Warning: This essay contains heretical ideas which, if adopted, are unlikely to make anyone rich.

For most of my long life, there really hasn't been any progress in understanding the mechanism of the migraine, i.e., how one thing leads to another, based on observations of typical sufferers and basic physics and chemistry.  Back in the 1970s, it was observed that ergot derivatives, which have a constricting effect, taken in the first two hours of the migraine (perhaps when the aura was happening), stopped it.  But since then, attention has drifted away from the role of the cardiovascular system and toward speculation about neurological, endocrinological, and even psychological aspects.  Many studies have zeroed in on specifics such as particular hormones, getting ever farther away from the big picture.  Treatment of migraines has been apparently pretty lucrative, however.

I would like to propose a new model: the classic migraine, consisting of an "aura" of well-known neurological symptoms as well as of the headache, is fundamentally a low-cholesterol condition.  Cholesterol is an important part of cell membranes, and in that role, modulates the flexibility of artery walls.  We all know what happens when there is too much cholesterol there, i.e., what's popularly called "hardening of the arteries": artery walls become too rigid to pump blood around the body.  But what if there is too little?  The artery walls could become extremely elastic and bulge out either when 1) too much salt or sugar is absorbed into these tissue cells, or 2) there are too little of these nutrients in the artery lumen, thereby drawing water into these tissue cells via osmosis.  If arteries in the brain bulge ("dilate") too far, they could block the lumen of the artery, temporarily starving the brain of nutrients.  This could be what triggers the aura, which typically causes visual hallucinations popularly called "scintillating scotomas" and miscellaneous other brain malfunctions.  In this case, the brain responds by constricting the artery walls, opening up the lumen but causing a headache as a result of the increased pressure. 

This constriction, which ends the aura and begins the headache, could have thrown researchers off, causing them to ditch the "dilation theory" when they found that migraine headaches were not accompanied by artery dilation; "they saw that people experimencing a migraine didn't appear to have dilated vessels as expected" (Hamzelou This is consistent with the model described above: dilation occurs only during the aura.

Why would low cholesterol be suspected on the basis of observed characteristics of migraine sufferers?  The classic target of the migraine seems to be a slender woman in her twenties who takes birth control pills; those who take statins, even older people, are also known to have migraines, especially if they take enough to get down to a total cholesterol level of 120 mg/dL.   Would our medical establishment be willing to consider that there is an ideal level of cholesterol in cell membranes, and that this is not as low as possible?

REFERENCES

Hamzelou J (2022) Taming Migraine.  New Scientist Spring 2022 16-20.  Retrieved 22 Apr 2022 from https://www.newscientist.com/article/mg25333713-100-we-are-finally-beginning-to-understand-migraines-and-how-to-treat-them/