Cachexia is a complex metabolic syndrome associated with underlying illness and characterized by loss of muscle with or without loss of fat mass. Cachexia most often accompanies tumors, chronic heart failure (CHF), chronic kidney disease (CKD), and chronic obstructive pulmonary disease (COPD). Its prevalence ranges from 5-15% in chronic heart failure to 50-80% in advanced cancer. The mortality of patients increases with the onset of cachexia. At the focal point of cachexia pathogenesis is an increased release of proinflammatory cytokines with IL-6, IL-1, and TNF being the most important ones. The loss of muscle mass occurs due to increased protein degradation, its decreased synthesis, and decreased differentiation of myocytes, while the main mechanism of fat tissue loss is increased lipolysis. Transcription factors NFкB, p38, and FOXO have the most important role in proteolyisis, while the activation of hormone sensitive lipase is important for lipolysis. Additionally, catabolism, anorexia, and hypermetabolism add up to loss of body mass. Cachexia is not only caused by proinflammatory cytokines, but also by other mediators that arise in illnesses mentioned above and intensify its development: in CHF the levels of circulatory myostatin and Ang II; in CKD the inflammation is intensified by uremic toxins, tumor tissues secrete PIF, HIF, ZAG, and LMF; in COPD hypoxemia increases thermogenesis. Cachexia, unlike malnutrition, cannot be cured by caloric supplementation, but its presentation is trying to be mitigated by substances that increase appetite. Most frequently mentioned are megestrol acetate, ghrelin, and cannabinoids.