The epidemic of obesity has become a major public health problem. Common-form obesity is underpinned by both environmental and genetic factors. Epidemiological studies have documented that increased intakes of energy and reduced consumption of high-fiber foods, as well as sedentary lifestyle, were among the major driving forces for the epidemic of obesity. Recent genome-wide association studies have identified several genes convincingly related to obesity risk, including the fat mass and obesity associated gene and the melanocortin-4 receptor gene. Testing gene-environment interaction is a relatively new field. This article reviews recent advances in identifying the genetic and environmental risk factors (lifestyle and diet) for obesity. The evidence for gene-environment interaction, especially from observational studies and randomized intervention trials, is examined specifically. Knowledge about the interplay between genetic and environmental components may facilitate the choice of more effective and specific measures for obesity prevention based on the personalized genetic make-up.

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The role of diet-associated inflammation in colorectal cancer is of interest. Accordingly, we aimed to examine whether the dietary inflammatory index (DII) was associated with the risk of colorectal cancer in a case-control study conducted in Korea. The DII was based on dietary intake, which was determined by a 106-item semi-quantitative food frequency questionnaire completed by 923 colorectal cancer cases and 1846 controls. Logistic regression was used to estimate odd ratios (ORs) and 95% confidence intervals (CIs). Subgroup analyses were conducted by the anatomical site of the cancer, sex, and other risk factors. Higher DII scores were associated with an increased incidence of colorectal cancer (OR (95% CI) = 2.16 (1.71, 2.73) for highest vs. lowest tertile). The magnitude differed by anatomical site and sex. This association was slightly weaker in subjects with proximal colon cancer (1.68 (1.08, 2.61)) and was stronger in women (2.50 (1.64, 3.82)). Additionally, stronger associations were observed in subjects who were older than 50 years (p for interaction = 0.004) and engaged in physical activity (p for interaction < 0.001). Results from this study suggest that diet-associated inflammation may increase the risk of colorectal cancer, and this effect may differ by certain factors, such as anatomical site, age, sex, and lifestyle.

Purpose Both genetic and lifestyle factors contribute to the risk of colorectal cancer, but each individual factor has a limited effect. Therefore, we investigated the association between colorectal cancer and the combined effects of genetic factors or/and lifestyle risk factors. Materials and Methods In a case-control study of 632 colorectal cancer patients and 1,295 healthy controls, we quantified the genetic risk score for colorectal cancer using 13 polymorphisms. Furthermore, we determined a combined lifestyle risk score including obesity, physical activity, smoking, alcohol consumption, and dietary inflammatory index. The associations between colorectal cancer and risk score using these factors were examined using a logistic regression model. Results Higher genetic risk scores were associated with an increased risk of colorectal cancer (odds ratio [OR], 2.57; 95% confidence interval [CI], 1.89 to 3.49 for the highest tertile vs. lowest tertile). Among the modifiable factors, previous body mass index, physical inactivity, heavy alcohol consumption, and a high inflammatory diet were associated with an increased risk of colorectal cancer. A higher lifestyle risk score was associated with an increased risk of colorectal cancer (OR, 5.82; 95% CI, 4.02 to 8.44 for the highest tertile vs. lowest tertile). This association was similar in each genetic risk category. Conclusion Adherence to a healthy lifestyle is associated with a substantially reduced risk of colorectal cancer regardless of individuals’ genetic risk.

BackgroundDiet is a major source of cadmium intake among the non-smoking general population. Recent studies have determined that cadmium exposure may produce adverse health effects at lower exposure levels than previously predicted. We conducted a meta-analysis to combine and analyze the results of previous studies that have investigated the association of dietary cadmium intake and cancer risk.MethodsWe searched PubMed, EMBASE, and MEDLINE database for case-control and cohort studies that assessed the association of dietary cadmium intake and cancer risk. We performed a meta-analysis using eight eligible studies to summarize the data and summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using a random effects model.ResultsOverall, dietary cadmium intake showed no statistically significant association with cancer risk (RR = 1.10; 95% CI: 0.99–1.22, for highest vs. lowest dietary cadmium group). However, there was strong evidence of heterogeneity, and subgroup analyses were conducted using the study design, geographical location, and cancer type. In subgroup analyses, the positive associations between dietary cadmium intake and cancer risk were observed among studies with Western populations (RR = 1.15; 95% CI: 1.08–1.23) and studies investigating some hormone-related cancers (prostate, breast, and endometrial cancers).ConclusionOur analysis found a positive association between dietary cadmium intake and cancer risk among studies conducted in Western countries, particularly with hormone-related cancers. Additional experimental and epidemiological studies are required to verify our findings.

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ObjectiveBoth variations in the interleukin-10 (IL10) gene and environmental factors are thought to influence inflammation and gastric carcinogenesis. Therefore, we investigated the associations between IL10 polymorphisms, Helicobacter pylori (H. pylori) infection, and smoking in noncardia gastric carcinogenesis in Koreans.MethodsWe genotyped three promoter polymorphisms (-1082A>G, -819T>C, and -592 A>C) of IL10 in a case-control study of 495 noncardia gastric cancer patients and 495 sex- and age-matched healthy controls. Multiple logistic regression models were used to detect the effects of IL10 polymorphisms, H. pylori infection, and smoking on the risk of gastric cancer, which was stratified by the histological type of gastric cancer.ResultsThe IL10-819C and -592C alleles were found to have complete linkage disequilibrium, and all three IL10 polymorphisms were associated with an increased risk of intestinal-type noncardia gastric cancer. These associations were observed only in H. pylori-positive subjects and current smokers. A statistically significant interaction between the IL10-592 genotype and H. pylori infection on the risk of intestinal-type gastric cancer was observed (P for interaction  = 0.047). In addition, H. pylori-positive smokers who were carriers of either the IL10-1082G (OR [95% CI]  = 17.76 [6.17−51.06]) or the -592C (OR [95% CI]  = 8.37 [2.79−25.16]) allele had an increased risk of intestinal-type gastric cancer compared to H. pylori-negative nonsmokers homozygous for IL10-1082A and -592A, respectively. The interaction between the IL10-1082 polymorphism and the combined effects of H. pylori infection and smoking tended towards significance (P for interaction  = 0.080).ConclusionsInflammation-related genetic variants may interact with H. pylori infection and smoking to increase the risk of noncardia gastric cancer, particularly the intestinal-type. These findings may be helpful in identifying individuals at an increased risk for developing noncardia gastric cancer.

This meta-analysis of geographically diverse epidemiological data suggests that smoking, particularly current smoking, may influence susceptibility to thyroid cancer. Further well-designed studies with larger sample sizes should be conducted.