This illness was seen in 400-600 live male births in the US (CDC, 2005). Muscular dystrophies affected children and adults; they were severe in nature and genetic in cause (Emery, 2008). The striate, voluntary, multi-nucleated skeletal muscles were affected by the illness (Fischman, 2009). French neurologist Guillaume-Benjamin-Armand-Duchenne (1806-1975) first published papers describing this illness in 1861; it was thereafter called Duchenne’s dystrophy in the founder’s memory (Johanson, 2008). The ill and the family were greatly affected by psychological and physiological challenges. Societies and support groups were also involved and joined hands with the families to uplift their general well-being. The disturbed motility and the emotional effects restricted the life of the ill and their families. Exercise, physiotherapy and surgery had a variable role in their existence. Schooling and career issues affected them. Genes, being the causative factors for the different varieties of muscular dystrophies, had been identified. Diagnosis was possible by molecular genetics. Prevention was done through genetic counseling (Emery, 2008). Muscular dystrophy patients had limited mobility or orophyangeal weakness (Motlagh et al, 2005). These led to nutritional deficiencies. Dysmotility of the gastrointestinal tract could be associated in muscular dystrophy and this was another cause for nutritional deficiencies caused by inadequate digestion and absorption. At various periods in the history of muscular dystrophies, different scientists had associated various nutritional deficiencies with muscular dystrophy. Vitamin E was the culprit by the anti-oxidant theory of which the main proponents were Alan Tappel in 1953 and Karl Folkers in 1960 (New Scientist, 1971). Folkers believed that the absence of ubiquinone caused a disturbance in the electron-transport system which then led to muscular dystrophy. In 1957, Klaus Schwarz indicated that selenium was as significant in the muscular dystrophy theories. In 1971, Lucy and Diplock had propounded that both selenium and Vitamin E were found on the membrane surfaces of cells in the process of electron transport (New Scientist, 1971). Johanson attributed the illness to the inability at the molecular level to synthesize the proteins needed to form and maintain healthy muscles (2008). Vitamin E had been considered an anti-oxidant apart from it being fat-soluble. Its anti-oxidant action in the interior part of the membranes protected the cell from the peroxidation of lipid (Rafique et al, 2001). The saturation of the membrane lipids depended on the distribution of the Vitamin E. Mitochondria were known to have an abundance of Vitamin E but it was not known which of the membranes, outer or inner, had more of the vitamin. Vitamin E or tocopherol joined with the free radicals to form anti-oxidant defenses. Its deficiency caused problems of lipid peroxidation and disturbances in the mitochondrial respiratory chain. “Ataxia, areflexia, large fiber sensory neuropathy and muscle weakness clinically similar to Frederich’s ataxia” constituted the neurological syndrome seen with Vitamin E deficiency (Rafique et al, 2001). Friedrich’s ataxia had been associated with a genetic mutation which involved a mitochondrial protein known to regulate handling of
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Nutritional deficiencies in muscular dystrophy patients Nutritional deficiencies in muscular dystrophy patients Nutritional deficiencies in muscular dystrophy patients Muscular dystrophy (MD) referred to a “group of more than 30 genetic diseases that caused progressive weakness and degeneration of skeletal muscles used during voluntary movement” (NINDS, 2011)…
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3 pages (750 words)Research Paper
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