Maybe it’s time to stop blaming junk food entirely for the nation’s ever-expanding waistline? New research out of the University of California-Los Angeles has found that it’s not only what we eat, but how our bodies respond to certain foods that contribute to obesity — and genetics are a critical factor in the equation.
The first-of-its-kind study, which is based on laboratory experiments involving mice, found body-fat responses to a typical fast-food diet can vary widely and are largely determined by the unique qualities and actions of several genes researchers believe may control those responses.
"Our research demonstrates that body-fat responses to high-fat, high-sugar diets have a very strong genetic component, and we have identified several genetic factors potentially regulating these responses," said Brian Parks, M.D., a researcher at the David Geffen School of Medicine at UCLA who helped lead the study, published in the journal Cell Metabolism.
"We found that obesity has similar genetic signatures in mice and humans, indicating the mice are a highly relevant model system to study obesity. Overall, our work has broad implications concerning the genetic nature of obesity and weight gain."
During the two-year study, the UCLA researchers examined the metabolic responses to a high-fat, high-sugar diet in more than 100 strains of mice. They also tracked the animals’ obesity traits, fat tissue, and genetic makeup — keying in on 11 DNA "regions" associated with obesity and fat gain due to high-fat, high-sugar intake. Editor’s Note: Editor’s Note: 3 Secrets to Never Get Sick Again. Get Super Immunity for Only $4.95. Click here.
The mice were placed on a normal diet for the first eight weeks of life, then switched to a high-fat, high-sugar “junk food” diet for eight weeks. Dr. Parks said researchers analyzed changes in fat and the relationship between obesity traits, genes, intestinal bacteria, and diet.
In general, he said, the results indicated that the type and amount of food consumed by the mice contributed only modestly to the degree of obesity. Certain strains of mice, with particular genetic traits, did not gain as much weight, suggesting “gain in body fat is resisted by genetic mechanisms,” the researchers said.
"Changes in body-fat percentage after high-fat, high-sugar feeding were also highly heritable, suggesting that dietary responses are strongly controlled by genetics," noted co-researcher Jake Lusis, M.D., a professor of medicine and human genetics and of microbiology, immunology, and molecular genetics at the Geffen School of Medicine.
The researchers noted the rise in obesity in recent decades has boosted rates of type 2 diabetes, heart disease, and cancer. While high-calorie diets containing high levels of fat and sugar, along with sedentary lifestyles, are significant contributing factors, the UCLA research suggests genetic factors also need to be considered in examining the problem and potential solutions.
"Our future studies will investigate the development of metabolic syndrome and diabetes after high-fat, high-sugar feeding," Dr. Parks said. "We will also begin to focus on specific, identified genetic factors and their role in dietary interactions and obesity."
The study was funded, in part, by the National Institutes of Health.