I was browsing through a magazine the other day while waiting in a doctor’s office and came across an interesting article that compelled me to research the subject in greater detail. The article stated that the types and amounts of bacteria we have in our intestinal tract help determine if we become fat or remain thin.
It’s an interesting concept to imagine. The article suggested that we might eventually be able to manipulate intestinal microbes to prevent obesity.
Since I hold both a clinical pharmacy degree and an advanced degree in nutrition, the idea of adjusting the microbe mix in our GI tract to control weight sounded bizarre and far-fetched. But as I researched deeper into the subject, the science made sense. Here’s what I found.
The current belief is that being overweight is simply a math issue. If you consume more calories than you use, you gain weight. If you consume fewer calories than needed, you lose weight. The science is simple, but the execution is much more difficult—for instance, I can never resist that piece of chocolate cake!
Now we may have a better answer. In 2005, Dr. Jeffery Gordon of Washington University in St. Louis began to investigate the relationship between diet, gut microbial ecology and obesity. By using mice in experiments, he found that the two main intestinal bacteria in mice are the same as in the human intestinal tract: Firmicutes and Baceroidetes.
As his research progressed, he discovered that obese mice had a greater amount of Firmicutes bacteria, while thin mice had more Bacteroidetes bacteria. Armed with this information, the research team gathered two sets of germ-free mice and infected one group with microbes taken from obese mice and infected the other group with bacteria from leaner mice. Both groups were fed the exact same diet.
The results showed that the mice given bacteria from the obese mice gained excessive weight. Specifically, two weeks after exposure to the obese mice bacteria, this group had a 47 percent increase in body fat. Conversely, the group of mice infected with bacteria from the thin group had only a 27 percent increase in body fat.
These results suggest that specific microbes absorb more energy from food and that the microbial mix in our GI tract determines if we gain weight.
In layman’s terms, the microbes associated with obesity required little food and energy to reproduce and thus transferred more calories to the host (more than the host needed to maintain weight). In contrast, microbes that kept the mice thin required far more calories to survive, leaving less for the host mice to process and use for energy. Therefore, these mice remained thin.
These studies, although preliminary and too primitive to extrapolate to humans at this point, suggest that one person might have bacteria in their intestinal tracts that consume more calories, leaving that person thinner. Whereas, another person might have a different bacterial mix and gain weight by consuming little more than water.
The studies make a strong argument that one day we might maintain our optimal weight simply by adjusting the microbes in our intestinal tracts.
The thought of having that piece of chocolate cake, and even second servings, without having to worry about gaining weight simply makes me smile—and it also makes me hungry for more of that cake!
Thoughts? Comments? I’d love to hear them!