Fasting alters the gut microbiome reducing blood pressure and body weight in metabolic syndrome patients.
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Authors
Maifeld, AndrásBartolomaeus, Hendrik
Löber, Ulrike
Avery, Ellen G
Steckhan, Nico
Markó, Lajos
Wilck, Nicola
Hamad, Ibrahim
Šušnjar, Urša
Mähler, Anja
Hohmann, Christoph
Chen, Chia-Yu
Cramer, Holger
Dobos, Gustav
Lesker, Till Robin
Strowig, Till

Dechend, Ralf
Bzdok, Danilo
Kleinewietfeld, Markus
Michalsen, Andreas
Müller, Dominik N
Forslund, Sofia K
Issue Date
2021-03-30
Metadata
Show full item recordAbstract
Periods of fasting and refeeding may reduce cardiometabolic risk elevated by Western diet. Here we show in the substudy of NCT02099968, investigating the clinical parameters, the immunome and gut microbiome exploratory endpoints, that in hypertensive metabolic syndrome patients, a 5-day fast followed by a modified Dietary Approach to Stop Hypertension diet reduces systolic blood pressure, need for antihypertensive medications, body-mass index at three months post intervention compared to a modified Dietary Approach to Stop Hypertension diet alone. Fasting alters the gut microbiome, impacting bacterial taxa and gene modules associated with short-chain fatty acid production. Cross-system analyses reveal a positive correlation of circulating mucosa-associated invariant T cells, non-classical monocytes and CD4+ effector T cells with systolic blood pressure. Furthermore, regulatory T cells positively correlate with body-mass index and weight. Machine learning analysis of baseline immunome or microbiome data predicts sustained systolic blood pressure response within the fasting group, identifying CD8+ effector T cells, Th17 cells and regulatory T cells or Desulfovibrionaceae, Hydrogenoanaerobacterium, Akkermansia, and Ruminococcaceae as important contributors to the model. Here we report that the high-resolution multi-omics data highlight fasting as a promising non-pharmacological intervention for the treatment of high blood pressure in metabolic syndrome patients.Citation
Nat Commun. 2021 Mar 30;12(1):1970. doi: 10.1038/s41467-021-22097-0.Affiliation
HZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.Publisher
NPGJournal
Nature communicationsPubMed ID
33785752Type
ArticleLanguage
enEISSN
2041-1723ae974a485f413a2113503eed53cd6c53
10.1038/s41467-021-22097-0
Scopus Count
The following license files are associated with this item:
- Creative Commons