Phase I single center trial of ketogenic diet for adults with traumatic brain injury

Arora, Niraj; Litofsky, N. Scott; Golzy, Mojgan; Aneja, Rachna; Staudenmyer, Danielle; Qualls, Kathyrn; Patil, Sachin

doi:10.1016/j.clnesp.2021.11.015

Cited by 10 publications

(26 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a single-center, open label, single-arm prospective intervention study conducted by our group we observed that ketogenic diet is well tolerated in TBI patients without significant adverse outcomes and the results are similar to patients with status epilepticus treated with ketogenic diet [40]. Another study by Kaul et al [41] showed that lower ratio ketogenic diet may be better tolerated in critically ill patients despite of not reaching therapeutic levels of BHB.…”

Section: Strategies To Modulate Beta-hydroxybutyratesupporting

confidence: 56%

Modulation of beta-hydroxybutyrate in traumatic brain injury

Arora,

Shastri,

Patel

et al. 2024

Current Opinion in Clinical Nutrition &Amp; Metabolic Care

Self Cite

View full text Add to dashboard Cite

Purpose of review Traumatic brain injury (TBI) is a significant public health concern with substantial morbidity and mortality rates in the United States. Current management strategies primarily focus on symptomatic approaches and prevention of secondary complications. However, recent research highlights the potential role of ketone bodies, particularly beta-hydroxybutyrate (BHB), in modulating cellular processes involved in TBI. This article reviews the metabolism of BHB, its effect in TBI, and its potential therapeutic impact in TBI. Recent findings BHB can be produced endogenously through fasting or administered exogenously through ketogenic diets, and oral or intravenous supplements. Studies suggest that BHB may offer several benefits in TBI, including reducing oxidative stress, inflammation, controlling excitotoxicity, promoting mitochondrial respiration, and supporting brain regeneration. Various strategies to modulate BHB levels are discussed, with exogenous ketone preparations emerging as a rapid and effective option. Summary BHB offers potential therapeutic advantages in the comprehensive approach to improve outcomes for TBI patients. However, careful consideration of safety and efficacy is essential when incorporating it into TBI treatment protocols. The timing, dosage, and long-term effects of ketone use in TBI patients require further investigation to fully understand its potential benefits and limitations.

show abstract

Section: Strategies To Modulate Beta-hydroxybutyratesupporting

confidence: 56%

Modulation of beta-hydroxybutyrate in traumatic brain injury

Arora,

Shastri,

Patel

et al. 2024

Current Opinion in Clinical Nutrition &Amp; Metabolic Care

Self Cite

View full text Add to dashboard Cite

show abstract

“…Based on that, we can say that the brain demands another source of energy, which can be provided by ketone bodies. Most recent studies also show that in patients with traumatic cerebral damage, in whom a ketogenic diet was applied, no clinical adverse effects were noted, and its safety and applicability were found [ 43 ]. The application of the ketogenic diet, through the mediation of β-hydroxybutyrate, can reduce demyelination, the death of oligodendrocytes (producing myelin) and the degeneration of axons caused by glucose deficiency [ 44 ].…”

Section: The Range and Mechanisms Of The Ketogenic Diet Effect In Neu...mentioning

confidence: 99%

“…In the study by Arora et al, no side effects of the ketogenic diet were found in adults with traumatic brain injury. The diet proved safe [ 43 ]. In a randomised controlled study on patients with Alzheimer’s disease, no major adverse effects were observed [ 171 ].…”

Section: Limitations and Potential Adverse Health Impacts Of The Keto...mentioning

confidence: 99%

The Role of Ketogenic Diet in the Treatment of Neurological Diseases

2022

View full text Add to dashboard Cite

Over a hundred years of study on the favourable effect of ketogenic diets in the treatment of epilepsy have contributed to a long-lasting discussion on its potential influence on other neurological diseases. A significant increase in the number of scientific studies in that field has been currently observed. The aim of this paper is a widespread, thorough analysis of the available scientific evidence in respect of the role of the ketogenic diet in the therapy of neurological diseases such as: epilepsy, Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS) and migraine. A wide range of the mechanisms of action of the ketogenic diet has been demonstrated in neurological diseases, including, among other effects, its influence on the reduction in inflammatory conditions and the amount of reactive oxygen species (ROS), the restoration of the myelin sheath of the neurons, the formation and regeneration of mitochondria, neuronal metabolism, the provision of an alternative source of energy for neurons (ketone bodies), the reduction in glucose and insulin concentrations, the reduction in amyloid plaques, the induction of autophagy, the alleviation of microglia activation, the reduction in excessive neuronal activation, the modulation of intestinal microbiota, the expression of genes, dopamine production and the increase in glutamine conversion into GABA. The studies discussed (including randomised controlled studies), conducted in neurological patients, have stressed the effectiveness of the ketogenic diet in the treatment of epilepsy and have demonstrated its promising therapeutic potential in Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS) and migraine. A frequent advantage of the diet was demonstrated over non-ketogenic diets (in the control groups) in the therapy of neurological diseases, with simultaneous safety and feasibility when conducting the nutritional model.

show abstract

“…Ketone bodies can provide an alternative energy substrate that bypasses glycolysis to be directly metabolized via the tricarboxylic acid cycle, leading to improvements in oxygen metabolism that support mitochondrial function, reducing oxidative stress and glutamate induced injury, and decrease the risk of posttraumatic seizures [29]. Studies on enteral ketone administration in TBI have shown safety and feasibility [30][31][32]. Other strategies to support mitochondrial function include substrates such as succinate that bypass complex 1 of the electron transport chain, which has been shown to be sensitive to damage following sepsis and TBI [33].…”

Section: Alternative Energy Substratesmentioning

confidence: 99%

Cerebral metabolic derangements following traumatic brain injury

Demers-Marcil

Coles

2022

Current Opinion in Anaesthesiology

View full text Add to dashboard Cite

Purpose of reviewOutcome following traumatic brain injury (TBI) remains variable, and derangements in cerebral metabolism are a common finding in patients with poor outcome. This review compares our understanding of cerebral metabolism in health with derangements seen following TBI. Recent findingsIschemia is common within the first 24 h of injury and inconsistently detected by bedside monitoring. Metabolic derangements can also result from tissue hypoxia in the absence of ischemic reductions in blood flow due to microvascular ischemia and mitochondrial dysfunction. Glucose delivery across the injured brain is dependent on blood glucose and regional cerebral blood flow, and is an important contributor to derangements in glucose metabolism. Alternative energy substrates such as lactate, ketone bodies and succinate that may support mitochondrial function, and can be utilized when glucose availability is low, have been studied following TBI but require further investigation.

show abstract

Phase I single center trial of ketogenic diet for adults with traumatic brain injury

Cited by 10 publications

References 40 publications

Modulation of beta-hydroxybutyrate in traumatic brain injury

Modulation of beta-hydroxybutyrate in traumatic brain injury

The Role of Ketogenic Diet in the Treatment of Neurological Diseases

Cerebral metabolic derangements following traumatic brain injury

Contact Info

Product

Resources

About