In a new post on my main blog I discussed my most recently published academic article, which explains what migraine is, what causes it, and also what can be used to help prevent it.

The blog article can be found here. I copy-paste here the blog:

What is Migraine?

I bet your answer is “headache” and some of you may also say “aura”. Many of you will say that it is a neurological disease and that it is a strong headache. Are any of you correct? A most recent article, published in the Frontiers in Nutrition, explained what migraine is, what causes it, how, why, who gets migraines, when, and why, eloquently. And I may say so since the author is me.

I summarize the article for you here in very short and add some information that was not part of the article.

Migraine vs Headache Defined

This definition is not part of the article. I define it here so that you can see the huge differences.

Migraine–Definition

1. Headache is optional
   • Unilateral headache (pain on one side of the head)–no exceptions
   • Pain is dull and doesn’t throb
   • Pain doesn’t move around in the head during the migraine phase
   • Pain lasts minimum 4 hours–typically 3 days
   • Doesn’t increase or decrease based on position–such as banding forward won’t increase pain
   • Pain starts low and intensifies over several hours
2. Aura optional
   • Classic color “rainbow” type
   • Black and white chainsaw type
   • Any kind of flickers, lines, dots, spots, blindspot, broken images (Alice in Wonderland), flashlight from the back of the eyes, fog, snow, rain, tunnel vision, etc., are visual disturbances that are referred to as scintillating scotomas, which are also auras but without definition.
3. Sensory disturbances, such as phantom sounds or odors, are optional but quite typical
4. Preceded by at least one prodrome. Some typical prodromes:
   • Ptosis of one eye
   • Visible edema around the eyes unevenly, bigger around one eye
   • Excessive urination
   • Nausea
   • Dizziness
   • Vertigo
   • Mood changes
   • Sensory sensitivity–increased sensitivity to light, sound, odor, touch, taste
   • Vomiting
   • Irritable Bowel Syndrome (IBS)
   • Cyclical Vomiting Syndrome (CVS)
5. The migraine itself
   • Possible pain
   • Possible aura
   • Comprehension difficulties
   • Usually nausea and/or vomiting
   • Possibly slurring of words or incomprehensible speaking
   • Possibly can’t hear or can’t speak or can’t see
   • Partial paralysis on one side in the case of Hemiplegic migraine presentation
   • Possible vertigo, dizziness, IBS, CVS
6. Postdrome

Headache–Definition

1. Headache is mandatory
2. Pain in the head anywhere
3. Pain can move from side to side to top of the head to back of the head, to face, whole head
4. It often throbs and intensifies when bending forward

Confusing Elements

I hear arguments all the time that migraine comes with, starts with, or is caused by cervicogenic pain. Cervicogenic (neck area) can most certainly be affected because there are some comorbidities with migraine. One of the most common comorbidities is Ehlers-Danlos Syndrome (EDS). People with EDS have weakened and overly stretchy connective tissues and so their vertebrae are weakly connected and tend to cause much pain. As a result, the cervicogenic area (neck and upper shoulders) is more sensitive for most migraineurs who have EDS as well. While the cervicogenic pain can add to a migraine and may even initiate stress responses that start migraine itself, cervicogenic pain is neither the cause of migraine, nor the outcome. It is a coincidental condition associated with EDS, which needs special attention.

Some people also mention TMJ–a condition with jaw bones misalignment–as a migraine cause. However, this too is just a connection rather than causation. Fixing the TMJ by proper dental care won’t prevent or cure migraine, but it will lessen the discomfort that is associated with TMJ and which is very specific to the chewing muscles and can cause strong headaches.

Migraine Cause

The cause of migraine is an electrolyte imbalance, specifically, not enough sodium in the extracellular space of the sensory neuron (s) to initiate action potential. Action potentials spread information in the nervous system to connected neurons and propagate commands to the periphery. If the action potential fails at any Node of Ranvier, the neuron’s communication is stopped, and instructions never reach their intended target. The neuron moves back into resting state with voltage-gated sodium channels closed. The symptoms resulting from blocked or malfunctioning sodium channels or insufficient sodium at the channels are: seizures, altered mental status, hypotension, prolonged QRS (ventricular depolarization in the heart), a terminal R-wave in lead to aVR (57), edema, swelling of the brain, coma, death, and I argue that this list should also include migraine…

The sensory neurons in the brain of a migraineur have more connections (73) than in the brain of those without migraine and these connections themselves also differ from the norm (74). Migraine brain seems to always be “on,” as migraineurs have only nominal changes in voltage between states of action potential and resting potential (75–77). Clearly, the brain of a migraineur is anatomically different from the brain of a non-migraineur, and as a result, it has been called the hypersensitive brain (78). The sensory neurons in mammals evolved during periods of high vulnerability levels, when vigilance was a major component of survivability, and the heightened sensory sensitivity presented a survival advantage.

Why Mostly Women & Children?

Most migraineurs are women and children in our modern world. Why? The article provides an explanation for that as well:

Why females and children are more vulnerable can also be explained by the hypothesis. Generally men were the hunters, carrying weapons, and the success rate of a predator killing a hunter was likely quite low. By contrast, women and children were left behind to gather—squatting or bending down without weapons, they are the ideal pray for a predator. As a consequence, this group developed and retained stronger sensory organ systems, especially for the time of their heightened vulnerability. Before puberty, more boys have migraines than girls (81). Boys became hunters at or shortly after puberty and correspondingly we see most boys losing their migraines after puberty (81). In our modern Western civilized world humans have no need for keen sensory organs against predators, and so it makes sense that such an energy sink would have devolved by adapting to a less sensitized human lifestyle with reduced ability to sense.

Nutrition, Salt, and Migraine

Overwhelming anecdotal evidence suggests that the application of any of the low carbohydrate diet forms: LCHF, ketogenic, and carnivore, provided they are well-formulated for health with sufficient protein and fats, should be helpful in preventing migraine, but the reason why it is so, is often misunderstood. For example, a small trial concluded that the ketogenic diet is likely beneficial because it helps people lose weight and migraine sufferers are overweight (188). Interestingly there are many studies pointing to migraineurs being overweight (189, 190), yet my experience in working with thousands of migraine sufferers from around the world is that they are not overweight—in fact many are underweight as a result of being unable to eat while they are so often in pain. Regardless, weight loss on its own is not likely to lead to the reduction of migraine given that it is a genetic condition of ionic channel variants and the brain’s glucose intolerance (191). Rather, with the help of the hypothesis laid out in this paper we can understand that it is the reduced carbohydrates in the ketogenic and other low carbohydrate diets, especially the carnivore diet, and the increased salt that provide relief for migraine sufferers…

Why any of the low carbohydrate diets are beneficial is clear considering the carbohydrate sensitivity of the brain and the associated osmolality changes. As noted earlier, ketones are the preferred fuel for the brain that has glucose metabolism difficulties (192). Ketones in the brain are 3β-Hydroxybutyrate (3HB) and acetoacetate, which are fatty acids of medium chain triglycerides that can easily cross the blood brain barrier (193) and provide the fuel with great efficiency (194–196). Ketogenic diets have had great success with epileptic seizures (197), as well as Alzheimer’s disease, Multiple Sclerosis, and a host of other neurodegenerative diseases. The use of ketones by most brain functions defers the use of glucose to the glial cells (198). When we reduce glucose to the brain, we are also reducing glucose to the body. The ensuing fundamental changes lead to reversal of metabolic disease and re-establishment of insulin sensitivity in general, which improves the brain’s insulin sensitivity as well (181, 182, 199, 200).

I hope you enjoy reading the article.

Comments are welcome, as always, and are moderated for appropriateness.

Angela