# Are the bacteria/parasites in your gut affecting your thinking?

There is a variety of science going on, mostly in mice, about how intestinal microbiota (bacteria/parasites/fungi?) can affect behavior, emotion, and mental development ([Review paper: The micro-biome gut-brain axis, 2011](http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2982.2010.01664.x/full). [Review paper 2009)](http://www.nature.com/nrgastro/journal/v6/n5/abs/nrgastro.2009.35.html). Does any of it have relevance to those of us who'd like to be better rationalists? I'm just beginning to look into this and I'm not a biologist, so I could use help. I'll reference some interesting papers here and give interesting excerpts.

To start off with something easy to read, here is an excerpt from a [press release](http://fhs.mcmaster.ca/main/news/news_2011/gut_anxiety_link_study.html) for this [2011 paper](http://www.gastrojournal.org/article/S0016-5085(11)00607-X/abstract) about effects on mice:

Working with healthy adult mice, the researchers showed that disrupting the normal bacterial content of the gut with antibiotics produced changes in behaviour; the mice _became less cautious or anxious_. This change was accompanied by an increase in brain derived neurotrophic factor (BDNF), which has been linked, to depression and anxiety.

When oral antibiotics were discontinued, bacteria in the gut returned to normal.

"This was accompanied by _restoration of normal behaviour_ and brain chemistry," Collins said.

To confirm that bacteria can influence behaviour, the researchers colonized germ-free mice with _bacteria taken from mice with a different behavioural pattern_. They found that when germ-free mice with a genetic background associated with passive behaviour were colonized with bacteria from mice with higher exploratory behaviour, _they became more active and daring_. Similarly, normally active mice _became more passive_ after receiving bacteria from mice whose genetic background is associated with passive behaviour.

While previous research has focused on the role bacteria play in brain development early in life, Collins said this latest research indicates that while many factors determine behaviour, the nature and stability of bacteria in the gut appear to influence behaviour and any disruption, from antibiotics or infection, might produce changes in behaviour.

The writing in the abstract is a lot more abstruse, but perhaps substantially more accurate too. I'd be happy to know if anyone can translate it more accurately than this press release. (E.g. they didn't just transfer bacteria)

Naturally, the experimenters are doing things to the mice they'd never get away with on people, and so less is known about the relevance to humans. For example, normal humans may already have reasonably healthy bacteria. College students, for example, did not have a significant reduction in exam-related anxiety by consuming yogurt rather than placebo \[[citation](http://www.ncbi.nlm.nih.gov/pubmed/20216564?dopt=Abstract)\]. Nor did healthy 1 to 3 year olds miss less school because by consuming a Gerber product with yogurt \[[citation](http://www.ncbi.nlm.nih.gov/pubmed/20216564?dopt=Abstract)\].

However, humans with chronic fatigue syndrome who consumed a potent pro-biotic had reduced anxiety (but not reduced depression): \[[citation](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2664325/?tool=pubmed)\]

> Chronic fatigue syndrome (CFS) is complex illness of unknown etiology. Among the broad range of symptoms, many patients report disturbances in the emotional realm, the most frequent of which is anxiety. Research shows that patients with CFS and other so-called functional somatic disorders have alterations in the intestinal microbial flora. Emerging studies have suggested that pathogenic and non-pathogenic gut bacteria might influence mood-related symptoms and even behavior in animals and humans. In this pilot study, 39 CFS patients were randomized to receive either 24 billion colony forming units of Lactobacillus casei strain Shirota (LcS) or a placebo daily for two months. Patients provided stool samples and completed the Beck Depression and Beck Anxiety Inventories before and after the intervention. We found a significant rise in both Lactobacillus and Bifidobacteria in those taking the LcS, and there was also a` _significant decrease in anxiety symptoms among those taking the probiotic vs controls_ (p = 0.01). These results lend _further support to the presence of a gut-brain interface_, one that may be mediated by microbes that reside or pass through the intestinal tract.

Interestingly, the ongoing [clinical trials](http://clinicaltrials.gov/ct2/results?term=chronic+fatigue+syndrome&type=Intr&rcv_s=01%2F01%2F2009&rcv_e=01%2F01%2F2013&pg=2) don't seem to be following up on this line of treatment, instead focusing mainly on drugs or alternative therapy. The jury seems to still be out in [inflammatory bowel disease](http://www.ncbi.nlm.nih.gov/pubmed/21992953).

Late-onset autism, is associated with bacterial irregularities \[[citation](http://www.de-poort.be/cgi-bin/Document.pl?id=33)\] and can respond to oral vancomycin (an antibiotic) \[[citation](http://www.ncbi.nlm.nih.gov/pubmed/21524713)\].

Going back to mice, these findings indicate that the bacteria that are present during development have a lasting effect:

[Hejitz et.al.: Normal gut microbiota modulates brain development and behavior, 2011](http://www.pnas.org/content/108/7/3047.full.pdf).

Here, we report that colonization by _gut microbiota impacts mammalian brain development and subsequent adult behavio_r. Using measures of motor activity and anxiety-like behavior, we demonstrate that germ free (GF) mice display increased motor activity and reduced anxiety, compared with specific pathogen free (SPF) mice with a normal gut microbiota. ... Hence, our results suggest that the microbial colonization process initiates signaling mechanisms that affect neuronal circuits involved in motor control and anxiety behavior.

They found that if they "conventionalized" the germ free mice early enough (i.e. if they infected them with the usual bacteria) that they'd be pretty much normal. However, if they tried to do this on adults, it was too late, so the absence of the bacteria during development had an enduring effect on behavior.

Encouraged by the observation that early colonization of GF mice could normalize several behavioral patterns of GF mice, we explored whether there is a sensitive/critical period for the effects of the normal gut microbiota on behavior. We therefore conventionalized adult GF mice and studied their behavior in open ﬁeld test as described above. Notably, conventionalization of adult mice failed to normalize the behavior of GF mice (Fig. 1F and Fig. S4).

Conversely, if the animal is subjected to stress, this can change the composition of microbiota. \[[citation](http://farncombe.mcmaster.ca/documents/CollinsBercikGastroenterology200913662003-14.pdf)\]

> Although many people are aware of the communication that occurs between the gastrointestinal (GI) tract and the central nervous system, fewer know about the ability of the central nervous system to influence the microbiota or of the microbiota's influence on the brain and behavior. Within the GI tract, the microbiota have a mutually beneficial relationship with their host that maintains normal mucosal immune function, epithelial barrier integrity, motility, and nutrient absorption. Disruption of this relationship alters GI function and disease susceptibility. Animal studies suggest that _perturbations of behavior, such as stress, can change the composition of the microbiota_; these changes are associated with increased vulnerability to inflammatory stimuli in the GI tract. The mechanisms that underlie these alterations are likely to involve stress-induced changes in GI physiology that alter the habitat of enteric bacteria. Furthermore, _experimental perturbation of the microbiota can alter behavior, and the behavior of germ-free mice differs from that of colonized mice_. Gaining a better understanding of the relationship between behavior and the microbiota could provide insight into the pathogenesis of functional and inflammatory bowel disorders.

Whew. That's a lot of material. And there's still so much more to find out. Let me know what you find, or what you think the next experiment should be.

DISCLAIMER: I am not an expert in medicine. Nothing here should be construed as medical advice. See your doctor.