Imperial College London

DrAbbasDehghan

Faculty of MedicineSchool of Public Health

Reader in Cardiometabolic Disease Epidemiology
 
 
 
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Contact

 

+44 (0)20 7594 3347a.dehghan CV

 
 
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Location

 

157Norfolk PlaceSt Mary's Campus

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Summary

 

Publications

Publication Type
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270 results found

Sedaghat S, Mattace-Raso FUS, Hoorn EJ, Uitterlinden AG, Hofman A, Ikram MA, Franco OH, Dehghan Aet al., 2015, Arterial Stiffness and Decline in Kidney Function, CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 10, Pages: 2190-2197, ISSN: 1555-9041

Journal article

Nino PKB, Durik M, Danser AHJ, de Vries R, Musterd-Bhaggoe UM, Meima ME, Kavousi M, Ghanbari M, Hoeijmakers JH, O'Donnell CJ, Franceschini N, Janssen GMJ, De Mey JGR, Liu Y, Shanahan CM, Franco OH, Dehghan A, Roks AJMet al., 2015, Phosphodiesterase 1 regulation is a key mechanism in vascular aging, CLINICAL SCIENCE, Vol: 129, Pages: 1061-1075, ISSN: 0143-5221

Journal article

van Leeuwen EM, Huffman JE, Bis JC, Isaacs A, Mulder M, Sabo A, Smith AV, Demissie S, Manichaikul A, Brody JA, Feitosa MF, Duan Q, Schraut KE, Navarro P, van Vliet-Ostaptchouk JV, Zhu G, Mbarek H, Trompet S, Verweij N, Lyytikäinen LP, Deelen J, Nolte IM, van der Laan SW, Davies G, Vermeij-Verdoold AJM, van Oosterhout AALJ, Vergeer-Drop JM, Arking DE, Trochet H, Medina-Gomez C, Rivadeneira F, Uitterlinden AG, Dehghan A, Franco OH, Sijbrands EJ, Hofman A, White CC, Mychaleckyj JC, Peloso GM, Swertz MA, Willemsen G, de Geus EJ, Milaneschi Y, Penninx BWJH, Ford I, Buckley BM, de Craen AJM, Starr JM, Deary IJ, Pasterkamp G, Oldehinkel AJ, Snieder H, Slagboom PE, Nikus K, Kähönen M, Lehtimäki T, Viikari JS, Raitakari OT, van der Harst P, Jukema JW, Hottenga JJ, Boomsma DI, Whitfield JB, Montgomery G, Martin NG, Polasek O, Vitart V, Hayward C, Kolcic I, Wright AF, Rudan I, Joshi PK, Wilson JF, Lange LA, Wilson JG, Gudnason V, Harris TB, Morrison AC, Borecki IB, Rich SS, Padmanabhan S, Psaty BM, Rotter JI, Smith BH, Boerwinkle E, Cupples LA, van Duijn Cet al., 2015, Fine mapping the CETP region reveals a common intronic insertion associated to HDL-C, npj Aging and Mechanisms of Disease, Vol: 1

© 2015 Japanese Society of Anti-Aging Medicine/Macmillan Publishers Limited. BACKGROUND: Individuals with exceptional longevity and their offspring have significantly larger high-density lipoprotein concentrations (HDL-C) particle sizes due to the increased homozygosity for the I405V variant in the cholesteryl ester transfer protein (CETP) gene. In this study, we investigate the association of CETP and HDL-C further to identify novel, independent CETP variants associated with HDL-C in humans. METHODS: We performed a meta-analysis of HDL-C within the CETP region using 59,432 individuals imputed with 1000 Genomes data. We performed replication in an independent sample of 47,866 individuals and validation was done by Sanger sequencing. RESULTS: The meta-analysis of HDL-C within the CETP region identified five independent variants, including an exonic variant and a common intronic insertion. We replicated these 5 variants significantly in an independent sample of 47,866 individuals. Sanger sequencing of the insertion within a single family confirmed segregation of this variant. The strongest reported association between HDL-C and CETP variants, was rs3764261; however, after conditioning on the five novel variants we identified the support for rs3764261 was highly reduced (βunadjusted = 3.179 mg/dl (P value = 5.25 × 10−509), βadjusted = 0.859 mg/dl (P value = 9.51 × 10− 25)), and this finding suggests that these five novel variants may partly explain the association of CETP with HDL-C. Indeed, three of the five novel variants (rs34065661, rs5817082, rs7499892) are independent of rs3764261. CONCLUSIONS: The causal variants in CETP that account for the association with HDL-C remain unknown. We used studies imputed to the 1000 Genomes reference panel for fine mapping of the CETP region. We identified and validated five variants within this region that may partly account for the association of the known variant (rs3764261), as well as o

Journal article

Ligthart S, van Herpt TTW, Leening MJG, Kavousi M, Hofman A, Stricker BHC, van Hoek M, Sijbrands EJG, Franco OH, Dehghan Aet al., 2015, Lifetime risk of developing impaired glucose metabolism and eventual progression from prediabetes to type 2 diabetes: a prospective cohort study, Lancet Diabetes and Endocrinology, Vol: 4, Pages: 44-51, ISSN: 2213-8595

BackgroundData are scarce for the lifetime risk of developing impaired glucose metabolism, including prediabetes, as are data for the risk of eventual progression from prediabetes to diabetes and for initiation of insulin treatment in previously untreated patients with diabetes. We aimed to calculate the lifetime risk of the full range of glucose impairments, from normoglycaemia to prediabetes, type 2 diabetes, and eventual insulin use.MethodsIn this prospective population-based cohort analysis, we used data from the population-based Rotterdam Study. We identified diagnostic events by use of general practitioners' records, hospital discharge letters, pharmacy dispensing data, and serum fasting glucose measurements taken at the study centre (Rotterdam, Netherlands) visits. Normoglycaemia, prediabetes, and diabetes were defined on the basis of WHO criteria for fasting glucose (normoglycaemia: ≤6·0 mmol/L; prediabetes: >6·0 mmol/L and <7·0 mmol/L; and diabetes ≥7·0 mmol/L or use of glucose-lowering drug). We calculated lifetime risk using a modified version of survival analysis adjusted for the competing risk of death. We also estimated the lifetime risk of progression from prediabetes to overt diabetes and from diabetes free of insulin treatment to insulin use. Additionally, we calculated years lived with healthy glucose metabolism.FindingsWe used data from 10 050 participants from the Rotterdam Study. During a follow-up of up to 14·7 years (between April 1, 1997, and Jan 1, 2012), 1148 participants developed prediabetes, 828 developed diabetes, and 237 started insulin treatment. At age 45 years, the remaining lifetime risk was 48·7% (95% CI 46·2–51·3) for prediabetes, 31·3% (29·3–33·3) for diabetes, and 9·1% (7·8–10·3) for insulin use. In individuals aged 45 years, the lifetime risk to progress from prediabetes to diabetes was 74·0% (

Journal article

Tamar Silva C, Kors JA, Amin N, Dehghan A, Witteman JCM, Willemsen R, Oostra BA, van Duijn CM, Isaacs Aet al., 2015, Heritabilities, proportions of heritabilities explained by GWAS findings, and implications of cross-phenotype effects on PR interval, HUMAN GENETICS, Vol: 134, Pages: 1211-1219, ISSN: 0340-6717

Journal article

Laugsand LE, Ix JH, Bartz TM, Djousse L, Kizer JR, Tracy RP, Dehghan A, Rexrode K, Lopez OL, Rimm EB, Siscovick DS, O'Donnell CJ, Newman A, Mukamal KJ, Jensen MKet al., 2015, Fetuin-A and risk of coronary heart disease: A Mendelian randomization analysis and a pooled analysis of AHSG genetic variants in 7 prospective studies, ATHEROSCLEROSIS, Vol: 243, Pages: 44-52, ISSN: 0021-9150

Journal article

van Loon J, Dehghan A, Tang W, Trompet S, McArdle WL, Asselbergs FW, Chen M-H, Lopez LM, Huffman JE, Leebeek FWG, Basu S, Stott DJ, Rumley A, Gansevoort RT, Davies G, Wilson JJF, Witteman JCM, Cao X, de Craen AJM, Bakker SJL, Psaty BM, Starr JM, Hofman A, Jukema JW, Deary IJ, Hayward C, van der Harst P, Lowe GDO, Folsom AR, Strachan DP, Smith N, de Maat MPM, O'Donnell Cet al., 2015, Genome-wide association studies identify genetic loci for low von Willebrand factor levels, EUROPEAN JOURNAL OF HUMAN GENETICS, Vol: 24, Pages: 1035-1040, ISSN: 1018-4813

Journal article

Maksimovic A, Hanewinckel R, Verlinden VJA, Ligthart S, Hofman A, Franco OH, van Doorn PA, Tiemeier H, Dehghan A, Ikram MAet al., 2015, Gait characteristics in older adults with diabetes and impaired fasting glucose: The Rotterdam Study, Journal of Diabetes and its Complications, Vol: 30, Pages: 61-66, ISSN: 1056-8727

AimsTo investigate the association of diabetes mellitus and impaired fasting glucose with gait in the general middle-aged and elderly population.MethodsWe performed a cross-sectional study on 3019 participants from the population-based Rotterdam Study (aged > 45 years, 54% women). The presence of diabetes mellitus and impaired fasting glucose was evaluated by measuring serum glucose levels and by documenting anti-diabetic treatment. Participants underwent gait analysis using an electronic walkway. Thirty gait variables were summarized into five independent gait domains for normal walking (Rhythm, Variability, Phases, Pace and Base of Support), one for turning (Turning) and one for walking heel to toe (Tandem), which were averaged into Global Gait. Linear regression analyses were performed to determine the association of diabetes, impaired fasting glucose and continuous glucose levels within the normal range with gait.ResultsDiabetes mellitus was associated with worse Global Gait (Z-score difference − 0.19, 95% confidence interval (CI) − 0.30; − 0.07), worse Pace (− 0.20, 95% CI − 0.30; − 0.10) and worse Tandem (− 0.21, 95% CI − 0.33; − 0.09), after adjusting for age, sex, height and weight. The association with Tandem remained significant after additional adjustment for cardiovascular risk factors. Impaired fasting glucose and continuous glucose levels within the normal range were not associated with any of the gait domains.ConclusionIn our population-based study diabetes mellitus was associated with worse Global Gait, which was mostly reflected in Pace and Tandem. These associations were partly driven by other cardiovascular risk factors, emphasizing the importance of optimal control of cardiovascular risk factor profiles in patients with diabetes.

Journal article

Chaker L, Heeringa J, Dehghan A, Medici M, Visser WE, Baumgartner C, Hofman A, Rodondi N, Peeters RP, Franco OHet al., 2015, Normal Thyroid Function and the Risk of Atrial Fibrillation: the Rotterdam Study, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 100, Pages: 3718-3724, ISSN: 0021-972X

Journal article

Kato N, Loh M, Takeuchi F, Verweij N, Wang X, Zhang W, Kelly TN, Saleheen D, Lehne B, Leach IM, Drong AW, Abbott J, Wahl S, Tan S-T, Scott WR, Campanella G, Chadeau-Hyam M, Afzal U, Ahluwalia TS, Bonder MJ, Chen P, Dehghan A, Edwards TL, Esko T, Go MJ, Harris SE, Hartiala J, Kasela S, Kasturiratne A, Khor C-C, Kleber ME, Li H, Mok ZY, Nakatochi M, Sapari NS, Saxena R, Stewart AFR, Stolk L, Tabara Y, Teh AL, Wu Y, Wu J-Y, Zhang Y, Aits I, Alves ADSC, Das S, Dorajoo R, Hopewell JC, Kim YK, Koivula RW, Luan J, Lyytikainen L-P, Nguyen QN, Pereira MA, Postmus I, Raitakari OT, Bryan MS, Scott RA, Sorice R, Tragante V, Traglia M, White J, Yamamoto K, Zhang Y, Adair LS, Ahmed A, Akiyama K, Asif R, Aung T, Barroso I, Bjonnes A, Braun TR, Cai H, Chang L-C, Chen C-H, Cheng C-Y, Chong Y-S, Collins R, Courtney R, Davies G, Delgado G, Do LD, Doevendans PA, Gansevoort RT, Gao Y-T, Grammer TB, Grarup N, Grewal J, Gu D, Wander GS, Hartikainen A-L, Hazen SL, He J, Heng C-K, Hixson JE, Hofman A, Hsu C, Huang W, Husemoen LLN, Hwang J-Y, Ichihara S, Igase M, Isono M, Justesen JM, Katsuy T, Kibriya MG, Kim YJ, Kishimoto M, Koh W-P, Kohara K, Kumari M, Kwek K, Lee NR, Lee J, Liao J, Lieb W, Liewald DCM, Matsubara T, Matsushita Y, Meitinger T, Mihailov E, Milani L, Mills R, Mononen N, Mueller-Nurasyid M, Nabika T, Nakashima E, Ng HK, Nikus K, Nutile T, Ohkubo T, Ohnaka K, Parish S, Paternoster L, Peng H, Peters A, Pham ST, Pinidiyapathirage MJ, Rahman M, Rakugi H, Rolandsson O, Rozario MA, Ruggiero D, Sala CF, Sarju R, Shimokawa K, Snieder H, Sparso T, Spiering W, Starr JM, Stott DJ, Stram DO, Sugiyama T, Szymczak S, Tang WHW, Tong L, Trompet S, Turjanmaa V, Ueshima H, Uitterlinden AG, Umemura S, Vaarasmaki M, van Dam RM, van Gilst WH, van Veldhuisen DJ, Viikari JS, Waldenberger M, Wang Y, Wang A, Wilson R, Wong T-Y, Xiang Y-B, Yamaguchi S, Ye X, Young RD, Young TL, Yuan J-M, Zhou X, Asselbergs FW, Ciullo M, Clarke R, Deloukas P, Franke A, Franks PW, Franks S, Friedlander Y, Gross MD, Guoet al., 2015, Trans-ancestry genome-wide association study identifies 12 genetic loci influencing blood pressure and implicates a role for DNA methylation, Nature Genetics, Vol: 47, Pages: 1282-1293, ISSN: 1546-1718

We carried out a trans-ancestry genome-wide association and replication study of blood pressure phenotypes among up to 320,251 individuals of East Asian, European and South Asian ancestry. We find genetic variants at 12 new loci to be associated with blood pressure (P = 3.9 × 10−11 to 5.0 × 10−21). The sentinel blood pressure SNPs are enriched for association with DNA methylation at multiple nearby CpG sites, suggesting that, at some of the loci identified, DNA methylation may lie on the regulatory pathway linking sequence variation to blood pressure. The sentinel SNPs at the 12 new loci point to genes involved in vascular smooth muscle (IGFBP3, KCNK3, PDE3A and PRDM6) and renal (ARHGAP24, OSR1, SLC22A7 and TBX2) function. The new and known genetic variants predict increased left ventricular mass, circulating levels of NT-proBNP, and cardiovascular and all-cause mortality (P = 0.04 to 8.6 × 10−6). Our results provide new evidence for the role of DNA methylation in blood pressure regulation.

Journal article

Huffman JE, de Vries PS, Morrison AC, Sabater-Lleal M, Kacprowski T, Auer PL, Brody JA, Chasman DI, Chen M-H, Guo X, Lin L-A, Marioni RE, Mueller-Nurasyid M, Yanek LR, Pankratz N, Grove ML, de Maat MPM, Cushman M, Wiggins KL, Qi L, Sennblad B, Harris SE, Polasek O, Riess H, Rivadeneira F, Rose LM, Goel A, Taylor KD, Teumer A, Uitterlinden AG, Vaidya D, Yao J, Tang W, Levy D, Waldenberger M, Becker DM, Folsom AR, Giulianini F, Greinacher A, Hofman A, Huang C-C, Kooperberg C, Silveira A, Starr JM, Strauch K, Strawbridge RJ, Wright AF, McKnight B, Franco OH, Zakai N, Mathias RA, Psaty BM, Ridker PM, Tofler GH, Voelker U, Watkins H, Fornage M, Hamsten A, Deary IJ, Boerwinkle E, Koenig W, Rotter JI, Hayward C, Dehghan A, Reiner AP, O'Donnell CJ, Smith NLet al., 2015, Rare and low-frequency variants and their association with plasma levels of fibrinogen, FVII, FVIII, and vWF, BLOOD, Vol: 126, Pages: E19-E29, ISSN: 0006-4971

Journal article

Nikpay M, Goel A, Won H-H, Hall LM, Willenborg C, Kanoni S, Saleheen D, Kyriakou T, Nelson CP, Hopewell JC, Webb TR, Zeng L, Dehghan A, Alver M, Armasu SM, Auro K, Bjonnes A, Chasman DI, Chen S, Ford I, Franceschini N, Gieger C, Grace C, Gustafsson S, Huang J, Hwang S-J, Kim YK, Kleber ME, Lau KW, Lu X, Lu Y, Lyytikainen L-P, Mihailov E, Morrison AC, Pervjakova N, Qu L, Rose LM, Salfati E, Saxena R, Scholz M, Smith AV, Tikkanen E, Uitterlinden A, Yang X, Zhang W, Zhao W, de Andrade M, de Vries PS, van Zuydam NR, Anand SS, Bertram L, Beutner F, Dedoussis G, Frossard P, Gauguier D, Goodall AH, Gottesman O, Haber M, Han B-G, Huang J, Jalilzadeh S, Kessler T, Koenig IR, Lannfelt L, Lieb W, Lind L, Lindgren CM, Lokki M-L, Magnusson PK, Mallick NH, Mehra N, Meitinger T, Memon F-U-R, Morris AP, Nieminen MS, Pedersen NL, Peters A, Rallidis LS, Rasheed A, Samuel M, Shah SH, Sinisalo J, Stirrups KE, Trompet S, Wang L, Zaman KS, Ardissino D, Boerwinkle E, Borecki IB, Bottinger EP, Buring JE, Chambers JC, Collins R, Cupples LA, Danesh J, Demuth I, Elosua R, Epstein SE, Esko T, Feitosa MF, Franco OH, Franzosi MG, Granger CB, Gu D, Gudnason V, Hall AS, Hamsten A, Harris TB, Hazen SL, Hengstenberg C, Hofman A, Ingelsson E, Iribarren C, Jukema JW, Karhunen PJ, Kim B-J, Kooner JS, Kullo IJ, Lehtimaki T, Loos RJF, Melander O, Metspalu A, Maerz W, Palmer CN, Perola M, Quertermous T, Rader DJ, Ridker PM, Ripatti S, Roberts R, Salomaa V, Sanghera DK, Schwartz SM, Seedorf U, Stewart AF, Stott DJ, Thiery J, Zalloua PA, O'Donnell CJ, Reilly MP, Assimes TL, Thompson JR, Erdmann J, Clarke R, Watkins H, Kathiresan S, McPherson R, Deloukas P, Schunkert H, Samani NJ, Farrall Met al., 2015, A comprehensive 1000 Genomes-based genome-wide association meta-analysis of coronary artery disease, Nature Genetics, Vol: 47, Pages: 1121-1130, ISSN: 1061-4036

Existing knowledge of genetic variants affecting risk of coronary artery disease (CAD) is largelybased on genome-wide association studies (GWAS) analysis of common SNPs. Leveragingphased haplotypes from the 1000 Genomes Project, we report a GWAS meta-analysis of 185thousand CAD cases and controls, interrogating 6.7 million common (MAF>0.05) as well as 2.7million low frequency (0.005<MAF<0.05) variants. In addition to confirmation of most knownCAD loci, we identified 10 novel loci, eight additive and two recessive, that contain candidategenes that newly implicate biological processes in vessel walls. We observed intra-locus allelicheterogeneity but little evidence of low frequency variants with larger effects and no evidence ofsynthetic association. Our analysis provides a comprehensive survey of the fine geneticarchitecture of CAD showing that genetic susceptibility to this common disease is largelydetermined by common SNPs of small effect size

Journal article

Sedaghat S, Cremers LGM, de Groot M, Hoorn EJ, Hofman A, van der Lugt A, Franco OH, Vernooij MW, Dehghan A, Ikram MAet al., 2015, Kidney function and microstructural integrity of brain white matter, NEUROLOGY, Vol: 85, Pages: 154-161, ISSN: 0028-3878

Journal article

Liefaard MC, Ligthart S, Vitezova A, Hofman A, Uitterlinden AG, Kiefte-de Jong JC, Franco OH, Zillikens MC, Dehghan Aet al., 2015, Vitamin D and C-Reactive Protein: A Mendelian Randomization Study, PLOS ONE, Vol: 10, ISSN: 1932-6203

Journal article

Milaneschi Y, Lamers F, Peyrot WJ, Abdellaoui A, Willemsen G, Hottenga JJ, Jansen R, Mbarek H, Dehghan A, Lu C, CHARGE inflammation working group, Boomsma DI, Penninx BWet al., 2015, Polygenic dissection of major depression clinical heterogeneity., Mol Psychiatry, Vol: 21, Pages: 516-522

The molecular mechanisms underlying major depressive disorder (MDD) are largely unknown. Limited success of previous genetics studies may be attributable to heterogeneity of MDD, aggregating biologically different subtypes. We examined the polygenic features of MDD and two common clinical subtypes (typical and atypical) defined by symptom profiles in a large sample of adults with established diagnoses. Data were from 1530 patients of the Netherlands Study of Depression and Anxiety (NESDA) and 1700 controls mainly from the Netherlands Twin Register (NTR). Diagnoses of MDD and its subtypes were based on DSM-IV symptoms. Genetic overlap of MDD and subtypes with psychiatric (MDD, bipolar disorder, schizophrenia) and metabolic (body mass index (BMI), C-reactive protein, triglycerides) traits was evaluated via genomic profile risk scores (GPRS) generated from meta-analysis results of large international consortia. Single nucleotide polymorphism (SNP)-heritability of MDD and subtypes was also estimated. MDD was associated with psychiatric GPRS, while no association was found for GPRS of metabolic traits. MDD subtypes had differential polygenic signatures: typical was strongly associated with schizophrenia GPRS (odds ratio (OR)=1.54, P=7.8e-9), while atypical was additionally associated with BMI (OR=1.29, P=2.7e-4) and triglycerides (OR=1.21, P=0.006) GPRS. Similar results were found when only the highly discriminatory symptoms of appetite/weight were used to define subtypes. SNP-heritability was 32% for MDD, 38% and 43% for subtypes with, respectively, decreased (typical) and increased (atypical) appetite/weight. In conclusion, MDD subtypes are characterized by partially distinct polygenic liabilities and may represent more homogeneous phenotypes. Disentangling MDD heterogeneity may help the psychiatric field moving forward in the search for molecular roots of depression.

Journal article

Ezzati M, Danaei G, Fahimi S, Lu Y, Zhou B, Hajifathalian K, Di Cesare M, Lo W, Reis-Santos B, Cowan MJ, Shaw JE, Bentham J, Lin JK, Bixby H, Magliano D, Bovet P, Miranda JJ, Khang Y, Stevens GA, Riley LM, Ali MKet al., 2015, Effects of diabetes definition on global surveillance of diabetes prevalence and diagnosis: a pooled analysis of 96 population-based studies with 331 288 participants, The Lancet Diabetes & Endocrinology, Vol: 3, Pages: 624-637, ISSN: 2213-8587

Background: Over time, diabetes has been defined based on different biomarkers, includingfasting plasma glucose (FPG) or 2-hour plasma glucose in an oral glucose tolerance test (2hOGTT) and,more recently, haemoglobin A1c (HbA1c). We examined the influence of diagnostic definitions on boththe population prevalence of diabetes and the classification of previously-undiagnosed individuals aswith vs. without diabetes in a pooled analysis of data from population-based health examinationsurveys in different world regions.

Journal article

de Vries PS, Boender J, Sonneveld MAH, Rivadeneira F, Ikram MA, Rottensteiner H, Hofman A, Uitterlinden AG, Leebeek FWG, Franco OH, Dehghan A, de Maat MPMet al., 2015, Genetic variants in the ADAMTS13 and SUPT3H genes are associated with ADAMTS13 activity, BLOOD, Vol: 125, Pages: 3949-3955, ISSN: 0006-4971

Journal article

Muka T, Trajanoska K, Kiefte-de Jong JC, Oei L, Uitterlinden AG, Hofman A, Dehghan A, Zillikens MC, Franco OH, Rivadeneira Fet al., 2015, The Association between Metabolic Syndrome, Bone Mineral Density, Hip Bone Geometry and Fracture Risk: The Rotterdam Study, PLOS ONE, Vol: 10, ISSN: 1932-6203

Journal article

Desikan RS, Schork AJ, Wang Y, Thompson WK, Dehghan A, Ridker PM, Chasman DI, McEvoy LK, Holland D, Chen C-H, Karow DS, Brewer JB, Hess CP, Williams J, Sims R, O'Donovan MC, Choi SH, Bis JC, Ikram MA, Gudnason V, DeStefano AL, van der Lee SJ, Psaty BM, van Duijn CM, Launer L, Seshadri S, Pericak-Vance MA, Mayeux R, Haines JL, Farrer LA, Hardy J, Ulstein ID, Aarsland D, Fladby T, White LR, Sando SB, Rongve A, Witoelar A, Djurovic S, Hyman BT, Snaedal J, Steinberg S, Stefansson H, Stefansson K, Schellenberg GD, Andreassen OA, Dale AMet al., 2015, Polygenic Overlap Between C-Reactive Protein, Plasma Lipids, and Alzheimer Disease, CIRCULATION, Vol: 131, Pages: 2061-2069, ISSN: 0009-7322

Journal article

Chaker L, Baumgartner C, den Elzen WPJ, Ikram MA, Blum MR, Collet T-H, Bakker SJL, Dehghan A, Drechsler C, Luben RN, Hofman A, Portegies MLP, Medici M, Iervasi G, Stott DJ, Ford I, Bremner A, Wanner C, Ferrucci L, Newman AB, Dullaart RP, Sgarbi JA, Ceresini G, Maciel RMB, Westendorp RG, Jukema JW, Imaizumi M, Franklyn JA, Bauer DC, Walsh JP, Razvi S, Khaw K-T, Cappola AR, Voelzke H, Franco OH, Gussekloo J, Rodondi N, Peeters RPet al., 2015, Subclinical Hypothyroidism and the Risk of Stroke Events and Fatal Stroke: An Individual Participant Data Analysis, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 100, Pages: 2181-2191, ISSN: 0021-972X

Journal article

Ghanbari M, Franco OH, de Looper HWJ, Hofman A, Erkeland SJ, Dehghan Aet al., 2015, Genetic Variations in MicroRNA-Binding Sites Affect MicroRNA-Mediated Regulation of Several Genes Associated With Cardio-metabolic Phenotypes, CIRCULATION-CARDIOVASCULAR GENETICS, Vol: 8, Pages: 473-486, ISSN: 1942-325X

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Muka T, Kiefte-de Jong JC, Hofman A, Dehghan A, Rivadeneira F, Franco OHet al., 2015, Polyunsaturated Fatty Acids and Serum C-Reactive Protein The Rotterdam Study, AMERICAN JOURNAL OF EPIDEMIOLOGY, Vol: 181, Pages: 846-856, ISSN: 0002-9262

Journal article

Steenaard RV, Ligthart S, Stolk L, Peters MJ, van Meurs JB, Uitterlinden AG, Hofman A, Franco OH, Dehghan Aet al., 2015, Tobacco smoking is associated with methylation of genes related to coronary artery disease, CLINICAL EPIGENETICS, Vol: 7, ISSN: 1868-7075

Journal article

Fall T, Hagg S, Ploner A, Maegi R, Fischer K, Draisma HHM, Sarin A-P, Benyamin B, Ladenvall C, Akerlund M, Kals M, Esko T, Nelson CP, Kaakinen M, Huikari V, Mangino M, Meirhaeghe A, Kristiansson K, Nuotio M-L, Kobl M, Grallert H, Dehghan A, Kuningas M, de Vries PS, de Bruijn RFAG, Willems SM, Heikkila K, Silventoinen K, Pietilainen KH, Legry V, Giedraitis V, Goumidi L, Syvanen A-C, Strauch K, Koenig W, Lichtner P, Herder C, Palotie A, Menni C, Uitterlinden AG, Kuulasmaa K, Havulinna AS, Moreno LA, Gonzalez-Gross M, Evans A, Tregouet D-A, Yarnell JWG, Virtamo J, Ferrieres J, Veronesi G, Perola M, Arveiler D, Brambilla P, Lind L, Kaprio J, Hofman A, Stricker BH, van Duijn CM, Ikram MA, Franco OH, Cottel D, Dallongeville J, Hall AS, Jula A, Tobin MD, Penninx BW, Peters A, Gieger C, Samani NJ, Montgomery GW, Whiteld JB, Martin NG, Groop L, Spector TD, Magnusson PK, Amouyel P, Boomsma DI, Nilsson PM, Jarvelin M-R, Lyssenko V, Metspalu A, Strachan DP, Salomaa V, Ripatti S, Pedersen NL, Prokopenko I, McCarthy MI, Ingelsson Eet al., 2015, Age- and Sex-Specific Causal Effects of Adiposity on Cardiovascular Risk Factors, DIABETES, Vol: 64, Pages: 1841-1852, ISSN: 0012-1797

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