To feed or to fast? Nutritional triggers in migraine: a narrative review

Background: Migraine attacks typically emerge in predisposed individuals after exposure to heterogeneous stimuli that vary widely across patients. A system-level perspective highlights migraine as a disturbance of homeostasis and allostasis: the brain integrates multiple inputs and generates adaptive responses to maintain physiological stability, but sustained physiological or paraphysiological stressors may impose excessive allostatic load. When compensatory mechanisms become energetically costly or insufficient, an “allostatic reset” may occur, clinically manifesting as a migraine attack. Within this framework, the concept of a migraine trigger is better viewed as a threshold modulator rather than a deterministic cause, i.e., a stimulus that lowers the attack threshold in susceptible individuals. Nutrition is among the most frequently implicated domains, including fasting, dehydration, specific foods and additives, and overall dietary patterns.

Methods: This narrative review synthesizes current evidence on dietary exposures as potential migraine precipitants and modulators of disease course.

Results: The most frequently reported food-related triggers include fasting, dehydration, alcohol, coffee and caffeine withdrawal, chocolate, milk and dairy products, processed and cured meats rich in nitrites and nitrates, citrus fruits, tea, onions, tomatoes, ice cream, nuts, spicy foods, and ultra-processed foods. Food additives such as monosodium glutamate, aspartame, sulfites, and other artificial sweeteners have also been repeatedly implicated, alongside dietary histamine and biogenic amines. Importantly, several studies suggest that overall dietary patterns, characterized by high glycemic load, irregular meal timing, excessive sugar and saturated fat intake, or ultra-processed foods, may exert a greater influence on migraine susceptibility than single food items.

Conclusions: Overall, the literature is fragmented and often contradictory, with a frequent mismatch between patient-reported triggers and results from blinded challenge studies, underscoring the roles of recall bias, expectancy effects, and prodromal symptoms (e.g., food cravings) misattributed to causation. Inter- and intra-individual variability – shaped by genetic background, metabolic state, gut-brain axis mechanisms, and comorbidities – suggests that “one-size-fits-all” dietary restrictions are inappropriate. Rather than endorsing broad exclusion lists, current evidence supports personalized trigger identification and prioritization of protective dietary patterns, regular hydration, and consistent meal timing to reduce attack susceptibility and overall disease burden.