TY - JOUR
T1 - Plasma and Dietary Linoleic Acid and 3-Year Risk of Type 2 Diabetes After Myocardial Infarction
T2 - A Prospective Analysis in the Alpha Omega Cohort
AU - Pertiwi, Kamalita
AU - Wanders, Anne J
AU - Harbers, Marjolein C
AU - Küpers, Leanne K
AU - Soedamah-Muthu, Sabita S
AU - de Goede, Janette
AU - Zock, Peter L
AU - Geleijnse, Johanna M
N1 - Funding Information:
The Alpha Omega Cohort emerged from the Alpha Omega Trial (ClinicalTrials.gov identifier NCT00127452), which was funded by the Dutch Heart Foundation (Hartstichting) (grant 200T401), National Institutes of Health National Heart, Lung, and Blood Institute (grant R01HL076200), and Office of Dietary Supplements. This research was supported in part by the Netherlands Organisation for Scientific Research (Nederlandse Organisatie voor Wetenschappelijk Onderzoek) through its Graduate Programme on Food Structure, Digestion and Health.
Funding Information:
Acknowledgments. The authors thank Eveline Waterham (Division of Human Nutrition and Health, WageningenUniversity)forlogisticsupportanddata management and Dr. Paul Hulshof, Robert Hove-nier, and Marlies Diepeveen-de Bruin (Division of Human Nutrition and Health, Wageningen University) for analysis of plasma FA. Funding. The Alpha Omega Cohort emerged from the Alpha Omega Trial (ClinicalTrials.gov identifier NCT00127452), which was funded by the Dutch Heart Foundation (Hartstichting) (grant 200T401), National Institutes of Health National Heart, Lung, and Blood Institute (grant R01HL076200), and Office of DietarySupplements.Thisresearchwassupported in part by the Netherlands Organisation for Scientific Research (Nederlandse Organisatie voor Wetenschappelijk Onderzoek) through its Graduate Programme on Food Structure, Digestion and Health. Duality of Interest. This research was supported in part by Upfield. Unilever R&D Vlaardingen provided financial support for plasma FA determinations in the Alpha Omega Cohort. A.J.W. and P.L.Z.areemployedbyUnilever,Vlaardingen,the Netherlands. J.M.G. received funding from Uni-lever R&D for epidemiological studies of dietary and circulating FAs and cardiovascular disease. Unilever is a producer of food consumer products. It divested its spreads business, which has operated since July 2018 under the name Upfield. No other potential conflicts of interest relevant to this article were reported. Author Contributions. K.P., A.J.W., and M.C.H. wrote the manuscript. K.P., A.J.W., M.C.H., L.K.K., S.S.S.-M., J.d.G., P.L.Z., and J.M.G. interpreted the results and critically revised the manuscript for intellectual content. K.P. and M.C.H. analyzed data. S.S.S.-M. and J.M.G. designed research. J.M.G. had primary responsibility for the final content and handled funding and supervision. All of the authors read and approved the final manuscript. J.M.G. is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Prior Presentation. Parts of this study were presented in abstract form at the EPI|Lifestyle 2018 Scientific Sessions of the American Heart Association, New Orleans, LA, 20–23 March 2018.
Publisher Copyright:
© 2019 by the American Diabetes Association.
PY - 2020/2/1
Y1 - 2020/2/1
N2 - OBJECTIVE: To study plasma and dietary linoleic acid (LA) in relation to type 2 diabetes risk in post-myocardial infarction (MI) patients. RESEARCH DESIGN AND METHODS: We included 3,257 patients aged 60-80 years (80% male) with a median time since MI of 3.5 years from the Alpha Omega Cohort and who were initially free of type 2 diabetes. At baseline (2002-2006), plasma LA was measured in cholesteryl esters, and dietary LA was estimated with a 203-item food-frequency questionnaire. Incident type 2 diabetes was ascertained through self-reported physician diagnosis and medication use. Hazardratios (with 95% CIs) were calculated by Cox regressions, in which dietary LA isocalorically replaced the sumofsaturated (SFA) and trans fatty acids (TFA). RESULTS: Mean ± SD circulating and dietary LA was 50.1 ± 4.9% and 5.9 ± 2.1% energy, respectively. Plasma and dietary LA were weakly correlated (Spearman r = 0.13, P < 0.001). During a median follow-up of 41 months, 171 patients developed type 2 diabetes. Plasma LA was inversely associated with type 2 diabetes risk (quintile [Q]5 vs. Q1: 0.44 [0.26, 0.75]; per 5%: 0.73 [0.62, 0.86]). Substitution of dietary LA for SFA+TFA showed no association with type 2 diabetes risk (Q5 vs. Q1: 0.78 [0.36, 1.72]; per 5% energy: 1.18 [0.59, 2.35]). Adjustment for markers of de novo lipogenesis attenuated plasma LA associations. CONCLUSIONS: In our cohort of post-MI patients, plasma LA was inversely related to type 2 diabetes risk, whereas dietary LA was not related. Further research is neededtoassess whether plasma LA indicates metabolic state rather than dietary LA in these patients.
AB - OBJECTIVE: To study plasma and dietary linoleic acid (LA) in relation to type 2 diabetes risk in post-myocardial infarction (MI) patients. RESEARCH DESIGN AND METHODS: We included 3,257 patients aged 60-80 years (80% male) with a median time since MI of 3.5 years from the Alpha Omega Cohort and who were initially free of type 2 diabetes. At baseline (2002-2006), plasma LA was measured in cholesteryl esters, and dietary LA was estimated with a 203-item food-frequency questionnaire. Incident type 2 diabetes was ascertained through self-reported physician diagnosis and medication use. Hazardratios (with 95% CIs) were calculated by Cox regressions, in which dietary LA isocalorically replaced the sumofsaturated (SFA) and trans fatty acids (TFA). RESULTS: Mean ± SD circulating and dietary LA was 50.1 ± 4.9% and 5.9 ± 2.1% energy, respectively. Plasma and dietary LA were weakly correlated (Spearman r = 0.13, P < 0.001). During a median follow-up of 41 months, 171 patients developed type 2 diabetes. Plasma LA was inversely associated with type 2 diabetes risk (quintile [Q]5 vs. Q1: 0.44 [0.26, 0.75]; per 5%: 0.73 [0.62, 0.86]). Substitution of dietary LA for SFA+TFA showed no association with type 2 diabetes risk (Q5 vs. Q1: 0.78 [0.36, 1.72]; per 5% energy: 1.18 [0.59, 2.35]). Adjustment for markers of de novo lipogenesis attenuated plasma LA associations. CONCLUSIONS: In our cohort of post-MI patients, plasma LA was inversely related to type 2 diabetes risk, whereas dietary LA was not related. Further research is neededtoassess whether plasma LA indicates metabolic state rather than dietary LA in these patients.
UR - http://www.scopus.com/inward/record.url?scp=85078368270&partnerID=8YFLogxK
U2 - 10.2337/dc19-1483
DO - 10.2337/dc19-1483
M3 - Article
C2 - 31727685
SN - 0149-5992
VL - 43
SP - 358
EP - 365
JO - Diabetes Care
JF - Diabetes Care
IS - 2
ER -