The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
astrocytes the helper cells of neurons would take up the glucose and process it to make lactate and then shuttle the lactate into the neuron because the neuron says i can digest lactate more efficiently than the glucose and i can produce atp with less damage so the neuronal favorite food is lactate and not glucose
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So the astrocytes in your brain do make lactate, because they’re glycolytic, and then neurons will take it up much like beta-hydroxybutyrate. They go through the same transporter. But, when there’s an abundance of lactate, and I don’t know if studies have been done on beta-hydroxybutyrate in the brain looking at this specific thing or not, but the glucose sparing that occurs is the glucose gets shunted into the pentose phosphate pathway to make NADPH, which is a precursor for glutathione synthesis. And so the idea is that under, like, a traumatic situation, like traumatic brain injury, when there’s a lot of oxidative stress happening, you need glutathione to counter from that.