Sodium Intake Is Linked to Increased Disease Activity in MS

A higher sodium intake is associated with increased clinical and radiologic disease activity among patients with multiple sclerosis (MS), according to research published online ahead of print August 28 in the Journal of Neurology, Neurosurgery, and Psychiatry.

Mauricio F. Farez, MD, from the Department of Neurology at Raúl Carrea Institute for Neurological Research in Buenos Aires, and colleagues conducted an observational study of 70 patients with relapsing-remitting MS who were followed for two years. The researchers estimated sodium intake from sodium excretion in urine samples and used regression analysis to estimate the effect of sodium intake on MS disease activity. The findings were subsequently replicated in a separate group of 52 patients with MS.

Dr. Farez’s group found a positive correlation between exacerbation rates and sodium intake in a multivariate model after adjusting for age, gender, disease duration, smoking status, vitamin D level, BMI, and treatment. The exacerbation rate was 2.75-fold higher in patients with medium or high sodium intake, compared with the rate in subjects who had a low sodium intake.

In addition, participants with a high sodium intake had a 3.4-fold greater risk of having a new lesion revealed by MRI. This group also had, on average, eight more T2 lesions on MRI than other participants. The investigators observed a similar relationship in the independent replication group.

The authors noted several study limitations, including a small cohort size and the inability to exclude potential confounders such as diet, role of commensal microbiota, stress, and other behavior that may affect food preference and treatment compliance or healthy overall behavior.

“Thus, even though an association between increased sodium intake and increased disease activity was shown, we cannot claim causality and we cannot exclude the possibility of reverse causation: individuals with more relapses received more steroids, and thus their salt intake and excretion is increased because they have higher disease activity, and not the other way around,” stated the researchers. “Another possible caveat relates to changes in salt consumption over time. We tried to overcome this [variation] by retesting the same patients at different time points, finding no significant changes.”

The investigators also noted that although studies have found that dietary salt has a role in regulating blood pressure, the effects of sodium on the risk of MS may involve additional factors. For example, sodium chloride has been shown to have pleiotropic effects on kidney homeostasis and T-cell function, and other evidence suggests a reciprocal relationship between sodium chloride and the immune system.

“Whether high blood pressure interacts with the typical autoimmune mechanisms associated with MS is an interesting question that remains to be answered,” commented Dr. Farez and colleagues. “Nevertheless, our findings suggest that clinical trials with a salt intake reduction as an intervention are needed to establish whether sodium intake control benefits patients with MS.”

—Colby Stong

A higher sodium intake is associated with increased clinical and radiologic disease activity among patients with multiple sclerosis (MS), according to research published online ahead of print August 28 in the Journal of Neurology, Neurosurgery, and Psychiatry.

Mauricio F. Farez, MD, from the Department of Neurology at Raúl Carrea Institute for Neurological Research in Buenos Aires, and colleagues conducted an observational study of 70 patients with relapsing-remitting MS who were followed for two years. The researchers estimated sodium intake from sodium excretion in urine samples and used regression analysis to estimate the effect of sodium intake on MS disease activity. The findings were subsequently replicated in a separate group of 52 patients with MS.

Dr. Farez’s group found a positive correlation between exacerbation rates and sodium intake in a multivariate model after adjusting for age, gender, disease duration, smoking status, vitamin D level, BMI, and treatment. The exacerbation rate was 2.75-fold higher in patients with medium or high sodium intake, compared with the rate in subjects who had a low sodium intake.

In addition, participants with a high sodium intake had a 3.4-fold greater risk of having a new lesion revealed by MRI. This group also had, on average, eight more T2 lesions on MRI than other participants. The investigators observed a similar relationship in the independent replication group.

The authors noted several study limitations, including a small cohort size and the inability to exclude potential confounders such as diet, role of commensal microbiota, stress, and other behavior that may affect food preference and treatment compliance or healthy overall behavior.

“Thus, even though an association between increased sodium intake and increased disease activity was shown, we cannot claim causality and we cannot exclude the possibility of reverse causation: individuals with more relapses received more steroids, and thus their salt intake and excretion is increased because they have higher disease activity, and not the other way around,” stated the researchers. “Another possible caveat relates to changes in salt consumption over time. We tried to overcome this [variation] by retesting the same patients at different time points, finding no significant changes.”

The investigators also noted that although studies have found that dietary salt has a role in regulating blood pressure, the effects of sodium on the risk of MS may involve additional factors. For example, sodium chloride has been shown to have pleiotropic effects on kidney homeostasis and T-cell function, and other evidence suggests a reciprocal relationship between sodium chloride and the immune system.

“Whether high blood pressure interacts with the typical autoimmune mechanisms associated with MS is an interesting question that remains to be answered,” commented Dr. Farez and colleagues. “Nevertheless, our findings suggest that clinical trials with a salt intake reduction as an intervention are needed to establish whether sodium intake control benefits patients with MS.”

—Colby Stong

A higher sodium intake is associated with increased clinical and radiologic disease activity among patients with multiple sclerosis (MS), according to research published online ahead of print August 28 in the Journal of Neurology, Neurosurgery, and Psychiatry.

Mauricio F. Farez, MD, from the Department of Neurology at Raúl Carrea Institute for Neurological Research in Buenos Aires, and colleagues conducted an observational study of 70 patients with relapsing-remitting MS who were followed for two years. The researchers estimated sodium intake from sodium excretion in urine samples and used regression analysis to estimate the effect of sodium intake on MS disease activity. The findings were subsequently replicated in a separate group of 52 patients with MS.

Dr. Farez’s group found a positive correlation between exacerbation rates and sodium intake in a multivariate model after adjusting for age, gender, disease duration, smoking status, vitamin D level, BMI, and treatment. The exacerbation rate was 2.75-fold higher in patients with medium or high sodium intake, compared with the rate in subjects who had a low sodium intake.

In addition, participants with a high sodium intake had a 3.4-fold greater risk of having a new lesion revealed by MRI. This group also had, on average, eight more T2 lesions on MRI than other participants. The investigators observed a similar relationship in the independent replication group.

The authors noted several study limitations, including a small cohort size and the inability to exclude potential confounders such as diet, role of commensal microbiota, stress, and other behavior that may affect food preference and treatment compliance or healthy overall behavior.

“Thus, even though an association between increased sodium intake and increased disease activity was shown, we cannot claim causality and we cannot exclude the possibility of reverse causation: individuals with more relapses received more steroids, and thus their salt intake and excretion is increased because they have higher disease activity, and not the other way around,” stated the researchers. “Another possible caveat relates to changes in salt consumption over time. We tried to overcome this [variation] by retesting the same patients at different time points, finding no significant changes.”

The investigators also noted that although studies have found that dietary salt has a role in regulating blood pressure, the effects of sodium on the risk of MS may involve additional factors. For example, sodium chloride has been shown to have pleiotropic effects on kidney homeostasis and T-cell function, and other evidence suggests a reciprocal relationship between sodium chloride and the immune system.

“Whether high blood pressure interacts with the typical autoimmune mechanisms associated with MS is an interesting question that remains to be answered,” commented Dr. Farez and colleagues. “Nevertheless, our findings suggest that clinical trials with a salt intake reduction as an intervention are needed to establish whether sodium intake control benefits patients with MS.”

—Colby Stong