This was a recent abstract (not formally published yet) which I found interesting. It was only a small study but showed a NEGATIVE TREND between increased salt intake and increased Multiple Sclerosis manifestations, both in terms of clinical events, like MS exacerbations, and in terms of new lesions on the MRI. Yikes.
The magic number was more than 4.8 grams a day. Once that number was reached, MS event relapse rates were 4 times higher than those who had less than 2 grams a day. Obviously, what to say about the in-between range is a grey area.
That being said the causal relationship is harder to prove. In other words, HOW this would be true is harder to determine and therefore the fundamental truth that salt itself is responsible also has to be further questioned. Other possibilities: Maybe people with worse, more aggressive MS are hungrier for more salt for some reason.
Theories on how salt would cause this are unclear. Many argue that salt causes and increased inflammatory condition in the human body or increased oxidative stress indirectly in the human body. It also may increase the permeability of the blood brain barrier which keeps the brain "locked off" from the body. This increased permeability would make it easier for the person to mistakenly "accidentally remember" that the myelin around the brain and spinal cord neurons is not part of you (of course, it is) and attack it again, inappropriately.
Interestingly a Big Mac alone contains almost 1gram.
versus
A cup of broccoli (29mg), a cup of grapes, a pre-made-pre-cooked chicken cordon blue (490 mg), an Oikos greek Yogurt (100mg) and a cup of milk chocolate Blue Bell ice cream (100mg).... is still only 719 mg of sodium.
I have included the full reader-friendly article below, and put a bold on my favorite part:
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COPENHAGEN -- Sodium intake was positively correlated with risk of increased disease activity in patients with multiple sclerosis, according to a small study reported here.
Each gram of estimated daily sodium intake above the average in a 52-patient sample was associated with an increase of 3.65 in MRI lesion counts, said Mauricio Farez, MD, PhD, of Buenos Aires.
Also, patients with estimated salt intake classified as high -- more than 4.8 g daily -- showed relapse rates that were 3.95 times greater (95% CI 1.39-11.21) than those with intakes less than 2 g/day, he told attendees at the European Committee for Treatment and Research in Multiple Sclerosis annual meeting.
Farez emphasized repeatedly that the findings did not prove that high salt intake caused the increased disease activity. He acknowledged that, if there is a causal relationship, it possibly could go in the reverse direction -- that patients with highly active MS may increase their salt intake as a result. But he said he did not view that as very likely.
The study in a total of 122 patients with relapsing-remitting MS grew out of previous research connecting salt intake with vitamin D levels and body mass index, he said. Numerous studies have indicated an association between vitamin D status and MS risk.
He and colleagues initially recruited 70 patients for a first phase of the observational study. They underwent a baseline MRI scan in November 2010, followed by MRI scans and analysis of urinary sodium excretion as a means of estimating sodium intake 1 year later. Finally, in November 2013, relapse rates for the preceding 2 years were calculated.
During this first phase, the MRI analyses included "combined unique activity" counts -- the total of new T2 lesions and new gadolinium-enhancing T1 lesions since the baseline scan.
A second group of 52 patients was examined in June 2013 with MRI scans and urinary sodium testing to provide replication data for the association between sodium intake and MRI lesion activity. Because this group had only a single scan and no follow-up, Farez and colleagues could only calculate T2 lesion loads, not the combined unique activity lesion counts nor relapse rates.
Farez acknowledged that an important limitation of the study was that it did not measure urinary sodium excretion with 24-hour urine collections, which he said were impractical since they require participants to carry a large container to capture all their urine for a whole day and night.
Instead, his team relied on spot urine collections and a published formula to estimate daily sodium excretion and, from that, daily sodium intake.
He reported that, in the first group of patients, not only those with high sodium intake (more than 4.8 g/day) but also those with "average" consumption showed increased risk of relapse. Participants with estimated daily intake of 2.0 to 4.8 g/day had relapse rates that were 2.75 times that of the low-intake group (95% CI 1.30-5.81).
Comparing both the average- and high-intake groups, the trend was significant at P=0.001, he reported.
Also in the first group, combined unique activity lesion counts were approximately three times greater in both the average- and high-intake groups compared with the low-intake group (P not reported), Farez said.
And, T2 lesion counts were similar in the first cohort's low- and average-intake groups at an average of about 6, but they reached a mean of approximately 14 in the high-intake group (P<0.05).
In the replication set of 52 patients, similar results were seen, Farez said. He and his colleagues calculated that each increment in intake of 1 g above the cohort average was associated with 3.65-lesion increase in T2 count (SD 0.77, P<0.001).
He did not specify the cohort average, but he said that the national average in Argentina has been measured at nearly 5 g/day, well above the U.S. mean of 3.4 g/day.
The World Health Organization has recommended a maximum daily intake of 2 g/day. In the U.S., several government agencies have jointly called for a maximum of 1.5 g/day-- but earlier this year, the Institute of Medicine complained that the scientific evidence did not a support such a low figure, instead backing an older standard of 2.3 g/day.
Farez and colleagues also measured serum sodium but found no relationship between it and clinical or MRI activity. It was also not significantly associated with estimated sodium intake, with an R2 value of just 0.0082.
Asked by the session moderator what a causal mechanism might be, Farez said previous studies had suggested that high salt levels can promote increased inflammatory activity throughout the body. Also, he said, it may increase permeability in the blood-brain barrier, which could contribute to inflammation in the central nervous system.
Whatever such a mechanism may be, he said, "it does not seem to occur in peripheral blood."
