Medical Bulletin 19/ February/ 2025
Here are the top medical news for the day:
New Study Identifies Genetic Link Between Sugar Digestion and IBS
The research points to sucrose, among other sugars, as a key trigger of bowel symptoms in individuals with a genetic predisposition to carbohydrate maldigestion, opening doors for personalized nutrition.
Sucrase-isomaltase (SI) is an intestinal enzyme critical for the digestion of dietary carbohydrates, particularly sucrose and starch.
Previous studies have suggested a genetic link between Sucrase-isomaltase defects and IBS, whereby certain DNA changes cause reduced enzymatic activity and inefficient digestion of carbohydrates, thus inducing symptoms like bloating, diarrhoea, and abdominal pain.
In the new study, the Gastrointestinal Genetics team now analysed genetic and health data from over 360,000 individuals in the UK Biobank, and found that individuals with defective sucrase variants were exposed to a significantly higher risk of IBS, while those with isomaltase defects were not affected. At the same time, sucrase defective carriers experienced more severe bowel symptoms, and were more likely to avoid sucrose-rich foods.
“On top of maltose from starch, sucrase has the unique ability to break down sucrose” said senior author Mauro D’Amato, Professor of Medical Genetics at LUM University and Ikerbasque Research Professor at CIC bioGUNE, “and it may be so that this sugar triggers bowel symptoms in individuals with genetic defects associated with reduced sucrase function. This not only contributes to understanding IBS risk in people predisposed to carbohydrate maldigestion, but also supports the idea of tailoring their dietary treatment based on genetics.”
IBS affects millions worldwide, often with unclear pathogenesis and limited treatment options. This study reinforces the importance of digestive enzyme genetics in IBS predisposition, and provides rationale for dietary modifications - such as reducing sucrose intake - in genetically susceptible individuals.
Ref: Domain-specific effects of sucrase-isomaltase genotype in irritable bowel syndrome. Torices L, Bonfiglio F, Esteban-Blanco C, Zamfir-Taranu A, Naim HY, D’Amato M. Gastroenterology. DOI: 10.1053/j.gastro.2025.01.242.
AI Screening Accelerates Heart Failure Clinical Trial Enrollment, Study Shows
Artificial intelligence (AI) can rapidly screen patients for clinical trial enrollment, according to a new study published in JAMA and led by Mass General Brigham researchers. Their novel AI-assisted patient screening tool significantly improved the speed of determining eligibility and enrollment in a heart failure clinical trial compared to manual screening. These findings suggest that using AI can be cheaper than conventional methods and speed up the research process, which could mean patients get earlier access to proven, effective treatments.
“Seeing this AI capability accelerate screening and trial enrollment this substantially in the context of a real-world randomized prospective trial is exciting,” said co-senior author Samuel (Sandy) Aronson, ALM, MA, executive director of IT and AI Solutions for Mass General Brigham Personalized Medicine and senior director of IT and AI Solutions for the Accelerator for Clinical Transformation.
The study randomized 4,476 patients to be either manually screened or screened using generative AI to see if they were eligible for the Co-Operative Program for Implementation of Optimal Therapy in Heart Failure (COPILOT-HF) trial.
In the AI arm of the study, a generative AI tool called RAG-Enabled Clinical Trial Infrastructure for Inclusion Exclusion Review (RECTIFIER) assessed clinical notes and other pieces of information in patients’ electronic health records to determine if they met key eligibility criteria for the heart failure study.
In the other arm of the study, research staff manually reviewed patients’ charts to determine if they met the eligibility criteria.
The rate of enrollment in the AI-enabled arm was almost double the rate of enrollment in the manual arm. This means that AI could almost halve the time it takes to complete enrollment in a trial,” said lead author Ozan Unlu, MD, a fellow in Clinical Informatics at Mass General Brigham and a fellow in Cardiovascular Medicine at Brigham and Women's Hospital.
Ref: Unlu, O et al. “Manual versus AI-Assisted Clinical Trial Screening Using Large-Language Models (MAPS-LLM)” JAMA DOI: doi:10.1001/jama.2024.28047
BMC Study Finds Higher Diabetes Risk in Psoriasis Patients
A recent study published in the Diabetology & Metabolic Syndrome journal found those that psoriasis patients have a 48% higher chance of getting diabetes. Nearly 23% of the link between psoriasis and diabetes was found to be caused by obesity, making it a significant mediator.
Diabetes is a chronic autoimmune condition characterized by high blood glucose levels and is a growing global health and financial burden, affecting nearly 10% of the population. Psoriasis which affects 2-4% of people is linked to depression, cardiovascular disease, oral health issues, and kidney disease. Obesity, another rising public health concern, increases the risk of diabetes, cardiovascular disease, and cancer. While obesity is a known risk factor for diabetes, the link between psoriasis and diabetes remains unclear. This study explored their relationship and assessed whether obesity serves as a mediator.
Data from a total of 21,835 NHANES participants between 2003–2006 to 2009–2014 were included in the study. Body mass index (BMI) and data on diabetes and psoriasis from questionnaires were included in the analysis.
The study discovered that people with psoriasis had a considerably greater incidence of diabetes after controlling for pertinent covariates. Diabetes incidence and BMI levels were found to be positively correlated in psoriasis patients, with a significant difference between the highest (Q4) and lowest (Q1) BMI quartiles.
In men, psoriasis was found to have an inflection point when BMI surpassed a particular threshold, at which point its prevalence started to decrease.
The prevalence of psoriasis also declined in younger persons over a certain BMI threshold. Also, psoriasis and diabetes were partially linked by obesity, which accounted for about 22.91% of this connection, according to mediation analysis. Overall, this study suggests a possible connection between diabetes and psoriasis, with fat perhaps acting as a mediating factor.
Ref: Xu, Z., Ma, K., Zhai, Y., Wang, J., & Li, Y. (2025). Obesity mediates the association between psoriasis and diabetes incidence: a population-based study. Diabetology & Metabolic Syndrome, 17(1). https://doi.org/10.1186/s13098-025-01622-x
New Treatment Strategy: Blocking Nerves to Combat Pancreatic Cancer
Pancreatic cancer is fueled by connections to the nervous system. This is reported by scientists from the German Cancer Research Center (DKFZ) and the Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM)* in their current publication in Nature. The team discovered that the tumor specifically reprograms the neurons for its own benefit. In mice, blocking nerve function inhibited cancer growth and increased the sensitivity of tumor cells to certain chemotherapies and immunotherapies.
When the researchers blocked the neural connection to the pancreatic tumor in a mouse modell using a targeted neurotoxin, the tumor became sensitive to the checkpoint inhibitor nivolumab again and the tumor mass shrank to one-sixth of the mass in control animals. “By blocking the nerves, were able to convert an immunologically cold tumor into one that was sensitive to immunotherapy,” says Simon Renders, also first author of the publication, summarizing the result.
The result underscores that both types of nerve cells have functional relevance for tumor growth. Complete blockade of the communication between nerves and tumor in combination with chemotherapy and/or immune checkpoint inhibitors is a promising approach for combating pancreatic cancer more effectively in the future.
Ref: Thiel, V., Renders, S., Panten, J. et al. Characterization of single neurons reprogrammed by pancreatic cancer. Nature (2025). https://doi.org/10.1038/s41586-025-08735-3
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