Author Topic: (Abst.) No link found between dietary sodium intake and MS risk  (Read 38 times)

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Offline agate

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From PubMed, August 27, 2017:

Quote
Neurology. 2017 Aug 25.

No association between dietary sodium intake and the risk of multiple sclerosis

Cortese M1, Yuan C2, Chitnis T2, Ascherio A2, Munger KL2.

Author information

1From 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.

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.

The abstract can be seen here.
MS Speaks--online for 13 years

SPMS, diagnosed 1980. Avonex 2001-2004. Copaxone 2007-2010.

 

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