@article {9464,
	title = {-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease: Pooling Project of 19 Cohort Studies},
	journal = {JAMA Intern Med},
	volume = {176},
	year = {2016},
	month = {Aug},
	pages = {1155{\textendash}1166},
	abstract = {-3 polyunsaturated fatty acids for primary prevention of coronary heart disease (CHD) remains controversial. Most prior longitudinal studies evaluated self-reported consumption rather than biomarkers.\ -3) for incident CHD.\ A global consortium of 19 studies identified by November 2014.\ -3 biomarkers and ascertained CHD.\ -6 levels, and FADS desaturase genes.\ Incident total CHD, fatal CHD, and nonfatal myocardial infarction (MI).\ -3 biomarkers ALA, DPA, and DHA were associated with a lower risk of fatal CHD, with relative risks (RRs) of 0.91 (95\% CI, 0.84-0.98) for ALA, 0.90 (95\% CI, 0.85-0.96) for DPA, and 0.90 (95\% CI, 0.84-0.96) for DHA. Although DPA was associated with a lower risk of total CHD (RR, 0.94; 95\% CI, 0.90-0.99), ALA (RR, 1.00; 95\% CI, 0.95-1.05), EPA (RR, 0.94; 95\% CI, 0.87-1.02), and DHA (RR, 0.95; 95\% CI, 0.91-1.00) were not. Significant associations with nonfatal MI were not evident. Associations appeared generally stronger in phospholipids and total plasma. Restricted cubic splines did not identify evidence of nonlinearity in dose responses.\ -3 fatty acids are associated with a modestly lower incidence of fatal CHD.},
	author = {Del Gobbo, L. C. and Imamura, F. and Aslibekyan, S. and Marklund, M. and Virtanen, J. K. and Wennberg, M. and Yakoob, M. Y. and Chiuve, S. E. and Dela Cruz, L. and Frazier-Wood, A. C. and Fretts, A. M. and Guallar, E. and Matsumoto, C. and Prem, K. and Tanaka, T. and Wu, J. H. and Zhou, X. and Helmer, C. and Ingelsson, E. and Yuan, J. M. and Barberger-Gateau, P. and Campos, H. and Chaves, P. H. and {\'e}, L. and Giles, G. G. and mez-Aracena, J. and Hodge, A. M. and Hu, F. B. and Jansson, J. H. and Johansson, I. and Khaw, K. T. and Koh, W. P. and Lemaitre, R. N. and Lind, L. and Luben, R. N. and Rimm, E. B. and rus, U. and Samieri, C. and Franks, P. W. and Siscovick, D. S. and Stampfer, M. and Steffen, L. M. and Steffen, B. T. and Tsai, M. Y. and van Dam, R. M. and Voutilainen, S. and Willett, W. C. and Woodward, M. and Mozaffarian, D.}
}
@article {9462,
	title = {740 adults from 20 prospective cohort studies},
	journal = {Lancet Diabetes Endocrinol},
	volume = {5},
	year = {2017},
	month = {Dec},
	pages = {965{\textendash}974},
	abstract = {The metabolic effects of omega-6 polyunsaturated fatty acids (PUFAs) remain contentious, and little evidence is available regarding their potential role in primary prevention of type 2 diabetes. We aimed to assess the associations of linoleic acid and arachidonic acid biomarkers with incident type 2 diabetes.\ We did a pooled analysis of new, harmonised, individual-level analyses for the biomarkers linoleic acid and its metabolite arachidonic acid and incident type 2 diabetes. We analysed data from 20 prospective cohort studies from ten countries (Iceland, the Netherlands, the USA, Taiwan, the UK, Germany, Finland, Australia, Sweden, and France), with biomarkers sampled between 1970 and 2010. Participants included in the analyses were aged 18 years or older and had data available for linoleic acid and arachidonic acid biomarkers at baseline. We excluded participants with type 2 diabetes at baseline. The main outcome was the association between omega-6 PUFA biomarkers and incident type 2 diabetes. We assessed the relative risk of type 2 diabetes prospectively for each cohort and lipid compartment separately using a prespecified analytic plan for exposures, covariates, effect modifiers, and analysis, and the findings were then pooled using inverse-variance weighted meta-analysis.\ 13).\ Findings suggest that linoleic acid has long-term benefits for the prevention of type 2 diabetes and that arachidonic acid is not harmful.\ Funders are shown in the appendix.},
	author = {Wu, J. H. Y. and Marklund, M. and Imamura, F. and Tintle, N. and Ardisson Korat, A. V. and de Goede, J. and Zhou, X. and Yang, W. S. and de Oliveira Otto, M. C. and ger, J. and Qureshi, W. and Virtanen, J. K. and Bassett, J. K. and Frazier-Wood, A. C. and Lankinen, M. and Murphy, R. A. and Rajaobelina, K. and Del Gobbo, L. C. and Forouhi, N. G. and Luben, R. and Khaw, K. T. and Wareham, N. and Kalsbeek, A. and Veenstra, J. and Luo, J. and Hu, F. B. and Lin, H. J. and Siscovick, D. S. and Boeing, H. and Chen, T. A. and Steffen, B. and Steffen, L. M. and Hodge, A. and Eriksdottir, G. and Smith, A. V. and Gudnason, V. and Harris, T. B. and Brouwer, I. A. and Berr, C. and Helmer, C. and Samieri, C. and Laakso, M. and Tsai, M. Y. and Giles, G. G. and Nurmi, T. and Wagenknecht, L. and Schulze, M. B. and Lemaitre, R. N. and Chien, K. L. and Soedamah-Muthu, S. S. and Geleijnse, J. M. and Sun, Q. and Harris, W. S. and Lind, L. and v, J. and Riserus, U. and Micha, R. and Mozaffarian, D.}
}
@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.}
}
