Long-term dietary intake influences the structure and activity of the trillions of microorganisms residing in the human gut1,2,3,4,5, but it remains unclear how rapidly and reproducibly the human gut microbiome responds to short-term macronutrient change. Here we show that the short-term consumption of diets composed entirely of animal or plant products alters microbial community structure and overwhelms inter-individual differences in microbial gene expression. The animal-based diet increased the abundance of bile-tolerant microorganisms (Alistipes, Bilophila and Bacteroides) and decreased the levels of Firmicutes that metabolize dietary plant polysaccharides (Roseburia, Eubacterium rectale and Ruminococcus bromii). Microbial activity mirrored differences between herbivorous and carnivorous mammals2, reflecting trade-offs between carbohydrate and protein fermentation. Foodborne microbes from both diets transiently colonized the gut, including bacteria, fungi and even viruses. Finally, increases in the abundance and activity of Bilophila wadsworthia on the animal-based diet support a link between dietary fat, bile acids and the outgrowth of microorganisms capable of triggering inflammatory bowel disease6. In concert, these results demonstrate that the gut microbiome can rapidly respond to altered diet, potentially facilitating the diversity of human dietary lifestyles.

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Gene Expression Omnibus

Data deposits

RNA-seq data have been deposited in the Gene Expression Omnibus under accession GSE46761; 16S and ITS rRNA gene sequencing reads have been deposited in MG-RAST under accession 6248.


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We would like to thank A. Murray, G. Guidotti, E. O’Shea, J. Moffitt and B. Stern for insightful comments; M. Delaney for biochemical analyses; C. Daly, M. Clamp and C. Reardon for sequencing support; N. Fierer for providing ITS primers; A. Luong and K. Bauer for technical assistance; J. Brulc and R. Menon for nutritional guidelines; A. Rahman for menu suggestions; A. Must and J. Queenan for nutritional analysis; and our diet study volunteers for their participation. This work was supported by the National Institutes of Health (P50 GM068763), the Boston Nutrition Obesity Research Center (DK0046200), and the General Mills Bell Institute of Health and Nutrition.

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Author notes

    • Lawrence A. David

    Present address: Molecular Genetics & Microbiology and Institute for Genome Sciences & Policy, Duke University, Durham, North Carolina 27708, USA.


  1. FAS Center for Systems Biology, Harvard University, Cambridge, Massachusetts 02138, USA

    • Lawrence A. David
    • , Corinne F. Maurice
    • , Rachel N. Carmody
    • , David B. Gootenberg
    • , Julie E. Button
    • , Benjamin E. Wolfe
    • , Rachel J. Dutton
    •  & Peter J. Turnbaugh
  2. Society of Fellows, Harvard University, Cambridge, Massachusetts 02138, USA

    • Lawrence A. David
  3. Division of Endocrinology, Children’s Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115, USA

    • Alisha V. Ling
    •  & Sudha B. Biddinger
  4. Department of Bioengineering & Therapeutic Sciences and the California Institute for Quantitative Biosciences, University of California, San Francisco, San Francisco, California 94158, USA

    • A. Sloan Devlin
    • , Yug Varma
    •  & Michael A. Fischbach


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L.A.D., R.J.D. and P.J.T. designed the study, and developed and prepared the diets. L.A.D., C.F.M., R.N.C., D.B.G., J.E.B., B.E.W. and P.J.T. performed the experimental work. A.V.L., A.S.D., Y.V., M.A.F. and S.B.B. conducted bile acid analyses. L.A.D. and P.J.T. performed computational analyses. L.A.D. and P.J.T. prepared the manuscript.

Competing interests

The authors declare no competing financial interests.

Corresponding author

Correspondence to Peter J. Turnbaugh.

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