Type 5 Diabetes: A Long-Ignored Condition Gets Its Moment

For more than 70 years, a distinct form of diabetes has quietly devastated populations across South Asia, sub-Saharan Africa, Latin America, and the Caribbean. It has been misdiagnosed, underfunded, and largely invisible to the institutions with the resources to study it. Now, malnutrition-related diabetes, formally designated type 5 diabetes,¹ is finally getting its moment.

At a joint American Diabetes Association (ADA)/International Diabetes Federation (IDF) symposium on the final day of ADA Scientific Sessions 2026, 4 experts traced the arc of a condition first reported in Jamaica in 1950, removed from the World Health Organization’s (WHO) classification list in 1997 for lack of consensus, and now on the cusp of its first formal diagnostic criteria and treatment guidelines. The stakes are not abstract: misclassification has been fatal. The science is now catching up to the clinical reality long known in low- and middle-income countries, and the framework being built around type 5 diabetes may reshape how the global diabetes community understands the disease itself, according to the experts, moderated by Mandeep Bajaj, MBBS, FRCP, vice chair for clinical affairs and professor, Department of Medicine, Baylor College of Medicine.

From J-Type to Type 5, a 70-Year History

It took 70 years, 3 naming conventions, 2 failed consensus meetings, and 1 blunt sentence from a colleague to get malnutrition-related diabetes the attention it deserves. Peter Schwarz, MD, PhD, MBA, president of the IDF, opened his discussion, “From J-Type Diabetes to Type 5 Diabetes: A 70-Year History of a Metabolic Conundrum,” by tracing that arc and not sparing the scientific community its share of blame.

In Jamaica in the 1950s, clinicians first identified a form of diabetes unlike anything in the Western literature: young patients, low body mass index (BMI), little insulin required, and no ketosis. It was called J-type diabetes for its Jamaican origins. Similar reports soon followed from Bangladesh, Ethiopia, Korea, Rwanda, and Uganda, he explained, a pattern emerging across low-resource, tropical environments that wealthy research institutions largely chose to ignore.

“The big organizations in Europe, in the US—the rich organizations—these are poor countries, poor environment,” he said. “They were not interested in it, and so it got forgotten."*

The WHO took an early leadership role, adding malnutrition-related diabetes to its official classification list in 1985 and convening an international expert group to build consensus around its physiology, diagnostic criteria, and treatment.² That effort collapsed. Scientists couldn’t agree on terminology or biological mechanisms, and in 1997, after nearly a decade on the list, WHO removed it. A quiet period followed.

The turning point came 29 years later, at a consensus meeting in Pune, India, where roughly 40 experts reconvened. It was there that Meredith Hawkins, MD, MS, founding director of the Global Diabetes Institute at Albert Einstein College of Medicine, delivered the sentence Schwarz called a personal shock: “Peter, this is a neglected disease, and we, as scientists, are guilty of it, because we are neglecting this disease.”

That meeting produced both a name, type 5 diabetes, and a commitment. The IDF launched working groups on physiology, diagnostics, and treatment, with formal guidelines expected at the World Diabetes Congress in April 2026.³

“Why type 5 diabetes,” Schwarz posed. “Because giving it a name, it’s becoming relevant.” He closed with a direct call to action: after 70 years of burden, it is time to act.

The Differential Diagnosis of Low-BMI Diabetes

A lean young patient, uncontrolled glucose, no ketosis, low C-peptide. The instinct may be to land on type 5 diabetes, said Nihal Thomas, MD, PhD, senior professor in endocrinology, Christian Medical College. He urged the room to slow down. First, clinicians must systematically rule out conditions that can look nearly identical, particularly where diagnostic tools are scarce. He led the discussion, “The Differential Diagnosis of Low-BMI Diabetes: A Global Perspective.”

“We’re looking for this disorder in areas that have no resources,” he said, “and that’s why we need to rule out the 4 or 5 other conditions, which are very, very important, with limited tests."*

Thomas opened with a type 5 case that met criteria cleanly: young male; low birth weight; low socioeconomic status; hepatic steatosis’ extremely low total body fat on DEXA scan, a procedure that measures bone mineral density via low-dose imaging⁴; suppressed C-peptide with a modest postprandial surge; and no ketosis. About half of such patients respond to oral agents; the other half require insulin, Thomas said.

A top critical differential diagnosis in tropical regions is fibrocalculous pancreatic diabetes (FCPD). Few patients with FCPD present with the classic triad of abdominal pain and steatorrhea, he explained, meaning CT imaging is often required to detect ductal dilation and calcification, a significant barrier in resource-poor settings. Left unmanaged, FCPD carries a significantly elevated lifetime risk of pancreatic malignancy.⁵

Thomas also walked through rarer but consequential mimics: HNF1B mutations presenting with pancreatic atrophy and renal cysts; mitochondrial disorders, where a mother’s pancreatic presentation preceded a daughter’s neurological one by years; atypical cystic fibrosis, where diabetes dominates; and lipodystrophy syndromes, which deceive by combining a lean appearance with markedly elevated triglycerides and high C-peptides, the inverse of type 5.

He closed with a caution on type 1 misclassification, citing YODA study findings (NCT05013346) showing antibody prevalence in certain ethnic populations is far lower than expected.⁶ “It is an important message that we cannot always use antibodies as a definitive cutoff to rule out type 1 for malnutrition modeling,” he said.

The message is practical: pancreatic imaging and accessible genetic testing are not luxuries. They are vital safeguard against a misdiagnosis that can prove fatal.

Defining the Phenotype of Type 5 Diabetes

For decades, clinicians encountering emaciated young patients with severe hyperglycemia did what seemed logical: they assumed insulin resistance and treated aggressively with high doses of insulin. Children died, however, pointed out Hawkins. She opened her talk, “Defining Type 5 Diabetes as a Unique Form of Diabetes: Comprehensive Phenotyping Studies,” with remarks on one of those deaths. A boy she met in a Ugandan village clinic in 2005 received a misdiagnosis of type 1 diabetes; he was given far more insulin than he needed and was eventually found dead of hypoglycemia.

“He was not the only child,” she stated. “I encountered many other such children in Uganda who died in a similar manner, and this is what catapulted me to learn more about this condition.”

That experience drove a length research partnership with Christian Medical College, one of the few settings outside the West with the infrastructure to conduct the rigorous metabolic phenotyping the question demanded. The central problem was glucose toxicity: patients presented so hyperglycemic that any measurement of insulin action would be confounded. Hawkins’s team would have to spend 2 to 3 weeks normalizing each patient’s glucose before conducting studies, including an 18-hour overnight insulin infusion the night before testing.

What the studies revealed overturned the prevailing assumption. Using stepped hyperinsulinemic-euglycemic clamps to isolate hepatic vs peripheral insulin sensitivity, and mixed meal tests with C-peptide deconvolution to assess secretion, Hawkins explained, she and her team found that patients with low BMI and diabetes were not insulin resistant at the liver or in peripheral tissues. Their insulin sensitivity was comparable to lean nondiabetic controls.

Body composition data reinforced the picture: profoundly low subcutaneous, visceral, and intramyocellular fat, with negligible intrahepatic lipid.⁷ However, the problem turned out to be insulin secretion—not where fat was going—which was markedly deficient, falling between type 1 and type 2 diabetes on the secretory spectrum.

The phenotype that emerged is biologically distinct: persistent life-course undernutrition, normal insulin sensitivity, negligible hepatic fat, and a severe β-cell secretory defect. That profile, Hawkins argued, is what separates type 5 from every other form of diabetes and what makes misclassification so dangerous.

Managing Type 5 From the Womb to the Clinic

Most clinical discussions of type 5 diabetes begin at the moment a patient presents with high blood sugar. Michael Boyne, MD, professor of endocrinology and metabolism, University of the West Indies, argued that by this point, the disease could already decades old. So must be its management, he noted. His presentation was, “Managing Malnutrition-Related Diabetes: The Way Forward.”

“I want to argue that the management begins much earlier, before birth, during recovery from malnutrition, and throughout the life course,” he said. “I’m going to take a sort of developmental way of looking at this aspect, and if that’s the case, if we’re going to be intervening, there are different time points that we can intervene.”

Boyne organized his framework around 4 intervention points. The first is preventing small for gestational age (SGA) births, which affect nearly 25% of births in low- and middle-income countries. Micronutrient supplementation alone can reduce SGA rates by roughly 9%, he said; adding macronutrient support is capable of producing measurable metabolic improvements in children as late as age 5. Evidence points to one clear prerequisite: interventions must begin at preconception. Boyne cited a randomized controlled trial in Sierra Leone combining supplementary food with malaria and infection treatment to improve birth anthropometrics.⁸

The second intervention point is severe acute malnutrition (SAM). Not all malnutrition is equivalent: the nonedematous marasmus phenotype carries significantly worse β-cell function and greater long-term diabetes risk than the edematous kwashiorkor type. Modern protocols combining maintenance calories, broad-spectrum antibiotics, and liberal micronutrients before advancing to high-calorie feeds have dramatically reduced SAM-related mortality. But survival creates its own risk, Boyne explained.

Catch-up growth is the third intervention point. Excessive post-SAM weight gain drives long-term fat accumulation and metabolic vulnerability. Ready-to-use therapeutic foods have helped moderate this, but the tension between short-term survival and long-term metabolic health remains unresolved.

By the time patients reach the clinic, Boyne proposed treating suspected type 5 diabetes—his fourth intervention point—with a C-peptide–directed approach: secretagogues such as DPP-4 inhibitors where β-cell reserve remains and basal insulin, starting at roughly 0.3 units/kg, where secretion is severely impaired. Sulfonylureas and metformin remain the most accessible options in low-resource settings, although hypoglycemia risk is real amid ongoing food insecurity.

What the field urgently needs, Boyne concluded, is a dedicated proof-of-concept trial comparing available agents in a true type 5 population, moving management from informed opinion to evidence-based guidelines. He cited the GRADE trial (NCT01794143) as a model for the comparative effectiveness study type 5 diabetes now requires.

References

1. Type 5 diabetes. International Diabetes Federation. Accessed June 15, 2026. https://idf.org/about-diabetes/type-5-diabetes/
2. Wadivkar P, Jebasingh F, Thomas N, et al. Classifying a distinct form of diabetes in lean individuals with a history of undernutrition: an international consensus statement. Lancet Glob Health. 2025;13(10):e1771-e1776. doi:10.1016/S2214-109X(25)00263-3.
3. Type 5 diabetes officially recognized thanks to Einstein research. Montefiore Einstein. April 13, 2026. Accessed June 15, 2026. https://montefioreeinsteinnow.org/update/2026-apr-13/type-5-diabetes-officially-recognized-thanks-einstein-research
4. Bone density text (DEXA or DEX). UC Sand Diego Health. Accessed June 15, 2026. https://health.ucsd.edu/care/imaging/dexa/
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8. Hendrixson DT, Smith K, Lasowski P, et al. A novel intervention combining supplementary food and infection control measures to improve birth outcomes in undernourished pregnant women in Sierra Leone: a randomized, controlled clinical effectiveness trial. PLoS Med. 2021;18(9):e1003618. doi:10.1371/journal.pmed.1003618