Infectious Obesity
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By about the age of 2, most of a person’s microbial community is established, and it looks much like any other person’s microbial community. But in the same way that it takes only a small percentage of our genome to make each of us unique, modest differences in our microflora may make a big difference from one person to another. It’s not clear what accounts for individual variations. Some guts may be innately more hospitable to certain microbes, either because of genetics or because of the mix of microbes already there. Most of the colonization probably happens in the first few years, which explains why the microflora fingerprints of adult twins, who shared an intimate environment (and a mother) in childhood, more closely resemble each other than they do those of their spouses, with whom they became intimate later in life.
No one yet knows whether an individual’s microflora community tends to remain stable for a lifetime, but it is known that certain environmental changes, like taking antibiotics, can alter it at least temporarily. Stop the antibiotics, and the microflora seems to bounce back — but it might not bounce back to exactly what it was before the antibiotics.
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Gordon first began studying the connection between the microflora and obesity when he saw what happened to mice without any microbes at all. These germ-free mice, reared in sterile isolators in Gordon’s lab, had 60 percent less fat than ordinary mice. Although they ate voraciously, usually about 30 percent more food than the others, they stayed lean. Without gut microbes, they were unable to extract calories from some of the types of food they ate, which passed through their bodies without being either used or converted to fat.
When Gordon’s postdoctoral researcher Fredrik Bäckhed transplanted gut microbes from normal mice into the germ-free mice, the germ-free mice started metabolizing their food better, extracting calories efficiently and laying down fat to store for later use. Within two weeks, they were just as fat as ordinary mice. Bäckhed and Gordon found at least one mechanism that helps explain this observation. As they reported in the Proceedings of the National Academy of Sciences in 2004, some common gut bacteria, including B. theta, suppress the protein FIAF, which ordinarily prevents the body from storing fat. By suppressing FIAF, B. theta allows fat deposition to increase. A different gut microbe, M. smithii, was later found to interact with B. theta in a way that extracts additional calories from polysaccharides in the diet, further increasing the amount of fat available to be deposited after the mouse eats a meal. Mice whose guts were colonized with both B. theta and M. smithii — as usually happens in humans in the real world — were found to have about 13 percent more body fat than mice colonized by just one or the other.