APIC and SHEA have issued a joint statement expressing concern that the President's executive order on childhood vaccine recommendations circumvents the established scientific review process. The organizations reaffirm that vaccines are safe, effective, and essential to protecting public health.

For decades, obesity medications produced only modest weight loss. But in recent years, Ozempic and related GLP-1 therapies have transformed the field, enabling sustained weight loss of 10 to 15% or more. Despite their success, however, scientists have not fully understood how these drugs work in the brain. 

Now, in a new study, Yale researchers have identified an unexpected mechanism of action that challenges a long-held assumption about the brain’s hunger circuitry: that agouti-related peptide (AgRP) neurons, known as drivers of hunger, functioned solely to oppose weight loss. However, the new study shows that GLP-1 therapies like Ozempic instead recruit these neurons to help sustain fat loss. 

“This completely changes how we think about the mechanism involved in these medications and provides new insight into the biology underlying their long-term effects, opening an avenue for the development of more efficient drugs,” said Mateus d’Ávila, a Ph.D. candidate in neuroscience working in Tamas Horvath’s lab in the Department of Comparative Medicine at Yale School of Medicine (YSM) and first author of the study.

A new study published in Diabetes Care finds that bone loss alone does not explain the increased fracture risk observed in some older adults with type 2 diabetes.

The article, "Type 2 Diabetes and Longitudinal Changes in Cortical and Trabecular Bone Density, Microarchitecture, and Strength: The Framingham Study," sought to better understand why people with type 2 diabetes are at greater risk of fractures.