NEWS.

A real-world study of about 330,000 matched patients published July 8 in Digestive Diseases and Sciences puts hard numbers on the GLP-1 gut toll: 31.9 percent had a gastrointestinal adverse event within a year, gastroparesis was 57 percent more likely, and drug-induced pancreatitis nearly tripled. But the same data cut both ways, with fewer bowel obstructions, null gallbladder findings, and fewer emergency-room visits and hospital admissions overall.

A meta-analysis of nine trials found the dual GLP-1 and glucagon agonist mazdutide cut weight by 6.6 to 11.1 percent across rising doses in obesity, and beat dulaglutide on weight and blood sugar in diabetes. The reviewers rated the obesity numbers very low certainty and the diabetes numbers moderate.

A study across 13 South Korean hospitals found adults who started semaglutide or liraglutide to lose weight were diagnosed with depression, anxiety, and other problems more often than matched non-users, with semaglutide carrying about 3.4 times the depression rate. The comparator was people not on the drug, so detection bias could be doing much of the work.

A retrospective study of 21,250 US patients found adults with chronic pancreatitis on GLP-1 drugs were 41 percent less likely to start long-term opioids, and had fewer nerve blocks, endoscopic procedures, and pancreatic surgeries. It is an association from hospital records, not proof the drugs ease the disease.

A network meta-analysis of 17 trials and 1,230 adolescents ranked semaglutide best for weight, dulaglutide for blood sugar, and others for glucose and blood pressure. But most comparisons were indirect and single-trial, so the leaderboard is a hypothesis, not a head-to-head result.

In 371 adults, semaglutide cut blood eosinophils, a driver of asthma inflammation, by about a third. The drop was bigger in leaner patients and independent of weight lost, pointing at a direct effect on type 2 inflammation.

A review of seven studies and 924 adults found GLP-1 drugs did not raise objectively measured physical activity. Structured exercise held steady; incidental daily movement dipped, by about 1,144 steps in one trial.

A 75,000-patient TriNetX cohort tied GLP-1 use to a 41 percent lower rate of atrial fibrillation in chronic kidney disease. The reduction held in people who were neither diabetic nor obese, where the usual metabolic explanation runs out.

A TriNetX study of GLP-1 receptor agonists found autoimmune thyroiditis went opposite directions by diabetes type: down in type 1 (hazard ratio 0.41), up in type 2 (1.23), with the type 2 signal holding against SGLT2 inhibitors. Thyroid cancer showed no change in any group.

A meta-analysis of 186,598 pregnancies found no significant rise in gestational diabetes, preterm birth, preeclampsia, or hypertension among women exposed to GLP-1 receptor agonists around conception.

An Israeli cohort of 2,721 matched pairs followed for up to 12.5 years found that, setting aside the price of the drugs and the operations themselves, GLP-1 patients cost the health system about $109 more per month than bariatric surgery patients. Hospital stays and other medications drove the gap, and it complicates the claim that the drugs are the cheaper path for people eligible for both.

In a records study of more than 4,200 patients, adults with type 2 diabetes and peripheral artery disease had about half the major amputations and a quarter fewer deaths on a GLP-1 drug versus metformin. The heart attacks, strokes, and kidney events the class usually moves did not differ.

A Korean national cohort ran the same GLP-1 patients against two comparison drugs and got two answers: no mental-health difference versus DPP-4 inhibitors, a 20 percent higher depression risk versus SGLT2 inhibitors. The comparator, not the drug, is driving the headline.

In 51,540 older adults with type 2 diabetes, tirzepatide was tied to about 35 percent less new open-angle glaucoma over two years than GLP-1-only drugs. The comparison isolates the drugs, not the disease, and the signal still needs a trial to confirm it.

Liver tumors that stop responding to lenvatinib rewire how they burn sugar, turning down the AMPK fuel gauge and ramping up glycolysis. In cells, a GLP-1 receptor agonist reversed that switch and restored the drug's effect, a preclinical mechanism for why GLP-1 drugs keep surfacing in cancer research.