Abstract and Introduction
Abstract
Objective: To assess whether alcohol intake is associated with the onset of migraine attacks up to 2 days after consumption in individuals with episodic migraine (EM).
Background: Although alcohol has long been suspected to be a common migraine trigger, studies have been inconclusive in proving this association.
Methods: This was an observational prospective cohort study among individuals with migraine who registered to use a digital health platform for headache. Eligible individuals were aged ≥18 years with EM who consumed alcohol and had tracked their headache symptoms and alcohol intake for ≥90 days. People who did not drink any alcohol were excluded. The association of alcohol intake ("Yes/No") and of the number of alcoholic beverages in the 2 days preceding a migraine attack was assessed accounting for the presence of migraine on day-2 and its interaction with alcohol intake on day-2, and further adjusted for sex, age, and average weekly alcohol intake.
Results: Data on 487 individuals reporting 5913 migraine attacks and a total of 40,165 diary days were included in the analysis. Presence of migraine on day-2 and its interaction with alcohol intake on day-2 were not significant and removed from the model. At the population level, alcohol intake on day-2 was associated with a lower probability of migraine attack (OR [95% CI] = 0.75 [0.68, 0.82]; event rate 1006/4679, 21.5%), while the effect of alcohol intake on day-1 was not significant (OR [95% CI] = 1.01 [0.91, 1.11]; event rate 1163/4679, 24.9%) after adjusting for sex, age, and average weekly alcohol intake. Similar results were obtained with the number of beverages as exposure.
Conclusions: In this English-speaking cohort of individuals with EM who identified themselves as mostly low-dose alcohol consumers, there was no significant effect on the probability of a migraine attack in the 24 h following consumption, and a slightly lower likelihood of a migraine attack from 24 to 48 h following use.
Introduction
Since primates began to eat fermenting fruit, the use of alcohol has had a profound effect upon humanity. Early Egyptian and Sumerian writings extoll the medicinal and dietary use of alcohol, and evidence has been found of use dating back to 7000–6600 BCE.[1] The relationship between alcohol and headache has also been described throughout history; the direct association with migraine, however, took much longer to develop.[2] The concept of migraine being separate or different from other headaches took centuries to be established, with the scientific definition still being modified today.[3]
The International Headache Society currently classifies alcohol-induced headache as a secondary headache, and distinguishes it from immediate and delayed (or hangover) headache.[4] Some individuals see an immediate reaction to alcohol (within 3 h from ingestion) with regards to stimulating a headache. More often, however, individuals experience a delayed effect of alcohol (5 h or more after ingestion). In both cases, the headache resolves spontaneously within 72 h.[4,5] People with migraine might find it difficult to distinguish between a migraine attack triggered by alcohol and a delayed alcohol-induced headache as symptoms may overlap.[5] Moreover, no specific clinical biomarkers have been found helpful in differentiating these conditions. Immediate alcohol-induced headache usually appears in people without migraine after consuming large amounts of alcohol, while smaller amounts may induce a migraine headache in persons with migraine.[4]
In this study we focused on the role of alcohol as a potential trigger of migraine attacks within 24–48 h after consumption. This delayed effect of alcohol on migraine attack onset may be more difficult to ascertain by an individual compared to an immediate effect. Consumption varies greatly between cultures, regions, and between individuals, a fact which may explain why different studies have found opposing results. An extensive review, including 22 studies in migraine populations in 13 different countries, found that overall close to one-third of participants self-reported retrospectively alcohol (any type) as an occasional trigger and about 10% as a consistent trigger.[6] The prevalence of alcohol as a trigger of migraine attacks estimated in prospective studies is lower.[7–9] One possible explanation is alcohol avoidance and/or low alcohol consumption in migraine populations.
The study of migraine triggers is complex. About 70% of people can identify a factor that is likely to predispose them to a migraine attack (triggers).[10] Among self-reported triggers there are endogenous events such as menses,[11] and exogenous events such as dietary factors[12] (including alcohol,[6,13] chocolate,[14,15] aspartame[16,17]), weather conditions,[18,19] and air pollution.[20,21] Interventional studies to test whether a potential trigger is indeed a trigger are rare. Oftentimes individuals with migraine give up trying to identify which of the multiple potential triggers reported in population-level analyses may apply to them. They may then decide to avoid those which they cannot confirm as a trigger or those for which they cannot develop some coping strategy.
Given that alcohol is a part of the social lives of many people, it would be useful to implement study designs and analytical techniques that may identify individuals for whom alcohol is indeed a trigger and individuals for whom it is not.
Individual-level analysis plays an important role in the study of migraine-associated exposures.[22] Mixed effects models may be the method of choice to study the association between potential triggers/protectors and migraine attacks. They provide specific estimates of the exposure effect for each individual while making optimal use of population-level data.[23] This balance between expected norms for the population and the individuals' experience may provide a more tailored approach to the issue and provide guidance for good self-care. In a recent individual-level analysis of the association between triggers and migraine attack onset among people with episodic migraine (EM), our group found that same-day alcohol consumption was associated with increased risk of an attack in less than 0.5% of drinkers.[9]
The objective of the present study is to explore the relationship between alcohol intake and risk of migraine attack onset at the individual level among people with EM who consume alcohol. We hypothesized that any alcohol intake as well as the number of alcoholic drinks on a given day may be associated with the onset of migraine attacks during the day after consumption or up to 2 days after consumption, and the effect of the association may vary among individuals.
Headache. 2022;62(10):1329-1338. © 2022 Blackwell Publishing
