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How does the Gut Microbiome really affect our health?

By Connor Young on

When I was in graduate school, I was working 3 teaching positions, running a clinical study, fulfilling my research data collection and analysis, studying for a “Qualifying Exam,” which would basically determine whether I became a PhD candidate or not, AND on top of that, training intensively for a ½ marathon. I didn’t know it at the time, but I was creating some major fluctuations in my microbiome, and not for the better.

Likely due to a combo of the above stressful events, little sleep, and ironically enough, poor nutrition, I developed an overgrowth of a bacteria called Helicobacter Pylori (it’s actually a common bacteria to have (1), and usually doesn’t show symptoms unless there’s an imbalance in beneficial to unhealthy bacteria). Because of my lack of time, I frequently grabbed food on the go, and these food choices weren’t always the healthiest. Combined with chronic stress, it was the perfect environment for the proliferation of unhealthy bacteria. For this H. Pylori overgrowth, I had to take a strong dose of two different antibiotics for 2 weeks. I did this round TWICE. Needless to say, this wiped out my microbiome completely and it took me years to re-flourish my healthy bacteria. Aside from the research we’re about to discuss, I will be the first to tell you:

Our Microbiome Matters.

So why is this a big deal? What happens when we get out of sync with our most optimal state?

People talk about the possible health effects of an imbalanced gut – cancer, obesity, and autoimmunity, to name a few, but how can the microbiome have so much of an impact? Does it really influence all of these things? Could it really be the next frontier in medicine?

Perhaps the word itself – microbe – suggests the topic is insignificant to the larger picture of health and self. Maybe we view our microbiome as something separate from us, or perhaps a byproduct of our internal environment and/or genetic makeup that we have no control over.

And maybe you’ve heard of probiotics or have only heard the word microbiome in passing. Or maybe you’re currently suffering from autoimmune issues, food allergies, indigestion, or some other health problem. Regardless, in the next few blog posts, we’ll discuss first what the microbiome is, why optimizing for microbiome health should be on your high priority list whether or not you’ve got any issues, and what you can do about it. After all, the gut microbiome—or, the ecosystem of bacteria living in your GI tract— happens to play a primary role in the following critical body processes:

On the Importance of the Microbiome – A 15,000 ft. View:

“All disease begins with the gut” – Hippocrates

The microbiome, or the ecosystem of microbes living within your GI tract, is incredibly important for many reasons.

It plays a huge role in:

  • Digestion
  • Harvesting nutrients otherwise inaccessible to us  
  • Lowering inflammation and developing an immune system
  • Determining whether one is lean or overweight
  • Absorbing nutrients
  • Producing vitamins
  • Metabolizing carcinogens
  • Preventing colonization by pathogens
  • The Central Nervous System, our brain, and our mood
  • Predisposing us to many different ailments IF in dysbiosis, including:
    • Inflammation, autoimmunity, cancer risk, metabolic disorders, obesity, depression, nutrient deficiency

Are we human? Or are we microbes?

The microbiome is linked to almost every part of our health (4, 5, 6, 7, 8, & 9). This is most evident, unfortunately, when things go wrong. A dysbiosis within this complex community can be associated with increases in asthma, allergies, metabolic disorder, diabetes, cancer, obesity, and autoimmune disease (10 & 11), to name just a few.

This, however, shouldn’t come as a surprise to us. We are, after all, 99% microbial and 1% “human” (2 & 3), which is to say our gut bacteria have one hundred times more genes and 10-fold more cells than our human counterpart, respectively (we have about 10 trillion cells, whereas our bacteria are comprised of approximately 100 trillion cells). These genomes are a product of 200,000 year co-evolution.

Single-celled organisms are roughly 3.5 billion years old; they help us break down and extract more energy from indigestible food (exponentially more than we would have been able to get without them), they help us efficiently utilize and store extra calories, they produce vitamins, make enzymes that help us break down and absorb vitamins & minerals, prevent colonization of other bacteria that may be pathogenic, and contribute to a healthy immune system (13). It’s clear that the microbiome evolved to contribute something to our health.

Interestingly, in any ecosystem (think rainforest for example), but especially our microbiome, diversity matters. Typically when diversity decreases, it’s not a good thing. According to some researchers, our ancestors had a more diverse gut microbiota than we currently have (13). Cultures such as the Hadza, who are an example of our “modern-day ancestors,” have been shown to have a wider diversity of microbes than what is noticed in Western society (13). And it turns out that the Hadza’s risk for many of the chronic diseases that we face, is almost absent. Though it doesn’t prove anything, this gives us some clues at why optimizing gut microbiome may be very critical. Similarly, it may not be a far stretch to assume that the rise of most major diseases present today came with a shift in our food system.

But how does this microbiome actually work its magic?

Our microbiome is seeded at birth

Before birth, we have very little, if any, bacteria. We become colonized with initial bacterial species AT birth, beginning with the the passage through the birth canal. One of the first exposures following this initial colonization is through breast milk, which surprisingly, babies can’t actually digest very well! (called milk oligosaccharides). At this point, the human GI tract contains about 90% colonization through the genus Bifidobacteria (17), along with Lactobacilli (16).

As an adult, we’re not good at breaking down complex carbohydrates (fiber, resistant starch, etc.) either, and co-evolved with microbes to help us with this task. As we get exposed to more food and the environment, our digestive system begins to slowly get colonized and diversified with other species, including Clostredium, Ruminococcus, Veilonella, and others (18). We become dominated by two main phyla of bacteria: Bacteroidetes and Firmicutes (18), and the percentage of each phyla is very important to health.

Why would evolution do this? Somehow nature knew to feed another important part of our physiology: the microbiota.

Processing indigestible stuff —> more nutrients

According to researchers Jeff Leach and the Sonnenberg Laboratory, our ancestors would eat 10 times as much fiber and resistant starches as we currently do (11,13, & 23 ). An average American eats 10-15 grams of fiber per day (still short of the recommended 30-35 daily grams). Compare this to the Hadza at 100-200 grams per day! On top of that, they ate seasonally (not sure they had a choice), further diversifying their microbiome by exposing themselves to all different kinds of foods, which in turn flourished different kinds of bacteria in their distal gut.

What about the outcome of that fiber? We can see in the fermentation of undigested foods that  bacteria produce end-products called short chain fatty acids (SCFA), including Acetate, Propionate, and Butyrate, which have regulatory mechanisms to our metabolism, appetite, and increasing T-regulatory cells (14). SCFA are also the main energy source to colonic cells, which make up the barrier that protects our immune cells from becoming exposed to the bacteria.

This is your brain on microbes

But wait, there’s more! No seriously, things get pretty interesting here. 100 million neurons line the GI tract from esophagus to rectum (5). When things get weird down there, your brain is listening. The microbiome is in charge of releasing enzymes and controlling blood flow, and it’s not just taking orders from the boss (brain) upstairs. This is a full blown conversation, and the influence may be bottoms up.

This is due to the tight connection between our microbes and and the brain-gut axis. Which is why what you eat influences your mood, your cravings, and your neural chemistry and affects serotonin, dopamine, epinephrine, GABA, catecholamines, and acetylcholine (5).

Altering our microbes changes US

There are also huge differences seen between the microbiomes of healthy vs. unhealthy individuals.

You can actually witness major shifts in health outcomes when you transplant the microbiota from one organism to another (i.e. obese to lean mouse turns the lean mouse obese, malnourished to non-malnourished turns the not sick now sick, and even anxiety-prone mouse to non anxiety-prone, turning the former into the latter).

For example, obese mice microbes transplanted to germ-free mice get fatter than if they were transplanted from lean mice microbes. This is a result of not only being able to harvest more energy from the food, but their behavior also changes! They are actually eating more! (10).

The same is true for an obese person’s microbes transplanted to a germ-free mouse, as opposed to transplanting from a lean person (yes, human to mouse). Similarly, individuals who have a C. difficile infection (think diarrhea up to 20x/day), that are transplanted with the microbes of a a non-infected donor exhibit relief of all symptoms, essentially resembling the donor’s community! (12).

Even more interesting, because 99% of our total genome is microbial, we can examine the microbes in an individual’s gut and predict with 90% accuracy whether a person is lean or obese. Examine the the human genome to predict the same information and that falls to approximately 60% accuracy, at best (12).


Who runs the show on inflammation and immunity?

Another fascinating observation is just how intelligent this micro-community really is. Bacteria in our gut are essentially struggling to create the most optimal environment for their own survival (which, happens to be that of our own). They can release inflammatory markers that in some way benefits them. This may lead to a feedback loop where the gut can become entrenched in an anti-inflammatory state, or conversely, an inflammatory state (Justin and Erica Sonnenberg). So we can’t just label bacteria as “pro” or “anti” inflammatory. Similarly, a disease state usually takes a long time to showcase itself- it’s not usually just that moment. Which is a good reason to play the long-game when it comes to overall health.

What happens if we starve, or even kill the little guys (read – ourself)? When our microbiota don’t have the nutrients to survive, they start eating away at our own mucus lining in the search for food. They eventually get closer and closer to the gut barrier where our immune cells are (side-note: our immune cells are not usually in contact with bacterial cells. Once in contact, an immune response is initiated, and immune cells are released and kill bacteria. Bacteria then release Lipopolysaccharide (LPS) endotoxin (20, 21), and if hyper-activated, leads to autoimmune diseases such as arthritis, multiple sclerosis, type I diabetes (22), and so on). Once mucin is being broken down, we’re not making as much! In other words, it’s a double-edged sword.

The death example posed above is essentially what happens when we take antibiotics. As we all know, or at least have read/heard, antibiotics are widely prescribed nowadays. Researchers mention that with each additional round of antibiotics, one is less likely to recover from wiping out all of our good bacteria.

So, is it all doom and gloom? Absolutely not. We can change our microbiome! In fact, it actually changes and adjusts relatively easily – by diet, by the environment, and by transplantation from another organism. The key is – you have to feed it – meaning there has to be foodstuff actually available to the microbiota. Most processed/easily digestible meals don’t get to the bacteria because we break it down first! (So there’s nothing left for them). The primary food substrate for the microbiome is fiber, and when the bacteria don’t have a food substrate to consume, they start eating away at our own mucus lining in the gut. That’s when problems start arising.

According to Justin and Erica Sonnenberg, if we can take away the bad bugs and give ourselves time to repair and achieve a new homeostasis, giving resources that will provide a less inflammatory state, THAT is the bacterial sweet spot. (of course prevention should be first line). With additional research, we may even find that our own unique microbiome might actually be the starting point in the pursuit of optimal health.

So that’s the 15,000 foot view. Over the next few weeks, we will look more closely into each of these aspects to see exactly what we can do to optimize that 99% part of our health.  



  1. http://www.nature.com/nature/journal/v445/n7130/abs/nature05562.html Linz, B., Balloux, F., Moodley, Y., Manica, A., Liu, H., Roumagnac, P., … & Yamaoka, Y. (2007). An African origin for the intimate association between humans and Helicobacter pylori. Nature, 445(7130), 915-918.
  2. http://www.sciencedirect.com/science/article/pii/S0163725811000362 Cani, P. D., & Delzenne, N. M. (2011). The gut microbiome as therapeutic target. Pharmacology & therapeutics, 130(2), 202-212.
  3. http://onlinelibrary.wiley.com/doi/10.1111/j.1462-2920.2005.00959.x/full Abdo, Z., Schüette, U. M., Bent, S. J., Williams, C. J., Forney, L. J., & Joyce, P. (2006). Statistical methods for characterizing diversity of microbial communities by analysis of terminal restriction fragment length polymorphisms of 16S rRNA genes. Environmental microbiology, 8(5), 929-938.
  4. https://www.ncbi.nlm.nih.gov/pubmed/22940212  LeBlanc, J. G., Milani, C., de Giori, G. S., Sesma, F., Van Sinderen, D., & Ventura, M. (2013). Bacteria as vitamin suppliers to their host: a gut microbiota perspective. Current opinion in biotechnology, 24(2), 160-168.
  5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367209/ Carabotti, M., Scirocco, A., Maselli, M. A., & Severi, C. (2015). The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems. Annals of gastroenterology: quarterly publication of the Hellenic Society of Gastroenterology, 28(2), 203.
  6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735932/#bib31 Den Besten, G., van Eunen, K., Groen, A. K., Venema, K., Reijngoud, D.-J., & Bakker, B. M. (2013). The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism. Journal of Lipid Research, 54(9), 2325–2340. http://doi.org/10.1194/jlr.R036012
  7. https://www.ncbi.nlm.nih.gov/pubmed/11581570 Alexander, C., & Rietschel, E. T. (2001). Invited review: bacterial lipopolysaccharides and innate immunity. Journal of endotoxin research, 7(3), 167-202.
  8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2327198/ Yoshino, S., Sasatomi, E., & Ohsawa, M. (2000). Bacterial lipopolysaccharide acts as an adjuvant to induce autoimmune arthritisin mice. Immunology, 99(4), 607–614. http://doi.org/10.1046/j.1365-2567.2000.00015.x
  9. Dietert, R. R., & Silbergeld, E. K. (2015). Biomarkers for the 21st century: listening to the microbiome. Toxicological Sciences, kfv013.
  10. https://knightlab.ucsd.edu/wordpress/?page_id=25 Accessed January 23, 2017.
  11. http://sonnenburglab.stanford.edu/ Accessed January 23, 2017.
  12. https://www.ted.com/talks/rob_knight_how_our_microbes_make_us_who_we_are Accessed January 21, 2017.
  13. https://www.amazon.com/Good-Gut-Taking-Control-Long-term-ebook/dp/B00OZ0TOV2
  14. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4756104/
  15. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4756104/
  16. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4053917/ Fijan, S. (2014). Microorganisms with claimed probiotic properties: an overview of recent literature. International journal of environmental research and public health, 11(5), 4745-4767.
  17. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3593662/pdf/nihms417420.pdf Garrido, D., Ruiz-Moyano, S., Jimenez-Espinoza, R., Eom, H. J., Block, D. E., & Mills, D. A. (2013). Utilization of galactooligosaccharides by Bifidobacterium longum subsp. infantis isolates. Food microbiology, 33(2), 262-270.
  18. http://www.sciencedirect.com/science/article/pii/S0092867416314477 Sharon, G., Sampson, T. R., Geschwind, D. H., & Mazmanian, S. K. (2016). The central nervous system and the gut microbiome. Cell, 167(4), 915-932.
  19. http://www.cell.com/cell/fulltext/S0092-8674(15)00248-2 Yano, J. M., Yu, K., Donaldson, G. P., Shastri, G. G., Ann, P., Ma, L., … & Hsiao, E. Y. (2015). Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis. Cell, 161(2), 264-276.
  20. http://diabetes.diabetesjournals.org/content/57/6/1470. Cani, P. D., Bibiloni, R., Knauf, C., Waget, A., Neyrinck, A. M., Delzenne, N. M., & Burcelin, R. (2008). Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet–induced obesity and diabetes in mice. Diabetes, 57(6), 1470-1481.
  21. http://www.sciencedirect.com/science/article/pii/S0016508512001588 Pendyala, S., Walker, J. M., & Holt, P. R. (2012). A high-fat diet is associated with endotoxemia that originates from the gut. Gastroenterology, 142(5), 1100-1101.
  22. http://link.springer.com/article/10.1007/s00125-007-0791-0 Cani, P. D., Neyrinck, A. M., Fava, F., Knauf, C., Burcelin, R. G., Tuohy, K. M., … & Delzenne, N. M. (2007). Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia. Diabetologia, 50(11), 2374-2383.
  23. http://humanfoodproject.com/ accessed Januray 25th, 2017.


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