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How can antioxidant nutrients contribute to cancer prevention?

May 14, 2014

A new study from the Netherlands suggests that adequate intakes of beta-carotene, lutein and the vitamins A, C and E may reduce the risk of developing colorectal cancer not only due to their antioxidant properties.

The case-control study (1), which used data from a large European cohort study (2), measured the blood concentrations and dietary intakes of beta-carotene, lutein and vitamins A, C, and E of 898 participants who received a colon cancer diagnosis, 501 who were diagnosed with rectal cancer and 1399 participants who had not developed cancer during the study period of 13 years. In addition, blood concentrations of reactive oxygen metabolites were measured in a subgroup of the participants to see whether their antioxidant status was related to the findings. The study results showed that higher blood levels of vitamin A (retinol) at the beginning of the study (before diagnosis) were associated with a 40% lower risk of developing colon cancer and a 55% lower risk of developing proximal colon cancer. Moreover, higher dietary intakes of vitamins C, E and beta-carotene were associated with a lower risk of developing colon cancer. In addition, obese partici- pants with higher lutein levels had a lower risk of colon cancer, and higher vitamin C levels reduced risk of colon cancer in overweight and obese subjects. The blood concentrations of reactive oxygen metabolites were not linked significantly to cancer risk reduction.

The researchers commented that earlier studies already associated higher dietary intakes and/or blood levels of carotenoids and/or the vitamins A, C or E with a reduced risk for colorectal cancer (3-5). However, pooled analyses of prospective studies showed no association between dietary intakes of these nutrients and colorectal cancer risk (6, 7), which may have resulted partly from measurement errors in dietary question- naire assessments (8). The lack of an effect of the antioxidant status (concentration of reactive oxygen metabolites) on cancer risk is a new finding. As in the new study only a single measurement of antioxidant status in a small proportion of the participants was used, a conclusion that there are reasons other than antioxidant activity why these nutrients could affect cancer risk is questionable, the scientists added.

It is thought that antioxidant nutrients prevent oxidative damage to cells and the resulting DNA mutations that may give rise to cancer. However, antioxidant nutrients can also have effects on the immune system, gene expression and DNA repair that could also affect cancer risk. For example, vitamin A (retinol) has found to be essential for the immune system, particularly in barrier cells of the intestines, and to modulate gene expression involved in the initiation of cancer (9).

References

  1. Leenders M. et al. Plasma and dietary carotenoids and vitamins A, C and E and risk of colon and rectal cancer in the European Prospective Investigation into Cancer and Nutrition. Int J Cancer. Published online April 2014.
  2. Riboli E. et al. European Prospective Investigation into Cancer and Nutrition (EPIC): study populations and data collection. Public Health Nutr. 2002; 5:1113–1124.
  3. Xu X. et al. Dietary intake of vitamins A, C, and E and the risk of colorectal adenoma: a meta-analysis of observational studies. Eur J Cancer Prev. 2013; 22(6):529–539.
  4. Jung S. et al. Carotenoid intake and risk of colorectal adenomas in a cohort of male health professionals. Cancer Causes Control. 2013; 24(4):705–717.
  5. Kabat G. C. et al. Repeated measurements of serum carotenoid, retinol and tocopherol levels in relation to colorectal cancer risk in the Women's Health Initiative. Eur J Clin Nutr. 2012; 66(5):549–554.
  6. Mannisto S. et al. Dietary carotenoids and risk of colorectal cancer in a pooled analysis of 11 cohort studies. Am J Epidemiol. 2007; 165:246–255.
  7. Park Y. et al. Intakes of vitamins A, C, and E and use of multiple vitamin supplements and risk of colon cancer: a pooled analysis of prospective cohort studies. Cancer Causes Control. 2010; 21:1745–1757.
  8. Potischman N. Biologic and methodological issues for nutritional biomarkers. J Nutr. 2003; 133:875S–880S.
  9. Eisinger A. L. et al. The adenomatous polyposis coli tumor suppressor gene regulates expression of cyclooxygenase-2 by a mechanism that involves retinoic acid. J Biol Chem. 2006; 281(29):20474–20482.