By Pooja Toshniwal Paharia Feb 22 2024 Reviewed by Lily Ramsey, LLM
In a recent review published in Frontiers in Oncology, researchers investigated eating patterns and indices related to gastric cancer and explored their association with stomach cancer risk.
Study: Review of dietary patterns and gastric cancer risk: epidemiology and biological evidence . Image Credit: Peakstock/Shutterstock.com Background
Gastric cancer is a common cancer worldwide, accounting for considerable global mortality. Despite attempts to minimize Helicobacter pylori prevalence and enhance food storage, the incidence and fatality rates of stomach cancer have decreased.
Epidemiological studies have found links between eating habits and stomach cancer risk. Individual dietary components, on the other hand, have produced inconsistent results in terms of the stated risk of stomach cancer.
Assessing eating patterns yields more reliable effect estimates and outcomes, emphasizing the need for comprehensive cancer prevention recommendations. About the review
In the present review, researchers reviewed existing data on the impact of diet on gastric cancer risk.
Diet patterns can be posteriori (formed from cohort population data) or a priori (created using existing information about food, nutrients, and illness). Posteriori patterns are determined using statistical approaches such as principal component analysis, factor analysis, and cluster analysis.
A priori patterns may derive from country-specific standards, chronic disease-preventive diets, or cultural eating habits. Association between a posteriori eating patterns and stomach cancer
In case-control studies, healthy eating patterns minimized the risk of stomach cancer, but an "unhealthy" dietary pattern raised the risk.
A comprehensive meta-analysis revealed that greater compliance with "prudent" diet patterns was related to a lower incidence of stomach cancer [odds ratio (OR) 0.8].
In contrast, increased compliance with Western diets increased the risk of total stomach cancer (odds ratio, 1.5). The association between poor eating habits and stomach cancer risk was more robust for cardia stomach cancers (OR, 2.1) than for distal stomach cancers (OR, 1.4).
Other meta-analyses showed that individuals consuming healthy foods had decreased stomach cancer risks (OR, 0.7) considerably.
In contrast, following unhealthy diets increased stomach cancer risk (OR, 1.6). A 2017 meta-analysis found that "Western" diets increase gastric cancer risk.
However, meta-analytical research of 13 case-control studies and eight studies of the prospective cohort type found that those abiding by "prudent" diets had a lower chance of developing stomach cancer. A priori dietary patterns, dietary indices, and gastric cancer
The relationship between eating habits and stomach cancer risk is complicated and nuanced. There is limited research on the link between high health eating index (HEI) or alternate HEI (AHEI) scores and the risk of stomach cancer.
A comprehensive review and meta-analysis found that higher adherence to HEI and AHEI dietary patterns was associated with a lower risk of total cancer-specific mortality.
New case-control research from Iran found that eating the dietary approaches to stop hypertension (DASH) diet was related to a 54% lower incidence of stomach cancer.
The DASH diet's components, such as excessive salt intake, red meat consumption, and fruits, have been linked to an increased risk of stomach cancer.
A Markov cohort state-transition model projected that a low sodium-DASH diet reduced stomach cancer risk by 25% in men and 21% in women.
Meta-analyses indicate that Mediterranean diet (MD) followers are less likely to develop stomach cancer.
MD vitamins and fibers reduce H. pylori colonization, whereas polyphenol-rich foods and extra-virgin olive oil (EVOO) reduce inflammation by inhibiting free radicals and lowering oxidative stress.
Omega-3 fatty acids reduce triglyceride levels and inflammation, methionine reduces body weight and insulin resistance, branched-chain amino acids improve insulin sensitivity, and short-chain fatty acids reduce trimethylamine N-oxide (TMAO) and inflammation and regulate autoimmunity factors. Patterns based on biological markers
Inflammation increases gastric cancer risk, particularly among men. Pro-inflammatory foods increase the incidence of intestinal and diffuse cancer subtypes.
The upregulation of cytokines and chemokines, which recruit several hematopoietic and progenitor cell types to inflamed stomach tissues, may cause chronic inflammation.
Gastric cancer-related inflammation includes inflammatory cytokines such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-α). IL-1 has an anti-tumor impact, whereas IL-6 is associated with tumor progression, invasion, and metastasis.
The ketogenic diet (KD) is associated with anti-cancer treatment in advanced gastric cancer patients. The KD alters glucose metabolism and inhibits insulin signaling and insulin-like growth factor 1 (IGF-1), the primary energy source for tumor cells. KD reduces nicotinamide adenine dinucleotide phosphate (NADPH) generation to increase oxidative stress in tumor cells.
Ad libitum KD therapy inhibits hypoxia-related and growth-driven proteins, influencing tumor progression.
Ketones enter cancer cells by monocarboxylate transporters (MCTs), limit lactate export, reduce cancer survival time, and prevent the activation of NLR family pyrin domain containing 3 (NLRP3), nuclear factor kappa B (NF-kB) and Signal transducer and activator of transcription 3 (STAT3) activation, lowering IL-1β expression.
The review findings indicate that dietary patterns can influence gastric cancer risk by influencing metabolites, gut microbiota, inflammation, and immune function.
Inconsistency in results might be owing to various factors such as meal types, recollection bias, overall energy consumption, and other confounders. Large-scale prospective cohort studies could improve the validity of the findings. Journal reference:
Pu K, Feng Y, Tang Q, Yang G, and Xu C (2024) Review of dietary patterns and gastric cancer risk: epidemiology and biological evidence. Front. Oncol. 14:1333623. doi: 10.3389/fonc.2024.1333623. https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2024.1333623/full?utm_source=S-TWT
