What part of the brain controls defecation?

Which part of the brain controls defecation, and how does the nervous system coordinate such a complex act? This article explains the brain control of defecation in clear, medically grounded terms. You’ll learn how cortical, brainstem, spinal, autonomic, and enteric circuits work together, why this system matters for everyday gut health, and how variability in biology and the gut microbiome can influence bowel regularity. We also discuss why symptoms alone rarely reveal the root cause of bowel issues and how microbiome testing can add useful context—especially when problems persist or remain unexplained.

Introduction

Defecation is not just a “plumbing” process—it is a finely tuned neurogastroenterological event. Understanding how the brain and nerves regulate bowel movements helps explain symptoms like constipation, urgency, and incontinence, and reveals why one-size-fits-all solutions often fall short. From the brainstem to the enteric nervous system (ENS), the neural regulation of bowel movements coordinates motility, sphincter tone, and sensation. Add the gut microbiome to this picture, and you have a dynamic brain–gut axis in which microbes can influence signaling molecules, reflexes, and motility patterns. This article connects these layers—from neural pathways to microbial metabolites—so you can better interpret your symptoms, appreciate individual variability, and know when deeper insight may be useful.

The Core Explanation: How the Brain Regulates Defecation

Neural Regulation of Bowel Movements: An Overview

The act of defecation begins with the movement of stool from the colon into the rectum and culminates in coordinated relaxation of the anal sphincters and abdominal/pelvic floor muscles. This sequence relies on overlapping control systems:

• Enteric nervous system (ENS): Often called the “second brain in the gut,” the ENS is embedded in the intestinal wall. It generates colonic motility patterns (e.g., mass movements) and mediates local reflexes like the rectoanal inhibitory reflex (RAIR), which transiently relaxes the internal anal sphincter when the rectum distends.
• Spinal cord circuits: A “sacral defecation center” (S2–S4) integrates rectal sensory input via pelvic nerves, coordinates reflexive responses, and provides parasympathetic outflow to the distal colon and rectum.
• Brainstem and higher centers: The brainstem integrates visceral signals (e.g., via the nucleus tractus solitarius) and communicates with cortical and subcortical regions that govern voluntary control, continence, and behavioral aspects of elimination.
• Somatic pathways: The pudendal nerve (originating from S2–S4) controls the external anal sphincter and the puborectalis muscle, enabling voluntary squeezing to delay defecation.

These systems interface with the autonomic nervous system—sympathetic and parasympathetic divisions—which modulate colonic motility, rectal sensitivity, and sphincter tone. Together, they form the neural pathways of stool elimination that respond to physiological needs and contextual factors (e.g., timing, social setting).

The Brain’s Involvement: Cortical and Subcortical Influence on Evacuation

While much of bowel function is reflexive, higher brain regions give humans voluntary control. The medial prefrontal and anterior cingulate cortices, along with supplementary motor areas, contribute to decision-making and motor planning for evacuation. These regions interact with subcortical structures and the brainstem, shaping awareness of rectal fullness, urgency, and the selection of appropriate responses (e.g., delay versus proceed).

The brainstem serves as a hub integrating afferent signals from the gut with efferent commands. Although the vagus nerve primarily modulates upper gut and proximal colon function, brainstem autonomic nuclei (including the dorsal motor nucleus of the vagus and associated circuits) participate in gastrointestinal reflexes and interoception. A pontine region—described in animal models as a defecation center—is thought to coordinate patterning between sphincters and abdominal musculature, akin to how the pontine micturition center coordinates urination. In humans, evidence points to distributed networks across the pontine tegmentum, periaqueductal gray, and related pathways that shape timing and synergy.

From the brain to the gut, neural pathways of stool elimination descend through the spinal cord to the sacral segments. Voluntary control travels via corticospinal and reticulospinal tracts to motor neurons (e.g., Onuf’s nucleus) that drive the external anal sphincter and pelvic floor. These commands interface with sacral parasympathetic output and the ENS to orchestrate rectal contraction, sphincter relaxation, and abdominal pressurization when appropriate.

The Role of the Autonomic Nervous System in Defecation

The autonomic nervous system in defecation balances readiness to evacuate with continence:

• Parasympathetic pathways (S2–S4 via pelvic splanchnic nerves) enhance colonic motility and facilitate rectal activity. They also promote internal anal sphincter relaxation during defecation, working in concert with ENS-mediated reflexes.
• Sympathetic pathways (primarily from L1–L3 via lumbar splanchnic nerves and the hypogastric plexus) generally inhibit colonic motility and enhance internal anal sphincter tone, supporting continence and delaying bowel movements during stress or activity.

Hormonal, metabolic, and circadian factors (e.g., the “gastrocolic reflex” after meals) influence this autonomic balance. At any given time, brainstem and hypothalamic signals bias sympathetic and parasympathetic outputs to match physiological demands and environmental context.

Why This Topic Matters for Gut Health

The Connection Between Neural Control and Digestive Wellness

Healthy bowel habits depend on stable communication across the brain–gut axis. Smooth colonic propulsion, timely rectal sensation, and appropriate sphincter responses require precise signaling. When these channels misfire—due to stress, neurological conditions, pelvic floor discoordination, or medication effects—people may experience constipation, urgency, incomplete evacuation, or incontinence. In day-to-day life, even small shifts in autonomic tone (e.g., chronic sympathetic arousal) can change motility and stool frequency.

Because the ENS operates semi-independently, it can buffer short-term disruptions but remains influenced by central and autonomic inputs. A further layer—the gut microbiome—modulates motility and sensation via microbial metabolites and immune–neural cross-talk. Digestive wellness thus emerges from the alignment of central neural circuits, spinal reflexes, enteric behavior, and microbial ecology.

Symptoms and Signals Indicating Potential Neural or Microbiome Issues

Common patterns can signal when neural or microbial contributors deserve attention:

• Constipation: Infrequent stools, hard consistency, straining, or incomplete evacuation may involve slow colonic transit, dyssynergic pelvic floor function, altered autonomic balance, or ENS dysregulation. Methane-producing microbes have been associated with slower transit in some individuals.
• Diarrhea or urgency: Rapid transit, heightened rectal sensitivity, or autonomic shifts can drive loose stools and urgency. Changes in bile acid metabolism or microbial fermentation patterns may be contributing factors.
• Fecal incontinence: May reflect sphincter weakness, pelvic floor dysfunction, neuropathy (e.g., pudendal), or central integration issues. The absence or impairment of the rectoanal inhibitory reflex (e.g., in certain developmental conditions) alters continence mechanisms.

These symptoms are not diagnostic on their own. They can arise from overlapping causes, including medications, dietary changes, hormonal states, or microbiome imbalances, which underscores the need for a stepwise, individualized assessment.

Beyond Symptoms: The Importance of Individual Variability and Uncertainty

Two people with identical symptoms can have very different underlying mechanisms. One may have a primarily neural pattern (e.g., dyssynergia of the external anal sphincter and puborectalis), while another’s presentation may be driven by microbial metabolites affecting motility or sensory thresholds. Genetic variation, prior surgeries, obstetric history, psychological stress, and comorbid conditions (e.g., diabetes, Parkinson’s disease, multiple sclerosis) all shape autonomic and enteric behavior. Recognizing this variability is central to responsible interpretation of bowel symptoms and helps avoid premature conclusions based solely on how those symptoms feel.

Limitations of Symptom-Based Diagnosis and the Need for Deeper Understanding

Why Symptoms Alone Do Not Reveal the Root Cause of Bowel Dysfunction

Constipation does not automatically mean “weak motility,” and diarrhea does not always reflect “too-fast transit.” For example, someone can feel constipated because of sensory hyposensitivity (delayed awareness of rectal filling) or outlet obstruction (pelvic floor discoordination), even if proximal colonic transit is normal. Similarly, urgency may be sensory hypersensitivity rather than inherently rapid transit. Medications (opioids, anticholinergics), metabolic factors (thyroid dysfunction, hypercalcemia), and neurologic injury (stroke, spinal cord lesions) can mimic or amplify these patterns. Symptom-based guessing frequently misses mixed presentations where neural regulation, biomechanics, and microbiota all contribute in varying proportions.

The Role of the Gut Microbiome in Neural Regulation of Bowel Movements

The microbiome shapes the neurochemical landscape of the gut. Microbial fermentation yields short-chain fatty acids (SCFAs)—like butyrate, acetate, and propionate—that influence motility, mucosal health, and ENS signaling. Certain microbes affect bile acid metabolism, altering colonic secretion and transit. Others modulate host serotonin (5-HT) production by enterochromaffin cells, a major regulator of peristalsis and sensation. Microbes also produce gases (e.g., methane, hydrogen, hydrogen sulfide) that may influence smooth muscle patterns; methane has been associated with slower transit in some individuals.

Through immune modulation, epithelial signaling, and vagal pathways, the microbiota participates in a bidirectional gut-brain axis that can calibrate autonomic outputs and enteric reflexes. Dysbiosis—an imbalance in microbial composition or function—may therefore tip neural regulation toward constipation, urgency, or hypersensitivity, depending on context.

Exploring the Gut Microbiome's Role in Defecation and Neural Regulation

Microbiome Imbalances and Their Impact on Bowel Function

In dysbiosis, functional shifts can alter motility and sensation:

• Reduced SCFA producers may impair mucosal support and neuromuscular coordination, influencing ENS function.
• Excess methanogens (e.g., Methanobrevibacter) have been associated with slower intestinal transit and harder stools in many, though not all, individuals.
• Bile-acid–transforming microbes can skew bile acid pools, affecting colonic secretion and motility and contributing to diarrhea or constipation phenotypes.
• Tryptophan-metabolizing microbes influence serotonergic signaling, potentially altering peristalsis and visceral sensation.

These effects are context-dependent. Diet, host genetics, ENS integrity, and autonomic setpoints interact with microbial outputs, so a given imbalance can present differently across people.

Understanding the Gut-Brain Axis: Connecting Microbiome and Neural Control

Microbial signals reach the nervous system through multiple channels:

• Enteroendocrine pathways: Microbiota influence enterochromaffin cell release of 5-HT and peptide hormones (e.g., PYY, GLP-1), which modulate motility and sensation.
• Neuroimmune crosstalk: Microbial components and metabolites affect mucosal immune tone and cytokines, which can sensitize or dampen ENS and afferent neurons.
• Vagal signaling: Changes in luminal chemistry and mucosal signals can alter vagal afferent firing, relayed to brainstem nuclei that influence autonomic outflow and gut behavior.

Hence, brainstem and gastrointestinal function are not isolated: they are continuously shaped by luminal inputs carried by the microbiome, contributing to the overall neural regulation of bowel movements.

How Microbiome Testing Can Offer Critical Insights

Because the same symptoms can arise from different mechanisms, identifying which microbial functions are prominent in your gut can be informative. A microbiome analysis may highlight:

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• Relative abundance of methanogens that may correlate with slower transit in some individuals.
• SCFA-producing communities and fiber fermentation capacity, relevant to neuromuscular coordination and mucosal health.
• Bile-acid–modifying bacteria that can influence stool liquidity and motility patterns.
• Markers of dysbiosis or low diversity that may affect resilience of gut-brain signaling.

Such data do not diagnose disease, but they provide context for discussions with clinicians and can guide personalized, education-based strategies. If you are exploring your gut ecology, consider reviewing an accessible option such as a microbiome test to illuminate patterns potentially relevant to motility and sensation.

Who Should Consider Microbiome Testing for Gut and Neural Health

Indicators That Microbiome Testing Might Be Valuable

Microbiome analysis may be useful if you experience:

• Chronic or unexplained bowel irregularity (constipation, loose stools, or alternating patterns) without a clear structural or neurological diagnosis.
• Symptoms resistant to standard measures, such as persistent straining, sense of incomplete emptying, or unpredictable urgency despite reasonable dietary and lifestyle changes.
• Suspected microbiota-related neural regulation issues, such as symptoms that fluctuate with dietary fermentable substrates, antibiotics, or probiotics—suggesting a microbially linked motility component.

When combined with clinical evaluation, microbiome data may help frame whether a motility pattern aligns with microbial gas production, bile acid transformation, or variability in SCFA profiles—each of which can modulate neural pathways of stool elimination.

The Benefits of Personalized Microbiome Insights in Managing Gut Disorders

Personalized microbial profiles support a more nuanced view of bowel function by mapping potential drivers of motility and sensation. For example, a profile indicating elevated methanogens or reduced butyrate-producing taxa can contextualize why certain foods or routines help or hinder. These insights can complement pelvic floor assessments, transit studies, or anorectal physiology testing. If you are seeking an introduction to your own microbial landscape, a well-structured gut microbiome analysis can serve as an educational foundation for collaborative decision-making with your care team.

Decision Support: When to Pursue Microbiome Testing

Practical Scenarios Favoring Microbiome Analysis

• Persistent constipation or diarrhea with unclear neural involvement: When physical exams and routine labs are unrevealing, microbial context may explain variability in motility or stool form.
• Bowel irregularities with neurological comorbidities: In conditions like Parkinson’s disease, MS, or after spinal injury, microbiome insights may add a layer to understanding symptom fluctuations beyond recognized neural deficits.
• Before advanced interventions: When considering invasive testing or procedures, microbiome data can round out the picture of functional contributors and help set expectations.

In these scenarios, a considerate approach mixes neural evaluation with microbial context rather than presuming a single cause.

How Microbiome Testing Complements Other Diagnostic Approaches

Microbiome analysis is not a replacement for clinical assessment. Instead, it can complement:

• Transit studies (e.g., radiopaque markers, scintigraphy) to distinguish slow-transit constipation from outlet dysfunction.
• Anorectal manometry and balloon expulsion tests to assess rectal sensation, sphincter function, and defecatory coordination.
• Imaging or endoscopy to address structural causes.

By adding microbial functional context (e.g., gas production potential, SCFA profiles), microbiome data can align expectations and guide tailored lifestyle discussions. If you decide to explore your microbial profile, choose a test that clearly explains methodology and limitations, and consider sharing the results with a clinician familiar with motility and the gut-brain axis.

The Core Explanation (Expanded): Putting It All Together from Brain to Bowel

From Rectal Filling to the Decision to Evacuate

When stool enters the rectum, stretch receptors activate. Afferent signals travel via the pelvic nerves to the sacral spinal cord and onward to brainstem and cortical structures, generating the conscious sensation of fullness. The ENS simultaneously triggers the rectoanal inhibitory reflex (RAIR): transient relaxation of the internal anal sphincter to “sample” rectal contents and fine-tune continence. If circumstances are appropriate, cortical decision centers facilitate relaxation of the external anal sphincter and puborectalis muscle, straighten the anorectal angle, and coordinate with abdominal and diaphragmatic muscles to create expulsive force.

Deferring Defecation: Continence and Autonomic Balance

If the moment is not appropriate, cortical influence on evacuation maintains continence by increasing external sphincter and puborectalis tone (via pudendal motor neurons in Onuf’s nucleus). Sympathetic tone supports continence by enhancing internal sphincter tone and dampening colonic contractions. The rectum may accommodate partially by adjusting tone and volume, with intermittent RAIR events occurring as stool moves or new content arrives.

Executing Defecation: Coordinated Relaxation and Propulsion

When the decision to defecate is made, parasympathetic outflow rises, promoting rectal contractions and facilitating internal sphincter relaxation. Simultaneously, the external sphincter and puborectalis relax under voluntary control, and abdominal musculature activates to generate pressure. The ENS coordinates local peristalsis around the rectal ampulla to optimize evacuation, while brainstem patterning helps synchronize muscle groups for efficient, comfortable stool passage.

Why Brain and Microbiome Interact in Real Life

Stress, Sleep, and Lifestyle Interactions

Chronic stress can shift autonomic balance toward sympathetic dominance, potentially slowing transit and changing rectal sensitivity. Sleep disruption affects circadian rhythms that influence colonic activity (e.g., morning gastrocolic reflex), while dietary patterns alter microbial fermentation and metabolite levels. Alcohol, caffeine, endurance exercise, and travel can further modulate motility, illustrating how brain–body context and the microbiome co-shape daily bowel patterns.

Medications and Comorbidities

Opioids, anticholinergics, and some antidepressants can slow motility or alter sphincter tone; metformin, magnesium supplements, or bile acid sequestrants can shift stool consistency or frequency. Diabetic autonomic neuropathy may dampen reflexes and sensation. Parkinson’s disease can slow colonic transit and alter rectal evacuation mechanics. In these settings, microbiome patterns can either buffer or amplify neural changes, contributing to symptom variability among patients with the same diagnosis.

Symptoms and Signals Revisited: Where Neural and Microbial Clues Overlap

Constipation Phenotypes

Constipation can be “slow transit,” “normal transit” (with perception of constipation), or “outlet dysfunction” (dyssynergia). Microbial clues might include elevated methanogen markers or decreased SCFA producers in slow transit patterns, whereas outlet dysfunction often reflects motor coordination issues detectable on physiology tests. However, overlap is common—some individuals have both motility delay and pelvic floor discoordination—and microbial changes may reflect adaptations to altered transit time.

Diarrhea, Urgency, and Fecal Incontinence

Diarrhea and urgency may align with increased bile acids in the colon, rapid fermentation of certain carbohydrates, or heightened visceral sensitivity. Fecal incontinence may reflect sphincteric weakness, sensory dysregulation, or impaired reflex integrity. In each case, microbial context can influence symptom thresholds; for instance, higher luminal bile acids can increase colonic secretion and urgency, while certain gas profiles may distend the rectum and alter reflex dynamics.

Limitations of Guessing: Why Personalized Insight Helps

The Risk of Over-Attributing to a Single Cause

It is tempting to blame all constipation on “the colon” or all urgency on “the nerves,” but lived experience often arises from converging contributors. Diet-derived fermentable substrates, microbial gas kinetics, ENS sensitivity, and autonomic bias can interact to produce the same outward symptom. Without objective context, adjustments may be trial-and-error, sometimes compounding the problem (e.g., adding excessive fiber in a methane-dominant, slow-transit pattern may worsen bloating).

How Microbiome Testing Informs, Not Diagnoses

Microbiome testing provides a snapshot of taxonomic composition and, in some platforms, potential functional capacity. This information can:

• Highlight gas-related signatures (e.g., methanogens) that may align with slower transit in some individuals.
• Show fiber-fermenting and SCFA-producing capacity, relevant to ENS support and motility.
• Indicate bile acid–modifying potential that could correlate with stool liquidity or urgency.

These insights are best integrated with clinical findings, diet history, and physiology testing. For a user-friendly starting point, an educational microbiome assessment can be one piece of a broader conversation about your brain–gut–microbiome network.

Practical Considerations: Interpreting Findings with Care

Contextualizing Results with Clinical Evaluation

Microbiome results make the most sense when paired with history, exam, and, where relevant, tests like anorectal manometry or transit studies. For example, high methanogen signals alongside objectively slow transit implicate gas-mediated motility effects, whereas dyssynergic defecation on manometry points toward neural–muscular coordination issues regardless of microbiome profile. Multifactorial cases are common; layered data help prioritize next steps without assuming a single culprit.

Variability and Change Over Time

Microbiomes are dynamic. Short-term diet changes, travel, infections, and medications can alter taxa and metabolites. Neural regulation also shifts with stress, activity, and sleep. Consequently, snapshots must be interpreted as part of a moving system. Recognizing this fluidity supports realistic expectations and iterative learning rather than rigid conclusions.

Key Takeaways

• Defecation is controlled by integrated circuits across cortex, brainstem, spinal cord, autonomic pathways, and the enteric nervous system.
• Parasympathetic activity supports motility and evacuation; sympathetic activity supports continence and delay.
• Voluntary control depends on cortical planning and pudendal nerve control of the external anal sphincter and pelvic floor.
• The microbiome influences motility and sensation via SCFAs, bile acid metabolism, gas production, and neuroimmune signaling.
• Similar symptoms can arise from distinct causes, so guessing based on symptoms alone often misleads.
• Microbiome testing does not diagnose disease, but it can reveal functional patterns (e.g., methanogens, SCFA producers) relevant to motility.
• Results are most useful when combined with clinical evaluation and, if needed, motility or anorectal physiology tests.
• Individual variability is the rule—biology, lifestyle, and microbes interact to shape bowel function over time.

Q&A: Brain Control of Defecation and the Gut Microbiome

Which part of the brain controls defecation?

There is no single “defecation center” in humans. Control is distributed across cortical areas (medial prefrontal, anterior cingulate, supplementary motor), the brainstem (including autonomic nuclei), and spinal circuits, with key reflexes handled by the enteric nervous system. A pontine region likely coordinates sphincter and abdominal patterning, based on animal and imaging studies.

What is the role of the spinal cord in bowel movements?

The sacral spinal cord (S2–S4) integrates rectal sensation and coordinates reflexes through parasympathetic outflow. It also houses motor neurons (Onuf’s nucleus) that control the external anal sphincter and pelvic floor via the pudendal nerve. Damage at this level can disrupt continence and evacuation reflexes.

How do the autonomic nervous system divisions affect defecation?

Parasympathetic pathways promote colonic motility and facilitate evacuation, while sympathetic pathways support continence by enhancing internal anal sphincter tone and reducing motility. The balance between these systems shifts with context, stress, and physiological needs.

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What is the rectoanal inhibitory reflex (RAIR)?

RAIR is an enteric reflex where rectal distension causes transient relaxation of the internal anal sphincter. This “sampling” reflex helps distinguish gas from stool and fine-tunes continence and the urge to defecate. It is intrinsic to the gut wall and does not require the brain to occur.

Can stress influence bowel movements through the brain?

Yes. Stress can increase sympathetic activity, potentially slowing transit, altering rectal sensitivity, or changing sphincter tone. Over time, this can contribute to constipation, urgency, or fluctuating patterns, especially in individuals with underlying motility sensitivity.

How does the gut microbiome affect motility?

Microbes produce metabolites (SCFAs), gases (like methane), and influence bile acid pools and serotonin signaling, all of which can affect muscle contractions and sensory thresholds. These effects vary by individual and diet, which is why microbiome context can be informative.

Is methane always linked to constipation?

Methane production has been associated with slower intestinal transit in many studies, but not universally. Some individuals with methane signals do not have constipation, and other factors (diet, ENS integrity, autonomic tone) can override or modify this association.

Do probiotics “fix” bowel dysfunction?

No single probiotic reliably resolves bowel dysfunction because underlying mechanisms vary. Some strains may influence stool form or frequency in certain people, but effects are inconsistent. Understanding personal mechanisms—neural, microbial, behavioral—helps set realistic expectations.

When might microbiome testing be useful?

It may be useful for persistent, unexplained bowel issues, symptoms resistant to standard strategies, or when neural and microbial factors seem to overlap (e.g., symptoms linked to fermentable foods or antibiotics). Testing provides context, not a diagnosis, and should be interpreted with clinical input.

Can neurological disorders cause bowel problems?

Yes. Conditions like Parkinson’s disease, multiple sclerosis, stroke, and spinal cord injury can disrupt autonomic outflow, ENS interactions, or pelvic floor control, leading to constipation, urgency, or incontinence. Microbiome factors can further modulate these symptoms.

Is anorectal manometry necessary to assess defecatory problems?

Not always, but it is valuable when outlet dysfunction or sensory abnormalities are suspected. Manometry and balloon expulsion tests can differentiate dyssynergia from slow-transit patterns and inform targeted strategies. Microbiome data can complement, not replace, such assessments.

What should I expect from a microbiome test result?

Expect a snapshot of microbial composition and potential functional traits (e.g., SCFA producers, methanogens). It can highlight patterns relevant to motility and sensation but does not diagnose disease. Use it as a tool for education and discussion with your care team.

Conclusion

Brain control of defecation emerges from a network of cortical, brainstem, spinal, autonomic, and enteric circuits that must work in concert. Because similar symptoms can arise from different combinations of neural regulation, pelvic floor mechanics, and microbial signals, a personalized lens is vital. Microbiome testing does not provide a diagnosis, but it can reveal functional patterns—such as gas kinetics, SCFA capacity, or bile acid modifiers—that help explain why your experience may differ from someone else’s. By connecting the dots across your brain–gut–microbiome network and integrating findings with clinical evaluation, you can move toward more informed, individualized strategies for bowel function and overall well-being.

Endnotes & Resources

• Bharucha AE, Rao SSC. An update on anorectal disorders for gastroenterologists. Gastroenterology. 2014.
• Rao SSC, Welcher KD, Leistikow JS. Obstructive defecation: a failure of rectoanal coordination. Am J Gastroenterol. 1998.
• Browning KN, Travagli RA. Central nervous system control of gastrointestinal motility and secretion and modulation of gastrointestinal functions. Compr Physiol. 2014.
• Mayer EA, Tillisch K, Gupta A. Gut/brain axis and the microbiota. J Clin Invest. 2015.
• Yano JM et al. Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis. Cell. 2015.
• Reigstad CS et al. Gut microbes promote colonic serotonin production through an effect of short-chain fatty acids. FASEB J. 2015.
• Chatterjee S, Park S, Low K, et al. The degree of breath methane production in IBS correlates with the severity of constipation. Am J Gastroenterol. 2007.
• Camilleri M. Bile acid diarrhea: prevalence, pathogenesis, and therapy. Gut Liver. 2015.
• Heitmann PT, Vollebregt PF, Knowles CH, et al. Neurological control of defecation and continence. Best Pract Res Clin Gastroenterol. 2010.

Keywords

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