Migraine: Types, Triggers, Treatments, and How to Build a Management Plan

What Is Migraine, Really?

Let’s start with what migraine is not: it is not just a headache. That distinction matters because it shapes how the condition is treated, researched, and taken seriously.

Migraine is a neurological disorder. It involves waves of abnormal electrical and chemical activity in the brain that affect blood vessels, nerves, and pain processing systems. A headache can be one part of a migraine attack, but migraine also involves changes in vision, sensation, cognition, mood, digestion, and energy that can begin hours before the head pain starts and linger for days after it stops.^[1]

The World Health Organization ranks migraine as the second leading cause of years lived with disability globally.^[2] It affects more than one billion people worldwide, roughly 12% of the population. Women are affected about three times more often than men, largely due to hormonal influences.

If you have migraine, you are dealing with a real, biologically-driven condition. It is not a character flaw, a stress problem, or something you should just push through.

Types of Migraine

Migraine is not a single entity. It comes in several forms, and knowing which type you have helps guide treatment.

Migraine Without Aura

This is the most common type, accounting for about 70-75% of all migraine. Attacks involve moderate to severe, usually one-sided pulsating head pain lasting 4-72 hours, accompanied by nausea, vomiting, and sensitivity to light and sound. There is no aura phase.

Migraine With Aura

About 25-30% of people with migraine experience aura, a set of neurological symptoms that typically develop over 5-20 minutes and last less than 60 minutes before the headache begins. Visual aura is the most common: you might see zigzag lines, shimmering spots, blind spots, or tunnel vision. Some people experience sensory aura (tingling or numbness in the face or hands) or speech disturbances.^[3]

Chronic Migraine

If you have headache on 15 or more days per month, with at least 8 of those days meeting migraine criteria, for more than 3 months, you have chronic migraine. This affects about 2% of the general population and is associated with greater disability and higher rates of depression and anxiety. Medication overuse can contribute to the progression from episodic to chronic migraine.^[4]

Episodic Migraine

Fewer than 15 headache days per month. Most people with migraine fall into this category, though episodic migraine can progress to chronic over time, particularly if attacks are not well managed.

Hemiplegic Migraine

A rare and dramatic form where the aura includes temporary weakness on one side of the body, mimicking a stroke. It can be familial (genetic) or sporadic. If you experience sudden one-sided weakness for the first time, go to the emergency room to rule out stroke, even if you have a history of migraine.^[5]

Vestibular Migraine

The primary symptom is dizziness or vertigo rather than head pain. Some attacks involve both; others involve vertigo alone. Vestibular migraine is the most common cause of episodic vertigo and is frequently misdiagnosed as inner ear problems or anxiety.^[6]

Ocular (Retinal) Migraine

This involves temporary, partial, or complete loss of vision in one eye, with or without headache. It is rare and should always be evaluated to rule out other causes of monocular vision loss.

Menstrual Migraine

Attacks that occur predictably around menstruation, typically in the two days before through the first three days of the period. They are driven by the natural drop in estrogen that happens at that time. Menstrual migraine attacks tend to be longer, more severe, and less responsive to treatment than non-menstrual attacks.^[7]

The Four Phases of a Migraine Attack

A migraine attack is not just the headache. It is a neurological event that unfolds in distinct phases, and understanding these phases can help you intervene earlier and more effectively.

Phase 1: Prodrome (Hours to Days Before)

Up to 77% of people with migraine experience prodromal symptoms. These are subtle changes that signal an attack is on its way:^[8]

• Yawning excessively
• Food cravings (especially for sweets or carbohydrates)
• Mood changes (irritability, depression, or euphoria)
• Neck stiffness
• Increased urination
• Difficulty concentrating
• Fatigue

Learning to recognize your prodrome is valuable because treating a migraine during this phase is often more effective than waiting until the headache hits.

Phase 2: Aura (5-60 Minutes Before Headache)

Not everyone experiences this phase. When it occurs, it reflects a wave of electrical activity (cortical spreading depression) moving across the brain. Visual disturbances are most common, but sensory, speech, and motor symptoms can also occur. Aura typically builds gradually and resolves before the headache starts, though overlap is possible.

Phase 3: Headache (4-72 Hours)

The headache phase involves moderate to severe pain, usually pulsating, often one-sided (though it can be bilateral). It worsens with physical activity. Associated symptoms include nausea or vomiting, photophobia (light sensitivity), phonophobia (sound sensitivity), and sometimes osmophobia (sensitivity to smells). Not every attack reaches the same intensity; some are milder than others.

Phase 4: Postdrome (“Migraine Hangover,” Up to 48 Hours After)

After the headache resolves, many people feel wiped out. Postdrome symptoms include fatigue, difficulty concentrating, mood changes, and a general feeling of being “off.” Some people describe it as feeling hungover. Moving too quickly back into normal activity during postdrome can sometimes retrigger the headache.^[9]

What Causes Migraine?

Migraine is primarily a genetic, neurological condition. If one of your parents has migraine, you have roughly a 50% chance of having it too. If both parents have it, that rises to about 75%.^[10]

The Brain Mechanisms

Several interconnected processes drive a migraine attack:

• Cortical spreading depression (CSD): A slow wave of neuronal excitation followed by suppression that spreads across the brain’s cortex. This is what produces the aura and may also activate pain pathways.
• Trigeminal nerve activation: The trigeminal nerve, which supplies sensation to the face and head, becomes activated and releases inflammatory neuropeptides, particularly calcitonin gene-related peptide (CGRP). This causes inflammation around brain blood vessels and sensitizes pain pathways.^[11]
• Serotonin fluctuations: Serotonin levels drop during migraine attacks, which may explain why triptans (serotonin receptor agonists) are effective treatments.
• Central sensitization: With repeated attacks, the brain’s pain processing systems can become increasingly sensitive, lowering the threshold for future attacks.

Common Triggers

Triggers do not cause migraine. They push an already susceptible brain past its threshold. Not everyone has the same triggers, and a trigger that provokes an attack one day might not the next. Context matters: triggers tend to stack.

The most commonly reported triggers include:

• Stress (and the letdown after stress, which is why weekend migraines are common)
• Hormonal changes (menstruation, ovulation, perimenopause)
• Sleep disruption (too little, too much, or irregular timing)
• Skipped meals or dehydration
• Weather changes (barometric pressure drops, heat, high humidity)
• Sensory overload (bright lights, loud noise, strong smells)
• Alcohol (especially red wine)
• Certain foods (aged cheese, processed meats, MSG, chocolate, though food triggers are highly individual and often overstated)
• Caffeine withdrawal

How Is Migraine Diagnosed?

Migraine is a clinical diagnosis, meaning it is based on your symptom pattern and medical history rather than a specific test. The International Classification of Headache Disorders (ICHD-3) criteria require at least five attacks meeting specific criteria for migraine without aura, or at least two attacks with typical aura features.^[12]

Brain imaging (MRI or CT) is not needed for a typical migraine presentation but should be done if there are unusual features: sudden onset of the worst headache of your life, neurological symptoms that do not fit typical aura patterns, new headache after age 50, or progressive worsening over weeks.

A headache diary is one of the most useful diagnostic tools. Track the timing, duration, intensity, associated symptoms, potential triggers, and response to treatment for at least a month before your appointment.

Conventional Treatments: Acute (Stopping an Attack)

The goal of acute treatment is to stop the attack quickly and completely, with minimal side effects and no recurrence. Timing matters enormously: most acute medications work best when taken early in the attack.

Triptans

These remain the gold standard for moderate to severe migraine attacks. Sumatriptan, rizatriptan, eletriptan, and others work by activating serotonin receptors, constricting dilated blood vessels, and blocking pain signal transmission in the trigeminal nerve. They are available as tablets, nasal sprays, and injections. Not all triptans work equally well for every person; it is worth trying a different one before concluding triptans do not work for you.^[13]

NSAIDs

For mild to moderate attacks, ibuprofen, naproxen, or aspirin can be effective, especially if taken early. Combining an NSAID with a triptan can improve response rates for stubborn attacks.

Gepants (CGRP Receptor Antagonists)

Ubrogepant (Ubrelvy) and rimegepant (Nurtec) represent a newer class of acute treatments. They block the CGRP receptor, targeting a key molecule in migraine pathophysiology. Unlike triptans, they do not constrict blood vessels, making them safe for people with cardiovascular risk factors. Rimegepant is also approved for prevention when taken every other day.^[14]

Ditans

Lasmiditan (Reyvow) targets serotonin receptors differently than triptans and does not cause vasoconstriction. It can cause dizziness and sedation, and driving is not recommended for 8 hours after taking it. It is an option for people who cannot take triptans.

Anti-Nausea Medications

Metoclopramide and prochlorperazine treat migraine-associated nausea and may have independent pain-relieving effects. They can also improve absorption of oral medications by reducing gastric stasis, which commonly occurs during migraine.

A Warning About Medication Overuse

Using acute migraine medications more than 10-15 days per month (depending on the type) can lead to medication overuse headache (MOH), a cycle where the treatment itself starts causing more frequent headaches. This is one of the most common reasons episodic migraine becomes chronic. If you are reaching for acute treatment more than twice a week regularly, it is time to discuss preventive therapy.^[15]

Conventional Treatments: Preventive (Reducing Attack Frequency)

Preventive treatment is recommended if you have four or more migraine days per month, if your attacks are particularly severe or long-lasting, or if acute treatments are not working well enough.

Oral Preventives

• Beta-blockers (propranolol, metoprolol): Among the oldest and best-studied preventives. They reduce attack frequency by about 50% in many patients.
• Topiramate: An antiepileptic medication with good evidence for migraine prevention. Common side effects include cognitive slowing (“brain fog”), tingling in hands and feet, and weight loss. These limit its tolerability for some people.
• Amitriptyline: A tricyclic antidepressant that is especially useful when migraine coexists with tension-type headache, insomnia, or depression. Usually dosed at night because it causes drowsiness.
• Candesartan and venlafaxine: Second-line options with reasonable evidence.

CGRP Monoclonal Antibodies

This class has transformed migraine prevention since arriving in 2018. Erenumab (Aimovig), fremanezumab (Ajovy), galcanezumab (Emgality), and eptinezumab (Vyepti) target either CGRP itself or its receptor. They are given as monthly or quarterly injections (eptinezumab is IV, quarterly). Side effects are minimal, mainly injection site reactions and constipation with erenumab. They work for both episodic and chronic migraine, including in patients who have failed multiple other preventives.^[16]

OnabotulinumtoxinA (Botox)

FDA-approved specifically for chronic migraine, Botox involves 31 injections across the head and neck every 12 weeks. It works by blocking CGRP release from nerve endings. Most people need at least two to three treatment cycles before seeing the full benefit.^[17]

Integrative and Complementary Approaches

Several non-pharmaceutical treatments have evidence strong enough that they are recommended in clinical guidelines. They can be used alone for mild cases or alongside medications for more frequent migraine.

Magnesium

Magnesium deficiency is common in people with migraine, and supplementation has been shown to reduce attack frequency by about 40% in some trials. Magnesium glycinate or citrate at 400-600 mg daily is the typical dose. It is one of the safest preventive options and is particularly helpful for menstrual migraine. The main side effect at higher doses is loose stools.^[18]

Riboflavin (Vitamin B2)

At a dose of 400 mg daily, riboflavin has shown significant migraine reduction in multiple trials. It is thought to improve mitochondrial energy metabolism in the brain. It is inexpensive, very well tolerated, and turns your urine bright yellow, which is harmless.^[19]

Coenzyme Q10 (CoQ10)

Another mitochondrial support supplement, CoQ10 at 100-300 mg daily has shown benefit in several trials, including in adolescents. It may take two to three months to see full effects.

Feverfew

This herbal remedy has been used for headache for centuries. Clinical evidence is mixed but generally positive for doses of 50-150 mg of dried leaf daily. It may work by inhibiting prostaglandin synthesis and serotonin release from platelets.

Butterbur

Petasites hybridus extract (butterbur) at 150 mg daily reduced migraine frequency by about 48% in a large RCT. However, safety concerns about hepatotoxicity from pyrrolizidine alkaloids mean that only PA-free preparations (like Petadolex) should be used, and availability varies by country.^[20]

Biofeedback

Biofeedback teaches you to control physiological responses like muscle tension, skin temperature, and heart rate variability. It has Grade A evidence for migraine prevention and is especially good for people who prefer non-drug approaches or who are pregnant. Several sessions with a trained therapist are typically needed before you can practice independently.^[21]

Acupuncture

A large Cochrane review found that acupuncture is at least as effective as preventive medications for migraine, with fewer side effects. Whether it works through specific meridian effects or general neurophysiological mechanisms is debated, but the clinical results are consistent.^[22]

Neuromodulation Devices

Several FDA-cleared devices are now available:

• Single-pulse TMS (sTMS): A handheld device placed on the back of the head that delivers a magnetic pulse to interrupt cortical spreading depression. Used for both acute treatment and prevention.
• External trigeminal nerve stimulation (Cefaly): A forehead-worn device that stimulates the supraorbital nerve. Used daily for prevention and on-demand for acute attacks.
• Non-invasive vagus nerve stimulation (gammaCore): Stimulates the vagus nerve through the neck. Approved for acute and preventive use.

Neurofeedback

This involves training your brain’s electrical patterns using real-time EEG feedback. While the evidence base is smaller than for biofeedback, preliminary studies show promise, particularly for patients with abnormal cortical excitability patterns.

Ketamine for Refractory Migraine

For people with chronic migraine who have not responded to standard treatments, low-dose intravenous ketamine is being studied as an option. It works through NMDA receptor antagonism and may help break cycles of central sensitization. This is an emerging therapy, not yet standard of care, and should only be administered in supervised clinical settings.^[23]

Migraine and Hormones

The strong female predominance of migraine (3:1 after puberty) points directly to hormonal influences. Estrogen is the key player.

Migraine often begins at menarche, fluctuates with the menstrual cycle, changes during pregnancy (often improves, especially in the second and third trimesters), and can worsen during perimenopause before sometimes improving after menopause.

Management strategies for hormone-related migraine include:

• Timed supplementation with magnesium and naproxen in the perimenstrual window
• Continuous hormonal contraception to eliminate the estrogen drop (with important caveats: combined estrogen-progestin methods may be contraindicated in migraine with aura due to increased stroke risk)
• Short-term estrogen supplementation during the perimenstrual period
• Frovatriptan taken preventively around menstruation

If you have migraine with aura, discuss contraceptive choices carefully with your doctor. Combined hormonal contraceptives (containing estrogen) are generally avoided due to a small but real increased risk of ischemic stroke.^[7]

Migraine in Children and Adolescents

Migraine often begins in childhood. Before puberty, boys and girls are affected equally. Attacks in children tend to be shorter (sometimes as brief as 2 hours), more often bilateral (across the forehead rather than one-sided), and more likely to include prominent nausea, vomiting, and abdominal symptoms.

Abdominal migraine, in which recurrent episodes of moderate to severe midline abdominal pain occur with nausea, vomiting, or pallor but minimal headache, is a recognized variant in children. Many of these children go on to develop typical migraine in adolescence or adulthood.

Treatment in children emphasizes lifestyle regularity (consistent sleep, meals, hydration, and physical activity), behavioral interventions (biofeedback and CBT have strong evidence in pediatric migraine), and cautious use of medications when needed. Ibuprofen and sumatriptan nasal spray have the best evidence for acute treatment in children. For prevention, amitriptyline and topiramate are commonly used, though a large NIH-funded trial (CHAMP) showed that neither was better than placebo for pediatric migraine when combined with lifestyle counseling.^[24]

When to Go to the Emergency Room

Most migraine attacks, even severe ones, can be managed at home or with your doctor’s guidance. But certain situations require urgent evaluation:

• Worst headache of your life (sudden, explosive onset): could indicate subarachnoid hemorrhage
• Headache with fever, stiff neck, and confusion: possible meningitis
• New neurological symptoms: weakness, difficulty speaking, or visual changes that do not fit your typical aura pattern
• Aura lasting more than 60 minutes or not followed by headache (if this is new for you)
• Headache after head injury
• Headache with seizure
• Status migrainosus: a migraine attack lasting more than 72 hours despite treatment, especially with dehydration from vomiting

When in doubt, seek evaluation. It is always better to be checked and reassured than to miss something serious.

Building Your Migraine Management Plan

Effective migraine management is rarely about a single solution. It is about building a personalized plan that addresses your specific pattern.

Step 1: Track Your Attacks

Use a headache diary or app (Migraine Buddy, N1 Headache) to record frequency, duration, severity, symptoms, potential triggers, and medication use. This data is invaluable for you and your doctor.

Step 2: Optimize Lifestyle Factors

These are not glamorous, but they form the foundation:

• Consistent sleep schedule (same bedtime and wake time, even on weekends)
• Regular meals (do not skip meals or go long periods without eating)
• Stay hydrated
• Regular aerobic exercise (30-40 minutes, 3-5 times per week; exercise is as effective as topiramate for prevention in some studies)
• Stress management (whatever works for you: meditation, breathing exercises, therapy, time in nature)

Step 3: Have an Acute Treatment Plan

Know which medication to take, when to take it (early), and what your backup plan is if the first option does not work. Stratified treatment, choosing your acute medication based on attack severity rather than stepping through options, is more effective.

Step 4: Consider Prevention If Needed

If you are having four or more attacks per month, using acute medication more than twice a week, or your attacks are significantly disabling, talk to your doctor about preventive options. You may start with supplements (magnesium, riboflavin, CoQ10) and add prescription prevention if needed.

Step 5: Build Your Support Team

A good primary care doctor or neurologist (ideally a headache specialist), a therapist familiar with chronic pain management, and the understanding of your close relationships make a real difference. Migraine can be isolating; it does not have to be.

Frequently Asked Questions

Can migraine be cured?

No. The guide describes migraine as not curable, but highly treatable. With the right combination of acute and preventive approaches, many people achieve a 50 to 75 percent reduction in attack frequency.

Which supplements have evidence for preventing migraine?

Several are covered with dosing. Magnesium (glycinate or citrate) at 400 to 600 mg daily reduced attack frequency by about 40 percent in some trials, with loose stools as the main side effect at higher doses. Riboflavin (vitamin B2) at 400 mg daily showed significant reduction in multiple trials and is inexpensive and well tolerated. CoQ10 at 100 to 300 mg daily may take two to three months for full effect, and butterbur (PA-free preparations only) at 150 mg daily reduced frequency by about 48 percent in a large randomized trial.

How long does Botox take to work for chronic migraine?

OnabotulinumtoxinA (Botox) is FDA-approved specifically for chronic migraine and is given as 31 injections across the head and neck every 12 weeks. According to the guide, most people need at least two to three treatment cycles before seeing the full benefit.

What are the risks of using acute migraine medication too often?

The guide warns that using acute migraine medications more than 10 to 15 days per month can lead to medication overuse headache (MOH). Specific drugs carry their own cautions too: ditans such as lasmiditan can cause dizziness and sedation, and driving is not recommended for 8 hours after taking them.

Are there non-drug options that actually work for migraine?

Yes. The guide notes biofeedback has Grade A evidence for migraine prevention and is especially suitable for people who prefer non-drug approaches or who are pregnant, though several sessions with a trained therapist are typically needed. Acupuncture is described as at least as effective as preventive medications with fewer side effects, and regular exercise (30 to 40 minutes, 3 to 5 times per week) was as effective as topiramate for prevention in some studies.

Do children with migraine need the same medications as adults?

Not necessarily. The guide points to a large NIH-funded trial (CHAMP) that showed neither amitriptyline nor topiramate was better than placebo for pediatric migraine when combined with lifestyle counseling. Children’s migraine can also look different, sometimes lasting as briefly as 2 hours and more often affecting both sides of the forehead rather than one side.

References

1. Goadsby PJ, Holland PR, Martins-Oliveira M, Hoffmann J, Schankin C, Akerman S. Pathophysiology of migraine: a disorder of sensory processing. Physiol Rev. 2017;97(2):553-622. doi:10.1152/physrev.00034.2015
2. Steiner TJ, Stovner LJ, Jensen R, Uluduz D, Katsarava Z. Migraine remains second among the world’s causes of disability, and first among young women. J Headache Pain. 2020;21(1):137. doi:10.1186/s10194-020-01208-0
3. Charles A. The pathophysiology of migraine: implications for clinical management. Lancet Neurol. 2018;17(2):174-182. doi:10.1016/S1474-4422(17)30435-0
4. Natoli JL, Manack A, Dean B, et al. Global prevalence of chronic migraine: a systematic review. Cephalalgia. 2010;30(5):599-609. doi:10.1111/j.1468-2982.2009.01941.x
5. Russell MB, Ducros A. Sporadic and familial hemiplegic migraine: pathophysiological mechanisms, clinical characteristics, diagnosis, and management. Lancet Neurol. 2011;10(5):457-470. doi:10.1016/S1474-4422(11)70048-5
6. Lempert T, Olesen J, Furman J, et al. Vestibular migraine: diagnostic criteria. J Vestib Res. 2012;22(4):167-172. doi:10.3233/VES-2012-0453
7. MacGregor EA. Migraine, menopause and hormone replacement therapy. Post Reprod Health. 2018;24(1):11-18. doi:10.1177/2053369117731172
8. Giffin NJ, Ruggiero L, Lipton RB, et al. Premonitory symptoms in migraine: an electronic diary study. Neurology. 2003;60(6):935-940. doi:10.1212/01.WNL.0000052998.58526.A9
9. Bose P, Goadsby PJ. The migraine postdrome. Curr Opin Neurol. 2016;29(3):299-301. doi:10.1097/WCO.0000000000000310
10. Gormley P, Anttila V, Winsvold BS, et al. Meta-analysis of 375,000 individuals identifies 38 susceptibility loci for migraine. Nat Genet. 2016;48(8):856-866. doi:10.1038/ng.3598
11. Edvinsson L, Haanes KA, Warfvinge K, Krause DN. CGRP as the target of new migraine therapies: successful translation from bench to clinic. Nat Rev Neurol. 2018;14(6):338-350. doi:10.1038/s41582-018-0003-1
12. Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018;38(1):1-211. doi:10.1177/0333102417738202
13. Cameron C, Kelly S, Hsieh SC, et al. Triptans in the acute treatment of migraine: a systematic review and network meta-analysis. Headache. 2015;55(Suppl 4):221-235. doi:10.1111/head.12601
14. Lipton RB, Dodick DW, Ailani J, et al. Effect of ubrogepant vs placebo on pain and the most bothersome associated symptom in the acute treatment of migraine. JAMA. 2019;322(19):1887-1898. doi:10.1001/jama.2019.16711
15. Diener HC, Dodick D, Evers S, et al. Pathophysiology, prevention, and treatment of medication overuse headache. Lancet Neurol. 2019;18(9):891-902. doi:10.1016/S1474-4422(19)30146-2
16. Ashina M, Saper J, Cady R, et al. Eptinezumab in episodic migraine: a randomized, double-blind, placebo-controlled study (PROMISE-1). Cephalalgia. 2020;40(3):241-254. doi:10.1177/0333102420905132
17. Dodick DW, Turkel CC, DeGryse RE, et al. OnabotulinumtoxinA for treatment of chronic migraine: pooled results from the double-blind, randomized, placebo-controlled phases of the PREEMPT clinical program. Headache. 2010;50(6):921-936. doi:10.1111/j.1526-4610.2010.01678.x
18. Mauskop A, Varughese J. Why all migraine patients should be treated with magnesium. J Neural Transm. 2012;119(5):575-579. doi:10.1007/s00702-012-0790-2
19. Schoenen J, Jacquy J, Lenaerts M. Effectiveness of high-dose riboflavin in migraine prophylaxis: a randomized controlled trial. Neurology. 1998;50(2):466-470. doi:10.1212/WNL.50.2.466
20. Lipton RB, Göbel H, Einhäupl KM, Wilks K, Mauskop A. Petasites hybridus root (butterbur) is an effective preventive treatment for migraine. Neurology. 2004;63(12):2240-2244. doi:10.1212/01.WNL.0000147290.68260.11
21. Nestoriuc Y, Martin A. Efficacy of biofeedback for migraine: a meta-analysis. Pain. 2007;128(1-2):111-127. doi:10.1016/j.pain.2006.09.007
22. Linde K, Allais G, Brinkhaus B, et al. Acupuncture for the prevention of episodic migraine. Cochrane Database Syst Rev. 2016;(6):CD001218. doi:10.1002/14651858.CD001218.pub3
23. Schwenk ES, Viscusi ER, Buvanendran A, et al. Consensus guidelines on the use of intravenous ketamine infusions for acute pain management. Reg Anesth Pain Med. 2018;43(5):456-466. doi:10.1097/AAP.0000000000000806
24. Powers SW, Coffey CS, Chamberlin LA, et al. Trial of amitriptyline, topiramate, and placebo for pediatric migraine. N Engl J Med. 2017;376(2):115-124. doi:10.1056/NEJMoa1610384
25. Magnesium: Types, Dosing, and What the Research Shows
26. CoQ10: Benefits, Dosing, and Clinical Evidence
27. The Vagus Nerve: Your Body’s Built-In Calming System
28. The Gut-Brain Connection: How Your Digestive System Affects Your Mind
29. Hormones and Headache: What Women Need to Know