Medical Bulletin 24/February/2026 - Video

Here are the top medical news for today:

Study Finds Red Blood Cells Improve Glucose Tolerance at High Altitude

Why do people living at high altitudes often have better blood sugar control—even though oxygen levels are lower? A new study published in Cell Metabolism suggests that red blood cells (RBCs) may act as an unexpected “glucose sink” under low-oxygen conditions, helping lower circulating glucose independently of insulin.

Epidemiological data show that populations living above 3,500 meters in regions such as Tibet and Peru have lower rates of type 2 diabetes and improved glucose tolerance compared to sea-level populations. To investigate the mechanism, researchers used a normobaric hypoxia mouse model. Eight-week-old male mice were housed in either normal oxygen (21%) or hypoxic conditions (8% oxygen, mimicking extreme altitude) for up to three weeks. The team monitored fasting glucose, glucose tolerance, insulin sensitivity, and body weight over time.

Blood glucose levels dropped significantly within two days of hypoxia exposure, and glucose tolerance improved for weeks—even after returning to normal oxygen. Surprisingly, insulin sensitivity did not improve, suggesting the glucose-lowering effect was insulin-independent.

Using advanced imaging with radiolabeled glucose tracers and stable isotope metabolic tracing, researchers found that traditional glucose-consuming organs—such as muscle and liver—accounted for only part of the increased glucose uptake. Instead, RBC numbers nearly doubled under hypoxia. When excess RBCs were removed through serial phlebotomy, glucose levels normalized. Conversely, transfusing RBCs from hypoxic mice into normal mice induced hypoglycemia without oxygen deprivation. This demonstrated that elevated RBC abundance was both necessary and sufficient for lowering blood glucose.

Further analysis revealed that individual RBCs under hypoxia increased glucose uptake by about 2.5-fold, with higher expression of glucose transporters GLUT1 and GLUT4. Metabolic tracing showed glucose was redirected into the Luebering-Rapoport shunt, increasing production of 2,3-diphosphoglycerate—a molecule that enhances oxygen release to tissues while consuming more glucose.

The findings suggest RBCs play an active role in systemic glucose regulation and may represent a novel therapeutic target for diabetes by harnessing controlled hypoxia or modulating RBC metabolism.

REFERENCE: Martí-Mateos Y, Safari Z, Bevers S, et al. (2026). Red blood cells serve as a primary glucose sink to improve glucose tolerance at altitude. Cell Metabolism. DOI: 10.1016/j.cmet.2026.01.019. https://www.cell.com/cell-metabolism/fulltext/S1550-4131(26)00018-5

Researchers Link Pneumonia-Causing Bacterium to Alzheimer’s Disease Risk

Could a common respiratory infection quietly contribute to Alzheimer’s disease? A new study suggests that Chlamydia pneumoniae—a bacterium best known for causing pneumonia and sinus infections—may invade the retina and brain, triggering inflammation and accelerating neurodegeneration. The research, led by scientists at Cedars-Sinai, was published in Nature Communications.

Alzheimer’s disease is characterized by the buildup of amyloid-beta plaques in the brain, along with chronic inflammation and progressive nerve cell loss. While genetics and aging are well-established risk factors, scientists have increasingly explored whether infections might also contribute to disease progression.

In this study, researchers analyzed retinal tissue from 104 individuals, including people with normal cognition, mild cognitive impairment, and Alzheimer’s disease. Using advanced imaging, molecular testing and protein analysis, they found significantly higher levels of Chlamydia pneumoniae in both the retinas and brains of patients with Alzheimer’s compared to cognitively healthy individuals. Higher bacterial levels were also linked to more severe cognitive decline.

The association was especially strong in individuals carrying the APOE4 gene variant, a known genetic risk factor for Alzheimer’s. This suggests a possible interaction between infection and genetic vulnerability.

To test causality, the team conducted laboratory experiments using human nerve cells and Alzheimer’s mouse models. Infection with Chlamydia pneumoniae led to increased inflammation, greater neuronal death and elevated production of amyloid-beta. Notably, researchers demonstrated for the first time that the bacterium can travel to and persist in the retina—activating immune responses that mirror changes occurring in the brain.

These findings support the concept of an “infection-inflammation axis” in Alzheimer’s disease. The retina, often described as a window to the brain, may serve as a noninvasive site for early detection through retinal imaging.

While further research is needed to confirm long-term causality, the study raises the possibility that early antibiotic treatment or anti-inflammatory therapies targeting chronic infection could represent novel strategies to slow or prevent Alzheimer’s progression.

REFERENCE: Bhakta Prasad Gaire, Yosef Koronyo, Jean-Philippe Vit, Alexandre Hutton, Lalita Subedi, Dieu-Trang Fuchs, Natalie Swerdlow, Altan Rentsendorj, Saba Shahin, Daisy Martinon, Edward Robinson, Alexander V. Ljubimov, Julie A. Schneider, Lon S. Schneider, Debra Hawes, Stuart L. Graham, Vivek K. Gupta, Mehdi Mirzaei, Keith L. Black, Jesse G. Meyer, Moshe Arditi, Timothy R. Crother, Maya Koronyo-Hamaoui. Identification of Chlamydia pneumoniae and NLRP3 inflammasome activation in Alzheimer’s disease retina. Nature Communications, 2026; 17 (1) DOI: 10.1038/s41467-026-68580-4

Study Highlights Immune Differences Between Coffee and Caffeine

A recent pilot study published in the European Journal of Nutrition explored whether coffee has different short-term effects on the immune system compared to pure caffeine. Coffee and caffeine are widely consumed and studied for their potential metabolic and immunological effects, but coffee is a complex mixture of bioactive compounds—not just caffeine. Understanding how these components interact in the body is important, especially since coffee is a common dietary exposure rather than a medical treatment.

The randomized crossover study involved 10 healthy adults aged 20 to 40 years who were regular coffee drinkers. On separate occasions, participants consumed coffee, a caffeine solution containing an equivalent dose (approximately 130 mg), or water as a control. All beverages were taken after a standardized meal to minimize variations in post-meal metabolic responses. Washout periods were included between sessions to avoid carryover effects. Researchers measured circulating inflammatory markers, including interferon-gamma and selected interleukins, as well as caffeine levels in the blood.

The findings showed modest but noticeable differences between coffee and pure caffeine. The caffeine solution produced a stronger short-term suppression of certain inflammatory cytokines compared to coffee. In contrast, coffee often triggered immune responses that were closer to those seen with water, despite containing the same amount of caffeine. This suggests that other components in coffee, such as polyphenols and other bioactive compounds, may influence or modify caffeine’s immunological effects.

Interestingly, blood caffeine exposure was slightly higher after consuming coffee than after the caffeine solution, indicating that the coffee “matrix” may affect caffeine absorption or metabolism. However, the authors cautioned that this was a small pilot study, and such findings should be interpreted carefully. Importantly, all immune changes were temporary and mild, with no clinically significant adverse effects observed.

Overall, the study suggests that coffee is not simply equivalent to isolated caffeine in terms of short-term immune responses.

REFERENCE: Kaltenbach et al. (2026). Acute effects of coffee versus caffeine on postprandial cytokine responses and caffeine pharmacokinetics. European Journal of Nutrition. DOI: 10.1007/s00394-026-03913-z, https://link.springer.com/article/10.1007/s00394-026-03913-z