June Waller at Scientific American has somehow posted this from the future (dated June 1, 2014). This article discusses research that shows not only are obese people missing bacteria from their guts that thin people have, they are missing a huge variety of them. They used more mouse tests. The part that is encouraging is that they actually made the mice obese and then thin by eliminating and then reintroducing the microbes! Hooray!
To demonstrate cause and effect, Gordon and his colleagues conducted an elegant series of experiments with so-called humanized mice, published last September in Science. First, they raised genetically identical baby rodents in a germ-free environment so that their bodies would be free of any bacteria. Then they populated their guts with intestinal microbes collected from obese women and their lean twin sisters (three pairs of fraternal female twins and one set of identical twins were used in the studies). The mice ate the same diet in equal amounts, yet the animals that received bacteria from an obese twin grew heavier and had more body fat than mice with microbes from a thin twin. As expected, the fat mice also had a less diverse community of microbes in the gut.
Gordon’s team then repeated the experiment with one small twist: after giving the baby mice microbes from their respective twins, they moved the animals into a shared cage. This time both groups remained lean. Studies showed that the mice carrying microbes from the obese human had picked up some of their lean roommates’ gut bacteria—especially varieties of Bacteroidetes—probably by consuming their feces, a typical, if unappealing, mouse behavior. To further prove the point, the researchers transferred 54 varieties of bacteria from some lean mice to those with the obese-type community of germs and found that the animals that had been destined to become obese developed a healthy weight instead. Transferring just 39 strains did not do the trick. “Taken together, these experiments provide pretty compelling proof that there is a cause-and-effect relationship and that it was possible to prevent the development of obesity,” Gordon says.
There are also some experiments showing how antibiotics are killing off the good bacteria, and then that causes obesity:
A new appreciation for the impact of gut microbes on body weight has intensified concerns about the profligate use of antibiotics in children. Blaser has shown that when young mice are given low doses of antibiotics, similar to what farmers give livestock, they develop about 15 percent more body fat than mice that are not given such drugs. Antibiotics may annihilate some of the bacteria that help us maintain a healthy body weight. “Antibiotics are like a fire in the forest,” Dominguez-Bello says. “The baby is forming a forest. If you have a fire in a forest that is new, you get extinction.” When Laurie Cox, a graduate student in Blaser’s laboratory, combined a high-fat diet with the antibiotics, the mice became obese. “There’s a synergy,” Blaser explains. He notes that antibiotic use varies greatly from state to state in the U.S., as does the prevalence of obesity, and intriguingly, the two maps line up—with both rates highest in parts of the South.
And there are human tests going on now as well, although not formally in the US:
A group in Amsterdam, meanwhile, is investigating whether transferring feces from lean to overweight people will lead to weight loss. U.S. researchers tend to view such “fecal transplants” as imprecise and risky. A more promising approach, says Robert Karp, who oversees National Institutes of Health grants related to obesity and the microbiome, is to identify the precise strains of bacteria associated with leanness, determine their roles and develop treatments accordingly. Gordon has proposed enriching foods with beneficial bacteria and any nutrients needed to establish them in the gut—a science-based version of today’s probiotic yogurts. No one in the field believes that probiotics alone will win the war on obesity, but it seems that, along with exercising and eating right, we need to enlist our inner microbial army.
I don’t know. The mice experiments kind of make it sound like probiotics alone might go a really long way. But then the other evidence points to the fact that you have to eat the right food to keep those good bacteria alive. So the eating right is for them, not you. “gotta feed the bugs”