Omega-3 fatty acids and individual variability in plasma triglyceride response: A mini-review
Amanda Rundblad,
Viviana Sandoval,
Kirsten B. Holven,
José M. Ordovás,
Stine M. Ulven
Affiliations
Amanda Rundblad
Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, P.O Box 1046 Blindern, 0317, Oslo, Norway
Viviana Sandoval
Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, P.O Box 1046 Blindern, 0317, Oslo, Norway; Escuela de Nutrición y Dietética, Facultad de Ciencias para el Cuidado de la Salud, Universidad San Sebastián, Gral. Lagos 1025, 5110693, Valdivia, Chile
Kirsten B. Holven
Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, P.O Box 1046 Blindern, 0317, Oslo, Norway; Norwegian National Advisory Unit on Familial Hypercholesterolemia, Oslo University Hospital, Norway
José M. Ordovás
Nutrition and Genomics Laboratory, USDA ARS, JM-USDA Human Research Center on Aging at Tufts University, Boston, MA, USA; Nutritional Genomics and Epigenomics Group, Precision Nutrition and Obesity Program, IMDEA Food, CEI UAM + CSIC, Madrid, Spain; Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, Madrid, Spain
Stine M. Ulven
Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, P.O Box 1046 Blindern, 0317, Oslo, Norway; Corresponding author.
Cardiovascular disease (CVD) is a leading cause of death worldwide. Supplementation with the marine omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) is associated with lower CVD risk. However, results from randomized controlled trials that examine the effect of omega-3 supplementation on CVD risk are inconsistent. This risk-reducing effect may be mediated by reducing inflammation, oxidative stress and serum triglyceride (TG) levels. However, not all individuals respond by reducing TG levels after omega-3 supplementation. This inter-individual variability in TG response to omega-3 supplementation is not fully understood. Hence, we aim to review the evidence for how interactions between omega-3 fatty acid supplementation and genetic variants, epigenetic and gene expression profiling, gut microbiota and habitual intake of omega-3 fatty acids can explain why the TG response differs between individuals. This may contribute to understanding the current controversies and play a role in defining future personalized guidelines to prevent CVD.
