It’s been theorized for a while that obesity can be “spread” between friends and family members due to the natural tendency to copy one another’s eating habits, but a new study suggests that obesity could actually be infectious.
The study, which was published online Feb. 1 in the journal Nature, showed that mice which were engineered to have a particular immune deficiency developed fatty liver disease and gained weight when fed a diet of Western-style foods. Surprisingly, when these immune-deficient mice were put in cages with healthy mice, the healthy mice started to develop symptoms of liver disease, and also gain weight.
The reason may be microbes in the stomachs of the mice. The disturbance in the immune systems of the mice may have affected the bacteria in their stomachs, according to study researcher Richard Flavell, a professor of immunobiology at Yale School of Medicine.
Flavell said that while beings normally live in symbiosis with the bacteria in the digestive system, in the study, the number of bacteria associated associated with disease increased 1,000-fold in mice with immune problems. These “bad” bacteria were transmitted from mouse to mouse, changing the microbes in the digestive system of the healthy mice, and making them fat.
Flavell said, “We could make a mouse fatter just by putting it in the same cage as the other mouse,”
It’s possible that humans could suffer similar effects, but much more research is necessary to find out, according to Flavell. The bacteria was transferred very easily in the study because mice tend to eat each other’s feces, a behavior that is not often seen in humans.
Fatty liver disease is very common among obese people, affecting between 75 percent and 100 percent of the obese population, according to researchers. In the past, if two family members living in the same household both became obese or developed liver disease, it would have blamed on genetics. The new study suggests that it could be more than that.
If the findings of the mouse study apply to people, they would suggest that changes need to be made in the approaces taken to obesit and fatty liver disease. Perhaps antibiotics or probitotics could be added to treatment plans to address gut microorganisms, according to Flavell.
Dr. Jasmohan Bajaj, an associate professor of gastroenterology, hepatology and nutrition at Virginia Commonwealth University,said, “This is a very thought-provoking study that underlines the role of the bugs that we all carry inside us in determining our susceptibility to liver disease and its complications.” Bajaj, who was not involved in the study, suggested that more research is needed with humans, who are considerably more complex than mice, to fully comprehend the role of digestive bacteria in liver disease, but “these experiments form a key step forward.”