Type 2 diabetes operates differently by BMI, yet treatment remains one-size-fits-all

A patient walks into a clinic in rural Ghana with blurred vision and high blood sugar. The doctor prescribes metformin, the standard first-line treatment for type 2 diabetes. The patient is lean—normal weight, even underweight by Western standards. The medicine does not help much. New research suggests why: the doctor is treating the wrong disease.

Scientists at Amsterdam UMC and the University of Ghana have discovered that type 2 diabetes is not one disease but two, split along a fault line of body weight. In people who are overweight, the condition stems from insulin resistance—the body's cells stop listening to the insulin signal, so the pancreas keeps pumping out more hormone in a futile effort to lower blood sugar. But in lean patients, the problem is the opposite. The pancreas itself is broken. It cannot make enough insulin in the first place. The two conditions look the same on the surface. They are treated identically. They are not the same at all.

This distinction matters most in Africa, where the disease wears a different face than it does in wealthy countries. In Europe and North America, type 2 diabetes is almost entirely a disease of excess weight—nine out of ten patients are overweight. In Africa, the picture inverts. Nearly four in ten African adults with type 2 diabetes are lean. In some rural areas of Ghana, the proportion climbs to six in ten. That means roughly ten million people across the African continent have a form of the disease that does not match the textbook description, yet they receive textbook treatment anyway.

The research team analyzed data from more than 3,300 African adults with type 2 diabetes across Ghana, Nigeria, Kenya, and Europe. What they found was stark: lean patients and overweight patients developed different complications from the same diagnosis. Lean diabetics suffered more eye damage—retinopathy—and strokes. Overweight diabetics faced high blood pressure and cardiovascular disease. Chronic kidney disease appeared equally in both groups. These divergent outcomes point to fundamentally different underlying biology. The amount of body fat, the researchers concluded, explained much of the variation. Lean patients often carried a history of malnutrition or low birth weight, conditions that can disrupt pancreatic development in childhood. Overweight patients typically had lifestyle-related risk factors. Same disease name. Different origins. Different trajectories.

Yet across Africa, both groups receive the same medications—metformin, sulfonylureas, and other oral tablets designed to combat insulin resistance. For lean patients whose problem is insufficient insulin production, these drugs are largely ineffective. They are receiving the wrong treatment, and until now, nobody had systematically documented the cost. The researchers did. Millions of people are probably getting worse outcomes than they should because the medicine in their hand was designed for a different condition.

The problem extends beyond Africa's borders. African migrants in Europe develop type 2 diabetes earlier than native Europeans and struggle to control their blood sugar despite following the same guidelines. Studies of the UK Biobank show that people of African descent reach the same diabetes risk at a BMI of 26 that Europeans do not reach until 30. A substantial portion of African patients in Europe likely have the lean-pancreatic form of the disease but are treated according to protocols written for the overweight-insulin-resistant form. Their control is demonstrably worse. There is no reason to think the mismatch stops at any border.

The researchers are calling for targeted clinical trials to identify which treatments actually work for lean-BMI diabetics. Until those trials happen, millions of patients will continue taking medications designed for a disease they do not have, watching their vision blur and their stroke risk climb, waiting for medicine that was never meant for them.