After several hints that gut microbes may be key players in the obesity epidemic, a new study provides a mechanistic explanation of how the intestinal inhabitants directly induce hunger, insulin resistance, and ultimately obesity in rodents.
…Many reports have observed that heavier patients appear more likely to come down with infections during a hospital stay, acquire weaker protection from vaccinations and, as with River, suffer more complications from the flu.
Weight alone may not be the entire explanation. A tantalizing line of evidence suggests that unhealthful foods — fatty, salty, sugary, processed foods — may disrupt the body’s defenses in a way that promotes inflammation, infection, autoimmune diseases and even illnesses like cancer.
Scientists have known for a while that gut bacteria can play a profound role in the weight of mice. Now we have a case report in humans that is not entirely surprising: A woman gained 36 pounds and became obese in the 16 months after a fecal transplant.
…It’s impossible to draw conclusions from any single patient, of course, but this case is interesting against the broader context of what we know about the gut microbiota and weight. A decade of studies in mice have found that those implanted with the gut microbiota of obese humans will become obese, too, despite eating the same diet as those given the microbiota of non-obese humans. Gastric bypass surgery in mice also drastically shifts the gut microbiota, and it could be one reason for why the surgery is so effective for losing weight.