Marianna Cortese1, Changzheng Yuan2, Tanuja Chitnis2, Alberto Ascherio2, Kassandra L Munger2. 1. From the Departments of Clinical Medicine and Global Public Health and Primary Care (M.C.), University of Bergen; The Norwegian Multiple Sclerosis Competence Center (M.C.), Haukeland University Hospital, Bergen, Norway; Departments of Nutrition (M.C., C.Y., A.A., K.L.M.) and Epidemiology (A.A.), Harvard T.H. Chan School of Public Health; Partners Multiple Sclerosis Center (T.C.), Brigham and Women's Hospital; and Channing Division of Network Medicine, Department of Medicine (A.A.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA. Marianna.Cortese@uib.no. 2. From the Departments of Clinical Medicine and Global Public Health and Primary Care (M.C.), University of Bergen; The Norwegian Multiple Sclerosis Competence Center (M.C.), Haukeland University Hospital, Bergen, Norway; Departments of Nutrition (M.C., C.Y., A.A., K.L.M.) and Epidemiology (A.A.), Harvard T.H. Chan School of Public Health; Partners Multiple Sclerosis Center (T.C.), Brigham and Women's Hospital; and Channing Division of Network Medicine, Department of Medicine (A.A.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
Abstract
OBJECTIVE: To prospectively investigate the association between dietary sodium intake and multiple sclerosis (MS) risk. METHODS: In this cohort study, we assessed dietary sodium intake by a validated food frequency questionnaire administered every 4 years to 80,920 nurses in the Nurses' Health Study (NHS) (1984-2002) and to 94,511 in the Nurses' Health Study II (NHSII) (1991-2007), and calibrated it using data from a validation study. There were 479 new MS cases during follow-up. We used Cox proportional hazards models to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the effect of energy-adjusted dietary sodium on MS risk, adjusting also for age, latitude of residence at age 15, ancestry, body mass index at age 18, supplemental vitamin D intake, cigarette smoking, and total energy intake in each cohort. The results in both cohorts were pooled using fixed effects models. RESULTS: Total dietary intake of sodium at baseline was not associated with MS risk (highest [medians: 3.2 g/d NHS; 3.5 g/d NHSII] vs lowest [medians: 2.5 g/d NHS; 2.8 g/d NHSII] quintile: HRpooled 0.98, 95% CI 0.74-1.30, p for trend = 0.75). Cumulative average sodium intake during follow-up was also not associated with MS risk (highest [medians: 3.3 g/d NHS; 3.4 g/d NHSII] vs lowest [medians: 2.7 g/d NHS; 2.8 g/d NHSII] quintile: HRpooled 1.02, 95% CI 0.76-1.37, p for trend = 0.76). Comparing more extreme sodium intake in deciles yielded similar results (p for trend = 0.95). CONCLUSIONS: Our findings suggest that higher dietary sodium intake does not increase the risk of developing MS.
OBJECTIVE: To prospectively investigate the association between dietary sodium intake and multiple sclerosis (MS) risk. METHODS: In this cohort study, we assessed dietary sodium intake by a validated food frequency questionnaire administered every 4 years to 80,920 nurses in the Nurses' Health Study (NHS) (1984-2002) and to 94,511 in the Nurses' Health Study II (NHSII) (1991-2007), and calibrated it using data from a validation study. There were 479 new MS cases during follow-up. We used Cox proportional hazards models to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the effect of energy-adjusted dietary sodium on MS risk, adjusting also for age, latitude of residence at age 15, ancestry, body mass index at age 18, supplemental vitamin D intake, cigarette smoking, and total energy intake in each cohort. The results in both cohorts were pooled using fixed effects models. RESULTS: Total dietary intake of sodium at baseline was not associated with MS risk (highest [medians: 3.2 g/d NHS; 3.5 g/d NHSII] vs lowest [medians: 2.5 g/d NHS; 2.8 g/d NHSII] quintile: HRpooled 0.98, 95% CI 0.74-1.30, p for trend = 0.75). Cumulative average sodium intake during follow-up was also not associated with MS risk (highest [medians: 3.3 g/d NHS; 3.4 g/d NHSII] vs lowest [medians: 2.7 g/d NHS; 2.8 g/d NHSII] quintile: HRpooled 1.02, 95% CI 0.76-1.37, p for trend = 0.76). Comparing more extreme sodium intake in deciles yielded similar results (p for trend = 0.95). CONCLUSIONS: Our findings suggest that higher dietary sodium intake does not increase the risk of developing MS.
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