Effect of egg ingestion on trimethylamine-N-oxide production in humans: a randomized, controlled, dose-response study , , ,

Miller, Colin; Corbin, Karen D.; Costa, Kerry Ann Da; Zhang, Shucha; Zhao, Xueqing; Galanko, Joseph A.; Blevins, Tondra; Bennett, Brian J.; O’Connor, Annalouise; Zeisel, Steven H.

doi:10.3945/ajcn.114.087692

Cited by 204 publications

(171 citation statements)

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“…An individual's eating habits over the short term as well as their dietary patterns over time have been shown to alter the concentration of certain species in the gut [15,54]. Furthermore, TMAO is a by-product of the metabolism of carnitine-and choline-containing food products [55,56]. Individuals with certain dietary preferences or restrictions persistent over time may have overly inflated or reduced TMAO levels based on the composition of the gut flora population and the provision of carnitine-and choline-containing food products.…”

Section: Discussionmentioning

confidence: 99%

Trimethylamine-N-oxide: A Novel Biomarker for the Identification of Inflammatory Bowel Disease

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Trimethylamine-N-oxide: A Novel Biomarker for the Identification of Inflammatory Bowel Disease

et al. 2015

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“…An obligatory role for gut microbiota in both TMA and TMAO formation from ingested PC was confirmed in animal model studies, which included germ-free mice (25), as well as human clinical investigations involving ingestion of egg yolk, isotope-labeled PC, and a cocktail of oral antibiotics (37). Recently, the association between acute egg yolk ingestion and increased plasma and urine TMAO concentrations was independently confirmed in humans (38). Additional studies have shown that L-carnitine, an alternative TMA-containing nutrient found almost exclusively in red meat, similarly serves as a dietary precursor to gut microbial production of TMA and TMAO in both mice and humans (ref.…”

Section: R E V I E W S E R I E S : G U T M I C R O B I O M Ementioning

confidence: 82%

“…Interestingly, only choline (and not betaine or lecithin) was found to produce a detectable rise in urine TMAO excretion in one small human study employing a variety of dietary exposures (30). More recent studies examining ingestion of either hard-boiled egg or egg yolk (37,38,62) or ingestion of trimethyld9-PC (37) have confirmed direct generation of TMAO from PC ingestion in humans. L-carnitine is a TMA nutrient that, in contrast to choline, is not required in our diets, since it is endogenously produced in mammals from dietary lysine, the single most abundant amino acid in plant and animal proteins (30,63,64).…”

Section: R E V I E W S E R I E S : G U T M I C R O B I O M Ementioning

confidence: 87%

“…TMA has long been recognized as an odorous byproduct of choline, PC, and L-carnitine during the decomposition of plants and animals, often by enterobacteria (31). Choline (free and esterified forms) and L-carnitine are the most common dietary nutrients ingested that produce TMA and TMAO (30,(37)(38)(39)55).…”

Section: R E V I E W S E R I E S : G U T M I C R O B I O M Ementioning

confidence: 99%

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The contributory role of gut microbiota in cardiovascular disease

2014

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R e v i e w s e R i e s : g u t m i c R o b i o m eSeries Editor: Martin J. Blaser IntroductionCardiovascular disease (CVD) remains the leading cause of death in both the United States and industrialized societies, with growing incidence in developing countries (1). Factors contributing to CVD arise from genetic sources, environmental sources, or a combination of genetic and environmental sources (2). Despite extensive investigations in search of causal genetic variants, such as large-scale GWAS, less than one-fifth of attributable cardiovascular risk has been accounted for from genetic determinants (3, 4). At the same time, major advances in the treatment of atherosclerosis beyond high-potency lipid-lowering agents has not yet materialized (5). Indeed, even with high-potency statin therapy, at least a 50% residual risk remains (6), with the majority of events unchecked. Therefore, there is still ample room for improving our understanding of the processes contributing to CVD pathogenesis, and for improved prevention and treatment of CVD. While the recognizable contribution of genetics to CVD will no doubt significantly increase with time, a reassessment of environmental contributions to CVD pathogenesis and risks for adverse events is certainly worthwhile.Our largest environmental exposure is what we eat. Technically speaking, food is a foreign object that we take into our bodies in kilogram quantities every day. From the latest National Health and Nutrition Examination Survey (NHANES, 2009(NHANES, -2010, the majority of individuals sampled achieved an intermediate or poor Healthy Eating Index (1). However, dietary composition is often difficult to assess, and even precise quantification of dietary intake may not necessarily reveal the many known and unknown factors that may influence the contributions of specific dietary nutrients to disease susceptibility (7). There has also been an overwhelming lack of appreciation at the bedside regarding the intricate and complicated processes that transform ingested food into the myriad metabolites that enter the circulation and fulfill or adversely affect various functional and metabolic processes in the body.Over the past decade we have increasingly begun to appreciate the ecological diversity of microbes living symbiotically within us, a large proportion of which reside within our intestines. We now know that the human gut harbors more than 100 trillion microbial cells, far outnumbering the human host cells of the body (8). Indeed, a sobering fact is that Homo sapiens DNA is estimated to represent less than 10% of the total DNA within our bodies, due to the staggeringly large numbers of microbes that reside in and on us, primarily within our gut (9). Our microbial symbiont guests have coevolved with us and affect a wide range of physiologic and metabolic processes of the body. The major taxa present in gut microbiota consist primarily of 2 major bacterial phyla, Firmicutes and Bacteroidetes, whose proportions appear to remain remarkably stable over time within individu...

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“…In a few other studies, TMAO levels in urine and plasma have also been associated 476 with intake of red meat, egg and dairy food (29,32,42,43 Table 7 for details on statistical results. T0 T2 T24 T0 T2 T24 T0 T2 T24 T0 T2 T24 T0 T2 T24 T0 T2 T24 T0 T2 T24 T0 T2 T24 T0 T2 T24 T0 T2 T24 T0 T2 T24 T0 T2 T24 W1 W2 W3 W1 W2 W3 W1 W2 W3 W1 W2 W3 A B…”

mentioning

confidence: 99%

A metabolomic study of biomarkers of meat and fish intake ,

Cheung

Keski‐Rahkonen

Assi

et al. 2017

The American Journal of Clinical Nutrition

175

161

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Background: Meat and fish intakes have been associated with various chronic diseases. The use of specific biomarkers may help to assess meat and fish intake and improve subject classification according to the amount and type of meat or fish consumed. Objective: A metabolomic approach was applied to search for biomarkers of meat and fish intake in a dietary intervention study and in free-living subjects from the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Design: In the dietary intervention study, 4 groups of 10 subjects consumed increasing quantities of chicken, red meat, processed meat, and fish over 3 successive weeks. Twenty-four-hour urine samples were collected during each period and analyzed by high-resolution liquid chromatography–mass spectrometry. Signals characteristic of meat or fish intake were replicated in 50 EPIC subjects for whom a 24-h urine sample and 24-h dietary recall were available and who were selected for their exclusive intake or no intake of any of the 4 same foods. Results: A total of 249 mass spectrometric features showed a positive dose-dependent response to meat or fish intake in the intervention study. Eighteen of these features best predicted intake of the 4 food groups in the EPIC urine samples on the basis of partial receiver operator curve analyses with permutation testing (areas under the curve ranging between 0.61 and 1.0). Of these signals, 8 metabolites were identified. Anserine was found to be specific for chicken intake, whereas trimethylamine-N-oxide showed good specificity for fish. Carnosine and 3 acylcarnitines (acetylcarnitine, propionylcarnitine, and 2-methylbutyrylcarnitine) appeared to be more generic indicators of meat and meat and fish intake, respectively. Conclusion: The meat and fish biomarkers identified in this work may be used to study associations between meat and fish intake and disease risk in epidemiologic studies. This trial was registered at clinicaltrials.gov as NCT01684917

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Effect of egg ingestion on trimethylamine-N-oxide production in humans: a randomized, controlled, dose-response study , , ,

Cited by 204 publications

References 31 publications

Trimethylamine-N-oxide: A Novel Biomarker for the Identification of Inflammatory Bowel Disease

Trimethylamine-N-oxide: A Novel Biomarker for the Identification of Inflammatory Bowel Disease

The contributory role of gut microbiota in cardiovascular disease

A metabolomic study of biomarkers of meat and fish intake ,

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