Evidence map›Paper›PMID 24362355›Full record

ReviewCurrent opinion in lipidology2014

Metaorganismal nutrient metabolism as a basis of cardiovascular disease.

J Mark Brown, Stanley L Hazen

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in lipidology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
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  5. Urinary metabolites and fatigue in a population-based metabolomics study: an exploratory analysis.Metabolomics : Official journal of the Metabolomic Society · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

J Mark BrownDepartment of Cellular and Molecular Medicine, Cleveland Clinic Lerner Research Institute, Cleveland, OH 44195, USA.
Stanley L Hazen
Cleveland Clinic · USCleveland Clinic Lerner College of Medicine · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024989 · NCRR · CASE WESTERN RESERVE UNIVERSITY · PI DAVIS, PAMELA B · 2007 to 2011
$53.7M
Structural Determinants Of Ceruloplasmin Inflammatory ActivityP01HL076491 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI PLOW, EDWARD FRANKLIN · 2004 to 2019
$27.3M
Regression of Atherosclerosis CoreP01HL098055 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI FISHER, EDWARD A · 2010 to 2014
$12.1M
Gut Flora Metabolism of Dietary Phosphatidylcholine and CVDR01HL103866 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI HAZEN, STANLEY L · 2010 to 2023
$10.8M
Functional Cardio-MetabolomicsP20HL113452 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI HAZEN, STANLEY L, TANG, WAI HONG WILSON · 2012 to 2016
$4.8M
Mechanisms Regulating Non-biliary Fecal Sterol LossR00HL096166 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BROWN, JONATHAN MARK · 2011 to 2013
$733k
NCRR NIH HHS 1UL1RR024989NCRR NIH HHS UL1 RR024989NHLBI NIH HHS P01 HL076491NHLBI NIH HHS P01 HL098055NHLBI NIH HHS P20 HL113452NHLBI NIH HHS R00 HL096166NHLBI NIH HHS R01 HL103866
6 · The paper itself

Abstract

purpose of reviewAtherosclerosis and associated cardiovascular disease (CVD) remains the leading cause of mortality in Western societies. It is well accepted that the consumption of foods abundant in saturated fats and cholesterol, like meats, egg yolk and high-fat dairy products, are associated with increased CVD risk. New evidence suggests that trimethylamine (TMA)-containing nutrients within these foods, including phosphatidylcholine, choline, and L-carnitine, can enter into a microbial metabolic pathway that promotes CVD. In this review, we highlight the role of gut microbiota-driven nutrient metabolism as a novel pathway promoting CVD. RECENT

findingsRecent studies demonstrate a link between ingestion of dietary phosphatidylcholine, choline, and L-carnitine and CVD risk. At the center of this pathway is gut microbiota-dependent synthesis of a metabolic intermediate called TMA, and subsequent host-driven conversion of TMA to trimethylamine-N-oxide (TMAO). Microbiota-dependent generation of TMAO is associated with increased risk of incident major adverse cardiovascular events in humans, and provision of TMAO promotes atherosclerosis in mice. SUMMARY: Microbial metabolism of TMA containing nutrients can lead to formation of the proatherogenic compound TMAO. Recent insights into this diet-microbe-host interaction provide new clues surrounding the pathogenesis of atherosclerosis, and may serve as a framework for new CVD therapies.

Indexed as

AnimalsAtherosclerosisCardiovascular DiseasesCarnitineDietHumansMethylaminesRiskCarnitineMethylaminestrimethyloxamine

Identifiers

PMID24362355
PMCPMC4018574
OpenAlexW2020141714

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.