Headache Medicine 2021, 12(1) p-ISSN 2178-7468, e-ISSN 2763-6178

ASAA

DOI: 10.48208/HeadacheMed.2021.4

Headache Medicine

Review

The association between obesity and migraine and possible

mechanisms of action: an integrative literature review

Dieniffer Aparecida Halaiko

Paulo Faro² Aline Andretta Levis

Bárbara Dal Molin Netto

Federal University of Paraná, Curitiba, Paraná, Brazil

Institute of Neurology of Curitiba – INC, Curitiba, Paraná, Brazil

Federal University of Paraná, Curitiba, Paraná, Brazil

Abstract

Introduction

Obesity is a multifactorial disease dened by the excessive accumulation of adipose tissue that

can cause harm to human health. The presence of obesity is an important risk factor for migraine

chronication. However, not much is known about the link between the two diseases.

Methods

In this study, an integrative literature review was conducted to better understand the mechanisms of

interaction between migraine and obesity. Therefore, a search of PubMed and the Virtual Health

Library (VHL) was performed with the following keywords:

enxaqueca e obesidade; enxaqueca

e obesidade e inamação; enxaqueca e obesidade e neuropeptídeos

; migraine and obesity;

migraine and obesity and inammation; migraine and obesity and neuropeptides.

Results

The search identied 22 articles. After reading and analyzing the articles, three thematic categories

emerged: 1) Obesity as an Aggravating Factor for Migraine, 2) Mechanisms Studied between

Obesity and Migraine and 3) The Effect of Weight Loss on Migraine Symptoms.

Conclusions

The chronic low-grade inammation associated with obesity can cause a predisposition to migraine

chronication. The abnormal secretion of adipokines, dysregulation of the sympathetic nervous

system, and hypothalamic dysfunction have been suggested to be the main shared mechanisms

between both diseases.

Dieniffer Aparecida Halaiko

Email: dienifferhalaiko@gmail.com

Bárbara Dal Molin Netto

Email: barbaradm@ufpr.br

Edited by

Mario Fernando Prieto Peres

Marcelo Moraes Valença

Keywords:

Migraine Disorders

Obesity

Inammation

Adipose Tissue

Risk Factors

Neuropeptides

Received: June 25, 2021

Accepted: August 5, 2021

ASAA

Halaiko DA, Faro P, Levis AA, Molin Netto BD

The association between obesity and migraine and possible mechanisms of action: an integrative literature review

Introduction

besity is a chronic disease dened by the excessive

accumulation of adipose tissue, resulting from an energy

imbalance, which can cause damage to human health.

The

worldwide prevalence of obesity practically tripled between

the years 1975 and 2016, and in 2016 more than 1.9 bil-

lion adults were overweight, of which over 650 million were

obese. Globally, there are more obese than underweight

individuals.

In Brazil, the prevalence of overweight is 60.3%,

affecting 96 million individuals, and one third of men and a

half of women are obese.

The etiology of obesity is multifactorial and involves genetic,

behavioral, socioeconomic and cultural factors.

The inade-

quate interaction between the aforementioned factors may

favor an imbalance in energy balance, which promotes lipo-

genesis and, consequently, body weight gain.

This accumula-

tion of adipose tissue and increase in body mass index (BMI)

increase the risk of developing chronic non-communicable

diseases, such as systemic arterial hypertension, dyslipidemia,

cardiovascular disease, diabetes mellitus, osteoarthrosis, ob-

structive sleep apnea syndrome, some types of cancer

and

even migraine.

7,8

In addition, obesity can also lead to mental

illnesses, such as depression.

Migraine is considered a common primary headache, and

is classied as the sixth most prevalent disorder worldwide

and as the rst cause of disability among men and women

under 50 years old.

10,11

It is known that the etiology of migraine is genetic

and that

obesity is an important risk factor for the worsening of its

symptoms. There is strong evidence showing an increased risk

of developing migraine in 50% of individuals with obesity

and migraine attacks appear to be associated with higher

BMIs.

Obesity also seems to interfere with the frequency

14,15

, dura-

tion and intensity of migraine symptoms

, in addition, it can

increase the susceptibility of migraine to chronicity.

17,18

Recent

studies prove this relationship and suggest some mechanisms

for the interaction between the two diseases, such as inam-

mation

, persistent states of hyperleptinemia

, irregular

hypothalamic function and sympathetic dysregulation.

Considering the above, the scientic literature was reviewed

in order to better understand the mechanisms of interaction

between obesity and migraine, in addition to their clinical

implications and the consequences for the health of the indi-

viduals affected by both diseases.

Methods

The present study is an integrative literature review, which

includes different types of studies (experimental, non-exper-

imental and reviews), since a broad understanding of the

phenomenon under study is sought.

To this end, the following steps were taken to develop the

integrative review: the denition of the problem to be re-

searched, a search of the literature (the selection of keywords,

outlining the criteria for selecting articles, and denition of

the databases). The search for articles was carried out in the

PubMed and Virtual Health Library (VHL) databases and the

inclusion criteria adopted were articles published between

2015 and 2020, written in Portuguese or English and that

presented in their discussions considerations about the role

of obesity in migraine. This search took place between the

months of August and September 2020.

To perform the search, the following keywords were used,

considered as descriptors DeCS (Descriptors in Health Scienc-

es), in Portuguese, and MeSH (Medical Subject Headings), in

English: enxaqueca e obesidade; enxaqueca e obesidade e

inamação; enxaqueca e obesidade e neuropeptídeos; mi-

graine and obesity; migraine and obesity and inammation;

migraine and obesity and neuropeptides.

The total number of articles found using the search terms de-

scribed was 54 in the Virtual Health Library (VHL) and 57 in

PubMed. The selection of articles for analysis was performed

through an exploratory reading of the title of all articles found

in each of the databases and summary of 45 articles, and

then 24 were selected for full reading. After the analytical

reading, 22 articles were selected that met the criteria and

answered the guiding question of this review. The steps taken

to develop the integrative review are described in Table 1.

Results and Discussion

After reading and analyzing the selected articles, they were

divided into three categories according to their approaches:

1) Obesity as an aggravating factor for migraine; 2) Mech-

anisms studied between obesity and migraine; and 3) The

effect of weight loss on migraine symptoms.

Obesity as an Aggravating Factor for Migraine

The review found a signicant amount of evidence showing

that there is a relationship between the diseases. The research

showed that overweight and obesity were considered risk

ASAA

Halaiko DA, Faro P, Levis AA, Molin Netto BD

The association between obesity and migraine and possible mechanisms of action: an integrative literature review

factors for migraine chronicity

and that obesity can increase

the risk of migraine by up to 50%, a risk that increases with

the increase in the degree of obesity.

Moreover, the evidence

suggests that the chance of having a daily migraine crisis

is associated with a higher BMI.

In addition, Miri et al.

found a positive association between individuals with obesity

and the presence of migraine with aura. Obese individuals

were 2.92 times more likely to have migraine with aura than

individuals with normal weight.

Corroborating these results,

Huang et al.

found that the higher the frequency of episodic

migraine attacks, the greater the BMI, but this association was

not observed between the severity and duration of headache,

nor in individuals with chronic migraine.

Although there appears to be a relationship between obe-

sity and the chronicity of migraine, several other risk factors

possibly inuence the relationship.

Increased adiposity and

the consequent low-grade chronic inammation can interfere

with the natural history of migraine

, and there is a clear

relationship between obesity and migraine; however, a num-

ber of other risk factors can also have a possible inuence

on migraine

including genetic predisposition, age and sex.

In respect of sex, for example, women with obesity are

more likely to have migraine when compared to men

8,18,25

especially women of reproductive age.

The increased risk

of migraine in women with obesity can be explained by

changes in sex hormones and low-grade inammation due

to the higher percentage of body fat present in obesity.

Furthermore, an experimental study carried out with rats

showed that female rats are more sensitive to light, and the

presence of obesity was shown to aggravate this symptom.

Another important factor in respect of this relationship is that

women with migraine and obesity tend to be less active than

obese women without migraine. The study by Bond et al.

concluded that women with obesity and migraine practiced

1.5 hours less daily physical activity when compared to

obese women without migraine.

There are also differences in the distribution and metabolic

function of adipocytes in relation to age and sex, which may

affect the relationship between obesity and migraine.

More-

over, the duration of obesity and the distribution of body fat

in women with obesity may also be inuenced by variations

in the hormonal concentrations of menstrual cycles during life,

which in turn may have an inuence on migraine.

Mechanisms Studied between Obesity and Migraine

Studies that analyze the mechanisms by which migraine is

associated with obesity are still incipient. The inammation

seen in patients with obesity may be one of the causes of the

high prevalence and progression of migraine in individuals

with both diseases.

14,18,19,22,28,29

The expansion of adipose

tissue, which happens with obesity, leads to an alteration in

the synthesis of pro-inammatory markers, favoring chronic

Table 1. Description of the completed steps for the development of the integrative review

Data base Keywords

Number of references

obtained

References

sorted by title

Abstracts

analyzed

References selected

for analysis

Total for review

PubMed Obesity/ 48 29 19 13 13

Migraine

Obesity/ 6 2 4 0 0

Migraine/

Inammation

Obesity/ 3 3 0 0 0

Migraine/

Neuropeptides

VHL Obesity/ 54 32 22 11 9

Migraine

Obesity/ 0 0 0 0 0

Migraine/

Inammation

Obesity/ 0 0 0 0 0

Migraine/

Neuropeptides

TOTAL 111 66 45 24 22

ASAA

Halaiko DA, Faro P, Levis AA, Molin Netto BD

The association between obesity and migraine and possible mechanisms of action: an integrative literature review

inammation and insulin resistance.

C-reactive protein (CRP),

tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-6

(IL-6), substance P and peptide related to the calcitonin gene

(CGRP) were found in high concentrations in individuals

with obesity and migraine, especially during crises, when

compared to individuals without obesity and without mi-

graine.

18,19,21

These inammatory mediators can sensitize the

central nervous system causing permanent damage to the

periaqueductal gray matter, an area closely related to the

pathophysiology of migraine and its modulation.

In turn, CGRP, which is an important inammatory mediator

in migraine, was also found at high levels in individuals with

obesity.

14,25

Substance P (SP), on the other hand, seems to

play a role in the accumulation of fat and in the beginning

of the inammatory cascade related to obesity, which may

be associated with an increase in susceptibility to trigeminal

stimulation and, consequently, leading to migraine attacks.

It is also important to highlight the possible effects of ele-

vated levels of proinammatory cytokines on the trigemi-

novascular system involved in stimulating migraine pain.

This may explain, at least partially, the more frequent and

severe headaches in individuals with obesity

and how these

changes in the trigeminal nociceptive pathway cause central

sensitization, which favors the evolution of the disease from

its episodic to chronic form.

Adipokines produced by adipose tissue, leptin and adi-

ponectin, have also been shown to be related to migraine.

In contrast to other adipokines, adiponectin is present in

higher concentrations in individuals classied with normal

BMI than in those with obesity. Changes in circulating levels

of adiponectin and leptin are strictly correlated with the devel-

opment of insulin resistance, inammatory processes, obesity

and regulation of adipogenesis.

21,30,31

On the other hand, the

literature contains conicting results regarding the effects of

changes in the serum concentrations of these adipokines on

the pathophysiology of migraine.

It is important to note that, as pointed out in a number of

the studies, adiponectin levels were found to be altered in

individuals both during crises and in the intercritical phase.

One study found that this adipokine appears to be below

normal levels during migraine attacks. It is assumed that low

levels of adiponectin may activate the production of TNF-α,

modulating the functions and phenotype of macrophages,

increasing inammation and nociceptive stimulation.

addition, other studies indicate that this adipokine can act to

worsen migraine by activating the nitric oxide pathway and

inducing a pro-inammatory state.

It should be noted that research on leptin in individuals with

migraine is not yet conclusive. There are assumptions about

a negative relationship between leptin and pain intensity,

since individuals with migraine have lower levels of leptin

during attacks and higher levels in the symptom-free phase.

Leptin may be involved in migraine through several mecha-

nisms.

A picture of hyperleptinemia seems to increase the

susceptibility to cortical spreading depression, since high

levels of leptin cause inhibition in the production and release

of serotonin and orexin-A, hormones that when at low levels

increase the frequency of cortical spreading depression.

Increased levels of leptin can also induce the secretion of

pro-inammatory cytokines, regulating immunoreaction and

inammatory reaction, such as IL-6 and TNF-α, arachidonic

acids and nitric oxide (NO) through the nuclear factor kappa

B (NFκB) signaling pathway.

16,19

In contrast, Ligong et al.

found no relationship between changes in leptin levels in

individuals with migraine.

The interaction between obesity and migraine also seems to

be shared by a bidirectional action involving hypothalamic

dysfunction

16,19,20,28

, since obesity results from a dysregula-

tion in energy metabolism and these changes have been

associated with migraine.

This hypothesis was reinforced

by the performance of imaging tests, which revealed great-

er hypothalamic activation, responsible for the control of

hunger, in the onset of migraine crises.

This may be due

to over-activation of the reward system, obesity linked to

overeating behaviors and migraine to overuse of medicines.

It is also noteworthy that the neuropeptides and neurotrans-

mitters (serotonin, adiponectin, leptin and orexin) that are

involved in the control of the energy balance, also seem to

be involved in the pathophysiology of migraine

7,28,32

. The

increase observed in the concentration of serotonin secret-

ed by platelets during crises may be one of the causes of

vasoconstriction of arteries that are part of the phenomenon

of cortical spreading depression.

Another possible mechanism is attributed to levels of orex-

in-A, as low concentrations were found in women with obe-

sity, and it is assumed that the deciency of this substance

promotes inammation of the trigeminal system contribut-

ing to the development of migraine.

High levels of orexin

were observed in the cerebrospinal uid of individuals with

migraine and was attributed to compensatory reactions

capable of increasing pain. The literature also suggests that

dysfunctions in orexigenic mechanisms can lead to increased

appetite and be related to homeostatic pathways that are

involved in the risk of generating the premonitory phase and

migraine headache.

ASAA

Halaiko DA, Faro P, Levis AA, Molin Netto BD

The association between obesity and migraine and possible mechanisms of action: an integrative literature review

Recent evidence indicates that dysregulation of the sympathet-

ic nervous system may be one of the links between obesity

and increased seizures in migraine patients. It is known that

individuals with obesity are often resistant to the action of

leptin in the central nervous system, which can contribute to an

increase in the risk of developing sympathetic hyperactivity.

High sympathetic tone is a common feature of obesity, which

can lead to a higher frequency of headache.

Figure 1. Shared mechanisms between obesity and migraine

The Eect of Weight Loss on Migraine Symptoms

In view of the strong evidence in the literature on the impact of

obesity on the frequency, duration and severity of migraine

and its transformation from episodic to chronic migraine, it is

important to consider approaches aimed at treating obesity

in migraine patients as it is a modiable risk factor.

Some studies have been developed to evaluate weight loss

as a treatment for migraine. The study by RazeghiJahromi

et al.

found that the surgical treatment of obesity through

gastric sleeve surgery in women with migraine promoted a

reduction in the severity and duration of crises, in addition

to providing a greater number of days without migraine.

Corroborating these ndings, a systematic review study with

bariatric patients observed a reduction in migraine frequen-

cy, headache-related disability and pain intensity 6 months

after surgery.

The improvement in migraine can be explained by the effects

of weight loss on metabolic abnormalities, decreased circu-

lating levels of inammatory adipokines related to migraine,

and decreased hormones produced by adipocytes due to

a reduction in the size of this cell.

Studies have shown that

gastric surgery can produce a signicant decrease in the

levels of glucose, insulin, leptin and adrenocorticotrophic

hormone (ACTH) one month after surgery.

Reinforcing the inuence of obesity on migraine, Di Vincenzo

et al.

compared surgical and non-surgical weight loss as

treatment methods for migraine, and reported positive re-

sults, with similar benets found in respect of the frequency,

intensity of pain, disability and duration of crisis, regardless

of the type of weight-loss treatment.

Bond et al.

sought

to evaluate the effects of two intervention methods on mi-

graine, conventional weight loss and a migraine control

educational protocol. Similar improvements in the frequency

of migraine were observed in respect of both interventions.

The authors suggest that the effects of conventional weight

loss on migraine are due to improvements in physiological,

psychological and behavioral factors, such as inammation,

depression and physical activity, respectively. In respect of

the migraine education, the benets can be attributed to

greater knowledge of the causes, triggers and behaviors

related to crises, as well as the correct way to manage them.

The mechanisms by which weight loss acts to control migraine

in individuals with obesity are not yet fully understood, as

studies have shown a reduction in the frequency of crises, the

intensity of the migraine and related disability even before

any signicant weight loss; it has been suggested that even

the small changes in the size of adipocytes following weight

loss programs can be benecial in respect of the release of

adipokines observed before any major changes in weight.

The negative energy balance resulting from different strat-

egies for weight reduction seems to generate a decrease

in circulating pro-inammatory cytokines and an increase

in anti-inammatory cytokines, which may have a positive

impact on the control of migraine crises.

Thus, the literature

indicates that normalizing adipokine levels through weight

loss can improve the pro-inammatory state responsible for

increasing the frequency and intensity of headache.

Several characteristics are shared between both diseas-

es and are involved in their triggering and/or worsening,

such as: depression, anxiety, uctuations in stress, stressful

events in childhood, short sleep duration, irregular meals,

more Westernized diets (rich in fats and sugars combined),

a sedentary lifestyle, as well as prolonged fasting and the

use of certain medications.

8,28

Moreover, the atherogenic

prole observed in individuals with migraine shares common

features with the prole of individuals with obesity, and is

possibly related to a higher incidence of migraine in indi-

viduals with obesity.

Limitations

Considering the studies evaluated in the present review on the

relationship between obesity and migraine, there are some

factors that can limit the expansion of knowledge about the

association of these disorders, such as:

ASAA

Halaiko DA, Faro P, Levis AA, Molin Netto BD

The association between obesity and migraine and possible mechanisms of action: an integrative literature review

a) Sample size and selectivity: since many of the studies

comprise samples of women of reproductive age who have

undergone weight loss, the results cannot be generalized to

other populations;

b) Absence of control groups with individuals with normal

weight and migraine;

c) Lack of differentiation between migraine and other types

of headache;

d) Use of migraine drugs in research aimed at evaluating the

symptoms of headache after weight loss;

e) Not following standard classications for migraine and

BMI. In addition, in order to have greater validity in respect

of the nutritional diagnosis, it is necessary to use methods

that assess body composition and levels of adipose tissue.

Conclusions

We conclude that the chronic low-grade inammation associ-

ated with obesity may predispose individuals to migraine, in

addition to increasing the number and severity of migraines

and the associated disability. Furthermore, abnormal adipo-

kine secretion, sympathetic dysregulation and hypothalamic

dysfunction have been suggested as mechanisms shared

between obesity and migraine. It should also be noted that

it is well established in the literature that weight loss can

decrease the frequency, intensity and duration of crises, as

well as migraine-related incapacity.

Conflict Of Interest: There is no conict of interest.

Author contributions: BDMN, DAH and AAL - Article plan-

ning, denition of research strategies and guiding question,

critical review of intellectual content; BDMN, DAH and PF

- Final approval of the version to be published.

Dieniffer Aparecida Halaiko

https://orcid.org/0000-0003-1074-7936

Paulo Faro

https://orcid.org/0000-0001-8932-4164

Aline Andretta Levis

https://orcid.org/0000-0001-7578-2375

Bárbara Dal Molin Netto

https://orcid.org/0000-0003-0748-7141

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