Alcohol & Migraine
Migraine is present in 12% of the world’s population and in women three times more than men. In one study 25% of women had migraine at age 42, and 6% of men had migraine at age 38, after which the incidence decreased. Migraine is the most common chronic medical problem for women. For women migraine is more common than diabetes, hypertension, heart disease, or arthritis.
Migraine headaches are frequently one sided, associated with moderate or severe throbbing headache pain, nausea, vomiting, and sensitivity to light and sound. Migraines are disabling with the patient often times missing work or social activities. There are many relationships which are thought to “trigger” or bring on a migraine headache such as menstruation for women, fasting, or stress. One of most commonly stated but not quite scientifically documented, migraine triggers is drinking alcohol, especially red wine. This article explores the neurology literature on this subject.
Alcohol &Migraine Alcohol is commonly stated to be a trigger by many patients and accepted by many doctors. The problem is that studying the relationship statistically gives some positive results, but also confusing results that limit the relationship.
1.Older personal, non-scientific statements. Older historical statements are stronger than newer, more carefully constructed scientific research studies. One of the earliest references connecting migraine and alcohol was made by Celsus (25 B.C.-50 A.D.) “the pain…is contracted…by drinking wine.” Another earlier statement was made by Paul of Aegina (625-690 A.D.) who commented on the relationship between drinking wine and the occurrence of migraine. Paulus Aeginata in the seventh century described migraine from “drinking of wine.” It has been thought that certain chemicals in alcohol such as tyramine and histamine act in the brain to set off a migraine headache.
2.Who educates about triggers? The National Headache Foundation, the American Headache Society, and many migraine web sites and doctors who write on migraine advocate attention to alcohol and dietary factors to avoid migraine and often provide a list of foods and chemicals that are suspected of doing this. However, the whole question of migraine worsened by various foods is controversial and confusing.
3.What do expert neurologists who write about migraine say? Lance, the famous Australian neurologist who first wrote about “ice pick headache” wrote in 1995: “…my patients with special food triggers have the same number of migraine attacks when they avoid triggers as before. The only thing on which they agreed is that alcohol precipitates attacks, specifically red wine. Otherwise, I think the question of dietary migraine is very suspect.”
4. What is a trigger? The American Headache Society web page states the following: “A migraine trigger is any factor that causes a headache in individuals who are prone to develop headaches. Only a small proportion of migraine sufferers, however, clearly can identify triggers. Examples of triggers include stress, sleep disturbances, fasting, hormones, bright or flickering lights, odors, cigarette smoke, alcohol, aged cheeses, chocolate, monosodium glutamate, nitrates, aspartame, and caffeine. For some women, the decline in the blood level of estrogen during the onset of menstruation is a trigger for migraine headaches. The interval between exposure to a trigger and the onset of headache varies from hours to two days. Exposure to a trigger does not always lead to a headache. Conversely, avoidance of triggers cannot completely prevent headaches.”
5. Migraine trigger literature review
Kelman writing in Cephalalgia in 2007 on “The triggers or precipitants of the acute migraine attack” listed stress at a frequency of 79 % and food at 26.9 %. The table of frequency of individual migraine triggers from his article is:
Hormones (in women) 65.1%
Not eating 57.3%
Sleep disturbance 49.8%
Perfume or odor 43.7%
Neck pain 38.4%
Light (s) 38.1%
Sleeping late 32.0%
Gallagher writing in Headache in 1988 on “Diet and Migraine” stated: “Alcohol is a nonspecific vasodilator that is thought to provoke migraine attacks in susceptible persons by depressing or altering the function of central vasomotor centers, since the direct effect of alcohol on blood vessels is insignificant. Of all the known precipitating agents, alcohol is the most consistent provoker of headache in the largest number of migraine patients.”
Littlewood, et al, wrote in the Lancet in 1988 on “Red wine as a Cause of Migraine.” They studied 19 migraine patients who thought they were sensitive to red wine, 5 migraineurs who thought they were not sensitive, and 8 control patients who neither had migraine nor red wine sensitivity. The study was for 11 patients sensitive to red wine to drink 300 mL of red wine, and the rest to drink 300 mL of vodka and lemonade. All drinks were taken cold from a brown glass bottle through a dark straw to conceal color and flavor; both the red wine and vodka mixture had the same alcohol content.
Nine of the 11 red-wine sensitive patients reported migraine after drinking wine but none of the 8 patients reported migraine after drinking vodka. The tyramine content of the wine was less than 1 mg and thought to not be responsible for inducing migraine. The authors concluded that “flavanoids,” substances that give red wine its color, and which are absent in white wine, cause the migraine headaches and they suggested that studies be done to discover the chemical agents provoking migraine.
Diamond writing in Neurology Forum in 1991 on “Dietary Factors in Vascular Headache” stated: “Many migraine patients will report an acute migraine attack precipitated by consumption of alcoholic beverages, such as red wine.”
Jarman, et al, described the “Release of (14C) 5-hydroxytryptamine from human platelets by red wine,” in Life Sciences in 1991. Jarman, et al, stated: “Since 5-HT, is probably released from body stores during migraine attacks and red wine is known to provoke migraine episodes in susceptible individuals, release of 5-HT, possibly from central stores, could represent a plausible mechanism for its mode of action.”
Spierings writing in Headache Quarterly in 1992 on “Headache Caused by Medications and Chemicals,” stated: “alcohol can also precipitate the so-called hangover headache in those who are not subject to headaches. Hangover headache occurs in up to 50% of subjects with an alcohol intake of 1.5 mL or more per Kg body weight. It is generalized in location, often throbbing in nature, and is accentuated by sudden movements of the head.[i]
Peatfield wrote in Headache in 1995 on “Relationships between food, wine, and beer-precipitated migrainous headaches.” Peatfield queried 577 consecutive patients attending the Princess Margaret Migraine Clinic from 1989 to 1991 about dietary precipitants of their headaches. Migraine occurred in 429 patients and 16.5% of these reported headaches brought on by cheese or chocolate, and nearly always both.
Of the migraineurs, 18.4% reported sensitivity to all alcoholic drinks, while another 11.8% were sensitive to red but not white wine. Beer provoked a migraine in 28% of the patients. There was a definite statistical association between sensitivity to cheese/chocolate and to red wine (P<0.001) and also to beer (P<0.001). None of the 40 patients with tension type headache reported sensitivity to foods, and only one was sensitive to alcoholic drinks. At the end of the article Peatfield stated:
It is concluded that cheese/chocolate and red wine sensitivity, in particular, have closely related mechanisms, in some way related more to migraine than to more chronic tension-type headache, while quite separate mechanisms play a major role in sensitivity to alcoholic drinks in general.
Kwasniewska, et al, writing in 2000 in Przegl Lek on “Red wine in medicine: panacea, fashion or…risk factor?” tried to put the red wine issue in perspective and acknowledged that red wine had been the subject of much interest in health care professionals representing different specialties of medicine. In general, the cardio-protective mechanisms of red wine, although not completely understood, are thought to relate to ethanol which increases high-density lipoprotein cholesterol (HDL) and inhibits platelet aggregation. Red wine also contains polyphenols (flavanoids, phenolic acids, and stilbenes) which have antioxidant, vasorelaxing, and antiplatelet properties.
Kwasniewska, et al, point out that there is a considerable body of evidence indicating that regular consumption of red wine at moderate doses (200-400 ml/day) provides protection against ischemic heart disease, perhaps diabetes, osteoporosis, and some cancers. The authors then stress the dangers of alcohol intake—dependence, alcoholism, organic disease, migraine, and allergies—and advise that “medical recommendations of red wine consumption be formulated very carefully.” One has to balance the good medicinal effects of red wine with the bad to get a clear picture.
Panconesi takes a similar global view of the place of red wine in health in an article entitled “Alcohol and migraine: trigger factor, consumption, mechanisms. A review” written in 2008 in J Headache Pain. This study utilized a MEDLINE search from 1988 to October 2007 for “headache and alcohol”, “headache and wine”, “migraine and alcohol,” and “migraine and wine.” In retrospective studies, about 1/3 of migraine patients reported alcohol as a frequent migraine trigger, but only 10% of migraine patients reported alcohol as a frequent migraine trigger. Recent studies showed that migraine patients consume less alcohol than controls. Red wine was reported to be the principal trigger of migraine, but other studies showed that white wine or other drinks were more frequently involved.
The study reported the different chemicals thought to be responsible for migraine. There was uncertainty in agreement on which chemicals were important yet biogenic amines, sulphites, flavonoid phenols, 5-hydroxytryptamline and vasodilating effects were discussed. The author concluded with the following statement: “The fact that few headache patients cannot tolerate some alcoholic drinks does not justify the consideration that alcohol is a major trigger and the suggestion of abstinence. In fact, low doses of alcohol can have a beneficial effect on patients such as migraineurs, who were reported to have an increased risk of cardiovascular disease.
Panconesi closed stating that “alcohol induced migraine is a very individual, specific reaction.”
Panconesi, et al, writing Alcohol and Migraine in 2013 as a legacy contribution from the American Headache Society Committee for Headache Education and the Fred Sheftall, MD Education center stated:
1.Alcohol is a migraine trigger, but its risk is overstated.
2.Alcohol can provoke two types of headache in migraine patients: an attack within a few hours and a delayed hangover headache.
3.Migraine patients consume alcohol less often than the general public.
4.Although migraine sufferers consider red wine the principal migraine trigger, studies show that other alcoholic drinks are equally or more frequently the cause.
5.Alcohol, and not a different constituent of the drink, is probably the trigger.
6.A small dose of alcohol, such as a 5-ounce glass of good wine, can be consumed if it does not trigger migraine frequently. Drink in small amounts to the benefit of your heart but use caution with breast cancer risks.
Panconesi, et al, asked “How important is alcohol as a trigger of migraine?”
Migraine patients consider many foods capable of triggering migraines. The food-trigger relationship is frequently equivocal. In fact, lists of triggers induce the migraineur to equate their migraine attack with a food just consumed. This is similar to crediting a new symptom to a drug they are taking at that moment. With full review, the cause and effect may or may not be true.
A food may be likely considered a trigger of a migraine attack If a) a strict time relationship exists between the consumption and the start of headache, or b) that this link is not occasional. From retrospective patient reports, it is very difficult to make sure a link exists. In fact, especially in the drug-new symptoms example, a possible link to other frequent triggers (stress, post-stress, fear, anxiety, menstruation, weather changes, etc.) must be considered.
When chocolate was studied to assess a chocolate trigger-headache link no connection was found with migraine and tension-type headache. Many consider alcohol to be a sure migraine trigger, but its importance is still debated.
In studies from different countries that collect date from the past, about one-third of migraine sufferers reported alcohol as a migraine trigger at least occasionally. In these retrospective studies, only 10% reported a frequent link. Curiously, in some countries the connection was negligible (1.4 to 6.1% of patients). The degree of alcohol habits perhaps explains these differences. No sex differences exist in alcohol susceptibility. The great majority of studies show no differences between migraine with or without aura. No difference exists between migraine and tension-type headache. Cluster headache patients have higher alcohol sensitivity (about 50-80%).
In a forward-looking study (PAMINA) published in 2007, Austrian researchers examined a large number of factors related to migraine. After an advanced data analysis, they found limited importance of nutrition, including alcoholic beverages in the precipitation of migraine. This work considered alcohol and other nutritional factors taken the day before onset of headache.
What is the interval from alcohol consumption to the start of headache?
Alcohol can trigger a migraine attack within a few hours (30 min to 3 hours). This is the typical headache induced by alcohol. Another type is the delayed alcohol-induced headache (DAIH). This hangover headache appears in the next morning after alcohol intake. At this time the blood alcohol level is falling and reaches zero. The symptom of headache is present in 2/3 of subjects with alcohol hangover.
The DAIH can be experienced by anyone, but people with migraine are more susceptible. Furthermore, migraine patients can develop headache with the ingestion of modest amounts of alcohol. All alcoholic drinks can provoke either immediate or delayed headache.
Alcohol consumption in migraine
Since alcohol can trigger a migraine attack, in a sense only a small number of migraineurs should drink alcohol. Population-based studies performed in various countries (US, Scandinavia, Netherlands, Japan, Italy) show that fewer migraine sufferers consume alcohol than those without headaches. Moreover, the more alcohol consumed the less likely the drinker reported migraine and non-migraine headache. This fact may be explained by sufferers of headache giving up alcohol since it is a trigger factor for their headache attacks.
However, an Italian study seems not to support this explanation. In this study, only a very small percentage of non-alcohol consuming female migraineurs reported that alcoholic drinks were a trigger. They concluded that this fact could not explain the large difference in alcohol consumption between migraine and the general public.
Is alcohol or another component of the drink the headache trigger?
Red wine is typically considered the most likely alcoholic drink trigger. In 1988, Littlewood and colleagues showed that 300 ml or ten ounces of red wine, but not vodka with an equivalent alcohol content, provoked headache in red wine sensitive migraineurs. Migraineurs not sensitive to wine and non-headache controls did not have headaches triggered. They suggested that red wine contains a migraine-provoking agent that is not alcohol.
Some studies in France and Italy report white wine as the major culprit. However, there are reports of also spirits, sparkling wine and beer triggering headache. Wine does not need to be ingested in large quantities to produce headache. In wine sensitive patients the time between drinking red wine and developing headache varied from 30 min to 3 hours. Only one or two glasses at most need be ingested.
The fundamental question still remains to be made definitely clear. Is alcohol or another component of the drink responsible for triggering headache? It remains difficult to answer this question. To provoke a migraine, attack a combination of factors may be necessary. These may include a given blood/brain alcohol level with degree of brain sensitivity along with the presence or not of other triggers.
Perhaps this combination activates the pathways necessary for headache to become active. Otherwise, if alcohol is not directly involved in producing headache per se, a substance present in the different alcoholic drinks seems responsible or facilitates the alcohol effect.
Some components of alcoholic beverages such as tyramine, phenylethylamine, histamine, sulfites, flavonoid phenols, have been considered possible triggers for migraine. This is due to their presence in various alcoholic drinks, and the belief the drink is capable of triggering migraine. However, this is not verified as studies are either negative or lack adequate proof to support their causal role.
Histamine is the substance most frequently mentioned. Some consider it an indicator of the wholesomeness of the food or food quality. Various foods such as fish, aged cheese, meat (sausage, salami), vegetables (eggplant, sauerkraut, spinach), contain much higher amounts of histamine than alcoholic drinks. In addition, many foods, including alcohol, may release histamine from bodily sources known as mast cells.
Histamine infused by vein is a time-tested way to provoke a migraine attack. However, other than headache, many symptoms of so-called “histamine intolerance” are not characteristic of a migraine attack. That antihistamine drugs do not prevent red wine headache further fails to support histamine as a critical trigger.
The same observations made on histamine are valid for sulfites. Much higher amounts are found in many foods compared to wine. These include dried fruits, chips, raisins, soy sauce, pickles, and juice fruits. So-called “sulfite sensitivity” provokes asthmatic responses rather than headache.
Tyramine is a naturally occurring monoamine that is not able to cross the blood-brain barrier. It is responsible for the so-called “cheese effect.” Its triggering relationship to migraine has been the most extensively studied. The studies have generally shown negative results. Considerable Tyramine is found in most meats and fermented foods, many condiments, figs, red plums, and raspberries among others. Tyramine is nearly impossible to avoid, as it is so widely distributed in foods. In addition, the Tyramine content of wine is negligible (1-2 mg/L) in comparison with the Tyramine doses utilized in oral challenge studies (100-200 mg).
Flavonoid phenols and tannins, both alike in character and action, are by-products of alcohol fermentation. These congeners, or alike minor chemical substances, give wine its distinctive character. Others known congeners include acetone, acetaldehyde, fuel oil, and furfural. These alcohol by-products have been suggested as responsible for triggering migraine. Darker colored drinks such as whiskey, brandy, and red wine have more of these by-products than lighter drinks such as vodka, gin, or white wine.
However, certain studies on white wine and spirits suggested more frequent involvement than with darker drinks. Bourbon has 37 times more of these substances than vodka. Recently, it was shown to cause a worse hangover than vodka, increasing the intensity of the hangover felt. Bourbon did not appear to increase the risk for impaired performance, sleep-disrupting effect, etc. The lack of a role for congeners in alcohol hangover was recently confirmed in an animal model of migraine.
Alcohol is probably the trigger of migraine. Increased artery size is the mechanism frequently suggested. This vasodilatation could explain the immediate headache provoked by high initial blood/brain levels. Vasodilatation cannot explain Delayed Alcohol-Induced Headache as the symptom of alcohol hangover appears when alcohol levels decline to reach zero. If vasodilatation is not responsible for alcohol-related headache, what other explanations might explain this effect?
Perhaps an action on nerve transmitters involved in central pain control is responsible. Specifically, serotonin (5-HT) release must be considered. Population surveys show that illicit/recreational drugs such as MDMA/ecstasy (amphetamine derivative) and ‘party pill’ BZP/TFMPP (piperazine derivatives), both serotonin and 5-HT releasing drugs, provoke headache in a high percentage of users. Young adults use recreational drugs very commonly in combination with alcohol (90%). Controlled studies show that BZP/TFMPP provoke headache/migraine in 2/3 of subjects.
Another piperazine derivative, mCPP is a nonselective serotonin activator. It is a liver-produced by-product of trazodone, an often-used sleeping aid. mCPP is extensively used to study altered serotonin nerve transmission and provokes migraine-like headache. This occurs in about 50% of subjects with oral mCPP. Migraine-like headache and many additional symptoms occur when given IV mCPP in research.
Should migraine patients avoid alcohol consumption?
Alcohol in low dose, especially of red wine, reduces the risk of cardiovascular disease. Migraine, specifically with aura or high frequency, increases the risk of some cardiovascular diseases. The unselective suggestion of alcohol abstinence for all migraine patients is not correct. In fact, patients with high migraine frequency with increased risk of ischemic stroke may benefit from a low dose of alcohol. Certainly, alcoholic drinks may trigger migraine and tension headache in some subjects.
This is probably much less likely than that suggested by patient’s recall. Moreover, it is frequently necessary to consume alcohol along with other factors (anxiety, stress events, emotions etc.) to trigger a headache attack. Before alcohol is considered responsible for a migraine attack, the patient should review certain factors. These include careful recording of the intake of the amount of alcohol, the specific drink types, the frequency of induced-headache to the amount and type and the 48 hours prior to headache and any “situation” or “stress” prior to the alcohol intake.
Panconesi, et al, closed with this statement, “If you find consistent agreement among these factors and the headache, alcohol is possibly causing headaches. However, when the factors do not associate together consistently, or extremely rarely, abstinence is not necessary. Since alcohol is considered a risk factor for breast cancer, know your risk for this disease.”
Krymchantowski, AF, et al writing in Headache, in 2014 Jun;54(6):967-75 on Wine and headache, performed a Medline search with the terms “headache, migraine, and wine.” The writers commented that “The notion of migraine attacks triggered by food and beverages has been posited for centuries. Red wine in particular has been acknowledged as a migraine trigger since antiquity when Celsus (25 B.C.-50 A.D.) described head pain after drinking wine.
Since then, references to the relationship between alcohol ingestion and headache attacks are numerous. The most common initiator of these attacks among alcoholic beverages is clearly wine. The aim of this review is to present and discuss the available literature on wine and headache.”
The authors commented that “Full papers specifically on headache and wine are scarce. General literature related to medicine and wine is available, but scientific rigor is typically lacking. The few studies on wine and headache were mostly presented as abstracts despite the common knowledge and patients' complaints about wine ingestion and headache attacks. These studies suggest that red wine, but not white and sparkling wines, do trigger headache and migraine attacks independently of dosage in less than 30% of the subjects.
Krymchantowski AF, et al, closed by saying: Wine, and specifically red wine, is a migraine trigger. Non-migraineurs may have headache attacks with wine ingestion as well. The reasons for that triggering potential are uncertain, but the presence of phenolic flavonoid radicals and the potential for interfering with the central serotonin metabolism are probably the underlying mechanisms of the relationship between wine and headache. Further controlled studies are necessary to enlighten this traditional belief.
Borkum, JM, wrote in Headache. 2016 Jan,6(1):12-35. On Migraine Triggers and Oxidative Stress: A Narrative Review and Synthesis. The author mentioned that, “The recent discovery that the TRPA1 ion channel transduces oxidative stress and triggers neurogenic inflammation suggests that oxidative stress may be the common denominator underlying migraine triggers.
Borkum performed a Medline search “crossing the terms "oxidative stress" and "brain" with "alcohol," "dehydration," "water deprivation," "monosodium glutamate," "aspartame," "tyramine," "phenylethylamine," "dietary nitrates," "nitrosamines," "noise," "weather," "air pollutants," "hypoglycemia," "hypoxia," "infection," "estrogen," "circadian," "sleep deprivation," "information processing," "psychosocial stress," or "nitroglycerin and tolerance." "Flavonoids" was crossed with "prooxidant."
The reference lists of the resulting articles were examined for further relevant studies. The focus was on empirical studies, in vitro and of animals, of individual triggers, indicating whether and/or by what mechanism they can generate oxidative stress.” Borkum concluded by saying, “Oxidative stress is a plausible unifying principle behind the types of migraine triggers encountered in clinical practice. The possible implications for prevention and for understanding the nature of the migraine attack are discussed.”
Onderwater, et al. writing in 2018 on “Alcoholic beverages as trigger factor and the effect on alcohol consumption behavior in patients with migraine.” In European Journal of Neurology, stated that: “Our study shows the effect that this trigger [e.g. alcoholic beverages] has on patients with over 25% of patients with migraine not consuming alcohol because of the (presumed) triggering effect.”
The study was done in Dutch adults aged 18-80 years of age with migraines (with or without aura). Of the 2,197 individuals in the study, 35.6% reported alcohol as a trigger. As a result, just over 25% of the participants reported abstaining from alcohol consumption. This was a web-based questionnaire study from individuals who participated in the Leiden
University Migraine Neuro-Analysis (LUMINA) study between February 2008 and January 2013. LUMINA is a study of Dutch adults with migraine with or without aura, recruited by advertisement, public announcement, or website. The questionnaire asked about number of alcoholic beverages consumed, triggers for migraine, reasons for abstinence, and time from alcohol consumption to migraine onset.
Among 2197 respondents, 70.4% reported drinking alcoholic beverages in the past three months. Among those who did not drink alcoholic beverages, about 25% had stopped drinking because of their presumed potential to trigger migraines.
A large majority of respondents (77.8%) considered wine, especially red wine, to be the most common alcoholic trigger for migraine. Only 8.8% of participants reported that drinking wine consistently lead to an attack. Among those who did not drink alcoholic beverages, about 25% had stopped drinking because of their presumed potential to trigger migraines. A large majority of respondents (77.8%) considered wine, especially red wine, to be the most common alcoholic trigger for migraine. Yet only 8.8% of participants reported that drinking wine consistently lead to an attack.
This inconsistency between drinking wine and migraine attacks suggests that alcohol alone may not be enough to trigger attacks, according to the authors. Instead, individual variation in trigger threshold may play a role, they suggested. One-third of participants had a quick onset of attack, within three hours of having a drink. Alcohol may have a quick onset of attack or a slow onset such as with hangover headache, which usually develops several hours later or the next day, as the blood ethanol level decreases over time. The shorter onset suggests a different mechanism r alcohol-triggered migraine, and that substances other than ethanol may be involved, they hypothesized.
Onderwater, et al, summary
Over 25% of migraineurs who abstain from alcohol do so because of its presumed potential to trigger attacks.
Among alcoholic drinks, red wine was reported as the most common trigger for attacks
Alcohol was inconsistently linked to attacks, suggesting individual variation in alcohol-triggered migraine threshold
Onset of attack was quick, within three hours of a drink.
Different studies report different findings on which type of wine triggers migraine the most. One European study found that 11% of migraineurs thought that red wine was their most common trigger, yet a French study showed that 54 % of alcohol induced attacks came after drinking white wine. Red wine has 20-200 times more histamine than white wine. Women have more migraines triggered by red wine than men.
1.So, is alcohol really a migraine trigger?
Migraine is an inherited, genetic medical problem. The genes for migraine with and without aura have been found and the data about this is published. You are born with migraine and you’re going to die with it, unless scientists learn how to change your genes. The exact relationship for and if alcohol aggravates migraine isn’t clear. Currently, migraine experts believe alcohol may cause a change in brain activity which affects neurochemicals and neuronal transmission.
2.What about Alcohol and Cluster Headache?
The Diagnostic Classification of Headache Disorders III refers to Cluster headache as one of the trigeminal autonomic neuralgias. The first classification of migraine used in the US published in the 1980’s considered cluster headache to be a kind of migraine, but today the two conditions are seen separately, but with some similar features. For instance, cluster headache, like migraine, responds to fast acting sumatriptan 6 mg given subcutaneously which acts in 10 minutes.
However, it is known that when a cluster headache patient consumes alcohol during their cluster headache time, 1-7 headaches a day for 6 weeks, alcohol will then trigger a cluster headache. This relationship is only true during their cluster time and they can drink at other times without fear pf a cluster headache if they are not currently having headaches.
3.What about the other migraine triggers? Are they real?
Many triggers are thought to trigger an attack of episodic migraine. Marmura, MJ writing in Curr Pain Headache Rep, 2018 Oct 5;22(12):81 stated that although the experimental trigger, glyceryl trinitrate, reliably produces migraine, “natural triggers are much less predictable and vary in importance between individuals.”
Many migraine triggers have been established based on patient surveys, diary studies, and clinical trials. The reliable well-known triggers are stress, menstrual cycle changes, weather changes, sleep disturbances, alcohol, and certain foods. Also, fasting, premenstrual periods in women, “letdown” after stress, and most likely low barometric pressure changes are migraine triggers.
Migraine may have early “prodrome-before the headache” symptoms such as neck pain, fatigue, sensitivity to light, sounds, and odors. “Multiple studies clearly demonstrate triggers in episodic migraine, often related to change in homeostasis or environment. Many common migraine triggers are not easily modifiable, and avoiding triggers may not be realistic. Healthy lifestyle choices such as exercise, adequate sleep, stress management, and eating regularly may prevent triggers and transformation to chronic migraine over time.”
Author note. In my book, Migraine, I have a chapter on triggers, with 28 entries.
4.Is there a difference between migraine trigger and aggravation?
Yes, ICHD III separates a “migraine trigger” from a “migraine aggravation” by time—usually 48 hours. I quote from my book, Migraine, “Since antiquity it has been recognized that the brain of a person with migraine is overly sensitive to different environmental, physical, and emotional factors, and that an attack of migraine may follow the episodic or the continual occurrence of one of these factors.
These provocative events are called either ”trigger factors” if they increase the probability of a migraine attack in the short term (usually 48 hours) or "aggravating factors" if they are associated with a relatively long-term increase in the severity or frequency of attacks (usually weeks to months).
ICDH-II gives examples of aggravating factors as “psychosocial factors, frequent intake of alcoholic beverages, other environmental factors.” Regarding trigger factors ICDH-II states: “Though some trigger factors have been reasonably well studied epidemiologically (e.g. menstruation) or in clinical trials (e.g., chocolate, aspartame), causal attribution in individual patients may be difficult.”
5.Can alcohol provoke 2 kinds of headache with migraine?
Yes, alcohol can trigger a migraine if the headache comes within 10 minutes after drinking alcohol. This immediate response is usually only found in persons with migraine. Alcohol can commonly cause a later occurring headache called a “hangover headache” in a non-migraineur, especially if they drink a lot and the headache comes after a delayed period of time, after sleep, the next morning. Persons with migraine may be more sensitive to hangovers than the ordinary person.
All the best.
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Britt Talley Daniel MD