Folate intake, post-folic acid grain fortification, and pancreatic cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial

Nutritional Epidemiology Branch, the Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA.
American Journal of Clinical Nutrition (Impact Factor: 6.77). 12/2009; 91(2):449-55. DOI: 10.3945/ajcn.2009.28433
Source: PubMed


Folate plays a critical role in DNA methylation, synthesis, and repair. Several epidemiologic studies suggest that higher folate intake is associated with decreased pancreatic cancer risk.
We investigated the association between dietary folate intake and pancreatic cancer in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) cohort.
Dietary data were collected with the use of a self-administered food-frequency questionnaire (1998-2005). Among the 51,988 male and 57,187 female participants, aged 55-74 y at enrollment, with complete dietary and multivitamin information, 162 men and 104 women developed pancreatic cancer during follow-up (January 1998 to December 2006; median: 6.5 y). We used Cox proportional hazards regression with age as the time metric to calculate hazard ratios (HRs) and 95% CIs.
The highest compared with the lowest quartile of food folate was associated with a significantly decreased pancreatic cancer risk among women (> or = 253.3 compared with < or = 179.1 microg/d; HR = 0.47; 95% CI: 0.23, 0.94; P for trend: 0.09) but not among men (> or = 229.6 compared with < or = 158.0 microg/d; HR = 1.20; 95% CI: 0.70, 2.04; P for trend: 0.67; P for interaction by sex: 0.03). There was also a significant inverse trend in risk of pancreatic cancer across increasing quartiles of total folate in women (P for trend: 0.04) but not in men (P for trend: 0.65). Folic acid supplements were not associated with pancreatic cancer.
These findings support an association between higher food and total folate intakes and decreased risk of pancreatic cancer in women but not in men.

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Available from: Li Jiao, Oct 01, 2015
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    • "Folate is crucial for normal DNA synthesis, repair and methylation (Martínez et al., 2004). Low folate level has been implicated in various types of cancer development (Glynn et al., 1996; Ibiebele et al., 2011; Keszei et al., 2009; Oaks et al., 2010; Shen et al., 2003; Stolzenberg-Solomon et al., 2006; Unnikrishnan et al., 2011). Our previous study showed that folate deficiency was correlated with the increased oxidative DNA damage, DNA strand breaks and global DNA hypomethylation in chromate exposed workers (Wang et al., 2012). "
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    ABSTRACT: Both hexavalent chromium [Cr (VI)] exposure and folate deficiency have been associated with increased cancer risks. Our previous studies have found folate deficiency in Cr (VI) exposed population. Here the relationship between some tumor markers and folate status in long-term Cr (VI) exposure was investigated carefully to show the multiple aspects of Cr (VI) carcinogenesis. A group of 115 workers occupationally exposed to chromate and 60 matched, unexposed controls in Shandong province of China were recruited. Environmental and biological exposure assessments including personal exposure to airborne Cr and Cr contents in erythrocytes were performed. Serum folate, plasma total homocysteine (tHcy) and plasma carcinoembryonic antigen (CEA), neuron specific enolase (NSE), squamous cell carcinoma antigen (SCC), cytokeratin fragment antigen 21-1 (CYFRA 21-1), cancer antigen 72-4 (CA72-4), as well as α-fetoprotein (AFP) were measured. Smoking index (SI) was also calculated to discriminate possible confounding effects of smoking status. Serum folate level decreased significantly, while plasma tHcy, CEA, NSE, SCC, CYFRA21-1, CA72-4 and AFP concentrations increased significantly after Cr (VI) exposure. Meanwhile, plasma CEA, NSE and SCC were negatively correlated with serum folate. SI was negatively correlated with serum folate but positively correlated with plasma tHcy, CEA and NSE levels. Present study suggests that folate deficiency was associated with increased cancer risks and might be affected by smoking in Cr (VI) exposed population. Folate might play a key role in Cr (VI) carcinogenesis although further detailed investigations are needed to clarify the mechanism of this process.
    International journal of hygiene and environmental health 04/2013; 217(1). DOI:10.1016/j.ijheh.2013.03.013 · 3.83 Impact Factor
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    • "However, folic acid from supplements did not show a protective effect. Other surveys have also confirmed the positive impact of folate [46, 47] on the prevention of pancreatic cancer, although not all of them [48, 49]. "
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    ABSTRACT: The aim of the study was to investigate the relationship between pancreatic cancer incidence and selected dietary factors, alcohol consumption, and tobacco smoking in Poland in 1960–2008. Data on pancreatic cancer morbidity were derived from the National Cancer Registry and on food consumption from the national food balance sheets. In 1960–1989 correlations were found between pancreatic cancer incidence rates and energy (0.60 for males and 0.57 for females), cholesterol (0.87 and 0.80), fibre (−0.84 and −0.89) and folate (−0.45 and −0.49) intake, the consumption of total fats (0.94 and 0.91), animal fats (0,90 and 0,82), sugar (0.88 and 0.87), cereals (−0.93 and −0.91), and alcohol (0.86 and 0.82). In 1990–2008 morbidity correlated with the consumption of red meat (0.67 and 0.48), poultry (−0.88 and −0.57), and fruit (−0.62 and −0.50). Correlation with tobacco smoking was observed in the whole studied period (0.55 and 0.44). Increased incidence of pancreatic cancer in 1960–1995 was probably related to adverse dietary patterns up to 1989, especially high consumption of fats, sugar, and alcohol. Further positive changes in the diet such as lowering red meat consumption and increasing fruit consumption could influence incidence reduction in recent years. Also changes in tobacco smoking could affect the morbidity.
    Gastroenterology Research and Practice 12/2012; 2012:682156. DOI:10.1155/2012/682156 · 1.75 Impact Factor
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