The Role of Ketogenic Diet in the Treatment of Neurological Diseases.
Damian DyńkaKatarzyna KowalczeAgnieszka PaziewskaPublished in: Nutrients (2022)
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.
Keyphrases
- multiple sclerosis
- weight loss
- reactive oxygen species
- physical activity
- cell death
- cerebral ischemia
- type diabetes
- randomized controlled trial
- stem cells
- spinal cord
- poor prognosis
- white matter
- ms ms
- newly diagnosed
- signaling pathway
- body mass index
- combination therapy
- gene expression
- chronic kidney disease
- clinical trial
- cognitive decline
- palliative care
- genome wide
- systematic review
- adipose tissue
- dna damage
- cell therapy
- study protocol
- replacement therapy
- transcription factor
- patient reported