Carbohydrates, Insulin, and Obesity
October 30, 2018
By Joseph E. Scherger, MD, MPH
Vice President, Primary Care, Eisenhower Medical Center; Clinical Professor, Keck School of Medicine, University of Southern California, Los Angeles
Dr. Scherger reports no financial relationships relevant to this field of study.
SYNOPSIS: Carbohydrate intake stimulates insulin secretion, which is the primary driver of weight gain. Besides driving glucose into cells, insulin causes fat storage, increases hunger, and lowers energy expenditure. High insulin blood levels lead to obesity with some genetic variation.
SOURCE: Astley CM, Todd JN, Salem RM, et al. Genetic evidence that carbohydrate-stimulated insulin secretion leads to obesity. Clin Chem 2018:64:192-200.
Astley et al used several large databases and meta-analyses to estimate the causal relationship between insulin secretion and body mass index (BMI). The data sources included summary results from the largest published studies of people from a predominately European ancestry for insulin secretion. Data also were drawn from the Cardiology and Metabolic Patient Cohort study at Massachusetts General Hospital to validate genetic associations with insulin secretion and to test the observational association of insulin with BMI.
Genetics is a partial determinant of insulin concentration in the blood 30 minutes after oral glucose, known as the insulin-30 index. In their research, Astley et al discovered that higher genetically determined insulin-30 was associated strongly with higher BMI consistent with a causal role in obesity.
COMMENTARY
Clinicians learn in medical school that the role of insulin is to drive glucose into cells so that it can be used for energy. That fundamental role is highlighted by the pathophysiology of type 1 diabetes. There are other important metabolic roles for insulin that become important in obesity and type 2 diabetes. Insulin causes fat storage (lipogenesis) and blocks the burning of fat (lipolysis). Insulin also increases hunger and lowers energy expenditure.1
Insulin causes the human body to burn glucose rather than fat. Any circulating glucose not needed for energy becomes fat through lipogenesis. High insulin blood levels reflect a stress to metabolism to burn glucose for energy rather than fat. High insulin levels also cause inflammation. When insulin levels become low, the body will burn fat for energy, resulting in ketosis. Researchers have demonstrated that burning fat to a degree that causes ketosis does not happen unless the fasting insulin level is less than 10 mcIU/mL.2
Ludwig, one of the authors of the study reviewed here, has conducted considerable research on the carbohydrate-insulin model of obesity and how excess high glycemic carbohydrates cause hunger, obesity, and type 2 diabetes.1,3 Despite opposition from the food industry, for whom refined carbohydrates are highly profitable, there is a clear path available to clinicians to combat obesity through low-carbohydrate nutrition augmented by intermittent fasting.2
REFERENCES
- Ludwig DS, Ebbeling CB. The carbohydrate-insulin model of obesity: Beyond “calories in, calories out.” JAMA Intern Med 2018;178:1098-1103.
- Fung J. The Obesity Code: Unlocking the Secrets of Weight Loss. Vancouver, BC: Greystone Books; 2016.
- Ludwig D. Always Hungry?: Conquer Cravings, Retrain Your Fat Cells, and Lose Weight Permanently. New York: Hachette Book Group; 2016.
Carbohydrate intake stimulates insulin secretion, which is the primary driver of weight gain. Besides driving glucose into cells, insulin causes fat storage, increases hunger, and lowers energy expenditure. High insulin blood levels lead to obesity with some genetic variation.
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