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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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.

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.