Electrolyte Homeostasis in Migraine

Abstract

Migraine is considered to be a neurovascular disease. Most research is aimed at reducing migraine pain by medications that either limit the activity of an overstimulated brain or add neurotransmitters that are presumed to be below ideal levels in a migraine brain (1, 2). In this presentation, a new view is discussed. Taking a closer look at metabolic deficits in migraineurs (3–9), we can see that it is their metabolic processes that disrupt electrolyte homeostasis prior to migraine. Some of these metabolic deficiencies are genetic and others are caused by medicines. The reestablishing of electrolyte homeostasis can prevent migraine. Migraineurs have special sensory sensitivities with sensory neurons that have more receptor connections than regular brains (10). Neurons that are more sensitized and have more receptor connections require higher ionic concentration electrolytes to keep their overactive work function. The lack of proper electrolyte is likely the cause of cortical depression and the ensuing cortical spreading depression—the wave that reaches the pain sensors in the meninges. A solution is offered for preventing pain without medical intervention by reducing electrolyte disrupting elements in the diet of migraineurs to the minimum required, such as glucose, and ensuring a constant proper electrolyte balance by a potassium and magnesium heavy diet with more sodium than what the average population uses. In the past three years of my observation of migraineurs in the Facebook group I specifically designed for reaching electrolyte homeostasis, all migraineurs can stop their medicines and remain migraine free—provided they maintain this balance.Support or Funding Informationno funding receivedno conflict of interest