What is the relationship between migraines and histamine?

What is the relationship between migraines and histamine?

We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

A family member suffers from migraines so I have been reading a little around the subject.

There seem to be any number of "triggers", but I have seen mention several times of the role of histamine in migraine activation as an active area of research. The suggestion is that high histamine levels in the body can cause migraines.

Is there solid evidence that histamine can trigger migraines? How does this mechanism operate?

Yes, this is true.

Histamine is thought to induce the enzyme Nitric Oxide (NO) Synthase. NO is then available to act locally on the vasculature as a vasodilator.

NO binds to guanylyl cyclase in vascular smooth muscle cells, which leads to the production of cyclic GMP, which in turn forms phosphorylated protein kinase G. PKG phosphorylates Ca2+ channels, slowing the influx of calcium into the cell, which leads to smooth muscle relaxation, and vasodilation, which leads to migraine.

The only silver lining is that there is a check in place: with the binding of histamine to H3 receptors on c-fibers in the central nervous system, feedback inhibition prevents the further release of histamine from these sites.


Akerman S, Williamson DJ, Kaube H, Goadsby PJ. (2002). The role of histamine in dural vessel dilation. Brain Res. 956(1):96-102.

Gupta, S., Nahas, S.J.,Peterlin, B.L. (2011) Chemical Mediators of Migraine: Preclinical and Clinical Observations. Headache: The Journal of Head and Face Pain, 51(6): 1029-1045.

I've experienced migraines for 10 years, and now for the last 14 months that I've taken anti histamine medicine to see if there would be a benifit I've had good results. The frequency has dropped from approx 3 times a month to a migraine approx every 6-8 weeks. For me thats a sizeable drop. The other benifit is the severity is less intense. Now I'm trying to find why my body produces too much histamine, so I hopefully can eliminate the anti histamine med's. Recently I've greatly reduced foods with refined sugar, also processed foods, and added more whole foods, and I'm seeing excellent results.

How a Migraine Happens

Older theories about migraines suggested that symptoms were possibly due to fluctuations in blood flow to the brain. Now many headache researchers realize that changes in blood flow and blood vessels don't initiate the pain, but may contribute to it.

Current thinking regarding migraine pain has moved more toward the source of the problem, as improved technology and research have paved the way for a better understanding. Today, it is widely understood that chemical compounds and hormones, such as serotonin and estrogen, often play a role in pain sensitivity for migraine sufferers.

One aspect of migraine pain theory explains that migraine pain happens due to waves of activity by groups of excitable brain cells. These trigger chemicals, such as serotonin, to narrow blood vessels. Serotonin is a chemical necessary for communication between nerve cells. It can cause narrowing of blood vessels throughout the body.

When serotonin or estrogen levels change, the result for some is a migraine. Serotonin levels may affect both sexes, while fluctuating estrogen levels affect women only.

For women, estrogen levels naturally vary over the life cycle, with increases during fertile years and decreases afterwards. Women of childbearing age also experience monthly changes in estrogen levels. Migraines in women are often associated with these fluctuating hormone levels and may explain why women are more likely to have migraines than men.

Some research suggests that when estrogen levels rise and then fall, contractions in blood vessels may be set off. This leads to throbbing pain. Other data suggest that lower levels of estrogen make facial and scalp nerves more sensitive to pain.


The patient with episodic cluster headaches should be started on prophylactic therapy as early as possible in the series in order to curtail the length of the cluster period and decrease the severity of the headaches. Cluster prophylaxis can involve several medications. Commonly used choices include corticosteroids, verapamil (a calcium channel blocking agent) and antiepileptic drugs such as divalproex sodium and topiramate. These agents are slowly tapered off and then discontinued as the headaches decrease and disappear. For patients with chronic cluster headaches, agents such as lithium or calcium channel blockers may be employed. Histamine desensitization and surgical intervention may be considered for chronic cluster headache patients who have not responded to other forms of standard therapy.

Because of the brief duration of an acute cluster attack, the abortive treatment of these headaches is difficult. Often, the acute headache has disappeared before the patient arrives at the emergency department or physician’s office to receive treatment. Oxygen inhalation by facial mask can be used at the first signs of a cluster attack and has been successful in aborting an acute cluster headache. The cluster patient may respond to ergotamine preparations, if used immediately at onset of symptoms. Some patients have gained some relief with the use of intranasal applications of a local anesthetic agent, such as lidocaine. Sumatriptan (Imitrex), a 5 HT agonist, is indicated for the abortive therapy of cluster headaches. It is available in injectable, nasal spray and tablet forms, although the latter is the least effective because of the time it takes before the onset of action. Any of these treatments should be used under the direction of a physician familiar with cluster headache therapy. The injectable form of sumatriptan (self-administered) is FDA approved for the acute treatment of cluster headache.


Olfactory stimulation and trigeminovascular system activation: pharmacology and anatomy

The California Bay laurel tree is also known as the "headache tree." Its leaves vaporize the volatile monoterpene ketone, umbellulone, a molecule that activates the transient receptor potential ankyrin-1 (TRPA-1) peptide on nociceptive neurons of the nasal mucosa, thereby activating the trigeminovascular system directly. TRPA-1 receptors are members of the transient receptor potential (TRP) receptor family and is co-expressed with the transient receptor potential vannilin-1 (TRPV-1) peptidergic sensory nerves. TRPA-1 and TRPV-1 receptors both co-localize on nociceptive C-fibers, transduce noxious stimuli, cold temperature, and are mechanosensitive. Theyਊlso respond to electrophilic agents and plant-derived volatile alkaloids. Nicotine activates and paracetamol, capsaicin, and caffeine suppress both receptors. Activation of TRPA-1 induces the release of SP and CGRP by trigeminovascular activation, explaining the generation of a migraine headache [15-17]. Olfactory stimulation also leads to increased activity of the limbic system and the dorsal pons, which induces inflammatory mediator (CGRP, SP) release and activation of nociceptors and vasodilation of meningeal vessels [14].

Odorants stimulate both the olfactory and trigeminal nerve endings in the nasal mucosa (chemosensation). The quality of a volatile molecule can elicit both an odor or a pungency (irritation). It was initially thought that the pungency of a substance may mask its odor however, a study by Cain SW et al. showed that pungency and odor are mutually exclusive, with pungency not masking the odor of an irritant agent [18].

Chemosensation begins in the nasal mucosa. Collaterals of the ophthalmic branch of the trigeminal nerve (SP- and CGRP-positive) synapse at the glomerular layer of the olfactory bulb, where mitral cells excite each other, intimately coupling the olfactory and trigeminal pathways [19-20].

The pharmacodynamics of estrogen and migraine generation

It is well-established that migraine is three times more frequent in women than men (sexual dimorphism). The sexually dimorphic area in the hypothalamus is the pre-optic region, known as the sexually dimorphic nucleus of the pre-optic area (SDN-POA). Here, along with the paraventricular nucleus, the transition to puberty is determined by the pulsatile release of the luteinizing hormone release hormone (LHRH). Opioids inhibit the pre-ovulatory LH surge via the mu- and kappa-opioid receptors [21-22].

The relationship between migraine and estrogen is non-linear implying that there is no straightforward proportionality. Specifically, whereas the estrogen withdrawal hypothesis (precipitation of migraine headache with a drop in estrogen levels below 40-50 pg/ml) generally holds true, this simple relationship breaks down in post-menopausal women, where hormone replacement therapy may actually increase the risk of migraine. Several days of exposure to estrogen are required prior to a drop of estrogen before a migraine is precipitated, a phenomenon known as priming [23-24].

Pharmacodynamically, estrogen increases endothelial cell nitric oxide synthetase activity and the production of nitrous oxide, a potent vasodilator. This effect heightens during the luteal phase, with a concomitant drop in serum serotonin [25]. When estrogens fall during the menses, two events occur due to membrane excitability: there is upregulation of inflammatory genes with a subsequent elaboration of cytokines and central sensitization of peptidergic neurons and increased pain [26]. In an in-vitro study of female rat trigeminal ganglia, estrogen-alfa receptors were localized in the cytoplasm of neurites and were associated with the upregulation of extracellular signal-regulated kinases (ERK-1), a protein associated with inflammatory painਊnd nociceptive neurons [27].

The pre-pubertal prevalence of migraine is 4%, equally in both boys and girls while post-pubertal prevalence is 18% for women and 6% for men, reflecting the prolific role of estrogen in the genesis of migraine [28]. The effects of the phase of the reproductive cycle on migraine genesis is outlined below (Table ​ (Table3) 3 ) [29].

Table 3

Peri-menstrual6014% of migraines are exclusively menstrual
Pregnancy23De novo genesis of migraine during pregnancy is rare < 3%
Oral contraception24.1Develops within a month. Only 30-40 % improve with discontinuation
Menopause14No consistent response with estrogen replacement therapy or oophorectomy

In a study of 98 women undergoing luteinizing hormone therapy to suppress ovarian estrogen release, the fall in serumꀗ-beta estradiol correlated with a surge in migraine headaches in 84% of the women undergoing in-vitro fertilization [30].

Barometric pressure, atmospheric chemistry, and migraine

Meteoropathy is the study of pain generated by a change in barometric pressure and other parameters of weather systems such as humidity and temperatures. In a study of 34 patients with migraines who developed a headache while in hospital, migraine was found to occur when the atmospheric pressure lay between 1003 and 1007 hectoPascal (hPA), the standard pressure being 1013 hPA [31]. In a study of 28 migraine patients, a drop of barometric pressure greater than 5 hPA was associated with headaches in 14 patients. The barometric pressure was measured two days prior and after headache onset, with a rise in barometric pressure of greater than 5 hPA associated with a reduced frequency of headaches [32].

Rats exposed to low barometric pressure showed increased discharge in the spinal trigeminal nucleus in the receptive fields of the cornea but not in the temporal muscle or dura mater. Therefore, one would speculate that a drop in barometric pressure may lead more to orbital pain in migraineurs sensitive to barometric pressure drop [33]. In a rat chronic pain model, a drop in barometric pressure was associated with increased sympathetic nerve activity and an increase in pain induced by chronic constriction of the sciatic nerve. This effect is abolished by an inner ear lesion suggesting that the barometric pressure sensor influencing pain behavior may be located in the inner ear [34-35]. Cellular forskolin (c-fos) expression, a marker of neuronal activity, was increased in the superior vestibular nucleus in rats subjected to a 5-27 hPA drop in barometric pressure [36].

Thunderstorms and hot desert winds generate positive ions and increase the ratio of positive-to-negative ions in inhaled air, which increases blood and brain serotonin levels. Negative atmospheric ions, in particular, superoxide ions, oxidize serotonin into tryptamine-4,5-dione and reduce serum and brain serotonin. Superoxide ions are generated by two mechanisms, a salubrious effect with the Lenard effect and a potentially harmful one with corona lightning਍ischarge (Table ​ (Table4) 4 ) [37].

Table 4

SOURCEwaterfalls, rain, cosmic rays, ultraviolet rayslightning, corona discharge
ION SPECIESsuperoxide only, attached to microclusters of water moleculessuperoxide and ozone
HALF-LIFE OF ION SPECIES60 secondsfew seconds
ACTIVITY ON SODincreasedecrease

The Lenard effect is the shearing of water molecules by spray electrification and the generation of negative superoxide ions, an effect common in waterfalls. The Lenard effect may improve red blood cell elasticity and improve aerobic metabolism. Low concentrations of superoxide ions, generated by the Lenard effect, stimulate the activity of superoxide dismutase (SOD), an enzyme that accelerates the metabolism of harmful free radicals [38-39].

A controversial but intriguing phenomenon is the "serotonin irritation syndrome,"ਊ clinical phenotype that has overlapping but less severe symptoms than the serotonin syndrome and is thought to arise during thunderstorms and with hot and dry desert winds (Table ​ (Table5) 5 ) [40-41].

Table 5

5-HT: 5-hydroxytryptophan 5-HIAA: 5-hydroxyindoleacetic

Sferics are very low-frequency radio waves generated by lightning in the ionosphere.

TRIGGERTwo or more serotonergic agents with different mechanisms of action: drug-induced - a toxic syndrome (toxidrome)Atmospheric sferics - cation excess - likely serotonin release from the hypothalamus: atmospheric induced - thunderstorm, hot and dry desert wind
CLINICAL PHENOTYPETriad: encephalopathy, autonomic, motor hyperactivityTriad: irritability, pain, and autonomic
TREATMENTSerotonin antagonists - cyproheptadine, benzodiazepines, and dopamine antagonistsAnion ionizers
MECHANISMSerotonin excess at synapses: 5HT-1A and 5-HT-2ACation-induced serotonin dysfunction: increased serum serotonin and reduced urinary metabolite (5-HIAA)

Alcoholic beverageਊnd food-induced migraine headaches: pharmacology and biochemistry

One-third of migraine patients are sensitive to alcohol. Histamine is stored in the granules of mast cells (tissues) and circulating basophils.ꃎntrally, it is found in high concentration in the hypothalamus. When injected experimentally into the hypothalamus, serotonin is released into the circulation. Histamine intolerance is due to diamine oxidase deficiency with impaired degradation of histamine. Red wine has 20-200 times the content of histamine than white wine. Histamine, an indicator of hygiene in foods, is released by food tissue mast cells. Alcohol can inhibit diamine oxidase leading to a higher histamine content of food. Red wine through two flavonoid extracts can lead to the release of serotonin into the blood from platelets. Meanwhile, white wine contains more sulfites than red wine. Sulfites can induce histamine release from mast cells [42], whereas a histamine H1 and H2 receptor blockade does not abort migraine headaches, the H3 receptor agonist has recently shown efficacy with aborting migraine headaches in small pilot clinical trials. The H3 and H4 receptors are found in the central nervous system (neurons and immune cells) and regulate neurogenic inflammation in the TVS. The H3 receptor is an auto-receptor and reduces the release of histamine [43].

Through the polyphenol resveratrol, both red and white wine can inhibit monoamine oxidase (MAO) activity and the reuptake of serotonin, thereby increasing its synaptic concentration. Red, more than white, wine can induce nitrous oxide release from endothelial cells, leading to direct vasodilatation or via਌GRP release. Phenolsulfatransferase (PST), which is found in the highest concentration in the intestine, exists in two forms: PST-M, which inactivates phenolic monoamines (tyramine, dopamine, and norepinephrine), and PST-P, which inactivates phenol, p-cresol, and synthetic phenols. Both enzymes catalyze sulfate conjugation. Phenolic compounds are found in a wide variety of foods, including fruits, dairy products, and alcoholic beverages.਎thylacetate and the flavonoids, found more in red more than white wine, can inhibit PST-P, which with other alcoholic drinks also inhibit platelet PST-P. Patients with dietary migraines have lower levels of platelet PST-P and PST-M than non-dietary migraine-sensitive patients [44].਎thanol also activates TRPV-1 in guinea pigs in trigeminal sensory afferents and activates TVS, thereby inducing neurogenic inflammation in meningeal blood vessels. This effect is blocked by CGRP antagonists [45].

A list of common migraine-provoking foods/beverages and their mechanisms of action are listed below. We add the pharmacological agent nitroglycerin to this list due to its ubiquity and historical significance (Table ​ (Table6) 6 ) [46].

Table 6

PEA: phenylethylamine mg: milligram

Hot dog headachehot dogs and cured meatsodium nitritenitric oxide-induced vasodilation 
Chinese restaurant syndromesoups and soy saucemonosodium glutamateglutamate-induced acetylcholine releaseHeadache, flushing, and palpitations: controversial syndrome.
Hangover headachehigh congener beverages such as cognac and bourbonaldehydes, methanol, and fusel alcohols (products of fermentation)alcohol dehydrogenase induced lactic acidosis with altered redox state and accumulation of acetaldehydewomen have lower levels of alcohol dehydrogenase
Dynamite headachenitroglycerin (dynamite factories), nitroglycerin sublingual (angina pectoris).nitrous oxidevasodilationcan be associated with amaurosis fugax
Chocolate headachechocolatePEAPEA crosses the blood-brain barrier, increases brain serotonin and cerebral blood flowAs low as 3 mg PEA can induce a headache, blocked by methysergide

Stress, sleep disturbance, hypothalamus, and allostatic loading

The concept of allostatic load refers to the pathophysiology of cerebral neuronal networks by repetitive physiological and psychological stressors. The hypothalamus is a major component of the central autonomic network and the key nexus in homeostatic regulation. The hypothalamus activates the SSN-SPG-GSPN parasympathetic arc, which mediates parasympathetic vascular tone and the activation of perivascular nociceptive fibers and is connected with the TVS [47]. It is well-known that a sphenopalatine block can abort a migraine headache and cranial autonomic symptoms can occur in up to two-thirds of migraine patients ipsilateral to the headache. It is also well-established that PET scans show the activation of the hypothalamus in addition to the midbrain (PAG) and dorsal pons (LC and DRN) during a migraine headache attack [48].

The hypothesis is that stressors such as sleep disturbance, hunger, emotional distress, and even cyclical events (seasonal changes, menopause, menstrual cycle) activate the hypothalamus indirectly via the SSN-SPG-GSPN arc or directly activate the TVS. Activation of the TVS cascades into the amygdala and basal forebrain explaining the irritability, emotionality, and mental fog associated with migraine [49].

These repeated stressors (allosteric load) over the long term lead to reduced gray matter volume of the cingulate and insula (the salience network) altering the valence or value of incoming afferent signals thereby altering the perception of pain and altering the emotional response to pain (anxiety and depression). This phenomenon correlates with migraine frequency [50].


Bei Patienten mit sogenanntem vaskulärem Kopfschmerz wurden die Histaminausscheidung sowie die Histaminurie nach intravenöser L-Histidinbelastung untersucht.

Es wurden folgende Ergebnisse gefunden: Bei 7 von 22 Patienten mit Bing-Horton-Kopfschmerz (cluster headache) war die Histaminausscheidung bei einer oder mehreren Gelegenheiten erhöht. Die Ausscheidung war an Tagen mit Anfällen signifikant höher als an anfallsfreien Tagen.

Bei 5 von 31 Patienten mit Migräne wurden an Tagen mit Anfällen eine erhöhte Ausscheidung gefunden. 7 von 24 Migränepatienten zeigten eine vermehrte Ausscheidung an anfallsfreien Tagen. Drei Patienten zeigten sowohl während als auch nach Kopfschmerzanfällen eine erhöhte Histaminurie. Die Ausscheidung an Tagen mit Anfällen war nicht signifikant verschieden von der an anfallsfreien Tagen.

Bei Patienten mit „cluster headache“ ergaben die Versuche mit L-Histidinbelastung an Tagen mit Anfällen keinerlei Hinweise für eine vermehrte Histaminbildung.

Der zugrunde liegende Mechanismus der vermehrten Histaminausscheidung beim „cluster headache“ kann entweder in einer vermehrten Bildung, einer verstärkten Freigabe oder einem veränderten Katabolismus bestehen. Das Auftreten von Histamin scheint eher eine Folge als die Ursache von Anfällen mit „cluster headache“ zu sein.

Why Are Some People More Susceptible to Histamine Intolerance?

There are several reasons someone may have decreased DAO activity. In my newest book, The 4-Phase Histamine Reset Plan, I go into all underlying causes and give you a detailed plan on how to stop histamine intolerance in it’s tracks. For this article, I will go into the mot common reasons for the development of HIT. First, there may be a genetic abnormality in the DAO gene, which limits its production, and decreases the amount of DAO you can produce, causing an issue breaking down histamine. These genes won’t be fully expressed until adulthood, which explains why 80% of individuals with HIT are middle-aged women over 40. 3,4 However, the primary explanation for HIT is poor gut health. Small intestinal bacterial overgrowth (SIBO) & leaky gut specifically. In SIBO, there is an overabundance of bacteria, which results in histamine production from the proteins of undigested food. Common symptoms include bloating, diarrhea, abdominal pain, and weight loss. Just to clarify, some bacteria in the small intestine is normal however, the type of organism in addition to the amount is important here. 6 Usually organisms in the small intestine are gram-positive, but with SIBO, it’s common to find more gram-negative bacteria, like E. Coli and Klebsiella pneumoniae. 7 While most are familiar with the type of havoc E.Coli can cause, Klebsiella can cause mucosal damage to the intestinal walls and lead to nutrient absorption issues, causing more serious problems like malnutrition, osteoporosis, etc. 8 With leaky gut, intestinal permeability causes inflammatory stress in the body which leads to decrease in the DAO enzyme production.

(p. 81) The relationship between mast cells and histamine

PRINTED FROM OXFORD MEDICINE ONLINE ( © Oxford University Press, 2021. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy and Legal Notice).

The amount of histamine that can be extracted from various body tissues has been studied extensively in recent years. However, little attention has been paid to the histology of tissues rich in histamine or to the changes which accompany histamine release. Since it is now believed that heparin in all species is produced by tissue mast cells . . . it seemed of interest to determine whether histamine also could arise from tissue mast cells. . . . Further evidence that substantial amounts of histamine are contained in, and can be released by, tissue mast cells is presented in this paper.

Access to the complete content on Oxford Medicine Online requires a subscription or purchase. Public users are able to search the site and view the abstracts for each book and chapter without a subscription.

Please subscribe or login to access full text content.

If you have purchased a print title that contains an access token, please see the token for information about how to register your code.

For questions on access or troubleshooting, please check our FAQs, and if you can't find the answer there, please contact us.

The science of migraines

SAN JOSE, CALIFORNIAIf you've ever had a migraine, you know it's no ordinary headache: In addition to throbbing waves of excruciating pain, symptoms often include nausea, visual disturbances, and acute sensitivity to sounds, smells, and light. Although there's no cure for the debilitating headaches, which affect roughly 10% of people worldwide, researchers are starting to untangle their cause and find more effective treatments. Here today at the annual meeting of AAAS (which publishes Science), Science sat down with Teshamae Monteith, a clinical neurologist at the University of Miami Health System in Florida, today to discuss the latest advances in the field.

Q: How is our understanding of migraine evolving?

A: It's more complicated than we thought. In the past, researchers thought of migraine as a blood vessel disorder, in part because some patients can feel a temple pulsation during a migraine attack. Now, migraine is considered a sensory perceptual disorder, because so many of the sensory systems—light, sound, smell, hearing — are altered. During an attack, patients have concentration impairments, appetite changes, mood changes, and sleeping is off. What fascinates me is that patients are often bothered by manifestations of migraine, such as increased sensitivity to light, in between attacks, suggesting that they may be wired differently, or their neurobiology may be altered. About two-thirds of patients with acute migraine attacks have allodynia, a condition that makes people so sensitive to certain stimuli that even steam from a shower can be incredibly painful. One way to view it is that migraineurs at baseline are at a different threshold for sensory stimuli.

Q: What is the most cutting-edge treatment today?

A: The mainstay acute treatment for migraines are a class of drugs called triptans, which act on serotonin receptors. Serotonin is thought to be the underlying neurotransmitter involved in migraine, based on a lower than normal level of serotonin (5-HT) which increases during attacks. There's also a strong relationship between depression [which is linked to abnormal serotonin levels] and migraines: People with depression are more likely to get migraines, and people with migraines are more likely to be depressed. It's not entirely clear how triptans work, but they are able to abort attacks in some patients. They are wonderful drugs, but not everyone responds. The field is now wide open for new drug targets, especially ones that do not constrict blood vessels like the triptans.

Q: What are some promising new treatments?

A: One new drug targets a substance called CGRP — calcitonin gene-related peptide — thought to be one of the peptides that's released during an acute migraine attack. A multicenter, randomized, double-blind placebo-controlled preventive study [in which different doses of the CGRP-targeting drug, telcagepant, were given to people with migraine] showed some liver enzyme abnormalities in a small subset of patients so it failed to pass the safety requirements although the data suggested a potential role. But now there's an antibody version that has completed the phase II studies and is considered the hottest new thing in the field. It was too small of a trial to really determine effectiveness, but it is still really exciting because it's the first trial which suggests that a drug which targets CGRP can be safe.

Q: To what extent is migraine inherited?

A: The genetics need some work because migraine so complicated, but for most patients we're able to tie it to a family history. As a medical resident in 2008, I learned about three genes associated with hemiplegic migraine, a condition in which people go weak on one side. Now, a number of additional genes have been associated with migraine. Some are associated with glutamate, a neurotransmitter associated with excitatory functioning. A lot of brain systems utilize glutamate — a major excitatory neurotransmitter — so blocking it may have some challenges.

Q: What risk factors have you found for migraine?

A: Migraine usually presents itself in adolescence or preadolescence women are more likely to have migraines around their menstrual cycles and the headaches seem to happen in response to hormonal changes in men as well. Low socioeconomic status as well as obesity, and poor sleep also increase the frequency of attacks. Lesions in brain tissue called infarctions are complications of migraine, and risk factors such as smoking and oral contraception may increase the risk.

Q: What are some challenges to studying migraine in the brain?

A: Right now we're stuck with animal models that don't exactly mimic the complexities of the human brain or even a migraine attack. Human brain imaging has a much greater potential and has exciting applications in migraine. With brain imaging, we are able to better understand the structures, connections, and chemicals that are involved in migraine. In addition, postmortem studies of the brains of people who have suffered migraine may be helpful in better understanding the etiology of white matter lesions commonly associated with migraine, currently of unknown etiology. However, it can be difficult to interpret such studies because what caused someone to expire — stroke, cancer, etc. — might change the brain.

Check out our full coverage of the AAAS annual meeting.

What message would you send into space? Tell us on Twitter and Vine with #msgtospace!

What Is The Prevention of Migraine Syndrome.

Of utmost importance in the pre­vention of attacks is a consideration of the personal problems of the patient. Patients with migraine headaches are anxious, striving, perfectionistic, order-loving, rigid persons who, during periods of threat or conflict, become progressively more tense, resentful, and fatigued. The person with migraine often attempts to gain approval by doing more and better than his fellows and to gain security by holding to a stable environment given system of excellent performance, even an n high cost of energy.

This pattern brings increased| responsibility and admiration, but little love. aSl that he feels greater and greater resentment at ism. pace he feels obliged to maintain. Then tensile associated with repeated frustration, sustained resentment and anxiety, often followed by fatigue and prostration, become the setting in which the migraine attack occurs. Treatment is best if it allows the patient free and repeated expression of his conflicts, resentments, and dissatisfactions, enables him to recognize the nature of his dilemma and its relationship to the physiologic basis of his pain, guides him toward accepting a more realistic appraisal of his needs, and establishes a more efficient regimen compatible with his individual equipment. About two of three patients can be appreciably helped by such aid.

For patients in whom attention to psychological attitudes and adjustment of life situations fail to bring significant relief, two forms of long-term pharmacotherapy have been useful. One is the monoamine oxidase inhibitor phenelzine sulfate, 45 mg. daily, which induces a significant reduction in headache frequency in most patients with migraine, and can be given indefinitely. The other is the serotonin antagonist methysergide, which in doses of 2 mg. three to four times daily is effec­tive in about two of three cases in preventing head­ache of the migraine type. However, methysergide must be used with great caution.

Both ergotamine tartrate and methysergide possess the ability to induce profound vasoconstriction and are contra­indicated in pregnancy, peripheral vascular dis­turbance, severe- hypertension, coronary artery disease, thrombophlebitis, and renal disease. Serious and unexpected vasospastic and psychic reactions have occasionally occurred with methy­sergide. Retroperitoneal fibrosis producing back pain and ureteral obstruction has been reported. Any of these serious complications necessitate prompt discontinuance of methysergide, and any single course of the drug should not outlast three months.

The Ultimate Guide to Foods That Trigger Migraine Attacks

You might already know about common migraine triggers like stress, lack of sleep, and even exercise (no, seriously), but did you know that what you’re eating could also be giving you migraines?

That's right—even if your migraines are typically triggered by visual stimuli like flashing lights, avoiding the foods below could help reduce the frequency or severity of your attacks.

Does food really trigger migraines?

Of course, the relationship between food and migraine isn’t clear-cut, and unfortunately, no single factor can be directly tied to your attacks. That said, there's scientific evidence that suggests migraines may be triggered by certain foods. Additionally, 27% of those who experience migraines believe that particular foods are personally triggering.

According to Dr. Sara Crystal, clinical neurologist and Cove Medical Director, certain foods and additives are more likely to trigger headaches in a higher percentage of migraineurs, but even among individuals, other factors like stress, hormonal changes, and lack of sleep can increase the likelihood of an attack after consuming a known trigger.

So, without further ado, here’s a list of the most common food triggers for migraine sufferers, in no particular order.

10 Migraine-Triggering Foods

1. Excessive Coffee

We know that some of you are probably groaning when you see this, but research shows that excessive caffeine consumption can trigger migraines, and both a 2016 study and a 2019 study suggest cutting back on coffee can help reduce migraines.

Now, if you can’t start your day without coffee, note the use of the word “excessive.” We know that the caffeine boost can feel like a lifesaver at times, and if that’s the case, drink it! But try to limit yourself to less than two cups per day.

2. Red Wine

Nope, it’s not just you. Studies confirm that alcoholic beverages are a common trigger, with certain chemicals in alcohol like tyramine and histamine believed to be the problem. Red wine, a commonly-reported trigger, contains a lot of histamine.

3. Aged Cheeses

Unfortunately for cheese lovers, this delicacy can also be a trigger for migraine symptoms. Again, the culprit is tyramine. Blue cheese, brie, cheddar, swiss, feta, mozzarella, and most other common cheeses are good to avoid.

4. Chocolate

We hate to (continue to) be the bearers of bad news, but chocolate can also sabotage your chances of avoiding migraines. One study found that, compared to a placebo, chocolate triggered a migraine in 42% of its subjects.

5. Citrus Fruits

While eating lots of fresh fruit is a great way to avoid migraines (and stay healthy!), you might want to be careful with citrus fruits. While some people say oranges, grapefruits, lemons, and limes give them migraines, they’re not as common a trigger as some of the other foods on this list. Try tracking your migraines to see if avoiding these fruits makes a difference for you.

6. Aspartame and Other Artificial Sweeteners

If you’ve got a sweet tooth, listen up: Research suggests that artificial sweeteners like aspartame commonly found in Diet Coke and other calorie-free drinks may increase the risk of migraine headaches.

7. Yeast

Foods that contain yeast—like sourdough bread and fresh-baked goods like donuts, cakes, and breads—have been known to trigger migraines. The sneaky ingredient is (you guessed it) tyramine, the same culprit found within alcohol and cheese.

8. Monosodium Glutamate (a.k.a. MSG)

MSG is a flavor enhancer used in a variety of processed foods, like frozen or canned foods, soups, snacks, seasoning, and more. A 2016 review of the available science concluded that MSG is no more likely to cause a headache or migraine than placebo, but many migraine sufferers say MSG is a trigger for them.

9. Processed and cured meats

Cured and processed meats (think: bacon, sausage, ham, and deli meats) often include nitrites and nitrates, known migraine triggers used to preserve their color and flavor. One study found that 5% of subjects with migraine history were statistically more likely to experience head pain on days they consumed nitrites, so make sure you check the ingredients you leave the grocery store with that pack of bacon.

10. Nuts and Certain Seeds

Addicted to almond butter? Prepare for some bad news: almonds, peanuts, and many other nuts and seeds contain tyramine, and you know what that means. Like all triggers, not all migraine sufferers are sensitive to nuts, so a trial and error may be the key to figuring out if you are.

A Few More Potential Trigger Foods

Even though we’d hate to take the fun out of even more of your favorite foods, we should let you know about these other potential trigger foods. According to the Cleveland Clinic, these foods are commonly reported as migraine triggers, but there’s no scientific evidence that they really cause them, so don’t clean out your fridge just yet. Instead, turn to a migraine tracker to see if any of these might be causing you pain.

  • Avocados
  • Chicken livers and other organ meats
  • Dairy products like buttermilk, sour cream, and yogurt
  • Dried fruits like dates, figs, and raisins
  • Garlic
  • Most beans including lima, fava, navy, pinto, garbanzo, lentils, and snow peas
  • Onions
  • Pickled foods like olives, sauerkraut, and, of course, pickles
  • Potato chips
  • Some fresh fruits like ripe bananas, papaya, red plums, raspberries, kiwi, and pineapple
  • Smoked or dried fish
  • Tomato-based products (including pizza!)

How Do You Identify Your Triggers?

So how do you know which of these foods (if any) are actually triggering your migraines? Since food affects all migraine sufferers differently, the best thing you can do is examine your eating habits and identify patterns that could be potential triggers. By slowly eliminating foods one-by-one, you can start to recognize what spurs your migraines. Food allergy testing can also be helpful, though you should still be wary of certain foods even if you aren’t allergic to them.

To keep track of your habits, Dr. Crystal recommends keeping a careful food diary for at least one month to record what you do and don’t eat. If something is a trigger, an attack will likely hit 12 to 24 hours post-consumption. You’ll be able to trace the pain back to the source—or at the very least, narrow it down.

We know reading this might make you feel like you’ll have to start living off of nothing but water if you want to avoid debilitating pain, but it’s important to remember that not all of these foods are triggers for every sufferer (and for many sufferers, hunger can be a bigger trigger than any specific food). Migraines are personal, and the only way to learn your specific triggers is to track your migraines, make one adjustment at a time, and see what helps.

And, of course, not all foods are your enemy. Check out this article for a list of migraine-safe foods. Looking for dinner ideas? Try this roundup of migraine-safe recipes.

Rather not change your whole diet to avoid migraines? Look into trying a preventive treatment, such as a supplement, that can help reduce your migraine frequency.

The information provided in this article is not a substitute for professional medical advice, diagnosis, or treatment. You should not rely upon the content provided in this article for specific medical advice. If you have any questions or concerns, please talk to your doctor.

Watch the video: What Is the Relationship Between Guru and Disciple? Sadhguru (May 2022).