The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here:

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Robert Koivula

Robert Koivula

Assistant researcher

Robert Koivula

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


  • Mohsen Mazidi
  • Ana M. Valdes
  • Jose M. Ordovas
  • Wendy L. Hall
  • Joan C. Pujol
  • Jonathan Wolf
  • George Hadjigeorgiou
  • Nicola Segata
  • Naveed Sattar
  • Robert Koivula
  • Tim D. Spector
  • Paul W. Franks
  • Sarah E. Berry

Summary, in English

BACKGROUND: Meal-induced metabolic changes trigger an acute inflammatory response, contributing to chronic inflammation and associated diseases. OBJECTIVES: We aimed to characterize variability in postprandial inflammatory responses using traditional (IL-6) and novel [glycoprotein acetylation (GlycA)] biomarkers of inflammation and dissect their biological determinants with a focus on postprandial glycemia and lipemia. METHODS: Postprandial (0-6 h) glucose, triglyceride (TG), IL-6, and GlycA responses were measured at multiple intervals after sequential mixed-nutrient meals (0 h and 4 h) in 1002 healthy adults aged 18-65 y from the PREDICT (Personalised REsponses to DIetary Composition Trial) 1 study, a single-arm dietary intervention study. Measures of habitual diet, blood biochemistry, gut microbiome composition, and visceral fat mass (VFM) were also collected. RESULTS: The postprandial changes in GlycA and IL-6 concentrations were highly variable between individuals. Participants eliciting an increase in GlycA and IL-6 (60% and 94% of the total participants, respectively) had mean 6-h increases of 11% and 190%, respectively. Peak postprandial TG and glucose concentrations were significantly associated with 6-h GlycA (r = 0.83 and r = 0.24, respectively; both P < 0.001) but not with 6-h IL-6 (both P > 0.26). A random forest model revealed the maximum TG concentration was the strongest postprandial TG predictor of postprandial GlycA and structural equation modeling revealed that VFM and fasting TG were most strongly associated with fasting and postprandial GlycA. Network Mendelian randomization demonstrated a causal link between VFM and fasting GlycA, mediated (28%) by fasting TG. Individuals eliciting enhanced GlycA responses had higher predicted cardiovascular disease risk (using the atherosclerotic disease risk score) than the rest of the cohort. CONCLUSIONS: The variable postprandial increases in GlycA and their associations with TG metabolism highlight the importance of modulating TG in concert with obesity to reduce GlycA and associated low-grade inflammation-related diseases.This trial was registered at as NCT03479866.


  • Genetic and Molecular Epidemiology
  • EpiHealth: Epidemiology for Health
  • EXODIAB: Excellence of Diabetes Research in Sweden

Publishing year







The American journal of clinical nutrition





Document type

Journal article


Oxford University Press


  • Nutrition and Dietetics


  • glycoprotein acetylation
  • inflammation
  • postprandial glycemia
  • postprandial lipemia
  • visceral fat mass



Research group

  • Genetic and Molecular Epidemiology


  • ISSN: 1938-3207