It's been known since the 1950s that feeding low doses of antibiotics to livestock increases weight gain. The practice, dubbed subtherapeutic antibiotic therapy, or STAT, lowers feed costs while increasing meat production. Nearly 80 percent of the antibiotics purchased in the United States are used for this purpose. The practice is suspected of facilitating evolution of antibiotic-resistant "superbugs" like methicillin-resistant Staphylococcus aureus, or MRSA, which infects both swine and people and is known to be especially common at pig farms. Meanwhile, it's finally coming to light that antibiotics can do to people what they do to livestock: make us fat.
Data has supported this hypothesis since a 1955 study in which antibiotics and placebos were given to three groups of Navy recruits. The placebo group showed the least weight gain, significantly lagging behind the two groups given different antibiotics. In general, the rates of obesity have risen with antibiotic use since their discovery, but as they say in science, correlation does not equal causation. Recent research, however, is turning up evidence that this correlation might not be a coincidence. The basic idea is that bacteria alter the body's microbial communities, also known as the microbiome, and this disruption changes the way our bodies metabolize and store food.
A study published Aug. 27 in Nature looked at how antibiotics affect the microbial balance in mice, and how this might affect weight-gain patterns. One group of mice was exposed to STAT, the other not. Bacteria from the guts of mice from these two groups was compared, and the researchers found antibiotics altered the microbial ecology in the guts of the exposed mice, changing their metabolism.
"By using antibiotics, we found we can actually manipulate the population of bacteria and alter how they metabolize certain nutrients," said Dr. Ilseung Cho, assistant professor of medicine and associate program director for the Division of Gastroenterology at New York University's School of Medicine, in a press release. "Ultimately, we were able to affect body composition and development in young mice by changing their gut microbiome through this exposure."
In other words, just like cows, pigs, and chickens that are exposed to antibiotics, the antibiotic-fed mice got fat.
Another paper, published Aug. 21 this year in Journal of Obesity, found a strong correlation between young children's exposure to antibiotics and later obesity. It also reports that a disproportionate number of obese children and adults were given antibiotics before the age of six months.
"It is possible that early exposure to antibiotics primes children for obesity later in life," said researcher Martin Blaser of NYU's School of Medicine.
Alas, before we can go any further I must first brief you on the topic of fecal transplants, in which one man's deposit becomes another man's suppository. The idea is that bacteria in feces will repopulate the guts of patients who have had their own bacterial communities disrupted.
A 2006 study demonstrated that the gut flora of obese mice are less diverse than those of healthy mice, and when one transplants feces from obese mice to healthy ones, without changing their diets, the healthy mice will gain weight. Researchers have found evidence that these introduced bacteria can influence the genes that regulate metabolism.
In Amsterdam, researchers are doing similar, but reverse, experiments on humans: giving fecal transplants to obese men. A control group receives their own feces, while the experimental group receives fecal transplants from lean donors. It appears that the experimental group's fecal transplants change the way the recipients' bodies metabolize sugar, giving rise to the idea that overhauling a dysfunctional microbiome could become a treatment for obesity.
The human gut contains more than 100 trillion individual bacterium from more than 500 different species, and 10 bacterial cells for every human cell. Of the 5 million genes identified in the human body, only 30,000 are found in human DNA; the rest are microbial genes. This drives home the idea that our bodies are not single autonomous creatures but symbiotic aggregations of multiple organisms.
The intricacies of how human health is influenced by the microbiome is a huge field of inquiry, the surface of which has barely been scratched. As Scientific American recently put it, "The recent literature on human symbionts is wondrous but still groping at the edge of understanding."
To help shed light on what these microbes are and how they influence human health, the National Institutes of Health launched the Human Microbiome Project in 2008. The purpose of the five-year, $157 million project is "to characterize microbial communities found at multiple human body sites and to look for correlations between changes in the microbiome and human health."
Antibiotics are crucial, lifesaving components of our medical system, but what this emerging field is telling us should lead to a more balanced respect for their powers. We may be going nuclear on our microbiomes unintentionally as we gun for the bad guys, creating even badder guys in the process. And we may be giving ourselves obesity via subtherapeutic antibiotic therapy, thanks to residue in the environment and the animal products we eat. Personally, I'll take my antibiotics as seldom as possible, and skip the fecal transplants.