@article {9806,
	title = {Meta-analysis of genome-wide association studies for height and body mass index in \~{}700000 individuals of European ancestry.},
	journal = {Human Molecular Genetics},
	volume = {27},
	year = {2018},
	pages = {3641-3649},
	abstract = {Recent genome-wide association studies (GWAS) of height and body mass index (BMI) in \~{}250000 European participants have led to the discovery of \~{}700 and \~{}100 nearly independent single nucleotide polymorphisms (SNPs) associated with these traits, respectively. Here we combine summary statistics from those two studies with GWAS of height and BMI performed in \~{}450000 UK Biobank participants of European ancestry. Overall, our combined GWAS meta-analysis reaches N~\~{}700000 individuals and substantially increases the number of GWAS signals associated with these traits. We identified 3290 and 941 near-independent SNPs associated with height and BMI, respectively (at a revised genome-wide significance threshold of P~<~1~{\texttimes}~10-8), including 1185 height-associated SNPs and 751 BMI-associated SNPs located within loci not previously identified by these two GWAS. The near-independent genome-wide significant SNPs explain \~{}24.6\% of the variance of height and \~{}6.0\% of the variance of BMI in an independent sample from the Health and Retirement Study (HRS). Correlations between polygenic scores based upon these SNPs with actual height and BMI in HRS participants were \~{}0.44 and \~{}0.22, respectively. From analyses of integrating GWAS and expression quantitative trait loci (eQTL) data by summary-data-based Mendelian randomization, we identified an enrichment of eQTLs among lead height and BMI signals, prioritizing 610 and 138 genes, respectively. Our study demonstrates that, as previously predicted, increasing GWAS sample sizes continues to deliver, by the discovery of new loci, increasing prediction accuracy and providing additional data to achieve deeper insight into complex trait biology. All summary statistics are made available for follow-up studies.},
	keywords = {BMI, Genetics, GWAS, Height},
	issn = {1460-2083},
	doi = {10.1093/hmg/ddy271},
	author = {Yengo, Loic and Sidorenko, Julia and Kathryn E Kemper and Zheng, Zhili and Andrew R Wood and Michael N Weedon and Timothy M Frayling and Joel N Hirschhron and Yang, Jian and Peter M Visscher}
}
@article {9988,
	title = {Meta-analysis of genome-wide association studies for height and body mass index in \~{}700000 individuals of European ancestry},
	journal = {Human Molecular Genetics},
	volume = {27},
	year = {2018},
	pages = {3641-3649},
	abstract = {Recent genome-wide association studies (GWAS) of height and body mass index (BMI) in similar to 250000 European participants have led to the discovery of similar to 700 and similar to 100 nearly independent single nucleotide polymorphisms (SNPs) associated with these traits, respectively. Here we combine summary statistics from those two studies with GWAS of height and BMI performed in similar to 450000 UK Biobank participants of European ancestry. Overall, our combined GWAS meta-analysis reaches N similar to 700000 individuals and substantially increases the number of GWAS signals associated with these traits. We identified 3290 and 941 near-independent SNPs associated with height and BMI, respectively (at a revised genome-wide significance threshold of P < 1 x 10(-8)), including 1185 height-associated SNPs and 751 BMI-associated SNPs located within loci not previously identified by these two GWAS. The near-independent genome-wide significant SNPs explain similar to 24.6\% of the variance of height and similar to 6.0\% of the variance of BMI in an independent sample from the Health and Retirement Study (HRS). Correlations between polygenic scores based upon these SNPs with actual height and BMI in HRS participants were similar to 0.44 and similar to 0.22, respectively. From analyses of integrating GWAS and expression quantitative trait loci (eQTL) data by summary-data-based Mendelian randomization, we identified an enrichment of eQTLs among lead height and BMI signals, prioritizing 610 and 138 genes, respectively. Our study demonstrates that, as previously predicted, increasing GWAS sample sizes continues to deliver, by the discovery of new loci, increasing prediction accuracy and providing additional data to achieve deeper insight into complex trait biology. All summary statistics are made available for follow-up studies.},
	keywords = {BMI, Genetics, GWAS, Height},
	issn = {0964-6906},
	doi = {10.1093/hmg/ddy271},
	author = {Yengo, Loic and Sidorenko, Julia and Kathryn E Kemper and Zheng, Zhili and Andrew R Wood and Michael N Weedon and Timothy M Frayling and Joel N Hirschhron and Yang, Jian and Peter M Visscher}
}
@article {9975,
	title = {Predictors and implications of accelerated cognitive aging},
	journal = {Biodemography and Social Biology},
	volume = {64},
	year = {2018},
	pages = {83-101},
	abstract = {Aging is a major risk factor for both normal and pathological cognitive decline. However, individuals vary in their rate of age-related decline. We developed an easily interpretable composite measure of cognitive age, and related both the level of cognitive age and cognitive slope to sociodemographic, genetic, and disease indicators and examined its prediction of dementia transition. Using a sample of 19,594 participants from the Health and Retirement Study, cognitive age was derived from a set of performance tests administered at each wave. Our findings reveal different conclusions as they relate to levels versus slopes of cognitive age, with more pronounced differences by sex and race/ethnicity for absolute levels of cognitive decline rather than for rates of declines. We also find that both level and slope of cognitive age are inversely related to education, as well as increased for persons with APOE ?4 and/or diabetes. Finally, results show that the slope in cognitive age predicts subsequent dementia among non-demented older adults. Overall, our study suggests that this measure is applicable to cross-sectional and longitudinal studies on cognitive aging, decline, and dementia with the goal of better understanding individual differences in cognitive decline.},
	keywords = {BMI, Cognition \& Reasoning, Risk Factors, Socioeconomic factors},
	issn = {1948-5565},
	doi = {10.1080/19485565.2018.1552513},
	url = {https://www.tandfonline.com/doi/full/10.1080/19485565.2018.1552513https://www.tandfonline.com/doi/pdf/10.1080/19485565.2018.1552513},
	author = {Morgan E. Levine and Harrati, Amal and Eileen M. Crimmins}
}
@article {9875,
	title = {Provider bias as a function of patient genotype: polygenic score analysis among diabetics from the Health and Retirement Study},
	journal = {Obesity Science \& Practice},
	volume = {4},
	year = {2018},
	month = {Jan-10-2018},
	pages = {448 - 454},
	abstract = {ObjectivePoor patient-provider interactions due to provider bias are associated with worse physiological and behavioural health outcomes for patients. Prior research has shown that patients with obesity perceive less favourable interactions compared with those with lower weights. This paper explores whether this association depends on patients{\textquoteright} cumulative polygenic score with respect to genes linked to obesity (i.e. a single variable quantifying the individual{\textquoteright}s genome-wide risk factors for high body mass index [BMI] or genetic liability) and whether providers react differentially to patients whose obesity is more genetic in nature compared with patients with diabetes caused by environmental factors. 

MethodsThe association between patients{\textquoteright} BMI category, their polygenic score for high BMI and their interaction was assessed for two measures of the patient-provider interaction within a sample of 521 older patients with diabetes from the Health and Retirement Study. 

ResultsParticularly for patients with obesity, the quality of the patient-provider interaction depended on genetic liability for high BMI controlling for demographic and clinical covariates. Providers responded less favourably to patients with diabetes influenced by environmental factors compared with individuals with high genetic liability. 

ConclusionsResults of this study suggest that a patient{\textquoteright}s genotype may elicit particular responses from their healthcare provider. When a provider judges a patient{\textquoteright}s high BMI to be environmentally driven rather than genetically oriented, patients receive reduced quality of care.},
	keywords = {Bias, BMI, Genotype, Health Care Outcomes, Patient-physician Relationship},
	doi = {10.1002/osp4.293},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6180716/},
	author = {Huibregtse, B. M. and Jason D Boardman}
}
@article {9299,
	title = {Religious Attendance and Body Mass: An Examination of Variations by Race and Gender.},
	journal = {Journal of Religion and Health},
	volume = {57},
	year = {2018},
	month = {12/2018},
	pages = {2140-2152},
	abstract = {Studies of the association between religious attendance and body mass have yielded mixed results. In this paper, we consider intersectional variations by race and gender to advance our understanding of these inconsistencies. We use data from the 2006-2008 Health and Retirement Study to examine the association between religious attendance and three indicators of body mass: overall body mass index, waist circumference, and waist-to-height ratio (n~=~11,457). For White women, attendance is either protective or unrelated to body mass. For Black women, attendance is consistently associated with increased body mass. We find that religious attendance is not associated with body mass among the men.},
	keywords = {BMI, Gender Differences, Racial/ethnic differences, Religion},
	issn = {1573-6571},
	doi = {10.1007/s10943-017-0490-1},
	author = {Godbolt, Dawn and Preeti Vaghela and Amy M. Burdette and Terrence D. Hill}
}
@mastersthesis {10315,
	title = {Selected Health Implications of Low Body Mass: Determinants and Health Outcomes},
	volume = {PhD},
	year = {2018},
	note = {Copyright - Database copyright ProQuest LLC; ProQuest does not claim copyright in the individual underlying works; Last updated - 2019-03-04},
	pages = {105},
	school = {University of Iowa},
	type = {phd},
	abstract = {While the role of obesity in health outcomes has been well described, the role of low body mass index (BMI), body weight relative to height, has largely been ignored. Those with low BMI are commonly excluded completely or combined with the normal BMI category in BMI studies. However, there have been some studies indicating poorer health outcomes among those with lower BMI, particularly that of increased risk of mortality. The purpose of this study is to explore the role of low BMI throughout the lifespan. Data from the Health and Retirement Study was used to evaluate 1) the association between childhood health and socioeconomic status (SES) exposures and low BMI in midlife adulthood, 2) the association between low BMI and health related outcomes in midlife adulthood (ages 50 to 65), and 3) the association between low BMI in midlife and health related outcomes, including mortality, over a longer follow-up (maximum of 20 years). To increase sample size, two low BMI definitions were used: the traditional <18.5 definition and a definition of <=20 based on the J-shaped curves found in BMI mortality studies. Few significant results were found. Low BMI status was consistently associated with older age and female gender as well as current smoking status. Childhood exposure of respiratory disease and greater SES disadvantages was more common among those with low BMI in adulthood. In midlife adulthood, low BMI status was associated with increased difficulties with activities of daily living with either definition of low BMI. Increased risk of fracture was associated with a low BMI definition of <18.5. Increased risk of lung disease and decreased risk of high blood pressure was associated with a low BMI definition of <=20. An analysis of those 30 years old or older found low BMI to be associated with increased risk of mortality and decreased risk of diabetes regardless of low BMI definition. When low BMI was defined as <18.5, those with low BMI were also more likely to experience difficulty with one or more activities of daily living. When low BMI was defined as <=20, low BMI status was associated with greater risk of lung disease and decreased risk of high blood pressure. Further research is needed to fully characterize the role of low BMI on health outcomes as well as the role of SES on low BMI. Additionally, there is a need for greater understanding of the potential biological mechanisms of low BMI for health outcomes. Currently, there are few studies evaluating health outcomes and SES of low BMI. Limiting studies to the extreme upper end of the BMI spectrum limits the overall understanding of the role of BMI in health and may overlook unique characteristics and challenges those with low BMI may face.},
	keywords = {0573:Public health, BMI, Health and environmental sciences, HRS, Life-course, Public Health, Underweight},
	isbn = {9780438870680},
	url = {https://ir.uiowa.edu/etd/6592/},
	author = {Holcombe,Andrea L.}
}
@article {9313,
	title = {Interaction between Social/Psychosocial Factors and Genetic Variants on Body Mass Index: A Gene-Environment Interaction Analysis in a Longitudinal Setting},
	journal = {International Journal of Environmental Research and Public Health},
	volume = {14},
	year = {2017},
	month = {09/2017},
	pages = {1153},
	abstract = {Obesity, which develops over time, is one of the leading causes of chronic diseases such as cardiovascular disease. However, hundreds of BMI (body mass index)-associated genetic loci identified through large-scale genome-wide association studies (GWAS) only explain about 2.7\% of BMI variation. Most common human traits are believed to be influenced by both genetic and environmental factors. Past studies suggest a variety of environmental features that are associated with obesity, including socioeconomic status and psychosocial factors. This study combines both gene/regions and environmental factors to explore whether social/psychosocial factors (childhood and adult socioeconomic status, social support, anger, chronic burden, stressful life events, and depressive symptoms) modify the effect of sets of genetic variants on BMI in European American and African American participants in the Health and Retirement Study (HRS). In order to incorporate longitudinal phenotype data collected in the HRS and investigate entire sets of single nucleotide polymorphisms (SNPs) within gene/region simultaneously, we applied a novel set-based test for gene-environment interaction in longitudinal studies (LGEWIS). Childhood socioeconomic status (parental education) was found to modify the genetic effect in the gene/region around SNP rs9540493 on BMI in European Americans in the HRS. The most significant SNP (rs9540488) by childhood socioeconomic status interaction within the rs9540493 gene/region was suggestively replicated in the Multi-Ethnic Study of Atherosclerosis (MESA) (p = 0.07).},
	keywords = {BMI, Genetics, Obesity},
	doi = {10.3390/ijerph14101153},
	url = {http://www.mdpi.com/1660-4601/14/10/1153http://www.mdpi.com/1660-4601/14/10/1153/pdf},
	author = {Wei Zhao and Erin B Ware and He, Zihuai and Sharon L R Kardia and Jessica Faul}
}
@article {8882,
	title = {Genetic studies of body mass index yield new insights for obesity biology.},
	journal = {Nature},
	volume = {518},
	year = {2015},
	month = {2015 Feb 12},
	pages = {197-206},
	abstract = {<p>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~{\texttimes}~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 \~{}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.</p>},
	keywords = {Age Factors, BMI, Continental Population Groups, Energy Metabolism, Europe, Female, Genome-Wide Association Study, Glutamic Acid, Humans, Insulin, Male, Obesity, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Synapses},
	issn = {1476-4687},
	doi = {10.1038/nature14177},
	author = {Locke, Adam E and Kahali, Bratati and Berndt, Sonja I and Justice, Anne E and Pers, Tune H and Day, Felix R and Powell, Corey and Vedantam, Sailaja and Buchkovich, Martin L and Yang, Jian and Croteau-Chonka, Damien C and T{\~o}nu Esko and Fall, Tove and Ferreira, Teresa and Gustafsson, Stefan and Kutalik, Zolt{\'a}n and Luan, Jian{\textquoteright}an and M{\"a}gi, Reedik and Randall, Joshua C and Thomas W Winkler and Andrew R Wood and Workalemahu, Tsegaselassie and Jessica Faul and Jennifer A Smith and Jing Hua Zhao and Wei Zhao and Chen, Jin and Rudolf Ferhmann and Hedman, {\r A}sa K and Karjalainen, Juha and Schmidt, Ellen M and Absher, Devin and Amin, Najaf and Anderson, Denise and Beekman, Marian and Bolton, Jennifer L and Bragg-Gresham, Jennifer L and Buyske, Steven and Demirkan, Ayse and Deng, Guohong and Georg B Ehret and Feenstra, Bjarke and Feitosa, Mary F and Fischer, Krista and Goel, Anuj and Gong, Jian and Jackson, Anne U and Kanoni, Stavroula and Kleber, Marcus E and Kristiansson, Kati and Lim, Unhee and Lotay, Vaneet and Mangino, Massimo and Irene Mateo Leach and Medina-Gomez, Carolina and Sarah E Medland and Michael A Nalls and Palmer, Cameron D and Pasko, Dorota and Pechlivanis, Sonali and Peters, Marjolein J and Prokopenko, Inga and Shungin, Dmitry and Stan{\v c}{\'a}kov{\'a}, Alena and Strawbridge, Rona J and Yun Ju Sung and Toshiko Tanaka and Teumer, Alexander and Trompet, Stella and van der Laan, Sander W and van Setten, Jessica and Jana V. van Vliet-Ostaptchouk and Wang, Zhaoming and Yengo, Loic and Zhang, Weihua and Isaacs, Aaron and Albrecht, Eva and {\"A}rnl{\"o}v, Johan and Arscott, Gillian M and Attwood, Antony P and Bandinelli, Stefania and Barrett, Amy and Bas, Isabelita N and Bellis, Claire and Bennett, Amanda J and Berne, Christian and Blagieva, Roza and Bl{\"u}her, Matthias and B{\"o}hringer, Stefan and Bonnycastle, Lori L and B{\"o}ttcher, Yvonne and Boyd, Heather A and Bruinenberg, Marcel and Caspersen, Ida H and Yii-Der I Chen and Robert Clark and Daw, E Warwick and de Craen, Anton J M and Delgado, Graciela and Dimitriou, Maria and Doney, Alex S F and Eklund, Niina and Estrada, Karol and Eury, Elodie and Folkersen, Lasse and Fraser, Ross M and Melissa E Garcia and Geller, Frank and Giedraitis, Vilmantas and Gigante, Bruna and Alan S Go and Golay, Alain and Goodall, Alison H and Gordon, Scott D and Gorski, Mathias and Hans-J{\"o}rgen Grabe and Grallert, Harald and Grammer, Tanja B and Gr{\"a}{\ss}ler, J{\"u}rgen and Gr{\"o}nberg, Henrik and Groves, Christopher J and Gusto, Ga{\"e}lle and Jeffrey Haessler and Hall, Per and Haller, Toomas and Hallmans, G{\"o}ran and Catharina A Hartman and Hassinen, Maija and Caroline Hayward and Heard-Costa, Nancy L and Helmer, Quinta and Hengstenberg, Christian and Oddgeir L Holmen and Jouke-Jan Hottenga and James, Alan L and Janina Jeff and Johansson, {\r A}sa and Jolley, Jennifer and Juliusdottir, Thorhildur and Kinnunen, Leena and Koenig, Wolfgang and Koskenvuo, Markku and Kratzer, Wolfgang and Laitinen, Jaana and Lamina, Claudia and Leander, Karin and Lee, Nanette R and Lichtner, Peter and Lars Lind and Lindstr{\"o}m, Jaana and Ken Sin Lo and Lobbens, St{\'e}phane and Lorbeer, Roberto and Lu, Yingchang and Mach, Fran{\c c}ois and Patrik K E Magnusson and Mahajan, Anubha and McArdle, Wendy L and McLachlan, Stela and Menni, Cristina and Merger, Sigrun and Mihailov, Evelin and Lili Milani and Moayyeri, Alireza and Monda, Keri L and Morken, Mario A and Mulas, Antonella and M{\"u}ller, Gabriele and M{\"u}ller-Nurasyid, Martina and Musk, Arthur W and Nagaraja, Ramaiah and Markus M N{\"o}then and Ilja M Nolte and Pilz, Stefan and Nigel W Rayner and Renstrom, Frida and Rettig, Rainer and Ried, Janina S and Ripke, Stephan and Neil R Robertson and Rose, Lynda M and Sanna, Serena and Scharnagl, Hubert and Scholtens, Salome and Schumacher, Fredrick R and Scott, William R and Seufferlein, Thomas and Jianxin Shi and Albert Vernon Smith and Smolonska, Joanna and Stanton, Alice V and Steinthorsdottir, Valgerdur and Kathleen E Stirrups and Heather M Stringham and Sundstr{\"o}m, Johan and Swertz, Morris A and Swift, Amy J and Syv{\"a}nen, Ann-Christine and Tan, Sian-Tsung and Bamidele O Tayo and Thorand, Barbara and Thorleifsson, Gudmar and Tyrer, Jonathan P and Uh, Hae-Won and Vandenput, Liesbeth and Verhulst, Frank C and Vermeulen, Sita H and Verweij, Niek and Vonk, Judith M and Lindsay L Waite and Warren, Helen R and Dawn M Waterworth and Michael N Weedon and Wilkens, Lynne R and Willenborg, Christina and Wilsgaard, Tom and Wojczynski, Mary K and Wong, Andrew and Alan F Wright and Zhang, Qunyuan and Brennan, Eoin P and Murim Choi and Dastani, Zari and Alexander W Drong and Eriksson, Per and Franco-Cereceda, Anders and G{\r a}din, Jesper R and Gharavi, Ali G and Goddard, Michael E and Handsaker, Robert E and Huang, Jinyan and Karpe, Fredrik and Kathiresan, Sekar and Keildson, Sarah and Kiryluk, Krzysztof and Kubo, Michiaki and Lee, Jong-Young and Liang, Liming and Lifton, Richard P and Ma, Baoshan and McCarroll, Steven A and McKnight, Amy J and Min, Josine L and Moffatt, Miriam F and Grant W Montgomery and Joanne M Murabito and Nicholson, George and Nyholt, Dale R and Okada, Yukinori and Perry, John R B and Dorajoo, Rajkumar and Reinmaa, Eva and Salem, Rany M and Sandholm, Niina and Scott, Robert A and Stolk, Lisette and Takahashi, Atsushi and Tanaka, Toshihiro and Ferdinand M van {\textquoteright}t Hooft and Anna A E Vinkhuyzen and Westra, Harm-Jan and Wei Zhang and Krina T Zondervan and Andrew C Heath and Arveiler, Dominique and Bakker, Stephan J L and Beilby, John and Bergman, Richard N and Blangero, John and Bovet, Pascal and Campbell, Harry and Caulfield, Mark J and Cesana, Giancarlo and Chakravarti, Aravinda and Daniel I Chasman and Chines, Peter S and Collins, Francis S and Crawford, Dana C and Cupples, L Adrienne and Cusi, Daniele and Danesh, John and de Faire, Ulf and Hester M den Ruijter and Dominiczak, Anna F and Erbel, Raimund and Erdmann, Jeanette and Johan G Eriksson and Farrall, Martin and Felix, Stephan B and Ferrannini, Ele and Ferri{\`e}res, Jean and Ford, Ian and Forouhi, Nita G and Forrester, Terrence and Franco, Oscar H and Gansevoort, Ron T and Gejman, Pablo V and Gieger, Christian and Gottesman, Omri and Gudnason, Vilmundur and Gyllensten, Ulf and Hall, Alistair S and Tamara B Harris and Andrew T Hattersley and Hicks, Andrew A and Hindorff, Lucia A and Aroon Hingorani and Hofman, Albert and Homuth, Georg and Hovingh, G Kees and Humphries, Steve E and Hunt, Steven C and Hypp{\"o}nen, Elina and Illig, Thomas and Jacobs, Kevin B and J{\"a}rvelin, Marjo-Riitta and J{\"o}ckel, Karl-Heinz and Johansen, Berit and Jousilahti, Pekka and Jukema, J Wouter and Jula, Antti M and Kaprio, Jaakko and Kastelein, John J P and Keinanen-Kiukaanniemi, Sirkka M and Lambertus A Kiemeney and Knekt, Paul and Kooner, Jaspal S and Charles Kooperberg and Kovacs, Peter and Kraja, Aldi T and Kumari, Meena and Kuusisto, Johanna and Lakka, Timo A and Langenberg, Claudia and Loic Le Marchand and Lehtim{\"a}ki, Terho and Lyssenko, Valeriya and M{\"a}nnist{\"o}, Satu and Marette, Andr{\'e} and Matise, Tara C and McKenzie, Colin A and McKnight, Barbara and Moll, Frans L and Morris, Andrew D and Morris, Andrew P and Murray, Jeffrey C and Nelis, Mari and Ohlsson, Claes and Oldehinkel, Albertine J and Ong, Ken K and Pamela A F Madden and Pasterkamp, Gerard and Peden, John F and Peters, Annette and Postma, Dirkje S and Pramstaller, Peter P and Price, Jackie F and Qi, Lu and Olli T Raitakari and Rankinen, Tuomo and Rao, D C and Rice, Treva K and Ridker, Paul M and Rioux, John D and Ritchie, Marylyn D and Rudan, Igor and Veikko Salomaa and Nilesh J Samani and Saramies, Jouko and Sarzynski, Mark A and Schunkert, Heribert and Schwarz, Peter E H and Peter Sever and Alan R Shuldiner and Sinisalo, Juha and Stolk, Ronald P and Strauch, Konstantin and T{\"o}njes, Anke and Tr{\'e}gou{\"e}t, David-Alexandre and Tremblay, Angelo and Tremoli, Elena and Virtamo, Jarmo and Vohl, Marie-Claude and V{\"o}lker, Uwe and Waeber, G{\'e}rard and Gonneke Willemsen and Witteman, Jacqueline C and Zillikens, M Carola and Adair, Linda S and Amouyel, Philippe and Asselbergs, Folkert W and Assimes, Themistocles L and Bochud, Murielle and Boehm, Bernhard O and Boerwinkle, Eric and Bornstein, Stefan R and Erwin P Bottinger and Bouchard, Claude and Cauchi, St{\'e}phane and Chambers, John C and Chanock, Stephen J and Cooper, Richard S and de Bakker, Paul I W and George Dedoussis and Luigi Ferrucci and Franks, Paul W and Froguel, Philippe and Leif C Groop and Christopher A Haiman and Hamsten, Anders and Hui, Jennie and Hunter, David J and Hveem, Kristian and Kaplan, Robert C and Mika Kivim{\"a}ki and Kuh, Diana and Laakso, Markku and Yongmei Liu and Nicholas G Martin and M{\"a}rz, Winfried and Melbye, Mads and Andres Metspalu and Moebus, Susanne and Munroe, Patricia B and Nj{\o}lstad, Inger and Ben A Oostra and Palmer, Colin N A and Nancy L Pedersen and Markus Perola and P{\'e}russe, Louis and Peters, Ulrike and Power, Chris and Quertermous, Thomas and Rauramaa, Rainer and Fernando Rivadeneira and Saaristo, Timo E and Saleheen, Danish and Sattar, Naveed and Eric E Schadt and Schlessinger, David and Eline P Slagboom and Snieder, Harold and Timothy Spector and Thorsteinsdottir, Unnur and Stumvoll, Michael and Tuomilehto, Jaakko and Andr{\'e} G Uitterlinden and Uusitupa, Matti and van der Harst, Pim and Walker, Mark and Wallaschofski, Henri and Wareham, Nicholas J and Watkins, Hugh and David R Weir and Wichmann, H-Erich and James F Wilson and Zanen, Pieter and Ingrid B Borecki and Deloukas, Panos and Caroline S Fox and Iris M Heid and Jeff O{\textquoteright}Connell and David P Strachan and Stefansson, Kari and Cornelia M van Duijn and Gon{\c c}alo R Abecasis and Lude L Franke and Timothy M Frayling and McCarthy, Mark I and Peter M Visscher and Scherag, Andre and Willer, Cristen J and Boehnke, Michael and Mohlke, Karen L and Lindgren, Cecilia M and Beckmann, Jacques S and Barroso, In{\^e}s and Kari E North and Ingelsson, Erik and Joel N Hirschhron and Ruth J F Loos and Elizabeth K Speliotes}
}
