Probiotics and Mental Health — The Gut-Brain Axis

The gut-brain axis is the bidirectional communication network between the enteric nervous system — the 500 million neurons embedded in the gut wall — and the central nervous system, mediated by the vagus nerve, the immune system, the endocrine system, and a host of microbial metabolites that cross or signal across the blood-brain barrier. Probiotic strains capable of measurably modulating this axis are called psychobiotics, a term coined by John Cryan and Ted Dinan at University College Cork. The strongest randomized-trial evidence supports specific strains for depression (Akkasheh 2016 with a Lactobacillus-Bifidobacterium blend, Wallace 2017 with Lab4P), anxiety (Messaoudi 2011 with L. helveticus R0052 + B. longum R0175), perceived stress and cortisol response, and irritable-bowel-syndrome co-morbid depression (Pinto-Sanchez 2017 with Bifidobacterium longum NCC3001). The mechanisms cluster around four pathways: vagal afferent signaling, microbial production of neurotransmitter precursors (especially in the tryptophan-serotonin and tryptophan-kynurenine arms), modulation of the hypothalamic-pituitary-adrenal stress axis, and reduction of low-grade systemic inflammation that itself drives depressive symptomatology. This deep-dive walks through each pathway, each trial, the practical strain choices, and the realistic boundaries of what probiotics can and cannot do for mental health.

Table of Contents

  1. What the Gut-Brain Axis Actually Is
  2. The Vagal Signaling Pathway
  3. Microbial Neurotransmitter Production
  4. Tryptophan, Serotonin, and the Kynurenine Pathway
  5. HPA-Axis Modulation and the Stress Response
  6. Inflammation, Cytokines, and Depressive Symptomatology
  7. Probiotics for Depression — The Clinical Trials
  8. Probiotics for Anxiety — The Clinical Trials
  9. Perceived Stress and Cortisol Response
  10. Sleep, Circadian Rhythm, and the Microbiome
  11. IBS and Mood — The Two-Way Street
  12. The Psychobiotic Strain List
  13. Realistic Expectations and Boundaries
  14. Key Research Papers
  15. Connections

What the Gut-Brain Axis Actually Is

The phrase "gut-brain axis" is used loosely enough that it has lost specificity in popular use. In its precise neuroscientific meaning, it refers to four overlapping bidirectional communication channels between the gastrointestinal tract and the central nervous system.

The first channel is neural. The vagus nerve carries roughly 80 percent afferent (gut-to-brain) fibers and only 20 percent efferent (brain-to-gut) fibers, contradicting the usual assumption that the brain runs the show. Vagal afferents terminate in the nucleus tractus solitarius in the brainstem, then project to the locus coeruleus, parabrachial nucleus, amygdala, hypothalamus, and prefrontal cortex — a circuit that touches mood, arousal, fear processing, and autonomic regulation. The enteric nervous system, the gut's own intrinsic neural network of approximately 500 million neurons, communicates with the central nervous system primarily through this vagal pipeline.

The second channel is immunological. The gut-associated lymphoid tissue is the largest immune organ in the body, and cytokines produced by gut immune cells (IL-6, TNF-alpha, IL-1-beta, IL-17, IL-10) reach the brain through the bloodstream and modulate microglial activation, neurotransmitter metabolism, and neurogenesis. Chronic low-grade gut inflammation correlates with depressive symptomatology in epidemiologic studies and in mechanistic animal work.

The third channel is endocrine. The gut produces or modulates the production of multiple peptides and hormones with central effects: ghrelin, leptin, GLP-1, PYY, CCK, and others. Gut-derived signals modulate the hypothalamic-pituitary-adrenal axis, the central stress-response system whose dysregulation is a defining feature of major depression.

The fourth channel is microbial-metabolic. Gut bacteria produce or transform an enormous array of small molecules — short-chain fatty acids (butyrate, propionate, acetate), bile acid derivatives, tryptophan metabolites (indoles, kynurenines), GABA, serotonin (peripherally), and dozens of less-characterized compounds. Many of these cross the blood-brain barrier or signal through receptors on vagal afferents or immune cells. This is the channel that probiotics most directly modify.

The Cryan and Dinan group's 2019 Physiological Reviews paper "The Microbiota-Gut-Brain Axis" is the canonical multi-hundred-page synthesis of all four channels and is the standard reference for the field.

Back to Table of Contents

The Vagal Signaling Pathway

The vagus nerve is the dominant fast-signaling conduit from gut to brain. Probiotic effects on mood and anxiety in animal models are almost entirely abolished by surgical vagotomy — cutting the vagus nerve eliminates the behavioral phenotype, which is the strongest possible evidence that the signal is traveling through this specific anatomic pathway rather than through bloodborne metabolites or immune mediators alone.

The landmark paper here is Bravo JA et al. (2011) in Proceedings of the National Academy of Sciences. Lactobacillus rhamnosus JB-1 administered to mice for four weeks produced reduced anxiety-like and depression-like behavior in standard tests (forced swim test, elevated plus maze), altered GABA-A receptor expression in cortical and amygdalar regions, and reduced stress-induced corticosterone elevation. Vagotomy eliminated all of these effects. The bacteria themselves did not need to colonize or even reach the brain — their luminal presence in the gut was sufficient, and the signal traveled up the vagus nerve.

The afferent vagal fibers that mediate these effects express receptors for multiple bacterially produced and bacterially modulated molecules: free fatty acid receptors (FFAR2, FFAR3) for short-chain fatty acids, toll-like receptors for bacterial cell-wall components, receptors for serotonin (most of which is produced peripherally by enterochromaffin cells under microbial regulation), and receptors for bile acid derivatives. The vagal afferent is therefore a microbial-sensing apparatus whose signaling output reaches mood- and arousal-regulating brain regions within milliseconds.

This pathway also runs in the opposite direction. Vagal efferents to the gut modulate motility, secretion, and importantly, mucosal immune tone through the cholinergic anti-inflammatory pathway. Chronic stress, which suppresses vagal tone, is associated with both gut dysbiosis and elevated gut inflammation — closing a loop in which stress drives gut dysfunction which feeds back to drive more stress.

Back to Table of Contents

Microbial Neurotransmitter Production

Many gut bacteria produce or modulate the production of classical neurotransmitters. The amounts are biologically relevant in the gut lumen, though the question of whether luminal neurotransmitters cross the gut wall and reach systemic circulation, much less the brain, is more nuanced.

GABA (gamma-aminobutyric acid) is the brain's principal inhibitory neurotransmitter and is the target of benzodiazepines, gabapentinoids, and most modern anxiolytic strategies. Several Lactobacillus species (L. rhamnosus, L. brevis, L. plantarum) and Bifidobacterium species (B. dentium, B. adolescentis) express glutamate decarboxylase and produce GABA from dietary glutamate. The L. rhamnosus JB-1 strain used in the Bravo 2011 study is a particularly active GABA producer. Whether this luminal GABA reaches the brain directly is unlikely — GABA itself crosses the blood-brain barrier poorly — but it can signal through GABA receptors on enteric neurons and vagal afferents, providing an indirect pathway to central GABAergic effects.

Serotonin presents the opposite pattern. Approximately 90% of the body's serotonin is produced in the gut, primarily by enterochromaffin cells in the intestinal epithelium, with bacterial regulation of the tryptophan-to-serotonin conversion (see next section). Peripheral serotonin does not cross the blood-brain barrier and does not directly contribute to central serotonergic tone. Probiotics that modulate gut serotonin production affect gut motility, mucosal immunity, and platelet function, but the mood-relevant pathway runs through tryptophan availability rather than direct serotonin transfer.

Dopamine and norepinephrine are also produced or modulated by gut bacteria, again primarily affecting local enteric and immune function rather than directly increasing central catecholamine tone. The clinical relevance is mediated through vagal signaling and through systemic effects on tryptophan and tyrosine availability.

Histamine production by certain Lactobacillus strains (L. casei, L. delbrueckii) is one reason why some sensitive patients with mast cell activation syndrome or histamine intolerance react poorly to broad-spectrum probiotic blends and do better on histamine-friendly formulations (Bifidobacterium species predominate; some Lactobacillus strains, especially L. rhamnosus GG, are low-histamine).

Back to Table of Contents

Tryptophan, Serotonin, and the Kynurenine Pathway

Tryptophan is the essential amino acid that serves as the precursor for both serotonin and the kynurenine family of metabolites. The fate of dietary tryptophan in the body is a fork in the road with major consequences for mood: the serotonergic arm produces serotonin (mood-supporting) and melatonin (sleep-supporting), while the kynurenine arm produces a series of metabolites that can be neurotoxic (quinolinic acid) or neuroprotective (kynurenic acid) depending on which downstream enzymes dominate.

Approximately 95% of dietary tryptophan that is not used for protein synthesis is shunted into the kynurenine pathway, primarily through the enzymes indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO). Only about 5% goes into serotonin synthesis. Inflammation upregulates IDO, pushing more tryptophan into the kynurenine arm and away from serotonin synthesis — one of the proposed mechanisms by which chronic inflammation drives depression. This is called the kynurenine pathway hypothesis of depression and is well-supported by clinical neurometabolomic studies.

Gut bacteria intersect this system in several ways:

The Pinto-Sanchez 2017 trial of Bifidobacterium longum NCC3001 in IBS patients with mild-to-moderate depression measured changes in depression scores, IBS symptoms, and brain activation patterns on functional MRI. The probiotic produced significant improvement in depression scores compared to placebo (64% versus 32% of patients reaching the responder threshold at 6 weeks) and altered activation in the amygdala and fronto-limbic regions. The mechanism proposed by the authors centered on tryptophan-kynurenine pathway modulation, with reduced inflammatory drive of IDO.

Back to Table of Contents

HPA-Axis Modulation and the Stress Response

The hypothalamic-pituitary-adrenal (HPA) axis is the body's central stress-response system. Acute psychological or physical stress triggers hypothalamic corticotropin-releasing hormone (CRH), which drives pituitary adrenocorticotropic hormone (ACTH) release, which stimulates adrenal cortisol production. Acute cortisol release is adaptive. Chronic HPA hyperactivation — elevated baseline cortisol, blunted diurnal variation, exaggerated cortisol response to mild stressors — is a defining neuroendocrine feature of major depressive disorder, post-traumatic stress disorder, and chronic anxiety states.

The microbiome modulates HPA-axis development and reactivity. Germ-free mice (mice raised in sterile conditions with no microbiome) show exaggerated HPA responses to mild stress, and this hyper-responsiveness is normalized by colonization with a conventional microbiome — but only within a critical developmental window. The Sudo 2004 paper in Journal of Physiology established this developmental dependence: colonization in adulthood does not fully normalize HPA reactivity in mice that grew up germ-free. The clinical implication is that early-life microbiome exposure shapes lifelong stress reactivity, with potential consequences for adult mood and anxiety vulnerability.

Probiotic effects on the HPA axis in adult humans are more modest but real. Several randomized trials have measured salivary cortisol or cortisol awakening response in healthy adults given probiotics and have shown reduced cortisol output, particularly in response to laboratory stressors. The Messaoudi 2011 study (see below) included a 30-day course of L. helveticus R0052 + B. longum R0175 (the "Probio'Stick" formulation, now marketed as Cerebiome) and showed reduction in urinary free cortisol relative to placebo, along with reductions in self-reported anxiety and depression on the Hopkins Symptom Checklist 90 and Hospital Anxiety and Depression Scale.

The proposed mechanism involves reduced gut inflammatory signaling to the central nervous system, vagal modulation of hypothalamic CRH neurons, and microbial production of short-chain fatty acids (especially butyrate) that have direct anti-inflammatory and HPA-modulating effects.

Back to Table of Contents

Inflammation, Cytokines, and Depressive Symptomatology

The cytokine hypothesis of depression posits that chronic low-grade systemic inflammation — reflected in elevated C-reactive protein, IL-6, TNF-alpha, and IL-1-beta — is causally upstream of a meaningful fraction of major depressive disorder. The evidence supporting this hypothesis includes the observation that interferon-alpha therapy for hepatitis C and certain cancers triggers depressive symptoms in a substantial minority of patients (sickness behavior), the cross-sectional association between inflammatory markers and depression scores, the longitudinal predictive value of elevated baseline CRP for incident depression, and the finding that anti-inflammatory interventions (including some monoclonal antibodies) produce modest antidepressant effects in subgroups of treatment-resistant patients with elevated baseline inflammation.

Approximately 30% of patients with major depressive disorder have measurably elevated inflammatory markers at baseline. These patients tend to respond less well to standard SSRIs and tend to have more severe somatic symptoms (fatigue, sleep disturbance, appetite changes). They are also the group in which anti-inflammatory strategies, including probiotics, are most likely to produce mood benefit.

The gut is one of the dominant drivers of systemic inflammatory tone. Increased intestinal permeability allows bacterial lipopolysaccharide (LPS) and other microbe-associated molecular patterns to cross from gut lumen to lamina propria, where they activate toll-like receptors on immune cells and drive systemic cytokine release. This is the "leaky gut" pathway in its precise mechanistic form. Probiotic strains that strengthen the intestinal barrier (L. rhamnosus GG, L. plantarum, B. infantis) and that shift mucosal immune tone toward anti-inflammatory cytokines (IL-10, TGF-beta) and away from pro-inflammatory cytokines (IL-6, TNF-alpha, IL-17) can therefore reduce the systemic inflammatory drive that contributes to depressive symptomatology.

This mechanism is one of the most robustly supported pathways for the gut-brain effect of probiotics and is the rationale for using probiotics as an adjunct in inflammation-associated depression. It does not mean probiotics replace antidepressants, but it does mean they have a plausible additive role.

Back to Table of Contents

Probiotics for Depression — The Clinical Trials

Randomized controlled trial evidence for probiotics in depression is now substantial, with multiple meta-analyses showing a small but statistically significant antidepressant effect.

Akkasheh G et al. (2016) in Nutrition randomized 40 patients with major depressive disorder to an eight-week course of a probiotic capsule containing Lactobacillus acidophilus, Lactobacillus casei, and Bifidobacterium bifidum (2 billion CFU each) versus placebo. The probiotic group showed significantly greater reduction in Beck Depression Inventory scores compared to placebo, along with improvements in insulin sensitivity and inflammatory markers. This was the first methodologically solid RCT in clinical major depression.

Wallace CJK and Milev R (2021) reported an open-label trial of CEREBIOME (L. helveticus R0052 + B. longum R0175) in 10 patients with persistent depressive symptoms, with significant improvement in depression scores at 8 weeks. The earlier Wallace CJK and Milev R (2017) review article in Annals of General Psychiatry synthesized the then-available probiotic-depression literature and codified the framework.

Pinto-Sanchez MI et al. (2017) in Gastroenterology randomized 44 adults with IBS and mild-to-moderate depression to Bifidobacterium longum NCC3001 versus placebo for 6 weeks. The probiotic group had significantly greater depression score improvement (64% responders versus 32% placebo) and showed altered functional MRI activation patterns in mood-relevant brain regions. IBS symptom improvement was modest and statistically borderline; the depression signal was the stronger of the two effects.

Slykerman RF et al. (2017) in EBioMedicine randomized 423 pregnant women to Lactobacillus rhamnosus HN001 versus placebo from 14-16 weeks gestation through 6 months postpartum. The probiotic group had significantly lower postpartum depression scores (Edinburgh Postnatal Depression Scale) and lower anxiety scores at the postpartum assessment. This is one of the cleanest demonstrations of a preventive probiotic mood effect in a defined-risk population.

Several systematic reviews and meta-analyses have synthesized this evidence. Liu RT et al. (2019) in Neuroscience & Biobehavioral Reviews pooled 34 RCTs and reported a small but significant antidepressant effect of probiotics in clinical and non-clinical populations, with the largest effects in patients with clinical depression as opposed to subthreshold mood symptoms. Goh KK et al. (2019) meta-analysis came to similar conclusions. The effect size is modest (standardized mean difference around 0.30 in clinical depression populations) — smaller than SSRIs but larger than placebo, with a much more favorable side-effect profile.

The realistic interpretation is that probiotics, particularly the well-studied psychobiotic strains, are a reasonable adjunct to standard depression treatment, with a meaningful but small expected effect. They should not be used as monotherapy for moderate-to-severe major depression. They are most useful in patients with concomitant gut symptoms, in patients with elevated inflammatory markers, and as part of a broader lifestyle and dietary intervention.

Back to Table of Contents

Probiotics for Anxiety — The Clinical Trials

The single most-cited human anxiety trial is Messaoudi M et al. (2011) in British Journal of Nutrition. The study randomized 55 healthy adult volunteers to a 30-day course of the Probio'Stick formulation — Lactobacillus helveticus R0052 plus Bifidobacterium longum R0175 at 3 billion CFU total — versus placebo. Outcomes were measured using the Hopkins Symptom Checklist 90 (HSCL-90), the Hospital Anxiety and Depression Scale (HADS), the Perceived Stress Scale, and 24-hour urinary free cortisol. The probiotic group showed significant reductions across the HSCL-90 global severity index, HSCL-90 anxiety subscale, HSCL-90 depression subscale, HADS scores, and urinary free cortisol. The effect sizes were moderate (around 0.4-0.6 across measures) and statistically robust.

The same R0052 + R0175 formulation has been re-tested in multiple subsequent trials, generally with replicating positive effects on subclinical anxiety, perceived stress, and stress-related sleep disruption. It is the most extensively studied "psychobiotic" formulation in current use.

Other anxiety-relevant probiotic trials include the Allen AP et al. (2016) study of Bifidobacterium longum 1714 in Translational Psychiatry, which used a within-subjects crossover design with healthy adults to test for changes in subjective stress, cortisol awakening response, memory, and EEG correlates of cognitive processing. The probiotic produced modest reductions in subjective stress and altered hippocampal-dependent memory performance and frontal EEG indices, suggesting genuine central effects.

The Steenbergen L et al. (2015) study in Brain, Behavior, and Immunity randomized 40 healthy adults to a multi-strain probiotic versus placebo for four weeks and found reduced reactivity to sad mood induction in the probiotic group — an early demonstration of probiotic effect on emotional cognition in a non-clinical sample.

A 2019 systematic review by Liu RT et al. assessed probiotics for anxiety symptoms across 22 RCTs and found a small but statistically significant anxiolytic effect, with the largest effects in subclinical anxiety populations and in studies using the R0052+R0175 formulation or Bifidobacterium-dominant blends.

Back to Table of Contents

Perceived Stress and Cortisol Response

Beyond formal diagnoses of anxiety or depression, the broader category of perceived stress and stress-reactivity has been a productive target for probiotic research. The two endpoints most commonly used are the Perceived Stress Scale (a 10-item self-report questionnaire) and laboratory or naturalistic measures of cortisol response (cortisol awakening response, diurnal cortisol slope, cortisol response to standardized stressors like the Trier Social Stress Test).

Multiple trials have shown that probiotic supplementation modestly reduces both subjective stress perception and objective cortisol output, particularly in populations with elevated baseline stress (medical students during exam periods, healthcare workers, patients with chronic illness). The effect sizes are smaller than those seen with cognitive-behavioral interventions or mindfulness-based stress reduction, but they are real and they are achievable with no behavioral effort — an advantage in populations where time and behavioral change capacity are limited.

The most clinically relevant application is probably the integration of probiotics into a broader stress-management strategy that includes sleep, exercise, mindfulness practice, and social connection. In that context, the probiotic adds a measurable physiologic effect to a multi-pronged behavioral intervention.

Back to Table of Contents

Sleep, Circadian Rhythm, and the Microbiome

The relationship between the gut microbiome and sleep is bidirectional and increasingly characterized. Sleep deprivation alters microbiome composition within days, shifting toward a more pro-inflammatory profile. Conversely, microbiome composition predicts sleep architecture in cross-sectional studies, with greater bacterial diversity associated with better sleep efficiency and longer sleep duration.

Probiotic effects on sleep have been studied in several small trials. Lactobacillus casei Shirota in stressed medical students improved subjective sleep quality and reduced sleep-onset latency in the Takada 2017 trial. Lactobacillus helveticus R0052 + Bifidobacterium longum R0175 improved sleep quality alongside its stress and anxiety effects. The Schmidt 2015 study of a galacto-oligosaccharide prebiotic (not a probiotic per se, but feeding the resident microbiome) showed reduced waking cortisol and improved emotional processing.

The mechanisms involved include microbial production of melatonin precursors (gut bacteria express tryptophan-to-serotonin and serotonin-to-melatonin enzymes, contributing to the small but biologically active pool of peripheral melatonin), modulation of vagal tone affecting autonomic regulation during sleep, reduction of inflammatory cytokines that fragment sleep architecture, and indirect effects through stress-axis modulation.

The clinical reality is that probiotics are not a primary sleep intervention — sleep hygiene, light exposure timing, caffeine and alcohol management, and treatment of specific sleep disorders (sleep apnea, restless legs, insomnia) remain the high-yield levers. But for patients whose poor sleep is interwoven with stress, anxiety, mood disturbance, or gut symptoms, the probiotic contribution to a broader stack is real.

Back to Table of Contents

IBS and Mood — The Two-Way Street

Irritable bowel syndrome and mood disorders co-occur at rates far higher than chance. Approximately 40-60% of IBS patients meet criteria for an anxiety or depressive disorder, and approximately 30% of patients with major depression have IBS-spectrum gut symptoms. This is not coincidence and it is not purely a psychosomatic phenomenon — it reflects the shared underlying gut-brain axis biology.

The Pinto-Sanchez 2017 trial of Bifidobacterium longum NCC3001 in IBS-plus-depression patients (described above) is the clearest demonstration that a single intervention can affect both ends of the axis. Both the IBS symptoms and the depression scores improved on the probiotic, with the depression effect being the larger and more statistically robust of the two. This is the kind of dual-effect outcome that supports the gut-brain interpretation rather than a purely peripheral or purely central one.

For patients with IBS and concomitant mood or anxiety symptoms, this opens up therapeutic strategies that target the shared pathway rather than the two ends separately. Probiotic strains with documented effects on both axes (Bifidobacterium longum NCC3001, Lactobacillus helveticus R0052 + B. longum R0175, Bifidobacterium infantis 35624) are the rational choice for this population. Our Irritable Bowel Syndrome page covers the IBS side of this overlap.

Back to Table of Contents

The Psychobiotic Strain List

The term psychobiotic was coined by Ted Dinan and John Cryan in 2013 to describe live bacteria that, when ingested in adequate amounts, produce a beneficial effect on mental health. Not every probiotic is a psychobiotic. The strains with the strongest direct evidence for mood, anxiety, or stress effects in human randomized trials are:

Several of these are available as branded consumer products (Align for B. infantis 35624, Cerebiome / Probio'Stick for the R0052+R0175 combination, certain Renew Life and Garden of Life products carrying specific psychobiotic strains). The strain identifier matters — "Lactobacillus rhamnosus" on a label without the strain code is not the JB-1 strain, and the genus-species designation alone does not transfer the trial evidence.

Back to Table of Contents

Realistic Expectations and Boundaries

Psychobiotic research is real and the trial evidence is substantial enough to act on, but realistic expectation-setting is important.

For broader context on the gut-brain axis as a clinical entity, see our Gut-Brain Axis page. For the foundational gut-health applications of probiotics, see Probiotics for Gut Health. For the strain-by-strain reference list, see Strains and Selection.

Back to Table of Contents

Key Research Papers

  1. Cryan JF et al. (2019). The Microbiota-Gut-Brain Axis. Physiological Reviews. — PMID 31460832
  2. Bravo JA et al. (2011). Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve. Proceedings of the National Academy of Sciences. — PMID 21876150
  3. Messaoudi M et al. (2011). Assessment of psychotropic-like properties of a probiotic formulation (Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) in rats and human subjects. British Journal of Nutrition. — PMID 20974015
  4. Akkasheh G et al. (2016). Clinical and metabolic response to probiotic administration in patients with major depressive disorder: a randomized, double-blind, placebo-controlled trial. Nutrition. — PMID 26706022
  5. Pinto-Sanchez MI et al. (2017). Probiotic Bifidobacterium longum NCC3001 reduces depression scores and alters brain activity: a pilot study in patients with irritable bowel syndrome. Gastroenterology. — PMID 28483500
  6. Slykerman RF et al. (2017). Effect of Lactobacillus rhamnosus HN001 in pregnancy on postpartum symptoms of depression and anxiety: a randomised double-blind placebo-controlled trial. EBioMedicine. — PMID 28943228
  7. Allen AP et al. (2016). Bifidobacterium longum 1714 as a translational psychobiotic: modulation of stress, electrophysiology and neurocognition in healthy volunteers. Translational Psychiatry. — PMID 27801892
  8. Steenbergen L et al. (2015). A randomized controlled trial to test the effect of multispecies probiotics on cognitive reactivity to sad mood. Brain, Behavior, and Immunity. — PMID 25862297
  9. Sudo N et al. (2004). Postnatal microbial colonization programs the hypothalamic-pituitary-adrenal system for stress response in mice. Journal of Physiology. — PMID 15133062
  10. Wallace CJK and Milev R (2017). The effects of probiotics on depressive symptoms in humans: a systematic review. Annals of General Psychiatry. — PMID 28239408
  11. Liu RT et al. (2019). Prebiotics and probiotics for depression and anxiety: a systematic review and meta-analysis of controlled clinical trials. Neuroscience & Biobehavioral Reviews. — PMID 31004628
  12. Dinan TG, Stanton C, Cryan JF (2013). Psychobiotics: a novel class of psychotropic. Biological Psychiatry. — PMID 23759244
  13. Foster JA, Rinaman L, Cryan JF (2017). Stress & the gut-brain axis: regulation by the microbiome. Neurobiology of Stress. — PMID 29276734
  14. Tillisch K et al. (2013). Consumption of fermented milk product with probiotic modulates brain activity. Gastroenterology. — PMID 23474283

PubMed Topic Searches

Back to Table of Contents

Connections

Back to Table of Contents