{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T11:40:52Z","timestamp":1791805252453,"version":"4.3.4"},"reference-count":47,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2016,10,3]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Clinical studies implicate trimethylamine N\u2010oxide (\n              <jats:styled-content style=\"fixed-case\">TMAO<\/jats:styled-content>\n              ; a gut microbiota\u2010dependent nutrient metabolite) in cardiovascular disease risk. There is a lack of population\u2010based data on the role of\n              <jats:styled-content style=\"fixed-case\">TMAO<\/jats:styled-content>\n              in advancing early atherosclerotic disease. We tested the prospective associations between\n              <jats:styled-content style=\"fixed-case\">TMAO<\/jats:styled-content>\n              and coronary artery calcium (\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              ) and carotid intima\u2010media thickness (\n              <jats:styled-content style=\"fixed-case\">cIMT<\/jats:styled-content>\n              ).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Data were from the Coronary Artery Risk Development in Young Adults Study (\n              <jats:styled-content style=\"fixed-case\">CARDIA<\/jats:styled-content>\n              ), a biracial cohort of\n              <jats:styled-content style=\"fixed-case\">US<\/jats:styled-content>\n              adults recruited in 1985\u20131986 (n=5115). We randomly sampled 817 participants (aged 33\u201355\u00a0years) who attended examinations in 2000\u20132001, 2005\u20132006, and 2010\u20132011, at which\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              was measured by computed tomography and\n              <jats:styled-content style=\"fixed-case\">cIMT<\/jats:styled-content>\n              (2005\u20132006) by ultrasound.\n              <jats:styled-content style=\"fixed-case\">TMAO<\/jats:styled-content>\n              was quantified using liquid chromotography mass spectrometry on plasma collected in 2000\u20132001. Outcomes were incident\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              , defined as Agatston units=0 in 2000\u20132001 and &gt;0 over 10\u2010year follow\u2010up,\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              progression (any increase over 10\u2010year follow\u2010up), and continuous\n              <jats:styled-content style=\"fixed-case\">cIMT<\/jats:styled-content>\n              . Over the study period, 25% (n=184) of those free of\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              in 2000\u20132001 (n=746) developed detectable\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              . In 2000\u20132001, median (interquartile range)\n              <jats:styled-content style=\"fixed-case\">TMAO<\/jats:styled-content>\n              was 2.6 (1.8\u20134.2) \u03bcmol\/L. In multivariable\u2010adjusted models,\n              <jats:styled-content style=\"fixed-case\">TMAO<\/jats:styled-content>\n              was not associated with 10\u2010year\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              incidence (rate ratio=1.03; 95%\n              <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n              : 0.71\u20131.52) or\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              progression (0.97; 0.68\u20131.38) in Poisson regression, or\n              <jats:styled-content style=\"fixed-case\">cIMT<\/jats:styled-content>\n              (beta coefficient: \u22120.009; \u22120.03 to 0.01) in linear regression, comparing the fourth to the first quartiles of TMAO.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              In this population\u2010based study,\n              <jats:styled-content style=\"fixed-case\">TMAO<\/jats:styled-content>\n              was not associated with measures of atherosclerosis:\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              incidence,\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              progression, or\n              <jats:styled-content style=\"fixed-case\">cIMT<\/jats:styled-content>\n              . These data indicate that\n              <jats:styled-content style=\"fixed-case\">TMAO<\/jats:styled-content>\n              may not contribute significantly to advancing early atherosclerotic disease risk among healthy early\u2010middle\u2010aged adults.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.116.003970","type":"journal-article","created":{"date-parts":[[2016,10,22]],"date-time":"2016-10-22T03:40:35Z","timestamp":1477107635000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":160,"title":["Microbiota\u2010Dependent Metabolite Trimethylamine N\u2010Oxide and Coronary Artery Calcium in the Coronary Artery Risk Development in Young Adults Study (CARDIA)"],"prefix":"10.1161","volume":"5","author":[{"given":"Katie A.","family":"Meyer","sequence":"first","affiliation":[{"name":"Department of Nutrition, Gillings School of Global Public Health &amp; School of Medicine, University of North Carolina, Chapel Hill, NC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas Z.","family":"Benton","sequence":"additional","affiliation":[{"name":"Nutrition Research Institute, University of North Carolina, Chapel Hill, NC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian J.","family":"Bennett","sequence":"additional","affiliation":[{"name":"Department of Nutrition, Gillings School of Global Public Health &amp; School of Medicine, University of North Carolina, Chapel Hill, NC"},{"name":"Nutrition Research Institute, University of North Carolina, Chapel Hill, NC"},{"name":"Department of Genetics, University of North Carolina, Chapel Hill, NC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr","given":"David R.","family":"Jacobs","sequence":"additional","affiliation":[{"name":"Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donald M.","family":"Lloyd\u2010Jones","sequence":"additional","affiliation":[{"name":"Department of Preventive Medicine, Northwestern University, Chicago, IL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Myron D.","family":"Gross","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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