Ten-Year Single-Center Experience of the Ketogenic Diet: Factors Influencing Efficacy, Tolerability, and Compliance

Wibisono, Cinthya; Rowe, Natalie; Beavis, Erin; Kepreotes, Helen; Mackie, Fiona; Lawson, John A.; Cardamone, Michael

doi:10.1016/j.jpeds.2014.12.018

Cited by 69 publications

(50 citation statements)

References 22 publications

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“…To compare nutritional differences and health status of mice on sHFLC and KD, body weight and blood analyses were performed. Patients on RKD report losing approximately 20% of their body weight (28), whereas patients on KD report initial body weight fat-loss followed by stabilization (29). Surprisingly, subcutaneous-L0 mice fed the sHFLC diet had a significant increase in body weight compared with the KD and control (Fig.…”

Section: The Shflc Diet Is Safe and Nutritionally Completementioning

confidence: 93%

A Supplemented High-Fat Low-Carbohydrate Diet for the Treatment of Glioblastoma

Martuscello

Vedam‐Mai

McCarthy

et al. 2016

Clinical Cancer Research

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Purpose: Dysregulated energetics coupled with uncontrolled proliferation has become a hallmark of cancer, leading to increased interest in metabolic therapies. Glioblastoma (GB) is highly malignant, very metabolically active, and typically resistant to current therapies. Dietary treatment options based on glucose deprivation have been explored using a restrictive ketogenic diet (KD), with positive anticancer reports. However, negative side effects and a lack of palatability make the KD difficult to implement in an adult population. Hence, we developed a less stringent, supplemented high-fat low-carbohydrate (sHFLC) diet that mimics the metabolic and antitumor effects of the KD, maintains a stable nutritional profile, and presents an alternative clinical option for diverse patient populations. Experimental Design: The dietary paradigm was tested in vitro and in vivo, utilizing multiple patient-derived gliomasphere lines. Cellular proliferation, clonogenic frequency, and tumor stem cell population effects were determined in vitro using the neurosphere assay (NSA). Antitumor efficacy was tested in vivo in preclinical xenograft models and mechanistic regulation via the mTOR pathway was explored. Results: Reducing glucose in vitro to physiologic levels, coupled with ketone supplementation, inhibits proliferation of GB cells and reduces tumor stem cell expansion. In vivo, while maintaining animal health, the sHFLC diet significantly reduces the growth of tumor cells in a subcutaneous model of tumor progression and increases survival in an orthotopic xenograft model. Dietary-mediated anticancer effects correlate with the reduction of mTOR effector expression. Conclusions: We demonstrate that the sHFLC diet is a viable treatment alternative to the KD, and should be considered for clinical testing. Clin Cancer Res; 22(10); 2482–95. ©2015 AACR.

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Section: The Shflc Diet Is Safe and Nutritionally Completementioning

confidence: 93%

A Supplemented High-Fat Low-Carbohydrate Diet for the Treatment of Glioblastoma

Martuscello

Vedam‐Mai

McCarthy

et al. 2016

Clinical Cancer Research

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“…In 1920, refractory epilepsia in children was treated in such a way with considerable success [114,115]. Currently, the ketogenic diet is an adjunct therapy of choice, supporting the pharmacological treatment of epilepsy, or as a principal treatment method in drug-resistant cases, highlighting the efficacy in decreasing seizure frequency, especially in children [116,117]. It has been suggested that some anti-convulsive effects of the ketogenic diet might be attributed to PPARα activation by medium and long chain fatty acids [118].…”

Section: Neuroprotective and Therapeutic Activity Of Ketone Bodiesmentioning

confidence: 99%

Regulation of Ketone Body Metabolism and the Role of PPARα

Grabacka

Pierzchalska

Dean

et al. 2016

IJMS

247

202

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Ketogenesis and ketolysis are central metabolic processes activated during the response to fasting. Ketogenesis is regulated in multiple stages, and a nuclear receptor peroxisome proliferator activated receptor α (PPARα) is one of the key transcription factors taking part in this regulation. PPARα is an important element in the metabolic network, where it participates in signaling driven by the main nutrient sensors, such as AMP-activated protein kinase (AMPK), PPARγ coactivator 1α (PGC-1α), and mammalian (mechanistic) target of rapamycin (mTOR) and induces hormonal mediators, such as fibroblast growth factor 21 (FGF21). This work describes the regulation of ketogenesis and ketolysis in normal and malignant cells and briefly summarizes the positive effects of ketone bodies in various neuropathologic conditions.

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“…The new clinical practice guidelines developed by van der Louw et al 4 will help child neurologists understand the growing evidence for intravenous ketogenic therapy and how best to administer it safely and effectively. There are several very important key messages from these consensus guidelines.…”

mentioning

confidence: 99%

“…3,4 It also provides reassurance that supplementation does not affect ketogenic diet efficacy. 3,4 It also provides reassurance that supplementation does not affect ketogenic diet efficacy.…”

mentioning

confidence: 99%

Intravenous ketogenic diet: guidelines for ketogenic parenteral therapy

Kossoff

2019

Develop Med Child Neuro

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This commentary is on the clinical practice guide by van der Louw et al. on pages 48-56 of this issue. REFERENCES 1. van der Louw E, van den Hurk D, Neal E, et al. Ketogenic diet guidelines for infants with refractory epilepsy. Eur J Paediatr Neurol 2016; 20: 798-809. 2. Arya R, Peariso K, Ga ınza-Lein M, et al. Efficacy and safety of ketogenic diet for treatment of pediatric convulsive refractory status epilepticus. Epilepsy Res 2018; 144: 1-6. 3. Rosenthal E, Weissman B, Kyllonen K. Use of parenteral medium-chain triglyceride emulsion for maintaining seizure control in a 5-year-old girl with intractable diarrhea. JPEN J Parenter Enteral Nutr 1990; 14: 543-5. 4. van der Louw E, Aldaz V, Harvey J, et al. Optimal clinical management of children receiving ketogenic parenteral nutrition: a clinical practice guide. Dev Med Child Neurol 2020; 62: 48-56.Commentaries 7

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Ten-Year Single-Center Experience of the Ketogenic Diet: Factors Influencing Efficacy, Tolerability, and Compliance

Cited by 69 publications

References 22 publications

A Supplemented High-Fat Low-Carbohydrate Diet for the Treatment of Glioblastoma

A Supplemented High-Fat Low-Carbohydrate Diet for the Treatment of Glioblastoma

Regulation of Ketone Body Metabolism and the Role of PPARα

Intravenous ketogenic diet: guidelines for ketogenic parenteral therapy

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