Why do patients become cachectic

The cachectic patient is like an accelerating car running out of petrol. Anorexia critically reduces fuel supply (by about 300-500 kcal (1254-2090 kJ) a day), while accelerated metabolic cycling (for example, glucose-lactate cycling) drives hypermetabolism (100-200 kcal a day). In addition, there are direct catabolic effects at the level of skeletal muscle (for example, activation of the ubiquitin-proteasome pathway) and adipose tissue. The mediators of these changes are complex and include proinflammatory cytokines, stress hormones, and tumour specific cachectic factors such as proteolysis inducing factor (PIF). The main energy (subcutaneous fat) and labile protein reserves (skeletal muscle) of the body are mobilised and the patient becomes prone to secondary effects such as insulin resistance and further muscle wasting due to immobility. These changes underlie a key paradox of cachexia in that while the metabolic rate may be increased, overall (or total) energy expenditure is decreased due to a fall in physical activity.

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