@article {6606,
	title = {Genome-wide meta-analysis identifies six novel loci associated with habitual coffee consumption.},
	journal = {Mol Psychiatry},
	volume = {20},
	year = {2015},
	month = {2015 May},
	pages = {647-56},
	abstract = {<p>Coffee, a major dietary source of caffeine, is among the most widely consumed beverages in the world and has received considerable attention regarding health risks and benefits. We conducted a genome-wide (GW) meta-analysis of predominately regular-type coffee consumption (cups per day) among up to 91,462 coffee consumers of European ancestry with top single-nucleotide polymorphisms (SNPs) followed-up in ~30 062 and 7964 coffee consumers of European and African-American ancestry, respectively. Studies from both stages were combined in a trans-ethnic meta-analysis. Confirmed loci were examined for putative functional and biological relevance. Eight loci, including six novel loci, met GW significance (log10Bayes factor (BF)>5.64) with per-allele effect sizes of 0.03-0.14 cups per day. Six are located in or near genes potentially involved in pharmacokinetics (ABCG2, AHR, POR and CYP1A2) and pharmacodynamics (BDNF and SLC6A4) of caffeine. Two map to GCKR and MLXIPL genes related to metabolic traits but lacking known roles in coffee consumption. Enhancer and promoter histone marks populate the regions of many confirmed loci and several potential regulatory SNPs are highly correlated with the lead SNP of each. SNP alleles near GCKR, MLXIPL, BDNF and CYP1A2 that were associated with higher coffee consumption have previously been associated with smoking initiation, higher adiposity and fasting insulin and glucose but lower blood pressure and favorable lipid, inflammatory and liver enzyme profiles (P<5 {\texttimes} 10(-8)).Our genetic findings among European and African-American adults reinforce the role of caffeine in mediating habitual coffee consumption and may point to molecular mechanisms underlying inter-individual variability in pharmacological and health effects of coffee.</p>},
	keywords = {Adaptor Proteins, Signal Transducing, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Brain-Derived Neurotrophic Factor, Coffea, Cytochrome P-450 CYP1A2, Food Habits, Genome-Wide Association Study, Humans, Phenotype, Polymorphism, Single Nucleotide},
	issn = {1476-5578},
	doi = {10.1038/mp.2014.107},
	author = {Cornelis, M C and Byrne, E M and Esko, T and Nalls, M A and Ganna, A and Paynter, N and Monda, K L and Amin, N and Fischer, K and Renstrom, F and Ngwa, J S and Huikari, V and Cavadino, A and Nolte, I M and Teumer, A and Yu, K and Marques-Vidal, P and Rawal, R and Manichaikul, A and Wojczynski, M K and Vink, J M and Zhao, J H and Burlutsky, G and Lahti, J and Mikkil{\"a}, V and Lemaitre, R N and Eriksson, J and Musani, S K and Tanaka, T and Geller, F and Luan, J and Hui, J and M{\"a}gi, R and Dimitriou, M and Garcia, M E and Ho, W-K and Wright, M J and Rose, L M and Magnusson, P K E and Pedersen, N L and Couper, D and Oostra, B A and Hofman, A and Ikram, M A and Tiemeier, H W and Uitterlinden, A G and van Rooij, F J A and Barroso, I and Johansson, I and Xue, L and Kaakinen, M and Milani, L and Power, C and Snieder, H and Stolk, R P and Baumeister, S E and Biffar, R and Gu, F and Bastardot, F and Kutalik, Z and Jacobs, D R and Forouhi, N G and Mihailov, E and Lind, L and Lindgren, C and Micha{\"e}lsson, K and Morris, A and Jensen, M and Khaw, K-T and Luben, R N and Wang, J J and M{\"a}nnist{\"o}, S and Per{\"a}l{\"a}, M-M and K{\"a}h{\"o}nen, M and Lehtim{\"a}ki, T and Viikari, J and Mozaffarian, D and Mukamal, K and Psaty, B M and D{\"o}ring, A and Heath, A C and Montgomery, G W and Dahmen, N and Carithers, T and Tucker, K L and Ferrucci, L and Boyd, H A and Melbye, M and Treur, J L and Mellstr{\"o}m, D and Hottenga, J J and Prokopenko, I and T{\"o}njes, A and Deloukas, P and Kanoni, S and Lorentzon, M and Houston, D K and Liu, Y and Danesh, J and Rasheed, A and Mason, M A and Zonderman, A B and Franke, L and Kristal, B S and Karjalainen, J and Reed, D R and Westra, H-J and Evans, M K and Saleheen, D and Harris, T B and Dedoussis, G and Curhan, G and Stumvoll, M and Beilby, J and Pasquale, L R and Feenstra, B and Bandinelli, S and Ordov{\'a}s, J M and Chan, A T and Peters, U and Ohlsson, C and Gieger, C and Martin, N G and Waldenberger, M and Siscovick, D S and Raitakari, O and Eriksson, J G and Mitchell, P and Hunter, D J and Kraft, P and Rimm, E B and Boomsma, D I and Borecki, I B and Loos, R J F and Wareham, N J and Vollenweider, P and Caporaso, N and Grabe, H J and Neuhouser, M L and Wolffenbuttel, B H R and Hu, F B and Hypponen, E and J{\"a}rvelin, M-R and Cupples, L A and Franks, P W and Ridker, P M and van Duijn, C M and Heiss, G and Metspalu, A and North, K E and Ingelsson, E and Nettleton, J A and van Dam, R M and Chasman, D I}
}
@article {6566,
	title = {Novel loci associated with usual sleep duration: the CHARGE Consortium Genome-Wide Association Study.},
	journal = {Mol Psychiatry},
	volume = {20},
	year = {2015},
	month = {2015 Oct},
	pages = {1232-9},
	abstract = {<p>Usual sleep duration is a heritable trait correlated with psychiatric morbidity, cardiometabolic disease and mortality, although little is known about the genetic variants influencing this trait. A genome-wide association study (GWAS) of usual sleep duration was conducted using 18 population-based cohorts totaling 47 180 individuals of European ancestry. Genome-wide significant association was identified at two loci. The strongest is located on chromosome 2, in an intergenic region 35- to 80-kb upstream from the thyroid-specific transcription factor PAX8 (lowest P=1.1 {\texttimes} 10(-9)). This finding was replicated in an African-American sample of 4771 individuals (lowest P=9.3 {\texttimes} 10(-4)). The strongest combined association was at rs1823125 (P=1.5 {\texttimes} 10(-10), minor allele frequency 0.26 in the discovery sample, 0.12 in the replication sample), with each copy of the minor allele associated with a sleep duration 3.1 min longer per night. The alleles associated with longer sleep duration were associated in previous GWAS with a more favorable metabolic profile and a lower risk of attention deficit hyperactivity disorder. Understanding the mechanisms underlying these associations may help elucidate biological mechanisms influencing sleep duration and its association with psychiatric, metabolic and cardiovascular disease. </p>},
	keywords = {Adult, African Americans, Aged, Dyssomnias, European Continental Ancestry Group, Female, Genetic Association Studies, Genome-Wide Association Study, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide, Self Report, Sleep},
	issn = {1476-5578},
	doi = {10.1038/mp.2014.133},
	author = {Gottlieb, D J and Hek, K and Chen, T-H and Watson, N F and Eiriksdottir, G and Byrne, E M and Cornelis, M and Warby, S C and Bandinelli, S and Cherkas, L and Evans, D S and Grabe, H J and Lahti, J and Li, M and Lehtim{\"a}ki, T and Lumley, T and Marciante, K D and P{\'e}russe, L and Psaty, B M and Robbins, J and Tranah, G J and Vink, J M and Wilk, J B and Stafford, J M and Bellis, C and Biffar, R and Bouchard, C and Cade, B and Curhan, G C and Eriksson, J G and Ewert, R and Ferrucci, L and F{\"u}l{\"o}p, T and Gehrman, P R and Goodloe, R and Harris, T B and Heath, A C and Hernandez, D and Hofman, A and Hottenga, J-J and Hunter, D J and Jensen, M K and Johnson, A D and K{\"a}h{\"o}nen, M and Kao, L and Kraft, P and Larkin, E K and Lauderdale, D S and Luik, A I and Medici, M and Montgomery, G W and Palotie, A and Patel, S R and Pistis, G and Porcu, E and Quaye, L and Raitakari, O and Redline, S and Rimm, E B and Rotter, J I and Smith, A V and Spector, T D and Teumer, A and Uitterlinden, A G and Vohl, M-C and Widen, E and Willemsen, G and Young, T and Zhang, X and Liu, Y and Blangero, J and Boomsma, D I and Gudnason, V and Hu, F and Mangino, M and Martin, N G and O{\textquoteright}Connor, G T and Stone, K L and Tanaka, T and Viikari, J and Gharib, S A and Punjabi, N M and R{\"a}ikk{\"o}nen, K and V{\"o}lzke, H and Mignot, E and Tiemeier, H}
}
