Nutrition
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Amyotrophic lateral sclerosis (ALS) is the most common form of progressive motor neuron disease and the most devastating neurodegenerative disorder. ALS is characterized by progressive paralysis and respiratory failure leading to death within 3 to 5 years after its onset. Protein-energy malnutrition is a frequent finding in ALS. ⋯ The use of fiber-enriched formulas may help prevent constipation. However, considering the complex metabolic abnormalities of ALS, standard and/or fiber-enriched formulas might not be sufficient to achieve optimal metabolic and nutritional support. Based on the most recent clinical and experimental evidence, it is tempting to hypothesize that personalized nutritional support including specific nutritional substrates could act on disease progression and improve the quality of life and the response to the few and yet scarcely effective, currently available pharmacologic therapies.
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The inflammatory process seen in multiple sclerosis is due to an excess production of proinflammatory cytokines interleukin-1 (IL-1), IL-6, tumor necrosis factor-α, interferons, macrophage migration inhibitory factor, HMGB1 (high mobility group B1), and, possibly, a reduction in antiinflammatory cytokines IL-10, IL-4, and transforming growth factor-β that leads to increased secretion of reactive oxygen species, including nitric oxide, resulting in neuronal damage. It is suggested that failure of production of adequate amounts of resolution-inducing molecules lipoxins, resolvins, and protectins that suppress inflammation and reactive oxygen species production, enhance wound healing, and have neuroprotective properties results in inappropriate inflammation and delay in the healing/repair process, and so neuronal damage continues, as seen in multiple sclerosis. Hence, methods designed to enhance the production and/or administration of lipoxins, resolvins, and protectins may form a new approach in the prevention and treatment of multiple sclerosis and other similar autoimmune diseases.