HoldsUp

George Brooks

George A. Brooks, Ph.D., is a researcher in physiology and metabolism known for developing the lactate shuttle hypothesis. His published research focuses on carbohydrate and lactate kinetics, muscle fuel utilization, and mitochondrial bioenergetics in the context of exercise and aging. He also investigates the potential therapeutic applications of lactate in neurological conditions and metabolic regulation.

36 claims checked on air: 1 context 1 contradicted 1 overstated 31 supported 2 unverified 2 flagged

What they said on air - flagged

9 citing their own research

0:29:41contradictedmoderateGeorge Brooks, Ph.D. on Lactate Shuttle Theory, Relevance fo

Following traumatic brain injury, cerebral glycolysis is impaired, leaving neurons starving for preferred lactate fuel.

"Now to answer your question about why is the injured brain suffering, for some reason the breakdown of sugar, or glycolysis, in the brain is impaired after injury. Now the product of that is lactate, and neurons run on lactate as the preferred fuel. So in part, the brain is starving." (said at 0:29:41)

The claim misstates the primary metabolic impairment that occurs following traumatic brain injury (TBI). Following TBI, cerebral glycolysis is typically accelerated (a phenomenon known as acute hyperglycolysis) rather than impaired. Lactate is the end product of glycolysis; its elevation in TBI results from increased glycolytic flux combined with downstream mitochondrial dysfunction (impaired oxidative phosphorylation in the TCA cycle) or hypoxia, which prevents efficient mitochondrial oxidation of pyruvate and lactate. If glycolysis were impaired, lactate production would be reduced rather than increased. Under the astrocyte-neuron lactate shuttle model, astrocytic glycolysis produces lactate that neurons can utilize as an energy substrate, but the brain's energetic deficit after TBI stems from mitochondrial dysfunction and metabolic uncoupling rather than an inability to break down glucose via glycolysis.

0:48:52overstatedlowtheir own paperGeorge Brooks, Ph.D. on Lactate Shuttle Theory, Relevance fo

When pyruvate is infused intravenously, red blood cells and the lungs convert it to lactate within seconds to a minute in one circulatory passage.

"when you infuse it in one circulatory passage, it's all lactate. So the lungs do that, and red blood cells do that. The red blood cells and the lungs are loaded with enzymes to convert pyruvate to lactate. So even if you want to try to give pyruvate, within seconds or a minute, it's going to be lactate anyway" (said at 0:48:52)

Evidence supports that red blood cells and pulmonary tissue rapidly take up and convert circulating pyruvate to lactate due to high lactate dehydrogenase (LDH) activity and monocarboxylate transporter (MCT) expression. However, claiming that pyruvate is completely converted ("it's all lactate") in a single circulatory passage overstates the magnitude of first-pass pulmonary extraction. In vivo tracer studies in animal models demonstrate a transpulmonary pyruvate fractional extraction of approximately 43% per circulatory transit, rather than complete conversion, though rapid equilibration toward lactate continues across subsequent passages and within erythrocytes.

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