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Anorexia

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A direct effect of systemic inflammation is appetite suppression. Cytokines directly result in feeding suppression and a lower intake of nutrients, and cachexia is nearly always accompanied by anorexia. IL‐1β and TNF‐α act on the glucose‐sensitive neurons in the ventromedial hypothalamic nucleus (a ‘satiety’ site) and the lateral hypothalamic area (a ‘hunger’ site).60

Acute illness is characterized by a spontaneous decrease in food intake despite an increased need for energy and nutrients.61 Although seemingly paradoxical, the voluntary suppression of food intake during illness is common to most species. Starvation induces autophagy as an adaptive and protective response to nutrient deprivation. Sickness‐associated anorexia appears to upregulate hepatic autophagy, improving the clearance of products such as lipopolysaccharides.62 Autophagy enhances the clearance of pathogens through actions in immune and non‐immune cells. However, underfeeding in acute disease may be detrimental, even in the early stages, depending on the exact mechanism of aggression against the body.62 The data suggest that cytokine levels are commonly associated with disease conditions characterized by cachexia and may play a role in mortality, weight loss, and appetite suppression. In contrast to starvation, cachexia is remarkably resistant to hypercaloric feeding.

Pathy's Principles and Practice of Geriatric Medicine

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