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Vitamin C, also known as ascorbic acid, is a water-soluble vitamin. Unlike most mammals and other animals, humans do not have the ability to make their own vitamin C. Therefore, we must obtain vitamin C through our diet. Severe vitamin C deficiency has been known for many centuries as the potentially fatal disease, scurvy. By the late 1700s the British navy was aware that scurvy could be cured by eating oranges or lemons, even though vitamin C would not be isolated until the early 1930s.
A large number of studies have shown that increased consumption of fresh fruits and vegetables is associated with a reduced risk for most types of cancer. Such studies were the basis for dietary guidelines endorsed by the U.S. Department of Agriculture and the National Cancer Institute, which recommended at least five servings of fruits and vegetables per day. U.S. government organizations currently recommend eating a variety of fruits and vegetables daily; the recommended serving number depends on total caloric intake, which is governed by age, gender, body composition, and physical activity level. A number of case-control studies have investigated the role of vitamin C in cancer prevention. Most have shown that higher intakes of vitamin C are associated with decreased incidence of cancers of the mouth, throat and vocal chords, esophagus, stomach, colon-rectum, and lung. Because the possibility of bias is greater in case-control studies, prospective cohort studies are generally given more weight when evaluating the effect of nutrient intake on disease. In general, prospective studies in which the lowest intake group consumed more than 86 mg of vitamin C daily have not found differences in cancer risk, while studies finding significant cancer risk reductions found them in people consuming at least 80 to 110 mg of vitamin C daily.
A prospective study that followed 870 men over a period of 25 years found that those who consumed more than 83 mg of vitamin C daily had a striking, 64% reduction in lung cancer compared with those who consumed less than 63 mg per day. However, a pooled analysis of eight prospective studies concluded that dietary vitamin C was not related to lung cancer when the analysis was controlled for other dietary factors. Although most large prospective studies observed no association between breast cancer and vitamin C intake, two studies found dietary vitamin C intake to be inversely associated with breast cancer risk in certain subgroups. In the Nurses' Health Study, premenopausal women with a family history of breast cancer who consumed an average of 205 mg/day of vitamin C from foods had a 63% lower risk of breast cancer than those who consumed an average of 70 mg/day. In the Swedish Mammography Cohort, overweight women who consumed an average of 110 mg/day of vitamin C had a 39% lower risk of breast cancer compared to overweight women who consumed an average of 31 mg/day.
A number of observational studies have found increased dietary vitamin C intake to be associated with decreased risk of stomach cancer, and laboratory experiments indicate that vitamin C inhibits the formation of carcinogenic compounds in the stomach. Infection with the bacteria, Helicobacter pylori (H. pylori), is known to increase the risk of stomach cancer and also appears to lower the vitamin C content of stomach secretions. Although two intervention studies did not find a decrease in the occurrence of stomach cancer with vitamin C supplementation, more recent research suggests that vitamin C supplementation may be a useful addition to standard H. pylori eradication therapy in reducing the risk of gastric cancer. Another intervention trial, a randomized, double-blind, placebo-controlled trial in more than 14,000 older men participating in the Physicians’ Health Study (PHS) II, reported vitamin C supplementation (500 mg/day) for an average of eight years had no significant effect on total cancer or site-specific cancers, including colorectal, lung, and prostate cancer. However, the PHS II had several limitations; see the Linus Pauling Institute’s response to the PHS II.