The 2011 ESPEN Arvid Wretlind lecture: cancer cachexia: the potential impact of translational research on patient-focused outcomes.

Cancer cachexia is a multifactorial syndrome characterised by loss of skeletal muscle that cannot be fully reversed by conventional nutritional support. Uncertainty continues as to its precise mediators and mechanisms. The pathophysiology is characterised by a variable combination of reduced food intake and abnormal metabolism. Recent evidence has suggested that there may be a genetic component to cachexia with emphasis on genes linked to systemic inflammation. Loss of skeletal muscle mass and function is a major contributor to the excess frailty, disability and increased mortality in cancer cachexia. Whilst muscle mass per se has been considered a key outcome measure in treating cachexia, it might be more rationale to choose a patient-centred outcome such as physical activity. Beyond good medical management, it is important that trials establish basic management for all patients (nutrition, exercise and anti-inflammatory treatment). Specific therapies for cachexia should focus on the key issues of reduced food intake and abnormal metabolism. Whilst combination regimens to treat these issues continue to be explored, there is also interest in biological therapies that target conserved molecular mechanisms of muscle growth/atrophy. The combination of approaches promises a new era for the management of cachexia in the context of supportive oncology.