Modified Atkins Diet Research Articles

MicroRNAs as potential biomarkers of response to modified Atkins diet in treatment of adults with drug-resistant epilepsy: A proof-of-concept study

BackgroundAccurate predictors of response to modified Atkins diet (MAD) are needed. MicroRNAs are potential biomarkers in epilepsy. This study aimed to explore the value of circulating miR-146a, miR-155, miR-22, miR-21 and miR-134 levels in predicting response to MAD. MethodsPatients who completed 3 months of MAD were selected from a prospective cohort of adults with DRE followed in a specialized MAD outpatient clinic. Patients were classified as responders if any reduction in seizure frequency at follow-up, calculated through seizure-calendars). The >50 % seizure reduction cut-off was also explored. Qualitative benefits in seizures and cognition were analysed. Blood samples were collected prior to initiate MAD and microRNAs were quantified by qRT-PCR. ResultsThirty-nine patients were included (56 %males, mean age=33.1±8.5yo, 62 %focal epilepsies, 59 %structural aetiology): 20(51 %) were responders [mean reduction in seizure frequency=54 %(17–100 %); 10 had ≥50 % reduction]; 25(64 %) reported qualitative benefit in seizures and 21(54 %) reported cognitive benefits. At pre-treatment baseline, a panel combining serum levels of all studied microRNAs predicted seizure reduction (AUC=0.839, p<0.0001), qualitative benefit in seizures (AUC=0.683, p=0.048) and in cognition (AUC=0.751, p<0.01) at 3months. miR-146a was the only significant microRNA when evaluated in isolation. There was no statistical correlation in the biomarkers when a ≥50 % seizure reduction was compared to <50 %. ConclusionsA panel combining pre-treatment serum levels of miR-146a, miR-155, miR-134, miR-21 and miR-22 predicted any reduction in seizures with MAD in adults with DRE at 3months. This panel may be a promising biomarker and a useful tool in the selection of patients.

Ketogenic diet in adult patients with mitochondrial myopathy

BackgroundThis study aimed to explore the feasibility, safety and efficacy of a Modified Atkins Diet (MAD) in patients with mitochondrial myopathy (MM). MethodsPatients with genetically proven mitochondrial disorder and exercise intolerance or muscle weakness followed a twelve week MAD. Feasibility was measured by diet duration and ketone levels. Safety was assessed by monitoring adverse events (AE). Efficacy was assessed by a maximal incremental test and a muscle performance test. ResultsEight out of twenty patients completed the twelve week intervention. Reasons to discontinue were the occurrence of AE: rhabdomyolysis (n = 3), vomiting (n = 1), fatigue (n = 6), constipation (n = 1), in combination with a lack of improvement and adherence difficulties. On an individual level, various positive effects were reported including improvements in VO2peak (n = 6), anaerobic threshold (n = 9), muscle fatigue resistance (n = 5), muscle strength (n = 7), fatigue (n = 6), glucose tolerance (n = 7), migraine (n = 3), sleep (n = 3), and gastrointestinal complaints (n = 2). Lipid profile improved and thirteen patients lost weight. All patients with mitochondrial DNA (mtDNA) deletions, experienced muscle related AE. The five patients with the m.3243A>G mutation achieved the longest diet duration. Discussion/conclusionMAD feasibility, safety and efficacy is variable in MD patients. MAD appears to be unsuitable for MD patients with mtDNA deletions. All patients should be monitored closely for adverse events when initiating the diet. Further research should focus on predictive factors to consider the diet, effectiveness of less stringent carbohydrate restricted diets.

Metabolic Reprogramming via Ketogenic Diet: A Novel Approach to Combating Neurological Diseases

Epilepsy is a chronic neurological disorder characterized by a persistent tendency for the brain to generate seizures, affecting approximately 0.5–1% of the global population. Despite advances in pharmacological treatments and surgical interventions, around 30% of individuals with epilepsy continue to experience seizures, leading to significant impacts on quality of life. Among these individuals, many suffer from drug-resistant epilepsy (DRE), where seizures persist despite optimal drug therapy or surgical interventions.In recent years, the ketogenic diet (KD)—a high-fat, low-carbohydrate dietary regimen—has emerged as an effective non-pharmacological strategy for managing DRE. The KD works by inducing ketosis, a metabolic state where the body uses fat as the primary energy source instead of carbohydrates, which has been associated with neuroprotective effects and significant seizure reduction. Variants of the KD, such as the Modified Atkins Diet (MAD) and Low Glycemic Index Treatment (LGIT), offer less restrictive alternatives that have shown similar efficacy in reducing seizure frequency.This review explores the cellular and molecular mechanisms of the KD, evaluates its safety and tolerability across different age groups, and assesses its efficacy in treating epilepsy, particularly DRE. The findings underscore the potential of personalized dietary interventions to serve as effective adjunctive therapies in the management of epilepsy, offering new hope for individuals who do not respond to conventional treatments.

Oral Administration of a Novel, Synthetic Ketogenic Compound Elevates Blood β-Hydroxybutyrate Levels in Mice in Both Fasted and Fed Conditions.

Elevating ketone levels with therapeutic nutritional ketosis can help to metabolically manage disease processes associated with epilepsy, diabetes, obesity, cancer, and neurodegenerative disease. Nutritional ketosis can be achieved with various dieting strategies such as the classical ketogenic diet, the modified Atkins diet, caloric restriction, periodic fasting, or the consumption of exogenous ketogenic supplements such as medium-chain triglycerides (MCTs). However, these various strategies can be unpleasant and difficult to follow, so that achieving and sustaining nutritional ketosis can be a major challenge. Thus, investigators continue to explore the science and applications of exogenous ketone supplementation as a means to further augment the therapeutic efficacy of this metabolic therapy. Here, we describe a structurally new synthetic triglyceride, glycerol tri-acetoacetate (Gly-3AcAc), that we prepared from glycerol and an acetoacetate precursor that produces hyperketonemia in the therapeutic range (2-3 mM) when administered to mice under both fasting and non-fasting conditions. Animal studies were undertaken to evaluate the potential effects of eliciting a ketogenic response systemically. Acute effects (24 h or less) were determined in male VM/Dk mice in both fasted and unfasted dietary states. Concentration levels of β-hydroxybutyrate in blood were elevated (βHB; 2-3 mM) under both conditions. Levels of glucose were reduced only in the fasted state. No detrimental side effects were observed. Pending further study, this novel compound could potentially add to the repertoire of methods for inducing therapeutic nutritional ketosis.

9356 Occurrence Of Dyslipidemia During Modified Atkins Diet In Children With Intractable Epilepsy And Effect Of Lipid-Lowering Agents On Dyslipidemia

Abstract Disclosure: J. Yoo: None. S. Kim: None. H. Chae: None. Introduction: The Modified Atkins Diet (MAD), as a type of Ketogenic diet (KD) therapy, is utilized as a treatment for intractable epilepsy. Compared to the classic KD, it has a lower ratio of fat to carbohydrate plus protein, resulting in higher compliance among patients. Dyslipidemia is known as a major complication of KD, but when it comes to MAD, there is a scarcity of long-term studies investigating lipid level alterations in children.In this study, our objective is to examine the impact of the MAD on serum lipid levels in children and adolescents with intractable epilepsy. Method: A total of 106 patients with intractable epilepsy aged under 19 who initiated MAD from January 2016 to December 2021 and maintained MAD for a minimum of 12 months were enrolled. Laboratory test for lipid level were conducted at baseline, 1 month, 3 months, 6 months, and subsequently at 6-month intervals after initiation of MAD. The prevalence rate of dyslipidemia and lipid levles by period after MAD was analyzed. Dyslipidemia is defined as having any one of the following criteria: total cholesterol ≥200 mg/dL, LDL (Low-density lipoprotein) ≥130 mg/dL, HDL (High-density lipoprotein) &amp;lt;40 mg/dL, and triglyceride ≥100 mg/dL for children aged 0-9 and ≥130 mg/dL for adolescents aged 10-18.3. Result: The prevalence rate of total dyslipidemia observed at baseline, 1 month, 3 months, 6 months, 12 months, 18 months, 24 months, 30 months, and 36 months, were 31.1%, 67.6%, 69.5%, 68.2%, 59.5%, 60.5%, 53.7%, 47.1%, and 31.3%, respectively. When the average value and prevalence rate for each type of dyslipidemia were analyzed, total cholesterol and LDL levels showed an increase from the 1-month period compared to the baseline, peaked at the 3-month period, and gradually decreased from the 6th month with statistical significance. In the case of triglycerides, the prevalence rate of hypertriglyceridemia was highest at 3 months, but the average value was highest at 1 month with statistical significance. However, in HDL, both the average value and the prevalence rate of hypo-HDL cholesterolemia did not exhibit a significant difference over the entire period. Conclusion: MAD increases the incidence of dyslipidemia until three months after initiation, but in most cases, it tends to decrease even without treatment after six months. Presentation: 6/1/2024

The effect of the modified Atkins diet and anti-seizure medications on lipid marker levels in adults with epilepsy.

Some anti-seizure medications (ASMs) are known to induce liver enzymes and impact lipid values that include total cholesterol (TC), low density lipoprotein cholesterol (LDL), high density lipoprotein cholesterol (HDL), and triglyceride (TG). In addition, use of ketogenic diet therapies, including the modified Atkins diet (MAD), has also influenced lipids. Here, we explored the combined impact of enzyme inducing ASMs (EIASMs) and MAD on lipid values in adults with epilepsy. Diet-naïve adults with epilepsy who began MAD were divided into three groups based on ASM use: EIASMs, non-EIASMs, and those on no ASMs. Demographic information, epilepsy-specific clinical history, anthropometrics and lipid values were obtained through retrospective chart review at baseline and after a minimum of 12 months of MAD use. Forty-two adults on MAD had baseline and follow up 12-month lipid outcomes. There was a significant increase in median levels of TC, LDL, non-HDL, and HDL after 12 months of MAD use. There was no change in median levels of TG. When separated according to ASM category, adults on non-EIASMs showed significant elevations in TC, HDL, and LDL after 12 months of MAD use. In contrast, adults on EIASMs only showed a significant increase in HDL after 12 months of MAD use. The increase in atherogenic cholesterol levels observed after 12 months of MAD use was most pronounced in adults with epilepsy on non-EIASMs and not observed in adults with epilepsy on EIASMs despite a higher proportion of abnormal cholesterol levels at baseline in those on EIASMs.

Effects of Modified Atkins Diet on Neurocognitive Function in Refractory Epilepsy

ABSTRACT Background: Diet therapy is an effective intervention to manage a wide range of seizures and has a wide range of acceptance. This anti-epileptic effect of the ketogenic diet and fasting has been linked with increased ketone levels and may lead to hypoproteinemia or growth issues. The modified Atkin diet is safe and can be taken without fluid or caloric restriction. Furthermore, the patient can use unlimited protein and fat. Objective: The study finds out the effects of the modified Atkins diet on fatigue and cognitive functional status in refractory epilepsy. Materials and Methods: Twenty-seven subjects (17 males, 10 females) suffering from refractory epilepsy were recruited. The mean age range was 09–15 years. The modified Atkins diet prescribed by diet specialists was introduced. The Visual Analog Scale was used for measuring fatigue levels, and the Quality of Life in Childhood Epilepsy was used to examine the effects on life quality in epileptic patients after 16 weeks. Results: The subject’s mean age was 11.7 ± 2.02 years. They had epilepsy for about 7.8 ± 3.1 years. The seizer frequency was about 2–5 days per week. The muscle fatigue level, seizer frequency, and quality of life were improved after 16 weeks (&lt;0.05). Conclusion: The modified Atkins diet exhibits some encouraging results in refractory epilepsy patients.

Factors associated with seizure response in adults with epilepsy on a modified Atkins diet

PurposeThis study investigated factors associated with improved seizure control in adults with epilepsy following a modified Atkins diet (MAD). MethodsFollow-up data collected from participants enrolled in a prospective study between March 2016 and November 2023 was analyzed. Demographic and clinical differences between diet responders and non-responders were evaluated. MAD response was defined as ≥ 50 % reduction in seizure frequency from baseline. ResultsMAD use led to clinical response in 48 % of study participants with 2–3 month follow-up and in 56 % of study participants with 6 month follow-up. No significant differences were found for gender, age at diet initiation, age at epilepsy diagnosis, or for number of current or past medications tried. However, a significant relationship emerged between epilepsy type and diet response at 6 months with a response of 100 % seen in adults with generalized epilepsy and a response of only 42 % in adults with focal epilepsy (p = 0.004). Those who responded to the diet showed non-significant increases in many of the measured lipid biomarkers. Levels of apolipoprotein-B and small low-density lipoprotein particles showed significant increases from baseline after 3 months in responders compared to non-responders (p = 0.004 and 0.049, respectively). ConclusionsThese findings support the continued use of MAD particularly for seizure management in adults with generalized epilepsy and highlight potential mechanisms of clinical response involving lipoprotein and energy metabolism.

Modified Atkins Diet in Adolescents and Adults with Drug Resistant Epilepsy: A Systematic Review and Meta-Analysis.

Epilepsy is one of the common neurological diseases which affects 65-70 million people worldwide. Modified Atkins diet (MAD) as a therapy is used as one of the treatments to reduce the seizures occurrence in epileptic patients. The purpose of this purpose is to review all evidence regarding the efficacy of the MAD from randomized controlled trials (RCTs) in adolescents and adults with drug resistant epilepsy (DRE). The total of three databases were searched (PubMed, Embase, and Cochrane Library) till 31 January 2023. Only RCTs with MAD as a one of the treatment arms were included in meta-analysis. The proportion of reduction of seizures in patients with epilepsy and relative risk to identify the relationship between MAD (as risk) to decrease the epileptic seizure was used as outcomes. The Jadad score with three domains was used to estimate the quality of RCTs included for meta-analysis. Only three RCTs were included following the stringent inclusion criteria in current meta-analysis. The pooled proportion from 142 patients going through MAD therapy shows the reduction in epileptic seizure ≥50%, by the random effect model was 0.23 (95% confidence interval [CI], 0.10 to 0.37). Our meta-analysis underlines a significant efficacy of MAD compared to the control group in seizure reduction ≥50%, The pooled relative risk was 6.47 (95% CI, 1.60 to 26.14; p-value <0.05). MAD therapy was efficacious and had better compliance for seizure reduction in subjects with DRE.

Sequential Treatment with Modified Atkins Diet and Low Glycemic Index Treatment for Drug-Resistant Epilepsy in Children.

The present study was designed to study the efficacy of sequential dietary therapy with a modified Atkins diet (mAD) followed by low glycemic index treatment (LGIT) in treating drug-resistant epilepsy in children. This interventional study was conducted from February 2021 to February 2022 among children aged 6 months to 5 years who had failed to respond to more than two conventional and correctly chosen antiseizure medications. The primary endpoint was the proportion of good responders, that is, children with more than 50% seizure reduction. Secondary outcome measures were the proportion of children with seizure freedom, > 90% seizure reduction, and the nature of parent-reported adverse events. A total of 45 children were recruited for the study, with 6 children being lost to follow-up at 12 weeks. At 12 weeks, 30 of 39 (76.9%) children were good responders with more than 50% seizure reduction. Of these 30 children, 11 (24.4%) had more than 90% seizure reduction, with 9 (20%) achieving complete spasm freedom. Constipation was the most common side effect of the diet among the enrolled subjects. Clinicians can consider sequential dietary therapy with a mAD in the first month followed by LGIT in the next 2 months for treating children who could not tolerate mAD beyond 1 month.

Potential therapeutic effect of a ketogenic diet for the treatment of lymphoedema: Results of an exploratory study.

Lymphoedema is a chronic and progressive disease characterised by excessive accumulation of lymph in the interstitial compartment, leading to tissue swelling and fibroadipose deposition. Lymphangiogenesis is partly regulated by ketone body oxidation, and a ketogenic diet (KD) has shown therapeutic efficacy in a preclinical mouse tail lymphoedema model. Therefore, we aimed to investigate the potential therapeutic effect of a KD in patients with secondary lymphoedema. Nine patients with unilateral stage 2 lymphoedema secondary to lymphadenectomy were included in this quasi-experimental exploratory study consisting of a short run-in phase to gradually induce ketosis, followed by a classic KD (CKD) and modified Atkins diet (MAD) phase during which patients consumed a CKD and MAD, respectively. Lymphatic function and oedema volume, the primary outcomes, were assessed at baseline and at the end of both the CKD and MAD phase. Secondary outcomes included health-related and lymphedema-specific quality of life (QoL). Seven out of nine patients completed the study protocol. Lymphatic function was improved upon consumption of both a CKD (dermal backflow score [mean ± SD]: 7.29 ± 2.98 vs. 10.86 ± 2.19 at baseline; p = 0.03) and MAD (6.71 ± 2.06; p = 0.02), whereas oedema volume did not decrease during the course of the study (excess limb volume [mean ± SD]: 20.13 ± 10.25% at end of CKD and 24.07 ± 17.77% at end of MAD vs. 20.79 ± 12.96% at baseline; p > 0.99 and p > 0.30, respectively). No changes were observed in health-related, nor lymphoedema-specific QoL at the end of CKD and MAD. The consumption of a KD improved lymphatic function and was associated with a clinically meaningful reduction in oedema volume in some patients (3/7 at end of CKD, 2/7 at end of MAD) with unilateral stage 2 secondary lymphoedema. These results highlight the potential of a KD to improve lymphatic function in patients with lymphoedema. However, further studies are required to substantiate our findings.

Effect of Classic Ketogenic Diet Versus Modified Atkins Diet over Electro-Encephalogram Findings in Children with Refractory Epilepsy

ABSTRACT Introduction: Ketogenic diet (KD) is well known for control of refractory epilepsy. We wanted to study the effect of the two types of diets: classic KD and modified Atkins diet (MAD) with Indian foods to children of refractory epilepsy on electroencephalogram (EEG). Aim: To determine the effect of KD on EEG on children with refractory epilepsy. Material and Methods: Ethics Committee approval was taken for randomized controlled trials. Sixty-five children of refractory epilepsy of 6 months to 12 years’ age from two tertiary care teaching institutes, of Pune and Mumbai, were selected and allocated to one of the two types of diets, classic KD and MAD, and followed over a period of 6 months. EEG was done in the beginning, at 3 months, and at 6 months of completion of therapy with standard techniques. Observations: The relationship of EEG findings at 3 months follow-up was statistically non-significant, but at the end of 6 months, when overall improved activity on EEG was compared, it had a significant difference of P-value = 0.01, stating KD better than MAD. Conclusion: Classic KD is better than MAD.

Application and Effectiveness of Dietary Therapies for Pediatric Migraine

Migraine is a representative type of primary headache and a common chronic neurological disease that accounts for a large proportion of headaches in children, adolescents, and adults. Unlike migraine in adulthood, pediatric migraine occurs when brain development is not yet complete. This characteristic may require a new perspective for the treatment and management of pediatric migraine. Dietary therapies, mainly the ketogenic diet and its variants, can have positive effects on pediatric migraine. Several recent studies have revealed that dietary therapies, such as the classic ketogenic diet, modified Atkins diet, and low glycemic index diet, improve various neurological diseases by improving dysbiosis of microbiota, reducing proinflammatory cytokines, and increasing mitochondrial function. Nonetheless, the mechanism through which active dietary therapy affects pediatric migraine requires further research. To achieve this, an important role is played by the neuro-nutritional team, which can develop and manage tolerable diets for pediatric migraine patients through mutual collaboration among pediatric neurologists, nurses, and nutritionists.

Ketogenic Diet in the Treatment of Epilepsy.

Epilepsy is one of the most disabling neurological diseases. Despite proper pharmacotherapy and the availability of 2nd and 3rd generation antiepileptic drugs, deep brain stimulation, and surgery, up to 30-40% of epilepsy patients remain drug-resistant. Consequences of this phenomenon include not only decreased a quality of life, and cognitive, behavioral, and personal disorders, but also an increased risk of death, i.e., in the mechanism of sudden unexpected death in epilepsy patients (SUDEP). The main goals of epilepsy treatment include three basic issues: achieving the best possible seizure control, avoiding the undesired effects of treatment, and maintaining/improving the quality of patients' lives. Therefore, numerous attempts are made to offer alternative treatments for drug-resistant seizures, an example of which is the ketogenic diet. It is a long-known but rarely used dietary therapy for intractable seizures. One of the reasons for this is the unpalatability of the classic ketogenic diet, which reduces patient compliance and adherence rates. However, its antiseizure effects are often considered to be worth the effort. Until recently, the diet was considered the last-resort treatment. Currently, it is believed that a ketogenic diet should be used much earlier in patients with well-defined indications. In correctly qualified patients, seizure activity may be reduced by over 90% or even abolished for long periods after the diet is stopped. A ketogenic diet can be used in all age groups, although most of the available literature addresses pediatric epilepsy. In this article, we focus on the mechanisms of action, effectiveness, and adverse effects of different variants of the ketogenic diet, including its classic version, a medium-chain triglyceride diet, a modified Atkins diet, and a low glycemic index treatment.

Ketogenic Diet Interventions in Inborn Errors of Metabolism: A Review Article

Objective: The ketogenic diet, which has been used in the treatment of epilepsy since the 1920s, is a diet containing high fat, sufficient protein, and low carbohydrate. The ketogenic diet mimics the metabolic effects of fasting by shifting metabolism towards fat utilization. The ketogenic diet, which has different variants, such as the classical ketogenic diet, modified Atkins diet, and medium-chain triglyceride diet, is used in inborn errors of metabolism to target the underlying metabolic state by bypassing the damaged metabolic pathway or to treat the clinical symptoms of inborn errors of metabolism, such as epileptic seizures. In this review, we assessed the evidence for ketogenic diet interventions in the treatment of inborn errors of metabolism.&#x0D; Methods: The Google Scholar search engine, PubMed, Scopus, and Science Direct databases were used to find studies on the use of ketogenic diet interventions in the treatment of inborn errors of metabolism.&#x0D; Results: The beneficial effects of different variants of the ketogenic diet on glucose transport type 1 deficiency syndrome and pyruvate dehydrogenase complex deficiency have long been recognized. There are also favorable data on its use in myopathic glycogen storage diseases, mitochondrial diseases, and nonketotic hyperglycinemia accompanied by epilepsy.&#x0D; Conclusion: The evidence is mostly based on individual case reports, case series, and clinical trials with small sample sizes and is insufficient to make recommendations.

A randomized feasibility trial of the modified Atkins diet in older adults with mild cognitive impairment due to Alzheimer's disease.

Alzheimer's disease (AD) is increasing in prevalence, but effective treatments for its cognitive impairment remain severely limited. This study investigates the impact of ketone body production through dietary manipulation on memory in persons with mild cognitive impairment due to early AD and explores potential mechanisms of action. We conducted a 12-week, parallel-group, controlled feasibility trial of a ketogenic diet, the modified Atkins diet (MAD), compared to a control diet in patients with cognitive impairments attributed to AD. We administered neuropsychological assessments, including memory tests, and collected blood samples at baseline and after 12 weeks of intervention. We performed untargeted lipidomic and targeted metabolomic analyses on plasma samples to detect changes over time. A total of 839 individuals were screened to yield 38 randomized participants, with 20 assigned to receive MAD and 18 assigned to receive a control diet. Due to attrition, only 13 in the MAD arm and nine in the control arm were assessed for the primary endpoint, with two participants meeting ketosis levels used to define MAD adherence criteria. The average change from baseline in the Memory Composite Score was 1.37 (95% CI: -0.87, 4.90) points higher in the MAD group compared to the control group. The effect size of the intervention on baseline MAD change was moderate (Cohen's D = 0.57, 95% CI: -0.67, 1.33). In the 15 participants (nine MAD, six control) assessed for lipidomic and metabolomic-lipidomics and metabolomics, 13 metabolites and 10 lipids showed significant changes from baseline to 12 weeks, including triacylglycerols (TAGs, 50:5, 52:5, and 52:6), sphingomyelins (SM, 44:3, 46:0, 46:3, and 48:1), acetoacetate, fatty acylcarnitines, glycerol-3-phosphate, and hydroxy fatty acids. Attrition was greatest between baseline and week 6. All participants retained at week 6 completed the study. Despite low rates of adherence by criteria defined a priori, lipidomic and metabolomic analyses indicate significant changes from baseline in circulating lipids and metabolites between MAD and control participants at 12-week postrandomization, and MAD participants showed greater, albeit nonsignificant, improvement in memory.

Efficacy and cognitive impact of modified Atkins diet in adults with drug-resistant epilepsy

This study aims to explore the efficacy and cognitive impact of the modified Atkins diet (MAD) in adults with drug-resistant epilepsy, as well as to analyze changes in epileptiform activity during ketogenic diet (KD) intervention. We performed a prospective, open-label study with patients aged 16 &amp;ndash; 60 years who met the International League Against Epilepsy (ILAE) criteria for drug-resistant epilepsy. Sixteen patients were enrolled in this study, and baseline clinical and electroencephalography (EEG) characteristics, along with neuropsychological tests, were collected before and after 3 months of KD. Patients were divided into responders (&amp;ge;50% seizure reduction) and non-responders (&lt;50% seizure reduction) according to the clinical efficacy of the KD. Results indicate that 37.5% of patients reported a &amp;ge;50% seizure reduction after 3 months. In terms of safety, 37.5% of patients reported adverse effects, including constipation, abdominal pain, and nausea. In addition, a statistically significant increase in the level of total cholesterol was observed (P = 0.037) after diet treatment. Regarding cognitive impact, there was a significant improvement in auditory verbal learning test (AVLT) instant recall scale scores (P = 0.017). In terms of EEG characteristics, MAD significantly reduces interictal epileptic discharge (IED) index in non-rapid eye movement 2 (NREM2) after 3 months. No clinical predictors or EEG characteristics of MAD efficacy were identified. In conclusion, MAD can be safely and effectively practiced by adults with drug-resistant epilepsy. KD treatment has a significant impact on AVLT instant recall and can reduce the IED index in NREM2.

The impact of ketogenic diet on drug-resistant epilepsy in children: A comprehensive review and meta-analysis.

The ketogenic diet (KD), characterized by high-fat and low-carbohydrate intake, is currently gaining widespread popularity as a treatment for drug-resistant epilepsy (DRE). In addition to the traditional ketogenic diet, several variants have been introduced to enhance compliance and flexibility, such as the modified Atkins diet (MAD) and the low glycemic index diet (LGID). These adaptations aim to provide patients with more manageable and sustainable options while harnessing the potential therapeutic benefits of DRE. The objective of this study is to evaluate the efficacy and safety of the KD in pediatric patients who exhibit DRE. In this study, we conducted a thorough review of existing literature by searching Cochrane, Embase, Medline, and PubMed. Our approach involved predefined criteria for data extraction and the assessment of study quality. Eleven RCTs with 788 participants were included in this study. The pooled effect estimates revealed a significant association between dietary interventions and seizure frequency reduction of > 50% (OR 6.68, 96% CI 3.52, 12.67) and > 90% (OR 4.37, 95% CI 2.04, 9.37). Dietary interventions also increased the odds of achieving seizure freedom (OR 4.13, 95% CI 1.61, 10.60). The common adverse effects included constipation (39.07%) and vomiting (10%). In conclusion, dietary interventions, notably the KD, hold promise for pediatric DRE, reducing seizures and achieving freedom. These non-pharmacological options improve the quality of life of non-responsive and non-surgical patients. The KD has emerged as a potential therapeutic approach. Further research is needed to address the limitations and investigate their long-term effects.

Hypocarnitinemia and its effect on seizure control in adult patients with intractable epilepsy on the modified Atkins diet.

Previous studies have demonstrated the safety and efficacy of the modified Atkins diet (MAD) in attenuating seizures in patients with intractable epilepsy. MAD works by achieving ketosis, which is heavily dependent on the metabolic compound, carnitine, to facilitate the transport of long-chain fatty acids across the mitochondria for beta-oxidation. The effect of carnitine on ketogenic diet therapy is not well-defined in the current literature. Thus, the purpose of our study is to investigate the effects of hypocarnitinemia on the efficacy of MAD. A retrospective chart review was conducted, and 58 adults with epilepsy undergoing MAD were evaluated. Generalized linear mixed effects models were used to compare the low carnitine status with normal carnitine group in patient measures of body mass index, seizure frequency and severity, number of anti-seizure medications, beta-hydroxybutyrate, triglyceride, and carnitine levels across baseline, 3-9-month follow-up (timepoint 1), 1-2-year follow-up (timepoint 2), and 2+ year follow-up (timepoint 3). Our study revealed that 38.3% of adult patients with epilepsy following MAD experienced low free carnitine at some point through the course of diet therapy. Patients with hypocarnitinemia at timepoint 2 showed a significant percent seizure increase while seizures continued to decrease in the normal carnitine group. Fasting triglyceride levels at timepoint 1 were significantly increased in the low carnitine group compared to normal carnitine group. Change in BHB, BMI, seizure severity, and number of ASMs showcased no significant differences between the low and normal carnitine groups. It may be important for clinicians to monitor for hypocarnitinemia in adults on MAD and provide carnitine supplementation when low. Further investigations into carnitine and MAD may inform clinical decisions on carnitine supplementation to maximize the efficacy of MAD therapy.

The Effectiveness of Modified Atkins Ketogenic Diet on Children with Intractable Epilepsy: A Pilot Study from Indonesia.

The ketogenic diet has recently been explored as a potential treatment approach for intractable epilepsy in children and has been applied in various parts of the world. The ketogenic diet is also effective for the treatment of mood disorders, especially for adolescent and young adults with epilepsy. The Modified Atkins Diet (MAD) is the less restrictive type of ketogenic diet with similar principles as the classic type. However, no study has been conducted to evaluate the use of MAD in children with severe epilepsy in Indonesia. This study aims to assess the effectiveness, tolerance, compliance, and the adverse effects of MAD in children with intractable epilepsy during a 6-month monitoring period. This is a pilot experimental study involving children aged 2-18 years old with intractable epilepsy at the Pediatric Neurology and the Pediatric Nutrition & Metabolic Diseases Clinics at the Dr. Cipto Mangunkusumo Hospital Jakarta between November 2021 and June 2022. A total of 31 subjects met the inclusion criteria and received the MAD in the first month, followed by 13 (41.9%) subjects in the third month, and 9 (29%) subjects in the sixth month. The MAD reduced the seizure frequency by 50% (p = 0.144), 62% (p = 0.221), and 83.3% (p = 0.028) in the first, third, and sixth months, respectively. The most frequent adverse effects are vomiting and diarrhea. Noncompliance was observed in 18 (58.1%) subjects. A sample of the MAD food menu guidebook was developed to make it easier for parents to adhere to the diet. The MAD reduces the mean seizure frequency in children with intractable epilepsy in the first, third, and sixth months, with a statistical significance in the sixth month. A further randomized, controlled, and multicenter clinical trial with a larger sample size and longer observation period is required. This trial is registered with Protocol ID 20-10-1323.