Abstract
There are still some controversies on the association between dietary folate intake and the risk of upper gastrointestinal cancers including esophageal, gastric and pancreatic cancers. Hence, a comprehensive meta-analysis on all available literatures was performed to clarify the relationship between dietary folate intake and risks of upper gastrointestinal cancers. An electric search was performed up to December 12th, 2016 within the PubMed, MEDLINE AND EMBASE databases. Ultimately, a total of 46 studies which evaluated the association between folate intake and risks of upper gastrointestinal cancers were included. According to the data from included studies, the pooled results showed significant association between folate intake and esophageal (OR = 0.545, 95%CI = 0.432-0.658), gastric (OR=0.762, 95%CI=0.648-0.876) and pancreatic (OR=0.731, 95%CI=0.555-0.907) cancers. Linearity dose-response analysis indicated that with 100μg/day increment in dietary folate intake, the risk of esophageal, gastric and pancreatic cancers would decrease by 9%, 1.5% and 6%, respectively. These findings indicated that higher level of dietary folate intake could help for preventing upper gastrointestinal cancers including esophageal, gastric and pancreatic cancers.
Highlights
Folate, named vitamin B9, is a naturally occurring nutrient and is found in many foods including fruits, vegetables legumes, cereals, and liver
These findings indicated that higher level of dietary folate intake could help for preventing upper gastrointestinal cancers including esophageal, gastric and pancreatic cancers
Folate plays an important role in the process of DNA synthesis, repair, and methylation, and was hypothesized to decrease risks of gastrointestinal cancers
Summary
Named vitamin B9, is a naturally occurring nutrient and is found in many foods including fruits, vegetables legumes, cereals, and liver. Folate plays an important role in the process of DNA synthesis, repair, and methylation, and was hypothesized to decrease risks of gastrointestinal cancers. The main carcinogenesis mechanisms of folate are inducing DNA strand breaks by causing uracil mis-incorporation into DNA and changing levels of DNA methylation [2]. These aberrant changes may result in potential alterations of critical proto-oncogene and tumor suppressor gene expressions [3]. Animal experiments referring mice and dogs suggested that high levels of folate intake affected DNA methylation and eventually decreased the risks of gastric cancer [4, 5]. The polymorphisms of genes in folate metabolizing pathway may modulate the susceptibility of several cancers
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