Researchers from the Linus Pauling Institute at Oregon State University, Children’s Hospital Oakland Research Institute, and the University of California, Davis report in the August, 2009 issue of the American Journal of Clinical Nutrition that reducing dietary zinc is associated with increased breakage of peripheral blood cell DNA strands, while restoring zinc to normal levels reduces breakage. Zinc deficiency is estimated to affect 2 billion people worldwide, and is believed to elevate the risk of several chronic diseases, including cancer. The ability of zinc to increase DNA repair, in addition to its role as an antioxidant, may be responsible for its protective effect.
For the first 13 days of the current study, nine healthy men received a diet that contained 11 milligrams zinc per day to ensure adequate zinc status. The subjects then underwent a period of zinc depletion during which they received liquid diets containing 0.6 milligrams zinc for seven days, followed by a diet containing 4 milligrams zinc for 35 days. During the first 21 days of the low zinc diet, participants received 1.3 grams per day of phytate, which inhibits zinc absorption. On the 56th day of the study, the participants were switched back to the zinc replete diet provided at the beginning of the study, and continued on this diet for 18 days with the addition of supplemental zinc for the first 7 days of this period. Fasting blood samples drawn at the beginning and end of the study and at several intermediate points were analyzed for DNA damage, plasma zinc levels, and antioxidant status.
By the end of the period during which the subjects received zinc-depleted diets, DNA strand breaks increased by an average of 57 percent compared to the beginning of the period, indicating that six weeks of reduced zinc intake significantly increases DNA damage in peripheral blood cells. These increases proved to be reversible by restoring adequate zinc intake, since DNA strand breaks decreased by 39.9 percent by the end of the study. The researchers also observed a decline in DNA damage during the 13 day baseline zinc-adequate period, suggesting that the participants may have had DNA damage prior to enrollment. Plasma F2-isoprostanes, which indicate oxidative stress, and total antioxidant capacity did not vary significantly over the course of the study.
The study is the first, to the authors’ knowledge, to report DNA damage in human peripheral blood cells associated with zinc deficiency. “Overall, these data suggest that dietary zinc status affects DNA damage in peripheral blood cells and that adequate zinc status may be essential to maintain DNA integrity in humans,” the authors write. “Importantly, the alterations in DNA integrity occurred before significant changes in plasma zinc were detected.”
Colorectal cancer develops through a process involving genetic change in the epithelial cells of the colon lining. The main factors that initiate colorectal cancer are consumption of cooked red meat (due to heterocyclic amines) (Gerhardsson de V et al 1991; Reddy S et al 1987), high intake of refined carbohydrates (Franceschi S et al 2001), poor vitamin and mineral intake, alcohol consumption, smoking, bile acids, fecal mutagens (DNA-damaging agents), fecal pH, and compromised detoxification enzymes (Winawer SJ et al 1992). An example of one important detoxification enzyme is N-acetyltransferase, which catalyzes the formation of DNA-damaging products from heterocyclic amines that form in cooked meats. Differences in the activity of this enzyme classify individuals as slow or fast acetylators. The level of red meat consumption in fast but not slow acetylators is associated with risk for colorectal cancer development (Welfare MR et al 1997).
In industrialized Western societies, both polyps and colon cancer occur more frequently due in part to diets low in fruits, vegetables, vegetable protein, and fiber (Satia-Aboutaj J et al 2003). Fecal mutagens are produced by certain diets such as those containing overcooked or burnt meat or fish. Increased intake of fiber, on the other hand, shortens the intestinal transit time, which in turn reduces the exposure of the colorectal lining to mutagens within the stool (Johansson G et al 1997).
Low folate intake, especially when combined with alcohol consumption and a low-protein diet, increases colorectal cancer risk (Kato I et al 1999). Dietary folate influences DNA methylation, synthesis, and repair. Abnormalities in these DNA processes enhance cancer development, particularly in rapidly growing tissues such as the colorectal mucosa (Lengauer C et al 1997; Feinberg AP et al 1983). Higher folate intake from either dietary sources or supplements may protect against the initiation of colorectal cancer (Giovannucci E 2002, 1998).
Low levels of selenium correlate with the presence of adenomas (benign tumors), whereas increased levels of selenium are associated with reduced risk of adenomas. Intervention trials have found a beneficial effect of selenium supplementation (Russo MW et al 1997).
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