RESTLESS LEGS SYNDROME Autoimmune disease patients are at an increased risk for developing restless legs syndrome (RLS) (a sleep disorder in which patients describe an urge to move their legs or other extremities during rest). For example, in the study entitled “Medical comorbidity of sleep disorders: sleep-related limb movements” the researchers stated: “RLS has also been found to be associated with a variety of rheumatological and immunological conditions, showing a prevalence of 20- 30% (two to six times that of the general population) among patients with rheumatoid arthritis, fibromyalgia, Sjögren’s syndrome, and scleroderma” (Dikeos, 2011). Patients with lupus, multiple sclerosis, diabetes, and hypothyroidism are also at an increased risk of developing RLS. For example, in the study entitled “Systemic lupus and risk of RLS” the researchers concluded: “These novel data indicate that RLS is more prevalent in women with SLE than in controls” (Hassan, 2011). The increased risk of developing RLS in patients with autoimmune disease would be due to an inability to properly metabolize iron and a lack of dopamine. In the following study the researchers concluded that there may be an “iron-dopamine” connection central to the pathophysiology of RLS for at least some if not most patients with the disorder. Dopamine and iron in the pathophysiology of restless legs syndrome (RLS). Allen, R. 2004. Sleep Med. 5(4):385-91. “…It is concluded that there may be an iron-dopamine connection central to the pathophysiology of RLS for at least some if not most patients with this disorder…” We have been discussing the lack of the essential amino acid phenylalanine (which is necessary to produce dopamine) found in patients with autoimmune disease. Essential amino acids, such as phenylalanine, are found in dietary proteins. Patients with autoimmune disease lack the enzymes necessary for protein digestion—protease. Protease are also required for the proper metabolism of iron. Without these enzymes the body would not be able to properly metabolize iron. In the following study the researchers concluded that the serine protease TMPRSS6 is an “essential component” of a pathway that detects iron deficiency and regulates iron absorption in the body. New insights into intestinal iron absorption. Hörl, W.H. 2008. Nephrol. Dial. Transplant. 23(10):3063-3064. “…Du et al. described the novel and exciting finding that the transmembrane serine protease 6 (TMPRSS6) senses iron deficiency…In their study, Du et al. described a mutant mouse, which is characterized by progressive loss of body hair and microcytic anaemia…Take home message: Iron deficiency activates the serine protease TM-PRSS6. The protease then inhibits hepcidin transcription and thereby allows intestinal iron absorption and cellular iron release.” Take home message: Patients with autoimmune disease are at an increased risk of developing RLS. Research has shown there is an “iron-dopamine” connection central to the pathophysiology of RLS. The inability to produce dopamine and to properly metabolize iron, due to a lack of protease (enzymes that digest proteins and metabolize iron), would explain the increased risk of developing RLS in patients with autoimmune disease.
Posted on: Wed, 04 Dec 2013 19:00:04 +0000
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