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Environmental Factor

May 2011

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Diet may protect against colon cancer, says NIEHS study

By Ed Kang
May 2011

Dan Shaughnessy, Ph.D.

Lead author Dan Shaughnessy is now a program administrator in the Susceptibility and Population Health Branch of the NIEHS Division of Extramural Research and Training.  (Photo courtesy of Steve McCaw)

Jack Taylor, M.D., Ph.D.

Taylor was principal investigator on the new study. (Photo courtesy of Steve McCaw)

Consuming meat cooked at high temperatures can cause DNA damage in the colon, whereas eating certain other foods may have a protective effect, according to a recent study from the Laboratory of Molecular Carcinogenesis (LMC) and the Epidemiology Branch at NIEHS. The study titled "Inhibition of Fried Meat-Induced Colorectal DNA Damage and Altered Systemic Genotoxicity in Humans by Crucifera, Chlorophyllin, and Yogurt" was published online in the journal PLoS ONE and is the result of a 4-week controlled feeding study of 16 volunteers.

The researchers explain that cooking meat at a high temperature (250°C versus 100°C) increases levels of carcinogens that are present in well-done, highly fried or burned meat. The study examined whether the negative effects of consuming this meat could be mitigated by a diet of yogurt, chlorophyllin (a derivative of chlorophyll), and cruciferous vegetables, such as green or red cabbage, broccoli, Brussels sprouts, and cauliflower.

"It's clear that cooking meat at a high temperature creates a large number of mutagens that contribute to DNA damage to colon cells," said lead author Dan Shaughnessy, Ph.D., who conducted the study while a postdoctoral fellow in the LMC. "But eating certain foods can reduce the damage and possibly the risk for cancer."

Colorectal cancer is the fourth most common cancer worldwide, and increased risk is associated with elevated levels of mutagenic compounds known as heterocyclic amines (HCAs). HCAs are formed when meats are cooked at high temperature, particularly by pan frying.

The cruciferous vegetables, chlorophyllin tablets, and yogurt containing lactobacilli were chosen based on previous studies showing their antimutagenic effects against the damage from HCAs, thus modulating cancer risks associated with meat consumption. The NIEHS study goes a step further by concurrently measuring urinary and fecal mutagenicity and DNA damage in the colon, and by demonstrating that dietary antimutagens can alter these characteristics.

"Although increased mutagenicity following consumption of highly fried meat is well established, to our knowledge, this is the first study to show that dietary factors can reduce DNA damage specifically in the colon," explained Jack Taylor, M.D., Ph.D., co-author and head of the LMC Molecular and Genetic Epidemiology Group. "The inhibitor diet decreased nearly twofold the DNA damage in colorectal cells." 

Although the study points to encouraging results, the investigators are quick to identify the need for further research. The authors caution that testing the effects of the three dietary factors together, rather than separately, limits conclusions about the relative importance of each dietary antimutagen and the mechanism of DNA-damage inhibition. Future studies may further evaluate the protective mechanisms and reveal any synergistic or even antagonistic relationship among the dietary antimutagens.

Participants were enrolled and studied at the University of North Carolina at Chapel Hill. Samples were analyzed at NIEHS, the U.S. Environmental Protection Agency, and the Lawrence Livermore National Laboratory.

Citation: Shaughnessy DT, Gangarosa LM, Schliebe B, Umbach DM, Xu Z, MacIntosh B, Knize MG, Matthews PP, Swank AE, Sandler RS, DeMarini DM, Taylor JA.( Exit NIEHS 2011. Inhibition of Fried Meat-Induced Colorectal DNA Damage and Altered Systemic Genotoxicity in Humans by Crucifera, Chlorophyllin, and Yogurt. PLoS ONE 6(4):e18707. doi:10.1371/journal.pone.0018707

(Ed Kang is a public affairs specialist in the Office of Communications and Public Liaison and a regular contributor to the Environmental Factor.)

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