WASHINGTON/ Jan. 2, 2018 (STL.NEWS) — Innovative research published in the Obesity issue of AACC’s journal, Clinical Chemistry, demonstrates that people are at greater risk for obesity if they produce higher than normal levels of insulin after eating processed carbohydrates. These findings support the still controversial theory that refined carbs are driving the obesity epidemic.
As obesity rates continue to increase, low-carb diets have gained popularity throughout the U.S. as a way to try to stave off weight gain. The main scientific model that supports the low-carb trend is the carbohydrate-insulin hypothesis, which postulates that eating fast-digesting carbohydrates (such as refined grains, potato products, and sugars) leads to obesity by increasing insulin production. In spite of the fact that many Americans now assume cutting carbs is healthy, no studies have definitively proven that the carbohydrate-insulin hypothesis is correct, and the healthcare community is still undecided on whether low-carb diets are beneficial.
In an effort to shine light on this dietary debate, a group of researchers led by David S. Ludwig, MD, PhD, of Harvard Medical School in Boston has completed the first Mendelian randomization (a type of genetic analysis) to determine whether carbohydrate-induced insulin production leads to weight gain. The researchers studied data from more than 26,000 individuals to identify genetic variants linked with high insulin levels 30 minutes after glucose administration (insulin-30). Statistical analysis of data from about 140,000 additional people revealed that these genetic variants were strongly associated with higher body-mass index. For example, based on the researchers’ findings, a 5’2″ to 5’9″ person with insulin-30 one standard deviation (SD) below average would weigh 5.5-6.8 lbs. less than the same person with above average insulin-30 (+1 SD). This indicates that a genetic predisposition to high insulin after carbohydrate consumption causes increased weight gain, and provides further evidence that the carbohydrate-insulin model of obesity is accurate.
“It appears that a lifetime of high glucose-stimulated insulin secretion … is obesogenic,” said Ludwig. “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.”
Dedicated to achieving better health through laboratory medicine, AACC brings together more than 50,000 clinical laboratory professionals, physicians, research scientists, and business leaders from around the world focused on clinical chemistry, molecular diagnostics, mass spectrometry, translational medicine, lab management, and other areas of progressing laboratory science. Since 1948, AACC has worked to advance the common interests of the field, providing programs that advance scientific collaboration, knowledge, expertise, and innovation. For more information, visit www.aacc.org.
Clinical Chemistry is the leading international journal of clinical laboratory science, providing 2,000 pages per year of peer-reviewed papers that advance the science of the field. With an impact factor of 8.008, Clinical Chemistry covers everything from molecular diagnostics to laboratory management.
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