Reposted from HCP Live
Increased salt intake may magnify the risk of relapses in patients with multiple sclerosis (MS).
According to researchers Farez et al in a study published on August 28, 2014, in the Journal of Neurology, Neurosurgery & Psychiatry,1 excess dietary sodium intake is associated with a higher level of disease activity in patients with relapsing-remitting MS (RRMS).
Previously, basic research found that sodium modulates differentiation of T-helper 17 (Th17) cells in both mice with experimental autoimmune encephalomyelitis and an in vitro model of human immune cell activity. To investigate whether or not high levels of salt intake affects MS disease activity, investigators conducted an observational, 2-year study in 70 patients with RRMS.
During the study, investigators monitored disease activity using clinical and radiologic measures. Data were later analyzed using a regression analysis adjusting for known factors associated with RRMS disease activity, including age, sex, disease duration, smoking status, vitamin D levels, baseline body mass index, and whether or not patients were undergoing treatment for MS.
Urine samples were obtained at 3, 6, and 9 months to assess the level of salt consumption in each patient. Investigators then divided patients into groups by salt consumption levels. In terms of daily salt consumption, patients in the low salt intake group consumed 2 g/day, patients in the moderate salt intake group consumed 2 to 4.8 g/day, and patients in the high-salt intake group consumed 4.8 g/day or more as part of their usual diet.
Compared with patients in the low-sodium intake group, the rate of MS exacerbation was 2.75 (95% confidence interval [CI], 1.3-5.8) times higher in patients with a medium sodium intake and 3.95 times (95% CI, 1.4-11.2) higher in patients with a high sodium intake. New MRI lesions were also more likely in patients receiving a high sodium diet, by a factor of 3 to 4.
An average of 8 more T2-enhancing lesions occurred over the course of the study in patients receiving a high salt diet compared with patients receiving a low salt diet. For a second group of 52 patients, investigators found similar results, confirming the findings of the initial 70-patient trial.
The relationship observed in this study adds to other factors that seem to affect the frequency of MS exacerbations, including vitamin D levels and infections with certain viruses, such as Epstein- Barr virus. Importantly, because this study was based on observational data, these results do not prove causality between disease activity in MS and increased sodium intake.
In fact, it is possible that MS disease activity affects salt consumption and not the other way around. The investigators acknowledged the possibility of reverse causality in this study, because damage to brain areas through disease activity may affect intake of salt among patients with MS.
Although the results of this study will require more investigation before being applied to clinical practice, the findings add to the growing volume of information about factors involved in the pathophysiology of MS. The study also invites the possibility of future prospective clinical trials to evaluate the effect of dietary changes in control of MS disease activity.
See more at HCP Live