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.

ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease

Abstract: ARIC was carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C), R01HL087641, R01HL59367 and R01HL086694; National Human Genome Research Institute contract U01HG004402; and National Institutes of Health contract HHSN268200625226C. The authors thank the staff and participants of the ARIC study for their important contributions. Infrastructure was partly supported by Grant Number UL1RR025005, a component of the National Institutes of Health and NIH Roadmap for Medical Research. CHS was supported by contracts HHSN268201200036C, HHSN268200800007C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086, and grant U01HL080295 from the National Heart, Lung, and Blood Institute (NHLBI), with additional contribution from the National Institute of Neurological Disorders and Stroke (NINDS). Additional support was provided by R01AG023629 from the National Institute on Aging (NIA). A full list of principal CHS investigators and institutions can be found at CHS-NHLBI.org. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health The Costa-Rican adult study was supported by grant R01HL081549 from the National Institutes of Health. EURAMIC was supported by the Commission of the European Communities, as a Concerted Action within Directorate General-XII, with additional support from Directorate General-V Europe against Cancer. The national studies were financed by the Dutch Ministry of Health. Ulster Cancer Foundation and Milk Intervention Board. Grant AKT76 from Cancer Research Switzerland. Swiss National Science Foundation Grant 32-9257-87. Spanish FIS and Ministry of Science and Education, and German Federal Health Office EPIC-Norfolk was funded by grants from Medical Research Council and Cancer Research UK. Dr. Imamura also received support from the Medical Research Council Epidemiology Unit Core Support (MC_UU_12015/5). HPFS was supported by the NIH grants UM1 CA167552, R01 HL35464, AA11181, HL35464, CA55075, HL60712 and P30 DK46200 The InChianti study was supported as a ‘targeted project’ (ICS 110.1\RS97.71) by the Italian Ministry of Health and in part by the Intramural Research Program of the NIH (Contracts N01-AG-916413 and N01-AG-821336 and Contracts 263 MD 9164 13 and 263 MD 821336) KIND (Kuopio Ischaemic Heart Disease Risk Factor Study) was supported by grants from the Academy of Finland, Helsinki, Finland (grants 41471, 1041086) MCCS (Melbourne Collaborative Cohort Study) recruitment was funded by VicHealth and Cancer Council Victoria. The MCCS was further supported by Australian NHMRC grants 209057, 251553 and 504711 and by infrastructure provided by Cancer Council Victoria. Cases and their vital status were ascertained through the Victorian Cancer Registry (VCR) and the Australian Institute of Health and Welfare (AIHW), including the National Death Index and the Australian Cancer Database. MESA and the MESA SHARe project are conducted and supported by the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with MESA investigators. Support for MESA is provided by contracts N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-MEHC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC-95169, UL1-TR-001079, and UL1-TR-000040. Funding for SHARe genotyping was provided by NHLBI Contract N02-HL-64278. Genotyping was performed at Affymetrix (Santa Clara, California, USA) and the Broad Institute of Harvard and MIT (Boston, Massachusetts, USA) using the Affymetric Genome-Wide Human SNP Array 6.0. NSHDS I & II (The Northern Sweden Health & Disease Study I & II) was supported by the Swedish Cancer Society and the Swedish Research Council NHS (Nurses’ Health Study) was supported by research grants UM1 CA186107, R01 CA49449, R01 HL034594, P01CA87969, R01HL034594, and R01HL088521 of the National Institutes of Health The PHS (Physician’s Health Study) was supported by grant R21 HL088081, CA-34944 and CA-40360, and CA-097193 from the National Cancer Institute and grants HL-26490 and HL-34595from the National Heart, Lung, and Blood Institute, Bethesda, MD. The 3C (Three-City) study was conducted under a partnership agreement between the Institut National de la Sante et de la Recherche Medicale (INSERM), the University Bordeaux 2 Victor Segalen and Sanofi-Aventis. The Fondation pour la Recherche Medicale funded the preparation and initiation of the study. The Three-City study was also supported by the Caisse Nationale Maladie des Travailleurs Salaries, Direction Generale de la Sante, MGEN, Institut de la Longevite, Conseils Regionaux d’Aquitaine et Bourgogne, Fondation de France, Ministry of Research-INSERM Programme “Cohortes et collections de donnees biologiques”, Agence Nationale de la Recherche (grant number COGINUT ANR-06-PNRA-005), the Fondation Plan Alzheimer (grant number FCS 2009-2012), and the Caisse Nationale pour la Solidarite et l’Autonomie (CNSA) . Dr Samieri was on a grant from the “Fondation Plan Alzheimer” SHHEC (Scottish Heart Health Extended Cohort) study was funded by the Scottish Health Department Chief Scientist Organization; British Heart Foundation; FP Fleming Trust. The authors would like to acknowledge Dr. Roger Tavendale for his work with the Scottish Heart Health Study. SCHS (Singapore Chinese Health Study) was supported by the Singapore National Medical Research Council (grant number: NMRC 1270/2010) and the U.S. NIH (grant numbers: R01CA 144034 and UM1 CA182876) ULSAM 50 and 70 were funded by the Swedish Research Council for Health, Working Life and Welfare (FORTE) Uppsala City Council (ALF) and Swedish Research Council

Coffee, Caffeine, and Health

Abstract: Coffee, Caffeine, and Health In many countries, a large majority of adults consume caffeine daily. This review summarizes the evidence about the varied physiological effects of caffeine and coffee ...

Breast-feeding and risk for childhood obesity : Does maternal diabetes or obesity status matter?

Abstract: OBJECTIVE — We sought to evaluate whether maternal diabetes or weight status attenuates a previously reported beneficial effect of breast-feeding on childhood obesity. RESEARCH DESIGN AND METHODS — Growing Up Today Study (GUTS) participants were offspring of women who participated in the Nurses’ Health Study II. In the present study, 15,253 girls and boys (aged 9–14 years in 1996) were included. Maternal diabetes and weight status and infant feeding were obtained by maternal self-report. We defined maternal overweight as BMI ≥25 kg/m 2 . Childhood obesity, from self-reported height and weight, was based on the Centers for Disease Control and Prevention definitions as normal, at risk for overweight, or overweight. Maternal status categories were nondiabetes/normal weight, nondiabetes/overweight, or diabetes. Logistic regression models used generalized estimating equations to account for nonindependence between siblings. RESULTS — For all subjects combined, breast-feeding was associated with reduced overweight (compared with normal weight) in childhood. Compared with exclusive use of formula, the odds ratio (OR) for exclusive breast-feeding was 0.66 (95% CI 0.53–0.82), adjusted for age, sex, and Tanner stage. Results did not differ according to maternal status (nondiabetes/normal weight OR 0.73 [95% CI 0.49–1.09]; nondiabetes/overweight 0.75 [0.57–0.99]; and diabetes 0.62 [0.24–1.60]). Further adjustment for potential confounders attenuated results, but results remained consistent across strata of maternal status ( P value for interaction was 0.50). CONCLUSIONS — Breast-feeding was inversely associated with childhood obesity regardless of maternal diabetes status or weight status. These data provide support for all mothers to breast-feed their infants to reduce the risk for childhood overweight.

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 …