Myasthenia gravis is an autoimmune disease that causes muscular weakness and fatigue, which is exacerbated by activity and improved with rest. Under normal circumstances antibodies are produced by the immune system largely to fight off infection. Myasthenia gravis causes the immune system to produce antibodies that target healthy cells, commonly affecting the cellular receptor in muscle cells for the neurotransmitter acetylcholine, which stimulates muscular contractions (Hoch 2001). The disease is characterized by fluctuating periods of muscular weakness, with easy fatigability representing a classic hallmark of the disease. Drooping eyelids, blurred vision, and difficulty chewing and swallowing are common symptoms. About 15–20% of people with myasthenia gravis develop severe, potentially life-threatening respiratory impairment, often within the first year of illness; this is a medical emergency called myasthenia crisis and necessitates mechanical ventilation (NINDS 2012; Juel 2004).
Myasthenia gravis affects an estimated 20 individuals per 100 000 people in the United States (Meriggioli 2012a; Jayam Trouth 2012). Women typically acquire the disease more frequently than men and at a younger age. Although initial signs of myasthenia gravis may emerge at any age, women most commonly develop symptoms under the age of 40, while symptoms among men usually develop after age 60 (NINDS 2012).
Scientists debate the predominant cause of the immune dysregulation associated with myasthenia gravis, though most theories agree that the thymus plays an important role in its development. The thymus is an organ behind the breastbone that produces certain immune cells called T cells (Rehan 2012). Approximately 10–15% of all people with myasthenia gravis have a thymic tumor and more than 50% have an increased number of cells (hyperplasia) in the thymus (Meriggioli 2012a). Recent, intriguing studies have suggested that inflammation and infection with the Epstein-Barr virus may also contribute to the development of this autoimmune disease (Cavalcante 2011).
Although the majority of patients with myasthenia gravis have antibodies that target muscle cell acetylcholine receptors, some researchers have discovered that some myasthenia gravis patients have antibodies against other proteins such as muscle-specific tyrosine kinase (MuSK) or the low-density lipoprotein receptor-related protein 4 (LRP4) (Zagoriti 2013).
Unfortunately, there is currently no cure for myasthenia gravis (MGFA 2010b). However, advances in treatment over the past few decades have enabled many myasthenia gravis patients to achieve prolonged remission with no signs or symptoms of the disease (Thanvi 2004). One of the most common treatments recommended for myasthenia gravis is removal of the thymus (Howard 2006; Ruckert 2011), but there is debate as to whether this procedure is effective in people who do not have thymic tumors (Diaz 2013; Spillane 2013; Corse 2014). Other common treatments include corticosteroids, which are used to inhibit the activity of immune cells short-term; acetylcholinesterase inhibitors, which allow the nerves to regain their ability to communicate with the muscles; and immunosuppressive drugs, which inhibit the body’s immune response long-term (Sathasivam 2011).
Physicians in the past believed that myasthenia gravis was a single disease, but now it has been suggested that it may represent several different clinical subtypes (Meriggioli 2012a; Meriggioli 2009). Clinicians are now able to test patients for the presence of different markers and tailor their treatments accordingly. Several recent clinical trials and laboratory experiments have suggested that agents used to treat other diseases, such as rituximab, which is used in the treatment of lymphomas and leukemias, may also be effective for the treatment of myasthenia gravis (Diaz-Manera 2012; Collongues 2012). Furthermore, additional studies have suggested that exercise and some integrative therapeutics, such as vitamin D3, astragalus extract, and creatine may also ease symptoms of myasthenia gravis (Askmark 2012; Stout 2001; Tu 1994).
In this protocol you will learn about the basics of myasthenia gravis and how it is typically treated by conventional medicine. A number of novel and emerging therapies for myasthenia gravis that have shown promise in clinical trials will be reviewed. Several dietary and lifestyle considerations that may mitigate myasthenia gravis symptoms will be presented, and a number of integrative, natural interventions that target some of the underlying mechanisms that contribute to myasthenia gravis will be outlined as well.