Ketogenic diet in adolescents and adults with epilepsy

Nei, Maromi; Ngo, Ly; Sirven, Joseph I; Sperling, Michael R.

doi:10.1016/j.seizure.2014.02.015

Cited by 146 publications

(65 citation statements)

References 11 publications

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“…In addition, high response rates and seizure freedom has been observed in adolescents and adults with juvenile myoclonic epilepsy with 2/3 of adults showing ≥50% seizure reduction and 1/6 adults seizure free in two separate small case series (Kossoff et al, 2013c, Kverneland et al, 2015). Similarly, a trend for increased benefit of diet therapy has been detected for patients with symptomatic generalized epilepsy compared to patients with focal epilepsies (Nei et al, 2014). …”

Section: Efficacy and Indications In Adultsmentioning

confidence: 97%

The role for ketogenic diets in epilepsy and status epilepticus in adults

Williams

Cervenka

2017

Clinical Neurophysiology Practice

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Section: Efficacy and Indications In Adultsmentioning

confidence: 97%

The role for ketogenic diets in epilepsy and status epilepticus in adults

Williams

Cervenka

2017

Clinical Neurophysiology Practice

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“…Another mechanism for the antiseizure action of the KD, suggested by Yudkoff et al ( 68 ), pertains to decreased availability of excitatory neurotransmitters (aspartate and glutamate) and increased availability of the inhibitory neurotransmitters [ ␥ -aminobutyric acid (GABA)], via stimulation of glutamic acid decarboxylase, which, in turn, increases GABA production from glutamate. Many studies have contributed in a variety of ways to our understanding of the benefi cial effect of KDs on epilepsy ( 60,62,(69)(70)(71)(72)(73)(74)(75)(76). However, despite the abundance of hypotheses, the basis for the antiseizure action of KBs remains unclear.…”

Section: Kesmentioning

confidence: 99%

Ketone body therapy: from the ketogenic diet to the oral administration of ketone ester

Hashim

VanItallie

2014

Journal of Lipid Research

121

108

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This article is available online at http://www.jlr.org family, its importance for purposes of this review is minimal.). KBs have been dubbed "metabolism's ugly duckling" because, in the mid-19th century, they were fi rst discovered in large quantities in the urine of patients succumbing to diabetic ketoacidosis. Thus, it is not surprising that physicians of the era considered KBs to be toxic byproducts of impaired carbohydrate metabolism. It took almost half a century for medical scientists to understand that KBs are normal metabolites manufactured by the liver in increasing amounts when dietary sources of carbohydrate and glucogenic amino acids are in short supply ( 1 ). Unfortunately, some physicians still fail to distinguish between the safe "physiological" hyperketonemia that occurs in healthy individuals during fasting or adherence to a ketogenic diet (KD), and the pathological, out-of-control hyperketonemia associated with insulin-defi cient diabetes.When Owen et al. ( 2 ) reported that during a prolonged fast KBs can provide 60% or more of the brain's daily energy requirement (thereby sparing ‫ف‬ 80 g/day of glucose that otherwise would have been derived largely from breakdown of the body's limited protein stores), it was finally acknowledged that, as in Hans Christian Andersen's 1843 fairy tale, the creature fi rst thought to be an ugly duckling was turning out to be an emerging swan. It became evident that the ketogenic response to starvation is an indispensable metabolic adaptation designed by nature to preserve strength and prolong life during times when food is unavailable ( 3 ) .It is now known that (in nondiabetic individuals), owing to the blood's effi cient buffering capacity, plasma KB Abstract Ketone bodies (KBs ), acetoacetate and ␤ -hydroxybutyrate ( ␤ HB), were considered harmful metabolic by-products when discovered in the mid-19th century in the urine of patients with diabetic ketoacidosis. It took physicians many years to realize that KBs are normal metabolites synthesized by the liver and exported into the systemic circulation to serve as an energy source for most extrahepatic tissues. Studies have shown that the brain (which normally uses glucose for energy) can readily utilize KBs as an alternative fuel. Even when there is diminished glucose utilization in cognition-critical brain areas, as may occur early in Alzheimer's disease (AD), there is preliminary evidence that these same areas remain capable of metabolizing KBs. Because the ketogenic diet (KD) is diffi cult to prepare and follow, and effectiveness of KB treatment in certain patients may be enhanced by raising plasma KB levels to у 2 mM, KB esters, such as 1,3-butanediol monoester of ␤ HB and glyceryl-tris-3-hydroxybutyrate, have been devised. When administered orally in controlled dosages, these esters can produce plasma KB levels comparable to those achieved by the most rigorous KD, thus providing a safe, convenient, and versatile new approach to the study and potential treatment of a variety of diseases, including epilepsy, ...

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“…The ketogenic diet, a high-fat and low-carbohydrate diet, is used to treat severe (difficult-to-control) epileptic cases in children -it reduces the frequency of epileptic seizures [15]. In fact, a long-term supplementation of this unbalanced diet was found to induce side effects in those patients, such as excessive bruising, bone fractures, and kidney stones [16,17].…”

Section: Discussionmentioning

confidence: 99%