Cardiac complications in pediatric patients on the ketogenic diet

Best, Thomas H.; Franz, David Neal; Gilbert, Donald L.; Nelson, David P.; Epstein, Menashe

doi:10.1212/wnl.54.12.2328

Cited by 148 publications

(99 citation statements)

References 7 publications

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“…Other reported, but rare, side effects of the KD are increased infection risk, bruising, raised serum uric acid, fractures, pancreatitis, lipid-aspiration pneumonia, and cardiac abnormalities [25,37,[49][50][51].…”

Section: Other Side Effectsmentioning

confidence: 99%

Ketogenic diet guidelines for infants with refractory epilepsy

Louw

Hurk

Neal

et al. 2016

European Journal of Paediatric Neurology

159

150

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Section: Other Side Effectsmentioning

confidence: 99%

Ketogenic diet guidelines for infants with refractory epilepsy

Louw

Hurk

Neal

et al. 2016

European Journal of Paediatric Neurology

159

150

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“…The longterm effects of a high-fat diet in mice have not been thoroughly investigated. In humans, the KD has been associated with increased risk of coronary heart disease (Best et al, 2000;Bergqvist et al, 2003;Dashti et al, 2003;Kwiterovich et al, 2003) among other adverse effects. It is unclear whether such adverse events played a role in the eventual death of KD fed Aldh5a1 −/− mice.…”

Section: Lifespanmentioning

confidence: 99%

A ketogenic diet rescues the murine succinic semialdehyde dehydrogenase deficient phenotype

Nylen

Velázquez

Likhodii

et al. 2008

Experimental Neurology

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Succinic semialdehyde dehydrogenase (SSADH) deficiency is an heritable disorder of GABA degradation characterized by ataxia, psychomotor retardation and seizures. To date, there is no effective treatment for SSADH deficiency. We tested the hypothesis that a ketogenic diet (KD) would improve outcome in an animal model of SSADH deficiency, the SSADH knockout mouse (Aldh5a1 −/− ). Using a 4:1 ratio of fat to combined carbohydrate and protein KD we set out to compare the general phenotype, in vivo and in vitro electrophysiology and [ 35 S]TBPS binding in both Aldh5a1 −/− mice and control (Aldh5a1 +/+ ) mice. We found that the KD prolonged the lifespan of mutant mice by >300% with normalization of ataxia, weight gain and EEG compared to mutants fed a control diet. Aldh5a1 −/− mice showed significantly reduced mIPSC frequency in CA1 hippocampal neurons as well as significantly decreased [ 35 S]TBPS binding in all brain areas examined. In KD fed mutants, mIPSC activity normalized and [ 35 S]TBPS binding was restored in the cortex and hippocampus. The KD appears to reverse toward normal the perturbations seen in Aldh5a1 −/− mice. Our data suggest that the KD may work in this model by restoring GABAergic inhibition. These data demonstrate a successful experimental treatment for murine SSADH deficiency using a KD, giving promise to the idea that the KD may be successful in the clinical treatment of SSADH deficiency.

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“…Aunque es infrecuente, por su gravedad, es indispensable la evaluación cardiológica periódica. [24][25][26] Con respecto al efecto que la dieta ejerce sobre el crecimiento, los últimos reportes indican que, con aporte calórico y proteico adecuados, se logra un ritmo de crecimiento normal. 27,28 En cada consulta, los datos de antropometría se evalúan y comparan con los patrones de crecimiento recomendados por la Sociedad Argentina de Pediatría.…”

Section: Efectos Adversos a Corto Y Largo Plazounclassified