The microorganisms in the human gut appear to play a pivotal role in determining whether a person is lean or obese, new research shows.
The study, published in Science, is the strongest evidence yet that what’s inside an individual’s digestive tract influences the risk of obesity and its related health problems, such as Type 2 diabetes. The work helps explain the nation’s 30-year run-up in excess weight—and it may supply a potential solution to the resulting epidemic, experts said.
“Many factors contribute to obesity,” said the study’s senior author, Dr. Jeffrey I. Gordon, director of the Center for Genome Sciences and Systems Biology at Washington University, St. Louis. For people whose gut organisms are not equipped to fight obesity, it may be possible to “add microbes to fill the vacancies” needed to keep a person lean and healthy, he said.
Gordon and a multinational group of scientists sought to isolate the gut microbiome’s effect on obesity from better-known influences such as genes, diet and exercise.
They recruited four sets of identical female twins in which one twin was lean and the other obese. Through stool samples, the researchers gathered a representative collection of the bacteria, viruses and protozoans flourishing in each woman’s gut. They transplanted that microscopic zoo into a large group of mice whose intestines were essentially a blank slate.
Almost immediately, the mix of living organisms inside a mouse’s digestive tract began to resemble the one inside its human donor. Soon the mice came to resemble more and more the women whose gut microbiomes they had adopted.
Despite eating about the same amount of the same low-fat chow, mice that got transplants from an obese twin began to gain weight and lay down fat deposits. The mice that got transplants from a lean twin remained lean.
The intestinal flora of the lean mice also worked better at breaking down and fermenting dietary sugars than did their counterparts in the obese mice. In the mice that got transplants from a lean twin, undigestible starches passed through the digestive system more speedily, resulting in thinner mice.
“It was a very, very clear, elegant, well-thought-out study,” said Dr. Lawrence J. Brandt, a gastroenterologist at the Albert Einstein College of Medicine in New York City who wasn’t involved in the research. By stripping out the effects of genes and diet, the experiment helps refine experts’ understanding of the specific ways that the gut’s living organisms influence a complex phenomenon like weight gain, he said.