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Carbohydrate-insulin theory

Genetic study supports carbohydrate-insulin obesity theory

Being genetically predisposed to have greater insulin secretion led to a higher a BMI but being genetically predisposed to have a higher BMI did not result in higher insulin secretion

A genetic study examining the carbohydrate–insulin model of obesity - that insulin secretion drives weight gain – has concluded that being genetically predisposed to have greater insulin secretion led to a higher a BMI. However, being genetically predisposed to have a higher BMI did not result in higher insulin secretion, therefore, the outcomes support the carbohydrate–insulin model of obesity.

In the study, ‘Genetic Evidence That Carbohydrate-Stimulated Insulin Secretion Leads to Obesity’, published in the Clinical Chemistry journal, the researchers from Boston Children’s Hospital used genetic variation to isolate and estimate the potentially causal effect of insulin secretion on body weight.

Data sources included summary results from the largest published meta-analyses of predominantly European ancestry for insulin secretion (n=26,037) and BMI (n=322,154), as well as individual-level data from the UK Biobank (n=138,541). Data from the Cardiology and Metabolic Patient Cohort study at Massachusetts General Hospital (n=1,675) were used to validate genetic associations with insulin secretion and to test the observational association of insulin secretion and BMI.

The researchers report that higher genetically determined insulin-30 was strongly associated with higher BMI, consistent with a causal role in obesity. Similar positive associations were noted in sensitivity analyses using other genetic variants as instrumental variables. By contrast, higher genetically determined BMI was not associated with insulin-30.

“We found that genetically-determined insulin secretion predicted body mass index with extremely high confidence and a potentially large effect across the population,” said lead researcher, Dr David Ludwig. “Of particular importance, the ‘reverse’ relationship was null. That is, genetically determined body mass index did not predict insulin secretion to any degree.”

The authors also stated that these results underscore the need for adequately powered clinical trials to explore how individuals with low vs high insulin secretion status respond to diets differing in glycaemic load.

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