Abstract

Tetanus is an acute infection caused by Clostridium tetani neurotoxin that attacks the neuromuscular system and causes progressive muscle spasms. Although it can be prevented through immunization, its prevalence in Indonesia is still recorded at 0.2 cases per 100,000 population per year. Research by Rampengan et al.(2016) showed that 45% of children with tetanus had not received immunization, and similar findings were also reported by Yusuflina (2017) that children with tetanus did not receive complete DPT immunization. At Dr. Wahidin Sudirohusodo Central General Hospital, there were 8 cases of pediatric tetanus reported in 2024, accounting for 0.005% of the total 145,289 visits. Delayed Immunization causes children to not have protective immunity against Clostridium tetani toxin, thus increasing the risk of tetanus infection resulting in disorders of the central nervous system. The resulting neurological complications can interfere with the ability to eat and reduce the child's nutritional intake, resulting in the risk of malnutrition (underweight and stunting) in children.

Azizah, Andi Sitti Nurul, Hikmawati Mas’ud, and Nusrah Ningsih. "Standardized Nutritional Care for Children with Moderate Tetanus." Journal of Health Care and Dietetic 1, no. 1 (2026): 62-67.

https://www.journalmpci.com/index.php/jhcd/article/download/606/589

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.

Abstract

Alzheimer’s disease (AD) is characterized by profound metabolic dysfunction and disturbances in gut–brain axis signaling. Ketogenic diet (KD) has demonstrated metabolic and cognitive benefits in both preclinical and clinical studies. However, factors that determine individual responsiveness or non-responsiveness to KD interventions remain poorly understood. Emerging evidence suggests that gut microbiome composition plays a critical role in modulating these factors. This study examined how KD responsiveness, determined by fecal microbiota transplantation (FMT) derived from human KD responders (RES) or non-responders (nRES)- influences cognition, gut barrier function, neuroinflammation, and microbial structure in 3xTg-AD mice. We further evaluated whether supplementing KD with a novel Synbiotic Yogurt (SY) formulated by our team could augment or restore responsiveness. We hypothesized that RES microbiota would confer superior KD-driven benefits and that KD-SY would synergistically improve metabolic and neurobiological outcomes, particularly among nRES recipients. Adult 3xTg-AD mice were antibiotic-cleansed and randomized to receive Control-, RES-, or nRES – FMT, while maintained on KD for four weeks. A second cohort received KD supplemented with SY or non-fat milk along with RES- or nRES-FMT. Behavioral tests, gut permeability assay, serum inflammatory markers, brain amyloid beta (Aβ), intestinal morphology, gene expression, and 16S rRNA microbial profiling were measured. RES-FMT recipients showed early improvements in spatial memory (Y-maze and novel object recognition) and consistently lower Aβ accumulation in cortex and hippocampus. They also showed higher synaptophysin and IL-10 expression. In contrast, nRES-FMT mice exhibited distinct microbiome clustering, lower microbial diversity, enrichment of Proteobacteria, and impaired gut barrier function relative to RES-FMT recipients. Functionally, specific taxa like Enterococcus, Enterobacter, and Paenibacillus were associated with greater vulnerability to AD-related pathology, while Akkermansia, Bifidobacterium, and Muribaculum were linked with lower vulnerability. SY supplementation improved metabolic and gut barrier indices across groups characterized by increased circulating ketone levels, lowered fasting glucose and glucose-ketone index, and decreased gut permeability. nRES-SY mice showed the strongest gains in recognition memory and reductions in brain Aβ1–42 burden. SY increased expression of barrier- and inflammation-modulating genes, including occludin, APLP2, and IL-10. Microbiome analysis demonstrated higher microbial diversity and enrichment of beneficial genera such as Paralactobacillus, Eubacterium, and Muribaculum. These findings show that KD responsiveness is strongly determined by gut microbiota composition and that SY supplementation can enhance or rescue metabolic, cognitive, and microbial outcomes, particularly in nonresponders. This supports a precision-microbiome strategy combining metabolic and Synbiotic interventions to improve gut–brain axis function in AD.

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.

Abstract

Background: Traumatic brain injury (TBI) affects 69 million individuals annually and represents a major global health burden. Ketogenic interventions have emerged as a potential therapy to address deficits following TBI. This scoping review updates previous work to synthesize evidence on ketogenic therapies for TBI, examining mechanistic insights, clinical feasibility, and barriers. Methods: A systematic search was conducted following the methodological framework of Arksey and O'Malley (2005) and JBI guidance. Findings are reported in accordance with PRISMA 2020 guidelines complemented by the PRISMA Extension for Scoping Reviews (PRISMA-ScR). Studies were included if they used TBI models in human or animal subjects; investigated ketogenic interventions; reported quantitative clinical, functional, or metabolic outcomes; and enrolled more than five participants in clinical trials. Studies were excluded if they were conducted in vitro, did not involve TBI or ketogenic interventions, were not original research, were duplicate publications, or lacked English full text manuscripts. Results: Out of 421 studies screened, 32 studies met the inclusion criteria. 25 animal studies and 7 human studies were analyzed. 68.0% of animal studies used exclusively male specimens. The total pooled male-to-female ratio across human studies was 53:24, reflecting an approximately twofold predominance of male participants. Studies were evaluated using clusters of the most-assessed frameworks. Animal investigations evaluated metabolic pathways in 23 out of 25 (92.0%) studies, neuroprotective effects in 15 out of 25 (60.0%) studies, and behavioral assays in 13 out of 25 (52.0%) studies. Human studies assessed feasibility in 7 out of 7 (100%) studies, safety in 5 out of 7 (83.33%) studies, and efficacy in 4 out of 7 (66.67%) studies. Clinical trials consistently demonstrated feasibility in monitored settings. Conclusions: Ketogenic interventions improve metabolic dysfunction in preclinical models with variable neuroprotective and functional effects. Clinical evidence demonstrates feasibility but lacks adequately powered efficacy trials. Larger controlled trials with standardized endpoints with balanced age and sex representation are needed to determine efficacy.

Quddus, Daaniyal, Serhat Aydin, Ayesha Akbar Waheed, Qazi Zeeshan, D. Kojo Hamilton, Nitin Agarwal, and Joseph C. Maroon. "Administration of Ketogenic Diet as a Potential Treatment During Post-Traumatic Brain Injury Recovery: A Scoping Review." Frontiers in Nutrition 13: 1848682.

Abstract

Objective: This study aimed to evaluate whether a ketogenic diet (KD) mitigates behavioral, metabolic, and peripheral tissue alterations in a rat model of propylthiouracil (PTU)-induced hypothyroidism.

Subjects and Methods: Adult female Sprague–Dawley rats (n = 28) were randomly assigned to Control, KD, PTU, and KD+PTU groups. Hypothyroidism was induced using 0.05% PTU for six weeks, while KD was administered during the final four weeks. Behavioral testing was conducted during the final phase of the experimental period, followed by biochemical and histological analyses at the end of the six-week protocol. Behavioral assessments included the open field, light/dark box, forced swim, and Morris water maze tests. Biochemical analyses evaluated serum free thyroxine (T4), thyroid-stimulating hormone (TSH), glucose, β-hydroxybutyrate, tumor necrosis factor alpha (TNFα), and interleukin 10 (IL-10). Histological evaluations targeted the thyroid gland, liver, white adipose tissue, and brown adipose tissue.

Results: PTU significantly reduced serum free T4 levels and impaired spatial learning and mood-related behaviors. KD effectively induced nutritional ketosis and improved systemic glucose metabolism but did not reverse cognitive impairment or depressive-like behaviors associated with hypothyroidism. Histologically, KD attenuated PTU-induced hepatic inflammation, white adipose tissue dysfunction, and brown adipose tissue whitening. Thyroid morphology and circulating TNF-α and IL-10 levels remained unchanged across groups.

Conclusion: KD exerts favorable metabolic and peripheral tissue effects in PTU-induced hypothyroidism but does not rescue associated neurobehavioral deficits, likely due to persistent thyroid hormone deficiency.

Akkaya, Erhan Caner, Rabia Ilgin, Servet Kızıldağ, Asuman Argon, and Ferda Hoşgörler. "Effects of Ketogenic Diet on Behavioral, Metabolic, and Peripheral Tissue Changes in a Propylthiouracil-Induced Hypothyroidism Model." Medical Principles and Practice (2026).

https://karger.com/mpp/article-pdf/doi/10.1159/000552101/4535722/000552101.pdf

Research Objectives

To evaluate the effects of a ketogenic diet (KD) versus standard hospital diet (SD) on neurologic recovery, metabolic function, and inflammatory markers in patients with acute spinal cord injury (SCI).

Design

Randomized controlled trial conducted during inpatient stay (∼3-5 weeks)

Setting

Inpatient hospital settings, including intensive care and inpatient rehabilitation

Participants

Patients with a T12 or higher level of SCI and ASIA Impairment Scale classification A, B, or C; enrolled within 72 hours of injury. Of 36 eligible patients, 19 consented to the study.

Interventions

Participants were randomized to KD (n=9) or SD (n=10) for the entirety of study enrollment. The KD consisted of approximately 70-80% of total caloric intake from fats, while the SD was comprised of standard hospital meals.

Main Outcome Measures

Neurological function was assessed using the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) at baseline and study conclusion. Blood serum samples were collected weekly for 3 weeks to analyze glucose metabolism (n=19), lipid profiles (n=16), and inflammatory markers (n=16).

Results

The KD group achieved sustained ketosis, evidenced by significantly elevated beta-hydroxybutyrate levels during the 3 weeks (p < 0.05 for all weeks). There is a trend for improved upper extremity motor scores (UEMS) over time in both groups—KD from a median of 34 (IQR: 5–45) to 47 (17–50) and SD from 28 (2–50) to 33 (4–50)—with a trend toward significance over time (ptime=0.08). While the between-group difference in UEMS change was not statistically significant, the effect size was moderate (r=0.30). Lower extremity motor scores and light touch sensation showed significant improvements over time (ptime=0.02), while pinprick sensation showed a trend for improvement (ptime=0.06), without diet and time interaction effect for all neurological outcomes. Metabolic, lipid, and inflammation markers analyses revealed no significant time or group effects for insulin, cholesterol, triglycerides, IFN-γ, or IL-8. Significant time effects were noted for glucose, HDL, IL-6, IL-10, and TNF-α (ptime < 0.05 for all), without significant interaction effects. LDL (p=0.07) and CRP (p=0.09) demonstrated weak time trends without interaction effects.

Conclusions

The KD induced sustained ketosis in acute SCI patients. A medium effect size in UEMS suggests the potential for clinically meaningful differences. The small sample size may have limited the detection of significant differences. Ongoing enrollment and analysis are expected to provide further insights.

Chahande, Sana, Jia Li, Ceren Yarar-Fisher, and Kristen Heitman. "Impact of Ketogenic Diet on Neurologic Recovery, Metabolic Function, and Inflammation in Acute Spinal Cord Injury: A Randomized Controlled Trial." Archives of Physical Medicine and Rehabilitation 107, no. 5 (2026): e127.

https://www.archives-pmr.org/article/S0003-9993(26)00393-X/abstract