By Benjamin Taimoorazy, MD FAHS - Nov 6, 2023
Migraine is a neurological dysfunction and a major cause of disability. It is estimated that about 15% of the general population suffer from this disabling headache disorder. In individuals predisposed to migraine headaches, certain areas within the brain react in an exaggerated manner to a variety of triggers which initiates the cascade of events resulting in the excruciating throbbing pain of migraine headaches with associated symptoms of nausea, light and sound sensitivity and dizziness.
Research into human brain activity reveals that migraine is a metabolic abnormality of the brain with increased oxidative stress and decreased antioxidant capacity. This susceptibility is due to abnormal metabolic activity and or lower levels of certain essential nutrients which ultimately results in an energy deficiency syndrome at the mitochondrial level in the brain. Mitochondria is the powerhouse of every cell in our body. This oxidative stress predisposes the brain of migraineurs to the start of a cascade of events that culminates in an inflammatory process resulting in the throbbing pain of migraine headaches.
The most important pathophysiological event is the release of a neurotransmitter called Glutamate and the activation of NMDA receptors. This event in turn initiates a process called cortical spreading depression or CSD. Cortical spreading depression basically is a slow wave of brain activity (depolarization) that travels across the surface of the brain and ultimately results in the trigeminal neuronal release of CGRP and substance P. The release of these neurochemicals is responsible for the vasodilation and mast cell degranulation which causes increased vascular permeability (leaky blood vessels), neurogenic inflammation and sensitization of the meningeal nerve fibers during an attack of migraine.
This nociceptive or painful information is then transmitted along the trigeminal nerve to the trigeminal nucleus in the brain stem and from there to the thalamic nuclei and the cerebral cortex where migraine pain is perceived. With its unique formulation and with supplementing the brain with the essential nutrients that it may be lacking, MiGuard may not only decrease the sensitivity of the brain to the migraine triggers but it may also disrupt all or most of the cascade of events that are responsible for the full blown headache of migraines. In that respect, nutritional supplementation has been shown to be very beneficial in managing this disabling primary headache disorder.
Watch this video below to learn more on how migraine affects your brain
The objectives for this clinical study were to compare the efficacy and safety of MiGuard with other popular nutritional supplements used to manage migraine headaches.
Study design: Retrospective comparative analytic study based on patient interviews and feedback.
Subjects: 100 patients, equally divided into Arm 1 and Arm 2, between ages of 18 to 50, suffering from 8 or more migraine headache attacks with or without aura (based on the International Classification of Headache Disorders, 3rd Edition - ICHD-3 criteria for migraine headaches) receiving MiGuard, which contains a proprietary formulation of Alpha Lipoic Acid (ALA), Magnesium, Ginger, Feverfew, Coenzyme Q-10 and Riboflavin (Arm 1), vs other nutritional supplements containing a combination of Magnesium, Coenzyme Q10, Riboflavin, and Butterbur (Arm2).
Methods: Review of outcomes in regards to safety and the decrease in frequency of migraine headaches after an uninterrupted use of the supplements in (Arm 1) and (Arm 2) for more than 90 days based on the manufacturers recommendations:
No severe adverse effects were reported by patients in either groups except for moderate increased frequency of bowel movements in (Arm 2) when 4 patients had to discontinue the use of the supplement. This was attributed to the high concentration of Magnesium in the (Arm 2) supplements. As expected both groups reported a neon yellow discoloration of the urine due to Riboflavin which is of no consequence.
After 90 days, the reported decrease in headache attacks was 74% in (Arm 1) as opposed to 42% in (Arm 2) of the study which was statistically significant.
Results: Recent evidence supports that migraine is a nutritional deficiency syndrome of the brain and causes a sterile neuroinflammatory reaction in the trigemino-vascular complex. It has been demonstrated that more than 90% of patients suffering from high frequency migraine headaches have significantly deficient levels of ALA in their bloodstream. MiGuard has a unique proprietary formulation to include ALA in conjunction with the other essential ingredients and provides the brain with anti-inflammatory, anti-Glutaminergic, anti-CGRP, anti-oxidant and neurostabizing properties. MiGuard provides the most physiologic and synergistic nutritional support for healthy brain function. Due to safety concerns (potential hepatotoxicity) Butterbur was not included in the formulation of MiGuard.
As Migraine could be decades long neurological dysfunction, the safety of nutritional supplementation especially if containing Butterbur (even PA free Butterbur) must be brought into question. Long term exposure to Butterbur has been associated with severe hepatic injury and liver failure. This side effect seems to be due to Pyrrolizidine Alkaloids (PA) present in some Butterbur products. Long term safety of PA free Butterbur is still not established.
Conclusion: Based on this retrospective study, MiGuard seems to be safe and highly effective in decreasing the frequency of migraine headaches with or without aura.
Correspondence:
Benjamin Taimoorazy, MD FAHS
Beverly Hills Migraine & Pain Management Institute
Beverly Hills, CA 90210
Guardian Headache & Pain management Institute
Bloomington IL 61704
Faculty of medicine, University of Illinois, Urbana/Champagne info@getmiguard.com