Migraine: It's not all in your head01 December 2018
“Intense throbbing pain, with a vice-like grip, and every bright spot of light, or minor sound becoming a searing aggravation”, are the words used to describe a migraine attack from a frequent sufferer (1). The official classification from the International Headache Society isn’t far different, defining migraines as episodic in nature, lasting between 4 and 72 hours, with symptoms including one-sided intense head pain, nausea, vomiting, and sensitivity to light or sound(2,3). In addition, some 25% of migraineurs experience sensory disturbances involving flashing lights or a loss of vision, known as auras(2,4).
It is estimated that migraine attacks effect one in seven people worldwide(5), with 1 in 10 in the UK suffering(6); so it is little wonder that migraines are the leading cause of neurological disability(5). Despite their prevalence, migraine mechanisms and pathways are yet to be fully understood due to the complex processes involved. In the last decade, the thinking around migraines has changed, as it was once considered a vascular disorder. Recently however, there has been a vast body of research data, that concludes a more integrated theory, that involves vascular symptoms as secondary events, with neuronal dysfunction as the primary driver(3).
Most individuals rely on orthodox treatment, whether prescription or over-the-counter medication, to mitigate and/or treat migraine attacks. Pharmacological treatment options often have adverse side effects, and are not without their limitations(7). It is therefore important to consider other treatment options, and an abundance of research is emerging on whether nutritional management can alter the mechanisms behind migraine, but is the research really conclusive enough to put into practice?
The mechanisms behind migraine explained
One mechanism termed ‘cortical spreading depression (CSD)’ can be described as a wave of electrical excitation that travels across the brain, and is believed to be the prominent underlying mechanism behind migraine aura. It is also thought to trigger the sensation of pain felt during a migraine via stimulation of the trigeminal nerve; the nerve responsible for sensation in the face(8). The stimulation of the trigeminal nerve has a trigger effect on the release of pro-inflammatory molecules, including Calcitonin Gene-Related Peptide (CGRP); which then gets to work sensitising nerve endings in the brain promoting and amplifying the feeling of pain(9).
CGRP has been shown to be responsible for many of the symptoms of migraines, including dilation of the arteries, inflammation and pain(3). Recent studies have demonstrated CGRP can induce migraines in susceptible individuals(10), so it is now the focus for many pharmaceutical companies to develop a suitable drug to block the action of CGRP(11).
Levels of CGRP are not only raised during neurogenic inflammation, but also increase rapidly during systemic inflammatory responses(12). This suggests that employing methods to reduce inflammation, may reduce levels of CGRP, which in turn may have a positive effect on migraines.
Why do some individuals suffer?
Migraines are thought to have a genetic element, which would explain why only the unlucky ones amongst us suffer. However not all individuals with the select genes experience migraines, so it is now thought that there must also be environmental influences(13). Certain risk factors that can’t be modified, such as being female or aged between 22-55(14,15,16) increases the likelihood of developing migraine attacks; but there are also some factors that we can do something about, including reducing our stress levels, shifting excess weight and eating an anti-inflammatory diet(17).
So what can be done?
Stress is thought to be a common trigger for the onset of migraine attacks, with 58% of 7,187 migraineurs identifying stress as the cause(18). Stress to the body can take on many forms, such as insufficient sleep, skipping meals, hormonal fluctuations or certain foods(15), so it is critical to identify personal trigger factors.
A change in lifestyle to include stress management activities can also be of benefit. Physical activity has been shown to reduce inflammation(19), and in addition, a 2011 study(20) reported “an improvement in migraine attack, frequency, symptom intensity and intake of medication, when an exercise programme based on indoor cycling three times a week was used”. Further, exercise insufficiency has been linked with a 21% increased risk of headaches in migraine susceptible individuals(21). Despite this, it is important to note, that for some exercise can be a trigger factor for migraines(20), so needs to be handled on a case-by-case basis.
A study by Dr. Wachholtz has shown meditation to be effective at reducing the number of headaches by 50%, where brief meditation training was given over four weekly 90-minute group sessions and meditation practice for 20 minutes per day was exercised(22). This positive reduction is based on the theory(22) that “migraines result in a significant increase in emotional and physiological stress, so by reducing stress this may lead to fewer headaches”.
For some people the consumption of gluten can be a huge stressor and also a source of inflammation in the body. Coeliac disease is an autoimmune condition where gluten induces an immune response that can lead to small intestinal damage. Non-coeliac gluten sensitivity has been termed for those that elicit many of the symptoms of coeliac disease, but where the diagnostic tests appear negative.
Abdominal pain, diarrhoea and nausea are frequent reported symptoms in these gut disorders, and also unexpectedly, migraines; with a prevalence of up to 30% in biopsy diagnosed coeliac disease(13). Whilst a correlation has been established, at present it remains unclear as to whether coeliac disease is causative of migraines, or is just a by-product of the disease.
Whilst gluten-free diets have become all the rage, and many are ‘jumping on the band wagon’ in the hope of following a ‘healthy’ lifestyle; they have shown to be successful in reducing migraines, with one study reporting nine out of ten patients that were experiencing episodic headaches with a gluten sensitivity, responding positively to the removal of gluten from their diet(23). Coeliac UK(24) estimates there are nearly half a million people in the UK who have coeliac disease but don’t know it, so if you suspected you have it, it is important to get help. Symptoms of coeliac disease can be found at www.coeliac.org.uk, and a free self-assessment questionnaire is available which advises whether its recommended to get tested - available at www.itiscoeliacdisease.org.uk. If in any doubt, speak to your GP who is able to test for and diagnose coeliac disease.
Weight Loss Diet
A consequence of carrying additional weight in migraine susceptible people is the induction of systemic inflammation. A clinic-based study back in 2005 showed the first connection between obesity and migraines, where obese patients were shown to be three times more likely to experience migraines when compared with normal weight people of the same age(25). It is thought, in short, that the inflammatory state in obesity may intensify the inflammatory response found in migraines(8). However, there is hope, as weight loss can reverse inflammation helping to improve migraine symptoms(26). In a year long study carried out at the University of Chieti in Italy(27), significant improvements in both adiposity, headache frequency and intensity were noted when weight loss was addressed through diet, physical activity and cognitive behaviour.
If you have weight to lose, the NHS advise to aim for around 0.5kg to 1kg weight loss a week, and the best way to lose weight is to make long-term changes to diet and physical activity(28).
Based on the connection between neurogenic inflammation and systemic inflammation, a diet incorporating anti-inflammatory foods may be of benefit to migraneurs. Anti-inflammatory foods work through a number of mechanisms to lower the inflammatory burden(26). A good base for incorporating more food sources is the Mediterranean diet, which focuses on fish, vegetables and olive oil. Oily fish, such as mackerel, salmon or trout are rich sources of omega 3 fatty acids, which have been splashed all over news headlines in recent years as potent anti-inflammatory agents. Although the research regarding omega 3 for migraine prevention is conflicting and in the early stages(29,30,31), it has firmly been confirmed as influential in reducing inflammation(26). Other sources that are worthy of note, include flaxseeds, chia seeds and walnuts; and of course omega 3 is available in supplement form. Vegetables are integral to the Mediterranean diet and also play a role in the lessening of inflammation where the predominant effect is thought to be through the suppression of pro-inflammatory agents(31).
Keep a diary
It is important to note, that almost anything can trigger an attack in someone predisposed, and the list of possible suspects is long and can be difficult to identify or recall(32). A trigger may also not cause an attack every time, and seems to only implement an attack when a threshold level is reached(33). The best way to recognise a trigger is to keep a detailed diary which can be helpful in identifying patterns preceding migraine attacks.
To conclude, the research appearing on the nutritional and lifestyle management of migraines is gaining speed and is showing promise; however further studies are needed to unlock this complex neurological disorder, proving there is much still to learn.
1.The Huffington Post (2014) This Is What A Migraine Feels Like. Available at: http://www.huffingtonpost.com/2014/03/03/what-a-mirgaine-feels-lik_n_4861163.html (Accessed: 7th April 2017).
2.Headache Classification Committee of the International Headache Society (IHS) (2013) ‘The international classification of headache disorders, 3rd edition (beta version)’, Cephalalgia: an international journal of headache, 33(9), pp. 629-808.
3.Malhotra, R. (2016) ‘Understanding migraine: Potential role of neurogenic inflammation’, Annals of Indian Academy of Neurology, 19(2), p. 175.
4.Migraine Research Foundation (2017) Migraine Facts. Available at: http://migraineresearchfoundation.org/about-migraine/migraine-facts/ (Accessed: 6th April 2017).
5.Steiner, T., Stovner, L. and Birbeck, G. (2013) ‘Migraine: the seventh disabler’, The Journal of Headache and Pain, 14(1), p. 1.
6.Thomas, S. (2015) ‘Migraine a huge burden on NHS services’, Available at: http://www.nhis.com/editorial/migraine-a-huge-burden-on-nhs-services#ii (Accessed: 21st March 2017).
7.Bunner, A., Agarwal, U., Gonzales, J., Valente, F. and Barnard, N. (2014) ‘Nutrition intervention for migraine: a randomized crossover trial’, The Journal of Headache and Pain, 15(1), p. 69.
8.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.
9.Lippi, G., Mattiuzzi, C. and Cervellin, G. (2014) ‘C-reactive protein and migraine. Facts or speculations?’, Clinical Chemistry and Laboratory Medicine, 52(9), pp. 1265-1272.
10.Kaiser, E. and Russo, A. (2013) ‘CGRP and migraine: Could PACAP play a role too?’, Neuropeptides, 47(6), pp. 451-461.
11.Russo, A. (2015) ‘Calcitonin Gene-Related Peptide (CGRP): A New Target for Migraine’, Annual Review of Pharmacology and Toxicology, 55(1), pp. 533-552.
12.Holzmann, B. (2011) ‘Modulation of immune responses by the neuropeptide CGRP’, Amino Acids, 45(1), pp. 1-7.
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15.Burstein, R., Noseda, R. and Borsook, D. (2015) ‘Migraine: Multiple Processes, Complex Pathophysiology’, Journal of Neuroscience, 35(17), pp. 6619-6629.
16.Martin, B. and Seaman, D. (2015) ‘Dietary and Lifestyle Changes in the Treatment of a 23-Year-Old Female Patient With Migraine’, Journal of Chiropractic Medicine, 14(3), pp. 205-211.
17.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.
18.Peroutka, S. (2014) ‘What Turns on a Migraine? A Systematic Review of Migraine Precipitating Factors’, Current Pain and Headache Reports, 18(10), pp. 1-6.
19. Khazaei, M. (2012) ‘Chronic Low-grade Inflammation after Exercise: Controversies’, Iranian journal of basic medical sciences, 15(5), pp.1008-1009.
20. Varkey, E., Cider, Å., Carlsson, J. and Linde, M. (2011) ‘Exercise as migraine prophylaxis: A randomized study using relaxation and topiramate as controls’, Cephalalgia, 31(14), pp. 1428-1438.
21. Chai, N., Bond, D., Moghekar, A., Scher, A. and Peterlin, B. (2014) ‘Obesity and Headache: Part II - Potential Mechanism and Treatment Considerations’, Headache: The Journal of Head and Face Pain, 54(3), pp. 459-471.
22. Wachholtz, A.B. (2013) ‘Brief Meditation Training for Migraineurs Affects Emotional and Physiological Stress Reactivity’, Psychiatry publications and presentations, 712.
23.Hadjivassiliou, M., Grunewald, R., Lawden, M., Davies-Jones, G., Powell, T. and Smith, C. (2001) ‘Headache and CNS white matter abnormalities associated with gluten sensitivity’, Neurology, 56(3), pp. 385-388.
24. Coeliac UK (2017) Key Challenges. Available at: https://www.coeliac.org.uk/about-us/what-we-do/key-challenges/ (Accessed: 6th April 2017).
25.Peres, M., Lerário, D., Garrido, A. and Zukerman, E. (2005) ‘Primary headaches in obese patients’, Arquivos de Neuro-Psiquiatria, 63(4), pp. 931-933.
26. Sears, B. and Ricordi, C. (2011) ‘Anti-Inflammatory Nutrition as a Pharmacological Approach to Treat Obesity’, Journal of Obesity, 2011, pp. 1-14.
27. Verrotti, A., Agostinelli, S., D’Egidio, C., Di Fonzo, A., Carotenuto, M., Parisi, P., Esposito, M., Tozzi, E., Belcastro, V., Mohn, A. and Battistella, P. (2012) ‘Impact of a weight loss program on migraine in obese adolescents’, European Journal of Neurology, 20(2), pp. 394-397.
28. National Health Service (NHS) (2017) Lose Weight. Available at: www.nhs.uk/Livewell/loseweight (Accessed: 7th April 2017).
29. Tajmirriahi, M., Sohelipour, M., Basiri, K., Shaygannejad, V., Ghorbani, A. and Saadatnia, M. (2012) ‘The effects of sodium valproate with fish oil supplementation or alone in migraine prevention: A randomized single-blind clinical trial’, Iranian journal of neurology, 11(1), p.21.
30. Sadeghi, O., Maghsoudi, Z., Khorvash, F., Ghiasvand, R. and Askari, G. (2015) ‘The relationship between different fatty acids intake and frequency of migraine attacks’, Iranian journal of nursing and midwifery research, 20(3), p.334.
31. 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.
32. The Migraine Trust (2017) The Migraine Trust – a patient focused, research driven UK charity. Available at: http://www.migrainetrust.org/ (Accessed: 7th April 2017).
33. Borkum, J. (2015) ‘Migraine Triggers and Oxidative Stress: A Narrative Review and Synthesis’, Headache: The Journal of Head and Face Pain, 56(1), pp. 12-3