Psychobiotic: how gut bacteria affect mood and stress

A psychobiotic is a probiotic with a documented impact on the psyche. We check which strains have studies in humans and how large the measured effect is.

Popular texts about the microbiome usually start like this: most serotonin is produced in the gut, so taking care of bacteria improves mood. The first part is true. The second does not follow from it, because serotonin produced in the gut does not pass to the brain; tryptophan, its precursor, crosses the blood-brain barrier. However, the influence of the microbiome on the psyche is real and described in randomized studies with specific strains of bacteria. A psychobiotic is precisely such a probiotic, with documented effects on mental health. This text separates evidence from shortcuts: it shows the pathways through which the gut actually reaches the brain, which strains have been studied in humans, and how large the measured effect turned out to be.

KEY INFORMATION
• The meta-analysis by Liu et al. (Neuroscience and Biobehavioral Reviews, 2019) included 34 controlled studies: probiotics had a small but significant effect on depression (d = -0.24), prebiotics did not differ from placebo.
• The term “psychobiotic” was introduced by Dinan, Stanton, and Cryan (Biological Psychiatry, 2013) as a name for a living organism that brings health benefits to people with mental disorders.
• The gastrointestinal tract contains most of the body’s serotonin, but this molecule does not reach the brain; the microbiome reaches there through other pathways.
• The best-documented strains are L. helveticus R0052 with B. longum R0175 and B. infantis 35624.

What is a psychobiotic and how does it differ from a regular probiotic?

A psychobiotic is a living organism that, taken in the right amount, brings health benefits to people suffering from a mental disorder. This is how Dinan, Stanton, and Cryan (Biological Psychiatry, 2013) defined it. It is not a separate species of bacteria, but a strain with clinical evidence.

The difference from a regular probiotic is therefore formal, not biological. Every psychobiotic is a probiotic; the reverse is not true. The authors of the original definition were more cautious than the market that later used it. They wrote about patients with mental illness, while most subsequent trials were conducted on healthy volunteers or on people with irritable bowel syndrome.

The mechanism they indicated is specific: these bacteria produce and deliver neuroactive substances, including gamma-aminobutyric acid and serotonin, acting on the gut-brain axis. Preclinical studies in rodents suggested antidepressant or anxiolytic effects, with the vagus nerve, spinal cord, or neuroendocrine system as intermediaries. The irritable bowel syndrome was the most widely studied at that time.

It is worth reading the last sentence of that work in full, as it sounds more modest than everything written after it: we are still waiting for the results of large placebo-controlled studies. Since 2013, such studies have appeared, and we return to them later in the text. However, they did not change the rule that evidence always concerns a single strain, not the category “probiotic”.

Is it true that serotonin from the gut controls mood?

Not in the form that the internet repeats. The gastrointestinal tract indeed contains most of the body’s serotonin, and the microbiome does regulate its production. However, this serotonin does not pass from the blood to the brain, and the brain produces its own from tryptophan supplied from the bloodstream.

How do we know that bacteria control gut serotonin? Yano et al. (Cell, 2015) showed that spore-forming bacteria from the microbiota of mice and humans stimulate the production of serotonin in enterochromaffin cells of the colon, and from there it reaches the mucosa, the lumen of the intestine, and circulating platelets. Increasing the concentration of selected bacterial metabolites in the intestinal lumen raised serotonin levels in the colon and in the blood of germ-free mice.

Note what effects this work measured. The authors mention gastrointestinal motility and platelet function. Not mood. Gut serotonin is a molecule of the digestive and coagulation system, not fuel for the brain.

This distinction has practical consequences. If someone promises mood improvement solely because serotonin is produced in the gut, they rely on a true premise and a conclusion that does not follow from it. Real pathways of influence exist, but they run elsewhere. A broad review describes them extensively, and a separate entry discusses the broader context of this axis in relation to the gut-brain axis.

Through which pathways does the microbiome reach the brain?

A review by Cryan et al. (Physiological Reviews, 2019) lists several parallel channels: the immune system, tryptophan metabolism, the vagus nerve along with the enteric nervous system, and bacterial metabolites, including short-chain fatty acids, branched-chain amino acids, and peptidoglycans. None of these channels rely on transmitting a ready-made neurotransmitter from the gut to the brain.

The scale of the phenomenon is sometimes exaggerated, so it is worth anchoring it. Sender, Fuchs, and Milo (PLoS Biology, 2016) calculated that in the body of a model man weighing 70 kg, there are about 38 trillion bacterial cells compared to 30 trillion human cells, and the entire population weighs about 0.2 kg. The often-repeated ratio of ten to one is inflated: the orders of magnitude are the same.

The strongest evidence for the role of the vagus nerve comes from animal studies. Bravo et al. (PNAS, 2011) administered the Lactobacillus rhamnosus JB-1 strain to mice and observed changes in GABA receptor mRNA expression dependent on the brain region, a decrease in stress-induced corticosterone, and less anxious and depressive behaviors. In mice with severed vagus nerves, there were neither neurochemical nor behavioral changes.

This is an important result, but it must be read literally. It concerns mice, and the changes in receptor expression went in both directions, depending on the brain structure. The popular summary that this strain works “the same way as benzodiazepines, just without addiction” adds a comparison that is not present in the available abstract of this work.

Which strains have the strongest clinical evidence?

In human studies, the weight of evidence rests on two strains: the combination of Lactobacillus helveticus R0052 with Bifidobacterium longum R0175 and the Bifidobacterium infantis 35624 strain. Besides these, aggregate data matter, as individual trials are small.

Messaoudi et al. (British Journal of Nutrition, 2011) conducted a two-part study: an experiment on rats and a trial with a double-blind, placebo-controlled parallel group of healthy volunteers who took the preparation for 30 days. Improvement was noted on the HSCL-90 scale, in its overall severity index, in the subscales of somatization, depression, and hostility, as well as in the overall score of the HADS scale. The anxiety subscale of HADS stopped at a p-value below 0.06, meaning it did not reach the usual significance threshold. Summaries that simply state “reduction of anxiety” omit this boundary.

The aggregate picture is provided by the meta-analysis by Liu, Walsh, and Sheehan (Neuroscience and Biobehavioral Reviews, 2019), which included 34 controlled studies. Probiotics had a small but significant effect on depression (d = -0.24) and anxiety (d = -0.10). Prebiotics did not differ from placebo. The effect grew in clinical and medical trials (d = -0.45), and in a preliminary analysis limited to psychiatric patients, it reached d = -0.73.

Study Who and how many Duration What was found
Messaoudi 2011, British Journal of Nutrition healthy volunteers, placebo trial 30 days improvement in HSCL-90 and overall HADS score, decrease in free cortisol in urine
O’Mahony 2005, Gastroenterology 77 people with irritable bowel syndrome 8 weeks B. infantis 35624 reduced abdominal pain and bloating, normalized IL-10 to IL-12 ratio
Schmidt 2015, Psychopharmacology 45 healthy volunteers 3 weeks B-GOS reduced morning cortisol spike; FOS had no effect
Liu 2019, Neurosci. Biobehav. Rev. meta-analysis of 34 controlled studies - probiotics d = -0.24 for depression; prebiotics no difference from placebo

How to choose a preparation is described in a separate entry on how to select a probiotic strain.

Does a psychobiotic lower cortisol?

In two independent human trials, yes, with two different indicators measured. In Messaoudi’s study, daily excretion of free cortisol in urine decreased, which is a measure of the hormone’s production over 24 hours. This is a statistically significant result obtained after 30 days of taking the preparation.

The second measurement concerned the morning cortisol spike and yielded a more interesting result, as it separated two components usually lumped together. Schmidt et al. (Psychopharmacology, 2015) administered one of two prebiotics, fructo-oligosaccharides or galacto-oligosaccharides B-GOS, or placebo in the form of maltodextrin to 45 healthy volunteers for three weeks. The salivary cortisol spike upon awakening was significantly lower after B-GOS than after placebo, and participants were less attentive to negative stimuli in the dot-probe test. No such effects were observed after fructo-oligosaccharides.

The conclusion is inconvenient for advertising slogans: prebiotics are not one category, just as probiotics are not. Two substances from the same chemical family, given in the same scheme and measured by the same method, yielded different results. The statement about “FOS and GOS prebiotics that lower reactivity to emotional stimuli” lumps together a position that worked with one that did not.

What do psychobiotics offer for irritable bowel syndrome?

This is the area with the longest history of research, as gastrointestinal and psychological symptoms co-occur frequently enough that one intervention can target both. Dinan et al. pointed to irritable bowel syndrome as the place where psychobiotics have been most widely studied.

O’Mahony et al. (Gastroenterology, 2005) randomly assigned 77 people with this diagnosis to three groups: Lactobacillus salivarius UCC4331, Bifidobacterium infantis 35624, or a malt beverage as placebo, for eight weeks. Each strain was administered at a dose of 10 billion live cells. Only B. infantis 35624 gained an advantage over placebo, both in the composite result and in individual assessments of abdominal pain, bloating, and difficulty with bowel movements.

The second result of this work concerns immunity. At the start, patients had an abnormal IL-10 to IL-12 ratio, indicating a predominance of the pro-inflammatory Th-1 profile. Administration of B. infantis 35624 normalized this ratio, which neither the other strain nor placebo did.

It is worth narrowing the conclusion to what this work measured: gastrointestinal symptoms and cytokine ratios. There are no psychiatric scales among the endpoints listed in the abstract, so the repeated statement about parallel psychological improvement in the same patients finds no confirmation in it. Separately, we wrote about irritable bowel syndrome in the context of cannabidiol and the microbiome.

Does the microbiome affect sleep?

Data in humans are correlational and come from small groups, so the answer is: probably yes, but the direction of the relationship remains undetermined. The most frequently cited work measured correlation, not the effect of intervention.

Smith et al. (PLoS ONE, 2019) combined actigraphy with microbiome sampling in 26 participants, exclusively men with an average age of about 22 years. Overall microbiome diversity positively correlated with sleep efficiency and total sleep time, and negatively with wake time after sleep onset. This same diversity also correlated with interleukin 6 levels, a cytokine previously linked to sleep. The group was small and homogeneously male, so this is a signal for further research, not a rule for the entire population.

The clock mechanism was described in mice. Thaiss et al. (Cell, 2016) showed that daily oscillations of the microbiota program the transcriptional and epigenetic rhythm of the host, and disrupting this rhythm not only abolishes normal oscillations but also induces new ones in the gut and liver. The work describes the transcriptional and epigenetic rhythm of the host; the quality of sleep is not addressed in its summary. The popular story about germ-free mice that sleep poorly and are fixed by probiotics attributes more to it than can be read from it.

What to eat to support the microbiome?

The strongest dietary evidence in this field concerns fermented foods, not capsules. Wastyk et al. (Cell, 2021) conducted a seventeen-week randomized study with 18 people per arm, comparing a diet rich in plant fiber with a diet rich in fermented products.

The results diverged clearly. The fermented arm systematically increased microbiota diversity and lowered inflammatory markers. In the high-fiber arm, the primary endpoint, the cytokine response index, did not change, and participants divided into three distinct immunological trajectories depending on the initial microbiota diversity. The authors concluded that fermented products may counteract the decline in diversity and the increase in inflammation typical of industrialized societies.

This translates simply into daily menus. Prebiotics are scattered throughout the kitchen, while fermented products stick to one shelf:

  • inulin and fructo-oligosaccharides: onion, garlic, leek, artichoke
  • beta-glucan: oats, barley
  • pectins: apples, citrus fruits
  • resistant starch: cooled potatoes, rice cooked the day before
  • polyphenols: berries, green tea
  • fermented products: natural yogurt, kefir, kimchi, sauerkraut, tempeh, miso

Keep in mind the lesson from Schmidt’s work: the name of the group does not determine the action. One galacto-oligosaccharide lowered morning cortisol, while fructo-oligosaccharide in the same study did not. Differences between prebiotics and probiotics are broken down in a separate entry on prebiotics and probiotics.

Frequently Asked Questions

What is a psychobiotic?

It is a living organism that, taken in the right amount, brings health benefits to people with mental disorders. The definition was formulated by Dinan, Stanton, and Cryan in Biological Psychiatry in 2013. It is not a separate species of bacteria, but a specific strain for which such an effect has been demonstrated in research.

Which psychobiotic strains have human studies?

The best-documented are two strains. Lactobacillus helveticus R0052 with Bifidobacterium longum R0175 was studied by Messaoudi and colleagues for 30 days in healthy volunteers. Bifidobacterium infantis 35624 was studied by O’Mahony’s team in 77 people with irritable bowel syndrome for eight weeks.

Can a psychobiotic replace an antidepressant?

No. A meta-analysis by Liu and colleagues from 2019 showed a small but statistically significant effect for probiotics, with a strength of d = -0.24 for depression. This is an order of magnitude incomparable to pharmacotherapy. In the case of diagnosed depressive or anxiety disorders, treatment by a physician is decisive.

How long did the studies on psychobiotics last?

From three weeks to seventeen. Schmidt administered prebiotics for three weeks, Messaoudi a probiotic preparation for 30 days, O’Mahony for eight weeks, and Wastyk conducted a dietary intervention for seventeen weeks. There are practically no shorter observations in this group of studies.

Does serotonin from the gut improve mood?

Not directly. Yano and colleagues demonstrated in 2015 that gut bacteria stimulate the production of serotonin in enterochromaffin cells, but the effects described in this work concern the motility of the gastrointestinal tract and blood platelets. This serotonin does not pass from the blood to the brain.

Does a prebiotic work the same as a probiotic?

No. In Liu’s 2019 meta-analysis, prebiotics did not differ from placebo either in depression or anxiety, while probiotics had a significant effect. Differences also occur within the prebiotic group itself: galacto-oligosaccharide worked in Schmidt’s study, while fructo-oligosaccharide did not.

Probiotic preparations and other supplements in the store ubucha.pl are collected in the supplements category.

This article is for informational and educational purposes and does not replace consultation with a doctor. If you are pregnant, breastfeeding, taking medications, or have chronic conditions, consult the use of supplements or herbs with a specialist.

Author: Michał Waluk · Published: 2026-05-29 · Updated: 2026-08-16

Podziel się:
Zaufanie
Dowiedz się więcej o nas
Darmowa wysyłka
Od 49PLN - paczkomatem
Łatwy kontakt
Masz pytania? Skontaktuj się z nami.
Lojalność
Jedyny taki program - zbieraj buchy

Strona tylko dla osób pełnoletnich.

Czy masz ukończone 18 lat?

Buch z Tobą