Dietary Intake of Linoleic Acid, Its Concentrations, and the Risk of Type 2 Diabetes: A Systematic Review and Dose-Response Meta-analysis of Prospective Cohort Studies

Abstract

Supplementary data Supplemental Table 2: Reason for exclusion of retrieved articles ReferencesReason for exclusion 1.

Dietary Linoleic Acid: Will Modifying Dietary Fat Quality Reduce the Risk of Type 2 Diabetes?

“…A further question is whether the observational finding of a reduced diabetes risk in this meta-analyses ( 6 ) reflects a causal association. Unfortunately, controlled trials provide limited evidence that modulating dietary LA affects important glycemic traits in individuals without diabetes ( 14 ); e.g., substitution of 5% energy from SFA by PUFA (thus mainly LA) does not significantly reduce fasting or 2-h glucose and insulin or HbA 1c .…”

“…In this issue of Diabetes Care , Mousavi et al ( 6 ) summarize data from such prospective studies. They first systematically identified cohort studies on either dietary intake or tissue biomarkers of LA status and diabetes incidence.…”

“…However, this observation seemed largely to be driven by the results of one individual cohort study, the Health Professionals Follow-up Study (HPFS) ( 7 ). In none of the other individual cohorts was a significant association observed, for several no indication for an inverse association was found at all, and leaving out the HPFS from analyses leads to attenuation and loss of significance ( 6 ).…”

“…Individual cohort studies evaluated LA levels in different tissues and compartments, ranging from plasma cholesterol esters to plasma or erythrocyte phospholipids to adipose tissue. Nevertheless, inverse associations between higher LA content and diabetes risk were evident in many individual studies and in all meta-analyses, with the exception of adipose tissue, where only data from one individual cohort were identified ( 6 ). These associations were overall very robust against different sensitivity analyses; e.g., the association was not driven by individual studies or dependent on the tissue used for biomarker determination.…”

“…Informative in this regard would be systematic investigations in cohort studies using specific macronutrient substitutions. Cohort studies included in the meta-analysis by Mousavi et al ( 6 ) considered different adjustment models, with only three cohorts evaluating a substitution of LA for SFA ( 7 ). Similarly important, LA phospholipid levels have been found to correlate with other PUFA but also different SFA (e.g., inverse with palmitic acid) ( 17 ).…”