One of the more useful things to understand about migraine is that the chocolate probably did not cause it.
People with migraine often notice they craved chocolate, or cheese, or something sweet, shortly before an attack — and conclude the food was the trigger. Studies of the migraine prodrome suggest the opposite in many cases: the craving is itself an early symptom of an attack that had already begun in the brain, hours before the pain. The food is a passenger, not the driver.
That single reframing changes how people manage the condition, and it is a good illustration of why migraine is poorly served by being lumped in with ordinary headaches.
Migraine is not a headache with extra steps
Migraine is a neurological disorder affecting roughly one in seven people worldwide, more commonly women. The head pain is one feature among several, and some people have migraines with no head pain at all.
An attack typically moves through phases:
Prodrome, hours to a couple of days before the pain. Yawning, food cravings, mood changes, neck stiffness, increased urination, difficulty concentrating, unusual fatigue or unusual energy. Many people learn to recognise their own prodrome reliably, which matters because treatment works better when started early.
Aura, in about a quarter of people. Most commonly visual: a shimmering blind spot, zigzag lines, or a slowly expanding arc of flickering light, usually developing over 5 to 20 minutes and resolving within an hour. Aura can also involve tingling that marches up an arm, or difficulty finding words. It reflects a slow wave of altered electrical activity spreading across the cortex.
Headache, typically but not always one-sided, throbbing, moderate to severe, worsened by movement, and accompanied by nausea and by sensitivity to light and sound. Untreated, it lasts 4 to 72 hours.
Postdrome, the "migraine hangover." Fatigue, foggy thinking, and a wrung-out feeling that can last another day.
What is actually happening
The old explanation — that migraine is fundamentally a blood-vessel problem — is outdated. Current understanding places the origin in the brain and nervous system, with vascular changes as a consequence rather than a cause.
The migraine brain appears to be hyperexcitable: less able to filter and habituate to sensory input. During an attack, the trigeminal nerve system becomes activated and releases inflammatory signalling molecules, notably a peptide called CGRP, which produces pain and sensitisation. This is why light, sound, smell, and even ordinary touch become unbearable — the sensory system's normal gating is failing.
Genetics play a substantial role. Migraine runs in families, and having a first-degree relative with migraine markedly increases risk.
Real triggers, and the ones that get blamed unfairly
Trigger identification is genuinely difficult, because attacks often require several factors to align, and because prodrome symptoms masquerade as triggers.
Reasonably well supported:
- Irregular sleep — both too little and too much, and especially disrupted schedules. Migraine is strongly tied to circadian rhythm.
- Skipped meals and dehydration.
- Hormonal fluctuation, particularly the drop in oestrogen before menstruation. Menstrual migraines are often more severe and more treatment-resistant.
- Alcohol, especially red wine, and often within a few hours rather than the next morning.
- Stress — but frequently the let-down after stress rather than the stress itself. Weekend and holiday migraines are a recognised pattern.
- Weather and barometric pressure changes, for a subset of people.
- Bright, flickering, or glaring light.
- Overuse of acute painkillers, which causes medication-overuse headache — a common and underdiagnosed cause of headaches becoming chronic.
Weaker than commonly assumed:
- Chocolate, cheese, citrus, and most other specific foods. Controlled challenge studies have generally failed to reproduce the effect.
- Monosodium glutamate, which has poor supporting evidence despite decades of reputation.
- Caffeine, which is genuinely double-edged: it helps acute attacks and is an ingredient in many migraine medications, but regular high intake and withdrawal both provoke headaches.
A headache diary — recording sleep, meals, stress, cycle, and attacks over two or three months — is more reliable than memory, which systematically over-attributes attacks to memorable causes like unusual foods.
What helps during an attack
Timing matters more than most people realise. Treating early, while pain is still mild, is substantially more effective than waiting to see whether it becomes severe.
Over-the-counter options work for many people, particularly NSAIDs, sometimes combined with an anti-nausea medication, because the stomach's emptying slows during an attack and oral drugs are absorbed poorly.
Triptans are migraine-specific prescription drugs and remain the standard acute treatment for moderate to severe attacks. They work best taken early. They are not appropriate for everyone, particularly people with certain cardiovascular conditions.
Newer options include gepants, which block CGRP directly, and ditans. These have expanded choices for people who cannot take triptans or do not respond to them.
Non-drug measures that many people find genuinely useful: a dark, quiet room; cold applied to the head or neck; sleep, which frequently aborts an attack outright; and avoiding the temptation to push through with screens and activity.
The critical caution is frequency. Using acute painkillers on more than about 10 to 15 days per month, depending on the drug, risks converting episodic migraine into chronic daily headache. If you are reaching for medication that often, that is the signal to discuss prevention rather than to take more.
Prevention
Preventive treatment is usually considered when attacks are frequent, disabling, or not responding well to acute treatment.
Established preventive medications include certain beta blockers, some antidepressants, and several anti-seizure drugs — all repurposed, all with their own trade-offs. More recently, monoclonal antibodies targeting CGRP or its receptor have been developed specifically for migraine prevention and are given monthly or quarterly. For chronic migraine, botulinum toxin injections have an established role.
Non-drug prevention with reasonable supporting evidence includes regular aerobic exercise, consistent sleep and meal timing, and cognitive behavioural approaches and biofeedback. Some supplements — magnesium, riboflavin, and coenzyme Q10 among them — have modest evidence, and are worth discussing with a doctor rather than self-prescribing indefinitely.
When to seek urgent assessment
Some headaches are not migraine and need immediate attention:
- A sudden, severe headache that reaches maximum intensity within seconds to a minute.
- Headache with fever, neck stiffness, confusion, weakness, or difficulty speaking.
- Headache after head injury.
- A significant change in your usual headache pattern, or a first severe headache after age 50.
- Headache that consistently worsens when lying down, coughing, or straining.
The short version
Migraine is a neurological condition with distinct phases, not a severe headache. Many perceived food triggers are actually prodrome symptoms. The best-supported lifestyle levers are regular sleep, regular meals, hydration, and managing stress let-down. Acute treatment works best taken early, and using it too often makes the problem worse. Effective prevention exists, including drugs designed specifically for migraine — so frequent attacks are a reason to see a doctor, not to keep buying larger boxes of painkillers.
This article is general information and not a substitute for individual medical advice.
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