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Hypertriglyceridemia: HELP
Articles from Massachusetts General Hospital
Based on 13 articles published since 2010
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These are the 13 published articles about Hypertriglyceridemia that originated from Massachusetts General Hospital during 2010-2020.
 
+ Citations + Abstracts
1 Review Genetics and causality of triglyceride-rich lipoproteins in atherosclerotic cardiovascular disease. 2014

Rosenson, Robert S / Davidson, Michael H / Hirsh, Benjamin J / Kathiresan, Sekar / Gaudet, Daniel. ·Mount Sinai Heart, Cardiometabolic Disorders, Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: robert.rosenson@mssm.edu. · Division of Cardiology, Pritzker School of Medicine, University of Chicago, Chicago, Illinois. · Mount Sinai Heart, Mount Sinai Hospital, New York, New York. · Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. · ECOGENE-21 and Lipid Clinic, Department of Medicine, Université de Montreal, Chicoutimi, Quebec, Canada. ·J Am Coll Cardiol · Pubmed #25500239.

ABSTRACT: Triglycerides represent 1 component of a heterogeneous pool of triglyceride-rich lipoproteins (TGRLs). The reliance on triglycerides or TGRLs as cardiovascular disease (CVD) risk biomarkers prompted investigations into therapies that lower plasma triglycerides as a means to reduce CVD events. Genetic studies identified TGRL components and pathways involved in their synthesis and metabolism. We advocate that only a subset of genetic mechanisms regulating TGRLs contribute to the risk of CVD events. This "omic" approach recently resulted in new targets for reducing CVD events.

2 Clinical Trial Characterizing familial chylomicronemia syndrome: Baseline data of the APPROACH study. 2018

Blom, Dirk J / O'Dea, Louis / Digenio, Andres / Alexander, Veronica J / Karwatowska-Prokopczuk, Ewa / Williams, Karren R / Hemphill, Linda / Muñiz-Grijalvo, Ovidio / Santos, Raul D / Baum, Seth / Witztum, Joseph L. ·Division of Lipidology and Hatter Institute for Cardiovascular Research in Africa, University of Cape Town, Cape Town, South Africa. Electronic address: dirk.blom@uct.ac.za. · Akcea Therapeutics Inc, Cambridge, MA, USA. · Ionis Pharmaceuticals, Carlsbad, CA, USA. · Department of Medicine, Massachusetts General Hospital, Boston, MA, USA. · Hospital Virgen del Rocío, Seville, Spain. · Heart Institute (InCor) University of Sao Paulo Medical School Hospital and Hospital Israelita Albert Einstein, Sao Paulo, Brazil. · Excel Medical Clinical Trials, Boca Raton, FL, USA. · Department of Medicine, University California San Diego, La Jolla, CA, USA. ·J Clin Lipidol · Pubmed #30318066.

ABSTRACT: BACKGROUND: Familial chylomicronemia syndrome (FCS) is a rare metabolic disorder caused by mutations in lipoprotein lipase (LPL) or genes required for LPL functionality and is characterized by hyperchylomicronemia that results in recurrent episodes of acute pancreatitis. Owing to the rarity of FCS, there are few case series describing the phenotypic variability in FCS patients in detail. OBJECTIVE: To provide baseline characteristics in the largest study population to date of patients with FCS. METHODS: We analyzed baseline demographic and clinical characteristics of adult FCS patients in the phase 3 APPROACH study of volanesorsen sodium (antisense inhibitor of apolipoprotein C-III). RESULTS: Sixty-six patients were included in the analysis. Mean (SD) age was 46 (13) years; and mean body mass index was 24.9 (5.7) kg/m CONCLUSIONS: Our data emphasize the severe hypertriglyceridemia characteristic of FCS patients despite restrictive low-fat diets and frequent use of existing hypolipemic therapies. Acute pancreatitis and recurrent acute pancreatitis are frequent complications of FCS. Diagnosis at an older age suggests likely underdiagnosis and underappreciation of this rare disorder.

3 Clinical Conference A 36-year-old woman with recurrent high-grade fevers, hypotension, and hypertriglyceridemia. 2010

Chou, Richard C / Dinarello, Charles A / Ferry, Judith A / Dal Cin, Paola. ·Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA. Richard.C.Chou@hitchcock.org ·Arthritis Care Res (Hoboken) · Pubmed #20191502.

ABSTRACT: -- No abstract --

4 Article Polygenic Hyperlipidemias and Coronary Artery Disease Risk. 2020

Ripatti, Pietari / Rämö, Joel T / Mars, Nina J / Fu, Yu / Lin, Jake / Söderlund, Sanni / Benner, Christian / Surakka, Ida / Kiiskinen, Tuomo / Havulinna, Aki S / Palta, Priit / Freimer, Nelson B / Widén, Elisabeth / Salomaa, Veikko / Tukiainen, Taru / Pirinen, Matti / Palotie, Aarno / Taskinen, Marja-Riitta / Ripatti, Samuli / Anonymous3831189. ·Institute for Molecular Medicine Finland, Helsinki Institute of Life Science (HiLIFE) (P.R., J.T.R., N.J.M., Y.F., J.L., C.B., I.S., T.K., A.S.H., P.P., E.W., T.T., M.P., A.P., S.R.), University of Helsinki, Helsinki, Finland. · Research Programs Unit, Diabetes and Obesity (S.S., M.-R.T.), University of Helsinki, Helsinki, Finland. · Department of Internal Medicine, Helsinki University Hospital, Helsinki, Finland (S.S.). · Department of Internal Medicine, University of Michigan, Ann Arbor, MI (I.S.). · Department of Public Health Solutions, Finnish Institute for Health and Welfare, Helsinki, Finland (A.S.H., V.S.). · Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behaviour, University of California, Los Angeles, CA (N.B.F.). · Department of Public Health, Clinicum, Faculty of Medicine (M.P., S.R.), University of Helsinki, Helsinki, Finland. · Department of Mathematics and Statistics, Faculty of Science (M.P.), University of Helsinki, Helsinki, Finland. · Program in Medical and Population Genetics (A.P.), Broad Institute of MIT and Harvard, Cambridge, MA. · Stanley Center for Psychiatric Research (A.P.), Broad Institute of MIT and Harvard, Cambridge, MA. · Psychiatric and Neurodevelopmental Genetics Unit, Department of Psychiatry (A.P.), Massachusetts General Hospital, Boston, MA. · Analytic and Translational Genetics Unit, Department of Medicine (A.P.), Massachusetts General Hospital, Boston, MA. · Department of Neurology (A.P.), Massachusetts General Hospital, Boston, MA. · Clinical Research Institute HUCH, Ltd, Helsinki, Finland (M.-R.T.). · Broad Institute of MIT and Harvard, Cambridge, MA (S.R.). ·Circ Genom Precis Med · Pubmed #32154731.

ABSTRACT: BACKGROUND: Hyperlipidemia is a highly heritable risk factor for coronary artery disease (CAD). While monogenic familial hypercholesterolemia associates with severely increased CAD risk, it remains less clear to what extent a high polygenic load of a large number of LDL (low-density lipoprotein) cholesterol (LDL-C) or triglyceride (TG)-increasing variants associates with increased CAD risk. METHODS: We derived polygenic risk scores (PRSs) with ≈6M variants separately for LDL-C and TG with weights from a UK Biobank-based genome-wide association study with ≈324K samples. We evaluated the impact of polygenic hypercholesterolemia and hypertriglyceridemia to lipid levels in 27 039 individuals from the National FINRISK Study (FINRISK) cohort and to CAD risk in 135 638 individuals (13 753 CAD cases) from the FinnGen project (FinnGen). RESULTS: In FINRISK, median LDL-C was 3.39 (95% CI, 3.38-3.40) mmol/L, and it ranged from 2.87 (95% CI, 2.82-2.94) to 3.78 (95% CI, 3.71-3.83) mmol/L between the lowest and highest 5% of the LDL-C PRS distribution. Median TG was 1.19 (95% CI, 1.18-1.20) mmol/L, ranging from 0.97 (95% CI, 0.94-1.00) to 1.55 (95% CI, 1.48-1.61) mmol/L with the TG PRS. In FinnGen, comparing the highest 5% of the PRS to the lowest 95%, CAD odds ratio was 1.36 (95% CI, 1.24-1.49) for the LDL-C PRS and 1.31 (95% CI, 1.19-1.43) for the TG PRS. These estimates were only slightly attenuated when adjusting for a CAD PRS (odds ratio, 1.26 [95% CI, 1.16-1.38] for LDL-C and 1.24 [95% CI, 1.13-1.36] for TG PRS). CONCLUSIONS: The CAD risk associated with a high polygenic load for lipid-increasing variants was proportional to their impact on lipid levels and partially overlapping with a CAD PRS. In contrast with a PRS for CAD, the lipid PRSs point to known and directly modifiable risk factors providing additional guidance for clinical translation.

5 Article Associations of homocysteine status and homocysteine metabolism enzyme polymorphisms with hypertension and dyslipidemia in a Chinese hypertensive population. 2020

Yuan, Xiaojie / Wang, Tingcai / Gao, Jie / Wang, Yunchao / Chen, Yajun / Kaliannan, Kanakaraju / Li, Xiaochun / Xiao, Jing / Ma, Tianyou / Zhang, Lei / Shao, Zhongjun. ·Department of Epidemiology, School of Public Health, Air Force Medical University, Xi'an, Shaanxi province, China. · Department of chronic disease control, Gansu Provincial Centre for Disease Control and Prevention, Lanzhou, Gansu province, China. · School of Public Health, Gansu University of Traditional Chinese Medicine, Lanzhou, Gansu province, China. · Laboratory for Lipid Medicine and Technology, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. · Department of chronic disease control, Center of disease control of Wuwei, Wuwei, Gansu province, China. · Institute of Endemic Diseases, Environment and Diseases-related Gene of Key Laboratory of Education Ministry, Medical School of Xi'an Jiaotong University, Xi'an, Shaanxi province, China. ·Clin Exp Hypertens · Pubmed #30786773.

ABSTRACT:

6 Article Coronary Artery Disease Risk and Lipidomic Profiles Are Similar in Hyperlipidemias With Family History and Population-Ascertained Hyperlipidemias. 2019

Rämö, Joel T / Ripatti, Pietari / Tabassum, Rubina / Söderlund, Sanni / Matikainen, Niina / Gerl, Mathias J / Klose, Christian / Surma, Michal A / Stitziel, Nathan O / Havulinna, Aki S / Pirinen, Matti / Salomaa, Veikko / Freimer, Nelson B / Jauhiainen, Matti / Palotie, Aarno / Taskinen, Marja-Riitta / Simons, Kai / Ripatti, Samuli. ·1 Institute for Molecular Medicine Finland HiLIFE University of Helsinki Finland. · 2 Research Programs Unit Clinical and Molecular Metabolism University of Helsinki Finland. · 3 Endocrinology Abdominal Center Helsinki University Hospital Helsinki Finland. · 4 Lipotype GmbH Dresden Germany. · 5 Łukasiewicz Research Network-PORT Polish Center for Technology Development Wroclaw Poland. · 6 Cardiovascular Division Department of Medicine Washington University School of Medicine St. Louis MO. · 7 Department of Genetics Washington University School of Medicine St. Louis MO. · 8 McDonnell Genome Institute Washington University School of Medicine St. Louis MO. · 9 National Institute for Health and Welfare Helsinki Finland. · 10 Department of Mathematics and Statistics Faculty of Science University of Helsinki Finland. · 16 Department of Public Health Clinicum Faculty of Medicine University of Helsinki Finland. · 11 Center for Neurobehavioral Genetics Semel Institute for Neuroscience and Human Behavior University of California Los Angeles CA. · 12 Minerva Foundation Institute for Medical Research Biomedicum Helsinki Finland. · 13 Program in Medical and Population Genetics and The Stanley Center for Psychiatric Research The Broad Institute of MIT and Harvard Cambridge MA. · 14 Psychiatric and Neurodevelopmental Genetics Unit Department of Psychiatry, Analytic and Translational Genetics Unit Department of Medicine, and the Department of Neurology Massachusetts General Hospital Boston MA. · 15 Max Planck Institute of Cell Biology and Genetics Dresden Germany. ·J Am Heart Assoc · Pubmed #31256696.

ABSTRACT: Background We asked whether, after excluding familial hypercholesterolemia, individuals with high low-density lipoprotein cholesterol ( LDL -C) or triacylglyceride levels and a family history of the same hyperlipidemia have greater coronary artery disease risk or different lipidomic profiles compared with population-based hyperlipidemias. Methods and Results We determined incident coronary artery disease risk for 755 members of 66 hyperlipidemic families (≥2 first-degree relatives with similar hyperlipidemia) and 19 644 Finnish FINRISK population study participants. We quantified 151 circulating lipid species from 550 members of 73 hyperlipidemic families and 897 FINRISK participants using mass spectrometric shotgun lipidomics. Familial hypercholesterolemia was excluded using functional LDL receptor testing and genotyping. Hyperlipidemias ( LDL -C or triacylglycerides >90th population percentile) associated with increased coronary artery disease risk in meta-analysis of the hyperlipidemic families and the population cohort (high LDL -C: hazard ratio, 1.74 [95% CI, 1.48-2.04]; high triacylglycerides: hazard ratio, 1.38 [95% CI, 1.09-1.74]). Risk estimates were similar in the family and population cohorts also after adjusting for lipid-lowering medication. In lipidomic profiling, high LDL -C associated with 108 lipid species, and high triacylglycerides associated with 131 lipid species in either cohort (at 5% false discovery rate; P-value range 0.038-2.3×10

7 Article Liver-specific deletion of IGF2 mRNA binding protein-2/IMP2 reduces hepatic fatty acid oxidation and increases hepatic triglyceride accumulation. 2019

Regué, Laura / Minichiello, Liliana / Avruch, Joseph / Dai, Ning. ·Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114. · Diabetes Unit of the Medical Services, Massachusetts General Hospital, Boston, MA 02114. · Department of Medicine, Harvard Medical School, Boston, MA 02115. · Department of Pharmacology, University of Oxford, Oxford OX1 3QT, United Kingdom. · Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114 avruch@molbio.mgh.harvard.edu. · Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114 ning@molbio.mgh.harvard.edu. ·J Biol Chem · Pubmed #31209109.

ABSTRACT: Insulin-like growth factor 2 mRNA-binding proteins 1-3 (IGF2BP1-3, also known as IMP1-3) contribute to the regulation of RNAs in a transcriptome-specific context. Global deletion of the mRNA-binding protein insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2 or IMP2) in mice causes resistance to obesity and fatty liver induced by a high-fat diet (HFD), whereas liver-specific IMP2 overexpression results in steatosis. To better understand the role of IMP2 in hepatic triglyceride metabolism, here we crossed mice expressing albumin-Cre with mice bearing a floxed

8 Article Comparison of novel and existing methods for detecting differentially methylated regions. 2018

Lent, Samantha / Xu, Hanfei / Wang, Lan / Wang, Zhe / Sarnowski, Chloé / Hivert, Marie-France / Dupuis, Josée. ·Department of Biostatistics, Boston University School of Public Health, 801 Massachusetts Avenue, 3rd Floor, Boston, MA, 02118, USA. lent@bu.edu. · Department of Biostatistics, Boston University School of Public Health, 801 Massachusetts Avenue, 3rd Floor, Boston, MA, 02118, USA. · Bioinformatics Program, Boston University, 44 Cummington Mall, Boston, MA, 02215, USA. · Obesity Prevention Program, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, 401 Park Drive, Suite 401 East, Boston, MA, 02215, USA. · Diabetes Unit, Massachusetts General Hospital, 50 Staniford Street, Suite 340, Boston, MA, 02144, USA. ·BMC Genet · Pubmed #30255775.

ABSTRACT: BACKGROUND: Single-probe analyses in epigenome-wide association studies (EWAS) have identified associations between DNA methylation and many phenotypes, but do not take into account information from neighboring probes. Methods to detect differentially methylated regions (DMRs) (clusters of neighboring probes associated with a phenotype) may provide more power to detect associations between DNA methylation and diseases or phenotypes of interest. RESULTS: We proposed a novel approach, GlobalP, and perform comparisons with 3 methods-DMRcate, Bumphunter, and comb-p-to identify DMRs associated with log triglycerides (TGs) in real GAW20 data before and after fenofibrate treatment. We applied these methods to the summary statistics from an EWAS performed on the methylation data. Comb-p, DMRcate, and GlobalP detected very similar DMRs near the gene CPT1A on chromosome 11 in both the pre- and posttreatment data. In addition, GlobalP detected 2 DMRs before fenofibrate treatment in the genes ETV6 and ABCG1. Bumphunter identified several DMRs on chromosomes 1 and 20, which did not overlap with DMRs detected by other methods. CONCLUSIONS: Our novel method detected the same DMR identified by two existing methods and detected two additional DMRs not identified by any of the existing methods we compared.

9 Article Comorbidities and Cardiometabolic Disease: Relationship With Longitudinal Changes in Diastolic Function. 2018

Nayor, Matthew / Enserro, Danielle M / Xanthakis, Vanessa / Larson, Martin G / Benjamin, Emelia J / Aragam, Jayashri / Mitchell, Gary F / Vasan, Ramachandran S. ·Framingham Heart Study, Framingham, Massachusetts; Cardiology Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. Electronic address: mnayor@mgh.harvard.edu. · Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts. · Framingham Heart Study, Framingham, Massachusetts; Section of Preventive Medicine, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts; Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts. · Framingham Heart Study, Framingham, Massachusetts; Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts. · Framingham Heart Study, Framingham, Massachusetts; Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts; Cardiology Section, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts. · Cardiovascular Division, Veterans Administration Hospital, West Roxbury, Massachusetts; Harvard Medical School, Boston, Massachusetts. · Cardiovascular Engineering, Inc., Norwood, Massachusetts. · Framingham Heart Study, Framingham, Massachusetts; Section of Preventive Medicine, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts; Cardiology Section, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts. ·JACC Heart Fail · Pubmed #29525334.

ABSTRACT: OBJECTIVES: This study sought to evaluate the course, correlates, and prognosis of longitudinal changes in left ventricular (LV) diastolic dysfunction (DD) in the community-based Framingham Heart Study. BACKGROUND: Relationships of clinical risk factors to longitudinal progression of DD are incompletely understood. METHODS: Diastolic function was assessed by echocardiography performed at consecutive examinations (visits 1 and 2, mean interval 5.6 years) in 1,740 participants (64 ± 8 years of age at visit 1, 59% women) with normal LV systolic function and no atrial fibrillation. RESULTS: Of 1,615 individuals with normal-to-mild DD at visit 1, 198 (12%) progressed to ≥ moderate DD at visit 2. Progression was more likely in women and with advancing age (p < 0.0001). Of 125 individuals with ≥ moderate DD at visit 1, 25 (20%) regressed to normal-to-mild DD by visit 2. Regression of DD was associated with younger age (p < 0.03). In stepwise regression models, age, female sex, baseline and changes in systolic blood pressure, diastolic blood pressure, body mass index, serum triglycerides, and diabetes were positively associated with worsening diastolic function (all p < 0.05). Noncardiac comorbidity tracked with progressive DD. Cardiovascular disease (CVD) or death events occurred in 44 of 1,509 participants free of CVD at visit 2, during 2.7 ± 0.6 years of post-visit 2 follow-up. Presence of ≥ moderate DD was associated with higher risk (age- and sex-adjusted hazard ratio for CVD or death: 2.14; 95% confidence interval: 1.06 to 4.32; p = 0.03). CONCLUSIONS: In a community-based cohort of middle-aged to older adults, cardiometabolic risk factors and noncardiac comorbidities were associated with DD progression. Moderate or worse DD was associated with higher risk of CVD or death.

10 Article Bi-directional analysis between fatty liver and cardiovascular disease risk factors. 2017

Ma, Jiantao / Hwang, Shih-Jen / Pedley, Alison / Massaro, Joseph M / Hoffmann, Udo / Chung, Raymond T / Benjamin, Emelia J / Levy, Daniel / Fox, Caroline S / Long, Michelle T. ·The Framingham Heart Study, Division of Intramural Research, National Heart, Lung, and Blood Institute, Framingham, MA, United States; Population Sciences Branch, Division of Intramural Research, National Heart, Lung, and Blood Institute, Framingham, MA, United States. · The Framingham Heart Study, Division of Intramural Research, National Heart, Lung, and Blood Institute, Framingham, MA, United States; Population Sciences Branch, Division of Intramural Research, National Heart, Lung, and Blood Institute, Framingham, MA, United States; Department of Mathematics and Statistics, Boston University, Boston, MA, United States. · Radiology Department, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States. · Liver Center, Gastrointestinal Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States. · The Framingham Heart Study, Division of Intramural Research, National Heart, Lung, and Blood Institute, Framingham, MA, United States; Department of Epidemiology, Boston University School of Public Health, Boston, MA, United States; Evans Department of Medicine, Whitaker Cardiovascular Institute and Cardiology Section, Boston University School of Medicine, Boston, MA, United States. · The Framingham Heart Study, Division of Intramural Research, National Heart, Lung, and Blood Institute, Framingham, MA, United States; Population Sciences Branch, Division of Intramural Research, National Heart, Lung, and Blood Institute, Framingham, MA, United States; Division of Endocrinology and Metabolism, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States. · Division of Gastroenterology, Evans Department of Medicine, Boston University School of Medicine, Boston, MA, United States. Electronic address: mtlong@bu.edu. ·J Hepatol · Pubmed #27729222.

ABSTRACT: BACKGROUND & AIMS: The relations of non-alcoholic fatty liver disease to cardiovascular disease (CVD) risk factors are not fully understood. The objective of our study is to explore the bi-directional relationships of fatty liver to CVD risk factors. METHODS: We prospectively evaluated whether liver fat predicted the development of CVD risk factors and whether CVD risk factors predicted new onset fatty liver during 6years of follow-up in middle- to older-aged Framingham Heart Study participants. We estimated liver fat using multi-detector computed tomography. RESULTS: We included 1051 participants (mean age 45±6years, 46% women). The prevalence of fatty liver was 18% at baseline. In participants without fatty liver at baseline, 101 participants developed incident fatty liver over approximately 6years. Baseline liver fat (per standard deviation increase) was associated with increased odds of incident hypertension (OR 1.42; 95% CI 1.15-1.76; p=0.001) and incident type 2 diabetes (OR 1.43; 95% CI 1.09-1.88, p<0.001). In a parallel analysis, individuals with hypertension (OR 3.34; 95% CI 2.04-5.49), hypertriglyceridemia (OR 3.04; 95% CI: 1.84-5.02), impaired fasting glucose (OR 2.92; 95% CI 1.76-4.82), or type 2 diabetes (OR 4.15; 95% CI 1.19-14.46) at baseline had higher odds of incident fatty liver compared to individuals without those conditions (all p<0.03). In both analyses, the observed associations remained similar after additional adjustments for measures of adiposity. CONCLUSIONS: The present study demonstrated bi-directional relationships between fatty liver and CVD risk factors among middle- to older-aged Framingham Heart Study participants. LAY SUMMARY: It is not fully understood whether non-alcoholic fatty liver (NAFLD) disease precedes or develops after increased cardiovascular disease (CVD) risk factors. The findings of our study suggest a bi-directional relationship between NAFLD and CVD risk factors.

11 Article Insulin resistance modifies the association between obesity and current asthma in adults. 2016

Cardet, Juan Carlos / Ash, Samuel / Kusa, Tope / Camargo, Carlos A / Israel, Elliot. ·Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA, USA Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Boston, MA, USA. · Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Boston, MA, USA. · Dept of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. · Dept of Emergency Medicine and Division of Rheumatology, Allergy, and Immunology, Dept of Medicine, Massachusetts General Hospital, Boston, MA, USA. · Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA, USA Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Boston, MA, USA eisrael@partners.org. ·Eur Respir J · Pubmed #27103388.

ABSTRACT: Insulin resistance potentiates the association between obesity and childhood asthma, but this relationship appears inconsistent in relatively small studies of adults. We investigated effect modification in adults using the National Health and Nutrition Examination Survey 2003-2012, a large, nationally representative database.Insulin resistance and a history of physician-diagnosed current asthma were obtained from 12 421 adults, ages 18-85 years. We used logistic regression to determine associations between obesity and current asthma, adjusting for age, sex, race/ethnicity, poverty income ratio and smoking status. An interaction term evaluated effect modification by insulin resistance of the obesity-asthma association.As expected, obesity was positively associated with current asthma. Insulin resistance modified this association, with obesity measured as body mass index, waist circumference or waist-to-height ratio. The relationship between obesity and current asthma was stronger with increasing insulin resistance tertiles (OR 2.05, 95% CI 2.76-3.00; p-value for interaction 0.03). This association was robust to adjustments for other components of the metabolic syndrome (hypertriglyceridaemia, hypertension, hyperglycaemia and systemic inflammation). None of these components were themselves effect modifiers of the obesity-asthma association.In this large, nationally representative sample, insulin resistance modified the association between obesity and current asthma in adults. Targeting insulin resistance may represent a novel therapeutic strategy for obese patients with asthma.

12 Article Sugar-Sweetened Beverage Intake Is Positively Associated with Baseline Triglyceride Concentrations, and Changes in Intake Are Inversely Associated with Changes in HDL Cholesterol over 12 Months in a Multi-Ethnic Sample of Children. 2015

Van Rompay, Maria I / McKeown, Nicola M / Goodman, Elizabeth / Eliasziw, Misha / Chomitz, Virginia R / Gordon, Catherine M / Economos, Christina D / Sacheck, Jennifer M. ·Friedman School of Nutrition Science and Policy, maria.vanrompay@tufts.edu. · Nutritional Epidemiology Program, Jean Mayer USDA Human Nutrition Research Center on Aging, and. · MassGeneral Hospital for Children, Boston, MA; Harvard Medical School, Boston, MA; and. · Department of Public Health and Community Medicine, School of Medicine, Tufts University, Boston, MA; · Divisions of Adolescent Medicine and Endocrinology, Hasbro Children's Hospital, Alpert Medical School of Brown University, Providence, RI. · Friedman School of Nutrition Science and Policy. ·J Nutr · Pubmed #26338888.

ABSTRACT: BACKGROUND: Intake of sugar-sweetened beverages (SSBs) is linked to greater cardiometabolic risk in adults. Although longitudinal evidence is sparse among children, SSB intake reduction is targeted to reduce cardiometabolic risk factors in this group. OBJECTIVE: We investigated characteristics associated with consumption of SSBs in a multi-ethnic sample of children/adolescents and measured cross-sectional and longitudinal associations between SSB intake and plasma HDL cholesterol and triglycerides (TGs) over 12 mo. METHODS: In a diverse cohort of children aged 8-15 y, cross-sectional associations (n = 613) between baseline SSB intake and blood lipid concentrations and longitudinal associations (n = 380) between mean SSB intake, changes in SSB intake, and lipid changes over 12 mo were assessed with multivariable linear regression. RESULTS: Greater SSB intake was associated with lower socioeconomic status, higher total energy intake, lower fruit/vegetable intake, and more sedentary time. In cross-sectional analysis, greater SSB intake was associated with higher plasma TG concentrations among consumers (62.4, 65.3, and 71.6 mg/dL in children who consumed >0 but <2, ≥2 but <7, and ≥7 servings/wk, respectively; P-trend: 0.03); plasma HDL cholesterol showed no cross-sectional association. In the longitudinal analysis, mean SSB intake over 12 mo was not associated with lipid changes; however, the 12-mo increase in plasma HDL-cholesterol concentration was greater among children who decreased their intake by ≥1 serving/wk (4.6 ± 0.8 mg/dL) compared with children whose intake stayed the same (2.0 ± 0.8 mg/dL) or increased (1.5 ± 0.8 mg/dL; P = 0.02). CONCLUSIONS: In a multi-ethnic sample of children, intake of SSBs was positively associated with TG concentrations among consumers, and changes in SSB intake were inversely associated with HDL cholesterol concentration changes over 12 mo. Further research in large diverse samples of children is needed to study the public health implications of reducing SSB intake among children of different racial/ethnic groups. The Daily D Health Study was registered at clinicaltrials.gov as NCT01537809.

13 Article Omega-3 fatty acids for atypical antipsychotic-associated hypertriglyceridemia. 2015

Freeman, Marlene P / McInerney, Kathryn / Sosinsky, Alexandra Z / Kwiatkowski, Molly A / Cohen, Lee S. ·Center for Women's Mental Health, Massachusetts General Hospital, Boston, Massachusetts, USA. E-mail: mfreeman@partners.org. ·Ann Clin Psychiatry · Pubmed #26247219.

ABSTRACT: BACKGROUND: The objective of this open-label, preliminary study was to assess the efficacy of omega-3 fatty acids for treating dyslipidemia associated with use of atypical antipsychotics. METHODS: Participants treated with atypical antipsychotics who had hypertriglyceridemia (> 200 mg/dL) and/or hypercholesterolemia (> 250 mg/dL) were enrolled in an open trial and received omega-3 fatty acids (Lovaza) for up to 16 weeks. Serum lipid profiles were re-assessed at 8 and 16 weeks. RESULTS: Twenty-eight participants with dyslipidemia enrolled in the trial; 16 were evaluable with post-baseline assessments. There was an average decrease in triglyceride levels of 54.13 ± 83.44 mg/dL (P = .04). A more pronounced benefit of omega-3 supplementation was observed in participants with elevated triglyceride levels at baseline (> 200 mg/dL), compared with those with elevated cholesterol values but normal or more modestly elevated triglyceride levels at enrollment. Participants with hypertriglyceridemia at baseline (n = 10, > 200 mg/dL) experienced a mean decrease in triglyceride levels of 75.8 ± 28.71 mg/dL, a significantly larger decrease than was observed among all participants (P = .005). CONCLUSIONS: Omega-3 supplementation reduced triglyceride levels but not levels of total cholesterol. Recruitment and retention in this study was challenging, and could indicate a lack of screening for dyslipidemia among atypical antipsychotic users/prescribers or could reflect the over-the- counter availability of omega-3 fatty acids.