Multiple sclerosis (MS) is an autoimmune disorder[1] characterized by muscle weakness and numbness, as well as problems with vision and bladder control. It is caused by the immune system attacking nerve-insulating myelin sheaths, which disrupts the communication between the brain and peripheral parts of the body. The disease is generally classified as either primary progressive MS or relapsing-remitting MS.
Primary-progressive MS is characterized by a progressively worsening neurological function that is evidenced by continuous symptoms, although these may change over time. Relapsing-remitting MS is characterized by clearly defined episodes that are separated by periods of remission from the disease. During remission there is a complete absence of symptoms with no apparent progression of the disease.
Oligodendrocytes are glial cells[2] that help create the myelin sheath around nerve axons in the central nervous system (CNS). These cells are critical for the development of the brain and ensure correct functioning of the nerve cells. The myelin sheath they produce acts as insulation that protects long nerve projections (known as axons) and facilitates the conduction of nerve signals.
During MS there is a loss of myelin in defined areas—known as lesion sites—in the brain and spinal cord. The process leading to lesions is summarized in Figure 1. MS is characterized[3] by a large array of invading immune cells, such as T-cells (tissue-infiltrating immune cells), B-cells (cells that secrete antibodies) and macrophages (a type of white blood cell that engulfs other cells and molecules). These cells attack and degrade the myelin sheath, the myelin-producing oligodendrocytes, and the nerve axon. Lesion sites develop over time and initially result in clinically benign symptoms, but they progress to significant disabilities.

References: Trapp B, Nave KA. Multiple Sclerosis: An Immune or Neurodegenerative Disorder? Annu. Rev. Neurosci, 2008.
Bar-Or A. The immunology of multiple sclerosis. Semin Neurol. Feb 2008.
Some studies on animal models of MS have suggested that various forms of dietary restriction, such as calorie restriction[4], intermittent fasting[5] and the ketogenic diet[6], protect neurons and reduce inflammation. Studies have also shown that periodic fasting[7] can improve cognitive function and reduce oxidative stress. A new study utilizing a diet that mimics fasting was tested to determine its effects on autoimmunity and inflammation.
Multiple sclerosis is an autoimmune disorder of the central nervous system during which the immune system attacks and destroys the myelin sheath around nerve axons. Most treatments for multiple sclerosis are immunosuppressive and do not alleviate autoimmunity or regenerate the damage already caused. New research hopes to determine the role diet and nutrition could have on overcoming multiple sclerosis.