Gut Motility and the Migrating Motor Complex

It’s estimated that 60 to 70 million Americans are affected by one or more digestive disorders, with 63 million people suffering from chronic constipation. In my experience as a practitioner, I observe that most people I see need to address an ongoing gut disturbance issue whether it be constipation, IBS, GERD, gastroparesis, or SIBO. Chronic constipation can accompany all of these issues, which can be a sign of an under functioning migrating motor complex.

It’s been established that neurodegenerative diseases such as Parkinson’s Disease are preceded by chronic constipation for as long as 20 years prior to diagnosis. In fact, chronic constipation is a warning sign for the potential development of Parkinson’s Disease. The reason for this is the loss of vagal nerve tone, impaired enteric nervous system functioning and the loss of gut motility.

Gut motility is dependent on communication between the autonomic and enteric nervous systems, also known as the gut-brain axis. Any disturbance in this axis from either the gut or the brain can cause decreased motility and therefore susceptibility to an impaired migrating motor complex (MMC). In order to restore proper digestive function and reduce the risk of a neurodegenerative condition such as Parkinson’s Disease, we have to focus on restoring the optimal functioning of the MMC.

What it is and the Role it Serves

It’s important to first gain an understanding of what the MMC is and how it functions so as to better understand its role in gut health and pathology. The MMC is the electromechanical activity in the gastrointestinal tract’s smooth muscle that’s engaged during the interdigestive states (periods between meals) and serves an important housekeeping role of “sweeping” undigested food from the stomach and small intestine into the large intestine.

The MMC serves two major purposes. First, it cleans the stomach and small intestine to receive new food for digestion and absorption of nutrients. Second, it prevents the build-up of bacterial populations in the small intestine that are a contributing factor for the pathogenesis of SIBO (Small Intestinal Bacterial Overgrowth). The activity of the MMC is actually a clinical marker for how well the GI tract is functioning. Issues such as gastroparesis, intestinal pseudo-obstruction, and SIBO have all been linked to a weakened MMC.

Periodicity and Phases of the MMC

The MMC has two distinct locations, the gastric and the intestinal/duodenal. Each consists of three primary phases with a brief fourth phase serving the role of transition between the third and first phases. A complete cycle lasts roughly 90 minutes and occurs every 90-120 minutes during fasting states. Though they operate in concert together, the duodenal MMC is controlled by different mechanisms than the gastric MMC.

Once the state of digestion comes to an end, approximately two hours after eating, the MMC cycle begins with Phase I, also known as the quiescent phase. This phase is characterized by little to no contractions and lasts 45-60 minutes. Phase II is marked by low-amplitude contractions that occur intermittently and gradually increase in frequency over a 30-minute period of time. Phase III consists of rapid, evenly spaced high-amplitude contractions and lasts anywhere from 5-15 minutes. During this phase, the pylorus remains open so all undigested food remaining in the stomach can move into the small intestine and eventually make its way into the large intestine.

How the MMC Functions

The MMC functions through the concerted effort of the nervous and endocrine systems. The two key hormones involved are motilin and ghrelin. Together with the vagus nerve, these hormones work synergistically to stimulate the various phases of both the gastric and duodenal MMC’s.

During gastric phase I, secretions of gastric, biliary, and pancreatic juices cause the pressure in the duodenum to rise. This increased pressure stimulates the release of 5-HT (serotonin), which initiates duodenal phase II. The gastric, biliary, and pancreatic secretions not only increase the pressure in the duodenum, but they also aid in the cleansing activity of the MMC and help to kill and reduce bacterial populations in the upper portion of the small intestine.

Once intestinal phase II is initiated, the duodenal pressure increases, stimulating the release of more serotonin. This enhances the amplitude of the contractions and leads to duodenal phase III and its rapid high-amplitude contractions. At this point, maximal pressure in the duodenum is achieved and motilin is released. Motilin stimulates large amounts of serotonin to act on the vagal afferent nerves leading to the brain stem. This stimulation by the vagal afferent activates the vagal efferent nerves leading back to the stomach, triggers the release of acetylcholine, which initiates the MMC and induces gastric phase III via vago-vagal reflex.

It’s important to understand that adequate levels of the neurotransmitters serotonin and acetylcholine are essential for the proper stimulation and optimal functioning of the MMC. Insulin surges, reactive hypoglycemia, inadequate protein intake, gut dysbiosis, and stress all impact the production of serotonin and acetylcholine and can lead to diminished amounts of these critical neurotransmitters and therefore decreased activity of the MMC.

Since the vagal efferent pathway is a key component to activating gastric phase III, it’s important to have healthy vagal nerve tone. In a time when chronic stress and trauma seem to be at an all-time high, sympathetic dominance is far too common. When a person is in long-term sympathetic dominance, vagal nerve tone diminishes and therefore so does its ability to stimulate the MMC.

How to Stimulate the MMC

Stress reduction and stress management techniques such as breath work, meditation, HeartMath, yoga, tai chi, and qigong are all important practices that can help increase vagal nerve tone. In addition, vigorous gargling, gagging yourself with a tongue depressor multiple times a day, singing loudly (when and where appropriate), humming or chanting, and coffee enemas are all ways to increase vagal nerve tone.

Since serotonin and acetylcholine are key neurotransmitters involved with activating the MMC supplements that promote the production of these can be supportive. 5-HTP, St. John’s Wort, SAMe, B6, methylfolate, and methylcobalamin can aid in serotonin production. Alpha-glycerolphosphorylcholine, phosphatidylcholine, and acetyl-L carnitine support the production of acetylcholine. Huperzine A can slow the activity of acetylcholinesterase, which can reduce the degradation of acetylcholine.

With a compromised MMC, it’s critical to focus on improving gut motility. Prokinetics (pro-movement), either herbal or pharmaceutical, can be an effective means to improving gastrointestinal movement.

Prokinetic herbs such as artichoke leaf and ginger have been shown in clinical trials to stimulate the MMC and improve gastric emptying. Taking a combination of ginger and artichoke leaf at dinner time and before bed improves gut motility and enhances the activity of the MMC. The digestive Ayurvedic formula Triphala shows a positive influence on the MMC, specifically the herb Haritaki (one of the three herbs included in the formula). Haritaki has been shown in clinical trials to improve GI muscle contractions and improve gastric emptying. In fact, when researchers compared the effect of Haritaki with that of the prokinetic drug Metoclopramide, they found that Haritaki increased gastric emptying by 86 percent, compared to 76 percent for Metoclopramide. 

There are also a number of prokinetic drugs such as Proculapride, Domperidone, Metoclopramide, and Erythromycin. These may all help with chronic constipation, bloating, feeling full too quickly, and gastroparesis, but they also come with a number of side effects. These include chest pain, irregular heartbeat, dizziness, headache, vomiting, diarrhea, abdominal pain, and trouble sleeping. 

Finally, making sure that there is 4-5 hours between meals, and nothing is eaten at least 4 hours prior to sleep, ensures an appropriate amount of time for the MMC to engage and completely cycle through all of its phases. Once food enters the system, the interdigestive state comes to an end and along with it, the activity of the MMC. Waiting 4-5 hours between meals can be a difficult task for a person with hypoglycemia who needs to have some protein every 2-3 hours. Eating in a way that satisfies hunger for a longer duration of time (a higher protein and fat diet with lower carbohydrates) and taking nutrients that support blood sugar regulation can all aid the hypoglycemic to be able to have more time in-between meals.

In Conclusion

When I encounter clients diagnosed with SIBO, IBS, gastroparesis, or complain of chronic constipation, feeling full too fast, bloating after meals, and chronic stress, I immediately look to improve the MMC. My standard protocol is to make sure that they allow for 4-5 hours in-between meals, don’t snack before bed or between meals, take a prokinetic, and do vagal nerve stimulating exercises. By following this protocol, they will be able to provide the time and space for the MMC to engage and perform its role, stimulate MMC activity, and increase vagal nerve tone, all of which are essential for an optimal functioning migrating motor complex.


Deloose, E., Janssen, P., Depoortere, I. et al. The migrating motor complex: control mechanisms and its role in health and disease. Nat Rev Gastroenterol Hepatol 9, 271–285 (2012) doi:10.1038/nrgastro.2012.57

Takahashi, T. Mechanism of interdigestive migrating motor complex. J Neurogastroenerol Motil., 2012 Jul;18(3):246-57 doi: 10.5056/jnm.2012.18.3.246. Epub 2012 Jul 10.

Tamhane MD, Thorat SP, Rege NN, Dahanukar SA. Effect of oral administration of Terminalia chebula on gastric emptying: an experimental study. J Postgrad Med 1997 Jan-Mar;43(1):12-3.)

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