Review of dietary patterns and gastric cancer risk: epidemiology and biological evidence

Abstract

Due to rapid research expansion on dietary factors and development of cancer prevention guidelines, the field of dietary pattern and its relationship to cancer risk has gained more focus. Numerous epidemiology studies have reported associations between Gastric Cancer (GC) and both data-driven posteriori dietary pattern and priori dietary pattern defined by predetermined dietary indexes. As dietary patterns have evolved, a series of patterns based on biological markers has advanced, offering deeper insights into the relationship between diet and the risk of cancer. Although researches on dietary patterns and cancer risk are booming, there is limited body of literature focusing specifically on GC. In this study, we compare the similarities and differences among the specific components of dietary patterns and indices, summarize current state of knowledge regarding dietary patterns related to GC and illustrate their potential mechanisms for GC prevention. In conclusion, we offer suggestions for future research based on the emerging themes within this rapidly evolving field.

Keywords: dietary patterns; gastric cancer; priori and posteriori; review; risk.

Figure 1

A posteriori and priori dietary patterns and cancer risk. The evidence is strongest for gastric cancer, where the alternative healthy eating index (AHEI-2010), Mediterranean diet score (MDS), and anti-inflammatory diets have been associated with reduced risk. There is no GC risk association with HEI-2005, Chinese food pagoda (CHFP), alternative mediterranean diets (AMED), and no consistent evidence for an association between the Dietary approaches to stop hypertension (DASH), vegetarian diets and gastric cancer.

Figure 2

The Healthy Eating Index (HEI)-1995 has ten components, encompassing five food groups, four nutrients, and a measure of food intake variety (15). The HEI-2005 introduced changes from the previous version. On density basis of foods and nutrients, it adopted new food groups, such as whole fruit, dark green and orange vegetables, legumes, whole grains, and oils. Additionally, it included a discretionary component, which accounted for calories from solid fat, alcohol, and added sugar (SoFAAS) (16, 17). Building upon the HEI-2005, the HEI-2010 further refined the scoring system. It replaced the dark green and orange vegetables and legumes component with the greens and beans component, expanded the protein group by adding seafood and plant proteins, replaced oils and saturated fat with a fatty acids ratio, and introduced a moderation component by assessing over-consumption of refined grains instead of total grains (18). The HEI-2015 retained the components of the HEI-2010, except for replacing empty calories with saturated fat and added sugars. This modification resulted in a total of 13 components. Notably, excessive energy from alcohol was no longer accounted for in a separate component but was included within the total energy calculation. Legumes were also treated differently in the HEI-2015, as they were counted towards all four components instead of being allocated to either the vegetable or protein foods components (19). The HEI-2020 maintains the same 13 components and scoring standards as the HEI-2015 (20). Each component is assigned a score, with a maximum possible index score of 100. HEI scores > 80 indicate a “good” diet, scores ranging from 51 to 80 reflect a diet that “needs improvement,” and scores < 51 imply a “poor” diet (21). The AHEI score was based on the intake of nine individual components. The components include vegetables, fruits, nuts and soy, the ratio of white to red meat, cereal fiber, trans fat, the ratio of polyunsaturated fatty acids to saturated fatty acids, multivitamin use, and alcohol intake. Each component had the potential to contribute 0-10 points, intermediate intakes were scored proportionately to receive points between 0 and 10. Multivitamin use was dichotomous, either 2.5 points (did not use) or 7.5 points (did use). All individual component scores were then summed to obtain an AHEI score, which ranged from 2.5 to 87.5 (22). The AHEI-2010 comprises 11 components, six are associated with higher intakes being beneficial: vegetables, fruit, whole grains, nuts and legumes, long-chain ω-3 fatty acids, and polyunsaturated fatty acids. Moderate intake is recommended for alcohol. Conversely, four components should be limited or avoided: sugar-sweetened drinks and fruit juice, red and processed meat, trans fats, and sodium. To calculate the total AHEI-2010 score, each component is scored on a scale of 0 to 10. The total AHEI-2010 score is sum of each component score, ranging from 0 to 110, with a higher score indicating higher adherence to a healthy diet (23). The AHEI-2010 maintains most dietary components of AHEI but encourages people to consume long-chain n-3 fatty acids and reduce sugar intake.

Figure 3

Collective mechanisms proposed to underlie the protective effect of Mediterranean diet against Gastric cancer.

Figure 4

Summary of the potential interplay in the molecular mechanisms of the ketogenic diet (KD) and cancers. (A) KD lower insulin and IGF-1 levels to suppress tumor cells’ insulin-stimulated GLUT4 trafficking by PI3K/Akt signing pathway. (B) Mitochondrial DNA dysfunctions triggering into reactive oxygen species (ROS) overdosage in tumor cells, resulting in NADPH and pyruvate increase via the pentose phosphate shunt and glycolysis way individually to reduce hydroperoxides to keep the steady state of oxidative stress. (C) KD can reduce NADPH generation to increase the oxidative stress in tumor cells, by impeding gluconeogenesis to form glucose-6-phosphate (G-6-P) that is necessity for the pentose phosphate shunt. (C) KD treated ad libitum could down-regulated hypoxia-related protein. (D) Ketones enter into the cancer cell by the monocarboxylate transporters (MCTs) that is responsible for lactate export, leading to competitive inhibition of lactate export. (E) KD had anti-tumor effects by hindering systematic inflammation. Ketone bodies supplements inhibited the activation of NLRP3 inflammasome mediated by inhibiting NF-κB and STAT3 activation, and finally lower the expression levels of IL-1β.