Research indicates a strong correlation between migraines and constipation, challenging the traditional view of migraines as solely a head-centered neurological event. People who experience migraines are four times more likely to have constipation than those without migraine. This connection is rooted in shared physiological pathways, requiring an examination of the complex communication system that ties the brain and the digestive system together.
Understanding the Gut-Brain Axis
The foundational link between a neurological disorder like migraine and a digestive issue like constipation lies in the Gut-Brain Axis (GBA). This axis represents a bidirectional communication system that constantly relays information between the central nervous system (CNS) and the enteric nervous system (ENS) in the gut. The ENS is sometimes referred to as the “second brain” because it manages the entire gastrointestinal tract, controlling functions like motility and secretion.
Communication along the GBA is facilitated by the vagus nerve, which acts like a superhighway connecting the two systems. This nerve transmits signals related to pain, inflammation, and stress between the brain and the gut. The stress and pain associated with a migraine attack can disrupt the normal rhythmic contractions of the intestines, potentially slowing down gut motility and leading to constipation.
The gut microbiome, the vast collection of bacteria residing in the intestines, also plays a significant role. Imbalances in this microbial community, known as dysbiosis, can affect systemic inflammation and alter nerve signaling, contributing to both migraine and constipation.
Shared Neurotransmitter Pathways
Specific chemical messengers are common to both migraine generation and the regulation of bowel movements. Serotonin (5-HT) is one such neurotransmitter, known for its dual role as a pain modulator in the brain and a primary regulator of peristalsis (the muscular contractions that move food through the gut). About 90% of the body’s serotonin is found in the gut, where it is released to stimulate digestive movement.
Fluctuations in serotonin signaling can affect both conditions simultaneously. In the brain, changes in serotonin levels are directly implicated in the migraine process, with a drop in levels often associated with the headache phase. Altered serotonin activity in the gut can lead to sluggish bowel movements, contributing to constipation.
Another powerful neuropeptide involved in this connection is Calcitonin Gene-Related Peptide (CGRP), which is widely recognized as a key molecule in migraine pain. CGRP is also present within the enteric nervous system, where it plays a physiological role in initiating propulsive motor activity and stimulating the secretion of water and ions into the intestinal lumen. In the gut, CGRP essentially acts to accelerate intestinal transit.
Systemic inflammation provides a further shared pathway. Inflammatory molecules triggered by conditions like gut dysbiosis can travel along the GBA. This heightened inflammatory state can increase pain sensitivity in the brain, contributing to migraine frequency, while also affecting the delicate balance required for proper gut function.
The Confounding Factor of Migraine Medication
While a physiological link exists between migraine and constipation, it is important to consider that the medications used to treat the head pain can often exacerbate or directly cause the digestive issue. Many acute and preventive migraine treatments have known gastrointestinal side effects that slow down gut motility.
Opioids, if used for severe acute migraine relief, are a major contributor to constipation due to their mechanism of slowing down intestinal contractions. Even common migraine preventives, such as certain anticonvulsants or older classes of antidepressants like tricyclics, can alter gut function. Tricyclic antidepressants, for instance, are known to have anticholinergic effects that directly inhibit the muscle contractions necessary for a bowel movement.
A prominent example involves newer treatments that target the CGRP pathway. Since CGRP naturally promotes intestinal movement, blocking its function with CGRP receptor antagonists or antibodies can interfere with the gut’s normal motility. This interference is a recognized mechanism for causing treatment-induced constipation. Patients should differentiate between the symptoms caused by the underlying condition and those that are a consequence of the necessary treatment.