A prospective study: Growth and nutritional status of children treated with the ketogenic diet

Liu, Yeou-mei Christiana; Williams, Shelley; Basualdo-Hammond, Carlota; Stephens, Derek; Curtis, R A

doi:10.1053/jada.2003.50136

Cited by 79 publications

(65 citation statements)

References 19 publications

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“…This was evidenced by significantly higher daily weight gain in the KD fed mutants. Clinically, the KD is associated with significantly attenuated growth compared to humans consuming a non-KD (Vining et al, 2002;Liu et al, 2003;Papandreou et al, 2006). This has also been shown in rats fed a KD (Zhao et al, 2004;Nylen et al, 2005;Nylen et al, 2006).…”

Section: Ataxia and Weightsmentioning

confidence: 59%

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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Section: Ataxia and Weightsmentioning

confidence: 59%

A ketogenic diet rescues the murine succinic semialdehyde dehydrogenase deficient phenotype

Nylen

Velázquez

Likhodii

et al. 2008

Experimental Neurology

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“…Also in patients with refractory epilepsy, short-term (3-4 mo) KD treatment resulted in decreased body weight (25,28). However, we now show that a prolonged KD is not associated with weight loss.…”

Section: Discussionmentioning

confidence: 70%

Long-term ketogenic diet causes glucose intolerance and reduced β- and α-cell mass but no weight loss in mice

Ellenbroek

Dijck

Töns

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

126

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Ellenbroek JH, van Dijck L, Töns HA, Rabelink TJ, Carlotti F, Ballieux BE, de Koning EJ. Long-term ketogenic diet causes glucose intolerance and reduced ␤-and ␣-cell mass but no weight loss in mice. Am J Physiol Endocrinol Metab 306: E552-E558, 2014. First published January 7, 2014 doi:10.1152/ajpendo.00453.2013.-High-fat, low-carbohydrate ketogenic diets (KD) are used for weight loss and for treatment of refractory epilepsy. Recently, short-time studies in rodents have shown that, besides their beneficial effect on body weight, KD lead to glucose intolerance and insulin resistance. However, the long-term effects on pancreatic endocrine cells are unknown. In this study we investigate the effects of long-term KD on glucose tolerance and ␤-and ␣-cell mass in mice. Despite an initial weight loss, KD did not result in weight loss after 22 wk. Plasma markers associated with dyslipidemia and inflammation (cholesterol, triglycerides, leptin, monocyte chemotactic protein-1, IL-1␤, and IL-6) were increased, and KD-fed mice showed signs of hepatic steatosis after 22 wk of diet. Long-term KD resulted in glucose intolerance that was associated with insufficient insulin secretion from ␤-cells. After 22 wk, insulin-stimulated glucose uptake was reduced. A reduction in ␤-cell mass was observed in KD-fed mice together with an increased number of smaller islets. Also ␣-cell mass was markedly decreased, resulting in a lower ␣-to ␤-cell ratio. Our data show that long-term KD causes dyslipidemia, a proinflammatory state, signs of hepatic steatosis, glucose intolerance, and a reduction in ␤-and ␣-cell mass, but no weight loss. This indicates that long-term high-fat, lowcarbohydrate KD lead to features that are also associated with the metabolic syndrome and an increased risk for type 2 diabetes in humans. pancreatic islet; ketogenic diet; glucose intolerance; ␤-cell; ␣-cell

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“…Vining et al 17 found that epileptic patients had decreased weight Z-scores after 3 months of treatment with KD, which led to a small decrease in the height Z-scores after 6 months of dietary intervention. Liu et al 9 reported that 14 children received classical KD and 11 received (MCT) ketogenic diet did not have statistically significant increases in height/age percentiles after 4 months of treatment with KD and a decrease in weight/ age percentiles by 10 percentiles. These results confirmed the importance of adequate monitoring of calorie and protein intake in order to promote health, reduce morbidity, and prevent weight and height deficits.…”

Section: Discussionmentioning

confidence: 99%

“…In 2003, Liu et al 9 compared micronutrient intake from the KD diet and vitamin supplements in patients with refractory epilepsy. The authors found that after 4 months of dietary intervention, the nutrient intakes and supplementation in these patients met the Dietary Reference Intakes (DRI) recommendations, except for phosphorus and folate.…”

Section: Discussionmentioning

confidence: 99%

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Ketogenic food pyramid for patients with refractory epilepsy: From theory to clinical practice

et al. 2017

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Objective: To develop a graphical representation in the form of a food pyramid for a ketogenic diet for dietary treatment in children and adolescents with refractory epilepsy. Methods: The pyramid was constructed based on: the estimation of energy requirements for different age groups, macronutrient distribution, food groups, and the number of servings and respective amounts of food according to the ketogenic diet. Serving sizes were based on the calculation of energy and macronutrient requirements according to age and nutritional status. Results: The pyramid was divided into three tiers and 5 food groups (fats, proteins, type 1 vegetables, type 2 vegetables, and fruits). Four portion size lists were defined for the following age groups: 1-3 years, 4-6 years, 7-10 years, and 11-19 years. Conclusion: The ketogenic diet food pyramid can be used as nutritional guidance for patients undergoing this dietary therapy by illustrating the variety of foods that can be eaten during the treatment, optimizing adherence to the treatment, and guaranteeing beneficial effects on seizure control.

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A prospective study: Growth and nutritional status of children treated with the ketogenic diet

Cited by 79 publications

References 19 publications

A ketogenic diet rescues the murine succinic semialdehyde dehydrogenase deficient phenotype

A ketogenic diet rescues the murine succinic semialdehyde dehydrogenase deficient phenotype

Long-term ketogenic diet causes glucose intolerance and reduced β- and α-cell mass but no weight loss in mice

Ketogenic food pyramid for patients with refractory epilepsy: From theory to clinical practice

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