@article {8536,
	title = {{Dairy Consumption and Body Mass Index Among Adults: Mendelian Randomization Analysis of 184802 Individuals from 25 Studies},
	journal = {Clin Chem},
	volume = {64},
	year = {2018},
	month = {01},
	pages = {183{\textendash}191},
	abstract = {Associations between dairy intake and body mass index (BMI) have been inconsistently observed in epidemiological studies, and the causal relationship remains ill defined.\ We performed Mendelian randomization (MR) analysis using an established dairy intake-associated genetic polymorphism located upstream of the lactase gene (LCT-13910 C/T, rs4988235) as an instrumental variable (IV). Linear regression models were fitted to analyze associations between (a) dairy intake and BMI, (b) rs4988235 and dairy intake, and (c) rs4988235 and BMI in each study. The causal effect of dairy intake on BMI was quantified by IV estimators among 184802 participants from 25 studies.\ Higher dairy intake was associated with higher BMI ({\^I}{\texttwosuperior} = 0.03 kg/m2 per serving/day; 95\% CI, 0.00-0.06; P = 0.04), whereas the LCT genotype with 1 or 2 T allele was significantly associated with 0.20 (95\% CI, 0.14-0.25) serving/day higher dairy intake (P = 3.15 {\~A}{\textemdash} 10-12) and 0.12 (95\% CI, 0.06-0.17) kg/m2 higher BMI (P = 2.11 {\~A}{\textemdash} 10-5). MR analysis showed that the genetically determined higher dairy intake was significantly associated with higher BMI ({\^I}{\texttwosuperior} = 0.60 kg/m2 per serving/day; 95\% CI, 0.27-0.92; P = 3.0 {\~A}{\textemdash} 10-4).\ The present study provides strong evidence to support a causal effect of higher dairy intake on increased BMI among adults.},
	author = {Huang, T. and Ding, M. and Bergholdt, H. K. M. and Wang, T. and Heianza, Y. and Sun, D. and Frazier-Wood, A. C. and Aslibekyan, S. and North, K. E. and Voortman, T. and Graff, M. and Smith, C. E. and Lai, C. Q. and Varbo, A. and Lemaitre, R. N. and de Jonge, M. E. A. L. and Fumeron, F. and Corella, D. and Wang, C. A. and Tj?nneland, A. and Overvad, K. and S?rensen, T. I. A. and Feitosa, M. F. and Wojczynski, M. K. and K?h?nen, M. and Renstr?m, F. and Psaty, B. M. and Siscovick, D. S. and Barroso, I. and Johansson, I. and Hernandez, D. and Ferrucci, L. and Bandinelli, S. and Linneberg, A. and Zillikens, M. C. and Sandholt, C. H. and Pedersen, O. and Hansen, T. and Schulz, C. A. and Sonestedt, E. and Orho-Melander, M. and Chen, T. A. and Rotter, J. I. and Allison, M. A. and Rich, S. S. and Sorl?, J. V. and Coltell, O. and Pennell, C. E. and Eastwood, P. and Hofman, A. and Uitterlinden, A. G. and van Rooij, F. J. A. and Chu, A. Y. and Rose, L. M. and Ridker, P. M. and Viikari, J. and Raitakari, O. and Lehtim?ki, T. and Mikkil?, V. and Willett, W. C. and Wang, Y. and Tucker, K. L. and Ordovas, J. M. and Kilpel?inen, T. O. and Province, M. A. and Franks, P. W. and Arnett, D. K. and Tanaka, T. and Toft, U. and Ericson, U. and Franco, O. H. and Mozaffarian, D. and Hu, F. B. and Chasman, D. I. and Nordestgaard, B. G. and Ellervik, C. and Qi, L.}
}
@article {8523,
	title = {{Quality of dietary fat and genetic risk of type 2 diabetes: individual participant data meta-analysis},
	journal = {BMJ},
	volume = {366},
	year = {2019},
	month = {07},
	pages = {l4292},
	abstract = {{To investigate whether the genetic burden of type 2 diabetes modifies the association between the quality of dietary fat and the incidence of type 2 diabetes.\ Individual participant data meta-analysis.\ Eligible prospective cohort studies were systematically sourced from studies published between January 1970 and February 2017 through electronic searches in major medical databases (Medline, Embase, and Scopus) and discussion with investigators.\ Data from cohort studies or multicohort consortia with available genome-wide genetic data and information about the quality of dietary fat and the incidence of type 2 diabetes in participants of European descent was sought. Prospective cohorts that had accrued five or more years of follow-up were included. The type 2 diabetes genetic risk profile was characterized by a 68-variant polygenic risk score weighted by published effect sizes. Diet was recorded by using validated cohort-specific dietary assessment tools. Outcome measures were summary adjusted hazard ratios of incident type 2 diabetes for polygenic risk score, isocaloric replacement of carbohydrate (refined starch and sugars) with types of fat, and the interaction of types of fat with polygenic risk score.\ Of 102 305 participants from 15 prospective cohort studies, 20 015 type 2 diabetes cases were documented after a median follow-up of 12 years (interquartile range 9.4-14.2). The hazard ratio of type 2 diabetes per increment of 10 risk alleles in the polygenic risk score was 1.64 (95\% confidence interval 1.54 to 1.75},
	author = {Merino, J. and Guasch-Ferr?, M. and Ellervik, C. and Dashti, H. S. and Sharp, S. J. and Wu, P. and Overvad, K. and Sarnowski, C. and Kuokkanen, M. and Lemaitre, R. N. and Justice, A. E. and Ericson, U. and Braun, K. V. E. and Mahendran, Y. and Frazier-Wood, A. C. and Sun, D. and Chu, A. Y. and Tanaka, T. and Luan, J. and Hong, J. and Tj?nneland, A. and Ding, M. and Lundqvist, A. and Mukamal, K. and Rohde, R. and Schulz, C. A. and Franco, O. H. and Grarup, N. and Chen, Y. I. and Bazzano, L. and Franks, P. W. and Buring, J. E. and Langenberg, C. and Liu, C. T. and Hansen, T. and Jensen, M. K. and S??ksj?rvi, K. and Psaty, B. M. and Young, K. L. and Hindy, G. and Sandholt, C. H. and Ridker, P. M. and Ordovas, J. M. and Meigs, J. B. and Pedersen, O. and Kraft, P. and Perola, M. and North, K. E. and Orho-Melander, M. and Voortman, T. and Toft, U. and Rotter, J. I. and Qi, L. and Forouhi, N. G. and Mozaffarian, D. and S?rensen, T. I. A. and Stampfer, M. J. and M?nnist?, S. and Selvin, E. and Imamura, F. and Salomaa, V. and Hu, F. B. and Wareham, N. J. and Dupuis, J. and Smith, C. E. and Kilpel?inen, T. O. and Chasman, D. I. and Florez, J. C.}
}
@article {8783,
	title = {{Epigenome-wide association meta-analysis of DNA methylation with coffee and tea consumption},
	journal = {Nat Commun},
	volume = {12},
	year = {2021},
	month = {05},
	pages = {2830},
	abstract = {10.1038/s41467-021-22752-6Coffee and tea are extensively consumed beverages worldwide which have received considerable attention regarding health. Intake of these beverages is consistently linked to, among others, reduced risk of diabetes and liver diseases; however, the mechanisms of action remain elusive. Epigenetics is suggested as a mechanism mediating the effects of dietary and lifestyle factors on disease onset. Here we report the results from epigenome-wide association studies (EWAS) on coffee and tea consumption in 15,789 participants of European and African-American ancestries from 15 cohorts. EWAS meta-analysis of coffee consumption reveals 11 CpGs surpassing the epigenome-wide significance threshold (P-value <1.1{\texttimes}10-7), which annotated to the AHRR, F2RL3, FLJ43663, HDAC4, GFI1 and PHGDH genes. Among them, cg14476101 is significantly associated with expression of the PHGDH and risk of fatty liver disease. Knockdown of PHGDH expression in liver cells shows a correlation with expression levels of genes associated with circulating lipids, suggesting a role of PHGDH in hepatic-lipid metabolism. EWAS meta-analysis on tea consumption reveals no significant association, only two CpGs annotated to CACNA1A and PRDM16 genes show suggestive association (P-value <5.0{\texttimes}10-6). These findings indicate that coffee-associated changes in DNA methylation levels may explain the mechanism of action of coffee consumption in conferring risk of diseases.},
	author = {Karabegovi{\'c}, I. and Portilla-Fernandez, E. and Li, Y. and Ma, J. and Maas, S. C. E. and Sun, D. and Hu, E. A. and K{\"u}hnel, B. and Zhang, Y. and Ambatipudi, S. and Fiorito, G. and Huang, J. and Castillo-Fernandez, J. E. and Wiggins, K. L. and de Klein, N. and Grioni, S. and Swenson, B. R. and Polidoro, S. and Treur, J. L. and Cuenin, C. and Tsai, P. C. and Costeira, R. and Chajes, V. and Braun, K. and Verweij, N. and Kretschmer, A. and Franke, L. and van Meurs, J. B. J. and Uitterlinden, A. G. and de Knegt, R. J. and Ikram, M. A. and Dehghan, A. and Peters, A. and Sch{\"o}ttker, B. and Gharib, S. A. and Sotoodehnia, N. and Bell, J. T. and Elliott, P. and Vineis, P. and Relton, C. and Herceg, Z. and Brenner, H. and Waldenberger, M. and Rebholz, C. M. and Voortman, T. and Pan, Q. and Fornage, M. and Levy, D. and Kayser, M. and Ghanbari, M.}
}
