Patients with chronic liver disease exhibit a progressive loss of fat and muscle mass leading to mixed protein-energy malnutrition. The severe loss of muscle mass and body cell mass have convincingly been shown to carry a grave prognosis. Cachexia is likely to progress due to increased requirements as a consequence of hypermetabolism on the one hand and reduced volitional food intake and malabsorption on the other. Hypermetabolism may be mediated by factors such as frequent episodes of endotoxinemia, an activation of the inflammatory cytokine and/or the beta-adrenergic system. Some of these factors may also be responsible for reduced appetite. Obviously, these mechanisms may also be operative in other disease entities but clearly, portal hypertension and portosystemic shunting pose the cirrhotic patient at a particular risk for such disturbances including that of malabsorption. Apart from the established value of providing sufficient nutritious substrate to meet requirements the use of beta-adrenergic blocking agents and endotoxinemia lowering strategies seem worthwhile options that merit further clinical evaluation.