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January 19, 2010
By: Sean Moloughney
Editor, Nutraceuticals World
Leafy green vegetables, folate and multivitamins may help to protect smokers from lung cancer, according to a study published recently in the journal Cancer Research. The study was supported by the National Cancer Institute, part of the National Institutes of Health. One promising approach for early detection of lung cancer is by monitoring gene promoter hypermethylation events in sputum. Epidemiologic studies have suggested that dietary fruits and vegetables and the micronutrients they contain may reduce risk of lung cancer. In this study, researchers evaluated whether diet and multivitamin use influenced the prevalence of gene promoter methylation in cells exfoliated from the aerodigestive tract of current and former smokers. The study population included 1101 people from the Lovelace Smokers Cohort, who completed the Harvard Food Frequency Questionnaire and provided a sputum sample that was assessed for promoter methylation of eight genes commonly silenced in lung cancer and associated with risk for this disease. Methylation status was categorized as low (fewer than two genes methylated) or high (two or more genes methylated). Logistic regression models were used to identify associations between methylation status and 21 dietary variables hypothesized to affect the acquisition of gene methylation. Significant protection against methylation was observed for leafy green vegetables [odds ratio (OR) = 0.83 per 12 monthly servings; 95% confidence interval (95% CI), 0.74–0.93] and folate (OR, 0.84 per 750 µg/d; 95% CI, 0.72–0.99). Protection against gene methylation was also seen with current use of multivitamins (OR, 0.57; 95% CI, 0.40–0.83). This is the first cohort-based study to identify dietary factors associated with reduced promoter methylation in cells exfoliated from the airway epithelium of smokers. Researchers concluded that novel interventions to prevent lung cancer should be developed based on the ability of diet and dietary supplements to affect reprogramming of the epigenome.
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