2.4 Playing Dirty (2)

Though humans and mice do not share the same microbial inhabitants nor do we have the same core metabolic functions, researchers did find parallels to the mouse studies in human volunteers. The analysis of the microbial fingerprint of 18 human individuals, including twins[1], revealed many mousey similarities[i]. As in mice, the ratio of Bacteriodetes to Firmicutes seemed related to microbial functional diversity and leanness in humans. Even though as Westerners, we have far more Firmicutes working in our gut market than any other phylum, the Bacteriodetes phylum has a greater diversity of metabolic functions.  Simply put, the higher the number of Bacteriodetes, the more diversity in your metabolic functions and the more lean you are likely to be[2].

Scientist Ruth Ley, while examining another aspect of gut microbiota, found a similar bloom of Firmicutes unique to obese people. Her team performed a broad analysis of the gut bionts of many species of animals which included ruminant animals, herbivores, carnivores, and omnivores as well as microbial samples from non-animal ecosystems. They then looked at the 16S rRNA signatures of the bacteria in the samples within a specific microbiome context and grouped them according to how related the bacteria were. What Ley’s group found is that types of microbes clustered in relatedness depending on which ecosystem they lived in. So, human microbes clustered together while microbes taken from, say, a termite gut clustered together. Surprisingly, within the human cluster, there was a unique subcluster of microbiomes: that of obese people. These microbiomes were unique, sharing only Firmicutes with the other human samples.

Are our gut ecosystem inhabitants making us fat and sick? Or are our diet and changes we’ve made to our internal ecosystem creating a niche for these diseased-linked microbes that wouldn’t have otherwise? Are they symptom or a cause?

It’s hard to say exactly. What we can determine is that specific metabolic and immune disorders to tend to have specific microbial fingerprints that are more like the disease individual than even genetically related healthy individuals. Obesity studies were the first place that we saw a direct link between microbes and a specific host phenotype. Thus, much of the initial research that explored our internal worlds centered on the connection between obesity and microbiota. Now, our exploration has expanded, and a disrupted gut ecosystem is implicated in many other previously considered “genetic” or mysterious diseases. As we refine our exploration of the gut ecosystem, we will have more and more information on the connection between our microbes and gut dis-biosis, but for now, we can learn a lot about holobiont function from looking at early obesity studies.

[1] Twin studies are very important in scientific research.  In examining identical twins (who share 100% genetic similarity) and fraternal twins (who share 50% genetic identity like any other brother or sister, the difference is that they are exposed to factors at the same point in time unlike conventionally spaced siblings), scientists can answer very important questions about environmental vs. genetic effects on humans.
[2] Whether an individual is lean or obese because of his microbial inhabitants or as a result of his BMI’s influence on his microbial inhabitants is proving to be a distinction that is harder to make than initially thought. Certainly, lean or germ-free mice do gain weight when they receive a transplant of obese microbiota; however, this effect may be transient.
[i] Peter J. Turnbaugh and Jeffrey I. Gordon, “The Core Gut Microbiome, Energy Balance and Obesity,” The Journal of Physiology 587, no. 17 (September 1, 2009): 4153–58, doi:10.1113/jphysiol.2009.174136.

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