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dc.contributor.authorVan Parys, Anthea
dc.contributor.authorDierkes, Jutta
dc.contributor.authorLysne, Vegard
dc.contributor.authorØyen, Jannike
dc.contributor.authorNygård, Ottar Kjell
dc.date.accessioned2022-01-18T08:55:19Z
dc.date.available2022-01-18T08:55:19Z
dc.date.created2022-01-14T15:08:45Z
dc.date.issued2020
dc.identifier.issn2666-1497
dc.identifier.urihttps://hdl.handle.net/11250/2837805
dc.description.abstractPlasma concentrations of trimethylamine N-oxide (TMAO) have been linked to cardiovascular disease (CVD) risk and mortality. TMAO is formed through the bacterial conversion of trimethylamine which is obtained either directly from food, generated from dietary precursors (e.g. choline) or derived from endogenous trimethyllysine (TML) production. In a previous article, we reported an increased risk of acute myocardial infarction with increased total choline intake in patients with stable angina pectoris. Due to the close link between TMAO, TML, choline metabolism and possibly CVD, we investigated whether plasma TMAO and TML modified the effect of total choline intake on acute myocardial infarction (AMI) risk in a post-hoc analysis. We found plasma TMAO and TML do not modify the association between higher dietary choline intake and increased AMI risk. Additionally, this association is not mediated via TMAO.en_US
dc.language.isoengen_US
dc.titleNo effect of plasma trimethylamine N-Oxide (TMAO) and plasma trimethyllysine (TML) on the association between choline intake and acute myocardial infarction risk in patients with stable angina pectorisen_US
dc.typeOthersen_US
dc.description.versionpublishedVersionen_US
dc.source.journalHuman Nutrition & Metabolismen_US
dc.identifier.doi10.1016/j.hnm.2020.200112
dc.identifier.cristin1981405
cristin.ispublishedtrue
cristin.fulltextoriginal


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