Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet

Abstract

Modern diets are largely heat-processed and as a result contain high levels of advanced glycation end products (AGEs). Dietary advanced glycation end products (dAGEs) are known to contribute to increased oxidant stress and inflammation, which are linked to the recent epidemics of diabetes and cardiovascular disease. This report significantly expands the available dAGE database, validates the dAGE testing methodology, compares cooking procedures and inhibitory agents on new dAGE formation, and introduces practical approaches for reducing dAGE consumption in daily life. Based on the findings, dry heat promotes new dAGE formation by >10- to 100-fold above the uncooked state across food categories. Animal-derived foods that are high in fat and protein are generally AGE-rich and prone to new AGE formation during cooking. In contrast, carbohydrate-rich foods such as vegetables, fruits, whole grains, and milk contain relatively few AGEs, even after cooking. The formation of new dAGEs during cooking was prevented by the AGE inhibitory compound aminoguanidine and significantly reduced by cooking with moist heat, using shorter cooking times, cooking at lower temperatures, and by use of acidic ingredients such as lemon juice or vinegar. The new dAGE database provides a valuable instrument for estimating dAGE intake and for guiding food choices to reduce dAGE intake.

High dietary advanced glycation end products are associated with poorer spatial learning and accelerated Aβ deposition in an Alzheimer mouse model

“…Advanced glycation end products (AGEs) are generated from multiple sources and mechanisms (Uribarri et al ., 2010). Chronic accumulation of AGEs is accelerated with aging and with aging‐related diseases such as diabetes, hyperlipidemia, and renal disease (Cho et al ., 2009).…”

Nϵ‐Carboxymethyllysine Increases the Expression of miR‐103/143 and Enhances Lipid Accumulation in 3T3‐L1 Cells

“…Exogenous AGEs, typically encountered in a Western diet, are at least partially absorbed into circulation where they add to the endogenous AGE level [Uribarri et al, 2005; Somoza et al, 2006; Sebekova et al, 2008; Birlouez‐Aragon et al, 2010]. Among the group of AGEs, N‐ϵ‐carboxymethyl‐ l ‐lysine (CML), a well‐characterized, stable [Ahmed et al, 1986; Kislinger et al, 1999; Uribarri et al, 2010] member, and major epitope of AGE‐modified proteins [Ikeda et al, 1996], has been detected in a wide range of foods, its concentration reaching up to 84.8 mg per average portion size in meat dishes [Hull et al, 2012]. In a study on the dose‐dependent utilization of CML in rats, 30% of dietary CML has been shown to enter the blood stream [Somoza et al, 2006].…”

The uremic toxin oxythiamine causes functional thiamine deficiency in end-stage renal disease by inhibiting transketolase activity

“…19 The use of vinegar in cooking has been proposed as beneficial in the diet of ESRD patients to decrease potassium and magnesium content of vegetables 22 and to decrease formation of advanced glycation endproducts (AGEs) in foods. 23 This requires reappraisal in light of the current studies. Low protein diets for renal patients will affect the exposure to oxythiamine if they concurrently decrease consumption of cooked thiamine-containing acidic foods.…”