Motility-Impaired Overlay: The Complete Guide to Slow & Dysregulated Gut Transit

If a meal sits in your stomach for hours, producing nausea, early satiety, and a sense of fullness long after the plate is empty; if your bowel movements come every 4-5 days and only with the help of magnesium or laxatives; if your SIBO comes back two months after every antimicrobial course; if you have diabetes, Parkinson's disease, scleroderma, or another condition associated with slow gut nerve function; if your gastroenterologist has used the word "gastroparesis" or "colonic inertia" — you may be living with a Motility-Impaired overlay. This overlay describes a gut where the coordinated, rhythmic contractions that move food from mouth to anus are weakened, mistimed, or absent — leaving food and bacteria to linger in places they should not, fermenting and accumulating instead of flowing through.

The Motility-Impaired overlay is distinct from the Slow Transit primary pattern in subtle but important ways. Slow Transit primary describes the typical clinical picture of chronic constipation as the dominant feature — infrequent stools, hard pellet consistency, straining. Motility-Impaired overlay describes a broader category of motility dysfunction that may manifest as gastroparesis (stomach), intestinal dysmotility (small bowel), colonic inertia (colon), or generalized dysmotility affecting all segments. Many patients with Slow Transit primary also have Motility-Impaired overlay; many patients with other primary patterns (Stress-Reactive, Inflammatory/Leaky-Prone, Meal-Timing Sensitive) have Motility-Impaired overlay as a contributor to their overall picture.

The cause of motility impairment varies widely. In some patients it is post-infectious (post-gastroenteritis autoimmune damage to enteric nerves, detected by anti-vinculin antibodies). In others it is medication-induced (opioids, anticholinergics, certain antidepressants, calcium channel blockers). In others it reflects a systemic condition (diabetic gastroparesis, scleroderma intestinal dysmotility, Parkinson's-related slowing, hypothyroidism). In a substantial subset, no clear cause can be identified — idiopathic dysmotility — but the functional impact is the same.

This guide is the practical companion to the GutIQ pattern pages and walks through what the Motility-Impaired overlay is, how it is scored, the physiology of normal versus impaired motility, structured testing and workup, the food strategy (smaller more frequent meals, low residue if severe, liquid nutrition options), supplement protocols (natural and prescription prokinetics, motility support), lifestyle interventions, severe-case strategies including when surgical or device-based interventions are appropriate, and an FAQ. By the end you will have a complete map for moving from "my gut barely works" to "I have a working plan to keep things moving."

A note on context: motility impairment can be a feature of serious underlying disease that requires specialist evaluation. If you have unexplained weight loss, vomiting that does not resolve, severe or worsening pain, blood in stool or vomit, or symptoms that progress rapidly, this guide is not a substitute for medical evaluation. The interventions discussed here are appropriate adjuncts to medical care, not replacements for it.

The Physiology: How Normal Motility Works (and Fails)

The migrating motor complex (MMC)

Between meals (the inter-digestive period), the gut runs a housekeeping program called the migrating motor complex. The MMC has four phases of approximately 90-120 minutes total, with Phase III being the dominant clearing wave — a powerful peristaltic contraction that sweeps from stomach through the small intestine, clearing bacteria, mucus, and undigested debris into the colon. The MMC only operates during fasting; eating immediately suppresses it and starts the digestive program. A healthy adult runs 3-4 MMC cycles per overnight fast. Impaired MMC function is one of the most common features of Motility-Impaired overlay and is the primary mechanism by which dysmotility predisposes to SIBO recurrence.

Gastric emptying

The stomach empties via coordinated antral contractions and pyloric relaxation. Normal gastric emptying half-time for a solid meal is 60-120 minutes. In gastroparesis, this can extend to 4-8+ hours, producing nausea, early satiety, post-prandial fullness, and bloating. Gastroparesis can be diabetic (the most common identifiable cause), idiopathic (the largest subgroup), post-surgical (vagal nerve injury), or related to systemic disease (scleroderma, amyloidosis, neurological disease).

Small intestinal transit

The small intestine moves contents from duodenum to ileocecal valve in approximately 3-4 hours. Slow small intestinal transit allows excess bacterial fermentation, contributes to SIBO formation, and produces post-meal bloating that persists for hours. Small intestinal dysmotility is harder to test for than gastric or colonic dysmotility but is increasingly recognized.

Colonic transit

The colon moves contents from cecum to rectum over 24-72 hours typically. Slow colonic transit produces classic constipation. Methane-producing archaea (relevant to Gas-Dominant overlay) directly slow colonic transit, creating a feedback loop where overgrowth slows the colon, which permits more overgrowth.

The enteric nervous system

The gut has its own "second brain" — the enteric nervous system (ENS) — with approximately 500 million neurons embedded in the gut wall. The ENS coordinates motility autonomously, communicates with the central nervous system via the vagus nerve, and is influenced by hormonal signals, mechanical stretch, microbiome metabolites, and emotional state. Damage to the ENS — from post-infectious autoimmunity (anti-vinculin antibodies), neurodegenerative disease (Parkinson's), metabolic disease (diabetic autonomic neuropathy), or surgical injury — impairs the ENS's ability to coordinate motility.

Post-infectious motility damage

One of the most under-recognized causes of motility impairment is the autoimmune sequel of food poisoning. The Pimentel research group identified that bacterial toxins (cytolethal distending toxin, CdtB) produced by common food poisoning pathogens (Campylobacter, Shigella, Salmonella, E. coli) share epitopes with vinculin, a host protein in interstitial cells of Cajal (the pacemaker cells of the gut). Anti-CdtB antibodies cross-react with vinculin, producing autoimmune damage to the pacemaker cells and chronic motility impairment. The IBSchek/IBS-Smart blood test detects these antibodies. Many patients with post-infectious IBS (PI-IBS) have detectable anti-vinculin antibodies and persistent motility impairment that responds well to prokinetic support but not to traditional IBS therapy.

Medication-induced motility impairment

Many common medications impair gut motility:

• Opioids (codeine, oxycodone, morphine, fentanyl) — major slow-transit driver
• Anticholinergics (antihistamines, antidepressants, anti-Parkinson medications, antipsychotics)
• Calcium channel blockers (verapamil, diltiazem)
• Iron supplements
• Aluminum-containing antacids
• Antispasmodics (paradoxically, used for cramping but slow transit)
• Ondansetron and other 5-HT3 antagonists
• GLP-1 agonists (semaglutide, tirzepatide) — delay gastric emptying intentionally; can cause significant nausea and constipation

Reviewing the medication list is one of the highest-yield interventions for Motility-Impaired overlay.

How GutIQ Scores the Motility-Impaired Overlay

The GutIQ assessment includes questions to identify Motility-Impaired overlay independent of primary pattern scoring. The overlay is scored based on: bowel movement frequency, stool consistency (Bristol scale), straining and incomplete evacuation, gastric symptoms (post-meal fullness, nausea, early satiety, vomiting of undigested food), recurrent SIBO history, motility-impairing medication use, and history of conditions associated with motility impairment (diabetes, Parkinson's, scleroderma, prior abdominal surgery, post-infectious symptoms).

A score below 25 indicates Motility-Impaired overlay is not clinically relevant. A score of 25-50 indicates mild motility issues — typically responds to Tier 1 natural prokinetics, dietary structure adjustment, and meal-timing optimization. A score of 51-75 indicates moderate motility impairment — warrants structured workup (gastric emptying study or colonic transit study), prokinetic trial, and possibly anti-vinculin antibody testing for post-infectious pattern. A score above 75 indicates severe motility impairment — requires gastroenterology consultation, comprehensive workup, and likely prescription prokinetic management.

The overlay scoring also identifies the predominant segment affected: gastric (nausea, fullness, early satiety dominant), small intestinal (post-meal bloating, recurrent SIBO dominant), or colonic (constipation dominant). This guides which testing and which interventions to prioritize.

Motility-Impaired Overlay Symptoms: The Full Picture

Gastric (gastroparesis spectrum)

• Post-meal fullness lasting hours
• Early satiety (feeling full after small portions)
• Nausea, especially in the morning or after meals
• Vomiting, sometimes of food eaten hours earlier
• Abdominal bloating in the upper abdomen
• Reflux that worsens with delayed gastric emptying
• Unintentional weight loss in severe cases
• Erratic blood glucose control (relevant for diabetic patients — slow gastric emptying disrupts insulin-meal timing)

Small intestinal

• Persistent bloating that worsens through the day
• Recurrent SIBO (3+ documented episodes in 18 months)
• Post-meal abdominal distension lasting 4-8 hours
• Nutritional deficiencies in severe cases (B12, iron, fat-soluble vitamins)
• Symptoms that worsen with dietary fiber (which has nowhere to go in a stagnant small intestine)

Colonic (constipation-dominant)

• Infrequent bowel movements (fewer than 3 per week)
• Hard, pellet-like stools (Bristol 1-2)
• Excessive straining
• Sense of incomplete evacuation
• Reliance on laxatives, suppositories, or enemas for evacuation
• Abdominal distension and discomfort that improves only after defecation

Generalized dysmotility

• Combinations of the above across multiple gut segments
• Erratic motility (constipation alternating with sudden urgency)
• Symptoms during travel or schedule changes that take days to weeks to recover from

Associated systemic symptoms

• Fatigue (delayed nutrient absorption, sleep disrupted by digestive symptoms)
• Poor blood sugar control if diabetic
• Skin and connective tissue features if scleroderma underlies
• Motor or cognitive features if Parkinson's underlies
• Anti-vinculin antibody positivity if post-infectious

How Motility-Impaired Overlay Combines With Primary Patterns

Slow Transit primary + Motility-Impaired overlay

The clinical picture is severe chronic constipation. Treatment combines the Slow Transit primary protocol (magnesium, psyllium, kiwi, prunes) with the motility-impaired overlay protocol (prokinetics, MMC support). Colonic transit study may guide whether colonic inertia is severe enough to consider colectomy in extreme refractory cases (rare).

Fermentation Sensitive primary + Motility-Impaired overlay

The classic post-infectious-SIBO picture. Anti-vinculin antibody testing is high-yield. Treatment combines SIBO eradication (antimicrobials) with aggressive long-term prokinetic support to prevent recurrence. Low-dose naltrexone, prucalopride, low-dose erythromycin, or natural prokinetics maintained indefinitely.

Meal-Timing Sensitive primary + Motility-Impaired overlay

The MMC is doubly compromised by mistimed eating plus underlying dysmotility. Treatment combines meal-timing structure (3-hour minimum between meals, last meal 3-4 hours before bed) with MMC-supportive prokinetics.

Stress-Reactive primary + Motility-Impaired overlay

Stress impairs motility through sympathetic dominance and CRH effects. Vagal tone work is critical alongside prokinetic support.

Fat/Bile Sensitive primary + Motility-Impaired overlay

Slow gastric emptying compounds the fat-tolerance problem. Treatment combines bile/enzyme support with prokinetics to accelerate gastric clearance.

Upper GI/Reflux primary + Motility-Impaired overlay

Delayed gastric emptying directly worsens reflux (more time for stomach contents to be available to refluxed). Prokinetics often substantially improve reflux symptoms by reducing post-prandial gastric volume.

Other primary patterns

Any primary pattern can have Motility-Impaired overlay. The personalized GutIQ report addresses your specific combination.

Testing & Workup for Motility-Impaired Overlay

Gastric emptying study (4-hour scintigraphy)

The gold standard for diagnosing gastroparesis. Eat a labeled standard meal (typically egg whites with technetium-99 sulfur colloid), and gamma camera scanning measures gastric emptying over 4 hours. Normal: greater than 90% emptied at 4 hours. Mild gastroparesis: 70-90%. Moderate: 50-70%. Severe: less than 50%. The 4-hour study is required — the older 2-hour version misses many cases.

Colonic transit study (Sitz marker test)

Swallow 24 radio-opaque markers and obtain plain abdominal radiographs at 24, 72, and 120 hours. The number of markers retained at 120 hours quantifies colonic transit time. Normal: less than 5 retained. Slow transit: greater than 5 retained, predominantly in left colon. Outlet dysfunction (pelvic floor): greater than 5 retained predominantly in rectum.

Anorectal manometry and balloon expulsion

For colonic-segment overlay with severe constipation. Identifies dyssynergic defecation (pelvic floor dysfunction) as a contributor — often missed and highly responsive to pelvic floor physical therapy.

Wireless motility capsule (SmartPill)

A swallowed capsule transmits pH and pressure data through the gut, measuring gastric emptying time, small intestinal transit, and colonic transit in a single test. Useful for global dysmotility assessment. Not universally available.

Anti-vinculin and anti-CdtB antibody testing (IBSchek/IBS-Smart)

Blood test that identifies post-infectious autoimmune motility damage. Positive results support a post-infectious etiology and predict response to long-term prokinetic prophylaxis. Available through Genova and other specialty labs.

SIBO breath test

If recurrent SIBO is suspected (see Gas-Dominant overlay), breath testing identifies hydrogen, methane, or H2S dominance and guides antimicrobial selection.

Targeted lab testing

• HbA1c, fasting glucose (rule out diabetes-related gastroparesis)
• TSH, free T4 (rule out hypothyroidism)
• Antinuclear antibody (ANA), scleroderma panel if connective tissue disease suspected
• Comprehensive metabolic panel including calcium and magnesium
• Vitamin B12, ferritin (deficiencies in chronic dysmotility)
• Celiac panel (TTG-IgA + total IgA)

Imaging

Abdominal CT, MR enterography, or contrast studies if obstruction, adhesions, or structural cause suspected.

Neurological evaluation

If symptoms suggest broader autonomic dysfunction (POTS, dysautonomia), neurology referral with autonomic function testing.

Food Strategy for Motility-Impaired Overlay

Meal structure: smaller, more frequent, lower-residue

The dysmotile gut cannot handle large or fibrous meals well. The standard approach:

• 4-6 smaller meals per day instead of 2-3 large meals
• Each meal under 500-600 calories typically
• Liquid or pureed components alongside solid foods (smoothies, soups, blended sauces)
• Lower fiber during severe phases (less than 15 g/day temporarily) — paradoxical advice but necessary when transit is severely slow because fiber accumulates without moving
• Limit high-fat meals (fat further delays gastric emptying)
• Sit upright for 1-2 hours after meals (gravity assistance)
• Walk after meals when possible (gentle activity supports motility)

Foods that support motility

• Ginger (fresh or in tea) — direct prokinetic effect
• Kiwifruit (2 per day) — evidence-based for constipation and overall transit
• Warm fluids in the morning (warm water with lemon, warm broth) — stimulates gastrocolic reflex
• Bitter foods (arugula, dandelion greens, radicchio) — pre-meal bitters stimulate motility via vagal pathways
• Olive oil with meals (small amounts can stimulate gastric emptying)
• Coffee in the morning — caffeine and chlorogenic acids stimulate gastrocolic reflex

Foods that may worsen motility (often)

• Very high-fat meals (delay gastric emptying)
• Very high-fiber meals during severe phase (accumulate in stagnant gut)
• Carbonated beverages (introduce gas into already-slow gut)
• Excessive raw vegetables (harder to digest in a slow gut)
• Tough cuts of meat (require strong gastric churn)
• Mushy/mucilaginous foods that compound stasis
• Late evening meals (compound MMC dysfunction)

Hydration

• 30 mL/kg body weight daily as a baseline
• Warm fluids preferred over cold (gentler on slow gut)
• Add electrolytes if loose stools occur during prokinetic initiation

Severe gastroparesis: liquid nutrition

In severe gastroparesis where solid foods cannot be tolerated, a liquid-predominant diet (smoothies, broths, blended soups, protein shakes, oral nutritional supplements) may be necessary. The Mayo Clinic gastroparesis diet provides a structured progression. Tube feeding (jejunostomy) is required in extreme refractory cases — coordinate with gastroenterology and registered dietitian.

Supplement Protocol for Motility-Impaired Overlay

Tier 1: Natural prokinetics

• Ginger 250-500 mg before main meals: Direct prokinetic; accelerates gastric emptying ~25%.
• Iberogast (STW-5) 20 drops three times daily before meals: Region-specific motility support; relaxes hypertonic regions while stimulating hypotonic regions.
• Artichoke leaf extract 320 mg before meals: Cephalic-phase digestion support and prokinetic.
• Magnesium glycinate 300 mg PM: Multimodal effects including parasympathetic support and mild laxative effect.
• Bitters (Urban Moonshine or liquid bitters) before meals: Vagal stimulation supports cephalic-phase signaling.

Tier 2: Targeted prokinetic support

• 5-HTP 50-100 mg in late afternoon — caution with SSRIs: Serotonin precursor; supports 5-HT4 receptor activation in the gut. Absolute contraindication with SSRI, SNRI, MAOI.
• Methylcobalamin (B12) 1,000-5,000 mcg daily if low: B12 deficiency can produce motility impairment. Methylated form is preferred.
• Thiamine (B1) 100-300 mg daily if neuropathy suspected: Important for autonomic nervous system function.
• L-carnitine 1,000-2,000 mg daily: Mitochondrial support for energy-demanding smooth muscle.
• Co-Q10 100-200 mg daily: Mitochondrial support.

Tier 3: Prescription prokinetics (with clinician)

• Prucalopride (Motegrity, Resolor) 1-2 mg daily: 5-HT4 agonist; particularly effective for chronic constipation and small intestinal motility. FDA-approved.
• Low-dose erythromycin 50-125 mg at bedtime: Motilin receptor agonist; effective for gastric emptying. Tachyphylaxis develops over weeks; cyclical use is sometimes preferred.
• Domperidone 10 mg three times daily before meals: Peripheral D2 antagonist; very effective for gastroparesis. Not available in US (FDA limited); available in Canada and Europe. Compounded versions accessible with prescription via certain pharmacies.
• Metoclopramide 5-10 mg before meals: Effective but limited to short-term use (less than 12 weeks) due to tardive dyskinesia risk.
• Low-dose naltrexone (LDN) 2.5-4.5 mg at bedtime: Off-label use; emerging evidence for motility improvement, particularly in post-infectious cases. Available through compounding pharmacies.
• Pyridostigmine 30-60 mg three times daily: Cholinesterase inhibitor; emerging evidence for intestinal pseudo-obstruction and small intestinal motility. Off-label.

Tier 4: Anti-recurrence prophylaxis (for post-SIBO patients)

After successful SIBO eradication, indefinite prokinetic maintenance reduces recurrence by 50-80%. Options:

• Natural prokinetics (Iberogast, ginger) — gentle but often sufficient for mild cases
• LDN 4.5 mg nightly — emerging preferred long-term option
• Prucalopride 1-2 mg daily — most evidence-supported prescription
• Low-dose erythromycin 50 mg nightly — useful but tachyphylaxis a concern

Lifestyle Interventions

Movement

Physical activity is one of the most underused tools for motility. Walking 10-15 minutes after each meal substantially accelerates gastric emptying and reduces post-meal bloating. Aerobic exercise 150+ minutes per week supports motility. Yoga poses targeting the abdomen (twists, gentle inversions, supine positions) can mobilize a sluggish gut. Avoid sedentary periods longer than 60 minutes during waking hours; even brief standing/walking breaks help.

Vagal tone work

The vagus nerve drives parasympathetic motility. Vagal tone exercises measurably improve motility over weeks:

• Diaphragmatic breathing 10-15 minutes daily
• Cold face splash (10 seconds of cold water on the face) — stimulates vagal reflex
• Humming, singing, gargling — stimulates vagal innervation of upper aerodigestive tract
• Slow exhalation breathing (4-second inhale, 8-second exhale)
• Gut-directed hypnotherapy (Nerva app) — combined vagal and central effects

Sleep and circadian rhythm

MMC depends on sleep architecture and overnight fasting. Prioritize:

• Consistent bedtime and wake time
• 7-9 hours of consolidated sleep
• Last meal 3-4 hours before bed
• Bright light exposure in morning, blue-light reduction in evening
• Address sleep apnea if present

Stress management

Chronic stress is a major motility suppressor. Daily mindfulness, breathwork, gut-directed hypnotherapy, and CBT for IBS all measurably improve motility over 4-12 weeks.

Toilet posture

For colonic-segment overlay, a squatting platform (Squatty Potty or equivalent) places the body in a more anatomically efficient position for evacuation. Reduces straining and improves complete evacuation.

Avoid motility-impairing medications when possible

Review medication list with prescriber. Often opioids can be replaced with non-opioid analgesics, anticholinergic antihistamines (diphenhydramine) replaced with non-anticholinergic options (loratadine, cetirizine), and similar substitutions can substantially improve motility.

Structured 12-Week Protocol

Weeks 1-2: Foundation and assessment

• Begin food/symptom journal (track meals, bowel movements, nausea, fullness on 0-10 scale)
• Begin Tier 1 supplements: ginger before meals, Iberogast 3x daily, magnesium glycinate PM
• Implement meal-structure changes: 4-5 smaller meals, last meal 3+ hours before bed
• Begin daily walking after meals
• Begin breathwork practice (10-15 min daily)
• Order baseline workup if not already done (gastric emptying study, SIBO breath test, anti-vinculin antibody, basic labs)

Weeks 3-6: Layer prokinetic support

• Continue Tier 1
• Add Tier 2 supplements as appropriate: B12, B1 if neuropathy, L-carnitine, Co-Q10
• If testing supports gastroparesis: discuss prescription prokinetic with gastroenterologist (domperidone if available, prucalopride, or short-course metoclopramide)
• If SIBO present: initiate antimicrobial protocol (see Gas-Dominant overlay guide) alongside prokinetic support
• Begin gut-directed hypnotherapy (Nerva app) for vagal/gut-brain support

Weeks 7-10: Optimize and assess response

• Continue Tier 1-2 supplements
• If prescription prokinetic started, assess effect at week 4 of use
• Re-evaluate diet: are smaller meals being tolerated? Is fiber tolerable yet?
• Address pelvic floor dysfunction if identified (physical therapy referral)
• Review and adjust motility-impairing medications

Weeks 11-12: Personalization and steady state

• Establish sustainable maintenance stack
• If post-infectious SIBO with anti-vinculin: plan for long-term prokinetic prophylaxis
• Reassess symptoms with same scoring tool as week 1
• Plan ongoing follow-up cadence

Long-term maintenance

• Personalized maintenance supplement stack (typically Tier 1 + targeted Tier 2)
• Prescription prokinetic if needed (often LDN or prucalopride long-term)
• Meal-structure discipline (smaller, more frequent, last meal early)
• Daily movement (walking after meals)
• Vagal tone practice (continued breathwork, hypnotherapy)
• Periodic re-evaluation (annual or symptom-driven)

Severe & Refractory Dysmotility Intensive Protocol

For patients with severe gastroparesis, intestinal pseudo-obstruction, or refractory dysmotility that has not responded to standard interventions:

Comprehensive evaluation

• Repeat gastric emptying study and small bowel manometry
• Autonomic function testing (HRV, tilt-table)
• Skin punch biopsy for small fiber neuropathy
• Genetic testing for mitochondrial disorders if appropriate
• Connective tissue disease workup (scleroderma, Ehlers-Danlos)
• Neurology consultation

Maximal pharmacological management

• Combination prokinetic therapy (e.g., prucalopride + low-dose erythromycin pulsed + LDN)
• Pyridostigmine for intestinal pseudo-obstruction
• Octreotide in selected cases of scleroderma intestinal dysmotility
• Antiemetics as adjuncts (ondansetron, prochlorperazine — though these can worsen motility paradoxically)

Device and procedural interventions

• Gastric electrical stimulation (Enterra): Implanted device for refractory diabetic or idiopathic gastroparesis. Modest evidence; FDA approved.
• Pyloroplasty or G-POEM (gastric per-oral endoscopic myotomy): Surgical or endoscopic disruption of the pyloric sphincter to improve gastric emptying. Emerging evidence.
• Botulinum toxin injection of the pylorus: Temporizing measure; evidence mixed.
• Jejunostomy tube feeding: Bypass the stomach when oral intake is inadequate.
• Colectomy with ileorectal anastomosis: Last resort for severe colonic inertia.

Nutritional support

• Coordinate with registered dietitian experienced with motility disorders
• Liquid nutritional supplements (Ensure, Boost) as needed
• Address specific deficiencies (B12 injections if oral absorption inadequate, iron infusion if severe)
• Monitor for refeeding syndrome if significant weight loss has occurred

Multidisciplinary care

Severe dysmotility benefits from a coordinated team: gastroenterologist with motility expertise, registered dietitian, possibly surgeon (for procedural options), pain medicine if chronic pain present, mental health support (chronic GI illness has substantial psychological burden), and primary care quarterbacking. Specialty motility centers (Cleveland Clinic, Mayo, UCLA, Beth Israel Deaconess, Cedars-Sinai) offer comprehensive evaluation.

Frequently Asked Questions

Get Your Personalized Motility-Impaired Plan

The Motility-Impaired overlay protocol in this guide is the evidence-based starting point. Your specific combination — primary pattern, overlay severity, segment of dysmotility (gastric, small intestinal, colonic), underlying cause, and overlapping conditions — shapes which interventions will work best for you. The GutIQ quiz takes the framework above and personalizes it.

Medical Disclaimer

This guide is for educational purposes and does not constitute medical advice. Motility impairment can share features with serious conditions including bowel obstruction, mesenteric ischemia, malignancy, severe inflammatory bowel disease, eating disorders, and neurodegenerative disease. If you have alarm features (unintentional weight loss, persistent vomiting, severe pain, blood in stool or vomit, fever, dramatic change in bowel habits over age 45, family history of colorectal cancer), see a gastroenterologist promptly. The supplements, doses, and prokinetic protocols in this guide assume normal kidney and liver function and no significant medication interactions. Prucalopride, domperidone, low-dose naltrexone, low-dose erythromycin, metoclopramide, and pyridostigmine are prescription medications requiring clinical supervision. Pregnancy and lactation require separate guidance. Brand examples are illustrative; choose based on quality marks and third-party testing. Evidence summaries reflect literature current as of April 2026.