Plasma and Dietary Linoleic Acid and 3-Year Risk of Type 2 Diabetes After Myocardial Infarction: A Prospective Analysis in the Alpha Omega Cohort

• Published in: Diabetes care Vol. 43; no. 2; pp. 358 - 365
• Main Authors: Pertiwi, Kamalita, Wanders, Anne J, Harbers, Marjolein C, Küpers, Leanne K, Soedamah-Muthu, Sabita S, de Goede, Janette, Zock, Peter L, Geleijnse, Johanna M
• Format: Journal Article
• Language: English
• Published: United States American Diabetes Association 01-02-2020
• Subjects: Aged; Aged, 80 and over; Biomarkers - blood; Cohort Studies; Diabetes; Diabetes mellitus; Diabetes mellitus (non-insulin dependent); Diabetes Mellitus, Type 2 - blood; Diabetes Mellitus, Type 2 - etiology; Diet; Dietary Fats - administration & dosage; Dietary Fats - blood; Epidemiology/Health Services Research; Esters; Fatty acids; Female; Follow-Up Studies; Health risk assessment; Health risks; Heart attacks; Humans; Linoleic acid; Linoleic Acid - administration & dosage; Linoleic Acid - blood; Lipogenesis; Male; Middle Aged; Myocardial infarction; Myocardial Infarction - blood; Myocardial Infarction - complications; Myocardial Infarction - epidemiology; Nutrition Surveys; Prospective Studies; Regression analysis; Research design; Risk; Risk Factors; Trans fatty acids; Trans Fatty Acids - administration & dosage; Trans Fatty Acids - blood
• ISSN: 0149-5992; 1935-5548; 1935-5548
• DOI: 10.2337/dc19-1483

To study plasma and dietary linoleic acid (LA) in relation to type 2 diabetes risk in post-myocardial infarction (MI) patients.
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. Hazard ratios (with 95% CIs) were calculated by Cox regressions, in which dietary LA isocalorically replaced the sum of saturated (SFA) and
fatty acids (TFA).
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
= 0.13,
< 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.
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 needed to assess whether plasma LA indicates metabolic state rather than dietary LA in these patients.