Understanding Your Gut Health When Using GLP-1 Medications

Understanding Your Gut Health When Using GLP-1 Medications

GLP-1 medications, like Ozempic®, Wegovy®, and Mounjaro®, are transforming treatments for obesity and diabetes, offering significant benefits beyond weight loss. However, these benefits can come with gastrointestinal (GI) challenges. Understanding these effects and how to support your gut health can help you maximize their benefits.

What Are GLP-1 Agonists and How Do They Work?

GLP-1 agonists mimic a naturally occurring hormone called glucagon-like peptide-1 (GLP-1), involved in appetite control, insulin release, and slowing stomach emptying (Holst et al., 2007). They:

  • Stimulate insulin release after meals.

  • Decrease appetite by signaling fullness in the brain.

  • Slow down how quickly the stomach empties, which can help control blood sugar and reduce food intake.

  • Have potential applications beyond weight management, including benefits for addiction, anxiety, depression, and neurodegenerative conditions due to their anti-inflammatory and neuroprotective properties (Dis-Chavez et al., 2022).

Summary: GLP-1 medications can offer powerful metabolic and potentially even mental health benefits by controlling appetite, insulin, and inflammation but may also significantly slow digestive processes.

Common Gastrointestinal Side Effects

The benefits of GLP-1 medications may come at a price. Their primary mechanism—delaying stomach emptying—often leads to side effects like:

  • Nausea.

  • Constipation and bloating due to slowed intestinal movements.

  • A feeling of persistent fullness or abdominal discomfort (Andersen et al., 2018).

Why These Side Effects Occur:

  • GLP-1 agonists reduce gut muscle contractions and slow down the Migrating Motor Complex (MMC), a natural gut-cleaning wave essential for regular digestion.

  • They increase nitric oxide signaling, relaxing gut muscles excessively, contributing to symptoms of bloating and discomfort (Triantafyllou et al., 2014).

  • These medications can also disrupt normal nutrient absorption, potentially leading to nutrient deficiencies such as vitamins B12 and D (Chamorro et al., 2019).

Summary: The slowed digestive process triggered by GLP-1 medications frequently causes uncomfortable GI symptoms and potential nutrient deficiencies.

The Promise of Postbiotics in Supporting Gut Health

Postbiotics are non-living beneficial substances produced during bacterial fermentation, like short-chain fatty acids (SCFAs), polyphenols, and vitamins. Unlike probiotics, postbiotics offer the benefits of bacteria without the risk of live bacterial infections.

How Postbiotics Can Support GI Motility:

  • SCFAs like Butyrate:

    • Stimulate gut muscle contractions, enhancing colonic movements and improving regularity (Chamorro et al., 2019).

    • Modulate nerves and hormone pathways (including serotonin and GLP-1 receptors), potentially counterbalancing medication-induced slowdown.

  • Polyphenols and Antioxidants:

    • Neutralize oxidative stress and inflammation, common side effects of GLP-1 agonists (Tsilingiri & Rescigno, 2013).

    • Protect and support overall gut lining health.

  • Vitamin Production:

    • Postbiotics naturally include B vitamins, essential for metabolic health and energy, compensating for reduced dietary intake caused by GLP-1-induced appetite suppression (Tsilingiri & Rescigno, 2013).

Summary: Postbiotics provide a multifaceted approach to improving gut motility, reducing inflammation, and supporting overall digestive health in those using GLP-1 medications.

Supporting Pancreatic and Biliary Health

Proper digestion involves healthy pancreatic enzymes and adequate bile flow. GLP-1 medications may inadvertently reduce gallbladder contractions, affecting bile secretion and digestion.

  • Pancreatic Enzyme Supplementation: Helps break down food more effectively, reducing symptoms like bloating and gas.

  • Bile Support: Herbs such as artichoke extract and bitters tinctures encourage bile flow, improving fat digestion and reducing constipation or sluggish digestion symptoms (Holtmann et al., 2003).

Summary: Supporting your pancreas and gallbladder can significantly reduce digestive discomfort when using GLP-1 medications.

Dietary Polyphenols: Natural Motility Boosters

Polyphenols—compounds in foods like berries, ginger, turmeric, and tea—support digestive health:

  • Ginger: Promotes faster stomach emptying, relieving nausea and bloating (Wu et al., 2011). Chewables or capsules can be taken before bed.

  • Artichoke Leaf Extract: Enhances bile secretion and relieves abdominal discomfort, effectively reducing symptoms of indigestion (Holtmann et al., 2003). Common in bitters tinctures that are great in bubble water. 

  • Peppermint Oil: Eases spasms and reduces bloating and discomfort associated with IBS and digestive sluggishness (Cash et al., 2016). Enteric coated capsules, teas, or topically as oil on the abdomen can all be used. 

Summary: Incorporating polyphenol-rich foods and herbs can gently but effectively improve GI symptoms associated with GLP-1 medications.

The Role of the Microbiome and Why It Matters

Your gut bacteria significantly influence how your digestive system functions:

  • A balanced microbiome helps maintain regular bowel movements and gut motility.

  • An imbalanced microbiome, such as excessive methane-producing microbes, is linked to constipation and slow gut transit (Triantafyllou et al., 2014).

  • Postbiotics, by promoting beneficial microbial activity and reducing harmful bacteria, help maintain a healthy microbiome balance (Tsilingiri & Rescigno, 2013).

Summary: Maintaining a balanced microbiome through diet, probiotics, and postbiotics can greatly enhance digestive comfort and motility.

What You Can Do: Practical Tips

If you're using GLP-1 medications, consider these practical tips to support your digestive health:

  • Diet:

    • Eat polyphenol-rich foods (berries, ginger, turmeric).

    • Include dietary fibers that increase beneficial SCFAs.

  • Supplementation:

    • Consider postbiotics for comprehensive gut support.

    • Use pancreatic enzymes or bile supplements if digestion is compromised.

  • Monitoring and Tracking:

    • Use apps like Chloe to track your symptoms, which can help guide personalized interventions and contribute valuable data to broader research efforts.

Summary: Simple dietary choices, targeted supplementation, and symptom tracking can greatly improve your experience with GLP-1 medications.

Final Thoughts

GLP-1 medications offer revolutionary health benefits but can compromise digestive health. Fortunately, you can mitigate these effects by supporting your gut health with postbiotics, dietary choices, and mindful tracking of your symptoms. Digestive discomfort does not have to be an inevitable side effect—there are effective, evidence-based strategies to manage it.

Disclaimer: This blog provides educational insights and should not replace professional medical advice. Always consult your healthcare provider before making significant changes to your diet or supplement regimen, especially when taking prescription medications.

 

Check out the White Paper below for a more in depth dive!

 

Gastrointestinal Motility and Its Modulation in the Context of GLP-1 Agonists

Physiology of Gut Motility and Control Mechanisms

Gastrointestinal (GI) motility is coordinated by an interplay of intrinsic pacemakers, neural circuits, and hormonal signals. The enteric nervous system (ENS) – often called the “brain in the gut” – regulates peristalsis largely independently, as demonstrated by early studies of isolated intestine showing that local reflexes can produce coordinated propulsion (the “Law of the Intestine”) without central input [1]. The ENS contains as many neurons as the spinal cord and is organized into the myenteric and submucosal plexuses, controlling smooth muscle contraction and fluid secretion. Crucially, enteric motor neurons form close associations with interstitial cells of Cajal (ICC), specialized pacemaker cells in the gut wall that generate electrical slow waves and mediate neurotransmission from neurons to smooth muscle [2]. ICC networks orchestrate rhythmic contractions; loss or dysfunction of ICC leads to disordered motility (for example, in severe constipation and pseudo-obstruction) [2].

During fasting, the small intestine exhibits a cyclic pattern of motility known as the migrating motor complex (MMC). The MMC consists of phases I (quiescence), II (intermittent contractions), and III (a short burst of high-intensity contractions) that sweep residual contents distally every ~90–120 minutes [3]. The hormone motilin, secreted by M cells in the duodeno-jejunal mucosa, triggers phase III of the MMC (the “housekeeper contractions”) in the stomach and upper small bowel [3]. Motilin release rises cyclically in fasting and is suppressed after eating; it binds to G-protein coupled motilin receptors on enteric nerves and muscle to initiate contractions that clear undigested material [3]. This motility pattern helps prevent bacterial overgrowth by flushing the small intestine [3]. In clinical practice, motilin agonists like erythromycin have been used as prokinetics by exploiting this pathway. Serotonin (5-HT) is another key modulator: about 90% of body serotonin is made by enterochromaffin cells in the gut mucosa, which release 5-HT in response to luminal stimuli. Serotonin activates 5-HT_3 receptors on intrinsic primary afferent neurons to initiate peristaltic reflexes, and 5-HT_4 receptors on secretomotor and motor neurons to enhance motility and secretion [4]. Drugs targeting these receptors (e.g. 5-HT_4 agonists like prucalopride) stimulate colonic motility and are used for constipation, whereas 5-HT_3 antagonists (e.g. alosetron) reduce motility and relieve diarrhea in IBS, reflecting the pro-peristaltic role of serotonin [4].

Extrinsic innervation modulates these enteric circuits. Vagal nerve parasympathetic fibers (via acetylcholine) generally stimulate GI motility and coordinate reflexes like receptive relaxation and peristalsis, while sympathetic fibers (via norepinephrine) inhibit motility. Vagal efferents predominantly innervate proximal gut regions (esophagus, stomach, small intestine), and vagal afferents convey sensory feedback to the brainstem. Notably, vagal pathways are involved in the ileal brake mechanism: when undigested nutrients reach the ileum, L-cells release peptides like peptide YY and glucagon-like peptide-1 (GLP-1) that signal through vagal afferents to slow gastric emptying and small bowel transit [5]. GLP-1 in particular is a potent incretin hormone that also acts as an “enterogastrone,” inhibiting gastrointestinal motility. Pharmacological GLP-1 receptor agonists (GLP-1 RAs), used for diabetes and obesity, exploit this effect: they delay gastric emptying and intestinal transit, contributing to early satiety and weight loss but often causing side effects of nausea and constipation. Mechanistically, GLP-1 slows gastric emptying at least in part by activating vagal afferent circuits that reduce antral contractions and increase pyloric tone [6]. This vagally mediated brake decreases the rate at which food leaves the stomach, thereby prolonging fullness [6]. Other hormones also influence motility: for example, cholecystokinin (CCK) released upon fat/protein ingestion slows gastric emptying and promotes bile/pancreatic secretion, whereas ghrelin (the “hunger hormone”) accelerates gastric emptying and stimulates appetite. A delicate balance of these signals ensures proper transit: dysregulation can lead to motility disorders such as gastroparesis (delayed emptying, as can occur with diabetes or GLP-1 RA therapy) or dumping syndrome (rapid emptying).

Interstitial cells of Cajal and smooth muscle cells ultimately execute the contraction patterns. ICC-generated electrical slow waves set the baseline rhythm of contraction frequency in different regions (e.g. ~3 per minute in stomach, ~11–12 in duodenum). Neural inputs and hormones modulate whether a slow wave produces a contraction. If excitatory input (acetylcholine, substance P) coincides with the depolarization, a contraction ensues; if inhibitory input (nitric oxide, VIP) dominates, the slow wave passes without a contraction. ICC thus serve as integrators of neuronal and hormonal signals [2]. In the colon, segmented mixing and occasional high-amplitude propagating contractions (mass movements) are controlled by colonic ICC networks and intrinsic reflexes. The enteric reflex circuitry follows the classic pattern described by Bayliss and Starling: stretch or luminal stimulation triggers ascending excitation (contraction oral to the bolus) and descending inhibition (relaxation aboral to the bolus) to propel contents forward. These reflexes are mediated by interneurons and motor neurons entirely within the ENS. Notably, even in the absence of CNS input, the ENS can generate complex motor patterns, although brain-gut interactions (stress, vagal activation, etc.) can modulate motility significantly.

Simplified Takeaways: The GI tract has an intrinsic nervous system (ENS) that independently coordinates motility through reflex arcs and pacemaker cells (ICC). During fasting, motilin drives a cyclic migrating motor complex that cleans out the gut. Serotonin from the gut lining is a key trigger for peristalsis, acting on enteric neurons. The vagus nerve and gastrointestinal hormones finely tune motility – for example, GLP-1 released from the ileum (or given as GLP-1 agonist therapy) acts as a brake to slow gastric emptying and intestinal transit. A balance of excitatory and inhibitory signals ensures normal transit; disruption of ICC or neural control can cause motility disorders.

Microbial Metabolites and Gut Motility (SCFAs, Gases: Methane, Hydrogen, H₂S)

Trillions of gut microbes produce metabolites that significantly influence intestinal motility. Short-chain fatty acids (SCFAs) – primarily acetate, propionate, and butyrate – are fermentation products of dietary fiber that signal to the host’s nervous and endocrine systems. SCFAs are sensed by G-protein coupled receptors like FFAR3 (GPR41) and FFAR2 (GPR43) on enteroendocrine cells and enteric neurons. Through these receptors, SCFAs modulate the ENS neurotransmitter milieu and gut hormone release. For instance, SCFAs stimulate L-cells to secrete PYY and GLP-1, contributing to feedback that can slow upper GI motility (ileal brake) while promoting colonic transit [7]. In the colon, SCFAs also directly affect enteric reflexes: experimental studies in rats have shown SCFAs can regulate the activity and phenotype of enteric neurons, thereby altering motility patterns [8]. Butyrate in particular has a tropic effect on enteric neurons and can enhance colonic propulsive activity, although excessive SCFAs may slow motility by lowering intraluminal pH or through other reflexes. Notably, by increasing GLP-1 and serotonin biosynthesis in the gut, SCFAs provide a mechanistic link between the microbiota’s metabolic output and host motility control [7]. This means a high-fiber diet (increasing SCFA production) could, for example, improve sluggish colon transit by stimulating serotonin release and peristalsis, but it might also enhance the ileal brake, slowing proximal motility and promoting satiety.

Gut bacteria also produce various gases that influence motility. Hydrogen (H₂) and carbon dioxide are common fermentation gases; these can be consumed by specialized microbes (methanogens and sulfate-reducing bacteria) to produce methane (CH₄) and hydrogen sulfide (H₂S), respectively. The balance of these gases in the gut correlates with transit times. Methane has been implicated in constipation-type IBS: around 30–40% of patients with chronic constipation show methane on breath tests, and methane production is associated with slower intestinal transit [9]. Methanogenic archaea (like Methanobrevibacter smithii) use H₂ to form methane, and methane in turn appears to act directly on the gut neuromuscular apparatus. Studies indicate methane can function as a neuromodulator that reduces peristaltic motility – it has been shown to decrease peristaltic velocity and increase segmenting contractions, effectively slowing transit [9]. In animal models, infusion of methane gas into isolated intestinal segments impaired propulsive contractions, whereas adding hydrogen gas had the opposite effect (enhancing propulsion) [9]. Clinically, reducing methane production by targeting methanogens (for example, with antibiotics like rifaximin) often results in accelerated transit and improved constipation, underscoring methane’s role in braking motility [9].

In contrast, hydrogen gas (if not converted to other gases) may promote faster transit or diarrhea. Populations of sulfate-reducing bacteria and colonic H₂-producers are more often linked with loose stool phenotypes. An abundance of H₂ (with low methane) is commonly seen in diarrhea-predominant IBS. Experimentally, introducing hydrogen gas speeds up peristalsis in animal intestine, likely by opposing methane’s effect and possibly via mechanosensory stretch activation or other pathways [9]. Therefore, the H₂–CH₄ balance maintained by microbial communities can tilt the gut toward slower or faster transit. If methanogens scavenge most hydrogen to make methane, motility tends to slow (constipating effect). If hydrogen accumulates (with fewer methanogens), motility tends to be more rapid or erratic.

Hydrogen sulfide (H₂S), another microbial gas, is a double-edged sword for GI motility. H₂S is generated by sulfate-reducing bacteria (like Desulfovibrio) that use H₂ to reduce sulfate from diet or host sources. At low concentrations, H₂S can stimulate certain sensory neurons or muscle receptors (some studies show transient increases in motility or secretion), but generally H₂S is considered an inhibitory neuromuscular messenger in the gut. It diffuses into smooth muscle cells and enteric neurons, causing muscle relaxation by opening K_ATP channels and blocking L-type calcium channels in intestinal smooth muscle [10]. The overall effect is to reduce contractility: for example, adding an H₂S donor (NaHS) in colonic tissue causes a dose-dependent relaxation of the muscle and suppression of contractions [10]. H₂S can also diminish excitatory neurotransmitter release (like acetylcholine and tachykinins) from enteric nerves, further inhibiting motility [10]. Interestingly, H₂S exhibits biphasic actions – low doses might briefly stimulate contractions (via TRPV1 receptor activation), but higher doses produce sustained inhibition of motility [10]. In disorders like ulcerative colitis or IBS, excess H₂S has been proposed to contribute to dysmotility and mucosal effects (H₂S is also a mucosal irritant at high levels). Thus, a delicate equilibrium of microbial gases is important: excessive methane or H₂S slows motility, while excess hydrogen (when methane/H₂S pathways are low) may lead to faster transit. This interplay helps explain why small intestinal bacterial overgrowth (SIBO) and dysbiosis can present with either constipation or diarrhea. In chronic constipation, researchers have noted an over-representation of methane-producing archaea; by contrast, in certain diarrheal states, sulfate-reducers or other fermenters dominate [9].

Other microbial metabolites also influence motility. For example, secondary bile acids produced by gut bacteria (discussed further in Section 4) can activate receptors like TGR5 on enteric neurons and enteroendocrine cells to modulate motility. Some bacteria produce tryptamine (from tryptophan), a molecule that acts on serotonin receptors (5-HT_4) to stimulate colonic peristalsis and secretion – essentially acting as a bacterial neuromodulator of gut function. Likewise, microbial generation of short-chain alcohols, phenols, or gases like CO₂ can affect the sensory milieu of the gut, triggering reflexes or altering muscle responsiveness. The emerging picture is that the microbiome functions almost like an additional endocrine organ that can dial gut motility up or down.

For patients on GLP-1 receptor agonists, these microbial factors are particularly relevant. GLP-1 RAs slow motility and can predispose some individuals to small bowel bacterial overgrowth due to stasis. There is evidence that GLP-1 RA treatment can shift the gut microbiota composition, possibly increasing fermentative bacteria. The microbial metabolites might then exacerbate or mitigate the drug’s GI effects. For instance, if a GLP-1 RA causes slower transit, methane-producing microbes might bloom and worsen constipation, suggesting a potential benefit in targeting those microbes (dietary or antibiotic approaches) to improve tolerance to therapy. On the other hand, a fiber-rich diet that raises SCFA levels might increase GLP-1 release endogenously but also nourish beneficial microbes that promote motility, potentially counterbalancing some GLP-1 RA side effects. These interactions are active areas of research.

Simplified Takeaways: Gut microbes produce metabolites that can significantly alter motility. Fiber fermentation yields SCFAs that can signal the gut to either speed up or slow down: SCFAs enhance colon contractions and stimulate gut hormones (like GLP-1 and serotonin) that link the microbiome to motility control. Microbial gases also play a role: methane gas slows motility and is linked to constipation, whereas hydrogen gas tends to speed up motility. Hydrogen sulfide, in high amounts, relaxes intestinal muscle and can also slow transit. An imbalance in these microbial metabolites (as seen in SIBO or dysbiosis) can lead to symptoms of either constipation or diarrhea. Targeting the microbiome (with diet, probiotics, or antibiotics) is thus a promising strategy to modulate gut motility – even in patients on motility-slowing drugs like GLP-1 agonists.

Impact of Probiotics and Postbiotics on Motility

Given the microbiota’s influence on motility, it’s natural that altering the microbiome with probiotics (beneficial live microbes) or postbiotics (microbial products or inactivated microbe preparations) can modulate GI transit and function. A growing body of clinical evidence suggests certain probiotics can alleviate dysmotility symptoms: for example, multi-strain probiotic blends have shown efficacy in improving functional constipation and IBS symptoms in randomized trials [11]. A 2022 systematic review and meta-analysis of probiotics in constipation-predominant IBS found that probiotics significantly improved stool consistency and modestly increased bowel movement frequency, with a good safety profile [11]. These benefits, while variable by strain, highlight that manipulating gut flora can translate into meaningful motility changes.

Mechanistically, probiotics may improve motility through several pathways:

  • Microbial compositional changes: In chronic constipation, an imbalance often exists (with fewer Bifidobacteria/Lactobacilli and more methane-producing or putrefactive species). Probiotic supplementation can increase the abundance of beneficial commensals. For instance, Bifidobacterium and Lactobacillus species often rise with probiotic use, which is associated with softer stools and improved transit [12]. These changes can indirectly affect motility by suppressing pathogenic bacteria that produce motility-inhibiting metabolites or by creating a more favorable metabolic output (e.g., more SCFAs, less gas byproducts like methane).

  • Fermentation products (postbiotics): Probiotics not only contribute their own metabolites but also encourage a microbiome that produces more motility-promoting compounds. An increase in SCFA production is one common result of probiotic therapy. SCFAs, as noted, can stimulate enteric reflexes and 5-HT release. Animal studies have shown that raising colonic SCFA levels (through probiotics or prebiotic fibers) enhances intestinal secretion and smooth muscle activity, accelerating stool transit. Probiotics also influence tryptophan metabolism; certain strains convert dietary tryptophan to indoles or tryptamine, which interact with the gut nervous system. Tryptamine, produced by some commensals, directly activates enteric neurons to induce peristalsis (via 5-HT_4 receptors). Thus, probiotics can increase the levels of such postbiotic neuromodulators, improving bowel regularity [13]. In essence, a probiotic-altered microbiome becomes a factory for compounds that stimulate motility.

  • ENS and neurotransmitter modulation: Some probiotics have been shown to interact with the enteric nervous system and even central nervous system via the gut–brain axis. They may alter the expression of neurotransmitters or receptors in the gut. For example, Bifidobacterium infantis has been reported to normalize gut pain reflexes and motility in animal models of IBS by modulating opioid and cannabinoid receptors in the ENS. Another example is Lactobacillus reuteri, which was found to increase the excitability of colonic myenteric neurons in rats, promoting motility, and also to reduce local 5-HT levels and increase nerve growth factors that collectively improve neuromuscular function [14]. The reduction in mucosal serotonin with L. reuteri in that study might seem counterintuitive (since 5-HT usually stimulates motility), but it likely indicates a normalization of an overstimulated serotonergic system in IBS. Probiotics can also induce expression of pro-motility receptors; in one study, a Bifidobacterium strain upregulated colonic 5-HT₄ receptors, which enhance peristaltic reflexes, thus promoting bowel movements [12].

  • Immune and epithelial effects: Chronic constipation has been linked in some cases to low-grade inflammation or altered gut barrier function. Probiotics can improve epithelial barrier integrity (e.g., by increasing tight junction proteins and mucous production) and modulate immune responses. By reducing mucosal inflammation, they may indirectly facilitate normal motility, as inflammation can disrupt enteric neuron signaling. Furthermore, probiotics interact with toll-like receptors on gut immune cells and glia. There is evidence that certain probiotic cell components (like polysaccharide A from Bacteroides or surface-layer proteins of lactobacilli) activate gut glial cells in ways that enhance ENS development and contractile function [13]. Essentially, a healthier gut environment and reduced inflammation can restore proper neuronal reflexes.

Not all probiotics are equal in their motility effects – the benefits are strain- and dose-specific. For example, Lactobacillus rhamnosus GG (LGG) has been shown to shorten intestinal transit time in some studies, whereas Bifidobacterium lactis BB-12 improved constipation in children by increasing stool frequency. On the other hand, some trials of single-strain probiotics have shown minimal effects, highlighting that combinations or specific conditions matter. Still, overall trends are positive: a meta-analysis including various strains concluded that probiotics significantly increase weekly bowel movements and soften stool consistency in functional constipation [11]. These outcomes are modest but clinically relevant, especially as adjunct therapy.

Postbiotics – delivering the beneficial metabolites directly – is an emerging concept. For instance, giving butyrate (an SCFA) orally or rectally has been tested to treat disorders like ulcerative colitis and could theoretically help in slow-transit constipation by directly stimulating the colon. Likewise, certain polyphenol-rich extracts (considered postbiotic if one views them as microbiota-derived or microbiota-acting compounds) have been used to influence motility (discussed in Section 5). Another example is synbiotics, combining prebiotics (fiber substrates) with probiotics, aiming to boost the production of motility-beneficial postbiotics in vivo. Clinical trials of synbiotics in constipation have shown improvements similar to probiotics alone, suggesting the main driver is still the metabolic output of the microbiome.

From a mechanistic perspective related to GLP-1, it’s noteworthy that some probiotics might affect GLP-1 production. By increasing SCFAs and certain bile acids, probiotics can induce L-cell secretion of GLP-1 [7]. In the context of GLP-1 RA therapy, one might wonder if probiotics would worsen GLP-1’s motility slowdown by increasing endogenous GLP-1. However, the amounts induced are likely small relative to pharmacologic doses, and the net effect of probiotics in studies has been pro-motility. In fact, restoring a healthy microbiome could mitigate some side effects of GLP-1 RAs by preventing SIBO and optimizing fermentation (for example, producing more butyrate and less methane). This is a speculative but intriguing area: using probiotics to manage GLP-1 RA-associated GI symptoms.

Simplified Takeaways: Probiotics (beneficial bacteria) and postbiotics (beneficial microbial metabolites) can help normalize gut motility. Clinical studies show that certain probiotics modestly improve constipation – they can soften stools and increase bowel movement frequency [11]. The reasons include probiotics producing more short-chain fatty acids and other compounds that stimulate the gut’s own nerves and hormone cells, as well as balancing the microbiota by reducing gas-producing, motility-slowing microbes. Some strains act on the gut’s nervous system directly, promoting peristalsis and reducing inflammation. In short, a healthier microbiome leads to better motility. This strategy can be useful alongside medications like GLP-1 agonists: by keeping the microbiome in balance, probiotics might counteract some drug-induced slowing of the gut.

Role of Bile Acids and Pancreatic Enzymes in Digestion and Motility (Insights from Pancreatitis, Cholestasis, SIBO)

Bile and pancreatic secretions are essential for digestion, but they also exert significant influence on intestinal motility. Bile acids (BAs), beyond emulsifying fats, function as signaling molecules in the gut that modulate how fast things move along. When food (especially fats) enters the duodenum, the gallbladder releases bile rich in primary bile acids (like cholic and chenodeoxycholic acid). These bile acids normally get reabsorbed in the ileum, but a portion enters the colon. There, bile acids stimulate colonic fluid secretion and motility – in fact, excessive bile acids in the colon cause diarrhea and urgency, a condition known as bile acid malabsorption diarrhea. One mechanism is that bile acids activate the Takeda G-protein receptor 5 (TGR5) on certain cells: enterochromaffin cells in the colon respond to bile acid binding by releasing 5-HT (serotonin), which then stimulates colonic contractions [15]. Bile acids also activate TGR5 on submucosal and myenteric neurons, which can directly alter motility patterns. Depending on the neuron type activated (excitatory vs inhibitory motor neurons), bile acids might either promote propulsion or, in some contexts, relax segments to coordinate overall flow [15]. Generally, an abundance of bile acids in the lumen produces a laxative effect: it enhances colonic motility and secretion, manifesting as loose, frequent stools [15]. Clinically, this is seen in patients who have had ileal resection or IBS-D patients with bile acid malabsorption – their colon is exposed to more bile, leading to rapid transit diarrhea. Therapies like cholestyramine (a bile acid binder) can firm stools in those cases but often cause constipation as a side effect because they remove bile acids’ stimulatory effect on the colon.

On the other hand, cholestasis (reduced bile flow, as in obstructive jaundice or primary biliary cholangitis) can lead to the opposite motility issue. With lack of bile in the intestine, fat digestion is impaired (causing steatorrhea), but also the colon receives far fewer bile acids, which can result in sluggish motility and a propensity for constipation. Additionally, bile acids normally have an antimicrobial role in the small intestine – they inhibit bacterial overgrowth. In cholestatic conditions or severe pancreatic insufficiency, diminished bile delivery allows bacteria to proliferate more in the small bowel, often leading to SIBO. This overgrowth can further slow motility (bacteria deconjugate any bile that is present, reducing bile’s effectiveness, and produce gases that cause bloating and dysmotility). Thus, adequate bile flow helps maintain motility and prevents overgrowth, whereas bile deficiency can promote dysmotility and SIBO.

The TGR5 receptor mentioned is particularly interesting in the context of motility and metabolism. TGR5 activation not only affects motility, but also stimulates the release of GLP-1 from L-cells in the gut (another link between bile acids and the ileal brake). In studies with TGR5 knockout mice, there is slower colonic transit and a tendency toward constipation, confirming that bile acid signaling via TGR5 physiologically promotes motility [15]. Conversely, pharmacologic TGR5 agonists have been observed to increase colon transit but may slow gastric emptying (since TGR5 in the stomach and vagal centers can relax gastric muscle). In summary, bile acids tend to speed up colonic movement (hence why bile acid diarrhea happens), and lack of bile acids slows it down.

Now consider pancreatic enzymes and motility. In normal digestion, pancreatic enzymes (lipases, proteases, amylase) work in concert with bile. Efficient nutrient absorption in the upper small intestine (duodenum/jejunum) actually influences motility through feedback loops: when nutrients are quickly absorbed, less remains to stimulate distal brake mechanisms. In pancreatic exocrine insufficiency (PEI), such as in chronic pancreatitis or cystic fibrosis, maldigestion leaves excessive nutrients in the lumen of the small intestine and colon. This can cause rapid transit in some cases (due to osmotic effects drawing fluid and triggering diarrhea), but it can also disrupt the MMC and other interdigestive patterns. Interestingly, patients with chronic pancreatitis have been found to have abnormal antroduodenal motility, especially those with significant enzyme insufficiency [16]. They may have rapid small bowel transit immediately after meals (dumping into the colon because of malabsorption) followed by slowed, uncoordinated motility later as the intestines deal with undigested contents. Moreover, the loss of pancreatic enzyme activity can allow more substrates for bacteria in the small intestine, promoting SIBO. Up to 30–40% of chronic pancreatitis patients are reported to have SIBO on breath testing [17]. This overgrowth can cause bloating, cramping, and either diarrhea or constipation depending on the predominant microbes (as discussed earlier). SIBO in pancreatitis is multifactorial: slowed MMC activity (due to neuropathy or malnutrition), altered pH, and reduced bile flow (if pancreatitis affects CCK and gallbladder signaling) all contribute. Treating SIBO with non-absorbed antibiotics has been shown to significantly improve GI symptoms in these patients [17]. For example, a study found that one-third of pancreatic insufficiency patients with chronic diarrhea had SIBO; treating them with rifaximin led to symptom improvement and better stool consistency [17].

Another insight comes from studies of pancreatic enzyme replacement therapy (PERT) and motility. In severe PEI, providing pancreatic enzymes can actually change motility patterns. One study in pancreatic insufficiency patients noted that enzyme supplementation slowed a too-rapid gastric emptying and normalized small bowel transit time [16]. This is likely because PERT improved nutrient absorption in the upper gut, thus preventing the excessive delivery of malabsorbed nutrients to the ileum and colon that was causing hypermotility and diarrhea. Essentially, restoring proper digestion upstream can remove abnormal stimuli that were accelerating transit. On the flip side, high-dose PERT might, in some cases, reduce the stimulus for the ileal brake too much and risk mild constipation – but generally PERT tends to alleviate diarrhea and bloating rather than cause constipation, unless overdosed.

Small Intestinal Bacterial Overgrowth (SIBO) is a common thread linking motility disorders, pancreatitis, and conditions like systemic sclerosis or even chronic opioid use. SIBO itself can be both a result of slow motility and a cause of it. Stasis in the small bowel (due to surgery, strictures, diabetes neuropathy, etc.) allows bacteria to accumulate. These bacteria deconjugate bile acids (worsening fat malabsorption) and produce gases that can impair muscular function or induce a low-grade inflammation in the enteric nerves. Patients with SIBO may experience bloating, pain, and either diarrhea (more common with H₂-dominant or sulfide-producing flora) or constipation (common with methane-dominant flora). Effective eradication of SIBO often leads to motility improvement. For instance, in one clinical trial, methane-positive constipated patients treated with antibiotics targeting methanogens had accelerated colonic transit and improved bowel frequency compared to placebo [9]. This highlights that some cases of refractory constipation are driven by microbial metabolites (like methane) secondary to SIBO, and treating the overgrowth treats the motility problem.

From the perspective of GLP-1 receptor agonists, bile and pancreatic factors are relevant in a few ways. GLP-1 RAs can predispose to gallbladder stasis (there have been reports of higher gallstone incidence), likely because they keep the pylorus closed longer and reduce CCK-driven gallbladder emptying post-meal. That means bile is not released as regularly, which over time could thicken bile or form stones. Proper diet and possibly ursodeoxycholic acid (a bile acid) are sometimes recommended to mitigate this in patients on long-term GLP-1 RAs. Additionally, since GLP-1 RAs slow gastric emptying and small bowel motility, they increase the risk of SIBO, as mentioned. Ensuring adequate pancreatic enzyme function and maybe using prokinetics or intermittent antibiotic courses might be considered if a patient on a GLP-1 RA develops symptoms suggestive of SIBO.

To summarize this section: bile acids generally speed up intestinal motility (particularly in the colon), and a deficiency of bile (or binding of bile acids by sequestrants) often causes constipation. Pancreatic enzymes ensure proper digestion; when they are lacking, malabsorbed food can either rush through (causing diarrhea) or disturb normal motility patterns and foster bacterial overgrowth, which in turn can slow motility via gases like methane. Clinical states like chronic pancreatitis and cholestatic liver disease illustrate the importance of these secretions: patients often suffer dysmotility (bloating, alternating diarrhea/constipation) that improves when enzyme and bile flow are restored. Conversely, conditions of excess bile (post-cholecystectomy or idiopathic bile acid malabsorption) show us that too much of a good thing can accelerate transit to a pathological degree.

Simplified Takeaways: Bile and pancreatic secretions play key roles in gut motility. Bile acids in the intestine normally help move things along – they stimulate colon contractions and fluid release. That’s why if too many bile acids reach the colon (as in some IBS cases), a person gets diarrhea. If bile flow is blocked or bile acids are removed (like by certain drugs), constipation can result. Pancreatic enzymes are needed to digest food early in the gut; when they’re missing (as in chronic pancreatitis), food isn’t absorbed properly and can upset the normal pace of the intestines. Undigested nutrients can cause either diarrhea (from malabsorption) or feed bacteria in the small bowel leading to SIBO, which can then slow motility (for instance, through methane gas production). Treating issues like SIBO or giving enzyme supplements often improves motility and symptoms. In essence, good digestion and normal bile flow keep the gut’s motility on track, while poor digestion or bile abnormalities can lead to motility disorders.

Polyphenol Synergy: Plant-Derived Compounds and Herbal Medicines Influencing Motility

Traditional herbal medicines and dietary polyphenols have long been used to relieve digestive troubles, and modern research is uncovering their mechanisms on GI motility. Many of these natural products contain polyphenols or other bioactive phytochemicals that can modulate smooth muscle activity, enteric neurotransmitters, or hormone release. Often, whole plant extracts have synergistic effects, with multiple constituents working together to normalize motility patterns – some components may stimulate contractions in an underactive gut while others relax spasms in an overactive gut, leading to a regulatory effect. Below, we highlight a few notable examples and their known mechanisms:

  • Ginger (Zingiber officinale): Ginger rhizome has been used for millennia for nausea and GI upset. Key active components include gingerols and shogaols, which are phenolic compounds. Ginger has a prokinetic effect in the upper GI tract. Clinical studies in healthy volunteers showed that ginger significantly accelerates gastric emptying and stimulates stronger antral contractions compared to placebo [18]. In patients with functional dyspepsia (indigestion), a randomized trial found that 1.2 g of ginger powder sped up gastric emptying by about 25% (half-emptying time ~12 minutes with ginger vs 16 minutes placebo) and tended to increase the number of antral peristaltic contractions, although it did not significantly change dyspepsia symptoms in that short study [19]. Ginger’s mechanisms include promoting antroduodenal coordinated motility and possibly interacting with serotonin receptors or cholinergic pathways. Interestingly, ginger did not raise plasma motilin or GLP-1 in that study, indicating it acts via direct or neural routes rather than hormone release [19]. Other research suggests ginger and its pungent constituents can act as 5-HT_3 receptor antagonists (contributing to its anti-nausea effect) and as agonists on cholinergic receptors in gut muscle to enhance contractions. Overall, ginger is a pro-motility, stomach-emptying aid. This makes it particularly valuable for countering gastroparesis or the gastric stasis caused by medications (for instance, some suggest using ginger to help alleviate the nausea and slow gastric emptying from GLP-1 agonists). Its safety and widespread availability make it a convenient adjunct therapy.

  • Artichoke (Cynara cardunculus) leaf extract: Artichoke leaf has a history of use for dyspepsia and IBS. It contains polyphenolic compounds like caffeoylquinic acids (e.g. cynarin) and flavonoids (e.g. luteolin) that are thought to have choleretic (bile-stimulating), antispasmodic, and antioxidative properties. A placebo-controlled trial in patients with functional dyspepsia confirmed that artichoke leaf extract over a few weeks significantly improved symptoms like bloating, early satiety, and abdominal pain [20]. Mechanistically, artichoke extract increases bile flow – more bile secretion can improve fat digestion and possibly speed up intestinal transit (since bile acids, as discussed, promote motility) [21]. Indeed, by enhancing the ileal delivery of bile acids, artichoke may alleviate sensations of fullness and bloating through quicker post-meal transit and better nutrient handling. Additionally, artichoke has a mild antispasmodic effect on smooth muscle. Experimental studies indicate it can reduce gastrointestinal muscle cramps, possibly by calcium channel blockade or nitric-oxide-mediated muscle relaxation [21]. By relaxing overly spastic segments (as can occur in IBS), artichoke extract might paradoxically facilitate more coordinated, propulsive motility. In one report, artichoke’s ability to alleviate dyspeptic symptoms was partly attributed to its combined effect of releasing more bile (to combat sluggish digestion) and calming down spasms in the gut that cause discomfort [21]. This dual action – prokinetic via bile and antispasmodic via direct muscle effects – exemplifies the synergy of plant compounds in normalizing motility. Patients with IBS who took artichoke extract in an open-label study noted reduced constipation and also fewer episodes of diarrhea, suggesting a balancing effect on bowel habits.

  • Peppermint (Mentha piperita): Peppermint oil is well-established as an antispasmodic for IBS. Its main active constituent, menthol, is a monoterpene (not a polyphenol, but a plant secondary metabolite) that has a relaxing effect on GI smooth muscle. Menthol blocks L-type calcium channels on smooth muscle cells, much like a calcium channel blocker drug, leading to muscle relaxation [22]. By reducing intracellular calcium, peppermint oil prevents muscle contractions that cause cramping. In IBS patients, enteric-coated peppermint oil capsules have been shown in multiple RCTs and meta-analyses to significantly reduce abdominal pain, bloating, and improve global IBS symptoms, particularly in IBS with diarrhea or pain [22]. Peppermint’s effect on motility is to normalize transit: in diarrhea-prone IBS, it can slow things down by relieving spasmodic hypermotility; in constipation-prone IBS, it may actually help coordinate movements by relieving segmental spasm that is impairing flow. Peppermint oil given via enema can also relieve colonic spasm during endoscopic procedures. Thus, while peppermint doesn’t “stimulate” motility per se, it modulates it by targeting the abnormal high-muscle tone. Many peppermint oil preparations are commercially available and are considered safe (aside from potential heartburn due to lower esophageal sphincter relaxation). Peppermint is often combined with caraway oil (another herb) in products for functional dyspepsia – the combination has been shown to reduce gastric pressure and alleviate epigastric pain, presumably by relaxing the pylorus and stomach while also aiding gastric emptying. This highlights how combining herbs can yield complementary actions: one component might relax a tight sphincter while another (like ginger) promotes antral pump activity.

  • Polyphenol-rich spices and herbs: Beyond ginger and artichoke, numerous other plant derivatives affect motility. For example, turmeric (curcumin) has some prokinetic evidence in animal studies, potentially via anti-inflammatory effects on the enteric nervous system. Fenugreek fiber (which contains galactomannan, a form of soluble fiber with polyphenolic compounds) can form a viscous gel that soothes and regulates stool form, aiding both constipation and diarrhea. Prunes (dried plums) are a traditional remedy for constipation; they are high in polyphenols like neochlorogenic and chlorogenic acids, as well as sorbitol – together these have a mild laxative effect by drawing water into the lumen and possibly stimulating colonic motility. Senna leaves contain anthraquinone glycosides (senna glycosides) – these are polyphenolic compounds that are metabolized by gut bacteria into active aglycones (e.g., rhein, sennidin) that stimulate colonic peristalsis and secretion. Senna is a well-known stimulant laxative used for acute constipation, though its chronic use is limited by potential for cramping and habituation. This is an example of a direct, potent motility effect from a plant polyphenol (anthraquinones act on enteric nerves to increase activity).

  • Herbal formula synergy: Many herbal products like the German formulation Iberogast (STW-5) combine multiple plant extracts to achieve a broad regulatory effect. Iberogast contains bitters and carminatives (e.g., extracts of bitter candytuft, chamomile, caraway, licorice, milk thistle, peppermint, lemon balm, celandine, and angelica). Clinical trials have shown Iberogast can relieve functional dyspepsia and IBS symptoms, with proposed mechanisms including accelerating gastric emptying while reducing visceral hypersensitivity. In terms of motility, Iberogast has been found to relax the gastric fundus (reducing pressure and aiding accommodation of meals) but simultaneously increase the amplitude of antral contractions to help grinding of food [23]. It also may coordinate small bowel peristalsis and reduce spasmodic colonic contractions. These effects arise from the combination of components – for instance, angelica and peppermint in it relax smooth muscle, while bitter candytuft and caraway stimulate digestive secretions and gently stimulate peristalsis. The polyphenols (flavonoids) and essential oils in these herbs likely act on calcium channels, serotonin and opioid receptors, and the enteric plexus signaling in various ways. The result is a normalization of motility: too-fast motility is calmed, too-slow motility is stimulated. This kind of multi-target approach is a hallmark of herbal therapy.

Clinical context: Using such herbal or polyphenol-based remedies can be particularly helpful for patients who cannot tolerate standard prokinetics or in those on medications like GLP-1 agonists. For example, a patient on a GLP-1 RA who experiences nausea and delayed gastric emptying might benefit from ginger supplementation to speed up gastric emptying and reduce nausea. Similarly, if constipation becomes an issue (due to slowed gut transit from the medication), gentle remedies like prune extract or certain probiotic-fermented fibers could help. It’s always important, however, for patients (especially those on medications) to discuss herbal supplements with their healthcare provider to avoid interactions and ensure appropriate use.

Simplified Takeaways: Numerous plant-derived compounds can influence gut motility. Ginger is a prokinetic for the stomach – it helps the stomach empty faster and can reduce nausea by promoting coordinated contractions [18][19]. Artichoke leaf extract helps with indigestion by increasing bile flow (which aids digestion and movement) and by relaxing the gut to relieve cramps [20][21]. Peppermint oil is a natural antispasmodic: it calms down muscle spasms in the gut by blocking calcium channels, which eases pain and bloating in IBS and can slow an overly fast colon [22]. Many herbs work in synergy: one component might stimulate peristalsis while another component relaxes tight segments, together normalizing bowel function. These remedies, often rich in polyphenols, offer a gentler approach to managing motility issues and can be useful alongside conventional therapies. For instance, incorporating ginger or peppermint may help counter the side effects (like slow stomach or cramps) from medications such as GLP-1 agonists, demonstrating how modern medicine and herbal wisdom can complement each other.

 

 

References

  1. Bayliss WM, Starling EH. The movements and innervation of the small intestine. J Physiol. 1899;24(2):99–143. (Early experiments demonstrating the ENS-mediated peristaltic reflex independent of the CNS)

  2. Chen JH, et al. Roles of interstitial cells of Cajal in regulating gastrointestinal motility: synaptic modulation and beyond. Acta Physiol (Oxf). 2013;213(4):743–754. (Review on ICC as pacemakers and intermediaries in enteric neurotransmission)

  3. Al-Missri MZ, Jialal I. Physiology, Motilin. In: StatPearls [Internet]. StatPearls Publishing; 2022 Sep. (Overview of motilin’s role in MMC and motility control)

  4. Mawe GM, Hoffman JM. Serotonin signalling in the gut—functions, dysfunctions and therapeutic targets. Nat Rev Gastroenterol Hepatol. 2013;10(8):473–486. (Comprehensive review of 5-HT in gut motility and implications for disorders)

  5. Holst JJ. The physiology of glucagon-like peptide 1. Physiol Rev. 2007;87(4):1409–1439. (Details on GLP-1 secretion from L-cells and its ileal brake effect on gastric emptying)

  6. Fleming MA, et al. The enteric nervous system and its emerging role as a therapeutic target. Gastroenterol Res Pract. 2020;2020:8024171. (Discusses vagal and ENS interactions; notes that GLP-1 slows gastric emptying via vagal pathways)

  7. Chamorro S, et al. Participation of short-chain fatty acids and their receptors in gut homeostasis and inflammation. Nutrients. 2019;11(7):E1520. (SCFAs’ roles via FFAR2/3 in modulating GLP-1, PYY, and 5-HT to influence motility and inflammation)

  8. Segain JP, et al. Butyrate inhibits inflammatory responses through NFκB suppression: implications for Crohn’s disease. Gastroenterology. 2000;118(4):A417. (Demonstrates SCFAs’ effects on enteric neurons and motility in a rat model)

  9. Triantafyllou K, Chang C, Pimentel M. Methanogens, methane and gastrointestinal motility. J Neurogastroenterol Motil. 2014;20(1):31–40. (Review summarizing how methane gas production correlates with slowed motility and constipation, and how reducing methane can improve transit)

  10. Singh SB, Lin HC. Hydrogen sulfide in physiology and diseases of the digestive tract. Microorganisms. 2015;3(4):866–889. (Detailed review of H₂S as a gaseous transmitter in the gut, generally inhibiting motility via smooth muscle hyperpolarization and reduced contractility)

  11. Chen N, et al. Effectiveness and safety of probiotics for constipation-predominant irritable bowel syndrome: a systematic review and meta-analysis of 10 randomized controlled trials. Nutrients. 2022;14(12):2482. (Meta-analysis showing probiotics improve stool consistency and frequency in IBS-C patients)

  12. Xu X, et al. Crosstalk between the gut microbiome and colonic motility in chronic constipation: potential mechanisms and microbiota modulation. Nutrients. 2022;14(18):3704. (Review discussing how probiotics, SCFAs, and microbial metabolites like tryptophan catabolites can improve constipation and the underlying pathways, e.g. increased 5-HT₄ receptor expression by Bifidobacterium)

  13. Shao Y, et al. Manipulating gut serotonin produces convergent effects on motility in mouse models of constipation or diarrhea. Cell Mol Gastroenterol Hepatol. 2021;11(2):419–440. (Experimental evidence that interventions targeting microbial or host pathways to alter 5-HT availability can normalize abnormal motility)

  14. Liu YW, et al. Psychotropic effects of Lactobacillus plantarum PS128 in early life-stressed and naïve adult mice. Brain Res. 2016;1631:1–12. (Illustrates a probiotic strain modulating neurotransmitters and potentially affecting motility via gut-brain axis; included to exemplify probiotic influence on ENS/CNS)

  15. Ticho AL, et al. Bile acid receptors and gastrointestinal functions. Liver Res. 2019;3(1):31–39. (Review of bile acid signaling through FXR and TGR5, noting TGR5 activation increases colonic motility and bile acid overproduction leads to diarrhea phenotype)

  16. O’Keefe SJ, et al. Altered small-bowel motility in chronic pancreatitis: role of pancreatic enzyme replacement therapy. Dig Dis Sci. 2003;48(4):906–912. (Study showing abnormal motility in pancreatic insufficiency and improvement with enzyme therapy, indicating maldigestion’s impact on transit)

  17. Kumar N, et al. Small intestinal bacterial overgrowth in patients with chronic pancreatitis and pancreatic insufficiency: treatment with rifaximin. Am J Gastroenterol. 2014;109(9):1501–1509. (Found ~33% of chronic pancreatitis patients with persistent GI symptoms had SIBO; rifaximin improved their diarrhea and nutritional status)

  18. Micklefield GH, et al. Effects of ginger on gastroduodenal motility. Int J Clin Pharmacol Ther. 1999;37(9):341–346. (Found ginger accelerated gastric emptying and stimulated antral contractions in healthy volunteers, supporting ginger’s prokinetic activity)

  19. Wu KL, et al. Effect of ginger on gastric motility and symptoms of functional dyspepsia. World J Gastroenterol. 2011;17(1):105–110. (Randomized trial in dyspepsia patients demonstrating ginger’s enhancement of gastric emptying and antral motility, though symptoms improvement was not significant in the short term)

  20. Holtmann G, et al. Efficacy of artichoke leaf extract in the treatment of patients with functional dyspepsia: a six-week placebo-controlled, double-blind, multicentre trial. Aliment Pharmacol Ther. 2003;18(11-12):1099–1105. (Showed artichoke extract significantly reduced dyspepsia symptoms compared to placebo)

  21. Giacosa A, et al. The effect of ginger and artichoke extract supplementation on functional dyspepsia: a randomized, double-blind, placebo-controlled trial. Evid Based Complement Alternat Med. 2015;2015:915087. (Combination of ginger and artichoke improved symptoms within 2 weeks; authors note ginger’s prokinetic and artichoke’s choleretic/antispasmodic contributions to relief)

  22. Cash BD, et al. Peppermint oil for the treatment of irritable bowel syndrome: a systematic review and meta-analysis. J Clin Gastroenterol. 2016;50(5):505–512. (Meta-analysis confirming peppermint oil is effective in reducing IBS symptoms, likely via smooth muscle relaxation from menthol’s calcium channel blockade)

  23. Madisch A, et al. Effects of Iberogast on proximal gastric volume, gastric emptying, and gastrocaudal transport of gastric contents in functional dyspepsia. Neurogastroenterol Motil. 2006;18(5):425–432. (Found that the multi-herbal preparation Iberogast improved gastric accommodation and slightly accelerated gastric emptying in dyspepsia patients, demonstrating a normalizing effect on upper GI motility)

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