How does sleep affect your gut microbiome?

And does this affect your health?

Go to the profile of Ben Libberton
Oct 27, 2016
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An interesting clinical study from Uppsala University came out this week investigating how changes in sleep can affect the gut microbiome in humans.

Researchers sampled the fecal microbiome of volunteers before and after 2 nights of altered sleep. The team reported the results cautiously. Senior author Jonathan Cedernaes said:

"Overall we did not find evidence that suggests that the diversity of the gut microbiota was altered by sleep restriction. This was somewhat expected given the short-term nature of the intervention and the relatively small sample size. In more specific analyses of groups of bacteria, we did however observe microbiota changes that parallel some of the microbiota changes observed when for instance obese subjects have been compared with normal-weight subjects in other studies, such as an increased ratio of Firmicutes to Bacteroidetes. Longer and larger clinical sleep interventions will be needed to investigate to what extent alterations of the gut microbiota may mediate negative health consequences attributed to sleep loss, such as weight gain and insulin resistance,"

So there was no loss of diversity. I think we can all breathe a sigh of relief there. Diversity loss in the microbiome is linked to loss of stability of the flora which could cause a whole host of heath issues. The prospect of this happening over two nights is not a pleasant one. However, there were significant shifts in the Firmicutes:Bacteroidetes ratio.

Is this important?

Well, from the study it is not clear. The authors point out that similar shifts are associated with obesity but no conclusions can be drawn within such a short time frame. However, the study clearly shows that despite the short time frame, changes can still be detected. They also raise important questions for future studies such as, can lack of sleep affect metabolism through shifts in the gut flora?



Changes to the microbial community in the human gut have been proposed to promote metabolic disturbances that also occur after short periods of sleep loss (including insulin resistance). However, whether sleep loss affects the gut microbiota remains unknown.


In a randomized within-subject crossover study utilizing a standardized in-lab protocol (with fixed meal times and exercise schedules), we studied nine normal-weight men at two occasions: after two nights of partial sleep deprivation (PSD; sleep opportunity 02:45-07:00h), and after two nights of normal sleep (NS; sleep opportunity 22:30-07:00h). Fecal samples were collected within 24 hours before, and after two in-lab nights, of either NS or PSD. In addition, participants underwent an oral glucose tolerance test following each sleep intervention.


Microbiota composition analysis (V4 16S rRNA gene sequencing) revealed that after two days of PSD vs. after two days of NS, individuals exhibited an increased Firmicutes:Bacteroidetes ratio and of the families Coriobacteriaceae and Erysipelotrichaceae, with decreases in Tenericutes (all P<0.05) – previously all associated with metabolic perturbations in animal or human models. However, no PSD vs. NS effect on beta diversity or on fecal short-chain fatty acid concentrations was found. Fasting and postprandial insulin sensitivity decreased after PSD (all P<0.05).


Our findings demonstrate that short-term sleep loss induces subtle effects on human microbiota. To what extent changes to the microbial community contribute to metabolic consequences of sleep loss warrants further investigations in larger and more prolonged sleep studies, to also assess how sleep loss impacts the microbiota in individuals who already are metabolically compromised.


Gut Microbiota and Glucometabolic Alterations in Response to Recurrent Partial Sleep Deprivation in Normal-weight Young Individuals

Christian Benedicta, Heike Vogelb, Wenke Jonasb, Anni Wotingd, Michael Blautd, Annette Schürmannb, Jonathan Cedernaesa,

Go to the profile of Ben Libberton

Ben Libberton

Communications Officer, MAX IV Laboratory

I'm a Communications Officer at MAX IV Laboratory in Lund, Sweden, formally a Postdoc in the biofilm field. I'm interested in how bacteria cause disease and look to technology to produce novel tools to study and ultimately prevent infection. Part of my current role is to find ways to use synchrotron radiation to study microorganisms.

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