There are many articles on the connection of metabolic disorder and migraines [1-7] but nearly all end with the statement “we do not yet understand the connection.” Well let’s end that non-understanding and convert it into full understanding: I will help you see it.

I summarize here some facts for easy understanding:

1) Migraine is a symptom of hyper sensory organ sensitivities that cause lack of enough energy simply because the migraine-brain uses more energy than the brain of a non-migraineur [8-10]

2) To retain enough energy, it is important to keep stable electrolyte with high concentration of sodium chloride (salt) [11]

3) Carbohydrates convert to glucose – simple carbohydrates convert very fast [12]

4) Glucose disrupts electrolyte balance [13]

5) Insulin and serotonin release at the same time to allow for metabolism, digestion, and excretion [14]

6) Serotonin medicines increase or enforce serotonin manufacturing thereby releasing insulin [15, 16]

7) Conclusion: serotonin medicines contribute to metabolic disorder in migraineurs

Though I pretty much captured the cause and effect above in the numbered points, let me elaborate further.

Migraine is considered to be a disease but it seems to actually be a symptom of a very different brain type. A migraine brain has more connections between sensory organ neurons. This is clearly recognizable by a few simple observations in addition to what is now visible in the scanners:

migraineurs see better in the dark so they are disturbed by bright light [17, 18]; migraineurs have deeper hearing range and/or better hearing because what seems to be normal noise for others is loud for migraineurs [9]; migraineurs smell better the things around them so if a strong scent is put under their nose they get pain from being over sensitized [19]. There are many other factors of sensitivity migraineurs share; I know since I am a migraineur. What is important to note is that migraineurs need more brain energy in order to keep their voltage going on continuously and at high level. Migraineurs’ brain generates more electricity even in resting potential state than a non-migraineur’s brain does [20].

To retain high level energy the electrolyte supply needs to be kept balanced and at a higher sodium chloride concentration level all the time. Unfortunately there is a major electrolyte disturbing agent without which we cannot survive and that is glucose. Glucose is converted from carbohydrates by insulin (highly simplified here) but look at what happens when glucose enters the blood:

“…serum Na+ falls by 1.4 mM for every 100-mg/dL increase in glucose, due to glucose-induced H2O efflux from cells” [13] page 4.

This implies that as glucose moves into our blood, it instantly disrupts electrolyte by removing water from the cells (H2O efflux) and holding onto water outside of the cells, causing edema (something that until now science held sodium responsible for but in fact it is glucose). Note also that glucose also reduces sodium (Na+). Thus two key elements of electrolytes are disturbed: water and sodium.

Given that electrolyte disturbance leads to lack of proper energy supply for the neurons in the brain of a migraineur, we can already see that glucose plays a large role in migraine pain. Note also that, as stated above, glucose and serotonin release at the same time. This is of little concern if the migraineur actually eats something that insulin can break down into glucose and serotonin can then aid in pushing it forth in the intestinal tract but has anyone ever asked what happens if we artificially give extra serotonin or induce the creation of serotonin in migraineurs by medicines while they are not eating?

Migraineurs receive several types of medications, two types of which are prominently serotonin based: pain abortive medications or triptans and pain preventives in the form of SSRIs (selective serotonin reuptake inhibitors) or other similar medicines. Triptans add serotonin to the brain of a migraineur and SSRIs force the brain to make more serotonin by plugging the neurons’ “reuptake” (sensor to how much serotonin was already made) and thus inhibiting the neurons’ ability to stop serotonin production. Neurons on SSRI never shut down serotonin production.

This begs the question: if insulin and serotonin work together and serotonin medicines also release insulin, what does that insulin do to the migraineur who is not eating anything?

Insulin floating in the blood endlessly is ignored by the insulin receptors (cry wolf scenario), which leads to insulin resistance. Insulin resistance is diabetes mellitus 2. Diabetes mellitus 2 is metabolic disorder. Serotonin is one the key contributors to migraineurs having metabolic disorder. Carbohydrate metabolism disrupting electrolytes is the second major contributor.

The first cause, the medicinal one, can only be stopped if migraineurs are stopped being prescribed serotonin medications! The second one can easily be stopped by using the Stanton Migraine Protocol^TM.

Please take migraines very seriously! migraine brain is a brain that does not need medicines but needs more energy and proper carbohydrate consumption process.

Read how to prevent your migraines in Fighting the Migraine Epidemic – paperback  or e-book.

Comments are welcomed!

Angela

References

1. Bhoi, S.K., J. Kalita, and U.K. Misra, Metabolic syndrome and insulin resistance in migraine. The Journal of Headache and Pain, 2012. 13(4): p. 321-326.
2. Casucci, G., et al., Migraine and metabolism. Neurological Sciences, 2012. 33(1): p. 81-85.
3. Gozke, E., et al., An Observational Study on the Association between Migraines and Tension Type Headaches in Patients Diagnosed with Metabolic Syndrome. ISRN Neurology, 2013. 2013: p. 4.
4. Guldiken, B., et al., Migraine in metabolic syndrome. The neurologist, 2009. 15(2): p. 55-58.
5. Sachdev, A. and M.J. Marmura, Metabolic Syndrome and Migraine. Frontiers in Neurology, 2012. 3: p. 161.
6. Salmasi, M., et al., Metabolic syndrome in migraine headache: A case-control study. Journal of Research in Medical Sciences : The Official Journal of Isfahan University of Medical Sciences, 2014. 19(1): p. 13-17.
7. Sinclair, A.J. and M. Matharu, Migraine, cerebrovascular disease and the metabolic syndrome. Annals of Indian Academy of Neurology, 2012. 15(Suppl 1): p. S72-S77.
8. Schwedt, T.J., Multisensory Integration in Migraine. Curr Opin Neurol, 2013: p. 248-253.
9. Tso, A.R., et al., The anterior insula shows heightened interictal intrinsic connectivity in migraine without aura. Neurology, 2015: p. 1043-50.
10. James, M.F., et al., Cortical spreading depression and migraine: new insights from imaging? TRENDS In Neuroscience, 2001: p. 226-271.
11. Campbell, D.A., E.M. Tonks, and K.M. Hay, An Investigation of the Salt and Water Balance in Migraine. British Medical Journal, 1951: p. 1424-1429.
12. Aronoff, S.L., et al., Glucose Metabolism and Regulation: Beyond Insulin and Glucagon. Diabetes Spectrum, 2004. 17(3): p. 183-190.
13. Longo, D.L., et al., Harrison’s Manual of Medicine 18th Edition. 2013, New York: McGraw Hill Medical.
14. Robinson, R., Serotonin’s Role in the Pancreas Revealed at Last. PLoS Biol, 2009. 7(10): p. e1000227.
15. Ohara-Imaizumi, M., et al., Serotonin regulates glucose-stimulated insulin secretion from pancreatic β cells during pregnancy. Proceedings of the National Academy of Sciences, 2013. 110(48): p. 19420-19425.
16. Paulmann, N., et al., Intracellular Serotonin Modulates Insulin Secretion from Pancreatic β-Cells by Protein Serotonylation. PLoS Biol, 2009. 7(10): p. e1000229.
17. Digre, K.B. and K.C. Brennan, Shedding Light on Photophobia, in J Neuroophthalmol. 2012. p. 68-81.
18. Rossi, H.L. and A. Recober, Photophobia in Primary Headaches. Headache, 2015: p. Epub ahead of print.
19. Benemei, S., et al., TRPA1 and other TRP channels in migraine. The Journal of Headache and Pain, 2013. 14(1): p. 71.
20. Liu, H., et al., Resting state brain activity in patients with migraine: a magnetoencephalography study, in The Journal of headache and Pain. 2015. p. 16-42.