All in the head - a nutritional approach to migraine management

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ION Archives

Issue: 
Spring
Year of publication: 
2001

Can the biochemical process that precedes a migraine be curbed or prevented? Martin Hum PhD, DHD pinpoints some of the common triggers associated with migraine and how nutritional therapy can help break the chain of events that precipitates an attack

Perhaps it starts with cold fingers or maybe your vision blurs and you can’t concentrate. Then you get that first dull ache above your eye and you know it’s happening again. You’re getting a migraine. Before long, you’ll have a relentless, excruciating, throbbing pain in your head, nausea and extreme sensitivity to light and noise.

The nightmare of migraine is all too real for around 25-30% of women and 15-20% of men in this country. These figures are estimates since surveys reveal that about 60% of migraine sufferers never consult a doctor about their condition. Of those who do, only about a third are satisfied with their treatment. In America, the incidence of migraine headaches has increased by 60% in less than fifteen years and there is little reason to believe that people in this country are faring better.

 

A CATALOGUE OF MISERY

Migraine is most common among 20 to 35 year olds, although it can affect people at any age, even children as young as two years. Migraines involve changes to the blood vessels in the brain, may be associated with nausea and typically affect one side of the head only. The word migraine comes from the Greek demi crania, meaning “half the head”. It can be classified into various types:

 

Classic migraine is a severe, throbbing pain on one side of the head, with nausea and sometimes vomiting. An “aura” of warning symptoms precedes many attacks, e.g. visual disturbances, cold extremities, anxiety, disturbed thoughts, fatigue and numbness or tingling of the limbs. Attacks typically start in the morning, last 6 to 24 hours and recur several times a month.
Common migraine rarely involves warning symptoms; the severe, throbbing pain may be on one or both sides of the head and nausea is usually absent. This kind of migraine headache can last for up to three days.
Cluster headache is no longer classified as migraine. It involves severe pain, usually localised around one eye. Headaches occur in clusters of one or more a day for a few days, separated by several weeks without symptoms.
Tension headaches, or “ordinary” headaches, are caused by muscular spasm. They usually start at the back of the head and are rarely one-sided. Current thinking is that most types of headaches involve both muscle tension and vascular changes, to some degree at least.

A CASCADE OF NEUROTRANSMITTERS

So what is going on in the body to cause these symptoms? Most researchers believe that constriction of the cranial arteries is involved, followed by over-dilation. Abnormal clumping, or “stickiness”, of blood platelets and the over-production of a neurotransmitter called “substance P” also occur during attacks. Making sense of the process underlying the symptoms of migraine is difficult because the conclusions of some studies contradict those of others. However, my own interpretation of the chain of events is as follows:

Catecholamine release. Chemicals called amines appear to play an important part in migraine biochemistry. Catecholamines are a group of highly active amines, including adrenaline and noradrenaline, that the body produces in response to a variety of stimuli (e.g. stress, caffeine, low blood sugar). Their release stimulates:
Serotonin over-production. Serotonin is another amine and a neurotransmitter that plays a vital part in normal brain physiology. Its over-production in migraine sensitive people may be linked to food sensitivity and is associated with:
Platelet stickiness. It is not certain whether abnormal serotonin release causes platelet stickiness or vice versa, or whether they could both be due to a third factor, such as increased levels of arachidonic acid. Amines in foods may also contribute to platelet stickiness. This leads to:
Vasoconstriction of the cerebral arteries. This seems to be the point of no return, after which the cascade of events leads inexorably to a migraine. Vasoconstriction may also be caused directly by catecholamines and by dehydration. It stimulates:
Adenosine release. Adenosine is a neurotransmitter that inhibits catecholamine release and tends to reverse its effects. Adenosine causes sensory disturbances of the kind often experienced in the classic migraine aura, as well as pain. It is also a potent vasodilator and causes:
Rebound vasodilation. The cranial arteries widen abnormally and dietary amines may aggravate this reaction. This stretches the nerves that enervate the arteries (part of the sympathetic nervous system), which may be the cause of:
Substance P release. This neurotransmitter is responsible for most of the pain associated with migraine. Stress can also have a direct effect on the sympathetic nervous system and may increase the production of substance P. Substance P in turn causes:
Inflammatory mediator release. The mast cells produce several inflammatory mediators, including histamine (another amine) and arachidonic acid. These can cause nausea and other symptoms. Arachidonic acid may promote further platelet stickiness and histamine causes vasoconstriction.
The above is an over-simplification of a process involving many more neurotransmitters and many more physiological effects. It does, however, provide a working model for understanding how diet can contribute to the migraine process, both positively and negatively.

 

 

 

LOCATING THE TRIGGERS

It is generally accepted that some foods, hormonal changes, environmental chemicals and sensory stimuli can be “triggers” for migraine. There is likely to be a threshold effect, in which potential migraine triggers summate without symptoms occurring, until the physiological balance tips and the chain of events described earlier ensues.

Food sensitivity is well documented as the most common single factor, linked to between 30% and 90% of migraines. The mechanism through which food sensitivity causes migraine is unclear, but possibly involves the overproduction of serotonin or inflammatory mediators. The major culprit is cow’s milk, followed fairly closely by wheat, eggs, oranges and tomatoes. However, as with other food sensitivity symptoms, almost any food could be implicated. (1, 2)

Other foods are known to cause migraine because of their chemical constituents. Many such foods naturally contain dietary amines, for instance figs, dates, raisins, pineapples, beans, potatoes, some fish and seafood, pork and turkey. Tyramine is the most notorious dietary amine and its content is increased by fermentation or ageing processes. Hard cheeses (especially blue cheese), yogurt, sauerkraut, yeast extract, pickled herrings and canned fish all have enhanced levels of tyramine. (3) Chocolate is another common migraine trigger, the guilty amines here being mainly phenylethylamine and phenylalanine. Some amines produced in the body are also present in foods, for instance serotonin in bananas and dopamine and histamine in cheese, sauerkraut, and cured meats.

Dietary amines are involved in several of the physiological steps down the road to a migraine. For most people, these compounds pose no threat, as they are broken down quickly by monoamine oxidase enzymes in the gut and the blood platelets. In migraine sensitive people, these enzymes may be deficient. There is also evidence that the amino-acid tyrosine is converted to tyramine more readily in migraine sufferers. Other chemicals naturally present in foods may also act as triggers. Red wine’s well known migraine-inducing properties are due both to its tyramine content and to other substances, probably flavonoids, that inhibit monoamine oxidase enzymes. Flavonoids in citrus fruits may act in the same way. Alcohol and gelatin do not cause migraine directly but increase the ability of trigger substances to enter the bloodstream. Bacterial toxins in foods are also suspect and may help explain the difficulty some migraine sufferers have in identifying specific foods as triggers. A food may be well tolerated when fresh but migraine-producing after a few days in the fridge. Artificial additives, such as monosodium glutamate (MSG), sweeteners (particularly aspartame), nitrites and nitrates in cured meats, flavourings and colourings can all trigger migraines, too.

Caffeine presents a paradox, since it can both cause and relieve migraines. One theory argues that virtually all migraines are caffeine withdrawal headaches. This may explain their common pattern of onset in the morning and at weekends (away from the office coffee pot) and their being more common in women than in men (oestrogen decreases the rate of caffeine breakdown). What is certain is that caffeine stimulates adrenaline production, which causes vasoconstriction. It can therefore contribute to the onset of a migraine during the vasoconstrictive phase or relieve the symptoms temporarily during the vasodilatory phase.

Stress, weather changes, smoking and too much or too little sleep can also cause migraine. They may all provoke hormonal or neurological changes that impact on the production of catecholamines. Low blood sugar and excess blood insulin levels, as a result of missed meals or sweet snacks, also promote catecholamine production. High oestrogen levels can in turn raise insulin output, leading to migraines linked to the menstrual cycle, the contraceptive pill and HRT. Liver problems can predispose towards migraine through a reduced ability to break down hormones in the blood and to deal with dietary and metabolic toxins.

 

 

BREAKING THE CHAIN

A nutritional treatment approach for migraine should take account of the mechanisms involved, so far as they are known or suspected, and aim to break the chain of events that leads to a migraine attack. The following eight point nutritional plan is likely to be of benefit.

Identify food sensitivities. An exclusion diet that initially eliminates dairy products, wheat and other gluten grains, eggs, oranges and tomatoes will cover about 90% of food sensitivity cases. Keep to this for a month and then, if no migraine has occurred, reintroduce one food at a time, allowing four days for a reaction to become apparent. Meat and animal fats should also be avoided during the elimination diet, since these tend to promote production of arachidonic acid (a precursor to series 2 prostaglandins which may produce unfavourable effects in the body).
Eliminate amines. Cut out any amine- containing foods known to be a problem and cut down on others as far as practicable. In particular, avoid chocolate, aged cheese, tinned and pickled fish, sauerkraut, dates, figs, raisins, pineapple, bananas and yeast extract.
Cut out caffeine. Coffee is often the villain of the piece, but tea and cola drinks may also contain appreciable amounts of caffeine. Gradual reduction is advisable to avoid a withdrawal headache. Drink plenty of water instead, since dehydration leads to histamine release and vasoconstriction. Stay clear of alcohol and tobacco, too.
Base your diet on the freshest, most natural foods you can obtain. Plan meals and shop frequently, so food doesn’t stay in your fridge for days. Avoid food additives as far as possible, especially nitrites in cured meats, MSG, tartrazine and aspartame.
Balance blood sugar. Include plenty of fibre from whole grains, fresh vegetables, salads and “safe” fruits e.g. apples, pears, cherries, plums, peaches and kiwi fruit. Avoid sweet foods and refined flour products (even if not wheat sensitive). Don’t rely on potatoes, as they can cause blood sugar levels to rise fast and are high in dietary amines. A supplement of chromium picolinate may help keep blood sugar stable.
Correct hormone imbalance. A natural diet and supplementation with essential fatty acids, B group vitamins (especially B6) and magnesium can help to avoid female sex hormone fluctuations, which can result in migraine. Herbs such as dong quai and agnus castus may help. Natural progesterone cream (only available on prescription in the UK) has also been shown to prevent menstrual cycle migraines. Use healing herbs. Feverfew can reduce migraine frequency in about two thirds of cases. Cayenne pepper, valerian, goldenseal and ginger have also been used successfully to prevent or treat migraine. Avoid St John’s Wort if you are a migraine sufferer, since it inhibits monoamine oxidase enzymes.
Take specific nutrients. Magnesium and calcium can reduce the severity of blood vessel spasms and prevent migraine onset. Vitamins B2, B3, B6, C and E can also help and seem to work by inhibiting platelet clumping or preventing vasoconstriction. Essential fatty acids reduce the production of inflammatory prostaglandins. Quercetin also inhibits inflammatory reactions.

 

REFERENCES

Egger J, Carter CM, Wilson J, Turner MW. Is migraine a food allergy? Lancet 1983; 2:865-9.
Grant EC. Food allergies and migraine. Lancet 1979; 1:966-9.
Leira R & Rodriguez R. Diet and migraine. Rev Neurol 1996; 129:534-8.

BIBLIOGRAPHY

Brainard, JB. Control of Migraine.WW Norton & Co, 1979.
Davies S & Stewart A. Nutritional Medicine. Pan Books, 1987.
Low R. Migraine. Henry Holt, New York, 1987.
Pizzorno J & Murray M. Migraine. Encyclopedia of Natural Medicine. Little, Brown & Co, 1995.

Martin Hum is a registered nutritional therapist who works in Central London and from his home in Southgate.

 

Keywords: 
HEALTH CONDITIONS
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