Relevant data, including study design, geographic region, participant characteristics, and results, were extracted from the selected studies. The Newcastle-Ottawa Scale was used to assess the quality of studies and rate them as having low, moderate, or high quality.

The associations between allergic diseases and the risk of lung cancer were assessed using random and fixed effects models. Heterogeneity was evaluated using the I-squared statistic and chi-squared test. Sensitivity analyses indicated that no single study significantly influenced the overall effect size, supporting the robustness of the findings.

The search protocol yielded 226 studies. Following deduplication, title/abstract screening, and full-text reviews, 10 studies were selected for the meta-analysis. Of these, eight were case-control studies and two were cohort studies, cumulatively encompassing over 3.8 million participants.

A new study from Aarhus University turns our understanding of how running injuries occur upside down. The research project, which is the largest of its kind ever conducted, shows that running-related overuse injuries do not develop gradually over time, as previously assumed, but rather suddenly—often during a single training session. The research is published in the British Journal of Sports Medicine.

“Our study marks a paradigm shift in understanding the causes of running-related overuse injuries. We previously believed that injuries develop gradually over time, but it turns out that many injuries occur because runners make training errors in a single training session,” explains Associate Professor Rasmus Ø. Nielsen from the Department of Public Health at Aarhus University, who is the lead author of the study.

The study followed 5,205 runners from 87 countries over 18 months and shows that injury risk increases exponentially when runners increase their distance in a single training session compared to their longest run in the past 30 days. The longer the run becomes, the higher the injury risk.

A gene called SDR42E1 has been identified as a key player in how our bodies absorb and process vitamin D. Researchers found that disabling this gene in colorectal cancer cells not only crippled their survival but also disrupted thousands of other genes tied to cancer and metabolism. This opens the door to highly targeted cancer therapies—by either cutting off vitamin D supply to tumors or enhancing the gene’s activity to boost health. The findings hint at vast possibilities in treating diseases influenced by vitamin D, though long-term impacts remain uncertain.

In a major advance for patients with Crohn’s disease, a new study led by researchers at Mount Sinai Health System found that guselkumab, a medication with a mechanism of action that is new to inflammatory bowel disease (IBD) treatment, outperformed an established standard of care in promoting intestinal healing and symptom relief.

These findings from two pivotal Phase III trials known as GALAXI 2 and 3, published in The Lancet, provided the basis for the recent Food and Drug Administration approval of guselkumab (brand name Tremfya) for the treatment of moderately to severely active Crohn’s disease.

Crohn’s disease affects roughly 780,000 people in the United States and often requires a lifetime of management. Despite numerous available biologic medications, many patients fail to achieve sustained remission. Guselkumab blocks the interleukin-23 (IL-23) pathway, a key driver of chronic intestinal inflammation.

Vitamin D is not only an essential nutrient, but also the precursor of the hormone calcitriol, indispensable for health. It regulates the uptake of phosphate and calcium necessary for bones by the intestines, as well as cell growth and the proper function of muscles, nerve cells, and the immune system.

Now, researchers have shown for the first time in Frontiers in Endocrinology that a particular gene called SDR42E1 is crucial for taking up vitamin D from the gut and further metabolizing it—a discovery with many possible applications in precision medicine, including cancer therapy.

“Here we show that blocking or inhibiting SDR42E1 may selectively stop the growth of cancer cells,” said Dr. Georges Nemer, a professor and associate dean for research at the University College of Health and Life Sciences at Hamad Bin Khalifa University in Qatar, and the study’s corresponding author.