Quality of life is a difficult concept to define and to measure. An hypothesis is proposed which suggests that the quality of life measures the difference, or the gap, at a particular period of time between the hopes and expectations of the individual and that individual's present experiences. Quality of life can only be described by the individual, and must take into account many aspects of life. The approach is goal-orientated, and one of task analysis. The hypothesis is developed in a diagramatic way, and several methods of testing the hypothesis suggested.
Summary pointsEpidemiological techniques, and the data generated from cancer registration, are powerful in identifying correlations between diseases and clinical outcomes. They do, however, have limitations in setting public policyIn understanding issues surrounding risk assessment, perception is a key aspect of understanding patient and public choice. Information sharing is criticalA proposal for clarifying the language of risk has been put forward for discussion and debate
This chapter presents some concluding thoughts from the authors. This book has sought to address a range of issues facing risk communication around a broad spectrum of public health concerns. At the same time, it has sought to show how these issues have evolved since the first edition of this collection was published. There is little doubt that the landscape in which policymakers and managers have to communicate risk has changed. The various public groups within our societies are also exposed to more diverse forms of information flows than were present even 10 years ago. Not all of it is accurate, and individuals now need to be able to filter, interpret, and make sense of the information that they are given, in increasingly sophisticated ways.
The aim of this study was to determine whether a ketogenic diet could decrease nitrogen losses in cachectic cancer patients and at the same time reduce the supply of glucose for tumor energy metabolism. Five patients with malignant disease and severe weight loss (mean 32%) were fed via a fine bore nasogastric tube. A normal diet was given for 6 d and this was followed by 7 d of an isonitrogenous, isocaloric, ketogenic diet. Both diets were well tolerated. At 7 d the mean ketone body concentration in the blood of patients fed the ketogenic diet was 1.21 +/- 0.33 mM. This ketosis was associated with a significant reduction of the concentration in blood of glucose, lactate, and pyruvate (p less than 0.05). There was, however, no significant alteration in host N balance or whole-body protein synthesis, degradation, or turnover rates. Whether the change from glucose- to fat-derived energy substrates might reduce tumor growth rates in the long term remains to be determined.
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