Medical Bulletin 18/November/2025

Aging in humans and animals often leads to cognitive decline, anxiety, and an increased risk of neurodegenerative diseases like Alzheimer’s. These issues are linked to brain changes such as shrinkage of the hippocampus, oxidative stress caused by harmful reactive oxygen species, and chronic inflammation. Aged garlic extract (AGE), rich in antioxidant and anti-inflammatory sulfur compounds, helps protect brain cells by reducing oxidative damage, calming inflammation, and supporting healthy neurotransmitter function. This makes AGE a promising natural option to counteract age-related brain deterioration.

In this controlled study, 48 male C57BL/6J mice were randomized to either a standard or AGE-supplemented diet and underwent extensive behavioral testing after 40 weeks. Tests assessed anxiety-related behavior, exploratory activity, learning, memory, sociability, and sensorimotor function. Findings showed significant improvements in anxiety and memory domains: AGE-fed mice spent more time in lighted areas (less anxious) and performed better in novel object recognition and spatial learning tasks, with no effect on general health or motor skills.

Proteomic analyses of hippocampal and cortical tissue highlighted molecular changes linked to synaptic signaling, apoptosis reduction, and neural plasticity, especially in the hippocampus. Key protein pathways affected involved tau, amyloid precursor protein, presenilin 1, and brain-derived neurotrophic factor, known players in aging and neurodegeneration.

While promising, the researchers caution that these results from mice require further validation for human application. The study supports aged garlic extract as a potential nutraceutical to enhance cognitive resilience and reduce anxiety during aging, inviting more research into its mechanisms and clinical relevance.

This work adds to a growing field exploring multi-targeted, natural approaches to aging-related neurological decline.

REFERENCE: Mony T, Jackson M, Zuckerman A, Yu W, Nguyen TT, Balderrama A, Li R, Sun GY, Cui J, Gu Z. Supplementation of aged garlic extract attenuates age-associated memory impairment and cognitive decline: Involvement of molecular pathways in the cortex and hippocampus. Biomedical Reports 2025, 24(1). DOI 10.3892/br.2025.2075, https://www.spandidos-publications.com/10.3892/br.2025.2075

Keto Diet Danger? Study Finds Serious Long-Term Health Risks of Keto Eating

A new study from University of Utah Health, published in Science Advances, raises important questions about the long-term safety of the ketogenic diet, a popular approach for weight loss and metabolic control. While keto is known for preventing weight gain and improving short-term metabolic markers, this research shows that extended ketogenic dieting may trigger hidden biological changes disrupting fat and sugar metabolism.

The ketogenic diet is a high-fat, very low-carbohydrate eating plan that forces the body into ketosis, a state where fat is burned for energy instead of glucose. Originally developed for epilepsy treatment, it has gained popularity for rapid weight loss and improved blood sugar control. While keto can reduce appetite and support metabolic health in the short term, it is restrictive and may cause nutrient deficiencies, digestive issues, and increased cholesterol levels. Long-term safety remains uncertain, with emerging evidence warning of potential liver and pancreatic stress, especially when followed for extended periods.

The study involved male and female mice fed a very high-fat, very low-carbohydrate ketogenic diet for over nine months. Researchers monitored body weight, blood fat levels, liver function, glucose, and insulin regulation, as well as gene expression and cellular health in the pancreas. While keto-fed mice maintained lower body weights compared to high-fat Western diet-fed mice, male mice developed fatty liver disease-a serious metabolic condition-and showed impaired liver function. Female mice did not develop fatty liver, highlighting significant sex differences.

Importantly, although keto mice had low fasting blood sugar and insulin, their blood sugar spiked excessively after carbohydrate intake, revealing impaired glucose regulation and metabolic inflexibility. This abnormal response was linked to severe stress and dysfunction in pancreatic beta cells responsible for insulin secretion, traced to disruptions in protein processing within these cells’ ER-Golgi transport system. Encouragingly, some of these metabolic issues reversed when mice returned to a normal diet.

This work challenges the perception of ketogenic diets as inherently safe over long periods. It suggests that while keto can achieve weight control, it may carry hidden risks—especially for liver and pancreatic health—and that sex, genetics, and lifestyle factors likely influence individual outcomes. The authors emphasize caution and recommend consulting healthcare providers before embarking on long-term ketogenic diets.

REFERENCE: Molly R. Gallop et al. ,A long-term ketogenic diet causes hyperlipidemia, liver dysfunction, and glucose intolerance from impaired insulin secretion in mice.Sci. Adv.11,eadx2752(2025).DOI:10.1126/sciadv.adx2752