Nutrition Facts in Multiple Sclerosis

Abstract

The question whether dietary habits and lifestyle have influence on the course of multiple sclerosis (MS) is still a matter of debate, and at present, MS therapy is not associated with any information on diet and lifestyle. Here we show that dietary factors and lifestyle may exacerbate or ameliorate MS symptoms by modulating the inflammatory status of the disease both in relapsing-remitting MS and in primary-progressive MS. This is achieved by controlling both the metabolic and inflammatory pathways in the human cell and the composition of commensal gut microbiota. What increases inflammation are hypercaloric Western-style diets, characterized by high salt, animal fat, red meat, sugar-sweetened drinks, fried food, low fiber, and lack of physical exercise. The persistence of this type of diet upregulates the metabolism of human cells toward biosynthetic pathways including those of proinflammatory molecules and also leads to a dysbiotic gut microbiota, alteration of intestinal immunity, and low-grade systemic inflammation. Conversely, exercise and low-calorie diets based on the assumption of vegetables, fruit, legumes, fish, prebiotics, and probiotics act on nuclear receptors and enzymes that upregulate oxidative metabolism, downregulate the synthesis of proinflammatory molecules, and restore or maintain a healthy symbiotic gut microbiota. Now that we know the molecular mechanisms by which dietary factors and exercise affect the inflammatory status in MS, we can expect that a nutritional intervention with anti-inflammatory food and dietary supplements can alleviate possible side effects of immune-modulatory drugs and the symptoms of chronic fatigue syndrome and thus favor patient wellness.

Correlation of Tissue Antibodies and Food Immune Reactivity in Randomly Selected Patient Specimens

“…Our study on the more common delayed immune responses, IgG+IgA, illustrates a need for some individuals to abstain from consuming dairy products. To improve clinical conditions, the dairy-free diet has been recommended for patients with nephrotic syndrome [59], osteoarthritis [60], diabetes [61,62], and neurological disorders [63,64]. Indeed, dairy protein antibodies have been shown to cross-react with glutamic acid decarboxylase (GAD)-65 [22], GAD-67, and insulin receptor-α [65], an important serological marker for type 1 diabetes and latent autoimmune diabetes in adults (LADA) [66].…”

Anti-inflammatory nutritional intervention in patients with relapsing-remitting and primary-progressive multiple sclerosis: A pilot study

“…This partial failure may be due to the fact that MS is a complex and multifactorial disease. In fact, in addition to the genetic and immunological components, various environmental and/or metabolic factors or conditions may have a role in its development: i) viral infections, [12][13][14] ii) heavy metal poisoning, 15,16 iii) smoking, 14,17 iv) childhood obesity, 18 v) incorrect life style, mostly including wrong dietary habits, 19,20 or vi) low vitamin D status. 21 The most significant difference between the different causative agents listed above is that, unlike the others, dietary habits and lifestyle (v) and vitamin D levels (vi) can be modified to provide beneficial effects on the course of the disease.…”

“…Fish oil and n-3 PUFA inhibit the pro-inflammatory transcription factor nuclear transcription factor-kB (NF-kB) and lower the level of the gelatinase B, also known as matrix metalloproteinase-9 (MMP-9) (another important mediator of inflammation). 20,25,26,34 In addition, n-3 PUFA have neuroprotective properties and may be very useful in the complementary treatment in MS patients. DHA is present at high concentration in the brain and its levels decreases dramatically in MS patients.…”

Metalloproteinases and their inhibitors as therapeutic targets for multiple sclerosis: current evidence and future perspectives

“…4,5 Several studies have shown that both anti-MS-specific therapies [6][7][8][9] and some antioxidant and anti-inflammatory compounds have the ability to downregulate MMPs, suggesting that inhibition of MMPs may represent an additional mechanism by which these agents decrease the development of new CNS lesions in the course of MS. [10][11][12] In this review, we summarize the general characteristics of the different MMPs and their regulatory mechanisms. The pathogenic role of MMPs in the development and progression …”