Medical Bulletin 06/January/2026

Type 2 diabetes (T2DM) has long been linked to higher risks of cancers like liver, colorectal, and breast cancer. Traditionally, this connection was thought to stem from high blood glucose, obesity, and insulin resistance. But the review highlights how diabetes itself—and the drugs used to treat it—could directly influence cancer progression through complex molecular pathways.

The researchers focused on three major drug groups: metformin, SGLT2 inhibitors, and GLP-1 receptor agonists. Drawing from human studies, laboratory experiments, and clinical databases, they found that metformin appears to have broad anti-cancer effects. It activates energy-regulating pathways such as AMPK and mTOR while reducing cancer-promoting signals through PI3K/AKT. These actions can slow tumor growth, cut off blood supply to cancer cells, and strengthen immune defenses within the tumor microenvironment.

For SGLT2 inhibitors and GLP-1 receptor agonists—newer classes of diabetes drugs—the evidence remains mixed. Some studies suggest they reduce inflammation, promote cell death (apoptosis), and may lower cancer risk. Others show no clear effect, hinting that their benefits may vary depending on drug type and cancer location. For example, metformin shows promise in preventing liver and colorectal cancers but has uncertain effects on breast cancer.

Experts like Dr. Linong Ji caution that while the emerging data are encouraging, many questions remain. The next step is long-term clinical research to confirm these effects in real-world settings. Still, the findings strengthen the case for a more personalized treatment approach—one that aligns diabetes care with cancer prevention and opens new avenues for therapy combining metabolic and oncology research.

REFERENCE: Meng Cao, Chu Lin, Xiaoling Cai, Fang Lv, Wenjia Yang, Linong Ji. Anti-diabetic medications and cancer: links beyond glycemic and body weight control. Precision Clinical Medicine, 2025; 8 (4) DOI: 10.1093/pcmedi/pbaf028

Daily meat consumption linked to nearly 20% higher UTI risk: Study

Your next urinary tract infection might not just come from poor hygiene—it could start in your kitchen. A new study from researchers at Kaiser Permanente and George Washington University has revealed that nearly one in five UTIs may be caused by foodborne E. coli from everyday meats like chicken, turkey, pork, and beef. Published recently in the mBio, the findings suggest that up to 20% of UTIs could originate from bacteria that jump from raw meat to human hosts through handling and food preparation.

Urinary tract infections are among the most common bacterial infections, affecting millions—especially women—each year. Historically, most cases were attributed to person-to-person contact, poor wiping practices, or weakened immune response. But this new research highlights another major source: zoonotic transmission, where bacteria spread from animals to humans. The team analysed DNA from over 2,300 UTI cases and compared them with E. coli strains isolated from 3,300 retail meat samples across Southern California. The results were surprising—18% of human infections shared identical bacterial fingerprints with those found in meats, confirming a direct link.

Among meat types, turkey samples topped the list—82% carried strains genetically similar to those infecting humans—followed by chicken (58%) and pork (54%). These strains readily colonized the gut before moving to the urinary tract, often aided by poor handwashing or undercooked preparation. Women were nearly twice as likely as men to contract foodborne UTIs, accounting for nearly 20% of related infections. Additionally, the study found that people living in lower-income areas faced a 60% higher risk—possibly due to limited access to refrigeration or proper kitchen facilities.

The researchers warned that these overlooked foodborne infections could account for more than 640,000 UTI cases each year in the U.S. alone. Experts recommend simple but crucial preventive steps: cook meat thoroughly, clean utensils separately, and wash hands for at least 20 seconds after touching raw products. Proper food hygiene, they say, can be as powerful as antibiotics in protecting against infection.

The findings shift how we think about UTIs—not just as a hygiene issue, but as a food safety concern—redefining prevention right from the chopping board.

REFERENCE: Aziz M, Park DE, Quinlivan V, Dimopoulos EA, Wang Y, Sung EH, Roberts ALS, Nyaboe A, Davis MF, Casey JA, Caballero JD, Nachman KE, Takhar HS, Aanensen DM, Parkhill J, Tartof SY, Liu CM, Price LB, . 2025. Zoonotic Escherichia coli and urinary tract infections in Southern California. mBio 16:e01428-25. https://doi.org/10.1128/mbio.01428-25

Intermittent fasting without calorie reduction shows no metabolic advantages, study finds

Skipping breakfast might not be the miracle health hack it’s made out to be. A new study from the German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE) and Charité – Universitätsmedizin Berlin has found that time-restricted eating—one of the most popular forms of intermittent fasting—offers no measurable boost to metabolism or heart health when calorie intake stays the same. Published in Science Translational Medicine, the “ChronoFast” study, led by Professor Olga Ramich, reveals that while meal timing can shift the body’s internal clock, it doesn’t necessarily enhance key metabolic markers.

Time-restricted eating (TRE) limits daily meals to a short window—typically eight to ten hours—followed by long fasting periods. The idea gained traction after early studies in animals and some human trials suggested that it improves insulin sensitivity, stabilises blood sugar, and helps with weight control. But scientists have questioned whether these benefits come from eating at specific hours or from people unintentionally cutting calories when fasting.

To find out, the ChronoFast team designed a carefully controlled, randomised crossover trial involving 31 women with overweight or obesity. Each participant followed two schedules for two weeks: early TRE (8 a.m. to 4 p.m.) and late TRE (1 p.m. to 9 p.m.). Importantly, every meal was identical in calories and nutrients, removing the variable of energy intake. Researchers then tracked insulin response, blood sugar, fats, and inflammation through blood tests and glucose monitoring. Physical activity was measured with motion sensors, and participants’ internal biological rhythms, or circadian clocks, were assessed using a specialised “BodyTime” blood assay.

The results? Despite adjusting their eating windows, participants showed no significant improvements in blood sugar control, insulin sensitivity, or lipid levels. However, meal timing did influence circadian rhythms—late eaters’ internal clocks shifted by about 40 minutes, and they also went to bed later.

The researchers conclude that future studies should explore combining calorie control with meal timing to truly optimise metabolic health.

REFERENCE: Beeke Peters, Julia Schwarz, Bettina Schuppelius, Agnieszka Ottawa, Daniela A. Koppold, Daniela Weber, Nico Steckhan, Knut Mai, Tilman Grune, Andreas F. H. Pfeiffer, Andreas Michalsen, Achim Kramer, Olga Pivovarova-Ramich. Intended isocaloric time-restricted eating shifts circadian clocks but does not improve cardiometabolic health in women with overweight. Science Translational Medicine, 2025; 17 (822) DOI: 10.1126/scitranslmed.adv6787