Ketogenic diet and other dietary treatments for epilepsy

Levy, Robert G; Cooper, Paul; Giri, Pratima; Weston, Jennifer

doi:10.1002/14651858.cd001903.pub2

Cited by 206 publications

(98 citation statements)

References 24 publications

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“…At 12 months after diet initiation 24 children (41%) remained on the diet. At 12 months 21 children (36%) had a ≥ 50% decrease in seizure frequency, whereas in other studies the efficacy rate at 12 months ranged from 9% to 83% [5]. Six patients (10%) were free of seizures at one year compared to 7% found by Freeman et al [12], 10% found by Vining et al [6] and 16% found by Maydell et al [13].…”

Section: Discussionmentioning

confidence: 76%

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Can we predict efficacy of the ketogenic diet in children with refractory epilepsy?

Vehmeijer

Louw

Arts

et al. 2015

European Journal of Paediatric Neurology

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Section: Discussionmentioning

confidence: 76%

“…Various studies showed an efficacy rate in the range of 27-62% at three months after diet initiation, with success being defined as ≥ 50% seizure reduction [4]. Reported efficacy rates at 12 months range between 9-83% [5].…”

Section: Introductionmentioning

confidence: 99%

Can we predict efficacy of the ketogenic diet in children with refractory epilepsy?

Vehmeijer

Louw

Arts

et al. 2015

European Journal of Paediatric Neurology

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“…Ketogenic diet promotes synthesis of glutamine (precursor of gamma-aminobutyric acid, an inhibitory neurotransmitter), which is structurally similar to GABA and would therefore have a direct antiepileptic effect. This treatment can be beneficial for children, 51,52 and it is the treatment of choice in cases of pyruvate dehydrogenase complex deficiency and lack of glucose transporter (GLUT-1). The treatment should be started at an early stage to allow the brain to use KB as an energy source 53 (LE III).…”

Section: Ketogenic Dietmentioning

confidence: 99%

Drug-resistant epilepsy: Definition and treatment alternatives

González

Osorio

Rein

et al. 2015

Neurología (English Edition)

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Introduction: Drug-resistant epilepsy affects 25% of all epileptic patients, and quality of life decreases in these patients due to their seizures. Early detection is crucial in order to establish potential treatment alternatives and determine if the patient is a surgical candidate. Development: PubMed search for articles, recommendations published by major medical societies, and clinical practice guidelines for drug-resistant epilepsy and its medical and surgical treatment options. Evidence and recommendations are classified according to the criteria of the Oxford Centre for Evidence-Based Medicine (2001) and the European Federation of Neurological Societies (2004) for therapeutic actions.Conclusions: Identifying patients with drug-resistant epilepsy is important for optimising drug therapy. Experts recommend rational polytherapy with antiepileptic drugs to find more effective combinations with fewer adverse effects. When adequate seizure control is not achieved, a presurgical evaluation in an epilepsy referral centre is recommended. These evaluations explore how to resect the epileptogenic zone without causing functional deficits in cases in which this is feasible. If resective surgery is not achievable, palliative surgery or neurostimulation systems (including vagus nerve, trigeminal nerve, or deep brain stimulation) may be an option. Other treatment alternatives such as ketogenic diet may also be considered in selected patients. Epilepsia resistente a fármacos. Concepto y alternativas terapéuticas ResumenIntroducción: La epilepsia resistente al tratamiento médico afecta a una cuarta parte de los pacientes con epilepsia. Como consecuencia de las crisis estos pacientes presentan una peor calidad de vida, por lo que es fundamental su diagnóstico para establecer posibles alternativas terapéuticas e iniciar una valoración prequirúrgica.Desarrollo: Búsqueda de artículos en PubMed y recomendaciones de las Guías de Práctica Clínica (GPC) y Sociedades Científicas más relevantes, referentes a epilepsia refractaria y al tratamiento médico y quirúrgico. Se clasifican las evidencias y recomendaciones según los criterios pronósticos del Oxford Centre for Evidence Based Medicine (2001) y de la European Federation of Neurological Societies (2004) para actuaciones terapéuticas.Conclusiones: La identificación de los pacientes con epilepsia refractaria es importante para optimizar el tratamiento farmacológico. Se recomienda el empleo de una politerapia racional de fármacos antiepilépticos, buscando combinaciones que aumenten la eficacia y minimicen los efectos adversos. Cuando no se consigue el control adecuado de las crisis es necesario realizar una valoración prequirúrgica en un centro especializado, con el fin de resecar la zona epileptógena sin producir déficits al paciente en los casos en los que sea posible. En caso contrario se recurrirá a procedimientos de cirugía paliativa o sistemas de neuroestimulación (vagal, trigeminal o cerebral). Otras alternativas, como la dieta cetógena, también pueden considerarse en pacientes...

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“…Accordingly, less rigid dietary regimens are being explored [42]. It seems possible that combination with pharmacological inhibition of CYP2E1 would permit a relaxation of dietary regimens, while still maintaining acetone levels in the therapeutic range.…”

Section: The Rationale For Supplementing the Ketogenic Diet With Cyp2mentioning

confidence: 99%

Combination treatment of epilepsy with ketogenic diet and concurrent pharmacological inhibition of cytochrome P450 2E1

Palmer

2013

Medical Hypotheses

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While most epileptic patients respond to treatment with existing antiepileptic drugs, there remains a considerable number of patients in whom these drugs do not suffice. Such patients, particularly children, are often treated using the ketogenic diet. This diet imposes a strict limit on carbohydrates; while providing for adequate protein, most of the calories are supplied as triacylglycerol, much of which is metabolized to ketone bodies.Animal experiments have provided evidence that the anticonvulsant effect of the ketogenic diet is mediated by acetone and correlates with acetone levels. Acetone can be converted in vivo to glucose via acetol and pyruvate; the initial conversion to acetol is catalyzed by cytochrome P450 2E1 (CYP2E1). When CYP2E1 knockout mice are subjected to starvation to induce ketogenesis, they develop blood acetone levels much higher than those observed in wild-type mice. Similarly, pharmacological inhibition of CYP2E1 significantly increases blood acetone levels in rat and man.Taken together, these observations suggest that pharmacological inhibition of CYP2E1 has the potential to significantly increase the antiepileptic effect of the ketogenic diet. With patients that respond insufficiently to the diet alone, increased acetone levels may improve response. With patients who respond sufficiently to the diet, CYP2E1 inhibitors might allow relaxation of the fairly severe diet regimen and so improve compliance and quality of life.An existing inhibitor of CYP2E1 is the drug disulfiram. This drug also inhibits the enzyme aldehyde dehydrogenase, which functions in alcohol degradation, and in this capacity has long been used in the treatment of alcohol addiction. Disulfiram inhibits CYP2E1 at conventional therapeutic dosages and increases blood acetone levels in humans and animals. It should therefore be a viable candidate for the proposed drug/diet combination treatment.2

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Ketogenic diet and other dietary treatments for epilepsy

Cited by 206 publications

References 24 publications

Can we predict efficacy of the ketogenic diet in children with refractory epilepsy?

Can we predict efficacy of the ketogenic diet in children with refractory epilepsy?

Drug-resistant epilepsy: Definition and treatment alternatives

Combination treatment of epilepsy with ketogenic diet and concurrent pharmacological inhibition of cytochrome P450 2E1

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