Author: "PAGE Consortium" / Topic: 3. good health - Searchworks@Jio Institute Digital Library Search Results

9 results on '"PAGE Consortium"'

1. Investigating the Causal Relationship of C-Reactive Protein with 32 Complex Somatic and Psychiatric Outcomes : A Large-Scale Cross-Consortium Mendelian Randomization Study

Author: Prins, Bram P., Abbasi, Ali, Wong, Anson, Vaez, Ahmad, Nolte, Ilja, Franceschini, Nora, Stuart, Philip E., Guterriez Achury, Javier, Mistry, Vanisha, Bradfield, Jonathan P., Valdes, Ana M., Bras, Jose, Shatunov, Aleksey, Lu, Chen, Han, Buhm, Raychaudhuri, Soumya, Bevan, Steve, Mayes, Maureen D., Tsoi, Lam C., Evangelou, Evangelos, Nair, Rajan P., Grant, Struan F. A., Polychronakos, Constantin, Radstake, Timothy R. D., van Heel, David A., Dunstan, Melanie L., Wood, Nicholas W., Al-Chalabi, Ammar, Dehghan, Abbas, Hakonarson, Hakon, Markus, Hugh S., Elder, James T., Knight, Jo, Arking, Dan E., Spector, Timothy D., Koeleman, Bobby P. C., van Duijn, Cornelia M., Martin, Javier, Morris, Andrew P., Weersma, Rinse K., Wijmenga, Cisca, Munroe, Patricia B., Perry, John R. B., Pouget, Jennie G., Jamshidi, Yalda, Snieder, Harold, Alizadeh, Behrooz Z., Williams, Julie, PAGE Consortium, International Stroke Genetics Consortium, Systemic Sclerosis consortium, Treat OA consortium, DIAGRAM Consortium, CARDIoGRAMplusC4D Consortium, ALS consortium, International Parkinson’s Disease Genomics Consortium, Autism Spectrum Disorder Working Group of the Psychiatric Genomics Consortium, CKDGen consortium, GERAD1 Consortium, International Consortium for Blood Pressure, Schizophrenia Working Group of the Psychiatric Genomics Consortium, Inflammation Working Group of the CHARGE Consortium, Life Course Epidemiology (LCE), Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Real World Studies in PharmacoEpidemiology, -Genetics, -Economics and -Therapy (PEGET), Epidemiology, Markus, Hugh [0000-0002-9794-5996], Perry, John [0000-0001-6483-3771], and Apollo - University of Cambridge Repository
Subjects: 0301 basic medicine, Knees, Social Sciences, Blood Pressure, Vascular Medicine, Biochemistry, PAGE Consortium, chemistry.chemical_compound, 0302 clinical medicine, Sociology, Consortia, Treat OA consortium, GENETIC-VARIANTS, Medicine and Health Sciences, CARDIoGRAMplusC4D Consortium, Medicine, ALS consortium, SUSCEPTIBILITY LOCUS, Musculoskeletal System, ALL-CAUSE MORTALITY, Schizophrenia Working Group of the Psychiatric Genomics Consortium, biology, Mental Disorders, COMMON VARIANTS, BIPOLAR DISORDER, Genomics, 11 Medical And Health Sciences, General Medicine, International Parkinson’s Disease Genomics Consortium, 3. Good health, C-Reactive Protein, Immune System Diseases, CARDIOVASCULAR-DISEASE, International Consortium for Blood Pressure, Legs, Anatomy, Autism Spectrum Disorder Working Group of the Psychiatric Genomics Consortium, Research Article, Biotechnology, medicine.medical_specialty, Genotype, Heart Diseases, Systemic Sclerosis consortium, Renal function, DIAGRAM Consortium, Polymorphism, Single Nucleotide, International Stroke Genetics Consortium, 03 medical and health sciences, Rheumatology, Metabolic Diseases, General & Internal Medicine, Statistical significance, Mental Health and Psychiatry, Osteoarthritis, Mendelian randomization, Genetics, Genome-Wide Association Studies, Journal Article, Humans, CORONARY-HEART-DISEASE, GENOME-WIDE ASSOCIATION, Psychiatry, Molecular Biology, Inflammation Working Group of the CHARGE Consortium, Creatinine, Mood Disorders, business.industry, Arthritis, Limbs (Anatomy), C-reactive protein, Biology and Life Sciences, Computational Biology, Human Genetics, Odds ratio, Cell Biology, Mendelian Randomization Analysis, Genome Analysis, GERAD1 Consortium, RISK LOCI, BODY-MASS INDEX, 030104 developmental biology, Blood pressure, chemistry, CKDGen consortium, Genetics of Disease, C400 Genetics, Schizophrenia, RC0321, biology.protein, business, Body mass index, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract: Background C-reactive protein (CRP) is associated with immune, cardiometabolic, and psychiatric traits and diseases. Yet it is inconclusive whether these associations are causal. Methods and Findings We performed Mendelian randomization (MR) analyses using two genetic risk scores (GRSs) as instrumental variables (IVs). The first GRS consisted of four single nucleotide polymorphisms (SNPs) in the CRP gene (GRSCRP), and the second consisted of 18 SNPs that were significantly associated with CRP levels in the largest genome-wide association study (GWAS) to date (GRSGWAS). To optimize power, we used summary statistics from GWAS consortia and tested the association of these two GRSs with 32 complex somatic and psychiatric outcomes, with up to 123,865 participants per outcome from populations of European ancestry. We performed heterogeneity tests to disentangle the pleiotropic effect of IVs. A Bonferroni-corrected significance level of less than 0.0016 was considered statistically significant. An observed p-value equal to or less than 0.05 was considered nominally significant evidence for a potential causal association, yet to be confirmed. The strengths (F-statistics) of the IVs were 31.92–3,761.29 and 82.32–9,403.21 for GRSCRP and GRSGWAS, respectively. CRP GRSGWAS showed a statistically significant protective relationship of a 10% genetically elevated CRP level with the risk of schizophrenia (odds ratio [OR] 0.86 [95% CI 0.79–0.94]; p < 0.001). We validated this finding with individual-level genotype data from the schizophrenia GWAS (OR 0.96 [95% CI 0.94–0.98]; p < 1.72 × 10−6). Further, we found that a standardized CRP polygenic risk score (CRPPRS) at p-value thresholds of 1 × 10−4, 0.001, 0.01, 0.05, and 0.1 using individual-level data also showed a protective effect (OR < 1.00) against schizophrenia; the first CRPPRS (built of SNPs with p < 1 × 10−4) showed a statistically significant (p < 2.45 × 10−4) protective effect with an OR of 0.97 (95% CI 0.95–0.99). The CRP GRSGWAS showed that a 10% increase in genetically determined CRP level was significantly associated with coronary artery disease (OR 0.88 [95% CI 0.84–0.94]; p < 2.4 × 10−5) and was nominally associated with the risk of inflammatory bowel disease (OR 0.85 [95% CI 0.74–0.98]; p < 0.03), Crohn disease (OR 0.81 [95% CI 0.70–0.94]; p < 0.005), psoriatic arthritis (OR 1.36 [95% CI 1.00–1.84]; p < 0.049), knee osteoarthritis (OR 1.17 [95% CI 1.01–1.36]; p < 0.04), and bipolar disorder (OR 1.21 [95% CI 1.05–1.40]; p < 0.007) and with an increase of 0.72 (95% CI 0.11–1.34; p < 0.02) mm Hg in systolic blood pressure, 0.45 (95% CI 0.06–0.84; p < 0.02) mm Hg in diastolic blood pressure, 0.01 ml/min/1.73 m2 (95% CI 0.003–0.02; p < 0.005) in estimated glomerular filtration rate from serum creatinine, 0.01 g/dl (95% CI 0.0004–0.02; p < 0.04) in serum albumin level, and 0.03 g/dl (95% CI 0.008–0.05; p < 0.009) in serum protein level. However, after adjustment for heterogeneity, neither GRS showed a significant effect of CRP level (at p < 0.0016) on any of these outcomes, including coronary artery disease, nor on the other 20 complex outcomes studied. Our study has two potential limitations: the limited variance explained by our genetic instruments modeling CRP levels in blood and the unobserved bias introduced by the use of summary statistics in our MR analyses. Conclusions Genetically elevated CRP levels showed a significant potentially protective causal relationship with risk of schizophrenia. We observed nominal evidence at an observed p < 0.05 using either GRSCRP or GRSGWAS—with persistence after correction for heterogeneity—for a causal relationship of elevated CRP levels with psoriatic osteoarthritis, rheumatoid arthritis, knee osteoarthritis, systolic blood pressure, diastolic blood pressure, serum albumin, and bipolar disorder. These associations remain yet to be confirmed. We cannot verify any causal effect of CRP level on any of the other common somatic and neuropsychiatric outcomes investigated in the present study. This implies that interventions that lower CRP level are unlikely to result in decreased risk for the majority of common complex outcomes., Using genetic instruments, Behrooz Z. Alizadeh and colleagues examine the hypothesis that increased CRP levels play a causal role in common somatic and psychiatric conditions., Editors' Summary Background Inflammation is an important part of the human immune response, the network of cells and molecules that protects the body from attack by pathogens (infectious organisms) and from harmful substances and foreign particles (for example, splinters). When human cells are attacked by pathogens or injured by trauma or chemicals, molecules called inflammatory mediators induce fluid leakage from the blood vessels into the damaged tissue and attract “phagocytes” (a type of immune cell) to the site of infection or injury to “eat” the germs and dead or damaged cells. The end result is inflammation, which is characterized by swelling, redness, heat, and pain. The inflammatory response, although unpleasant, limits the damage caused by foreign invaders or chemicals by preventing further contact with body tissues. Sometimes, however, inflammation can be harmful. Persistent dysregulation of the inflammatory response is implicated in numerous somatic disorders (diseases that affect the body, such as cardiovascular disease) and neuropsychiatric disorders (mental disorders attributable to diseases of the nervous system, such as schizophrenia). Why Was This Study Done? Observational studies suggest that increased blood levels of C-reactive protein (CRP, an inflammatory protein) are associated with certain somatic and neuropsychiatric disorders. But observational studies cannot prove that changes in CRP levels actually cause any of these disorders. It could be that the individuals who develop a specific disease and who have a high CRP level also share another unknown characteristic that is actually responsible for disease development (confounding). Alternatively, it could be that the disease itself increases CRP levels (reverse causation). It is important to know whether CRP is causally involved in the development of specific diseases because it might then be possible to prevent or treat these diseases using drugs that control CRP levels. Here, the researchers undertake a Mendelian randomization study to determine whether CRP has a causal relationship with 32 common complex somatic and neuropsychiatric outcomes. Because gene variants are inherited randomly, they are not prone to confounding and are free from reverse causation. So, if CRP levels actually cause a specific somatic or neuropsychiatric disease, genetic variants that affect CRP levels should be associated with an altered risk for that disease. What Did the Researchers Do and Find? The researchers used data collected by several consortia involved in large genome-wide association studies (studies that ask whether specific genetic changes across the whole human genome, or blueprint, are associated with specific diseases) to look for associations between 32 somatic and neuropsychiatric outcomes and two genetic risk scores (GRSs) for CRP level. GRSCRP consisted of four single nucleotide polymorphisms (SNPs; a type of genetic variant) in the gene encoding CRP; GRSGWAS consisted of 18 SNPs that were associated with CRP level in a genome-wide association study. The researchers report that a genetically increased CRP level was significantly associated with a reduced risk of schizophrenia (a significant association is one unlikely to have arisen by chance). In addition, they found a nominally significant association (an association that needs to be confirmed) between genetically increased CRP levels and an increased risk of knee osteoarthritis, raised diastolic and systolic blood pressure, and bipolar disorder. Notably, there was no evidence for an effect of genetically increased CRP levels on any of the other 27 outcomes studied. What Do These Findings Mean? These findings suggest that genetically raised levels of CRP are causally associated with protection against schizophrenia, an unexpected finding given other recent studies that suggest that raised CRP levels and brain inflammation predispose individuals to schizophrenia. The findings also provide preliminary evidence that genetically raised levels of CRP may be causally associated with an increased risk of raised blood pressure, knee arthritis, and bipolar disorder. The lack of any association between genetically raised levels of CRP and the other outcomes studied suggests, however, that many previously identified disease-associated rises in CRP levels might be a response to the disease process rather than a cause of these diseases. Like all Mendelian randomization studies, the reliability of these findings depends on the validity of several assumptions made by the researchers and on the ability of the GRSs used in the study to explain variations in CRP level. Importantly, however, these findings suggest that interventions designed to lower CRP level are unlikely to decrease the risk of people developing the majority of common complex somatic and neuropsychiatric outcomes. Additional Information This list of resources contains links that can be accessed when viewing the PDF on a device or via the online version of the article at http://dx.doi.org/10.1371/journal.pmed.1001976. Wikipedia has pages on inflammation, C-reactive protein, and Mendelian randomization (note: Wikipedia is a free online encyclopedia that anyone can edit; available in several languages) The MedlinePlus encyclopedia has a page on C-reactive protein (in English and Spanish) The American Heart Association provides a short article on inflammation and heart disease A UK National Health Service “Behind the Headlines” article explains a recent study that found an association between immune activity in the brain and schizophrenia
Published: 2016
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2. Generalization and Dilution of Association Results from European GWAS in Populations of Non-European Ancestry: The PAGE Study

Author: Christopher S Carlson, Tara C Matise, Kari E North, Christopher A Haiman, Megan D Fesinmeyer, Steven Buyske, Fredrick R Schumacher, Ulrike Peters, Nora Franceschini, Marylyn D Ritchie, David J Duggan, Kylee L Spencer, Logan Dumitrescu, Charles B Eaton, Fridtjof Thomas, Alicia Young, Cara Carty, Gerardo Heiss, Loic Le Marchand, Dana C Crawford, Lucia A Hindorff, Charles L Kooperberg, and PAGE Consortium
Subjects: Native Hawaiian or Other Pacific Islander, QH301-705.5, Population, Population genetics, Genome-wide association study, Biology, Polymorphism, Single Nucleotide, White People, General Biochemistry, Genetics and Molecular Biology, Body Mass Index, 03 medical and health sciences, 0302 clinical medicine, Gene Frequency, Genetic variation, Genetic model, Humans, Genetic Predisposition to Disease, Biology (General), education, Allele frequency, 030304 developmental biology, Genetics, 0303 health sciences, education.field_of_study, Asian, General Immunology and Microbiology, General Neuroscience, Genetic Variation, Hispanic or Latino, Lipids, Genetic architecture, 3. Good health, Black or African American, Diabetes Mellitus, Type 2, Genetic epidemiology, Indians, North American, Synopsis, Metagenomics, General Agricultural and Biological Sciences, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract: The vast majority of genome-wide association study (GWAS) findings reported to date are from populations with European Ancestry (EA), and it is not yet clear how broadly the genetic associations described will generalize to populations of diverse ancestry. The Population Architecture Using Genomics and Epidemiology (PAGE) study is a consortium of multi-ancestry, population-based studies formed with the objective of refining our understanding of the genetic architecture of common traits emerging from GWAS. In the present analysis of five common diseases and traits, including body mass index, type 2 diabetes, and lipid levels, we compare direction and magnitude of effects for GWAS-identified variants in multiple non-EA populations against EA findings. We demonstrate that, in all populations analyzed, a significant majority of GWAS-identified variants have allelic associations in the same direction as in EA, with none showing a statistically significant effect in the opposite direction, after adjustment for multiple testing. However, 25% of tagSNPs identified in EA GWAS have significantly different effect sizes in at least one non-EA population, and these differential effects were most frequent in African Americans where all differential effects were diluted toward the null. We demonstrate that differential LD between tagSNPs and functional variants within populations contributes significantly to dilute effect sizes in this population. Although most variants identified from GWAS in EA populations generalize to all non-EA populations assessed, genetic models derived from GWAS findings in EA may generate spurious results in non-EA populations due to differential effect sizes. Regardless of the origin of the differential effects, caution should be exercised in applying any genetic risk prediction model based on tagSNPs outside of the ancestry group in which it was derived. Models based directly on functional variation may generalize more robustly, but the identification of functional variants remains challenging.
Published: 2013
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3. Genome-wide physical activity interactions in adiposity - A meta-analysis of 200,452 adults

Author: Graff, Mariaelisa, Scott, Robert A, Justice, Anne E, Young, Kristin L, Feitosa, Mary F, Barata, Llilda, Winkler, Thomas W, Chu, Audrey Y, Mahajan, Anubha, Hadley, David, Xue, Luting, Workalemahu, Tsegaselassie, Heard-Costa, Nancy L, Den Hoed, Marcel, Ahluwalia, Tarunveer S, Qi, Qibin, Ngwa, Julius S, Renström, Frida, Quaye, Lydia, Eicher, John D, Hayes, James E, Cornelis, Marilyn, Kutalik, Zoltan, Lim, Elise, Luan, Jian'an, Huffman, Jennifer E, Zhang, Weihua, Zhao, Wei, Griffin, Paula J, Haller, Toomas, Ahmad, Shafqat, Marques-Vidal, Pedro M, Bien, Stephanie, Yengo, Loic, Teumer, Alexander, Smith, Albert Vernon, Kumari, Meena, Harder, Marie Neergaard, Justesen, Johanne Marie, Kleber, Marcus E, Hollensted, Mette, Lohman, Kurt, Rivera, Natalia V, Whitfield, John B, Zhao, Jing Hua, Stringham, Heather M, Lyytikäinen, Leo-Pekka, Huppertz, Charlotte, Willemsen, Gonneke, Peyrot, Wouter J, Wu, Ying, Kristiansson, Kati, Demirkan, Ayse, Fornage, Myriam, Hassinen, Maija, Bielak, Lawrence F, Cadby, Gemma, Tanaka, Toshiko, Mägi, Reedik, Van Der Most, Peter J, Jackson, Anne U, Bragg-Gresham, Jennifer L, Vitart, Veronique, Marten, Jonathan, Navarro, Pau, Bellis, Claire, Pasko, Dorota, Johansson, Åsa, Snitker, Søren, Cheng, Yu-Ching, Eriksson, Joel, Lim, Unhee, Aadahl, Mette, Adair, Linda S, Amin, Najaf, Balkau, Beverley, Auvinen, Juha, Beilby, John, Bergman, Richard N, Bergmann, Sven, Bertoni, Alain G, Blangero, John, Bonnefond, Amélie, Bonnycastle, Lori L, Borja, Judith B, Brage, Søren, Busonero, Fabio, Buyske, Steve, Campbell, Harry, Chines, Peter S, Collins, Francis S, Corre, Tanguy, Smith, George Davey, Delgado, Graciela E, Dueker, Nicole, Dörr, Marcus, Ebeling, Tapani, Eiriksdottir, Gudny, Esko, Tõnu, Faul, Jessica D, Fu, Mao, Færch, Kristine, Gieger, Christian, Gläser, Sven, Gong, Jian, Gordon-Larsen, Penny, Grallert, Harald, Grammer, Tanja B, Grarup, Niels, Van Grootheest, Gerard, Harald, Kennet, Hastie, Nicholas D, Havulinna, Aki S, Hernandez, Dena, Hindorff, Lucia, Hocking, Lynne J, Holmens, Oddgeir L, Holzapfel, Christina, Hottenga, Jouke Jan, Huang, Jie, Huang, Tao, Hui, Jennie, Huth, Cornelia, Hutri-Kähönen, Nina, James, Alan L, Jansson, John-Olov, Jhun, Min A, Juonala, Markus, Kinnunen, Leena, Koistinen, Heikki A, Kolcic, Ivana, Komulainen, Pirjo, Kuusisto, Johanna, Kvaløy, Kirsti, Kähönen, Mika, Lakka, Timo A, Launer, Lenore J, Lehne, Benjamin, Lindgren, Cecilia M, Lorentzon, Mattias, Luben, Robert, Marre, Michel, Milaneschi, Yuri, Monda, Keri L, Montgomery, Grant W, De Moor, Marleen HM, Mulas, Antonella, Müller-Nurasyid, Martina, Musk, AW, Männikkö, Reija, Männistö, Satu, Narisu, Narisu, Nauck, Matthias, Nettleton, Jennifer A, Nolte, Ilja M, Oldehinkel, Albertine J, Olden, Matthias, Ong, Ken K, Padmanabhan, Sandosh, Paternoster, Lavinia, Perez, Jeremiah, Perola, Markus, Peters, Annette, Peters, Ulrike, Peyser, Patricia A, Prokopenko, Inga, Puolijoki, Hannu, Raitakari, Olli T, Rankinen, Tuomo, Rasmussen-Torvik, Laura J, Rawal, Rajesh, Ridker, Paul M, Rose, Lynda M, Rudan, Igor, Sarti, Cinzia, Sarzynski, Mark A, Savonen, Kai, Scott, William R, Sanna, Serena, Shuldiner, Alan R, Sidney, Steve, Silbernagel, Günther, Smith, Blair H, Smith, Jennifer A, Snieder, Harold, Stančáková, Alena, Sternfeld, Barbara, Swift, Amy J, Tammelin, Tuija, Tan, Sian-Tsung, Thorand, Barbara, Thuillier, Dorothée, Vandenput, Liesbeth, Vestergaard, Henrik, Van Vliet-Ostaptchouk, Jana V, Vohl, Marie-Claude, Völker, Uwe, Waeber, Gérard, Walker, Mark, Wild, Sarah, Wong, Andrew, Wright, Alan F, Zillikens, M Carola, Zubair, Niha, Haiman, Christopher A, Lemarchand, Loic, Gyllensten, Ulf, Ohlsson, Claes, Hofman, Albert, Rivadeneira, Fernando, Uitterlinden, André G, Pérusse, Louis, Wilson, James F, Hayward, Caroline, Polasek, Ozren, Cucca, Francesco, Hveem, Kristian, Hartman, Catharina A, Tönjes, Anke, Bandinelli, Stefania, Palmer, Lyle J, Kardia, Sharon LR, Rauramaa, Rainer, Sørensen, Thorkild IA, Tuomilehto, Jaakko, Salomaa, Veikko, Penninx, Brenda WJH, De Geus, Eco JC, Boomsma, Dorret I, Lehtimäki, Terho, Mangino, Massimo, Laakso, Markku, Bouchard, Claude, Martin, Nicholas G, Kuh, Diana, Liu, Yongmei, Linneberg, Allan, März, Winfried, Strauch, Konstantin, Kivimäki, Mika, Harris, Tamara B, Gudnason, Vilmundur, Völzke, Henry, Qi, Lu, Järvelin, Marjo-Riitta, Chambers, John C, Kooner, Jaspal S, Froguel, Philippe, Kooperberg, Charles, Vollenweider, Peter, Hallmans, Göran, Hansen, Torben, Pedersen, Oluf, Metspalu, Andres, Wareham, Nicholas J, Langenberg, Claudia, Weir, David R, Porteous, David J, Boerwinkle, Eric, Chasman, Daniel I, CHARGE Consortium, EPIC-InterAct Consortium, PAGE Consortium, Abecasis, Gonçalo R, Barroso, Inês, McCarthy, Mark I, Frayling, Timothy M, O'Connell, Jeffrey R, Van Duijn, Cornelia M, Boehnke, Michael, Heid, Iris M, Mohlke, Karen L, Strachan, David P, Fox, Caroline S, Liu, Ching-Ti, Hirschhorn, Joel N, Klein, Robert J, Johnson, Andrew D, Borecki, Ingrid B, Franks, Paul W, North, Kari E, Cupples, L Adrienne, Loos, Ruth JF, and Kilpeläinen, Tuomas O
Subjects: Epigenomics, Male, Genotype, Waist-Hip Ratio, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, 3. Good health, Body Mass Index, Humans, Female, Genetic Predisposition to Disease, Obesity, Waist Circumference, Exercise, Adiposity, Genome-Wide Association Study
Abstract: Physical activity (PA) may modify the genetic effects that give rise to increased risk of obesity. To identify adiposity loci whose effects are modified by PA, we performed genome-wide interaction meta-analyses of BMI and BMI-adjusted waist circumference and waist-hip ratio from up to 200,452 adults of European (n = 180,423) or other ancestry (n = 20,029). We standardized PA by categorizing it into a dichotomous variable where, on average, 23% of participants were categorized as inactive and 77% as physically active. While we replicate the interaction with PA for the strongest known obesity-risk locus in the FTO gene, of which the effect is attenuated by ~30% in physically active individuals compared to inactive individuals, we do not identify additional loci that are sensitive to PA. In additional genome-wide meta-analyses adjusting for PA and interaction with PA, we identify 11 novel adiposity loci, suggesting that accounting for PA or other environmental factors that contribute to variation in adiposity may facilitate gene discovery.

4. Understanding pneumococcal serotype 1 biology through population genomic analysis

Author: Chaguza, Chrispin, Cornick, Jennifer E., Harris, Simon R., Andam, Cheryl P., Bricio-Moreno, Laura, Yang, Marie, Yalcin, Feyruz, Ousmane, Sani, Govindpersad, Shanil, Senghore, Madikay, Ebruke, Chinelo, Du Plessis, Mignon, Kiran, Anmol M., Pluschke, Gerd, Sigauque, Betuel, McGee, Lesley, Klugman, Keith P., Turner, Paul, Corander, Jukka, Parkhill, Julian, Collard, Jean-Marc, Antonio, Martin, von Gottberg, Anne, Heyderman, Robert S., French, Neil, Kadioglu, Aras, Hanage, William P., Everett, Dean B., Bentley, Stephen D., and PAGe Consortium
Subjects: 2. Zero hunger, 3. Good health

5. Understanding pneumococcal serotype 1 biology through population genomic analysis

Author: Chaguza, Chrispin, Cornick, Jennifer E, Harris, Simon R, Andam, Cheryl P, Bricio-Moreno, Laura, Yang, Marie, Yalcin, Feyruz, Ousmane, Sani, Govindpersad, Shanil, Senghore, Madikay, Ebruke, Chinelo, Du Plessis, Mignon, Kiran, Anmol M, Pluschke, Gerd, Sigauque, Betuel, McGee, Lesley, Klugman, Keith P, Turner, Paul, Corander, Jukka, Parkhill, Julian, Collard, Jean-Marc, Antonio, Martin, Von Gottberg, Anne, Heyderman, Robert S, French, Neil, Kadioglu, Aras, Hanage, William P, Everett, Dean B, Bentley, Stephen D, and PAGe Consortium
Subjects: 2. Zero hunger, Recombination, Genetic, Asia, Antibiotic resistance, Evolution, Tetracycline Resistance, ST217, Genetic Variation, Serogroup, Pneumococcal Infections, 3. Good health, Phylogeography, Pneumococcal serotype 1, Streptococcus pneumoniae, Nasopharynx, Africa, Drug Resistance, Bacterial, Humans, Selection, Genetic, Phylogeny
Abstract: BACKGROUND: Pneumococcus kills over one million children annually and over 90 % of these deaths occur in low-income countries especially in Sub-Saharan Africa (SSA) where HIV exacerbates the disease burden. In SSA, serotype 1 pneumococci particularly the endemic ST217 clone, causes majority of the pneumococcal disease burden. To understand the evolution of the virulent ST217 clone, we analysed ST217 whole genomes from isolates sampled from African and Asian countries. METHODS: We analysed 226 whole genome sequences from the ST217 lineage sampled from 9 African and 4 Asian countries. We constructed a whole genome alignment and used it for phylogenetic and coalescent analyses. We also screened the genomes to determine presence of antibiotic resistance conferring genes. RESULTS: Population structure analysis grouped the ST217 isolates into five sequence clusters (SCs), which were highly associated with different geographical regions and showed limited intracontinental and intercontinental spread. The SCs showed lower than expected genomic sequence, which suggested strong purifying selection and small population sizes caused by bottlenecks. Recombination rates varied between the SCs but were lower than in other successful clones such as PMEN1. African isolates showed higher prevalence of antibiotic resistance genes than Asian isolates. Interestingly, certain West African isolates harbored a defective chloramphenicol and tetracycline resistance-conferring element (Tn5253) with a deletion in the loci encoding the chloramphenicol resistance gene (cat pC194), which caused lower chloramphenicol than tetracycline resistance. Furthermore, certain genes that promote colonisation were absent in the isolates, which may contribute to serotype 1's rarity in carriage and consequently its lower recombination rates. CONCLUSIONS: The high phylogeographic diversity of the ST217 clone shows that this clone has been in circulation globally for a long time, which allowed its diversification and adaptation in different geographical regions. Such geographic adaptation reflects local variations in selection pressures in different locales. Further studies will be required to fully understand the biological mechanisms which makes the ST217 clone highly invasive but unable to successfully colonise the human nasopharynx for long durations which results in lower recombination rates.

6. Investigating the Causal Relationship of C-Reactive Protein with 32 Complex Somatic and Psychiatric Outcomes: A Large-Scale Cross-Consortium Mendelian Randomization Study

Author: Prins, BP, Abbasi, A, Wong, A, Vaez, A, Nolte, I, Franceschini, N, Stuart, PE, Guterriez Achury, J, Mistry, V, Bradfield, JP, Valdes, AM, Bras, J, Shatunov, A, PAGE Consortium, International Stroke Genetics Consortium, Systemic Sclerosis Consortium, Treat OA Consortium, DIAGRAM Consortium, CARDIoGRAMplusC4D Consortium, ALS Consortium, International Parkinson’s Disease Genomics Consortium, Autism Spectrum Disorder Working Group Of The Psychiatric Genomics Consortium, CKDGen Consortium, GERAD1 Consortium, International Consortium For Blood Pressure, Schizophrenia Working Group Of The Psychiatric Genomics Consortium, Inflammation Working Group Of The CHARGE Consortium, Lu, C, Han, B, Raychaudhuri, S, Bevan, S, Mayes, MD, Tsoi, LC, Evangelou, E, Nair, RP, Grant, SFA, Polychronakos, C, Radstake, TRD, Van Heel, DA, Dunstan, ML, Wood, NW, Al-Chalabi, A, Dehghan, A, Hakonarson, H, Markus, HS, Elder, JT, Knight, J, Arking, DE, Spector, TD, Koeleman, BPC, Van Duijn, CM, Martin, J, Morris, AP, Weersma, RK, Wijmenga, C, Munroe, PB, Perry, JRB, Pouget, JG, Jamshidi, Y, Snieder, H, and Alizadeh, BZ
Subjects: C-Reactive Protein, Genotype, Heart Diseases, Immune System Diseases, Metabolic Diseases, Mental Disorders, Humans, Mendelian Randomization Analysis, Polymorphism, Single Nucleotide, 3. Good health, Genome-Wide Association Study
Abstract: BACKGROUND: C-reactive protein (CRP) is associated with immune, cardiometabolic, and psychiatric traits and diseases. Yet it is inconclusive whether these associations are causal. METHODS AND FINDINGS: We performed Mendelian randomization (MR) analyses using two genetic risk scores (GRSs) as instrumental variables (IVs). The first GRS consisted of four single nucleotide polymorphisms (SNPs) in the CRP gene (GRSCRP), and the second consisted of 18 SNPs that were significantly associated with CRP levels in the largest genome-wide association study (GWAS) to date (GRSGWAS). To optimize power, we used summary statistics from GWAS consortia and tested the association of these two GRSs with 32 complex somatic and psychiatric outcomes, with up to 123,865 participants per outcome from populations of European ancestry. We performed heterogeneity tests to disentangle the pleiotropic effect of IVs. A Bonferroni-corrected significance level of less than 0.0016 was considered statistically significant. An observed p-value equal to or less than 0.05 was considered nominally significant evidence for a potential causal association, yet to be confirmed. The strengths (F-statistics) of the IVs were 31.92-3,761.29 and 82.32-9,403.21 for GRSCRP and GRSGWAS, respectively. CRP GRSGWAS showed a statistically significant protective relationship of a 10% genetically elevated CRP level with the risk of schizophrenia (odds ratio [OR] 0.86 [95% CI 0.79-0.94]; p < 0.001). We validated this finding with individual-level genotype data from the schizophrenia GWAS (OR 0.96 [95% CI 0.94-0.98]; p < 1.72 × 10-6). Further, we found that a standardized CRP polygenic risk score (CRPPRS) at p-value thresholds of 1 × 10-4, 0.001, 0.01, 0.05, and 0.1 using individual-level data also showed a protective effect (OR < 1.00) against schizophrenia; the first CRPPRS (built of SNPs with p < 1 × 10-4) showed a statistically significant (p < 2.45 × 10-4) protective effect with an OR of 0.97 (95% CI 0.95-0.99). The CRP GRSGWAS showed that a 10% increase in genetically determined CRP level was significantly associated with coronary artery disease (OR 0.88 [95% CI 0.84-0.94]; p < 2.4 × 10-5) and was nominally associated with the risk of inflammatory bowel disease (OR 0.85 [95% CI 0.74-0.98]; p < 0.03), Crohn disease (OR 0.81 [95% CI 0.70-0.94]; p < 0.005), psoriatic arthritis (OR 1.36 [95% CI 1.00-1.84]; p < 0.049), knee osteoarthritis (OR 1.17 [95% CI 1.01-1.36]; p < 0.04), and bipolar disorder (OR 1.21 [95% CI 1.05-1.40]; p < 0.007) and with an increase of 0.72 (95% CI 0.11-1.34; p < 0.02) mm Hg in systolic blood pressure, 0.45 (95% CI 0.06-0.84; p < 0.02) mm Hg in diastolic blood pressure, 0.01 ml/min/1.73 m2 (95% CI 0.003-0.02; p < 0.005) in estimated glomerular filtration rate from serum creatinine, 0.01 g/dl (95% CI 0.0004-0.02; p < 0.04) in serum albumin level, and 0.03 g/dl (95% CI 0.008-0.05; p < 0.009) in serum protein level. However, after adjustment for heterogeneity, neither GRS showed a significant effect of CRP level (at p < 0.0016) on any of these outcomes, including coronary artery disease, nor on the other 20 complex outcomes studied. Our study has two potential limitations: the limited variance explained by our genetic instruments modeling CRP levels in blood and the unobserved bias introduced by the use of summary statistics in our MR analyses. CONCLUSIONS: Genetically elevated CRP levels showed a significant potentially protective causal relationship with risk of schizophrenia. We observed nominal evidence at an observed p < 0.05 using either GRSCRP or GRSGWAS-with persistence after correction for heterogeneity-for a causal relationship of elevated CRP levels with psoriatic osteoarthritis, rheumatoid arthritis, knee osteoarthritis, systolic blood pressure, diastolic blood pressure, serum albumin, and bipolar disorder. These associations remain yet to be confirmed. We cannot verify any causal effect of CRP level on any of the other common somatic and neuropsychiatric outcomes investigated in the present study. This implies that interventions that lower CRP level are unlikely to result in decreased risk for the majority of common complex outcomes.

7. The global distribution and diversity of protein vaccine candidate antigens in the highly virulent Streptococcus pnuemoniae serotype 1

Author: Cornick, Jennifer E., Tastan Bishop, Özlem, Yalcin, Feyruz, Kiran, Anmol M., Kumwenda, Benjamin, Chaguza, Chrispin, Govindpershad, Shanil, Ousmane, Sani, Senghore, Madikay, du Plessis, Mignon, Pluschke, Gerd, Ebruke, Chinelo, McGee, Lesley, Sigaùque, Beutel, Collard, Jean-Marc, Bentley, Stephen D., Kadioglu, Aras, Antonio, Martin, von Gottberg, Anne, French, Neil, Klugman, Keith P., Heyderman, Robert S., Alderson, Mark, Everett, Dean B., and PAGe consortium
Subjects: 3. Good health

8. Genetic studies of body mass index yield new insights for obesity biology

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G, Kretzler, Matthias, Fraser, Ross M, Colhoun, Helen M, Panduru, Nicolae Mircea, Gu, Harvest F, Brismar, Kerstin, Zerbini, Gianpaolo, Hadjadj, Samy, Marre, Michel, Groop, Leif, Lajer, Maria, Bull, Shelley B, Garcia, Melissa E, Waggott, Daryl, Paterson, Andrew D, Savage, David A, Bain, Stephen C, Martin, Finian, Hirschhorn, Joel N, Godson, Catherine, Florez, Jose C, Groop, Per-Henrik, Maxwell, Alexander P, Geller, Frank, Willer, Cristen J, Schmidt, Ellen M, Sengupta, Sebanti, Peloso, Gina M, Gustafsson, Stefan, Kanoni, Stavroula, Ganna, Andrea, Chen, Jin, Buchkovich, Martin L, Mora, Samia, Giedraitis, Vilmantas, Beckmann, Jacques S, Bragg-Gresham, Jennifer L, Chang, Hsing-Y, Demirkan, Ayşe, Den Hertog, Heleen M, Do, Ron, Donnelly, Louise A, Ehret, Georg B, Esko, Tõnu, Feitosa, Mary F, Gigante, Bruna, Ferreira, Teresa, Fischer, Krista, Fontanillas, Pierre, Freitag, Daniel F, Gurdasani, Deepti, Heikkilä, Kauko, Hyppönen, Elina, Isaacs, Aaron, Jackson, Anne U, Esko, Tonu, Go, Alan S, 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EN., Warrington, NM., Alavere, H., Barroso, I., Berenson, GS., Blackburn, H., Busonero, F., Chen, W., Couper, D., Easton, DF., Eriksson, J., Foroud, T., Geller, F., Hernandez, DG., Kilpeläinen, TO., Li, S., Melbye, M., Murray, JC., Murray, SS., Nelis, M., Ness, AR., Northstone, K., Peacock, M., Pennell, CE., Pharoah, P., Rafnar, T., Rice, JP., Ring, SM., Schork, NJ., Segrè, AV., Sovio, U., Srinivasan, SR., Tammesoo, ML., Tyrer, J., van Meurs JB., Weedon, MN., Wichmann, H., Young, L., Bierut, LJ., Boyd, HA., Econs, MJ., Van T'Hooft, Ferdinand M., Njølstad, Inger, Abecasis, Gonçalo R., Barroso, Inɥ, The MIGEN Consortium, Investigator, Casari, GIORGIO NEVIO, Other departments, ACS - Amsterdam Cardiovascular Sciences, Vascular Medicine, Landsteiner Laboratory, Clinical Haematology, Damage and Repair in Cancer Development and Cancer Treatment (DARE), Guided Treatment in Optimal Selected Cancer Patients (GUTS), Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Life Course Epidemiology (LCE), Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Groningen Research Institute for Asthma and COPD (GRIAC), Groningen Institute for Organ Transplantation (GIOT), Lifestyle Medicine (LM), Groningen Kidney Center (GKC), Cardiovascular Centre (CVC), Center for Liver, Digestive and Metabolic Diseases (CLDM), Stem Cell Aging Leukemia and Lymphoma (SALL), Locke, A, Kahali, B, Berndt, S, Justice, A, Pers, T, Day, F, Powell, C, Vedantam, S, Buchkovich, M, Yang, J, Croteau-Chonka, D, Esko, T, Fall, T, Ferreira, T, Gustafsson, S, Kutalik, Z, Luan, J, Magi, R, Randall, J, Winkler, T, Wood, A, Workalemahu, T, Faul, J, Smith, J, Zhao, J, Zhao, W, Chen, J, Fehrmann, R, Hedman, A, Karjalainen, J, Schmidt, E, Absher, D, Amin, N, Anderson, D, Beekman, M, Bolton, J, Bragg-Gresham, J, Buyske, S, Demirkan, A, Deng, G, Ehret, G, Feenstra, B, Feitosa, M, Fischer, K, Goel, A, Gong, J, Jackson, A, Kanoni, S, Kleber, M, Kristiansson, K, Lim, U, Lotay, V, Mangino, M, Leach, I, Medina-Gomez, C, Medland, S, Nalls, M, Palmer, C, Pasko, D, Pechlivanis, S, Peters, M, Prokopenko, I, Shungin, D, Stancakova, A, Strawbridge, R, Sung, Y, Tanaka, T, Teumer, A, Trompet, S, van der Laan, S, van Setten, J, Van Vliet-Ostaptchouk, J, Wang, Z, Yengo, L, Zhang, W, Isaacs, A, Albrecht, E, Arnlov, J, Arscott, G, Attwood, A, Bandinelli, S, Barrett, A, Bas, I, Bellis, C, Bennett, A, Berne, C, Blagieva, R, Bluher, M, Bohringer, S, Bonnycastle, L, Bottcher, Y, Boyd, H, Bruinenberg, M, Caspersen, I, Chen, Y, Clarke, R, Daw, E, de Craen, A, Delgado, G, Dimitriou, M, Doney, A, Eklund, N, Estrada, K, Eury, E, Folkersen, L, Fraser, R, Garcia, M, Geller, F, Giedraitis, V, Gigante, B, Go, A, Golay, A, Goodall, A, Gordon, S, Gorski, M, Grabe, H, Grallert, H, Grammer, T, Grassler, J, Gronberg, H, Groves, C, Gusto, G, Haessler, J, Hall, P, Haller, T, Hallmans, G, Hartman, C, Hassinen, M, Hayward, C, Heard-Costa, N, Helmer, Q, Hengstenberg, C, Holmen, O, Hottenga, J, James, A, Jeff, J, Johansson, A, Jolley, J, Juliusdottir, T, Kinnunen, L, Koenig, W, Koskenvuo, M, Kratzer, W, Laitinen, J, Lamina, C, Leander, K, Lee, N, Lichtner, P, Lind, L, Lindstrom, J, Lo, K, Lobbens, S, Lorbeer, R, Lu, Y, Mach, F, Magnusson, P, Mahajan, A, Mcardle, W, Mclachlan, S, Menni, C, Merger, S, Mihailov, E, Milani, L, Moayyeri, A, Monda, K, Morken, M, Mulas, A, Muller, G, Muller-Nurasyid, M, Musk, A, Nagaraja, R, Nothen, M, Nolte, I, Pilz, S, Rayner, N, Renstrom, F, Rettig, R, Ried, J, Ripke, S, Robertson, N, Rose, L, Sanna, S, Scharnagl, H, Scholtens, S, Schumacher, F, Scott, W, Seufferlein, T, Shi, J, Smith, A, Smolonska, J, Stanton, A, Steinthorsdottir, V, Stirrups, K, Stringham, H, Sundstrom, J, Swertz, M, Swift, A, Syvanen, A, Tan, S, Tayo, B, Thorand, B, Thorleifsson, G, Tyrer, J, Uh, H, Vandenput, L, Verhulst, F, Vermeulen, S, Verweij, N, Vonk, J, Waite, L, Warren, H, Waterworth, D, Weedon, M, Wilkens, L, Willenborg, C, Wilsgaard, T, Wojczynski, M, Wong, A, 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Ormel, J, Rosmalen, J, Slaets, J, Lagou, V, Welch, R, Wheeler, E, Rehnberg, E, Rasmussen-Torvik, L, Lecoeur, C, Johnson, P, Sennblad, B, Salo, P, Timpson, N, Evans, D, St Pourcain, B, Bielak, L, Horikoshi, M, Navarro, P, Raychaudhuri, S, Chen, H, Rybin, D, Willems, S, Song, K, An, P, Marullo, L, Jansen, H, Pankow, J, Edkins, S, Varga, T, Oksa, H, Antonella, M, Kong, A, Herder, C, Antti, J, Small, K, Miljkovic, I, Atalay, M, Kiess, W, Smit, J, Campbell, S, Fowkes, G, Rathmann, W, Maerz, W, Watanabe, R, de Geus, E, Penninx, B, Toenjes, A, Peyser, P, Korner, A, Dupuis, J, Cucca, F, Balkau, B, Bouatia-Naji, N, Purcell, S, Musunuru, K, Ardissino, D, Mannucci, P, Anand, S, Engert, J, Morgan, T, Spertus, J, Stoll, M, Girelli, D, Mckeown, P, Patterson, C, Merlini, P, Berzuini, C, Bernardinelli, L, Peyvandi, F, Tubaro, M, Celli, P, Fetiveau, R, Marziliano, N, Casari, G, Galli, M, Ribichini, F, Rossi, M, Bernardi, F, Zonzin, P, Piazza, A, Yee, J, Friedlander, Y, Marrugat, J, Subirana, I, Sala, J, Ramos, R, Williams, G, Nathan, D, Macrae, C, Berglund, G, Asselta, R, Duga, S, Spreafico, M, Daly, M, Nemesh, J, Korn, J, Surti, A, Gianniny, L, Parkin, M, Burtt, N, Gabriel, S, Wright, B, Ball, S, Schunkert, I, Linsel-Nitschke, P, Lieb, W, Fischer, M, Grosshennig, A, Preuss, M, Scholz, M, Chen, Z, Wilensky, R, Matthai, W, Qasim, A, Hakonarson, H, Devaney, J, Pichard, A, Kent, K, Satler, L, Lindsay, J, Waksman, R, Knouff, C, Scheffold, T, Berger, K, Huge, A, Martinelli, N, Olivieri, O, Corrocher, R, Xie, C, Ahmadi, K, Ainali, C, Bataille, V, Bell, J, Buil, A, Dermitzakis, E, Dimas, A, Durbin, R, Glass, D, Hassanali, N, Ingle, C, Knowles, D, Krestyaninova, M, Lowe, C, Meduri, E, Di Meglio, P, Montgomery, S, Nestle, F, Nica, A, Nisbet, J, O'Rahilly, S, Parts, L, Potter, S, Sekowska, M, Shin, S, Surdulescu, G, Travers, M, Tsaprouni, L, Tsoka, S, Wilk, A, Yang, T, Higashio, J, Williams, R, Nato, A, Ambite, J, Deelman, E, Manolio, T, Heiss, G, Taylor, K, Avery, C, Graff, M, Lin, D, Quibrera, M, Cochran, B, Kao, L, Umans, J, Cole, S, Maccluer, J, Person, S, Gross, M, Fornage, M, Durda, P, Jenny, N, Patsy, B, Arnold, A, Buzkova, P, Haines, J, Murdock, D, Glenn, K, Brown-Gentry, K, Thornton-Wells, T, Dumitrescu, L, Bush, W, Mitchell, S, Goodloe, R, Wilson, S, Boston, J, Malinowski, J, Restrepo, N, Oetjens, M, Fowke, J, Spencer, K, Pendergrass, S, Le Marchand, L, Park, L, Tiirikainen, M, Kolonel, L, Cheng, I, Wang, H, Shohet, R, Stram, D, Henderson, B, Monroe, K, Anderson, G, Carlson, C, Prentice, R, Lacroix, A, Wu, C, Carty, C, Rosse, S, Young, A, Kocarnik, J, Lin, Y, Jackson, R, Duggan, D, Kuller, L, He, C, Sulem, P, Barbalic, M, Broer, L, Byrne, E, Gudbjartsson, D, Mcardle, P, Porcu, E, van Wingerden, S, Zhuang, W, Lauc, L, Broekmans, F, Burri, A, Chen, C, Corre, T, Coviello, A, D'Adamo, P, Davies, G, Deary, I, Ebrahim, S, Fauser, B, Ferreli, L, Folsom, A, Hankinson, S, Hass, M, Janssens, A, Karasik, D, Keyzer, J, Kiel, D, Lahti, J, Lai, S, Laisk, T, Laven, J, Liu, J, Lopez, L, Louwers, Y, Marongiu, M, Klaric, I, Masciullo, C, Melzer, D, Newman, A, Pare, G, Peeters, P, Pop, V, Raikkonen, K, Salumets, A, Stacey, S, Starr, J, Stathopoulou, M, Styrkarsdottir, U, Tenesa, A, Tryggvadottir, L, Tsui, K, van Dam, R, van Gils, C, van Nierop, P, Vink, J, Voorhuis, M, Widen, E, Wijnands-Van Gent, C, Yerges-Armstrong, L, Zgaga, L, Zygmunt, M, Buring, J, Crisponi, L, Demerath, E, Streeten, E, Murray, A, Visser, J, Lunetta, K, Elks, C, Cousminer, D, Koller, D, Lin, P, Smith, E, Warrington, N, Alavere, H, Berenson, G, Blackburn, H, Busonero, F, Chen, W, Couper, D, Easton, D, Foroud, T, Kilpelainen, T, Li, S, Murray, S, Ness, A, Northstone, K, Peacock, M, Pennell, C, Pharoah, P, Rafnar, T, Rice, J, Ring, S, Schork, N, Segre, A, Sovio, U, Srinivasan, S, Tammesoo, M, van Meurs, J, Young, L, Bierut, L, Econs, M, The ADIPOGen Consortium, The AGEN-BMI Working Group, The CARDIOGRAMplusC4D Consortium, The CKDGen Consortium, The GLGC, The ICBP, The MAGIC Investigators, The MuTHER Consortium, The MIGen Consortium, The PAGE Consortium, The ReproGen Consortium, The GENIE Consortium, The International Endogene Consortium, Berndt, Sonja I, Justice, Anne E, Hyppönen, Elina Tuulikki, Epidemiology and Data Science, NCA - Neurobiology of mental health, and EMGO - Lifestyle, overweight and diabetes
Subjects: Male, LOCI, Genome-wide association study, Continental Population Groups/genetics, VARIANTS, Body Mass Index, Insulin Secretion, Insulin, Age Factor, Adiposity, ddc:616, Adipogenesis, Genetic Predisposition to Disease/genetics, Synapse, 3. Good health, Continental Population Group, Urological cancers Radboud Institute for Health Sciences [Radboudumc 15], GENOME-WIDE ASSOCIATIONPROVIDES INSIGHTSGLYCEMIC TRAITSLOCIMETAANALYSISVARIANTSINDIVIDUALSHIPPOCAMPALARCHITECTURETOPIRAMATE, ddc:500, Adipogenesis/genetics, Single Nucleotide/genetics, Age Factors, Continental Population Groups, Energy Metabolism, Europe, Female, Genetic Predisposition to Disease, Glutamic Acid, Humans, Obesity, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Synapses, Genome-Wide Association Study, Multidisciplinary, genetics [Adiposity], Human, Socio-culturale, genetics [Energy Metabolism], ta3111, genetic, body mass index, obesity, SDG 3 - Good Health and Well-being, GLYCEMIC TRAITS, genetics [Continental Population Groups], Genetic variability, Polymorphism, GENOME-WIDE ASSOCIATION, genetics [Adipogenesis], METAANALYSIS, Genetic association, Adipogenesi, genetics [Quantitative Trait Loci], ta1184, metabolism [Glutamic Acid], ta1182, PATHWAYS, metabolism [Synapses], ta3121, medicine.disease, metabolism [Insulin], Adiposity/genetics, Clinical Medicine, Quantitative Trait Loci/genetics, Body mass index, HUMAN HEIGHT, BIO/12 - BIOCHIMICA CLINICA E BIOLOGIA MOLECOLARE CLINICA, Synapses/metabolism, Medizin, Obesity/genetics, Bioinformatics, genetic basis, Obesity/metabolism, genetics [Obesity], body mass index (BMI), genetics [Genetic Predisposition to Disease], ethnology [Europe], 2. Zero hunger, Genetics, ARCHITECTURE, Genetics of obesity, Medicine (all), Single Nucleotide, Polymorphism, Single Nucleotide/genetics, Insulin/metabolism/secretion, Glutamic Acid/metabolism, genetics [Polymorphism, Single Nucleotide], EXPRESSION, Insulin/metabolism, PROVIDES INSIGHTS, genetics [Racial Groups], Biology, Obesity/genetics/metabolism, Europe/ethnology, metabolism [Obesity], Mendelian randomization, medicine, Energy Metabolism/genetics, body mass, genetic analysis, obesity, Klinisk medicin
Abstract: Item does not contain fulltext Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P < 5 x 10(-8)), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for approximately 2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.
Published: 2015
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9. Genome-wide physical activity interactions in adiposity - A meta-analysis of 200,452 adults

Author: Amélie Bonnefond, Nancy L. Heard-Costa, Julius S. Ngwa, Jennifer E. Huffman, Tanja B. Grammer, Jaakko Tuomilehto, Lu Qi, Nicholas G. Martin, Massimo Mangino, Henrik Vestergaard, Penny Gordon-Larsen, Reedik Mägi, Natalia V. Rivera, Charles Kooperberg, Alain G. Bertoni, Sarah H. Wild, Robert Luben, Veikko Salomaa, Claude Bouchard, Lynda M. Rose, Patricia A. Peyser, Graciela E. Delgado, Jessica D. Faul, Tuija Tammelin, John C. Chambers, Tsegaselassie Workalemahu, Kari E. North, David J. Porteous, Peter Vollenweider, Kennet Harald, Claire Bellis, Serena Sanna, Nicholas D. Hastie, Robert J. Klein, Marie-Claude Vohl, Ruth J. F. Loos, Jian Gong, Igor Rudan, Unhee Lim, Christopher A. Haiman, Martina Müller-Nurasyid, Konstantin Strauch, Mark A. Sarzynski, Albert V. Smith, Mark Walker, Tapani Ebeling, Göran Hallmans, Nicole Dueker, Caroline S. Fox, Sven Bergmann, Keri L. Monda, Thorkild I. A. Sørensen, André G. Uitterlinden, Johanne Marie Justesen, Aki S. Havulinna, Torben Hansen, Ivana Kolcic, Cecilia M. Lindgren, Marcel den Hoed, Richard N. Bergman, Mariaelisa Graff, Alan R. Shuldiner, Dorota Pasko, James F. Wilson, John Whitfield, Joel Eriksson, Jaspal S. Kooner, Mette Hollensted, Winfried März, Gonçalo R. Abecasis, Weihua Zhang, Harold Snieder, Rajesh Rawal, Tao Huang, Åsa Johansson, Lydia Quaye, Ying Wu, Benjamin Lehne, Matthias Nauck, Caroline Hayward, Linda S. Adair, Michel Marre, Tanguy Corre, Alan James, Frida Renström, Jian'an Luan, Zoltán Kutalik, Kurt Lohman, Jennifer A. Smith, Mao Fu, Jennifer L. Bragg-Gresham, Tamara B. Harris, Claudia Langenberg, Tõnu Esko, Mattias Lorentzon, Ken K. Ong, Blair H. Smith, Fabio Busonero, Alan F. Wright, Gemma Cadby, Andrew D. Johnson, Steve Buyske, Anubha Mahajan, Antonella Mulas, Gérard Waeber, Lori L. Bonnycastle, Daniel I. Chasman, Jennie Hui, Audrey Y. Chu, Uwe Völker, Albertine J. Oldehinkel, Jing Hua Zhao, Robert A. Scott, Ilja M. Nolte, Loic LeMarchand, Yu-Ching Cheng, David P. Strachan, Jie Huang, Gerard van Grootheest, John D. Eicher, Marcus E. Kleber, Francis S. Collins, Cornelia M. van Duijn, Timothy M. Frayling, Pau Navarro, Leo-Pekka Lyytikäinen, Cinzia Sarti, Paul M. Ridker, John-Olov Jansson, Shafqat Ahmad, Philippe Froguel, Albert Hofman, Inga Prokopenko, Vilmundur Gudnason, Anne U. Jackson, David R. Weir, Lyle J. Palmer, Alexander Teumer, Ulf Gyllensten, Mette Aadahl, Niels Grarup, Beverley Balkau, Oluf Pedersen, Cornelia Huth, Dorret I. Boomsma, Harry Campbell, Charlotte Huppertz, Ingrid B. Borecki, Juha Auvinen, Soren Snitker, Yuri Milaneschi, Iris M. Heid, Barbara Thorand, Wouter J. Peyrot, Lavinia Paternoster, Sian-Tsung Tan, Anne E. Justice, Dena G. Hernandez, Marcus Dörr, Nicholas J. Wareham, Marilyn C. Cornelis, Claes Ohlsson, Amy J. Swift, Ozren Polasek, Brenda W.J.H. Penninx, James E. Hayes, Stephanie A. Bien, Jana V. van Vliet-Ostaptchouk, Eric Boerwinkle, Louis Pérusse, Peter J. van der Most, Ulrike Peters, Pirjo Komulainen, Lynne J. Hocking, Catharina A. Hartman, William R. Scott, Jeffrey R. O'Connell, Stefania Bandinelli, Tuomo Rankinen, Timo A. Lakka, Leena Kinnunen, Markus Perola, John Blangero, Sharon L.R. Kardia, Veronique Vitart, Mika Kähönen, Marie Neergaard Harder, Diana Kuh, Kai Savonen, Kristin L. Young, Jeremiah Perez, Nina Hutri-Kähönen, George Davey Smith, Toshiko Tanaka, Barbara Sternfeld, Jennifer A. Nettleton, Jouke-Jan Hottenga, Christian Gieger, Gonneke Willemsen, Soren Brage, Mika Kivimäki, Lucia A. Hindorff, Steve Sidney, Tarunveer S. Ahluwalia, Liesbeth Vandenput, Loic Yengo, Markku Laakso, Yongmei Liu, Arthur W. Musk, Harald Grallert, Kirsti Kvaløy, Rainer Rauramaa, Satu Männistö, Tuomas O. Kilpeläinen, M. Carola Zillikens, Hannu Puolijoki, Luting Xue, Oddgeir L. Holmens, Sandosh Padmanabhan, Inês Barroso, Ching-Ti Liu, L. Adrienne Cupples, Judith B. Borja, Karen L. Mohlke, Matthias Olden, Henry Völzke, Myriam Fornage, Michael Boehnke, Pedro Marques-Vidal, John Beilby, Fernando Rivadeneira, Maija Hassinen, Najaf Amin, Kristian Hveem, Gudny Eiriksdottir, Lenore J. Launer, Johanna Kuusisto, Dorothée Thuillier, Heather M. Stringham, Sven Gläser, Min A. Jhun, Marjo-Riitta Järvelin, Niha Zubair, Annette Peters, Llilda Barata, Paula J. Griffin, Markus Juonala, Wei Zhao, Andres Metspalu, Christina Holzapfel, Lawrence F. Bielak, Thomas W. Winkler, Alena Stančáková, Anke Tönjes, Narisu Narisu, David Hadley, Peter S. Chines, Andrew Wong, Günther Silbernagel, Kati Kristiansson, Eco J. C. de Geus, Grant W. Montgomery, Elise Lim, Laura J. Rasmussen-Torvik, Terho Lehtimäki, Heikki A. Koistinen, Meena Kumari, Qibin Qi, Ayse Demirkan, Francesco Cucca, Allan Linneberg, Reija Männikkö, Jonathan Marten, Olli T. Raitakari, Mary F. Feitosa, Paul W. Franks, Kristine Færch, Mark I. McCarthy, Marleen H.M. de Moor, Joel N. Hirschhorn, Toomas Haller, Graff, Mariaelisa [0000-0001-6380-1735], Young, Kristin L [0000-0003-0070-6145], Winkler, Thomas W [0000-0003-0292-5421], Heard-Costa, Nancy L [0000-0001-9730-0306], Renström, Frida [0000-0001-6053-298X], Barroso, Inês [0000-0001-5800-4520], Strachan, David P [0000-0001-7854-1366], Liu, Ching-Ti [0000-0002-0703-0742], Klein, Robert J [0000-0003-3539-5391], Apollo - University of Cambridge Repository, University of Helsinki, Institute for Molecular Medicine Finland, Quantitative Genetics, Clinicum, Department of Medicine, Endokrinologian yksikkö, HUS Internal Medicine and Rehabilitation, Complex Disease Genetics, Læknadeild (HÍ), Faculty of Medicine (UI), Heilbrigðisvísindasvið (HÍ), School of Health Sciences (UI), Háskóli Íslands, University of Iceland, CHARGE Consortium, EPIC-InterAct Consortium, PAGE Consortium, Edwards, Todd L., Biological Psychology, APH - Mental Health, APH - Health Behaviors & Chronic Diseases, APH - Personalized Medicine, Amsterdam Neuroscience - Mood, Anxiety, Psychosis, Stress & Sleep, Clinical Child and Family Studies, APH - Methodology, School of Medicine / Biomedicine, Public and occupational health, Psychiatry, Amsterdam Neuroscience - Complex Trait Genetics, APH - Digital Health, Life Course Epidemiology (LCE), Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Center for Liver, Digestive and Metabolic Diseases (CLDM), Epidemiology, Medical Microbiology & Infectious Diseases, Erasmus MC other, Child and Adolescent Psychiatry / Psychology, and Internal Medicine
Subjects: Netherlands Twin Register (NTR), Epigenomics, Male, Genome-wide association study, genome, obesity, BMI, Body Mass Index, 0302 clinical medicine, Cell Signaling, Public and Occupational Health, GENE-EXPRESSION, Adiposity, Genetics & Heredity, ADIPOCYTE DIFFERENTIATION, 1184 Genetics, developmental biology, physiology, Genomics, Functional Genomics, 3. Good health, Meta-analysis, Physical Sciences, REACTIVE PROTEIN-LEVELS, Waist Circumference, Statistics (Mathematics), Waist, Genotype, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Single-nucleotide polymorphism, Locus (genetics), BINDING PROTEIN, 03 medical and health sciences, SDG 3 - Good Health and Well-being, Genome-Wide Association Studies, Genetics, Humans, Statistical Methods, Molecular Biology, Exercise, Ecology, Evolution, Behavior and Systematics, 0604 Genetics, Science & Technology, ASSOCIATION METAANALYSIS, Physical activity, ta1184, Biology and Life Sciences, Computational Biology, Physical Activity, 030104 developmental biology, Genetic Loci, Body mass index, Mathematics, 030217 neurology & neurosurgery, Meta-Analysis, Developmental Biology, BODY-MASS INDEX, IDENTICAL-TWINS, ACTIVITY QUESTIONNAIRES, FAT DISTRIBUTION, FOOD-INTAKE, 0301 basic medicine, Cancer Research, Medicin och hälsovetenskap, Offita, Physiology, FTO gene, Genome-wide association studies, Medical and Health Sciences, Mathematical and Statistical Techniques, Waist–hip ratio, Medicine and Health Sciences, Genetics (clinical), Public Health, Global Health, Social Medicine and Epidemiology, Physiological Parameters, Female, Genomic Signal Processing, Life Sciences & Biomedicine, Research Article, Signal Transduction, lcsh:QH426-470, Biology, Research and Analysis Methods, Hreyfing (heilsurækt), Journal Article, Erfðafræði, Genetic Predisposition to Disease, Obesity, Waist-Hip Ratio, Body Weight, Human Genetics, Cell Biology, Rannsóknir, Genome Analysis, lcsh:Genetics, Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi, 3111 Biomedicine, Genome-Wide Association Study
Abstract: Physical activity (PA) may modify the genetic effects that give rise to increased risk of obesity. To identify adiposity loci whose effects are modified by PA, we performed genome-wide interaction meta-analyses of BMI and BMI-adjusted waist circumference and waist-hip ratio from up to 200,452 adults of European (n = 180,423) or other ancestry (n = 20,029). We standardized PA by categorizing it into a dichotomous variable where, on average, 23% of participants were categorized as inactive and 77% as physically active. While we replicate the interaction with PA for the strongest known obesity-risk locus in the FTO gene, of which the effect is attenuated by ~30% in physically active individuals compared to inactive individuals, we do not identify additional loci that are sensitive to PA. In additional genome-wide meta-analyses adjusting for PA and interaction with PA, we identify 11 novel adiposity loci, suggesting that accounting for PA or other environmental factors that contribute to variation in adiposity may facilitate gene discovery., The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services. Funding for this study was provided by the Aase and Ejner Danielsens Foundation; Academy of Finland (102318; 104781, 120315, 123885, 129619, 286284, 134309, 126925, 121584, 124282, 129378, 117787, 250207, 258753, 41071, 77299, 124243, 1114194, 24300796); Accare Center for Child and Adolescent Psychiatry; Action on Hearing Loss (G51); Agence Nationale de la Recherche; Agency for Health Care Policy Research (HS06516); Age UK Research into Ageing Fund; Åke Wiberg Foundation; ALF/LUA Research Grant in Gothenburg; ALFEDIAM; ALK-Abello´ A/S (Hørsholm, Denmark); American Heart Association (13POST16500011, 10SDG269004); Ardix Medical; Arthritis Research UK; Association Diabète Risque Vasculaire; AstraZeneca; Australian Associated Brewers; Australian National Health and Medical Research Council (241944, 339462, 389927, 389875, 389891, 389892, 389938, 442915, 442981, 496739, 552485, 552498); Avera Research Institute; Bayer Diagnostics; Becton Dickinson; Biobanking and Biomolecular Resources Research Infrastructure (BBMRI –NL, 184.021.007); Biocentrum Helsinki; Boston Obesity Nutrition Research Center (DK46200); British Heart Foundation (RG/10/12/28456, SP/04/002); Canada Foundation for Innovation; Canadian Institutes of Health Research (FRN-CCT-83028); Cancer Research UK; Cardionics; Center for Medical Systems Biology; Center of Excellence in Complex Disease Genetics and SALVECenter of Excellence in Genomics (EXCEGEN); Chief Scientist Office of the Scottish Government; City of Kuopio; Cohortes Santé TGIR; Contrat de Projets État-Région; Croatian Science Foundation (8875); Danish Agency for Science, Technology and Innovation; Danish Council for Independent Research (DFF–1333-00124, DFF–1331-007308); Danish Diabetes Academy; Danish Medical Research Council; Department of Psychology and Education of the VU University Amsterdam; Diabetes Hilfs- und Forschungsfonds Deutschland; Dutch Brain Foundation; Dutch Ministry of Justice; Emil Aaltonen Foundation; Erasmus Medical Center; Erasmus University; Estonian Government (IUT20-60, IUT24-6); Estonian Ministry of Education and Research (3.2.0304.11-0312); European Commission (230374, 284167, 323195, 692145, FP7 EurHEALTHAgeing-277849, FP7 BBMRI-LPC 313010, nr 602633, HEALTH-F2-2008-201865-GEFOS, HEALTH-F4-2007-201413, FP6 LSHM-CT-2004-005272, FP5 QLG2-CT-2002-01254, FP6 LSHG-CT-2006-01947, FP7 HEALTH-F4-2007-201413, FP7 279143, FP7 201668, FP7 305739, FP6 LSHG-CT-2006-018947, HEALTH-F4-2007-201413, QLG1-CT-2001-01252); European Regional Development Fund; European Science Foundation (EuroSTRESS project FP-006, ESF, EU/QLRT-2001-01254); Faculty of Biology and Medicine of Lausanne; Federal Ministry of Education and Research (01ZZ9603, 01ZZ0103, 01ZZ0403, 03ZIK012, 03IS2061A); Federal State of Mecklenburg - West Pomerania; Fédération Française de Cardiologie; Finnish Cultural Foundation; Finnish Diabetes Association; Finnish Foundation of Cardiovascular Research; Finnish Heart Association; Food Standards Agency; Fondation de France; Fonds Santé; Genetic Association Information Network of the Foundation for the National Institutes of Health; German Diabetes Association; German Federal Ministry of Education and Research (BMBF, 01ER1206, 01ER1507); German Research Council (SFB-1052, SPP 1629 TO 718/2-1); GlaxoSmithKline; Göran Gustafssons Foundation; Göteborg Medical Society; Health and Safety Executive; Heart Foundation of Northern Sweden; Icelandic Heart Association; Icelandic Parliament; Imperial College Healthcare NHS Trust; INSERM, Réseaux en Santé Publique, Interactions entre les déterminants de la santé; Interreg IV Oberrhein Program (A28); Italian Ministry of Economy and Finance; Italian Ministry of Health (ICS110.1/RF97.71); John D and Catherine T MacArthur Foundation; Juho Vainio Foundation; King's College London; Kjell och Märta Beijers Foundation; Kuopio University Hospital; Kuopio, Tampere and Turku University Hospital Medical Funds (X51001); Leiden University Medical Center; Lilly; LMUinnovativ; Lundbeck Foundation; Lundberg Foundation; Medical Research Council of Canada; MEKOS Laboratories (Denmark); Merck Santé; Mid-Atlantic Nutrition Obesity Research Center (P30 DK72488); Ministère de l’Économie, de l’Innovation et des Exportations; Ministry for Health, Welfare and Sports of the Netherlands; Ministry of Cultural Affairs of the Federal State of Mecklenburg-West Pomerania; Ministry of Education and Culture of Finland (627;2004-2011); Ministry of Education, Culture and Science of the Netherlands; MRC Human Genetics Unit; MRC-GlaxoSmithKline Pilot Programme Grant (G0701863); Municipality of Rotterdam; Netherlands Bioinformatics Centre (2008.024); Netherlands Consortium for Healthy Aging (050-060-810); Netherlands Genomics Initiative; Netherlands Organisation for Health Research and Development (904-61-090, 985-10-002, 904-61-193, 480-04-004, 400-05-717, Addiction-31160008, Middelgroot-911-09-032, Spinozapremie 56-464-14192); Netherlands Organisation for Health Research and Development (2010/31471/ZONMW); Netherlands Organisation for Scientific Research (10-000-1002, GB-MW 940-38-011, 100-001-004, 60-60600-97-118, 261-98-710, GB-MaGW 480-01-006, GB-MaGW 480-07-001, GB-MaGW 452-04-314, GB-MaGW 452-06-004, 175.010.2003.005, 175.010.2005.011, 481-08-013, 480-05-003, 911-03-012); Neuroscience Campus Amsterdam; NHS Foundation Trust; Novartis Pharmaceuticals; Novo Nordisk; Office National Interprofessionel des Vins; Paavo Nurmi Foundation; Påhlssons Foundation; Päivikki and Sakari Sohlberg Foundation; Pierre Fabre; Republic of Croatia Ministry of Science, Education and Sport (108-1080315-0302); Research Centre for Prevention and Health, the Capital Region for Denmark; Research Institute for Diseases in the Elderly (014-93-015, RIDE2); Roche; Russian Foundation for Basic Research (NWO-RFBR 047.017.043); Rutgers University Cell and DNA Repository (NIMH U24 MH068457-06); Sanofi-Aventis; Scottish Executive Health Department (CZD/16/6); Siemens Healthcare; Social Insurance Institution of Finland (4/26/2010); Social Ministry of the Federal State of Mecklenburg-West Pomerania; Société Francophone du Diabète; State of Bavaria; Stroke Association; Swedish Diabetes Association; Swedish Foundation for Strategic Research; Swedish Heart-Lung Foundation (20140543); Swedish Research Council (2015-03657); Swedish Medical Research Council (K2007-66X-20270-01-3, 2011-2354); Swedish Society for Medical Research; Swiss National Science Foundation (33CSCO-122661, 33CS30-139468, 33CS30-148401); Tampere Tuberculosis Foundation; The Marcus Borgström Foundation; The Royal Society; The Wellcome Trust (084723/Z/08/Z, 088869/B/09/Z); Timber Merchant Vilhelm Bangs Foundation; Topcon; Torsten and Ragnar Söderberg's Foundation; UK Department of Health; UK Diabetes Association; UK Medical Research Council (MC_U106179471, G0500539, G0600705, G0601966, G0700931, G1002319, K013351, MC_UU_12019/1); UK National Institute for Health Research BioResource Clinical Research Facility and Biomedical Research Centre; UK National Institute for Health Research (NIHR) Comprehensive Biomedical Research Centre; UK National Institute for Health Research (RP-PG-0407-10371); Umeå University Career Development Award; United States – Israel Binational Science Foundation Grant (2011036); University Hospital Oulu (75617); University Medical Center Groningen; University of Tartu (SP1GVARENG); National Institutes of Health (AG13196, CA047988, HHSN268201100046C, HHSN268201100001C, HHSN268201100002C, HHSN268201100003C, HHSN268201100004C, HHSC271201100004C, HHSN268200900041C, HHSN268201300025C, HHSN268201300026C, HHSN268201300027C, HHSN268201300028C, HHSN268201300029C, HHSN268201500001I, HL36310, HG002651, HL034594, HL054457, HL054481, HL071981, HL084729, HL119443, HL126024, N01-AG12100, N01-AG12109, N01-HC25195, N01-HC55015, N01-HC55016, N01-HC55018, N01-HC55019, N01-HC55020, N01-HC55021, N01-HC55022, N01-HD95159, N01-HD95160, N01-HD95161, N01-HD95162, N01-HD95163, N01-HD95164, N01-HD95165, N01-HD95166, N01-HD95167, N01-HD95168, N01-HD95169, N01-HG65403, N02-HL64278, R01-HD057194, R01-HL087641, R01-HL59367, R01HL-086694, R01-HL088451, R24-HD050924, U01-HG-004402, HHSN268200625226C, UL1-RR025005, UL1-RR025005, UL1-TR-001079, UL1-TR-00040, AA07535, AA10248, AA11998, AA13320, AA13321, AA13326, AA14041, AA17688, DA12854, MH081802, MH66206, R01-D004215701A, R01-DK075787, R01-DK089256, R01-DK8925601, R01-HL088451, R01-HL117078, R01-DK062370, R01-DK072193, DK091718, DK100383, DK078616, 1Z01-HG000024, HL087660, HL100245, R01DK089256, 2T32HL007055-36, U01-HL072515-06, U01-HL84756, NIA-U01AG009740, RC2-AG036495, RC4-AG039029, R03 AG046389, 263-MA-410953, 263-MD-9164, 263-MD-821336, U01-HG004802, R37CA54281, R01CA63, P01CA33619, U01-CA136792, U01-CA98758, RC2-MH089951, MH085520, R01-D0042157-01A, MH081802, 1RC2-MH089951, 1RC2-MH089995, 1RL1MH08326801, U01-HG007376, 5R01-HL08767902, 5R01MH63706:02, HG004790, N01-WH22110, U01-HG007033, UM1CA182913, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-32119, 32122, 42107-26, 42129-32, 44221); USDA National Institute of Food and Agriculture (2007-35205-17883); Västra Götaland Foundation; Velux Foundation; Veterans Affairs (1 IK2 BX001823); Vleugels Foundation; VU University’s Institute for Health and Care Research (EMGO+, HEALTH-F4-2007-201413) and Neuroscience Campus Amsterdam; Wellcome Trust (090532, 091551, 098051, 098381); Wissenschaftsoffensive TMO; and Yrjö Jahnsson Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Published: 2017
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