Frank B. Hu

Bio: Frank B. Hu is an academic researcher from Harvard University. The author has contributed to research in topics: Type 2 diabetes & Diabetes mellitus. The author has an hindex of 250, co-authored 1675 publications receiving 253464 citations. Previous affiliations of Frank B. Hu include Southwest University & Brigham and Women's Hospital.

Association of Coffee Consumption With Total and Cause-Specific Mortality in 3 Large Prospective Cohorts

Abstract: Background The association between consumption of caffeinated and decaffeinated coffee and risk of mortality remains inconclusive. Methods and results We examined the associations of consumption of total, caffeinated, and decaffeinated coffee with risk of subsequent total and cause-specific mortality among 74,890 women in the Nurses' Health Study (NHS), 93,054 women in the Nurses' Health Study II, and 40,557 men in the Health Professionals Follow-up Study. Coffee consumption was assessed at baseline using a semiquantitative food frequency questionnaire. During 4,690,072 person-years of follow-up, 19,524 women and 12,432 men died. Consumption of total, caffeinated, and decaffeinated coffee were nonlinearly associated with mortality. Compared with nondrinkers, coffee consumption of 1 to 5 cups per day was associated with lower risk of mortality, whereas coffee consumption of more than 5 cups per day was not associated with risk of mortality. However, when restricting to never smokers compared with nondrinkers, the hazard ratios (and 95% confidence intervals) of mortality were 0.94 (0.89-0.99) for 1.0 or less cup per day, 0.92 (0.87-0.97) for 1.1 to 3.0 cups per day, 0.85 (0.79-0.92) for 3.1 to 5.0 cup per day, and 0.88 (0.78-0.99) for more than 5.0 cup per day (P value for nonlinearity = 0.32; P value for trend Conclusions Higher consumption of total coffee, caffeinated coffee, and decaffeinated coffee was associated with lower risk of total mortality.

Plasma uric acid and the risk of type 2 diabetes in a Chinese community.

Abstract: Background: Previous cross-sectional studies have shown hyperuricemia to be prevalent among individuals with metabolic syndrome, but the evidence from prospective studies of an association between uric acid and diabetes risk is limited. We prospectively investigated the association between plasma concentrations of uric acid and the incidence of type 2 diabetes in Chinese individuals. Methods: We conducted a community-based prospective cohort study of 2690 participants (age range, 35–97 years) in the Chin-Shan Community Cardiovascular Cohort Study, who were found to be free of diabetes and cardiovascular disease during baseline assessment at study entry in 1990. During a median 9.0-year follow-up, 548 participants developed type 2 diabetes. Results: High plasma uric acid concentrations were associated with a higher prevalence of metabolic syndrome. After adjustment for age, sex, body mass index, and other covariates, the relative risks (RR) of diabetes according to uric acid quintile were 1.11, 1.29, 1.40, and 1.63 [95% confidence interval (CI), 1.20–2.23; P for trend <0.001]. After additional adjustment for metabolic syndrome, the RR for comparing the participants in the fifth and first uric acid quintiles was 1.40 (95% CI, 1.02–1.92; P for trend = 0.027). In joint analyses, participants who were in the highest uric acid quintile and also had metabolic syndrome had a 3.3-fold greater risk of diabetes (95% CI, 2.27–4.94) than those in the lowest uric acid quintile and without metabolic syndrome. Conclusions: These findings suggest a modest positive association between plasma uric acid concentration and the incidence of type 2 diabetes in Chinese individuals. The association between hyperuricemia and diabetes was partly mediated through the metabolic syndrome.

Genome-wide meta-analysis uncovers novel loci influencing circulating leptin levels

Abstract: Leptin is an adipocyte-secreted hormone, the circulating levels of which correlate closely with overall adiposity. Although rare mutations in the leptin (LEP) gene are well known to cause leptin deficiency and severe obesity, no common loci regulating circulating leptin levels have been uncovered. Therefore, we performed a genome-wide association study (GWAS) of circulating leptin levels from 32,161 individuals and followed up loci reaching P<10(-6) in 19,979 additional individuals. We identify five loci robustly associated (P<5 × 10(-8)) with leptin levels in/near LEP, SLC32A1, GCKR, CCNL1 and FTO. Although the association of the FTO obesity locus with leptin levels is abolished by adjustment for BMI, associations of the four other loci are independent of adiposity. The GCKR locus was found associated with multiple metabolic traits in previous GWAS and the CCNL1 locus with birth weight. Knockdown experiments in mouse adipose tissue explants show convincing evidence for adipogenin, a regulator of adipocyte differentiation, as the novel causal gene in the SLC32A1 locus influencing leptin levels. Our findings provide novel insights into the regulation of leptin production by adipose tissue and open new avenues for examining the influence of variation in leptin levels on adiposity and metabolic health.

Vitamin D Deficiency

Abstract: Once foods in the United States were fortified with vitamin D, rickets appeared to have been conquered, and many considered major health problems from vitamin D deficiency resolved. But vitamin D deficiency is common. This review considers the role of vitamin D in skeletal and nonskeletal health and suggests strategies for the prevention and treatment of vitamin D deficiency.

Diagnosis and Management of the Metabolic Syndrome An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement

Abstract: The metabolic syndrome has received increased attention in the past few years. This statement from the American Heart Association (AHA) and the National Heart, Lung, and Blood Institute (NHLBI) is intended to provide up-to-date guidance for professionals on the diagnosis and management of the metabolic syndrome in adults. The metabolic syndrome is a constellation of interrelated risk factors of metabolic origin— metabolic risk factors —that appear to directly promote the development of atherosclerotic cardiovascular disease (ASCVD).1 Patients with the metabolic syndrome also are at increased risk for developing type 2 diabetes mellitus. Another set of conditions, the underlying risk factors , give rise to the metabolic risk factors. In the past few years, several expert groups have attempted to set forth simple diagnostic criteria to be used in clinical practice to identify patients who manifest the multiple components of the metabolic syndrome. These criteria have varied somewhat in specific elements, but in general they include a combination of both underlying and metabolic risk factors. The most widely recognized of the metabolic risk factors are atherogenic dyslipidemia, elevated blood pressure, and elevated plasma glucose. Individuals with these characteristics commonly manifest a prothrombotic state and a pro-inflammatory state as well. Atherogenic dyslipidemia consists of an aggregation of lipoprotein abnormalities including elevated serum triglyceride and apolipoprotein B (apoB), increased small LDL particles, and a reduced level of HDL cholesterol (HDL-C). The metabolic syndrome is often referred to as if it were a discrete entity with a single cause. Available data suggest that it truly is a syndrome, ie, a grouping of ASCVD risk factors, but one that probably has more than one cause. Regardless of cause, the syndrome identifies individuals at an elevated risk for ASCVD. The magnitude of the increased risk can vary according to which components of the syndrome are …