Obesity and migraine
A population study
Citation Manager Formats
Make Comment
See Comments

Abstract
Objective: To assess the influence of body mass index (BMI) on the prevalence, attack frequency, and clinical features of migraine.
Methods: In a population-based telephone interview study, the authors gathered information on headache, height, and weight. The 30,215 participants were divided into five categories, based on BMI: 1, underweight (<18.5), normal weight (18.5 to 24.9), overweight (25 to 29.9), obese (30 to 24.9), and morbidly obese (≥35). Migraine prevalence and modeled headache features were assessed as a function of BMI, adjusting by covariates (age, sex, marital status, income, medical treatment, depression).
Results: Subjects were predominantly female (65% female) and in middle life (mean age 38.4). BMI group was not associated with the prevalence of migraine, but was associated with the frequency of headache attacks. In the normal weight group, 4.4% had 10 to 15 headache days per month, increasing to 5.8% of the overweight (odds ratio [OR] = 1.3), 13.6% of the obese (OR = 2.9), and 20.7% of the morbidly obese (OR = 5.7). The proportion of subjects with severe headache pain increased with BMI, doubling in the morbidly obese relative to the normally weighted (OR = 1.9). Similar significant associations were demonstrated with BMI category for disability, photophobia, and phonophobia.
Conclusion: Though migraine prevalence is not associated with body mass index, attack frequency, severity, and clinical features of migraine increase with body mass index group.
Both migraine and obesity are highly prevalent disorders in the population. Migraine affects 12% of the adults in the United States,1 whereas results of the National Health and Nutrition Examination Survey indicate that an estimated 64% of U.S. adults are either overweight or obese.2
Obesity is comorbid with a number of chronic pain syndromes, including fibromyalgia, back pain, and neck pain.3,4 A longitudinal study showed that the relative odds of chronic daily headaches (CDHs), within individuals with episodic headaches, are five times higher in obese individuals (body mass index [BMI] ≥30) than in the normally weighted.5
Little is know about the influence of baseline weight status on the prevalence, severity, and disability of episodic migraine. Migraine and obesity may, however, be linked from a biochemical perspective. It is know that obesity is a pro-inflammatory (adipocytes secrete a variety of cytokines, including interleukin [IL] 6 and tumor necrosis factor [TNF] α, which promote inflammation)6 and pro-thrombotic state7 and that migraine is associated with neurovascular inflammation.8 Migraine and obesity are independent risk factors for cardiovascular disorders, particularly stroke.9,10
As obesity is a risk factor for CDH, herein we predicted that obesity might be associated with the prevalence and severity of migraine. We report a large population study investigating 1) the influence of the BMI on the prevalence of migraine; and 2) the influence of the BMI on the migraine clinical features, including headache frequency, pain severity, disability, and associated symptoms.
Methods.
Population sample.
A validated computer-assisted telephone interview (CATI)11,12 was conducted from 1997 to 2000 in three large metropolitan U.S. areas to identify individuals with selected health problems, including primary headache disorders. The study was performed in participants of Baltimore, Atlanta, and Philadelphia, selected to facilitate the conduct of population-based clinical trials.13
Households were selected using random digit dialing methods. No less than 10 attempts were made to contact each household. At the time of initial telephone contact, a census of the household was obtained from the person who answered the phone. Gender and age of each eligible household member were ascertained. Finally, age-eligible individuals (≥18 years) were selected for the interview. Verbal informed consent (institutional review board approved) was obtained, and the purpose of the survey was described to the respondent.
CATI.
Respondents who agreed to participate in the research were subsequently scheduled for an interview with trained interviewers, using a CATI and computer scripts. The validity of the CATI for the diagnosis of migraine was previously assessed by comparing the telephone-based diagnosis for migraine with an independent diagnosis assigned by a headache specialist. For the diagnosis of migraine, the CATI had high sensitivity (91%) and specificity (98%).11,12
In the CATI headache interview, participants were first asked if they had at least one headache not due to a head injury, hangover, pregnancy, or an illness such as a cold or flu. They were subsequently asked if they had at least five headaches in the previous year. For those who responded positively, they were then asked about how many different types of headache they had. Detailed questions were initially asked about the most severe headache type that the respondent had in the last 12 months. The most severe headache type was initially self-defined. If respondents had a second and different self-defined headache, the same questions were also asked about this headache.
Questions covered all the diagnostic features of migraine with and without aura, as specified by the first edition of the International Classification of Headache Disorders (ICHD-1; 1988).14 The criteria for migraine remain essentially unchanged in the second edition of the ICHD (2004).15 Each headache feature reported in the affirmative (ever vs never) was followed by a question about how often the feature occurred with the specific headache type. The response options included never, rarely, less than half the time, and half the time or more. When nausea, photophobia, or phonophobia was reported in the affirmative, a follow-up question was also asked about the severity (mild, moderate, or severe) of the symptom. Subjects with CDH, defined by 15 or more headache days per month, were excluded from the analyses.
The survey also assessed demographic information (age, gender, race, educational level, marital status) and health status (history of several other medical conditions). Respondents were requested to provide their weight and height at the time of the interview. Headache severity and headache-related disability were assessed in a 10-point scale (from no severe/disabling at all to as severe/disabling it could be). Finally, the questionnaire assessed the amount of over-the-counter, prescribed analgesic medication for headache and prescribed analgesic medication used for other pain conditions, in the prior month and prior 3 months.
Analysis.
Analyses were performed using Stata (Intercooled Stata 6.0 for Windows, College Station, TX). Data were summarized using frequency counts and descriptive statistics. BMI was calculated according to the following formula: BMI = (wt [lbs]/ht2 [in]) * 703. We defined five categories based on BMI: underweight (<18.5), normal weight (18.5 to 24.9), overweight (25 to 29.9), obese (30 to 34.9), and morbidly obese (≥35). The χ2 test was used to compare proportions. We modeled headache features (frequency of headache, duration of headache, headache-related disability, presence and severity of associated symptoms) as dependent variables, using BMI, use of acute or preventive medication, age, race, and socioeconomic status as dependent variables. Based on the 10-point severity scale, headaches were defined as mild (scored from 1 to 3), moderate (scored from 4 to 7), or severe (scored from 8 to 10). Similar definition was used for disability. Multivariate logistic regression was used to estimate the odds ratios (ORs) for each explanatory variable. Continuous independent variables were evaluated for nonlinearity using squared and higher-order terms. Backwards stepwise maximum likelihood estimation was used to arrive at a parsimonious model.
Results.
Description of the sample.
Our sample consists of 30,215 subjects with complete CATI headache history and who provided weight and height. The demographic characteristics of our sample are summarized in table 1. In brief, respondents were predominantly female (65%) and Caucasian (65.7%). Age ranged from 18 to 89 years (mean 38.7). The majority had completed high school. Overall, most of our sample had a normal BMI (51.3%). A total of 30.6% were overweight, 10.4% were obese, and 4.6% were morbidly obese. A minority of subjects (3.1%) was underweight (table 1).
Table 1 Demographic characteristics of the study population
Persons with migraine had a median of 33 headache days per year, and control subjects had a median of 30 nonmigraine headache days per year. A total of 1,246 participants had 15 or more days of headache per month and were excluded from further analyses. Consistently, a total of 25,150 individuals were defined as controls. Control subjects had no headaches on the prior year or had episodic headaches (<15 days per month) not filling criteria for migraine (table 1).
Headache status and BMI.
Migraine was diagnosed in 3,791 individuals (1-year prevalence of 12.5%). Table 2 shows migraine prevalence in female and males, by demographic features. The crude prevalence of migraine was higher in underweight subjects (15.8%) than the normal weight group (13.1%; p < 0.05). Relative to normal weighted, migraine prevalence was not significantly different for overweight (11.8%), obese (11.9%), or morbidly obese (14%) subjects. This pattern held true after stratifying the prevalence by gender. For women, in the normal weight group, the prevalence of migraine was 15.5% and was not significantly different in the other weight groups. In men of normal weight, the crude prevalence of migraine was 7.2%; it was higher only in those with morbid obesity (8.8%; p < 0.01). However, after adjusting for, age, race (table 2), and education (data not shown), the prevalence of migraine was not significantly different by BMI group overall or in any age or gender.
Table 2 Prevalence of migraine by demographic characteristics and body mass index
Headache frequency and BMI.
Although the prevalence of migraine did not increase as a function of body weight, it was associated with high attack frequency (figure). With use of the normal weight group as a reference, whereas just 4.4% of them had 10 to 15 headache days per month, 5.8% of the overweight (OR = 1.3, 95% CI 1.1 to 1.9), 13.6% of the obese (OR = 2.9, 1.9 to 4.4), and 20.7% of the morbidly obese (OR = 5.7, 3.6 to 8.8) had it. Consequently, fewer individuals who were obese (66.3%; OR = 0.8, 0.6 to 0.99, p = 0.04) or morbidly obese (58.1%; OR = 0.5, 0.4 to 0.8, p < 0.01) had less than 3 headache days per month compared with the normal weighted (71.6%) (table 3). No significant changes were seen in the proportion of those with intermediate frequency of attacks (3 to 9 days per month) according to the BMI group. The number of days with headache per month experienced by underweight did not significantly differ from the values for those with normal weight.
Figure. Proportion of migraine subjects with 10 or more headache days per month.
Table 3 Number of days with headache per month according to the body mass index
Headache features and BMI.
BMI was also a predictor of a number of headache features. The proportion of subjects reporting severe migraine attacks increased with BMI group from 53% in the normal weighted group to 57% in the overweight (OR = 1.25 vs normal weight, 95% CI 1.1 to 1.5), 59% in the obese (OR = 1.31, 1.03 to 1.66), and 65% in the morbidly obese (OR = 1.9, 1.2 to 2.4). The proportion of severe attacks in the underweight group was not statistically different from that in the normal weighted.
Similarly, obese (OR = 1.5, 1.2 to 1.9) and morbidly obese (OR = 2, 1.5 to 2.8) subjects more frequently reported having missed at least 1 day of work or school because of their headaches in the prior 3 months compared with the normal weight group. The other groups did not significantly differ.
Exacerbation by physical activities was also more common in the morbidly obese vs the normal weighted (OR = 1.7, 1.2 to 2.2), with nonsignificant trends in the overweight and underweight groups.
The proportion of subjects reporting that typically the pain was unilateral or throbbing did not significantly differ by BMI group among persons with migraine (see table E-1 on the Neurology Web site; go to www.neurology.org). Finally, the duration of pain did not vary according to the BMI group.
The BMI was significantly associated with the proportion of migraine patients that reported photophobia and phonophobia in more than 50% of their migraine attacks (table E-2). With use of the normal weight group as a reference, photophobia in 50% or more of the attacks was reported by 78% of those with normal weight vs 88% of those morbidly obese (OR = 2.0, 1.3 to 3.2). The other groups did not significantly differ. Phonophobia was reported by 75% of those with normal weight, 80% of the overweight (OR = 1.4, 1.2 to 1.7), 82% of the obese (OR = 1.5, 1.3 to 2.1), and 85% of those morbidly obese (OR = 1.8, 1.5 to 2.1). The proportion of subjects reporting nausea or visual symptoms suggestive of aura did not vary significantly by BMI group (see table E-2).
In the logistic regression model, after adjusting for covariates (gender, age, use of headache medications, sleep problems, education status, and depression), frequency of migraine attacks varied as a function of BMI (p < 0.001). BMI higher than 30 was also significantly associated with high severity of pain, high disability, and proportion of attacks accompanied by photophobia and phonophobia.
Discussion.
We conducted a large population-based cross-sectional study to investigate the influence of BMI on the prevalence and clinical attributes of migraine. Our findings suggest the following: 1) Migraine and obesity are not comorbid. The prevalence of migraine in the population does not significantly vary as a function of the BMI group. 2) Obesity is significantly associated with the number of headache days per month among migraineurs, particularly for very frequent headaches (10 to 14 days per month), even after adjusting for covariates. 3) BMI is also significantly associated with the severity of attacks experienced by migraine sufferers, the perception that attacks are worsened by physical activity, and the migraine-related disability. 4) Finally, the BMI influences some associated symptoms, such as photophobia and phonophobia, but not nausea. It does not seem to have an influence on aura. These associations also held true after correcting for several potential confounders.
It has been previously reported that obesity may be associated with the development of CDH.10 In cross-sectional analyses, being overweight (OR = 1.26, 95% CI 1.0 to 1.7) or obese (1.34, 95% CI 1.0 to 1.8) was associated with prevalent CDH. In a subsequent longitudinal study, the odds for the new onset of CDH over the course of 1 year were increased in obese subjects was 5.53 (CI 1.4 to 21.8), relative to the normal weighted. This study addresses the issue of directionality, demonstrating that obesity is a risk factor for new-onset CDH and not the opposite.
Whereas CDH and obesity are comorbid,10 in the current study, migraine and obesity were not. However, we found that obesity was related with the severity and frequency of headache attacks experienced by migraineurs as well as with some associated symptoms.
The mechanisms that link obesity with migraine attack frequency and severity are uncertain. Plasma calcitonin gene-related peptide (CGRP) levels are elevated in obese individuals, particularly in women; fat intake may also be associated with increased CGRP secretion.16 CGRP is significantly higher in obese subjects relative to controls.16 After weight loss, CGRP concentrations remain unchanged. The same study showed that a high-fat meal caused a significant rise in CGRP levels. The authors suggested that elevated plasma CGRP levels may constitute a primary phenomenon in obese women and that fat intake may be associated with increased CGRP secretion.16 This may be important in migraine, where it is well known that CGRP is an important postsynaptic mediator of the migraine trigeminovascular inflammation17 and experimental CGRP inhibitors are effective in the acute treatment of migraine.18
Additionally, obesity itself is a pro-inflammatory (adipocytes secrete a variety of cytokines, including IL-6 and TNF-α, which promote inflammation)16 and pro-thrombotic state.6 Obesity is currently characterized by a chronic, systemic low-grade state of inflammation.19 Biomarkers of inflammation, such as the leukocyte count, TNF-α, IL-6, and C-reactive protein, are increased in obesity, are associated with insulin resistance, and predict the development of type 2 diabetes and cardiovascular disease. The adipocyte is an active participant in the generation of the inflammatory state in obesity. Adipocytes secrete a variety of cytokines that promote inflammation. Moreover, recent studies suggest that obesity is associated with an increase in adipose tissue macrophages, which also participate in the inflammatory process through the elaboration of cytokines. It has been recently suggested that an improved understanding of the role of adipose tissue in the activation of inflammatory pathways may suggest novel treatment and prevention strategies aimed at reducing obesity-associated morbidities and mortality. This may be particularly important for migraine, which is associated with neurovascular inflammation.20–22 Furthermore, migraine, just as obesity, is comorbid with several cardiovascular disorders, as well as a risk factor for stroke, especially in women who have migraine with aura.23
Some caution is required in assessing these results. There is some evidence for participation bias. For example, women are overrepresented, probably because interviews were conducted during business hours most of the time. We addressed this issue by stratifying by gender and modeling the data including demographic features Second, although we modeled our data adjusting for covariates, several other potential confounders, such as the influence of specific food triggers (obese subjects may be exposed to them more often) and exercises could not be assessed. Third, we cannot exclude that some obese individuals have idiopathic intracranial hypertension. However, this pathology is usually associated with daily headaches, not sporadic attacks as in our study. Additionally, although depression symptoms were assessed, a formal depression diagnosis was not obtained. Finally and most important, BMI was calculated based on weight and height that were self-reported. This is critical in the analysis and clearly a weakness of our article. Recent research has investigated this particular issue. Differences between self-reported (over the phone) and measured stature, weight, and BMI were investigated for a sample of 3,797 Minnesota adolescents. Gender, age, race/ethnicity, socioeconomic status, and measured body size were examined as potential factors associated with errors in self-reports. It was concluded that, at least for adolescents, self-reports of stature, weight, and BMI are, on the average, valid representations of their measured counterparts.24 In adults, self-assessment of weight and height has been used to conduct large epidemiologic studies. The National Health Interview Survey interviewed 68,556 adults, and calculated their BMI using CATI assessments of weight and height that were identical to ours, generating data adopted by health-policy makers.25 CATI with self-reported weight has also been used to estimate the impact of obesity on the health-related quality of life26 as well as the comorbidity between obesity and other health problems.27 Nonetheless, it is reasonable to suppose that obese individuals would tend to underestimate their reported weight. If that is so, this creates a bias in our study that is difficult to assess, and this should be taken into consideration.
Although not comorbid with migraine, we found that obesity is associated with the frequency, severity, and some other clinical features of migraine. This refines our knowledge on the clinical manifestations of migraine and also provides insights to the process of migraine chronification. Prospective studies should focus on whether the reduction of weight in obese subjects is associated with a decrease in the burden of migraine.
Footnotes
-
Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the February 28 issue to find the title link for this article.
This article was previously published in electronic format as an Expedited E-Pub on December 14, 2005, at www.neurology.org.
Disclosure: Ortho-McNeil Neurologics funded the analysis of this study. Drs. Bigal and Lipton have received honoraria from Ortho-McNeil Neurologics unrelated to this study.
Received July 14, 2005. Accepted in final form October 26, 2005.
References
- 1.↵
- 2.↵
National Center for Chronic Disease Prevention and Health Promotion. Overweight and obesity: obesity trends. Available at: http://www.cdc.gov/nccdphp/dnpa/obesity/trend/maps/index.htm. Accessed 04/18/2005.
- 3.↵
- 4.
- 5.↵
- 6.↵
Lee YH, Pratley RE. The evolving role of inflammation in obesity and the metabolic syndrome. Curr Diabetes Rep 2005;5:70–75.
- 7.↵
Alessi MC, Lijnen HR, Bastelica D, Juhan-Vague I. Adipose tissue and atherothrombosis. Pathophysiol Haemost Thromb 2004;33:290–297.
- 8.↵
- 9.↵
- 10.↵
Kurth T, Gaziano JM, Rexrode KM, et al. Prospective study of body mass index and risk of stroke in apparently healthy women. Circulation 2005;111:1992–1998.
- 11.↵
Stewart WF, Lipton RB, Whyte J, Dowson A, Kolodner K, Liberman JN, Sawyer J. A multi-national study to assess reliability of the Migraine Disability Assessment (MIDAS) score. Neurology 1999;53:988–994.
- 12.
Stewart WF, Lipton RB, Liberman J. Variation in migraine prevalence by race. Neurology 1996;47:52–59.
- 13.↵
- 14.↵
Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias, and facial pain. Cephalalgia 1988;8 (suppl):1–128.
- 15.↵
Headache Classification Committee of the International Headache Society. The International Classification of Headache Disorders. Cephalalgia 2004;24:1–160.
- 16.↵
- 17.↵
- 18.↵
- 19.↵
- 20.↵
- 21.
- 22.
Stang PE, Carson AP, Rose KM, et al. Headache, cerebrovascular symptoms, and stroke: The Atherosclerosis Risk in Communities Study. Neurology 2005;64:1573–1577.
- 23.↵
Kurth T, Slomke MA, Kase CS, et al. Migraine, headache, and the risk of stroke in women. Neurology 2005;64:1020–1026.
- 24.↵
- 25.↵
- 26.↵
- 27.↵
Letters: Rapid online correspondence
- Obesity and migraine: A population study
- Yasuo Iwasaki, Toho University Omori Hospital, 6-11-1,Omorinishi,Ota-ku,Tokyo ,Japan[email protected]
- Ken Ikeda
Submitted August 07, 2006 - Obesity and migraine: A population study
- Gordon J. Gilbert, Dept. of Physiology and Biophysics, University of South Florida School of Medicine, 500 Pasadena Avenue South, St. Petersburg, FL 33707[email protected]
Submitted August 07, 2006 - Reply from the authors
- Marcelo E. Bigal, Albert Einstein College of Medicine, [email protected]
- Richard B. Lipton
Submitted August 07, 2006
REQUIREMENTS
You must ensure that your Disclosures have been updated within the previous six months. Please go to our Submission Site to add or update your Disclosure information.
Your co-authors must send a completed Publishing Agreement Form to Neurology Staff (not necessary for the lead/corresponding author as the form below will suffice) before you upload your comment.
If you are responding to a comment that was written about an article you originally authored:
You (and co-authors) do not need to fill out forms or check disclosures as author forms are still valid
and apply to letter.
Submission specifications:
- Submissions must be < 200 words with < 5 references. Reference 1 must be the article on which you are commenting.
- Submissions should not have more than 5 authors. (Exception: original author replies can include all original authors of the article)
- Submit only on articles published within 6 months of issue date.
- Do not be redundant. Read any comments already posted on the article prior to submission.
- Submitted comments are subject to editing and editor review prior to posting.
You May Also be Interested in
Hastening the Diagnosis of Amyotrophic Lateral Sclerosis
Dr. Brian Callaghan and Dr. Kellen Quigg
► Watch
Topics Discussed
Alert Me
Recommended articles
-
Articles
Obesity is a risk factor for transformed migraine but not chronic tension-type headacheMarcelo E. Bigal, Richard B. Lipton et al.Neurology, July 24, 2006 -
Views & Reviews
Obesity, migraine, and chronic migrainePossible mechanisms of interactionMarcelo E. Bigal, Richard B. Lipton, Philip R. Holland et al.Neurology, May 21, 2007 -
Articles
Tracing transformationChronic migraine classification, progression, and epidemiologyRichard B. Lipton et al.Neurology, February 02, 2009 -
Articles
Prevalence and characteristics of allodynia in headache sufferersA population studyM. E. Bigal, S. Ashina, R. Burstein et al.Neurology, April 21, 2008