Medical Bulletin 13/November/2025 - Video

Here are the top medical news for the day:

New Study Reveals Unexpected Link Between Sugar Metabolism and Alcohol Addiction

Scientists from the University of Colorado Anschutz have discovered a surprising link between the body's sugar metabolism and alcohol addiction, opening new possibilities for treating both alcohol use disorder (AUD) and alcohol-associated liver disease (ALD). Their study, published in Nature Metabolism, reveals that alcohol consumption stimulates an internal production of fructose — the same sugar common in sweet foods — through the enzyme ketohexokinase (KHK). This pathway appears to encourage further drinking and worsens liver damage.

The team conducted experiments using mice genetically engineered to lack KHK, observing that these mice showed significantly reduced alcohol preference and consumption. Tests included voluntary drinking and reward-based models. Additionally, blocking KHK, either genetically or with medication, prevented liver injury typically caused by alcohol. This included reductions in liver fat buildup, inflammation, and scarring.

"This shows alcohol doesn't just harm the liver directly, it hijacks our sugar metabolism to reinforce drinking and accelerate liver injury," said lead researcher Dr. Miguel Lanaspa. The findings suggest that targeting fructose metabolism could break this harmful cycle.

Moreover, since both ALD and metabolic-associated steatotic liver disease (MASLD) involve fructose-driven damage, therapies inhibiting fructose metabolism may benefit a broad group of patients suffering from liver disease related to diet or alcohol.

Co-author Dr. Richard Johnson emphasized this unexpected intersection between sugar and alcohol metabolism, highlighting its potential to spur new treatments addressing the root metabolic pathways common to these liver illnesses.

This discovery offers hope in tackling two pressing health challenges — alcohol addiction and liver disease — with innovative strategies focused on controlling fructose production and activity in the body.

REFERENCE: Andres-Hernando, A., et al. (2025). Identification of a common ketohexokinase-dependent link driving alcohol intake and alcohol-associated liver disease in mice. Nature Metabolism. doi: 10.1038/s42255-025-01402-x. https://www.nature.com/articles/s42255-025-01402-x

Daily Coffee Consumption May Lower AFib Risk by 39 Percent, Study Finds

Scientists have challenged the long-held belief that coffee worsens heart rhythm problems, revealing that a daily cup may actually reduce outbreaks of atrial fibrillation (AFib) by 39%. Published in JAMA and part of the DECAF trial, this research overturns previous guidance advising AFib patients to avoid caffeine, instead suggesting coffee could have protective effects.

AFib is a common heart rhythm disorder causing rapid, irregular beats that increase stroke and heart failure risk. Rates are rising globally alongside aging populations and obesity. The DECAF study, led by researchers from UC San Francisco and the University of Adelaide, enrolled 200 regular coffee drinkers diagnosed with persistent AFib or atrial flutter. All participants underwent electrical cardioversion to restore normal heart rhythm, then were randomized to either drink at least one cup of caffeinated coffee daily or abstain for six months.

The coffee group experienced a significantly lower risk of recurrent AFib episodes (47%) compared to the abstainers (64%), with no increase in adverse events. Researchers propose several coffee components may contribute: caffeine boosts physical activity, which is known to reduce AFib risk; caffeine’s diuretic effect may lower blood pressure; and anti-inflammatory compounds in coffee may protect cardiac tissue.

Lead author Dr. Christopher Wong described the results as “astounding,” given the widespread advice for AFib patients to minimize caffeine. Senior author Dr. Gregory Marcus added that coffee consumption seemed safe and likely beneficial, highlighting a shift in understanding coffee’s impact on heart health.

This landmark clinical trial opens new possibilities for AFib management, encouraging clinicians and patients to reconsider caffeine restrictions. While future studies are needed to assess effects across different caffeine doses and starting habits, this finding offers hope for safer, approachable lifestyle modifications that can reduce AFib recurrence and improve cardiovascular outcomes.

REFERENCE: Christopher X. Wong, Christopher C. Cheung, Gabrielle Montenegro, Hannah H. Oo, Isabella J. Peña, Janet J. Tang, Samuel J. Tu, Grace Wall, Thomas A. Dewland, Joshua D. Moss, Edward P. Gerstenfeld, Zian H. Tseng, Henry H. Hsia, Randall J. Lee, Jeffrey E. Olgin, Vasanth Vedantham, Melvin M. Scheinman, Catherine Lee, Prashanthan Sanders, Gregory M. Marcus. Caffeinated Coffee Consumption or Abstinence to Reduce Atrial Fibrillation. JAMA, 2025; DOI: 10.1001/jama.2025.21056

New Study Identifies Hidden Weakness That Causes Prostate Cancer to Self-Destruct

Scientists have discovered a critical weakness in prostate cancer cells involving two enzymes, PDIA1 and PDIA5, that protect the androgen receptor (AR)—a protein driving prostate cancer growth. A recent study published in the Proceedings of the National Academy of Sciences found that blocking these enzymes destabilizes the AR, causing cancer cells to die and tumors to shrink both in lab cultures and animal models.

Prostate cancer is the second most common cancer in men worldwide, and resistance to hormone therapies remains a significant challenge. Targeting PDIA1 and PDIA5 offers a novel strategy to overcome such resistance and improve patient outcomes, paving the way for more effective, combination treatment options in advanced prostate cancer management.

Prostate cancer cells rely on PDIA1 and PDIA5 as molecular bodyguards to maintain AR stability and resist treatment. When these enzymes were inhibited, the AR could not function properly and began breaking down. This not only led to cancer cell death but also made tumors more responsive to existing therapies like enzalutamide, a commonly prescribed AR-targeting drug.

Researchers from Flinders University, Australia, and South China University of Technology performed extensive experiments including patient-derived tumor samples and mouse models. Their findings showed impressive tumor shrinkage and enhanced treatment efficacy when PDIA1 and PDIA5 inhibitors were combined with enzalutamide.

Beyond AR protection, these enzymes help cancer cells manage stress and maintain energy production by supporting mitochondria, the cell’s powerhouses. Blocking PDIA1 and PDIA5 damages mitochondria, increases oxidative stress, and deprives cancer cells of energy—essentially cutting off both the “fuel” and “engine” that sustain tumor growth.

Lead researchers, including Professor Luke Selth and Dr. Jianling Xie, highlighted this dual impact as a promising therapeutic avenue. Although current inhibitors show potential, they require refinement to ensure safety and selectivity, as some may affect healthy cells.

REFERENCE: Jianling Xie, Kaikai Shen, Wenken Liang, Zijian Kuang, Raj K. Shrestha, Adrienne R. Hanson, Scott L. Townley, Meiling He, Sishu Yu, Peiwen Zhou, Liangzhen Zhu, Zhiwen Gong, Xiang Ao, Sushma R. Rao, Qing Zhang, Kaijie Chen, Jinfen Wei, Shashikanth Marri, Marten F. Snel, Swati Irani, Liye Chen, Ling Wang, Daniel P. McDougal, John B. Bruning, Minglin Ou, Shaobo Wang, Christopher G. Proud, Hongli Du, Lisa M. Butler, Luke A. Selth. Protein disulfide isomerases regulate androgen receptor stability and promote prostate cancer cell growth and survival. Proceedings of the National Academy of Sciences, 2025; 122 (42) DOI: 10.1073/pnas.2509222122