More than a third of adults in the US are obese, according to the Centers for Disease Control and Prevention. As these rates escalate, researchers are working to figure out obesity's causes in the hopes of developing more effective and less invasive treatments than doctors currently are relying on.
Recent research shows a surprising obesity predictor: intestinal
bacteria. In 2010, Andrew Gewirtz, Ph.D., now a professor at Georgia
State University's Center for Inflammation, Immunity & Infection,
led a seminal study in this particular field. He and his team found that
mice without a gene for toll-like receptor 5 (TLR5), a gene which helps
cells control and detect bacteria, ate about 10 percent more than
normal mice. Given limited food, mice without TLR5 still had insulin
resistance, and when given high-fat diets, they gained more weight and
developed diabetes and fatty liver disease.
In short, an inability to detect the presence of bacteria led mice to develop metabolic syndrome-that dangerous cocktail of obesity, insulin resistance, elevated triglycerides and elevated cholesterol, which puts people at risk for type 2 diabetes, heart disease and certain kinds of cancer.
How does this work? TLR5 detects flagellin, a component of bacteria's flagella, which propel their movement. If there's no TLR5, which acts like a sort of "border patrol", bacteria has the ability to multiply without inhibition.
Surprisingly, the composition of one's intestinal bacteria is not only a matter of genetics. When Gewirtz and his colleagues transferred the intestinal bacteria of TLR5-deficient mice to healthy mice, they exhibited the same dangerous eating behaviors and associated weight gain. "What this means is that when you transfer bacteria from one group of mice to another, you can transfer this predisposition for obesity and its related metabolic diseases," says Gewirtz.
So, what does this mean for us? "While adult humans may not efficiently transfer bacteria to each other, transmission to a newborn baby is very efficient," explains Gewirtz. "Thus, what our results may mean to humans is that the bacteria one acquires from their early development, especially their parents, may have a big impact upon one's tendency to develop obesity and/or type 2 diabetes over a lifetime."
Another study conducted by Mihai Covasa, Ph.D., and his colleagues at the French National Institute for Agricultural Research (INRA) has confirmed and built on these findings. The researchers bred obesity-prone and obesity-resistant rats-the former weren't actually obese, but actually came from a lineage of rats that had a tendency to gain weight and fatten quickly when fed high-fat foods. The researchers extracted microbiota from the rats' feces and implanted them into the stomachs of mice that had been germ-free since birth. For eight weeks, adequate time for the maturation of the intestinal microflora, the mice ate either a regular or a high-fat diet.
The results? The mice implanted with the obesity-prone gut bacteria ate more and gained more weight and fat-regardless of whether they were fed a high- or low-fat diet-compared to all other groups.
The upshot is that proneness to obesity can be inherited not just genetically, but also by simply transferring intestinal bacteria such as from parent to child. Also, the composition of your microbiota is controlled by a variety of factors, your environment and antibiotics, as well as your diet. "Diet can affect bacteria, but bacteria can affect appetite," notes Gewirtz. "So it's an interrelated factor." When discussing obesity, he says, "Most people have focused on diet and lifestyle or lack of exercise, but this is another potential contributor."
That said, there's no clear-cut cause-and-effect here-and researchers are still trying to unravel how those changes in gut bacteria could influence obesity in humans. "We speculate that those changes do influence obesity in humans," he says, "but it is indeed not established fact."
So what is in a bacterial profile that could make people prone to obesity? Could it be the amount of bacteria, or are there specific bacteria that present a problem? Both Drs. Covasa and Gewirtz say there are a lot of unknowns here and that the answer is not so simple. Preliminary findings, according to Covasa, show that obese individuals may have reduced microbial diversity. And Gewirtz's follow-up work has indicated that the issue is largely a matter of bacteria's instability. In healthy mice, the composition of intestinal bacteria doesn't change frequently, but in obesity-prone mice, the population shifts from week to week.
The current research is on mice, not humans, but Gewirtz and his team have found preliminary indications that their findings apply to us, too. A certain percentage of people are TLR5 deficient, and thus far, it looks as though they may be prone to obesity, just like mice. But only one in 250 people are TLR5-deficient-a tiny percentage of the obese population-so the point isn't to show that TLR5-deficiency is a significant cause of obesity, but rather that the mouse work applies to humans. The research is also meant to show that something that alters humans' bacterial composition can affect their metabolism.
One thing you shouldn't take away from these findings is the idea that if you have this or that bacterial profile, you're screwed. Both Gewirtz's and Covasa's research has shown that, no matter what your intestinal bacterial profile, you do have to eat more for the adverse metabolic effects to take hold.
Right now, some doctors rely on invasive gastric bypass surgery to treat obesity; these findings indicate that there might be another way. The end goal is to isolate just what a healthy bacterial profile looks like and, if possible, which types of bacteria are particularly important. From there, researchers could develop a way of manipulating obese people's microbiota to potentially decrease their proneness to metabolic syndrome-and protect their health.
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