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(searched for: doi:10.3389/fnut.2018.00075)
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Rajesh N. Gacche
Published: 1 November 2021
Dietary Research and Cancer pp 47-60; https://doi.org/10.1007/978-981-16-6050-4_5

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Muhammad Asyraf Abduraman, Nurul Ain Azizan, ,
Published: 25 December 2020
Obesity Research & Clinical Practice, Volume 15, pp 10-18; https://doi.org/10.1016/j.orcp.2020.12.001

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, Jeff Volek, Angela Poff, Dominic P D'Agostino
Published: 12 December 2020
by BMJ
BMJ Nutrition, Prevention & Health, Volume 3, pp 363-373; https://doi.org/10.1136/bmjnph-2020-000167

Abstract:
The ketogenic diet (KD) is a low-carbohydrate, high-fat, adequate-protein diet proven to be effective for the reversal of obesity, metabolic syndrome and type 2 diabetes, and holding therapeutic potential for the prevention and treatment of other chronic diseases. Genetic and dynamic markers of KD response may help to identify individuals most likely to benefit from KD and point to individuals at higher risk for adverse health outcomes. Here, we provide a clinician-friendly review of state-of-the-art research on biomarkers of KD response for a variety of outcomes including weight loss, body composition and cognitive performance drawing data from both intervention trials and case reports of rare inborn errors of metabolism. We also present a selection of the most promising candidate genes to evaluate in future studies and discuss key aspects of study design and variant interpretation that may help accelerate the implementation of these biomarkers in clinical practice.
Yuri Zilberter, Tanya Zilberter
Published: 9 November 2020
Abstract:
The ketogenic diet (KD) has been successfully used for a century for treating refractory epilepsy and is currently seen as one of the few viable approaches to the treatment of a plethora of metabolic and neurodegenerative diseases. Empirical evidence notwithstanding, there is still no universal understanding of KD mechanism(s). An important fact is that the brain is capable of utilizing ketone bodies for fuel. Another critical point is that glucose's functions span beyond its role as an energy substrate, and in most of these functions glucose is irreplaceable. By acting as a supplementary fuel, ketone bodies may free up glucose for its other crucial and exclusive function. We propose that this glucose-sparing effect of ketone bodies may underlie the effectiveness of KD in epilepsy and major neurodegenerative diseases, which are all characterized by brain glucose hypometabolism. Significance Statement The ketogenic diet (KD) was created in the 1920s as a therapy for refractory epilepsy. Since then, evidence accumulated showing its potential for other major neurodegenerative disorders. The exact mechanism of KD's protective activity still remains unknown, nonetheless. In the brain, ketone bodies can be utilized for cellular energy, at least partially substituting glucose as brain fuel. However, glucose has essential functions beyond those of just energy supply that cannot be provided by alternative substrates. We propose that the glucose-sparing effect of ketone bodies may underlie the effectiveness of KD in epilepsy and other major neurodegenerative diseases which are all characterized by brain glucose hypometabolism.
, Shireen Sindi, Anna Sandebring-Matton, Ingemar Kåreholt, Makrina Daniilidou, Ulrika Akenine, Karin Nordin, Staffan Rosenborg, Tiia Ngandu, Miia Kivipelto
Published: 15 April 2020
Frontiers in Nutrition, Volume 7; https://doi.org/10.3389/fnut.2020.00040

Abstract:
Introduction: Medium-chain-triglycerides (MCT), formed by fatty acids with a length of 6–12 carbon atoms (C6–C12), constitute about two thirds of coconut oil (Coc). MCT have specific metabolic properties which has led them to be described as ketogenic even in the absence of carbohydrate restriction. This effect has mainly been demonstrated for caprylic acid (C8), which constitutes about 6–8% of coconut oil. Our aim was to quantify ketosis and blood glucose after intake of Coc and C8, with and without glucose intake. Sunflower oil (Suf) was used as control, expected to not break fasting ketosis, nor induce supply-driven ketosis. Method: In a 6-arm cross-over design, 15 healthy volunteers—age 65–73, 53% women—were tested once a week. After a 12-h fast, ketones were measured during 4 h after intake of coffee with cream, in combination with each of the intervention arms in a randomized order: 1. Suf (30 g); 2. C8 (20 g) + Suf (10 g); 3. C8 (20 g) + Suf (10 g) + Glucose (50 g); 4. Coc (30 g); 5. Coc (30 g) + Glucose (50 g); 6. C8 (20 g) + Coc (30 g). The primary outcome was absolute blood levels of the ketone β-hydroxybutyrate, area under the curve (AUC). ANOVA for repeated measures was performed to compare arms. Results: β-hydroxybutyrate, AUC/time (mean ± SD), for arms were 1: 0.18 ± 0.11; 2: 0.45 ± 0.19; 3: 0.28 ± 0.12; 4: 0.22 ± 0.12; 5: 0.08 ± 0.04; 6: 0.45 ± 0.20 (mmol/L). Differences were significant (all p ≤ 0.02), except for arm 2 vs. 6, and 4 vs. 1 & 3. Blood glucose was stable in arm 1, 2, 4, & 6, at levels slightly below baseline (p ≤ 0.05) at all timepoints hours 1–4 after intake. Conclusions: C8 had a higher ketogenic effect than the other components. Coc was not significantly different from Suf, or C8 with glucose. In addition, we report that a 16-h non-carbohydrate window contributed to a mild ketosis, while blood glucose remained stable. Our results suggest that time-restricted feeding regarding carbohydrates may optimize ketosis from intake of MCT. Clinical Trial Registration: The study was registered as a clinical trial on ClinicalTrials.gov, NCT03904433.
Sarah Lévesque, , Gladys Ferrere, Lorenzo Galluzzi, ,
Published: 3 April 2019
Abstract:
Dietary interventions have a profound impact on whole body metabolism, including oncometabolism (the metabolic features allowing cancer cells to proliferate) and immunometabolism (the catabolic and anabolic reactions that regulate immune responses). Recent preclinical studies demonstrated that multiple dietary changes can improve anticancer immunosurveillance of chemo-, radio- and immunotherapy. These findings have fostered the design of clinical trials evaluating the capacity of dietary interventions to synergize with treatment and hence limit tumor progression. Here, we discuss the scientific rationale for harnessing dietary interventions to improve the efficacy of anticancer therapy and present up-to-date information on clinical trials currently investigating this possibility.
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