Sleep problems are often blamed on stress, screens, or a restless environment. But growing evidence suggests another influence may be working quietly in the background – the gut.
A new review suggests that people with insomnia and other sleep disorders often share a similar microbiome pattern, including fewer “helpful” bacteria that thrive on fiber.
It’s not proof that fiber fixes sleep, but it does point to a biological pathway worth taking seriously.
The research was led by Zhe Wang and a team at Shandong First Medical University in China. They pulled together results from 53 earlier studies that compared the gut microbiota of people with sleep disturbances against those without.
Gut bacteria with lower diversity
Across the studies, one signal kept showing up. People with sleep conditions tended to have lower “alpha diversity,” meaning their guts hosted fewer different bacterial species overall.
That kind of drop in diversity has been tied to a range of health issues, and here it appears again in the context of sleep.
The review also found a more specific signature in several conditions, including insomnia, obstructive sleep apnea, and REM sleep behavior disorder.
In these groups, there was a consistent decrease in certain anti-inflammatory, butyrate-producing bacteria, alongside an increase in bacteria that tend to be linked with inflammation.
Bacteria that may be linked
One of the bacteria that stood out was Faecalibacterium, often discussed as a beneficial gut microbe. The review suggests it shows up less in people with these sleep disorders.
At the same time, microbes described as more pro-inflammatory, such as Collinsella, appeared more abundant.
This doesn’t automatically mean these bacteria are causing the sleep problems. But when the same microbial “shape” keeps appearing across different datasets, it raises the possibility that the microbiome is not just a bystander.
Fiber and gut chemistry
The fiber angle comes from the chemistry of what these microbes do. Faecalibacterium is known for producing butyrate, a short-chain fatty acid made when gut bacteria ferment dietary fibre.
Butyrate matters because it helps fuel colon cells, supports the gut barrier, and is generally associated with lower inflammation.
So if people with certain sleep disorders have less Faecalibacterium, one plausible downstream effect is lower butyrate production.
And if that shift nudges the body toward more inflammation, it could help explain why the microbiome might be linked to sleep quality.
The review’s findings also hint at something clinically practical. The authors suggest that this microbial signature might eventually help distinguish diagnosed sleep disorders from more general complaints about sleep.
That could, in theory, help clinicians target treatments more precisely. But that idea is still at an early stage, because it depends on more consistent testing methods and clearer definitions across studies.
The evidence is still limited
Outside experts quoted in the article largely see the pattern as plausible, especially the focus on butyrate-producing microbes.
Katherine Maki at the US National Institutes of Health in Maryland said the results align with work her group has been doing.
They highlight a microbiome-metabolite pathway linking sleep and host physiology. As a result, direct testing in future mechanistic and interventional studies would be highly beneficial.
Other researchers acknowledges a possible link but emphasize that the evidence remains limited and that scientists cannot yet establish causality.
The data could just as plausibly reflect insomnia altering appetite, food choices, and daily routines rather than diet driving changes in sleep.
If that leads to lower fiber intake, it could reduce Faecalibacterium levels. The other direction is the reverse. Lower Faecalibacterium could mean less butyrate, which might influence sleep through inflammation or other signaling pathways.
Diet choices and sleep
Even if the biology is intriguing, the review does not translate into a simple takeaway like “eat oats, sleep like a baby.” Maki is careful to stress that point.
She says it is still too early to recommend dietary fiber specifically as a sleep treatment, even though higher fiber intake is broadly beneficial for overall health.
That caution matters, especially because there is already solid evidence that certain dietary habits can actively interfere with sleep.
Caffeine is the most obvious example. At higher doses or later in the day, it can delay sleep onset and shorten total sleep time.
Alcohol presents another common trap. While it can initially make people feel drowsy, it often fragments sleep later in the night, which helps explain why drinking can leave people feeling less rested the next day.
Meal timing also plays a role. Eating close to bedtime is frequently associated with poorer sleep quality.
For those looking for a possible “bedtime boost,” Maki points to tart cherry juice, which has shown promise in some studies. Higher overall diet quality, often including more fiber, is consistently linked with better sleep in broader research.
Gut microbes gain attention
What this review adds most clearly is a sharper shortlist of microbial suspects. Earlier studies often linked sleep problems to a less diverse gut microbiome. Which specific bacteria mattered, however, remained unclear.
By highlighting repeated shifts in butyrate-producing bacteria such as Faecalibacterium, along with increases in microbes linked to inflammation, the new analysis gives researchers more concrete targets to test.
If future intervention studies confirm a causal pathway, it could open new avenues for supporting sleep that go beyond sedatives or behavioral techniques alone.
Those approaches might include dietary changes, targeted prebiotics, or other strategies designed to boost butyrate production while reducing inflammation.
For now, the most honest message remains cautious. The gut-sleep link is looking increasingly real, and dietary fiber appears to be a strong candidate in the story.
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