Neuroscientists are now looking at lactate with a much more positive eye, considering it a possible replacement “fuel” for the brain in the immediate //hours after a traumatic brain injury instead of glucose, the current standard. If they are right, it could change how emergency room physicians and intensive care physicians treat patients with brain injuries in the first critical hours after injury.

Previous work by Dr. Neil Martin, professor and chief of neurosurgery at the David Geffen School of Medicine at UCLA, and Thomas Glenn, a UCLA adjunct assistant professor in the department of neurosurgery, showed that the brain takes up lactate after traumatic injury. Now, thanks to a $275,000 grant from the National Institute for Neurological Diseases and Stroke at the National Institutes of Health, the investigators will determine why the brain does this. Is it actually using lactate to help it recover after injury?

“The prevailing theory for the brain after traumatic injury is that, just as in normal circumstances, glucose is the primary source for energy,” Glenn said. “Further, it was thought the brain’s metabolic process produces lactate, long considered a harmful waste product of a dysfunctional metabolism, one that causes further cell death via acidosis, an abnormally high buildup of acid in blood and tissue.”

Instead, the researchers found that in the first 12 to 48 hours following traumatic injury, the brain takes up and apparently consumes more lactate than at any other time. They discovered this by measuring the levels of lactate in blood entering and leaving the brain. To determine if lactate was being used by the brain, the researchers, in collaboration with George Brooks, a professor in the department of integrative biology at the University of California, Berkeley, labeled lactate with C13, a non-radioactive and stable isotope, then added it to the patient’s standard intravenous solution. The isotope served as a marker t
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