Longitudinal study shows no link between salt intake and MS disease activity
The cause of multiple sclerosis (MS) remains largely unknown; genetic, environmental and lifestyle factors have all been linked to MS, and the question of how an individual’s diet impacts MS progression has been of considerable interest and spurred research studies in recent years. Specifically, the relationship between salt intake and MS has been examined in a small number of animal experiments and human observational studies. While these studies demonstrate that increased levels of dietary salt promote inflammation and lead to more severe MS-like symptoms, they possess a number of methodological limitations. Additional studies involving pediatric MS patients showed no connection between dietary sodium intake and MS. Conflicting evidence calls for further research to understand the role of sodium in the cause and progression of MS.
A recently published article in Annals of Neurology from Dr. Alberto Ascherio and colleagues including MS Society-funded researcher Mark Freedman from the Ottawa Hospital Research Institute, assess whether sodium intake is associated with MS activity.
The research team analyzed urine samples from over 400 participants who took part in the Betaferon/Betaseron in Newly Emerging Multiple Sclerosis for Initial Treatment (BENEFIT)clinical trial. The 5-year trial was designed to evaluate if interferon beta-1b compared to placebo could reduce conversion to MS in people who had their first clinical event suggestive of MS, called clinically isolated syndrome (CIS).
Trial participants provided urine samples during clinic visits that took place at the start of the trial (baseline), every 3 months until month 12, and then every 6 months until the end of the trial, which were later analyzed to determine sodium intake levels. As sodium intake varies throughout the day, the best measure is to obtain multiple urine samples over a 24-hour period. As urine samples were not taken for a full 24 hours in the BENEFIT trial, 24-hour sodium excretion value was estimated using a validated formula that takes into consideration the amount of sodium in the urine, the amount of creatinine in the urine (measure of kidney health), age, height and weight. Clinical and imaging outcomes measures used in the trial were evaluated to assess the relationship between sodium intake and MS outcomes.
While there was a link between higher sodium levels and sex, body mass index as well as less lesions seen prior to the start of interferon beta-1b and placebo treatments, the researchers found no relationship between sodium levels and rate of conversion to MS from CIS after 6 months. Furthermore, there were no associations between sodium levels and relapse rates, changes in Expanded Disability Status Score (EDSS), development of new lesions or change in brain volume from month 6 to month 60. Additional analyses were carried out to look at other potential associations, but the researchers could not identify any link between sodium changes over time and changes in MS outcomes.
Based on the findings from this study, the research team discovered no association between sodium intake and progression of MS in patients treated with interferons, as measured by conversion to MS from CIS, relapse rates, changes in EDSS and MRI activity. A limitation of the study is participants were treated with interferon beta-1b, thus the results may not be the same for individuals with MS on other therapies. Furthermore, the study does not exclude the idea that higher levels of dietary sodium could be risk factor for MS, and the inclusion of primarily Caucasian patients from Europe and Canada makes it difficult to ascertain the impact of sodium intake in other populations and ethnicities. Nevertheless the study adds to the growing body of research on diet and MS and provides strong evidence to individuals with MS and their health care teams that help them make informed decisions about their health.
Fitzgerald KC et al. (2017) Sodium intake and multiple sclerosis activity and progression in BENEFIT. Ann Neurol. 10.1002/ana.24965. [Epub ahead of print].
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