Dietary Advanced Glycation End Products and Risk Factors for Chronic Disease: A Systematic Review of Randomised Controlled Trials

Nutrients. 2016 Mar 1;8(3):125. doi: 10.3390/nu8030125.

Abstract

Dietary advanced glycation end-products (AGEs) form during heating and processing of food products and are widely prevalent in the modern Western diet. Recent systematic reviews indicate that consumption of dietary AGEs may promote inflammation, oxidative stress and insulin resistance. Experimental evidence indicates that dietary AGEs may also induce renal damage, however, this outcome has not been considered in previous systematic reviews. The purpose of this review was to examine the effect of consumption of a high AGE diet on biomarkers of chronic disease, including chronic kidney disease (CKD), in human randomized controlled trials (RCTs). Six databases (SCOPUS, CINHAL, EMBASE, Medline, Biological abstracts and Web of Science) were searched for randomised controlled dietary trials that compared high AGE intake to low AGE intake in adults with and without obesity, diabetes or CKD. Twelve dietary AGE interventions were identified with a total of 293 participants. A high AGE diet increased circulating tumour necrosis factor-alpha and AGEs in all populations. A high AGE diet increased 8-isoprostanes in healthy adults, and vascular cell adhesion molecule-1 (VCAM-1) in patients with diabetes. Markers of CKD were not widely assessed. The evidence presented indicates that a high AGE diet may contribute to risk factors associated with chronic disease, such as inflammation and oxidative stress, however, due to a lack of high quality randomised trials, more research is required.

Keywords: advanced glycation end-products; cardiovascular disease; chronic kidney disease; diabetes; diet; inflammation; systematic review.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review
  • Systematic Review

MeSH terms

  • Biomarkers / blood
  • Diet / adverse effects*
  • Dinoprost / analogs & derivatives
  • Dinoprost / blood
  • Glycation End Products, Advanced / adverse effects*
  • Glycation End Products, Advanced / metabolism
  • Humans
  • Inflammation / etiology*
  • Inflammation / metabolism
  • Inflammation Mediators / blood
  • Oxidative Stress
  • Renal Insufficiency, Chronic / etiology*
  • Renal Insufficiency, Chronic / metabolism
  • Risk Assessment
  • Risk Factors
  • Tumor Necrosis Factor-alpha / blood
  • Vascular Cell Adhesion Molecule-1 / blood

Substances

  • Biomarkers
  • Glycation End Products, Advanced
  • Inflammation Mediators
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • 8-epi-prostaglandin F2alpha
  • Dinoprost