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Previously, it was thought safe to withdraw from the diet in the late teens or early twenties, after the central nervous system was fully developed; recent studies suggest some degree of relapse, and a continued phenylalanine-restricted diet is now recommended. [4] PKU or hyperphenylalaninemia may also occur in persons without the PKU genotype.
A low-protein diet is used as a therapy for inherited metabolic disorders, such as phenylketonuria and homocystinuria, and can also be used to treat kidney or liver disease. Low protein consumption appears to reduce the risk of bone breakage, presumably through changes in calcium homeostasis. [ 1 ]
The E.S.PKU executive board is elected by the annual general meeting every three years and consists of volunteers. The Scientific advisory committee oversees projects like the European Guidelines and collects data [2] to support studies in the field of phenylketonuria.
Phenylketonuria is inherited in an autosomal recessive fashion. PKU is an autosomal recessive metabolic genetic disorder. As an autosomal recessive disorder, two PKU alleles are required for an individual to experience symptoms of the disease. For a child to inherit PKU, both parents must have and pass on the defective gene. [17]
Individuals with phenylketonuria (PKU) must keep their intake of phenylalanine – an essential amino acid – extremely low to prevent a mental disability and other metabolic complications. Phenylalanine is a component of the artificial sweetener aspartame, so people with PKU need to avoid low calorie beverages and foods with this ingredient. [49]
varied by: 1) provision of general calorie recommendations, 2) provision of specific calorie information, and 3) whether high- or low-calorie items were more easily accessible. Results suggest that a strictly informational approach may be less effective than subtle guidance in enticing fast-food customers towards healthier meals.
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