The ketogenic diet in disease and development

Barry, Denis; Ellul, Sarah; Watters, Lindsey; Lee, David; Haluska, Robert; White, Robin

doi:10.1016/j.ijdevneu.2018.04.005

Cited by 48 publications

(42 citation statements)

References 110 publications

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“…Around 60% of the patients on KD become seizure-free, suggesting that 4-carbon KBs can compensate a glucose deficit. The results of KD in GLUT1 management [56] and other forms of intractable epilepsy and other conditions [ 57 – 59 ] exemplify the potential of energy metabolism as a therapeutic approach in neurodevelopmental diseases.…”

Section: Energy Metabolism and Neurodevelopment: Where Are We Now?mentioning

confidence: 99%

Energy metabolism in childhood neurodevelopmental disorders

Oyarzábal

Musokhranova

et al. 2021

eBioMedicine

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Whereas energy function in the aging brain and their related neurodegenerative diseases has been explored in some detail, there is limited knowledge about molecular mechanisms and brain networks of energy metabolism during infancy and childhood. In this review we describe current insights on physiological brain energetics at prenatal and neonatal stages, and in childhood. We then describe the main groups of inborn errors of energy metabolism affecting the brain. Of note, scarce basic neuroscience research in this field limits the opportunity for these disorders to provide paradigms of energy utilization during neurodevelopment. Finally, we report energy metabolism disturbances in well-known non-metabolic neurodevelopmental disorders. As energy metabolism is a fundamental biological function, brain energy utilization is likely altered in most neuropediatric diseases. Precise knowledge on mechanisms of brain energy disturbance will open the possibility of metabolic modulation therapies regardless of disease etiology.

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Section: Energy Metabolism and Neurodevelopment: Where Are We Now?mentioning

confidence: 99%

Energy metabolism in childhood neurodevelopmental disorders

Oyarzábal

Musokhranova

et al. 2021

eBioMedicine

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“…Ketones are effectively oxidised by the fasting brain, more reluctant than other tissues to renounce glucose and metabolise FFAs [38]. The use of FFAs and ketones as energy sources reduces the respiratoryexchange ratio (RER), compared with the fed state, indicating a greater metabolic efficiency of energy production during weight loss leading to ketosis [25].…”

Section: The Metabolic Switchmentioning

confidence: 99%

Unravelling the health effects of fasting: a long road from obesity treatment to healthy life span increase and improved cognition

et al. 2020

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In recent years a revival of interest has emerged in the health benefits of intermittent fasting and long-term fasting, as well as of other related nutritional strategies. In addition to meal size and composition a new focus on time and frequency of meals has gained attention. The present review will investigate the effects of the main forms of fasting, activating the metabolic switch from glucose to fat and ketones (G-to-K), starting 12-16 h after cessation or strong reduction of food intake. During fasting the deactivation of mTOR regulated nutrient signalling pathways and activation of the AMP protein kinase trigger cell repair and inhibit anabolic processes. Clinical and animal studies have clearly indicated that modulating diet and meal frequency, as well as application of fasting patterns, e.g. intermittent fasting, periodic fasting, or long-term fasting are part of a new lifestyle approach leading to increased life and health span, enhanced intrinsic defences against oxidative and metabolic stresses, improved cognition, as well as a decrease in cardiovascular risk in both obese and non-obese subjects. Finally, in order to better understand the mechanisms beyond fasting-related changes, human studies as well as non-human models closer to human physiology may offer useful clues. KEY-MESSAGES 1. Biochemical changes during fasting are characterised by a glucose to ketone switch, leading to a rise of ketones, advantageously used for brain energy, with consequent improved cognition. 2. Ketones reduce appetite and help maintain effective fasting. 3. Application of fasting patterns increases healthy life span and defences against oxidative and metabolic stresses. 4. Today's strategies for the use of therapeutic fasting are based on different protocols, generally relying on intermittent fasting, of different duration and calorie intake. 5. Long-term fasting, with durations between 5 and 21 days can be successfully repeated in the course of a year.

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“…They serve as energy source when glucose is not readily available (Laffel, ), and this could be during fasting, starvation, prolonged exercise, etc. Although primarily aimed at ameliorating seizures and abnormal behavior in intractable epilepsy, KD is currently used for treating a wide‐range of dysfunctions and diseases, including metabolic and mitochondrial disorders, cancer, movement disorders, and neurodegeneration, through its effects on brain, fatty adipose tissue, and muscle (Figure ) (Barry et al, ). Nutritional KD is generally safe and harmless in adults, involving self‐regulation of ketone body concentration and excretion of the excess, and has gained a significant popularity in recent decades with increasing numbers of KD‐based advisory clinics, worldwide (Kossoff & Hartman, ).…”

Section: Kd and General Healthmentioning

confidence: 99%

Ketogenic diets and protective mechanisms in epilepsy, metabolic disorders, cancer, neuronal loss, and muscle and nerve degeneration

Liu

et al. 2020

J Food Biochem

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Ketogenic diet (KD), the “High‐fat, low‐carbohydrate, adequate‐protein” diet strategy, replacing glucose with ketone bodies, is effective against several diseases, from intractable epileptic seizures, metabolic disorders, tumors, autosomal dominant polycystic kidney disease, and neurodegeneration to skeletal muscle atrophy and peripheral neuropathy. Key mechanisms include augmented mitochondrial efficiency, reduced oxidative stress, and regulated phospho‐AMP‐activated protein kinase, gamma‐aminobutyric acid‐glutamate, Na+/K+ pump, leptin and adiponectin levels, ghrelin levels, lipogenesis, ketogenesis, lipolysis, and gluconeogenesis. In cancer cells, KD targets glucose metabolism, suppresses insulin‐like growth factor‐1 and PI3K/AKT/mTOR pathways, and reduces cancer cachexia and muscle waste and fatigue. An associated increased skeletal proliferator‐activated receptor‐γ coactivator‐1α activity alters systemic ketone body homeostasis, contributing toward attenuated diabetic hyperketonemia. Antioxidative and anti‐inflammatory properties enable KD enhance endurance and sports performances while preventing exercise‐induced muscle and organ debility. KD reduces metabolic syndromes‐associated allodynia and promotes peripheral axonal and sensory regeneration. This review enlightens effects of KD on various disease conditions. Practical applications It is increasingly being realized that diet plays a very important role in our fight against several diseases. This can range from neurological disorders to diabetes and cancer. In this context, the potential of KD, the “High‐fat, low‐carbohydrate, adequate‐protein” diet strategy, is increasingly being realized. In this article, we provide a comprehensive analysis of the benefits of KD against many diseases and discuss the underlying biochemical mechanisms. We hope that our write‐up will stimulate further research on KD and help generate an interest for the populations to adopt this healthy diet. It can help overcome the problems associated with weight and dysregulated metabolism.

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The ketogenic diet in disease and development

Cited by 48 publications

References 110 publications

Energy metabolism in childhood neurodevelopmental disorders

Energy metabolism in childhood neurodevelopmental disorders

Unravelling the health effects of fasting: a long road from obesity treatment to healthy life span increase and improved cognition

Ketogenic diets and protective mechanisms in epilepsy, metabolic disorders, cancer, neuronal loss, and muscle and nerve degeneration

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