Migraine is not a bad headache. It is a neurological condition involving cortical spreading depression, trigeminal nerve activation, and a sensitization of pain pathways that can last for hours to days. The pain is typically pulsating, usually on one side, moderate to severe, and worsened by routine activity. Most migraines come with nausea or vomiting, and significant sensitivity to light and sound. About 30% come with aura — visual disturbances, tingling, or speech difficulty that precede the headache.
Migraine is the second most disabling condition in the world by years lived with disability. It affects approximately 15% of the global population and is three times more common in women than men. In India, it is systematically under-recognised and undertreated — a large proportion of people with frequent migraines are told they have “tension headaches” or “sinusitis,” diagnose themselves with both, and take inappropriate medication that worsens the condition over time.
What actually triggers a migraine
Migraine has a threshold, not a single cause. Think of it as a bucket: the brain’s migraine threshold determines how full the bucket is before it overflows into an attack. Triggers do not cause migraines — they tip an already filling bucket over the edge. This matters because removing one trigger often does not stop attacks; the bucket needs to be emptied by raising the threshold.
The most reliable triggers across the literature: sleep disruption (both too little and too much — the “weekend migraine” from sleeping in is common), hormonal fluctuation (many women have attacks premenstrually when estrogen drops sharply), dehydration, fasting or skipping meals, strong sensory stimulation (bright light, strong smells, loud noise), weather changes, and alcohol (particularly red wine and beer).
One of the most useful things to do is keep a headache diary for at least eight weeks — recording the date, duration, severity, sleep the previous night, meals, menstrual cycle, and any identifiable exposures. A pattern often emerges, and identifying it is usually more useful than an elimination diet.
The medication overuse trap
This is the issue I see most often in patients who present with daily or near-daily headaches. Taking pain medication or triptans more than 10–15 days per month causes medication overuse headache (MOH) — a condition where the treatment becomes part of the cause. The brain downregulates its pain suppression systems in response to frequent pain medication, making it more sensitive to pain over time.
Common culprits in India: combination analgesics with caffeine (Saridon, Dart), paracetamol, NSAIDs, and triptans. If you are taking any of these more than 10–15 days per month for headaches, you likely have MOH contributing to your headache frequency, regardless of the original migraine pattern.
Managing MOH usually means stopping the overused medicine under your doctor’s guidance, which can be uncomfortable for two to six weeks as the brain readjusts — combined with preventive migraine therapy. This is a conversation that requires a neurologist or a doctor experienced with headache medicine, but understanding the mechanism is the first step.
Magnesium: a low-risk option worth discussing with your doctor
Magnesium deficiency is more common in migraineurs than in the general population, and migraine attacks are associated with reduced magnesium in cerebrospinal fluid. Intravenous magnesium is used in hospital settings to abort acute attacks. Oral magnesium supplementation (400–600 mg of magnesium glycinate or citrate daily) has consistent evidence for reducing migraine frequency in preventive trials — the 2012 American Headache Society guidelines classify it as probably effective for prevention.
I start most of my migraine patients on magnesium unless there is a contraindication. It takes six to eight weeks to see the full effect. Side effects are minimal at this dose (loose stools if too much is taken, which resolves with dose reduction). The cost is trivial and the evidence is reasonable. It is one of the interventions I would recommend starting before moving to prescription preventives in episodic migraine.
Riboflavin (vitamin B2) and CoQ10
Riboflavin at 400 mg daily has evidence for migraine prevention from several small randomized trials. It is thought to work through mitochondrial energy metabolism — migraine brains may have impaired mitochondrial function between attacks, and riboflavin addresses this. It is well-tolerated (turns urine bright yellow, which is harmless), inexpensive, and classified as probably effective by headache societies.
Coenzyme Q10 at 300 mg daily has similar evidence and similar proposed mechanism. Either alone or combined with magnesium and riboflavin, these nutritional supplements have a reasonable evidence base and a favorable side effect profile. They are not a replacement for prescription preventives in patients with frequent or severe migraine — but they are a sensible starting point for patients with less frequent attacks who prefer to avoid daily medication.
Sleep — perhaps the single most modifiable risk factor
Sleep disruption is both a trigger for individual attacks and a driver of migraine frequency over time. Poor sleep increases central sensitization — the brain’s pain amplification — making migraine attacks more likely and more severe. Consistent sleep timing (the same bedtime and wake time every day, including weekends) is one of the most reliably effective lifestyle modifications for migraine frequency. The “weekend migraine” pattern I mentioned is often largely a sleep timing problem.
For patients with insomnia and migraine: treating the insomnia is as important as treating the migraine. They are often mutually reinforcing — migraines disturb sleep, and poor sleep triggers migraines. Breaking this cycle requires addressing both.
Regular meals and hydration
Fasting and meal skipping are among the most common and easily modifiable migraine triggers. The mechanism involves hypoglycemia and cortisol fluctuation. For patients whose migraines reliably follow missed meals: eating every four to five hours, including protein at each meal, and keeping a regular meal schedule significantly reduces attack frequency in many patients.
Dehydration is similarly well-documented as a trigger. 2–2.5 litres of fluid daily, spread through the day, is a reasonable target. This is not about over-hydrating but about avoiding the dehydration that many patients sustain chronically by drinking mainly when thirsty.
Exercise and migraine — a nuanced relationship
Regular aerobic exercise reduces migraine frequency over time in multiple studies — the mechanism is thought to involve endorphin release, reduced central sensitization, and improved sleep quality. However, vigorous exercise can trigger an acute attack in some people, particularly in those who are dehydrated, have not eaten, or are at a vulnerable point in their hormonal cycle. The approach: begin exercise gradually, stay hydrated, eat before vigorous sessions, and aim for consistency at moderate intensity rather than occasional intense effort.
When to seek preventive medication
Preventive medication is appropriate when: migraines occur more than four days per month, individual attacks are severely disabling, acute medications are needed more than eight days per month, or lifestyle and supplement approaches have been optimally applied for two to three months without adequate response. First-line preventives include beta-blockers (propranolol, metoprolol), topiramate, valproate, and amitriptyline. CGRP antagonists are newer and highly effective but currently expensive in India.
The most important thing about migraine treatment: it is not just about stopping the pain — it is about reducing the frequency. Acute medication manages attacks; preventive treatment reduces how often they happen. Both are necessary for patients with frequent migraine, and neither alone is sufficient.
