r/ketoscience
Healthy eating improves memory, but sugary diets may cause lasting damage
uts.edu.auNocturnal fat oxidation is lower in older individuals with overweight/obesity, including those with type 2 diabetes, and is associated with fasting triglyceride levels (2026)
link.springer.comMeta-analysis of blood metabolomics reveals dysregulated amino acid, neurotransmitter, and energy pathways in depression (2026)
sciencedirect.comLong-Chain Fatty Acids as Drivers of Neuroinflammation in Neurodegeneration: Mechanistic Links to Lipid Peroxidation, Ferroptosis, and Mitochondrial Dysfunction (2026)
mdpi.comMultiorgan observations following consumption of ketogenic diet in prolonged experimental diabetes mellitus
Abstract
Oxidative stress and inflammation have been identified as key mediators in either the progression, or amelioration of diabetes mellitus. Dietary interventions, especially ketogenic diet, has been reported to exert ameliorative effects in diabetes mellitus. However, its likely benefit in prolonged diabetes mellitus is unclear. This study was designed to evaluated the likely beneficial effects of ketogenic diet on systemic and selected organ oxidative stress and inflammation in experimentally induced diabetic Wistar rats. Wistar rats (N=40) were equally divided into Control and Diabetic (streptozotocin 55mg/kg in 2% citrate buffer) animals. Control (I-II) and diabetic animals (III-IV) where divided into 2 groups (n=10) and exposed to either standard chow (SC) or ketogenic diet (KD), for 14 days, respectively. Animals were exposed to the different diets, 7 days after induction of diabetes mellitus. Thereafter, blood samples were obtained and evaluated for blood glucose, lipid profile, liver and renal function tests, and serum oxidative stress and inflammations indices. Cardiac, renal, knee joint and hepatic samples were also obtained and evaluated for histology, and oxidative stress and inflammation indices. Blood glucose, systemic, cardiac, renal and knee joint oxidative stress and inflammation were elevated while hepatic and renal functions were impaired in the SC exposed diabetic group compared to controls. Exposure of diabetic animals to KD resulted in reduced blood glucose and alleviated systemic inflammation in varying degrees. Impaired renal and hepatic functions were however not reversed. Similarly, tissue specific oxidative stress and inflammation though somewhat ameliorated, were however still persistent. This study suggests that consumption of ketogenic diet alone in preexisting or prolonged diabetes mellitus may ameliorate fasting blood glucose and reduces systemic inflammation but does not reverse completely, tissue-specific aberrations caused by diabetic mellitus.
This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Seven Years of 700 Cholesterol Without Coronary Atherosclerosis: A Lean Mass Hyper-Responder Case Report
Abstract
Background: While reducing LDL cholesterol (LDL-C) remains central focuses of conventional preventive cardiology, substantial heterogeneity exists in the cardiovascular risk associated with even extreme LDL-C elevations, likely depending heavily on the broader metabolic context. Specifically, the lean mass hyper-responder (LMHR) phenotype—characterized by markedly elevated LDL-C with elevated high-density lipoprotein cholesterol (HDL-C) and low triglycerides in the setting of a ketogenic diet—has recently been described, though its long-term risk profile remains poorly defined. Case Presentation: We describe a male in his 30s without any congenital dyslipidemia who adopted a ketogenic diet for the management of ulcerative colitis and who subsequently exhibited a sixfold increase in LDL-C from a baseline of 95 mg/dL to 574 mg/dL, with total cholesterol of up to 705 mg/dL, HDL-C at 124 mg/dL, and triglycerides at 34 mg/dL. Despite maintaining these extreme lipid levels for nearly seven years, he demonstrated no coronary plaque or stenosis on coronary computed tomography angiography (CCTA; CAD-RADS = 0). Additionally, quantification of coronary plaque as assessed by AI-guided quantified analysis by Heartflow^(®) identified 0 mm^(3) plaque in any vessels, placing him in the lowest percentile for atherosclerotic plaque. Conclusions: This case represents an extreme and extensively characterized example of the LMHR phenotype and highlights the limitations of extrapolating cardiovascular risk from LDL-C levels alone without consideration of broader patient context and the etiology of hypercholesterolemia. While a single case cannot redefine clinical practice, this well-characterized case is consistent with emergent literature on LMHR, and careful study of such individuals may provide valuable insights into lipid metabolism, atherosclerosis biology, and precision cardiovascular risk assessment.
Norwitz, Nicholas G., David Feldman, and Adrian Soto-Mota. "Seven Years of 700 Cholesterol Without Coronary Atherosclerosis: A Lean Mass Hyper-Responder Case Report." Diseases 14, no. 5 (2026): 168.