The Science of Concussions & Ketones
Post-Injury, Glucose uptake is impaired.
“Under these post-brain injury conditions of impaired glycolytic metabolism, glucose becomes a less favorable energy substrate. Ketone bodies are the only known natural alternative substrate to glucose for cerebral energy metabolism. While it has been demonstrated that other fuels (pyruvate, lactate, and acetyl-L-carnitine) can be metabolized by the brain, ketones are the only endogenous fuel that can contribute significantly to cerebral metabolism.” - Prins, Matsumoto, 2014
The collective therapeutic potential of cerebral ketone metabolism in traumatic brain injury
Ketones are an effective energy source.
“Although much feared by clinicians, the ability to produce ketones has allowed humans to withstand prolonged periods of starvation. At such times, ketones can supply up to 50% of basal energy requirements. More interesting, however, is the fact that ketones can provide as much as 70% of the brain's energy needs, more efficiently than glucose. Studies suggest that during times of acute brain injury, cerebral uptake of ketones increases significantly.” - White, Venkatesh, 2011
Ketones can be produced by diet, but it takes 3-5 days to reach therapeutic levels.
Ketone Ester reaches therapeutic levels within 30 mins.
“In terms of clinical use, the benefits of endogenously produced ketone bodies are limited due to the timeframe of inducing ketosis through a ketogenic diet containing low carbohydrates and high fats in the form of medium chain triglycerides. Endogenous ketone body production through a ketogenic diet and/or fasting takes 3–5 days to reach therapeutic blood ketone body levels. However, exogenous ketone supplementation can achieve therapeutic levels of blood ketone levels within 30 minutes of administration” - Daines, 2021
The Therapeutic Potential and Limitations of Ketones in Traumatic Brain Injury
Timing of using Ketone Ester post-injury.
“The timing and duration of exogenous ketone administration could also have significant consequences on TBI outcomes and warrants further investigation. Following a TBI, changes in cerebral energy metabolism occurs in two stages. The first stage is an acute period of hypermetabolism associated with excitotoxicity and increased glucose utilization. The second stage is a prolonged period of hypometabolism associated with the inhibition of glycolysis and mitochondrial dysfunction…
…In this study, researchers found that, in males, administering exogenous β-hydroxybutyrate in the hypometabolic state improved all measures of metabolic function, including mitochondrial function, reactive oxygen species production, and tricarboxylic acid cycle intermediate production.” - Daines, 2021
The Therapeutic Potential and Limitations of Ketones in Traumatic Brain Injury