In this week’s issue of The Savvy Diabetic:
- Notice of Boycott of the American Diabetes Association
- The ADA Controversy Continues
- Community Voices on the Events at the ADA Scientific Sessions
- A New Path Toward a Type 1 Diabetes Cure
- Regenerating the Body’s Own Insulin-Producing Beta Cells
- Could Type 1 Diabetes Actually Be Two Distinct Diseases?
- Sernova and Seraxis Merge to Advance T1D Cell Therapy
- SGLT Inhibitors for Heart and Kidney Disease in Type 1 Diabetes
- How to Stop GLP-1s Without Regaining Weight
- How Much Protein Can Your Body Use in One Meal?
- Four Plant-Based Proteins for People With Diabetes
News from T1Dto100
- Could Popular Supplements Harm the Aging Brain?
- The Muscle Ability We Lose Fastest With Age — and How to Preserve It
NOTICE OF BOYCOTT OF THE AMERICAN DIABETES ASSOCIATION
There continues to be significant concern and controversy within the diabetes medical, scientific and patient communities following events at the American Diabetes Association’s 86th Scientific Sessions in New Orleans. A group of people with diabetes, advocates, researchers and healthcare professionals has now organized a Notice of Boycott of the American Diabetes Association, with separate petitions for people with diabetes/supporters and for ADA members and healthcare providers.
Sign the Petition: For People with Diabetes and Supporters
Sign the Petition: For ADA Members and Healthcare Providers
THE CONTROVERSY CONTINUES: Troubling new details emerge on diabetes ouster controversy, by Jennifer Ouellette for Ars Technica, July 17, 2026
The controversy began June 5, when prominent diabetes researchers and physicians were removed from the ADA Scientific Sessions in New Orleans after distributing copies of an editorial published in Diabetes Care that criticized federal actions affecting scientific and medical research. Those removed included Diabetes Care Editor-in-Chief Dr. Steven Kahn, former ADA President Dr. Desmond Schatz, Dr. Aaron Kelly, Dr. Justin Ryder and Dr. Irl Hirsch. Dr. Maureen Gannon was also removed from the conference.
The ADA subsequently apologized for how the incident was handled, but the controversy did not end there. According to Ars Technica, the deputy editors of Diabetes Care subsequently attempted to publish an editorial and seven accompanying opinion pieces addressing what happened. They report that the ADA refused to publish the articles.
The collection includes additional allegations about the events in New Orleans, including claims that ADA leadership knew beforehand that the editorial would be distributed and that security and police involvement had been planned in advance. These allegations remain disputed and raise unanswered questions about how and why the researchers were removed.
The authors have called for a thorough investigation, greater transparency, protection of editorial independence and stronger ADA advocacy for scientific research and research funding.
Savvy Note: I don’t usually lead Savvy Updates with organizational controversy. But this is bigger than personalities or politics. Scientific freedom, open discussion, research funding, and the ability of medical-journal editors to operate independently matter enormously to those of us whose lives depend upon continued diabetes research. I believe our community deserves transparency about what happened — and what happens next.
Read more: Troubling new details emerge on diabetes ouster controversy
Community Voices: On the Events of the American Diabetes Association 86th Scientific Sessions, July 16, 2026
The editors, researchers, and physicians involved have made their collection of articles publicly available through the Zenodo research repository after they said the articles could not be published as planned in Diabetes Care.
The collection includes perspectives from a remarkable group of diabetes leaders, including Elizabeth Selvin, Cheryl Anderson, Steven Kahn, Maureen Gannon, Aaron Kelly, Justin Ryder, Desmond Schatz, Mark Atkinson, John Buse, Irl Hirsch, C. Ronald Kahn and David Nathan, among others.
Their central message is simple and important: the ADA exists “to prevent and cure diabetes and to improve the lives of all people affected by diabetes,” and its actions should remain focused on that mission.
Read more: Community Voices
A New Path Toward a Type 1 Diabetes Cure, from Stanford Medicine, July 10, 2026
Stanford endocrinologist Dr. Marina Basina discusses the Stanford Pancreatic Islet Replacement and Immune Tolerance Program (SPIRIT) — and an approach that could potentially overcome one of the biggest obstacles to islet transplantation: lifelong immunosuppression.
In May 2025, Stanford performed its first allogeneic islet-cell transplant using its tolerance-induction protocol. Allogeneic means that the insulin-producing cells come from another person; tolerance induction is designed to teach the recipient’s immune system to accept those cells rather than attack them. The approach introduces donor blood stem cells along with the beta-cell transplant. The goal is to create mixed chimerism, in which immune cells from both donor and recipient coexist, allowing the immune system to recognize the transplanted cells as “self.”
Why is this so important? Current immunosuppressive drugs carry substantial risks, including infection, cancer and kidney damage. Some can also be toxic to the very islet cells they are intended to protect.
And the early result from Stanford’s first patient is certainly attention-getting: time in range greater than 90% and approximately an 80% reduction in insulin requirements. The patient reportedly returned to full-time work, began running again and experienced a substantial improvement in quality of life.
For now, Stanford is focusing primarily on adults with T1D who have hypoglycemia unawareness, for whom recurrent severe hypoglycemia can be life-threatening.
Savvy Note: THIS is why I continue to follow cell-replacement research so closely. Making insulin-producing cells is no longer the only hurdle. Keeping them alive without trading T1D for lifelong immunosuppression may be the bigger challenge. Stanford’s approach to immune tolerance is another fascinating path toward solving that problem.
Read more: A New Path Toward a Type 1 Diabetes Cure
Kura Oncology spins out diabetes pipeline with $50M and Lilly’s help, from Endpoints News, September 9, 2026
Kura Oncology has launched a new company, Caspian Therapeutics, with $50 million in financing to develop a potentially disease-modifying approach to diabetes — one aimed at increasing the body’s own insulin-producing beta cells.
Caspian is built around KO-7246, a next-generation menin inhibitor designed specifically for chronic metabolic diseases. Menin acts, in part, as a brake on pancreatic beta-cell proliferation. Blocking it may allow beta cells to multiply, potentially increasing the body’s own insulin production rather than simply replacing insulin from outside the body. In preclinical studies, KO-7246 selectively expanded pancreatic beta cells, increased endogenous insulin production and improved glucose control in models of both Type 1 and Type 2 diabetes.
Researchers have also observed beta-cell proliferation and improved beta-cell function in human pancreatic islet models. Importantly, improvements in animal studies persisted after treatment stopped, suggesting a potentially durable increase in functional beta-cell capacity.
BVF Partners led the $50 million financing, which includes the T1D Fund, Eli Lilly, and other investors. Kura retains approximately half of Caspian. Additional preclinical data on KO-7246 are scheduled to be presented at the EASD Annual Meeting on September 29.
Savvy Note: This one definitely caught my attention. Much of the current excitement in T1D cure research involves replacing beta cells. This is a very different idea — trying to stimulate and restore our own insulin-producing capacity. It is still preclinical, but absolutely one to watch!
Read more: Kura Oncology with $50M and Lilly’s help
Type 1 Diabetes May Hide Two Distinct Diseases, Large GWAS Suggests, by David Nield for ScienceAlert/CRBC News, September 2026
Could what we call Type 1 diabetes actually include biologically different forms of the disease?
An international genome-wide association study (GWAS) involving 9,091 people with T1D and 14,157 controls separated T1D cases according to two important genetic risk haplotypes, HLA-DR3 and HLA-DR4. Researchers found evidence suggesting two genetically distinct T1D subtypes. The DR3-associated form pointed toward immune pathways involving mast cells, while DR4-associated T1D showed stronger evidence of T-cell-mediated beta-cell destruction.
This matters because T1D has always been remarkably variable. Age at diagnosis, speed of beta-cell destruction, associated autoimmune diseases, insulin requirements and other characteristics can differ substantially from one person to another.
If these findings are confirmed, researchers say they could eventually help with more precise risk prediction, better-designed clinical trials and therapies targeted to particular biological forms of T1D. But replication in additional populations is essential before we start redefining the disease.
Savvy Note: Fascinating! Anyone who has spent enough time around people with T1D knows that we don’t all seem to have exactly the same disease. This research begins to ask whether there may actually be different biological pathways hiding underneath our single T1D label. Don’t start calling them Type 1A and Type 1B yet — but this could eventually help explain why T1D behaves so differently among us.
Read more: Type 1 Diabetes May Hide Two Distinct Diseases
Diabetes cell-therapy biotechs Sernova and Seraxis to merge, from Endpoints News, September 8, 2026
Two companies pursuing cell-replacement therapies for Type 1 diabetes — Sernova Biotherapeutics and Seraxis — have agreed to merge, creating a new company called BetaNova Biotherapeutics. The combination is particularly interesting because it brings together two different pieces of the T1D cell-replacement puzzle: Seraxis’ stem cell-derived pancreatic islet cells and manufacturing capabilities with Sernova’s Cell Pouch Bio-hybrid Organ, an implantable device designed to support survival, engraftment and function of transplanted islet cells.
The proposed BetaNova will focus on advancing cell-replacement therapies for T1D. The company plans to advance SR-02, Seraxis’ stem cell-derived islet-cell therapy, with human clinical testing anticipated in 2027. Next-generation development is intended to incorporate gene editing that could help protect transplanted cells from immune attack — potentially moving toward the ultimate goal of cell replacement without chronic immunosuppression.
Savvy Note: The cells are only one part of the T1D cure puzzle. We need a reliable source of insulin-producing cells, somewhere for them to live and become vascularized, AND a way to prevent the immune system from destroying them. This merger is an interesting attempt to put several of those pieces together.
Read more: Diabetes cell-therapy biotechs Sernova and Seraxis to merge
SGLT Inhibitors for Heart and Kidney Disease in Type 1 Diabetes, by Jonathan Rosen and Ian H. de Boer, Diabetes Care, September 3, 2026
SGLT inhibitors have transformed the prevention and treatment of heart and kidney disease in people with Type 2 diabetes and, increasingly, in people without diabetes. But people with Type 1 diabetes have largely been left behind. In this important Perspective in Diabetes Care, Jonathan Rosen of Breakthrough T1D and Dr. Ian de Boer of the University of Washington argue that developing a safe path forward for the use of SGLT inhibitors for heart and kidney disease in T1D is essential.
The problem, of course, is diabetic ketoacidosis (DKA). SGLT inhibitors can lower glucose while increasing the risk of ketosis and DKA — sometimes with glucose levels that are not dramatically elevated. That risk resulted in significant caution and regulatory barriers to their use in T1D.
But people with T1D also develop chronic kidney disease and cardiovascular disease, and the remarkable cardiorenal benefits demonstrated with SGLT inhibition elsewhere raise an important question: Are people with T1D being denied potentially valuable heart and kidney protection because we haven’t yet developed an adequately safe way to use these drugs?
The authors call for renewed research and a deliberate path toward evaluating these therapies in T1D, including strategies to reduce DKA risk and identify appropriate patients.
Savvy Note: This is an important conversation. We should absolutely respect the very real DKA risk — but that shouldn’t necessarily end the discussion. As more of us live long lives with T1D, protecting our hearts and kidneys becomes increasingly important. Rather than simply saying “not for T1D,” I’d like to see the research determine whether these drugs can be used safely in carefully selected people with appropriate education, ketone monitoring and safeguards.
Read more: SGLT Inhibitors for Heart and Kidney Disease in Type 1 Diabetes. )Article may require purchase/subscription)
We may finally know how to stop taking GLP-1s without regaining weight, by Greg Noone for BBC Science Focus, August 30, 2026
One of the big questions surrounding GLP-1 medications is what happens when someone stops taking them. The short answer: weight regain is common.
GLP-1 drugs suppress appetite, and once the medication is withdrawn, hunger tends to return. Research cited in the article suggests people may regain roughly 0.4 kg (about 0.9 pounds) per month, with some newer medications associated with even faster regain after discontinuation. A meta-analysis of 48 studies found that people retained about one-quarter of their GLP-1-associated weight loss after stopping treatment.
The article argues that the period before stopping may be critical. Patients need more than instructions to “eat healthy.” They may benefit from practical training and behavioral strategies that help them respond when appetite returns.
Some clinicians favor gradually reducing the GLP-1 dose over several months rather than abruptly stopping, although the best discontinuation strategy has not yet been established. Researchers are also studying lower-dose or “microdosing” approaches and other interventions to help maintain weight loss.
Savvy Note: For those of us using GLP-1s with T1D, there is another wrinkle: these medications can substantially change appetite, carbohydrate intake and insulin requirements. Starting, reducing OR stopping one can therefore mean insulin needs change too. This is definitely a conversation to have with the clinician managing both medications rather than simply stopping on your own.
Read more: We may finally know how to stop taking GLP-1s without regaining weight
The truth about how much protein your body can absorb in one meal, by Anahad O’Connor for The Washington Post, September 10, 2026
You’ve probably heard that your body can use only about 20–30 grams of protein at one meal, and that anything beyond that is essentially wasted. Apparently, that’s another nutrition “rule” that isn’t really a rule.
Researchers say the body can digest and use considerably more protein at one sitting. In at least one study, people consumed 100 grams of protein in a single meal and still metabolized and used it. The longstanding 20–30 gram idea comes partly from studies of muscle-protein synthesis, but building muscle isn’t the only thing the body does with amino acids. Protein is used throughout the body — in muscles, organs, skin, enzymes, hormones and the immune system.
For most healthy adults, the National Academy of Medicine’s recommended daily allowance is 0.8 grams of protein per kilogram of body weight (0.36 grams per pound), although needs can be higher depending upon age, activity level and health.
Savvy Note: For those of us getting older, the more useful question may not be “Did I eat too much protein at lunch?” but “Am I getting enough protein overall to help preserve muscle?” And for anyone with kidney disease, protein targets deserve an individualized discussion with your healthcare team.
Read more: The truth about how much protein your body can absorb in one meal. Washington Post subscription may be required.
4 Plant-Based Proteins for People With Diabetes, by Madeline Kennedy for diaTribe, last reviewed July 28, 2025
Looking for ways to eat a little less meat without sacrificing protein? diaTribe offers four diabetes-friendly alternatives: tempeh, beans and other legumes, seitan and tofu. Plant-based proteins are generally lower in saturated fat than many animal proteins and can also provide fiber — helpful for satiety, cardiovascular health and glucose management.
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- Tempeh, made from fermented soybeans, is relatively low in carbohydrates, high in protein and contains all nine essential amino acids.
- Beans, chickpeas and lentils combine protein with lots of fiber and valuable nutrients including potassium, magnesium and iron.
- Seitan, made from wheat gluten, is high in protein and low in saturated fat and provides a soy-free alternative — although obviously not an option for people avoiding gluten. Prepared seitan can also be high in sodium.
- And tofu is another complete protein, low in saturated fat and a good source of iron and calcium.
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And, of course, carbohydrates still count! Beans and legumes in particular contain carbohydrates, so those of us dosing insulin still need to account for them.
Read more: 4 Plant-Based Proteins for People With Diabetes
FROM T1Dto100
Why scientists are starting to worry popular supplements could harm the aging brain, by Ariana Eunjung Cha for The Washington Post, September 10, 2026
Here’s one that made me stop and read. Vitamin D. Omega-3 fish oil. Glucosamine. They’re among the most familiar supplements used by older adults — often precisely because we’re trying to stay healthier as we age.
But emerging research is asking an unexpected question: Could something beneficial or harmless earlier in life behave differently in the aging brain?
Recent studies have reported associations between vitamin D supplementation and faster cognitive decline among some older adults whose vitamin D levels were already normal; between omega-3 supplementation and cognitive deterioration in adults 55 and older; and between glucosamine use and progression from mild cognitive impairment to dementia.
BUT — and this is important — these findings are preliminary. Much of the research is observational, meaning it can identify an association but cannot establish that the supplements caused the cognitive changes. Some of the findings also conflict with earlier research showing possible benefits.
The emerging theory is interesting: aging changes the ways our brains handle fats, calcium, glucose and inflammation. Something that affects a younger brain one way might therefore have a different effect later in life. The researchers aren’t suggesting that everyone empty the supplement cabinet. Instead, they’re raising the possibility that supplements, like prescription drugs, may eventually require more age-specific consideration.
Savvy/T1Dto100 Note: I think the most important message here is NOT “stop taking your supplements.” It’s ask questions. Why am I taking this? Do I still need it? Has anyone checked my blood level? Is the dose still appropriate at my age and with my kidney function, medications and other health conditions? Aging changes us — and perhaps our supplement lists deserve the same periodic review as our prescriptions.
Read more: 9. https://diatribe.org/diabetes-recipes/4-plant-based-proteins-people-diabetes May require subscription to WashingtonPost.com
The muscle ability you lose fastest with age — and how to preserve it, by Gretchen Reynolds for The Washington Post, September 2, 2026
We talk a lot about losing muscle strength as we age. But there’s another important ability that may decline even faster: muscle power.
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- Strength is your ability to produce force. It’s power that helps us rise quickly from a chair, climb a step, catch ourselves when we stumble or react fast enough to prevent a fall.
- Power is your ability to produce that force quickly.Muscle power typically begins declining in our 40s and accelerates with age. But the encouraging news is that it’s never too late to work on it.
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And that difference matters in everyday life.
Power training doesn’t necessarily mean heavy weights or explosive gym workouts. It can mean performing the lifting portion of an appropriate resistance exercise more quickly — while remaining controlled and safe. Research suggests older adults, including people in their 70s and beyond, can improve muscular power with properly designed training.
Savvy/T1Dto100 Note: This one REALLY matters to our T1Dto100 community. We’re always talking about balance, falls, neuropathy, mobility and maintaining independence. Strength matters — but being able to summon that strength quickly enough when we trip may be what keeps us on our feet. Obviously, anyone with significant balance problems, neuropathy, osteoporosis or other mobility issues should work with a PT or qualified professional rather than suddenly trying “power training” alone!
Read more: The muscle ability you lose fastest with age — and how to preserve it May require subscription to WashingtonPost.com
News from T1Dto100
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- Prepare for Open Enrollment with our 2027 Medicare Plan Guide!
- Smart walker boosts walking efficiency & dynamic balance in older adults
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