3 February 2014
Category: Uncategorized
3 February 2014,

How Healthy Poop Can Help Your Mood

My nephews are in the phase when even the word ‘toilet’ elicits reams of laughter. Yet, healthy poop and the micriobiome that is responsible for its maintenance, is no laughing matter ****(I'll do my best to avoid terrible jokes to side step the gross factor of this post. Promise).  In fact, the gut microbiome is becoming a critical area within neuroscientific, psychiatric, and psychological research. 

I’m not suggesting you bring up this blog post over dinner or canapés, but it’s worth a read if you haven’t had a chance to learn about the ways unhealthy poop can lead to psychological distress. It’s not just a tummy ache; chronic stomache pain can reflect a series of deeper issues. Here are a few insights into this burgeoning field of research.

Mind/ Body Links

Last year, the director of the National Institute of Mental Health made reference to recent studies of microbiota: 

‘Our bodies are ……a complex ecosystem in which human cells represent a paltry 10% of the population. But beyond the sheer numbers, we now know about the profound diversity of this ecosystem and striking individual differences. How these differences in our microbial world influence the development of brain and behavior will be one of the great frontiers of clinical neuroscience in the next decade"

Dysregulated cross-talk between the brain and the gut immune system may contribute to the pathogenesis of several conditions; including schizophrenia, mood disorders, obsessive-compulsive disorder, autism, attention-deficit/hyperactivity disorder, anorexia nervosa, narcolepsy, and chronic fatigue syndrome (Hornig, 2013).

Quick Biological Facts about the Microbiome, the Gut, and Brain Development

It is estimated that 10^14 microorganisms reside in the adult GI tract which amounts to ten times the number of human cells in the body (Arumugam et al., 2011). The bacteria and fungi that inhabit our bodies vastly outnumber our human cells.

The 100 trillion bacterial residents in the human gut comprise approximately 4 lb of fecal matter. These bacteria maintain a high population density by deriving nutrients from food sources, and this may serve as an energy source for the intestinal epithelial lining.  In this way, healthy poop may also contribute to increased satiety (Tilg & Kaser, 2011): the healthier your epithelial lining,  the more effectively you can obtain nutrients from food. So, you’ll eat less if your intestines are healthy.

In some of the earlier studies into the gut/brain axis, Sudo et al., (2004) provide insight into the role of the intestinal microbiota in the development of the Hypothalamic Pituaitary Adrenal axis (overstimulation of the HPA is a sign of stress):

In Germ Free mice, a mild restraint stress induces an exaggerated release of stress hormones compared with the specific pathogen free (SPF) control animals. The stress response in Germ Free mice is partially reversed by exchanging fecal matter with the Pathogen Free animals (Sudo et al., 2004).

The previous study is important, demonstrating that the microbial content of the gut is critical to the development of an appropriate stress response later in life. Also, authors suggest that there is a narrow window in early life where appropriate colonization of poop must occur to ensure normal development of the HPA axis


Gross!! But… Cool?

Healthy poop plays such an important role in physiological process, that researchers began to question whether fecal microbiota transplant (FMT) could enhance the health of the overall organism.  In fact, for difficult bacterial infections (appropriately named C. Difficile) fecal transplant is becoming a relatively accepted treatment option (Agito, Atreja, & Rizk, 2013). Here are some other bullet points on the topic:

·       Fecal transplants from obese mice transplanted into lean germ- free mice have been found to induce obesity (Vrieze et al., 2012)

·      A recent study found an improvement in insulin resistance in obese individuals who received fecal transplants from lean individuals compared with those who received a control version (Vrieze et al., 2012).

And, although we all know 'correlation isn't causation,' researchers found a significant positive relationship between gut microbiome profiles and type 2 diabetes in a Chinese population. The relationship was strong to the extent that composition of the gut microbiota predicted the disorder in a second cohort (Qin et al., 2012)


How? Why?


How does it work?

Turnbaugh et al. (2009) showed that switching from a low-fat, polysaccharide-rich diet to a high-fat, high-sugar diet shifted the structure of the microbiota within a single day and changed the representation of metabolic pathways in the microbiome, thus indicating how fragile this community of 'commensal bacteria' is. Commensal refers to the point that it doesn't just 'take' but acts cooperatively.

The microbiota has been shown to impact bile acid production, insulin resistance, glucose metabolism and inflammation, which of course have an impact and contribute to metabolic disease (Tremaroli & Backhed, 2012). Certain microbial populations secrete enzymes, which are not encoded in the human genome, that allow synthesis of calories from otherwise indigestible polysaccharides in our diet (Backhed et al. 2005).

The consequent increase in bacterial fermentation products, short chain fatty acids (SCFAs) which include acetate, propionate and butyrate influence various aspects of metabolism.

The latter Short Chain Fatty Acid is an energy substrate for cellular metabolism in the colonic epithelium (the lining of the colon). Acetate and propionate are substrates for metabolizing sugars and fat in the liver (and other peripheral organs). These processes coordinate and promote lipid storage in the host (Backhed et al. 2004).

The microbiota has been shown to impact bile acid production, insulin resistance, glucose metabolism and inflammation, all of which can contribute to metabolic disease (Tremaroli & Backhed, 2012). However, the specific mechanisms for making an unhealthy gut healthier is still the focus of significant research.

For example…


Although this field of research is still in its infancy, an exciting new field of development is in psychobiotics, which is a class of probiotic (i.e. what your yogurt claims to have loads of). Psychobiotics are capable of producing and delivering neuroactive substances such as gamma-aminobutyric acid (GABA) and serotonin, which act on the brain-gut axis. This is the focus of significant research at the University of Cork (Dinan, Stanton, & Cryan, 2013) (and beyond).


Repopulate (Repoolulate?) the Microbiome?

Of course… there is much controversy and debate over whether a core healthy microbiota profile exists. Metagenomics, is a new field of research that applies high-throughput screening techniques to characterise the microbial community at a genome-level in health and disease (Turnbaugh & Gordon, 2009) . This whole arena has undergone massive advancement, and further efforts will allow insight into the composition, diversity and functions of the human microbiome.

In terms of using this information for psychological conditions… WELL.I'm not sure how or when an anti depressant that targets the gut will ever be available. However, the advantage to incorporating this information is quite clear, particularly if you've ever had to take anti depressants. Current psychopharmacological products only target psychological systems within the brain, as opposed to the organism in full. The news about the gut-microbiome-brain axis lends itself to a better understanding of the entire gestaldt of the human body; indeed this provides insight for treating disorders like IBS, but maybe even depression.

Anti depressants are effective, but some people suffer a variety of uncomfortable side effects with their use. Our increasing understanding of the gut-brain axis will likely offer new possibilities for more effective medicine, and higher quality of life. For a look into some of the innovation to make this less disgusting, have a look at some new steps taken by Canadian researchers

Repoopulate a sterile, healthy poop substitute used to re-establish a healthy gut- and it looks like it may begin to be included in more formal therapy settings (hospitals, etc). Despite this exciting news, however, I'm not mentioning any of this to anyone under the age of 30. My nephews would have a field day!

And so, to end the post (finally)…Sorry for making your Monday even sh*ttier. 


:) MyL





Agito, M. D., Atreja, A., & Rizk, M. K. (2013). Fecal microbiota transplantation for recurrent C difficile infection: ready for prime time? Cleve Clin J Med, 80(2), 101-108. doi: 10.3949/ccjm.80a.12110

Arumugam, M., Raes, J., Pelletier, E., Le Paslier, D., Yamada, T., Mende, D. R., . . . Bork, P. (2011). Enterotypes of the human gut microbiome. Nature, 473(7346), 174-180. doi: 10.1038/nature09944

Dinan, T. G., Stanton, C., & Cryan, J. F. (2013). Psychobiotics: a novel class of psychotropic. Biol Psychiatry, 74(10), 720-726. doi: 10.1016/j.biopsych.2013.05.001

Hornig, M. (2013). The role of microbes and autoimmunity in the pathogenesis of neuropsychiatric illness. Curr Opin Rheumatol, 25(4), 488-795. doi: 10.1097/BOR.0b013e32836208de

Qin, J., Li, Y., Cai, Z., Li, S., Zhu, J., Zhang, F., . . . Wang, J. (2012). A metagenome-wide association study of gut microbiota in type 2 diabetes. Nature, 490(7418), 55-60. doi: 10.1038/nature11450

Sudo, N., Chida, Y., Aiba, Y., Sonoda, J., Oyama, N., Yu, X. N., . . . Koga, Y. (2004). Postnatal microbial colonization programs the hypothalamic-pituitary-adrenal system for stress response in mice. J Physiol, 558(Pt 1), 263-275. doi: 10.1113/jphysiol.2004.063388

Tilg, H., & Kaser, A. (2011). Gut microbiome, obesity, and metabolic dysfunction. J Clin Invest, 121(6), 2126-2132. doi: 10.1172/JCI58109

Tremaroli, V., & Backhed, F. (2012). Functional interactions between the gut microbiota and host metabolism. Nature, 489(7415), 242-249. doi: 10.1038/nature11552

Turnbaugh, P. J., & Gordon, J. I. (2009). The core gut microbiome, energy balance and obesity. J Physiol, 587(Pt 17), 4153-4158. doi: 10.1113/jphysiol.2009.174136

Vrieze, A., Van Nood, E., Holleman, F., Salojarvi, J., Kootte, R. S., Bartelsman, J. F., . . . Nieuwdorp, M. (2012). Transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome. Gastroenterology, 143(4), 913-916 e917. doi: 10.1053/j.gastro.2012.06.031


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