Ketogenic Diet Research Articles

Epithelial-mesenchymal transition-related signaling pathways in gastric Cancer cells distinctively respond to long-term experimental ketosis.

The interrelationship between cellular metabolism and the epithelial-to-mesenchymal transition (EMT) process has made it an interesting topic to investigate the adjuvant effect of therapeutic diets in the treatment of cancers. However, the findings are controversial. In this study, the effects of glucose limitation along and with the addition of beta-hydroxybutyrate (bHB) were examined on the expression of specific genes and proteins of EMT, Wnt, Hedgehog, and Hippo signaling pathways, and also on cellular behavior of gastric cancer stem-like (MKN-45) and non-stem-like (KATO III) cells. The expression levels of chosen genes and proteins studied in cancer cells gradually adopted a low-glucose condition of one-fourth, along and with the addition of bHB, and compared to the unconditioned control cells. The long-term switching of the metabolic fuels successfully altered the expression profiles and behaviors of both gastric cancer cells. However, the results for some changes were the opposite. Glucose limitation along and with the addition of bHB reduced the CD44+ population in MKN-45 cells. In KATO III cells, glucose restriction increased the CD44+ population. Glucose deprivation alleviated EMT-related signaling pathways in MKN-45 cells but stimulated EMT in KATO III cells. Interestingly, bHB enrichment reduced the beneficial effect of glucose starvation in MKN-45 cells, but also alleviated the adverse effects of glucose restriction in KATO III cells. The findings of this research clearly showed that some controversial results in clinical trials for ketogenic diet in cancer patients stemmed from the different signaling responses of various cells to the metabolic changes in a heterogeneous cancer mass.

Triheptanoin Did Not Show Benefit versus Placebo for the Treatment of Paroxysmal Movement Disorders in Glut1 Deficiency Syndrome: Results of a Randomized Phase 3 Study.

Paroxysmal movement disorders are common in Glut1 deficiency syndrome (Glut1DS). Not all patients respond to or tolerate ketogenic diets. The objective was to evaluate the effectiveness and safety of triheptanoin in reducing the frequency of disabling movement disorders in patients with Glut1DS not receiving a ketogenic diet. UX007G-CL301 was a randomized, double-blind, placebo-controlled, phase 3 crossover study. After a 6-week run-in, eligible patients were randomized 1:1 to the first sequence (triheptanoin/placebo or placebo/triheptanoin) titration plus maintenance, followed by washout and the opposite sequence titration plus maintenance. The placebo (safflower oil) matched the appearance, taste, and smell of triheptanoin. Open-label triheptanoin was administered in the extension. The frequency of disabling paroxysmal movement disorder events per 4 weeks (recorded by diary during maintenance; primary endpoint) was assessed by Wilcoxon rank-sum test. Forty-three patients (children, n = 16; adults, n = 27) were randomized and treated. There was no difference between triheptanoin and placebo in the mean (interquartile range) number of disabling paroxysmal movement disorder events (14.3 [4.7-38.3] vs. 11.8; [3.2-28.7]; Hodges-Lehmann estimated median difference: 1.46; 95% confidence interval, -1.12 to 4.36; P = 0.2684). Treatment-emergent adverse events were mild/moderate in severity and included diarrhea, vomiting, upper abdominal pain, headache, and nausea. Two patients discontinued the study because of non-serious adverse events that were predominantly gastrointestinal. The study was closed early during the open-label extension because of lack of effectiveness. Seven patients continued to receive triheptanoin compassionately. There were no significant differences between the triheptanoin and placebo groups in the frequency of disabling movement disorder events during the double-blind maintenance period. © 2024 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Gender Differences in Liver Steatosis and Fibrosis in Overweight and Obese Patients with Metabolic Dysfunction-Associated Steatotic Liver Disease before and after 8 Weeks of Very Low-Calorie Ketogenic Diet

Obesity and metabolic syndrome are linked to steatotic liver disease (SLD), the most common form of chronic liver disease. Lifestyle modifications and dieting are strategies that can prevent metabolic dysfunction-associated steatotic liver disease (MASLD). The very low-calorie ketogenic diet (VLCKD) is a helpful treatment for MASLD and has been recommended for people affected by obesity; we evaluated the effect of gender on steatosis and fibrosis in a cohort of 112 overweight or obese patients undergoing an eight-week treatment with a VLCKD. Differences between the genders in terms of anthropometric measures, body composition, and metabolic indicators were examined before, during, and after the nutritional intervention. At baseline, there were significant differences between men and women in terms of anthropometric parameters, blood pressure, Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), fasting insulin, hepatic markers, and lipid profile. Men had considerably higher levels of liver steatosis (measured by CAP) and liver stiffness (measured by E) under basal conditions than women. After the VLCKD, there were reductions in both genders of controlled attenuation parameter (CAP), body weight, body mass index (BMI), waist circumference, systolic and diastolic blood pressure, insulin resistance, fat mass (FM), free fat mass (FFM), and fasting blood glucose, insulin, glycated hemoglobin (HbA1c), triglycerides, total cholesterol, low-density lipoprotein (LDL) cholesterol, alanine transaminase (ALT), gamma-glutamyl transferase (γGT), and uric acid levels. Only in men, liver stiffness, aspartate aminotransferase (AST), creatinine, and C-reactive protein (CRP) levels significantly decreased. Moreover, men had significantly greater levels of liver steatosis: the male gender featured an increase of 23.96 points of the Fibroscan CAP. Men exhibited higher levels of steatosis and fibrosis than women, and these differences persist despite VLCKD. These gender-specific variations in steatosis and fibrosis levels could be caused by hormonal and metabolic factors, suggesting that different therapeutic strategies might be required depending on the gender.

Ketogenic Diet Induced Shifts in the Gut Microbiome Associate with Changes to Inflammatory Cytokines and Brain-Related miRNAs in Children with Autism Spectrum Disorder

In this interventional pilot study, we investigated the effects of a modified ketogenic diet (KD) on children with autism spectrum disorder (ASD). We previously observed improved behavioral symptoms in this cohort following the KD; this trial was registered with Clinicaltrials.gov (NCT02477904). This report details the alterations observed in the microbiota, inflammation markers, and microRNAs of seven children following a KD for a duration of 4 months. Our analysis included blood and stool samples, collected before and after the KD. After 4 months follow up, we found that the KD led to decreased plasma levels of proinflammatory cytokines (IL-12p70 and IL-1b) and brain-derived neurotrophic factor (BDNF). Additionally, we observed changes in the gut microbiome, increased expression of butyrate kinase in the gut, and altered levels of BDNF-associated miRNAs in the plasma. These cohort findings suggest that the KD may positively influence ASD sociability, as previously observed, by reducing inflammation, reversing gut microbial dysbiosis, and impacting the BDNF pathway related to brain activity.

Acetoacetate and D- and L-β-hydroxybutyrate have distinct effects on basal and insulin-stimulated glucose uptake in L6 skeletal muscle cells.

Ketone bodies (acetoacetate and β-hydroxybutyrate) are oxidized in skeletal muscle mainly during fasting as an alternative source of energy to glucose. Prior studies suggest that there is a negative relationship between increased muscle ketolysis and muscle glucose metabolism in mice with obesity and/or type 2 diabetes. Therefore, we investigated the connection between increased ketone body exposure and muscle glucose metabolism by measuring the effect of a 3-hour exposure to ketone bodies on glucose uptake in differentiated L6 myotubes. We showed that exposure to acetoacetate at a typical concentration (0.2 mM) resulted in increased basal glucose uptake in L6 myotubes, which was dependent on increased membrane GLUT4 translocation. Basal and insulin-stimulated glucose uptake was also increased with a concentration of acetoacetate reflective of diabetic ketoacidosis or a ketogenic diet (1 mM). We found that β-hydroxybutyrate had a variable effect on basal glucose uptake, in that a racemic mixture of the two β-hydroxybutyrate enantiomers (D and L) appeared to decrease basal glucose uptake, while 3 mM D-β-hydroxybutyrate alone increased basal glucose uptake. However, the effects of the ketone bodies individually were not observed when acetoacetate was present in combination with β-hydroxybutyrate. These results provide insight that will help elucidate the effect of ketone bodies in the context of specific metabolic diseases and nutritional states (e.g., type 2 diabetes and ketogenic diets).

A ketogenic diet as feasible treatment for post bariatric weight regain

A ketogenic diet as feasible treatment for post bariatric weight regain

Ketogenic diet (KD) as a nutritional therapeutical option for women suffering from polycystic ovary syndrome

Ketogenic diet (KD) as a nutritional therapeutical option for women suffering from polycystic ovary syndrome

Remission of type 2 diabetes: opportunities of different nutrition styles

Last time there are a lot of date, published systematic reviews and meta-analyses about relationship between eating behavior and incidence type 2 diabetes. It is known that more than 80% of cases of type 2 diabetes are associated with obesity. In this regard, the nutritional factor is of particular importance in the formation of treatment goals for patients with type 2 diabetes. Today, the disease is no longer a sentence, because achieving remission of type 2 diabetes is possible with the help of nutritional correction. The results of studies shown that a significant decrease in body weight is a predictor of remission of type 2 diabetes. However, the question of the best dietary recommendations for patients with type 2 diabetes remains open. Various dietary patterns (Mediterranean, paleo diet, DASH system, etc.) contribute to the improvement of glycemia, however, there is not enough data indicating a regression of symptoms of type 2 diabetes. In all likelihood, achieving remission is possible only with a significant reduction in daily caloric intake. The ketogenic diet, especially popular in recent times, also improves glycemic control. At the same time, according to the results of a meta-analysis, carbohydrates from whole grains and cereal fibers should not be neglected, because this category of products helps reduce the risk of developing diabetes.

The effect of ketogenic diet versus mediterranean diet on clinical and biochemical markers of inflammation in patients with obesity and psoriatic arthritis

The effect of ketogenic diet versus mediterranean diet on clinical and biochemical markers of inflammation in patients with obesity and psoriatic arthritis

Evaluating the impact of a moderately low-calorie ketogenic diet on mafld in patients with obesity: the role of magnetic resonance imaging

Evaluating the impact of a moderately low-calorie ketogenic diet on mafld in patients with obesity: the role of magnetic resonance imaging

Ketone Bodies after Cardiac Arrest: A Narrative Review and the Rationale for Use.

Cardiac arrest survivors suffer the repercussions of anoxic brain injury, a critical factor influencing long-term prognosis. This injury is characterised by profound and enduring metabolic impairment. Ketone bodies, an alternative energetic resource in physiological states such as exercise, fasting, and extended starvation, are avidly taken up and used by the brain. Both the ketogenic diet and exogenous ketone supplementation have been associated with neuroprotective effects across a spectrum of conditions. These include refractory epilepsy, neurodegenerative disorders, cognitive impairment, focal cerebral ischemia, and traumatic brain injuries. Beyond this, ketone bodies possess a plethora of attributes that appear to be particularly favourable after cardiac arrest. These encompass anti-inflammatory effects, the attenuation of oxidative stress, the improvement of mitochondrial function, a glucose-sparing effect, and the enhancement of cardiac function. The aim of this manuscript is to appraise pertinent scientific literature on the topic through a narrative review. We aim to encapsulate the existing evidence and underscore the potential therapeutic value of ketone bodies in the context of cardiac arrest to provide a rationale for their use in forthcoming translational research efforts.

Reappraisal of Traditional Persian Medicine in the Treatment of Epilepsy and Seizure

Reappraisal of Traditional Persian Medicine in the Treatment of Epilepsy and Seizure

Abstract PO3-02-03: Ketogenic diet and letrozole to inhibit PI3K signaling in ER+ breast cancer

Abstract Obesity is associated with an increased risk of breast cancer recurrence, similar in magnitude to the reduction in risk seen with the use of adjuvant chemotherapy. However, whether and how obesity causes that increased risk of recurrence remains unknown. Plausible mechanisms include obesity-mediated increases in estrogen signaling, inflammatory conditions resulting from obesity, or effects on insulin or other growth factor signaling pathways resulting from the insulin-resistant state that often accompanies obesity. While phosphatidyl inositol 3-kinase (PI3K) signaling is the normal, biological effector of insulin signaling, abnormal activation of PI3K is of particular concern in breast cancer, where it is associated with resistance to endocrine therapies and HER2-targeted therapies. We hypothesize that at least part of the adverse outcome associated with obesity results from aberrant activation of PI3K signaling in tumors. This may confer resistance to established therapies, or directly stimulate tumor growth (particularly in tumors with existing PI3K pathway mutations), or both. We tested a dietary intervention designed to alter insulin resistance pathophysiology coupled with endocrine therapy in the well-established neoadjuvant treatment paradigm in breast cancer. This will allow us to study the effects of the dietary intervention directly on tumor biology. The primary objective of this neoadjuvant study was to assess feasibility and tolerability of 2 weeks of a very low-carbohydrate ketogenic diet in combination with letrozole for patients with early stage operable ER+ disease. Up to 36 patients will be enrolled for this pilot and feasibility study (24 in the treatment group and 12 controls). Baseline metabolic parameters will be measured and the treatment group will begin a dietitian-supervised 2-week diet to induce a ketogenic state, along with letrozole 2.5 mg daily. The control group will receive only letrozole. At the end of 2 weeks, patients will proceed with surgical treatment of their breast cancer. We will report the primary outcome measure of feasibility, assessed by determining 1) the proportion of patients in the diet group achieving ketosis, 2) adherence to the diet and 3) participant-reported measures of stress, fatigue, and emotional health. For both groups, cell proliferation will be measured in a tumor biopsy obtained from the surgical specimen and compared with the pre-treatment diagnostic biopsy. Correlative studies will evaluate tumor markers of insulin/PI3K signaling before and after the intervention and between diet and control. Citation Format: Brent Rexer, Vandana Abramson, Sara Nunnery, Sonya Reid, Laura Kennedy, Melinda Sanders, Jessica Bennett, Paula Gonzalez-Ericsson, Violeta Sanchez. Ketogenic diet and letrozole to inhibit PI3K signaling in ER+ breast cancer [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO3-02-03.

A very-low-calorie ketogenic diet normalises obesity-related enhanced levels of erythropoietin compared with a low-calorie diet or bariatric surgery.

Nutritional ketosis synergistically with body-weight loss induced by a very-low-calorie ketogenic diet (VLCKD) has proven to be effective in improving obesity-related pathophysiology. Recently, growing attention has been focused on the relation between erythropoietin (EPO) and obesity. Thus, this study aims to investigate whether nutritional ketosis and weight loss induced by a VLCKD modify the circulating levels of EPO in patients with obesity in comparison with the effect of low-calorie diet (LCD) or bariatric surgery (BS). EPO levels, iron status and body composition parameters were evaluated in 72 patients with overweight or obesity and 27 normal-weight subjects at baseline and after the three different weight-reduction therapies (VLCKD, LCD and BS) in 69 patients with excess body weight. β-hydroxybutyrate levels were also measured in the VLCKD group. The follow-up was established at 2-3months and 4-6months. It was found that EPO levels were higher in morbid obesity and correlated with higher basal weight, fat mass (FM) and fat-free mass (FFM) in the overall sample. High baseline EPO levels were also correlated with higher impact on the course of weight loss and changes in FM and FFM induced by the three weight-loss interventions. Furthermore, the VLCKD induced a decrease in EPO levels coinciding with maximum ketosis, which was maintained over time, while statistically significant changes were not observed after LCD and BS. The obesity-related increased EPO levels are restored after VLCKD intervention at the time of maximum ketosis, suggesting a potential role of the nutritional ketosis induced by the VLCKD. Baseline EPO levels could be a biomarker of response to a weight-loss therapy.

Abstract PO5-12-02: Landscape analysis of oncology nutrition research among patients being treated for breast cancer

Abstract The American Institute for Cancer Research/World Cancer Research Fund and the American Cancer Society regularly conduct systematic reviews on the evidence supporting nutrition interventions during cancer treatment. These reviews have found that the evidence to support clinical oncology nutrition practice guidelines is limited. It is unclear how many oncology nutrition studies are currently being conducted, especially among patients being treated for breast cancer. The goal of this project was to conduct a landscape analysis of nutrition research being conducted among breast cancer patients over the past 10 years. Methods: This analysis was part of a larger effort to describe the oncology nutrition research landscape for all cancer sites. Searches of ClinicalTrials.gov were performed on 1/8/2023 using the following search terms/combinations: “cancer AND nutrition”, “cancer nutrition”, “oncology AND nutrition”, “diet AND cancer”, “cancer, oncology, neoplasms, nutrition, diet”. Search results were downloaded as .csv files and uploaded to RStudio for merging and data cleaning (elimination of duplicates, and exclusion of studies registered in ClinicalTrials.gov before 1/1/2013 or after 12/31/2022). The resulting harmonized dataset was then uploaded to REDCap, and each entry was reviewed for eligibility by one of the authors. To be included in this landscape analysis, studies must have included data collection from patients who were actively receiving cancer treatment at the time of the study and the study had to be first posted to ClinicalTrials.gov between 1/1/2013 and 12/31/2022. Studies were excluded if they: 1) focused on the role of diet in primary cancer prevention, 2) focused on cancer survivors who had completed primary treatment for their cancers. Following eligibility review, the study datafile was returned to RStudio for further cleaning and analysis. Results: The initial ClinicalTrials.gov search identified 4,345 unique study listings. After review, 1,267 studies met the inclusion criteria, of which 132 (10.4%) studies were specific to breast cancer (117 intervention studies and 15 observational studies). Among breast cancer studies, reasons for exclusion were: study focused on diet/nutrition in the prevention of a primary cancer diagnosis (n=40), study participants had already completed their cancer treatment (n=128), study did not include a diet/nutrition intervention or assessment (n=31). The largest number of breast cancer specific studies were based in the United States (n=55, 41.6%), Italy (n=11, 8.3%), France (n=10, 7.6%) and Canada (n=9, 6.8%). Dietary supplement interventions were the most common type of intervention (n=50 studies, 42.7%), followed by behavior change interventions (n=22, 18.8%), diet in relation to a drug intervention (n=25, 21.4%), diet in relation to a device/procedure/radiation intervention (n=16, 14%), fasting/time-restricted feeding studies (n=13, 11.1%) and ketogenic diet interventions (n=3, 2.6%). Changes in weight or body composition (n=52, 39.4%), quality of life (n=45, 34.1%), adverse events (n=24, 18.2%), survival (n=20, 15,2%) and fatigue (n=17, 12.9%) were the most common outcome measures. Sixteen (12.1%) studies were supported by NIH funding and 9 (6.8%) studies were industry funded, although the majority (n=124, 93.9%) reported funding from “other” sources. Of the 41 studies that started between 2013-2017 (five years prior to the January 2023 ClinicalTrials.gov search), only 21 (51.2%) were listed as being “completed” and of those, only 7 were listed as “has results”. Conclusion: More research is needed to support evidence-based supportive care guidelines for oncology nutrition interventions during breast cancer treatment. Efforts should be made to support researchers in completing studies and disseminating research findings. Citation Format: Kim Robien, Heather Wopat. Landscape analysis of oncology nutrition research among patients being treated for breast cancer [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO5-12-02.

The effects of ketogenic diet on brain gene expressions in type 2 diabetes background

Type 2 diabetes mellitus (T2DM) is a major risk factor of a number of neurodegenerative diseases (NDDs). Ketogenic diet (KD) has significant beneficial effects on glycemic control and may act effectively against NDDs, but the mechanism remains unclear. In this study, we aimed to investigate the potential effects of KD on gene expressions in the brains of T2DM model mice. Male db/db mice at the age of 9 weeks were fed with KD or normal diet to the age of 6 months, and the whole brains were subjected to mRNA-seq analysis for differentially expressed genes. KD significantly lowered fasting glucose and body weights in db/db mice (P<0.05), and the expression of 189 genes in the brain were significantly changed (P<0.05, |log2|>1). Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses revealed that the differentially expressed genes upon KD are involved in inflammatory responses and the functions of biosynthesis. In inflammatory responses, NF-κB signaling pathway, viral protein interaction with cytokine and cytokine receptor, and cytokine-cytokine receptor interaction pathways were enriched, and in biosynthesis pathways, genes functioning in lipid and amino acid metabolism, protein synthesis, and energy metabolism were enriched. Moreover, consistent with the gene set enrichment analysis results, proteasomal activity measured biochemically were enhanced in KD-fed T2DM mice. These data may facilitate the understanding of how KD can be protective to the brain in T2DM background. KD could be a new strategy for the prevention of NDDs in T2DM patients.

The ketogenic diet does not improve cardiac function and blunts glucose oxidation in ischemic heart failure.

Cardiac energy metabolism is perturbed in ischemic heart failure and is characterized by a shift from mitochondrial oxidative metabolism to glycolysis. Notably, the failing heart relies more on ketones for energy than a healthy heart, an adaptive mechanism that improves the energy-starved status of the failing heart. However, whether this can be implemented therapeutically remains unknown. Therefore, our aim was to determine if increasing ketone delivery to the heart via a ketogenic diet can improve the outcomes of heart failure. C57BL/6J male mice underwent either a sham surgery or permanent left anterior descending (LAD) coronary artery ligation surgery to induce heart failure. After 2 weeks, mice were then treated with either a control diet or a ketogenic diet for 3 weeks. Transthoracic echocardiography was then carried out to assess in vivo cardiac function and structure. Finally, isolated working hearts from these mice were perfused with appropriately 3H or 14C labelled glucose (5 mM), palmitate (0.8 mM), and ß-hydroxybutyrate (0.6 mM) to assess mitochondrial oxidative metabolism and glycolysis. Mice with heart failure exhibited a 56% drop in ejection fraction which was not improved with a ketogenic diet feeding. Interestingly, mice fed a ketogenic diet had marked decreases in cardiac glucose oxidation rates. Despite increasing blood ketone levels, cardiac ketone oxidation rates did not increase, probably due to a decreased expression of key ketone oxidation enzymes. Furthermore, in mice on the ketogenic diet no increase in overall cardiac energy production was observed, and instead there was a shift to an increased reliance on fatty acid oxidation as a source of cardiac energy production. This resulted in a decrease in cardiac efficiency in heart failure mice fed a ketogenic diet. We conclude that the ketogenic diet does not improve heart function in failing hearts, due to ketogenic diet-induced excessive fatty acid oxidation in the ischemic heart and a decrease in insulin-stimulated glucose oxidation.

Dietary intervention in acne management: review of the literature and future prospective

Acne is a common skin disease, affecting millions of subjects worldwide. Several processes and mechanisms have been identified in acne pathogenesis. Among these, it is known that acne or its worsening is also related to metabolic factors and nutritional influences. In this scenario, we carried out a review of the current literature in order to investigate the role of diet in acne disease, offering a wide perspective for possible clinical applications. A total of 55 manuscripts were considered. In particular, the role of the Western diet, glycemic index, glycemic load, dairy products, fats, fatty acids, Mediterranean diet, ketogenic diet, and dietary supplements in acne management has been investigated. On one hand, dairy products, foods with high glycemic load and glycemic index, fatty acids and fats seem to worsen the severity; on the other hand, Mediterranean and ketogenic diet, and oral supplements seem to improve the disease. Despite the conflicting results and conclusions in the scientific literature about the impact of nutrition in acne, mainly related to the severla limitations of the study design, several prospective, controlled, well-designed studies have recently demonstrated the role of some specific nutrition influenced mediators on acne severity.

ESPEN Guideline on Nutrition and Hydration in Dementia – Update 2024

Background & aimsDementia is accompanied by a variety of changes that result in an increased risk of malnutrition and low-intake dehydration. This guideline update aims to give evidence-based recommendations for nutritional care of persons with dementia in order to prevent and treat these syndromes. MethodsThe previous guideline version was reviewed and expanded in accordance with the standard operating procedure for ESPEN guidelines. Based on a systematic search in three databases, strength of evidence of appropriate literature was graded by use of the SIGN system. The original recommendations were reviewed and reformulated, and new recommendations were added, which all then underwent a consensus process. Results40 recommendations for nutritional care of older persons with dementia were developed and agreed, seven at institutional level and 33 at individual level. As a prerequisite for good nutritional care, organizations caring for persons with dementia are recommended to employ sufficient qualified staff and offer attractive food and drinks with choice in a functional and appealing environment. Nutritional care should be based on a written care concept with standardized operating procedures. At the individual level, routine screening for malnutrition and dehydration, nutritional assessment and close monitoring are unquestionable. Oral nutrition may be supported by eliminating potential causes of malnutrition and dehydration, and adequate social and nursing support (including assistance, utensils, training and oral care). Oral nutritional supplements are recommended to improve nutritional status but not to correct cognitive impairment or prevent cognitive decline. Routine use of dementia-specific ONS, ketogenic diet, omega-3 fatty acid supplementation and appetite stimulating agents is not recommended. Enteral and parenteral nutrition and hydration are temporary options in patients with mild or moderate dementia, but not in severe dementia or in the terminal phase of life. In all stages of the disease, supporting food and drink intake and maintaining or improving nutrition and hydration status requires an individualized, comprehensive approach. Due to a lack of appropriate studies, most recommendations are good practice points. ConclusionNutritional care should be an integral part of dementia management. Numerous interventions are available that should be implemented in daily practice. Future high-quality studies are needed to clarify the evidence.

Opinion: Are mental health benefits of the ketogenic diet accompanied by an increased risk of cardiovascular disease?

Opinion: Are mental health benefits of the ketogenic diet accompanied by an increased risk of cardiovascular disease?