To evaluate the role of dietary factors in the etiology of inflammatory bowel disease (IBD), we conducted a multicenter hospital-based case-control study in a Japanese population. Cases were IBD patients aged 15 to 34 years [ulcerative colitis (UC) 111 patients; Crohn's disease (CD) 128 patients] within 3 years after diagnosis in 13 hospitals. One control subject was recruited for each case who was matched for sex, age, and hospital. A semiquantitative food frequency questionnaire was used to estimate preillness intakes of food groups and nutrients. All the available control subjects (n = 219) were pooled, and unconditional logistic models were applied to calculate odds ratios (ORs). In the food groups, a higher consumption of sweets was positively associated with UC risk [OR for the highest versus lowest quartile, 2.86; 95% confidence interval (CI), 1.24 to 6.57], whereas the consumption of sugars and sweeteners (OR, 2.12; 95% CI, 1.08 to 4.17), sweets (OR, 2.83; 95% CI, 1.38 to 5.83), fats and oils (OR, 2.64; 95% CI, 1.29 to 5.39), and fish and shellfish (OR, 2.41; 95% CI, 1.18-4.89) were positively associated with CD risk. In respect to nutrients, the intake of vitamin C (OR, 0.45; 95% CI, 0.21 to 0.99) was negatively related to UC risk, while the intake of total fat (OR, 2.86; 95% CI, 1.39 to 5.90), monounsaturated fatty acids (OR, 2.49; 95% CI, 1.23 to 5.03) and polyunsaturated fatty acids (OR, 2.31; 95% CI, 1.12 to 4.79), vitamin E (OR, 3.23; 95% CI, 1.45 to 7.17), and n-3 (OR, 3.24; 95% CI, 1.52 to 6.88) and n-6 fatty acids (OR, 2.57; 95% CI, 1.24 to 5.32) was positively associated with CD risk. Although this study suffers from the shortcoming of recall bias, which is inherent in most retrospective studies (prospective studies are warranted to confirm the associations between diet and IBD risk), the present findings suggest the importance of dietary factors for IBD prevention.

OBJECTIVETo identify novel type 2 diabetes gene variants and confirm previously identified ones, a three-staged genome-wide association study was performed in the Japanese population.RESEARCH DESIGN AND METHODSIn the stage 1 scan, we genotyped 519 case and 503 control subjects with 482,625 single nucleotide polymorphism (SNP) markers; in the stage 2 panel comprising 1,110 case subjects and 1,014 control subjects, we assessed 1,456 SNPs (P < 0.0025, stage 1); additionally to direct genotyping, 964 healthy control subjects formed the in silico control panel. Along with genome-wide exploration, we aimed to replicate the disease association of 17 SNPs from 16 candidate loci previously identified in Europeans. The associated and/or replicated loci (23 SNPs; P < 7 × 10–5 for genome-wide exploration and P < 0.05 for replication) were examined in the stage 3 panel comprising 4,000 case subjects and 12,569 population-based samples, from which 4,889 nondiabetic control subjects were preselected. The 12,569 subjects were used for overall risk assessment in the general population.RESULTSFour loci—1 novel with suggestive evidence (PEPD on 19q13, P = 1.4 × 10–5) and three previously reported—were identified; the association of CDKAL1, CDKN2A/CDKN2B, and KCNQ1 were confirmed (P < 10–19). Moreover, significant associations were replicated in five other candidate loci: TCF7L2, IGF2BP2, SLC30A8, HHEX, and KCNJ11. There was substantial overlap of type 2 diabetes susceptibility genes between the two populations, whereas effect size and explained variance tended to be higher in the Japanese population.CONCLUSIONSThe strength of association was more prominent in the Japanese population than in Europeans for more than half of the confirmed type 2 diabetes loci.

This study provides insight into the architecture of common genetic variation contributing to CRC etiology and improves risk prediction for individualized screening.

Epidemiologic evidence on the relation between nutrition and stomach cancer is reviewed. Stomach cancer shows a distinct international variation and dramatic worldwide decline. These descriptive features suggest that dietary factors are important in determining the risk of stomach cancer. The authors assessed relevant data regarding specific dietary hypotheses in the etiology of stomach cancer. A negative association with fresh vegetables and fruits is highly consistent in numerous case-control studies in different populations. Both epidemiologic and experimental data suggest that vitamins C and carotenoids lower risk of stomach cancer. Evidence is sparse and inconsistent as to protective effects of vitamin E and selenium. Epidemiologic studies have not lent, and will not provide, supportive evidence for an etiologic role of nitrate intake. High salt intake has been associated with an increased risk in many case-control studies and limited cohort studies. Taken together with animal data, it is considered that high salt intake is a risk factor for stomach cancer. Both epidemiologic and experimental data are inconclusive as to whether high-starch diets confer an increased risk. Cohort studies using quantitative dietary assessment and biologic measurement of micronutrients are needed for further understanding of etiologic roles of dietary factors in the causation of stomach cancer.

The relationship between drinking habit surveyed in 1965 and cause-specific mortality over 19 years was investigated in 5135 male Japanese physicians taking into account smoking habit and separating ex-drinker from non-drinker. As compared with non-drinkers, daily drinkers with high consumption had a significantly increased mortality from all causes. Drinking was significantly related to the so-called alcohol-related causes of death; upper aerodigestive cancer, liver cancer and liver cirrhosis. Mortality from acute myocardial infarction was inversely related to drinking, whereas other coronary heart disease showed a somewhat higher mortality among men consuming a large amount of alcohol than among non-drinkers. There was a weak, but significant, association between stroke and drinking, and the relation did not differ between haemorrhagic stroke and other stroke. No obvious relationship with drinking was observed for cancers of the stomach, large bowel, pancreas and lung.