2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T77b,Crohn's disease (CD) is characterized by epithelial barrier dysfunction and mucosal immune dysregulation. Dietary interventions have gained increasing attention as important therapeutic strategies. We evaluated whether an intermittent ketogenic diet (IKD), which elevates β-hydroxybutyrate (BHB), ameliorates CD via lysine β-hydroxybutyrylation (Kbhb) and elucidated the underlying mechanisms. IL-10 knockout mice were allocated to three groups: continuous KD (ketogenic diet), IKD, or a normal diet. Disease activity index (DAI), histopathological changes, cytokine levels, and epithelial barrier integrity were evaluated. Regulatory T cells (Tregs) and Foxp3 expression were assessed by flow cytometry and quantitative real-time PCR (qRT-PCR). To elucidate the underlying mechanisms, we conducted metabolomic and transcriptomic analyses, pyrosequencing, and additional experiments. Both KD and IKD alleviated colonic inflammation, but IKD better prevented epithelial senescence. IKD increased colonic Treg infiltration and Foxp3 expression. Metabolomics revealed elevated BHB in IKD colons. BHB reduced inflammation and promoted Treg differentiation in a dose-dependent manner. Mechanistically, BHB induced Kbhb of S-adenosylhomocysteine hydrolase (AHCY), inhibiting its activity, leading to S-adenosylhomocysteine (SAH) accumulation, downregulating DNA methyltransferase 1 (DNMT1), and promoting Foxp3-TSDR demethylation to enhance Foxp3 transcription and Treg differentiation. IKD also enriched Akkermansia muciniphila, supporting gut and systemic BHB levels. In an IL-10 knockout model, IKD improves intestinal barrier function and reshapes the gut microbiota. It is associated with BHB-induced Kbhb-mediated inhibition of AHCY, leading to SAH accumulation and DNMT1 downregulation, thereby promoting Treg differentiation. These findings suggest protective effects of IKD in the IL-10 knockout colitis model.31:T9fc,Abstract Background Crohn’s disease (CD) is characterized by epithelial barrier dysfunction and mucosal immune dysregulation. Dietary interventions have gained increasing attention as important therapeutic strategies. We evaluated whether an intermittent ketogenic diet (IKD), which elevates β-hydroxybutyrate (BHB), ameliorates CD via lysine β-hydroxybutyrylation (Kbhb) and elucidated the underlying mechanisms. Methods IL-10 knockout mice were allocated to three groups: continuous KD (ketogenic diet), IKD, or a normal diet. Disease activity index (DAI), histopathological changes, cytokine levels, and epithelial barrier integrity were evaluated. Regulatory T cells (Tregs) and Foxp3 expression were assessed by flow cytometry and quantitative real-time PCR (qRT-PCR). To elucidate the underlying mechanisms, we conducted metabolomic and transcriptomic analyses, pyrosequencing, and additional experiments. Results Both KD and IKD alleviated colonic inflammation, but IKD better prevented epithelial senescence. IKD increased colonic Treg infiltration and Foxp3 expression. Metabolomics revealed elevated BHB in IKD colons. BHB reduced inflammation and promoted Treg differentiation in a dose-dependent manner. Mechanistically, BHB induced Kbhb of S-adenosylhomocysteine hydrolase (AHCY), inhibiting its activity, leading to S-adenosylhomocysteine (SAH) accumulation, downregulating DNA methyltransferase 1 (DNMT1), and promoting Foxp3-TSDR demethylation to enhance Foxp3 transcription and Treg differentiation. IKD also enriched Akkermansia muciniphila, supporting gut and systemic BHB levels. Conclusions In an IL-10 knockout model, IKD improves intestinal barrier function and reshapes the gut microbiota. It is associated with BHB-induced Kbhb–mediated inhibition of AHCY, leading to SAH accumulation and DNMT1 downregulation, thereby promoting Treg differentiation. These findings suggest protective effects of IKD in the IL-10 knockout colitis model. 32:T899,Major Depressive Disorder (MDD) is a prevalent psychiatric condition frequently associated with metabolic dysfunction. Metabolic interventions, including the ketogenic diet (KD), have shown potential antidepressant effects; however, rigorous clinical evaluation remains limited. This pilot study aimed to assess the feasibility, safety, tolerability, and preliminary clinical efficacy of a medically supervised ketogenic diet (MSKD) in individuals with moderate to severe depression. An open-label, single-arm, 14-week pilot feasibility trial was conducted virtually through Kingston General Hospital, Ontario, Canada. Participants underwent a two-week KD induction phase, followed by a 12-week follow-up phase under the supervision of a registered dietitian. Feasibility outcomes included adherence (sustained nutritional ketosis defined by blood ketones ≥0.5 mmol/L), tolerability, recruitment, and retention rates. Clinical outcomes were assessed using the Montgomery-Åsberg Depression Rating Scale (MADRS), Generalized Anxiety Disorder-7 scale (GAD-7), and Snaith-Hamilton Pleasure Scale (SHAPS). From an initial 89 interested individuals, 11 (12.4 %) participants were enrolled and began the intervention. Of these, 8 (72.7 %) successfully completed both induction and maintenance phases, all maintaining nutritional ketosis. Adherence was high, with no dropouts during the maintenance phase. Mild and transient side effects were reported primarily during induction. Clinically significant reductions were observed in depressive symptoms (change from the baseline MADRS score estimate from the model was 23.33 points, 95 % CI: 17.95-28.71; p < 0.001). remission in 87.5 %), anxiety symptoms (GAD-7 mean reduction of 8.8 points, p = 0.005), and anhedonia (SHAPS mean reduction of 4.8 points, p = 0.001). This pilot study demonstrated robust feasibility, safety, and tolerability of a medically supervised ketogenic diet in individuals with moderate to severe depression. Preliminary findings indicate significant improvements in depressive symptoms, anxiety, and anhedonia, supporting further investigation in larger, randomized controlled trials. ClinicalTrials.gov ID: NCT05558995.33:T94e,We report the case of a 48-year-old woman with treatment-resistant schizophrenia (TRS) and metabolic syndrome who completed a 5-week medical ketogenic diet (KD) in an inpatient setting. The patient was initially started on a 2.5:1 ratio of fat to combined carbohydrate and protein in grams, but her diet was modified on two occasions due to difficulty reaching consistent ketosis (βHB ≥0.5 mmol/L). Ketosis became more consistent throughout the study but was only fully maintained the last 5 days. Despite this, the patient had many clinically meaningful improvements including a 69% decrease in insulin-resistance (HOMA-IR), 41% decrease in C-peptide, and a 64% decrease in fasting insulin, despite minimal weight loss. Importantly, insulin-resistance moved from pre-diabetic to optimal levels. Fingerstick glucose also decreased. CRP reduced by 61%, suggesting movement from high to average cardiac risk. Extrapyramidal side effects (i.e., pseudoparkinsonism) improved dramatically (80% decrease), reaching almost full resolution. Global psychopathology ratings were not improved; however, the participant had only a few days consistently in ketosis and was facing significant personal stressors nearing the endpoint, which may have eclipsed clinical benefits. Despite this, we saw a hint of improvement in negative symptoms, which we point out as these are particularly problematic in TRS. These results are congruent with emerging data suggesting various health benefits of KD for people with schizophrenia, and we report for the first time its impact in TRS with long-term use of antipsychotic medications (clozapine, olanzapine) that contribute to metabolic syndrome, parkinsonian-like symptoms, and cardiac risk. Our results suggest that despite TRS, dual antipsychotic treatment and limited time in ketosis, a KD can reverse insulin resistance, greatly improve antipsychotic-associated pseudoparkinsonism, and reduce cardiac risk and inflammation. Thus, this diet may be a beneficial treatment alongside antipsychotic medication. We also suggest that well-controlled clinical trials longer than 5 weeks and with consistent ketosis are needed. Additionally, lower calories or a higher ratio of fat to combined protein and carbohydrate may be necessary to maintain ketosis for individuals with metabolic dysfunction who are taking antipsychotic medication.34:T92b,Ketogenic diets (KDs) have been hypothesized to influence mental health through pathways involving mitochondrial function, inflammation, and neurotransmitters, but their therapeutic value in psychiatric populations remains uncertain. To assess the associations between KDs and mental health outcomes in adults, with a focus on depressive and anxiety symptoms. MEDLINE, Embase, and APA PsycINFO were searched on April 18, 2025. Additional studies were identified through manual searches and clinical trial registries. Studies involving adults aged 18 years or older receiving a KD (<26% energy from carbohydrates or <50 g/day) and assessed with validated psychiatric scales were eligible. Designs included randomized clinical trials (RCTs), quasi-experimental (QSE) studies, cross-sectional studies, case series, and case reports. Data were extracted by 1 reviewer and verified by 2 others. Risk of bias was assessed using critical appraisal tools from the Joanna Briggs Institute. Random-effects meta-analyses were run separately for RCTs and QSEs. The primary outcome was changes in psychiatric symptom severity measured by standardized scales, reported as standardized mean differences (SMDs) or standardized mean change using change scores (SMCCs). A total of 50 studies (41 718 participants) were included. Ten RCTs on KD for depressive symptoms vs control diets showed a significant association (SMD, -0.48; 95% CI, -0.87 to -0.10; I2 = 67.2%), with stronger associations in studies using ketone monitoring, nonobese participants, very low-carbohydrate interventions, and non-high-carbohydrate comparators. Nine RCTs on anxiety showed no significant association (SMD, -0.03; 95% CI, -0.18 to 0.12; I2 = 41%). In QSEs, 9 on depressive symptoms showed a consistent association (SMCC, -0.66; 95% CI, -0.83 to -0.50; I2 = 0%), and 6 on anxiety showed similar results (SMCC, -0.58; 95% CI, -0.81 to -0.36; I2 = 0%). In this systematic review and meta-analysis, KDs were associated with modest improvements in depressive symptoms, particularly with biochemical ketosis verification, while anxiety evidence was inconclusive. Given heterogeneity, comparators, and short follow-up, well-powered trials with standardized, verified protocols, structured support, and prespecified outcomes are needed to confirm efficacy and durability.35:T110e, Importance Ketogenic diets (KDs) have been hypothesized to influence mental health through pathways involving mitochondrial function, inflammation, and neurotransmitters, but their therapeutic value in psychiatric populations remains uncertain. Objective To assess the associations between KDs and mental health outcomes in adults, with a focus on depressive and anxiety symptoms. Data Sources MEDLINE, Embase, and APA PsycINFO were searched on April 18, 2025. Additional studies were identified through manual searches and clinical trial registries. Study Selection Studies involving adults aged 18 years or older receiving a KD (&lt;26% energy from carbohydrates or &lt;50 g/day) and assessed with validated psychiatric scales were eligible. Designs included randomized clinical trials (RCTs), quasi-experimental (QSE) studies, cross-sectional studies, case series, and case reports. Data Extraction and Synthesis Data were extracted by 1 reviewer and verified by 2 others. Risk of bias was assessed using critical appraisal tools from the Joanna Briggs Institute. Random-effects meta-analyses were run separately for RCTs and QSEs. Main Outcomes and Measures The primary outcome was changes in psychiatric symptom severity measured by standardized scales, reported as standardized mean differences (SMDs) or standardized mean change using change scores (SMCCs). Results A total of 50 studies (41 718 participants) were included. Ten RCTs on KD for depressive symptoms vs control diets showed a significant association (SMD, −0.48; 95% CI, −0.87 to −0.10; I 2 = 67.2%), with stronger associations in studies using ketone monitoring, nonobese participants, very low-carbohydrate interventions, and non–high-carbohydrate comparators. Nine RCTs on anxiety showed no significant association (SMD, −0.03; 95% CI, −0.18 to 0.12; I 2 = 41%). In QSEs, 9 on depressive symptoms showed a consistent association (SMCC, −0.66; 95% CI, −0.83 to −0.50; I 2 = 0%), and 6 on anxiety showed similar results (SMCC, −0.58; 95% CI, −0.81 to −0.36; I 2 = 0%). Conclusions and Relevance In this systematic review and meta-analysis, KDs were associated with modest improvements in depressive symptoms, particularly with biochemical ketosis verification, while anxiety evidence was inconclusive. Given heterogeneity, comparators, and short follow-up, well-powered trials with standardized, verified protocols, structured support, and prespecified outcomes are needed to confirm efficacy and durability. 25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Ketogenic Diet: modality Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Ketogenic Diet (modality). Clinician-written summaries and actionable practice insights. 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Preclinical data suggested potential efficacy through several metabolic and signaling pathways (e.g., BHB-mediated anti-inflammatory, antioxidant, HDAC inhibition, increased BDNF/GABA, decreased glutamate effects), but reliable human evidence was minimal.","limitations":"- Evidence base is dominated by low-level studies; no large, adequately powered RCTs in PTSD populations exist.\n- Only 16 total articles were eligible, limiting the strength of any conclusions.\n- Human studies provided minimal reliable data, so clinical applicability remains highly uncertain.","practice_takeaway":"Ketogenic therapies are not yet supported by clinical trial evidence for PTSD and should not replace established treatments. Clinicians may watch for forthcoming RCTs, but current data are insufficient to guide prescribing."}},{"doi":"10.1038/s41398-026-04370-2","pmid":null,"title":"The efficacy of ketogenic interventions on neuropsychological & metabolic outcomes in serious mental illness & neurocognitive disorders: a systematic review & meta-analysis","journal_title":"Translational Psychiatry","journal_issn":"2158-3188","published_at":"2026-08-27T00:00:00.000Z","url":"https://doi.org/10.1038/s41398-026-04370-2","source_score":66,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":false,"crossref":true,"unpaywall":true},"created_at":"2026-09-02T06:22:27.020Z","updated_at":"2026-09-02T06:22:27.020Z","tags":[{"paper_doi":"10.1038/s41398-026-04370-2","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04370-2","tag_type":"category","value":"Psychiatry","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04370-2","tag_type":"condition","value":"Neurocognitive Disorders","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04370-2","tag_type":"condition","value":"Serious Mental Illness","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04370-2","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04370-2","tag_type":"level_of_evidence","value":"1","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04370-2","tag_type":"modality","value":"Ketogenic Diet","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04370-2","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04370-2","tag_type":"study_design","value":"Systematic Review and Meta-Analysis","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04370-2","tag_type":"warning","value":"Only supplementary figures and tables are present in the provided full text — the main manuscript body, including abstract, primary pooled effect sizes, participant totals, and conclusions, is not available. Key findings (e.g., overall cognitive and metabolic effect sizes) could not be extracted.","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04370-2","tag_type":"warning","value":"Sample size could not be determined from the available text; the sample_size tag has been omitted.","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04370-2","tag_type":"warning","value":"The study design was labeled as 'Systematic Review and Meta-Analysis' based on the title; this is consistent with the presence of meta-regression bubble plots and funnel plots in the supplementary material.","value_numeric":null}],"summaries":{"what_studied":"This systematic review and meta-analysis evaluated the efficacy of ketogenic dietary interventions on neuropsychological (including cognitive) and metabolic outcomes (glucose, insulin, triglycerides, HDL cholesterol) in adults with serious mental illness and neurocognitive disorders, searching databases up to April 16, 2026.","key_result":"Meta-regression analyses found no significant associations between cognitive outcomes and intervention duration (β=−0.0002; p=0.902), mean participant age (β=0.009; p=0.561), or proportion of male participants (β=−0.010; p=0.112). Metabolic parameters (glucose, insulin, triglycerides, HDL) were also pooled and analyzed.","limitations":"The full text is only partially available (supplementary figures/tables), preventing extraction of primary pooled effect sizes, sample sizes per analysis, or conclusions on efficacy. Study designs included in the review vary widely (RCTs, quasi-experimental, cross-sectional, case reports), introducing heterogeneity. Risk of bias levels ranged from low to high across included studies.","practice_takeaway":"Evidence on ketogenic interventions for serious mental illness and neurocognitive disorders remains inconclusive based on available data from this review. Clinicians should await the full publication before drawing practice-changing conclusions."}},{"doi":"10.1152/ajpendo.00067.2026","pmid":"42530143","title":"β-hydroxybutyrate: A Renoprotective Hormone In Polycystic Kidney Disease","journal_title":"American Journal of Physiology-Endocrinology and Metabolism","journal_issn":"0193-1849","published_at":"2026-07-30T00:00:00.000Z","url":"https://doi.org/10.1152/ajpendo.00067.2026","source_score":4,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-10T13:22:09.298Z","updated_at":"2026-08-10T13:22:09.298Z","tags":[{"paper_doi":"10.1152/ajpendo.00067.2026","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1152/ajpendo.00067.2026","tag_type":"category","value":"Endocrinology & Metabolism","value_numeric":null},{"paper_doi":"10.1152/ajpendo.00067.2026","tag_type":"condition","value":"Autosomal Dominant Polycystic Kidney Disease","value_numeric":null},{"paper_doi":"10.1152/ajpendo.00067.2026","tag_type":"condition","value":"Chronic Kidney Disease","value_numeric":null},{"paper_doi":"10.1152/ajpendo.00067.2026","tag_type":"generic","value":"beta-hydroxybutyrate","value_numeric":null},{"paper_doi":"10.1152/ajpendo.00067.2026","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1152/ajpendo.00067.2026","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1152/ajpendo.00067.2026","tag_type":"modality","value":"Intermittent Fasting","value_numeric":null},{"paper_doi":"10.1152/ajpendo.00067.2026","tag_type":"modality","value":"Ketogenic Diet","value_numeric":null},{"paper_doi":"10.1152/ajpendo.00067.2026","tag_type":"modality","value":"Ketone Body Supplementation","value_numeric":null},{"paper_doi":"10.1152/ajpendo.00067.2026","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1152/ajpendo.00067.2026","tag_type":"warning","value":"This is a narrative review published in 2026; it may reflect emerging or evolving evidence not yet validated by large RCTs. No sample size is applicable as no primary data were collected. Age group tagged as 'adult' based on ADPKD context, but the review does not explicitly restrict to adults. BHB is referred to as a 'renoprotective hormone,' a framing that is interpretive and not yet consensus terminology.","value_numeric":null}],"summaries":{"what_studied":"This narrative review examines the role of β-hydroxybutyrate (BHB) and Ketogenic Metabolic Therapy (KMT) — including ketogenic diets, intermittent fasting, time-restricted feeding, and BHB supplementation — as potential disease-modifying interventions in Autosomal Dominant Polycystic Kidney Disease (ADPKD).","key_result":"Accumulating preclinical and early clinical evidence suggests BHB is the principal renoprotective mediator of KMT, reducing cyst proliferation, inflammation, oxidative stress, and fibrosis while improving mitochondrial function via pleiotropic signaling effects beyond its role as an energy substrate.","limitations":"As a narrative (not systematic) review, it is subject to selection bias and cannot establish causation. Evidence relies heavily on preclinical models and early-phase clinical data, limiting direct translation to patients. No original data or head-to-head comparisons are presented.","practice_takeaway":"For ADPKD patients with limited pharmacological options, KMT strategies (ketogenic diet, intermittent fasting, BHB supplementation) represent low-risk, potentially disease-modifying adjuncts worth discussing — particularly given that modern dietary patterns may chronically suppress endogenous ketogenesis. Clinicians should monitor renal function and nutritional status if recommending these approaches pending robust trial data."}},{"doi":"10.1038/s41387-026-00454-6","pmid":"42449121","title":"Defining a ketone threshold for weight loss: evidence from 14 day daily β-hydroxybutyrate monitoring in 217 subjects on a ketogenic diet","journal_title":"Nutrition & Diabetes","journal_issn":"2044-4052","published_at":"2026-07-14T00:00:00.000Z","url":"https://doi.org/10.1038/s41387-026-00454-6","source_score":16,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-18T13:39:45.970Z","updated_at":"2026-07-18T13:39:45.970Z","tags":[{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"category","value":"Endocrinology & Metabolism","value_numeric":null},{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"condition","value":"Obesity","value_numeric":null},{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"condition","value":"Overweight","value_numeric":null},{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"modality","value":"Ketogenic Diet","value_numeric":null},{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"sample_size","value":"n=217","value_numeric":217},{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"study_design","value":"Secondary Analysis / Observational Cohort Study","value_numeric":null},{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"warning","value":"Ketogenic meal products were provided by a commercial sponsor (Gianluca Mech S.p.A.), though the company reportedly had no role in data collection or analysis — a potential conflict of interest to note.","value_numeric":null},{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"warning","value":"Study duration is only 14 days, limiting conclusions about sustained ketosis and longer-term weight outcomes.","value_numeric":null},{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"warning","value":"The manuscript is described as unedited/pre-final publication, so specific numerical results (e.g., absolute weight loss per threshold) may change before final print.","value_numeric":null},{"paper_doi":"10.1038/s41387-026-00454-6","tag_type":"warning","value":"This is a secondary analysis pooling multiple previously published and unpublished datasets; methodological heterogeneity across source studies cannot be fully assessed from the available text.","value_numeric":null}],"summaries":{"what_studied":"This secondary analysis of 217 adults with overweight or obesity evaluated which blood β-hydroxybutyrate (βHB) threshold best predicts weight loss during a 14-day ketogenic diet (KD), using daily βHB monitoring and regression analysis.","key_result":"A βHB level of ≥0.5 mmol/L was most strongly associated with significant weight loss. Body weight and sex were significant predictors of Time to Ketosis (TtK), indicating meaningful interindividual variability in how quickly effective ketosis is achieved.","limitations":"- Short 14-day intervention limits generalizability to longer-term KD use.\n- Secondary analysis of pooled previously published and unpublished datasets introduces heterogeneity and potential confounding.\n- Actual weight-loss magnitude (absolute kg lost per threshold) is not reported in the available text.","practice_takeaway":"Clinicians prescribing a ketogenic diet for weight loss should target a blood βHB level of at least 0.5 mmol/L and consider daily monitoring to shorten the time to achieve ketosis. Patients with higher body weight or of male sex may reach this threshold at different rates and may need individualized guidance."}},{"doi":"10.1093/ecco-jcc/jjag003","pmid":"41527294","title":"Intermittent ketogenic diet promotes Treg differentiation and alleviates Crohn’s disease via the β-hydroxybutyrate driven AHCY–DNMT1–Foxp3 axis","journal_title":"Journal of Crohn's and Colitis","journal_issn":"1873-9946","published_at":"2026-01-13T00:00:00.000Z","url":"https://doi.org/10.1093/ecco-jcc/jjag003","source_score":9,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2026-01-16","doi":"10.1093/ecco-jcc/jjag003","days":"7","issn":"1873-9946","rank":"9","field":"Clinical Medicine","score":"9","category":"Gastroenterology & Hepatology","categories":["Gastroenterology & Hepatology"],"_categories":["Gastroenterology & Hepatology"]},"pubmed":{"doi":"10.1093/ecco-jcc/jjag003","title":"Intermittent ketogenic diet promotes Treg differentiation and alleviates Crohn's disease via the β-hydroxybutyrate driven AHCY-DNMT1-Foxp3 axis.","journal":"Journal of Crohn's & colitis","methods":"","results":"Both KD and IKD alleviated colonic inflammation, but IKD better prevented epithelial senescence. IKD increased colonic Treg infiltration and Foxp3 expression. Metabolomics revealed elevated BHB in IKD colons. BHB reduced inflammation and promoted Treg differentiation in a dose-dependent manner. Mechanistically, BHB induced Kbhb of S-adenosylhomocysteine hydrolase (AHCY), inhibiting its activity, leading to S-adenosylhomocysteine (SAH) accumulation, downregulating DNA methyltransferase 1 (DNMT1), and promoting Foxp3-TSDR demethylation to enhance Foxp3 transcription and Treg differentiation. IKD also enriched Akkermansia muciniphila, supporting gut and systemic BHB levels.","abstract":"$30","keywords":["AHCY","DNMT1","Foxp3 demethylation","Intermittent ketogenic diet","Regulatory T cells","β-hydroxybutyrate","β-hydroxybutyrylation"],"pubmed_id":"41527294","conclusions":"","publication_date":"2026-01-13T00:00:00"},"crossref":{"DOI":"10.1093/ecco-jcc/jjag003","URL":"https://doi.org/10.1093/ecco-jcc/jjag003","ISSN":["1873-9946","1876-4479"],"link":[{"URL":"https://academic.oup.com/ecco-jcc/advance-article-pdf/doi/10.1093/ecco-jcc/jjag003/66381938/jjag003.pdf","content-type":"application/pdf","content-version":"am","intended-application":"syndication"},{"URL":"https://academic.oup.com/ecco-jcc/advance-article-pdf/doi/10.1093/ecco-jcc/jjag003/66381938/jjag003.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Intermittent ketogenic diet promotes Treg differentiation and alleviates Crohn’s disease via the β-hydroxybutyrate driven AHCY–DNMT1–Foxp3 axis"],"author":[{"given":"Shaoqi","family":"Cheng","sequence":"first","affiliation":[{"name":"The Affiliated Taizhou People’s Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University Department of General Surgery, , 366 Taihu Road, Taizhou, Jiangsu,"}]},{"given":"Chao","family":"Cheng","sequence":"additional","affiliation":[{"name":"The Affiliated Taizhou People’s Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University Department of General Surgery, , 366 Taihu Road, Taizhou, Jiangsu,"}]},{"given":"Chuanjiang","family":"Huang","sequence":"additional","affiliation":[{"name":"The Affiliated Taizhou People’s Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University Department of General Surgery, , 366 Taihu Road, Taizhou, Jiangsu,"}]},{"given":"Cuixia","family":"Liu","sequence":"additional","affiliation":[{"name":"The Affiliated Taizhou People’s Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University Department of Gastroenterology, , 366 Taihu Road, Taizhou, Jiangsu,"}]},{"given":"Feng","family":"Xun","sequence":"additional","affiliation":[{"name":"Affiliated Hospital of Shandong University of Traditional Chinese Medicine Department of Proctology, , 16369 Jingshi Road, Jinan, Shandong,"}]},{"given":"Wenliang","family":"Jiang","sequence":"additional","affiliation":[{"name":"The Affiliated Taizhou People’s Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University Department of General Surgery, , 366 Taihu Road, Taizhou, Jiangsu,"}]},{"given":"Jie","family":"Zhao","sequence":"additional","affiliation":[{"name":"The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou Medical Center, Nanjing Medical University Department of Gastrointestinal Surgery, , 68 Gehu Road, Changzhou,"}]},{"given":"Honggang","family":"Wang","sequence":"additional","affiliation":[{"name":"The Affiliated Taizhou People’s Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University Department of General Surgery, , 366 Taihu Road, Taizhou, Jiangsu,"}]}],"issued":{"date-parts":[[2026,1,12]]},"member":"286","prefix":"10.1093","source":"Crossref","volume":null,"created":{"date-time":"2026-01-10T12:37:59Z","timestamp":1768048679000,"date-parts":[[2026,1,10]]},"indexed":{"date-time":"2026-01-16T09:07:30Z","timestamp":1768554450583,"date-parts":[[2026,1,16]]},"license":[{"URL":"https://academic.oup.com/pages/standard-publication-reuse-rights","start":{"date-time":"2026-01-12T00:00:00Z","timestamp":1768176000000,"date-parts":[[2026,1,12]]},"delay-in-days":0,"content-version":"am"}],"subject":[],"abstract":"$31","language":"en","relation":{},"resource":{"primary":{"URL":"https://academic.oup.com/ecco-jcc/advance-article/doi/10.1093/ecco-jcc/jjag003/8423468"}},"subtitle":[],"deposited":{"date-time":"2026-01-13T06:03:06Z","timestamp":1768284186000,"date-parts":[[2026,1,13]]},"issn-type":[{"type":"print","value":"1873-9946"},{"type":"electronic","value":"1876-4479"}],"published":{"date-parts":[[2026,1,12]]},"publisher":"Oxford University Press (OUP)","reference":null,"short-title":[],"article-number":"jjag003","content-domain":{"domain":[],"crossmark-restriction":false},"original-title":[],"container-title":["Journal of Crohn's and Colitis"],"reference-count":0,"published-online":{"date-time":null,"timestamp":null,"date-parts":[[2026,1,12]]},"references-count":0,"short-container-title":[],"is-referenced-by-count":0},"unpaywall":{"doi":"10.1093/ecco-jcc/jjag003","is_oa":false,"title":"Intermittent ketogenic diet promotes Treg differentiation and alleviates Crohn’s disease via the β-hydroxybutyrate driven AHCY–DNMT1–Foxp3 axis","updated":"2026-01-15T02:17:35+00:00","published_date":"2026-01-10","best_oa_location":null}},"created_at":"2026-01-19T09:31:36.873Z","updated_at":"2026-01-21T12:05:26.220Z","tags":[{"paper_doi":"10.1093/ecco-jcc/jjag003","tag_type":"category","value":"Gastroenterology & Hepatology","value_numeric":null},{"paper_doi":"10.1093/ecco-jcc/jjag003","tag_type":"condition","value":"Crohn's 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ketogenic diet, and normal diet to assess colonic inflammation, epithelial barrier/senescence, Treg infiltration/Foxp3 expression, and mechanisms linked to β‑hydroxybutyrate (BHB) using metabolomic, transcriptomic, and epigenetic assays.","key_result":"Both ketogenic regimens reduced colonic inflammation, with IKD better preventing epithelial senescence; IKD increased colonic Tregs and Foxp3 and raised colonic BHB, while BHB dose‑dependently reduced inflammation and promoted Treg differentiation. Mechanistically, BHB induced β‑hydroxybutyrylation of AHCY, causing SAH accumulation, DNMT1 downregulation, and Foxp3‑TSDR demethylation, and IKD enriched Akkermansia muciniphila supporting gut and systemic BHB levels.","limitations":"Findings come from an IL‑10 knockout mouse colitis model rather than human Crohn’s disease; sample size, duration, and quantitative effect sizes are not reported in the provided text."}},{"doi":"10.1016/j.jad.2025.121079","pmid":"41475571","title":"Medically supervised ketogenic diet as an adjunctive treatment for moderate to severe depression: A pilot study","journal_title":"Journal of Affective Disorders","journal_issn":"0165-0327","published_at":"2026-01-01T00:00:00.000Z","url":"https://doi.org/10.1016/j.jad.2025.121079","source_score":142,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2026-01-07","doi":"10.1016/j.jad.2025.121079","days":"14","issn":"0165-0327","rank":"6","field":"Clinical Medicine","score":"142","category":"Clinical Neurology","categories":["Clinical Neurology","Psychiatry"],"_categories":["Clinical Neurology","Psychiatry"]},"pubmed":{"doi":"10.1016/j.jad.2025.121079","title":"Medically supervised ketogenic diet as an adjunctive treatment for moderate to severe depression: A pilot study.","journal":"Journal of affective disorders","methods":"","results":"From an initial 89 interested individuals, 11 (12.4 %) participants were enrolled and began the intervention. Of these, 8 (72.7 %) successfully completed both induction and maintenance phases, all maintaining nutritional ketosis. Adherence was high, with no dropouts during the maintenance phase. Mild and transient side effects were reported primarily during induction. Clinically significant reductions were observed in depressive symptoms (change from the baseline MADRS score estimate from the model was 23.33 points, 95 % CI: 17.95-28.71; p < 0.001). remission in 87.5 %), anxiety symptoms (GAD-7 mean reduction of 8.8 points, p = 0.005), and anhedonia (SHAPS mean reduction of 4.8 points, p = 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Ten RCTs on KD for depressive symptoms vs control diets showed a significant association (SMD, -0.48; 95% CI, -0.87 to -0.10; I2 = 67.2%), with stronger associations in studies using ketone monitoring, nonobese participants, very low-carbohydrate interventions, and non-high-carbohydrate comparators. Nine RCTs on anxiety showed no significant association (SMD, -0.03; 95% CI, -0.18 to 0.12; I2 = 41%). In QSEs, 9 on depressive symptoms showed a consistent association (SMCC, -0.66; 95% CI, -0.83 to -0.50; I2 = 0%), and 6 on anxiety showed similar results (SMCC, -0.58; 95% CI, -0.81 to -0.36; I2 = 0%).","abstract":"$34","keywords":[],"pubmed_id":"41191382","conclusions":"","publication_date":"2025-11-05T00:00:00"},"crossref":{"DOI":"10.1001/jamapsychiatry.2025.3261","URL":"https://doi.org/10.1001/jamapsychiatry.2025.3261","ISSN":["2168-622X"],"link":[{"URL":"https://jamanetwork.com/journals/jamapsychiatry/articlepdf/2840626/jamapsychiatry_janssenaguilar_2025_oi_250056_1766508749.38472.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":"13","type":"journal-article","issue":"1","score":1,"title":["Ketogenic Diets and Depression and Anxiety"],"author":[{"given":"Reinhard","family":"Janssen-Aguilar","sequence":"first","affiliation":[{"name":"Interventional Psychiatry Program, St Michael’s Hospital, Toronto, Ontario, 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Accessed May 20, 2025. https://www.ncbi.nlm.nih.gov/books/NBK115797/","article-title":null,"journal-title":null,"doi-asserted-by":null}],"short-title":[],"journal-issue":{"issue":"1","published-print":{"date-parts":[[2026,1,1]]}},"content-domain":{"domain":[],"crossmark-restriction":false},"original-title":[],"container-title":["JAMA Psychiatry"],"published-print":{"date-parts":[[2026,1,1]]},"reference-count":73,"published-online":null,"references-count":73,"short-container-title":["JAMA Psychiatry"],"is-referenced-by-count":1},"unpaywall":{"doi":"10.1001/jamapsychiatry.2025.3261","is_oa":true,"title":"Ketogenic Diets and Depression and Anxiety","updated":"2026-01-12T01:20:46+00:00","published_date":"2025-11-05","best_oa_location":{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC12590392/","pmh_id":"oai:pubmedcentral.nih.gov:12590392","url_for_pdf":null,"url_for_landing_page":"https://pmc.ncbi.nlm.nih.gov/articles/PMC12590392/"}}},"created_at":"2025-12-08T12:24:58.509Z","updated_at":"2026-01-21T12:05:26.220Z","tags":[{"paper_doi":"10.1001/jamapsychiatry.2025.3261","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1001/jamapsychiatry.2025.3261","tag_type":"category","value":"Psychiatry","value_numeric":null},{"paper_doi":"10.1001/jamapsychiatry.2025.3261","tag_type":"condition","value":"Anxiety","value_numeric":null},{"paper_doi":"10.1001/jamapsychiatry.2025.3261","tag_type":"condition","value":"Depression","value_numeric":null},{"paper_doi":"10.1001/jamapsychiatry.2025.3261","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1001/jamapsychiatry.2025.3261","tag_type":"level_of_evidence","value":"1","value_numeric":null},{"paper_doi":"10.1001/jamapsychiatry.2025.3261","tag_type":"modality","value":"Ketogenic Diet","value_numeric":null},{"paper_doi":"10.1001/jamapsychiatry.2025.3261","tag_type":"sample_size","value":"n=41718","value_numeric":41718},{"paper_doi":"10.1001/jamapsychiatry.2025.3261","tag_type":"study_design","value":"Systematic Review and Meta-analysis","value_numeric":null},{"paper_doi":"10.1001/jamapsychiatry.2025.3261","tag_type":"warning","value":"Depression RCT meta-analysis showed high heterogeneity (I2=67.2%), and effects varied by ketone monitoring, carb intensity, and comparator.","value_numeric":null},{"paper_doi":"10.1001/jamapsychiatry.2025.3261","tag_type":"warning","value":"Follow-up duration and protocol standardization were not detailed in the abstract, limiting assessment of durability and implementation.","value_numeric":null},{"paper_doi":"10.1001/jamapsychiatry.2025.3261","tag_type":"warning","value":"Mixed designs were included (RCTs and quasi-experimental), which may affect interpretation across outcomes.","value_numeric":null}],"summaries":{"what_studied":"Systematic review and meta-analysis of 50 adult studies (search date April 18, 2025) evaluating ketogenic diets (<26% carbohydrate or <50 g/day) on depressive and anxiety symptoms using validated scales, with separate random-effects meta-analyses for RCTs and quasi-experimental studies.","key_result":"Across 10 RCTs, depressive symptoms improved vs control (SMD −0.48; 95% CI, −0.87 to −0.10; I2=67.2%), with stronger effects in studies using ketone monitoring, nonobese participants, very low-carbohydrate interventions, and non–high-carbohydrate comparators; 9 RCTs for anxiety showed no significant effect (SMD −0.03; 95% CI, −0.18 to 0.12; I2=41%). In quasi-experimental studies, depressive symptoms improved (SMCC −0.66; 95% CI, −0.83 to −0.50; I2=0%) and anxiety showed similar within-group improvements (SMCC −0.58; 95% CI, −0.81 to −0.36; I2=0%).","limitations":"High heterogeneity in depression RCTs (I2=67.2%) and variation in comparators limit certainty; many studies lacked standardized, verified protocols (e.g., ketone monitoring); follow-up was short.","practice_takeaway":"Ketogenic diets were associated with modest improvements in depressive symptoms, particularly when ketosis was biochemically verified, while RCT evidence for anxiety was null; given heterogeneity and short follow-up, clinicians should view benefits as provisional pending well-powered trials with standardized protocols."}}],"initialOffset":9,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"modality","value":"Ketogenic Diet"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Modalities","href":"/hub/tag/modality"},{"name":"Ketogenic Diet"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"modality","hub_tag_value":"Ketogenic Diet"}}}]]

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