Remission of OCD and ulcerative colitis with a ketogenic diet: Case Report DOI Creative Commons
Lori Calabrese

Frontiers in Psychiatry, Journal Year: 2025, Volume and Issue: 16

Published: April 3, 2025

There is little research describing the clinical use of a ketogenic diet in obsessive-compulsive disorder (OCD) or inflammatory bowel disease. We describe first application adult OCD with ulcerative colitis (UC) resulting complete remission OCD, UC, and improved metabolic health. A 37-year-old obese woman longstanding was treated for 12 weeks personalized whole-food (KMT 1:5:1 ratio) specialized psychiatry clinic. Adherence assessed by capillary beta-hydroxybutyrate (BHB) photojournaling food intake. Remission Yale-Brown Obsessive Compulsive Scale (Y-BOCS), Florida Inventory scale (FOCI), Clinical Global Impression-Improvement/Severity (CGI-S/I). Patient Health Questionnaire-9 (PHQ-9) Yale Food Addictions 2.0 (YFAS 2.0) depression addiction. UC Partial Mayo Score (PMS) Ulcerative Colitis Patient-Reported Outcome (UC-PRO). Metabolic health laboratories bioimpedance. Quality life using validated scales flourishing, resilience, self-compassion, subjective narrative. occurred within 3 (PMS 0, UC-PRO 0). Progressive improvement inversely related to oscillating BHB, FOCI 0 at 9 weeks, (Y-BOCS CGI-S 1). Body weight decreased 12.2%, significant decreases percentage body fat visceral fat. Flourishing, self-compassion 2- 20-fold. Complete marked well-formulated ratio 1:5:1) meaningful positive impact on quality improvements self-compassion.

Language: Английский

Ketogenesis supports hepatic polyunsaturated fatty acid homeostasis via fatty acid elongation DOI Creative Commons
Eric D. Queathem, Zahra Moazzami, David B. Stagg

et al.

Science Advances, Journal Year: 2025, Volume and Issue: 11(5)

Published: Jan. 29, 2025

Ketogenesis is a dynamic metabolic conduit supporting hepatic fat oxidation particularly when carbohydrates are in short supply. Ketone bodies may be recycled into anabolic substrates, but physiological role for this process has not been identified. Here, we use mass spectrometry–based 13 C-isotope tracing and shotgun lipidomics to establish link between ketogenesis lipid anabolism. Unexpectedly, mouse liver primary hepatocytes consumed ketone support fatty acid biosynthesis via both de novo lipogenesis (DNL) polyunsaturated (PUFA) elongation. While an acetoacetate intermediate was absolutely required source DNL, PUFA elongation activation of by cytosolic acetoacetyl–coenzyme A synthetase (AACS). Moreover, AACS deficiency diminished free esterified PUFAs hepatocytes, while ketogenic insufficiency depleted increased triacylglycerols. These findings suggest that influences metabolism, representing molecular mechanism through which could influence systemic physiology chronic diseases.

Language: Английский

Citations

1
The cyclic metabolic switching theory of intermittent fasting DOI
Mark P. Mattson

Nature Metabolism, Journal Year: 2025, Volume and Issue: unknown

Published: March 14, 2025

Language: Английский

Citations

1
Gut microbiota regulates hepatic ketogenesis and lipid accumulation in ketogenic diet-induced hyperketonemia by disrupting bile acid metabolism DOI Creative Commons
Zhengzhong Luo, Yixin Huang, Kang Yong

et al.

Gut Microbes, Journal Year: 2025, Volume and Issue: 17(1)

Published: April 23, 2025

The ketogenic diet (KD) induces prolonged hyperketonemia, characterized by elevated circulating level of β-hydroxybutyrate. However, the KD can negatively affect host metabolic health altering gut microbial community. Despite this, regulatory effect microbiota on hepatic ketogenesis and triacylglycerol (TAG) accumulation during a remains poorly understood. Here, we hypothesized that commensal bacterium regulates lipid metabolism in association with KD-induced hyperketonemia. disrupts remodeling following antibiotic-induced depletion. capacity for severity TAG liver closely correlated changes composition up-regulation farnesoid X receptor (FXR), peroxisome proliferator-activated alpha (PPARα), diacylglycerol O-acyltransferase 2 (DGAT2), which were modulated bile acid through gut-liver axis. Clostridium perfringens type A is particularly implicated exacerbating steatosis disrupting secondary metabolism. increased conversion deoxycholic to 12-ketolithocholic represents critical pathway C. colonization. These findings illuminate adverse effects adaptation highlight role ketonic states.

Language: Английский

Citations

0
High Fat Low Carbohydrate Diet Is Linked to CNS Autoimmunity Protection DOI Creative Commons
Duan Ni, Jian Tan,

Julen Gabirel Araneta Reyes

et al.

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: March 27, 2025

Abstract Multiple sclerosis (MS) is an inflammatory and neurodegenerative disease of the central nervous system (CNS) believed to be driven by autoimmune mechanisms. Genetic environmental factors are implicated in MS development, among latter, diets nutrients emerging as potential critical contributors. However, a comprehensive understanding their impacts underlying mechanisms involved lacking. Harnessing state‐of‐the‐art nutritional geometry analytical methods, it first revealed that globally, increased carbohydrate supply associated with burden, while fat has opposite effect. Furthermore, mouse model, experimental encephalomyelitis (EAE), found isocaloric diet high aggravated EAE, enriched (HF) fully protective. This reflected reduced neuroinflammation skewing toward anti‐inflammatory phenotypes. The protective effects from HF multifaceted. Metabolically, lipid storage immune cells, correlating IL‐10 production. Transcriptionally epigenetically, feeding preprogrammed naïve T cells less activated but more tolerogenic phenotype. It showcased manipulating potentially efficient cost‐effective approach prevent and/or ameliorate EAE. exhibits translational potentials for prevention/intervention possibly other diseases.

Language: Английский

Citations

0
Remission of OCD and ulcerative colitis with a ketogenic diet: Case Report DOI Creative Commons
Lori Calabrese

Frontiers in Psychiatry, Journal Year: 2025, Volume and Issue: 16

Published: April 3, 2025

There is little research describing the clinical use of a ketogenic diet in obsessive-compulsive disorder (OCD) or inflammatory bowel disease. We describe first application adult OCD with ulcerative colitis (UC) resulting complete remission OCD, UC, and improved metabolic health. A 37-year-old obese woman longstanding was treated for 12 weeks personalized whole-food (KMT 1:5:1 ratio) specialized psychiatry clinic. Adherence assessed by capillary beta-hydroxybutyrate (BHB) photojournaling food intake. Remission Yale-Brown Obsessive Compulsive Scale (Y-BOCS), Florida Inventory scale (FOCI), Clinical Global Impression-Improvement/Severity (CGI-S/I). Patient Health Questionnaire-9 (PHQ-9) Yale Food Addictions 2.0 (YFAS 2.0) depression addiction. UC Partial Mayo Score (PMS) Ulcerative Colitis Patient-Reported Outcome (UC-PRO). Metabolic health laboratories bioimpedance. Quality life using validated scales flourishing, resilience, self-compassion, subjective narrative. occurred within 3 (PMS 0, UC-PRO 0). Progressive improvement inversely related to oscillating BHB, FOCI 0 at 9 weeks, (Y-BOCS CGI-S 1). Body weight decreased 12.2%, significant decreases percentage body fat visceral fat. Flourishing, self-compassion 2- 20-fold. Complete marked well-formulated ratio 1:5:1) meaningful positive impact on quality improvements self-compassion.

Language: Английский

Citations

0