Berries contain vitamin C and are also a rich source of phytochemicals, especially anthocyanins which occur along with other classes of phenolic compounds, including ellagitannins, flavan-3-ols, procyanidins, flavonols and hydroxybenzoate derivatives. This review examines studies with both human subjects and animals on the absorption of these compounds, and their glucuronide, sulphate and methylated metabolites, into the circulatory system from the gastrointestinal tract and the evidence for their localisation within the body in organs such as the brain and eyes. The involvement of the colonic microflora in catabolising dietary flavonoids that pass from the small to the large intestine is discussed along with the potential fate and role of the resultant phenolic acids that can be produced in substantial quantities. The in vitro and in vivo bioactivities of these polyphenol metabolites and catabolites are assessed, and the current evidence for their involvement in the protective effects of dietary polyphenols, within the gastrointestinal tract and other parts of the body to which they are transported by the circulatory system, is reviewed.

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Berry flavonoids and phenolics: bioavailability and evidence of protective effects

Ingested nitrate and nitrite and stomach cancer risk: An updated review

Folate: metabolism, genes, polymorphisms and the associated diseases.

The potential associations between dietary consumption of nitrates, nitrites, and nitrosamines and gastric cancer risk have been investigated by several studies, but yielded inconclusive results. We conducted a meta-analysis to provide a quantitative assessment of their relationships. Relevant articles were identified by a systematic literature searching of PubMed and Embase databases prior to August 2015. Random-effects models were employed to pool the relative risks. A total of 22 articles consisting of 49 studies-19 studies for nitrates, 19 studies for nitrites, and 11 studies for N-nitrosodimethylamine (NDMA)-were included. The summary relative risk of stomach cancer for the highest categories, compared with the lowest, was 0.80 (95% confidence interval (CI), 0.69-0.93) for dietary nitrates intake, 1.31 (95% CI, 1.13-1.52) for nitrites, and 1.34 (95% CI, 1.02-1.76) for NDMA (p for heterogeneity was 0.015, 0.013 and <0.001, respectively). The study type was found as the main source of heterogeneity for nitrates and nitrites. The heterogeneity for NDMA could not be eliminated completely through stratified analysis. Although significant associations were all observed in case-control studies, the cohort studies still showed a slight trend. The dose-response analysis indicated similar results as well. High nitrates intake was associated with a weak but statistically significant reduced risk of gastric cancer. Whereas increased consumption of nitrites and NDMA seemed to be risk factors for cancer. Due to the lack of uniformity for exposure assessment across studies, further prospective researches are warranted to verify these findings.

Dietary Nitrates, Nitrites, and Nitrosamines Intake and the Risk of Gastric Cancer: A Meta-Analysis

Dietary polyphenols are substrates for colonic microbiota. They and their metabolites contribute to the maintenance of gastrointestinal health by interacting with epithelial cells, and largely by modulating the gut microbial composition. Polyphenols may act as promoting factors of growth, proliferation, or survival for beneficial gut bacteria—mainly Lactobacillus strains—and thus, exerting prebiotic actions and inhibiting the proliferation of some pathogenic bacteria such as Salmonella and Helicobacter pylori species. To date the interactions affecting metabolic pathways and numerous metabolites of dietary polyphenols have been widely documented. However, the effects of dietary polyphenols on the modulation of the intestinal ecology and on the growth of gut microbial species are still poorly understood. This paper summarizes data on the influence of dietary polyphenols on gut microbiota and the main interactions between dietary polyphenols and beneficial and pathogenic intestinal bacteria.

Dietary Polyphenols and Human Gut Microbiota: a Review

N-nitroso compounds (NOC) are potent animal carcinogens and potential human carcinogens. The primary source of exposure for most individuals may be endogenous formation, a process that can be inhibited by dietary polyphenols. To estimate the risk of gastric cancer (GC) in relation to the individual and combined consumption of polyphenols and NOC precursors (nitrate and nitrite), a population-based case-control study was carried out in Mexico City from 2004 to 2005 including 257 histologically confirmed GC cases and 478 controls. Intake of polyphenols, nitrate and nitrite were estimated using a food frequency questionnaire. High intakes of cinnamic acids, secoisolariciresinol and coumestrol were associated with an approximately 50% reduction in GC risk. A high intake of total nitrite as well as nitrate and nitrite from animal sources doubled the GC risk. Odds ratios around 2-fold were observed among individuals with both low intake of cinnamic acids, secoisolariciresinol or coumestrol and high intake of animal-derived nitrate or nitrite, compared to high intake of the polyphenols and low animal nitrate or nitrite intake, respectively. Results were similar for both the intestinal and diffuse types of GC. Our results show, for the first time, a protective effect for GC because of higher intake of cinnamic acids, secoisolariciresinol and coumestrol, and suggest that these polyphenols reduce GC risk through inhibition of endogenous nitrosation. The main sources of these polyphenols were pears, mangos and beans for cinnamic acids; beans, carrots and squash for secoisolariciresinol and legumes for coumestrol.

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Dietary intake of polyphenols, nitrate and nitrite and gastric cancer risk in Mexico City.

DNA methylation is an important epigenetic process for transcriptional control of human genome including those genes involved in cancer initiation and progression. Clinical studies have suggested that biological explanation to the protective effect of some nutrients could be linked with the DNA methylation. Folate is a primary methyl donor nutrient; it has been shown to play a key role in DNA methylation, repair and synthesis, by acting as co-factors and/or substrates in this metabolic pathway. Likewise, activity of a key enzyme, the methylenetetrahydrofolate reductase (MTHFR) has also been shown to influence DNA methylation. Overall, these findings support the notion that dietary intake as well as genetic factors play a role in one-carbon metabolism. This study is to evaluate the dietary intake of nutrients involved in one-carbon metabolism and the genotype of MTHFR 677 C > T with respect to GC risk. We carried out in January 2004 a population-based case–control study in the metropolitan area of Mexico City. A total of 248 histological confirmed GC patients were recruited from nine tertiary hospitals, along with 478 age and sex-matched controls. Nutrient intake was estimated from food frequency questionnaire; the MTHFR 677C > T genotype was determined by PCR-RFLP analysis. A significant reduction in diffuse GC risk was observed for MTHFR 677 TT genotype among individuals with high consumption of folate (OR = 0.23; 95% CI 0.06–0.84), choline (OR = 0.55; 95% CI 0.33–0.9) and Vitamin B6 (OR = 0.59; 95% CI 0.36–0.96) compared to MTHFR 677 CC + CT carriers. Among subjects with low consumption of methionine, a reduced risk of diffuse GC was also detected (OR = 0.40; 95% CI 0.16–0.97). In contrast, carriers of the MTHFR 677 TT genotype with a low consumption of folate had a significant increased risk of intestinal GC (OR = 1.88 95% CI 1.02–3.47). A folate–MTHFR 677 C > T interaction in the borderline of significance (P = 0.055) was detected. It is probable that GC prevention requires dietary recommendations according to the individual genotype; nevertheless, the available information to this respect is still very limited.

Oswaldo Palma-Coca

Papers

Dietary intake of polyphenols, nitrate and nitrite and gastric cancer risk in Mexico City.

Gastric cancer in relation to the intake of nutrients involved in one-carbon metabolism among MTHFR 677 TT carriers.