2011; Wang et al., 2010). Darveau said, “It actually takes something that is already functioning and modulates that.”

Vincent Young, associate professor at the University of Michigan Medical School, expanded on the theme that disease reflects an imbalance in the microbiome. Using Clostridium difficile as an example, he discussed how medical thinking around infectious disease is shifting. When he was a medical student, the paradigm revolved around finding the lone “bad bug” and the “drug for bug.” Young teaches his students to consider instead bad versus good communities of microbes. He described a series of experiments that he and colleagues have conducted to better understand what factors influence whether an indigenous gut microbiota resists or succumbs to C. difficile colonization and disease (Chang et al., 2008). Evidence suggests that C. difficile illness is a function of how resilient the indigenous microbiota is following an antibiotic assault, with some communities able to restore balance following withdrawal of the antibiotic and others not. Recurrence is also a common problem with C. difficile, with 25 percent of patients becoming sick again after ending antibiotic treatment due to continued imbalance of the gut microbiota. Restoring balance in the indigenous microbiota—for example, by adding a “good bug” or combination of “good bugs”—could be the basis for a novel therapeutic approach to managing C. difficile disease.


Although research on the microbiome is considered an emerging science, scientists already have made tremendous progress in understanding the microbial makeup of the microbiome and associating microbiome diversity with human disease. Moreover, they are beginning to make headway in understanding how the microbiome impacts human health and disease. It is likely that much of this impact is mediated through diet. Growing evidence suggests that gut microbes influence what the human host is able to extract from its diet, including energetically.

Peter Turnbaugh, Bauer fellow in the FAS Center for Systems Biology at Harvard University, summarized some of what is known about how the gut microbiome influences host energetics based on a series of mouse model studies demonstrating that gut microbes influence obesity (Backhed et al., 2004; Ley et al., 2005; Turnbaugh et al., 2006, 2008). For example, when the gut microbiota of obese mice is transplanted into germ-free mice, the mice gain more body fat compared to initially germ-free mice that receive microbiota transplants from lean mice; furthermore, the obese microbiome has been shown to extract more energy from the same amount of kilocalories compared to the lean microbiome (Turnbaugh et al., 2006, 2008). Other mouse data from Turnbaugh’s lab suggest that the microbiome impacts host

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