Why do diets cause headaches

About It was also noted that IR might correlate with attacks duration in migraine suffers [ 62 ]. Migraine and metabolic syndrome are usually comorbid, though no causal relationship has yet been established [ 60 ]. Moreover, the association between metabolic syndrome components and migraine characteristics including frequency of headache attacks, severity and duration needs further studies [ 60 ].

Although no specific treatment for migraine and concurrent metabolic syndrome has been proposed to date, general recommendations are given on following a weight reduction plan including diet and physical activity, proper sleep duration, and reducing stress levels [ 60 ]. The hypothetical relationship between obesity and migraine has been linked to an elevated release of pro-inflammatory markers and neuroinflammation that might be principally involved in migraine pain genesis [ 28 ].

Among the studied proinflammatory agents, elevated level of C-reactive protein CRP , which is known as a marker of systemic inflammation, has been reported both in obese individuals and patients with migraine.

It seems there could be an epidemiological association between CRP and migraine headache onset [ 63 , 64 ]. These events finally lead to a persistent low-grade inflammatory status [ 20 — 22 ]. In addition, due to the important role of CGRP in migraine pathogenesis, the neuropeptide and its receptors are predominantly important targets for migraine treatment [ 29 ].

On the other hand, evidence proposed an increase in plasma CGRP level in adults with obesity, which is also observed in patients with migraine [ 29 , 30 , 70 , 71 ]. Moreover, it has been proposed that the administration of CGRP induces the accumulation of fat in obese animal models.

Also in murine model, an elevation of CGRP level was reported before obesity onset [ 70 — 73 ]. Substance P SP in another factor which is likely to play a role in migraine attack pathogenesis that was also detected in adipose tissue and shares a role in fat accumulation and the start of the inflammatory cascade related to obesity [ 70 ]. Further, in recent years, the relationship between adipocytes released factors, known as adipokines e.

Although more studies are required to make a definite conclusion, the current evidence propose that adiponectin concentration might be increased between attack phases whereas it may be decreased during migraine attacks [ 23 , 24 ]. It has also been mentioned that the level of this factor might be mediated following prophylactic treatment of migraine with topiramate [ 23 ].

Thus, it could be hypothesized that chronic rise in adiponectin level might be beneficial in migraine improvement [ 23 ]. This issue might be related to the reported correlation of low level of adiponectin with proinflammatory cytokine secretion and platelet aggregation [ 22 , 74 ].

Thus, at lower than normal levels, adiponectin might be nociceptive [ 58 ]. On the other hand, reduced adiponectin level appears be involved in increasing the risk of developing obesity, atherosclerosis and diabetes [ 22 , 75 ]. The current findings reported leptin administration in Wistar rats could diminish the threshold of pain [ 76 ]. On the flip side, enhancement of leptin levels following weight reduction has been noted [ 23 ].

However, the results of the researches concerning the association between leptin levels and migraine have not been conclusive yet [ 23 ]. Nonetheless, it is likely that migraineurs might have lower leptin levels in ictal phases and higher levels of leptin during inter attack periods.

Besides, there may be a negative relationship between leptin and pain intensity [ 23 ]. Some neurotransmitters, such as serotonin 5HT , are responsible for food consumption and body weight regulation which are controlled by hypothalamus and seems to be involved in sense of fullness [ 25 ]. On the other hand, the increment in serotonin concentrations in ictal periods in migraine can possibly be attributed to the secretion of serotonin from platelets that induce vasoconstriction of arteries and affects CSD development [ 26 , 27 ].

Another appetite regulator, which also might be contributed to migraine, is orexin A. An increase in CSF level of orexin has been observed in migraineurs [ 63 ]. Orexin A could have antinociceptive characteristic and may probably play a role in compensatory reaction to pain and also contribute to hunger perception [ 63 ]. Additionally, orexinergic system dysfunction may be associated with homeostatic pathways which are involved in risk of attack generation, migraine nociception and characteristics, as well as its premonitory stage including appetite alteration [ 77 ].

Evidence showed that orexin A administration in murine model stimulates hunger and postpones the sense of fullness [ 63 ]. Therefore, applying the medications that can affect the orexinergic system may ameliorate migraine associated gastrointestinal features [ 77 ]. However, more studies are needed in order to address the association between orexin A and migraine headache in obese and non-obese individuals and explore the effects of drugs that target this system in migraineurs.

Besides, available data suggest that hypothalamic NPY may contribute to the etiology of weight gain among migraineurs who received prophylactic treatment [ 77 ]. For instance, NPY concentrations in plasma of migraine suffers may be elevated following treatment with flunarizine or amitriptyline. It has been also proposed that the weight gain following drug therapy may probably be related to changes in leptin transport system or sensitivity to leptin [ 77 ].

In , a trial conducted to assess the role of fat-reduced diet for migraine control in 54 adults. They reported a notable reduction in headache frequency, intensity, and need for abortive medication [ 78 ].

An open-label, randomized cross-over trial investigated the effect of a diet change in comparison with a placebo supplement on migraine patients. Then after a 4-week washout period was considered and the studied subjects in either group crossed over to the other group. A decrease in headache intensity, frequency, and use of abortive medication were observed following the intervention; However, in the mentioned trial, details regarding dietary fat composition were not noted [ 79 ].

Additionally, based on the theory of the probable effects of different fat types on headache characteristics, a randomized study assessed the effect of omega-3 and omega-6 intake. Fifty-five adults with CM were either reduced omega-6 fats intake or reduced omega-6 fats along with increased omega-three consumption. Headache frequency was also reduced in all treatment groups incl. Amount and type of fat intake affect inflammatory responses [ 16 ].

The balance between the omega-6 and omega-3, two main fatty acids that compete with arachidonic acid as eicosanoid biosynthesis precursor, contribute to inflammatory control in response to the environmental metabolic changes. Prostaglandins PG , which are made from essential fatty acids, take part in platelet function and regulation of vascular tone.

PGs also play the principal role in controlling acute and chronic inflammation [ 16 ]. PGE1, downstream metabolite of linoleic acid omega-6 , is one of the most potent vasodilators. PGE1 has been shown to cause headache [ 83 ]. On the other hand, omega-3 fatty acids i.

It is generally believed that high-fat diet elevates plasma LDL-cholesterol and consequently increases platelet agreeability [ 86 ]. Studies reported hypercoagulation in serum samples obtained from healthy subjects after a high-fat meal [ 78 , 87 ]. On the flip side, it has been suggested that migraine attack could be initiated following and condition that causes platelet aggregation, through serotonin secretion and its consequent effects on blood vessels, and NO and PGs production.

The secretion of these factors simultaneously may contribute to head pain initiation in migraine [ 88 ]. In particular, it is proposed that vulnerability to migraine is likely to be related to constant low concentration of serum serotonin and increased sensitivity to serotonin agonists during attacks, probably due to a defect in serotonin metabolism [ 26 , 27 ].

In this regard, suppressing platelet aggregation might have therapeutic value in migraine prevention [ 88 ]. Therefore, any modalities in dietary fat intake that results in modulating plasma free fatty acids and plasma lipid profile and consequently reducing platelet aggregation, seems to decrease the frequency and duration of migraine headache [ 78 , 88 ].

Each headache patients may have a specific trigger or a unique set of triggers. It is known that certain types of foods and beverages can act as headache triggers [ 13 ].

Cheese, chocolate, citrus fruit, alcohol, coffee, tomatoes, carbohydrates, leavened products and red wine are among the proposed foods that may trigger migraine attacks [ 13 , 89 , 90 ]. However, there is not any consensus between previous studies on identifying food triggers in headache. For example, as mentioned, chocolate have been introduced as one of triggering foods of headache; while a double-blind trial by Marcus et al.

However, after administration of chocolate and carob both two samples , there was not any differences in provocative effects of these agents on headache [ 91 ]. In the following paragraphs, the studies regarding elimination diets in headache patients have been described. A few studies assessed the effect of elimination diets in controlling headache among adults.

Two randomized controlled trials RCT , applied the personalized method for eliminating trigger food in migraine suffers, using IgG antibodies to food antigens [ 92 , 93 ]. Although, the week parallel-group trial on patients with migraine like headaches that examined the impact of the elimination diet compared to a sham diet failed to show any differences between the 2 studied arms [ 93 ], the other study demonstrated beneficial effects in reducing migraine headaches [ 92 ].

In this research, the effect of the eliminating diet in migraineurs, who also suffered from irritable bowel syndrome was explored. It was reported that a diet excluding provocative foods in comparison with provocation diet could effectively attenuate the symptoms of both disorders with positive effects on patients quality of life [ 92 ]. Similarly, a small cross-over RCT showed that individualized elimination diet could reduce migraine frequency and abortive medication need, compared to a standard diet after six-week [ 18 ].

Some headache suffers report that specific foods only provoke headache in combination with stress or extended physical exercise. Both conditions are identified as headache triggers and lead to the production of proinflammatory cytokines [ 18 ]. Therefore, it seems that applying elimination diets in headache patients with food sensitivities could be effective in preventing migraine attacks, though more studies are needed [ 94 ].

Some patients may also be sensitive to other triggers like histamine, which is related to impairment of detoxification caused by low activity of di-amino-oxidase. Histamine thus, may play an additional role which should be considered in the elimination diets [ 18 ]. A sample of 28 patients who suffered from chronic headache attacks were assigned to complete a histamine-free diet for 4 weeks.

Also, the number of headache attacks and analgesic medication consumption significantly decreased following the histamine-free diet [ 95 ]. With respect to the probable link between migraine and allergy [ 96 , 97 ], and due to the beneficial effects of histamine-reduced diet on histamine intolerance symptoms and allergic disorders [ 98 , 99 ], it can be hypothesized that this type of diet might be promising in migraine control particularly among allergic patients.

The mechanisms of IgG-mediated food allergy have not been entirely clarified, but it has been suggested that an increase in production of pro-inflammatory mediators and IgG antibodies through food allergy reaction can induce an inflammatory state that may play a crucial role in the migraine pathophysiology [ 92 ].

In both migraine and food sensitivities, inflammation induced by food could make the pro-inflammatory environment which is needed for the induction of headache by other triggers [ 18 ].

In this regard, when we focus on inflammation caused by food, a specific indicator is required. Except for IgG4, all IgG subclasses can cause an inflammatory response in exposure to the respective antigen [ 18 ]. Accordingly, specific IgG can thus be considered as an ideal tool for a vast number of foods to identify individually suspected food items and enables adjusting eating habits in order to prevent chronic inflammation and occurrence of migraine in sensitized patients [ 18 ].

According to the findings of a large sample population-based cohort study there might be a negative relationship between blood pressure and headache occurrence [ ].

Therefore, it may be logical to anticipate that dietary interventions that reduce blood pressure, could also lower headache occurrence. In this regard, certain nutritional strategies for lowering blood pressure including dietary approach to stop hypertension DASH diet and controlling the amount of sodium intake [ , ], could be considered as a matter of interest in studies on headache prophylaxis. Available evidence on sodium intake in relation to headache has mainly focused on monosodium glutamate MSG intake on headache initiation [ ].

However, the result of the only multicenter, randomized clinical trial on the effect of DASH and low-sodium diet on headache is to somehow different. The study was performed on participants in three days phases i. The occurrence of headaches was not different in DASH group compared to controls, following either phases of low, intermediate and high sodium diets. However, headache risk was lower in low versus high sodium intake, both in DASH diet and control groups [ ].

In sum, according to these findings, the current data on the effects of dietary sodium intakes on headache characteristic is not conclusive yet. Thereby, except for those migraineurs suffering from concurrent hypertension [ ], more researches are needed to be able to make certain advice for optimal sodium intake in migraine patients. Dietary sodium may aggregate headache attacks via direct influence on increasing blood pressure or through inducing endothelial dysfunction [ ].

However, due to lack of well-designed clinical trials, and according to the current findings, there is not a persuasive basis for probable beneficial effects of a low sodium diet on migraine. According to the present review, different nutritional interventions might be effective in migraine and their associated symptoms. There are different types of diets that are thought to attenuate migraine headache. For example, KD and MAD might play a role in neuroprotection, mitochondrial function and energy metabolism, compensating serotoninergic dysfunction, decreasing CGRP level, suppressing neuro-inflammation and CSD, all may be involved in the pathophysiology of migraine.

Moreover, obesity and headaches especially migraine could be attributed to each other through mechanisms like inflammation, and irregular hypothalamic function.

These dietary approaches could affect inflammatory responses, platelet function and regulation of vascular tone. Regarding elimination diet, it could mostly be effective in migraine patients with food sensitivities to prevent the headaches. Because in some sections it was not possible to differentiate headache and migraine in included articles, and given there is a dearth of rigorous RCTs in the field of diet and migraine, the results of present review should be should be completed by the future studies.

Authors thank Dr. All authors contributed equally. All authors contributed with data interpretation, drafting, revision of the manuscript and approved the final manuscript.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Soodeh Razeghi Jahromi, Email: ri. Paolo Martelletti, Email: ti. Christian Lampl, Email: ta. Mansoureh Togha, Email: ri. Supplementary information accompanies this paper at National Center for Biotechnology Information , U.

Journal List J Headache Pain v. J Headache Pain. Published online Nov Author information Article notes Copyright and License information Disclaimer. Corresponding author. Received Jul 1; Accepted Oct This article has been cited by other articles in PMC. A description of the studies on dietary interventions in adults with headache. Additional file 2:Table S2. A description of the studies on dietary interventions in children and adolescents with headache.

Abstract The global prevalence of migraine as a primary headache has been estimated as Introduction Headache epidemiology and etiology According to the reports of global burden of headache, [ 1 ], The global prevalence of migraine as a primary headache has been estimated as Suggested mechanisms for the effects of ketosis on headache with a focus on migraine pathogenesis Despite several animal studies have been conducted on the effects of ketosis on different aspects of metabolism [ 52 , 53 ], the exact pathway by which it may affect on CSD, and trigeminal activation has not yet been clarified.

Weight loss strategies The relationship between primary headaches and obesity was first suggested by Scher and colleagues in [ 56 ]. Migraine and metabolic syndrome In addition to obesity, hypertension, dyslipidemia, insulin resistance, and augmented inflammation, that all are believed to be components of metabolic syndrome, tend to be highly prevalent diseases in migraineurs [ 49 , 60 ].

Suggested mechanisms for the association between obesity and headache with a focus on migraine pathogenesis Three dimensional effect of inflammation, headache, and obesity The hypothetical relationship between obesity and migraine has been linked to an elevated release of pro-inflammatory markers and neuroinflammation that might be principally involved in migraine pain genesis [ 28 ].

Adipokines and migraine Further, in recent years, the relationship between adipocytes released factors, known as adipokines e. Effect of irregular hypothalamic function on weight and headache Some neurotransmitters, such as serotonin 5HT , are responsible for food consumption and body weight regulation which are controlled by hypothalamus and seems to be involved in sense of fullness [ 25 ].

Suggested mechanisms for the association between dietary fat and headache with a focus on migraine pathogenesis Fat intake, inflammation, hypercoagulability and hyperaggregability Amount and type of fat intake affect inflammatory responses [ 16 ]. From symptoms of exhaustion to incessant cravings, you must have experienced an array of issues in the process.

A deficit in calorie consumption can also attribute to health issues such as headaches and lightheadedness. Is your weight loss diet giving you a headache as well? From insufficient calorie intake to caffeine withdrawal, every subtle diet tweak can give you headaches, but the exact cause may differ from one individual to another. My simple advice would be to start dieting at least a week after you start exercising to let your body get adjusted with the routine.

Then incorporate a healthy diet and tapering carbohydrate and sugar. According to the dietician, a person trying to shed the extra kilos should avoid:. This is especially common when sodium levels get too low. Lindora Clinic patients often take a potassium supplements during the weight loss phase to maintain normal potassium levels and fight off symptoms, like headaches.

If you are being treated for chronic disease, high blood pressure, or taking potassium-sparing diuretics, you should not take extra potassium supplements without first consulting your physician. Hypoglycemia The brain needs a continuous supply of glucose from the blood in order to function properly. When glucose levels drop as in hypoglycemia the brain is one of the first organs affected, resulting in symptoms such as headache, migraine, confusion, nausea, sweating, faintness, and hypothermia low body temperature.

To prevent low blood glucose levels, eat small and frequent low-sugar meals, never miss breakfast or skip meals, and eat a healthy afternoon snack to appease hunger. Dehydration This condition results from a decrease in total body water content due to less intake or greater fluid loss.