Fecal microbiota transplantation of vegan donor did not lower arterial wall inflammation

Effect of Vegan Fecal Microbiota Transplantation on Carnitine- and Choline-Derived Trimethylamine-N-Oxide Production and Vascular Inflammation in Patients With Metabolic Syndrome

Literature - Smits LP, Kootte RS, Levin E, et al. - J Am Heart Assoc. 2018;7:e008342

Introduction and Methods

Evidence suggests that gut microbiota contribute to atherosclerosis [1]. Intestinal bacteria produce trimethylamine (TMA) from endogenous and dietary phosphatidyl-choline and carnitine, which are mainly present in animal-derived food products. TMA is oxidized in the liver to trimethylamine-N-oxide (TMAO), an intestinal microbiota–related metabolite related to atherosclerosis and incident CV disease [2-4]. Omnivorous metabolic syndrome patients have increased TMAO production compared with lean vegan individuals [5].

In this double-blind, randomized, controlled, pilot study, it was investigated whether a single lean vegan-donor fecal microbiota transplantation (FMT) affects the intestinal microbiota composition and the conversion of both choline and carnitine to TMA and TMAO in omnivorous metabolic syndrome patients, compared with autologous (own feces) FMT.

For this purpose, 20 obese metabolic syndrome patients, aged 21-69 years, without a history of CV disease, cholecystectomy, or immunodeficiency who were not taking any medication, were randomized to lean vegan-donor or autologous FMT. FMT was performed after bowel lavage, and feces from either the donor (vegan-donor FMT) or the patient (autologous FMT) were infused through a naso-duodenal tube.

At baseline and 2 weeks later, an oral stable isotope–labeled choline and carnitine challenge test (CCCT) was performed, and the effect of vegan-donor FMT on vascular inflammatory tone was evaluated, by measuring aortic wall vascular inflammation, as assessed by 18F-fluorodeoxyglucose (18F-FDG) uptake positron emission tomography/computed tomography (PET/CT) scanning, which is reported to be increased in metabolic syndrome patients.

Main results

  • There was a nonsignificant trend toward decreased fecal microbial diversity in vegans versus metabolic syndrome patients (Shannon index: 5.9; IQR: 5.8–6.0; vs 6.0; IQR: 5.9–6.1; P=0.08).
  • Fasting plasma concentrations of TMAO did not differ significantly between metabolic syndrome patients and vegan donors (3.7 lmol/L; IQR: 2.7–4.9 lmol/L; vs 2.8 lmol/L; IQR: 1.9–3.4 lmol/L; P=0.13).
  • 24-hour urinary excretion of TMAO was significantly higher in metabolic syndrome patients compared with vegan donors (529 lmol; IQR: 239–1407 lmol; vs 178 lmol; IQR: 98–338 lmol; P=0.03), although 24-hour urinary TMA excretion was not significantly different between the 2 groups at baseline.
  • There were no changes in fecal microbiota diversity (Shannon index) 2 weeks after either vegan donor FMT (from 6.0; IQR: 5.9–6.1; to 6.1; IQR: 5.9–6.2; P=0.260) or autologous FMT (from 6.0; IQR: 5.9–6.0; to 6.0; IQR: 5.7–6.1; P=0.721).
  • Vegan-donor FMT changed intestinal microbiota composition towards a vegan profile in some, but not all, metabolic syndrome patients.
  • FDG uptake in the aortic wall was not significantly different between metabolic syndrome patients and vegan donors (maximized target to background: 3.25±0.8 versus 2.83±0.9; P=0.27).


Single lean vegan-donor fecal microbiota transplantation in obese male patients with metabolic syndrome resulted in changes in intestinal microbiota composition of some subjects, but this did not translate into altered carnitine- or choline-to-TMAO conversion, nor did it affect markers of arterial wall inflammation.


1. Koren O, Spor A, Felin J, et al. Human oral, gut, and plaque microbiota in patients with atherosclerosis. Proc Natl Acad Sci USA. 2011;108(suppl):4592–4598.

2. Bennett BJ, de Aguiar Vallim TQ, Wang Z, et al. Trimethylamine-N-oxide, a metabolite associated with atherosclerosis, exhibits complex genetic and dietary regulation. Cell Metab. 2013;17:49–60.

3. Wang Z, Klipfell E, Bennett BJ, et al. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature. 2011;472:57–63.

4. Tang WH, Wang Z, Levison BS, et al. Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk. N Engl J Med. 2013;368:1575–1584.

5. Org E, Blum Y, Kasela S, et al. Relationships between gut microbiota, plasma metabolites, and metabolic syndrome traits in the METSIM cohort. Genome Biol. 2017;18:70.

Find this article online at J Am Heart Assoc

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