Cancer cachexia, a multifactorial syndrome characterised by body weight loss, muscle and adipose tissue wasting, affects cancer patients. Over time, the definition of cachexia has been modified, including inflammation as one of the main causal factors.

Evidences have suggested that a range of pro-inflammatory mediators may be involved in the regulation of intracellular signalling, resulting in enhanced resting energy expenditure, metabolic changes, and muscle atrophy, all of which are typical features of cachexia. Physiologically speaking, however, inflammation is a response aimed at facing potentially damaging events.

Along this line, its induction in the cancer hosts could be an attempt to restore the physiological homeostasis. Interesting observations have shown that cytokines such as interleukins 4 and 6 could improve muscle wasting, supporting the view that the same mediator may exert pro- or anti-inflammatory activity depending on the immune cells involved as well as on the tissue metabolic demand.

In conclusion, whether inflammation is crucial to the occurrence of cachexia or just one contributor among others, is still unclear. Indeed, inflammation could trigger cachexia, but it could also be the response to alterations of energy and protein metabolism and hormonal homeostasis.

Probably both aspects are true, supporting the view that inflammation could be a crucial issue or just another player. Whether the causative role prevails over the compensatory one likely depends on the tumour type and stage, on patient lifestyle, on the presence of comorbidities, on the response to anticancer treatments, paving the way to a holistic, personalized approach to cancer cachexia.