In human infants, ketones provide 12.8% of the brain energy in a fed state, and 30% after 9 hr of fasting (Kraus et al., 1974). Throughout the animal kingdom, the importance of ketone metabolism appears to be positively related to the brain/body ratio (Cahill, 2006). While the latter is predominantly glucose, the role of ketones may become relevant depending on species, age, caloric balance, diet composition, and pathophysiological state. The energy supply to neurons is provided by metabolic pathways that utilize oxygen and a caloric substrate. Hematic levels of ketones are directly proportional to the effect size of neuroprotection. Ketosis exerts a potent neuroprotection against acute damage to the mammalian CNS in terms of reduction of mortality, of neuronal damage and dysfunction. Only the magnitude of intervention was a predictor of neuroprotection (g 0.07, SE 0.03, p 0.01 per every mmol/L increase in ketone levels). Reduction of mortality was particularly pronounced in the adult subgroup (g 2.71, SE 0.57, p < .01). The selected publications were 49 experimental murine studies (period 1979–2020). Meta-regression evaluated timing, type, and magnitude of intervention as predictors of neuroprotection. Subgroup analyses evaluated the modulatory effect of age, insult type, and injury site. Secondary endpoints were a reduction in neuronal damage and dysfunction, and an ‘aggregated advantage’ (composite of all primary and secondary endpoints). Primary endpoint was a reduction in mortality. Search engines were interrogated to identify experimental studies comparing the mitigating effect of ketosis (intervention) versus non-ketosis (control) on acute CNS damage. To evaluate the neuroprotection exerted by ketosis against acute damage of the mammalian central nervous system (CNS).
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