“Vitamin C injections can destroy cancer”, the Daily Express reported. Widespread media attention was given to a study that found that high dose injections of vitamin C could slow the growth of cancers. The newspapers said that tests in mice showed that this treatment could halve the size of pancreatic, brain, and ovarian tumours. Most reports mentioned that the concentrations of vitamin C used in the study could not be achieved simply by eating vitamin C-rich foods or by taking supplements. In addition, Dr Alison Ross from Cancer Research UK called for more research, and cautioned, “there is currently no evidence from clinical trials in humans that injecting or consuming vitamin C is an effective way to treat cancer. Some research even suggests that high doses of antioxidants can make cancer treatment less effective, reducing the benefits of radiotherapy and chemotherapy.”
Although this research may prompt other studies into the potential anticancer effects of vitamin C, it should not be taken as proof that vitamin C injections will necessarily have the same effects in humans. More research is needed before it is possible to be certain what the effects of this treatment might be.
Where did the story come from?
Dr Qi Chen and colleagues from the National Institute of Diabetes and Digestive and Kidney Diseases, and other research institutions in the USA, carried out the research. The study was funded in part by the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health. The study was published in the peer-reviewed medical journal: Proceedings of the National Academy of Sciences.
What kind of scientific study was this?
This experimental laboratory study looked at the effects of high doses of ascorbic acid (vitamin C) on tumour cells grown in the laboratory, and on transplanted tumours in mice. Ascorbic acid is an essential part of the diet, and is considered to be an antioxidant, thought to protect cells from free radicals which have been linked to cell damage and cancer. In this study, the researchers considered the possibility that in high concentrations, ascorbate is in fact a pro-oxidant, and generates the chemical hydrogen peroxide, which can kill tumour cells.
The researchers took 43 different cancer cell types (including rat, mouse, and human cancers) and five different normal cell types grown in the laboratory, called cell lines. After exposing these cell lines to varying concentrations of ascorbic acid for up to two hours, they looked at whether the cells died, what concentration of ascorbic acid was needed to kill half the cells, and whether this was different for cancer and normal cells. To ascertain whether hydrogen peroxide was involved, they tested whether the cells would still die if they added an enzyme that breaks down hydrogen peroxide.
The researchers then took a selection of the cell lines that were most susceptible to ascorbic acid and transplanted them into mice and allowed them to grow. Once the mice had developed tumours that were 5-7mm in diameter, some of them (between 9 and 18 mice) received daily injections of high concentration ascorbic acid into their abdominal cavity for 30 days. The remaining mice were injected with salt water (the control groups, which included between 10 and 18 mice). The researchers compared tumour growth in these two groups of mice.
Finally, the researchers looked at whether they could achieve the concentrations of ascorbate seen in mice in humans, using intravenous injections of ascorbic acid.
What were the results of the study?
The researchers found that ascorbic acid killed most of the different mouse, rat and human cancer cells at a lower concentration than that which killed normal cells. Some human cancer cells also survived these lower concentrations. Experiments showed that hydrogen peroxide was involved in killing the cells.
In the second phase of the experiment, the researchers injected mice with cancer cell lines that were susceptible to ascorbic acid in their first set of experiments - a human ovarian cancer cell line, a rat brain tumour cell line, and a mouse pancreatic cancer cell line. They found that injecting these mice with ascorbic acid reduced tumour growth and weight compared to controls. They found that about a third of the control mice injected with the brain tumour cells had metastases (tumours spread from the original tumour), but none of the ascorbic acid treated mice had metastases.
The mice did not seem to experience adverse effects from the ascorbic acid injections. The researchers found that they could achieve similar concentrations to those seen in mice in humans by using intravenous injections.
What interpretations did the researchers draw from these results?
The researchers concluded that ascorbic acid “may have benefits in cancers with poor prognosis and limited therapeutic options.”
What does the NHS Knowledge Service make of this study?
This is a very preliminary study looking at the effects of high levels of vitamin C on tumour cells grown in the lab, or in small numbers of mice. It is worth noting that not all of the tumour cells grown in the laboratory were susceptible to ascorbic acid, and only one of the cancer cell lines that was tested in mice was a human cell line.
Although this study may lead to further research into the anticancer effects of vitamin C, it cannot prove that vitamin C injections will necessarily have the same effects in humans. The authors report that the concentrations of vitamin C used could not be achieved orally; therefore it certainly should not be assumed that taking vitamin C orally would have similar effects.
Sir Muir Gray adds...
Vitamin C won't do any harm and may do some good, but as a supplement to conventional treatment and not an alternative.
Analysis by Bazian
Edited by NHS Website
Links to the headlines
Daily Express, 5 August 2008
The Independent, 5 August 2008
The Mirror, 5 August 2008
The Daily Telegraph, 5 August 2008
The Guardian, 5 August 2008
Daily Mail, 5 August 2008
BBC News, 5 August 2008
Links to the science
Cochrane Database Syst Rev 2004, Issue 4
PNAS 2008; Published online before print August 4