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JNNP Online First, published on August 28, 2014 as 10.1136/jnnp-2014-307928
Multiple sclerosis

RESEARCH PAPER

Sodium intake is associated with increased disease
activity in multiple sclerosis
Mauricio F Farez,1 Marcela P Fiol,1 María I Gaitán,1 Francisco J Quintana,2
Jorge Correale1
▸ Additional material is
published online only. To view
please visit the journal online
(http://dx.doi.org/10.1136/
jnnp-2014-307928).
1

Department of Neurology,
Raúl Carrea Institute for
Neurological Research (FLENI),
Buenos Aires, Argentina
2
Center for Neurologic
Diseases, Brigham and
Women’s Hospital, Harvard
Medical School, Boston,
Massachusetts, USA
Correspondence to
Dr Mauricio F Farez,
Department of Neurology, Raúl
Carrea Institute for
Neurological Research, FLENI.
Montañeses 2325, Buenos
Aires 1428, Argentina;
mauriciofarez@gmail.com
Received 18 February 2014
Revised 25 May 2014
Accepted 30 June 2014

ABSTRACT
Background Recently, salt has been shown to
modulate the differentiation of human and mouse Th17
cells and mice that were fed a high-sodium diet were
described to develop more aggressive courses of
experimental autoimmune encephalomyelitis. However,
the role of sodium intake in multiple sclerosis (MS) has
not been addressed. We aimed to investigate the
relationship between salt consumption and clinical and
radiological disease activity in MS.
Methods We conducted an observational study in
which sodium intake was estimated from sodium
excretion in urine samples from a cohort of 70 relapsingremitting patients with MS who were followed for
2 years. The effect of sodium intake in MS disease
activity was estimated using regression analysis. We then
replicated our findings in a separate group of 52
patients with MS.
Results We found a positive correlation between
exacerbation rates and sodium intake in a multivariate
model adjusted for age, gender, disease duration,
smoking status, vitamin D levels, body mass index and
treatment. We found an exacerbation rate that was
2.75-fold (95% CI 1.3 to 5.8) or 3.95-fold (95% CI 1.4
to 11.2) higher in patients with medium or high sodium
intakes compared with the low-intake group.
Additionally, individuals with high-sodium intake had a
3.4-fold greater chance of developing a new lesion on
the MRI and on average had eight more T2 lesions on
MRI. A similar relationship was found in the
independent replication group.
Conclusions Our results suggest that a higher sodium
intake is associated with increased clinical and
radiological disease activity in patients with MS.

INTRODUCTION

To cite: Farez MF, Fiol MP,
Gaitán MI, et al. J Neurol
Neurosurg Psychiatry
Published Online First:
[please include Day Month
Year] doi:10.1136/jnnp2014-307928

Multiple sclerosis (MS) is an inflammatory demyelinating disease caused by an autoimmune response
against the central nervous system that is presumed
to result from a complex interplay between genes
and the environment.1
The autoimmune response directed against the
central nervous system involves several immune cell
types. Of particular interest is the Th17 T-cell
subset, which has gained particular attention in
recent years.2
Studies showing a shifting incidence of MS in
migrant populations and its geographical distribution indicate that environmental factors play a
major role in disease pathogenesis. Consequently, it
has been demonstrated that several environmental
factors, such as vitamin D,3 Epstein-Barr virus

infection,4 systemic infections,5 parasitical infections6 and immunisations,7 might play a role in the
onset, as well as the clinical, radiological and
immunological courses of MS.
Recently, salt (NaCl, sodium chloride) has been
shown to modulate the differentiation of human
and mouse Th17 cells.8 9 Moreover, mice that were
fed a high-sodium diet were described to develop
more aggressive courses of experimental autoimmune encephalomyelitis (EAE), the animal
model of MS.8 9
However, the role of sodium intake in MS has
not been addressed. In this study, we investigated
the effect of sodium intake on the clinical and
radiological activity of MS.

MATERIALS AND METHODS
Study population and design
The study was approved by the Institutional Ethics
Committee, and all participants signed an informed
consent form. The study included two participants
of patients: group 1 and group 2 (figure 1). The
first group consisted of a traditional cohort to test
our main hypothesis, and the second group was
made up of a cross-sectional sample recruited for
replication purposes. Group 1 consisted of 70
patients with relapsing–remitting MS according to
the McDonald criteria10 who were seen at the MS
clinic at the Raúl Carrea Institute for Neurological
Research and were consecutively invited to participate in a longitudinal cohort study in which an
MRI was required at baseline and clinical, radiological and sodium intake data were collected
throughout the follow-up period (from September
2010 until November 2012). Group 2 consisted of
a cross-sectional sample of 52 relapsing–remitting
patients with MS according to the McDonald criteria who were recruited from June to July 2013.
Pregnant patients and patients with hyponatraemia
were excluded from enrolment in both groups.
Blood and urine samples were taken 12 months
after enrolment for patients in group 1. Sodium
and creatinine levels in urine and serum sodium
and vitamin D levels were measured via routine
analysis in our hospital’s clinical laboratory. For
group 2, casual urine samples were collected and
analysed by following the same procedures as those
used for the initial cohort.
The relationship between salt consumption and
MS disease activity was tested by applying crosssectional and longitudinal analyses. In the former,
correlations between T2 lesion load and sodium
intake were investigated. This analysis was

MF, et
al. J Neurol Neurosurg
2014;0:1–6.
doi:10.1136/jnnp-2014-307928
Copyright Article author (orFarez
their
employer)
2014.Psychiatry
Produced
by BMJ
Publishing Group Ltd under licence.

1

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Multiple sclerosis
Figure 1 Study design. Two subsets
of patients were included in this study,
group 1 and group 2. The first group
consisted of a cohort of 70 patients
recruited in September 2010; this
cohort was followed for two years. All
patients had a baseline MRI and an
MRI at least yearly. At the middle of
the follow-up, coinciding with the
yearly MRI, a morning first-urine
sample was taken and sodium intake
was calculated. Neurological
assessments were performed every 3–
6 months until the end of the
follow-up. The main outcome was the
number of relapses at the end of
follow-up with radiological activity as
secondary outcomes. The second group
was recruited as a replication group,
casual urine sample was taken, and
the T2 lesion load was the comparator
outcome.
performed first in group 1 (at month 12 when a urine sample
was taken and an MRI was performed) and then repeated for
validation in group 2. The longitudinal cohort (group 1)
follow-up lasted 2 years (sample taken at month 12), and the
association between salt consumption and increased clinical and
radiological activity during follow-up was tested.

Sodium intake assessment
We estimated sodium excretion in urine as a proxy of sodium
intake because 80–90% of ingested sodium is eliminated
through urine.11 Twenty-four hour urine collection is the most
reliable method for measuring sodium excretion and therefore
intake but collecting 24 h urine is cumbersome and can lead to
inaccurate measurement due to patients skipping some urine
collection throughout the day.12 Thus, alternative methods have
been developed to estimate sodium excretion; Tanaka’s equation
uses excreted sodium and creatinine in spot urine to estimate
the total sodium excretion,13 has been widely assessed in the
general population, and has been recommended as a reliable
and convenient method for calculating salt intake via hypertension guidelines.14
Tanaka’s equation is as follows:
21:98 ðurinary sodium=urinary creatinine ð 2:04
age þ 14:89 weight þ 16:14 height 2244:45ÞÞ0:392 :
Patients were asked to provide urine from their first morning
urination on a weekday. All patients were required to provide
urine samples after 3, 6 and 9 months to assess potential
changes in salt consumption with time and to test method reliability. Patients in group 2 were asked to provide urine on the
same day of recruitment regardless of time or number of previous voidings that day. Urine samples were separated at least for
90 days since last steroid administration.
Sodium intake was then divided into three levels according to
the recommendations of the WHO as the target to avoid highblood pressure-related disorders: patients with less than 2 g/day,
patients with an average intake according to national standards
(between 2 and 4.8 g/day) and patients whose intake was above
average (more than 4.8 g).15
2

Clinical data
Clinical data were retrieved from our patient with MS database.
The Expanded Disability Status Scale (EDSS) score was assessed
at baseline and at the end of follow-up. The number of relapses
during follow-up was counted during this period. Additionally,
disease duration was calculated from the date of diagnosis until
the end of follow-up. Other features extracted were gender, age,
treatment history, body weight, height, vitamin D level (measured at the same timepoints as sodium intake) and smoking
status (measured at baseline).
Exacerbation was defined as development of a new symptom
or worsening of pre-existing symptoms confirmed via neurological examination, lasting at least 48 h and preceded by stability or improvement lasting at least 30 days.

MRI assessment
Brain and spinal cord MRI was performed at baseline and
at 3-month or 6-month follow-up visits on a 1.5-T MRI
unit (General Electric, Milwaukee, Wisconsin, USA). Axial
5 mm-thick slices with no gap and a 192×256 matrix with subcallosum alignment were obtained with T2-weighted, proton
density, fast spin-echo, fluid-attenuated inversion recovery and
T1-weighted sequences prior to and after the administration of
gadolinium (0.1 mmol/kg).
In addition to the neuroradiologist report, a blinded assessment of MRI was performed by JC and MFF. T2 lesions and
gadolinium-enhancing lesions were noted. Additionally, the
combined unique activity (CUA) was calculated by adding new
or enlarging T2 lesions to the gadolinium-enhancing lesions as
previously reported.16 Conflicts in MRI assessment were solved
by discussion between JC and MFF.

Statistical analysis
The primary outcome of the study was the number of relapses
occurring from the time of recruitment to the time of the last
follow-up. Secondary outcomes were the CUA and the T2
lesion load on MRI. The primary predictor for the analysis was
the estimated sodium intake.
Demographical, clinical and radiological baseline characteristics between the low, medium and high salt-consuming groups

Farez MF, et al. J Neurol Neurosurg Psychiatry 2014;0:1–6. doi:10.1136/jnnp-2014-307928

Downloaded from jnnp.bmj.com on September 1, 2014 - Published by group.bmj.com

Multiple sclerosis
were compared using the Kruskal-Wallis test and χ2 when
appropriate.
A Poisson regression model was used to assess the impact of
sodium intake on the number of clinical relapses, generating an
incidence rate ratio and corresponding 95% CIs. Fitness of the
Poisson regression model over the zero-inflated Poisson model
was tested with the Vuong test. Unadjusted and adjusted values
were calculated for all analyses including potential confounders
such as age (salt intake may vary with age), gender (there are
reported differences in sodium intake with gender), disease duration (increase lesion load occurring over time may confound
the association), treatment (there may be an unknown association between treatment and dietary preferences, untreated and
patients with immunomodulatory drugs were grouped and used
as baseline in comparison to patients treated with immunosuppressive drugs), vitamin D levels (there may be a correlation
between sodium intake and vitamin D levels), body mass index
(BMI, obesity has been linked to sodium intake) and smoking
status (smoker, non-smoker, we included this because it may be
related to health consciousness). The effects of salt intake on
EDSS progression (dichotomised in individuals who increased
their score and individuals who maintained or improved their
score) were analysed via logistic regression. The association
between sodium consumption and T2 lesion load was evaluated
using the same method for group 1 and 2 with an adjusted
linear regression model with heteroskedasticity-robust SDs. All
statistical analyses were performed using Stata V.12 software.

RESULTS
Clinical and demographic characteristics of the study
participants
The clinical and demographic characteristics of the study participants are presented in table 1 and online supplementary table.
A total of 70 patients were included in the initial cohort, and 52
were included in group 2; thus, a total of 122 patients were
included. For the initial cohort, the mean follow-up time was
24 months (range 22–26 months). None of the patients suffered
from hypertension or had been prescribed diuretics. None of
the patients were on vitamin supplementation, and four patients
started multivitamin supplements during follow-up. None of the
patients were on a weight-loss diet. The 70 initial cohort participants experienced a total of 44 relapses with an annualised
relapse rate of 0.31. The replication group was similar to the
initial cohort in terms of age ( p=0.41), disease duration
( p=0.42) and EDSS ( p=0.21); however, the replication group
had more males ( p=0.007; see online supplementary table).

Table 1

Estimated sodium intake
The mean estimated daily sodium intake for the entire population was 4.12±1.6 g/day, which is in the range estimated for
Argentina (4–4.8 g). As previously reported,11 males had significantly higher levels of sodium intake compared with females
(5.3±1.8 vs 3.78±1.4 ( p<0.001)). There were no significant
differences in sodium intake between treatment groups
(p=0.45).
Similar results were found for the replication group, which
had an average daily sodium intake of 4.45±1.5 ( p=0.24), and
no differences between treatment groups (p=0.34) were
observed. Unlike the initial cohort, males from the replication
group did not significantly differ from females in terms of salt
intake ( p=0.87).

Sodium intake and clinical outcomes
The relationship between exacerbation rate and sodium intake
levels is shown in table 2. To assist in analysing the association
between sodium intake and clinical activity, sodium intake was
categorised into three groups: a baseline group comprising
patients with the WHO recommended intake (under 2 g/day),
patients within the national average (2–4.8 g) and patients with
an above average intake (4.8 g or more).
We found a positive correlation between exacerbation rate
and sodium intake in a multivariate model adjusted for age,
gender, disease duration, treatment, vitamin D levels, BMI and
smoking status (smoker or non-smoker). Compared with the
baseline intake group (intake below 2 g/day), the average intake
(2–4.8 g/day) and above average intake groups (≥4.8 g/day) presented an exacerbation rate of 2.75 (95% CI 1.3 to 5.8) and
3.95-fold higher (95% CI 1.4 to 11.2) than the baseline group
(p<0.001 for trend). No significant differences were found in
terms of EDSS either at baseline or at the end of follow-up
(data not shown).

Sodium intake and MRI outcomes
We then correlated sodium intake levels with radiological activity. As with clinical disease activity, a significant correlation
between sodium intake and MRI activity was found including
total T2 lesion load and CUA (the combination of new Gd+
lesions and new or enlarging T2 lesions; see table 3).
Individuals with a sodium intake above the national average had
a 3.4-fold increased chance of developing a new lesion on MRI
and had, on average, eight more T2 lesions.

Baseline and clinical characteristics of the study participants

Age (years, means±SD)
Female:male (n)
Disease duration (years, median, range)
EDSS (median, range)
Treatment (n)
None
Interferon
Glatiramer acetate
Natalizumab
Fingolimod

All participants
(n=70)

Low-sodium intake
(n=21)

Medium sodium intake
(n=37)

High-sodium intake
(n=12)

p Value

37.5±8.9
54:16
5 (1–16)
1 (0–3·5)

42.27±10.1
20:1
4 (1–16)
1 (0–3)

35.66±8.3
28:9
3 (1–16)
0 (0–3.5)

40.6±8.9
6:6
4 (1–14)
0 (0–2.5)

0.73
0·05
0.18
0.83

1
30
22
4
13

0
11
8
0
2

0
15
9
4
9

1
4
5
0
2

EDSS, Expanded Disability Status Scale.

Farez MF, et al. J Neurol Neurosurg Psychiatry 2014;0:1–6. doi:10.1136/jnnp-2014-307928

3

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Multiple sclerosis
Table 2 Association between sodium intake and exacerbation
rate in a regression analysis
IRR
IRR of exacerbation (univariate model)
Sodium intake (g/day)
<2
2–4.8
>4.8
IRR of exacerbation (adjusted model)
Sodium intake (g/day)
<2
2–4.8
>4.8
Age (1-year increment)
Gender (male)
Disease duration (1-year increment)
Vitamin D (1 ng increase)
Smoking (smoker)
BMI (1 unit increase)
Treatment (immunosuppressant
vs immunomodulators/untreated)

95% CI

Table 3
activity

Association between sodium intake and radiological

p Value

1 (baseline)
2.56
3.37


1.3 to 4.9
1.5 to 9.55


0.005
0.001

1 (baseline)
2.75
3.95
0.992
1.09
0.99
1
1.13
0.97
1.46


1.3 to 5.8
1.4 to 11.2
0.96 to 1.02
0.49 to 2.42
0.98 to 1.01
0.96 to 1.04
0.56 to 2.28
0.87 to 1.07
0.79 to 2.73


0.008
0.01
0.59
0.82
0.08
0.85
0.73
0.58
0.22

IRR
CUA in MRI (univariate model)
Sodium intake (g/day)
<2
2–4.8
>4.8
CUA in MRI (adjusted model)
Sodium intake (g/day)
<2
2–4.8
>4.8
Age (1-year increment)
Gender (male)
Disease duration
(1-year increment)
Vitamin D (1 ng increase)
Smoking (smoker)
BMI (1 unit increase)
Treatment
(immunosuppressant
vs immunomodulators/
untreated)
Average T2 lesion count

BMI, body mass index; IRR, incidence rate ratio.

Correlation between salt intake and MRI activity is also
present in group 2

Sodium levels in serum are not linked to clinical or
radiological outcomes
We then tested whether the aforementioned association
observed between sodium intake and clinical and radiological
activity extended to sodium serum levels. Owing to its importance in general metabolism, sodium levels are tightly regulated
within narrow levels regardless of large variations in dietary
sodium consumption.17 Therefore, overall consumption should
not significantly affect serum levels. We did not detect a significant correlation between daily sodium intake and serum sodium
after adjusting for BMI, age, gender, vitamin D levels and
smoking status ( p=0.692), nor there was a correlation between
serum sodium and clinical or radiological disease activity (data
not shown). Thus, if salt intake has any causal role beyond its
association, it does not appear to occur in the peripheral blood.

DISCUSSION
In this study, the risk of clinical or radiological MS exacerbation
was increased in (longitudinally followed) individuals with highsodium intakes. We replicated our results using a cross-sectional
analysis of a separate group of 52 patients.
This study has some limitations including a relatively small
cohort size and the inability to exclude potential confounders
(such as diet, role of commensal microbiota, stress and other
4

Sodium intake (g/day)
<2
2–4.8
>4.8

p Value

1 (baseline)
2.68
3.56


1.4 to 4.9
1.7 to 7.55


0.002
0.001

1 (baseline)
2.86
3.42
0.97
0.57
1.05


1.52
1.37
0.93
0.24
0.96

to 5.4
to 8.55
to 1.00
to 1.34
to 1.15


0.001
0.008
0.869
0.920
0.25

0.96
0.19
0.86
0.22

to 1
to 1.33
to 1
to 1.06

0.1
0.17
0.06
0.06

0.94
0.51
0.92
0.45

Mean

We conducted several analyses to test the robustness of the
results such as retesting the same patients at different time
points, using a different equation to estimate sodium intake (see
online supplementary material) and repeating the analysis in a
different subset of patients. We recruited an additional independent cohort to perform a cross-sectional analysis on salt
intake and MRI T2 lesion count and CUA to replicate the
results found for the original longitudinal cohort. Despite some
differences between cohorts (as described previously), there was
a positive correlation between salt intake and MS disease severity in the replication group (see table 4).

95% CI

6.45
7.14
14.13

SEM

1.84
0.88
1.98

p Value
(vs baseline)

0.743
0.005

BMI, body mass index; CUA, combined unique activity; IRR, incidence rate ratio.

conducts that may have an impact on 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. Another
possible caveat relates to changes in salt consumption over time.
We tried to overcome this by retesting the same patients at different time points, finding no significant changes.
Another potential confounder involves patients with increased
disease activity who may have hypothalamic lesions and therefore develop inappropriate antidiuretic hormone secretion, as
has been reported in patients with MS,18 and who therefore
excrete higher amounts of sodium. However, we ruled out this
possibility by measuring the sodium concentration in the serum
and by excluding patients with hyponatraemia. There is evidence that sodium intake is linked to obesity and changes in
body fat composition,19 and although obesity has been linked to
MS risk, appear to occur in childhood and adolescence.20
Nevertheless, we included this variable in our adjusted models
to account for potential confounding factors.
There is widespread evidence from epidemiological and
animal studies as well as from clinical trials that dietary salt
(sodium chloride) plays a key role in regulating blood pressure.11 21 However, the effects of salt consumption on MS may
go beyond the effects of elevated blood pressure. Specifically,
sodium chloride has been shown to have pleiotropic effects on

Farez MF, et al. J Neurol Neurosurg Psychiatry 2014;0:1–6. doi:10.1136/jnnp-2014-307928

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Multiple sclerosis
Table 4 Association between sodium intake and radiological
activity in group 2

CUA in MRI (univariate model)
Sodium intake (g/day)
<2
2–4.8
>4.8
CUA in MRI (adjusted model)
Sodium intake (g/day)
<2
2–4.8
>4.8
Gender (male)
Disease duration
(1-year increment)
EDSS (1 unit increase)
BMI (1 unit increase)
Treatment (immunosuppressant
vs immunomodulators/untreated)
Average T2 lesion count

Sodium intake (g/day)
<2
2–4.8
>4.8

IRR

95% CI

1 (baseline)
3.9
1.82


0.98 to 15.6
0.4 to 7.7

1 (baseline)
3.81
1.86
0.58
1.1
1.1
1.08
1.1


1.1 to
0.4 to
0.2 to
0.9 to

14.6
7.7
1.9
1.2

0.8 to 1.7
0.9 to 1.2
0.2 to 5.2

p Value


0.054
0.41


0.05
0.39
0.4
0.5
0.5
0.4
0.9

Mean

SEM

p Value
(vs baseline)

9.43
15.08
24.44

2.26
1.57
2.43


0.055
<0.001

BMI, body mass index; CUA, combined unique activity; EDSS, Expanded Disability
Status Scale; IRR, incidence rate ratio.

kidney homeostasis and T-cell function.22–24 There appears to
be a reciprocal relationship between sodium chloride and the
immune system: a lack of T and B cells is associated with lower
hypertension levels in mice,25 and higher IL-17 levels have been
observed in some hypertensive individuals.26 Despite the potential relationship between sodium consumption and the immune
system, there is scarce evidence of its role in autoimmune diseases. Twenty years ago a potential relationship between salt and
asthma was described,27 and a recent systematic review found
evidence that a low sodium diet may improve lung function in
exercise induced-asthma, with no clear evidence on the overall
control of asthma.28 Other reports have linked sodium intake to
mortality in type 1 diabetes, but in this case the involvement of
the immune system is less clear and it is probably linked to renal
integrity.29
Th17 cells and IL-17 are thought to be major players in MS
pathogenesis.3 30 31 yet their relationship to sodium chloride
levels has been only recently addressed.8 9 Increasing sodium
chloride concentrations in an in vitro system by 40 mM boosts
highly pathogenic human Th17 generation in an serum and
glucocorticoid kinase 1-dependent fashion with no significant
effects on other effector T-cell subsets.9 Furthermore, mice fed
a high-salt diet had an exacerbated clinical and histological EAE
course that was associated with increased IL-17.8 9 Thus, the
aforementioned effects of sodium on Th17 cells could at least
partly explain the association found in our study.
Future studies should address whether the effects of sodium
in MS are mediated by Th17 or additional mechanisms. Sodium
chloride intake has many physiological effects such as blood
pressure and renin angiotensin system modulation.32
Interestingly, the activation of renin and angiotensin has been
implicated in EAE pathogenesis.33 Moreover, increases in

systolic blood pressure similar to those observed with high-salt
consumption have recently been shown to be associated with
the disruption of white matter integrity in young normotensive
individuals.34 Whether high-blood pressure interacts with the
typical autoimmune mechanisms associated with MS is an interesting question that remains to be answered.
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.
Contributors MFF was involved in drafting/revising the manuscript, study concept
and design, analysis and interpretation of the data, statistical analysis, study
supervision and coordination, funding acquisition. MPF and MIG were involved in
drafting/revising the manuscript, study concept and design, acquisition of data. FJQ
was involved in drafting/revising the manuscript, study concept and design. JC
drafting/revising the manuscript, study concept and design, acquisition of data,
funding acquisition.
Funding This study was supported by funding from the Raúl Carrea Institute for
Neurological Research FLENI, by a grant from Novartis Argentina, and Merck-Serono
Argentina.
Competing interests MFF received honoraria and professional travel/
accommodations stipends from Merck-Serono Argentina and Novartis Argentina.
MPF received honoraria from Merck-Serono, Genzyme and Bayer Argentina. MIG has
nothing to disclose. FJQ received reimbursement for developing educational
presentations for Novartis, and research in his lab is partially supported by EMDSerono, Novartis, Sanofi and Questcor. JC is a board member of Merck-Serono
Argentina, Novartis Argentina, Biogen-Idec LATAM and Merck-Serono LATAM. JC
received reimbursement to develop educational presentations for Merck-Serono
Argentina, Merck-Serono LATAM, Biogen-Idec Argentina, Novartis Argentina,
Novartis LATAM, Genzyme Argentina and TEVA-Tuteur Argentina as well as
professional travel/accommodation stipends.
Ethics approval Institutional Ethics Committee.
Provenance and peer review Not commissioned; externally peer reviewed.

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Farez MF, et al. J Neurol Neurosurg Psychiatry 2014;0:1–6. doi:10.1136/jnnp-2014-307928

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Farez MF, et al. J Neurol Neurosurg Psychiatry 2014;0:1–6. doi:10.1136/jnnp-2014-307928

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Sodium intake is associated with increased
disease activity in multiple sclerosis
Mauricio F Farez, Marcela P Fiol, María I Gaitán, et al.
J Neurol Neurosurg Psychiatry published online August 28, 2014

doi: 10.1136/jnnp-2014-307928

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