I am slowly moving migraine as a metabolic disease in front of as many scientists as possible. As some of you know, I was elected to become a member of the American College of Nutrition (ACN) last year and finished their keto training course under the American Nutrition Association (ANA), which is a member of (or part of) the ACN. They have a conference coming up in November in San Diego, my neck of the woods, so I applied and got accepted into the poster session. This is the first nutrition-based academic organization where I present a poster on migraine, so it is exciting!
If you will be part of this conference, let me know! It would be great to meet. It is an academic conference, so it is not free to enter.
Because it is in a session on From Chronic Disease to Regeneration by Nutrition, the title of my submission contains the the session title.
Here is what was accepted:
Migraine: From Chronic Disease to Regeneration by Nutrition
Migraines are misunderstood by scientists and physicians. Migraines are either considered to be vascular disease(1), neurological disease(2), the combination of to two(3) or “mental disease”(4). Research also suggests that migraineurs may suffer from metabolic syndrome(5). Migraine is a form of channelopathy, where the brain places ionic and metabolic limitation on what a migraineur can safely eat without generating a migraine. Migraine is genetic and is defined by the following states: hyper-sensory brain(6); increased neuronal connections(7); extra voltage used by extra connections(8,9); channelopathy(10); glucose entering cells causes sodium efflux(11); migraine brain uses more sodium(12); kidney increase sodium by wasting potassium(13,14) and water; the renal system increases blood pressure(15); the reduced amount of sodium in circulation triggers increased production of aldosterone, cortisol, and adrenaline(16); cortisol and adrenaline increase glucose in the blood(17); when glucose enters the cells, sodium and water leave the cell, reducing sodium, which initiates the previous steps with adrenaline and cortisol11. This catch 22 cycle builds up to electrolyte imbalance, starting migraine. In this presentation, I hope to connect these disparate dots to form a coherent picture of migraine is and show how the proper nutrition may prevent migraines.
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2 Lipton, R. B. & Pan, J. Is migraine a progressive brain disease? JAMA 291, 493-494, doi:10.1001/jama.291.4.493 (2004).
3 Fabjan, A., Zaletel, M., #x17d & van, B. Is There a Persistent Dysfunction of Neurovascular Coupling in Migraine? BioMed Research International 2015, 11, doi:10.1155/2015/574186 (2015).
4 Antonaci, F. et al. Migraine and psychiatric comorbidity: a review of clinical findings. The Journal of Headache and Pain 12, 115-125, doi:10.1007/s10194-010-0282-4 (2011).
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8 Liu, H. et al. Resting state brain activity in patients with migraine: a magnetoencephalography study. The Journal of Headache and Pain 16, 42, doi:10.1186/s10194-015-0525-5 (2015).
9 Xue, T. et al. Intrinsic Brain Network Abnormalities in Migraines without Aura Revealed in Resting-State fMRI. PLOS ONE, e52927 (2012).
10 Albury, C. L., Stuart, S., Haupt, L. M. & Griffiths, L. R. Ion channelopathies and migraine pathogenesis. Molecular Genetics and Genomics 292, 729-739, doi:10.1007/s00438-017-1317-1 (2017).
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13 Huang, C.-L. & Kuo, E. Mechanism of Hypokalemia in Magnesium Deficiency. Journal of the American Society of Nephrology 18, 2649-2652, doi:10.1681/asn.2007070792 (2007).
14 Muto, S., Asano, Y., Okazaki, H. & Kano, S. Renal Potassium Wasting in Distal Renal Tubular Acidosis : Role of Aldosterone. Internal Medicine 31, 1047-1051, doi:10.2169/internalmedicine.31.1047 (1992).
15 Sharma, R. S., Sandeep;. in Physiology, Blood Volume (StatPearls Publishing, 2018).
16 Goldstein, D. S. Adrenal responses to stress. Cellular and molecular neurobiology 30, 1433-1440, doi:10.1007/s10571-010-9606-9 (2010).
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