top of page
  • Writer's pictureAmie Butler

Food for thought: migraine headaches.

If you suffer from migraine headaches you are not alone. If fact you will join the one in seven people globally.

A woman holding her head

Current research now understands that migraine headaches are a complex, genetic neurological disorder however, the exact mechanisms still remain much of a mystery. In recent studies, the role of dietary triggers and functional nutrients have been raised as possible targets for new migraine therapies consequently this provides scope for a personalised nutritional therapeutic approach to help those who suffer with this debilitating disorder.

What is a migraine?

Migraines are a complex phenomenon, however they can be defined as a sporadic headache disorder characterised by recurrent severe head pain along with nausea, vomiting, sensitivity to light and sound. Some may also experience visual, hearing and speech disturbances as well as physical numbness. Unlike other pain disorders, migraines do not have a diagnostic test which can make them easy to misdiagnose. This is because migraine symptoms and patterns vary from person to person. Every migraine sufferer has a different experience which makes migraines all the more complex.

Anyone who suffers from migraines will tell you that they can be extremely debilitating and incapacitating, particularly as they can sometimes last for days. They have an enormous impact on the quality of everyday life both at home and at work and have been estimated to account for twenty five million lost days from work or school each year. Migraines often begin during puberty and affect most adults between the ages of thirty five and forty five years. However, migraines are a predominantly female disorder as there are associations with migraines and the hormonal menstrual cycle.. Migraines are also now only just being understood as a hereditary disorder.

Current Treatments

For many years the main consensus was that abnormal blood flow to brain was the key factor contributing to the disorder. General orthodox treatments for migraines consist of over the counter pain killers, anti-inflammatory painkillers, anti-sickness medicines and prescribed triptans. Triptans are a well-established drug and were developed to selectively constrict the pain producing blood vessels and restore blood flow to the brain. However, a notorious drawback has been their chronic overuse and the paradoxical side effect of medication withdrawal migraines. Approximately thirty percent of migraines are now thought to be caused by medication overuse, worryingly ‘Medication Overuse Headaches’ (MOH) is now a common and well recognised term to describe this disorder.

Although orthodox treatments rely on medication, it is now generally understood within health care practice that pain medication does not prevent or improve migraine frequency/severity without additional diet, lifestyle and trigger interventions. Studies have found a number of factors can trigger migraines some of which include stress, fatigue, sleep deprivation, hormonal changes, nutrient deficiencies, allergies, alcohol as well as some foods such as cheese, chocolate and food additives18. Similarly, disorders such as obesity and celiac disease as well as depression and anxiety have been linked to migraines. The exact cause of migraines is still largely an unknown, however advances in the last decade have focused upon the neurological process of the trigeminovascular system, the sensory pain pathway in the brain9. Two neurological mechanisms which are thought to be involved are called Cortical spreading depression (CSD) and Calcitonin Gene Related Peptide (CGRP).

Cortical Spreading Depression

Up to a third of migraine suffers report visual or sensory changes known as migraine auras. The most common described aura is visual and involves flashing lights, tunnel vision or blind spots in the eyes which can last from five minutes up to an hour. Researchers now believe that the phenomenon CSD is the likely initial trigger event which is involved in migraine auras and subsequent migraine attacks. This is thought to be due to waves of spontaneous electrical activity followed by waves of inactivity which spread across the visual or sensory parts of the brain. CSD has also been suggested to be the underlying reason why migraine attacks are so painful. Although unproven in humans, CSD has been found to induce the brains trigeminal nerve system and heighten the sensitive sensory pain receptors. This theory explains that CSD could be a primary migraine event which then initiates the pain-related areas in the brain causing migraine headache.

There are many suggestions as to what may trigger CSD. Genetics may play a part as a brain more susceptible to migraine attacks may be due to hereditary factors, but there could also be a hormonal predisposition. The hormones oestrogen and progesterone have both been found to increase the frequency of CSD which could be one reason to explain why women are more prone to migraines. In animal studies changes in calcium channels which play a role in the process of neurotransmitter release has also been suggested. It is also now understood that magnesium deficiency can promote CSD and effect various neurotransmitters in the brain. Studies have shown that magnesium deficiency is significantly more prevalent in migraine sufferers and various trials have had successful results in migraine management when magnesium status had been rectified. Stress and lack of sleep which provoke inflammatory molecules have also been suggested to provoke or exacerbate CSD and migraine frequency.

Calcitonin Gene Related Peptide

The theory that CSD is the primarily cause of migraines remains disputed, however the idea that a hypersensitive trigeminovascular system, the sensory pathway in the brain, is still regarded as the main culprit of painful migraines. Specifically, the neurotransmitter CGRP which is released from the trigeminovascular nerves, has been found to be a pivotal inflammatory messenger which causes migraine pain. Levels of CGRP were found to be high in a study which tested migraine patients suggesting they could be strong factor in understanding migraine pain.

Similar to CSD, there appears to be many theories as to what may cause or contribute to CGRP9. Particular foods have been associated with increasing as well decreasing CGRP in the brain, highlighting the possible link between diet and migraine. Food components that activate CGRP include isoflavones found in soya, and nitrates which increase nitric oxide which are found in foods such as processed meats, wine and chocolate. Likewise foods such as ginger and grape extracts have been found to decrease CGRP. Recent research has also found that the prevalence of migraines with gastrointestinal inflammation disorders such as celiac disease, may be connected to the release of CGRP. Interestingly several studies which tested a gluten free diet on migraine sufferers found that their symptoms improved .

Migraines are a very personal disorder and every person will have their own unique triggers.

Given the myriad of possible migraine triggers involved in the neurological processes of a migraine and the unreliability and side effects of current migraine medication, there is now an increasing demand for tailored individualised and natural support for migraines. Migraines are a very personal disorder and every person will have their own unique triggers. This is where nutritional therapy can provide support by addressing the individual causes of migraines and not simply the symptoms.

What can I do to help?

Here are some dietary and lifestyle functional medicine approaches which may provide relief and positively impact on migraine symptoms.

Eliminate processed foods.

Try to eat foods as close to their natural state as possible. Food additives, preservatives and nitrates found in processed and prepared foods are well known migraine triggers and have been linked to CGRP release. Aim to make up the majority of your diet from fresh, organic is preferable, fruits and vegetables and whole unrefined foods as these will contain less trigger additives/preservatives.


It is now estimated that magnesium deficiency plays a role in most migraine headaches most likely because it is so essential for the regulation of neurotransmitters in the brain. Some studies have found that magnesium supplementation helped ameliorate migraine auras and the painful effects of CSD. Furthermore, a deficient magnesium status also contributes to symptoms of stress and anxiety which are both well-known migraine triggers. Food sources of magnesium include almonds, green leafy vegetables and pulses.

Go Gluten Free.

Gluten has been found to provoke migraine headaches via release of CGRP. A recent study found that migraines sufferers responded to a gluten free diet with fewer and reduced hadaches. Eliminating gluten from your diet for four to six weeks may help in determining whether gluten containing foods could be contributing to migraine symptoms.


Studies have found that ginger root may help in reducing migraine pain, this is because ginger has anti-inflammatory properties which prevent CGRP release and blood vessel changes in the brain. In studies which compared ginger and triptans for migraine pain, a 250 milligram capsule of powered ginger was found to be equally affective in relieving headaches with very little side effects. Ginger can be taken as a 250 milligram supplement when a migraine begins or could be used fresh grated into food or in juices.


One of the most effective ways to reduce migraines is reduce stress. Stress has been found to correlate in the production of CSD which leads to migraine pain which can create more stress and so the cycle continues. Introducing effective stress management strategies and techniques to cope with stressful situations may help reduce migraine frequency. Incorporating regular light exercise daily such as jogging three times a week or practicing yoga with meditation have both been proven to reduce migraine frequency and intensity.

If you would like help to support your migraines or health then contact Amie.

Registered Nutritional Therapist , DipION, mBANT, CNHC

Reference List

1. Steiner, T., Scher, A., Stewart, W., Kolodner, K., Liberman, J. and Lipton, R. (2003). The Prevalence and Disability Burden of Adult Migraine in England and their Relationships to Age, Gender and Ethnicity. Cephalalgia, 23(7), Abstract only. Available at: [Accessed 24 Mar. 2018].

2. NICE (2018). Migraine - NICE CKS. Available at:!topicsummary [Accessed 19 Mar. 2018].

3. Ying, G., Fan, W., Li, N., Wang, J., Li, W., Tan, G. and Zhou, J. (2014). Clinical Characteristics of Basilar-Type Migraine in the Neurological Clinic of a University Hospital. Pain Medicine, 15(7), pp.1230-1235. Available at: [Accessed 18 Mar. 2018].

4. NHS (2018). Diagnosis. Available at: [Accessed 18 Mar. 2018].

5. Migranetrust (2018). Facts and figures - The Migraine Trust. The Migraine Trust. Available at: [Accessed 18 Mar. 2018].

6. WHO (2016). Headache disorders. World Health Organization. Available at: [Accessed 23 Mar. 2018].

7. Arulmozhi, D., Veeranjaneyulu, A. and Bodhankar, S. (2005). Migraine: Current concepts and emerging therapies. Vascular Pharmacology, 43(3), pp.176-187. Available at: [Accessed 23 Mar. 2018].

8. Buse, D., Scher, A., Dodick, D., Reed, M., Fanning, K., Manack Adams, A. and Lipton, R. (2016). Impact of Migraine on the Family: Perspectives of People With Migraine and Their Spouse/Domestic Partner in the CaMEO Study. Mayo Clinic Proceedings, 91(5), pp.596-611. Available at: [Accessed 24 Mar. 2018].

9. Burstein, R., Noseda, R. and Borsook, D. (2015). Migraine: Multiple Processes, Complex Pathophysiology. Journal of Neuroscience, 35(17), pp.6619-6629. Available at: [Accessed 18 Mar. 2018].

10. Noseda, R. and Burstein, R. (2013). Migraine pathophysiology: anatomy of the trigeminovascular pathway and associated neurological symptoms, CSD, sensitization and modulation of pain. Pain, 154(Suppl), pp.S44–S53. Available at: [Accessed 24 Mar. 2018].

11. (2018). Migraine Treatment and Medication | Triptans. Available at: [Accessed 24 Mar. 2018].

12. Kristoffersen, E. and Lundqvist, C. (2014). Medication-overuse headache: epidemiology, diagnosis and treatment. Therapeutic Advances in Drug Safety, 5(2), pp.87-99. Available at: [Accessed 24 Mar. 2018].

13. Ahn, A. and Basbaum, A. (2005). Where do triptans act in the treatment of migraine?. Pain, 115(1), pp.1-4. Available at: [Accessed 24 Mar. 2018].

14. Bigal, M. and Lipton, R. (2006). Modifiable Risk Factors for Migraine Progression. Headache: The Journal of Head and Face Pain, 46(9), pp.1334-1343. Available at: [Accessed 25 Mar. 2018].

15. Weatherall, M. (2015). The diagnosis and treatment of chronic migraine. Therapeutic Advances in Chronic Disease, 6(3), pp.115-123. Available at: [Accessed 24 Mar. 2018].

16. Sun-Edelstein, C. and Mauskop, A. (2009). Foods and Supplements in the Management of Migraine Headaches. The Clinical Journal of Pain, 25(5), p.Abstract only. Available at: [Accessed 26 Mar. 2018].

17. Park, J., Chu, M., Kim, J., Park, S. and Cho, S. (2016). Analysis of Trigger Factors in Episodic Migraineurs Using a Smartphone Headache Diary Applications. PLOS ONE, 11(2), p.e0149577. Available at: [Accessed 26 Mar. 2018].

18. Alpay, K., Ertaş, M., Orhan, E., Üstay, D., Lieners, C. and Baykan, B. (2010). Diet restriction in migraine, based on IgG against foods: A clinical double-blind, randomised, cross-over trial. Cephalalgia, 30(7), pp.829-837. Available at: [Accessed 26 Mar. 2018].

19. Bond, D., Roth, J., Nash, J. and Wing, R. (2010). Migraine and obesity: epidemiology, possible mechanisms and the potential role of weight loss treatment. Obesity Reviews, 12(5), pp.e362-e371. Available at: [Accessed 26 Mar. 2018].

20. Swanson, S., Zeng, Y., Weeks, M. and Colman, I. (2013). The contribution of stress to the comorbidity of migraine and major depression: results from a prospective cohort study. BMJ Open, 3(3), p.e002057. Available at: [Accessed 27 Mar. 2018].

21. Cui, Y., Kataoka, Y. and Watanabe, Y. (2014). Role of cortical spreading depression in the pathophysiology of migraine. Neuroscience Bulletin, 30(5), pp.812-822. Available at: [Accessed 27 Mar. 2018].

22. The Migraine Trust (2018). Migraine with aura - The Migraine Trust. The Migraine Trust. Available at: [Accessed 27 Mar. 2018].

23. Charles, A. and Brennan, K. (2009). Cortical Spreading Depression—New Insights and Persistent Questions. Cephalalgia, 29(10), pp.1115-1124. Available at: [Accessed 29 Mar. 2018].

24. De Simone, R., Ranieri, A., Montella, S. and Bonavita, V. (2013). Cortical spreading depression and central pain networks in trigeminal nuclei modulation: time for an integrated migraine pathogenesis perspective. Neurological Sciences, 34(S1), pp.51-55. Available at: [Accessed 31 Mar. 2018].

25. Pietrobon, D. (2010). Insights into migraine mechanisms and CaV2.1 calcium channel function from mouse models of familial hemiplegic migraine. The Journal of Physiology, 588(11), pp.1871-1878. Available at: http://Insights into migraine mechanisms and CaV2.1 calcium channel function from mouse models of familial hemiplegic migraine [Accessed 29 Apr. 2018].

26. Mauskop, A. and Varughese, J. (2012). Why all migraine patients should be treated with magnesium. Journal of Neural Transmission, 119(5), p.abstract only. Available at: [Accessed 30 Mar. 2018].

27. Yeh, T., Huang, Y., Chen, P. and Chiu, H. (2016). Effects of Intravenous and Oral Magnesium on Reducing Migraine: A Meta-analysis of Randomized Controlled Trials. Pain Physician, 19(1). Available at: [Accessed 1 Apr. 2018].

28. O’Hare, M. and Cowan, R. (2017). Sleep and Headache. Sleep and Neurologic Disease, p.Abstract only. Available at: [Accessed 1 Apr. 2018].

29. Zhao, J., Harada, N., Kurihara, H., Nakagata, N. and Okajima, K. (2011). Dietary isoflavone increases insulin-like growth factor-I production, thereby promoting hair growth in mice. The Journal of Nutritional Biochemistry, 22(3), pp.227-233. Available at: [Accessed 1 Apr. 2018].

30. Gonzalez, A., Hyde, E., Sangwan, N., Gilbert, J., Viirre, E. and Knight, R. (2016). Migraines Are Correlated with Higher Levels of Nitrate-, Nitrite-, and Nitric Oxide-Reducing Oral Microbes in the American Gut Project Cohort. mSystems, 1(5), pp.e00105-16. Available at: [Accessed 1 Apr. 2018].

31. Slavin, M., Bourguignon, J., Jackson, K. and Orciga, M. (2016). Impact of Food Components on in vitro Calcitonin Gene-Related Peptide Secretion—A Potential Mechanism for Dietary Influence on Migraine. Nutrients, 8(7), p.406. Available at: [Accessed 2 Apr. 2018].

32. Mormile, R. (2014). Celiac disease and migraine: is there a common backstage?. International Journal of Colorectal Disease, 29(12), pp.1571-1571. Available at: [Accessed 3 Apr. 2018].

33. Doulberis, M., Saleh, C. and Beyenburg, S. (2017). Is there an Association between Migraine and Gastrointestinal Disorders?. Journal of Clinical Neurology, 13(3), p.215. Available at: [Accessed 3 Apr. 2018].

34. NIH (2018). Office of Dietary Supplements - Magnesium. Available at: [Accessed 4 Apr. 2018].

35. Costa, C., Tozzi, A., Rainero, I., Cupini, L., Calabresi, P., Ayata, C. and Sarchielli, P. (2013). Cortical spreading depression as a target for anti-migraine agents. The Journal of Headache and Pain, 14(1). Available at: [Accessed 3 Apr. 2018].

36. Boyle, N., Lawton, C. and Dye, L. (2017). The Effects of Magnesium Supplementation on Subjective Anxiety and Stress—A Systematic Review. Nutrients, [online] 9(5), p.429. Available at: [Accessed 6 Apr. 2018].

37. Lucía,, A., Farez, M., Calandri, I. and Goicochea, M. (2015). Headache In Patients With Celiac Disease And Its Response To Gluten-Free Diet (P3.043). Neurology, 84(15), p.Abstract only. Available at: [Accessed 7 Apr. 2018].

38. Maghbooli, M., Golipour, F., Moghimi Esfandabadi, A. and Yousefi, M. (2013). Comparison Between the Efficacy of Ginger and Sumatriptan in the Ablative Treatment of the Common Migraine. Phytotherapy Research, 28(3), pp.412-415. Available at: [Accessed 7 Apr. 2018].

39. Darabaneanu, S., Overath, C., Rubin, D., Lüthje, S., Sye, W., Niederberger, U., Gerber, W. and Weisser, B. (2011). Aerobic Exercise as a Therapy Option for Migraine: A Pilot Study. International Journal of Sports Medicine, 32(06), p.Abstract only. Available at: [Accessed 7 Apr. 2018].

40. Sathyaprabha, T., Kisan, R., Adoor, M., Nalini, A., Kutty, B., ChindandaMurthy, B., Sujan, M., Rao, R. and Raju, T. (2014). Effect of Yoga on migraine: A comprehensive study using clinical profile and cardiac autonomic functions. International Journal of Yoga, 7(2), p.126. Available at: [Accessed 7 Apr. 2018].


bottom of page