In clinics from southern India to parts of East and Central Africa, physicians still encounter a familiar, uneasy picture. A lean young adult arrives with blood sugar soaring and a long history of stomach pain and scant meals in childhood. Imaging shows a pancreas freckled with calcifications. This is diabetes, but not the kind most readers know. It is a form rooted in early-life deprivation, not genetics or autoimmunity.
The diabetes that begins with hunger
For decades, researchers have described a variant of diabetes strongly linked to chronic undernutrition in childhood and adolescence. Historically it carried names that reflected where and how it was first recognized. In the 1950s, clinicians in the Caribbean and later in South and Southeast Asia described a ketosis-resistant diabetes in undernourished young people. In the 1980s, the World Health Organization grouped these cases under malnutrition-related diabetes mellitus, with two subtypes: protein-deficient pancreatic diabetes and fibrocalculous pancreatic diabetes. The latter involves scarring and stones in the pancreatic ducts that show up on scans.
Medical taxonomy evolves. In 1999, the WHO revised its classification, concluding that the evidence fit better within broader categories. Today most specialists consider these patients to have diabetes due to diseases of the exocrine pancreas, often labeled type 3c. The link to poor nutrition remains central in many regions, even if the old terminology has faded. What persists is a pattern of damage that begins early and declares itself years later.
How it looks in the exam room
Unlike classic type 1 diabetes, which is driven by autoimmune destruction of insulin-producing cells, or type 2, which is dominated by insulin resistance and often accompanied by overweight, malnutrition-linked diabetes tends to appear in people who are thin and have a history of limited protein and micronutrient intake. Many report abdominal pain or steatorrhea, a sign that the pancreas is not producing enough digestive enzymes. Imaging may reveal calcifications in the pancreas. Bloodwork often shows diminished insulin production rather than primary insulin resistance, which is why these patients frequently need insulin to control blood sugar.
Clinically there are familiar complications. Eyes, kidneys, and nerves are vulnerable, just as in other forms of diabetes. But there are also challenges that are specific to the underlying pancreatic damage. People may need pancreatic enzyme replacement to digest food. They often require careful nutritional support to restore protein and micronutrient stores, even as they start insulin or oral diabetes medications. In resource-limited settings, the practicalities are stark. Insulin has to be available and affordable. Reliable refrigeration and glucose monitoring must be in place. Without those, a treatable condition becomes perilous.
A category that slipped through the cracks
The naming debate can feel academic until it affects care. For years, malnutrition-related diabetes was a distinct box on paper. When that box disappeared from official classifications, many cases began to be coded as either type 1 or type 2. In places where undernutrition remains common, that can lead to misdiagnosis and mismanagement. A person with malnutrition-linked diabetes might be told to lose weight they do not have or to try pills that will not work if the pancreas is already failing.
Specialists now encourage a more deliberate approach. If a patient is young, lean, and has a history of early-life undernutrition, and if imaging suggests pancreatic disease or there is evidence of fat malabsorption, clinicians should think about diabetes of the exocrine pancreas. C-peptide testing, which gauges how much insulin the body is making, can help. So can ultrasound or CT scans when available. Labeling the condition correctly is not just a matter of taxonomy. It guides therapy and opens doors to nutrition support and enzyme replacement.
Why it emerges, and why it still matters
Hunger leaves fingerprints. Prolonged deficiencies in protein and micronutrients during growth can stunt organ development, including the pancreas. Repeated infections and environmental toxins may add stress. In some regions, diets heavy in cassava, which contains naturally occurring cyanogenic compounds, and the burden of chronic pancreatitis are part of the story. The result is a pancreas that struggles both to digest food and to regulate blood sugar.
As economies grow and diets diversify, this form of diabetes has become less common in many cities. But it has not vanished. Rural poverty, climate shocks, conflict, and economic crises continue to push households into food insecurity. Health workers in low-resource settings still see young adults with pancreatic calcifications and brittle blood sugars. Even in wealthier countries, severe childhood deprivation can echo in adult metabolism. The lesson is blunt. Conditions that damage the pancreas early do not politely abide by our modern type 1 and type 2 shorthand.
What patients and families should know
- This is not a new type number. The catchy labels that circulate online can obscure more than they explain. The current medical consensus places malnutrition-associated cases under diabetes due to exocrine pancreatic disease, often referred to as type 3c.
- History matters. A clinician evaluating unexplained diabetes in a lean young adult should ask about early diet, growth, and gastrointestinal symptoms. Evidence of poor pancreatic enzyme output or calcifications on imaging strengthens the case.
- Treatment is possible. Insulin is often required. When exocrine function is impaired, pancreatic enzyme replacement and a protein- and micronutrient-adequate diet are part of care. Regular eye, kidney, and nerve screening is as important as in any other form of diabetes.
- Prevention begins far upstream. Reliable access to nutritious food during pregnancy, infancy, and adolescence may prevent the pancreatic damage that sets the stage for this disease.
The bigger picture of diabetes
It is tempting to think in twos. Type 1. Type 2. That shorthand fits headlines but not biology. Gestational diabetes emerges in pregnancy. There are monogenic forms like maturity-onset diabetes of the young. There is diabetes after chronic pancreatitis or cystic fibrosis. There is steroid-induced hyperglycemia. The list is longer than common parlance suggests, and it reflects a simple truth. Different paths can lead to the same destination of high blood sugar.
For malnutrition-linked diabetes, the path is etched by deprivation. The pancreas is both an endocrine organ that makes insulin and an exocrine organ that releases digestive enzymes. Starve a growing body of building blocks and the organ that emerges may never work as intended. Years later, the bill comes due.