Dietary advanced glycation end products intake, genetic predisposition and risk of coronary heart disease: a prospective study.

Abstract

Objective: Dietary advanced glycation end products (AGEs) intake may be associated with coronary heart disease (CHD) risk. We aimed to investigate the association between dietary AGEs intake and CHD risk and to further investigate whether this association could be influenced by genetic risk.

Methods: Data from UK Biobank were used. Dietary AGEs intake, including Nε-(carboxymethyl) lysine (CML), Nε-(1-Carboxyethyl)-L-lysine (CEL), and Nd-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1) were calculated by coupling the consumption of food items from 24-hour dietary recall with the dietary AGEs database. Baseline dietary information was first collected through Oxford WebQ 24 h food recall between April 2009 and September 2010. From February 2011 to June 2012, the Oxford WebQ survey was conducted online in four rounds. The association between dietary AGEs and CHD risk was estimated using multivariable-adjusted Cox proportional risk models. The association between dietary AGEs intake and genetic risk with CHD risk was further explored via the multiplicative interaction analyses.

Results: During a median follow-up of 12.2 years, 4,348 participants developed CHD. In the fully adjusted model, a higher intake of dietary AGEs, CML and MG-H1 (highest tertile vs. lowest tertile) was associated with a higher risk of CHD [HR, (95% CI):1.12 (1.03,1.23), 1.15 (1.05,1.26) and 1.10 (1.00,1.20), respectively (all P trend < 0.05)]. Among participants with intermediate to high genetic risk, HRs (95% CI) were 1.63 (1.39, 1.91) and 2.45 (2.10, 2.85) for AGEs, 1.67 (1.42, 1.97) and 2.60 (2.23, 3.02) for CML, 1.48 (1.26 1.74) and 2.34 (2.01, 2.72) for CEL, and 1.64 (1.40, 1.92) and 2.31 (1.99, 2.69) for MG-H1, respectively.

Conclusions: Higher intakes of dietary AGEs, CML and MG-H1 were associated with an increased risk of coronary heart disease, and there was an interaction between dietary AGEs intake and genetic predisposition on the risk of CHD.