Meal-induced inflammation: postprandial insights from the Personalised REsponses to DIetary Composition Trial (PREDICT) study in 1000 participants

Inflammation is chronically and acutely affected by diet.  Chronic effects include those linked to the generation of reactive oxygen species (ROS), haemostatic function, lipoprotein remodelling, and endotoxemia.  These are mainly thought to be associated with postprandial spikes in insulin and triglycerides (TG) that are linked with the consumption of dietary CHO and fat.  Acute inflammatory responses are a physiological defence mechanism however a continuous activated response may result in a persistent low-grade inflammation and an increased risk of CVD.

Quick takes:

  • Current dietary approaches aimed to lower CVD risk are not aimed at reducing inflammation
  • The postprandial effect of diet can last up to 18 hours therefore the reduction of an individual’s postprandial inflammatory response could provide a dietary preventative mechanism against CVD
  • IL-6 is the only inflammatory marker consistently changing postprandially
  • Glycoprotein acetylation (GlycA) is an emerging inflammatory biomarker, with low intra-individual variability. High levels are linked with fatty liver disease, type 2 diabetes, some cancers, CVD and mortality
  • GlycA concentrations show a composite measure of systematic inflammation, unlike traditional markers like CRP and IL-6
  • This study shows an independent and cumulative association between postprandial glycemia and lipemia with GlycA
  • Lipemia and adiposity play a key role in food-induced inflammation
  • Potential dietary strategies to control fasting and postprandial TG include consumption of low GI foods, fibre, high intake of Omega 3 fatty acids, low alcohol consumption, and consumption of polyphenols / antioxidant rich foods.  Exercise and consuming larger meals earlier in the day are also recommended as lifestyle modification strategies
  • The large interindividual variability in postprandial inflammation highlights the potential for personalised strategies to target obesity and post prandial metabolic responses associated with low-grade inflammation

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