For years, weight loss has been seen as the main goal for preventing type 2 diabetes. But new research published in Nature Medicine suggests the number on the scale may not tell the whole story.
Researchers in Germany followed more than 1,100 adults with prediabetes for up to nine years. They found that participants who managed to bring their blood sugar back to normal levels through diet and exercise cut their risk of developing type 2 diabetes by 71%, even if they didn’t lose weight or, in some cases, gained weight. That protection was nearly identical to those who did lose weight (73%).
“Restoring a normal fasting blood sugar level is the most important goal in preventing type 2 diabetes and not necessarily the number on the scale,” said study leader Prof. Dr. Andreas Birkenfeld of the University of Tübingen and Helmholtz Munich.
The analysis also pointed to fat distribution as a key factor. Visceral fat, the deep abdominal fat that wraps around organs, is strongly linked to insulin resistance and higher diabetes risk. Participants who normalized blood sugar without losing weight showed a drop in visceral fat, while those who stayed in the prediabetes range did not.
The findings suggest that focusing only on weight loss may overlook other meaningful health improvements.
“Exercise and a balanced diet have a positive effect on blood sugar levels, regardless of whether weight is reduced,” Birkenfeld said.
Coauthor Prof. Dr. Reiner Jumpertz-von Schwartzenberg added that guidelines should pay closer attention to blood sugar control and fat distribution patterns, not just body weight.
The takeaway: a healthy lifestyle remains the best recipe for preventing diabetes, but its benefits go beyond weight loss. Improving diet quality and staying active can normalize blood sugar, trim harmful visceral fat and lower long-term risk, even if the scale doesn’t budge.
This study was supported by the German Center for Diabetes Research with funding from the German Federal Ministry for Education and partner states, as well as grants from the German Research Foundation, Helmholtz Munich, and the University of Tübingen. Additional support came from European organizations including the European Foundation for the Study of Diabetes, Independent Research Fund Denmark, and the Novo Nordisk Foundation, along with contributions from the U.S. National Institute of Diabetes and Digestive and Kidney Diseases and the Diabetes Prevention Program Research Group. Open access funding was provided by Helmholtz Zentrum München.