Medical Bulletin 17/February/2026

The 7.5-week trial included 39 overweight or obese adults aged 36 to 75. Participants were assigned either to extend their overnight fasting window to 13–16 hours or to maintain their usual 11–13 hour fasting period. Those in the intervention group stopped eating at least three hours before bedtime and dimmed lights in the evening to support circadian alignment. Adherence was high, at nearly 90%.

Compared with the control group, participants who adjusted their eating schedule experienced measurable improvements. Nighttime blood pressure fell by 3.5%, and heart rate decreased by 5%, reflecting a healthier day–night cardiovascular rhythm. Stronger nighttime dips in blood pressure and heart rate are associated with better heart health.

Daytime glucose control also improved. When given glucose, participants in the extended fasting group showed more effective insulin release, suggesting improved pancreatic responsiveness and steadier blood sugar regulation.

Researchers emphasized that cardiometabolic health depends not only on how much or what people eat, but also on meal timing relative to sleep. With only a small percentage of U.S. adults meeting criteria for optimal cardiometabolic health, aligning eating patterns with natural sleep–wake cycles may offer a practical, non-pharmacological strategy to reduce long-term risk. Larger multi-center trials are planned to confirm these findings.

REFERENCE: Daniela Grimaldi, Kathryn J. Reid, Sabra M. Abbott, Kristen L. Knutson, Phyllis C. Zee. Sleep-Aligned Extended Overnight Fasting Improves Nighttime and Daytime Cardiometabolic Function. Arteriosclerosis, Thrombosis, and Vascular Biology, 2026; DOI: 10.1161/ATVBAHA.125.323355

Higher Plant-Based Diet Intake Linked to Lower Breast Cancer Risk, Major Global Study Finds

A large prospective study published in Frontiers in Nutrition examined whether adherence to healthful plant-based diets and intake of specific micronutrients were associated with breast cancer risk and survival. The findings suggest that stronger adherence to a healthy plant-based diet is linked to a lower risk of developing breast cancer and reduced mortality after diagnosis, though the results are observational and do not establish causation.

Researchers analyzed data from two cohorts: the UK Biobank and the Chinese Longitudinal Healthy Longevity Survey (CLHLS). The UK Biobank sample included 67,045 cancer-free participants and 3,397 women with breast cancer at baseline. Plant-based diet adherence was measured using the Healthful Plant-Based Diet Index (HPDI) and the Alternate Mediterranean Diet (AMED) score.

In the UK Biobank, women in the highest HPDI tertile were 11% less likely to develop breast cancer compared to those in the lowest tertile. Among women already diagnosed, those with the highest HPDI adherence had a 28% lower risk of all-cause mortality. Each standard deviation increase in HPDI was associated with a 4% lower incidence risk and an 11% reduction in mortality risk.

Micronutrient analyses revealed that higher intakes of calcium, magnesium, copper, and vitamin C were associated with lower breast cancer risk. Among patients, greater intake of calcium, phosphorus, magnesium, and vitamin B2 was linked to reduced mortality. In contrast, higher sodium intake increased mortality risk by 15% per standard deviation increase.

Predictive modeling showed modest accuracy overall. Micronutrients were better predictors of incidence, while HPDI more strongly predicted five-year mortality. Combined models performed best at 10 years.

Although the study benefits from large sample sizes and advanced statistical methods, its observational design limits causal interpretation. Dietary data were collected at baseline only, and some risk factors were unavailable. Larger and longer studies are needed to clarify clinical implications.

REFERENCE: Xu, W., Gu, W., Huang, Y., Li, S., Liu, H., Zhu, X. (2026). Plant-based dietary patterns, micronutrient status and breast cancer outcomes: a joint analysis of UK Biobank and Chinese longitudinal healthy longevity survey. Frontiers in Nutrition, 12. DOI: 10.3389/fnut.2025.1748611, https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2025.1748611/full

Study Examines Bidirectional Causal Link Between MASLD and Sarcopenia

A new study, published in the Journal of Clinical and Translational Hepatology, has shed light on the close and potentially harmful relationship between metabolic dysfunction-associated steatotic liver disease (MASLD) and sarcopenia, a condition marked by loss of muscle mass and strength. While the two disorders often occur together, it has remained unclear whether one directly causes the other or how they biologically interact.

To explore this, researchers used Mendelian randomization, a genetic method that helps assess cause-and-effect relationships. Their analysis showed that reduced muscle mass and poor muscle function increase the risk of developing MASLD. This adds to previous evidence suggesting that MASLD itself can also contribute to sarcopenia, pointing toward a two-way causal relationship.

The team also conducted experiments in multiple mouse models, including diet-induced MASLD, genetic MASLD models, a steatotic model, and a drug-induced muscle atrophy model. Mice with MASLD showed clear signs of muscle loss, reduced strength, and abnormal fat accumulation within skeletal muscle. On the other hand, mice with muscle atrophy developed worse liver damage, including increased fat buildup, inflammation, and fibrosis.

Further analysis using multi-tissue transcriptomic profiling of liver and muscle tissues revealed important molecular changes. Sarcopenia disrupted liver metabolic balance by increasing fatty acid uptake and reducing oxidative phosphorylation. Meanwhile, MASLD worsened muscle health by promoting inflammation and metabolic dysfunction.

Importantly, the researchers identified two key signaling molecules involved in liver–muscle communication: C-C motif chemokine ligand 2 (CCL2), a muscle-derived factor that promotes MASLD, and adrenomedullin (ADM), a liver-derived hormone that contributes to muscle loss.

Overall, the findings highlight that MASLD and sarcopenia are interconnected conditions that may fuel each other. Targeting this liver–muscle signaling axis could offer new therapeutic strategies, though further studies are needed to clarify disease progression and underlying pathways.

REFERENCE: Song, Y., et al. (2026). Bidirectional Regulation between Metabolic Dysfunction-associated Steatotic Liver Disease and Sarcopenia via Liver-muscle Crosstalk. Journal of Clinical and Translational Hepatology. DOI: 10.14218/jcth.2025.00538. https://www.xiahepublishing.com/2310-8819/JCTH-2025-00538