The old adage “you are what you eat” might not be as correct as saying you are your bacteria (that feed on the food you ingest). Ok, I know this is pretty gross, but bear with me here! It’s actually way cooler than it is disgusting. If who we are was really as simple as what we ate, then your friends whom you do paleo diet fads with or the boozy brunch club you meet with on the weekends should think and feel the same as you. When you really think about it, the way in which we process information, perceive our social interactions, and regulate our emotions can’t be as simple as the food we eat (although it certainly does play a crucial moderating role).
By now you have probably heard about the microbiome — the collection of microbes (bacteria, archae, viruses, fungi) that share a body cavity with us — and have heard the staggering factoid that you are more microbes than you are you (over 100 times as many microbial genes reside in your body than human genes) (1). Over the past couple of decades, microbiome research has exploded and has been primarily concerned with characterizing the types and composition of bacteria living in our gastrointestinal tracts (the “gut microbiome”) and how these community structures differ between “healthy” humans and those with disease states (like obesity, cancer, inflammatory bowel disease, and even autism). A lot of this blossoming program of research owes thanks to the biotechnological advances that allow us to not only sequence our entire meta-genomes (figure out what types of bacteria we have and their community composition) but also characterize our metabolomes (the collection of metabolites that we and these microbes produce that influence our health).
So why would I posit that when considering what makes us “us,” we should think more about the bacteria living in our guts than the food we put in them? Before completely throwing the baby out with the bathwater, I first need to pay this old adage some respect in that it does emphasize the correct location, just not the right players. Did you know that the gastrointestinal tract is densely innervated with neural fibers (the enteric nervous system) and connected with the vagus nerve, which essentially acts like a bidirectional highway between your brain and your gut? In fact, the GI tract is so densely innervated that it is referred to as your “second brain,” a fitting title given that it is home to the majority of your microbiome, which in total weighs approximately the same amount as your brain. These bacteria also produce neurotransmitters like GABA and serotonin that can directly communicate with the neurons of the enteric nervous system. Recognizing the direct relationship between the gut and the brain, researchers from psychologists to microbiologists have begun interrogating what we are referring to as the “gut-brain connection.”
How does the gut-brain connection impact what makes you “you?” Depending on who you talk to, there are a lot of different conceptions of the self and what makes us who we are. In terms of genetics, you are certainly your bacteria. But going beyond the genome, in my program of research, I emphasize the role of cognition (how we think) and emotion regulation (the way we generate and respond to emotions) in what makes us who we are, recognizing that the two processes are intricately intertwined. Psychological researchers have been uncovering the impact of the immune system on our brains for quite some time, and given that our gut bacteria can influence immune processes like the inflammatory response, it makes sense that we begin to look at how our bacteria can modulate immune-to-brain communication. If you didn’t know before reading my last paragraph, you’d probably laugh at the idea of events taking place in our guts having any impact on how we think and experience emotions. But even before this article, you inherently did know this fact to be the case — have you ever felt something was wrong in your gut? Did you ever make a decision based on gut feelings? See, you’ve been experiencing the gut-brain connection this entire time!
Most of the work done in probing the influence of bacteria on cognition has been conducted in animal models (2). This is because in order to support a role of causation, we must be able to directly control the variable of interest. But it’d be pretty hard, and frankly unethical, to control for the microbiome in humans. Therefore, researchers have developed mouse models that are completely germ-free, which allow us to directly interrogate the influence of the microbiome on behavior. How? We can observe how these germ-free mice behave under various experimental conditions compared to their microbial-rich friends: germ-free mice have been shown to have cognitive deficits in short-term recognition and working memory (3). We can assess the role of the microbiome in cognitive functioning in humans through observing patient populations with diseases characterized by microbial dysbiosis, like inflammatory bowel diseases (IBD). Not only are individuals diagnosed with IBD more likely to be diagnosed with depression and anxiety, they also have decreased cognitive function compared to controls (as measured by verbal IQ) (4).
While we can’t make a human completely germ-free, we can influence the types of bacteria that populate their guts. The one case where I think “you are what you eat” really holds up is in probiotics (ingestible microorganisms). Researchers at UCLA conducted a randomized experiment in which they instructed some healthy women to drink a fermented milk drink and others to drink a milk drink that did not contain any probiotics or nothing at all twice daily for 4 weeks (5). They subjected all participants to an emotion-eliciting task while in an fMRI scanner and found that this short probiotic intervention affected activity of brain regions that control central processing of emotion and sensation. Another group of researchers conducted a similar study and found that subjects who received a probiotic treatment showed reduced cognitive reactivity to sad mood, and this effect could be explained by reduced rumination and aggressive thoughts (6). In another study linking cognitive processes and emotion regulation, researchers found that participants who were administered probiotics for just 30 days demonstrated decreased self-blame scores and increased problem solving scores (7). These results were found in a healthy population and may have implications for cognitive affective processes in patient populations, which are crucial to coping with disease.
So, the next time you think about who you are, and why you think and feel the way you do, make sure to consider that your body is a universe that provides a home to trillions of microbes, and that we coevolved with these tiny inhabitants since the dawn of time. In fact, we wouldn’t be us at all without them.
1. Qin J, Li R, Raes J, et al. A human gut microbial gene catalogue established by metagenomic sequencing. Nature. 2010;464(7285):59-65. doi:10.1038/nature08821.
2. Allen AP, Dinan TG, Clarke G, Cryan JF. A psychology of the human brain–gut–microbiome axis. Soc Personal Psychol Compass. 2017;11(4):1-22. doi:10.1111/spc3.12309.
3. Gareau MG, Wine E, Rodrigues DM, et al. Bacterial infection causes stress-induced memory dysfunction in mice. Gut. 2011;60(3):307-317. doi:10.1136/gut.2009.202515.
4. Dancey CP, Attree EA, Stuart G, Wilson C, Sonnet A. Words fail me: The verbal IQ deficit in inflammatory bowel disease and irritable bowel syndrome. Inflamm Bowel Dis. 2009;15(6):852-857. doi:10.1002/ibd.20837.
5. Tillisch K, Labus J, Kilpatrick L, et al. Consumption of Fermented Milk Product With Probiotic Modulates Brain Activity. Gastroenterology. 2013;144(7):1394-1401.e4. doi:10.1053/j.gastro.2013.02.043.
6. Steenbergen L, Sellaro R, van Hemert S, Bosch JA, Colzato LS. A randomized controlled trial to test the effect of multispecies probiotics on cognitive reactivity to sad mood. Brain Behav Immun. 2015;48:258-264. doi:10.1016/j.bbi.2015.04.003.
7. Messaoudi M, Lalonde R, Violle N, et al. Assessment of psychotropic-like properties of a probiotic formulation ( Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) in rats and human subjects. Br J Nutr. 2011;105(5):755-764. doi:10.1017/S0007114510004319.