@article {13628, title = {A longitudinal study of polygenic score and cognitive function decline considering baseline cognitive function, lifestyle behaviors, and diabetes among middle-aged and older US adults.}, journal = {Alzheimer{\textquoteright}s research \& therapy}, volume = {15}, year = {2023}, pages = {196}, abstract = {

BACKGROUND: Genomic study of cognition decline while considering baseline cognition and lifestyle behaviors is scarce. We aimed to evaluate the impact of a polygenic score for general cognition on cognition decline rate, while considering baseline cognition and lifestyle behaviors, among the general population and people with diabetes, a patient group commonly affected by cognition impairment.

METHODS: We tested associations of the polygenic score for general cognition with annual changing rates of cognition measures in 8~years of follow-up among 12,090 White and 3100 Black participants of the Health and Retirement Study (HRS), a nationally representative sample of adults aged 50~years and older in the USA. Cognition measures including word recall, mental status, and total cognitive score were measured biannually. To maximize sample size and length of follow-up, we treated the 2010 wave of survey as baseline, and follow-up data until 2018 were analyzed. Baseline lifestyle behaviors, APOE status, and measured cognition were sequentially adjusted. Given racial differences in polygenic score, all analyses were conducted by race.

RESULTS: The polygenic score was significantly associated with annual changing rates of all cognition measures independent of lifestyle behaviors and APOE status. Together with age and sex, the polygenic score explained 29.9\%, 15.9\%, and 26.5\% variances of annual changing rates of word recall, mental status, and total cognitive scores among Whites and explained 17.2\%, 13.9\%, and 18.7\% variance of the three traits among Blacks. Among both White and Black participants, those in the top quartile of polygenic score had the three cognition measures increased annually, while those in the bottom quartile had the three cognition measures decreased annually. After further adjusting for the average cognition assessed in 3 visits around baseline, the polygenic score was still positively associated with annual changing rates of all cognition measures for White (P <= 2.89E - 19) but not for Black (P >= 0.07) participants. In addition, among participants with diabetes, physical activity offset the genetic susceptibility to decline of mental status (interaction P <= 0.01) and total cognitive scores (interaction P = 0.03).

CONCLUSIONS: Polygenic score predicted cognition changes in addition to measured cognition. Physical activity offset genetic risk for cognition decline among diabetes patients.

}, keywords = {Adult, Aged, Apolipoproteins E, Cognition, Cognitive Dysfunction, Diabetes Mellitus, Humans, Life Style, Longitudinal Studies, Middle Aged}, issn = {1758-9193}, doi = {10.1186/s13195-023-01343-1}, author = {Liu, Tingting and Li, Changwei and Zhang, Ruiyuan and Millender, Eugenia Flores and Miao, Hongyu and Ormsbee, Michael and Guo, Jinzhen and Westbrook, Adrianna and Pan, Yang and Wang, Jing and Kelly, Tanika N} } @article {12145, title = {Association Between Baseline Buccal Telomere Length and Progression of Kidney Function: The Health and Retirement Study.}, journal = {The Journals of Gerontology, Series A}, volume = {77}, year = {2022}, pages = {471-476}, abstract = {

We aimed to evaluate associations of baseline telomere length with overall and annual change in estimated glomerular filtration rate (eGFR) and trajectory of kidney function during an 8-year follow-up. A total of 3,964 participants of the Health and Retirement Study (HRS) were included. We identified three trajectory groups of kidney function: consistently normal (n=1,163 or 29.3\%), normal to impaired (n=2,306 or 58.2\%), and consistently impaired groups (n=495 or 12.5\%). After controlling for age, sex, race, education, smoking, drinking, diabetes, heart disease, blood pressure, body mass index, total cholesterol, and hemoglobin A1c, participants with longer telomere length were 20\% less likely (odds ratio [OR]=0.80, 95\% confidence interval [CI]: 0.69-0.93, P=0.003) to have a normal to impaired kidney function trajectory than a consistently normal function trajectory. Telomere length was not associated with changing rate of eGFR over 8 years (P=0.45). Participants with longer telomere length were more likely to have consistently normal kidney function.

}, keywords = {Kidney disease, Kidney function, Telomere}, issn = {1758-535X}, doi = {10.1093/gerona/glac004}, author = {Westbrook, Adrianna and Zhang, Ruiyuan and Shi, Mengyao and Razavi, Alexander C and Huang, Zhijie and Chen, Jing and He, Jiang and Tanika N Kelly and Shen, Ye and Li, Changwei} } @article {12102, title = {The Brain-Derived Neurotrophic Factor Functional Polymorphism and Hand Grip Strength Impact the Association between Brain-Derived Neurotrophic Factor Levels and Cognition in Older Adults in the United States.}, journal = {Biological Research for Nursing}, volume = {24}, year = {2022}, pages = {226-234}, abstract = {

INTRODUCTION: Aging is associated with subtle cognitive decline in attention, memory, executive function, processing speed, and reasoning. Although lower brain-derived neurotrophic factor (BDNF) has been linked to cognitive decline among older adults, it is not known if the association differs among individuals with various Val66Met (rs6265) genotypes. In addition, it is not clear whether these associations vary by hand grip strength or physical activity (PA).

METHODS: A total of 2904 older adults were included in this study using data from the Health and Retirement Study. Associations between serum BDNF and measures of cognitive function were evaluated using multivariable linear regression models stratified by Met allele status. PA and hand grip strength were added to the model to evaluate whether including these variables altered associations between serum BDNF and cognition.

RESULTS: Mean age was 71.4~years old, and mean body mass index was 28.3~kg/m. Serum BDNF levels were positively associated with higher total cognitive score (beta = 0.34, = .07), mental status (beta = 0.16, = .07), and word recall (beta = 0.22, =.04) among Met carriers, while serum BDNF levels were negatively associated with mental status (beta = -0.09, = .07) among non-Met carriers. Furthermore, associations changed when hand grip strength was added to the model but not when PA was added to the model.

CONCLUSIONS: The Val66Met variant may moderate the association between serum BDNF levels and cognitive function in older adults. Furthermore, such associations differ according to hand grip strength but not PA.

}, keywords = {Brain-Derived Neurotrophic Factor, Cognition, Exercise, Gene-Environment Interaction, Hand Strength}, issn = {1552-4175}, doi = {10.1177/10998004211065151}, author = {Liu, Tingting and Li, Hongjin and Conley, Yvette P and Primack, Brian A and Wang, Jing and Li, Changwei} } @article {12732, title = {The Influence of the Val66Met Variant on the Association Between Physical Activity/Grip Strength and Depressive Symptoms in Persons With Diabetes.}, journal = {Clinical Nursing Research}, year = {2022}, abstract = {

The rs6265 in the (BDNF) is associated with depression in people with diabetes. Both physical activity (PA) and grip strength are negatively associated with depression. We conducted cross-sectional analyses of the wave 10 survey data for a nationally representative sample of 1,051 diabetes participants of the Health and Retirement Study. Both greater PA (β = -.15) and stronger grip strength (β = -.02) were independently associated with depression. Although the interaction between rs6265 and PA on depressive symptoms was not significant, the negative PA-depression association was stronger among female non-Met carriers (β = -.19) and male Met carriers (β = -.14). Meanwhile, grip strength was associated with depression only in Met carriers (β = -.04), and similar association was observed in both males and females. In conclusion, female non-Met carriers and male Met carriers may benefit from PA, and Met carriers may benefit from grip strength to relieve depression.

}, keywords = {Brain-Derived Neurotrophic Factor, Depressive symptoms, Diabetes, Grip strength, Physical activity}, issn = {1552-3799}, doi = {10.1177/10547738221119343}, author = {Zeng, Bin and Yue, Yan and Liu, Tingting and Ahn, Hyochol and Li, Changwei} } @article {12127, title = {Gene-educational attainment interactions in a multi-ancestry genome-wide meta-analysis identify novel blood pressure loci.}, journal = {Mol Psychiatry}, volume = {26}, year = {2021}, pages = {2111-2125}, abstract = {

Educational attainment is widely used as a surrogate for socioeconomic status (SES). Low SES is a risk factor for hypertension and high blood pressure (BP). To identify novel BP loci, we performed multi-ancestry meta-analyses accounting for gene-educational attainment interactions using two variables, "Some College" (yes/no) and "Graduated College" (yes/no). Interactions were evaluated using both a 1 degree of freedom (DF) interaction term and a 2DF joint test of genetic and interaction effects. Analyses were performed for systolic BP, diastolic BP, mean arterial pressure, and pulse pressure. We pursued genome-wide interrogation in Stage 1 studies (N = 117 438) and follow-up on promising variants in Stage 2 studies (N = 293 787) in five ancestry groups. Through combined meta-analyses of Stages 1 and 2, we identified 84 known and 18 novel BP loci at genome-wide significance level (P < 5 {\texttimes} 10). Two novel loci were identified based on the 1DF test of interaction with educational attainment, while the remaining 16 loci were identified through the 2DF joint test of genetic and interaction effects. Ten novel loci were identified in individuals of African ancestry. Several novel loci show strong biological plausibility since they involve physiologic systems implicated in BP regulation. They include genes involved in the central nervous system-adrenal signaling axis (ZDHHC17, CADPS, PIK3C2G), vascular structure and function (GNB3, CDON), and renal function (HAS2 and HAS2-AS1, SLIT3). Collectively, these findings suggest a role of educational attainment or SES in further dissection of the genetic architecture of BP.

}, keywords = {Blood pressure, Epistasis, Genetic, Genetic Loci, Genome-Wide Association Study, Humans, Hypertension, Polymorphism, Single Nucleotide}, issn = {1476-5578}, doi = {10.1038/s41380-020-0719-3}, author = {de Las Fuentes, Lisa and Yun Ju Sung and Noordam, Raymond and Thomas W Winkler and Feitosa, Mary F and Schwander, Karen and Bentley, Amy R and Brown, Michael R and Guo, Xiuqing and Alisa Manning and Daniel I Chasman and Aschard, Hugues and Traci M Bartz and Bielak, Lawrence F and Campbell, Archie and Cheng, Ching-Yu and Dorajoo, Rajkumar and Hartwig, Fernando P and Horimoto, A R V R and Li, Changwei and Li-Gao, Ruifang and Liu, Yongmei and Marten, Jonathan and Musani, Solomon K and Ntalla, Ioanna and Rankinen, Tuomo and Melissa Richard and Sim, Xueling and Smith, Albert V and Tajuddin, Salman M and Bamidele O Tayo and Vojinovic, Dina and Warren, Helen R and Xuan, Deng and Alver, Maris and Boissel, Mathilde and Jin-Fang Chai and Chen, Xu and Christensen, Kaare and Divers, Jasmin and Evangelou, Evangelos and Gao, Chuan and Giorgia G Girotto and Sarah E Harris and He, Meian and Hsu, Fang-Chi and K{\"u}hnel, Brigitte and Laguzzi, Federica and Li, Xiaoyin and Lyytik{\"a}inen, Leo-Pekka and Ilja M Nolte and Poveda, Alaitz and Rauramaa, Rainer and Riaz, Muhammad and Rueedi, Rico and Shu, Xiao-Ou and Snieder, Harold and Sofer, Tamar and Takeuchi, Fumihiko and Verweij, Niek and Erin B Ware and Weiss, Stefan and Yanek, Lisa R and Amin, Najaf and Dan E Arking and Donna K Arnett and Bergmann, Sven and Boerwinkle, Eric and Brody, Jennifer A and Broeckel, Ulrich and Brumat, Marco and Burke, Gregory and Cabrera, Claudia P and Canouil, Micka{\"e}l and Chee, Miao Li and Chen, Yii-Der Ida and Cocca, Massimiliano and Connell, John and de Silva, H Janaka and de Vries, Paul S and Eiriksdottir, Gudny and Jessica Faul and Fisher, Virginia and Forrester, Terrence and Fox, Ervin F and Friedlander, Yechiel and Gao, He and Gigante, Bruna and Giulianini, Franco and Gu, Chi Charles and Gu, Dongfeng and Tamara B Harris and He, Jiang and Heikkinen, Sami and Heng, Chew-Kiat and Hunt, Steven and Ikram, M Arfan and Irvin, Marguerite R and K{\"a}h{\"o}nen, Mika and Kavousi, Maryam and Khor, Chiea Chuen and Kilpel{\"a}inen, Tuomas O and Koh, Woon-Puay and Komulainen, Pirjo and Kraja, Aldi T and Krieger, J E and Langefeld, Carl D and Li, Yize and Liang, Jingjing and David C Liewald and Liu, Ching-Ti and Liu, Jianjun and Kurt Lohman and M{\"a}gi, Reedik and McKenzie, Colin A and Meitinger, Thomas and Andres Metspalu and Milaneschi, Yuri and Lili Milani and Dennis O Mook-Kanamori and Michael A Nalls and Nelson, Christopher P and Norris, Jill M and Jeff O{\textquoteright}Connell and Ogunniyi, Adesola and Padmanabhan, Sandosh and Palmer, Nicholette D and Nancy L Pedersen and Thomas T Perls and Peters, Annette and Petersmann, Astrid and Peyser, Patricia A and Polasek, Ozren and David J Porteous and Raffel, Leslie J and Rice, Treva K and Rotter, Jerome I and Rudan, Igor and Rueda-Ochoa, Oscar-Leonel and Sabanayagam, Charumathi and Babatunde Salako and Schreiner, Pamela J and Shikany, James M and Stephen Sidney and Sims, Mario and Sitlani, Colleen M and Smith, Jennifer A and John M Starr and Strauch, Konstantin and Swertz, Morris A and Teumer, Alexander and Tham, Yih Chung and Andr{\'e} G Uitterlinden and Vaidya, Dhananjay and van der Ende, M Yldau and Waldenberger, Melanie and Wang, Lihua and Wang, Ya-Xing and Wei, Wen-Bin and David R Weir and Wen, Wanqing and Yao, Jie and Yu, Bing and Yu, Caizheng and Yuan, Jian-Min and Zhao, Wei and Alan B Zonderman and Becker, Diane M and Bowden, Donald W and Ian J Deary and D{\"o}rr, Marcus and T{\~o}nu Esko and Freedman, Barry I and Froguel, Philippe and Paolo P. Gasparini and Gieger, Christian and Jost Bruno Jonas and Kammerer, Candace M and Kato, Norihiro and Lakka, Timo A and Leander, Karin and Lehtim{\"a}ki, Terho and Patrik K E Magnusson and Marques-Vidal, Pedro and Brenda W J H Penninx and Nilesh J Samani and van der Harst, Pim and Wagenknecht, Lynne E and Wu, Tangchun and Zheng, Wei and Zhu, Xiaofeng and Bouchard, Claude and Cooper, Richard S and Correa, Adolfo and Michele K Evans and Gudnason, Vilmundur and Caroline Hayward and Horta, Bernardo L and Tanika N Kelly and Stephen B Kritchevsky and Levy, Daniel and Walter R Palmas and Pereira, A C and Province, Michael M and Psaty, Bruce M and Ridker, Paul M and Charles N Rotimi and Tai, E Shyong and van Dam, Rob M and Cornelia M van Duijn and Wong, Tien Yin and Kenneth Rice and Gauderman, W James and Alanna C Morrison and Kari E North and Sharon L R Kardia and Caulfield, Mark J and Elliott, Paul and Munroe, Patricia B and Franks, Paul W and Rao, Dabeeru C and Myriam Fornage} } @article {10869, title = {Association of Low to Moderate Alcohol Drinking With Cognitive Functions From Middle to Older Age Among US Adults}, journal = {JAMA Network Open}, volume = {3}, year = {2020}, abstract = {Studies examining the association of low to moderate drinking with various cognitive functions have yielded mixed findings.To investigate whether associations exist between low to moderate alcohol drinking and cognitive function trajectories or rates of change in cognitive function from middle age to older age among US adults.A prospective cohort study of participants drawn from the Health and Retirement Study (HRS), a nationally representative sample of US adults, with mean (SD) follow-up of 9.1 (3.1) years. In total, 19 887 participants who had their cognitive functions measured in the HRS starting in 1996 through 2008 and who had participated in at least 3 biennial surveys were included. The data analysis was conducted from June to November 2019.Alcohol consumption and aging.Trajectories and annual rates of change for the cognitive domains of mental status, word recall, and vocabulary and for the total cognitive score, which was the sum of the mental status and word recall scores. Participants were clustered into 2 cognitive function trajectories for each cognition measure assessed based on their scores at baseline and through at least 3 biennial surveys: a consistently low trajectory (representing low cognitive scores throughout the study period) and a consistently high trajectory (representing high cognitive scores throughout the study period).The mean (SD) age of 19 887 participants was 61.8 (10.2) years, and the majority of the HRS participants were women (11 943 [60.1\%]) and of white race/ethnicity (16 950 [85.2\%]). Low to moderate drinking (\<8 drinks per week for women and \<15 drinks per week for men) was significantly associated with a consistently high cognitive function trajectory and a lower rate of cognitive decline. Compared with never drinkers, low to moderate drinkers were less likely to have a consistently low trajectory for total cognitive function (odds ratio [OR], 0.66; 95\% CI, 0.59-0.74), mental status (OR, 0.71; 95\% CI, 0.63-0.81), word recall (OR, 0.74; 95\% CI, 0.69-0.80), and vocabulary (OR, 0.64; 95\% CI, 0.56-0.74) (all P \< .001). In addition, low to moderate drinking was associated with decreased annual rates of total cognitive function decline (β coefficient, 0.04; 95\% CI, 0.02-0.07; P = .002), mental status (β coefficient, 0.02; 95\% CI, 0.01-0.03; P = .002), word recall (β coefficient, 0.02; 95\% CI, 0.01-0.04; P = .01), and vocabulary (β coefficient, 0.01; 95\% CI, 0.00-0.03; P = .08). A significant racial/ethnic difference was observed for trajectories of mental status (P = .02 for interaction), in which low to moderate drinking was associated with lower odds of having a consistently low trajectory for white participants (OR, 0.65; 95\% CI, 0.56-0.75) but not for black participants (OR, 1.02; 95\% CI, 0.74-1.39). Finally, the dosage of alcohol consumed had a U-shaped association with all cognitive function domains for all participants, with an optimal dose of 10 to 14 drinks per week.These findings suggested that low to moderate alcohol drinking was associated with better global cognition scores, and these associations appeared stronger for white participants than for black participants. Studies examining the mechanisms underlying the association between alcohol drinking and cognition in middle-aged or older adults are needed.}, keywords = {Aging, Cognition, moderate alcohol drinking}, isbn = {2574-3805}, doi = {10.1001/jamanetworkopen.2020.7922}, author = {Zhang, Ruiyuan and Shen, Luqi and Toni Miles and Shen, Ye and Cordero, Jose and Qi, Yanling and Liang, Lirong and Li, Changwei} } @article {11164, title = {The Influence of the BDNFVal66Met Polymorphism on the Association of Regular Physical Activity With Cognition Among Individuals With Diabetes.}, journal = {Biological Research for Nursing}, year = {2020}, abstract = {

INTRODUCTION: Diabetes is associated with cognitive dysfunction that comes with substantial lifetime consequences, such as interference with diabetes self-management and reduced quality of life. Although regular physical activity has been consistently shown to enhance cognitive function among healthy subjects, significant interpersonal differences in exercise-induced cognitive outcomes have been reported among (BDNF) Val/Val vs. Met carriers. However, the evidence on how the Val66Met variant influences the relationship between regular physical activity and cognition among individuals with diabetes is currently lacking.

METHODS: A total of 3,040 individuals with diabetes were included in this analysis using data from the Health and Retirement Study. Associations among moderate and vigorous physical activities (MVPA) and measures of cognitive function were evaluated using multivariable linear regression models within each stratum of the Val66Met genotypes.

RESULTS: MVPA was more strongly associated with total cognitive score, mental status, and words recall among Met/Met carriers, compared to Val/Val and Val/Met carriers.

CONCLUSIONS: This study provided preliminary findings on how variants may modulate the exercise-induced cognitive benefits among mid-aged and older adults with diabetes. Given the limitations of the current study, it is necessary for randomized controlled trials to stratify by genotypes to more conclusively determine whether Met carriers benefit more from increased physical activity. In addition, future research is needed to examine how the interplay of Val66Met variants, DNA methylation, and physical activity may have an impact on cognitive function among adults with diabetes.

}, keywords = {Brain-Derived Neurotrophic Factor, Cognition, Diabetes Mellitus, Exercise, Gene-Environment Interaction}, issn = {1552-4175}, doi = {10.1177/1099800420966648}, author = {Liu, Tingting and Canon, McKenzie D and Shen, Luqi and Marples, Benjamin A and Colton, Joseph P and Lo, Wen-Juo and Gray, Michelle and Li, Changwei} } @article {12128, title = {Multi-ancestry study of blood lipid levels identifies four loci interacting with physical activity.}, journal = {Nature Communications}, volume = {10}, year = {2019}, pages = {376}, abstract = {

Many genetic loci affect circulating lipid levels, but it remains unknown whether lifestyle factors, such as physical activity, modify these genetic effects. To identify lipid loci interacting with physical activity, we performed genome-wide analyses of circulating HDL cholesterol, LDL cholesterol, and triglyceride levels in up to 120,979 individuals of European, African, Asian, Hispanic, and Brazilian ancestry, with follow-up of suggestive associations in an additional 131,012 individuals. We find four loci, in/near CLASP1, LHX1, SNTA1, and CNTNAP2, that are associated with circulating lipid levels through interaction with physical activity; higher levels of physical activity enhance the HDL cholesterol-increasing effects of the CLASP1, LHX1, and SNTA1 loci and attenuate the LDL cholesterol-increasing effect of the CNTNAP2 locus. The CLASP1, LHX1, and SNTA1 regions harbor genes linked to muscle function and lipid metabolism. Our results elucidate the role of physical activity interactions in the genetic contribution to blood lipid levels.

}, keywords = {Adolescent, Adult, Aged, Aged, 80 and over, Asians, Blacks, Brazil, Calcium-Binding Proteins, Cholesterol, Cholesterol, HDL, Cholesterol, LDL, Exercise, Female, Genetic Loci, Genome-Wide Association Study, Genotype, Hispanic or Latino, Humans, LIM-Homeodomain Proteins, Lipid Metabolism, Lipids, Male, Membrane Proteins, Microtubule-Associated Proteins, Middle Aged, Muscle Proteins, Nerve Tissue Proteins, Transcription Factors, Triglycerides, Whites, Young Adult}, issn = {2041-1723}, doi = {10.1038/s41467-018-08008-w}, author = {Kilpel{\"a}inen, Tuomas O and Bentley, Amy R and Noordam, Raymond and Yun Ju Sung and Schwander, Karen and Thomas W Winkler and Jakupovi{\'c}, Hermina and Daniel I Chasman and Alisa Manning and Ntalla, Ioanna and Aschard, Hugues and Brown, Michael R and de Las Fuentes, Lisa and Franceschini, Nora and Guo, Xiuqing and Vojinovic, Dina and Aslibekyan, Stella and Feitosa, Mary F and Kho, Minjung and Musani, Solomon K and Melissa Richard and Wang, Heming and Wang, Zhe and Traci M Bartz and Bielak, Lawrence F and Campbell, Archie and Dorajoo, Rajkumar and Fisher, Virginia and Hartwig, Fernando P and Horimoto, Andrea R V R and Li, Changwei and Kurt Lohman and Marten, Jonathan and Sim, Xueling and Smith, Albert V and Tajuddin, Salman M and Alver, Maris and Amini, Marzyeh and Boissel, Mathilde and Jin-Fang Chai and Chen, Xu and Divers, Jasmin and Evangelou, Evangelos and Gao, Chuan and Graff, Mariaelisa and Sarah E Harris and He, Meian and Hsu, Fang-Chi and Jackson, Anne U and Jing Hua Zhao and Kraja, Aldi T and K{\"u}hnel, Brigitte and Laguzzi, Federica and Lyytik{\"a}inen, Leo-Pekka and Ilja M Nolte and Rauramaa, Rainer and Riaz, Muhammad and Robino, Antonietta and Rueedi, Rico and Heather M Stringham and Takeuchi, Fumihiko and van der Most, Peter J and Varga, Tibor V and Verweij, Niek and Erin B Ware and Wen, Wanqing and Li, Xiaoyin and Yanek, Lisa R and Amin, Najaf and Donna K Arnett and Boerwinkle, Eric and Brumat, Marco and Brian E Cade and Canouil, Micka{\"e}l and Chen, Yii-Der Ida and Concas, Maria Pina and Connell, John and de Mutsert, Ren{\'e}e and de Silva, H Janaka and de Vries, Paul S and Demirkan, Ayse and Ding, Jingzhong and Charles B Eaton and Jessica Faul and Friedlander, Yechiel and Gabriel, Kelley P and Ghanbari, Mohsen and Giulianini, Franco and Gu, Chi Charles and Gu, Dongfeng and Tamara B Harris and He, Jiang and Heikkinen, Sami and Heng, Chew-Kiat and Hunt, Steven C and Ikram, M Arfan and Jost Bruno Jonas and Koh, Woon-Puay and Komulainen, Pirjo and Krieger, Jose E and Stephen B Kritchevsky and Kutalik, Zolt{\'a}n and Kuusisto, Johanna and Langefeld, Carl D and Langenberg, Claudia and Lenore J Launer and Leander, Karin and Lemaitre, Rozenn N and Lewis, Cora E and Liang, Jingjing and Liu, Jianjun and M{\"a}gi, Reedik and Manichaikul, Ani and Meitinger, Thomas and Andres Metspalu and Milaneschi, Yuri and Mohlke, Karen L and Thomas H Mosley and Murray, Alison D and Michael A Nalls and Nang, Ei-Ei Khaing and Nelson, Christopher P and Nona, Sotoodehnia and Norris, Jill M and Nwuba, Chiamaka Vivian and Jeff O{\textquoteright}Connell and Palmer, Nicholette D and Papanicolau, George J and Pazoki, Raha and Nancy L Pedersen and Peters, Annette and Peyser, Patricia A and Polasek, Ozren and David J Porteous and Poveda, Alaitz and Olli T Raitakari and Rich, Stephen S and Neil Risch and Robinson, Jennifer G and Rose, Lynda M and Rudan, Igor and Schreiner, Pamela J and Scott, Robert A and Stephen Sidney and Sims, Mario and Smith, Jennifer A and Snieder, Harold and Sofer, Tamar and John M Starr and Sternfeld, Barbara and Strauch, Konstantin and Tang, Hua and Kent D Taylor and Tsai, Michael Y and Tuomilehto, Jaakko and Andr{\'e} G Uitterlinden and van der Ende, M Yldau and van Heemst, Diana and Voortman, Trudy and Waldenberger, Melanie and Wennberg, Patrik and Wilson, Gregory and Xiang, Yong-Bing and Yao, Jie and Yu, Caizheng and Yuan, Jian-Min and Zhao, Wei and Alan B Zonderman and Becker, Diane M and Boehnke, Michael and Bowden, Donald W and de Faire, Ulf and Ian J Deary and Elliott, Paul and T{\~o}nu Esko and Freedman, Barry I and Froguel, Philippe and Paolo P. Gasparini and Gieger, Christian and Kato, Norihiro and Laakso, Markku and Lakka, Timo A and Lehtim{\"a}ki, Terho and Patrik K E Magnusson and Oldehinkel, Albertine J and Brenda W J H Penninx and Nilesh J Samani and Shu, Xiao-Ou and van der Harst, Pim and Jana V. van Vliet-Ostaptchouk and Vollenweider, Peter and Wagenknecht, Lynne E and Wang, Ya X and Wareham, Nicholas J and David R Weir and Wu, Tangchun and Zheng, Wei and Zhu, Xiaofeng and Michele K Evans and Franks, Paul W and Gudnason, Vilmundur and Caroline Hayward and Horta, Bernardo L and Tanika N Kelly and Liu, Yongmei and Kari E North and Pereira, Alexandre C and Ridker, Paul M and Tai, E Shyong and van Dam, Rob M and Fox, Ervin R and Sharon L R Kardia and Liu, Ching-Ti and Dennis O Mook-Kanamori and Province, Michael A and Redline, Susan and Cornelia M van Duijn and Rotter, Jerome I and Charles Kooperberg and Gauderman, W James and Psaty, Bruce M and Kenneth Rice and Munroe, Patricia B and Myriam Fornage and Cupples, L Adrienne and Charles N Rotimi and Alanna C Morrison and Rao, Dabeeru C and Ruth J F Loos} }