The recent BBC article made waves for finally recognizing what people with migraine have known all along: migraine isn't just a headache.
The BBC migraine article is a step in the right direction. But here's what the article, and most mainstream migraine research, still gets wrong.
The BBC article got one thing very right: many migraine "triggers" are actually early symptoms of an attack that's already begun.¹
For years, people with migraines have been told to avoid chocolate, cheese, perfume, light, stress, the list goes on. But what if it's not a sensitivity to chocolate, what if the brain is already energy-compromised, and the craving for chocolate is the body trying to signal that something's off?
This reframing matters. It moves us away from blaming external factors and toward understanding migraine as a pre-existing biological state that makes the brain more reactive to normal stimuli.
At Health By Principle, we've been saying this for years: migraine doesn't start when the pain starts. The attack begins hours, sometimes days, before you feel it. Our article Pre-Migraine Signs Explained breaks this down in more detail.
The BBC article does an excellent job cataloging what happens during a migraine:¹
Abnormal electrical waves in the brain (cortical spreading depression)
High levels of CGRP (calcitonin gene-related peptides)
Activation of the hypothalamus
Inflammation in the meninges
But here's the problem: these are all downstream mechanisms. They describe what migraine looks like once it's happening, not why it happens in the first place.
It's like describing a car overheating without asking why the engine is failing.
While the BBC focuses on genetic risk, electrical instability, and molecular markers, it never answers the fundamental question: Why does the migraine brain enter this unstable state at all?
The answer lies in brain energy and electrolyte balance.²⁻³
Migraine is not a random neurological event. It's a predictable metabolic failure that occurs when the brain doesn't have the energy or electrolytes it needs to maintain stable electrical function.²⁻⁴
When sodium-dependent neurons can't maintain proper ion gradients, the brain becomes electrically unstable.³⁻⁵ That instability cascades into:
Abnormal electrical waves (cortical spreading depression)⁶
Release of inflammatory molecules like CGRP⁷⁻⁸
Activation of pain pathways in the meninges⁹
All the symptoms mainstream medicine treats as the "disease"
But those aren't diseases. They're the alarm system.
The article celebrates CGRP-blocking drugs as a major breakthrough, noting that 70% of patients saw significant improvement.¹
And yes, those drugs can reduce suffering. But they don't restore normal brain function, they just mute the alarm.
Think of it this way: if your smoke detector keeps going off, you could remove the batteries. The alarm stops. But the fire is still burning.
CGRP drugs such as Aimovig (erenumab), Ajovy (fremanezumab), and Emgality (galcanezumab) silence pain signaling without addressing the underlying metabolic instability.¹⁰ Long-term, that means:
The brain remains energy-deficient
The risk of future attacks continues
Protective immune and vascular functions may be disrupted
Symptom suppression is not the same as healing.
A key limitation in the BBC article is how it describes migraine as a "cocktail of things going on," as illustrated by this line:¹
"There are multiple ways to get migraine and everybody's got a cocktail of things going on."
That's true. But the "cocktail" isn't random; it's metabolic.
Every factor the article lists: stress, fasting, hormonal fluctuations, sleep disruption, acidity changes affect brain energy and electrolyte balance.²⁻³
Stress increases energy demand
Fasting depletes glucose and sodium
Hormonal shifts affect fluid and electrolyte regulation
Sleep loss impairs cellular repair and ion balance
The BBC frames these mysterious, overlapping pathways. Health by Principle sees them as variations of the same underlying problem: the brain doesn't have what it needs to stay stable.
If you experience migraines, you don't need another drug that blocks a molecule. You need to restore the foundational conditions your brain requires to function without going into crisis mode.
That means:
Consistent electrolyte support (sodium, potassium, magnesium)
Stable blood sugar (to avoid glucose-driven crashes)
Adequate hydration (not just water, but mineralized fluids)
Vitamin D3 for immune and neurological baseline
Reducing inflammatory triggers in your diet
This isn't about perfection. It's about consistency.
Migraine research is finally moving in the right direction, recognizing that this is a whole-brain, whole-body condition with biological roots, not a personality flaw or a random curse.
But until mainstream science asks why the brain becomes unstable, not just what happens when it does, people with migraine will keep getting treatments that silence symptoms without solving the problem.
What does the brain actually need to stay stable, and how do we give it consistently?
The answer isn't blocking molecules. It's in restoring balance
Want to support your brain's foundational needs?
Read our other blog: Pre-Migraine Signs Explained
Explore our Electrolytes, Complete Magnesium, and Vitamin D3 formulas, designed for daily resilience, not just symptom management.
¹ BBC Future. "What Really Causes Migraines." February 2026. https://www.bbc.com/future/article/20260127-what-really-causes-migraines
² Stanton A. Electrolyte Homeostasis in Migraine. The FASEB Journal. 2017;31(1_supplement):1027.1. https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fasebj.31.1_supplement.1027.1
³ Zhang X, et al. Energy metabolism disorders in migraine: triggers, pathways, and therapeutic repurposing. Frontiers in Neurology. 2025;16:1561000. https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2025.1561000/full
⁴ Harrington M, et al. Is there a relationship between dietary sodium and potassium intake and clinical findings of a migraine headache? British Journal of Nutrition. 2021;126(9):1387-1397.
⁵ Antunes A, et al. Energy metabolism disturbance in migraine: From a mitochondrial point of view. Frontiers in Physiology. 2023;14:1133528.
⁶ Lauritzen M. Cortical spreading depression in migraine. Cephalalgia. 1994;14(1):47-54.
⁷ Iyengar S, et al. CGRP and the Trigeminal System in Migraine. Headache: The Journal of Head and Face Pain. 2019;59(5):659-681.
⁸ Durham PL. Calcitonin Gene-Related Peptide (CGRP) and Migraine. Headache. 2006;46(Suppl 1):S3-S8.
⁹ Russo AF. Calcitonin gene-related peptide (CGRP): Role in migraine pathophysiology and therapeutic targeting. Headache. 2015;55(9):1230-1242.
¹⁰ Deen M, et al. Blocking CGRP in migraine patients – a review of pros and cons. The Journal of Headache and Pain. 2017;18(1):96.