Could Obesity Be an Infectious Disease?

Is there anything to the notion that the rapid increase in obesity worldwide is due in part to obesity being an infectious disease? Obesity has doubled in adults in the U.S. in the last 30 years and has tripled in children, and with the exception of infectious diseases, no other chronic disease in history has advanced so rapidly. Two studies in the last year add provocative evidence toward the concept of obesity as a communicable disease.

These two recent studies are interesting as the rapid expansion of human obesity, even in poorer countries, has led to reservations that overeating and lack of exercise are the only factors in the obesity epidemic.

In the journal Nature, researchers studying mice found that obesity and a common type of liver disease (NAFLD) could be caused by proteins that change microbe populations in the stomach. Researchers studied proteins — known as inflammasomes — that start the immune system’s inflammatory response and act as regulators of the microbial environment in the intestines. A deficiency in parts of two particular types of inflammasomes in mice caused changes in the intestinal tract’s microbial population. These changes were associated with increased bacteria that control the severity of obesity and NAFLD in the mice. Remarkably the changed intestinal environment that led to obesity and NAFLD was infectious among the community of mice studied.

In the more recent research paper in the ISME Journal, investigators studied a human developed endotoxin bacterium inserted into germfree mice. They found it cause obesity, suggesting that the bacterium may cause the development of obesity in its human host.

Researchers describe finding that Enterobacter — a bacterial class of opportunistic, endotoxin-producing pathogens — made up 35% of the gut bacteria in an extremely obese volunteer who suffered from diabetes and other serious metabolic disorders. Investigators took an isolated Enterobacter strain from this person and injected it into germfree mice. The mice inoculated with the bacterial sample put on substantial weight, became insulin resistant, and showed many alterations in their lipid and glucose handling pathways. This research suggests that the expansion of an endotoxin-producing gut bacterium is a causal factor to and not a consequence of the metabolic worsening in its human host.

Even if the link between microbes and obesity is proven, weight gain is a complex issue that involves a person’s genetics, environment, and culture, and not just the viruses or bacterium in the body. Of course, much more research is required, but consider that at one time the idea that stomach ulcers and cancer could be caused by H. pylori was thought to be absurd.

Click here to read the review of the Nature study in the Huffington Post, click here to read the Corante In the Pipeline blog about the Enterobacter paper, or click here to read the original ISME Journal study.

E. coli image by Eric Erbe / Wikimedia