News Note: More evidence that high-glycemic diets cause obesity

a high-glycemic diet

A large genetic analysis lends credence to the idea that insulin spikes after eating high-glycemic foods promote weight gain. People genetically predisposed to produce higher than normal levels of insulin after eating processed carbohydrates — “bad carbs” like white bread, potatoes and refined sugar — were more likely to be obese, the study found.

The researchers, led by David Ludwig, MD, PhD, of Boston Children’s Hospital, Joel Hirschhorn, MD, PhD, of Boston Children’s and the Broad Institute, and Jose Florez, MD, PhD, of the Broad Institute and Massachusetts General Hospital, tapped a collection of large-scale genome-wide association studies. Analyzing data from more than 26,000 people who had glucose challenges, they identified genetic variants linked with high insulin levels 30 minutes after the challenge.

Next, the team analyzed data from about 140,000 additional people and found that these genetic variants were strongly associated with a higher body-mass index (BMI).

“It appears that a lifetime of high glucose-stimulated insulin secretion is obesogenic,” said Ludwig in a press release. “These findings lend additional support to the carbohydrate-insulin model of weight regulation, which postulates that diets high in glycemic load promote weight gain through the anabolic effects of increased insulin secretion.”

Capturing causality

The study used a technique called Mendelian randomization to get at causality. It minimizes confounding factors and reverse causation — i.e., obesity causing a tendency to produce more insulin, rather than the other way around. Indeed, having a genetic tendency toward a greater BMI did not predict higher insulin secretion.

The researchers believe their findings also lend support for a “precision medicine” approach to dietary interventions for weight loss, since there’s evidence that low-glycemic-index diets work best in high insulin secreters.

Christina Astley, MD, ScD and Jennifer Todd, MD of Boston Children’s were co-first authors on the study. See the report, in the January issue of Clinical Chemistry, for a full list of authors. The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases (K12DK094721, K12DK094721, K24DK082730, R01DK075787, K24DK110550) and the National Heart, Lung and Blood Institute (R00HL122515).