Listen to the audio version of this article (generated by AI).
• 60%+ of African youth with type 1 diabetes lack autoimmune markers.
• They are insulin-deficient but non-autoimmune.
• This may represent a new subtype of diabetes.
• Global diagnostic systems may miss these cases.
• Findings have relevance for Black populations worldwide.
For decades, researchers defined type 1 diabetes as an autoimmune condition in which the body attacks its own insulin-producing beta cells. This definition has shaped global diagnostic criteria, training and treatment pathways. But new evidence from sub-Saharan Africa is challenging this long-held theory and raising questions about how diabetes is understood, diagnosed and managed worldwide.
The Young-Onset Diabetes in Sub-Saharan Africa (YODA) study, published in 2025, found that most young people diagnosed with type 1 diabetes in the region lack the autoimmune markers traditionally used to define the condition. Instead, many appear to live with a distinct form of diabetes that is insulin-deficient but non-autoimmune.
Among young people diagnosed with type 1 diabetes in clinics across sub-Saharan Africa, the picture is more complex than it first appears. As Dr Jean-Claude Katte, one of the lead researchers of the YODA study, explains: “Within the group of young people who present as having type 1 diabetes in clinics in sub-Saharan Africa, there are two distinct entities. While some have the classic autoimmune form, there is also another group who are insulin-deficient but do not have the immunologic or genetic markers of type 1 diabetes.”
Findings from this study do more than expand scientific knowledge. They show where we can improve our understanding of diabetes and access to diagnosis, and why care approaches need to better reflect the needs of different populations.
The YODA study was led by researchers working across several countries in sub-Saharan Africa, including Cameroon, Uganda and South Africa. Its aim was simple but long overdue: to understand how diabetes presents in young people in African settings, rather than assuming that patterns observed in Europe or North America apply everywhere.
The researchers’ findings challenged those assumptions. Around two-thirds of young people diagnosed with type 1 diabetes did not have pancreatic islet autoantibodies — the blood markers that signal autoimmune destruction of insulin-producing beta cells. Despite this, they were clearly insulin-deficient. Many were diagnosed at a young age, had a low body mass index (BMI), and sometimes presented with diabetic ketoacidosis (DKA).
In other words, they appeared as people with type 1 diabetes who need insulin to survive. But they did not fit the autoimmune definition that underpins most global guidelines.
Around two-thirds of young people diagnosed with type 1 diabetes lacked pancreatic islet autoantibodies
Increasingly, we recognise diabetes as a condition with many forms, driven by different biological pathways. However, we most often apply this complexity to type 2 diabetes, while we still describe type 1 diabetes as a single, uniform condition.
The YODA findings challenge that view. Researchers identified two distinct groups among young people treated for type 1 diabetes in sub-Saharan Africa. One group showed the expected autoimmune and genetic markers of classic type 1 diabetes. The other — the larger group — was insulin-deficient but lacked both autoimmune markers and the genetic risk profiles typically associated with type 1 diabetes.
Importantly, this second group also did not show features of type 2 diabetes. They were not living with obesity, did not have high levels of naturally produced insulin, and did not carry a high genetic risk for type 2 diabetes.
Taken together, the evidence points to a distinct subtype of diabetes — one that sits outside current classification systems and raises important questions about diabetes diagnoses and treatment around the world.
Most diagnostic criteria for type 1 diabetes are based on studies in people of white European ancestry. These criteria assume that autoimmunity is the defining feature of the condition. In African settings, this assumption can be misleading.
As the YODA research emphasises, the knowledge about diabetes rests on what is “transposed” from European and North American populations, without sufficient validation in other contexts. This matters because genetics, early-life nutrition, exposure to infections and environmental factors vary widely across regions. All of these can influence how diseases and conditions develop.
That complexity, Katte argues, exposes a broader problem in how diabetes is understood and classified globally. Much of today’s clinical guidance, he notes, is rooted in evidence from Europe: “Most of what we know about diabetes was translated from studies conducted in European populations, but we know this is not always correct for African settings. Applying the same diagnostic frameworks everywhere risks misclassification and inequity in care.”
When diagnostic tools do not reflect this diversity, people are more likely to be given the wrong diagnosis. For people living with diabetes, a misdiagnosis is not an abstract issue. It can shape access to insulin, glucose monitoring technologies, education and long-term support.
Much of what is known about diabetes is “transposed” from European and North American populations, without sufficient validation in other contexts
Could undernutrition be the cause?
If this form of diabetes is not autoimmune, what might be driving beta-cell damage? The YODA study does not yet provide definitive answers, but it raises important hypotheses. Researchers point to possible environmental contributors, including early-life undernutrition, recurrent infections, exposure to toxins, or interactions between genetic susceptibility and environmental stressors.
The biological mechanisms behind these differences are still unfolding. For Katte, the lack of clear genetic signals pointed researchers in a new direction: “The absence of a clear genetic predisposition to classic type 1 diabetes made us think that the destruction of beta cells in these young people may be driven by environmental factors. There may be complex interactions between genetics and environment that we do not yet fully understand.”
Undernutrition is a salient factor in this mix. Some researchers speculate that reduced beta-cell mass early in life may be linked to poor nutrition during pregnancy or childhood. This could weaken the pancreas, making it less able to cope with later stresses or damage. Other researchers are exploring whether viral, bacterial or parasitic infections found in some settings could play a role. These questions underline how much remains unknown and how urgently context-specific research is needed.
For healthcare professionals in sub-Saharan Africa, the YODA findings confirm what many already experience in practice: it is often impossible to distinguish diabetes subtypes using clinical features alone.
Access to diagnostic tools is a major barrier. Many healthcare settings lack routine testing for islet autoantibodies or C-peptide, a marker of endogenous insulin production. According to surveys cited by the researchers, a significant number of healthcare professionals in the region need access to these tests.
Accurate classification matters. While insulin remains essential for anyone with insulin deficiency, misclassification can affect access to technologies, follow-up care and long-term planning, particularly in health systems where resources are already stretched.
Researchers stress that treatment decisions should prioritise physiology over labels. If a person is not producing enough insulin, they need insulin, regardless of whether their diabetes fits a textbook definition.
While insulin remains essential for anyone with insulin deficiency, misclassification can affect access to technologies, follow-up care, and long-term planning
Although the YODA study focuses on sub-Saharan Africa, its implications are global. When researchers examined data from the United States, they found that a smaller but significant proportion of young people of African ancestry showed a similar non-autoimmune, insulin-deficient pattern. This was not observed among young people of white European ancestry in the same datasets.
These findings from the US suggest similar patterns elsewhere, with Katte highlighting that: “We identified 9-15% of young Black American children with diabetes who showed the same non-autoimmune, insulin-deficient profile. This suggests that this subtype extends beyond Africa and has implications for diagnosis and treatment worldwide.”
For people living with diabetes, particularly those who were reclassified or misdiagnosed, this research brings validation. It reminds us that biology does not always follow neat or universal rules. Nor can it be separated from lived realities such as food systems, infectious disease burden or early-life deprivation.
At its core, the YODA study highlights a structural problem in global health research: whose bodies define “normal”, and whose experiences shape medical knowledge?
Type 1 diabetes research has historically received less attention and funding than type 2 diabetes research, particularly in low- and middle-income countries. Within that limited research, African populations have been underrepresented.
Recognising diversity in diabetes is not about creating ever-narrower labels. It is about ensuring that diagnostic tools, guidelines and treatments are grounded in the realities of the people they are meant to serve.
As the researchers argue, understanding this non-autoimmune form of diabetes could open new biological pathways, inform prevention strategies, and improve care—not only in Africa, but globally.
Type 1 diabetes research has historically received less attention and funding than type 2 diabetes research, particularly in low- and middle-income countries
The YODA findings arrive at a moment when global health systems are grappling with rising diabetes prevalence and persistent inequities in care. They point to the need for action on several fronts. This includes greater investment in inclusive research that reflects the genetic, environmental and social diversity of global populations. It also means improving access to diagnostics such as autoantibody and C-peptide testing, particularly in under-resourced settings, and updating clinical guidelines to recognise the heterogeneity of diabetes presentation.
Most importantly, they underscore the significance of centering people living with diabetes, so classification systems support, rather than restrict, access to appropriate and timely care.
Diabetes does not look the same everywhere. Recognising that fact is not a challenge to science; it is an opportunity to make science more accurate, equitable, and humane.
As diabetes communities work towards better outcomes for all, the YODA study is a reminder that listening to data, to healthcare professionals, and to lived experience is where progress begins.
