Kenji Wakai

BACKGROUND: In western populations, coffee consumption is associated with a reduced risk for type 2 diabetes; however, the effect of green, black, and oolong teas is unclear. OBJECTIVE: To examine the relationship between consumption of these beverages and risk for diabetes. DESIGN: Retrospective cohort study. SETTING: 25 communities across Japan. PARTICIPANTS: A total of 17,413 persons (6727 men and 10,686 women; 49% of the original study population) who were 40 to 65 years of age; had no history of type 2 diabetes, cardiovascular disease, or cancer at the baseline lifestyle survey; and completed the 5-year follow-up questionnaire. There was no difference in body mass index levels at baseline between respondents and nonrespondents. MEASUREMENTS: Questionnaire on consumption of coffee; black, green, and oolong teas; and physician-diagnosed diabetes. RESULTS: During the 5-year follow-up, there were 444 self-reported new cases of diabetes in 231 men and 213 women (5-year event rates, 3.4% and 2.0%, respectively). Consumption of green tea and coffee was inversely associated with risk for diabetes after adjustment for age, sex, body mass index, and other risk factors. Multivariable odds ratios for diabetes among participants who frequently drank green tea and coffee (> or =6 cups of green tea per day and > or =3 cups of coffee per day) were 0.67 (95% CI, 0.47 to 0.94) and 0.58 (CI, 0.37 to 0.90), respectively, compared with those who drank less than 1 cup per week. No association was found between consumption of black or oolong teas and the risk for diabetes. Total caffeine intake from these beverages was associated with a 33% reduced risk for diabetes. These inverse associations were more pronounced in women and in overweight men. LIMITATIONS: Diabetes was self-reported, no data were available on consumption of soda, and the follow-up rate was low. CONCLUSIONS: Consumption of green tea, coffee, and total caffeine was associated with a reduced risk for type 2 diabetes.

BACKGROUND AND PURPOSE: The objectives of the present study were to estimate an annual number of patients with moyamoya disease in Japan and to describe the clinicoepidemiological features of the disease. METHODS: The study consisted of 2 questionnaire surveys, which were distributed to randomly selected departments of neurosurgery, internal medicine, neurology, cerebrovascular medicine, and pediatrics in hospitals throughout Japan. The first survey inquired about the number of the patients treated in 2003, and the second requested additional detailed clinicoepidemiological information about each patient identified in the first survey. RESULTS: In 2003, the total number of patients treated in Japan was estimated at 7700 (95% confidence interval, 6300 to 9300). Sex ratio (women to men) of the patients was 1.8. For men, the peak of moyamoya disease was observed in patients aged 10 to 14 years and for women aged 20 to 24 years. Annual rate of newly diagnosed cases in 2003 was 0.54 per 100,000 population. Family history of moyamoya disease was found in 12.1% of the patients. The majority (77.9%) were treated as outpatients. CONCLUSIONS: Although the clinicoepidemiological features of the patients in the present study were almost similar to those obtained in previous ones, the estimated prevalence of moyamoya disease in Japan has almost doubled during the recent decade (3900 in 1994 and 7700 in 2003). The increase could partly be explained by the increase in newly diagnosed cases (0.35 in 1994 and 0.54 in 2003 per 100,000 population).

Gout based on hyperuricemia is a common disease with a genetic predisposition, which causes acute arthritis. The ABCG2/BCRP gene, located in a gout-susceptibility locus on chromosome 4q, has been identified by recent genome-wide association studies of serum uric acid concentrations and gout. Urate transport assays demonstrated that ABCG2 is a high-capacity urate secretion transporter. Sequencing of the ABCG2 gene in 90 hyperuricemia patients revealed several nonfunctional ABCG2 mutations, including Q126X. Quantitative trait locus analysis of 739 individuals showed that a common dysfunctional variant of ABCG2, Q141K, increases serum uric acid. Q126X is assigned to the different disease haplotype from Q141K and increases gout risk, conferring an odds ratio of 5.97. Furthermore, 10% of gout patients (16 out of 159 cases) had genotype combinations resulting in more than 75% reduction of ABCG2 function (odds ratio, 25.8). Our findings indicate that nonfunctional variants of ABCG2 essentially block gut and renal urate excretion and cause gout.