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Severe Headache or Migraine History Is Inversely Correlated With Dietary Sodium Intake: NHANES 1999–2004
Author(s) -
Pogoda Janice M.,
Gross Noah B.,
Arakaki Xianghong,
Fonteh Alfred N.,
Cowan Robert P.,
Harrington Michael G.
Publication year - 2016
Publication title -
headache: the journal of head and face pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.14
H-Index - 119
eISSN - 1526-4610
pISSN - 0017-8748
DOI - 10.1111/head.12792
Subject(s) - medicine , migraine , national health and nutrition examination survey , odds ratio , body mass index , headaches , confidence interval , population , environmental health , surgery
Objective We investigated whether dietary sodium intake from respondents of a national cross‐sectional nutritional study differed by history of migraine or severe headaches. Background Several lines of evidence support a disruption of sodium homeostasis in migraine. Design Our analysis population was 8819 adults in the 1999–2004 National Health and Nutrition Examination Survey (NHANES) with reliable data on diet and headache history. We classified respondents who reported a history of migraine or severe headaches as having probable history of migraine. To reduce the diagnostic conflict from medication overuse headache, we excluded respondents who reported taking analgesic medications. Dietary sodium intake was measured using validated estimates of self‐reported total grams of daily sodium consumption and was analyzed as the residual value from the linear regression of total grams of sodium on total calories. Multivariable logistic regression that accounted for the stratified, multistage probability cluster sampling design of NHANES was used to analyze the relationship between migraine and dietary sodium. Results Odds of probable migraine history decreased with increasing dietary sodium intake (odds ratio = 0.93, 95% confidence interval = 0.87, 1.00, P  = .0455). This relationship was maintained after adjusting for age, sex, and body mass index (BMI) with slightly reduced significance ( P  = .0505). In women, this inverse relationship was limited to those with lower BMI ( P  = .007), while in men the relationship did not differ by BMI. We likely excluded some migraineurs by omitting frequent analgesic users; however, a sensitivity analysis suggested little effect from this exclusion. Conclusions This study is the first evidence of an inverse relationship between migraine and dietary sodium intake. These results are consistent with altered sodium homeostasis in migraine and our hypothesis that dietary sodium may affect brain extracellular fluid sodium concentrations and neuronal excitability.

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