Properties

Ewan Cameron, Ava Helen and Linus Pauling. Glasgow, Scotland, October 1976.

[An analysis of Ewan Cameron and Linus Pauling’s book, Cancer and Vitamin C. This is part 2 of 9.]

In their 1979 book, Cancer and Vitamin C, Ewan Cameron and Linus Pauling argued that vitamin C could be used to effectively treat cancer. With such a bold claim having been issued, vitamin C now needed to do a lot of heavy lifting. More specifically, Pauling and Cameron needed to prove that vitamin C could a) effectively treat cancer and also b) do so better than other substances being used to treat and cure cancer. As such, the authors devoted nearly half of their book to exploring vitamin C’s unique properties, with particular attention naturally paid to its cancer-fighting abilities.

In doing so, Cameron and Pauling first examined known cancer-causing agents on the cellular level and then investigated how vitamin C interreacted with these agents. One such substance was the enzyme hyaluronidase. When Pauling and Cameron were writing their book, it was widely recognized that certain malignant tumors released this enzyme and that, when exposed to healthy tissues, the enzyme would break down the glycosaminoglycans, which might be likened to the “cement” that makes tissues strong. As the cement became weaker, the tissues grew more vulnerable to being penetrated by cancer cells. By extension, it was believed that hyaluronidase promoted the spread of malignant cells within the body. It was also suspected that cancer cells released a different enzyme, collagenase, which would break down the collagen in tissues, further weakening cells and making them more susceptible to disease.

Having established this, Pauling and Cameron then illustrated the role that vitamin C could play in obstructing this process. Studies had found that vitamin C naturally helps to produce a hyaluronidase inhibitor, which in effect blocks the enzyme and stops the destruction of the tissue cement. Furthermore, vitamin C is known to be a necessary component for the building of collagen, and it was proposed that increased intake of vitamin C could boost collagen production and strengthen cells even more.

When Pauling and Cameron published their first edition, some of the ideas regarding hyaluronidase and collagenase were speculative. Pauling and Cameron were also relying on their collective scientific expertise to develop a model for vitamin C’s interactions with these enzymes. Pauling was not shy about making informed inferences to explain scientific phenomena, and in the case of vitamin C and these two enzymes, his thinking appears to have been correct. Since the publication of the first edition of Cancer and Vitamin C, two different research teams have published articles (in 2001, 2004, 2010, and 2011) which found evidence that vitamin C does in fact help to inhibit hyaluronidase.

More recent research has also suggested that high levels of vitamin C generate hydrogen peroxide. While it is not clear what the exact mechanism is that causes this, it is known that hydrogen peroxide can lead to a type of cell death that turns out to be useful in the cancer fight. Most healthy cells are not impacted by hydrogen peroxide because of the presence of an enzyme, catalase, that neutralizes its impact. Cancer cells, on the other hand, are not equipped with catalase; or if they are, the amount is negligible. So it is now well-established that hydrogen peroxide can kill cancer cells, but getting sufficient quantities of hydrogen peroxide to cancer cells inside the body has proven challenging. By administering large doses of vitamin C, it is hoped that clinicians may someday be able to provide targeted hydrogen peroxide therapy to patients who could benefit from it.


While Pauling and Cameron were able to provide data-based connections between vitamin C and its ability to fight cancer, their book also includes more anecdotal ideas that support their argument. One such observation was that patients who were given vitamin C for cancer treatment tended to experience less severe side effects from chemotherapeutics than those who did not take vitamin C. Although it was hard to quantify, Pauling and Cameron noted several instances where bed-ridden patients under Cameron’s care would take vitamin C and soon be capable of moving about. Cameron also observed that patients who stopped taking vitamin C often saw their symptoms rapidly return.

More notably, several of Cameron’s patients who were given vitamin C were found to go into remission. Because of ethical concerns related to placebo trials, Cameron and Pauling did not have any controls to support their claims. However, many of the patients took no treatment other than vitamin C, and Cameron, who had been a practicing physician for many years prior to beginning work on vitamin C therapy, understood that remissions for many of these cancers was not at all common.

To further support the notion that there was something special about vitamin C, Pauling and Cameron also observed that healthy people could not tolerate as much supplemental vitamin C as could those suffering from cancer. That is to say, healthy patients could take only so much vitamin C before they began to experience side effects, such as diarrhea, than was the case with cancer patients. This anecdote suggested to the authors that cancer patients needed a large amount of vitamin C – all of it was, in effect, being used, and as such there were no negative side effects. In fact, the appropriate dosage was often determined by giving a patient as much as they could tolerate before experiencing side effects.


Pauling and Cameron knew that vitamin C helped fight cancer. They saw that their patients were getting better and, from a molecular viewpoint, the mechanisms involved made sense, even if the data wasn’t in hand to prove everything. But there was more to support vitamin C as a model substance for treating cancer, and that had to do with its connection to scurvy, which we will explore in our next post.

Hydrogen Peroxide

Linus Pauling in the laboratory. 1940.

I am planning to carry out during the next few days some experiments on the resistance of concentrated peroxide to shock by detonators and by rifle bullets, and I shall let you know the results of the experiments.

-Linus Pauling, letter to T. K. Sherwood, November 14, 1940.

Beginning in early 1940, Dr. Paul A. Giguere, a visiting researcher from Laval University, began a study of the properties of concentrated hydrogen peroxide at the Caltech labs. Under Pauling’s watch, Giguere spent several months performing electron diffraction analyses on samples of hydrogen peroxide and hydrazine. By November, the testing had been completed and the two men wrote a brief report on their findings. Pauling, already deeply involved in the development of the oxygen meter for the National Defense Research Committee (NDRC), felt that his and Giguere’s work might net the Institute another war research contract.

On November 14 he sent Thomas K. Sherwood, his primary NDRC contact, an enthusiastic letter detailing the initial findings. One early indication of Guigere’s work was that hydrogen peroxide might be used to absorb shock from explosives or rifle bullets. He also thought it possible to develop a means of controlling the evolution of hydrogen peroxide, suggesting that it could be used to produce oxygen for respirators. The laboratory intended to begin shock resistance tests immediately so that a clean set of data might be prepared, pending Sherwood’s response.

Pauling received an encouraging reply from Sherwood, but it is unclear at what point further work on the hydrogen peroxide project began. Fully two months after the initial correspondence exchange, Sherwood sent a letter to Caltech requesting a progress report from Pauling. In response, Pauling appears to have sent two letters: one detailing work on the oxygen meter and the other containing information on the hydrogen peroxide project. Unfortunately, it seems Pauling’s archives are incomplete as only the first letter remains extant. Whatever information may have been included in the second letter is lost, though we do know that Sherwood responded positively and sent Pauling data on hydrogen peroxide as a chemical fuel for combustion engines.

Thomas K. Sherwood, ca. 1960s. National Academy of Sciences image.

Bizarrely, following this last communication from Sherwood, no further mention of the hydrogen peroxide problem appears in Pauling’s papers until February 1943, in the form of a letter from Giguere demanding to know why Pauling’s article – presumably on his hydrogen peroxide research – had never been published. In response, Pauling reported that he and Dr. Verner Schomaker had only recently completed the manuscript and would send it on to Giguere shortly. Interestingly, this report too appears to be absent from the archives. What’s more, only a single page of hydrogen peroxide research remains in Pauling’s research notebooks.  This page details the decomposition of hydrogen peroxide in blood – a tantalizing entry that gives little indication of the nature of his research.

It is surprising that Pauling, who maintained comprehensive records of his scientific activities, possessed so few notes on his work with hydrogen peroxide. One might speculate that perhaps certain of the materials related to this project were turned over to higher authorities within the government, as has been confirmed with other projects in which Pauling was engaged.

Whatever the cause may have been for this lapse in the record, it seems plausible that Pauling’s early hydrogen peroxide work did have some long-term consequences.  In 1942 Pauling began work on a war research project on the development of a plasma substitute eventually known as oxypolygelatin. This work was spawned from his private Caltech-based research into bovine gamma-globulin, possibly the cause of Pauling’s initial experiments with blood and hydrogen peroxide. It may have also been this initial investigation that led Pauling to use hydrogen peroxide in the creation of oxypolygelatin.

Unfortunately, without letters, reports or laboratory data to review, it is impossible to know exactly what Pauling’s hydrogen peroxide research entailed or how it affected his later research. It seems then, that this particular project will remain one of many small mysteries in Pauling’s life.