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Fasting – the voluntary withholding of food – is a common practice in many religions. Depending on the type of fast, weight loss may occur. Participants in a fast may develop negative sodium balance and have high rates of gluconeogenesis with amino acids as the primary substrates. Ketosis develops and ketones replace glucose as the primary energy source in the central nervous system, thereby decreasing the need for gluconeogenesis and sparing protein catabolism. Several hormonal changes occur during fasting, including a fall in insulin and T3 levels and a rise in glucagon and reverse T3 levels [1]. However, the effect of fasting on neurological diseases, direct or indirect (for instance through affecting medication adherence), are not well known. The mass participation in, and clear regulations of, Ramadan fasting make it an ideal opportunity to study these issues.
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