You are only 76% human [1].

This may feel strange to know, but you share your body with a rich and dynamic ecosystem of bacteria contained in your mouth, in your gastrointestinal tract, and on your skin [1].

These bacteria are not biologically inert: taken together, the trillions of microbes express 100-times as many genes as the human genome [2]. This relationship, termed the ‘extended genome,’ is the result of a co-evolution between our species and bacteria that is now recognised to be essential for human health [2][3].

In recent years, there has been an immense surge of interest in this complicated world of bacteria with whom we share our bodies. This complex field has led to some interesting hypotheses, learned insights, and – typical of nutrition and health science taken into the mainstream – hyperbole and some misinformation.

This article will take a look into the world of the microbiome, providing a definition for the terminology, a basic understanding of the structure of the ecosystem, and then a focus on the role of diet and nutrition in shaping and influencing the microbiome toward health or disease.

 

Defining Terms: What is the “Microbiome”?

First, let’s get the terminology down:

  • The “microbiome”: the term for the ‘extended genome’ provided by the bacteria in the human gut, i.e. what functions do they perform?
  • The “microbiota”: the term for the different bacteria in the ecosystem, i.e. what bacteria are there, and in what proportions?
  • “Bacteria”: single-cell organisms that are highly adaptable.
  • “Dysbiosis”: the term for disturbances in the composition of the microbiota, influencing disease states.

Where did this system come from, and why? At a basic level, we can say that as a species we provide a very attractive residence for different bacteria, from our UV-exposed, aerobic skin to the anaerobic, dark, moist, and energy-rich gut which is the primary residence for bacteria in humans [4].

In the course of their evolution, human beings have colonised every corner of the planet, adopting diverse diets in radically different natural environments and climates. Our gastrointestinal tract is one of the largest interfaces (250-400m2) with our external environment, providing for both the digestion and assimilation of essential nutrients, and the first line of immune defence for host health [5]. The exceptional diversity in our gut microbiota may thus reflect diversity of environment, food sources, and consequent adaptations influencing host health [4][5].

Whatever the evolutionary origins of this symbiotic relationship, bacteria like humans as a residence and – depending on how we shape them and feed them – can enhance our health or promote conditions which may precipitate disease.

To understand this more, let’s look at the structure of the system.

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Structure, Composition & Function of the Human Microbiota

As an ecosystem of living organisms, the microbiota has taxonomic (the categorisation of living organisms) layers of organisation. At the broadest level, there are 4 main divisions, known as ‘phyla’: Firmicutes, Bacteroidetes, Actinobacteria and Proteobacteria [3].

These phyla are considered our “bacterial core,” with the majority of bacterial types belonging to two major phyla: the Firmicutes and Bacteroidetes, and significant contributions from Actinobacteria and Proteobacteria [6][7].

Within each phylum, there are a multitude of different genus, and within the genus, individual species. The following table contains two examples of this taxonomic organisation:

Phylum: Bacteroidetes Firmicutes
Genus: Prevotella Lactobacillus
Species: Prevotella copri (P.copri) Lactobacillus acidophilus (L.acidophilus)

 

While at a phylum level the human microbiota does not have as much variation as other ecosystems such as soil for example, it is within the composition of each phyla – at the genus and species level – that significant inter-individual variability is observed [3][4].

Diversification in the human gut thus reflects the depth and breadth of variability within each major phylum [3]. For example, in analysis of 124 Nordic and Mediterranean subjects, there was not one single abundant species shared between any 2 persons [6]. In each faecal sample, up to 160 bacterial species were identified in each sample, with a total of 3.3-million genes in the study cohort [6].

In relation to location, the primary site of bacterial colonisation in humans is in the large intestine. In the stomach and small intestine (duodenum, jejunum, and ileum), there are small numbers of primarily aerobic bacteria, but these compartments of the GI system are not major locations for bacteria [5]. The acidic environment of the stomach, pancreatic secretions and bile salts in the small intestine, coupled with the presence of oxygen and short transit time, create an environment that limits large-scale colonisation [8].

In the colon, however, there is increasing predominance of anaerobic bacterial species provided with fermentable substrates from the foods we consume, in particular complex carbohydrates which pass undigested through the small intestine. This coupled with a long transit time results in an extensively colonised large intestine with a dense and diverse bacterial community [8].

Surrey NUT MED 07-04-2017 BJ Campbell

While our understanding of the full spectrum of functions of the microbiota is still emerging, a number of important roles have been elucidated which influence host health, including:

  1. Facilitating maturation of the epithelial layer of the intestines;
  2. Facilitating maturation of the immune system [intimately linked to a) above];
  3. Regulating inflammation;
  4. Interacting with the gut-brain axis to influence neurological processes and mood;

  5. Synthesising of certain vitamins and minerals;
  6. Production of secondary metabolites which influence host health, e.g. short-chain fatty acid [SCFA] production in the colon [9][10][11][12][13].
  7. The variability of the microbiota between and within individuals reflects a dynamic system that is influenced by geographical variability, life-stage (including birth delivery and feeding method), age, antibiotic use, and diet [10]. These ongoing variables are associated with shaping, reshaping, and influencing the composition of the microbiota and as a consequence, health or disease processes [10].

 

Shaping the Microbiota

The composition of the microbiota is shaped from minute one of life. Whether the in-utero environment is sterile, and a foetus develops in a bacteria-free environment, is still a matter of debate [14].

The primary determinant of an infant’s bacterial community is birth delivery method. The microbiota of babies delivered via the birth canal reflects maternal vaginal composition, which is typically stable [14]. Conversely, the microbiota of babies delivered via caesarean-section reflects the bacterial composition of skin of the mother and delivery room attendees, and the microbiota of skin is highly variable [14].

There are marked differences in the composition of the microbiota, relative to delivery method. Birth canal deliveries are abundant in Lactobacillus and Prevotella genus, while C-section deliveries are abundant in Staphylococcus [15]. While the microbiota of a birth canal-delivered infant will reflect maternal composition within 3-7 day post-delivery, the microbiota of a C-section delivered infant may be disturbed for up to 6-months [15]. While the long-term consequences of such an altered microbiota are yet emerging, C-section deliveries are associated with higher prevalence of asthma and allergy, and certain autoimmune conditions, in particular Coeliac and Diabetes Type-1 [15].

Feeding method follows on from delivery method as a vital early life-stage variable influencing the microbiota. An important feature of the microbiota in this life-stage, contrasted with the adult microbiota, is that the composition of the infant microbiota is not intended for diversity [16]. The microbiota of breastfed infants is dominated by specific species of the Bifidobacterium genus, specialising in the degradation of human milk oligosaccharides [16].

Conversely, formula-fed infants display higher levels of pro-inflammatory Proteobacteria, resembling adult patterns of colonisation – which is not a positive feature for the infant gut that thrives on selective functions of a limited number of species [16]. In breastfed infants, these species – in particular Bifidobacteria – utilise the complex sugars found in human milk to populate the gut, express anti-inflammatory genes, increase host immune tolerance, and enhance gut barrier function [16].

Geographic region is another important variable; however, it is arguable that the primary difference here is the composition of traditional diets vs. Western diets. In comparative analysis of populations from Malawi, Peru, and Philadelphia, the US subjects exhibited the least microbial diversity [11]. While the African and South American subjects were distinguishable, the distinction was not as extreme as between the traditional diets vs. the Western diet: both African and South American groups were dominated by Prevotella, a genus of specialised fibre-degrading bacteria [11].

The analysis also confirmed that the composition of the adult microbiota evolves over the first 3-years of life, after which it is relatively stable [11]. In the infants in the cohort, however, Bifidobacterium dominated in all subjects, indicating that shifts to an adult composition are strongly influenced by feeding method and duration, and habitual diet following weaning [11].

These early life-stage variables are largely determined for us. However, the significant differences in the microbiota of African and South American subjects consuming traditional diets, and US subjects consuming a Western diet, indicates that diet is a primary driver of variation in the human microbiome [11][17].

 

The Influence of Diet on the Human Microbiome

Alterations in the composition of the microbiota reflect humans’ ability to respond to nutritional changes in the short and long-term. Microbes are specialised in the fermentation of different dietary substrates, thus dietary choices and patterns provide substrates for the selective growth of specific species [17].

In both African children and adults consuming a diet low in animal protein and fat, and high in fibre and non-starch polysaccharides [NSP], high levels of Prevotella and other microbial species required for metabolism of indigestible carbohydrates are found consistently [18][19]. The microbiome of populations consuming diets rich in indigestible carbohydrates display greater microbial diversity than Western diets, which corresponds to the diversity of complex carbohydrate structures, including resistant starch [RS], prebiotic fibres and other NSP, in traditional diets, and is associated with host health [20][17].

The benefit of diets high in fibre is broadly attributable to structurally diverse, non-digestible carbohydrates, including resistant starch [RS], NSP, and other prebiotic fibres which reach the colon and undergo selective microbial fermentation [21]. High intake of fibre/NSP results in a shift to increased populations of short-chain fatty acid [SCFA] producing microbes [22][18]. SCFA’s, in particular butyrate, exert anti-inflammatory effects in the colon, and are associated with inhibition of tumorigenesis, carcinogenic detoxification, and antineoplastic activity [19].

Conversely, ‘Western’ diets high in fat, sugar, animal protein, and low in fibre, negatively impact the microbiome, with effects seen as early as one year of age [18]. European children consuming a Western diet showed 2-times more abundant levels of Firmicutes and lower Bacteroidetes, and had significantly lower levels of SCFA [18]. This profile is associated with increased levels of pro-inflammatory proteobacteria, and increased secondary bile acid metabolites, which are potentially carcinogenic and increase levels of pathogenic bile-tolerant bacteria [23][24]. These changes are driven by specific characteristics of the Western diet. High fat intake alters the microbiome through driving increased bile acid production and increasing bile-acid tolerant bacteria levels (20). However, fat subtype is important. The evidence suggests monounsaturated fats do not significantly influence microbial composition [25][24]. Omega-3 fish oil polyunsaturates may increase some beneficial Actinobacteria and Lactobacilli, and modify bile acid composition [24][25].

High animal protein intake is another feature of the Western diet and is associated with increased protein putrefaction into potentially toxic and carcinogenic metabolic by-products, decreased SCFA’s, and decreases in butyrate-producing bacteria [20]. However, protein is also strongly correlated with increased microbial diversity [24], and beneficial compounds produced through proteolytic fermentation [7]. The detriment to high animal protein is mediated by the presence or absence of fibre, and has been shown where a high protein intake is coupled with fibre of 8-12g/d [26]. With fibre intake at 31g/d, no evidence of increased putrefaction, toxic metabolites, or decrease in SCFA’s was noted despite high protein intake [27]. Alterations in the microbiome are thus primarily associated with the presence or absence of fibre. [21]

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