The risk for disordered oropharyngeal swallowing (dysphagia) increases with age. Loss of swallowing function can have devastating health implications including dehydration, malnutrition, and pneumonia, as well as reduced quality of life. Age-related changes place older adults at risk for dysphagia for two major reasons: One is that natural, healthy aging takes its toll on head and neck anatomy and physiologic and neural mechanisms underpinning swallowing function. This progression of change contributes to alterations in the swallowing in healthy older adults and is termed presbyphagia, naturally diminishing functional reserve. Second, disease prevalence increases with age and dysphagia is a co-morbidity of many age-related diseases and/or their treatments. Sensory changes, medication, sarcopenia and age-related diseases are discussed herein. Relatively recent findings that health complications are associated with dysphagia are presented. Nutrient requirements, fluid intake and nutritional assessment for older adults are reviewed relative to their relations to dysphagia. Dysphagia screening and the pros and cons of tube feeding as a solution are discussed. Optimal intervention strategies for elders with dysphagia ranging from compensatory interventions to more rigorous exercise approaches are presented. Compelling evidence of improved functional swallowing and eating outcomes resulting from active rehabilitation focusing on increasing strength of head and neck musculature is provided. In summary, while oropharyngeal dysphagia may be life-threatening, so are some of the traditional alternatives, particularly for frail, elderly patients. While the state of the evidence calls for more research, this review indicates the behavioral, dietary and environmental modifications emerging in this past decade are compassionate, promising and in many cases preferred alternatives to the always present option of tube feeding.

Background: Phenylketonuria (PKU) requires a lifelong lowphenylalanine diet that provides the majority of protein from a phenylalanine-free amino acid (AA) formula. Glycomacropeptide (GMP), an intact protein formed during cheese production, contains minimal phenylalanine. Objective: The objective was to investigate the effects of substituting GMP food products for the AA formula on acceptability, safety, plasma AA concentrations, and measures of protein utilization in subjects with PKU. Design: Eleven subjects participated in an inpatient metabolic study with two 4-d treatments: a current AA diet (AA diet) followed by a diet that replaced the AA formula with GMP (GMP diet) supplemented with limiting AAs. Plasma concentrations of AAs, blood chemistries, and insulin were measured and compared in AA (day 4) and GMP diets (day 8). Results: The GMP diet was preferred to the AA diet in 10 of 11 subjects with PKU, and there were no adverse reactions to GMP. There was no significant difference in phenylalanine concentration in postprandial plasma with the GMP diet compared with the AA diet. When comparing fasting with postprandial plasma, plasma phenalyalanine concentration increased significantly with the AA but not with the GMP diet. Blood urea nitrogen was significantly lower, which suggests decreased ureagenesis, and plasma insulin was higher with the GMP diet than with the AA diet. Conclusions: GMP, when supplemented with limiting AAs, is a safe and highly acceptable alternative to synthetic AAs as the primary protein source in the nutritional management of PKU. As an intact protein source, GMP improves protein retention and phenylalanine utilization compared with AAs.

Phenylketonuria (PKU) is caused by deficient activity of the enzyme phenylalanine hydroxylase, needed to convert the essential amino acid (AA) phenylalanine (phe) to tyrosine. In order to prevent neurological damage, lifelong adherence to a low-phe diet that is restricted in natural foods and requires ingestion of a phe-free AA formula to meet protein needs is required. The goal of nutritional management for those with PKU is to maintain plasma phe concentrations that support optimal growth, development, and mental functioning while providing a nutritionally complete diet. This paper reviews developing a lifelong dietary prescription for those with PKU, outcomes of nutritional management, compliance with the low-phe diet across the life cycle, and new options for nutritional management. An individualized dietary prescription is needed to meet nutrient requirements, and the adequacy of phe intake is monitored with assessment of blood phe levels. Elevated phe concentrations may occur due to illness, excessive or inadequate phe intake, or inadequate intake of AA formula. Although normal growth and development occurs with adherence to the low-phe diet, it is important to monitor vitamin, mineral and essential fatty acid status, especially in those who do not consume sufficient AA formula. Given the growing population of adults with PKU, further research is needed to understand the risks for developing osteoporosis and cardiovascular disease. There are promising new options to liberalize the diet and improve metabolic control such as tetrahydrobiopterin therapy or supplementation with large neutral AAs. Moreover, foods made with glycomacropeptide, an intact protein that contains minimal phe, improves the PKU diet by offering a palatable alternative to AA formula. In summary, continued efforts are needed to overcome the biggest challenge to living with PKU – lifelong adherence to the low-phe diet.

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