@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 {8270,
	title = {{Associations of circulating very-long-chain saturated fatty acids and incident type 2 diabetes: a pooled analysis of prospective cohort studies},
	journal = {Am. J. Clin. Nutr.},
	volume = {109},
	year = {2019},
	month = {04},
	pages = {1216{\textendash}1223},
	abstract = {Saturated fatty acids (SFAs) of different chain lengths have unique metabolic and biological effects, and a small number of recent studies suggest that higher circulating concentrations of the very-long-chain SFAs (VLSFAs) arachidic acid (20:0), behenic acid (22:0), and lignoceric acid (24:0) are associated with a lower risk of diabetes. Confirmation of these findings in a large and diverse population is needed.\ We investigated the associations of circulating VLSFAs 20:0, 22:0, and 24:0 with incident type 2 diabetes in prospective studies.\ Twelve studies that are part of the Fatty Acids and Outcomes Research Consortium participated in the analysis. Using Cox or logistic regression within studies and an inverse-variance-weighted meta-analysis across studies, we examined the associations of VLSFAs 20:0, 22:0, and 24:0 with incident diabetes among 51,431 participants.\ There were 14,276 cases of incident diabetes across participating studies. Higher circulating concentrations of 20:0, 22:0, and 24:0 were each associated with a lower risk of incident diabetes. Pooling across cohorts, the RR (95\% CI) for incident diabetes comparing the 90th percentile to the 10th percentile was 0.78 (0.70, 0.87) for 20:0, 0.84 (0.77, 0.91) for 22:0, and 0.75 (0.69, 0.83) for 24:0 after adjustment for demographic, lifestyle, adiposity, and other health factors. Results were fully attenuated in exploratory models that adjusted for circulating 16:0 and triglycerides.\ Results from this pooled analysis indicate that higher concentrations of circulating VLSFAs 20:0, 22:0, and 24:0 are each associated with a lower risk of diabetes.},
	author = {Fretts, A. M. and Imamura, F. and Marklund, M. and Micha, R. and Wu, J. H. Y. and Murphy, R. A. and Chien, K. L. and McKnight, B. and Tintle, N. and Forouhi, N. G. and Qureshi, W. T. and Virtanen, J. K. and Wong, K. and Wood, A. C. and Lankinen, M. and Rajaobelina, K. and Harris, T. B. and Djouss?, L. and Harris, B. and Wareham, N. J. and Steffen, L. M. and Laakso, M. and Veenstra, J. and Samieri, C. and Brouwer, I. A. and Yu, C. I. and Koulman, A. and Steffen, B. T. and Helmer, C. and Sotoodehnia, N. and Siscovick, D. and Gudnason, V. and Wagenknecht, L. and Voutilainen, S. and Tsai, M. Y. and Uusitupa, M. and Kalsbeek, A. and Berr, C. and Mozaffarian, D. and Lemaitre, R. N.}
}
@article {8455,
	title = {{Fatty acids in the de novo lipogenesis pathway and incidence of type 2 diabetes: A pooled analysis of prospective cohort studies},
	journal = {PLoS Med},
	volume = {17},
	year = {2020},
	month = {06},
	pages = {e1003102},
	abstract = {De novo lipogenesis (DNL) is the primary metabolic pathway synthesizing fatty acids from carbohydrates, protein, or alcohol. Our aim was to examine associations of in vivo levels of selected fatty acids (16:0, 16:1n7, 18:0, 18:1n9) in DNL with incidence of type 2 diabetes (T2D).\ Seventeen cohorts from 12 countries (7 from Europe, 7 from the United States, 1 from Australia, 1 from Taiwan; baseline years = 1970-1973 to 2006-2010) conducted harmonized individual-level analyses of associations of DNL-related fatty acids with incident T2D. In total, we evaluated 65,225 participants (mean ages = 52.3-75.5 years; \% women = 20.4\%-62.3\% in 12 cohorts recruiting both sexes) and 15,383 incident cases of T2D over the 9-year follow-up on average. Cohort-specific association of each of 16:0, 16:1n7, 18:0, and 18:1n9 with incident T2D was estimated, adjusted for demographic factors, socioeconomic characteristics, alcohol, smoking, physical activity, dyslipidemia, hypertension, menopausal status, and adiposity. Cohort-specific associations were meta-analyzed with an inverse-variance-weighted approach. Each of the 4 fatty acids positively related to incident T2D. Relative risks (RRs) per cohort-specific range between midpoints of the top and bottom quintiles of fatty acid concentrations were 1.53 (1.41-1.66; p < 0.001) for 16:0, 1.40 (1.33-1.48; p < 0.001) for 16:1n-7, 1.14 (1.05-1.22; p = 0.001) for 18:0, and 1.16 (1.07-1.25; p < 0.001) for 18:1n9. Heterogeneity was seen across cohorts (I2 = 51.1\%-73.1\% for each fatty acid) but not explained by lipid fractions and global geographical regions. Further adjusted for triglycerides (and 16:0 when appropriate) to evaluate associations independent of overall DNL, the associations remained significant for 16:0, 16:1n7, and 18:0 but were attenuated for 18:1n9 (RR = 1.03, 95\% confidence interval (CI) = 0.94-1.13). These findings had limitations in potential reverse causation and residual confounding by imprecisely measured or unmeasured factors.\ Concentrations of fatty acids in the DNL were positively associated with T2D incidence. Our findings support further work to investigate a possible role of DNL and individual fatty acids in the development of T2D.},
	author = {Imamura, F. and Fretts, A. M. and Marklund, M. and Ardisson Korat, A. V. and Yang, W. S. and Lankinen, M. and Qureshi, W. and Helmer, C. and Chen, T. A. and Virtanen, J. K. and Wong, K. and Bassett, J. K. and Murphy, R. and Tintle, N. and Yu, C. I. and Brouwer, I. A. and Chien, K. L. and Chen, Y. Y. and Wood, A. C. and Del Gobbo, L. C. and Djousse, L. and Geleijnse, J. M. and Giles, G. G. and de Goede, J. and Gudnason, V. and Harris, W. S. and Hodge, A. and Hu, F. and Koulman, A. and Laakso, M. and Lind, L. and Lin, H. J. and McKnight, B. and Rajaobelina, K. and Riserus, U. and Robinson, J. G. and Samieri, C. and Senn, M. and Siscovick, D. S. and Soedamah-Muthu, S. S. and Sotoodehnia, N. and Sun, Q. and Tsai, M. Y. and Tuomainen, T. P. and Uusitupa, M. and Wagenknecht, L. E. and Wareham, N. J. and Wu, J. H. Y. and Micha, R. and Lemaitre, R. N. and Mozaffarian, D. and Forouhi, N. G.}
}
@article {9460,
	title = {{Trans Fatty Acid Biomarkers and Incident Type 2 Diabetes: Pooled Analysis of 12 Prospective Cohort Studies in the Fatty Acids and Outcomes Research Consortium (FORCE)},
	journal = {Diabetes Care},
	volume = {45},
	year = {2022},
	month = {Apr},
	pages = {854{\textendash}863},
	abstract = {Trans fatty acids (TFAs) have harmful biologic effects that could increase the risk of type 2 diabetes (T2D), but evidence remains uncertain. We aimed to investigate the prospective associations of TFA biomarkers and T2D by conducting an individual participant-level pooled analysis.\ 18 years without prevalent diabetes. Each cohort conducted de novo harmonized analyses using a prespecified protocol, and findings were pooled using inverse-variance weighted meta-analysis. Heterogeneity was explored by prespecified between-study and within-study characteristics.\ 0.1).\ Circulating individual trans-18:2 TFA biomarkers were not associated with risk of T2D, while trans-16:1n-9, total trans-18:1, and total trans-18:2 were inversely associated. Findings may reflect the influence of mixed TFA sources (industrial vs. natural ruminant), a general decline in TFA exposure due to policy changes during this period, or the relatively limited range of TFA levels.},
	author = {Lai, H. T. M. and Imamura, F. and Korat, A. V. A. and Murphy, R. A. and Tintle, N. and Bassett, J. K. and Chen, J. and ger, J. and Chien, K. L. and Senn, M. and Wood, A. C. and Forouhi, N. G. and Schulze, M. B. and Harris, W. S. and Vasan, R. S. and Hu, F. and Giles, G. G. and Hodge, A. and Djousse, L. and Brouwer, I. A. and Qian, F. and Sun, Q. and Wu, J. H. Y. and Marklund, M. and Lemaitre, R. N. and Siscovick, D. S. and Fretts, A. M. and Shadyab, A. H. and Manson, J. E. and Howard, B. V. and Robinson, J. G. and Wallace, R. B. and Wareham, N. J. and Chen, Y. I. and Rotter, J. I. and Tsai, M. Y. and Micha, R. and Mozaffarian, D.}
}
