Migraines and Ionic Variances

Chronic migraine is considered to be a disabling neurological disease, treated with dangerous and often brain damaging medicines. A good summary of recent findings labels migraine as “an inherited, episodic disorder involving sensory sensitivity” 9 . While crucial findings like this have been made, and even with the medical community's understanding and acceptance of the previous section's genetic explanation, research of dietary factors is still missing. Why? There are several reasons but one of the fundamental ones is the belief that migraine is a disease. Research showed in 1951 that migraineurs excrete 50% more sodium in their urine than non‐migraineurs do and have “busy brains”. These findings suggest an important clue for the mechanism of migraines even without the understanding of the genetic connection. This clue led me to the recognition of a promising hypothesis, namely, the possibility that in some manner sodium depletion is involved in migraine onset and persistence. As far as I could ascertain, the question of “Why sodium is depleted?” has not been asked—though some resent research found support for an inverse relationship between migraines and the amount of dietary sodium consumed: the more sodium was consumed, the fewer migraines appeared. Migraineurs are much more likely to have metabolic disorders than non‐migraineurs. This is likely connected to electrolyte disturbance caused by exogenous glucose. The extreme response is caused by genetic variations of glucose transporters, ionic channels that manage electrolyte homeostasis, and associated proteins. Migraineurs appear to genetically be predisposed to other forms of metabolic diseases as well. Some of the most critical genetic variances that affect migraineurs are as follows (GeneCards database): CACNA1A Calcium voltage gated channel ATP1A2 ATPase, Na/K transporting SCN1A Sodium voltage gated channel NOTCH3 intercellular signaling pathway that plays a key role in neural development PRRT2 Proline Rich Transmembrane Protein 2; α‐amino acid that is used in the biosynthesis of proteins; potential endogenous excitotoxin KCNK18 potassium channel EDNRA Endothelin Receptor Type A activation result in elevation of intracellular‐free calcium SLC2A1 Solute Carrier Family 2 Member 1 facilitative transporters (allow solutes to flow downhill with their electrochemical gradients); secondary active transporters (allow solutes to flow uphill against their electrochemical gradient by coupling to transport of a second solute that flows downhill with its gradient such that the overall free energy change is still favorable) MTHFR Methylation of folate SLCxxx just about all solute carriers Together, these hint at major electrolyte dysregulation potential if proper nutrition is not provided. Migraine appears to share much in common with channelopathy. More research is needed to specifically examine the electrolyte dysfunction caused by exogenous glucose consumption in migraineurs and the associated CSD and migraine pain. Support or Funding Information The author received no funding or support. There is no conflict of interest. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .