Do Antibiotics in Early Life Contribute to Obesity?

In recent years, science has made great strides in its understanding of the microbiome, discovering that it plays a role in regulating many body processes. One area of study is the microbiomes interaction and influence on host metabolic processes. Studies using both mice and humans have established a clear correlation between obesity and the composition of the microbiome, identifying a microbiome unique to obese individuals. Furthermore, experiments with germ-free mice have shown that the microbiome effects host metabolism, causing germ free mice to increase in mass when inoculated with normal microbiota. Inoculation with microbiota from obese mice yielded greater increases in mass, showing the obesogenic effect of the microbiota. The mechanisms through which the microbiome can contribute to obesity are enhanced extraction of energy from food, and increased capacity for nutrient uptake in the gut, and alteration of metabolic pathways by suppressing fasting induced adipose factor and decreasing AMPK activity. Many of these pathways show increased activity in obese mice. The enhanced energy extraction coupled with greater deposition of fat mediated by altered metabolic pathways can contribute to obesity. The role of the microbiota in obesity, combined with decades-old observations that antibiotics, particularly early in life, increased the weight of livestock, led to a hypothesis that antibiotics can disrupt the development of the microbiome, causing metabolic changes, leading to obesity. Recently, this hypothesis has been tested, both in studies utilizing mice, and in many epidemiological studies. This paper will evaluate the available evidence to determine if exposure to antibiotics early in life can lead to increased incidence of obesity later