Department of Internal Medicine and Medical Specialties, Rheumatology, Sapienza University of Rome, Italy
Dietary Habits Bursting into the Complex Pathogenesis of Autoimmune Diseases: The Emerging Role of Salt from Experimental and Clinical Studies.
The incidence and prevalence of autoimmune diseases have increased in Western countries over the last years. The pathogenesis of these disorders is multifactorial, with a combination of genetic and environmental factors involved. Since the epidemiological changes cannot be related to genetic background, which did not change significantly in that time, the role of environmental factors has been reconsidered. Among these, dietary habits, and especially an excessive salt, typical of processed foods, has been implicated in the development of autoimmune diseases. In this review, we summarize current evidence, deriving both from experimental models and clinical studies, on the capability of excessive salt intake to exacerbate proinflammatory responses affecting the pathogenesis of immune-mediated diseases. Data on several diseases are presented, including rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, and Crohn's disease, with many of them supporting a proinflammatory effect of salt. Likewise, a hypertonic microenvironment showed similar effects in experimental models both in vivo and in vitro. However, murine models of spontaneous autoimmune polyneuropathy exposed to high salt diet suggest opposite outcomes. These results dictate the need to further analyse the role of cooking salt in the treatment and prevention of autoimmune diseases, trying to shape a fine tuning between the possible advantages of a restricted salt intake and the changes in circulating metabolites, mediators, and hormones which come along salt consumption and could in turn influence autoimmunity.
1. I have learned recently that the body, for the most part, regulates its sodium level naturally to the optimum level it needs just as it does for many other nutrients.
2. Life on this planet evolved from the oceans and salt apparently was a primary factor. Without salt on this planet, there would likely be no life as we know it.
3. Salt is likely necessary for good health and life.
The so called experts have been insisting for many, many years that sodium should be avoided. I always avoided adding salt to my foods and avoided salty foods. There is ample evidence now including the info you present that salt is a good and necessary nutrient. My sodium level has not really changed since I added sodium back into my diet a few years ago. I now consume salt, typically Himalayan pink salt, on a daily basis, which is considered one of the most nutrient rich sources of sodium available.
Benefits of salt include:
contracting and relaxing muscles
maintaining proper fluid balance and preventing dehydration
sending nervous system impulses
preventing low blood pressure
Recent research has suggested that eating salt can reduce the risk of infection and kill harmful bacteria.
One study on animals has also led researchers to infer that salt may have a positive effect on symptoms of depression.
Some interesting info on Himalayan salt include:
Pink Himalayan salt is chemically similar to table salt. It contains up to 98 percent sodium chloride. The rest of the salt consists of trace minerals, such as potassium, magnesium, and calcium. These give the salt its light pink tint.
These minerals also explain why Himalayan salt tastes different from regular table salt.
Here is an interesting article detailing this phenomenon titled "How the body regulates salt levels"
Some sources say that pink Himalayan salt contains up to 84 different trace minerals.
As it contains up to 98 percent sodium chloride, this means that only around 2 percent is made up of these various trace minerals. Given the relatively limited quantities in which people normally consume salt, and the tiny quantity of these minerals in the salt, they are unlikely to provide any measurable or significant health benefits.
Here is a link to an interesting article titled "How the body regulates salt levels"
https://www.nih.gov/news-events/nih-res ... alt-levels
Department of Neurology and Neuroimmunology, Johns Hopkins School of Medicine, Baltimore
Sodium intake and multiple sclerosis activity and progression in BENEFIT
To assess whether a high-salt diet, as measured by urinary sodium concentration, is associated with faster conversion from clinically isolated syndrome (CIS) to multiple sclerosis (MS) and MS activity and disability.
BENEFIT was a randomized clinical trial comparing early versus delayed interferon beta-1b treatment in 465 patients with a CIS. Each patient provided a median of 14 (interquartile range = 13-16) spot urine samples throughout the 5-year follow-up. We estimated 24-hour urine sodium excretion level at each time point using the Tanaka equations, and assessed whether sodium levels estimated from the cumulative average of the repeated measures were associated with clinical (conversion to MS, Expanded Disability Status Scale [EDSS]) and magnetic resonance imaging (MRI) outcomes.
Average 24-hour urine sodium levels were not associated with conversion to clinically definite MS over the 5-year follow-up (hazard ratio [HR] = 0.91, 95% confidence interval [CI] = 0.67-1.24 per 1g increase in estimated daily sodium intake), nor were they associated with clinical or MRI outcomes (new active lesions after 6 months: HR = 1.05, 95% CI = 0.97-1.13; relative change in T2 lesion volume: -0.11, 95% CI = -0.25 to 0.04; change in EDSS: -0.01, 95% CI = -0.09 to 0.08; relapse rate: HR = 0.78, 95% CI = 0.56-1.07). Results were similar in categorical analyses using quintiles.
Our results, based on multiple assessments of urine sodium excretion over 5 years and standardized clinical and MRI follow-up, suggest that salt intake does not influence MS disease course or activity. Ann Neurol 2017;82:20-29.
Department of Neurology, Division of Neurobiology, Medical University of Innsbruck, Innsbruck, Austria
High-salt Diet Does Not Boost Neuroinflammation and Neurodegeneration in a Model of α-Synucleinopathy
https://pubmed.ncbi.nlm.nih.gov/3198004 ... einopathy/
Aim: Pre-clinical studies in models of multiple sclerosis and other inflammatory disorders suggest that high-salt diet may induce activation of the immune system and potentiate inflammation. However, high-salt diet constitutes a common non-pharmacological intervention to treat autonomic problems in synucleinopathies such as Parkinson's disease and multiple system atrophy. Since neuroinflammation plays an important pathogenic role in these neurodegenerative disorders, we asked here whether high-salt diet may aggravate the disease phenotype in a transgenic model of multiple system atrophy.
Methods: Nine-month-old PLP-hαSyn and matched wildtype mice received normal or high-salt diet for a period of 3 months. Behavioral, histological, and molecular analyses were performed to evaluate the effect of high-salt diet on motor decline, neuroinflammation, neurodegeneration, and α-synuclein accumulation in these mice.
Results: Brain subregion-specific molecular and histological analyses showed no deleterious effects of high-salt diet on the level of microglial activation. Moreover, neuroinflammation-related cytokines and chemokines, T cell recruitment or astrogliosis were unaffected by high-salt diet exposure. Behavioral testing showed no effect of diet on motor decline. High-salt diet was not related to the deterioration of neurodegeneration or α-synuclein accumulation in PLP-hαSyn mice.
Conclusions: Here, we demonstrate that high-salt diet does not aggravate neuroinflammation and neurodegeneration in PLP-hαSyn mice. Our findings discard a deleterious pro-neuroinflammatory effect of high-salt diet in multiple system atrophy.