Human Gut Microbiome – 10 Considerations
Published on the 23 November 2016
Published on the 23 November 2016
The human microbiome is a diverse and complex microbial community that resides in our gastrointestinal tracts and has been coined a forgotten target metabolic ‘organ’. With the advent and application of next generation gene sequencing, the microbiome has become appreciated as integral to a number of physiological functions including endocrine, neurology and acquisition of nutrition, and immunity.
The state of a healthy biome is a function of diversity and compositional balance. Dynamic alterations to the microbiome have been attributed to a number of factors such as diet, environmental toxins, and medication such as antibiotics. A state of dysbiosis is the abnormal microbial colonisation of the intestine where changes in quantity and quality of flora become pathological and harmful. Dysbiosis has been attributed to significant impacts on health and multiple chronic disease states. There are many implications to understanding this relatively new area of research and the potential for future treatment approaches and options.
As a nurse you would have undoubtedly come across spectacular claims and speculation of how the human gut microbiome is interrelated to aspects of our health, wellbeing and disease states. Words of wisdom and snippets of discoveries have most likely filtered your way in the form of faecal microbiota transplantation (FMT), probiotic use, and rethinking the use of broad spectrum antibiotics, to allegations that C-sections result in increased rates of autism.
This article is a starting point in defining the human microbiome (MB); identifying what is known, and what continues to be further studied for clinical significance and potential application for human health and disease.
The human microbiome (MB) is a diverse and complex microbial community that resides in our gastrointestinal tracts and has been coined a forgotten target metabolic ‘organ’ (Blasser 2014). It is estimated that throughout our gastrointestinal tract we harbour 100 trillion microbes, representing 500 different species that outnumber human cells by 10:1. The microbiome is composed of archaea (strict anaerobes) and bacteria (aerobes and anaerobes), viruses, fungi, and is considered to be one of the most complex ecological system on the planet (Hollister et al. 2014).
The largest proportion of the MB resides in the colon. Traditionally, investigative studies of the MB have been limited due to culture-based methods that proved difficult to culture the majority of anaerobically-living commensal gut microbiome (Alien 2015). The capacity to investigate the MB role in disease and health has come to the limelight through the development of culture-independent approaches, and has been made possible through advances in gene sequencing technology (Evans et al. 2013). This technology gave rise to the 2002 human genome project, and birth to metagenomics. Now extension to the human metagenome has led investigators to the necessary tools to study the DNA microbiome human gastrointestinal tract.
MB research is in its infancy and large metagenome projects (National Institute of Health, Human Microbiome Project (HMP)) are identifying the ‘who and what’ of the MB (Blasser 2014). This research has lead to the significant development of ‘the second genome’: one inherited from our parents and the other acquired, i.e. the MB. Because of the dynamic nature of the MB, the question is not whether the MB has a role in health and disease, but rather for current research to provide insight into how the MB contributes, promotes, and sustains a healthy MB (Evans et al. 2013).
A healthy MB is defined by high diversity and an ability to resist change under physiological stress (Lloyd-Price et al. 2016). The far reach understanding of the MB as integral to health and disease comes from an appreciation of the multiple metabolic and physiological functions that have been attributed to the MB. These include: energy harvesting through nutrient extraction and fermentation of indigestible food substances, synthesis of key substances such as vitamins (B12 and K), neurotransmitters such as serotonin, maintenance of gut barrier (mucosa), immune functions such as protection against infection, systemic immunity and autoimmune disease protection (Calafiore et al 2012).
In contrast, MB associated with disease is defined by lower species diversity, fewer beneficial microbes and the presence of pathogenic microbes. Disease states are known to influence the MB and/or be the result of dysbiosis. Dysbiosis is an imbalance (compositional or diversity changes) in the intestinal bacteria that precipitates changes in the normal activities of the gastrointestinal tract (D’Argenio & Salvatore 2015). A state of dysbiosis that changes in quantity and quality of flora results in a pathological and harmful MB.
Dynamic alterations to the microbiome have been attributed to a number of factors such as diet, environmental toxins, and medications such as antibiotics. This state of imbalance has been implicated in a number of gastrointestinal diseases such as inflammatory bowel disease, irritable bowel disease and colorectal cancer. In addition, a complex relationship between diet, microbes and the gut epithelium has implications in systemic diseases such as obesity, diabetes, atherosclerosis and non-alcoholic fatty liver disease (Chan et al. 2013).
MB is a complex and dynamic internal ecosystem. Various ecological principles provide a new appreciation to a dynamic interplay between health and diseases (Rook 2013). For example, symbiosis is the relationship between two or more organisms that live closely together as commensal, mutualistic or independent. In the MB, pathogenic and commensal bacteria coexist and have certain functions (Blasser, 2011). Commensals can be opportunists, and an opportunist in one host can be a primary pathogen in another host. Successful microbes of both classes must find ways to coexist symbiotically to ultimately evolve. Pathogenic MB does not necessarily become pathogenic unless the internal environment does not sustain symbiosis as in the case of c-difficile infections resulting in colitis. Location and niche of commensal colonisation can result in opportunistic pathogens when the microbe crosses anatomical and biochemical barriers in the host that serve to limit colonisation by commensals. For example, E. coli that cause diarrhoea and urinary tract infections do not occupy the same niche as the commensal strains of E. coli in the colon (Institute of Medicine (US) 2006). The greater application of ecological principles to the MB supports a paradigm shift in understanding ‘germs’ as greater than ‘the bad guys that make us sick’ (Blasser 2014). Rather, the state of dysbiosis results in an imbalance between protective and harmful bacteria (Chan et al. 2013).
Continued in part two: What Factors Create and Sustain a Healthy Microbiome?
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Michelle Woods completed her Doctorate of Nursing and Master of Science Nursing (Nurse Practitioner) at the University of Colorado with an emphasis in adult primary health care. Her expertise as a Nurse Practitioner started in the United States, working in primary care and endocrinology practices. She has been certified both in the USA and Australia as a diabetes educator. Her current practice is with the Royal Hobart Hospital Diabetes Centre. She has a clinical management focus in complex care.