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The management of chronic kidney disease (CKD) includes nutritional interventions aimed at slowing disease progression and mitigating complications. This review examines various dietary approaches for CKD treatment, focusing on carbohydrate intake modulation, ketogenic diets, and plant-based diets. Standard guidelines recommend carbohydrate intake within 45% to 65% of total calories, but there is growing interest in reducing carbohydrate consumption to preserve kidney function. Low-carbohydrate diets (<25% of total calories) have shown benefits in glycemic control and weight reduction but may pose long-term adherence challenges. High-protein, low-carbohydrate diets are discouraged due to associations with hyperfiltration and CKD progression. Limiting fructose intake has been linked to reductions in blood pressure and uric acid levels. Intermittent fasting and ketogenic diets, which promote ketone body production and reduce inflammation, have shown promise in animal models and some human studies, particularly in autosomal dominant polycystic kidney disease, though more research is needed. Plant-based diets, such as the Mediterranean and DASH (Dietary Approaches to Stop Hypertension) diets, offer cardiovascular benefits and may reduce CKD risk but require careful management of potassium intake. Overall, dietary interventions should be individualized, considering potential risks like hyperkalemia and ensuring nutritional adequacy. [ABSTRACT FROM AUTHOR]

Medium chain fatty acids are commonly consumed as part of diets for endurance sports and as medical treatment in ketogenic diets where these diets regulate energy metabolism and increase adenosine levels. However, the role of the equilibrative nucleoside transporter 1 (ENT1), which is responsible for adenosine transport across membranes in this process, is not well understood. Here, we investigate ENT1 activity in controlling the effects of two dietary medium chain fatty acids (decanoic and octanoic acid), employing the tractable model system Dictyostelium. We show that genetic ablation of three ENT1 orthologues unexpectedly improves cell proliferation specifically following decanoic acid treatment. This effect is not caused by increased adenosine levels triggered by both fatty acids in the presence of ENT1 activity. Instead, we show that decanoic acid increases expression of energy-related genes relevant for fatty acid β-oxidation, and that pharmacological inhibition of ENT1 activity leads to an enhanced effect of decanoic acid to increase expression of tricarboxylicacid cycle and oxidative phosphorylation components. Importantly, similar transcriptional changes have been shown in the rat hippocampus during ketogenic diet treatment. We validated these changes by showing enhanced mitochondria load and reduced lipid droplets. Thus, our data show that ENT1 regulates the medium chain fatty acid-induced increase in cellular adenosine levels and the decanoic acid-induced expression of important metabolic enzymes in energy provision, identifying a key role for ENT1 proteins in metabolic effects of medium chain fatty acids. [ABSTRACT FROM AUTHOR]

The management of chronic kidney disease (CKD) includes nutritional interventions aimed at slowing disease progression and mitigating complications. This review examines various dietary approaches for CKD treatment, focusing on carbohydrate intake modulation, ketogenic diets, and plant-based diets. Standard guidelines recommend carbohydrate intake within 45% to 65% of total calories, but there is growing interest in reducing carbohydrate consumption to preserve kidney function. Low-carbohydrate diets (

There is currently a growing interest in diets and physical activity patterns that may be beneficial in preventing and treating breast cancer (BC). Mounting evidence indicates that indeed, the so-called Mediterranean diet (MedDiet) and regular physical activity likely both help reduce the risk of developing BC. For those who have already received a BC diagnosis, these interventions may decrease the risk of tumor recurrence after treatment and improve quality of life. Studies also show the potential of other dietary interventions, including fasting or modified fasting, calorie restriction, ketogenic diets, and vegan or plant-based diets, to enhance the efficacy of BC therapies. In this review article, we discuss the biological rationale for utilizing these dietary interventions and physical activity in BC prevention and treatment. We highlight published and ongoing clinical studies that have applied these lifestyle interventions to BC patients. This review offers valuable insights into the potential application of these dietary interventions and physical activity as complimentary therapies in BC management. [ABSTRACT FROM AUTHOR]

Aim: Drug‐resistant epilepsy (DRE) is a neurological disorder characterized by uncontrolled seizures. It affects between 10%–40% of the patients with epilepsy worldwide. Drug‐resistant patients have been reported to have a different microbiota composition compared to drug‐sensitive patients and healthy controls. Importantly, fecal microbiota transplantations (FMTs), probiotic and dietary interventions have been shown to be able to reduce seizure frequency and improve the quality of life in drug‐resistant patients. The classic ketogenic diet (KD) and its modifications may reduce seizures in DRE in some patients, whereas in others they do not. The mechanisms mediating the dietary effects remain elusive, although it is known that gut microbes play an important role in transmitting dietary effects to the host. Indeed, specific commensal microbes differ even between responders and non‐responders to KD treatment. Methods: In this narrative mini‐review, we summarize what is known about the gut microbiota changes and ketogenic diets with special focus on patients with DRE. Results and Conclusions: By highlighting unanswered questions and by suggesting future research directions, we map the route towards future improvement of successful DRE therapy. [ABSTRACT FROM AUTHOR]

Humans can flexibly switch between two primary metabolic modes, usually distinguished by whether substrate supply from glucose can meet energy demands or not. However, it is often overlooked that when glucose use is limited, the remainder of energy needs may still be met more or less effectively with fat and ketone bodies. Hence a fat-based metabolism marked by ketosis is often conflated with starvation and contexts of inadequate energy (including at the cellular level), even when energy itself is in ample supply. Sleep and satiation are regulated by common pathways reflecting energy metabolism. A conceptual analysis that distinguishes signals of inadequate energy in a glucose-dominant metabolism from signals of a fat-based metabolism that may well be energy sufficient allows a reexamination of experimental results in the study of sleep that may shed light on species differences and explain why ketogenic diets have beneficial effects simultaneously in the brain and the periphery. It may also help to distinguish clinically when a failure of a ketogenic diet to resolve symptoms is due to inadequate energy rather than the metabolic state itself.

Carbohydrate restriction has gained increasing popularity as an adjunctive nutritional therapy for diabetes management. However, controversy remains regarding the long-term suitability, safety, efficacy and potential superiority of a very low carbohydrate, ketogenic diet compared to current recommended nutritional approaches for diabetes management. Recommendations with respect to a ketogenic diet in clinical practice are often hindered by the lack of established definition, which prevents its capacity to be most appropriately prescribed as a therapeutic option for diabetes. Furthermore, with conflicted evidence, this has led to uncertainty amongst clinicians on how best to support and advise their patients. This review will explore whether a ketogenic diet has a place within clinical practice by reviewing current evidence and controversies. [ABSTRACT FROM AUTHOR]

This article, titled "Editorial: Ketone bodies: friend or foe?" explores the therapeutic use of ketone bodies (KBs) in various health conditions. Ketogenic diets (KDs), which increase KB levels, have been found to be beneficial for epilepsy, Parkinson's disease, diabetes, and cancer. However, recent studies have raised concerns about potential off-target effects of KBs, particularly on cardiac health. The article includes a review and several research articles that provide insights into the role of KBs in stem cell biology, neurodegenerative conditions, epilepsy, and diabetic kidney disease. Overall, the article highlights the potential of KDs and KB supplementation in therapeutic settings and calls for further research in this area. [Extracted from the article]

There is currently a growing interest in diets and physical activity patterns that may be beneficial in preventing and treating breast cancer (BC). Mounting evidence indicates that indeed, the so-called Mediterranean diet (MedDiet) and regular physical activity likely both help reduce the risk of developing BC. For those who have already received a BC diagnosis, these interventions may decrease the risk of tumor recurrence after treatment and improve quality of life. Studies also show the potential of other dietary interventions, including fasting or modified fasting, calorie restriction, ketogenic diets, and vegan or plant-based diets, to enhance the efficacy of BC therapies. In this review article, we discuss the biological rationale for utilizing these dietary interventions and physical activity in BC prevention and treatment. We highlight published and ongoing clinical studies that have applied these lifestyle interventions to BC patients. This review offers valuable insights into the potential application of these dietary interventions and physical activity as complimentary therapies in BC management.

Overactivation of the NLRP3 inflammasome is implicated in chronic low-grade inflammation associated with various disease states, including obesity, type 2 diabetes, atherosclerosis, Alzheimer's disease, and Parkinson's disease. Emerging evidence, mostly from cell and animal models of disease, supports a role for ketosis in general, and the main circulating ketone body beta-hydroxybutyrate (BHB) in particular, in reducing NLRP3 inflammasome activation to improve chronic inflammation. As a result, interventions that can induce ketosis (e.g., fasting, intermittent fasting, time-restricted feeding/eating, very low-carbohydrate high-fat ketogenic diets) and/or increase circulating BHB (e.g., exogenous ketone supplementation) have garnered increasing interest for their therapeutic potential. The purpose of the present review is to summarize our current understanding of the literature on how ketogenic interventions impact the NLRP3 inflammasome across human, rodent and cell models. Overall, there is convincing evidence that ketogenic interventions, likely acting through multiple interacting mechanisms in a cell-, disease- and context-specific manner, can reduce NLRP3 inflammasome activation. The evidence supports a direct effect of BHB, although it is important to consider the myriad of other metabolic responses to fasting or ketogenic diet interventions (e.g., elevated lipolysis, low insulin, stable glucose, negative energy balance) that may also impact innate immune responses. Future research is needed to translate promising findings from discovery science to clinical application.

Numerous studies have examined the effects of ketogenic diets (KD) on health-related outcomes through meta-analyses. However, the presence of biases may compromise the reliability of conclusions. Therefore, we conducted an umbrella review to collate and appraise the strength of evidence on the efficacy of KD interventions. We conducted a comprehensive search on PubMed, EMBASE, and the Cochrane Database until April 2023 to identify meta-analyses that investigated the treatment effects of KD for multiple health conditions, which yielded 23 meta-analyses for quantitative analyses. The evidence suggests that KD could increase the levels of low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C), the respiratory exchange rate (RER), and could decrease total testosterone and testosterone levels (all p-random effects: <0.05). The combination of KD and physical activity can significantly reduce body weight and increase the levels of LDL-C and cortisol. In addition, KD was associated with seizure reduction in children, which can be explained by the ketosis state as induced by the diet. Furthermore, KD demonstrated a better alleviation effect in refractory childhood epilepsy, in terms of median effective rates for seizure reduction of ≥50%, ≥90%, and seizure freedom. However, the strength of evidence supporting the aforementioned associations was generally weak, thereby challenging their credibility. Consequently, future studies should prioritize stringent research protocols to ascertain whether KD interventions with longer intervention periods hold promise as a viable treatment option for various diseases. [ABSTRACT FROM AUTHOR]

Conventional hypocaloric diets, providing continuous energy restriction, are considered to be the cornerstone of dietary management of obesity. Although energy-restricted diets are overall safe, healthy, and modestly effective, their long-term adherence is difficult to accomplish. Intermittent fasting and ketogenic diets have emerged as attractive alternative dietary options for weight loss and improvement in cardiometabolic risk. Intermittent fasting is a unique dietary pattern characterized by periods of eating alternated with periods of fasting. Ketogenic diets are very low in carbohydrate, modest in protein, and high in fat. Several systematic reviews and meta-analyses of randomized controlled trials (RCTs) have reported beneficial but short-lived effects of intermittent fasting and ketogenic diets on various obesity-related health outcomes. Although for both diets, the current evidence is promising and steadily evolving, whether they are better than traditional calorie-restricted diets, whether they can safely lead to sustained weight loss and overall health benefits, and their effects on body composition, weight loss maintenance, energy intake and expenditure, diet quality, and cardiometabolic risk factors are still not unequivocally proven. The aim of the present review is to summarize the current state of evidence regarding the effects of these two popular modern diets, namely intermittent fasting and ketogenic diets. We describe the rationale and characteristics of different dietary protocols, we analyze the major mechanisms explaining their weight loss and cardiometabolic effects, and we provide a concise update on their effects on body weight and cardiometabolic risk factors, focusing on meta-analyses of RCTs. We also discuss knowledge gaps in the field of these diets, and we indicate directions for future research.

BackgroundMultiple sclerosis (MS) is a neurodegenerative disorder. Individuals with MS frequently present symptoms such as functional disability, obesity, and anxiety and depression. Axonal demyelination can be observed and implies alterations in mitochondrial activity and increased inflammation associated with disruptions in glutamate neurotransmitter activity. In this context, the ketogenic diet (KD), which promotes the production of ketone bodies in the blood [mainly β-hydroxybutyrate (βHB)], is a non-pharmacological therapeutic alternative that has shown promising results in peripheral obesity reduction and central inflammation reduction. However, the association of this type of diet with emotional symptoms through the modulation of glutamate activity in MS individuals remains unknown.AimTo provide an update on the topic and discuss the potential impact of KD on anxiety and depression through the modulation of glutamate activity in subjects with MS.DiscussionThe main findings suggest that the KD, as a source of ketone bodies in the blood, improves glutamate activity by reducing obesity, which is associated with insulin resistance and dyslipidemia, promoting central inflammation (particularly through an increase in interleukins IL-1β, IL-6, and IL-17). This improvement would imply a decrease in extrasynaptic glutamate activity, which has been linked to functional disability and the presence of emotional disorders such as anxiety and depression.

Conventional hypocaloric diets, providing continuous energy restriction, are considered to be the cornerstone of dietary management of obesity. Although energy-restricted diets are overall safe, healthy, and modestly effective, their long-term adherence is difficult to accomplish. Intermittent fasting and ketogenic diets have emerged as attractive alternative dietary options for weight loss and improvement in cardiometabolic risk. Intermittent fasting is a unique dietary pattern characterized by periods of eating alternated with periods of fasting. Ketogenic diets are very low in carbohydrate, modest in protein, and high in fat. Several systematic reviews and meta-analyses of randomized controlled trials (RCTs) have reported beneficial but short-lived effects of intermittent fasting and ketogenic diets on various obesity-related health outcomes. Although for both diets, the current evidence is promising and steadily evolving, whether they are better than traditional calorie-restricted diets, whether they can safely lead to sustained weight loss and overall health benefits, and their effects on body composition, weight loss maintenance, energy intake and expenditure, diet quality, and cardiometabolic risk factors are still not unequivocally proven. The aim of the present review is to summarize the current state of evidence regarding the effects of these two popular modern diets, namely intermittent fasting and ketogenic diets. We describe the rationale and characteristics of different dietary protocols, we analyze the major mechanisms explaining their weight loss and cardiometabolic effects, and we provide a concise update on their effects on body weight and cardiometabolic risk factors, focusing on meta-analyses of RCTs. We also discuss knowledge gaps in the field of these diets, and we indicate directions for future research. [ABSTRACT FROM AUTHOR]

Epilepsy is an important medical problem with approximately 50 million patients globally. No more than 70% of epileptic patients will achieve seizure control after antiepileptic drugs, and several epileptic syndromes, including Lennox-Gastaut syndrome (LGS), are predisposed to more frequent pharmacoresistance. Ketogenic dietary therapies (KDTs) are a form of non-pharmacological treatments used in attempts to provide seizure control for LGS patients who experience pharmacoresistance. Our review aimed to evaluate the efficacy and practicalities concerning the use of KDTs in LGS. In general, KDTs are diets rich in fat and low in carbohydrates that put the organism into the state of ketosis. A classic ketogenic diet (cKD) is the best-evaluated KDT, while alternative KDTs, such as the medium-chain triglyceride diet (MCT), modified Atkins diet (MAD), and low glycemic index treatment (LGIT) present several advantages due to their better tolerability and easier administration. The literature reports regarding LGS suggest that KDTs can provide ≥50% seizure reduction and seizure-free status in a considerable percentage of the patients. The most commonly reported adverse effects are constipation, diarrhea, and vomiting, while severe adverse effects such as nephrolithiasis or osteopenia are rarely reported. The literature review suggests that KDTs can be applied safely and are effective in LGS treatment. [ABSTRACT FROM AUTHOR]

Numerous studies have examined the effects of ketogenic diets (KD) on health-related outcomes through meta-analyses. However, the presence of biases may compromise the reliability of conclusions. Therefore, we conducted an umbrella review to collate and appraise the strength of evidence on the efficacy of KD interventions. We conducted a comprehensive search on PubMed, EMBASE, and the Cochrane Database until April 2023 to identify meta-analyses that investigated the treatment effects of KD for multiple health conditions, which yielded 23 meta-analyses for quantitative analyses. The evidence suggests that KD could increase the levels of low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C), the respiratory exchange rate (RER), and could decrease total testosterone and testosterone levels (all p-random effects:

A ketogenic diet characterized by high fat and low carbohydrate can drive the body to produce a large number of ketone bodies, altering human metabolism. Unlike normal cells, tumor cells have difficulty in consuming ketone bodies. Therefore, the application of ketogenic diets in cancer therapy is gaining attention. However, the effect of ketogenic diets on body parameters of cancer patients is not well established. This meta-analysis aimed to summarize the effects of ketogenic diets on cancer patients in earlier controlled trials. PubMed, Embase, and Cochrane Library were searched for clinical trials that enrolled cancer patients who received ketogenic diets intervention. Ten controlled trials were included in this meta-analysis. Data were extracted and checked by three authors independently. Pooled effect sizes revealed a significant effect of ketogenic diets on body weight (SMD −1.83, 95% CI −2.30 to −1.35; p < 0.00001) and fat mass (SMD −1.52, 95% CI −1.92 to −1.07; p < 0.00001). No significant effect on blood glucose, insulin, or lipid profile except triglycerides was found in the analysis. It had no effect on liver and kidney function except that GGT were decreased a little. There were no significant changes in IGF-1 and TNF-α related to tumor growth. Mental health improvement of cancer patients was supported by several trials. Taken together, findings in this study confirmed that the ketogenic diet was a safe approach for cancer patients reducing body weight and fat mass. In addition, cancer treatment-related indicators changed insignificantly. Ketogenic diets may be beneficial to the quality of life of cancer patients. However, intervention duration in most studies is shorter than 6 months, and the effect of a long-term ketogenic diet is still required further validation. More trials with a larger sample size are necessary to give a more conclusive result; PROSPERO registration number: CRD42021277559. [ABSTRACT FROM AUTHOR]

Food addiction, specifically ultra-processed food addiction, has been discussed in thousands of peer-reviewed publications. Although 20% of adults meet criteria for this condition, food addiction is not a recognized clinical diagnosis, leading to a dearth of tested treatment protocols and published outcome data. Growing numbers of clinicians are offering services to individuals on the basis that the food addiction construct has clinical utility. This audit reports on clinical teams across three locations offering a common approach to programs delivered online. Each team focused on a whole food low-carbohydrate approach along with delivering educational materials and psychosocial support relating to food addiction recovery. The programs involved weekly sessions for 10-14 weeks, followed by monthly support. The data comprised pre- and post-program outcomes relating to food addiction symptoms measured by the modified Yale Food Addiction Scale 2.0, ICD-10 symptoms of food related substance use disorder (CRAVED), mental wellbeing as measured by the short version of the Warwick Edinburgh Mental Wellbeing Scale, and body weight. Sample size across programs was 103 participants. Food addiction symptoms were significantly reduced across settings; mYFAS2 score -1.52 (95% CI: -2.22, -0.81), CRAVED score -1.53 (95% CI: -1.93, -1.13) and body weight was reduced -2.34 kg (95% CI: -4.02, -0.66). Mental wellbeing showed significant improvements across all settings; short version Warwick EdinburghMentalWellbeing Scale 2.37 (95% CI: 1.55, 3.19). Follow-up data will be published in due course. Further research is needed to evaluate and compare long-term interventions for this complex and increasingly burdensome biopsychosocial condition. [ABSTRACT FROM AUTHOR]

Context: Ketogenic diets and ketone supplements have gained popularity among endurance runners given their purported effects: potentially delaying the onset of fatigue by enabling the increased utilization of the body's fat reserve or external ketone bodies during prolonged running., Objective: This systematic review was conducted to evaluate the effects of ketogenic diets (>60% fat and <10% carbohydrates/<50 g carbohydrates per day) or ketone supplements (ketone esters or ketone salts, medium-chain triglycerides or 1,3-butadiol) on the aerobic performance of endurance runners., Data Sources: A systematic search was conducted in PubMed, Web of Science, Pro Quest, and Science Direct for publications up to October 2023., Study Selection: Human studies on the effects of ketogenic diets or ketone supplements on the aerobic performance of adult endurance runners were included after independent screening by 2 reviewers., Study Design: Systematic review., Level of Evidence: Level 3., Data Extraction: Primary outcomes were markers of aerobic performance (maximal oxygen uptake [VO 2 max], race time, time to exhaustion and rate of perceived exertion)., Results: VO 2 max was assessed by incremental test to exhaustion. Endurance performance was assessed by time trials, 180-minute running trials, or run-to-exhaustion trials; 5 studies on ketogenic diets and 7 studies on ketone supplements involving a total of 132 endurance runners were included. Despite the heterogeneity in study design and protocol, none reported benefits of ketogenic diets or ketone supplements on selected markers of aerobic performance compared with controls. Reduction in bodyweight and fat while preserving lean mass and improved glycemic control were reported in some included studies on ketogenic diets., Conclusion: This review did not identify any significant advantages or disadvantages of ketogenic diets or ketone supplements for the aerobic performance of endurance runners. Further trials with larger sample sizes, more gender-balanced participants, longer ketogenic diet interventions, and follow-up on metabolic health are warranted., Competing Interests: The authors report no potential conflicts of interest in the development and publication of this article.

Food addiction, specifically ultra-processed food addiction, has been discussed in thousands of peer-reviewed publications. Although 20% of adults meet criteria for this condition, food addiction is not a recognized clinical diagnosis, leading to a dearth of tested treatment protocols and published outcome data. Growing numbers of clinicians are offering services to individuals on the basis that the food addiction construct has clinical utility. This audit reports on clinical teams across three locations offering a common approach to programs delivered online. Each team focused on a whole food low-carbohydrate approach along with delivering educational materials and psychosocial support relating to food addiction recovery. The programs involved weekly sessions for 10–14 weeks, followed by monthly support. The data comprised pre- and post- program outcomes relating to food addiction symptoms measured by the modified Yale Food Addiction Scale 2.0, ICD-10 symptoms of food related substance use disorder (CRAVED), mental wellbeing as measured by the short version of the Warwick Edinburgh Mental Wellbeing Scale, and body weight. Sample size across programs was 103 participants. Food addiction symptoms were significantly reduced across settings; mYFAS2 score −1.52 (95% CI: −2.22, −0.81), CRAVED score −1.53 (95% CI: −1.93, −1.13) and body weight was reduced −2.34 kg (95% CI: −4.02, −0.66). Mental wellbeing showed significant improvements across all settings; short version Warwick Edinburgh Mental Wellbeing Scale 2.37 (95% CI: 1.55, 3.19). Follow-up data will be published in due course. Further research is needed to evaluate and compare long-term interventions for this complex and increasingly burdensome biopsychosocial condition.

Humans can flexibly switch between two primary metabolic modes, usually distinguished by whether substrate supply from glucose can meet energy demands or not. However, it is often overlooked that when glucose use is limited, the remainder of energy needs may still be met more or less effectively with fat and ketone bodies. Hence a fat-based metabolism marked by ketosis is often conflated with starvation and contexts of inadequate energy (including at the cellular level), even when energy itself is in ample supply. Sleep and satiation are regulated by common pathways reflecting energy metabolism. A conceptual analysis that distinguishes signals of inadequate energy in a glucose-dominant metabolism from signals of a fat-based metabolism that may well be energy sufficient allows a reexamination of experimental results in the study of sleep that may shed light on species differences and explain why ketogenic diets have beneficial effects simultaneously in the brain and the periphery. It may also help to distinguish clinically when a failure of a ketogenic diet to resolve symptoms is due to inadequate energy rather than the metabolic state itself., Competing Interests: The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 O'Hearn.)

While the prevalence of cardio-metabolic diseases (CMDs) has become a worldwide epidemic, much attention is paid to managing CMDs effectively. A ketogenic diet (KD) constitutes a high-fat and low-carbohydrate diet with appropriate protein content and calories. KD has drawn the interests of clinicians and scientists regarding its application in the management of metabolic diseases and related disorders; thus, the current review aimed to examine the evidences surrounding KD and the CMDs to draw the clinical implications. Overall, KD appears to play a significant role in the therapy of various CMDs, which is manifested by the effects of KDs on cardio-metabolic outcomes. KD therapy is generally promising in obesity, heart failure, and hypertension, though different voices still exist. In diabetes and dyslipidemia, the performance of KD remains controversial. As for cardiovascular complications of metabolic diseases, current evidence suggests that KD is generally protective to obese related cardiovascular disease (CVD), while remaining contradictory to diabetes and other metabolic disorder related CVDs. Various factors might account for the controversies, including genetic background, duration of therapy, food composition, quality, and sources of KDs. Therefore, it's crucial to perform more rigorous researches to focus on clinical safety and appropriate treatment duration and plan of KDs. [ABSTRACT FROM AUTHOR]

Background: The Warburg effect, also termed "aerobic glycolysis", is one of the most remarkable and ubiquitous metabolic characteristics exhibited by cancer cells, representing a potential vulnerability that might be targeted for tumor therapy. Ketogenic diets (KDs), composed of high-fat, moderate-protein and low carbohydrates, are aimed at targeting the Warburg effect for cancer treatment, which have recently gained considerable attention. However, the efficiency of KDs was inconsistent, and the genotypic contribution is still largely unknown. Methods: The bulk RNA-seq data from The Cancer Genome Atlas (TCGA), single cell RNA sequencing (scRNA-seq), and microarray data from Gene Expression Omnibus (GEO) and Cancer Cell Line Encyclopedia (CCLE) were collected. A joint analysis of glycolysis and ketone bodies metabolism (KBM) pathway was performed across over 10,000 tumor samples and nearly 1,000 cancer cell lines. A series of bioinformatic approaches were combined to identify a metabolic subtype that may predict the response to ketogenic dietary therapy (KDT). Mouse xenografts were established to validate the predictive utility of our subtypes in response to KDT. Results: We first provided a system-level view of the expression pattern and prognosis of the signature genes from glycolysis and KBM pathway across 33 cancer types. Analysis by joint stratification of glycolysis and KBM revealed four metabolic subtypes, which correlated extensively but diversely with clinical outcomes across cancers. The glycolytic subtypes may be driven by TP53 mutations, whereas the KB-metabolic subtypes may be mediated by CTNNB1 (β-catenin) mutations. The glycolytic subtypes may have a better response to KDs compared to the other three subtypes. We preliminarily confirmed the idea by literature review and further performed a proof-of-concept experiment to validate the predictive value of the metabolic subtype in liver cancer xenografts. Conclusions: Our findings identified a metabolic subtype based on glycolysis and KBM that may serve as a promising biomarker to predict the clinical outcomes and therapeutic responses to KDT. [ABSTRACT FROM AUTHOR]

While the prevalence of cardio-metabolic diseases (CMDs) has become a worldwide epidemic, much attention is paid to managing CMDs effectively. A ketogenic diet (KD) constitutes a high-fat and low-carbohydrate diet with appropriate protein content and calories. KD has drawn the interests of clinicians and scientists regarding its application in the management of metabolic diseases and related disorders; thus, the current review aimed to examine the evidences surrounding KD and the CMDs to draw the clinical implications. Overall, KD appears to play a significant role in the therapy of various CMDs, which is manifested by the effects of KDs on cardio-metabolic outcomes. KD therapy is generally promising in obesity, heart failure, and hypertension, though different voices still exist. In diabetes and dyslipidemia, the performance of KD remains controversial. As for cardiovascular complications of metabolic diseases, current evidence suggests that KD is generally protective to obese related cardiovascular disease (CVD), while remaining contradictory to diabetes and other metabolic disorder related CVDs. Various factors might account for the controversies, including genetic background, duration of therapy, food composition, quality, and sources of KDs. Therefore, it’s crucial to perform more rigorous researches to focus on clinical safety and appropriate treatment duration and plan of KDs.

BackgroundThe Warburg effect, also termed “aerobic glycolysis”, is one of the most remarkable and ubiquitous metabolic characteristics exhibited by cancer cells, representing a potential vulnerability that might be targeted for tumor therapy. Ketogenic diets (KDs), composed of high-fat, moderate-protein and low carbohydrates, are aimed at targeting the Warburg effect for cancer treatment, which have recently gained considerable attention. However, the efficiency of KDs was inconsistent, and the genotypic contribution is still largely unknown.MethodsThe bulk RNA-seq data from The Cancer Genome Atlas (TCGA), single cell RNA sequencing (scRNA-seq), and microarray data from Gene Expression Omnibus (GEO) and Cancer Cell Line Encyclopedia (CCLE) were collected. A joint analysis of glycolysis and ketone bodies metabolism (KBM) pathway was performed across over 10,000 tumor samples and nearly 1,000 cancer cell lines. A series of bioinformatic approaches were combined to identify a metabolic subtype that may predict the response to ketogenic dietary therapy (KDT). Mouse xenografts were established to validate the predictive utility of our subtypes in response to KDT.ResultsWe first provided a system-level view of the expression pattern and prognosis of the signature genes from glycolysis and KBM pathway across 33 cancer types. Analysis by joint stratification of glycolysis and KBM revealed four metabolic subtypes, which correlated extensively but diversely with clinical outcomes across cancers. The glycolytic subtypes may be driven by TP53 mutations, whereas the KB-metabolic subtypes may be mediated by CTNNB1 (β-catenin) mutations. The glycolytic subtypes may have a better response to KDs compared to the other three subtypes. We preliminarily confirmed the idea by literature review and further performed a proof-of-concept experiment to validate the predictive value of the metabolic subtype in liver cancer xenografts.ConclusionsOur findings identified a metabolic subtype based on glycolysis and KBM that may serve as a promising biomarker to predict the clinical outcomes and therapeutic responses to KDT.

Background: Alzheimer's disease is the most common neurodegenerative disorder in our society, mainly characterized by loss of cognitive function. However, other symptoms such as anxiety and depression have been described in patients. The process is mediated by alterations in the synaptic and extrasynaptic activity of the neurotransmitter glutamate, which are linked to a hypometabolism of glucose as the main source of brain energy. In that respect, Ketogenic diet (KD) has been proposed as a non-pharmacological treatment serving as an alternative energy source to the neurons increasing the fat percentage and reducing the carbohydrates percentage, showing promising results to improve the cognitive symptoms associated with different neurodegenerative disorders, including AD. However, the association of this type of diet with emotional symptoms and the modulation of glutamate neurotransmission systems after this dietary reduction of carbohydrates are unknown.Objective: The aim of this short review is to provide update studies and discuss about the relationship between KD, anxiety, depression, and glutamate activity in AD patients.Discussion: The main results suggest that the KD is an alternative energy source for neurons in AD with positive consequences for the brain at different levels such as epigenetic, metabolic and signaling, and that the substitution of carbohydrates for fats is also associated with emotional symptoms and glutamate activity in AD.

Epilepsy is an important medical problem with approximately 50 million patients globally. No more than 70% of epileptic patients will achieve seizure control after antiepileptic drugs, and several epileptic syndromes, including Lennox-Gastaut syndrome (LGS), are predisposed to more frequent pharmacoresistance. Ketogenic dietary therapies (KDTs) are a form of non-pharmacological treatments used in attempts to provide seizure control for LGS patients who experience pharmacoresistance. Our review aimed to evaluate the efficacy and practicalities concerning the use of KDTs in LGS. In general, KDTs are diets rich in fat and low in carbohydrates that put the organism into the state of ketosis. A classic ketogenic diet (cKD) is the best-evaluated KDT, while alternative KDTs, such as the medium-chain triglyceride diet (MCT), modified Atkins diet (MAD), and low glycemic index treatment (LGIT) present several advantages due to their better tolerability and easier administration. The literature reports regarding LGS suggest that KDTs can provide ≥50% seizure reduction and seizure-free status in a considerable percentage of the patients. The most commonly reported adverse effects are constipation, diarrhea, and vomiting, while severe adverse effects such as nephrolithiasis or osteopenia are rarely reported. The literature review suggests that KDTs can be applied safely and are effective in LGS treatment.

A ketogenic diet characterized by high fat and low carbohydrate can drive the body to produce a large number of ketone bodies, altering human metabolism. Unlike normal cells, tumor cells have difficulty in consuming ketone bodies. Therefore, the application of ketogenic diets in cancer therapy is gaining attention. However, the effect of ketogenic diets on body parameters of cancer patients is not well established. This meta-analysis aimed to summarize the effects of ketogenic diets on cancer patients in earlier controlled trials. PubMed, Embase, and Cochrane Library were searched for clinical trials that enrolled cancer patients who received ketogenic diets intervention. Ten controlled trials were included in this meta-analysis. Data were extracted and checked by three authors independently. Pooled effect sizes revealed a significant effect of ketogenic diets on body weight (SMD −1.83, 95% CI −2.30 to −1.35; p < 0.00001) and fat mass (SMD −1.52, 95% CI −1.92 to −1.07; p < 0.00001). No significant effect on blood glucose, insulin, or lipid profile except triglycerides was found in the analysis. It had no effect on liver and kidney function except that GGT were decreased a little. There were no significant changes in IGF-1 and TNF-α related to tumor growth. Mental health improvement of cancer patients was supported by several trials. Taken together, findings in this study confirmed that the ketogenic diet was a safe approach for cancer patients reducing body weight and fat mass. In addition, cancer treatment-related indicators changed insignificantly. Ketogenic diets may be beneficial to the quality of life of cancer patients. However, intervention duration in most studies is shorter than 6 months, and the effect of a long-term ketogenic diet is still required further validation. More trials with a larger sample size are necessary to give a more conclusive result; PROSPERO registration number: CRD42021277559.

Many studies show that glucose metabolism in epileptic brain areas can be impaired. Energy is crucial to maintain normal brain function, including ion and neurotransmitter balances. Energy deficits can lead to disruption of ion gradients, which can trigger neuronal depolarization and generation of seizures. Thus, perturbed metabolic processing of glucose in epileptogenic brain areas indicates a specific nutritional need for people and animals with epilepsy, as they are likely to benefit from auxiliary brain fuels other than glucose. Ketogenic diets provide the ketone bodies acetoacetate and β‐hydroxybutyrate, which can be used as auxiliary fuel by the brain. In approximately 50% children and adults with certain types of epilepsy, who can tolerate and maintain these dietary regimens, seizure frequency can be effectively reduced. More recent data demonstrate that addition of medium chain triglycerides (MCTs), which provide the medium chain fatty acids octanoic and decanoic acid, as well as ketone bodies as auxiliary brain energy, can be beneficial in rodent seizure models, and dogs and humans with epilepsy. Here, this evidence is reviewed, including tolerance in 65% of humans, efficacy studies in dogs, possible anticonvulsant mechanisms of actions of MCTs, and specifically decanoic acid as well as metabolic and antioxidant mechanisms. In conclusion, MCTs are a promising adjunct to standard pharmacological treatment for both humans and dogs with epilepsy, as they lack central nervous system side effects found with current antiepileptic drugs. There is now a need for larger clinical trials in children, adults, and dogs to find the ideal composition and doses of MCTs and the types of epilepsy that respond best. [ABSTRACT FROM AUTHOR]

Ketogenic diets (KDs) are very high-fat low-carbohydrate diets that promote nutritional ketosis and are widely used for weight loss, although concerns about potential adverse cardiovascular effects remain. We investigated a very high-fat KD's vascular impact and plasma metabolic signature compared to a non-ketogenic high-fat diet (HFD). Apolipoprotein E deficient (ApoE −/−) mice were fed a KD (%kcal:81:1:18, fat/carbohydrate/protein), a non-ketogenic high-fat diet with half of the fat content (HFD) (%kcal:40:42:18, fat/carbohydrate/protein) for 12 weeks. Plasma samples were used to quantify the major ketone body beta−hydroxybutyrate (BHB) and several pro-inflammatory cytokines (IL-6, MCP-1, MIP-1alpha, and TNF alpha), and to targeted metabolomic profiling by mass spectrometry. In addition, aortic atherosclerotic lesions were quantified ex-vivo by magnetic resonance imaging (MRI) on a 14-tesla system. KD was atherogenic when compared to the control diet, but KD mice, when compared to the HFD group (1) had markedly higher levels of BHB and lower levels of cytokines, confirming the presence of ketosis that alleviated the well-established fat-induced systemic inflammation; (2) displayed significant changes in the plasma metabolome that included a decrease in lipophilic metabolites and an increase in hydrophilic metabolites; (3) had significantly lower levels of several atherogenic lipid metabolites, including phosphatidylcholines, cholesterol esters, sphingomyelins, and ceramides; and (4) presented significantly lower aortic plaque burden. KD was atherogenic and was associated with specific metabolic changes but alleviated the fat-induced inflammation and lessened the progression of atherosclerosis when compared to the HFD. [ABSTRACT FROM AUTHOR]

Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disease leading to kidney failure. To date, there is no cure for the disease although there is one approved disease-modifying therapy: tolvaptan. In this context, a common question that ADPKD patients ask in clinical practice is whether there is anything they can do to slow their disease by modifying their diet or lifestyle. Recent evidence from experimental PKD models has shown the potential benefits of caloric restriction, high water intake and especially ketogenic diets in preserving kidney function. Whether these benefits are translatable to humans remains unknown. In this issue of CKJ , Strubl et al. report results of a self-enrolled survey of autosomal dominant polycystic kidney disease (ADPKD) patients who have self-administered a ketogenic diet [ 1 ]. These results provide interesting insights into the tolerability, potential benefits and harms of such an intervention that could inform a future clinical trial. [ABSTRACT FROM AUTHOR]

Diabetes mellitus is a collection of metabolic disorders marked by elevated levels of glucose in the blood due to irregularities in the generation or functioning of insulin. Medical nutrition therapy and weight loss are crucial elements in the management of diabetes and the prevention of complications. Several diets have become popular over time for the goal of achieving weight loss, but their popularity has declined due to a lack of reliable scientific evidence. This study classifies popular diets into three categories: diets that manage the composition of macronutrients, diets that restrict specific foods or food groups, and diets that manipulate meal timing. The review includes research studies that investigated the effects of popular diets on the prevention, management, and complications of diabetes. It is clear that different popular diets can have positive effects on both preventing and treating diabetes and preventing and treating complications related to diabetes. However, it is not practical to determine which diet is the most effective option for preventing or controlling diabetes. Thus, the main focus should be on common underlying factors that support well-being, such as decreasing the intake of refined grains and added sugar, choosing non-starchy vegetables, and giving priority to whole foods over processed foods whenever possible, until there is stronger evidence supporting the specific benefits of different dietary patterns., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Şahin Bayram et al.)

The purpose of the present review is to describe how human physiology at very low carbohydrate intakes relates to the criteria for nutritional essentiality. Although we did not limit ourselves to one particular type or function of carbohydrates, we did primarily focus on glucose utilisation as that function was used to determine the recommended daily allowance. In the general population, the human body is able to endogenously synthesise carbohydrates, and does not show signs of deficiency in the absence of dietary carbohydrates. However, in certain genetic defects, such as glycogen storage disease type I, absence of dietary carbohydrates causes abnormalities that are resolved with dietary supplementation of carbohydrates. Therefore, dietary carbohydrates may be defined as conditionally essential nutrients because they are nutrients that are not required in the diet for the general population but are required for specific subpopulations. Ketosis may be considered a physiological normal state due to its occurrence in infants in addition to at very low carbohydrate intakes. Although sources of dietary carbohydrates can provide beneficial micronutrients, no signs of micronutrient deficiencies have been reported in clinical trials of low-carbohydrate ketogenic diets. Nonetheless, more research is needed on how micronutrient requirements can change depending on the dietary and metabolic context. More research is also needed on the role of dietary fibre during a low-carbohydrate ketogenic diet as the beneficial effects of dietary fibre were determined on a standard diet and several studies have shown beneficial effects of decreasing non-digestible carbohydrates. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a multifactorial and chronic neurodegenerative disorder that interferes with memory, thinking, and behavior. The consumption of dietary fat has been considered a vital factor for AD as this disease is related to blood-brain barrier function and cholesterol signaling. The ε4 allele of apolipoprotein E (APOE4) is a primary genetic risk factor that encodes one of many proteins accountable for the transport of cholesterol and it is deemed as the leading cholesterol transport proteins in the brain. In case of AD development, the causative factor is the high level of serum/plasma cholesterol. However, this statement is arguable and, in the meantime, the levels of brain cholesterol in individuals with AD are extremely inconstant and levels of cholesterol in the brain and serum/plasma of AD individuals do not reflect cholesterol as a risk factor. In fact, APOE4 is neither fundamental nor sufficient for the advancement of AD; it just acts as a synergistic and increases the danger of AD. Another noticeable characteristic of AD is area-specific decreases in the metabolism of brain glucose. It has been found that the brain cells cannot efficiently metabolize fats; hence, they totally rely upon glucose as a vitality substrate. Thus, suppression of glucose metabolism can possess an intense effect on brain actions. Hypometabolism is frequently found in AD and has quite recently achieved impressive consideration as a plausible target for interfering in the progression of the disease. One promising approach is to keep up the normal supply of glucose to the brain with ketone bodies from the ketogenic diet signifies a potential therapeutic agent for AD. Therefore, this review represents the role of ketogenic diets to combat AD pathogenesis by considering the influence of APOE. [ABSTRACT FROM AUTHOR]

This study investigated the effect of ketogenic diet on monosodium glutamate (MSG)-induced testicular dysfunction. Forty-six male rats (180 ± 40 g) were grouped into two groups (23 rats each); control group and MSG-induced group (4 mg/kg bw) for 28 days. At the 29th day, 5 rats from both group were sacrificed to establish testicular dysfunction. The remaining animals from the control group was further divided into three sub-groups and treated for 42 days; untreated group, ketogenic diet only and curcumin only as the standard drug (150 mg/kg bw). In the pre-treatment, the administration of MSG resulted in a significant (p

Background:epilepsy is one of the common neurological disorders and approximately 0.5-1% of populations suffers from it. Unfortunately, despite of treatment by antiepileptic drugs, between 20-30% of patients cannot be controlled completely. There are a lot of supplementary therapies for this group of patients and in this study, L-arginine was used as an additional therapy in refractory epileptic patients. Methods: Two groups of epileptic patients (n=21) were selected randomly. Group 1 received lactose as a placebo, and group 2 received L-arginine (twofold of daily need) as a drug for three months. We used a standard questionnaire for evaluating the effect of L-arginine on the quality of life before and after the study. Results: we did not find significant change in the quality of life of patients after using L-arginine, but the epileptic attacks decreased in L-arginine group significantly. Conclusion: L-arginine therapy is safe and can decrease the rate of seizure attacks in refractory epileptic patients, and can be an alternative of ketogenic diets. [ABSTRACT FROM AUTHOR]

Gut microbiota (GM) is a key contributor to host metabolism and physiology. Data generated on comparing diseased and healthy subjects have reported changes in the GM profile between both health states, suggesting certain bacterial composition could be involved in pathogenesis. Moreover, studies reported that reshaping of GM could contribute actively to disease recovery. Interestingly, ketogenic diets (KD) have emerged recently as new economic dietotherapeutic strategy to combat a myriad of diseases (refractory epilepsy, obesity, cancer, neurodegenerative diseases...). KD, understood in a broad sense, refers to whatever dietetic approximation, which causes physiological ketosis. Therefore, high fat-low carbs diets, fasting periods or caloric restriction constitute different strategies to produce an increase of main ketones bodies, acetoacetate and β-hydroxybutyrate, in blood. Involved biological mechanisms in ketotherapeutic effects are still to be unravelled. However, it has been pointed out that GM remodelling by KD, from now on "keto microbiota", may play a crucial role in patient response to KD treatment. In fact, germ-free animals were resistant to ketotherapeutic effects; reinforcing keto microbiota may be a powerful contributor to host disease recovery. In this review, we will comment the influence of gut microbiota on host, as well as, therapeutic potential of ketogenic diets and keto microbiota to restore health status. Current progress and limitations will be argued too. In spite of few studies have defined applicability and mechanisms of KD, in the light of results, keto microbiota might be a new useful therapeutic agent. [ABSTRACT FROM AUTHOR]

Headaches are among the most prevalent and disabling neurologic disorders and there are several unmet needs as current pharmacological options are inadequate in treating patients with chronic headache, and a growing interest focuses on nutritional approaches as non-pharmacological treatments. Among these, the largest body of evidence supports the use of the ketogenic diet (KD). Exactly 100 years ago, KD was first used to treat drug-resistant epilepsy, but subsequent applications of this diet also involved other neurological disorders. Evidence of KD effectiveness in migraine emerged in 1928, but in the last several year’s different groups of researchers and clinicians began utilizing this therapeutic option to treat patients with drug-resistant migraine, cluster headache, and/or headache comorbid with metabolic syndrome. Here we describe the existing evidence supporting the potential benefits of KDs in the management of headaches, explore the potential mechanisms of action involved in the efficacy in-depth, and synthesize results of working meetings of an Italian panel of experts on this topic. The aim of the working group was to create a clinical recommendation on indications and optimal clinical practice to treat patients with headaches using KDs. The results we present here are designed to advance the knowledge and application of KDs in the treatment of headaches.

Medical ketogenic diets (KDs) are effective yet resource-intensive treatment options for drug-resistant epilepsy (DRE). We investigated dietetic care contact time, as no recent data exist. An online survey was circulated to ketogenic dietitians in the UK and Ireland. Data were collected considering feeding route, KD variant and type of ketogenic enteral feed (KEF), and the estimated number of hours spent on patient-related activities during the patient journey. Fifteen dietitians representing nine KD centres responded. Of 335 patients, 267 (80%) were 18 years old or under. Dietitians spent a median of 162 h (IQR 54) of care contact time per patient of which a median of 48% (IQR 6) was direct contact. Most time was required for the classical KD taken orally (median 193 h; IQR 213) as a combined tube and oral intake (median 211 h; IQR 172) or a blended food KEF (median 189 h; IQR 148). Care contact time per month was higher for all KDs during the three-month initial trial compared to the two-year follow-up stage. Patients and caregivers with characteristics such as learning or language difficulties were identified as taking longer. Twelve out of fifteen (80%) respondents managed patients following the KD for more than two years, requiring an estimated median contact care time of 2 h (IQR 2) per patient per month. Ten out of fifteen (67%) reported insufficient official hours for dietetic activities. Our small survey gives insight into estimated dietetic care contact time, with potential application for KD provision and service delivery

Overactivation of the NLRP3 inflammasome is implicated in chronic low-grade inflammation associated with various disease states, including obesity, type 2 diabetes, atherosclerosis, Alzheimer's disease, and Parkinson's disease. Emerging evidence, mostly from cell and animal models of disease, supports a role for ketosis in general, and the main circulating ketone body beta-hydroxybutyrate (BHB) in particular, in reducing NLRP3 inflammasome activation to improve chronic inflammation. As a result, interventions that can induce ketosis (e.g., fasting, intermittent fasting, time-restricted feeding/eating, very low-carbohydrate high-fat ketogenic diets) and/or increase circulating BHB (e.g., exogenous ketone supplementation) have garnered increasing interest for their therapeutic potential. The purpose of the present review is to summarize our current understanding of the literature on how ketogenic interventions impact the NLRP3 inflammasome across human, rodent and cell models. Overall, there is convincing evidence that ketogenic interventions, likely acting through multiple interacting mechanisms in a cell-, disease- and context-specific manner, can reduce NLRP3 inflammasome activation. The evidence supports a direct effect of BHB, although it is important to consider the myriad of other metabolic responses to fasting or ketogenic diet interventions (e.g., elevated lipolysis, low insulin, stable glucose, negative energy balance) that may also impact innate immune responses. Future research is needed to translate promising findings from discovery science to clinical application., (© 2023 The Authors. Published by Elsevier B.V. on behalf of Chang Gung University. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).)

Background Gliomas are the most dreaded primary brain tumour because of their dismal cure rates. Ketogenic-type diets (KDS) are high-fat, low-protein, and low-carbohydrate diets; the modified Atkins diet (MAD) is a less-stringent version of a KD that still generates serum ketones in patients. The purpose of the present study was to retrospectively examine the feasibility of attaining ketosis and the safety of the mad in patients undergoing radiation and chemotherapy treatment for glioma. The rate of pseudoprogression (PSP) after treatment was also assessed as a marker of radiation sensitization. To our knowledge, this dataset is the largest published relating to patients with glioma undergoing KD during radiation and chemotherapy. Methods We retrospectively studied 29 patients with grades ii–iv astrocytoma following the MAD during standard radiation and chemotherapy. Feasibility of attaining ketosis was assessed though levels of beta hydroxybutyrate in blood. Pre- and post-radiation magnetic resonance images were evaluated for PSP by a neuroradiologist blinded to patient data. Results In the 29 patients who started the MAD during radiation, ketosis was achieved in all 29 (100%). No serious adverse events occurred secondary to the MAD. Of those 29 patients, 19 had glioblastoma multiforme. Of the latter 19 patients, 11 (58%) showed PSP after mad and radiation and temozolomide therapy. Conclusions A modified Atkins diet is feasible and safe for glioma patients during radiation and chemotherapy treatment. The MAD and resulting ketosis could play a role as a radiation sensitizer. [ABSTRACT FROM AUTHOR]

Ketogenic states are of 3 major types: total starvation and those resulting from the consumption of semistarvation, ketogenic diets, and eucaloric ketogenic diets. All are characterized by little or no dietary carbohydrate, resulting in a fat-based metabolism with sustained ketonemia of varying degrees in each state. The latter 2 diets are clinically useful with important impacts on both aspects of the energy balance equation with increased satiety and less hunger on the intake side and probably increased energy expenditure on the output side; both may have important implications for the successful long-term management of obesity. Consideration of older research regarding the hormonal response to carbohydrate-free dieting and recent findings on hepatic glycogen status that occurs with sustained ketonemia support the likelihood that there are profound differences in 24-hour gluconeogenesis rates between ketogenic diets and balanced diets containing substantial carbohydrate. This metabolic distinction could have a meaningful impact to increase the thermic effect of feeding and daily energy expenditure amounting to 100 kcal/d or more with each of the ketogenic diets. [ABSTRACT FROM AUTHOR]

The existence of a common mesenchymal cell progenitor shared by bone, skeletal muscle, and adipocytes cell progenitors, makes the role of the skeleton in energy metabolism no longer surprising. Thus, bone fragility could also be seen as a consequence of a “poor” quality in nutrition. Ketogenic diet was originally proven to be effective in epilepsy, and long-term follow-up studies on epileptic children undergoing a ketogenic diet reported an increased incidence of bone fractures and decreased bone mineral density. However, the causes of such negative impacts on bone health have to be better defined. In these subjects, the concomitant use of antiepileptic drugs and the reduced mobilization may partly explain the negative effects on bone health, but little is known about the effects of diet itself, and/or generic alterations in vitamin D and/or impaired growth factor production. Despite these remarks, clinical studies were adequately designed to investigate bone health are scarce and bone health related aspects are not included among the various metabolic pathologies positively influenced by ketogenic diets. Here, we provide not only a narrative review on this issue, but also practical advice to design and implement clinical studies on ketogenic nutritional regimens and bone health outcomes. Perspectives on ketogenic regimens, microbiota, microRNAs, and bone health are also included.

The provision or restriction of select nutrients in an athlete’s diet can elicit a variety of changes in fuel utilization, training adaptation, and performance outcomes. Furthermore, nutrient availability can also influence athlete health, with one key system of interest being iron metabolism. The aim of this review was to synthesize the current evidence examining the impact of dietary manipulations on the iron regulatory response to exercise. Specifically, we assessed the impact of both acute and chronic carbohydrate (CHO) restriction on iron metabolism, with relevance to contemporary sports nutrition approaches, including models of periodized CHO availability and ketogenic low CHO high fat diets. Additionally, we reviewed the current evidence linking poor iron status and altered hepcidin activity with low energy availability in athletes. A cohesive understanding of these interactions guides nutritional recommendations for athletes struggling to maintain healthy iron stores, and highlights future directions and knowledge gaps specific to elite athletes.