Even though we all seem to settle into a similar pattern of microbiota after we start eating solid foods, it doesn’t mean that we are healthy. Just as early man’s farming practices left the soil progressively more salty over the years, eventually affecting agriculture in that area centuries

later, our earliest gut homesteaders could shape our metabolism in such a way that haunts us our entire lives. There is still much to be determined about what microbes do in the infant developing gut.

As we discussed in the previous section, all infants progress over the course of the first one to two years of life to an “normal” adult microbial community no matter how they were born (c-section vs vaginal), fed (formula vs breast milk), or any other factor.  By age two, a healthy individual will have an established “adult” gut with a microbial population that is nicely settled into its niches.  This population remains remarkably constant over time despite transient changes that can occur (when taking antibiotics, a temporary shift in diet, etc …)^[1].

It makes sense that, at a species level, we should get the most information about the core functions of our GI ecosystem. However, this focus has proven that the human holobiont is not so easy to classify. One study of microbial species in 124 Europeans drew a broad picture of both the specificity within an individual and diversity among individuals in the microbiome^[i].  Even more important, this study was able to correlate its findings with other studies from Japan and the US.  The European study found that as a group, these 124 people had over three million microbial genes expressed from about 1000 species.  Each individual, though, only harbored about 160 species of microbes with about 57 of these shared across everyone.

Think about it as if everyone has a box of crayons—these are the species.  In everyone’s box, there are 160 different colors—the types of species.  And 57 of those colors are in everyone’s box.  However, the number of crayons of the shared colors may differ among individuals; while we all have the color red in our boxes, I, Breeann, might have three red crayons and you might have 300.  The colors and amounts of colors of crayons in my box (variations in microbial populations on the species level) is my microbial fingerprint (to use another analogy).  And like my actual fingerprint, my microbial fingerprint is unique to me and me alone—even identical twins do not have the same microbial fingerprint^[2].  This study along with others shows that your microbial fingerprint can tell doctors and scientists a lot about you. From your microbial fingerprint, scientists can determine if you are lean, obese, or have a specific bowel disease such as Crohn’s or IBD. Are microbes the cause of these diseases or are they merely adapting to the niches that these diseases create in the gut? Probably a bit of both just like the winding path of the Euphrates influenced early agriculture even as humans manipulated its course.

^[1] Most current research focuses on microbes in the gut because their metabolic contributions are the most evident. However, this focus is quickly shifting as we begin to realize that the sheer volume of genetic influence of the phage population cannot be discounted. We aren’t sure exactly how viruses influence the gut, but many researchers believe that it has something to do with microbial pressure and selection. We will discuss the possibility of viral overlords in the next chapter when we address the importance of our genetic narratives.

^[2] However, if you examine our microbes at a genus level, you will see some similarity between related individuals.  Not surprisingly, on a genus level, I am more like my parents and brothers than I am like my husband because my parents are the primary source of my initial microbial inoculation, and my brothers and I not only share an inoculation source but also ate the food as children.

^[i] Junjie Qin et al., “A Human Gut Microbial Gene Catalogue Established by Metagenomic Sequencing,” Nature 464, no. 7285 (March 4, 2010): 59–65, doi:10.1038/nature08821.