It's In the News - a look at the top diabetes headlines and stories happening now. Our top stories: More information about type 1 and COVID, including the vaccine, why is the latest GLP-1 medication, not yet FDA approved, showing up all over the place, what table sugar and vinegar could mean for drug costs, a new inhaled insulin study and much more I'll see you at Friends for Life next week. Come find me at Table T18 Learn more about our in-person events here: https://diabetes-connections.com/events/ Announcing Community Commericals! Learn how to get your message on the show here. Learn more about studies and research at Thrivable here Please visit our Sponsors & Partners - they help make the show possible! Omnipod - Simplify Life All about Dexcom All about VIVI Cap to protect your insulin from extreme temperatures The best way to keep up with Stacey and the show is by signing up for our weekly newsletter: Sign up for our newsletter here Here's where to find us: Facebook (Group) Facebook (Page) Instagram Check out Stacey's books! Learn more about everything at our home page www.diabetes-connections.com Transcript & links: Okay.. our top story this week: XX A large Swedish study found that the increased risk of being diagnosed with type 1 diabetes after COVID-19 infection is mostly limited to the first 30 days after infection and does not continue long term. Researchers followed nearly the entire Swedish population under age 80 from 2020 through 2023 and found that while SARS-CoV-2 infection was linked to a temporary rise in new type 1 diabetes diagnoses, the risk declined over time. The study also found no evidence that COVID-19 vaccination increases the long-term risk of developing type 1 diabetes. Vaccination did not significantly change the relationship between COVID-19 infection and diabetes risk, and any small increase in diagnoses seen among adults shortly after a first vaccine dose was not seen after later doses or during longer follow-up. The researchers concluded that their findings do not support changing current COVID-19 vaccination recommendations because of concerns about type 1 diabetes risk. https://www.infectiousdiseaseadvisor.com/news/covid19-infection-may-increase-short-term-type-1-diabetes-risk/ XX Two new studies are challenging the traditional view that type 1 diabetes develops solely because the immune system attacks insulin-producing beta cells. Researchers from Indiana University found evidence that beta cells themselves may play an active role in determining whether they survive or succumb to the stresses that lead to type 1 diabetes. In the first study, scientists discovered that some healthy human beta cells can quickly activate an antiviral defense system when exposed to interferon-alpha, an immune signal often produced during viral infections. This response relies on molecules called reactive oxygen species (ROS), which are usually associated with cell damage but, in this case, appeared to help switch on protective antiviral genes. Researchers found this defense program in healthy cells and in people at risk for type 1 diabetes, but not in beta cells from people who already had the disease. The findings suggest that losing this built-in defense mechanism may make beta cells more vulnerable during the development of type 1 diabetes. The second study focused on autophagy, the process cells use to recycle damaged or worn-out components. Using a new imaging technique, researchers observed that beta cells in a mouse model of type 1 diabetes showed defects in autophagy before blood sugar levels began to rise and even before a full immune attack was underway. This suggests that problems inside the beta cells may occur early in the disease process rather than being caused entirely by the immune system. Together, the studies point to a more complex picture of type 1 diabetes. While they do not show that beta-cell defects cause the disease, they suggest that differences in how beta cells respond to stress, viral signals, and cellular damage may influence who develops type 1 diabetes and how the disease progresses. https://medicalxpress.com/news/2026-06-beta-cells-players-diabetes.html XX Researchers have created the most detailed map yet of how the human pancreas develops during childhood, offering new clues about why children are especially vulnerable to developing diabetes. The study, published in Nature Communications, examined pancreatic tissue from 123 children without diabetes, ranging from newborns through age 10. Using advanced imaging techniques, scientists tracked how insulin-producing islet cells grow and mature during the first decade of life. The researchers found that pancreas size varies dramatically at birth, with some infants having pancreases nearly four times larger than others. They also discovered that insulin-producing beta cells grow more slowly after birth than previously thought, suggesting that much of a person's lifelong beta cell capacity may be established before birth and during early childhood. Other findings showed that insulin-producing cells mature earlier than glucagon-producing cells and that new hormone-producing cells may continue to form after birth. The researchers hope this new understanding of pancreas development will help scientists identify diabetes risk earlier and develop better strategies for prevention and treatment in children. https://news.vumc.org/2026/06/29/unlocking-diabetes-secrets-pediatric-organ-donors-help-map-a-path-to-a-cure-and-prevention/ XX At the American Diabetes Association annual meeting, 2-year results from the SUPPRESS-EARLY trial showed that initiating tirzepatide (Mounjaro, Zepbound) early in the course of type 2 diabetes led to substantially higher rates of near-normal glycemic control and also led to broader metabolic improvements compared with intensive conventional therapy. In this MedPage Today video, investigator Stefano Del Prato, MD, of the University of Pisa in Italy, discusses the findings. Following is a transcript of his remarks: What happened is that in the tirzepatide-treated arm, 85% of the population at the end of the second year was on the maximum dose of tirzepatide 15 mg. And then the remaining 15 with the different doses. Interestingly, in the population that had been treated with the intensive conventional approach, 85% of them ended up to have, on top of metformin, a GLP-1 receptor agonist, mainly represented by subcutaneous semaglutide [Ozempic, Wegovy], 60+%, another 15% on oral semaglutide [Rybelsus], and the remaining on dulaglutide [Trulicity]. And I have to say that maybe the recommendation to really push along the line to try to achieve and to strive to achieve [glycemic] control was successful in these individuals. Because the population that had been recruited in the study started off with a baseline A1C of 7.8% and it went down to 6.3% in the conventionally intensive treatment, which is not bad at all, on average is below the target of 6.5%. However, when we look at the effect of tirzepatide, the final level of A1C at the end of the second year was 5.6%, which is on average below the upper limit of the normal range for A1C, 5.7%. This also translates into more people not only achieving normal glycemia, if we can define normal glycemia as A1C below 5.7%, greater than what we observed in conventionally treated individuals. So it was around three times more people achieving an A1C of 5.7%, in the range of around 65%, as compared to 28% with people on a conventional optimized treatment. Now, this is not surprising knowing the potency of tirzepatide. But again, going back to the rationale of the design, can we change what is the natural history of the disease? This seems to be at least of interest and it's possibly changing the trajectory of the disease for glycemic control, as I mentioned, but also in terms of the body weight and waist circumference because both body weight and waist circumference went much lower with tirzepatide compared to the conventional treatment. Tirzepatide also was associated with an improvement in the lipid profile, in particular with the LDL, triglycerides, and the triglyceride concentration and non-HDL cholesterol, and also with a statistically significantly lower systolic blood pressure with a numerical reduction in the diastolic blood pressure. And also the other thing that probably will ... become more apparent with the study continuing is that the investigators were allowed to add on any other treatment ... needed to achieve their target. So tirzepatide was just metformin and tirzepatide. In the control group, there was already 10% of people who were receiving two drugs on top of the metformin. So another potential result of the trial is that it's possible to achieve and maintain better glycemic or better metabolic control over the time without really needing to increase the number of medications in order to achieve that goal. And we know that type 2 diabetes is a progressive condition often requiring intensification of the treatment. So these initial results really stand for a great opportunity with tirzepatide. Of course, we need to wait for the 4 years just to confirm that this is indeed the case, but the initial result seems to point along that line. https://www.medpagetoday.com/meetingcoverage/adavideopearls/121967 XX A study from the University of Virginia found that high blood pressure is extremely common among people with diabetes, even among those who believe their blood pressure is under control. Researchers measured blood pressure in 172 adults with type 1 or type 2 diabetes during routine eye clinic visits and found that only 8% had normal readings. About half had stage 2 hypertension, and more than 10% had blood pressure levels high enough to be considered a medical em
