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Background The financial implications of central nervous system (CNS) cancers are substantial, not only for the healthcare service and payers, but also for the patients who bear the brunt of direct, indirect, and intangible costs. This study sought to investigate the impact of healthcare spending on CNS cancer survival using recent US data. Methods This study used public data from the Disease Expenditure Project 2016 and the Global Burden of Disease Study 2019. The primary outcome was the annual healthcare spending trend from 1996 and 2016 on CNS tumors adjusted for disease prevalence, alongside morbidity and mortality. Secondary outcomes included drivers of change in healthcare expenditures for CNS cancers. Subgroup analysis was performed stratified by age group, expenditure type, and care type provided. Results There was a significant increase in total healthcare spending on CNS cancers from $2.72 billion (95% CI: $2.47B to $2.97B) in 1996 to $6.85 billion (95% CI: $5.98B to $7.57B) in 2016. Despite the spending increase, the mortality rate per 100 000 people increased, with 5.30 ± 0.47 in 1996 and 7.02 ± 0.47 in 2016, with an average of 5.78 ± 0.47 deaths per 100 000 over the period. The subgroups with the highest expenditure included patients aged 45 to 64, those with private insurance, and those receiving inpatient care. Conclusions This study highlights a significant rise in healthcare costs for CNS cancers without corresponding improvements in mortality rate, indicating a mismatch of healthcare spending, contemporary advances, and patient outcomes as it relates to mortality. [ABSTRACT FROM AUTHOR]

Energy metabolism in the human brain is not fully understood. Classically, glucose is regarded as the major energy substrate. However, lactate (conventionally a product of anaerobic metabolism) has been proposed to act as an energy source, yet whether this occurs in man is not known. Here we show that the human brain can indeed utilize lactate as an energy source via the tricarboxylic acid cycle. We used a novel combination of 13C-labelled cerebral microdialysis both to deliver 13C substrates into the brain and recover 13C metabolites from the brain, and high-resolution 13C nuclear magnetic resonance. Microdialysis catheters were placed in the vicinity of focal lesions and in relatively less injured regions of brain, in patients with traumatic brain injury. Infusion with 2-13C-acetate or 3-13C-lactate produced 13C signals for glutamine C4, C3 and C2, indicating tricarboxylic acid cycle operation followed by conversion of glutamate to glutamine. This is the first direct demonstration of brain utilization of lactate as an energy source in humans. [ABSTRACT FROM PUBLISHER]