What Else Is New? ATTD 2026 Conference Catch-Up

Welcome to The Deep Dive. We have a really incredible mission for you today. We really do. Yeah, so we're looking at two huge presentations from a very recent highly exclusive diabetes technology conference. And the goal today is to explore two ground breaking shifts in the world of Type 1 diabetes or T1D. Right. And the source material we're pulling from is, well, it's pretty heavy stuff. One is a brand new consensus report on safely using those massive weight loss drugs, you know, the GLP and GIPs like, go Zempik and Munjar, right? Exactly. But using them specifically for T1D patients. And the second source breaks down this massive European roadmap for universally screening and detecting T1D before it becomes an absolute crisis. Okay, let's unpack this because everything that people thought they knew about Type 1 diabetes is turning out to be completely wrong. Oh, completely. I mean, the assumption has always been that it primarily affects the lean and that it's usually caught early because, you know, you have a family history of it, but throw those assumptions out. Yeah, these sources, they aren't just minor medical updates. We're talking about a fundamental paradigm shift in how we understand and manage a chronic disease. Totally. So before we even dive into the new treatments, we kind of have to look at how the patients themselves have changed. Or you have to understand the biology of what's happening now. Because I was looking at the data, Dr. Satish Garg presented and he pulled this statistic straight from the CDC and it just sets the stage for everything. The obesity statistic. Yes. Right now, 70% of the US adult population is classified as either overweight or obese. And historically, doctors use weight to distinguish between Type 1 and Type 2. It was like a visual shorthand. Exactly. Type 2 was weight gain and metabolic syndrome. And Type 1 patients were lean because their body stopped making insulin and they lost weight before diagnosis. But that visual distinction is just, well, it's gone now. Right. T1D patients are now completely indistinguishable from the general population regarding weight. They're mirroring that 70% statistic. Which honestly makes perfect biological sense when you look at how we treat the disease today. How so? Well, people with T1D are obviously navigating the same, you know, modern food environment as everyone else. But they have this incredibly complex added layer. Intensive insulin therapy is a weight promoting treatment. Right. Because insulin is a growth hormone. Exactly. Its primary evolutionary job is to tell the body to store energy and often that means storing it as fat. And if you're managing T1D right now, you totally know the catch 22 of modern automated insulin delivery systems. Smart pumps. Right. The smart pumps. They are engineering marvels at keeping your blood sugar in range. But to do that, they are constantly micro-bulleting, just, you know, dripping more insulin into your system all day. Which inherently forces the body to store more fat. And then that creates a vicious cycle, right? Because more fat means more insulin resistance. Yes. So your pump has to deliver even more insulin to hit the same glucose target, which leads to more weight gain. Patients and doctors are just desperate to break this cycle. But there aren't many options. I mean, the only FDA-proved non-insulin therapy for T1D is Pramlin Tide. And nobody uses it. Literally nobody. Because to get any real benefit, you have to take multiple extra daily injections right before meals. And the GI side effects are notoriously harsh. It's just a massive burden. So it's basically a required software update for medical textbooks. The classic character sheet for a T1D patient is officially outdated. It really is. And because doctors have their backs against the wall with this weight gain cycle, they're turning to off-label treatments. The GLPs. Exactly. The massive wave of GLP and GIP medications. The prescription rate for these increase in therapies in T1D is just exploding. But this is off-label, meaning up until this new consensus report, there were basically zero official guidelines on how to do this safely. None. And doing it wrong puts the patient in extreme danger. And that danger is what really stood out to me in Dr. Guards real-world clinical case studies. It shows just how volatile mixing GLPs with insulin can be. It's an absolute balancing act. Right. So let's look at Case 1. He had this young woman. Her BMI was 39 and she was taking 75 units of insulin a day. Which is a pretty hefty dose. Yeah. So he puts her on a weekly GLP. And the standard unofficial clinic practice they've developed is to reduce the patient's insulin by 20% right off the bat to prevent low blood sugar since they'll be eating less. A standard cautious starting line. But for her, 20% wasn't even close to enough. Her insulin resistance vanished so rapidly that she actually ended up in the ER with severe hyperglycemia. Oh wow. Yeah, she needed a 35% reduction just to stabilize. And then you look at Case 2, which is the exact opposite reaction. Yes. This is the one that really highlights the danger of a one size fits all approach. So Case 2 was an older patient. She had lived with T1D for 30 years. Okay. She gets prescribed to her's appetite and the doctor warns her about hyperglycemia. Which is terrifying if you've had T1D for three decades. Exactly. It's your worst nightmare. So she panicked. She ignored the 20% rule and just slashed her basal insulin, her treceba by 60%. Oh no. There's a fundamental misunderstanding of basal insulin. Right. Because that triggered self-induced ketosis. Yeah. Because by cutting it that drastically, she starved her liver of the baseline insolent needs. Her body thought it was starving and started rapidly oxidizing fatty acids into ketones. But wait, I have to point out this fascinating medical trap from the source. Okay. What is it? Well, the known side effects of GLPs are nausea and vomiting, right? Right. So if you're a T1D patient taking this drug and you start throwing up, how do you know if the drug is just making you sick or if you're actually in life-threatening ketosis like that second patient? What's fascinating here is you've actually isolated the exact mechanism that stalled these drugs in T1D clinical trials for years. Really? Just symptom overlap? Yes. It's a massive clinical blinds butt. Nausea from the drugs delayed gastric emptying looks exactly like the nausea from acidic blood in DKA. That is exactly why the consensus rule is so strict. Go slow. You know, type two patients might push up to 15 milligrams of tersepatite. But T1D patients can't handle that? No, wildly inappropriate for their endocrine system. They usually find success around 7.5 to 10 milligrams. It requires hyper individualized care. So knowing all those risks, recalibrating insulin, the mast DKA, why take the risk at all? Because the potential benefits are massive. Right. So let's get into the big picture benefits. The Cleveland Clinic did a study of 4,000 T1D patients using these meds. A huge cohort? Yeah. And first of all, tersepatite, which is the dual GIP and GLP, showed 30 to 40 percent more weight loss and a much greater insulin reduction compared to stomach luteide. The GIP component really supercharges it. But it wasn't just weight. The study showed lower two-year all-cause mortality for those on GLP's. That's the real headline. Totally. And with no overall increase in severe hypoglycemia or DKA, plus their cardioreal biomarkers significantly improved after nearly two years. You're actively shielding the heart and kidneys from the damage that fluctuating glucose causes. But there is a catch. The source had a massive warning about the eyes. The retinopathy risk. Yes. If a patient starts with really poor glucose control, like an A1C of 8.5 or 9, and this drug drops their A1C rapidly, they are at high risk for retinopathy. It's called early worsening of diabetic retinopathy. And it comes down to osmotic shock. Wait, explain that. Why does fixing the blood sugar hurt the eyes? So when patient has chronically high blood glucose, their blood is actually thicker, higher osmolarity. Okay. And the cells lining the tiny blood vessels in the retina adapt to that toxic pressure. But if you drop the glucose levels too fast with the GLP, that gradient shifts violently. The pressure changes. Exactly. Water rushes into those adapted cells. They swell and sometimes they literally burst. Oh my gosh. So a baseline eye exam is absolutely critical before starting. Non-negotiable. Here's where it gets really interesting though, because it's not just insulin they have to monitor. These drugs change how the body processes everything. Right. Entirely separate conditions. Yeah. Like if you're on thyroid medication, your TSH levels might change or uric acid levels shift. Blood pressure drops as you lose weight. So hypertension meds need to be dialed back. And cardiologists are even debating taking T1D patients off statins because their lipid panels are dropping so much. Treating T1D is no longer just about managing blood sugar. It's this holistic balancing act of overall metabolic health, which is amazing for adults. But as we transition to the second source, a really urgent problem emerges. Yeah, we are fundamentally failing to catch the disease early in the first place. Let's rewind the clock. Dr. Sufian Hussain presented data that is just terrifying. Right now, 40 to 42% of children and adolescents newly diagnosed with T1D present with DKA. There are already in a catastrophic crisis. Right. And DKA isn't just a bad stomach ache. It causes acute kidney injury, cerebral edema, which is brain swelling. Yeah. And it has long term cognitive impacts not to mention the severe psychological trauma for the families. Oh, so you might be thinking, you know, listener, in the year 2026 with all our medical advancements, how are nearly half of kids only finding out they have type one diabetes when they are literally an organ failure? And the answer is the biggest misconception about the disease. Yeah. Most of these cases happen in kids with zero family history of T1D. Zero. None. And the international consensus paper makes it clear because there's no family history. Doctors aren't looking for it. So a kid gets lethargic or really thirsty and the pediatrician just thinks it's a summer virus. Exactly. Until the child collapses. So the only solution mathematically is general population screening. Testing millions of healthy people. Yes. Screening for eyelid, auto, and abotties to catch the disease in its silent early stages, months or years before symptoms start. But logistically, how do we actually do that? Well, that's where the European roadmap comes in. Right. The International Diabetes Federation, Europe, the IDF, Europe, they released a nine-step national rollout plan for policymakers. And it starts with public awareness. Because they desperately need campaigns to clear up the confusion between type one and type two, parents still think it's about diet and exercise. Which is completely false for T1D. But the testing mechanism is the key. The consensus advocates for remote or at-home testing. Using a finger prick or a salivary swab? Yeah, making it easier so they can reach rural, deprived, and minority communities who are usually left out of clinical studies. You have to bring the test to the kitchen table. But it took a tragedy to catalyze this. In Italy, the deaths of two children from DKA actually forced lawmakers to act. Right. Italy is implementing screening now. And the consensus is pleading with the rest of Europe. Please don't wait for more tragedies. But I have a practical concern here. Okay, what is it? If you screen a healthy five-year-old and tell the parents they have the markers for an incurable disease that might not strike for years, aren't you just replacing physical illness with intense psychological anxiety? It's a really valid point. And the consensus agrees that exact issue is why they dictate that psychological support absolutely must be a foundational pillar of any screening program. You can't just drop that news and leave them alone. Exactly. But there's another reason we screen. It allows patients to access new preventative therapies. Like T'plizumab. Yes, it's a drug that can actively delay the clinical onset of the disease. But you can't give it to them if you don't know who has the antibodies. Right. So to summarize this whole journey listener, we've really looked at the extreme ends of the Type 1 diabetes timeline today. We really have. On one end, you've got veterans of the disease navigating these new GLP therapies, battling changing waistlines and balancing volatile insulin doses. Trying to protect their organs for the long haul. Yeah. And on the other end, a massive policy push is underway to catch the disease in kids before the trauma of DKA even occurs. Which is just incredible. And you know, if we connect this to the bigger picture, it leaves you with this really profound thought. What's it at? If remote screening becomes universal, and pipeline drugs can delay the onset of the disease for years, are we moving toward a future where Type 1 diabetes is no longer defined as a chronic condition you live with, but as a preventable genetic quirk that we just keep indefinitely paused. Well, paused disease. Wow. I mean, that is a future worth completely tearing up the medical textbooks for. Definitely. Thank you so much for joining us on this deep dive into the evolving science of T1D. We will see you next time.