CoEnzyme Q10 and riboflavin: the mitochondrial connection

Abstract

Objective: We conducted a short review of relevant literature which contends that migraine is associated with a wide-spread metabolic abnormality of mitochondrial oxidative metabolism, leading to the use of riboflavin and coenzyme Q10 as prophylactic therapy for migraine.

Background: Riboflavin and coenzyme Q10 supplementation has been recommended widely as safe and effective prophylactic therapy for migraine. The background neurophysiological studies that led to the development of this therapy, which are extremely complex, deserve wider distribution.

Methods: A brief review of the relevant literature was conducted and summarized.

Results: Brain energy metabolism in migraine has been found to be abnormal in all types of migraine, making the migrainous brain hyper-responsive to many stimuli. The metabolic abnormalities are more severe in the more-severe types of migraine, such as hemiplegic migraine and migrainous stroke, but they are present both during and between attacks. The metabolic abnormality in migraine extends beyond the brain to platelets and muscles, as proven by techniques of biochemistry, muscle morphology, and nuclear magnetic spectroscopy. There are strong similarities between migraine and certain inborn errors of metabolism, the metabolic encephalomyopathies, in which patients suffer genetic abnormalities in mitochondrial energy production to produce lactic acidosis, stroke, and migraine headaches. The theory of migraine as a mitochondrial disorder seems to have abundant evidence. However, aside from the genetic abnormalities discovered for the familial hemiplegic migraines, molecular genetic studies in migraine have been negative until recently, when whole genome sequencing has now reported positive results.

Conclusion: Arising from these extensive neurophysiological studies, the treatment of metabolic encephalomyopathies with pharmacological doses of riboflavin and coenzyme Q10 has shown positive benefits. The same treatment has now been applied to migraine, adding clinical support to the theory that migraine is a mitochondrial disorder.