Obesity and Headache: Part <scp>II</scp> – Potential Mechanism and Treatment Considerations

Chai, Nu Cindy; Bond, Dale S.; Moghekar, Abhay; Scher, Ann I.; Peterlin, B. Lee

doi:10.1111/head.12297

Cited by 73 publications

(67 citation statements)

References 88 publications

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“…Limited data in uncontrolled studies suggest that morbidly obese episodic and chronic migraineurs who undergo bariatric surgery have a reduction in monthly frequency and headache severity 3 to 6 months after surgery. [32][33][34][35] In addition, although several well-designed aerobic exercise trials have demonstrated efficacy for reducing headache days and pain severity in those with migraine, it remains unclear as to whether this is related to the exercise itself or as a result of weight loss. 32 We also found that being underweight (BMI , 18.5) was associated with a small increased risk of migraine.…”

Section: Neurology 88 May 9 2017 1801mentioning

confidence: 99%

“…[32][33][34][35] In addition, although several well-designed aerobic exercise trials have demonstrated efficacy for reducing headache days and pain severity in those with migraine, it remains unclear as to whether this is related to the exercise itself or as a result of weight loss. 32 We also found that being underweight (BMI , 18.5) was associated with a small increased risk of migraine. After adjusting for age and sex, the risk of migraine in underweight individuals was increased by 13% and remained significant after multivariate adjustments.…”

Section: Neurology 88 May 9 2017 1801mentioning

confidence: 99%

“…1 Human data support that several of these obesityrelated signaling molecules are altered in those with migraine at baseline when pain-free (e.g., adiponectin, resistin) and during acute migraine pain (adiponectin, IL-6). 32 Further, recent animal data have demonstrated that obesity is associated with both an augmented basal and acute trigeminovascular response to stimulation and may be capable of priming the trigeminovascular system to be responsive to otherwise innocuous stimuli. 38,39 Finally, it is also possible other factors such as changes in physical activity, medications, the presence of comorbidities (e.g., depression), or other medical conditions contribute to the relationship between migraine and obesity and underweight status.…”

Section: Neurology 88 May 9 2017 1801mentioning

confidence: 99%

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Body composition status and the risk of migraine

et al. 2017

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Objective: To evaluate the association between migraine and body composition status as estimated based on body mass index and WHO physical status categories.Methods: Systematic electronic database searches were conducted for relevant studies. Two independent reviewers performed data extraction and quality appraisal. Odds ratios (OR) and confidence intervals (CI) were pooled using a random effects model. Significant values, weighted effect sizes, and tests of homogeneity of variance were calculated.Results: A total of 12 studies, encompassing data from 288,981 unique participants, were included. The age-and sex-adjusted pooled risk of migraine in those with obesity was increased by 27% compared with those of normal weight (odds ratio [OR] 1.27; 95% confidence interval [CI] 1.16-1.37, p , 0.001) and remained increased after multivariate adjustments. Although the age-and sex-adjusted pooled migraine risk was increased in overweight individuals (OR 1.08; 95% CI 1.04, 1.12, p , 0.001), significance was lost after multivariate adjustments. The age-and sex-adjusted pooled risk of migraine in underweight individuals was marginally increased by 13% compared with those of normal weight (OR 1.13; 95% CI 1.02, 1.24, p , 0.001) and remained increased after multivariate adjustments. Conclusions:The current body of evidence shows that the risk of migraine is increased in obese and underweight individuals. Studies are needed to confirm whether interventions that modify obesity status decrease the risk of migraine. Both migraine and obesity are conditions associated with substantial personal and societal burdens.1 As obesity is a potentially modifiable risk factor, the relationship between migraine and obesity has been a focus of research interest for the last decade. [1][2][3] Although several studies support that obesity is associated with an increased risk of migraine, results are inconsistent with regards to included populations, how obesity status is categorized, and other features of individual study design and conduct, and the conclusions drawn.

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Section: Neurology 88 May 9 2017 1801mentioning

confidence: 99%

Section: Neurology 88 May 9 2017 1801mentioning

confidence: 99%

Section: Neurology 88 May 9 2017 1801mentioning

confidence: 99%

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Body composition status and the risk of migraine

et al. 2017

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“…Obesity may enhance the frequency and severity of headache attacks and appears to increase the risk for having migraine (1). Experimental results indicate multiple areas of overlap between migraine pathophysiology and the mechanisms related to excess body fat (2,3). Adipose tissue has significant endocrine functions by producing bioactive molecules that serve as regulators of metabolism and also possess immunoregulatory functions (4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Diet-induced obesity alters dural CGRP release and potentiates TRPA1-mediated trigeminovascular responses

et al. 2016

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Background Clinical studies suggest a link between obesity and the primary headache disorder migraine. In our study we aimed to reveal the effect of obesity on meningeal nociceptor function in rats receiving a high-fat, high-sucrose diet. Methods Transient receptor potential ankyrin 1 (TRPA1) receptor activation-induced changes in meningeal blood flow, release of calcitonin gene-related peptide (CGRP) from trigeminal afferents and TRPA1 protein expression in the trigeminal ganglia were measured in control and obese rats. Metabolic parameters of the animals were assessed by measuring glucose and insulin homeostasis as well as plasma cytokine concentrations. Results The present experiments revealed an enhanced basal and TRPA1 receptor agonist-induced CGRP release from meningeal afferents of obese insulin-resistant rats and an attenuated CGRP release to potassium chloride. Obesity was also associated with an augmented vasodilatation in meningeal arteries after dural application of the TRPA1 agonist acrolein, a reduction in TRPA1 protein expression in the trigeminal ganglia and elevations in circulating proinflammatory cytokines IL-1β and IL-6 in addition to increased fasting blood glucose and insulin concentrations. Conclusions Our results suggest trigeminal sensitisation as a mechanism for enhanced headache susceptibility in obese individuals after chemical exposure of trigeminal nociceptors.

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“…[5][6][7] Studies evaluating interictal LEP levels in migraineurs have been inconclusive. [8][9][10][11][12] No previous studies have evaluated ictal LEP or resistin levels in migraineurs. …”

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confidence: 99%

Ictal adipokines are associated with pain severity and treatment response in episodic migraine

et al. 2015

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Objective: To evaluate ictal adipokine levels in episodic migraineurs and their association with pain severity and treatment response.Methods: This was a double-blind, placebo-controlled trial evaluating peripheral blood specimens from episodic migraineurs at acute pain onset and 30 to 120 minutes after treatment with sumatriptan/naproxen sodium vs placebo. Total adiponectin (T-ADP), ADP multimers (high molecular weight [HMW], middle molecular weight, and low molecular weight [LMW]), leptin, and resistin levels were evaluated by immunoassays.Results: Thirty-four participants (17 responders, 17 nonresponders) were included. In all partici- Conclusions: Both pretreatment migraine pain severity and treatment response are associated with changes in adipokine levels. Adipokines represent potential novel migraine biomarkers and drug targets. Neurology ® 2015;84:1409-1418 GLOSSARY ADP 5 adiponectin; CI 5 confidence interval; CV 5 coefficient of variation; HMW 5 high molecular weight; ICHD-2 5 International Classification of Headache Disorders, second edition; IL-6 5 interleukin 6; LEP 5 leptin; LMW 5 low molecular weight; MMW 5 middle molecular weight; NRS 5 numeric rating scale; suma/nap 5 sumatriptan/naproxen sodium; T-ADP 5 total adiponectin; TNF-a 5 tumor necrosis factor a.Adipokines are biologically active proteins, predominantly secreted from adipose tissue, that participate in multiple processes, including the drive to feed and pain processesing. [1][2][3][4] Adiponectin (ADP), leptin (LEP), and resistin are 3 such adipokines. These adipokines modulate inflammation and endothelial function-processes that overlap with the proposed mechanisms of migraine pathophysiology. In addition, receptors for these adipokines are expressed in key structures implicated in migraine, including the hypothalamus and the cerebral microvasculature. [1][2][3][4] Previous studies have reported that interictal ADP levels are increased in those with migraine, and that ictal ADP levels decline with successful abortive treatment in women episodic migraineurs. [5][6][7] Studies evaluating interictal LEP levels in migraineurs have been inconclusive. [8][9][10][11][12] No previous studies have evaluated ictal LEP or resistin levels in migraineurs.

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Obesity and Headache: Part II – Potential Mechanism and Treatment Considerations

Cited by 73 publications

References 88 publications

Body composition status and the risk of migraine

Body composition status and the risk of migraine

Diet-induced obesity alters dural CGRP release and potentiates TRPA1-mediated trigeminovascular responses

Ictal adipokines are associated with pain severity and treatment response in episodic migraine

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