Medical Bulletin 27/January/2026 - Video

Here are the top medical news for today:

Genetic Study Connects Vitamin B1 Metabolism to Gut Motility, IBS Risk

A new study published in Gut sheds light on how genetics and vitamin B1 metabolism influence gut motility, offering potential new treatment targets for common digestive disorders like irritable bowel syndrome (IBS).

The research focused on stool frequency (SF) as a practical proxy for gastrointestinal (GI) motility, which is essential for nutrient absorption, waste elimination, and overall digestive health. Disrupted motility underlies conditions ranging from constipation-predominant IBS to diarrhea-predominant IBS, yet treatments are often limited due to incomplete understanding of underlying mechanisms.

Researchers analyzed data from 268,606 participants across six biobanks, including five European and one East Asian population. Genetic analysis identified 479 significant variants across 18 genomic regions, corresponding to 21 independent genetic signals and 197 protein-coding genes. Notably, three variants were highlighted: rs12407945 (Europeans), rs2581260, and rs12022782 (multi-ancestry).

The top variant affects SLC35F3, a gene transporting vitamin B1 (thiamine) into cells, while another affects XPR1, a phosphate exporter needed to activate thiamine into thiamine pyrophosphate. These findings suggest that the way the body processes vitamin B1 plays a key role in regulating gut motility through interactions between the enteric and central nervous systems.

Observational data from 98,449 participants further supported this link: higher thiamine intake was associated with increased SF, with effects depending on an individual’s genetic variants. Other genes implicated include KLB, which regulates bile acid metabolism, and COLQ, involved in gut nerve signaling and linked to diverticular disease risk.

Drug signature analysis highlighted 831 compounds that could theoretically modulate gut motility, offering avenues for repurposing medications or developing new interventions. While stool frequency is a proxy measure and dietary thiamine intake was observational, these findings uncover a previously underappreciated role for vitamin B1 in bowel regulation and pave the way for mechanistic and clinical studies to improve treatments for motility disorders.

REFERENCE: Díaz-Muñoz C, Bozzarelli I, Lopera-Maya EA, et al. (2026) Genetic dissection of stool frequency implicates vitamin B1 metabolism and other actionable pathways in the modulation of gut motility. Gut. DOI: 10.1136/gutjnl-2025-337059. https://gut.bmj.com/content/early/2026/01/05/gutjnl-2025-337059

Study Finds Genetic Factor Linked to Staying Mentally Sharp for Life

A recent study in Alzheimer’s & Dementia reveals that “super agers”—adults over 80 whose cognitive abilities resemble those decades younger—carry fewer Alzheimer’s risk genes and more protective ones. Led by Vanderbilt University Medical Center, the research examined genetic data from 18,080 participants across eight national aging cohorts, making it the largest study of super agers to date.

The study focused on the APOE gene, where the ε4 variant strongly increases Alzheimer’s disease (AD) risk, while the ε2 variant appears protective. Results showed super agers were 68% less likely to carry APOE-ε4 compared with peers over 80 with Alzheimer’s dementia. Even relative to cognitively healthy adults in the same age group, super agers were still 19% less likely to carry the risk variant.

Conversely, the protective APOE-ε2 variant was more frequent among super agers. They were 28% more likely to carry ε2 than cognitively normal peers and 103% more likely than those with Alzheimer’s dementia. These findings suggest that genetic factors play a key role in enabling exceptional cognitive aging.

Super ager status was determined by memory performance, requiring participants over 80 to outperform the average memory score of cognitively normal adults aged 50–64. The study included diverse participants: 1,412 non-Hispanic white super agers, 211 non-Hispanic Black super agers, alongside 8,829 individuals with AD dementia and 7,628 cognitively normal controls.

“This is the largest study to date linking APOE allele frequency with super-ager status and the first to show an association with APOE-ε2,” said Leslie Gaynor, PhD. The findings highlight the super-ager phenotype as a promising model for studying resilience to Alzheimer’s and may guide future research into mechanisms that protect the aging brain.

REFERENCE: Alaina Durant, Shubhabrata Mukherjee, Michael L. Lee, Seo‐Eun Choi, Phoebe Scollard, Brandon S. Klinedinst, Emily H. Trittschuh, Jesse Mez, Lindsay A. Farrer, Katherine A. Gifford, Carlos Cruchaga, Jason Hassenstab, Adam C. Naj, Li‐San Wang, Sterling C. Johnson, Corinne D. Engelman, Walter A. Kukull, C. Dirk Keene, Andrew J. Saykin, Michael L. Cuccaro, Brian W. Kunkle, Margaret A. Pericak‐Vance, Eden R. Martin, David A. Bennett, Lisa L. Barnes, Julie A. Schneider, William S. Bush, Jonathan L. Haines, Richard Mayeux, Badri N. Vardarajan, Marilyn S. Albert, Paul M. Thompson, Angela L. Jefferson, Paul K. Crane, Logan Dumitrescu, Derek B. Archer, Timothy J. Hohman, Leslie S. Gaynor. Evaluating the association of apolipoprotein E genotype and cognitive resilience in SuperAgers. Alzheimer-'s, 2026; 22 (1) DOI: 10.1002/alz.71024

Study Explains Why Some People Catch Bad Colds, Others Don’t

A new study in Cell Press Blue reveals that the speed and strength of your nasal defenses may determine how sick you get from the common cold. Rhinovirus, the leading cause of colds, triggers nasal cells to launch coordinated antiviral responses. Researchers from Yale School of Medicine found that these early cellular defenses often matter more than the virus itself in shaping illness severity.

To study this, the team created lab-grown human nasal tissue from stem cells, producing structures that mimic the real nasal lining. This model included multiple cell types, such as mucus-producing cells and ciliated cells that help clear particles. “Since rhinovirus infects humans but not other animals, organotypic tissue models are especially valuable,” explained senior author Ellen Foxman.

The study revealed that interferons—proteins that block viral replication—play a central role. Nasal cells release interferons upon detecting the virus, activating antiviral defenses in both infected and neighboring healthy cells. Rapid interferon responses contained infections effectively, whereas blocking these responses allowed the virus to spread widely, causing extensive cell damage.

Researchers also observed that when viral growth exceeds early defenses, a separate pathway triggers excess mucus and inflammatory signals, contributing to airway inflammation and breathing difficulties. These mechanisms could offer targets for therapies that reduce symptoms while preserving antiviral defenses.

The model has limitations, as it lacks immune cells present in real infections. Future research will examine how these additional cells and environmental factors affect antiviral responses. First author Bao Wang noted that understanding the body’s defense mechanisms opens opportunities for novel therapeutics: “Our study highlights that how the body responds to a virus is critical in determining both whether illness occurs and its severity.”

REFERENCE: Bao Wang, Julien A.R. Amat, Valia T. Mihaylova, Yong Kong, Guilin Wang, Ellen F. Foxman. Rhinovirus triggers distinct host responses through differential engagement of epithelial innate immune signaling. Cell Press Blue, 2026; 100001 DOI: 10.1016/j.cpblue.2025.100001