Study reveals type 2 diabetes in lean Africans requires different treatment approach

A study published in Diabetologia has upended a fundamental assumption about type 2 diabetes: that it is, essentially, one disease. Researchers from Amsterdam UMC and the University of Ghana have found that the condition operates through two entirely different biological mechanisms depending on whether a patient carries excess weight. In heavier individuals, the pancreas produces insulin normally, but the body resists it. In lean patients, the pancreas itself fails to manufacture enough insulin. Yet across Africa, both groups receive identical medications—drugs designed to combat insulin resistance, not insulin shortage.

The scale of this mismatch is staggering. In wealthy nations, roughly nine in ten people with type 2 diabetes are overweight, making the disease appear synonymous with excess weight. Africa tells a different story. Nearly four in ten African adults with type 2 diabetes are lean, with normal or even low body weight. In rural areas like Ghana, the proportion climbs to six in ten. This means approximately ten million lean Africans are living with a condition that does not fit the standard textbook picture—yet they are being treated as though it does.

First author Sabrina Esmail articulated the core problem: for these lean patients, the issue is not a reduced response to insulin but an absolute shortage of it. The medications typically prescribed—metformin and sulfonylureas—are calibrated to address insulin resistance. For someone whose pancreas cannot produce enough hormone in the first place, these drugs offer little help. Until now, no one had systematically examined what happens when millions of people receive treatment mismatched to their actual disease.

The researchers analyzed data from more than 3,300 African adults with type 2 diabetes across Ghana, Nigeria, Kenya, and Europe. What emerged was a pattern of divergent harm. Lean patients developed eye damage, known as retinopathy, and strokes at higher rates. Overweight patients faced high blood pressure and increased cardiovascular risk. Chronic kidney disease appeared equally in both groups. Senior author Felix Chilunga noted that body fat composition explained much of this variation, pointing to genuinely distinct disease processes at work.

The roots of these two conditions differ as well. Overweight-driven diabetes is often linked to lifestyle factors. Lean-patient diabetes frequently traces back to malnutrition or low birth weight—conditions that disrupt pancreatic development during critical windows. This is not a matter of individual choice or behavior. It is a matter of early deprivation leaving lasting biological marks.

The implications extend beyond Africa. Africans living in Europe face a similar bind. Research from the UK Biobank shows that people of African descent with a BMI of 26 carry the same diabetes risk as Europeans with a BMI of 30. Across Europe, African migrants develop type 2 diabetes earlier, achieve worse blood sugar control, and face higher disease burden than native populations—all while following treatment guidelines written for a disease pattern they do not have. Charles Agyemang, project leader at Amsterdam UMC, observed that there is no reason to assume the treatment mismatch stops at any border.

The researchers are now calling for targeted clinical trials to identify which treatments actually work for lean diabetic patients. Until those trials happen, millions of people across Africa and the African diaspora will continue receiving medications unlikely to address their underlying condition. The disease is the same in name only. The biology is different. The treatment remains unchanged.