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Suzuki R.,Research Center for Cancer Prevention and Screening | Iwasaki M.,Research Center for Cancer Prevention and Screening | Inoue M.,Research Center for Cancer Prevention and Screening | Inoue M.,National Cancer Center | And 105 more authors.
International Journal of Cancer

Epidemiological studies have evaluated whether the impact of alcohol intake on breast cancer risk is modified by use of exogenous estrogens, folate intake, body weight and smoking status, but results have been inconsistent. Further, effect modification by intake of isoflavones and alcohol-induced facial flushing, which are prevalent in Asian populations, have not been investigated. We investigated the association between alcohol intake and breast cancer risk and whether the association is modified by these factors among 50,757 premenopausal and postmenopausal women (aged 40-69 years) in the population-based Japan Public Health Center-based Prospective Study. Alcohol consumption and other related factors were assessed using self-reported questionnaires. Through to the end of 2006, 572 patients were identified. Relative risks (RRs) and 95% confidence intervals (CIs) were estimated by hazard ratios derived from Cox proportional hazards regression models. Compared with never-drinkers, regular alcohol drinkers (>150 g of ethanol/week) had a higher risk of the development of breast cancer; the multivariable-adjusted RRs were 1.75 (95% CI = 1.16-2.65; ptrend 5 0.035) for overall, 1.78 (95% CI = 1.09-2.90) for premenopausal and 1.21 (95% CI = 0.53-2.75) for postmenopausal women. There was no statistical evidence for effect modification by menopausal status, use of exogenous estrogens, intakes of isoflavone and folate, body weight, alcohol-induced facial flushing or smoking (All p interactions ≥ 0.15). Excessive alcohol intake was associated with an increase in the risk of breast cancer in this population. There was no statistical evidence for effect modification. © 2009 UICC. Source

Inoue M.,Research Center for Cancer Prevention and Screening | Tsugane S.,Research Center for Cancer Prevention and Screening | Sobue T.,National Cancer Center | Hanaoka T.,National Cancer Center | And 99 more authors.
Journal of Epidemiology and Community Health

Background: Few studies have examined the impact of weight change in different periods of lifetime on type 2 diabetes risk, and the association of weight loss with type 2 diabetes is unclear. We prospectively investigated the association of weight change since age 20 y and that during middle-to-late adulthood with the incidence of type 2 diabetes. Methods: Subjects were 52 014 men and women aged 45-75 y who participated in the Japan Public Health Center-Based Prospective Study and had no history of diabetes. ORs of self-reported physician-diagnosed type 2 diabetes for weight change between age 20 y and baseline survey (mean age 50.6 y) and during 5 y between baseline and second surveys were estimated using logistic regression analysis. Results: During the 5-year period following 5-year survey, 989 newly diagnosed cases of type 2 diabetes were self-reported. Weight gain from age 20 y was associated with an increased risk of type 2 diabetes. The multivariate-adjusted OR (95% CI) for a weight gain of ≥5 kg versus a stable weight were 2.61 (2.11 to 3.23) in men and 2.56 (1.95 to 3.35) in women. A weight gain of ≥5 kg over the 5-y following the baseline survey was also associated with an increased risk in women. No association with weight loss was observed for either period. Conclusions: These results suggest that long-term weight gain from early adulthood to middle-age increases risk of type 2 diabetes in men and women and that risk is further enhanced by weight gain in later life in women. Source

Michikawa T.,Japan National Institute of Environmental Studies | Michikawa T.,Research Center for Cancer Prevention and Screening | Inoue M.,Research Center for Cancer Prevention and Screening | Sawada N.,Research Center for Cancer Prevention and Screening | And 118 more authors.
Preventive Medicine

Objective: The purpose of the present study was to develop a risk estimation model for the 10-year risk of hepatocellular carcinoma (HCC) that could be easily used in a general population to aid in the prevention of HCC. Methods: Our prediction model was derived from data obtained on 17,654 Japanese aged 40 to 69. years who participated in health checkups (follow-up: 1993-2006). Cox proportional hazards regression was applied to obtain coefficients for each predictor. Results: During follow-up, a total of 104 cases of HCC were newly diagnosed. After checking the model fit, we incorporated age, sex, alcohol consumption, body mass index, diabetes, coffee consumption, and hepatitis B and C virus infection into the prediction model. The model showed satisfactory discrimination (Harrell's c-index = 0.94) and was well calibrated (the overall observed/expected ratio = 1.03, 95% confidence interval = 0.83-1.29). We also developed a simple risk scoring system. Those subjects with total scores of 17 or more under this system (score range: - 1 to 19) had an estimated 10-year HCC risk of over 90%; those with 4 points or less had an estimated risk of less than 0.1%. Conclusion: We developed a simple 10-year risk prediction model for HCC in the Japanese general population as a public education tool. © 2012 Elsevier Inc. Source

Saito E.,Epidemiology and Prevention Group | Saito E.,University of Tokyo | Inoue M.,Epidemiology and Prevention Group | Inoue M.,University of Tokyo | And 137 more authors.
Annals of Epidemiology

Purpose: We examined the association between green tea consumption and mortality due to all causes, cancer, heart disease, cerebrovascular disease, respiratory disease, injuries, and other causes of death in a large-scale population-based cohort study in Japan. Methods: We studied 90,914 Japanese (aged between 40 and 69years) recruited between 1990 and 1994. After 18.7years of follow-up, 12,874 deaths were reported. The association between green tea consumption and risk of all causes and major causes of mortality was assessed using the Cox proportional hazards regression model with adjustment for potential confounders. Results: Hazard ratios for all-cause mortality among men who consumed green tea compared with those who drank less than 1 cup/day were 0.96 (0.89-1.03) for 1-2 cups/day, 0.88 (0.82-0.95) for 3-4 cups/day, and 0.87 (0.81-0.94) for more than 5 cups/day (P for trend <.001). Corresponding hazard ratios for women were 0.90 (0.81-1.00), 0.87 (0.79-0.96), and 0.83 (0.75-0.91; P for trend <.001). Green tea was inversely associated with mortality from heart disease in both men and women and mortality from cerebrovascular disease and respiratory disease in men. No association was found between green tea and total cancer mortality. Conclusions: This prospective study suggests that the consumption of green tea may reduce the risk of all-cause mortality and the three leading causes of death in Japan. © 2015 Elsevier Inc. Source

Hidaka A.,Epidemiology and Prevention Group | Sasazuki S.,Epidemiology and Prevention Group | Sasazuki S.,National Cancer Center | Matsuo K.,Kyushu University | And 135 more authors.

The association between alcohol consumption, genetic polymorphisms of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) and gastric cancer risk is not completely understood. We investigated the association between ADH1B (rs1229984), ADH1C (rs698) and ALDH2 (rs671) polymorphisms, alcohol consumption and the risk of gastric cancer among Japanese subjects in a population-based, nested, case-control study (1990-2004). Among 36 745 subjects who answered the baseline questionnaire and provided blood samples, 457 new gastric cancer cases matched to 457 controls were used in the analysis. The odds ratios (OR) and corresponding 95% confidence intervals (CI) were calculated using logistic regression models. No association was observed between alcohol consumption, ADH1B (rs1229984), ADH1C (rs698) and ALDH2 (rs671) polymorphisms and gastric cancer risk. However, considering gene-environmental interaction, ADH1C G allele carriers who drink ≥150 g/week of ethanol had a 2.5-fold increased risk of gastric cancer (OR = 2.54, 95% CI = 1.05-6.17) relative to AA genotype carriers who drink 0 to <150 g/week (P for interaction = 0.02). ALDH2 A allele carriers who drink ≥150 g/week also had an increased risk (OR = 2.08, 95% CI = 1.05-4.12) relative to GG genotype carriers who drink 0 to < 150 g/week (P for interaction = 0.08). To find the relation between alcohol consumption and gastric cancer risk, it is important to consider both alcohol consumption level and ADH1C and ALDH2 polymorphisms. © The Author 2014. Source

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