The vote to endorse the category took place on April 8, during the International Diabetes Federation’s (IDF’s) World Diabetes Congress, held in Bangkok, Thailand. In January 2025, a panel met in India to draft a consensus statement about the condition, due to be published soon, Meredith Hawkins, MD, professor of medicine at Albert Einstein College of Medicine, Bronx, New York, told Medscape Medical News.
“Malnutrition-related diabetes has historically been vastly underdiagnosed and poorly understood. The IDF’s recognition of it as ‘type 5 diabetes’ is an important step toward raising awareness of a health problem that is so devastating to so many people,” Hawkins said.
According to the American Diabetes Association,
•“type 3” diabetes indicates specific types due to other causes such as single genes, exocrine pancreatic diseases such as cystic fibrosis, or drug/chemical-induced diabetes.
• “Type 4” is gestational diabetes
Malnutrition-related diabetes was first described in Jamaica in 1955. It is seen most commonly in young men in low- and middle-income countries (LMICs) who have a body mass index < 19. They are often misdiagnosed as having type 1 diabetes, but they don’t develop ketonuria or ketosis despite high blood glucose levels and high insulin requirements.
In 1985, the World Health Organization officially classified “malnutrition-related diabetes mellitus” as a distinct diabetes type, but then in 1999 dropped the category, citing a lack of evidence that malnutrition or protein deficiency causes diabetes.
Hawkins became aware of malnutrition-related diabetes in 2005 while teaching at global health meetings. In 2010, she founded Einstein’s Global Diabetes Institute to study it. In 2022, she and her colleagues published findings from state-of-the-art metabolic testing in 73 Asian Indian men, including 20 with what is now called “type 5 diabetes” following exclusion of all other known forms of diabetes by immunogenetic analysis. Another 15 had type 1 diabetes, 13 had type 2 diabetes, 16 were lean without diabetes, and nine were overweight without diabetes.
Among the findings were lower total insulin secretion in the “type 5” group than in both the lean group without diabetes and the T2D group, significantly lower endogenous glucose production and significantly higher glucose uptake in the type 5 group than in the T2D group, and significantly lower visceral adipose tissue and hepatocellular lipids in the type 5 group than in the T2D group.
These findings contradict the previous belief that malnutrition-associated diabetes was associated primarily with insulin resistance. “It turns out people with this form of diabetes have a profound defect in the capacity to secrete insulin, which wasn’t recognized before. This finding has revolutionized how we think about this condition and how we should treat it,” Hawkins said.
She told Medscape Medical News it’s important to differentiate type 5 from type 1 diabetes because giving too much insulin can rapidly prove fatal. Although there aren’t clear guidelines yet for treating type 5, some data suggest that very small amounts of insulin combined with oral agents may be the most effective.
And, Hawkins added, “I suspect that their nutrition should include much higher amounts of protein and lower amounts of carbohydrates, plus attention to deficient micronutrients…but this needs to be carefully studied now that there is global will and an official mandate from the International Diabetes Federation to do so.”
Hawkins lectures on this topic often at universities in LMICs. “They frequently ask, ‘Why is it we see so much of it and yet never read about it in textbooks?’ Turns out those textbooks are written in the West, where it is not encountered. This will change soon…I’m excited that the tide is turning on a condition that is so prevalent among the world’s poor yet so neglected in Western literature.”
A working group has been tasked with developing formal diagnostic and therapeutic guidelines for type 5 diabetes over the next 2 years.
From www.medscape.com
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An Atypical Form of Diabetes Among Individuals With Low BMI
Eric Lontchi-Yimagou, Meredith Hawkins et al
OBJECTIVE
Diabetes among individuals with low BMI (<19 kg/m2) has been recognized for >60 years as a prevalent entity in low- and middle-income countries (LMICs) and was formally classified as “malnutrition-related diabetes mellitus” by the World Health Organization (WHO) in 1985. Since the WHO withdrew this category in 1999, our objective was to define the metabolic characteristics of these individuals to establish that this is a distinct form of diabetes.
RESEARCH DESIGN AND METHODS
State-of-the-art metabolic studies were used to characterize Indian individuals with “low BMI diabetes” (LD) in whom all known forms of diabetes were excluded by immunogenetic analysis. They were compared with demographically matched groups: a group with type 1 diabetes (T1D), a group with type 2 diabetes (T2D), and a group without diabetes. Insulin secretion was assessed by C-peptide deconvolution. Hepatic and peripheral insulin sensitivity were analyzed with stepped hyperinsulinemic-euglycemic pancreatic clamp studies. Hepatic and myocellular lipid contents were assessed with 1H-nuclear magnetic resonance spectroscopy.
RESULTS
The total insulin secretory response was lower in the LD group in comparison with the lean group without diabetes and the T2D group. Endogenous glucose production was significantly lower in the LD group than the T2D group (mean ± SEM 0.50 ± 0.1 vs. 0.84 ± 0.1 mg/kg · min, respectively; P < 0.05). Glucose uptake was significantly higher in the LD group in comparison with the T2D group (10.1 ± 0.7 vs. 4.2 ± 0.5 mg/kg · min; P < 0.001). Visceral adipose tissue and hepatocellular lipids were significantly lower in LD than in T2D.
CONCLUSIONS
These studies are the first to demonstrate that LD individuals in LMICs have a unique metabolic profile, suggesting that this is a distinct entity that warrants further investigation.
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From the Discussion
In summary, this study is the first to comprehensively evaluate the metabolic profile of individuals with antibody-negative, ketosis-resistant LD without significant microvascular or macrovascular complications in comparison with individuals with clearly defined T1D and T2D from India.
When glucose toxicity was corrected, this unique group of patients displayed a phenotype that is fundamentally different from T1D or T2D.
Specifically, results of this study demonstrate that the cardinal physiologic feature of LD is a defect in insulin secretory capacity as opposed to insulin resistance, as had been previously suggested. Moreover, T2D is associated with an increase in hepatic glucose output and decrease in peripheral glucose uptake, neither of which is a prominent feature in LD, emphasizing that LD is unlikely to be a subtype of T2D.
However, much remains to be learned about this distinctive metabolic entity, including its epidemiology, pathophysiology, natural history, and optimal treatment strategies, especially in low-resource clinical settings in LMICs.
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