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MainThe uncontrolled cellular growth and local tissue disruption produced by tumorigenesis elicit a complex host response, including chronic inflammation, metabolic reprogramming and endocrine dysfunction1,2. These systemic changes can emerge early and persist throughout the disease course, contributing to profound alterations in appetite, energy balance, tissue composition and immune function3,4. Together, they underlie debilitating syndromes such as fatigue, anorexia and cachexia. Understanding these pathophysiologies in human patients with cancer requires integrated, longitudinal measurements of host physiology and tumor biology. Cancer cachexia (herein, ‘cachexia’) is a paraneoplastic metabolic syndrome characterized by progressive, unintentional weight loss3,5,6 accompanied by muscle wasting7 that affects approximately half of all patients with cancer3,8. Cachexia is associated with reduced quality of life9,10, premature termination of therapy, increased treatment complications and elevated risk of death11,12,13. Despite its prevalence and well-acknowledged consequences for morbidity and mortality, the underlying causes of cachexia are poorly understood.